powerpoint · pdf filereferences goldfrank’s toxicologic emergencies, tenth edition....
TRANSCRIPT
Title Text
Heartbreakers
Michael Emswiler MD Division of Clinical Toxicology VCU Medical Center Virginia Poison Center
Objectives Physiology review Cardiac action potential Vaughn-Williams Classification
Discuss mechanism of selected toxins Beta-blockers CCB digoxin others
Discuss treatment options
Tox 101 Identify the patient Decontamination Antidote Enhanced elimination
Relevant anatomy
httpwwwtexasheartorgHICAnatomyanatomy2cfm
Myocytes Contractile cells Conducting cells SA node interatrial AV node bundle of His Purkinje fibers
httpswwwurmcrochestereduEncyclopediaGetImageaspxImageID=125477
We want action Action potentials are the same in the atria and
ventricles Long duration (when compared to skeletal muscle) Longer the AP ndash longer the refractory periods
Sinoatrial node action potential Automaticity ndash spontaneously generates action
potentials without neuronal input Unstable resting membrane potential No sustained plateau
Ventricular action potential
Costanzo Physiology 3rd edition 2006
Refractory period
httpswwwstudybluecomnotesnotenphysiology-cardiovascular-part-1deck4279768
Definitions Chronotropic-effects on HR Inotropic-effects on contractility Dromotropic-effects on conduction velocity
Back to the bedside P wave ndash represents atrial depolarization PR interval ndash represents AV node conduction QRS ndash depolarization of the ventricles T wave ndash repolarization of the ventricles QT interval ndash first ventricular depolarization to last
ventricular repolarization
Bringing it together
Text
httpwesleytoddblogspotcom201311action-potentialshtml
Vaughn-Williams Classification Class I Fast sodium channel blockers 1a Quinidine procainamide
1b Lidocaine phenytoin 1c Flecainide
Class I Beta blockers Propranolol esmolol metroprolol atenolol
Class III Potassium channel blockers Amiodarone Sotalol dofetilide Class IV Slow calcium channel blockers
Verapamil diltiazem
Class V Variable mechanism Adenosine Digoxin
Lastly where does BP come from BP = CO x PVR CO = SV x HR
Letrsquos review Pacemaker cells with automaticity Different action potential
Atria and ventricles have prolonged action potential Work together to function as a syncyticum Electrolytes are critically important to normal function
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Heartbreakers
Michael Emswiler MD Division of Clinical Toxicology VCU Medical Center Virginia Poison Center
Objectives Physiology review Cardiac action potential Vaughn-Williams Classification
Discuss mechanism of selected toxins Beta-blockers CCB digoxin others
Discuss treatment options
Tox 101 Identify the patient Decontamination Antidote Enhanced elimination
Relevant anatomy
httpwwwtexasheartorgHICAnatomyanatomy2cfm
Myocytes Contractile cells Conducting cells SA node interatrial AV node bundle of His Purkinje fibers
httpswwwurmcrochestereduEncyclopediaGetImageaspxImageID=125477
We want action Action potentials are the same in the atria and
ventricles Long duration (when compared to skeletal muscle) Longer the AP ndash longer the refractory periods
Sinoatrial node action potential Automaticity ndash spontaneously generates action
potentials without neuronal input Unstable resting membrane potential No sustained plateau
Ventricular action potential
Costanzo Physiology 3rd edition 2006
Refractory period
httpswwwstudybluecomnotesnotenphysiology-cardiovascular-part-1deck4279768
Definitions Chronotropic-effects on HR Inotropic-effects on contractility Dromotropic-effects on conduction velocity
Back to the bedside P wave ndash represents atrial depolarization PR interval ndash represents AV node conduction QRS ndash depolarization of the ventricles T wave ndash repolarization of the ventricles QT interval ndash first ventricular depolarization to last
ventricular repolarization
Bringing it together
Text
httpwesleytoddblogspotcom201311action-potentialshtml
Vaughn-Williams Classification Class I Fast sodium channel blockers 1a Quinidine procainamide
1b Lidocaine phenytoin 1c Flecainide
Class I Beta blockers Propranolol esmolol metroprolol atenolol
Class III Potassium channel blockers Amiodarone Sotalol dofetilide Class IV Slow calcium channel blockers
Verapamil diltiazem
Class V Variable mechanism Adenosine Digoxin
Lastly where does BP come from BP = CO x PVR CO = SV x HR
Letrsquos review Pacemaker cells with automaticity Different action potential
Atria and ventricles have prolonged action potential Work together to function as a syncyticum Electrolytes are critically important to normal function
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Objectives Physiology review Cardiac action potential Vaughn-Williams Classification
Discuss mechanism of selected toxins Beta-blockers CCB digoxin others
Discuss treatment options
Tox 101 Identify the patient Decontamination Antidote Enhanced elimination
Relevant anatomy
httpwwwtexasheartorgHICAnatomyanatomy2cfm
Myocytes Contractile cells Conducting cells SA node interatrial AV node bundle of His Purkinje fibers
httpswwwurmcrochestereduEncyclopediaGetImageaspxImageID=125477
We want action Action potentials are the same in the atria and
ventricles Long duration (when compared to skeletal muscle) Longer the AP ndash longer the refractory periods
Sinoatrial node action potential Automaticity ndash spontaneously generates action
potentials without neuronal input Unstable resting membrane potential No sustained plateau
Ventricular action potential
Costanzo Physiology 3rd edition 2006
Refractory period
httpswwwstudybluecomnotesnotenphysiology-cardiovascular-part-1deck4279768
Definitions Chronotropic-effects on HR Inotropic-effects on contractility Dromotropic-effects on conduction velocity
Back to the bedside P wave ndash represents atrial depolarization PR interval ndash represents AV node conduction QRS ndash depolarization of the ventricles T wave ndash repolarization of the ventricles QT interval ndash first ventricular depolarization to last
ventricular repolarization
Bringing it together
Text
httpwesleytoddblogspotcom201311action-potentialshtml
Vaughn-Williams Classification Class I Fast sodium channel blockers 1a Quinidine procainamide
1b Lidocaine phenytoin 1c Flecainide
Class I Beta blockers Propranolol esmolol metroprolol atenolol
Class III Potassium channel blockers Amiodarone Sotalol dofetilide Class IV Slow calcium channel blockers
Verapamil diltiazem
Class V Variable mechanism Adenosine Digoxin
Lastly where does BP come from BP = CO x PVR CO = SV x HR
Letrsquos review Pacemaker cells with automaticity Different action potential
Atria and ventricles have prolonged action potential Work together to function as a syncyticum Electrolytes are critically important to normal function
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Tox 101 Identify the patient Decontamination Antidote Enhanced elimination
Relevant anatomy
httpwwwtexasheartorgHICAnatomyanatomy2cfm
Myocytes Contractile cells Conducting cells SA node interatrial AV node bundle of His Purkinje fibers
httpswwwurmcrochestereduEncyclopediaGetImageaspxImageID=125477
We want action Action potentials are the same in the atria and
ventricles Long duration (when compared to skeletal muscle) Longer the AP ndash longer the refractory periods
Sinoatrial node action potential Automaticity ndash spontaneously generates action
potentials without neuronal input Unstable resting membrane potential No sustained plateau
Ventricular action potential
Costanzo Physiology 3rd edition 2006
Refractory period
httpswwwstudybluecomnotesnotenphysiology-cardiovascular-part-1deck4279768
Definitions Chronotropic-effects on HR Inotropic-effects on contractility Dromotropic-effects on conduction velocity
Back to the bedside P wave ndash represents atrial depolarization PR interval ndash represents AV node conduction QRS ndash depolarization of the ventricles T wave ndash repolarization of the ventricles QT interval ndash first ventricular depolarization to last
ventricular repolarization
Bringing it together
Text
httpwesleytoddblogspotcom201311action-potentialshtml
Vaughn-Williams Classification Class I Fast sodium channel blockers 1a Quinidine procainamide
1b Lidocaine phenytoin 1c Flecainide
Class I Beta blockers Propranolol esmolol metroprolol atenolol
Class III Potassium channel blockers Amiodarone Sotalol dofetilide Class IV Slow calcium channel blockers
Verapamil diltiazem
Class V Variable mechanism Adenosine Digoxin
Lastly where does BP come from BP = CO x PVR CO = SV x HR
Letrsquos review Pacemaker cells with automaticity Different action potential
Atria and ventricles have prolonged action potential Work together to function as a syncyticum Electrolytes are critically important to normal function
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Relevant anatomy
httpwwwtexasheartorgHICAnatomyanatomy2cfm
Myocytes Contractile cells Conducting cells SA node interatrial AV node bundle of His Purkinje fibers
httpswwwurmcrochestereduEncyclopediaGetImageaspxImageID=125477
We want action Action potentials are the same in the atria and
ventricles Long duration (when compared to skeletal muscle) Longer the AP ndash longer the refractory periods
Sinoatrial node action potential Automaticity ndash spontaneously generates action
potentials without neuronal input Unstable resting membrane potential No sustained plateau
Ventricular action potential
Costanzo Physiology 3rd edition 2006
Refractory period
httpswwwstudybluecomnotesnotenphysiology-cardiovascular-part-1deck4279768
Definitions Chronotropic-effects on HR Inotropic-effects on contractility Dromotropic-effects on conduction velocity
Back to the bedside P wave ndash represents atrial depolarization PR interval ndash represents AV node conduction QRS ndash depolarization of the ventricles T wave ndash repolarization of the ventricles QT interval ndash first ventricular depolarization to last
ventricular repolarization
Bringing it together
Text
httpwesleytoddblogspotcom201311action-potentialshtml
Vaughn-Williams Classification Class I Fast sodium channel blockers 1a Quinidine procainamide
1b Lidocaine phenytoin 1c Flecainide
Class I Beta blockers Propranolol esmolol metroprolol atenolol
Class III Potassium channel blockers Amiodarone Sotalol dofetilide Class IV Slow calcium channel blockers
Verapamil diltiazem
Class V Variable mechanism Adenosine Digoxin
Lastly where does BP come from BP = CO x PVR CO = SV x HR
Letrsquos review Pacemaker cells with automaticity Different action potential
Atria and ventricles have prolonged action potential Work together to function as a syncyticum Electrolytes are critically important to normal function
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Myocytes Contractile cells Conducting cells SA node interatrial AV node bundle of His Purkinje fibers
httpswwwurmcrochestereduEncyclopediaGetImageaspxImageID=125477
We want action Action potentials are the same in the atria and
ventricles Long duration (when compared to skeletal muscle) Longer the AP ndash longer the refractory periods
Sinoatrial node action potential Automaticity ndash spontaneously generates action
potentials without neuronal input Unstable resting membrane potential No sustained plateau
Ventricular action potential
Costanzo Physiology 3rd edition 2006
Refractory period
httpswwwstudybluecomnotesnotenphysiology-cardiovascular-part-1deck4279768
Definitions Chronotropic-effects on HR Inotropic-effects on contractility Dromotropic-effects on conduction velocity
Back to the bedside P wave ndash represents atrial depolarization PR interval ndash represents AV node conduction QRS ndash depolarization of the ventricles T wave ndash repolarization of the ventricles QT interval ndash first ventricular depolarization to last
ventricular repolarization
Bringing it together
Text
httpwesleytoddblogspotcom201311action-potentialshtml
Vaughn-Williams Classification Class I Fast sodium channel blockers 1a Quinidine procainamide
1b Lidocaine phenytoin 1c Flecainide
Class I Beta blockers Propranolol esmolol metroprolol atenolol
Class III Potassium channel blockers Amiodarone Sotalol dofetilide Class IV Slow calcium channel blockers
Verapamil diltiazem
Class V Variable mechanism Adenosine Digoxin
Lastly where does BP come from BP = CO x PVR CO = SV x HR
Letrsquos review Pacemaker cells with automaticity Different action potential
Atria and ventricles have prolonged action potential Work together to function as a syncyticum Electrolytes are critically important to normal function
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
We want action Action potentials are the same in the atria and
ventricles Long duration (when compared to skeletal muscle) Longer the AP ndash longer the refractory periods
Sinoatrial node action potential Automaticity ndash spontaneously generates action
potentials without neuronal input Unstable resting membrane potential No sustained plateau
Ventricular action potential
Costanzo Physiology 3rd edition 2006
Refractory period
httpswwwstudybluecomnotesnotenphysiology-cardiovascular-part-1deck4279768
Definitions Chronotropic-effects on HR Inotropic-effects on contractility Dromotropic-effects on conduction velocity
Back to the bedside P wave ndash represents atrial depolarization PR interval ndash represents AV node conduction QRS ndash depolarization of the ventricles T wave ndash repolarization of the ventricles QT interval ndash first ventricular depolarization to last
ventricular repolarization
Bringing it together
Text
httpwesleytoddblogspotcom201311action-potentialshtml
Vaughn-Williams Classification Class I Fast sodium channel blockers 1a Quinidine procainamide
1b Lidocaine phenytoin 1c Flecainide
Class I Beta blockers Propranolol esmolol metroprolol atenolol
Class III Potassium channel blockers Amiodarone Sotalol dofetilide Class IV Slow calcium channel blockers
Verapamil diltiazem
Class V Variable mechanism Adenosine Digoxin
Lastly where does BP come from BP = CO x PVR CO = SV x HR
Letrsquos review Pacemaker cells with automaticity Different action potential
Atria and ventricles have prolonged action potential Work together to function as a syncyticum Electrolytes are critically important to normal function
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Sinoatrial node action potential Automaticity ndash spontaneously generates action
potentials without neuronal input Unstable resting membrane potential No sustained plateau
Ventricular action potential
Costanzo Physiology 3rd edition 2006
Refractory period
httpswwwstudybluecomnotesnotenphysiology-cardiovascular-part-1deck4279768
Definitions Chronotropic-effects on HR Inotropic-effects on contractility Dromotropic-effects on conduction velocity
Back to the bedside P wave ndash represents atrial depolarization PR interval ndash represents AV node conduction QRS ndash depolarization of the ventricles T wave ndash repolarization of the ventricles QT interval ndash first ventricular depolarization to last
ventricular repolarization
Bringing it together
Text
httpwesleytoddblogspotcom201311action-potentialshtml
Vaughn-Williams Classification Class I Fast sodium channel blockers 1a Quinidine procainamide
1b Lidocaine phenytoin 1c Flecainide
Class I Beta blockers Propranolol esmolol metroprolol atenolol
Class III Potassium channel blockers Amiodarone Sotalol dofetilide Class IV Slow calcium channel blockers
Verapamil diltiazem
Class V Variable mechanism Adenosine Digoxin
Lastly where does BP come from BP = CO x PVR CO = SV x HR
Letrsquos review Pacemaker cells with automaticity Different action potential
Atria and ventricles have prolonged action potential Work together to function as a syncyticum Electrolytes are critically important to normal function
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Ventricular action potential
Costanzo Physiology 3rd edition 2006
Refractory period
httpswwwstudybluecomnotesnotenphysiology-cardiovascular-part-1deck4279768
Definitions Chronotropic-effects on HR Inotropic-effects on contractility Dromotropic-effects on conduction velocity
Back to the bedside P wave ndash represents atrial depolarization PR interval ndash represents AV node conduction QRS ndash depolarization of the ventricles T wave ndash repolarization of the ventricles QT interval ndash first ventricular depolarization to last
ventricular repolarization
Bringing it together
Text
httpwesleytoddblogspotcom201311action-potentialshtml
Vaughn-Williams Classification Class I Fast sodium channel blockers 1a Quinidine procainamide
1b Lidocaine phenytoin 1c Flecainide
Class I Beta blockers Propranolol esmolol metroprolol atenolol
Class III Potassium channel blockers Amiodarone Sotalol dofetilide Class IV Slow calcium channel blockers
Verapamil diltiazem
Class V Variable mechanism Adenosine Digoxin
Lastly where does BP come from BP = CO x PVR CO = SV x HR
Letrsquos review Pacemaker cells with automaticity Different action potential
Atria and ventricles have prolonged action potential Work together to function as a syncyticum Electrolytes are critically important to normal function
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Refractory period
httpswwwstudybluecomnotesnotenphysiology-cardiovascular-part-1deck4279768
Definitions Chronotropic-effects on HR Inotropic-effects on contractility Dromotropic-effects on conduction velocity
Back to the bedside P wave ndash represents atrial depolarization PR interval ndash represents AV node conduction QRS ndash depolarization of the ventricles T wave ndash repolarization of the ventricles QT interval ndash first ventricular depolarization to last
ventricular repolarization
Bringing it together
Text
httpwesleytoddblogspotcom201311action-potentialshtml
Vaughn-Williams Classification Class I Fast sodium channel blockers 1a Quinidine procainamide
1b Lidocaine phenytoin 1c Flecainide
Class I Beta blockers Propranolol esmolol metroprolol atenolol
Class III Potassium channel blockers Amiodarone Sotalol dofetilide Class IV Slow calcium channel blockers
Verapamil diltiazem
Class V Variable mechanism Adenosine Digoxin
Lastly where does BP come from BP = CO x PVR CO = SV x HR
Letrsquos review Pacemaker cells with automaticity Different action potential
Atria and ventricles have prolonged action potential Work together to function as a syncyticum Electrolytes are critically important to normal function
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Definitions Chronotropic-effects on HR Inotropic-effects on contractility Dromotropic-effects on conduction velocity
Back to the bedside P wave ndash represents atrial depolarization PR interval ndash represents AV node conduction QRS ndash depolarization of the ventricles T wave ndash repolarization of the ventricles QT interval ndash first ventricular depolarization to last
ventricular repolarization
Bringing it together
Text
httpwesleytoddblogspotcom201311action-potentialshtml
Vaughn-Williams Classification Class I Fast sodium channel blockers 1a Quinidine procainamide
1b Lidocaine phenytoin 1c Flecainide
Class I Beta blockers Propranolol esmolol metroprolol atenolol
Class III Potassium channel blockers Amiodarone Sotalol dofetilide Class IV Slow calcium channel blockers
Verapamil diltiazem
Class V Variable mechanism Adenosine Digoxin
Lastly where does BP come from BP = CO x PVR CO = SV x HR
Letrsquos review Pacemaker cells with automaticity Different action potential
Atria and ventricles have prolonged action potential Work together to function as a syncyticum Electrolytes are critically important to normal function
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Back to the bedside P wave ndash represents atrial depolarization PR interval ndash represents AV node conduction QRS ndash depolarization of the ventricles T wave ndash repolarization of the ventricles QT interval ndash first ventricular depolarization to last
ventricular repolarization
Bringing it together
Text
httpwesleytoddblogspotcom201311action-potentialshtml
Vaughn-Williams Classification Class I Fast sodium channel blockers 1a Quinidine procainamide
1b Lidocaine phenytoin 1c Flecainide
Class I Beta blockers Propranolol esmolol metroprolol atenolol
Class III Potassium channel blockers Amiodarone Sotalol dofetilide Class IV Slow calcium channel blockers
Verapamil diltiazem
Class V Variable mechanism Adenosine Digoxin
Lastly where does BP come from BP = CO x PVR CO = SV x HR
Letrsquos review Pacemaker cells with automaticity Different action potential
Atria and ventricles have prolonged action potential Work together to function as a syncyticum Electrolytes are critically important to normal function
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Bringing it together
Text
httpwesleytoddblogspotcom201311action-potentialshtml
Vaughn-Williams Classification Class I Fast sodium channel blockers 1a Quinidine procainamide
1b Lidocaine phenytoin 1c Flecainide
Class I Beta blockers Propranolol esmolol metroprolol atenolol
Class III Potassium channel blockers Amiodarone Sotalol dofetilide Class IV Slow calcium channel blockers
Verapamil diltiazem
Class V Variable mechanism Adenosine Digoxin
Lastly where does BP come from BP = CO x PVR CO = SV x HR
Letrsquos review Pacemaker cells with automaticity Different action potential
Atria and ventricles have prolonged action potential Work together to function as a syncyticum Electrolytes are critically important to normal function
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Vaughn-Williams Classification Class I Fast sodium channel blockers 1a Quinidine procainamide
1b Lidocaine phenytoin 1c Flecainide
Class I Beta blockers Propranolol esmolol metroprolol atenolol
Class III Potassium channel blockers Amiodarone Sotalol dofetilide Class IV Slow calcium channel blockers
Verapamil diltiazem
Class V Variable mechanism Adenosine Digoxin
Lastly where does BP come from BP = CO x PVR CO = SV x HR
Letrsquos review Pacemaker cells with automaticity Different action potential
Atria and ventricles have prolonged action potential Work together to function as a syncyticum Electrolytes are critically important to normal function
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Lastly where does BP come from BP = CO x PVR CO = SV x HR
Letrsquos review Pacemaker cells with automaticity Different action potential
Atria and ventricles have prolonged action potential Work together to function as a syncyticum Electrolytes are critically important to normal function
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Letrsquos review Pacemaker cells with automaticity Different action potential
Atria and ventricles have prolonged action potential Work together to function as a syncyticum Electrolytes are critically important to normal function
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Beta blockers
Properties of β-adrenergic receptor blockers
Drug Cardioselectivity Lipophilicity Protein Binding Intrinsic sympathomimetic activity Membrane Stabilizing Effect
Time to peak plasma concentration (hours)
Elimination t frac12 (hours)
Acebutolol β1 Low 25 Yes Yes 2-4 2-4
Atenolol β1 Low lt5 No No 2-4 5-8
Carvedilol β1β2α1 High 95-98 No Yes 1-2 6-10
Labetalol β1β2α1 Low-moderate 50 No No 1-2 8
Metoprolol β1 Moderate 10 No No 15-2 3-4
Nadolol β1β2 Low 30 No No 3-4 10-20
Nebivolol β1 High 98 No No 15-4 12-19
Propranolol β1β2 High 90 No Yes 1-2 3-5
Sotalol β1β2 Low 0 No No 204 10-20
Timolol β1β2 Low-moderate lt10 No No 1-2 2-4
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Beta receptors Beta receptors are located
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Beta blockers
Certainly good in therapeutic doses Buthellip
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Beta blockers Can be life threatening in overdose
Who needs treatment
And how do you treat them
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Identifying potential adverse reactions Children
Individuals with suspicion for self-harm
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Treatment Consider GI decontamination
Two large bore Ivs
Crystalloid IVF
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Treatment What else are you going to do
What pressor(s) are available to you
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Any other therapies IVF calcium glucagon IV
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Goldfrankrsquos Toxicologic Emergencies 10th edition
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Any other therapies Hyperinsulinemia-euglycemia
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Calcium channel blockers Where are they located Heart nerves pancreas muscles
Primarily antagonize (block) L-type Calcium channels
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
CCB
Class Specific drugs Phenylalkylamine Verapamil Benzothiazepine Diltiazem Dihydropyridines Amlodipine
Clevidipine Felodipine Isradipine Nicardipine Nifedipine Nimodipine Nisoldipine
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
CCB While the mechanism seems clear
In overdose ndash you lose specificity
May also see hyperglycemia
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Clinical presentation Hypotension and bradycardia
Fatigue dizziness AMS
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Treatment Consider GI decontamination
Two large bore IVs
Crystalloid IVF
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Pharmacologic treatment Atropine Calcium Glucagon
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Pharmacologic treatment Pressors HIE Intralipid
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Pharmacologic treatment Intralipid
wwwthepoisonreviewcom
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Digoxin Well known mechanism Characteristic EKG findings Narrow therapeutic index
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Digoxin
httplifeinthefastlanecomecg-librarydigoxin-effect
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Digoxoin Cause Treatment Antidote
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Next case 28 yo male present with altered mental status after
performing poorly on his semester grades Has seemed depressed to his roommates over the past few days
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Treatment Text
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
TCA Text
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
TCA Pharmacology SNRI Antimuscarinic H1 Antagonist Alpha 1 antagonist Fast Na Ch blockade 1A effect
Clincal effect Seizures Anticholinergic sxs Sedation Hypotension Cardiotoxicity
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Itrsquos widehellipand itrsquos tox Na channel blockers TCAs Diphenhydramine Venlafaxine
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
QT prolongation
Definition Inherited causes Medications
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
QT prolongation - Medications
Amiodarone Dofetilide Procainamide Sotalol Chloroquine Chlorpromazine Haloperidol
Methadone Droperidol
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Whatrsquos the problem with a little QT Torsade de pointes ndash twisting of the points
httpmstcparamedicpbworkscomwpage21902876Torsades20de20Pointes
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
The most common cardiac toxin
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Hyperkalemia Most commonly AKI or ESRD But really anything that either Increases absorption (increased intake) Decreased excretion (AKI medications etc)
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Hyperkalemia Text
httplifeinthefastlanecomecg-librarybasicshyperkalaemia
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
References Goldfrankrsquos Toxicologic Emergencies Tenth edition 2015
Rosenrsquos Emergency Medicine Seventh edition
Charlotte van Noord12 Mark Eijgelsheim1 and Bruno H Ch Strickerr Drug- and non-drug-associated QT interval prolongation Br J Clin Pharmacol 2010 Jul 70(1) 16ndash23
Drug-Induced Prolongation of the QT Interval
Roden D Drug-Induced Prolongation of the QT interval NEJM 2004 3501013-1022 2004
Evans KJ1 Greenberg A Hyperkalemia a review J Intensive Care Med 2005 Sep-Oct20(5)272-90
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-
Questions Call anytime anywhere
- Title
- Heartbreakers
- Objectives
- Tox 101
- Slide Number 5
- Slide Number 6
- Relevant anatomy
- Myocytes
- We want action
- Sinoatrial node action potential
- Ventricular action potential
- Refractory period
- Definitions
- Back to the bedside
- Bringing it together
- Slide Number 16
- Lastly where does BP come from
- Letrsquos review
- Beta blockers
- Beta receptors
- Beta blockers
- Beta blockers
- Identifying potential adverse reactions
- Treatment
- Treatment
- Any other therapies
- Any other therapies
- Calcium channel blockers
- CCB
- CCB
- Clinical presentation
- Treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Pharmacologic treatment
- Digoxin
- Digoxin
- Digoxoin
- Next case
- Treatment
- TCA
- TCA
- Itrsquos widehellipand itrsquos tox
- QT prolongation
- QT prolongation - Medications
- Whatrsquos the problem with a little QT
- The most common cardiac toxin
- Hyperkalemia
- Hyperkalemia
- Hyperkalemia
- Slide Number 52
- Slide Number 53
- References
- Questions Call anytime anywhere
-