applied clinical pharmacology

8/10/2019 Applied Clinical Pharmacology

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Muhammad Yusuf Muharam,

MBBS (UM), MMed. Emergency (USM)

Emergency & Trauma Department,

Hospital Queen Elizabeth

Kota Kinabalu, Sabah

23rd September 2014


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Introduction

Resuscitative drugs

Pharmacology

Summary


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Severe, often life-threatening consequences

can occur if paramedics

make a mistake.

??? Pharmacology

scientific study of how various

substances interact with or

alter the function of living

organisms.

Chemicals have been used

for centuries.


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Formal scientific study began in the 17th and18th centuries.

Some ancient remedies are still used today.Atropa belladonna, poppy seed Papaver

somniferum etc

EBM guidelines assist clinicians usingpharmacologic interventions.

Medications undergo extensive testing and

clinical trials.


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Medications for desired effect in the body.

Pharmacodynamics: as a medication is

administered, it alters a function or processof the body.

Any medication can cause toxic effects.


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Pharmacokinetics: action of the body on a

medication

Process of medication administration (ADME): Absorption

Distribution

Metabolism/Biotransformation

Elimination


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Cardiac Output = HR X SV

Heart Rate x Stroke Volume

stroke volume cardiac output stroke volume cardiac output

heart rate cardiac output

heart rate cardiac output

SV = EDV ESV


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Mean (average) Arterial Pressure (MAP)

(Diastolic Pressure + Pulse Pressure) / 3

DBP + 1/3 (SBP-DBP)

Blood Flow (vascular system) = CardiacOutput

relatively constant but will vary in the individualorgans.

At rest:

brain 13%

internal organs 24% heart 4%

skeletal muscle 20%

kidneys 20%


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Blood pressure is affected

by cardiac output and

resistance.

Cardiac output is affected

by blood volume.

So blood volume alsoaffects blood pressure.


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Adrenaline /

epinephrine

Amiodarone

Atropine

Adenosine

Magnesium sulphate

Dopamine

Dobutamine

Sodium Bicarbonate


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Indications

Cardiac arrest

VF; Pulseless VT; asystole; PEA

Anaphylaxis; severe allergic reactions

Combine with large fluid volume; corticosteroids;

antihistamines

Severe hypotension


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Systemic vascular resistance

Systemic arterial pressure

Heart rate

Contractile state

Myocardial oxygen requirement

Improved cerebral and myocardialblood flow from vasoconstriction andincreased perfusion pressure


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Precautions

May increase myocardial ischemia, angina, and

oxygen demand

High doses do not improve survival; may be

detrimental

Standard preparation

1 mg/ml ampoule

S/E:

tachy, HPT, arrhythmias


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ADRENALINE

(1 mg/ml)

Strength

1:1000)

CPRall

pulseless

conditions

1 mg every 3

5 min Undiluted

Anaphylaxis

IV: 0.1 mg every 10 mins

as required

+ 9 ml NS

(0.1 mg/ml)

I.M: 0.20.5 mg (1:1000)

every 515 mins -

Hypotension

/ Shock

Start 220 mcg/min

Or220 ml/hr

3mg in 47ml of D5%

(0.06mg/ml) or

-


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Amiodarone useful in treating both supra- andventricular tachydysrhythmias.

Increase the rate of survival from cardiac arrest,BUThas not been shown to increase survival tohospital discharge.

In PSVT, Amiodarone is a second-line agent, andcan be used when adenosine fails.


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The maximum dose in 24 hour: not exceed 2.2

grams.

AMIODARONE

(150 mg/3ml)

Cardiac arrestPulseless VT or

VF

Initial 300 mg, may repeat

dose at 150 mg

Non-cardiac arrest

Stable VT/ SVT

Atrial

fibrillation

Loading dose:

Step 1: 150 mg stat

Maintenance dose:

Step 2: 360 mg over 6 hrs (run

33.3 ml/hr)

Step 3: 540 mg over 18 hrs (run

16.7 ml/hr)


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hyper/hypothyroidism,

bradycardia,

proarrhythmia, nausea,

anorexia,

photosensitivity,

corneal microdeposits.

Pulmonary toxicity

(pneumonitis)


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Atropine

For symptomatic bradycardia that are due toincreased parasympathetic tone.

Atropine should not be used when infranodalpathology is suspected such as with second-degree AV blocks.

Heart transplant??? Atropine is ineffective in the setting of previous heart

transplant and may worsen ischemia during amyocardial infarction.


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Mechanism of Action

Inhibits the actions of acetycholine on structuresinnervated by postganglionic sites

(smooth/cardiac muscle, SA/AV nodes)


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Indications

First line drug for symptomatic sinus bradycardia

Organophosphate poisoning; large dose may beneeded

Precautions

Not effective for type II 2nd

or 3rd

degree block (mayslow the rhythm)

Doses < 0.5 mg may cause a paradoxical slowing


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ATROPINE

(1 mg/ml)

CPRAsystole,

PEA

1 mg every 35 mins

(Max: 0.04 mg/kg)

Symptomatic

bradycardia

0.5 mg every 35 mins

(Max : 3 mg total dose)

Organo-phosphate

poisoning

12 mg and with doubling of

each subsequent dose every 3-5

minutes until full atropinisation

effect.

Dont delay pacing forseverely symptomatic(unstable) patients.


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HA,

convulsion,

VT,

paradoxical bradycardia, eye dryness,

dry mouth,

constipation, flushed skin


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Indications

1stdrug for stable, narrow complex, regular SVT

May consider for unstable SVT while preparing for

cardioversion


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Place supine or mild reverse Trendelenburg,

IV nearest to the heart

Ampoule: 6mg / 2 ml

Half-life???


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ADENOSINE

(6 mg/2ml)

Supraventricular

tachycardia (SVT)

612 mg - 12 mg

(Max. single dose:

12 mg)

f/by 20 ml NS

bolus


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Contraindications/Precautions

2ndand 3rddegree block is contraindicated

Transient side effects; flushing, CP, asystole, brady,

ectopy, bronchospasm

Transient periods of sinus brady or ventricularectopy common after termination of SVT

Safe in pregnancy


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Transcient brady,

Complete HB

Ventricular standstill

DyspnoeaNausea

Angina like chest pain

Bronchospasm Raised ICP


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Mechanism of Action

Increases magnesium levels in cases whereprolonged QT interval is thought to be

secondary to hypomagnesemia.


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Indications

Torsades is suspected in cardiac arrest

Life-threatening ventricular dysrhythmias in

digitalis OD

Precautions

Fall in BP with rapid administration

Dosing

Arrest 1-2 g over 5-20 min.

Torsades w/ pulse 1-2 g over 5-60 min.


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MAGNESIUM

SULPHATE

(2.47 g/5ml)

AEBA 2 g (4 ml) over 20 min

Torsade de pointes 12 g over 15 mins

Treatment for

hypomagnesemia12 g over 5 to 60 mins

Pre-eclampsia/

Eclampsia

45 g over 20 mins, followed

by 1

2 g/hr

(Max: 40 g/24 hr)

20gm (40ml) in 450NS

40m /ml


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Bradycardia

Diplopia

HA

HypotensionNausea, SOB

Vomiting

Weakness

Reduce reflex


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Mechanism of Action

Stimulates adrenergic receptors

(dose dependent)


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Indications

Second-line drug for symptomatic bradycardia

Hypotension with signs and symptoms of shock

Precautions

Correct hypovolemia with volume before initializing

May cause tachydysrhythmias; excessive vasoconstriction

Dont mix with sodium bicarbonate


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DOPAMINE

(200 mg/5 ml)

Hypotension

/ shock

120 mcg/kg/min

(Max: 20 mcg/kg/min)

(200mg in 45 ml of NS:4mg/ml)


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chest pain;

fast, slow, or pounding heartbeats; arrythmia

weakness, confusion,

swelling in your feet or ankles,

N,V


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Mechanism of action

Direct beta-adrenergic stimulator

Potent inotropic effect but less chronotropic Renal and mesenteric flow follows cardiac

output

Myocardial work is balanced by increases in

coronary flow at clinical doses


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Indications

Congestive heart failure

Cardiogenic shock

Hemodynamically significant hypotension


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DOBUTAMINE

(250 mg/20 ml)

Hypotension/

shock

2.520 mcg/kg/min

(Max: 20 mcg/kg/min)

(250mg in 30 ml: 5mg/ml)


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Generally dose related, uncommon

if < 10mcg/kg/min

TachycardiaArrhythmias

Tremors

HPT

Angina like chest pain

Nausea

Vomiting


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Mechanism of action

Reacts with H+ ion, as in metabolic acidosis

HCO3- + H+ H2CO3 CO2+ H20

No definite evidence of benefit in arrest

Indication

Consider in severe metabolic acidosis eg.

Cardiac arrest


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Dose

1 mmol/kg initially, OR 50-100 ml of 8.4%

NaHCO3 over 30-60 mins

Precautions

Worsened intracellular acidosis from CO2formation and retention

Hyperosmolality and hypernatremia

Metabolic alkalosis

Acute hypokalemia


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Indication

PEA d/t; HyperK, hypoCa, CCB overdose

Dose:

10 ml of 10% calcium gluconate (6.8 mmol/L Ca)

S/E:

Brady,

Arrythmias, tissue irrtation (local)


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MUST KNOW DRUGSin Emergency

Department

Local protocol of drug

Always re-confirm before giving ANY drugs to

patient

Reportany drug reaction


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applied clinical pharmacology

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