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Page 1: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Cardiac Meds

Cardiac Output

Stroke Volume Heart Rate

Meds Sympathetic Stimulation

Afterload Preload Contractility

X

=

PVR

Viscosity

Aortic Impedance

Venous Return

Ventricular

Compliance

Page 2: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Preload

• Function of the volume of blood to the LV and the compliance (ability of the ventricle to stretch) of the ventricles at the end of diastole (LVEDP)

• Factors affecting are: venous return, total blood volume and atrial kick

• Hypovolemic patient has too little preload• Heart failure patient has too much preload

Page 3: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Afterload

• Ventricular wall tension or stress during systolic ejection

• Increase in afterload relates to an increase in the work of the heart

• Increased afterload R/T:– Aortic stenosis– Vasoconstriction and SVR– Blood volume and viscosity

• To decrease, use vasodilators, decrease myocardial oxygen demand

Page 4: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Contractility

• Inotrophy or enhancing strength, can be positive or negative

• Sympathetic medications increase contractility• Ca++ is a medication that will increase

contractility by increasing actin and myosin contractions

• Digoxin also works to increase Ca++ channels by slowing the Na/Ca pump

Page 5: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Control of Heart Rate• SNS- sympathetic nervous system

– Fight or flight– Increase HR, BP, respirations, dilate pupils

• PNS- parasympathetic system– Decreases contractility, rate– Vagus nerves to the SA and AV nodes

• Baroreceptors- pressure sensors in carotids and aortic arches• Chemoreceptors- pH levels in aortic arch• ANF- atrial natriuretic factor- hormone secreted by the atria in

response to atrial pressure– Causes Na and water to be excreted and also vasodilates

Page 6: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Control of Stroke Volume

• Preload– Increase use:

• Fluid resusitation

– Decrease use:• Diuretics and vasodilators

• Afterload– Increase use:

• Vasopressors• Volume expanders

• Afterload– Decrease use:

• Vasodilators• Diuretics• Decrease sympathetic

stimulation

• Contractility– Increase use:

• Sympathetic stimulants– Decrease use:

• CCB’s• Decrease sympathetics

Page 7: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Vasopressors

• Sympathomimetic-inotrophic• Medications that mimic the sympathetic

system, work on alpha, beta and dopamineric receptors

• Require continuous monitoring of BP and heart rate

• Alpha: vasoconstricts peripheral arterioles• Beta 1: Increased HR, contractility• Beta 2: Bronchodilation

Page 8: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Vasopressor

• Dopamine – Stimulates alpha and

beta receptors– In small doses (2-5

mcg/kg/min) produces renal vasodilation

– Larger doses (max 20 mcg/kg/min) alpha and beta stimulation

– Increases HR and BP

• Precautions:– Give IV only, can

sloughing of tissue with extravasation, if it does infiltrate, give phentolamine IV to the site

– Tachyarrhythmias, palpations, hypotension if not hydrated, headache, dyspnea

Page 9: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Vasopressor

• Epinephrine– Alpha-Adrenergic, beta 1

and beta 2 stimulant– Produces

bronchodilation and vasoconstriction

– Increases HR, BP and bronchodilates

– Given IV, SQ and inhalation

– Max is 20 mcg/min

• Precautions:– Tachyarrhythmias– Angina– Nervousness, tremors– Hypertension– Works almost

immediately IV– Watch for chest pain and

HR >120, can cause cardiac arrest with too last a rate

Page 10: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Vasopressor

• Norepinephrine– Stimulates alpha, beta

receptors– Need to hydrate patient– Lacks beta 2 effects– Marked alpha

vasoconstriction– Used in shock states– Max is 16 mcg/min

• Precautions:– Closely monitor HR and

BP, can elevate quickly– Monitor for peripheral

vasoconstriction, in high doses, can constrict all extremities

– Can decrease the C.O. if rate is too high

Page 11: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Vasopressor

• Dobutamine– Synthetic

cathecholamine with mainly beta effects

– Mild stimulation of beta 2

– Increases myocardial contractility

– Useful with heart failure patients

– Max is 20 mcg/kg/min

• Precautions:– Monitor for increased

HR and BP– PVC’s and angina– Watch for shortness of

breath– May be given over a long

infusion for heart failure patients

Page 12: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Vasopressors- Phosphodiesterase Inhibitors

• Cause increased levels of AMP and Ca++

• Medications:– Amrinone (Inocor)– Milrinone (Primacor)

• Cause an increase in cardiac output and some decreased afterload

• Effective in heart failure patients to increase C.O.

• Precautions:– Given as a continuous IV

infusion– Can cause PVC’s and V tach

because of increased contraction

– Monitor for drops in BP R/T decreased afterload

– Watch for thrombocytopenia and abnormal liver function

Page 13: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Other Vasopressors

• Phenylephrine (neo-synephrine)– Stimulates alpha

receptors only– Used by anesthesia– Can increase myocardial

demand– Works very quickly

• Vasopressin (antidiuretic hormone)– Nonadrenergic

peripheral vasoconstrictor

– Used in VF and pulseless VT, 40Units

– Used as an IV infusion in sepsis with peripheral vasodilation

Page 14: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Vasodilators- Direct Smooth Muscle Relaxants

• Decrease PVR• Arterial and venous dilation• Improves cardiac output• Medications:

– Nitroprusside (Nipride)– Nitroglyceride– Hydralazine (Apresoline)

• Precautions:– Closely monitor BP, can drop

dramatically, especially nipride

– Long term nitroprusside therapy can lead to thiocyanate toxicity

– NTG is used with unstable angina (given 5-300 mcg/min

– Apresoline is not a continuous infusion, major side effect is tachycardia

Page 15: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Vasodilators- Ca++ Channel Blockers

• Arterial vasodilation• Reduce the influx of

calcium and decrease resistance

• Used mostly for hypertension

• Also to slow rapid rhythms, such as SVT, and Atrial fib

• Medications:– Nicardipine (Cardene)– Nifedipine (Procardia)– Diltiazem (Cardizem)– Verapamil (Calan)

• Side effects:– Hypotension,

bradycardia, nausea, heart failure and peripheral edema

Page 16: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Vasodilators-ACE inhibitors

• Vasodilate by blocking the conversion of angiotensin I to angiotensin II, decreases PVR

• May drop BP dramatically if volume depleted

• Stops Na and water retention

• Medications:– Captopril (Capoten)– Enalapril (Vasotec)

• Precautions:– Hypotension, chronic

cough, neutropenia and elevated liver enzymes

Page 17: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Vasodilators- Alpha adrenergic blockers

• Block peripheral alpha receptors in arteries and veins

• Orthostatic changes may result

• May lead to fluid retention

• Medications:– Labetalol (normadyne)

• Alpha & beta blocker• Decreased BP without

increased HR• Used in aortic dissections

– Phentolamine (Regitine)• Peripheral alpha blocker,

decreases afterload• Used with

pheochromocytomas

Page 18: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Vasodilators- DA-1 receptor agonists & Synthetic BNP

• Dopamine DA-1 receptor agonists, vasodilates peripheral and renal arteries

• Medication:– Fenoldopam (Corlapam)

• Hypertensive emergencies

• Watch for hypotension and tachycardia

• Natrecor:– Brain naturietic peptide– Used for decompensated

HR with dyspnea– Vasodilates pulmonary

bed, reduces SVR and PVR

– Lowers BNP levels– Infusion runs for 6-48

hours

Page 19: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Vaughn Williams Classification- Used for Antiarrhythmics

• Class I agents interfere with the sodium (Na+) channel.

• Class II agents are anti-sympathetic nervous system agents. Most agents in this class are beta blockers.

• Class III agents affect potassium (K+) efflux. • Class IV agents affect calcium channels and the

AV node. • Class V agents work by other or unknown

mechanisms.

Page 20: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Class Ia

• Medications:– Quinidine– Procainamide– Disopyramide

• Type:– Na+ channel block

intermediate

• Use:• Ventricular arrhythmias• Prevents recurrent atrial

fib, triggered by overactive vagal stimulation (Wolff-Parkinson-White syndrome)

Page 21: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Class Ib

• Medication:– Lidocaine– Phenytoin– Mexiletine

• Type:– Na+ channel block fast

• Use:– Ventricular tachycardia– Atrial fib– Prevention during and

immediately after an MI, but it is now discouraged R/T increased risk of asystole

Page 22: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Class Ic

• Medications:– Flecainide– Propafenone– Moricizine

• Type:– Na+ channel block slow

• Use:– Prevents paroxysmal

atrial fib– Treats recurrent

tachyarrhythmias of abnormal conduction system

Page 23: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Class II• Medications:

– Propranolol– Esmolol– Timolol– Metoprolol– Atenolol

• Type:– Beta Blocker

• Use:– Decrease myocardial

infarction mortality, used post MI

– Prevent recurrence of tachyarrhythmias

– Decrease Beta 1 and 2 stimulation, decrease HR and BP

– Side effects of bradycardia, fatigue, wt. gain, impotence, depression

Page 24: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Class III

• Medications:– Amiodarone– Sotalol (also a Beta)– Ibutilide– Dofetilide

• Type:– K+ channel blocker

• Use:– Ventricular tachyarrhythmias– Atrial flutter and atrial fib– Wolff-Parkinson-White

syndrome• Side effects:

– SOB, bronchospasm, renal or hepatic insufficiency

– Photosensitive, use sunscreen and sunglasses, may cause bluing of periphery

Page 25: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Class IV

• Medications:– Verapamil– Diltiazem

• Type:– Ca++ channel blocker

• Use:– Prevent recurrence of

paroxysmal SVT– Reduce ventricular rate in

patients with atrial fib– Decrease the contraction of

muscle tissue, prevents slide of actin and myosin

– Avoid grapefruit juice it can increase serum levels, as do high fat meals

– Monitor thyroid function

Page 26: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Class VMedications:

AdenosineDigoxin

Type:Work by other methods,

direct nodal inhibitionNa/Ca pump

Use: Supraventricular arrhythmias Contraindicated in ventricular

arrhythmiasSide effects:

Digoxin- bradycardia, anorexia, nausea & vomiting, yellow/green halos, heart blocks, arrhythmias, causes hypocalcemia and hypokalemia

Page 27: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Aspirin

• Acts to reduce inflammation by inhibiting the production of prostaglandins

• Decreases platelet aggregation, decreases the incidence of TIA’s and MI

• Dosage of 81 mg maintenance, not enteric coated in MI

• Monitor for GI bleeding, exfoliative dermatitis, Stevens-Johnson syndrome, tinnitus

Page 28: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Other Emergency Medications

• Atropine:– Parasympathicolytic, enhances

the SA node and AV node conduction

– Used for bradycardia and asystole

– Side effects:• Tachycardia, urinary

retention, blurred vision, bowel obstruction, not for Complete heart block

• Calcium Cl:– Enhances myocardial

contractility for pts with elevated K, Mg and low Ca and CCB toxicity

– Side effects:• Coronary and cerebral

vasospasm, ventricular irritability, cautious if on Digoxin

Page 29: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Other Emergency Medications

• Magnesium– Reduces post infarction

arrhythmias and pump failure– Hypomagnesemia can cause

refractory V fib and sudden cardiac death

– Side effects:• Flushing, sweating,

hypotension, sensation of heat, flaccid paralysis, circulatory collapse

• Diprivan (Propofol)– Short acting sedative,

used for sedation with patients who have airway and ventilatory support

– Side effects:• Hypotension, rebound

tachycardia and increased ICP when wean off, hepatotoxicity

Page 30: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Other Emergency Medications

• Lorazepam (Ativan)– Benzodiazepine sedative– Effects last 6-8 hours– If given intraarterial can cause

gangrene and limb loss– CNS depression is prominent if

over 50– Contraindicated if glaucoma– Watch for airway depression

• Midazolam (Versed)– Benzodiazepine sedative– Effects last 1.5-2 hours– Depresses respiratory rate,

apnea, can cause hypotension– Hiccups, headache, nausea,

amnesia, confusion– Can be reserved with romazicon

(flumazenil)

Page 31: Cardiac Meds Cardiac Output Stroke VolumeHeart Rate Meds Sympathetic Stimulation AfterloadPreload Contractility X = PVR Viscosity Aortic Impedance Venous

Other Emergency Medications

• Succinylcholine– Neuromuscular blocking agent– Rapid acting agent for intubation– Side effects:

• Hypotention, tachycardia, hyperkalemia, severe in neurologic patients myoglobinuria, malignant hyperthemia

• Rocuronium or vecuronium– Neuromuscular blocking agent– Lasts 20-60 minutes– Can cause tachycardia,

hypotension and bronchospasm in some patients, prolonged weakness if renal involvement


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