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74 Cards in this Set

  • Front
  • Back
drug of choice for HF
ACE inhibitors

block enzyme that cleaves angiotensin I to form the potent vasoconstrictor angiotensin II

also diminish the rate of bradykinin inativation (bradykinin is a vasodilator)

also decrease the secretion of aldosterone, resulting in decreased sodium and water retention

also decrease output of sympathetic nervous system

(vasodilation of vascular smooth muscles)
pharm-kinetics for ACE inhibitors
orally administered

take on an empty stomach

these are prodrugs (except for captopril) that require activation of hydrolysis via hepatic enzymes

renal elimination is key
Adverse effects of ACE inhibitors
postural hypotension, renal insufficiency, hyperkalemia, angioedema, and a persistent dry cough

do NOT use in pregnant women
angiotensin receptor blockers
orally active compounds

extremely potent competitive antagonists of the angiotensin type 1 receptor
ARBs action on CV system
treatment of hypertension based on clinical efficacy in lowering BP and reducing morbidiy and mortality

(can be used as a substitute for ACE inhibitors in those patients with severe cough or angioedema)
Pharmacokinetics of ARBs
orally active and require once a day dosing

Losartan: different in that it undergoes extensive first pass hepatic metabolism, including conversion to an active metabolite

other drugs have inactive metabolites

elimination of metabolites occurs in the urine and feces

have large volume of distributions

(ARBs are contraindicated in pregnancy)
Beta blockers
may seem counterintuitive to give in HF, BUT has shown improved systolic functioning and reverse cardiac remodeling in patients receiving beta-blockers

has an ability to prevent the changes that occur because of the chronic activation of the sympathetic nervous system, including decreasing the heart rate and inhibiting the release of renin
nonselective beta-adrenoreceptor antagonist

also blocks alpha adrenoreceptors
longer acting

Beta-1 selective antagonist

shown to reduce mortality in patients with heart failure
Use loop diuretics...
when patients require extensive diuresis and those with renal insufficiency

overdoses of loop diuretics can lead to profound hypovolemia
Calcium channel blockers should be avoided in patients with CHF
if patient is intolerant of ACE inhibitors or beta-blockers, the combination of hydralazine and isosorbide dinitrate is most commonly used

positive inotropic agents

result of an increased cytoplasmic calcium concentration that enhances the contractility of cardiac muscle

influence the sodium and calcium ion flows in cardiac muscle, thereby increasing contraction of the atrial and ventricular myocardium (positive inotropic action)

have a low therapeutic index (small difference between a therapeutically effective dose and doses that are toxic or even fatal)
Digoxin and the Na/Ca pump
by inhibiting the ability of the myocyte to actively pump Na from the cell, cardiac glycosides decrease the Na concentration gradient, and consequently the ability of the Na/Ca exchanger to move calcium out of the cell

more Ca is retained intracellulary, a small increase occurs in the free Ca that is available at next contraction cycle of the cardiac muscle

(increase in contractility leads to a decrease in EDV...thus increasing the efficiency of contraction)
Therapeutic uses of digoxin
indicated in patients with severe left-ventricular systolic dysfunction after initiation of diuretic, ACE inhibitor, and beta-blocker therapy

not indicated in patients with RHF
stimulates Beta 1 and beta 2
Pharmacokinetics of digoxin
relatively short half life, allows better treatment of toxic reactions

more rapid onset of action, making it useful in emergency situations

eliminated largely unchanged in the urine

extensively metabolized by the liver before excretion in the feces, and patients with hepatic diseases may require a decreased dose
Digitalis toxicity
most commonly encountered adverse drug reactions

must determine serum potassium levels first...

in general, decreased serum levels of potassium predispose a patient to digoxin toxicity

levels must be closely looked at in presence of renal insufficiency

severe toxicity resulting in ventricular tachycardia may require administration of antiarrhythmic drugs and the use of antibodies to digoxin
Cardian adverse reactions with digitalis
1. Cardiac effects: more severe dysrhythmia...moving from decreased or blocked AV nodal conduction to paroxysmal VT, to conversion of Atrial flutter to atrial fibrillation, premature ventr. depolarization, VF and finally complete heart block

a decrease in intracellular potassium is the primary predisposing factor in these effects
CNS adverse reactions with digitalis
headache, fatigue, confusion, blurred vision, alteration of color perception, and halos on dark objects...
Predisposing to digitalis toxicity
hypokalemia can precipitate serious arrhythmia (most observed in patients using thiazide or loop diuretics...can be prevented using k-sparing diuretics)

hypercalcemia also predispose to digitalis toxicity
Drugs that stimulate digitalis toxicity
quinidine, verapamil, and amiodarone can cause digoxin displacing digoxin from tissue protein binding sites and by competing with digoxin for renal excretion
Dobutamine is the...
most commonly used inotropic agent other than digitalis

leads to an increase in intracellular cAMP which results in the activation of protein kinase...when slow calcium channels are phosphorylated, the entry of calcium into the myocardial cells increases, thus enhancing contraction

dobutamine must be given by IV infusion and is primarly used in the treatment of acute HF
direct antagonist of aldosterone, thereby preventint salt retention, myocardial hypertrophy, and hypokalemia

should be reserved for the most advanced cases of HF

promotes potassium retenion, therefore patients should not be taking potassium supplements

adverse side effects: gastric disturbances, CNS effects (lethargy, confusion) and endocrine abnormalities (decreased libido)

does not treat acute pulmonary edema
Primary drugs for Positive chronotropic/dromotropic agents
Secondary drugs for positive chronotropic/dromotropic drugs
calcium cholride

isoproterenol (beta agonist)

Primary drugs for positive inotropic effects

dopamine (alpha 1, beta 1, and beta 2 agonist)


Secondary drugs for positive inotropic effects
propranolol (for ASH, IHSS)

dobutamine (beta agonist)

milrinone (a PDE inhibitor that increases the intracellular concentration of cAMP)
Primary drugs for afterload reducing agents (vasodilators)





(secondary: enalapril)
Primary preload reducing agents
Primary drugs to inhibit inappropriate proliferation/remodeling



(can also use other beta blockers and losartan)
conduction velocity
if we have low preload
we increase volume
if the HR is too slow

(chronotropic, dromotropic)
we use: atropine, isoproterenol, and a pacemaker
If the HR is too fast or disorganized we use...
cardioversion or antiarrhythmic drugs
If we have a diminished inotropic state we use...
epinephrine, dopamine, dobutamine, amrinone, calcium, glucagon, digoxin, carvedilol, correct acid/base, correct hypoxemia
If we have pathologic peripheral vasoconstriction we use...
(captopril), enalapril, lisinopril, hydralazine, prazosin, carvedilol, nitroglycerin, or nitroprusside
If we have excessive, abnormal contractility (diastolic dysfunction) we use...
propranolol, verapamil
blocks muscarinic receptors

acts both centrally and peripherally

at low doses: decreases HR (bradycardia)

higher doses: the M2 receptors on the SA node are blocked and the cardiac rate increases modestly

drug can also block the effects of excess acetylcholine resulting from acetylcholinesterase inhibitors

also used as an antispasmodic agent to relax the GI tract and bladder
direct acting synthetic catecholamine that predominantly stimulates both Beta 1 and beta 2 adrenergic receptors

its non-selectivity is one of its drawbacks

Beta receptors in SA node, AV node, ventricles

beta receptors in bronchioles...
prototypical drug producing mixed alpha 1, beta 1 and beta 2 effects
epinephrine...CV effects
strengthens contractility of the myocardium and increases its rate of contraction

constricts arterioles in the skin, mucous membranes, and viscera (alpha effects) and dilates vessels going to the liver and skeletal muscle (beta 2 effects)

cumulative effect: increase in systolic BP coupled with slight decrease in diastolic pressure)

use during cardiac arrest with asystole

fine ventricular fibrillation

use after open heart surgery
Epinephrine...respiratory effects
powerful bronchodilation by acting directly on bronchial smooth muscle (beta 2)

use in the case of anaphylactic shock (drug of choice)
Drug class of Dopamine
adrenergic receptor and dopaminergic receptor agonist
Therapeutic class of dopamine
inotropic agent and vasopressor
Pharmacodynamics of dopamine
stimulates dopaminergic, beta-1 adrenergic, and alpha 1 adrenergic receptors

these receptors respond to different concentrations, achieved by different rates of infusion...increase levels of cAMP within cells
Pharmacokinetics of dopamine
not given by mouth

onset after IV administration in several minutes

almost entirely metabolized in the liver, kidneys, and plasma (MAO) to inactive metabolites

half life is brief (minutes)

Toxicity of dopamine
ectopy (disturbance of the electrical conductance of the heart), tachycardia, angina, nausea, vomiting
Interactions of dopamine with other drugs
monoamine oxidase inhibitors may prolong and intensify the effects of dopamine

obvious interactions with alpha and beta blockers
Special considerations with dopamine
correct hypovolemia

if present, administer through large vein

prevent extravasation

monitor patient closely
Dose/route for dopamine
low to higher doses: adjunct in shock to increase CO, BP, and urine flow

for short term treatment of severe, refractory, chronic congestive heart failure (use lower dose)
Drug class of Amrinone
bipyridine derivative administered as an inotropic agent and vasodilator
Pharmacodynamics of amrinone
primary vasodilating effects on peripheral arteries

mech not clear (book says PDE inhibitor...possible increases in cAMP leading to more Ca)
Pharmacokinetics of amrinone
IV administration only

onset of action in 2-5 minutes

effects persist for several hours

metabolized in the liver to products of unknown activity

also excreted in the urine with a terminal half life of 4 hours
Precations and adverse drug reactions of amrinone
known allergy to amrinone or sulfites (preservative)

valvular disease, hypertrophic cardiomyopathy

patients with acute MI (may cause arrhythmia)

If amrinone is used with ____ it may cause hypotension
Special considerations with amrinone
do not mix with furosemide

monitor platelet counts and patient closely

fourth line drug after digoxin, diuretics, and vasodilators
Indications and dose/route for amrinone
used for the short term management of CHF...given as an IV loading dose over 2-3 minutes, then a continuous infusion
Lisinopril names
Prinivil, captopril, enalapril, ramipril
Pharm class of Lisinopril
ACE inhibitor
Therapeutic class of Lisinopril
antihypertensive, treatment of CHF, preserving renal function, preserving LV function after MI, acute management of MI
Pharmacodynamics of Lisinopril
inhibits the conversion of AT I to AT II by ACE

diminishes both vasoconstriction and stimulation of aldosterone secretion by AT II
Pharmacokinetics of Lisinopril
well absorbed

onset 1 hour

peak 6 hours

duration 24 hours

given once a day is fine

excreted primarly in the urine as and unchanged drug
Toxicity of lisinopril
orthostatic hypotension

use with caution in patients with impaired renal function or renal artery stenosis

be careful in patients on diuretics or those with aortic stenosis


acute renal failure
Interactions of Lisinopril with other drugs
additive effects with most other antihypertensives

NSAIDs may reduce ability to lower BP

hypercalemia with KCL
Special considerations of lisinopril
often discontinue diuretics prior to beginning use to reduce hypotension

category C/D pregnancy

abnormal cartilage development

(monitor: BP, weight, edema, K, BUN, creatinine, and cough)
Use of vasodilators to improve CHF (afterload reduction)
1. lisinopril (biggest study with Ramipril)

2. Hydralazing (direct acting vasodilator)

3. Prazosin (vasodilator by alpha 1 adrenoceptor antagonist)

4. Nitroprusside

5. in general, pure vasodilators (hydralazine and nitroprusside) have NOT been shown to improve patient survival
vasodilator by alpha 1 adrenergeric antagonist
Preload reducing agents
loop diuretics (furosemide, torsemide, bumetanide)

thiazide diuretics (hydrochlorothiazide)

other diuretics (spironolactone)
Some neurohumoral responses may work well in the short run to increase CO, but are harmful in the long run...
salt and water retention

sympathetic mediated vasoconstriction

cardiac stimulation
some vasodilators can improve survival...
ACE inhibitors, hydralazine/TNG
Can worsen remodeling...
beta-receptor stimulation


Aldosterone...why we have a benefit from such drugs as beta blockers, ACE inhibitors, and spironolactone
Benefit of beta blockers
annual mortality dropped from 12% down to 8%

Benefit of ACE inhibitors
enalapril and AT receptor blockers (losartan)
Benefit of spironolactone
30% relative decrease in mortality

30% lower rate of hospitalizations

when added to ACE inhibitor, loop diuretic, and digoxin