module 6 Flashcards
Heart Failure Drugs
The heart is unable to pump blood in sufficient amounts from the ventricles to meet the body’s metabolic needs Symptoms depend on the cardiac area affected Systolic dysfunction Diastolic dysfunction • Less common
Heart Failure: Causes
Cardiac defect Myocardial infarction Valve deficiency Defect outside the heart Coronary artery disease Pulmonary hypertension Diabetes Supraventricular dysrhythmias Atrial fibrillation Atrial flutter
Drug Therapy for Heart Failure
Positive inotropic drugs Increase the force of myocardial contraction Positive chronotropic drugs Increase heart rate Positive dromotropic drugs Accelerate cardiac conduction Used to treat heart muscle failure
Drug Therapy for Heart Failure
ACE inhibitors Angiotensin II receptor blockers B-type natriuretic peptides Phosphodiesterase inhibitors Cardiac glycosides
ACE inhibitors
end in pril
Prevent sodium and water resorption by
inhibiting aldosterone secretion
Diuresis results, which decreases preload, or
the left ventricular end-volume, and the work
of the heart
Examples: lisinopril, enalapril, captopril
lisinopril(Prinivil, Zestril) (C in women in 1st trimester; D in 2nd & 3rd can cause fetal death in these trimesters)
Ace inhibitor; used for HTN, HF & acute MI;
Hyperkalemia ma occur with any ACE inhibitor & K+ supplmentaion or K+ sparing diuretics need to be used with caution. SE-dry cough & possible decreased renal function
enalapril,
Hyperkalemia ma occur with any ACE inhibitor & K+ supplmentaion or K+ sparing diuretics need to be used with caution. SE-dry cough & possible decreased renal function
captopril
Hyperkalemia ma occur with any ACE inhibitor & K+ supplmentaion or K+ sparing diuretics need to be used with caution. SE-dry cough & possible decreased renal function
Angiotensin II Receptor Blockers(ARB)
end in artan
Potent vasodilators; decrease systemic
vascular resistance (afterload)
Examples: valsartan, candesartan, losartan
valsartan(Diovan) (D)
ARBS are potent vasodilators; used alone or in combo with other drugs such as diuretics in tx of HTN & HF.Most commonly used; Less likely to cause cough or hyperkalemia
candesartan(Atacand)(D)
ARBS are potent vasodilators; used alone or in combo with other drugs such as diuretics in tx of HTN & HFMost commonly used; Less likely to cause cough or hyperkalemia
losartan(Cozaar) (D)
ARBS are potent vasodilators; used alone or in combo with other drugs such as diuretics in tx of HTN & HFMost commonly used; Less likely to cause cough or hyperkalemia
B-type Natiuretic Peptides
nesiritide (Natrecor)
Used in se ere life threatening heart fail re
severe, life-failure
B-type Natiuretic Peptides:
Mechanism of Action
Vasodilating effects on arteries and veins
Indirectly increases cardiac output
Suppresses renin-angiotensin system
Diuresis
Phosphodiesterase Inhibitors
Work by inhibiting the enzyme phosphodiesterase Results in: Positive inotropic response Vasodilation Two drugs (inodilators) Inamrinone and milrinone
Inamrinone
Phosphodiesterase Inhibitors,Work by inhibiting the enzyme phosphodiesterase
Results in:
Positive inotropic response
Vasodilation(inodilators)
milrinone
Phosphodiesterase Inhibitors,Work by inhibiting the enzyme phosphodiesterase
Results in:
Positive inotropic response
Vasodilation(inodilators)
Phosphodiesterase Inhibitors:
Indications
Short-term management of heart failure
Given when patient does not respond to treatment with digoxin, diuretics, and/or vasodilators
AHA and ACC advise against weekly infusions
No improvement of clinical status
Phosphodiesterase Inhibitors:
Adverse Effects
*inamrinone Thrombocytopenia Dysrhythmia, nausea, hypotension Elevated liver enzymes with long-term use * milrinone Dysrhythmia, mainly ventricular Hypotension, angina, hypokalemia, tremor, thrombocytopenia
Cardiac Glycosides
No longer used as first-line treatment
Originally obtained from Digitalis plant,
foxglove
Digoxin
Used in heart failure and to control ventricular
response to atrial fibrillation or flutter
Cardiac Glycosides:
Mechanism of Action
Increase myocardial contractility Change electrical conduction properties of the heart Decrease rate of electrical conduction Prolong the refractory period • Area between SA node and AV node
Cardiac Glycosides:
Drug Effects
Positive inotropic effect
Increased force and velocity of myocardial contraction
Negative chronotropic effect
Reduced heart rate
Negative dromotropic effect
Decreased automaticity at SA node, decreased AV nodal
conduction
Cardiac Glycosides:
Drug Effects
Increased stroke volume
Reduction in heart size during diastole
Decrease in venous BP and vein engorgement
Increase in coronary circulation
Promotion of diuresis due to improved blood circulation
decreased exertional and paroxysmal nocturnal dyspnea, cough, and cyanosis
Cardiac Glycosides:
Indications
Heart failure
Supraventricular dysrhythmias
Atrial fibrillation and atrial flutter
