Deja review Cardio/Renal agents - Congestive heart failure agents Flashcards

1
Q

What is the cardiac output equation?

A

Cardiac output (CO) = heart rate (HR) X stroke volume (SV)

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2
Q

What is normal CO?

A

5L/min

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3
Q

What is the most common course of right sided heart failure?

A

Left sided heart failure

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4
Q

Name 3 compensatory physiological responses seen in CHF

A

1) Fluid retention
2) INC sympathetic drive
3) Hypertrophy of cardiac muscle

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5
Q

Define preload

A

The pressure stretching the ventricular walls at the onset of ventricular contraction, related to left ventricular end-diastolic volume pressure

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6
Q

Define afterload

A

The load or force developed by the ventricle during systole

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7
Q

What drugs are used to DEC preload?

A

Diuretics, vasodilators, angiotensin-converting enzyme inhibitors (ACEIs), angiotensin II receptor blockers (ARBs), nitrates

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8
Q

What drugs are used to DEC afterload?

A

Vasodilators, ACEIs, ARBs, hydralazine

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9
Q

What drugs are used to INC contractility?

A

Digoxin, phosphodiesterase inhibitors (amrinone and milrinone), ß-adrenoceptor agonists

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10
Q

What is MOA of digoxin?

A

Inhibition of the Na+/K+-ATPase pump which leads to positive inotropic action (via INC intracellular sodium ions that exchanges with extracellular calcium ions, resulting INC in intracellular calcium ions leads to INC force of contraction

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11
Q

What are the 2 digitalis glycosides?

A

1) Digoxin

2) Digitoxin

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12
Q

What are the adverse effects of digoxin?

A

Arrhythmias, nausea, vomiting, anorexia, headache, confusion, blurred vision, visual disturbances, such as yellow halos around light sources

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13
Q

What electrolyte disturbances predispose to digoxin toxicity?

A

Hypokalemia, hypomagnesemia, hypercalcemia

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14
Q

Digoxin can cause what types of arrhythmias?

A

Supraventricular tachycarias, AV nodal tachycardias, AV block, ventricular tachycardias, ventricular fibrillation, complete heart block

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15
Q

Can digoxin be used in WPW (wolf-parkinson-white) syndrome?

A

Np. Since digoxin slows conduction thru the AV node, the necessary pathway present in WPW is left unopposed, leading to supraventricular tachycardias and atrial arrhythmias

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16
Q

How is digoxin toxicity treated?

A

Correction of electrolyte disturbances, antiarrhythmics, anti-digoxin Fab antibody (Digibind)

17
Q

What drugs can INC digoxin concentrations?

A

Quinidine, amiodarone, erythromycin, verapamil

18
Q

What drugs can DEC digoxin concentrations?

A

Loop diuretics, thiazide diuretics, corticosteroids

19
Q

Dpes digoxin therapy in CHF lead to prolonged survival?

A

No, it is of symptomatic benefit only, improving quality, but not necessarily duration of life

20
Q

What classes of medications have been shown to INC survival in CHF patients?

A

ACEs, ARBs, ß-blockers

21
Q

How does dobutamine work in CHF?

A

ß-adrenergic agonist (sympathomimetic that binds to (ß1 adrenoceptors) that INC force of contraction and vasodilation via INC cAMP

22
Q

How do amrinone and milrinone work in CHF?

A

Inhibits phosphodiesterase (PDE) thus INC cAMP levels, INC cAMP leads to INC intracellular calcium, INC intracellular calcium leads to INC force of contraction, INC cAMP also leads to INC vasodilation

23
Q

What are the side effects of PDEIs?

A

Milrinone may actually DEC survival in CHF, amrinone may cause thrombocytopenia

24
Q

How do diuretics work in CHF?

A

DEC in intravascular volume, thus DEC in preload, reduce pulmonary and peripheral edema often seen in CHF patients

25
Q

How can INC sympathetic activity in CHF be counteracted?

A

ß-blockers

26
Q

What 2 ß-blockers have specific indications for the treatment of CHF?

A

1) Metoprolol

2) Carvedilol (mixed α-/ß blocker)

27
Q

What is the MOA of nesiritide?

A

Recombinant B-type natriuretic peptide that binds to guanylate cyclase receptors on vascular smooth muscle and endothelial cells, thus INC cyclic guanosine monophosphate (cGMP) evels; INC cGMP leads to INC relaxation of vascular smooth muscle

28
Q

How do ACEIs work in CHF?

A

Inhibition of angiotensin-II (AT-II) production thus DEC total peripheral resistance (TPR) and thus afterload prevents left ventricular remodeling