Cardiac meds

Question 1

cardiac glycosides/inotropic meds:
(digoxin)

Answer 1

tx of HF-not seen as often but still occasionally used, especially when associated with low cardiac output used to improve cardiac contractility

Question 2

ACE-I/ARBs

Answer 2

decrease afterload and improve myocardial contractility
(ACE-I side effect is hyperkalemia; most common side effect= cough)

Question 3

Diuretics

Answer 3

loop, thiazide

Question 4

Vasodilators

Answer 4

decrease afterload and improve contractility

Question 5

Morphine

Answer 5

decrease afterload, decreases preload, dilates coronary vessels

Question 6

Human B-type natriuretic peptides

Answer 6

vasodilates

Question 7

beta adrenergic blockers

Answer 7

decrease myocardial oxygen demand

Question 8

CCB

Answer 8

• Generally CCB should not be used in HF with decreased ejection fraction. 1st generation (diltiazem, verapamil) worsens outcomes.
• CCB are categorized by chemical structure: nondihydropyridines vs dihydropyridines
• Pharm interactions: Vitamin D may interfere with CCB. Inform pt to talk with HCP about taking vitamin D if started on CCB

Question 9

CCB nondihydropyridines

Answer 9

(ex. diltiazem {cardizem}, verapamil {Calan})
- are more myocardial selective and tend to decrease heart rate
- are contraindicated because of the possibility of causing bradycardia and worsening cardiac output

Question 10

CCB dihydropyridines

Answer 10

(ex. amlodipine, felodipine, nicardipine, nifedipine)
- more vascular selective so therefore may be utilized as secondary treatment option
- if CCB are used, they are used as secondary treatment options- relax blood vessels and increase oxygen and blood supply to the heart while decreasing workload (ex. amlodipine {Norvasc}, nifedipine {Procardia, Adalat})

Question 11

Suffixes, such as -pril

Answer 11

ACE inhibitors

Question 12

Suffixes, such as -sartan

Answer 12

ARBs

Question 13

Antihypertensives may act by blocking the renin-angiotensin-aldosterone system (RAAS), by blocking the sympathetic nervous system (SNS), or by causing vasodilation. Understanding the mechanism of action helps to determine possible adverse effects and contraindications.

Question 14

ACE inhibitors and ARBs block the RAAS. This lowers blood pressure and protects renal function, but it increases the risk for hyperkalemia as well as hypotension. Angioedema is a serious adverse effect.

Question 15

Beta-blockers, alpha-1 adrenergic receptor blockers, and centrally-acting alpha adrenergics all block the SNS but in different locations. Monitoring the pulse is necessary for both beta-blockers and centrally-acting alpha adrenergics. Blocking the SNS also results in lowered blood glucose and a masking of the symptoms of hypoglycemia.

Question 16

Calcium channel blockers and direct-acting vasodilators work by causing vasodilation. However, peripheral edema may be an adverse effect.

Question 17