Cardiovascular Flashcards

1
Q

What is angina?

A

a supply/demand problem (suppl of blood to myocardium is not sufficient to meet the demands)

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2
Q

What is perfusion?

A

blood flow

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3
Q

What are the consequences of angina?

A

decreased myocardial perfusion so decreased metabolite removal and decreased oxygenation

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4
Q

Which drug is often administered for acute angina attacks?

A

Nitroglycerin (usually sublingual for fast acting effect)

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5
Q

What are the methods of administration of nitroglycerin?

A

Sublingual tablets and spray (acute)

transdermal patches and ointment (chronic/prophylactic)

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6
Q

Nitroglycerin mechanism of action?

A

pro drug: enters smooth muscle and converted to nitric oxide
can limit platelet adhesion and aggregation
dilates vessels intrinsically (heart) and extrinsically (peripheral vessels)

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7
Q

Describe the timeframe of nitroglycerin action.

A

2 minutes: starts to work
4 minutes: PEAK
10 minutes: max effect
30-60 minutes: duration

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8
Q

Nitroglycerin side effects?

A

flushing, headache, dizziness, reflex tachy

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9
Q

What should be done to reduce side effects of nitroglycerin?

A

Pt should be seated to reduce pooling of blood to the legs which causes side effects.
When seated, the venous dilatation in the legs causes a decrease in blood pressure.

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10
Q

What is the max dose of nitroglycerin for an acute attack?

A

3 tabs (distributed one at a time at 5 minute intervals)

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11
Q

What if 3 nitroglycerin tabs don’t work?

A

Patient is probably having an MI (or the tabs have expired/deteriorated)

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12
Q

What is mechanism of action of beta adrenergic blockers?

A

decrease myocardial oxygen consumption by reducing myocardial contractility, HR, and BP

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13
Q

Why avoid sudden withdrawal of beta adrenergic blockers (especially with angina or post-MI therapy)?

A

risk for acute MI and sudden death

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14
Q

What is mechanism of action of Ca Channel blockers?

A

dilate systemic arteries and main coronary arteries; heart pumps against less resistance; decreases myocardial oxygen consumption

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15
Q

Ca Channel blockers (especially verapamil) may cause what changes?

A

decreased heart rate and myocardial contractility

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16
Q

Causes of CHF?

A

ischemic heart disease, HTN, cardiomyopathy, vavular and pericardial disease

17
Q

CHF non-pharmacological interventions?

A

stop smoking, control HTN, dec sodium, moderate exercise, dec stress

18
Q

CHF pharmacological management is “mix and match” including:

A
ace inhibitors (usually first line of therapy)
thiazide loop diuretics, a-adrenergic blockers (B-Blockers), digoxin, hydralazine/isosorbine also used
19
Q

ACE inhibitors have names usually ending in -____.

A

-pril.

20
Q

What is mechanism of action of ACE inhibitors?

A

indirectly dec. aldosterone secretion
inhibits vascular smooth muscle contraction
VASODILATION
dec. peripheral resistance

21
Q

Side effects of ACE inhibitors?

A

cough, decreased/loss of taste perception, hypotension, potassium retention

22
Q

Angiotensin II Receptor Antagonists mechanism of action?

A

VASODILATION

increased sodium and water excretion

23
Q

Diuretic Classes (3)

A

thiazides
loop diuretics (lasix)
potassium-sparing diuretics

24
Q

Effect of diuretics?

A

control excessive fluid and edema, dec. workload on the heart

25
Q

Diuretics and CHF?

A

Used in combination for CHF: inc. effects and safety of ACEIs and Beta Blockers (but diuretics should not be used alone for CHF)

26
Q

Digoxin (Lanoxin) mechanism of action?

A

positive inotropic effect (increase strength of muscular contractions)

27
Q

Digoxin (Lanoxin) side effects?

A

side effects/adverse effects with toxicity can be FATAL: cardiac arrhythmia, CNS (mental status change, disorientation, blurred vision)

28
Q

What patients is Digoxin (Lanoxin) best for?

A

pts with abnormal contractility (often atrial flutter/fibrillation) or rapid ventricular rate

29
Q

What is usual dose of Digoxin (Lanoxin)?

A

0.125 mg

remember, toxicity is a huge problem ~25% of patients experience signs of toxicity

30
Q

Digoxin (Lanoxin) drug interactions?

A

diuretics - due to hypokalemia - directly increases risk of toxicity

31
Q

Vasodilator that has direct effect on smooth muscles of arterioles but no effect on veins:

A

Hydralazine (often used in combination with a diuretic and/or B-Blocker)

32
Q

What is the effect of B-blockers to notice with exercise?

A

muted cardiovascular response