CPVR Unit I Flashcards

(25 cards)

1
Q

HfrEF Rx

A

NYHA Class I-IV Stage C: ACEI/ ARB and Beta-blocker
For all volume overload, NYHA Class II-IV: add loop diuretics.
For symptomatic AA Class III-IV: add hydral-nitrates.
For Class II-IV with >30ml/min creatine and <5mEq/dL K+, add aldosterone antagonist.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Vasodilators

A

Hydralazine: arterial vasodilation (po TID/ QID, SLE and headache)
Isosorbide Dinitrate: venous dilation (TID, hypotension, headache, and dizziness)
Improved EF, but ACEI better in reducing mortality, unless in AA receiving BB, ACEI, and Aldosterone antagonist.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ACEI and Dosing

A

Block ACE and Kinase II. Reduced mortality and hospitalizations. Recommended to reduce morbidity and mortality unless contraindicated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Angiotensin II

A

Increase arteriolar constriction, CO, Na Resorption, Na and H2O retention, ADH, and thirst.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ACEI Patient Considerations

A

Side effects: cough, hyperkalemia, angiedema, renal dysfunction, neutropenia, hypotension.
Monitoring: Chemistry-7 with MG and Ca and BP once every 2 weeks x 1 month, then monthly; CBC once a month.
DDI: Lithium, NSAIDS, Salt Substitutes, Loop diuretics, K+sparing diuretics.
Contraindications: Pregnancy, bilateral renal artery stenosis, renal failure, angioedema, hyperkalemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ARBs (Angiotensin Receptor Blockers)

A

Dosing: Candesartant work.

Indicated when patient is intolerant to ACEI.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ARBs Patient Consideration

A

Similar to ACEI, but without the cough.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Beta-receptors Biological Response

A

Cardiac myocyte growth, positive inotropic and chronotropic response, and if overstimulated myocyte toxicity and apoptosis. Too much stimulation = increase in NE= decrease in survival.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Benefits of Beta-Blocker

A

Prevent downregulation of B1 receptors, apoptosis/oxidative stress, increased arrhythmia potential, hypertrophy/fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Classes of Beta-Blocker

A

First generation: non-selective for B1 and B2 blockade, no ancillary properties (pro and tim)
Second: Selective for B1 and B2 blockade, no ancillary properties (met, as, bis)
Third: Selective or non-selective with ancillary (car and nep) properties.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Appropriate Patients for Therapy

A

Mild to severe symptoms of HF, LVEF <40%, receiving Rx with ACEI and diuretic, any age and either sex, CAD or nonischemic dilated cardiomyopathy. Diabetic and Non-Diabetic. COPD without reactive airway disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Neprilysin (LCZ696)

A

Action similar to Kinase II. Inhibits neprilysin from breaking down natriuretic peptides. Even better than ACEI.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

HFpEF Rx

A

Can Tx HTN with BB, ACEI, and ARBs. ARBs might be considered to decrease hospitalizations in HFpEF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Digoxin Patient Considerations

A

Sinus rhythm or atrial fibrillation with HF despite ACEI, ARBs, BB,and diuretics. Patients who have symptoms of HF!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Digoxin

A

Beneficial in pts with HFrEF, unless contraindicated, to decrease hospitalizations for HF. No role in HFpEF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Inotropic Therapy

A

Dobutamine: B1 agonist to increase contractility, slight peripheral vasodilation.
Milronone: PDE inhibitor, augments myocyte Ca2+ utilization,moderate peripheral vasodilation.
Indications: ADHF short-term management- Cold and Wet. To relieve symptoms and end-organ function, <90 systolic pressue, symptomatic hypotension despite adequate filling pressures, unresponsive to, or intolerant of intravenous dilators.

17
Q

Dopamine

A

endogenous precursor of NE- exerts its effect by directly stimulating adrenergic receptors, as well as, release noepi from nerve terminals.

18
Q

Aortic Stenosis

A

Crescendo-descrendo systolic ejection murmur. LV&raquo_space; aortic pressure during systole. Loudest at hear base; radiates to carotids. Pulsus parvus et tardus. Syncope, angina, and dyspnea on exertion.

19
Q

MR/TR

A

Holosystolic, high-pitched “blowing murmur”. Mitral- loudestat apex and radiates towards axilla. MR is often due to ischemic heart disease, LV dilatation.

20
Q

Mitral Valve Prolapse

A

Late systolic crescendo murmur with midsystolic click (due to sudden tensing of chordae tendinae). Loudest just before S2. Usually benign. Can be caused by myxomatous degeneration.

21
Q

Ventricular Septal Defect

A

Holosystolic, harsh sounding murmur. Loudest at tricuspid area.

22
Q

Aortic Regurgitation

A

High-pitched blowing early diastolic descrendo murmur. Long dyastolic murmur and signs of hyperdynamic pulse. when severe and chronic. Aortic root dilation, bicuspid, endocarditis, RF. Progresses to HF.

23
Q

Mitral Stenosis

A

Follows opening snap. Delayed rumbling late diastolic murmur. LA&raquo_space; LV pressure. Can lead to LA dilatation.

24
Q

Loop Diuretics

A

Furosemide, torsemide, bumetanide (High loops). Thiazide (low loops). Acts on ascending limb (K+ wasting), Inhibits NaCl transport. po/iv if congested. High loops 25-30% of filtered Na+ reabsorbed. Use spironolactone to enhance diuresis and ameliorate potassium wasting. Hyperuricemia. Sulfa allergy.

25
Aldosterone Antagonists
Spironolactone (also a hormone receptor) and eplerone. Use because ACEI/ ARB aldosterone block is incomplete.