Treatment of CHF Flashcards

1
Q

What are the common causes of acute CHF?

A
  • Acute MI
  • Global Myocardial Ischemia
  • Viral Myocarditis
  • Acute Valvular Regurgitation
  • Arrhythmia (VT/VF)
  • Acute Pericardial Tamponade
  • Massive Pulmonary Embolism
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2
Q

What are common causes of chronic CHF?

A
  • Ischemic Cardiomyopathy
  • Hypertrophic Cardiomyopathy
  • Dilated Cardiomyopathy
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3
Q

What is the most common cause of CHF in the US?

A

Ischemic Cardiomyopathy

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4
Q

What are the treatment objectives in Acute CHF?

A
  • Early recognition
  • Reduce pulmonary congestion
  • Increase CO
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5
Q

What is used to treat pulmonary congestion?

A

Loop diuretics and venodilators (nitroglycerin)

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6
Q

How do diuretics affect pulmonary congestion?

A

Reduces volume which will reduce the preload and the pulmonary venous pressure and pulmonary edema.

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7
Q

Why do diuretics have little effect on CO output on patients with acute CHF?

A

Preload reduction may have little effect because patient in CHF will have a very flat Frank Starling curve making changes in the LVEDP have little impact on the CO

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8
Q

How do nitrates alleviate pulmonary congestion?

A

Venodilation will decrease the venous return to the heart which will lead to the reduction of pulmonary symptoms.

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9
Q

Nisertide MOA

A

hBNP and it activates smooth muscle NPR1 and 2 which raises cGMP causing vasodilation and decreases Na reabsorption in the DT

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10
Q

What are the drugs use to increase inotropy in acute CHF?

A

Beta Adrenergics

Phosphodiesterase Inhibitors

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11
Q

How does nitroprusside increase CO?

A

Reduces afterload

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12
Q

What are the treatment objectives in chronic CHF?

A
  • Prevent ventricular remodeling
  • Reduce pulmonary congestion and edema
  • Increase CO
  • Prolong survival
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13
Q

Digitalis Glycoside MOA

A

Partial inhibition of Na/K ATPase leads to increase [Na] intracellularly which will enhance the Na/Ca exchange, increasing [Ca] in the cell and stored in the SR.

More Ca is release from the SR with each contraction increasing the contractility.

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14
Q

Digitalis Glycoside SE

A
  • Delayed afterdepolarizations (DAD’s) and abnormal automaticity - arrhythmias
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15
Q

Digitalis Glycoside Indications

A

Because of potential for side-effects, digoxin is now primarily used in patients with CHF and Atrial Fibrillation with rapid ventricular response

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16
Q

What is used to reverse digitalis toxicity?

A

Digibind antibodies used to treat life-threatening Digitalis Toxicity

17
Q

What are the vasodilators used for acute CHF?

A
  • Nitroprusside

- Nitroglycerin

18
Q

What are the vasodilators used for chronic CHF?

A
  • ACE Inhibitors
  • Angiotensin II Receptor Blockers
  • Hydralazine
  • Minoxidil
  • Prazosin
19
Q

How do ACE inhibitors improve survival in CHF?

A

Prevent ventricular remodeling

20
Q

What is the MOA of ACE-I in prevention of ventricular remodeling?

A
  • Angiotensin II is a potent cardiomyocyte growth factor (hypertrophy) and fibroblast mitogen (hyperplasia)
  • Inhibition of local RAAS System (autocrine/paracrine
    effects)
  • ACE Inhibitors also reduce systolic and diastolic wall stress, decreasing stretch-induced hypertrophy and remodeling
21
Q

What is LCZ696?

A

Combination of Valsartan (An ARB) and Sacubitril

22
Q

LCZ696 MOA

A
  • Valsartan blocks AT1a receptor on cardiac and vascular smooth muscle.
  • Sacubitril is converted into a neutral endopeptidase inhibitor. Neutral endopeptidases degrade natriuretic peptides, bradykinin, and adrenomedullin. Thus, sacubitril increases the levels of these peptides, causing vasodilation and reduction of ECF volume via sodium excretion.
23
Q

What is “Destination Therapy?”

A

LVADs given to patients who are not candidates for heart transplants and it is used to carry on their life as far as it can go

24
Q

What agents have been proven to improve survival in chronic CHF?

A
  • Carvedilol

- Spironolactone

25
Q

What is cardiac resynchronization therapy?

A

It resynchronizes the contractions of the heart’s ventricles by sending tiny electrical impulses to the heart muscle, which can help the heart pump blood throughout the body more efficiently.

26
Q

What is the rationale for using arteriolar vasodilators to treat acute CHF?

A

Increased C.O. and it will reduce pulmonary capillary wedge pressure

27
Q

How does intravenous nitroglycerin decrease pulmonary edema in acute CHF?

A

Venodilation. Reduced preload will ultimately reduce pulmonary capillary hydrostatic pressure and filtration of fluid across capillary membrane, thus reducing interstitial edema formation.

28
Q

What is the goal of diuretic therapy in acute CHF?

A

Reduce pulmonary congestion and edema

29
Q

Why do inotropic drugs like dobutamine cause an increase in urine output in acute CHF?

A

Increase CO will increase perfusion to the kidneys and hence increase urine output

30
Q

What are the hemodynamic effects of dopamine and how do they differ from the effects of dobutamine?

A

Dopamine will decrease the TPR via D1 receptors and has a splanchnic vasodilatory effect that is protective of the kidneys.

31
Q

How is niseritide beneficial in acute decompensation of chronic congestive heart failure?

A

Induces vasodilatation and natriuresis

32
Q

What is the mechanism by which digoxin increases cardiac contractility?

A

Partial inhibition of Na/K ATPase leads to more Ca2+ in the SR

33
Q

What are the beneficial effects of digoxin on the autonomic nervous system in CHF?

A

Sensitizes baroreceptors
Increases central vagal stimulation
Prolongs AV nodal conduction velocity

34
Q

What is the rationale for using arteriolar vasodilators to treat chronic CHF?

A

Increase CO

35
Q

How does captopril decrease pulmonary edema formation in chronic CHF?

A

Increases urine and Na excretion

36
Q

What agents have been proven to improve survival in chronic CHF?

A

ACE-I
Spironolactone
Beta blockers

37
Q

How would nitroglycerin be beneficial in chronic CHF?

A

Aim of therapy is to increase venous capacitance and reduce venous filling pressure - reduces edema

38
Q

Why are beta-blockers given to patients with chronic CHF?

A
  • Increase survival rate and prevent deterioration of LV

performance over time in patients with mild-moderate chronic CHF