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
What is cardiac resynchronization therapy?
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
What is the rationale for using arteriolar vasodilators to treat acute CHF?
Increased C.O. and it will reduce pulmonary capillary wedge pressure
27
How does intravenous nitroglycerin decrease pulmonary edema in acute CHF?
Venodilation. Reduced preload will ultimately reduce pulmonary capillary hydrostatic pressure and filtration of fluid across capillary membrane, thus reducing interstitial edema formation.
28
What is the goal of diuretic therapy in acute CHF?
Reduce pulmonary congestion and edema
29
Why do inotropic drugs like dobutamine cause an increase in urine output in acute CHF?
Increase CO will increase perfusion to the kidneys and hence increase urine output
30
What are the hemodynamic effects of dopamine and how do they differ from the effects of dobutamine?
Dopamine will decrease the TPR via D1 receptors and has a splanchnic vasodilatory effect that is protective of the kidneys.
31
How is niseritide beneficial in acute decompensation of chronic congestive heart failure?
Induces vasodilatation and natriuresis
32
What is the mechanism by which digoxin increases cardiac contractility?
Partial inhibition of Na/K ATPase leads to more Ca2+ in the SR
33
What are the beneficial effects of digoxin on the autonomic nervous system in CHF?
Sensitizes baroreceptors Increases central vagal stimulation Prolongs AV nodal conduction velocity
34
What is the rationale for using arteriolar vasodilators to treat chronic CHF?
Increase CO
35
How does captopril decrease pulmonary edema formation in chronic CHF?
Increases urine and Na excretion
36
What agents have been proven to improve survival in chronic CHF?
ACE-I Spironolactone Beta blockers
37
How would nitroglycerin be beneficial in chronic CHF?
Aim of therapy is to increase venous capacitance and reduce venous filling pressure - reduces edema
38
Why are beta-blockers given to patients with chronic CHF?
- Increase survival rate and prevent deterioration of LV | performance over time in patients with mild-moderate chronic CHF