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Heart Pharm > Treatments of Congestive Heart Failure > Flashcards

Treatments of Congestive Heart Failure Flashcards

1
Q

What are 7 causes of ACUTE congestive heart failure?

A
  1. Acute myocardial infarction
  2. Global Myocardial Ischemia
  3. Acute viral myocarditis
  4. Acute Valvular Regurgitation
  5. Arrhythmias
  6. Acute pericardial tamponade
  7. Massive Pulmonary Embolism
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2
Q

What are 3 common causes of CHRONIC congestive heart failure?

A
  1. Ischemic Cardiomyopathy
  2. Hypertrophic cardiomyopathy
  3. Dilated Cardiomyopathy
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3
Q

How do you treat acute CHF?

A
  1. Reduce Pulmonary congestion
    a. loop diuretic
    b. venodilators (nitroglycerine)
    c. Nesiritide
  2. Increase cardiac output
    a. increase contractility
    - Beta agonists and phosphodiesterase inhibitors
    b. reduce afterload
    - nitroprusside
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4
Q

Nesiritide

A

Human Recombinant brain natriuretic peptide

  • raises cGMP levels in VSMC-vasodilation
  • decreases Na reabsorption in the distal tubule

vasodilation & natriuresis

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5
Q

What are inotropic agents used to treat acute CHF?

A
  1. beta adrenergic agonists
    - isoproterenol-B agonist-Tachy
  • dopamine-D,B1,Alpha
  • low dose=lowBP
  • high dose=ischemia
  • dobutamine-B1 agonist
  • norepinephrine-no B2
  1. Phosphodiesterase Inhibitors
    - Inamrinone aka Amrinone
    - Milrinone
    * inhibit degradation of cAMP-used when beta receptors have been down regulated
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6
Q

What do arteriolar vasodilators like nitroprusside do?

A

-increase cardiac output by reducing afterload

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7
Q

Why are Ca channel blockers contraindicated in CHF even though they are potent vasodilators?

A

Negative inotropic effects

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8
Q

What are some non pharmacological therapies for acute CHF?

A
  1. PCI/Surgical therapy
    - acute revascularization
    - urgent valve repair/replacement
  2. ultrafiltration
  3. intra-aortic balloon pump
  4. ventricular assist devices
    - Impella percutaneous LVAD
    - Implantable LVAD
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9
Q

What are the treatment objectives in chronic CHF?

A
  1. Early recognition of ventricular dysfunction even in the ABSENCE of symptoms
  2. Prevent ventricular Remodeling
    a. ACEi/ARB’s/LCZ969
    b. Beta Blockers
    c. Aldosterone Antagonists

Decrease Symptoms

  1. reduce pulmonary congestion and edema formation
    a. Thiazides, Loop Diuretics, Aldosterone Antagonists
    b. Venodilators
    - ACE inhibitors, ARBs, Nitrates
  2. Increase Cardiac Output
    a. increase contractility
    - Digitalis
    b. Reduce Afterload
    - ACEi, ARBs, hydralazine
  3. Prolong survival
    a. ACEi
    b. Nitrates+hydrazines
    c. Beta Blockers
    - carvedilol, metoprolol
    d. Aldosterone antagonists
    - spironolactone, eplerenone
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10
Q

MOA Digitalis

A
  1. Partial inhibition of Na/K ATPase pump
  2. Increased NA leads to extrusion of Na out of cell and Ca into cell via Na/Ca exchanger (reverse mode Na/Ca exchanger)
  3. Increased Ca in SR
  4. increase Ca released from SR stores during each contraction
  • ->increased velocity of fiber shortening and force of contraction
  • ->increased ventricular emptying
  • ->decreased end systolic and end diastolic volume
  1. increased CO
  2. increased renal perfusion
  3. Decreased sympathetic tone (reduced HR, vasoconstriction)
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11
Q

Digitalis SE

A
  • therapeutic range 1-2ng/ml
  • renal clearance

Cardiac Toxicity

  • DADs and abnormal automaticity
  • Digitalis Intoxication-VPB, Vtach, junctional tach
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12
Q

Clinical use of digitalis

A

CHF

Atrial fibrillation with rapid ventricular response

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13
Q

What can treat digitalis toxicity?

A

digibind antibodies

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14
Q

What do you use for a vasodilator (which increases cardiac output by reducing afterload) in acute CHF vs. chronic CHF?

A
  1. Acute CHF (IV, rapid onset)
    - Nitroprusside
    - Nitroglycerin
  2. Chronic CHF (oral, slow onset)
    - ACEi
    - ARB
    - Hydralazine
    - Minoxidil
    - Prazosin
    - LCZ696 (valsartan+sacubitril)
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15
Q

What does ACEi improve survival in? Why?

A

Chronic LV dysfunction and CHF

MOA

  1. Angiotensin 2 is a potent cardiomyocyte growth factor and fibroblast mitogen
  2. ACEi also reduce systolic and diastolic wall stretch
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16
Q

LCZ969

A

Combination of Valsartan (ARB) and Sacubitril ( a neprilysin inhibitor)

  1. Valsartan blocks AT receptor on cardiac and vascular smooth muscle
  2. Sacubitril is converted into endopeptidase inhibitor
    - Endopeptidase degrades natriuretic peptides, bradykinin, adrenomedullin
    - so this increases the levels of these peptides, causing vasodilation and reduction of ECF volume via sodium excretion
17
Q

Beta blockers also increase survival and prevent deterioration of LV performance over time in patients with mild-moderate CHF, what is the mechanism?

A

reduction in HR and prevention of deleterious effects of chronic sympathetic stimulation
-prevents fetal gene program

18
Q

Does spironolactone improve survival in CHF?

A

yes

Heart Pharm (14 decks)

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