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CV 3 > Heart Failure Pharmacology > Flashcards

Heart Failure Pharmacology Flashcards

1
Q

WHat are the types of drugs that are used for heart failure?

A
  • Diuretics
  • Inhibitors of the RAA system
    • ACE inhibitors
    • Angiotensin receptor blockers
    • aldosterone antagonists
  • B adrenergic receptor blockers
  • vasodilators
  • positive inotropic agents
  • heart rate reducing agents
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2
Q

what is the flow of the renin-angiotensin system?

A

Angiotensinogen

****Renin****

Angiotensin I

****ACE****

Angiotensin II

**** AT receptor****

Aldosterone release

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3
Q

What are the positive inotropes for chronic heart failure?

A

Digoxin

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4
Q

What is Digoxin used for? What are its mechanisms of action?

A

Digoxin is used for Heart Failure w Left Ventricular systolic dysfunction, A fib, or in pts who are in sinus rhythm but are symptomatic and have tried other drugs. Does not decrease mortality/prolong survival, but does provide moderate symptomatic releif (Atrial Fibrillation and SVT to control ventricular response rate)

  • Positive Inotrope: Directly increases contractile state of myocardium and increases SV
    • Inhibits Na/K/ATPase (pumps 3 Na out, 2 K in)
      • Increases intracellular Na, which decreases drive for Na/Ca Exchanger (uses Na gradient rushing in to pump Ca out) so intracellular Ca increases which increases contractility
      • K competes against Digoxin for the Na/K/Exchanger
  • Increase Vagal tone: (slow conduction at the AV node)
    • Secondary effects: decrease HR, arterial/venous dilation, decrease venous pressure (bc of lessened Neuro-hormonal activation (due to Increase vagal))
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5
Q

What are the pharmacokinetics and adverse effects of digoxin?

A
  • Pharmacokinetics: t1/2=36 hours so daily dosing, orally absorbed, excreted unchaged by the kidneys (renal elimination)
  • Adverse Effects: low TI and affects all excitable tissues. Toxicity enhanced with hypokalemia (bc K competes w Digoxin at the Na/K/ATPase)
    • GI (most common): anorexia, nausea, vomiting, diarrhea
    • Visual disturbances: blurred vision, photophobia, color disturbances
    • Neurologic: disorientation, hallucinations
    • Muscular: muscle weakness, fatigue
    • Cardiac: arrhythmias (any type)
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6
Q

What is the overall function/ goal of diuretics?

A

promote elimination of sodium and water to reduce intravascular volume and venous return to the heart. Decrease preload, filling pressure falls out of range that leads to pulmonary congestion. Reduce EDP without reducing SV

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7
Q

What are the 3 types of diuretics and what do they do?

A
  • Loop Diuretics: Furosemide
    • Widely used to maintain euvolemia
    • Promote K loss- hypokalemia
  • Thiazide diuretics: Chlorothiazide
    • Rarely used alone
    • Used in combo w loop diuretics in pts who are refractory to loop alone
    • Promote K loss- hypokalemia
  • K Sparing Diuretics: amiloride, triamterene
    • Weak diuretic activity, but limited K and Mg wasting
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8
Q

What are the effects of Angiotensin II? WHat are the effects of Aldosterone?

A
  • Angiotensin II:
    • potent arterial constrictor
    • Na and H20 retention bc acts on glomerulr filtration by stimulating aldosterone secretion
    • enhances sympathetic activity by promoting neuronal and adrenal catecholamine release
    • Arrhythmogenic
    • Promotes cardiac remodeling: myocardial hypertrophy, fibrosis, apoptosis
  • Aldosterone
    • promotes Na and H20 retention
    • promotes cardiac remodeling (fibrosis)
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9
Q

What are the ACE inhibitors and what are they used for? What beneficial effects do they have? what are the adverse effects?

A

ACE Inhibitors: captopril, enalopril: Reduce Heart Failure symptoms, decrease need for hospitalizations, extend survival

  • Stop production of AngII (ACE converts AngI to AngII)
    • Decrease afterload (AngII arterial constrict)
    • Decrease intravascular volume and systemic/ pulmonary congestion (AngII signals Aldosterone release via AT receptor which= Na/H20 retention)
    • Limits maladaptive ventricular remodeling
  • Adverse: (note ACE breaks down bradykinin to inactive peptides)
    • Hyperkalemia esp. if used with K sparing or K supplementation
    • Angioedema (increased bradykinin), dry cough (bradykinin), hypotension, renal failure
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10
Q

What kind of drug is Sacubitrin/Valsartan and what is the use? What does is drug in this combo do?

A

Angiotensin Receptor Blocker/ Neprilysin Inhibitor Combination

use: Sacubitrin/Valsartan: superior to enalapril in reducing risk of death and hospitalization for heart failure

Sacubitril: neprilysin inhibitor, Valsartan: angiotensin blocker

  • Neprilysin inhibits ANP and BNP, bradykinin etc. therefore their levels increase which counters neurohormonal activation that contributes to vasoconstriction, sodium retention, and maladaptive remodeling
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11
Q

What are the aldosterone antagonists? what are their uses? What are the adverse effects?

A
  • Aldosterone Antagonists: Spironolactone, Eplerenone: reduce edema, anti-arrhythmic, decrease fibrosis in the myocardium and vessels. Improve mortality and symptoms
  • Block effects of Aldosterone
  • AE: Hyperkalemia
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12
Q

What do venous dilators do? How about arterial? how about mixed?

A
  • Venous:
    • decreases pre-load (LV-EDV),
    • decreases wall stress with little effect on SV
  • Arterial:
    • reduces afterload by decreasing systemic vascular resistance
    • results in increased SV and decreased wall stress
  • Mixed:
    • reduces preload and after load (systemic vascular resistance)
    • increased SV adn decreased wall stress
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13
Q

WHat are the 3 different kinds of dilators? what are examples of each as well as their effects?

A
  • Venous: Nitrates-decrease preload, decrease wall stress, little effect on SV
  • Arterial: Hydralazine- reduce afterload, increase SV, decrease wall stress
  • Mixed Acting: ACE inhibitors, AT1 inhibitors, nitroprusside- reduce preload and afterload, increase SV, decrease wall stress
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14
Q

What is the use of Isosorbide Dinitrate/Hydralazine combo

A
  • improve survival in pts with HF, but less efficacious than ACE inhibitors. Substitute if can’t use ACE inhibitor or angiotensin receptor blocker (ie due to renal dysfunction). More efficacious in African Americans
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15
Q

use and effect of beta blockers in heart failure with reduced ejection fraction?

A

heart failure, symptoms, survival time, ventricular function

  • Decrease arrhythmias, oxygen demand, blood pressure
  • Prevent disease progression (remodeling-caused by aldosterone from sympathetics NH)
  • Inhibit cardiotoxic effects of catecholamines
  • Reduce B1 receptor downregulation
  • Initially worsens cardiac function, so start on low dose and gradually increase to maximally tolerated dose
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16
Q

what is the use of Ivabradine? what does it do?

A

​used in heart failure pts. with HR> 70bpm even if taking B blocker. Prolongs survival time

  • Slows heart rate by blocking If channel in pacemaker cells
17
Q

WHat are some non drug therapies for heart failure with reduced ejection fraction?

A
  • Salt restriction, rehab/exercise therapy, Bi-ventricular pacing or cardiac resynchronization therapy (CRT-pacemaker that stimulate both ventricles simultaneously, which synchronizes contraction), Implantable cardio-defibrilator devices (reduces likelihood of SCD), Mechanical circulatory support (ventricular assist devices-VAD, Implantable artificial hearts), heart transplant, cell therapy
18
Q

How do you treat HFpEF?

A
  • Renin-angiotensin-aldosterone system blockade and b blockers have limited utility
    • May be some benefit of aldosterone receptor blockade
  • Because contractile function is preserved, inotropic
    drugs have no role in this condition
  • Address correctable causes of impaired diastolic function
  • Diuretics to reduce pulmonary congestion and peripheral
    edema
    • Use cautiously to avoid under filling of LV
    • Could reduce stroke volume
19
Q

how do pts w acute heart failure present?

A

urgent life-threatening symptomology often in a previously asymptomatic patient. but can also be a complicaiton of compensated chronic heart failure following a precipitating trigger

20
Q

Classification and approach to therapy of acute heart failure is based on presence or absence of _______ and ________

What are the 3 profiles of acute heart failure?

A
  • Classification and approach to therapy of acute heart failure is based on
    • volume overload (“wet” vs “dry”) consequent of elevated filling pressures
    • decreased cardiac output (“cold” vs “warm”) consequent of reduced tissue perfusion
  • Profile A: normal hemodynamic
  • Profile B and C: acute pulmonary edema
    • B: “wet” lungs but preserved “warm” tissues
    • C: in addition to pulmonary congetsion, impaired forward output results in marked systemic vasoconstriction
  • Profile L: “cold” extremities due to ow cardiac output but no signs of vascular congestion
    *
21
Q

what is pulmonary edema? what is wedge pressure?

A
  • Elevated capillary hydrostatic
    pressures cause rapid
    accumulation of fluid within the
    interstitium and alveolar spaces
    of the lung
  • Develops when the pulmonary
    capillary wedge pressure (which
    reflects LV diastolic pressure)
    exceeds 20-25 mmHg
  • Results in hypoxemia and
    severe dyspnea
  • Life-threatening emergency that
    requires immediate
    improvement of systemic
    oxygenation and elimination of
    the underlying cause
  • Wedge pressure translates into LV end- diastolic pressure
22
Q

what are the goals of therapy for acute pulmonary edema?

A
  • normalize ventricular filling pressure
  • restore adequate filling pressure
  • patient profile-type guides:
    • Profile B – requires diuretic and/or
      vasodilator for pulmonary edema –
    • Profile C – may additionally require
      intravenous inotropic therapy to
      increase cardiac output
23
Q

what diuretics are typically used for acute pulmonary edema and how do they work?

A
  • Loop Diuretics (furosemide)
    • Rapid and potent diuresis, IV administration, reduce blood volume and therefore preload
24
Q

What vasodilators are used for acute pulmonary edema

A
  • Nitroprusside: severe heart failure w elevated systemic vascular resistance
    • IV, direct NO donor that dilates both arteries and veins (mixed)
    • Reduces ventricular filling pressure (preload) and systemic vascular resistance (afterload) combined effect increases cardiac function (SV)
  • Nitroglycerin: acute dysfunction due to acute ischemia
    • IV, Primarily induces venodilation and reduces ventricular filling pressure (preload)
25
Q

What are the inotropic drugs for acute pulmonary edema?

A
  • Dobutamine
    • B1 adrenergic receptor stimulation
    • Increase contractility and stroke volume
    • Little effect on peripheral vascular resistance and arterial pressure
  • Dopamine
    • Dose dependent effect:
      • Low dose (D1) dilation of renal and mesenteric arteries
      • Intermediate dose (D1 and B1 receptors) renal effect plus increases heart rate and contractility
      • High dose: (D1, B1, a1 receptors) vasoconstriction
26
Q

What is Milrinone

A
  • Phosphodiesterase inhibitor (PDE3 isoform)
  • Decreases degradation of cAMP resulting in elevation of cAMP levels in cardiac and smooth muscle
  • Positive inotropic effect
  • Balanced arterial and venodilator
  • Combined effects increase SV
  • IV

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