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BIOM 3090 > Unit 0.4: Treatment of Heart Failure > Flashcards

Unit 0.4: Treatment of Heart Failure Flashcards

1
Q

what is heat failure

A

when heart is unable to pump enough blood

  • the delivery of blood or CO is inadequate for oxygen and the nutritional needs of the body
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2
Q

what are the causes of heart failure?

A
  • myocardial damage (>80%), hypertension, infection, genetric/congential abnormality and chemical toxicity
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3
Q

what are the two types of heart failure

A
  • systolic heart failure: reduced contractility of the heart
  • Diastolic heart failure: reduced filling of the heart
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4
Q

how does the body compensate for decreases in CO

A
  • inc SNS activity, activate the renin angiotensin system inc force on contraction of the heart and centricular hypertrophy
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5
Q

how does the SNS compensate for heart failure

A
  • decrease in CO is monitored by baroreceptors and signals an inc in SNS and dec in PSNS activity
  • changes result in an increase in HR, force of contraction and peripheral vascular resistance
  • compensatory mechansisms contribute to some of the symptoms of heart failure like tachycardia and sweating
  • also results in fluid retnetnion via renin-angiotensin system
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6
Q

Describe the renin angiotensin system

A
  • decrease in CO and SNS medicated vasoconstriction causes a decrease in blood flow to the kidneys
  • this decreases glomerular filtration
  • SNS activity activates β1 receptors in the kidneys, inc renin relase and conversion of angiotensin I to angiotensin II
  • results in decrease in fluid removed from blood and dec in urine output

*occurs bc of an increase in vasocontriction and sodium and water rentention - BP and PVR are increased

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7
Q

describe the neurohumoral effects of heart failure

A
  • Compromised cardiac function -> dec arterial BP -> Baroreceptor reflex -> inc sympathetic outlfow (α and β Adrenergic sympathetic outflow)
  • α: vasoconstriction -> INC afterload -> greater pressure against which the heart must contract -> inc myocardial demand
  • β: inc juxtaglomerular cell release of renin -> inc AT II (directly acts as vasoconstrictor but also) ->inc aldosterone synthesis and secretion -> inc collecting duct Na+ reabsorption eading to intravascular volume expansion and inc preload

*net is inc afterload and preload which inc myocardial O2 demand - if heart if already compromised this inc stress can lead to worsening heart failure

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8
Q

How does contractility compensate for heart failure

A
  • fluid retnetion combined with vasocontriction = increased contractility
  • when blood volume increases in veins there is an increase in pressure in blood returning to heart

* cardiac muscle stretching to increase strength of contraction called Frank-Starling Law

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9
Q

describe the frank starling relationship in heart failure and treatment with positive inotrope

A

*left panel

normal frank starling relatinship shows a steep increase in CO w/ increasing ventricular end-diastolic pressure (preload)

point A = the end diastolic pressure and CO of a normal HR at rest

  • contractile dysfunction (untreated HR), cardiac output falls (B_ and frank starling curve flatterns - increasing preload translated to only modest inc in CO
  • inc in CO acompanied by dyspnea

= treatment with positive inotrope shifts curve upwards and CO increases - imporvement in myocardial contractility supports a sufficient reduction in preload that the venous congestion is relieved (E)

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10
Q

how does afterlad reduction and preload reduction influence the stank starling curve

A
  • afterload reduction (ACE inhibitors) (F) inc CO at any given preload - elevate the frank-starling relationship
  • Preload reduction (G) alleviates congestive symptoms by decreasing ventricular end diastolic pressure along same rnak starling curve
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11
Q

what is ventircular hypertrophy

A

thickening of ventricular cell calls

  • results if damage to heart causes a decrease in CO or the heart is chronically stressed and cardiac muscle cells increase in size to compensate
  • heart can function normally at rest but can fail due to exercise or stress
  • if compensatory mechansims return CO to normal levels then renal output also reutnrs to normal - if does not return to norma levels end result is decompensated heart failure
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12
Q

what is a decompensated heart

A
  • severely damaged heart that cannot be compensated by SNS activity, renin-angiotensin system or ventricular hypertrophy
  • excessive stretching of heart muscle weakens heart further and excess fluid in venous system can leak into tissues (ie fluid in lungs = pulmonary edema)
  • decompensated heart combined with edema is reffered to as congestive heart failure
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13
Q

what is congestive heart failure

A
  • insufficient CO to supply the organs in the body with nutrients and oxygen
  • fluid accumulation in extremities and/or lungs (which results in decreased oxygenation of blood) is also contributing factor
  • when normal CO cannot be achieved, reflex mechanisms that are used to compensate for heart failure decrease cardiac function even more
  • body canot respond to CHF - there is a high mortality rate associated with the disease
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14
Q

what are symptoms of CHF caused by compensatory responses to decrease CO

A
  • tachycardia, shortness of breath, sweating, peripheral/pulmonary edema, decreased exercise tolerance, enlargement of heart (cardiomegaly), hypotension and urine retention
  • therapeutic strategies are aimed at reducing the work load of the heart
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15
Q

how is heart failure treated

A
  1. reccomend lifestyle changes - decreasing activity level, weight and stress. restrict sodium instake from diet and stop smoking
  2. use of pharmacological agenets like diuretics, ACH inhibitors/ARBs, cardiac glycosides, beta-blockers and vasodilators

*patients with severe HR usually requrie combination therapy (diuretic, ACE inhibitor and cardiac glycoside)

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16
Q

describe calss 1 heart failure

A

mild

No limitation of physical activity

Ordinary physical activity does not cause undue fatigue, palpitation, or dyspnea (shortness of breath).

17
Q

describe class II heart failure

A

Slight limitation of physical activity

Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea.

18
Q

Describe class III heart failure

A

moderate

Marked limitation of physical activity

Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea.

19
Q

describe class IV heart failure

A

severe

Unable to carry out any physical activity without discomfort.

Symptoms of cardiac insufficiency at rest.

If any physical activity is undertaken, discomfort is increased

20
Q

how is mild heart failure treated? Patients with left ventricular dysfunction but no edema? left ventricular dysfunction with edema?

A
  • ACE inhibitors (enalapril), ARBs (lorartan), thaizide diuretics or loop diuretic (furosemide) if a more powerful agent is required
  • patients with elft venticular dysfunction but no edema can receieve ACE inhibitiors (enalarpil) or ARBs (lorartain) and those with edema require vasodilators or diuretics.
21
Q

what are patients with excessive tachycardiac prescribed

A

low dose beta-blockers (metoprolol) but must be monitored closely to ensure sufficient cardiac output

22
Q

how are patients with CHF combined with atrial fibrillation or an enlarged/dysfunctional left ventricle

A
  • require cardiac glycosides (digoxin)
  • absorbed and dsitrbuted well and has direct and indirect cardiovascular effects on heart and baroreceptors respectively
23
Q

what is the mechanism of action of Digoxin: direct pathway

A
  • inhibition of Na+/K+ ATPase
  • for the direct pathway the concentration of Na+ inc inside cardiac muscle cells due to inhibition of Na+/K+ ATPase

*result = decrease in Ca2+ efflu via Na+/Ca+ exchanger

  • intracellualr Ca2+ builds up which inc interaction between actin and myosin

*overall effect is an increase in cardiac contractility

24
Q

describe the mechanism of digoxin - indirect pathway

A
  • increase PSNS activity and decreases SNS actiivty
  • increased force and decreased rate of contraction

*occurs at least in part from the imporved CO )detected by baroreceptors

25
Q

digoxin treatment - half life, therapeutic index, dosing, administration, side effects

A
  • long half life ~ 40 hours and narrow therapeutic index (0.5-1.5 ng/mL)
  • toxicity observed at >2 ng/mL
  • pateints given large initial dose (digitalization) and then daily maintenance doses - maintenace doses adjusted per pateints by monitoring plasma digoxin levels
  • toxicities associated include adverse cardiac and GI effects
  • can develop arrhythmias from pateints with decrease K+ levels (from diuretics or diarrhea) can lead to tachycardia and fibrilation
  • GI toxicity includes anorexia, nausea, vomiting and diarrhea
26
Q

what is quinidine

A

anti-arrhythmic

reduces digoxin clearance and therefore increases toxicity if administered in tandem with digoxin

GI toxicity includes anorexia, nausea, vomiting and diarrhea.

27
Q

describe the poritive inotropic mechanism of digoxin

A
  1. digoxin selectively binds to and inhibits Na+/K+-ATPase.
    • Dec Na+ extrusion (dashed arrows) -> increased concentration of cytosolic Na+
  2. Inc intracellular Na+ decreases teh driving force for the Na+/Ca2+ exchanger
    • leads to decreased extrusion of Ca2+ from cardiac myocyte into extracellular space and to increase cytoslic Ca2+
  3. ince Ca2+ is pumped by SERCA Ca2+ ATPase into sarcoplasmic reticulum
    1. creates a net increase in Ca2+ that is available for release during subsequnt contractions
  4. During each contraction, the increased Ca2+ release from SR leads to increased myofibril contraction =? INC cardiac inotropy

BIOM 3090 (22 decks)

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