Heart Failure I - Pathophysiology Flashcards

1
Q

Discuss the major significance of heart failure in the United States, including how it is a common chronic health care problem that affects survival, quality of life, and health care costs.

A

• Prevalence: approx 5,000,000
• Annual incidence: 550,000
• Mortality: 250,000
• Cost: $37.5 billion.
• HF is a highly symptomatic and progressive disease. Consequently, decreased quality of life, hospitalizations, and death are common. For patients with HF, half will be dead within 5 years, making HF more deadly than most cancers.
• Incidence and prevalence are increasing for a number of reasons:
o Aging population
o Increased survival of initial cardiac disease
o Therapies generally stabilize HF, but do not often cure it

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2
Q

Heart failure as a syndrome:

A

o Heart failure is the inability of the heart to pump blood forward at a sufficient rate to meet the metabolic demands of the body (forward failure), or the ability to do so only if the cardiac filling pressures are abnormally high (backward failure).

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3
Q

what can cause HF?

A
-	Poor forward blood flow
	Low flow →↓CO
-	Backward buildup of pressure
	Congestion→↑filling pressure
	Typically a response to low flow.
•	Decrease in cardiac output and an increase in filling pressure are fundamental to the pathophysiology of heart disease
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4
Q

Systolic dysfunction:

A

a problem with squeeze→↓contraction→↓inotropy.
o Hallmark: decreased ejection fraction and entricular enlargement
 Decreased ejection fraction
 Heart failure with reduced ejection fraction=HFrEF
 Left ventricular systolic dysfunction=LVSD
 Ventricular enlargement
 Dilated cardiomyopathy= DCM

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5
Q

primary causes of systolic dysfunction

A

 Direct destruction of heart muscle cells→myocardial infarction, viral myocarditic, peripartum cardiomyopathy, idiopathic dilated cardiomyopathy, alcohol.
 Overstressed heart muscle→tachycardia-mediated HF, meth abuse, catecholamine mediated.
 Volume overloaded heart muscle→mitral regurgitation, high cardiac output

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6
Q

Diastolic dysfunction:

A

a problem with filling→↓lusitropy/decrease in relaxation.
o Hallmark: normal ejection fraction and ventricular wall thickening.
 Normal ejection fraction:
 HF with preserved ejection fraction=HFpEF
 Preserved systolic function=PSF
 Ventricular wall thickening:
 Left ventricular hypertrophy=LVH
 Hypertrophic cardiomyopathy=HCM→genetic

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7
Q

Primary causes of diastolic dysfunction:

A

 High afterload/pressure afterload→hypertension, aortic stenosis, dialysis (inadequate volume removal)
 Myocardial thickening/fibrosis→HCM, primary restrictive cardiomyopathy
 External compression (may not be HF since it doesn’t involve heart itself)→pericardial fibrosis/constrictive pericarditis, pericardial effusion.

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8
Q

Compensatory responses to decreased cardiac output

A
  • neurohormonal activation
  • F-S increases in preload
  • Ventricular remodeling via hypertrophy and dilation
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9
Q

Frank-Starling increases in preload

A

 ↑LV filling→↑SV

 stroke volume is preserved by increasing the end diastolic filling/pressure.

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10
Q

Neurohormonal activation

A

 ↓filling/↓SV→↓CO
 Juxtaglomerular apparatus in kidney senses lower flow→renin-angiotensin-aldosterone (RAAS) activation
 ↑Sodium retention
 vasoconstriction
 Carotid sinus/aortic baroreceptors sense lower pressure→autonomic nervous system/adrenergic activation
 ↑HR
 vasoconstriction
 ↑sodium retention + vasoconstriction + ↑HR →↑volume→↑LV filling

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11
Q

Ventricular remodelling via hypertrophy and dilation

A
	Long term increases in cardiac workload and increased metabolic demands promote adverse myocardial remodelling.
	Ventricular hypertrophy
	Ventricular dilation
	Myocardial damage/apoptosis
	Myocardial fibrosis
	Overtime remodelling causes:
	Decreased contractile force
	Decreased dynamic function
	Increased diastolic stiffness
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