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Flashcards in Heart Failure Pathophysiology Deck (22)
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heart failure

clinical syndrome

happens when the heart cannot produce enough cardiac output to meet the metabolic demands of the body


can only produce enough cardiac output at the expense of high cardiac filling pressures


both 1 and 2


Stage A HF

no symptoms

+ risk factors for developing HF


Stage B HF

no symptoms

 + structural disease that is strongly associated with the development of HF


Stage C HF

symptomatic heart failure associated with underlying structural heart disease


Stage D HF

advanced structural heart disease and marked symptoms of HF at rest despite maximal medical therapy


equation for wall stress

wall stress (sigma) = (P x r)/2h


What causes increased filling pressures?

impaired LV or RV relaxation

reduced LV or RV compliance (increased stiffness)

fluid overload (ex. renal failure)


systolic HF vs systolic dysfunction

systolic dysfunction:

implies contractile dysfunction

clinically usually manifests as decreased EF

may or may not have signs or symptoms of HF

does not equal systolic HF

systolic HF:

systolic dysfunction along with signs/symptoms of HF

most patients will have decreased CO and increased filling pressures


diastolic dysfunction vs. diastolic HF

diastolic dysfunction:

implies slowed relaxation, noncompliant ventricle, or both

clincially manifests as increased filling pressures

may or mat not hav signs of HF

diastolic HF:

diastolic dysfunction + signs/symptoms of HF

EF is normal


ejection fraction cutoffs

reduced means EF < 40-45%

preserved means EF > 45-50%


What is the main difference between SHF and DHF?

the anatomical structure and function of the myocardium and myocytes


clinical features of DHF vs SHF

both have symptoms

both have a congestive state (edema)

both have neurohomonal activation (increased BNP, SNS, RAAS)


LV structure and function of DHF vs SHF (LV ejection fraction, LV mass, relative wall thickness, LV EDV, LV EDP and LA size)


normal LV ejection fraction

increased LV mass

increased relative wall thickness

normal LV EDV

increased LV EDP and left atrial size


decreased LV EF

increased LV mass

decreased relative wall thickness

increased LV EDV

increased LV EDP and left atrial size


exercise of DHF vs. SHF


decreased exercise capacity

decreased CO augmentation

increased EDP


decreased exercise capacity

decreased CO augmentation

increased EDP


hemodynamic hypothesis of SHF

the sympathetic tone is maxed out so the only way to increase CO is by increasing LV filling pressures


arginine vasopression (AVP)

aka antidiuretic  hormone (ADH)

arterial baroreceptors and angiotensin II stimulate the posterior pituitary to secrete AVP which results in vasoconstriction (V1A), LV hypertrophy (V1A) and remodeling, and water retention (V2) depending on the receptor

V1B receptors lead to ACTH and beta-endorphin release


natriuretic peptides

released into the circulation when the myocardium is under stress

beneficial homones that counterace the effects of the SNS, RAAS, and AVP


B-type natriuretic peptide (BNP)

developed into a blood test to diagnose HF

increased levels increase the likelihood of a cardiac cause of dyspnea and elevated levels indicate a poor prognosis

can be elevated in cases of pulmonary embolism and acute coronary syndrome


Why is neurohormonal activation bad?

except for antriuretic peptide,s activation of other neurohormones, though initially helpful, quickly cause worsening HF due to increased congestion, worsening CO

angiotensin II and aldosterone trigger fibrosis int he myocardium


eccentric hypertrophy

caused by volume overload

LV dilation, globular shape, systolic dysfunction predominates

mitral regurgitation

sacromeres grow in series, making myocytes longer


concentric hypertrophy

due to chronic pressure overload

normal cavity size, concentric LVH, diastolic dysfunction predominates

increased, wall thickness, decreased chamber compliance, increased filling pressures

more at risk for ischemia

parallel growth of sarcomeres


three common types of electrical problems in HF

scar formation = focal re-entry = ventricular tachycardia

atrial enlargement/overload = atrial fibrosis = atrial fibrillation/atrial flutter

electric remodeling = intra- and interventricular dyssynchrony -> further determioration in cardiac output