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Flashcards in Heart failure physiology Deck (31):

HF definition

-A syndrome caused by cardiac dysfunction (from myocardial muscle dysfxn or loss) and characterized by either LV dilation, hypertrophy, or both
-HF leads to neurohormonal and circulatory abnormalities including fluid retention, SOB, fatigue and DOE
-Beneficial heart remodeling can be result of therapy or spontaneously
-HF is usually accompanied by pulmonary or systemic venous congestion, or both
-Also often accompanied by inadequate O2 delivery (at rest or stress) due to cardiac dysfxn


Components of HF

-Abnormal LV function (systolic, diastolic, or both)
-Abnormal hemodynamic profile
-Activation of neurohormonal systems
-Activation of inflammatory markers, endothelial dysfxn
-Signs and Sx (edema, hepatomegaly, pulm edema, tachycardia)


Heart dysfxns

-Ventricular remodeling
-Wall motion abnormalities (desynchrony)
-Endothelial dysfxn
-Electrical abnormalities (arrhythmias)
-Reduced longevity


Relevant heart terms

-Contractility (independent of preload and after load)
-SV, CO (based on SV and HR)
-Preload: based on venous pressure (return), approximated as EDV
-Afterload: based on TPR
-Ejection fraction (EF): SV/EDV (the fraction of the EDV that is ejected)
-Normal EF is 55-75%
-Compliance: change in pressure/ change in volume (how easily it changes volume)


HF ventricular function curve

-In VF curves, SV (y axis) is compared to preload (EDV, x axis)
-Normal curves are at the top, w/ HF curves down and to the right (+ inotropes up and to left)
-Increasing EDV will increase SV to a point, but after that it has little effect on increasing SV
-But lowering EDV by decreasing blood volume will move a point on a curve down/left on the same curve


HF force-tension curves

-In FT curves, SV (y axis) is compared to afterload (TPR, x-axis)
-Normal curves at the tope, w/ HF curves down and to left
-Lower TPR means a larger SV, but during HF there is smaller SV at the same TPR as a normal heart
-However, lowering TPR (after load) in HF can increase SV (positive inotropic effect)
-This moves the curve up one curve


Changing the ventricular function curve 1

-Want to move the curve up and to the left (increasing SV while decreasing EDV)
-This is b/c want to decrease EDV to reduce work the heart must do, but also want to increase SV instead of losing SV to increase CO
-In order to accomplish this, certain drugs are required
-Drugs that decrease EDV move the point on a curve down (to the left) the same curve, and drugs that decrease TPR move the point directly up to a new curve (those that do both move the point up and to the left


Changing the ventricular function curve 2

-Diuretics: decrease blood volume (thus decreasing EDV), so they move a point on a curve to the left
-Positive-inotropic effects (anything that vasodilates arteries: hydralazine, ACEIs, nitroprusside) moves the point up to a new curve
-Vasodilators can move the curves variably, based on where they vasodilate


Changing the ventricular function curve 3

-Isorbide dinitrate (venous only) moves the point down the curve, nitroprusside (both) moves the point up and to the left (also ACEIs, b/c they cause arteriole dilation and decrease EDV), and hydralazine (arteries only) moves the point up
-Combining drugs also can achieve the desired effect, as in giving a diuretic and hydralazine (moves the curve up and to the left)


Systolic dysfxn

-Diminished capacity of the ventricle to eject blood due to impaired myocardial contractility or volume overload
-There is reduced SV and increased EDV in return (leads to larger ventricle w/ limited capacity to generate force), therefore EF goes down
-Usually seen w/ dilated ventricle remodeling (LV systolic function impaired)


Diastolic dysfxn

-Impaired early diastolic relaxation, increased stiffness of ventricular wall (reduced compliance)
-But LV retains normal systolic function
-There is reduced EDV and reduced SV, thus EF doesn't change
-Lower compliance leads to increased ED pressure, thus the low EDV/SV
-Hypertrophy usually due to pressure overload (HTN)
-Heart must work more to generate same CO so there is often LV hypertrophy remodeling, exacerbating the low compliance of the ventricle and HF


Risk factors for HF

-CAD or Hx of MI
-HTN, diabetes
-EtOH, drugs (coke, meth)
-Age, obesity, smoking, etc


Right sided HF

-Cardiac causes: L sided HF, RV infarction, pulm stenosis
-Pulmonary diseases: pulm HTN (often from L sided HF), pulm embolism, COPD, chronic lung infection, etc


Compensatory mechanisms

-Frank starling: decrease in SV leads to increase in EDV to increase SV back to normal (leads to dilated LV b/c of constantly large EDV)
-Laplace law: when after load increases the ventricle must compensate by increasing wall thickness (which also decreases radius of ventricle) to maintain normal wall stress (leads to LVH)


Myocardial hypertrophy

-First stage of HF, can be either concentric (small ventricle) or eccentric (larger ventricle)
-Concentric hypertrophy is due to pressure overload leading to increased systolic wall stress and remodeling to thick walls
-Sarcomeres in parallel
-Eccentric hypertrophy due to volume overload leading to increased diastolic wall stress and remodeling to dilated walls (same thickness)
-Sarcomeres in series


Neurohormonal stimulation

-Adrenergic NS stimulation
-Renin angiotensin aldosterone system
-Natriuretic peptide


Effects of SNS

-Increased HR and contraction by B1
-Increased BP from A1 vasoconstriction
-These lead to increased myocardial O2 consumption and ischemia, and can limit CO
-Can provide short term benefit but long term can be very damaging


Renin-angiotensin-aldosterone system (RAAS)

-Activated due to decreased blood flow to kidneys due to decreased BP and by sympathetic activation of kidneys due to detection of low BP in baroreceptors
-Overall, angiotensin II causes vasoconstriction directly (arteries and veins) and increased Na/H2O retention (via aldosterone/ADH) to increase blood volume
-These two effects thus increase preload and increase after load


Effects of Angiotensin II

-Leads to fibrosis of the heart, kidneys, other organs
-Enhances release of NE from SNS
-Stimulates adrenals to produce aldosterone and activates release of ADH, leading to increased blood volume
-Stimulates thirst center to consume more water
-Angiotensin II has multiple receptors, but the AT1 receptors cause the problems (cause vasoconstriction, aldosterone secretion, etc)
-AT1 receptors target for angiotensin receptor blockers (ARBs)


RAAS pathway 1

-Liver secretes angiotensinogen, which is converted to angiotensin I by renin (from kidneys)
-Angiotensin I converted to angiotensin II by ACE (secreted from lungs)
-Angiotensin II leads to secretion of aldosterone from adrenal cortex, ADH from post pituitary


RAAS pathway 2

-ATII also causes vasoconstriction of arteries/veins, GF stimulation (LVH), and sympathetic activation (catecholamine release)
-Aldosterone also has many effects that contribute to HF, such as increased fibroblast collagen synthesis, increased AT1 receptors, increased ACE activity, increased VSMC hypertrophy, increased endothelin1, etc


Overall effects of aldosterone

-Causes edema by increasing Na/H2O absorption and blood volume
-Decreases vascular and ventricular compliance
-Can cause arrhythmias by increasing fibrosis
-Can increase endothelial dysfxn and lead to ischemia/worsening HF


Vasopressin and endothelin1

-ADH released in response to increase in plasma osmolality, leads to water retention
-Elevated levels in pts w/ HF
-Endothelin1 has many effects similar to angiotensin II, and increases ATII effects, as well as the effects of catecholamines


Counter neurohormonal systems

-Increased production of prostaglandins PGE2 and PGI2, causes vasodilation and Na excretion
-(!) natriuretic peptide (NPs): causes vasodilation, Na/H2O excretion, and decreases thirst
-Most important NPs: ANP (atria) and BNP (brain, ventricles)
-Hallmark of HF is BNP resistance
-BNP most important biomarker in HF


Symptoms of HF

-Exercise intolerance and water retention are primary Sx
-DOE, fatigue, orthopnea, PND very common
-Also: nocturnal cough, nocturia, abdominal discomfort, decreased appetite


Signs of HF

-Tachycardia, low BP, tachypnea, elevated JVP, pulses alternance (alternating strong and weak beats)
-Displaced and diffuse LV impulse, right ventricular heave, S3, MR and TR murmurs
-Pulmonary rales, liver enlargement, nocturia
-Leg edema, ascites, cold extremities


Classes of HF

-Class I: asymptomatic
-Class II: symptomatic w/ normal exercise
-Class III: symptomatic w/ little exercise
-Class IV: symptomatic at rest


ECG results indicating HF

-Atrial enlargement
-Post MI
-Conduction abnormalities (wide QRS, BBB)



-Pulmonary edema
-Pleural effusion
-Upper zone vascular redistribution


HF on echo

-Dilated chambers
-Wall motion abnormalities
-Mitral/tricuspid/Ao regurg
-Increase pulmonary pressure
-Pericardial effusion
-Pleural effusion


Hemodynamics of HF

-Increased RAP, pulmonary artery pressure
-Decreased SV and CO
-Increased TPR and pulmonary vascular resistance