Week 3: heart failure Flashcards
Define ejection fraction (EF).
EF=stroke volume/EDV
normal is 55-75%
Define compliance
property of heart muscle that accounts for changes in the strength of contraction, independent of preload and after load.
=change in pressure/change in volume
Describe the movement on the Frank-Starling Curve of someone going from normal left ventricle function to heart failure after an MI for example.
- on a EDV vs. SV curve
- The curve for heart failure is shifted downward due to decreased contractility. A person who had an MI would shift down and to the right after developing systolic dysfunction (slightly increased EDV and decreased SV)
- increasing LV filling via fluid retention can shift the person to the right along the heart failure curve to have greater EDV and slightly increased SV, and result in pulmonary congestion
Describe the effects of varying preload, afterload, and contractility on the pressure-volume loop.
- increasing preload
-increasing preload (EDV): higher SV but constant ESV - increasing afterload (ESV): decreasing SV with increasing ESV. increasing end systolic pressure.
- Increasing contractility: smaller ESV, higher SV. Shifts End systolic pressure-volume relation upward and leftward.
ESPVR-end systolic pressure volume relation, linear relationship depicting dependence of ESV on afterload
Define systolic dysfunction.
-Diminished capacity of the ventricle to eject blood due to impaired myocardial contractility or pressure overload
What are conditions that lead to systolic dysfunction (reduced ejection fraction)?
- Impaired contractility
- CAD: MI, transient myocardial ischemia
- chronic volume overload: mitral/aortic regurg
- dilated cardiomyopathies - Increased afterload (chronic pressure overload)
- advanced aortic stenosis
- uncontrolled severe hypertension.
Define diastolic dysfunction.
(preserved ejection fraction)
- heart failure caused by abnormalities of diastolic relaxation or ventricular filling
- preserved LV systolic function
What conditions can lead to diastolic dysfunction?
- left ventricular hypertrophy
- restirctive cardiomyopathy
- myocardial fibrosis
- transient myocardial ischemia
- pericardial constriction or tamponade
Describe the effect of systolic dysfunction or heart failure with reduced EF on pressure volume curve.
- ESPVR shifted downward, increased ESV, and decreased stroke volume
- EDV increases since normal pulmonary venous return is added to an increased ESV. Compensatory (partial) rise in stroke volume via frank-starling.
Describe the effect of diastolic dysfunction on the pressure volume curve.
(increased stiffness of ventricle)
- shift upward of the diastolic pressure-volume curve, at any diastolic volume, ventricular pressure is higher than normal.
- reduced EDV bc of less filling of a stiffened ventricle at a higher than normal pressure
- no change in ESV
Describe the following compensatory mechanism in heart failure: Frank Starling mechanism.
- In systolic dysfunction: increased ESV leads to increased EDV with normal venous return, stretching myofibers and inducing greater contraction. Helps increase cardiac output.
- however, in severe heart failure, curve is nearly flat at higher EDVs, reducing increases in CO with increasing EDV. And higher EDV and pressure transmits to left atrium, pulmonary veins, capillaries–>pulmonary congestion and edema
Describe the following compensatory mechanism in heart failure: neurohormonal alterations.
- adrenergic nervous system
-increase sympathetic output: increase HR, contractility, and vasoconstriction - renin-angiotensin-aldosterone system
-increased renin releases. Cleaves angiotensinogen to angiotensin I, which is cleaved by ACE (angiotensin converting enzyme) to angiotensin II, a vasoconstrictor.
-AII stimulates thirst
-AII increases aldosterone secretion, which promotes Na reabsorption–>rise in intravascular volume–>higher EDV - increased antidiuretic hormone (ADH) or vasopressin
-made in hypothalamus, released by posterior pituitary, promotes water retention in distal nephron - Endothelin-1: vasoconstriction
These all serve to increase systemic vascular resistance to maintain arterial perfusion (since BP=CO X TPR)
-HOWEVER, chronically elevated levels of AII and aldosterone leads to fibrosis, adverse remodeling, edema, arrhythmia,
Describe role of natriuretic peptides in heart failure.
- secreted in response to increased intracardiac pressure.
- ANP-atrial natriuretic peptide
- BNP-B type natriuretic peptide
- result in excretion of Na+ and water, vasodilatation, inhibition of renin secretion, and antagonism of effects of AII (angiotensin II) on aldosterone and vasopressin levels.
- however not enough to fully contract vasoconstriction and volume retaining effects of the other hormonal system
- increased BNP concentration seen in increasing CHF severity
Describe the following compensatory mechanism in heart failure: ventricular hypertrophy
- increased wall stress leads to myocardial hypertrophy
- helps to maintain contractile force and counteracts elevated ventricular wall stress (according to LaPlaces formula)
- eccentric hypertrophy: myocytes elongate, synthesis of sacromeres in series, in respond to volume overload
- concentric hypertrophy: myocytes thicken, sacromeres synthesized in parallel, in response to chronic pressure overload
- however increased ventricular diastolic pressure from increased stiffness in wall–>increased atrial pressure–>backward failure, i.e. pulmonary congestion
what are the symptoms of chronic heart failure?
LEFT sided -dyspnea -fatigue -orthopnea -paroxysmal nocturnal dyspnea (PND) -nocturnal cough -nocturnia (waking up to pee) RIGHT sided -peripheral edema -right upper quad discomfort from hepatic enlargement -abdominal discomfort -decreased appetite
