Heart Failure Flashcards
What is the difference between preload and afterload?
PRELOAD = left ventricular end-diastolic volume or pressure (volume of blood in ventricles before contraction)
AFTERLOAD = resistance/pressure the ventricles are pumping against
(left CO = right CO)
How is MAP calculated? CO?
MAP = CO x SVR
CO = SV x HR
What is heart failure? What 4 things does it lead to?
inability of the heart to maintain normal venous/capilary pressures, CO, and/or systemic BP that occurs secondary to severe, overwhelming cardiac disease
- volume overload
- pressure overload
- impaired LV filling (pump/myocardial failure)
- primary myocardial disease
What are 3 of the heart’s priorities?
- maintain normal systemic arterial pressure
- maintain normal tissue blood flow
- maintain normal systemic and pulmonary capillary pressures
Why is heart failure a vicious cycle?
the heart overcompensates and the mechanisms meant to preserve function leads to failure
What are 6 mechanisms used for cardiac compensation (that can ultimately lead to failure)?
- Starling’s Law
- endocrine - RAAS
- sympathetic nervous system
- neurohormones
- renal effects
- remodeling to accommodate for changes in volume and pressure
What are the 3 major causes of CHF?
- decreased CO - infarction, myocarditis, volume/pressure overload, genetics
- renal responses - water and sodium retention, vasoconstriction, cardiac remodeling (RAAS, aldosterone, ADH, sympathetic NS, neurohormones)
- decompensation - pulmonary edema, ascites, pleural effusion
What are 4 results of compensated heart failure?
- no clinical signs
- increased RAAS
- increased adrenergic systems
- cardiac remodeling
What are 3 results of decompensated heart failure (CHF)?
- clinical signs - water retention exceeds vessel capacity, leading to accumulation of fluid in body cavities
- increased RAAS
- increased adrenergic systems
How does the activation of the RAAS progress throughout heart disease?
- mechanical or functional abnormalities of the valves upregulates the RAAS with no clinical signs for years
- onset of clinical signs begins years later, ultimately leading to death within months
How does right-sided and left-sided heart failure compare?
RIGHT - blood cannot pump blood into the heart properly, so it backs up in the BODY, resulting in ascites, poor organ function, and distended veins
LEFT - blood cannot pump into the heart properly, so it backs up in the LUNGS, resulting in pulmonary edema
What is the Frank Starling mechanism? What does this result in?
acute increases in ventricular filling (preload) induces greater contraction force and blood ejection, allowing for beat-to-beat adjustments that balance the output of the 2 ventricles in response to acute increases in hemodynamic load
ventricular output increases as preload increases = heart can change its force of contraction and SV
What role does the Frank Starling mechanism take part in during compensation for heart failure? How is it limited?
buffers the fall in CO to preserve sufficient blood pressure when there is poor emptying and higher preload by stretching to allow for better contraction and preservation of CO
can cause muscle failure —> poor compensation leading to end diastolic volume and left ventricular pressure increase —> pulmonary edema
Cardiac compensation:
increase in catecholamines is not enough to increase contraction enough at a certain point
How does heart failure affect the endocrine system? When does this activate?
increases RAAS and ADH, resulting in water and sodium retention to increase circulating volume
later in heart disease when there is renal artery hypoperfusion, resulting in decreased filtered Na reaching the macula densa which increases SNS activity and renin release
RAAS:
things that cause renin release are targeted by cardiac drugs
What 2 local effects does angiotensin II have on the heart? What else does it do?
- enhances sympathetic affections
- promotes tissue remodeling - hypertrophy, inflammation, fibrosis
- vasoconstrictor
- releases aldosterone from adrenal cortex —> increases thirst and salt appetite
- stimulated ADH release
What 2 local effects does aldosterone have on the heart and kidneys? What else does it do?
- mediates inflammation and fibrosis
- pathologic cardiac changes
- promotes sodium and chloride reabsorption in renal collection tubules
- promotes potassium and hydrogen secretion in collection tubules
How does heart failure affect the nervous system? How does it do this?
decreased CO activates the SNS to compensate by stimulating beta receptors and increase contractility and HR
maintains CO by causing vasoconstriction and increased inotropy/chronotropy to increase venous return
What inhibitory and excitatory inputs affect SNS activation with heart failure?
INHIBITORY - baroreceptors, mechanoreceptors (maintain pressure)
EXCITATORY - non-baroreflex peripheral chemoreceptors, muscle metaboreceptors
What are 4 results of chronic SNS activation with heart failure? What ultimate response is seen?
- increased afterload stress
- increased myocardial O2 demands
- cellular damage
- myocardial fibrosis
persistent sympathetic innervation reduces cardiac sensitivity to catecholamines, resulting in arrhythmias in later disease
What are 3 other neurohormones that play a role in abnormal cardiovascular hypertrophy or fibrosis?
- free radicals from oxidative stress
- cytokines - TNFa
- endothelins - ET-1, 2, and 3 produced in response to hypoxia and vascular mechanical factors, angiotensin II, ADH, NE, and cytokines act as potent vasoconstriction
What role do most neurohormones play in heart failure? What happens as failure worsens?
prolonged vasoconstriction = increases workload by reducing forward CO and exacerbating valvular regurgitation
neurohormone activation increases —> increased endothelins and inflammatory cytokines
What are 5 endogenous mehanisms that oppose the vasoconstrictor responses caused by heart failure? Why does heart failure often still result?
- natriuretic peptides - natriuresis/diuresis, vasodilation, inhibits RAAS and SNS (ANP, CNP, NT-proBNP)
- vasodilatory prosraglandins - PGE2, PGI2
- adrenomedullin
- nitric oxide
- bradykinin
as heart failure progresses, the influence of vasoconstriction predominates despote activation of vasodilatory mechanisms
How do the kidneys respond to heart failure? What happens with chronic heart failure? What effects do diuretics have?
efferent glomerular arteriolar constriction - maintains GFR in the face of reduced cardiac output and renal blood flow, enhances reabsorption of tubular fluid and sodium (promoted by angiotensin II)
clinical edema and effusions
magnify azotemia and electrolyte loss and further reduces CO and activates NH mechanisms
What different responses happen with pressure overload and volume overload?
PRESSURE = concentric hypertrophy, thickening
VOLUME = eccentric hypertrophy, dilation (spreading of muscle)
Cardiac remodeling:
What causes eccentric hypertrophy? What 3 things does this result in?
volume overload
- addition of sarcomeres in series (elongated)
- increased LV lumen diameter
- poor contractility
What causes concentric hypertrophy? What 3 things does this result in?
pressure overload
- addition of sarcomeres in parallel (side by side)
- increased cross-sectional area
- decreased LV luminal diameter and compliance, which impairs relaxation (diastolic dysfunction)
What are 3 causes of eccentric hypertrophy?
- valvular insufficiency - MMVD, aortic insufficiency
- systolic dysfunction - DCM, myocarditis, nutritional cardiomyopathy
- congenital volume overload - PDA, ASD, VSD
What are 3 causes of concentric hypertrophy?
- pressure overload - aortic/pulmonic stenosis, systemic hypertension, hyperthyroidism, systolic anterior motion of mitral valve (SAM)
- genetic - hypertrophic cardiomyopathy, myocarditis, nutritional cardiomyopathy
- infiltrative - neoplasia, amyloidosis, lysosomal disorders
CHF causes:
Diuretics:
