Pathophysiology of Heart Failure Flashcards
how does the heart respond to stress?
- concentric hypertrophy (wall thickening):
-response to increased end-systolic wall stress (afterload)
-lays down sarcomeres in parallel
-pressure overload hypertrophy
-ex. systemic arterial hypertension - eccentric hypertrophy (chamber dilation, wall thickness stays the same)
-response to end-diastolic wall stress (pre-load)
-sarcomeres laid down in series
-volume overload hypertrophy
contrast heart success to heart failure
heart success: enough blood is ejected to
-maintain MAP!!!!!!!!!!!!!
-meet body’s metabolic demands
-adequately drain pulmonary and systemic veins to maintain appropriate distribution of circulating pool
heart failure: inability of heart to pump enough blood
-to maintain metabolic demands of peripheral tissues (forward heart failure) and/or
-to meet these demands WITHOUT the trade-off of increased heart filling pressures and poor venous drainage (backwards/congestive heart failure)
-usually present with a little bit of both forward and backward failure
heart failure is an end stage result of severe heart disease, many causes!
describe congestive heart failure
- increased venous/capillary hydrostatic pressure upstream of the heart, resulting in tissue edema and/or cavitary effusion
- maladaptive response to heart disease, mediated by neuro-hormonal changes intended to maintain normal MAP above all else!
-phase I: initiation; heart disease/injury = can no longer maintain normal stroke volume, cardiac output goes down and so does MAP (body HATES this)
-phase II: compensation via activation of neurohormonal systems that increase the cardiac workload!
–SNS activation, RAAS activation, overexpression of endothelin, vasopressin/ADH, and pro-inflammatory cytokines
-phase III: diseased heart has decreased capacity to respond to the increased workload, so we cause further damage and eventually lead to congestive-ness
what is the NUMBER ONE priority of the heart?
maintaining mean arterial pressure!!
MAP = CO x SVR
CO = HR x SV
SV = end diastolic volume - end systolic volume and determined by preload, afterload, and contractility
the body will manipulate
-SVR
-HR
-preload
-contractility
in response to the reduced CO of heart disease (also drug targets!)
what are 2 examples of diseases causing congestive heart failure?
- degenerative mitral valve disease
-primary problemL misdirection of blood flow (regurgitation) leading to decreased forward stroke volume - hypertrophic cardiomyopathy:
-primary problem: stiff left ventricle leading to poor diastolic filling and decreased forward stroke volume
describe the response of the sympathetic nervous system in early response to heart disease (baroreceptor reflex)
- heart disease decreases CO which decreases MAP
- decreased stretch of arterial baroreceptors decreases firing rate of the baroreceptors
- the baroreceptors send signals to the vasomotor center in the brain which
-increases sympathetic nervous system outflow, which increases systemic vasoconstriction (alpha receptors), increases heart rate and contractility (B1), and activates RAAS (B1) AND
-decreases parasympathetic nervous system outflow, which increases heart rate and contractility
-this leads to restoration of normal MAP in the short term but is detrimental chronically by increasing the workload on an already-injured heart and promote further injury
describe RAAS in intermediate and long term response to heart disease
- stimuli for renin release:
-decreased blood pressure (afferent arteriole of kidney)
-adrenergic stimulation (B1 adrenergic receptors)
-decreased Na+ delivery to distal tubule (macula densa) - angiotensin I: increases thirst and salt hunger, increases ADH release, and increases activity of sympathetic nervous system
- angiotensin II: increases myocardial contractility and Na+/H2O reabsorption
- angiotensin II: leads to overall vasoconstriction!!
- net effects of RAAS are: increased preload, increased heart rate, increased contractility, and increased SVR
describe the frank-starling relationship of CHF
- increased preload = increased stroke volume = increased cardiac output (normal frank-starling relationship)
- diseased heart can’t maintain output at normal preload and can’t respond fully to preload increases
-frank-starling relationship shifts downward and flattens
-body tries to normalize cardiac output by increasing preload via neurohormonal (SNS and RAAS) activation
-blood volume may be 30% > normal
-initial cardiac response = eccentric hypertrophy - eventually excess preload = increased diastolic (filling) pressure = increased venous and capillary hydrostatic pressures (congestion)
-if venous pressure > 20-25 mmHg (normal 5-15mmHg): fluid leak from capillaries > lymphatic drainage, edema/cavitary effusions occur
describe cardiogenic pulmonary interstitial edema (left-sided CHF); compare to normal microvascular fluid exchange in the lung
normal microvascular fluid exchange in lung:
-small amount of fluid moves from capillary to interstitium
-fluid removed by lymphatics and returned to circulation
-no fluid enters alveoli due to tight cell junctions
fluid exchange in chronic left-sided heart disease:
-increased left-sided filling pressure transmitted to pulmonary veins (no valve to protect them) = increased pulmonary capillary hydrostatic pressure
-if fluid movement out of capillaries > fluid drainage by pulmonary lymphatics, CHF occurs
-when left atrial pressure = 20-25mmHg (normal = 0-5mmHg), interstitial fluid (edema) accumulates
-at LAP > 25 mmHg, fluid floods alveoli, which interferes with normal gas exchange
describe the harm of increased afterload in heart disease and failure
- frank-starling mechanism also explains how the heart adjusts to acute changes in afterload
- for practical purposes, increases in afterload do not put substantially reduce stroke volume and cardiac output unless:
-afterload is severely increased
-the heart is diseased (vasoconstriction, diseased heart can’t handle it)
