5. heart failure (clinical aspects, medical therapy, emergency treatment of cardiac diseases) Flashcards
heart failure definition
- heart don’t pump blood satisfactorily
- cardiac output is not enough to deliver nessecary amount to tissues
- generally chronic process
- cellular remodeling
consequence of heart fail
physical
neurohormonal
inflammatory
physical consequences of heart fail
CO: decreased, not enough preload increased contractility increased afterload increased heart rate increased distensibility increased
general preload
initial stretching of cardiac myocytes (left ventricle filling at end of diastole)
if preload increase -> CO increase
-> congestion and increased oxygen demand
can decrease preload with diuretics, ventilators
general contractility
the ability of the heart to contract
change in rhythm causes change in contractility
increased contractility -> increased CO -> increased energy and oxygen demand
general afterload
the pressure the heart works against to eject blood in ventricular systole
determined by vascular resistance
increased after load - decreased CO -> hypertrophy and oxygen demand increase
general heart rate
the number of times heart beats per minute
increased HR: first increased CO then decreased CO
general distensibility
the stretching ability of the heart
increased distensability -> increased CO -> pathological dilatation, increased oxygen and energy demand
general CO
cardiac output = the volume of blood the heart pumps per minute
stroke volume x heart rate
neurohormonal consequences
compensation of heart failure
compensatory mechanism
- systain arterial pressure to vital organs
- systain arterial pressure to other organs
- keep systemic venous blood pressure reasonably low (preload)
neurohormonal consequences
what
increased sympathetic outflow from brainstem
catecholamine levels in blood increase
neurohormonal consequences
how
elevate heart rate
increase myocardial activity
peripheral vasoconstriction
increased blood volume (RAAS)
role of RAAS in compensation prosess
increased renin synthesis -> angiotensinogen ->-> angiotensin 2
-> vasoconstriction
water and sodium retention
inflammatory reactions
permanent RAAS activation
increased heart rate
insufficient O2 and energy supply of myocytes
ENDOTHELIN release
free radicals
inflammatory mediators - cytokine, TNF, IL
=> all lead to further myocardial injury, decrease contractility
endothelin
most potent vasoconstrictor
synthesized in endothelium and myocardium
lead to vasoconstriction and cardiac hypertrophy
