what is heart failure
inability of the heart to maintain tissue perfusion at normal filling pressure
what does the frank starling curve show
as we increase the end diastolic pressure of the left ventricle the stroke volume in systole increases
what does increased adrenaline do to the heart
increases heart rate and force of contraction to increase stroke volume
why does heart failure decrease starlings curve
heart does not have enough force to pump blood around the body but there is a high LV end diastolic pressure
what is systolic dysfunction
impaired ventricular contraction/ inotropy
what is diastolic dysfunction
impaired ventricular relaxation
what are the physiological effects of heart failure
what is preload
volume of blood in the ventricles after diastole
what is afterload
resistance left ventricle overcomes to overcome circulating blood
what are neurohormonal changes in heart failure
compensation for the lack of oxygen that is reaching the body so increases neuronal and hormonal firing
what is the maladaptive remodelling in heart failure
issues are not helped or corrected then they become worse and cycle starts again
what are the electrophysical changes in heart failure
what causes an increase in heart contraction
why is digoxin used in heart failure
why is dobutamine used in heart failure
why is milrinone used in heart failure
why don’t inotropic agents not always work
heart works faster as stimulation increased but is less efficient
what are the pro-arrhythmogenic changes in heart failure
increase inward current + decreased outward current = action potential prolongation causing arrhythmias
what causes an increase in sympathetic overactivity in heart failure
how is beta1 adrenergic signalling altered in heart failure
what are the beta 1 adrenergic mediated effects
how is the RAAS system activated
stages of vasoconstriction as neurohormonal signalling compensation
how does Na+ and H2O retention increase preload