Heart Failure Flashcards
ventricular stroke volume is dependent on which three factors
preload
afterload
contractility
how is preload approximated
by measuring ventricular end-diastolic volume
what is preload
ventricular wall tension at the end of DIASTOLE
what is afterload
ventricular wall tension during SYSTOLE
how is afterload approximated
systolic arterial/ventricular pressure
what is ventricular end-systolic volume dependant on/
afterload and contractility but not preload
how is ventricular wall stress estimated and what is its relationship to wall thickness and chamber radius
Laplace’s relationship
wall tension is proportional to radius and inversely proportional to wall thickness
besides the side of heart failure, heart failure can be divided into two categories. Name them and briefly describe them
PRESERVED ejection fraction or DIASTOLIC dysfunction- abnormality in ventricular filling
REDUCED ejection fraction or SYSTOLIC dysfunction - an abnormality in ventricular filling from impaired contractility or increased afterload
name 5 conditions which impair ventricular filling
conditions which impair early diastolic relaxation (as this is an active process) or increase the stiffness of the ventricular wall
- left ventricular hypertrophy
- restrictive cardiomyopathy
- transient myocardial ischaemia
- myofibrosis
- pericardial constriction or tamponade
name three things which impair contractility of the ventricles
coronary artery disease (MI/transient ischaemia)
chronic volume overload (mitral or aortic regurg)
dilated cardiomyopathies
name two conditions which can increase afterload in heart failure
aortic stenosis
uncontrolled HTN
describe two conditions which are non-cardiac in origin which cause heart failure
inadequate perfusion (severe haemorrhage)
increased metabolic demand (hyperthyroid)
outline three pathophysiological processes which occur in cardiac muscle leading to decrease in contractility
- change in gene expression (from adult to foetal)
- less efficient energetics
- impaired calcium handling (impair calcium release –> systolic dysfunction; impaired pumping of calcium outside of the cell impairs relaxation)
name three mechanisms of heart failure compensation
the Frank-Starling mechanism
neurohormonal adaptations
ventricular hypertrophy and remodelling
all of these mechanisms eventually become maladaptive
how does the Frank-Starling compensatory mechanism restore cardiac output
reduced stroke volume leads to incomplete ventricular emptying
on the next cardiac cycle this means the diastolic volume is increased.
This means that there is an increased stretch in the heart muscle and therefore increased contraction
which three neurohumoral alterations help compensate heart failure
- the adrenergic nervous system
- RAAS
- incr production of ADH
what are the three immediate effects from activation of the sympathetic nervous system in the context of heart failure compensation
increased contractility
increased heart rate
increased vasoconstriction (via alpha receptors in arteries and veins)
how does venous vasoconstriction increase cardiac output
it increases the venous return to the heart (increasing preload) which leads to increased stroke volume
what are the stimuli for renin release from the juxtaglomerular cells in the kidney in heart failure patients
1) decreased renal perfusion following reduced CO
2) decreased salt delivery to macula densa
3) direct stimulation of beta-2 receptors in juxtaglomerular apparatus via the sympathetic nervous system
name two ways angiotensin II increases the intravascular volume
1) at the hypothalamus it stimulates thirst
2) increases aldosterone secretion at the adrenal cortex
when is BNP released
it is not normally detected but is released when the ventricular myocardium undergoes haemodynamic stress
what is endothelin-1 and what is its significance in heart failure
a potent vasoconstrictor from endothelial cells
in heart failure endothelin-1 levels correlate with adverse outcomes
how does chronic volume overload alter the ventricular musculature
it results in ECCENTRIC hypertrophy - addition of new sarcomeres in series
this impairs filling as the wall become stiffer
how does chronic pressure overload alter the ventricular musculature
it results in CONCENTRIC hypertrophy - addition of new sarcomeres in parallel
this alters the wall tension owing the Laplaces law as the ventricle becomes thicker
