Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
13 Cards in this Set
- Front
- Back
what is cardiac reserve?
what is it's significance with heart failure patients? |
this is the ability to increase CO during increased activity.
people with heart failure often use their cardiac reserve at rest |
|
very basically, what is the pathophysiology of heart failure?
|
- a reduction in the pumping ability of the heart
- the adaptive mechanisms that serve to maintain CO but which also contribute to the progression of the disease |
|
what is PRE-LOAD?
what determines this |
it is the STRETCH relative to the volume of blood stretching the heart at the end of ventricular diastole.
largely determines by venous return |
|
what is AFTERLOAD?
what are the main determining components? |
the force the contracting heart must generate in order to eject blood from the heart
main components are TPR and ventricular wall tension |
|
what is CONTRACTILITY?
|
the mechanical performance of the heart
|
|
6 adaptive responses that maintain CO and lead to progression of heart failure
|
-Frank-Starling mechanism
-sympathetic nervous system activity -RAA system -natriuretic peptides -local vasoactive products (endothelin) -myocardial hypertrophy and remodelling |
|
adaptive responses that maintain CO and lead to progression of heart failure
-Frank-Starling mechanism..... --flowchart of how this works in heart failure --chronic effects -sympathetic nervous system activity -RAA system -natriuretic peptides -local vasoactive products (endothelin) -myocardial hypertrophy and remodelling |
-reduced CO
-reduced renal flow and increased salt and water retention -increased blood volume, venous return, EDV, PRELOAD -more optimal approximation of actin and myosin filaments, increasing the strength of the next contraction -chronically --the pressure is transmitted leading to oedema --overfilling of the ventricle reduces wall thickness and increases wall tension leading to increased myocardial oxygen demand leading to ischaemia, further impairment and dysfunction |
|
adaptive responses that maintain CO and lead to progression of heart failure
-Frank-Starling mechanism -sympathetic nervous system activity... --including chronic effects -RAA system -natriuretic peptides -local vasoactive products (endothelin) -myocardial hypertrophy and remodelling |
-increases catecholamine levels
-increased HR, contractility, peripheral and visceral vasoconstriction (maintain cerebral and coronary circulation) -chronically --increased TPR lead to increased AFTERLOAD --reduced flow to skin, muscle, kidneys, abdominal organs --high levels of catecholamines may contribute to arrythmias |
|
adaptive responses that maintain CO and lead to progression of heart failure
-Frank-Starling mechanism -sympathetic nervous system activity -RAA system -natriuretic peptides -local vasoactive products (endothelin) -myocardial hypertrophy and remodelling |
-decreased CO - reduced renal flow and GFR - salt and water retention
-increased RENIN release -increased ANGIOTENSIN II- vasoconstriction (increasing AFTERLOAD), also a GROWTH FACTOR for cardiac muscle and fibroblasts contributing to adverse cardiac remodelling -increased ALDOSTERONE - increased reabsorption of Na+ and H2O |
|
adaptive responses that maintain CO and lead to progression of heart failure
-Frank-Starling mechanism -sympathetic nervous system activity -RAA system -natriuretic peptides... -local vasoactive products (endothelin) -myocardial hypertrophy and remodelling |
-atrial natriuretic peptide
-released from atria in response to increased pressure and stretch -causes diuresis, natriuresis, loss of potassium in urine -inhibits RENIN and ALDOSTERONE secretion -antagonist for ANGIOTENSIN II -inhibits release of noradrenaline from presynaptic nerve terminals brain natriuretic peptide - similar action but stored in ventricular cells circulating levels of ANP and BNP are raised in heart failure |
|
adaptive responses that maintain CO and lead to progression of heart failure
-Frank-Starling mechanism -sympathetic nervous system activity -RAA system -natriuretic peptides -local vasoactive products (endothelin) -myocardial hypertrophy and remodelling |
-produced mainly in ENDOTHELIUM
-vasoconstrictors -myocyte hypertrophy -smooth muscle cell proliferation |
|
adaptive responses that maintain CO and lead to progression of heart failure
-Frank-Starling mechanism -sympathetic nervous system activity -RAA system -natriuretic peptides -local vasoactive products (endothelin) -myocardial hypertrophy and remodelling --including stimuli |
-increased workload
-increased production of sarcomeres and mitochondria -increased size of myocyte -reduced capillary density, increased intercapillary distance, increased synthesis leading to myocardial fibrosis and ventricular wall stiffness -stimuli --mechanical stress --angiotensin II --endothelins --ANP BNP |
|
explain
symmetric, concentric and eccentric hypertrophy |
SYMMETRIC - proportionate increase in length and width (as in athletes)
CONCENTRIC - in response to pressure overload - increase in wall thickness ECCENTRIC - in response to volume overload - increase in wall length, diastolic volume and wall tension, decrease in wall thickness |