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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