Heart Flashcards
What is heart failure
Inability to provide adequate output to support needs of the tissue
What are normal circulation values
Systemic veins: 5mmHg
Pulmonary artery: 30mmHg
Pulmonary veins: 8mmHg
Aorta: 100mmHg
What do baroreceptors do
In the aorta and bifurcation of the carotids - ensure aortic pressure is cosntant
What is right sided heart failure
Cannot pump blood effectively into pulmonary circulation. Blood backs up behind right ventricle. Only systemic venous pressure changes to 10mmHg as right ventricular end-diastolic pressure increases
What is left sided heart failrue
Impaired pumping causes CO to fall to 6mmHg. Blood backs up in to the left side of heart. Pulmonary venous pressure rises because left end-diastolic pressure is increased. Elevated venous pressure transmitted through lungs to increase pulmonary artery pressure
What is congestive heart failure
Failure of left side puts strain on the right. Increase of pulmonary vein pressure due to left side back up, increase of pulmonary artery pressure as lungs back up, increase of systemic veins as right side backs up
What pressure is kept constant
Aortic
What are the three causes of heart failure
Pressure overload, volume overload, contractile dysfunction
What are examples of pressure overload
Hypertension, aortic stenosis - obstruction in the outflow tract
What are examples of volume overload
Aortic or mitral valve regurgitation - ventricles have too much blood at the wrong time
What are examples of contractile dysfunction
Ischaemic heart disease, myocardial disease, pregnancy - changes to hormonal balance, congenital cardiomyopathies)
What is Laplace’s law
For a fixed wall stress, a small ventricle can generate high pressure than a large ventricle. When a heart gets bigger, for the heart to generate the same pressure it must either increase the amount of work done by the fibres or increase the wall thickness
What occurs to heart muscles during pressure overload
Increase in left ventricular pressure -> increase wall stress. Muscles have to work harder to muscles enter concentric hypertrophy (R becomes smaller) -> heart starts to dilate, which further increases wall stress
What occurs to heart muscles during volume overload
Valve regurgitation, increasing radius -> wall stress increases
Wall stress normalised by dilated hypertrophic myocardium -> eventually enters myocardial failure
What occurs to heart muscles during dilated cardiomyopathy
Hypertrophy equals degree of chamber enlargement -> excessive chamber enlarge and inadeqaute hypertrophy
What occurs to heart muscles in hypertrophic cardiomyopathy (normal relation between wall thickness and wall stress)
Development of dilation leads to myocardial failure
What is the normal weight of the heart
Less than 450g in males and less than 400g in females
Ratio of LV/body height should be less than 36
What happens in the cardiac compensatory mechanism
Acute overload -> myocyte growth - hypertrophy -> physiological hypertrophy (normal) or -> concentric hypertrophy (fatter) or eccentric hypertrophy (longer) - these both have increased expression of embryonic genes
What are the 3 phases of heart failrue
Short term acute: functional reserves overwhelmed by overload Compensated hypertrophy (can last up to 10 years): heart enlarges and adapts Chronic failure: exhaustion, cell death and necrosis
Describe the steps of the neurohumoral compensatory mechanism
LV failure -> CO falls -> BP falls -> baroreceptor reflex sympathetic stimulation -> peripheral vasoconstriction and increased HR and contractility -> constriction of renal arteries to retain slat and water -> CO returns to normal and BP returns to normal
Describe the renal compensatory mechanism
Sympathetic stimulation -> renal artery vasoconstriction -> sodium and water retention -> RAAS pathway -> increased CVP -> increased end diastolic pressure
How does the RAAS pathway work
Renin secretion by juxtaglomerular cells kidney -> convert angiotensinogen to angiotensin I -> angiotensin II by ACE -> AGII causes vasoconstriction at tissues and raises blood pressure and releases aldosterone from adrenal lands -> slat and water retention
How do ANPs work
Rise in CNP cause release of ANP. Diuretic action - vasodilates and inhibits aldosterone secretion, noradrenaline release. ANP is an endogenous antagonist for AGII.
Why do the beneficial effects of ANP not dominate
Increase in ANP overwhelmed by vasoconstriction and slat and water retention induced by activation of RAAS. ANP secretion becomes down regulated and vascular ANP receptors desensitised