19. The Pathophysiology of Heart Failure Flashcards
What is heart failure?
A state in which the heart fails to maintain an adequate circulation for the needs of the body despite an adequate filling pressure.
What is the primary cause of heart failure?
Ischaemic heart disease.
What are the four classes of heart failure progression according to the NYHA functional classing?
Class I - asymtpomatic limitation of physical activity.
Class II - slight limitation of physical activity, normal activity results in symptoms, but none at rest.
Class III - marked limitation of physical activity, less than normal activity results in symptoms, but none at rest.
Class IV - symptoms with any physical activity, even some at rest, discomfort increases with degree of physical activity.
What are the 6 year mortality rates for Class I, II, and III heart failure?
Class I - 60%.
Class II and III - 40%.
What is the 3 year mortality rate for Class IV heart failure?
80%.
What is Starling’s law for cardiac output and filling?
The force developed in a muscle fibre depends on the degree to which the fibre is stretched.
What happens to Starling’ curve for cardiac output and filling with mild heart failure and gross heart failure?
Mild - output increases with filling, but not to the efficient extent of normal heart function.
Gross - output increases with filling to an extent but then starts to decrease again.
What is the pathology of systolic dysfunction?
There is an increase left ventricular capacity, but reduced cardiac output. This leads to thinning of the myocardial wall and mitral valve incompetence as the ventricle dilates but the valve is the same size. This can lead to cardiac arrhythmias.
What happens structurally to the heart with systolic dysfunction?
Loss of muscle which is replaced by scar tissue, that can’t contract. There is uncoordinated contraction of the myocardium. More collagen in the extracellular matrix. Myocyte hypertrophy.
What is involved in neuro-hormonal activation on the heart?
The sympathetic nervous system, renin-angiotensin-aldosterone system, natriuretic hormones, anti-dieuretic hormone, endothelin, prostaglandins/ nitric oxide, kallikrien system, tissue necrosis factor.
What is the early compensatory mechanism to increase CO from the sympathetic nervous system acting on the failing heart?
Baroreceptor-mediated response to raise cardiac contractility, cause vasovonstriction of arteries and veins, and also tachycardia.
How is the sympathetic nervous system’s compensatory reaction to heart failure deleterious long term?
The B-adrenergic receptors are down-regulated/ uncoupled. Noradrenaline induces cardiac hypertrophy/ myocyte apoptosis and necrosis via a-receptors.
What happens to angiotensinogen in the RAAS?
Angiotensinogen is cleaved to angiotensin I, which is cleaved to angiotensin II, which acts on AT1R and AT2R receptors. Angiotensin I and II are hydrolysed by NEP to angiotensin III.
What does an increase in angiotensin II cause in the RAAS?
Acts on AT2R receptors which raise nitric oxide levels.
What happens to bradykinin in the RAAS?
It goes to Bk2R which raises nitric oxide levels.
Which receptor does angiotensin II act on to cause damage?
AT1R.
