heart failure

Question 1

define heart failure

Answer 1

complex clinical syndrome resulting from any structural or functional impairment of ventricular filling or ejection of the blood. cardinal manifestations of HF are dyspnoea which may limit exercise tolerance and fluid retention, which may lead to pulmonary and/ splanchnic congestion /peripheral oedema

fatigue
dyspnoea
some have no symptoms of volume overload
no single diagnostic test for HF - PE + hx

Question 2

HF in ireland

Answer 2

2% of pop
2-4% have left ventricular dysfunction - high risk for heart failure

Hf is major drain on health care spending - 2-4% of total healthcare budget

HF prevalence continues due to:
ageing pop
improved survival post MI
obesity htn t2dm - difficulty managing cardio-metabolic diseases

Question 3

HF classification

Answer 3

Patients with HF are commonly stratified into 2 groups based on the contractile function of the left ventricular myocardium:
HF with reduced ejection fraction (HFrEF) or
HF with preserved ejection fraction (HFpEF).

Patients with HFrEF have a left ventricular ejection fraction (EF) less than 40% and have an inadequate stroke volume and cardiac output as the primary manifestation.
Patients with HFpEF have relatively normal contractile abilities of the left ventricle (EF >50%) with pathophysiologic manifestations of the disease process defined by impaired relaxation of the left vent

Question 4

renin angiotensin aldosteron system

Answer 4

Stimulation of the renin-angiotensin-aldosterone system leads to increased concentrations of renin, plasma angiotensin II, and aldosterone. Angiotensin II is a potent vasoconstrictor of the renal (efferent arterioles) and systemic circulation, where it stimulates release of noradrenaline from sympathetic nerve terminals, inhibits vagal tone, and promotes the release of aldosterone. This leads to the retention of sodium and water and the increased excretion of potassium.

Question 5

atrial natriuretic peptide and brain natriuretic peptide

Answer 5

ANP is released from the atria in response to stretch, leading to natriuresis (excretion of sodium in the urine) and vasodilatation.

BNP is also released from the heart, predominantly from the ventricles, and its actions are similar to those of ANP.

The ANP and BNP increase in response to volume expansion and pressure overload of the heart and act as physiological antagonists to the effects of angiotensin II on vascular tone, aldosterone secretion, and renal-tubule sodium reabsorption