Chronic Heart Failure

Chronic Heart Failure – etiology, pathogenesis, circulatory disturbances, classification, clinical features, diagnosis, treatment

Clinical syndrome that develops when the heart cannot maintain adequate output, or can do so only at the expense of elevated ventricular filling pressures

Etiology

Pathophysiology

Cardiac output is determined by
- Preload – volume and pressure of blood in the ventricles at the end of diastole
- Afterload – pressure required to open the aortic valve
- Myocardial contractility
Impairment of ventricular myocardial function is main abnormality – leads to a fall in cardiac output (CO)
- Can be due to impaired systolic contraction and/or impaired diastolic relaxation
This activates counter-regulatory neurohormonal mechanisms – leads to ↑preload and afterload
Reduced CO and therefore renal perfusion stimulates activation of Renin – angiotensin – aldosterone system (RAAS)
Stimulation of RAAS → vasoconstriction; Na + water retention; SNS activation
- Mediated by angiotensin II – which is a potent constrictor of arterioles in kidney and systemic circulation
ANS – SNS activity initially ↑contractility (inotropy) and heart rate (HR) (chronotrophy) – sustains CO
- But prolonged stimulation causes negative effects – cardiomyocyte apoptosis, hypertrophy, necrosis
- SNS also causes peripheral vasoconstriction and arrhythmias
Aldosterone and ADH (vasopressin) release promotes retention of Na and water
- Natriuretic peptides (BNP/ANP) released from the atria in response to atrial stretch antagonise the fluid-conserving effect of aldosterone

Remodelling

LV remodelling is a process of progressive alteration of ventricular size, shape and function due to the influence of mechanical, neurohormonal and genetic factors
- Seen in MI, cardiomyopathy, HTN
Hypertrophy, loss of myocytes, interstitial fibrosis

Types of heart failure

Left, Right and Biventricular heart failure

Left heart failure
- Reduction of LV output and increase in left arterial pressure (LAP) and pulmonary venous pressure
- An acute rise in LAP causes pulmonary congestion and oedema
- A gradual rise in LAP leads to reflex pulmonary vasoconstriction – protect pt from pulm congestion, but in turn leads to PHTN, which can then impair RV function
Right heart failure (RHF)
- Reduction in RV output and increase in LAP and systemic venous pressure
- Causes of isolated RHF – corpulmonale, PE, pulmonary valve stenosis
Biventricular heart failure
- Diseases such as ischemic heart disease/dilated CMO affect both ventricles

Systolic dysfunction –HFrEF (reduced ejection fraction)

Diastolic dysfunction – HfpEF (preserved ejection fraction)

Increased stiffness and decreased compliance of LV – leads to impaired diastolic ventricular filling and ↓CO
MC in elderly hypertensive pts

High output failure

Excessively high CO due to arteriovenous shunt, Beri-beri , anaemia, thyrotoxicosis

Acute and chronic HF

Acute HF (decompensated) – can develop suddenly. Presents overtly (PCWP >16mmHg = poor prognosis)
- E.g. HF in MI
Chronic HF (compensated) – adaptive, compensatory mechanisms prevent the development of overt HF
- E.g. in valvular diseases

Clinical features

Chronic HF pts have a relapsing and remitting course – periods of stability and then periods of decompensation
Fatigue, restlessness, poor effort tolerance, cold peripheries – due to ↓CO
Oliguria, uraemia – due to poor renal perfusion
Dyspnoea, Pulmonaryoedema – LHF
High JVP, hepatic congestion, peripheral oedema – RHF
Cardiac cachexia – GI congestion causes impaired absorption

Complications

Renal failure, hypo/hyperkalaemia, hyponatremia, impaired liver function, thromboembolism, arrhythmias

Diagnosis

Blood test – FBC, U+E, LFT, BNP, thyroid function
Monitor – FLUID, FUNCTION, RHYTHM
CXR – cardiomegaly, pulmonary congestion, Kerley B lines
ECG
ECHO – chamber size, systolic/diastolic function, valvularabnormalities, cardiomyopathies. Stress ECHO w/ dobutamine
Cardiac MRI – cardiac structure, function and viability
Cardiac catheterisation – dx of IHD and measurement of pulmonary artery pressure, LAP (wedge)

Treatment

Drug therapy –aim to increase contractility, optimise preload and decrease afterload

Diuretics – ↓preload, improves pulmonary and systemic venous congestion
- Loop + thiazides can be combined for resistant oedema
Mineral corticoid receptor antagonist – can cause hyperkalemia when combined with ACEi
ACE inhibitors – interrupts vicious circle of neurohormonal activation (prevents conversion of AT I → AT II)
- Prevents peripheral vasoconstriction, SNS activity, Na + salt retention
ARBs – block the action of AT II
- Better tolerated than ACEi
Vasodilators
- Nitrates (venodilators) – reduce preload
- Hydralazine (arterial dilators) – reduce afterload
Beta blockers – counteract effects of ↑SNS activity, reduces risk of arrhythmias and sudden death
- Contra-indicated in acute HF due to negative inotropic effects
Ivabradine – acts on I_f inward current on the SAN, results in ↓HR
Digoxin – rate control

ICDs + resynchronisation

Heart transplant