Heart failure Flashcards
Define
DEFINITION: inability of the cardiac output to meet the body’s demands despite normal venous pressures
Causes
LOW OUTPUT Cardiac Failure (reduced cardiac output)
Left Heart Failure
Ischaemic heart disease
Hypertension
Cardiomyopathy
Aortic valve disease
Mitral regurgitation
Right Heart Failure
Secondary to left heart failure (in which case it is called congestive cardiac failure)
Infarction
Cardiomyopathy
Pulmonary hypertension/embolus/valve disease
Chronic lung disease
Tricuspid regurgitation
Constrictive pericarditis/pericardial tamponade
Biventricular Failure
Arrhythmia
Cardiomyopathy (dilated or restrictive)
Myocarditis
Drug toxicity
HIGH OUTPUT Cardiac Failure (increased demand)
Anaemia
Beri beri
Pregnancy
Paget’s disease
Hyperthyroidism
Arteriovenous malformation
Epidemiology
10% > 65 yrs old
Symptoms
Left Heart Failure - symptoms caused by pulmonary congestion
Dyspnoea - divided based on the New York Heart Association classification:
1 - no dyspnoea
2 - dyspnoea on ordinary activities
3 - dyspnoea on less than ordinary activities
4 - dyspnoea at rest
Orthopnoea
Paroxysmal nocturnal dyspnoea
Fatigue
Acute Left Ventricular Failure
Dyspnoea
Wheeze
Cough
Pink frothy sputum
Right Heart Failure
Swollen ankles
Fatigue
Increased weight (due to oedema)
Reduced exercise tolerance
Anorexia
Nausea
Signs
Left Heart Failure
Tachycardia
Tachypnoea
Displaced apex beat
Bilateral basal crackles
S3 gallop (caused by rapid ventricular filling)
Pansystolic murmur (due to functional mitral regurgitation)
Acute Left Ventricular Failure
Tachypnoea
Cyanosis
Tachycardia
Peripheral shutdown
Pulsus alternans
Arterial pulse waveforms showing alternating strong and weak beats
Sign of left ventricular systolic impairment
Explanation:
In left ventricular dysfunction, ejection fraction significantly decreases leading to a reduction in stroke volume
This causes an increase in end-diastolic volume
This means that the left ventricle is stretched more for the next contraction
Due to Starling’s Law, the increased stretch of the left ventricle caused by the increased end-diastolic volume following the previous beat leads to an increase in the strength of the myocardial contraction
This results in a stronger systolic pulse
Gallop rhythm
Wheeze (cardiac asthma)
Fine crackles throughout lung
Right Heart Failure
Raised JVP
Hepatomegaly
Ascites
Ankle/sacral pitting oedema
Signs of functional tricuspid regurgitation
Investigations
Bloods
FBC
U&E
LFTs
CRP
Glucose
Lipids
TFTs
In ACUTE Left Ventricular Failure
ABG
Troponin
BNP
Raised plasma BNP suggests diagnosis of cardiac failure
Low plasma BNP rules out cardiac failure (90% sensitivity)
CXR
Alveolar shadowing
Kerley B lines
Cardiomegaly
Upper Lobe Diversion
Pleural Effusion
ECG
May be normal
May show ischaemic changes (pathological q waves, t wave inversion)
May show arrhythmia or left ventricular hypertrophy
Echocardiogram
Assess ventricular contraction
Systolic dysfunction = LV ejection fraction < 40%
Diastolic dysfunction = decreased compliance of the myocardium leads to restrictive filling defect
Swan-Ganz Catheter
Allows measurement of right atrial, right ventricular, pulmonary artery, pulmonary wedge and left ventricular end-diastolic pressures
Management
Acute Left Ventricular Failure
Treating Cardiogenic Shock:
This is severe cardiac failure with low blood pressure
Requires the use of inotropes (e.g. dobutamine)
Managed in ITU
Treating Pulmonary Oedema:
Sit the patient up
60-100% Oxygen (and consider CPAP)
Diamorphine (venodilator + anxiolytic)
GTN infusion (venodilator –> reduced preload)
IV furosemide (venodilator and later diuretic effect)
Monitor:
BP
Respiratory rate
Oxygen saturation
Urine output
ECG
TREAT THE CAUSE! (e.g. MI, arrhythmia)
Chronic Left Ventricular Failure
TREAT THE CAUSE (e.g. hypertension)
TREAT EXACERBATING FACTORS (e.g. anaemia)
ACE Inhibitors
Inhibits renin-angiotensin system and inhibits adverse cardiac remodelling
They slow down the progression of heart failure and improve survival
Beta-Blockers
Blocks the effects of a chronically activated sympathetic system
Slows progression of heart failure and improves survival
The benefits of ACE inhibitors and beta-blockers are additive
Loop Diuretics
Alongside dietary salt restriction, can correct fluid overload
Aldosterone Antagonists
Improves survival in patients with NYHA class III/IV symptoms on standard therapy
Monitor K+ (as these drugs may cause hyperkalaemia)
Angiotensin Receptor Blockers
May be added in patients with persistent symptoms despite the use of ACE inhibitors and beta-blockers
Monitor K+ (as these drugs may cause hyperkalaemia)
Hydralazine and a Nitrate
May be added in patients (particularly Afro-Caribbeans) with persistent symptoms despite the use of ACE inhibitors and beta-blockers
Digoxin
Positive inotrope
Reduces hospitalisation but does NOT improve survival
N-3 Polyunsaturated Fatty Acids
Provide a small beneficial advantage in terms of survival
Cardiac Resynchronisation Therapy
Biventricular pacing improves symptoms and survival in patients with a left ventricular ejection fraction < 35%, cardiac dyssynchrony (QRS > 120 msec) and moderate-severe symptoms
These patients are also candidates for implantable cardioverter defibrillator (ICD)
They may receive a combined device
CAUTION: avoid drugs that could adversely affect a patient with heart failure due to systolic dysfunction (e.g. NSAIDs, non-dihydropyridine CCBs)
Complication
Respiratory failure
Cardiogenic shock
Death
Prognosis
50% with cardiac failure die within 2 years
