Cardiac failure (acute and chronic) Flashcards
Define cardiac failure
Inability of the cardiac output to meet the body’s demands despite normal venous pressures
Explain the aetiology and risk factors of low output cardiac failure
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
Explain the aetiology and risk factors of high output cardiac failure
Anaemia Beri beri Pregnancy Paget's disease Hyperthyroidism Arteriovenous malformation
Summarise the epidemiology of cardiac failure
10% > 65 yrs old
Recognise the presenting symptoms of cardiac failure
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
Recognise the signs of cardiac failure on physical examination
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 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
What is Pulsus alternans?
Arterial pulse waveforms showing alternating strong and weak beats. Sign of left ventricular systolic impairment
In left ventricular dysfunction, ejection fraction decreases leading to a reduction in stroke volume. Causes an increase in end -diastolic volume -> 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
Identify appropriate investigations for cardiac failure
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 - ABCDE 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 pressure
Generate a management plan for Acute left ventricle 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)
Generate a management plan for chronic left ventricle 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
Identify the possible complications of cardiac failure
Respiratory failure
Cardiogenic shock
Death
Summarise the prognosis for a patient with cardiac failure
50% with cardiac failure die within 2 years
