Heart Failure
Definition: failure of the heart to maintain an adequate CO resulting in insufficient tissue
perfusion; and congestive cardiac failure occurs when plasma volume increases and fluid
accumulate in the lungs, abdominal organs and peripheral tissues.
Cardiac dysfunction precipitates changes in vascular function, blood volume, and
neurohumoral status. Initially these changes serve as compensatory mechanisms to help
maintain cardiac output (primarily by the Frank-Starling mechanism) and arterial blood
pressure (by systemic vasoconstriction).
The figures below summarise cardiac and vascular changes and compensatory
mechanisms in heart failure.
However, these compensatory changes over months and years can worsen cardiac
function. Therefore, some of the most effective treatments for chronic heart failure
involve modulating non-cardiac factors such as arterial and venous pressures by
administering vasodilator and diuretic drugs.
Cardiac Function
The cardinal feature of heart failure is decreased cardiac output due to decreased
stroke volume. Stroke volume decrease either because of systolic dysfunction,
diastolic dysfunction, or a combination of the two. Systolic dysfunction results from
poor contractility: due to dysrrhythmia or from the loss of viable, contracting muscle
as occurs following acute myocardial infarction. Diastolic dysfunction refers to the
diastolic properties of the ventricle and occurs when the ventricle becomes less
compliant (i.e., "stiffer"), which impairs ventricular filling. Therapeutic interventions
to improve cardiac function in heart failure include the use of cardio-stimulatory
drugs (e.g., beta-agonists and digitalis) that stimulate heart rate and contractility, and
vasodilator drugs that reduce ventricular afterload and thereby enhance stroke
volume.
Neurohumoral Status
Neurohumoral responses include activation of sympathetic nerves and the renin-
angiotensin system, and increased release of antidiuretic hormone (vasopressin) and
atrial natriuretic peptide. The net effect of these neurohumoral responses is to
produce arterial vasoconstriction , venous constriction and increased blood volume.
In general, these neurohumoral responses can be viewed as compensatory
mechanisms, but they can also aggravate heart failure by increasing ventricular
afterload (which depresses stroke volume) and increasing preload to the point where
pulmonary or systemic congestion and edema occur. Therefore some drug treatments
for heart failure involve reversing the effects of the neurohumoral changes.
Classification of heart failure
Acute HF: sudden e.g. MI
Chronic HF: gradual onset e.g. progressive valvular disease
Left ventricular failure: Reduced cardiac output with or without increased pulmonary
pressure eg. Hypertension, Coronary artery disease,Persistent dustus arteriosus
Right ventricular failure: reduced cardiac output on the right side e.g. Cor
pulmonale,Mitral stenosis
Biventricular/ congestive cardiac failure: e.g. in dilated cardiomyopathy, Ischemic
heart disease
High output: persitent high cardiac output leading ventricular dysfunction eg. Severe
anaemia, thyrotoxicosis
Causes of heart failure
cause features examples
Ventricular outflow Hypertrophy, hypertension,aortic
obstruction dilatation of stenosis,Pulmonary hypertension
ventricles
Ventricular inflow Small vigourous Mitral Stenosis,Triscuspid
obstruction ventricle + dilated Stenosis,constrictive pericarditis
atrium, atrial
fibrillation
Ventricle volume Dilatation, Mitral/Aortic Regurgitation,
overload hypertrophy Ventricular Septal Defect,
Thyrotoxicosis
Reduced vent Progressive vent Myocarditis,Myocardial
contractility dilatation Infection,Cardiomyopathy,
dysrrhythmia
Clinical Features
Symptoms depend on predominant side.
LVF: Fatigue, breathlessness, nocturnal cough, orthopnoea, paroxysmal nocturnal
dyspnoea due to Pulmonary congestion. Dyspnoea on exertion or rest. Pink frothy
sputum, Diffuse apex beat, basal crepitations, tachycardia,gallop rhythm,
peripheral cyanosis due to poor tissue perfusion
RVF: Fatigue, Abdomenal/ neck fullness, Tender Rt hypochondrium, Ankle
swelling, Tender hepatomegaly, Pitting oedema of dependent par
Pulmonary oedema: it is a life threatening acute LVF with sudden onset. There is fluid
shift into interstitial and alveoli.
Symptoms and signs
Extreme dyspnoea
Deep cyanosis
Tachypnea
Hyperpnea
Restlessness
Maybe thready pulse and BP low
Fine crepitations and laboured breathing
±wheeze
hypoxia
ACUTE LEFT VENTRICULAR FAILURE
Heart failure may develop suddenly as after myocardial infarction MI. The above
outlined compensatory mechanisms do not come into play. The patients with acute left
ventricular failure usually complain of sudden onset of rapidly increasing breathlessness;
occasionally this is accompanied by wheezing. The patient is usually sweating, breathless
and anxious, and on examination has basal crepitations due to pulmonary oedema, a
raised jugular venous pressure and gallop heart sounds. Acute left ventricular failure is a
life threatening emergency.
CAUSES OF LVF
1. Ischaemic Heart Disease - Many a times acute myocardial infarction first presentation
is acute LVF
2. Hypertension
3. Rheumatic heart disease
4. Congenital heart disease
5. High altitude
PRECIPITATING FACTORS
1. Tachyarrhythmia - Atrial fibrillation with fast ventricular rate
2. Infective endocarditis
3. Myocarditis
4. Severe physical exertion
5. Fluid overload
Clinical Features
1. Dyspnoea - Pt. is acutely breathless, restless, anxious, profusely sweating, often
cyanosed and orthopnoeic. Extremities are cold.
2. Cough - Patient gets cough with frothy white or pink sputum.
3. Pulse – is rapid and BP is high in hypertension. BP is low in low output states like
mitral stenosis, massive myocardial infarction.
4. Auscultation - Gallop rhythm present. Murmur of underlying heart disease may be
present. Respiratory system auscultation reveals basal crepitations, from first crackling
sound to bubbling crepitations all over. Sometimes rhonchi may be heard.
DIFFERENTIAL DIAGNOSIS
The following conditions are the important ones to remember.
Br. asthma : Previous H/o allergy and br. asthma present. There are more rhonchi,
extremities are warm, no gallop rhythm. X-ray chest may be normal or hyperinflated.
Pneumonia : H/O fever with chest pain, bronchial breathing localised crepitation may be
heard. X-ray will show the consolidation.
Pneumo-thorax : H/o trauma or thin individual tall person, previous history of TB
pneumothorax site of chest movement is restricted intercostal spaces are full on that side.
Breath sounds are absent. On percussion there is hyper resonance. X-ray will reveal the
diagnosis.
Pulmonary Embolism : H/O Bed rest giving rise to DVT, h/o Oral Contraceptive use,
H/O Valvular heart disease. Chest pain with difficulty in breathing, crepitation may be
heard on auscultation. X-ray chest may be normal or shows shadow of consolidation.
Renal Asthma : H/O Renal disease, acidotic breathing, rhonchi, no gallop or murmur. BP
is usually high. Creatinine is high and urine shows casts.
Anxiety Neurosis : Common in females, extremities are cold, anxious dramatising, no
gallop or murmur, no crepitation.
DIAGNOSIS/ INVESTIGATIONS
Symptoms and signs very helpful
Chest xray- all patients
Pulmonary congestion
Kerley B lines
Pleural effusions
ECG: nonspecific but provide etiology hint
Echocardiogram: may show reduced ejection fraction. It may also detect chamber
enlargement or valvular disease or wall motion abnormality in case of an infarct.
Blood electrolytes, creatinine,glucose, albumin
TREATMENT
Arrange for the patient to be transferred to hospital immediately .
While waiting for the ambulance, ddo the following
Prop up the patient i.e put the patient in a sitting position
start drug treatment.
• high concentration oxygen (unless you suspect COPD) by nasal catheter or venti
mask.
• furosemide (frusemide) 40-80mg IV can be repeated depending on recovery. Up to
500-800mg can be given
• repeat doses of furosemide and diamorphine if there is no improvement
after 20 minutes.
Sublingual nifedipine 5 mg in case of hypertension with LVF. Can be repeated every
10 minutes. till the BP drops to 150/100 mm Hg
Tab. Captopril 6.25 mg crushed sublingually provided BP is normal or high.
Treatment of the underlying cause can wait.
CHRONIC HEART FAILURE
Appoint When heart failure develops gradually as in chronic anaemia, hypertension or
progressive valvular damage, the above mentioned compensatory mechanisms may take
place. Symptoms and signs depend on which of these mechanisms take place.
Compensated heart failure is when these adaptive mechanisms prevent developing of
clinically overt heart failure. In this instance, minor events may precipitate a compesated
case into frank heart failure. These include:
1. Inappropriate reduction of therapy e.g. a patient not compliant to medication
2. Conditions associated with increased metabolic demands e.g. anaemia, pregnancy,
thyrotoxicosis, infections
3. Tachyarrhythmia - Atrial fibrillation with fast ventricular rate
4. Infective endocarditis
5. Myocarditis, myocardial infarction
6. Severe physical exertion
7. Fluid overload
8. administration of negative inotropic drugs e.g.
TREATMENT
Bed rest: increases renal blood flow
Reduced dietary salt intake and fluids
Drug treatment:
Increase removal of body fluids: Diuretics increase loss of urinary Na+ and thus fluids
leading to reduction of preload. This improves pulmonary congestion.
Reduce after-load (peripheral resistance) or preload using arteriole dilators or veno-
dilators respectively.
Increase cardiac contractility: Digoxin
