Heart Failure

17/08/2013 by admin | Cardiology


Occurs when the heart is unable to maintain sufficient cardiac output to meet demands of the body (in essence left ventricular systolic dysfunction = LVSD)

Low output cardiac failure = congestive heart failure (‘pump failure’).

High output cardiac failure = when the body’s requirements for oxygen and nutrients are increased, and demand outstrips what the heart can provide = severe anaemia

Rare causes of HF:

  1. Gram negative septicaemia
  2. beriberi (vitamin B1/thiamine deficiency)
  3. thyrotoxicosis
  4. Paget’s disease
  5. arteriovenous fistulae
  6. arteriovenous malformations


Functional classification relies on the New York Heart Association Functional Classification (1 = no change, IV = debilitating)


10% >65 years suffer atherosclerosis

1% have HF


  1. Right heart failure (RHF) = systemic oedema and symptoms
  2. LHF: pulmonary symptoms.
    1. o HFREF: normal HF picture = fluid retention, LVH, systolic dysfunction.
    2. o HF with normal ejection fraction (HFNEF): >50% EF, non-dilated LV, due to:
    3. Isolated diastolic dysfunction (=restricted LV filling due to hypertrophy/AS/constrictive pericarditis/restrictive cardiomayopathy).
    4. Shortened diastolic filling time (tachy/AF)



  1. Fatigue
  2. Ankles swollen
  3. Cerebral signs
  4. Increased urinary frequency and renal congestion
  5. Anorexia
  6. Liver congestion
  7. Palpitations
  8. Ascites
  9. Nausea


Physical signs are usually more prominent:

  1. Jugular venous distension = raised JVP
  2. Tender smooth hepatic enlargement (maybe pulsatile)
  3. Dependent pitting oedema
  4. Development of free abdominal fluid (ascites)
  5. Pleural transudates (non-inlflammatory)


Chest xray changes of heart failure



  1. Alveolar oedema
  2. Kerley B-lines
  3. Cardiomegaly
  4. Dilated prominent upper lobe vessels
  5. Pleural Effusion


Left heart failure (LHF) = LUNGS!!!

  1. Fatigue
  2. Exertional dyspnoea
  3. Orthopnoea
  4. Paraoxysmal nocturnal dyspnoea


On examination

  1. Murmur, pansystolic
  2. Apex beat is displaced
  3. Tachycardia
  4. Crackles
  5. Auscultation reveals 3rd heart sound (Gallop rhythm, rapid ventricular filling)
  6. Tachypnoea


HF differentials:

CHF, COPD, chronic respiratory infection, arrhthymia, anaemia, nephrotic syndrome, PE, asthma, pneumothorax.


  1. Blood tests (=Trop T/I, CK)
  2. Chest xray (=ABCDE)
    1. o Kerley lines
  3. Electrocardiogram
  4. Natriuretic peptide (BNP in chronic HF [LV stretch])
  5. Echocardiography for cardiomegally
  6. Cardiac MRI
  7. PET scan


Aetiology – cause, risk factors

Main causes of heart failure:

  1. Ischaemic heart disease
  2. Cardiomyopathy (dilated)
  3. Hypertension
  4. Valvular disease
  5. Pregnancy
  6. Amyloid
  7. Sarcoidosis (=conduction abnormalities of ventricular arrhythmias)


Risk Factors:

  1. Dyslipidaemia
  2. Obesity/sedentary lifestyle
  3. Tobacco
  4. DM and MS
  5. Oestrogen deficiency and premature menopause
  6. Microalbuminaemia
  7. Age


  1. Male gender
  2. PMH of CVD
  3. HTN
  4. High homocysteine


Multiple RFs in synergy = increased risk!

Extra causes right heart failure (RHF)

  1. Chronic lung disease (cor pulmonale)
  2. Pulmonary embolism or pulmonary hypertension
  3. Tricuspid or pulmonary valve disease
  4. Left-to-right shunts
  5. Mitral valve disease with pulmonary hypertension


Extra cause left heart failure (LHF)

  1. Mitral regurgitation
  2. Aortic valve disease



When heart fails, compensatory mechanisms attempt to maintain cardiac output and peripheral perfusion.

Sympathetic nervous system

Improves ventricular function by increasing heart rate and myocardial contractility.

Constriction of venous capacitance vessel redistributes flow centrally.

Increased venous return to the heart (preload) further augments ventricular function via the Starling mechanism.

Stroke volume is directly proportional to the diastolic filling (ventricular end-diastolic pressure/pre-load).

As preload increases, stroke volume increases.

Contractility increases, stroke volume increases.

Sympathetic stimulation also leads to vasoconstriction, reducing pre-load and reducing cardiac output.

Renin-angiotensin system

Decrease cardiac output and increase sympathetic tone (increased TPR due to activation of angiotensin-II) lead to decreased renal perfusion, activation of RAA and therefore increased fluid retention.

Salt and water retention cause increase venous pressure and maintain stroke volume – promote suffiicent perfusion = oedema and dyspnoea.

Angiotensin II causes arteriolar constriction, increased afterload and work of the heart.


Increased BP = distension of atria = release peptides which have vasodilator and natriuretic properties.

Compensatory response leading to reduced cardiac output.

Ventricular dilation

Myocardial failure leads to a reduction of the volume of blood ejected with each heart beat.

Get increase in volume of blood remaining after systole.


  1. o General lifestyle advice
  2. o Education
  3. o Obesity control
  4. o Dietary modification
  5. o Smoking


  1. o Physical activity
  2. o Vaccination
    1. Pneumococcal
    2. Influenza


Drug management – do not use CCBs in HF!!

Stages of heart failure and treatment options:

Stage A: High risk with no symptoms Risk factor reduction, patient and family education.
Treat hypertension, diabetes, dyslipidaemia: ACE inhibitors (act on RAA pathway and slow progression) or ARBs in some patients
Stage B: Structural heart disease, no symptoms ACE inhibitors or ARBs in all patients, beta blockers in selected patients
Stage C: Structural disease, previous or current symptoms ACE inhibitors and beta-blockers in all patients
Dietary sodium restriction, diuretics and digoxin (+ve ionotrope)
Cardiac resynchronisation if bundle branch block present
Revascularisation, mitral valve surgery
Consider multidisciplinary team
Aldosterone antagonist (spironolactone), nesiritide
Stage D: Refractory symptoms requiring special intervention Inotropes
VAD, transplantation
Hospice = palliative



Patients with angina and left ventricular dysfunction have a higher mortality from surgery (10-20%), but have most to gain in terms of improved symptoms and prognosis.

  1. o CABG: use synthetic tubing or long saphenous vein
  2. o Transplant
  3. o Implantable cardioverter defibrillator (ICD)
  4. o Pacemaker


Use: Support myocardial function in patients with acute left ventricular failure and following cardiac surgery.
Drug Mechanism
Dobutamine (beta-1 selective) act on the beta1-adrenoceptor, increasing intracellular cyclic AMP. Increases calcium availability for myocardial contraction.

Causes peripheral vasodilation by an anti-alpha-adrenergic effect

Dopexamine (beta-2 selective) Selective beta2-agonist with an additional action on peripheral dopamine receptors. Theoretically results in improved renal perfusion.
Dopamine (non-selective) Less selective Used in low dose to improve renal perfusion.



50 – 70% die in 5 years (half of pump failure / half of conductance failure)

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