Heart Failure is…

  • Inability of the heart to pump adequate amounts of blood to meet the body’s metabolic demands
  • End stage of all heart diseases
  • Accounts for 5 in 1000 hospital admission each year in the UK


  • Systolic HF – inability of the heart to contract efficiently to eject adequate volumes of blood to meet the body metabolic demand [most common].
  • Diastolic HF – reduction in the heart compliance resulting in compromised ventricular filling and therefore ejection [pericardial disease, restrictive cardiomyopathy, tamponade]
  • Left HF –  inability of the left ventricle to pump adequate amount of blood leading to pulmonary circulation congestions and pulmonary edema. Usually results in RHF due to pulmonary hypertension.
  • Right HF –  inability of the right ventricle to pump adequate amount of blood leading to systemic venous congestion, therefore peripheral edema and hepatic congestion and tenderness.
  • Congestive HF –  failure of both right and left ventricles, which is more common.
  • Low-output HF –  heart failure resulting from reduced cardiac output [Most common]
  • High-output HF –  heart failure that occurs in normal or high cardiac output due to metabolic demand and supply mismatch, either due to reduced blood oxygen carrying capacity [Anemia] or increase body metabolic demand [thyrotoxicosis]
  • Acute HF –  acute onset of symptom presentation usually due to acute event [MI, persistent arrhythmia, Mechanical event (ruptured valve, ventricular aneurysm)]
  • Chronic HF – slow symptoms presentation usually due to slow progressive underlying disease [CAD, HTN etc…]
  • Acute-on-chronic; acute deterioration of a chronic condition, usually following an acute event [anemia, infections, arrhythmias, MI]

Causes of HF

Ischemic heart disease
Valvular disease
Pericardial disease
  • Pericarditis
  • Pericardial effusion
  • Alcohol
  • Cocaine
  • Chemotherapeutic drugs [Beta-blockers]
  • Bradycardia
  • Tachycardia
  • Atrio-ventricular miss-match due to Atrial or ventricular arrhythmia
  • Congestive ‘dilated’
  • Hypertrophic
  • Restrictive
Severe Anemia
Pulmonary hypertension- Pulmonary pathologies


IHD –  infarction causes impaired ventricular function, therefore reduced contractility function and HF. IHD are the most common cause of HF along with HTN
HTN –  increase strain on the heart, since the heart have to pump blood against a high afterload, leading to hypertrophy which increase the chances of arrhythmias. The heart would eventually gets too big for the coronary system to perfuse leading to IHD and compromised ventricular function
Cardiomyopathy –  disease of the heart muscle that is not secondary to IHD, HTN, valvular, congenital or pericardial disease. Several types;

  • Congestive; weakening and dilation of ventricular walls leading to overstretching, therefore reduced contractile efficiency. Most common cause of HF in the absence of IHD, valvular disease and HTN. Might have a familial link
  • Hypertrophic; thickening of the heart muscle wall leading to reduced compliance and therefore reduced CO. The thickening involves an increase in fibrous tissue of the heart, which increases the chances of arrhythmias such as ventricular fibrillation, which is a common cause of death in young adults. This disease has a strong familial link.
  • Restrictive; reduced heart compliance without significant increase in muscle wall thickness leading to reduced EDV and CO. This can be caused by infiltrative disease such as sarcoidosis, amyloidosis, hemachromatosis and endocardial fibrosis.


  • Bradycardia – CO = HR X SV. Therefore reduced HR reduces CO
  • Tachycardia –Reduced ventricular filling duration, increased heart oxygen demand and ventricular dilatation
  • Abnormal atrial and ventricular contractions àAF removes active ventricular filling leading to reduced EDV and CO. VT also causes reduced EDV due to reduced ventricular filling period.

Alcohol – Acute heart failure, arrhythmias such as AF and dilated cardiomyopathy in alcoholics
Infections – due to toxic effects of infection on heart itself along with vasodilation and tachycardia increase myocardial oxygen demand. Patients with chronic HF are more susceptible to infections
Myxedema – can cause HF due to direct effects on myocardium, bradycardia and pericardial disease


  • MAP = CO X TPR
  • CO = SV X Heart Rate
  • SV = EDV – ESV
HF causes a drop in MAP that initially stimulates baroreceptors that feed back into the medullary cardiovascular center [MCVC]. MCVC tries to increase and maintain the MAP by reducing vagal tone and increase sympathetic tone leading to increase heart contractility and rate therefore output. The sympathetic system also stimulates the contraction of arteries [inc. TPR] and veins [inc. venous return] and the release of adrenaline from adrenal medulla, which stimulate all of the above actions. Renin-angiotensis-system [RAS] is also stimulated in heart failure due to reduced kidney perfusion caused by reduced MAP and vasoconstriction and direct sympathetic stimulations. The end product, Angiotensin II, causes vasoconstriction, aldosterone release and ADH release causing Na and water retention by the kidneys. These mechanisms are beneficial initially as they increase blood volume, therefore venous return and SV, TPR and HR, therefore maintaining a high CO, however, chronically these compensatory mechanisms act to worsen the situation;

Increase TPR

  • Increase afterload therefore increasing workload and strain on the heart
  • Tissue underperfusion leading to ischemia
  • RAS system stimulation

Increase HR

  • Increase workload and therefore oxygen demand of the heart

Fluid retention

  • Increase stretching of the heart eventually leading to dilatation of ventricles which possess reduced contractility
  • Fluid build up causes fluid transudation into interstitial tissue causing peripheral and pulmonary edema
  • Hyponatremia and hypokalemia

Clinical presentations

 Fatigue, lethargy and exercise intolerance
 Peripheral Swelling [edema]
 Weight loss
 Paroxysmal Nocturnal Dyspnea
 Peripheral Edema History
 Elevated JVP [venous congestion]
 Pulsus alternans
 Displaced Apex Beat [sign of cardiomegaly]
 Gallop [S3]
 Bilateral Crepitations
 Cardiomegaly on CXR
 Cachexia [dec. appetite, weight loss, lethargy, muscle atrophy]
Hepatic Tenderness
  • Dyspnea due to pulmonary edema and respiratory muscle weakness
  • Orthopnea dyspnea that occurs just after lying down [fast developing]
  • PND dyspnea that occurs during lying down/sleeping forcing sudden awakening of the patient. This occurs due to blood redistribution during lying down causing increase venous blood in the lungs causing transudation of plasma into the alveolar spaces [Pulmonary edema]
  • Fatigue, Lethargy and Exercise Intolerance exercise intolerance occurs due to inability of the heart to raise the CO during exercise as it has used its cardiac reserve by fluid retention. Fatigue and lethargy occurs due to the compromised CO leading to tissue hypoperfusion. Muscle tissue are one of the tissues that undergo atrophy and altered metabolism due to hypoperfusion, causing lethargy and fatigue, as well as exercise intolerance when it involves respiratory muscles
  • Peripheral edema occurs predominantly due to right heart failure causing blood congestion in systemic circulation, causing increased venous pressure, therefore fluid transudation into the interstitial spaces. These spaces can be the lungs, ankles/sacrum and liver.

Diagnosis of Congestive Heart Failure – the Framingham Criteria
A formal set of diagnostic criteria for congestive heart failure (CHF) resulted from the well-known Framingham Heart Study (an excellent example of a prospective study, to be mentioned in any public health examinations!). As with other diagnostic criteria systems this one makes use of Major and Minor criteria which, apart from being study aids in themselves, are sure to impress finals examiners if you can remember them (mnemonics provided for this purpose!). Diagnosis of congestive heart failure using the Framingham criteria requires simultaneous presence of 2 Major or 1 Major and 2 Minor criteria, which provide for a 100% sensitivity (but 78% specificity) value when diagnosing the symptoms and signs of CHF.

  • Major
    • S3 heart sound present (‘gallop’ sound)
    • Acute pulmonary oedema (left side of heart is unable to clear fluid from lungs)
    • Weight loss of more than 4.5kg in 5 days when treated (patients lose their retained fluids)
    • Paroxysmal nocturnal dyspnoea
    • Abdominojugular reflux (JVP waveform rises when pressure applied over liver area)
    • Neck vein distended (i.e. JVP elevated at rest)
    • Increased cardiac shadow on X-ray (cardiomegaly: heart occupies more than ≈50% of chest diameter)
    • Crackles heard in lungs
  • Minor
    • Hepatomegaly
    • Effusion, pleural
    • Ankle oedema bilaterally
    • exeRtional dyspnoea
    • Tachycardia
    • Vital capacity decreased by a third of maximum value
    • Nocturnal cough

Small print is that the Minor criteria can only be used if they are not attributable to other medical conditions (eg. pleural effusions cannot be due to infection, malignancy, etc).

One set of mnemonics for the criteria is the following: SAW PANIC for the Major, and HEART ViNo for the Minor. Although, there are probably infinite other (less tame) personalized mnemonics out there!

Classification of HF
New York Heart Association [NYHA]
  • Class 1 – no limitation of life activities
  • Class 2 –  slight limitation of moderate exercise, comfortable in rest
  • Class 3 –  considerable limitation on exercise, only comfortable at rest
  • Class 4 –  breathlessness and fatigue during rest


  • Depends on the Age, sex and severity of the disease
  • Overall 8 years survival rate of all NYHA classes is 30%
  • One year mortality rate of NYHA class 4 is over 60%
Survival Rates for comparison with heart failure
Time from Dx
1 Year
2 Years
5 Years
Heart Failure

Complications of HF

  1. Muscle underperfusion causing muscle weakness and atrophy causing fatigue, exercise intolerance and dyspnea
  2. Increase risk of thromboembolism and stroke development. This is due to blood stasis, arrhythmias and existing atheromas.
  3. Arrhythmias – arrhythmias are tightly associated with HF and are responsible for a large proportion of death in patients with HF. Arrhythmias usually results from increase in fibrous tissue deposition during tissue remodeling post-insults. Arrhythmias themselves lead to HF therefore they worsen the situation when they exist. AF is the most common atrial arrhythmia that co-exists with HF and is associated with increased risk of thromboembolism and stroke development. Ventricular Tachycardia [VT] is common in advanced HF, which may evolve into ventricular arrhythmias and cardiac arrest. Beta-blockers treatments are used to minimize these VT, hence sudden death
  4. Increased risks of infections that can initiate an acute-on-chronic event


CXR- may show several changes depending on the severity of the heart failure; ABCDE

  • Cardiomegaly [CTR (cardiothoracic ratio)>50% on PA]
    • L or RVH
    • Pericardial effusion if cardiac silhouette has a global appearance

ECG – may indicate the underlying cause of the heart failure such as;

  1. Myocardial infarction/ischemia
  2. Bundle Branch Block
  3. Ventricular hypertrophy
  4. Pericardial disease
  5. Arrhythmias

Blood tests – to detect any underlying causes and the severity of the disease

  1. Anemia
  2. Hyponatremia [in severe disease due to dilution]
  3. Hypokalemia/Hyperkalemia
  4. LFT’s to detect extent of liver congestion/damage
  5. RFT’s to detect the severity of the disease [inc. creatinine/urea]
  6. TFT’s to rule out thyrotoxicosis or myxedema.

Echocardiogram –  the only sensitive, non-invasive investigation that can confirm HF by detecting the ejection fraction, ventricular wall thickness and cardiac kinetics. Can also be used to detect underlying causes such as valvular diseases
Angiography – can be used to assess the extent of IHD
Pulmonary function tests – to exclude lung disease causing breathlessness


Non-pharmacological intervention;
  • Exercise
    • Involve in supervised physical activity as this increase general wellbeing
  • Diet
    • Increase in healthy food intake
    • Reduce salt intake
    • Monitor weight
  • Reduce alcohol intake as it’s a cause of AF and HF
  • Quit smoking as it leads to deterioration of cardiac function
  • Flu vaccination

Pharmacological intervention

A(ACEi), B(b-blocker), C(Ca blockers and vasodilators), D(diuretics, digoxin)

ACE inhibitors [enalapril, lisinopril, captopril]

  • Reduce afterload and fluid retention therefore slowing down left ventricular disease progression
  • Can cause Dry cough, if intolerable use Angiotensin II inhibitors
  • Angiotensin II receptor blockers [losartan]


  • Hydralazine + Nitrates in patient intolerant to ACEI and ARB’s


  • Loop diuretic [frusemide] – SE; Electrolyte imbalance, gout
  • Thiazides [bendroflumethiazide] – SE; Electrolyte imbalances K/Na/Mg, acute gout, hyperglycemia
  • Potassium sparing à spironolactone [SE: gynecomastia]

Beta-blockers [carvedilol] – reduce afterload and heart rate to prevent arrhythmias
Digoxin; considered in;

  1. Sinus rhythm patients that remains symptomatic even after full pharmacological interventions
  2. Patients with severely impaired left ventricular function
  3. Recurrent hospital admissions

Amiodarone in arrhythmic patients

Improve Prognosis
Improve Symptoms
Cardioselective β- blockers (β1)
E.g.  atenolol, bisoprolol, carvedilol
Angiotensin-II receptor antagonists

Surgical intervention

  • Revascularization in IHD [CABG or Angioplasty (PTA)]
  • Valvular replacement
  • Implanted Automatic cardiodefibrillator or pacemaker
  • Heart transplant

Emergency management

HF can present acutely as acute HF or acute-on-chronic HF

Acute HF
Usual clinical presentations are dyspnea, anxiety and tachycardia. Acute HF can evolve into cardiogenic shock, which is an acute circulatory failure due to improper/inappropriate fluid distribution. Pallor and Hypotension [systolic <90], reduced CO and oliguria characterize cardiogenic shock. SHOCK CAC
Acute HF usually results from an acute event such as MI, arrhythmias, mechanical disease [valve rupture], pericardial disease etc…
Management involves;

  • Sit up and 100% oxygen flow
  • Do an ECG, FBC, U/E, Cardiac enzymes, ABG, CXR
  • Sublingual 2 puffs nitrates or oral to enhance myocardial perfusion
  • IV opiates [diamorphine 2.5-5mg] to reduce anxiety and preload
  • IV frusemide 40-80mg i.v. to reduce fluid retention, hence pulmonary edema
  • If Systolic>90 then give IV infusion isosorbide dinitrate 2-10mg/h, if Sys<90 then treat as cardiogenic shock

In advanced situation can consider;

  • IV inotropic drug [dobutamine] to increase contractility and CO
  • IV Dopamine to enhance renal perfusion to prevent renal failure
  • IV aminophylline to enhance contractility and bronchodilate [slow]
  • Assisted ventilation

Acute-on-Chronic HF

  • Chronic HF is characterized by a slow progressive onset of symptom development. Patients in a stable chronic HF have a compensated heart, which undergo decompensation by acute events such as myocardial ischemia/infarction, infections, persistent arrhythmias, anemia, electrolyte imbalance etc…
  • Patient can either present as acute pulmonary edema i.e. like acute HF with acute dyspnea, tachycardia, anxiety and frothy productive cough, or can present as worsening of chronic HF symptoms i.e. increase breathlessness, fatigue and malaise. In either case, the management stays the same, along with identification and treatment of decompensation cause.

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