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Flashcards in Cardiac Failure Deck (18)
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Heart failure definition

Pathophysiological state in which the heart is unable to pump enough blood to meet the requirements of tissue metabolism, or needs an elevated filling pressure to do so. 


Pathiphysiology of HF

Reduced CO leads to sympathic activation and release of noradrenaline form adrenergic cardiac nerves. The RAAS and adrenergic system is activated. 

  • The high LVEDP, LAP therefore high PCP. 
  • Increased hydrostatic pressure gradient - increased fluid in interstitial tissues. 
  • Increased pulmonary lymph flow
  • If lymphatic transport maximum exceeded then interstitial fluid accumulates. 
  • If marked then alveolar fluid 'invasion'.
  • Low CO leads to redistribution of blood flow, preserving flow to brain and heart at expense of skin, muscle, gut and kidney. 
  • Ventricular remodelling with hypertrophy. 
  • Endothelial dysfunction. 
  • Over time, myocytes die, leading to fibrosis, reduced capillary density (hypertrophy, fibrosis) but added work (noradrenaline) leading to further ischaemic necrosis.


Natriurretic peptides

  • BNP: found in ventricles and atria
  • ANP: found in atria

Both released with increase in pressure and/or volume

  • Both cause natriuresis, vasodilatation. 
  • BNP now used in diagnosis, assessment of severity and progress of treatment. 


Affects of the RAAS system

Activation of renin-angiotensin-aldosterone system.

  • Retention of Na and water
    • Increased LVEDV therefore LVEDP
    • The rise in LVEDP is reflected back to LA and pulmonary veins and capillaries. 
  • Angiotensin-2 potent vasoconstrictor
    • increased SVR
  • Angiotensin-2 potent stimulus to cell proliferation
    • hypertrophy
    • fibrosis. 


Effects of the adrenergic system

Activation of adrenergic system

  • Increase in myocardial noradrenaline, toxic to myocytes 

  • Increased SVR 

  • Increased cardiac work 

  • Progression of myocardial ischaemia 


Mechanisms of cardiac failure

Systolic failure

  • Reduced contractility (measured by ejection fraction)

Diastolic failure

  • Impaired relaxation
  • Increased wall stiffness


Mechanisms of pulmonary oedema

  • Fluid movement into lung interstitial spaces depends on the balance offorces driving fluid out of the capillaries versus those forces holding fluid in the capillaries; and
  • Capillary surface are; and
  • Capillary permeability

Fluid fremoval from interstitial spaces via pulmonary lymphatics



Pulmonary capillary pressure depends on LAP - which itself depends on LVEDP.


Diastolic dysfunction causes

Generally due to delayed relaxation (ischaemia) and reduced compliance with either LVH or myocardial infiltration or fibrosis as main causes. 


Intersitital fluid pressure


Usually negative (effect of the pressure generated by normal inspiration and surface tension in alveoli).

IntP rarely affects the rate of fluid movement except where marked increase in alveolar surface tension (e.g. loss of surfactant) or during mechanical ventilation where gas is pushed into lungs by  positive pressures.  


Oncotic forces

Capillary normally impermeable to protein. 

  • Plasma onconic pressure (Pl OncP) principally due to albumen and usually abotu 25mmHg. 
  • Interstitial oncotic pressure (Int OncP) usually about 8-10mmHg. 

Usual net balance is about +2-3mmHg causing a small fluid movement into interstitial space. 

  • All entirely depenent on normal capillary permeability. 

If this lost then fluid movement solely on hydrostatic pressure gradients. 


Presentation of cardiac failure


  • Dramatic onset
  • Pulmonary oedema
  • 'small' heart
  • RHF rare


  • Slowly progressive onset
  • Pulmonary oedema rare
  • Cardiomegaly
  • RHF common


Causes of cardiac failure

  • HTN
  • Ischaemic heart disease
  • Dilated cardiomyopathy
    • Specific
    • Idiopathic
    • Tachycardia induced
  • Valvular heart disease
  • Dysrhythmias
  • HOCM
  • Restrictive cardiomyopathy


Right heart failure

  • Usually secondary to left heart fialure or chronically raised pulmonary capillary pressure and pulmonary hypertension. 
  • COPD (cor pulmonale)
  • Primary pulmonary HTN
  • Other causes of RHF:
    • RV infarction - rare
    • RV cardiomyopathy - rare


Symptoms of cardiac failure

  • Dyspnoea and fatigue
    • Significant exercise
    • Mild exercise
    • Trivial exercise
    • At rest
  • Orthopnoea
  • PND
  • Fatigue and exhaustion
  • Cough
  • Peripheral oedema
  • Tachycardia
  • Elevated venous pressure
  • Gallop rhythm
  • Lung crackles
  • Hepatomegaly
  • Peripheral vasoconstriction


Investigation of cardiac failure

  • ECG
  • Echocardiogram
  • CXR
  • Standard blood plus lipids and glucose


Echo in cardiac failure

  • Regional dysfunction vs global, plus guesstimate of EF
  • LVH
  • State of values and severity of valve disease
  • HOC including outflow tract gradient
  • Diastolic dysfunction


Management of cardiac failure

Establish cause - treat if possible. 

  • IHD: consider angiography re vascularisation
  • Valvular disease: repair or replace the valve
  • HOCM: consider if role for surgical reduction or outflow tract gradient. 
  • Treat any specific cardiomyopathy: sarcoid, amyloid, alcohol etc. 

Volume control 

  • diuretic, daily weight

Lifestyle measure

  • Salt restriction, physical activity

Block RAA system

  • ACEI
  • Receptor blockers

Block adrenergic system

  • Specific beta blockers: carvedilol, bisprolol improve outcome


  • Spironolactone improves outcome NYHA 3-4 failure
  • Epleronone improves outcome

Surgical management

  • Impanted defibrillator
  • Synchronised biventircular pacing
  • Left ventricular assist devices
  • Cardiac transplantation