Cardiac Failure Flashcards
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
PCP
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
(IntP)
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
Acute
- Dramatic onset
- Pulmonary oedema
- ‘small’ heart
- RHF rare
Chronic
- 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
