Pathophysiology of Heart Failure

• Heart failure is:

  • Where the heart fails to deliver enough blood for the needs of the body - old physiological definition
  • A clinical syndrome with multiple causes, which includes breathlessness, fatigue and oedema

  
• Types of heart failure:

  • Acute or chronic
  • Acute is pulmonary oedema with breathlessness at rest
  • Right-sided or left-sided
  • Often both together
  • Right-sided causes peripheral oedema and raised jugular venous pressure
  • Left-sided causes raised pulmonary venous pressure and pulmonary oedema
• Chronic heart failure:

  • Several underlying cardiac causes
  • Aggravated by dysfunctional neuro-hormonal regulation
  • Associated with high mortality
  • Patients have high risk of complications of general anaesthesia
• In cardiac failure, the heart itself is damaged, or its function is restricted:

  • Heart muscle disease (cardiomyopathy or ischaemic heart disease) - 'Left Ventricular Systolic Dysfunction'
  • Excessive volume load (valvular regurgitation)
  • Excessive pressure load (hypertension, aortic stenosis, pulmonary hypertension)
  • Sustained abnormal rhythm
  • Tachycardias and bradycardias
• Non-cardiac causes of heart failure syndrome:

  • Excessive demand in high output heart failure
  • Arteriovenous shunts
  • Anaemia - need to pump more blood around the body in order to get enough oxygen to the muscles
  • Hyperthyroidism
  • Fluid overload from other causes
  • IV therapy
  • Renal failure
• Commonest causes of heart failure:

  • Ischaemic heart disease
  • Myocardial infarction results in left ventricular weakness
  • Hypertension
  • Increased LV afterload
  • Valvular heart disease (any type)
  • Valve stenosis and valve regurgitation
  • Chronic obstructive pulmonary disease (COPD)
  • Cor pulmonale - right sided heart failure due to pulmonary hypertension in chronic lung disease
• Symptoms of heart failure:

  • Breathlessness - pulmonary oedema, pulmonary venous congestion
  • Fluid retention leading to oedema, usually ankles - systemic venous congestion
  • Fatigue - poor cardiac output

  Not all these symptoms may be present in any one case
• Physical signs of heart failure:

  • Pulmonary oedema - breathless, cyanosis, basal lung crackles on auscultation
  • Peripheral oedema - pitting
  • Other fluid overload - ascites, pleural effusions
  • Raised jugular venous pressure
  • Signs of the underlying cause eg irregular pulse, heart murmur, anaemia
• Investigations of heart failure - heart:

  • Chest x-ray showing heart and lungs - heart may be enlarged and lungs may be congested with excess fluid, pulmonary oedema or pleural effusions
  • ECG - look for signs of myocardial infarction or previous MI or atrial fibrillation
  • Echocardiogram - ultrasound that shows heart in real time to see how well the different chambers are contracting
• Investigations of heart failure - other causes/consequences:

  • U&E (urea and electrolytes) - check kidney function
  • FBC (full blood count) - check for anaemia
  • Thyroid - overactive thyroid can cause heart failure and atrial fibrillation
• Conflicting neurohormonal compensatory mechanisms:

  • Reduced cardiac output and blood pressure resembles dehydration or haemorrhage:
  • Activates renin-angiotensin-aldosterone system to retain salt and water
  • Activates sympathetic nervous system to vasoconstrict (maintain blood pressure) and stimulate heart (maintain cardiac output)
• Conflicting neurohormonal compensatory mechanisms:

  • Increased intracardiac pressures detected by 'stretch receptors' - resembles fluid overload:
  • Atrial and 'brain' natriuretic peptides stimulate sodium excretion
  • Atrial natriuretic peptide comes from atria BUT
  • So-called 'brain' natriuretic peptide comes from ventricles (was first found in brain tissue and name stuck)
• Renin-angiotensin-aldosterone system - the details:

  • Reduced renal blood flow stimulates secretion of renin from the kidney
  • Renin stimulates Angiotensin-Converting Enzyme (ACE)
  • ACE catalyses production of Angiotensin II (from Angiotensin I, already present)
  • Angiotensin II
  • Acts as a vasoconstrictor through the AT1 receptor
  • Stimulates aldosterone secretion from the adrenal cortex
  • Aldosterone is a mineralocorticoid, which increases sodium retention in the kidney
• Renin-angiotensin-aldosterone system - the details:

  • Aldosterone is a mineralocorticoid, which increases sodium retention in the kidney
  • Sodium retention indirectly stimulates water retention through vasopressin (= Antidiuretic Hormone, ADH) from the posterior pituitary
  • RESULT = increased circulating volume, oedema, and vasoconstriction
• Sympathetic system - adrenaline and noradrenaline:

  • Stimulate heart rate and contractility
  • Vasoconstriction
  • Thereby raises low blood pressure
• Pharmacological correction of heart failure:

  • ACE inhibitors - -pril
  • Angiotensin II receptor blockers - -sartan
  • Aldosterone antagonists - spironolactone and eplerenone
  • Beta blockers - -olol
  • Vasodilators - hydralazine, nitrates
  • Loop diuretics to treat symptoms due to fluid overload
  • New sacubitril-valsartan treatment blocks both the AT1 receptor and neprilysin - an enzyme that degrades natriuretic and vasoactive peptides
• Left-sided heart failure:

  • Presents mainly with pulmonary oedema
  • As the left ventricle fails, blood dams back in the pulmonary veins where the venous pressure rises causing the alveoli in the lungs to fill with fluid
  • This causes dyspnoea (breathlessness)
  • On effort, then at rest and when lying down (orthopnoea)
  • Other symptoms
  • Cough
  • Pink frothy sputum
  • Paroxysmal nocturnal dyspnoea
• Right-sided heart failure:

  • Congestion of the systemic and portal veins
  • Affecting the liver, kidneys, gastrointestinal tract and subcutaneous tissues
  • Subcutaneous oedema
  • Ankles
  • Sacral
  • Fatigue
  • Abdominal distension and discomfort
  • Hepatic congestion
  • Ascites
• Non-pharmacological treatment of heart failure:

  • Cardiac resynchronisation pacemaker for severe left ventricular systolic dysfunction with wide QRS (ventrical contraction time)
  • Cardiac surgery - valve replacement, repair, transplantation
• The ECG:

  • P wave = atrial contraction
  • QRS = ventricular contraction
  • T wave = ventricular repolarisation
• Rhythm disturbances:

  • Too fast - tachycardia
  • Any heart rate greater than 100 bpm
  • Too slow - bradycardia
  • Any heart rate lower than 60 bpm
  • Normal rate
  • Any heart rate between 60 bpm and 100 bpm

  Not all tachycardias and bradycardias are abnormal
• Examples of tachycardias:

  • Sinus tachycardia
  • Atrial fibrillation
  • Ventricular tachycardia
• Sinus tachycardia:

  • A normal response to exercise or emotion
  • Hyperthyroidism, hypovolaemia, fever, heart failure
  • Normal p-waves visible on ECG
• Atrial fibrillation:

  • The most common rhythm disturbance
  • Uncoordinated and ineffectual atrial contraction (fibrillation)
  • Results in rapid & irregular ventricular rate
  • Reduces efficiency of the heart - heart failure
• Ventricular tachycardia:

  • Rate is usually faster than 140 bpm
  • Often associated with ischaemic heart disease
  • Sometimes caused by drugs
  • Complexes are wide, since not conducted by His-Purkinje system
• Bradycardias:

  • Sinus bradycardia may be normal in a young person: often found in athletes
  • Heart Block - atrioventricular block
  • May cause blackouts or dizzy spells
• Extrasystoles are the most common type of intermittent rhythm disturbance - single extra beats arising from atria or ventricles:

  • Sensation of missed beats, or of extra beats
  • Usually of no clinical significance
• Ventricular fibrillation:

  • Uncoordinated and ineffective electrical activity of the ventricles
  • No cardiac output - cardiac arrest
  • Rapid loss of consciousness and death within minutes
  • A common cause of sudden death
  • Acute coronary ischaemia (myocardial infarction)
  • Cocaine, digitalis overdose, cardiomyopathy
• Asystole:

  • Absence of electrical activity and contraction
  • Cardiac arrest
  • There may be evidence of atrial activity
  • Causes sudden loss of consciousness and death
• Treatments for arrhythmias:

  • Anti-arrhythmic drugs - beta-blockers, amiodarone
  • DC cardioversion
  • Emergency for ventricular fibrillation or other life-threatening tachycardias
  • Elective for atrial fibrillation
  • Electrophysiological studies and catheter ablation of abnormal tissue
  • Pacemakers for bradycardias
• Treatments for arrhythmias:

  • Implantable defibrillators for ventricular tachycardia or ventricular fibrillation
  • Note electrical devices can be subject to electrical interference eg from electro-cautery equipment
  • Atrial fibrillation - commonest chronic arrhythmia:
  • Rate-controlling drugs - digoxin or beta blockers
  • Anticoagulation with warfarin or DOAC to reduce risk of stroke from embolisation of left atrial thrombus
• Anticoagulants in dentistry:

  • Warfarin - check INR is in range, no need to reverse. Local haemostatic measures.
  • DOACs
  • Dabigatran, rivaroxaban, apixaban
  • Others in development, mostly '-xaban' as they inhibit factor Xa
  • No need to stop, use local haemostatic measures