Heart Failure Flashcards
Heart failure definition
Failure to maintain an adequate cardiac output to meet the demands of the body
Structural or functional abnormality - impairs ability of ventricles to eject blood or fill
CO
HR x SV
Preload
Is affected by venous blood pressure and the rate of venous return to the heart
This, in turn, is affected by venous tone and volume of circulating blood
Preload increases with increasing blood volume and vasoconstriction
Preload decreases with blood volume loss and vasodilatation
Frank-Starling Law
An increase in volume of blood filling the heart stretches the heart muscle fibres causing greater contractile forces which, in turn, increases the stroke volume
Afterload
It is the pressure in the aorta/pulmonary artery that the left/right ventricular muscle must overcome to eject blood
The greater the aortic/pulmonary pressure, the greater the afterload on the left/right ventricle respectively
Afterload increase with hypertension and vasoconstriction
Afterload decreases with vasodilatation
As the afterload increases, cardiac output decreases
LOHF
Systolic heart failure
Diastolic heart failure
HOHF
The heart itself is functioning normally but cannot keep up with the unusually high demand for blood to one or more organs in the body
Causes: thyrotoxicosis, profound anaemia, pregnancy, pagets disease, acromegaly, sepsis
Systolic heart failure
Progressive deterioration myocardial contractile function
Ischaemic injury
Volume overload
Pressure overload
Diastolic heart failure
Inability of the heart chamber to relax, expand and fill sufficiently during diastole to accommodate an adequate blood volume
Significant left ventricular hypertrophy (LVH) e.g HCM
Infiltrative disorders
Constrictive pericarditis
Restrictive cardiomyopathy
HF causes
Coronary Heart Disease Hypertensive Heart Disease Valvular Heart Disease Myocardial Disease/ Cardiomyopathies Congenital Heart Disease
Activation of neurohormonal system
Release of Noradrenaline – increases heart rate and myocardial contractility. Causes vasoconstriction
Release of ANP/BNP
Activation of renin-angiotensin – aldosterone system
Compensatory mechanisms
Vasoconstriction
Na and water retention
Excessive Tachycardia
Pressure Overload
Concentric left ventricular hypertrophy
E.g. Hypertension or aortic stenosis
Augmented muscle may reduce the cavity diameter
Cross sectional areas of the myocytes are increased
Volume overload
Chamber dilatation with increased ventricular pressure
E.g. mitral or aortic regurgitation
Deposition of new sarcomeres
Increased cell length and width
Muscle mass and wall thickness are increased in proportion to chamber diameter
Left side HF
Blood backs up progressively from the left atrium to the pulmonary circulation
Causes: Ischaemic heart disease Hypertension Valvular heart disease Myocardial disease
Left side HF - lungs
Breathlessness
Orthopnoea
Paroxysmal nocturnal dyspnoea
Left side HF - kidneys
Decreased cardiac output
Reduction in renal perfusion
Activation of renin - angiotensin – aldosterone system
Retention of salt and water with consequent expansion of interstitial fluid and blood volumes
Left side HF - brain
Hypoxic encephalopathy Irritability Loss of attention Restlessness Stupor and coma
Right side HF
Usually as a consequence of left sided heart failure (congestive cardiac failure
Cor-pulmonale:
Right sided HF due to significant pulmonary hypertension due to increased resistance within the pulmonary circulation
Usually as a result of respiratory disease e.g. COPD or pulmonary emboli
Right side HF- Cor Pulmonale
Right sided HF due to significant pulmonary hypertension due to increased resistance within the pulmonary circulation
Usually as a result of respiratory disease e.g. COPD or pulmonary emboli
Right side HF - other causes
Valvular heart disease
Congenital heart disease
RHF - liver and portal system
Congestive hepatomegaly
Centrilobular necrosis when severe
Cardiac cirrhosis
RHF - spleen
Congestive splenomegaly
RHF - abdomen
Ascites - accumulation of transudate in peritoneal cavity
RHF - subcutaneous tissue
Peripheral oedema of dependent portions of the body esp. ankle and pretibial oedema
Sacral oedema if bedridden
RHF - Pleural and pericardial space
Effusions
RHF systemic effects
Liver and portal system Spleen Abdomen Subcutaneous tissue Pleural and pericardial space
Biventricular failure
Either due to the same pathological process on each side of the heart
OR
Consequence of left heart failure leading to volume overload of the pulmonary circulation and eventually the right ventricle causing right ventricular failure
HF clinical presentation
Due to excess fluid accumulation Dyspnoea Orthopnoea, paroxysmal nocturnal dyspnoea Oedema Hepatic congestion Ascites
Due to reduction in cardiac output
Fatigue
Weakness
HF clinical presentation - due to excess fluid accumulation
Dyspnoea Orthopnoea, paroxysmal nocturnal dyspnoea Oedema Hepatic congestion Ascites
HF clinical presentation - Ddue to reduction in cardiac output
Fatigue
Weakness
Classification of HF
I: No limitation
II: Slight limitation
III: Marked limitation
IV: Severe limitation
Clinical signs of cardiac failure
Cool, pale, cyanotic extremities Tachycardia Elevated JVP Third heart sound (S3) – gallop rhythm Displaced apex (LV enlargement) Crackles or decreased breath sounds at bases on chest auscultation Peripheral oedema Ascites Hepatomegaly
Acute Pulmonary Oedema
Acute Breathlessness Pallor Cyanosis Sweating Rapid Pulse Hypoxia Crackles in Lungs
Clinical tests in HF
CXR ECG Blood investigations Echocardiogram / Cardiac MRI or CT / CT-PET CTCA / Coronary angiography
Current drug treatment
Aldosterone antagonists ARNI ACEi/ARBs Beta-blockers SA Node Blockade
Current drug treatment - ACEi / ARBs
Enalapril, Ramipril, Perindopril
Losartan, Candesartan, Irbesartan
Current drug treatment - ARNI
Sacubitril Valsartan
Current drug treatment - Aldosterone antagonists
Spironolactone, Eplerenone
Current drug treatment - Beta-blockers
Carvedilol, Bisoprolol, Metoprolol
Current drug treatment -SA Node Blockade
Ivabradine
Current drug treatment - Diuretics
Loops – Furosemide, Bumetanide
Thiazides – Bendrofluamethiazide, Indapamide
Quinazolines - Metolazone
Loop diuretics
FRUSEMIDE, BUMETANIDE
Inhibit Na+ re-absorption from the proximal tubule
K+ loss from distal tubule
Can be given iv or orally
Potent – can lead to:
electrolyte abnormalities
hypovolaemia and diminished renal perfusion
Mineralocorticoid Receptor Antagonists
EPLERENONE, SPIRONOLACTONE
Acts on distal tubule
Promotes Na+ excretion and K+ re-absorption
Reduces hypertrophy and fibrosis
Principle Side-Effects
Gynaecomastia (esp. Spironolactone)
Electrolyte (K+ high) and renal function abnormalities
ACE Inhibitors
RAMIPRIL, PERINDOPRIL, ENALAPRIL, CAPTOPRIL, LISINOPRIL
Act on activated renin - angiotensin system
Given orally in small doses with slow titration
Block production of angiotensin:
Vasodilatation
BP lowering
Reduce cardiac work
Principle Side-Effects: cough, hypotension, renal impairment
ARNI
SACUBITRIL VALSARTAN
Acts on activated renin - angiotensin system
Also blocks breakdown of ANP/BNP
Block production of angiotensin:
Vasodilatation, BP lowering, reduce cardiac work
Promote natriuresis
Sodium excretion, vasodilatation, reduce hypertrophy and fibrosis
Principle Side-Effects: hypotension, renal impairment
Beta blockers
BISOPROLOL, CARVEDILOL, METOPROLOL
Block the action of adrenaline and noradrenaline on adrenergic beta receptors
Slow HR, reduce BP
Given orally in small doses with slow titration
(treat arrhythmias)
Principle Side-Effects
Bronchospasm
Claudication
SAN blockade
IVABRADINE
Blocks the If channel within the SA node
Slow HR, no effect on BP
Given orally with dose titration
Principle Side-Effects
Visual aura
Bradycardia
Digoxin
Action:
Increases myocardial contractility
Slows conduction at the AV node (use in AF)
Excreted by kidney - Toxicity important
Given:
Acute HF especially in AF
Chronic HF in selected cases
Treatment of Acute Pulmonary Oedema - Immediate
High flow oxygen
IV Morphine
IV Nitrates
IV Frusemide
+/- Assisted Ventilation
Treatment of Acute Pulmonary Oedema - Definitive
Identify Cause
Oral diuretics
Medical Therapy
Revascularisation if appropriate
Other therapies
Cardiac Resynchronisation Therapy (CRT) Implantable Cardioverter Defibrillator (ICD) Dialysis & Ultrafiltration Ventricular Assist Device (LVAD/RVAD) Intra-aortic balloon pump Cardiac transplantation (Stem cell therapy)
CRT (Biventricular pacing)
Standard pacemakers equipped with two wires (or “leads”) conduct pacing signals to specific regions of heart. Biventricular pacemakers have an additional third lead designed to conduct signals directly into the left ventricle. Combination of all three leads promote synchronised pumping of ventricles, increasing efficiency of each beat and pumping more blood on the whole.
