HEART FAILURE

Inability of the heart to perfuse metabolising tissues adequately due to insufficient cardiac output.
Cardiac output> cardiac demand

TYPES
Right vs Left
High output vs Low output
Systolic vs diastolic
Most commonly due to CAD, usually following MI
LV is usually dilated and fails to contract normally
Diastolic
Common causes: CAD, HTN, hypertrophic cardiomyopathy
Results from impaired myocardial relaxation with ↑ stiffness in the ventricular wall and decreased LV
compliance  ↓ diastolic ventricular filling  ↓CO

Forward vs Backwards
Compensated vs Decompensated
Compensated: Sx are stable and absence of overt features of fluid retention
Decompensated: Acute or continuing deterioration of CO and Sx progression)

PATHOPHYSIOLOGY
Myocardial ischaemia and cell death  myocardial failure  ↓cardiac output  ↑sympathetic stimulation
(aims the improve CO and will do so in early stages)  Tachycardia (and fatal arrhythmias) & Peripheral
vasoconstriction (↑ afterload)  ↑ myocardial 02 consumption  myocardial ischaemia and cell death

↓CO  Activation of the renin-angiotensin system  via angiotensin II  aldosterone  Na and water
retention  ↑ end diastolic volume  ↑ myocardial 02 consumption

Renin-angiotensin system is activated because:

1. Stimulation of the beta1-adrenergic receptors on the juxtaglomerular apparatus
2. ↓renal perfusion  activated baroreceptor in the renal arterioles to stimulate renin production

Natriuretic peptides
1. Atrial
2. Brain
3. C-natriuretic peptide
ANP & BNG ↑ in heart failure
Causes:
Water excretion
Also cause peripheral vasodilatation
Cytokines
Thought be involved in cardiac dysfunction. Levels are ↑ in heart failure

Endothelin
Powerful vasoconstrictor
Produced by endothelial cells
↑ IN cardiac failure  ↑ myocardial strain
CAUSES
MYOCARDIAL DYSFUNCTION
- Coronary artery disease
- Systemic HTN
- Cardiomyopathies
o Dilated (large floppy heart)
o Hypertrophic (genetic autosomal dominant, usually LVH)
o Restrictive
- ETOH cardiomyopathy
o Direct toxin to myocardium
o Not much reversibility
VOLUME OVERLOAD
- Valvular regurgitation (mitral/aortic)

OUTFLOW OBSTRUCTION
- Aortic stenosis
- Hypertrophic obstructive cardiomyopathy
- Systemic HTN
OBLIGATORY HIGH OUTPUT
- Anaemia
- Thyrotoxicosis
- Pregnancy
- Sepsis (usually gram –ve)
↓ VENTRICULAR FILLING
- Restrictive cardiomyopathy
- Constrictive pericarditis
- Pericardial tamponade

ARRHYTHMIAS
- Bradycardia/ heart block
- Atrial fibrillation
OTHERS
- Autoimmune disease
- Chemotherapy: anthracyclines, doxorubicin (used in breast cancer, non-Hodgkin’s lymphoma)

Causes of LHF Causes of RHF

CAD/IHD LHF
Systemic HTN Cor pulmonale
- Chronic lung disease e.g. fibrosis
- Acute lung disease e.g. PE
Mitral & Aortic valvular disease Tricuspid & Pulmonary valvular disease
(regurgitation/stenosis) (regurgitation/stenosis)
Cardiomyopathies Left-to-Right shunts e.g. VSD

Causes of Systolic HF Causes of Diastolic HF

Cad/IHD HTN
Systemic HTN CAD
Valvular disease Diabetes
Others Others
- Idiopathic dilated cardiomyopathy - Valvular disease
- Ischaemic cardiomyopathy - Hypertrophic cardiomyopathy
- Inflammatory cardiomyopathy - Restrictive cardiomyopathy
 - Arrhythmia
- Thyroid dysfunction
- Drug-induced cardiomyopathy

PRECIPITANTS
An acute exacerbation of cardiac failure is related to a precipitating event other than the underlying cause.
Common precipitants are:
- Reduction of or non-compliance with therapy, or fluid retention due to drugs, such as NSAIDS
- Recent infection – esp pulmonary infection
o Infection ↑ metabolic rate  causes tachycardia  ↑ demand on the heart
- MI – may trigger heart failure
- Tachy- or Bradyarrhythmias
o AF results in a loss of atrial component to CO  ↓ efficiency of vent. Filling
o Bradycardia requires ↑ in stroke volume to maintain CO w a lower heart rate (may not be
possible w failing heart)

CLINICAL FEATURES
Forward effects
Applies to the left ventricle
- Poor renal perfusion  prerenal failure
- Poor perfusion of extremities  cold extremities
- ↑ lactic acid production in underperfused skeletal muscle  weakness and fatigue
- Hypotension
Right ventricle:
- ↓ pulmonary flow  dyspnoea & under filling of the
heart of the left ventricle

Backward effects
↓ CO + Na & H2O retention  accumulation of blood in the atria
and the venous system  tissue congestion + progressive
dilatation of L&R ventricles

LVF  ↑ pulmonary venous pressure  extravasation of fluid in

alveolar spaces  Pulmonary oedema
Hence untreated LVH  RHF
RVF  ↑ backpressure in venous system  fluid extravasation at:
- The peripheries  subcutaneous oedema felt in the legs
- The liver  Hepatic congestion tender hepatomegaly
 cirrhotic changes
FIGURE 1 CCF LIVER; ALTERNATING ZONES OF PALE FATTY
- The abdominal cavity  ascites CHANGE & DARK CONGESTION PRODUCING A 'NUTMEG'
LIVER

SIGNS AND SYMPTOMS

LEFT HEART FAILURE
Systolic heart failure:
Inadequate cardiac output  ↑ left atrial pressures  then give:
- Exertional dyspnoea (most common) Dyspnoea secondary to APO & lactic
- Orthopnoea
acidosis
- Paroxysmal nocturnal dyspnoea
- Fatigue  due to poor cardiac output and lactic acidosis
- Wheeze (‘cardiac asthma’)
 - Cough
o Nocturnal dry cough due to bronchial oedema or cardiac asthma
o Productive pink frothy sputum due to pulmonary oedema
- Haemoptysis (rare)

Signs include:
- Tachypnoea
- Tachycardia
- Pulsus alternans (alternating large and small-volume pulse)
- Peripheral cyanosis and low pulse volume
- Cardiomegaly
- Third heart sound (S3 gallop)
- Functional mitral regurgitation secondary to dilatation of the mitral valve annulus
- Basal crepitations  APO
- Pleural effusion
- Hypotension, cold peripheries and renal impairment – due to poor LV output
- Signs of fluid retention
RIGHT HEART FAILURE
May occur secondary to:
- Chronic lung disease
- Multiple pulmonary emboli
- Primary pulmonary HT
- Right heart valve disease
- Left-to right shunts
- Isolated right ventricular cardiomyopathy

Symptoms
- Fatigue – poor LV filling (& poor cardiac output and lactic acidosis)
- Nausea
- Wasting
- Swollen ankles
- Abdominal discomfort
- Anorexia – oedema of the gut
- Breathlessness – poor pulmonary perfusion
Signs include:
- ↑ JVP
- Hypotension, cold peripheries and renal impairment – due to poor LV output
- Smooth hepatomegaly
- Liver tenderness
- Pitting oedema
- Ascites
- Functional tricuspid regurgitation
- Tachycardia
- Right ventricular third heart sound

CLASSIFICATION
New York Heart Association functional classification:
Class I – no limitation of physical activity
Class II – slight limitation. Comfortable at rest. Ordinary physical activity  fatigue, palpitations, dyspnoea or
angina
Class III – Marked limitation of physical activity. Patients are comfortable; at rest, less-than-ordinary activity
leads to Sx
Class IV – inability to carry on any physical activity w/out discomfort
INVESTIGATIONS
FBE
Chronic anaemia  cardiac failure
Leucocytosis secondary to infections may exacerbate CCF

U&E
Hypokalaemia and hyponatraemia are common in pts w diuretic therapy
Hyponatraemia (pts not on diuretics) – due to sodium restrictions and high circulating vasopressin levels
(dilutional hyponatraemia)
Hyperkalaemia – K-sparing diuretics (e.g. amiloride or spironolactone), ACE inhibitors (ramipril or perindopril)
or Ang II receptor blockers (Iosartan or candesartan)
Renal impairment due to hypoperfusion or diuretic therapy

LFT
Liver congestion
↑ AST, ALT & bilirubin

CK/ TROPONIN
If acute onset, exclude acute coronary syndromes
TFT
Thyrotoxicosis
ECG
IHD, arrhythmias, LVH
CSR
Cardiomegaly, alveolar oedema ‘bat’s wings shadowing’, prominent upper lobe vessels, Kerley B lines, pleural
effusions
ECHO
Gold standard Ix
Assess ventricular valvular function
Ejection fraction <45% = systolic dysfunction

OTHER TESTS
Exercise testing: functional severity
Cardiac catheterization: assess & treat ischaemic/valve lesions
Nuclear techniques: ejection fraction, cardiac function and reversible ischaemia
Brain (B-type) natriuretic peptide: marker of ventricular dysfunction

MANAGEMENT
THERAPY

M ANAGEMENT OF ACUTE LVF

Management Notes
1. Sit patient up Reduce venous return to the heart
2. 100% oxygen via facial mask Improves arterial oxygen tension ↓ myocardial 02
debt & improve myocardial function
3.Establish peripheral intravenous access and
administer:
IV diamorphine Good anxiolytic and venodilator, ↓ load
IV Metoclopramide Prevents vomiting secondary to diamorphine
IV furosemide Venodilator to ↓ load, also powerful diuretic and will
cause Na & h2o excretion
↓ load  ↓ backpressure on the pulmonary
circulation  relieve APO by allowing resorption of
fluid back from the ECF  ICF
Urinary catheter
IV nitrates Vasodilating both veins and arterioles
Dose is titrate to prevent hypotension (common SE)
CPAP Very effective – pushes fluid out of the alveoli back
into the circulation

A CUTE RVF
1. Diuretics
2. Nitrates

C HRONIC CCF
- Lifestyle advice (Exercise, Salt restriction, quit smoking, ↓ETOH)
- Vaccination: pneumococcus, influenza
- Pharmacological
o ACE-I/A2RB, beta blockers & diuretics (loop+/- spironolactone)
o NB: Ca-channel blockers are good for angina & diastolic HF – causes vasodilation & afterload
 NOT for systolic HF because ↓ contractility
o Others: Nitrates, adrenergic agonists, digoxin, anticoagulants

P ROVEN BENEFITS
Only use A2rBs if ACE-I are contraindicated. ACE-I ↓ mortality.
Beta-blockers used in chronic stable HF, NOT acute. ↓ mortality
Spironolactone. Beware with renal failure + ACE-I
Hydralazine + nitrates – useful if ACE-I are contraindicated

S X RELIEF
Loop diuretics – Thiazide or frusemide
Digoxin – should be used in AF, beware in renal failure, last resort
Anti-arrhythmics – amiodarone only
Anticoagulants – HF is a/w ↑ stroke risk (x4)

C ONTRAINDICATED DRUGS
Ca-Channel blockers: NOT in systolic HF
+ve inotropic agents (dobutamine, adrenaline): only used for acute Mx
NSAIDs
Steroids
Tricyclic antidepressants

SURGICAL
- Revascularisation
- Pacemaker
- Transplant