A complex clinical syndrome in which the heart is incapable of maintaining a cardiacoutputadequateto accommodate metabolicrequirementsand the venousreturn
New York Heart Association Classification
Class I: No symptoms with ordinary activity
Class II: Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, dyspnoea, or anginal pain
Class III: Marked limitation of physical activity. Comfortable at rest, but less than ordinary physical activity results in fatigue, palpitation, dyspnoea or anginal pain
Class IV: Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency may be present even at rest.
HF Classification: Evolution and Disease Progression
Stage A: Patient at high risk for developing HF with no structural disorder of the heart
Stage B: Patient with structural disorderwithoutsymptoms of HF
Stage C: Patient with past or current symptoms of HFassociatedwithunderlyingstructuralheartdisease
An increase in EDV increases the stretch on actin-myosin filaments, causing greater contraction and, therefore, increased stroke volume and decreased end-systolic volume.
If the heart is overstretched, a less forceful contraction occurs, decreasing stroke volume, increasing end-systolic volume, and raising the end-diastolic volume.
The graph becomes more linear. A large increase in EDV does not cause a larger increase in SV
Symtomology?
Increase in ventricular end-diastolic pressure
Left atrial pressure increase
Pulmonary capillary pressure increases
Pulmonary congestion
LV dysfunction - systolic and diastolic (symptoms)
Dyspnoea on exertion
Paroxysmal nocturnal dyspnoea (PND)
Tachycardia
Cough
Haemoptysis
Fatigue
LV dysfunction - systolic and diastolic (physical signs)
Basilar Rales
Pulmonary oedema
S3 Gallop (systolic dysfunction)
Pleural effusion
Cheyne-stokes respiration
RV failure - Systolic and diastolic (symptoms)
Abdominal pain
Anorexia
Nausea
Bloating
Swelling
RV failure - systolic and diastolic (physical signs)
Peripheral oedema
Jugular venous distention
Abdominal-jugular reflux
Hepatomegaly
Compensation?
How does the body adjust to having this pain.
Frank-starling mechanism
Neurohormonal activation
Ventricular remodelling
Compensatory mechanism (Frank-starling mechanism)
At rest, no HF
HF due to LV systolic dysfunction
Advanced HF
Neurohormonal activation
Sympatheticnervoussystem
Renin-angiotensin-aldosterone system
Vasopressin (antidiuretic hormone, ADH)
Compensatory mechanism 

MAP = (SV x HR) x TPR
Beta-Blockers
Beta-blockers decrease myocardial contractility and increase EF after 1-3 months of use
When combined with conventional HF therapy, beta-blockers reduce the combined risk of morbidity and mortality or disease progression.
Beta 1 - cardiac
Lowers blood pressure by reducing contractility of the heart
Aldosterone antagonists
Reducesheartfailure-relatedmorbidity and mortality
Reserved for patients with NYHA class III-IV HF
Side effects include hyperkalaemia and gynecomastia. Potassium and creatinine levels should be closely monitored
Angiotensin Receptor Blockers (ARBs)
Block AT1 receptors, which bind circulating angiotensin II
Examples valsartan, candesartan, losartan
Should be used to treat patients who are ACE intolerant or who develop angioedema
Cardiac Resynchronization Therapy (CRT)
Increases efficiency by improving the co-ordination
LVAD & Transplant
The biggest problem is the rejection
Patients immune system will attack it
Lack of donors
ACE inhibitor
Reducesbloodpressure by preventingvasoconstriction