Heart failure

    Cards (22)

    • What is heart failure?
      A complex clinical syndrome in which the heart is incapable of maintaining a cardiac output adequate to accommodate metabolic requirements and the venous return
    • 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 disorder without symptoms of HF
      • Stage C: Patient with past or current symptoms of HF associated with underlying structural heart disease
      • Stage D: Patient with end-stage disease who requires specialised treatment strategies
    • Causes of heart failure?
      • Ischemic heart disease
      • Hypertension
      • Idiopathic cardiomyopathy
      • Infections
      • Toxins
      • Valvular disease
      • Prolonged arrhythmias
    • Left ventricular dysfunction
      Systolic: Impaired contractility/ejection
      Diastolic: Impaired filling/relaxation
    • Frank Starlings law
      CO = HR X SV
      • 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
      • Sympathetic nervous system
      • 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
      • Reduces heart failure-related morbidity 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
      Reduces blood pressure by preventing vasoconstriction
    • Diuretic
      Reduces blood pressure by decreasing circulating blood volume
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