6.2 - Left-Sided Heart Failure

left-sided heart failure

caused by ischemic heart disease, systemic hypertension, valve disease, and disease of myocardium

• creates two major problems:

  1. blood does not get pumped adequately into systemic circulation

     • results in decreased systemic perfusion

  2. blood backed up into pulmonary circulation

     • increases pulmonary pressure (hydrostatic pressure)

     • results in pulmonary congestion / edema

morphologic features of left heart failure

left ventricle typically enlarged, and increased pressure in pulmonary veins cause increased hydrostatic pressure

• congestion

  • heart failure cells — macrophages with hemosiderin

    1. high pulmonary venous pressure causes RBCs to extravasate into alveoli

    2. alveolar macrophages phagocytose RBCs

    3. hemoglobin iron becomes hemosiderin

    4. phagocytosis by macrophages

• edema

• pleural effusion

• boggy texture → fluid-filled, squishy tissue that rebounds

clinical features of left heart failure — pulmonary

• dyspnea (SOB) → congested/edematous lungs harder to inflate

• cough → related to pulmonary congestion

• orthopnea → dyspnea when lying down

  • supine position increases venous return, so more blood returns to already congested pulmonary circulation

• paroxysmal nocturnal dyspnea → waking from sleep with SOB bordering on sensation of suffocation

• rales at lungs base → from opening edematous pulmonary alveoli

clinical features of left heart failure — cardiac

• enlarged heart

• tachycardia

• third heart sounds

• systolic murmur → ventricular dilation results in papillary muscle displacement

  • mitral valve cannot close normally, causing mitral regurgitation

• atrial fibrillation → from chronic dilation of left atrium

  • chaotic, uncoordinated flow results in reduced ventricular stroke volume and stasis

    • blood pools and forms thrombus, potentially leading to stroke

• diminished renal perfusion → due to diminished cardiac output

  • triggers RAAS for increased volume and vascular tone

  • exacerbates pulmonary edema, further reducing renal perfusion

  • eventually causes pre-renal azotemia

    • impaired excretion of nitrogenous wastes

    • increased metabolic derangement

• diminished cerebral perfusion → causes hypoxic encephalopathy

  • results in irritability, diminished cognition, restlessness, potential stupor and coma