Pocket ICU Management

Systolic and Diastolic Dysfunction

First Things First (assess & treat for the following)

  • Is there evidence for isolated systolic dysfunction?
    • LV ejection fraction < 50%
  • Is there evidence for isolated diastolic dysfunction?
    • Ejection fraction >50%, but
    • Impaired ventricular filling on echocardiography
  • Signs of heart failure/cardiogenic shock? (i.e., low/“inadequate” cardiac output)
    • Heart failure is a clinical diagnosis (symptoms and signs).
    • Treat reversible causes (tamponade, coronary ischemia, pulmonary embolism, thyrotoxicosis, severe anemia, etc.).
    • Optimize cardiac output and treat symptoms.
      • Inotropic support (drugs, assist devices, etc.)
      • Vasodilator therapy and/or afterload reduction
      • Diuresis as tolerated

History and Physical (assess for the following):

  • *= best feature in each category

History (precipitating causes)

  • *Past history of heart failure
  • *PND
  • *Presence of S3 gallop
  • *Atrial fibrillation (irregularly irregular: confirm by EKG)
    • (Dyspnea on exertion more likely pulmonary disease than heart failure)
  • Coronary ischemia/myocardial infarction (±VSD)
  • Hypertension (renal or stimulant drug-induced)
  • Arrhythmias (e.g., new-onset atrial fibrillation)
  • Valvular disease or infective endocarditis
  • Myocarditis (viral or drug-induced)
  • Pericarditis
  • Thyrotoxicosis, pregnancy, anemia, infection, etc. (high-output failure)
  • Pulmonary embolism
  • Dietary and environmental factors

Physical exam

  • Orthopnea or dyspnea ± wheezing
  • Basal/dependent pulmonary rales
  • Pleural effusions
  • Cheyne-Stokes respiration
  • Tachycardia or pulsus alternans
  • Apically displaced focal impulse
  • Cool/mottled extremities/gangrene of digits if on vasopressors
  • Pitting edema (sacral and pedal)
  • Jugular venous distention
  • Hepatic congestion with abdominojugular reflex
  • Ascites

Diagnostic Tests

  • CXR (PA and lateral)
    • *Presence of pulmonary venous congestion
    • Pleural effusions
  • 12-lead EKG
    • Echocardiography
      • Ejection fraction (systolic dysfunction =< 50%)
        • Echocardiography (or radionuclide ventriculography)
      • Rule out valvular pathology.
      • Doppler echocardiography to assess diastolic dysfunction
        • Impaired relaxation (mitral inflow E/A wave reversal)
        • Pseudonormal (“normal” E/A pattern with blunted systolic PV flow)
        • Restrictive (high velocity/short duration E-wave pattern)
      • Tissue Doppler echocardiography to assess ventricular dysfunction
        • Reduced peak systolic (Sm) and early diastolic (Em) mitral annulus velocities
      • Rule out RV dysfunction.
        • May lead to LV diastolic dysfunction (interventricular interdependence)
  • Left heart catheterization
    • Diagnosis of ischemic and/or valvular etiology
  • Right heart catheterization findings
    • Low cardiac output
    • Elevated PA pressures
    • Elevated wedge pressure
      • Wedge pressure >25 mmHg is consistent with pulmonary edema.
    • Elevated central venous pressure
  • Myocardial biopsy
    • Hemochromatosis
    • Eosinophilia
    • Amyloidosis
    • Transplant rejection
  • Laboratory tests (nonspecific but important for management)
    • ABG: severe uncompensated metabolic acidosis suggests cardiogenic shock
    • CBC, hemoglobin A1C, fasting blood glucose, lipid profile
    • s-Electrolytes (including calcium and magnesium), BUN and creatinine
    • Urinalysis
    • Elevated liver enzymes and INR
    • Thyroid-stimulating hormone to rule out thyrotoxicosis
    • Elevated BNP
      • Not useful as screening for asymptomatic ventricular dysfunction
      • Level < 100 pg/ml rules out heart failure
      • Level >500 pg/ml is typically present in heart failure
      • Metoprolol increases levels unrelated to NYHA class

General Management Principles

Heart failure

  • Both systolic and diastolic dysfunction may lead to heart failure.
  • Diuretics & ACE inhibitors have emerged as first-line therapy.
  • Angiotensin receptor antagonists can be substituted for ACE inhibitors (angioedema risk remains!).
  • Low-dose aldosterone antagonists (e.g., spironolactone) should be considered in patients with moderately severe or severe HF symptoms and recent decompensation, or with LV dysfunction early after MI.
  • Digitalis can be beneficial in patients with current or prior symptoms of heart failure and reduced LVEF to decrease re-hospitalizations.
  • Beta-blockers and ACE inhibitors should be used in all patients with a recent or remote history of MI regardless of EF orpresence of HF.
  • Beta-blockers are indicated in all patients (even without a history of MI) who have a reduced LVEF.
  • Beta-blockers (using 1 of the 3 proven to reduce mortality [i.e., bisoprolol, carvedilol, and sustained-release metoprolol succinate]) are recommended for all stable patients with current or prior symptoms of HFand reduced LVEF, unless contraindicated
  • Arrhythmia management
    • Biventricular pacing and/or AICD (based on history and EF)
  • Diet control: reduction of salt intake
  • Reduction of physical & emotional distress

Isolated diastolic dysfunction

  • Usually some of degree of systolic dysfunction is present too.
  • Diuretic treatment reduces symptoms.
  • No additional symptombenefit from added ACE or ARB treatment
  • Inotropic agents are relatively contraindicated unless systolic failure is present.
  • Calcium channel blockers to assist in diastolic relaxation, but no clear current recommendations are available.
  • Beta-blocker therapy for long-term therapy to modify underlying pathophysiology
  • Heart rate reduction as long as diastolic filling is improved – otherwise may lead to worsening failure
  • Maintain sinus rhythm (to optimize diastolic filling).

Specific Treatment

Acute heart failure

  • Oxygen by nasal cannula or mask, BiPAP or endotracheal intubation
  • Sitting position to increase venous pooling/decrease venous return
  • IV morphine (1-2 mg) provides pre- & afterload reduction as well as a reduction in anxiety & sympathetic override.
  • Furosemide (10-40 mg IV) provides diuresis and venous & arterial vasodilatation.
  • Vasodilator therapy (nitroglycerin, nicardipine, nesiritide or nitroprusside, etc.)
    • Pre-existing renal insufficiency is not worsened by nesiritide.
  • Inotropic support
    • Dobutamine 3-5 mcg/kg/min
    • Milrinone (0.1-0.7 mcg/kg/min)
    • Epinephrine (0.03-0.1 mcg/kg/min) for those in cardiogenic shock
  • Mechanical support (if cardiogenic shock present)
    • Intra-aortic balloon pump counterpulsation
    • Tandem heart (temporary left heart support)
    • Mechanical assist devices (left and/or right)
    • Rarely ECMO ± IABP as bridge to mechanical assist device/heart transplant

Ongoing Assessment

  • Ongoing assessment of cardiac output (PA catheter, etc.)
  • Assess and treat for RV dysfunction/failure.
    • Pulmonary vasodilators (oxygen, inhaled prostacyclin or i-NO)
    • Optimize RV perfusion: consider norepinephrine and/or vasopressin
    • Drain effusions, assisted ventilation, etc. to decrease PVR
  • Optimize inotropic therapy vs. vasodilator therapy.
  • Consider surgical consult (L or R heart assist devices vs. heart transplant).
  • Isolated diastolic dysfunction
    • Monitored diuresis
    • Afterload reduction as tolerated
    • Continue to evaluate for ischemia, valve abnormalities & pericardial effusion.
    • Treat non-sinus rhythm aggressively.


Systolic/diastolic dysfunction

  • Respiratory distress (pulmonary edema)
  • Arrhythmias (including atrial fibrillation, V tach, VF, etc.)
  • Worsening coronary ischemia (MI, etc.)
  • Electrolyte imbalances (hyperkalemia with spironolactone, ACE inhibitor)
  • Drug toxicity and side effects (digoxin, amiodarone, milrinone, etc.)

Heart failure with end-organ failure

  • Renal failure (prerenal azotemia)
  • Respiratory failure
  • Hepatic insufficiency
  • Ascites
  • Pulmonary embolism
  • Gangrene of limbs/digits (vasopressors)
  • Stroke (embolic from A fib, LV thrombus)


  • Written by Mark A. Cannon, MD
  • Revised by Charl J. De Wet, MBChB

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