Cardiogenic Shock

Cardiogenic Shock

1. Etiology

   • Impaired blood flow, oxygen, nutrients to cardiac muscle cells
     • Right or left ventricular dysfunction
     • End-stage cardiomyopathy
     • Papillary muscle dysfunction
     • Free wall rupture
     • Congenital Heart Defect
     • Myocardial Infraction (most common)
     • Cardiac tamponade

2. Pathogenesis

   • Low cardiac output
     • Decreased peripheral perfusion
       • Sympathetic Nervous System Response
         • Catecholamine Release
         • Activation of renin-angiontensin-aldosterone system
           • Increases preload, stroke volume, and heart rate. Sodium and water retention by the kidneys due to RAAS causes intravascular volume to increase along with blood pressure. Increased systemic vascular resistance occurs due to the release of hormones (catecholamines) increasing heart rate and afterload. Cardiac muscles have to work harder to pump and subsequently the heart's oxygen demand increases.
             • Cardiac tissue necrosis and ischemia increases
       • Cyanosis, cool clammy skin, decreased cap-refill
   • High left ventricular preload
     • Increase left ventricular end diastolic pressure

3. Diagnosis

4. Assessment Findings

   • • Hypoxemia
   • Altered LOC. Anxiety, confusion, and agitation from decreased cerebral perfusion
   • Decreased Urine Output due to RAAS
   • Narrow pulse pressure
     • Decrease systolic pressure due to low stroke volume

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