1. References:
    1. A., Lenneman, H., H Ooi, & X., Ren. (2012). Cardiogenic Shock. Medscape: Drugs & Diseases. Retrieved from http://emedicine.medscape.com/article/152191-overview
    2. Lewis, S. M., & Dirksen, S. R. (2014). Medical-surgical nursing: Assessment and management of clinical problems (Ninth ed.). St. Louis, MO: Elsevier Inc
  2. "Typical" Patient
    1. Patient description
      1. A 67 year old male presented to the Emergency Department for Substernal Chest Pain, diaphoresis, and dyspnea at rest. Further assessment findings noted a family history of Acute coronary syndrome (father died at age 50 from MI), previous anterior MI 6 months prior, PCI of Proximal LAD with stent, Hx of diabetes, hyperlipidemia, and a 3 pack-year smoking history who quite 8 years prior to assessment. Vitals on arrival: BP-156/92, P-110, RR-22, O2 Sat-89% on Rm air, Temp-98.7 F.
  3. Risk factors
    1. Age 65 or older
    2. Having a history of heart failure/previous heart attack and diabetes
    3. Having blockages (coronary artery disease) in several of your heart's main arteries
  4. Pathophysiology
    1. Cardiogenic shock is caused by systolic or diastolic dysfunction of the heart’s pumping action to propel the blood forward, which causes reduced cardiac output (CO).
    2. Systolic dysfunction affects the left ventricle. However, it can affect the right side and causes a reduced flow of blood to the pulmonary circulation.
    3. The most common cause of systolic dysfunction is a myocardial infarction (MI).
    4. Cardiogenic shock death is the number one cause of death from an MI (Lewis, 2014, pg. 1633).
    5. Patient will have tachycardia, chest pain and be hypotensive, they will have lung crackles, cyanosis, pallor, diaphoresis weak pulses, cool skin and delayed cap refill. Anxiety and confusion may also happen because of poor cerebral perfusion.
    6. Diagnostic findings consist of increased cardiac markers, increased BNP, increased blood glucose, and increased BUN
  5. Clinical Manifestations
    1. Shortness of breath
    2. Tachycardia
    3. Tachypnea
    4. Confusion/ altered mental status
    5. Loss of consciousness
    6. Weak and thready pulses
    7. Diaphoresis
    8. Pallor
    9. Cool extremities
    10. Often a result of MI
  6. ADPIE
    1. Assessment
      1. Tachypnea
      2. Crackles
      3. Increased PAWP, SVV, and pulmonary vascular resistance
      4. Cyanosis, pallor, diaphoresis, cool/clammy skin, prolonged capillary refill
      5. Edema and decreased urine output
      6. Anxiety
      7. Confusion
      8. Agitation
      9. Result of decreased cerebral perfusion
      10. Result of pulmonary congestion
      11. Result of hypoperfusion and poor renal blood supply
    2. Diagnosis
      1. Increased cardiac markers
      2. Increased BNP
      3. Increased Blood Glucose
      4. Increased BUN
      5. ECG
      6. Echocardiogram
      7. CXR
      8. DX Imaging
      9. DX labs
    3. Planning
      1. Assess for and report s/s of cardiac dysrhythmia
      2. Implement measures to maintain adequate cardiac output and myocardial perfusion
      3. Assess for and report s/s of heart failure
      4. DVT prophylaxis
      5. Assess for s/s of pain
    4. Intervention
      1. Initiate cardiac monitoring
      2. Restrict activity if indicated
      3. Daily weights
      4. Administer medications as ordered
        1. Dobutamine
          1. Will increase myocardial contractility, decrease ventricular filling pressure, decrease SVR and PAWP, increase cardiac output and stroke volume, and affect the heart's rate
        2. Dopamine
          1. Is a positive inotrope that will increase myocardial contractility, automaticity, and AV conduction, it will increase HR and cardiac output, as well as BP and MAP (can cause progressive vasoconstriction at high doses
        3. Norepinephrine
          1. (after MI)
          2. Renal and splanchnic vasoconstriction, cardiac stimulation, peripheral vasoconstriction, increase BP, increase MAP
        4. Epinephrine
          1. Is a beta-adrenergic agonist and at low doseswill cause cardiac stimulation, bronchodilation, peripheral vasodilation, also increase HR, contractility, and cardiac output
        5. Nitroglycerin
          1. Dilates coronary arteries
          2. Most often used vasodilator for cardiogenic shock
        6. Diuretics = reduce preload
        7. Vasodilators = reduce afterload
        8. Beta-adrenergic blockers = reduce heart rate and contractility
        9. Nitrates = reduce workload
      5. Oxygen therapy as prescribed
      6. Cardiac catheterization
    5. Evaluation
      1. Patient will have stable or improved mental status
      2. Patient will have systolic BP greater than 80 mmHg
      3. Patient will have palpable peripheral pulses
      4. Patient will have stable or improved skin temperature and color
      5. Patient will have urine output of at least 30ml/hr
      6. Patient will have stable vital signs
      7. Patient will have stabilizing cardiac enzymes
      8. The patient will report tolerable pain
      9. Patient will be free of dyspnea
      10. Patient will have clear breath sounds