Scenario 3: Cardiogenic Shock

Sam Smith is a 50-year-old executive. He is five feet 10 inches tall and weighs 225 lbs. (102 kg). He
takes a statin for his cholesterol and an occasional over-the-counter acid reducer for indigestion. He
does not smoke and drinks occasionally. He does not exercise regularly because he is busy with family
and work. Recently, he has been experiencing intermittent bouts of chest pressure while on a business
trip, but these bouts always had resolved quickly, so he dismissed them as indigestion. At home one
evening, he developed chest pain that did not resolve as it usually had. He began sweating, was
flushed and short of breath. His wife called 911. When the paramedics arrived, Mr. Smith's vitals were
BP = 160/86; HR = 122; Resp = 30; pulse oximetry = 88 percent. He was started on 4 L nasal
cannula, given sublingual nitroglycerin and transferred to the hospital.
Mr. Smith arrived in the ED and a 12-lead ECG confirmed he an MI. He had bilateral rales about
halfway up. His BP was now 80/66; HR = 142; Resp = 36; pulse oximetry = 91 percent on 4 L. An
arterial blood gas (ABG) revealed respiratory alkalosis: pH 7.67, pHCO3 28, pO2 80, PCO2 40.
Mr. Smith was growing more anxious by the minute. These bouts of chest discomfort had always
resolved quickly, but this time was different. Mr. Smith knew something "bad" was happening. A Foley
catheter was inserted, which revealed minimum urine output. The interventional cardiologist examined
Mr. Smith in the ED, and arrangements were made for an emergency cardiac angiogram with possible
angioplasty, the cardiologist ordered aspirin 325 mg to be chewed and Lopressor 5 mg IVP every 5
minutes for three doses. The cardiologist also ordered dopamine 10 mcg/kg/min; dobutamine 10
mcg/kg/min IV, and milrinone 50 mcg/kg IV loading dose over 10 minutes followed by 0.5
mcg/kg/min continuous IV. The nurse monitors the patient closely for cardiogenic shock related to
acute MI.

Decreased cardiac output related to inadequate cardiac contractility AEB angina, bilateral rales
ausculated in the lungs, low urine output, tachycardia, rapid respirations with dypsnea, low O2
status despite supplemental oxygen, diagnosed respiratory alkalosis per ABG results and
confirmed MI per EKG.
This is a high priority nursing diagnosis because the patient is experiencing inadequate perfusion
of oxygen to his tissues due to decreased cardiac output caused by the recent MI. His symptoms
correspond to poor perfusion (low urine output, altered EKG, angina, low blood pressure with
rapid respirations, tachycardia) secondary to the MI. Cardiogenic shock is the primary concerninadequate blood flow to the tissues caused by cardiac malfunction. In this case the ability for the
heart to contract appropriately is the issue- MI is the primary cause for decrease in cardiac
contractility. The nurses were charged with monitoring the patient for cardiogenic shock and the
physicians initiated vasoactive and inotropic drug therapy to aid in preventing this complication
sometimes seen after an acute MI.
2. Goal:The client will demonstrate adequate cardiac output as evidenced by blood pressure
within normal range for the client, apical heart rate between 60-100 beats/min, urine output of at
least 30ml/hr, decrease in angina and dypsnea, palpable peripheral pulses, and 2 saturation
greater than 90% during the next 12 hours.
Interventions:

1) Administer O2 per physician's order- Supplemental oxygen increases oxygen availability to

the myocardium- cardiogenic shock is caused by demand for O2 by the heart and tissues
exceeding the available amount of oxygen.
2)Titrate inotropic and vasoactive medications within defined parameters to maintain
contractility, preload and afterload per physician directions. - Pts presenting with low BP, low
cardiac output with heart failure can benefit from inotropic drugs to help maintain systemic
perfusion and organ function