Case Study
A rapid response event was initiated by the bedside nurse after the patient had sudden acute shortness of breath and severe chest pain. On prompt arrival of the rapid response team, the patient’s telemetry showed tachycardia with a regular rhythm. Chart review showed a 70-year-old male with a known history of coronary artery disease with coronary artery bypass grafting in the past, peripheral vascular disease, hyperlipidemia, type 2 diabetes, and hypertension. He was admitted earlier for chest pain and a syncopal event, which was being evaluated.
Vital Signs
Temperature: 96.2 °F, axillary
Blood Pressure: 70/42 mmHg
Heart Rate: 120 beats per min (bpm) – regular rhythm
Respiratory Rate: 30 breaths per min
Pulse Oximetry: 86% oxygen saturation on room air, with saturation improving to 93% on 15 L/min via non-rebreather
Focused Physical Examination
The patient was an elderly man in severe distress. He was alert but not oriented, responding to questions with yes and no intermittently. His cardiac exam showed tachycardia with normal heart sounds. He had distended neck veins, cold skin, and decreased intensity of the distal pulses. No peripheral edema was noted. Hepatojugular reflex was not checked because of patient distress. A lung exam showed tachypnea and fine bibasilar crackles. His abdomen was soft, non-tender, and non-distended.
Interventions
A cardiac monitor and pacer pads were attached immediately. A stat electrocardiogram (EKG) showed tachycardia, irregular rhythm with a narrow QRS complex. He was also noted to have ST elevations in leads V5, V6, and leads I and aVL. The patient was given 2 mg intravenous (IV) morphine for dyspnea and pain. Norepinephrine and dopamine infusions were started for vasopressor support in the setting of suspected cardiogenic shock. Laboratory tests included complete blood count, chemistry panel, electrolytes, troponins, lactate, prothrombin time, international normalized ratio, and type and screen were ordered. A stat chest X-ray was obtained, which showed diffuse pulmonary infiltrates ( Fig. 12.1 ). The patient was given 40 mg of IV furosemide. A stat consult was called to cardiology, and a working diagnosis of acute ST-elevation myocardial infarction with cardiogenic shock was established. The patient was transferred to the cardiac catheterization lab immediately for revascularization.
Final Diagnosis
Cardiogenic shock in the setting of STEMI.
Acute Cardiogenic Shock
Shock is a state of circulatory failure defined as a state of hypoxia at a tissue and cellular level because of either reduced delivery of oxygen, increased consumption of oxygen leading to mismatch, or inability to utilize the delivered oxygen adequately. Shock is classified into four etiologies based on the underlying pathophysiology: distributive, cardiogenic, hypovolemic, and obstructive ( Table 12.1 ). Undifferentiated shock is the presence of shock without a clearly defined underlying mechanism.
| Type of shock | Cardiac output | Systemic vascular resistance | Mean arterial pressure | Pulmonary capillary wedge pressure | Central venous O 2 saturation | Examples |
|---|---|---|---|---|---|---|
| Distributive | High/Normal | Low | Low | Low/Normal | Normal/High | Sepsis, anaphylaxis |
| Cardiogenic | Low | High | Low | High | Low | Acute MI |
| Hypovolemic | Low | High | Low | Low | Low | Hemorrhage |
| Obstructive | Low | High | Low | High/Normal | Low | Pulmonary embolism, tamponade |
Acute decompensated heart failure or cardiogenic shock is the sub-type of shock caused by an inability of the heart to pump an adequate amount of blood. The reduction in tissue perfusion results in decreased oxygen and nutrient delivery to the tissues and can lead to end-organ damage and multi-system failure if present for a long time.
Pathophysiology
Failure of the left ventricle (LV) or right ventricle (RV) to pump an adequate amount of blood is the primary cause of cardiogenic shock. The fall in cardiac output leads to a compensatory rise in systemic vascular resistance (SVR) in an effort to maintain the mean arterial pressure. This response is mediated by endogenous vasoconstrictors such as epinephrine, norepinephrine, and angiotensin II. An increase in SVR exerts a strain on the already strained heart even further, leading to a vicious cycle and further fall in cardiac output, producing the classical “cold and wet” appearance.
Acute myocardial infarction (MI) is the most common cause of cardiogenic shock (see Table 12.2 for different etiologies of cardiogenic shock). Older age, co-morbidities such as hypertension, diabetes, multi-vessel coronary artery disease, prior MI, prior history of heart failure, and infarction of the anterior wall of the LV are risk factors for the development of heart failure in acute MI. The diagnosis of cardiogenic shock in the setting of acute MI can be made clinically with reasonable surety based on history, presentation, lab work, EKG, and chest X-ray. Specific diagnostic studies can be obtained in equivocal cases ( Table 12.3 ).
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