A 55-year-old man is immediately brought to the hospital after experiencing a sudden collapse at home 20 minutes ago. The patient reported chest pain and then collapsed to the floor while trying to sit down. Medical history is significant for type 2 diabetes mellitus and hypertension. Temperature is 36.7 C (98.1 F), blood pressure is 80/50 mm Hg, pulse is 120/min, and respirations are 22/min. On examination, the patient is in marked respiratory distress. Bilateral crackles are present. An S3 is audible. ECG reveals ST-segment elevation in leads V2 through V6. Which of the following hemodynamic changes are most likely present in this patient?
Hemodynamic measurements in shock | ||||
Parameter | Hypovolemic | Cardiogenic | Obstructive | Distributive shock |
CVP | ↓ | ↑ | ↑ | ↓ |
PCWP | ↓ | ↑ | ↓* | ↓ |
Cardiac index | ↓ | ↓ | ↓ | ↑** |
SVR | ↑ | ↑ | ↑ | ↓ |
SvO2 | ↓ | ↓ | ↓ | ↑** |
*In tamponade, left-sided preload is decreased, but measured PCWP is paradoxically increased due to external compression by pericardial fluid. **Cardiac index & SvO2 are usually decreased in neurogenic shock due to impaired sympathetic reflexes. CVP = central venous pressure; LV = left ventricular; PCWP = pulmonary capillary wedge pressure; SvO2 = mixed venous oxygen saturation; SVR = systemic vascular resistance. | ||||
This patient with sudden-onset chest pain and ST-segment elevation in contiguous ECG leads has an ST-elevation myocardial infarction (MI). Hypotension, pulmonary crackles, and an audible S3 suggest MI-induced acute left ventricular (LV) failure and cardiogenic shock.
In cardiogenic shock, LV systolic failure causes increased LV end-diastolic pressure, which is transmitted backward to cause increased pulmonary capillary wedge pressure (PCWP) (an estimate of left atrial pressure) and pulmonary edema. The increased pressure also impairs right ventricular function, resulting in increased central venous pressure (CVP). Markedly decreased cardiac output leads to hypotension with decreased coronary perfusion pressure (as coronary perfusion pressure is driven by aortic diastolic pressure) (Choices C and E). In response to the reduced cardiac output, compensatory peripheral vasoconstriction occurs to increase systemic vascular resistance in an effort to maintain organ and tissue perfusion.
(Choice A) Decreased CVP, PCWP, and coronary perfusion pressure are expected with hypovolemic and septic shock.
(Choice B) Increased CVP with decreased PCWP and coronary perfusion pressure are expected with obstructive shock due to pulmonary embolism (ie, blood flow blocked at the pulmonary arteries) or tension pneumothorax (ie, blood flow blocked at the right atrium due to thoracic pressure–induced vena cava collapse).
Educational objective:
Myocardial infarction may be complicated by acute left ventricular failure (LV) and cardiogenic shock. In cardiogenic shock, increased LV end-diastolic pressure is transmitted backward to cause increased pulmonary capillary wedge pressure (evidenced by pulmonary edema) and increased central venous pressure. There is markedly decreased cardiac output, which causes hypotension and decreased coronary perfusion pressure.