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1
Question:

A 56-year-old man is admitted to the intensive care unit after being hospitalized 3 days ago for sepsis and acute respiratory failure due to community-acquired pneumonia.  Medical history is remarkable for hypertension and moderate aortic stenosis that was last evaluated by echocardiography 2 years ago.  On admission, the patient was intubated and placed on mechanical ventilation.  He was also treated with intravenous fluids and antibiotics and required vasopressor therapy for 12 hours, after which he showed clinical improvement.  While still intubated this morning, the patient develops sudden-onset hypotension and tachycardia.  Temperature is 98.6 F (37 C), blood pressure is 82/54 mm Hg, pulse is 120/min, and respirations are 26/min.  Cardiac examination shows regular rhythm with a rapid rate, and lung auscultation reveals bilateral breath sounds with crackles in the right lower lung field.  The patient is rapidly infused with 2 L of normal saline with minimal improvement in his blood pressure.  Pulmonary arterial catheterization is performed and shows:

Central venous pressure14 mm Hg (normal: 6-8)
Pulmonary capillary wedge pressure6 mm Hg (normal: 6-12)

Which of the following is the most likely cause of this patient's shock?

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Explanation:

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This patient's pulmonary arterial catheterization findings are most consistent with obstructive shock due to an acute pulmonary embolism (PE).

The expected hemodynamic parameters in obstructive shock include elevated central venous pressure (CVP) and low cardiac output; however, pulmonary capillary wedge pressure (PCWP), an estimate of left atrial pressure and representation of left-sided preload, can vary depending on the location of the obstruction.

  • Prepulmonary obstructive shock (due to massive PE or tension pneumothorax) is most common and results from obstruction involving the right atrium, right ventricle, or pulmonary arteries.  Because blood is unable to pass from the right side of the heart to the left side, PCWP is low or normal. 
  • Postpulmonary obstructive shock typically involves obstruction within the left side of the heart or aorta; PCWP is elevated, making the hemodynamic parameters the same as those expected in cardiogenic shock.

Of note, cardiac tamponade causes prepulmonary obstructive shock as blood is unable to fill the compressed right-sided heart chambers.  Despite reduced left-sided preload, the expected PCWP is paradoxically elevated due to external compression of the left atrium, a rare exception when left-sided preload and PCWP are discordant.

(Choices A and E)  Aortic dissection is a potential cause of postpulmonary obstructive shock because the dissecting aortic wall can create a false aortic lumen that obstructs blood flow in the true aortic lumen.  Severe aortic stenosis can also cause postpulmonary obstructive shock.  Elevated PCWP is expected with these postpulmonary obstructions.  Aortic dissection may also cause hemorrhagic (hypovolemic) shock; however, low CVP is expected.

(Choice B)  Low CVP and low PCWP are expected in septic shock.

(Choice C)  Left ventricular failure can result from acute myocardial infarction and leads to cardiogenic shock characterized by elevated CVP and PCWP.  Right ventricular myocardial infarction and failure will demonstrate elevated CVP and low or normal PCWP, the same findings expected in prepulmonary obstructive shock.

Educational objective:
Most cases of obstructive shock result from prepulmonary obstruction (eg, due to massive pulmonary embolism or tension pneumothorax) with hemodynamic parameters showing high central venous pressure (CVP), low pulmonary capillary wedge pressure (PCWP), and low cardiac output.  Postpulmonary obstructive shock (eg, due to aortic dissection or severe aortic stenosis) leads to the same findings as cardiogenic shock with high CVP, high PCWP, and low cardiac output.