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Difficulty: Very hardPhysiological Adaptation

A nurse is analyzing the clinical profile of a client who abruptly developed severe dyspnea, pleuritic chest pain, and a feeling of impending doom. A massive pulmonary embolism is confirmed, and the client is currently exhibiting signs of obstructive shock. Which of the following hemodynamic and laboratory findings are consistent with this physiological decompensation? Select all that apply.

  1. Central venous pressure (CVP) of 16 mm HgAnswer
  2. B
    Decreased systemic vascular resistance (SVR) with bounding peripheral pulses
  3. C
    Pulmonary artery wedge pressure (PAWP) of 24 mm Hg
  4. Arterial blood gas results demonstrating pH 7.52, PaCO2 29 mm Hg, and PaO2 54 mm HgAnswer

Answer

The findings consistent with obstructive shock secondary to a massive pulmonary embolism are an elevated CVP (16 mm Hg) and respiratory alkalosis with hypoxemia (pH 7.52, PaCO2 29 mm Hg, PaO2 54 mm Hg).
A massive pulmonary embolism creates a sudden mechanical obstruction in the pulmonary vasculature. This dramatically increases pulmonary vascular resistance, causing acute right ventricular failure (cor pulmonale). Consequently, blood backs up into the systemic venous circulation, leading to a significantly elevated Central Venous Pressure (CVP of 16 mm Hg; normal is 2-8 mm Hg). Simultaneously, the severe ventilation-perfusion (V/Q) mismatch causes profound hypoxemia (PaO2 54 mm Hg). In response to the hypoxemia and physiological stress, the client hyperventilates, which blows off excessive carbon dioxide and results in an early respiratory alkalosis (pH 7.52, PaCO2 29 mm Hg).

Step-by-Step Solution

1
Analyze the pathophysiology of a massive pulmonary embolism (PE).
A large embolus creates a mechanical obstruction in the pulmonary artery, drastically increasing pulmonary vascular resistance.
Understanding the location of the obstruction is required to trace upstream and downstream hemodynamic effects.
2
Evaluate the upstream (right-sided) hemodynamic effects of the obstruction.
The right ventricle dilates and fails against the high resistance (acute cor pulmonale), causing blood to back up into the systemic venous system, resulting in an elevated CVP.
This identifies why central venous pressure rises significantly in obstructive shock.
3
Evaluate the downstream (left-sided) hemodynamic effects of the obstruction.
Because blood cannot pass through the pulmonary circulation, left ventricular preload is severely diminished. Consequently, PAWP remains low or normal, and cardiac output plummets.
This differentiates obstructive shock from cardiogenic shock, where PAWP would be highly elevated.
4
Assess the compensatory mechanisms and gas exchange alterations.
The ventilation-perfusion (V/Q) mismatch causes profound hypoxemia. The client's compensatory tachypnea blows off excessive CO2, producing an early respiratory alkalosis. Sympathetic activation increases SVR.
This correlates the ABG values and systemic vascular resistance findings with the acute disease process.

Key Concept

Hemodynamic profile and arterial blood gas alterations in obstructive shock secondary to massive pulmonary embolism.
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Physiological Adaptation

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