Critical care case study - Pulmonary embolism: Nursing

Nurse Joe works in the emergency department and is caring for Rachel, a 64-year-old who was diagnosed with a pulmonary embolism, or PE. Nurse Joe goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Rachel’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.

First, Nurse Joe recognizes important cues, including Rachel’s vital signs which are temperature 99.7° F, or 37.6° C, heart rate 110 beats per minute, respirations 26 breaths per minute, blood pressure 94/62 mmHg, and oxygen saturation 86 percent on 6 L/min nasal cannula. Upon assessment, Nurse Joe notes Rachel is apprehensive, short of breath, coughing, and has crackles in her bilateral lower lobes. She reports a sharp pain in her chest that worsens with inspiration that she rates as 4 on a 10-point numeric scale.

Next, Nurse Joe analyzes these cues. He reviews the electronic health record, or EHR, and notes Rachel has a history of factor V Leiden, a genetic disorder that increases the risk of blood clots, and that she returned home from a long, overnight flight last night. He also reviews her ECG which shows sinus tachycardia and her CT that confirms a PE in her left lung.

Nurse Joe knows a PE can occur when a clot or plug of material travels to the lungs and lodges in the small pulmonary vessels, obstructing blood flow. He realizes Rachel’s history of factor V Leiden and prolonged immobility during her flight place her at risk for venous thromboembolism, or VTE. VTE is when a deep vein thrombosis, or DVT, which is a blood clot that develops in a vein in an extremity, travels to the lungs, causing a PE.

As the PE obstructs blood flow, it creates a ventilation-perfusion, or V/Q, mismatch where, in the affected area of the lung, there’s enough oxygen but not enough blood to pick it up. This results in ventilatory dead space, inadequate gas exchange, and hypoxemia, triggering tachypnea. Initial compensation occurs as blood is shunted from poorly perfused areas of the lungs to areas where there’s normal perfusion, a process called compensatory shunting.

The obstruction also initiates the release of inflammatory mediators, which constricts the pulmonary blood vessels, further decreasing blood flow throughout the lungs. This decreases production of surfactant, leading to atelectasis, a condition where all or part of a lung collapses.

Inflammatory mediators also cause bronchoconstriction of the small airways, which, together with atelectasis, worsen hypoxemia even more.

On top of that, increasing pulmonary vascular resistance increases right ventricular afterload, which can eventually lead to right ventricular failure.

Meanwhile, peripheral chemoreceptors respond to hypoxemia by sending signals to the brain to increase ventilation, leading to hyperventilation. This leads to hypocapnia and respiratory alkalosis, as carbon dioxide is blown off.

Nurse Joe recognizes that Rachel needs prompt management of her PE.

Now, using the information he’s gathered, Nurse Joe chooses a priority hypothesis of impaired gas exchange. Then, he generates solutions to address Rachel’s impaired gas exchange, including pharmacologic and non-pharmacologic interventions; and he establishes the expected outcome that after intervening, Rachel’s oxygen saturation will improve to 92% or greater within 15 minutes.