Why a pulmonary embolism makes clients blow off carbon dioxide

A blocked vessel creates dead space and mismatch

An embolus lodges in a pulmonary artery and stops blood reaching the alveoli beyond it. Those alveoli are still ventilated, but no gas exchange occurs there, so they act as dead space. MSD lists hypoxaemia from ventilation and perfusion mismatch among the effects of larger emboli, along with a reflex increase in ventilation.

Blood is diverted to other parts of the lung, which may now receive more flow than their ventilation can handle. Atelectasis and changes in surfactant add to the mismatch. The overall result is that oxygen uptake suffers, while carbon dioxide, which diffuses much more easily, can still be cleared by faster breathing.

Why breathing speeds up and PaCO2 falls

MSD describes respiratory alkalosis as a primary fall in PaCO2 caused by an increase in respiratory rate or depth, most often as a physiologic response to hypoxia, and notes that pain and anxiety also drive it. In pulmonary embolism, several of these triggers act together, along with reflex stimulation from the lung itself.

Carbon dioxide forms carbonic acid in the blood. When the client breathes off more carbon dioxide than the body produces, acid falls and pH rises. Early arterial blood gases can therefore show a low PaCO2 and high pH, sometimes with low PaO2. MSD stresses that embolism often occurs without hypoxia, so a normal saturation does not exclude it.

What the nurse sees at the bedside

MSD lists tachycardia and tachypnoea as the most common signs of pulmonary embolism, and dyspnoea and pleuritic chest pain as common symptoms. MedlinePlus adds anxiety, lightheadedness or fainting, cough that may bring up blood, low oxygen, and leg pain or swelling from a clot source. Many findings are nonspecific.

The alkalosis itself can add symptoms. MSD notes acute respiratory alkalosis can cause lightheadedness, confusion, paresthesias, cramps and carpopedal spasm. MSD also warns that embolism should be strongly considered before attributing hyperventilation to anxiety alone. A client with sudden breathlessness and tingling fingers needs an assessment for a cause, not just reassurance.

Why a rising CO2 in a tiring client is a warning

Fast breathing takes effort. If the embolus is large, hypoxaemia persists, or the client has limited reserve, the breathing muscles can tire. As the respiratory rate slows or breaths become shallow, PaCO2 that was low may rise back toward normal and then above it. A normal PaCO2 in that context is not reassuring.

Concerning trends include falling oxygen saturation despite oxygen, a slowing respiratory rate with increasing drowsiness, new hypotension, or signs of right ventricular strain such as distended neck veins. MSD notes death from embolism is often due to right ventricular failure. Escalate immediately and prepare for interventions under local protocol rather than waiting for repeat blood gases.

Work a hypothetical blood gas scenario

Imagine a hypothetical postoperative client who develops sudden breathlessness, pleuritic chest pain and a fast heart rate. The first blood gas shows a high pH and low PaCO2. An hour later the client is drowsy, breathing more slowly, and the repeat PaCO2 is near normal. Options include documenting that the gas has normalised, offering a paper bag to rebreathe, or escalating urgently.

Escalating urgently is correct. The early alkalosis reflected compensatory hyperventilation; a return toward normal PaCO2 with drowsiness and slower breathing suggests the client is tiring and ventilation is failing. Calling it normalised misses the clinical context. Rebreathing into a bag is inappropriate because it can worsen hypoxaemia in a client whose problem is a clot, not anxiety.

Sources and further reading

Pulmonary Embolism (MSD Manual Professional Edition). Reflex tachypnoea, V/Q mismatch hypoxaemia, atelectasis; tachycardia and tachypnoea as common signs; dyspnoea and pleuritic pain; death often from right ventricular failure.

Respiratory Alkalosis (MSD Manual Professional Edition). Primary fall in PaCO2 from hyperventilation, often a response to hypoxia, pain or anxiety; acute symptoms; PE often without hypoxia and should be considered before attributing hyperventilation to anxiety.

Pulmonary embolus (MedlinePlus Medical Encyclopedia). Symptoms including chest pain worse with breathing, fast breathing, fast heart rate, anxiety, hypoxaemia, leg swelling and cough with blood.