Pulmonary Thromboembolism

22 Pulmonary Thromboembolism



Erin M. Portillo



1. What is a pulmonary thromboembolism (PTE)?

A PTE occurs when a clot obstructs a pulmonary vessel. This can occur within the vessel itself (thrombus) or the clot can originate elsewhere and migrate to the pulmonary vasculature and become lodged (thromboembolism), therefore obstructing blood flow.


2. What is Virchow’s triad?

Virchow’s triad is composed of three elements that are risk factors for thrombosis. These include (1) vascular alteration or injury, (2) blood stasis or impairment of flow, and (3) hypercoagulability resulting from a defect in coagulation.


3. When should I be concerned about a PTE in my dogs?

In animals with one of the components of Virchow’s triad, there should be concern. PTE has been associated with the following conditions: cardiac disease, protein-losing nephropathy, neoplasia, immune-mediated disease, hypercortisolism, diabetes mellitus, infectious disease, trauma, surgical procedures, necrotizing pancreatitis, and atherosclerosis. A recent study suggested that 60% of dogs diagnosed with thromboembolic disease had underlying protein-losing nephropathy or neoplasia.


Although these conditions are favorable for thrombosis, occurrence of a PTE is unpredictable and should be suspected if clinical signs become apparent.


4. Describe the pathophysiologic effects of PTE.
• A thromboembolic event to the pulmonary vasculature within a normal lung may be well tolerated because of significant reserve capacity. However, if there is cardiac or pulmonary compromise, clinically significant pulmonary or hemodynamic sequelae may ensue.

• The degree of vascular obstruction will dictate the severity of the consequences. A major problem is ventilation-perfusion (V/Q) mismatch. This is a ratio that expresses the difference between alveolar ventilation and alveolar blood flow. If perfusion is adequate to an area of lung that is inadequately ventilated or the reverse if there is inadequate flow to a well-ventilated lung then the result is a compromise in respiratory exchange. In a total occlusion, which is rare, ventilation will continue despite absence of blood flow to the affected region.

• Arterial hypoxemia may follow partially the result of the V/Q mismatch. Cardiac disease resulting in decreased cardiac output or pulmonary disease resulting in diffusion impairment may also contribute to hypoxemia.

• Hyperventilation is a common consequence of hypoxemia, which, depending on the severity, can lead to hypocapnia. This may or may not be adequate to alleviate the hypoxemia.

• If the pulmonary arterial occlusion is complete, then the decreased blood flow to the type II pneumocytes, which make surfactants is compromised, resulting in depletion of surfactant, edema, and atelectasis. This can occur within 24 hours of the PTE event.

• Hemodynamic consequences also relate to the magnitude of the obstruction. There is a large reserve capacity of the pulmonary vasculature but after this is overloaded, pulmonary vascular resistance will increase and right ventricular afterload occurs. These are poor prognostic indicators because increased afterload leads to increased ventricular oxygen requirements; if these requirements are not met, ventricular failure and decreased cardiac output can occur.
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Jul 31, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Pulmonary Thromboembolism

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