Does high blood pressure (hypertension) occur in pulmonary embolism (PE)?

Blood Pressure in Pulmonary Embolism

Pulmonary embolism typically causes systemic hypotension rather than hypertension, particularly in severe cases, due to right ventricular failure and decreased cardiac output. 1

Pathophysiology of Blood Pressure Changes in PE

• Acute PE interferes with both circulation and gas exchange, with right ventricular (RV) failure due to acute pressure overload being the primary cause of death in severe PE 1
• The abrupt increase in pulmonary vascular resistance (PVR) results in RV dilation and dysfunction, which alters the contractile properties of the RV myocardium via the Frank-Starling mechanism 1
• While compensatory mechanisms including systemic vasoconstriction temporarily stabilize systemic blood pressure, the extent of adaptation is limited as the thin-walled RV cannot generate a mean pulmonary artery pressure >40 mmHg 1
• Prolonged RV contraction time leads to leftward bowing of the interventricular septum, causing desynchronization of the ventricles and impeded LV filling in early diastole 1
• This cascade ultimately leads to reduced cardiac output and contributes to systemic hypotension and hemodynamic instability in severe PE 1

Blood Pressure Patterns in PE

Hypotension in PE

• Sustained hypotension (systolic blood pressure <90 mmHg for at least 15 minutes or requiring inotropic support) is a defining feature of massive PE 1
• Hypotension in PE is associated with significantly increased mortality - the 90-day mortality rate for patients with acute PE and systolic blood pressure ≤90 mmHg at presentation was 52.4% versus 14.7% in normotensive patients 1
• Recent research shows that even moderate decreases in blood pressure are concerning - systolic BP ≤120 mmHg and diastolic BP ≤65 mmHg at admission are associated with elevated risk of in-hospital death 2

Hypertension and PE

• Arterial hypertension is actually listed as a weak risk factor (OR <2) for developing venous thromboembolism, rather than being a consequence of PE 1
• There is no evidence in current guidelines suggesting that high blood pressure occurs as a direct result of acute PE 1
• The pathophysiological response to PE involves compensatory mechanisms including systemic vasoconstriction to temporarily maintain blood pressure, but this typically prevents hypotension rather than causing hypertension 1

Clinical Implications

• Blood pressure monitoring is crucial in PE patients as hypotension is a critical marker of severity and poor prognosis 1
• High-risk PE is defined by hemodynamic instability including hypotension, pulselessness, or persistent profound bradycardia 1
• ROC analysis shows systolic BP ≤119.5 mmHg and diastolic BP ≤66.5 mmHg are predictive cutoffs for in-hospital mortality 2
• Systemic hypotension in PE can further compromise the situation by impairing coronary driving pressure to the already overloaded right ventricle, potentially leading to RV ischemia 1

Long-term Considerations

• In some cases, unresolved PE can lead to chronic thromboembolic pulmonary hypertension (CTEPH), but this refers to pulmonary (not systemic) hypertension 1, 3
• CTEPH develops in approximately 3.8% of patients within 2 years after an initial PE episode, with risk factors including delayed treatment and location of embolism 1, 3
• This condition involves elevated pulmonary artery pressure (≥25 mmHg) due to persistent obstruction of pulmonary vessels, but does not typically cause systemic hypertension 1

Common Pitfalls

• Mistaking pulmonary hypertension (elevated pressure in pulmonary circulation) for systemic hypertension (elevated arterial blood pressure) 1
• Failing to recognize that even modest decreases in blood pressure (systolic BP ≤120 mmHg) can indicate increased mortality risk in PE patients 2
• Overlooking that arterial hypertension is actually a risk factor for developing PE rather than a consequence of it 1