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..................................................................................................... 6 Treatment in the acute phase

6.1 Haemodynamic and respiratory

support 6.1.1 Oxygen therapy and ventilation Hypoxaemia is one of the features of severe PE, and is mostly due to the mismatch between ventilation and perfusion. Administration of supplemental oxygen is indicated in patients with PE and SaO2 <90%. Severe hypoxaemia/respiratory failure that is refractory to conventional oxygen supplementation could be explained by right-to-left shunt through a patent foramen ovale or atrial septal defect.67 Further oxygenation techniques should also be considered, including high-flow oxygen (i.e. a high-flow nasal cannula)236,237 and mechanical ventilation (non-invasive or invasive) in cases of extreme instability (i.e. cardiac arrest), taking into consideration that correction of hypoxaemia will not be possible without simultaneous pulmonary reperfusion. Patients with RV failure are frequently hypotensive or are highly susceptible to the development of severe hypotension during induction of anaesthesia, intubation, and positive-pressure ventilation. Consequently, intubation should be performed only if the patient is unable to tolerate or cope with non-invasive ventilation. When feasible, non-invasive ventilation or oxygenation through a high-flow nasal cannula should be preferred; if mechanical ventilation is used, care should be taken to limit its adverse haemodynamic effects. In particular, positive intrathoracic pressure induced by mechanical ventilation may reduce venous return and worsen low CO due to RV failure in patients with high-risk PE; therefore, positive end-expiratory pressure should be applied with caution. Tidal volumes of approximately 6 mL/kg lean body weight should be used in an attempt to keep the end-inspiratory plateau pressure <30 cm H2O. If intubation is needed, anaesthetic drugs more prone to cause hypotension should be avoided for induction. 6.1.2 Pharmacological treatment of acute right ventricular failure Acute RV failure with resulting low systemic output is the leading cause of death in patients with high-risk PE. The principles of acute right heart failure management have been reviewed in a statement from the Heart Failure Association and the Working Group on Pulmonary Circulation and Right Ventricular Function of the ESC.68

An overview of the current treatment options for acute RV failure is provided in Table 9. If the central venous pressure is low, modest (<_500 mL) fluid challenge can be used as it may increase the cardiac index in patients with acute PE.238 However, volume loading has the potential to overdistend the RV and ultimately cause a reduction in systemic CO.239 Experimental studies suggest that aggressive volume expansion is of no benefit and may even worsen RV function.240 Cautious volume loading may be appropriate if low arterial pressure is combined with an absence of elevated filling pressures. Assessment of central venous pressure by ultrasound imaging of the IVC (a small and/or collapsible IVC in the setting of acute high-risk PE indicates low volume status) or, alternatively, by central venous pressure monitoring may help guide volume loading. If signs of elevated central venous pressure are observed, further volume loading should be withheld. Use of vasopressors is often necessary, in parallel with (or while waiting for) pharmacological, surgical, or interventional reperfusion treatment. Norepinephrine can improve systemic haemodynamics by bringing about an improvement in ventricular systolic interaction and coronary perfusion, without causing a change in PVR.240 Its use should be limited to patients in cardiogenic shock. Based on the results of a small series, the use of dobutamine may be considered for patients with PE, a low cardiac index, and normal BP; however, raising the cardiac index may aggravate the ventilation/perfusion mismatch by further redistributing flow from (partly) obstructed to unobstructed vessels.241 Although experimental data suggest that

5.7 Recommendations for prognostic assessment

Recommendations Classa Levelb

Initial risk stratification of suspected or confirmed PE, based on the presence of haemodynamic instability, is recommended to identify patients at high risk of early mortality.218,219,235 I B In patients without haemodynamic instability, further stratification of patients with acute PE into intermediate- and lowrisk categories is recommended.179,218,219,235 I B In patients without haemodynamic instability, use of clinical prediction rules integrating PE severity and comorbidity, preferably the PESI or sPESI, should be considered for risk assessment in the acute phase of PE.178,226,229 IIa B Assessment of the RV by imaging methodsc or laboratory biomarkersd should be considered, even in the presence of a low PESI or a negative sPESI.234 IIa B In patients without haemodynamic instability, use of validated scores combining clinical, imaging, and laboratory PE-related prognostic factors may be considered to further stratify the severity of the acute PE episode.218223 IIb C

PE = pulmonary embolism; PESI = Pulmonary Embolism Severity Index; RV = right ventricle; sPESI = simplified Pulmonary Embolism Severity Index. aClass of recommendation. bLevel of evidence. cTransthoracic echocardiography or computed tomography pulmonary angiography. dCardiac troponins or natriuretic peptides. Downloaded from academic.oup.com/eurheartj/article/41/4/543/5556136 by guest on 07 October 2026