2022-12-05 20:22:46
#Pulmonary_Embolism_7 #PE
PE treatment part 1 #ESC
Haemodynamic and respiratory support:
Administration of supplemental oxygen is indicated in patients with PE and SaO, <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.
Further oxygenation techniques should also be considered, including high-flow oxygen (ie. a high-flow nasal cannula) and mechanical ventilation (non-invasive or invasive) in cases of extreme instability (e. cardiac arrest), taking into consideration that correction of hypoxaemia will not be possible without simultaneous pulmonary reperfusion.
Patients with RV failure :
This pt 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 particutar, 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
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.
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 However, volume loading has the potential to overdistend the RV and ultimately cause a reduction in systemic CO
Experimental studies suggest that aggressive volume expansion is of no benefit and may even worsen RV function 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
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.
Although experimental data suggest that levosimendan may restore RV-pulmonary arterial coupling in acute PE by combining pulmonary vasodilation with an increase in RV contractility, no evidence of clinical benefit is available.
Vasodilators decrease PAP and PVR, but may worsen hypotension and systemic hypoperfusion due to their lack of specificity for the pulmonary vasculature after systemic [intravenous ( I.V.)]
administration.
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