Pulmonary embolism (PE) is a consequence of the embolization of venous thrombi in the
branches of the pulmonary arteries. It affects approximately 1 in 1,000 people per year
worldwide and represents the third cause of cardiovascular death.
The degree of hemodynamic compromise due to PE can be determined by imaging studies, such
as computed tomography angiography, transthoracic echocardiography (TTE), and
transesophageal echocardiography (TEE). Additionally, laboratory tests may suggest
circulatory compromise, such as elevated levels of cardiac troponin and N-terminal pro
b-type natriuretic peptide (NT-proBNP) at the time of PE presentation.
There are different classifications to evaluate the severity of PE and we consider the
presence of hemodynamic instability to differentiate high-risk PE from intermediate-risk
PE. The presence of hemodynamic instability includes a state of obstructive shock (signs
of hypoperfusion associated with a systolic blood pressure (SBP) <90mmHg, and/or SBP ≥
90mmHg with the need for vasoactive drugs), persistent hypotension (SBP<90mmHg for ≥ 15
min or SBP decrease ≥ 40mmHg compared to baseline) or cardiac arrest with the need for
cardiopulmonary resuscitation (CPR). The high risk of PE also includes the existence of
some parameter included in the sPESI such as: history of cancer, age over 80 years, heart
rate ≥ 110 bpm, history of chronic obstructive pulmonary disease, SBP <100 mmHg and SpO2
<90%.
Patients with high-risk and/or intermediate/high-risk pulmonary embolism benefit from
immediate reperfusion therapy, such as systemic thrombolysis, catheter-directed
thrombolysis, catheter thrombectomy or surgery. Although the incidence of complications
and mortality in high-risk PE patients has been determined, the incidence and immediate
causes of hemodynamic and/or respiratory deterioration before, during, and after
pulmonary thrombectomy are unknown. Pulmonary thrombectomy is a technique that consists
of the extraction or dissolution, using endovascular devices, of the thrombus that
partially or totally obstructs a pulmonary artery. It is generally associated with the
local intra-thrombus administration of thrombolytic drugs. The increase in pulmonary
intravascular pressure generated during the procedure can trigger the appearance of
complications (arrhythmias, acute overload of the right ventricle, hemodynamic and/or
respiratory instability, shock, cardiovascular arrest). These complications usually
require an increase in hemodynamic support (with an increase in vasoactive drugs) and/or
respiratory support (orotracheal intubation and mechanical ventilation), and even
mechanical support with ECMO, usually veno-arterial ECMO for cardiovascular assistance.
Also, the type of anesthesia performed can precipitate the hemodynamic and/or respiratory
compromise of patients due to the possible presence of hypoxia and hypercapnia in
patients who present hypoventilation, and the increase in airway pressures caused by
orotracheal intubation and mechanical ventilation. In some cases, the use of mechanical
circulatory support, usually ECMO, may be justified; but it is currently unclear whether
VA-ECMO should be initiated in all high-risk PE patients. It must be considered that
VA-ECMO is associated with innumerable complications (bleeding, thrombi, vascular
complications), which increase the longer the duration of support.
Determining the incidence and causes or context of the onset of hemodynamic and/or
respiratory deterioration (leading to shock, need for orotracheal intubation,
cardiopulmonary arrest and/or mechanical support with ECMO), before, during and after
thrombectomy pulmonary disease, could help reduce the morbidity and mortality of these
patients.