Acute pulmonary embolism (PE) is a common disease encountered by pulmonologists, cardiologists, and critical care physicians throughout the world. For patients with high risk (defined by systemic hypotension) and intermediate high-risk (defined by the absence of systemic hypotension but the presence of numerous other concerning clinical and imaging features) acute PE, intensive care is often necessary. Initial management strategies should focus on optimization of right ventricular (RV) function while decisions about advanced interventions are being considered. Here we review the existing literature of various vasoactive agents, intravenous fluids and diuretics, and pulmonary vasodilators in both animal models and human trials of acute PE. We also review the potential complications of endotracheal intubation and positive pressure ventilation in acute PE. Finally, we review the data of veno-arterial extracorporeal membrane oxygen use in acute PE. The above interventions are discussed in the context of the underlying pathophysiology of acute RV failure in acute PE with corresponding illustrations. Norepinephrine is a reasonable first choice for hemodynamic support with vasopressin as an adjunct. Intravenous loop diuretics may be useful if there is evidence of RV dysfunction or volume overload. Fluids should only be given if there is concern for hypovolemia and absence of RV dilatation. Supplemental oxygen administration should be considered even without hypoxemia. Positive pressure ventilation should be avoided if possible. VA-ECMO cannulation should be implemented early if ongoing deterioration occurs despite these interventions.

Recovery after acute pulmonary embolism occurs on a continuum from complete restoration of flow to persistent perfusion defects causing pulmonary hypertension. An under-recognized complication of pulmonary embolism is chronic thromboembolic disease (CTED), a condition characterized by abnormal perfusion but no resting pulmonary hypertension. These patients often present with dyspnea on exertion. In this review, we discuss the epidemiology of CTED and the physiologic reasons that dyspnea on exertion manifests, namely increased dead space ventilation and exercise-induced pulmonary hypertension. We present the protocol used for invasive cardiopulmonary exercise testing with right heart catheterization necessary to differentiate these two phenotypes of CTED and exclude other causes of dyspnea on exertion such as exercise-induced diastolic dysfunction. Finally, we discuss the potential management options for symptomatic CTED including pulmonary thromboendarterectomy and balloon pulmonary angioplasty.

Background and Objective: The COVID-19 pandemic magnified the importance of gas exchange abnormalities in early respiratory failure. Pulse oximetry (SpO₂) has not been universally effective for clinical decision-making, possibly because of limitations. The alveolar gas monitor (AGM100) adds exhaled gas tensions to SpO₂ to calculate the oxygen deficit (OD). The OD parallels the alveolar-to-arterial oxygen difference (AaDO₂) in outpatients with cardiopulmonary disease. We hypothesized that the OD would discriminate between COVID-19 patients who require hospital admission and those who are discharged home, as well as predict need for supplemental oxygen during the index hospitalization. Methods: Patients presenting with dyspnea and COVID-19 were enrolled with informed consent and had OD measured using the AGM100. The OD was then compared between admitted and discharged patients and between patients who required supplemental oxygen and those who did not. The OD was also compared to SpO₂ for each of these outcomes using receiver operating characteristic (ROC) curves. Results: Thirty patients were COVID-19 positive and had complete AGM100 data. The mean OD was significantly (p = 0.025) higher among those admitted 50.0 ± 20.6 (mean ± SD) vs. discharged 27.0 ± 14.3 (mean ± SD). The OD was also significantly (p < 0.0001) higher among those requiring supplemental oxygen 60.1 ± 12.9 (mean ± SD) vs. those remaining on room air 25.2 ± 11.9 (mean ± SD). ROC curves for the OD demonstrated very good and excellent sensitivity for predicting hospital admission and supplemental oxygen administration, respectively. The OD performed better than an SpO₂ threshold of <94%. Conclusions: The AGM100 is a novel, noninvasive way of measuring impaired gas exchange for clinically important endpoints in COVID-19.

OBJECTIVES: Although proning is beneficial to acute respiratory distress syndrome, impressions vary about its efficacy. Some providers believe that paralysis is required to facilitate proning. We studied impact of paralysis on prone-induced gas exchange improvements and provider attitudes regarding paralytics. DESIGN: Observational. SETTING: University of California San Diego. PATIENTS: Intubated COVID acute respiratory distress syndrome patients. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: 1) Changes in Pao ₂:Fio ₂ and Spo ₂:Fio ₂ ratios before and after proning with and without paralytics, 2) adverse events during proning with and without paralytics, and 3) nurse and physician attitudes about efficacy/safety of proning with and without paralytics. Gas-exchange improvement with proning was similar with and without paralytics (with no serious adverse events). Survey results showed similar attitudes between nurses and physicians about proning efficacy but differing attitudes about the need for paralytics with proning. CONCLUSIONS: Findings support use of proning and may help in design of randomized trials to assess paralytics in acute respiratory distress syndrome management.