High-altitude Pulmonary Edema in Emergency Department: A Review

High altitude pulmonary Edema (HAPE) is a severe form of high-altitude disease that, if left untreated, can result in death in up to half of those who are affected. Lowlanders who rapidly go to elevations more than 2500-3000 m are more likely to develop high altitude pulmonary Edema (HAPE). Individual sensitivity owing to a low hypoxic ventilatory response (HVR), quick pace of climb, male sex, usage of sleep medicine, high salt consumption, chilly ambient temperature, and intense physical effort are all risk factors. HAPE may be totally and quickly reversed if caught early and correctly treated. Slow climb is the most effective technique of prevention. A fall of at least 1000 meters, is the best and most certain treatment choice in HAPE. Supplemental oxygen, portable hyperbaric chambers, and pulmonary vasodilator medications (nifedipine and phosphodiesterase-5 inhibitors) may be beneficial. In this article we’ll be looking at the disease etiology, epidemiology, diagnosis and management.

Chronic thromboembolic pulmonary hypertension: anticoagulation and beyond

Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare complication in pulmonary embolism (PE) survivors, characterized by chronic vascular occlusion and pulmonary hypertension. The identification and diagnosis of CTEPH requires a stepwise approach, starting with symptom evaluation, functional evaluation, screening imaging, and progressing to interventional hemodynamic assessment. On the backbone of anticoagulation, CTEPH management necessitates a multidisciplinary approach. Surgical pulmonary thromboendarterectomy (PTE) is the only potentially curative option. In nonoperable disease or residual disease after PTE, interventional balloon pulmonary angioplasty and/or pulmonary-vasodilator therapies can be offered, in collaboration with interventional and vascular pulmonary colleagues. As it is a disease that can cause high morbidity and mortality, CTEPH requires a high index of suspicion to diagnose and treat in patients following PE.

The Use of Inhaled Epoprostenol for Acute Respiratory Distress Syndrome Secondary due to COVID-19: A Case Series

Introduction Inhaled epoprostenol (iEpo) is a pulmonary vasodilator used to treat refractory respiratory failure, including that caused by Coronavirus 2019 (COVID-19) pneumonia. Aim of Study To describe the experience at three teaching hospitals using iEpo for severe respiratory failure due to COVID-19 and evaluate its efficacy in improving oxygenation. Methods Fifteen patients were included who received iEpo, had confirmed COVID-19 and had an arterial blood gas measurement in the 12 hours before and 24 hours after iEpo initiation. Results Eleven patients received prone ventilation before iEpo (73.3%), and six (40%) were paralyzed. The partial pressure of arterial oxygen to fraction of inspired oxygen (P/F ratio) improved from 95.7 mmHg to 118.9 mmHg (p=0.279) following iEpo initiation. In the nine patients with severe ARDS, the mean P/F ratio improved from 66.1 mmHg to 95.7 mmHg (p=0.317). Ultimately, four patients (26.7%) were extubated after an average of 9.9 days post-initiation. Conclusions The findings demonstrated a trend towards improvement in oxygenation in critically ill COVID-19 patients. Although limited by the small sample size, the results of this case series portend further investigation into the role of iEpo for severe respiratory failure associated with COVID-19.

Increased incidence of Persistent Pulmonary Hypertension of the Newborn following third trimester maternal COVID-19 infection

Background Novel coronavirus (COVID-19) has been a world concern since December 2019. The knowledge about vertical transmission and fetal morbidity and mortality from maternal COVID-19 infection is limited. We detected an increase in the number of cases of term and near-term neonates with persistent pulmonary hypertension (PPHN) during the COVID-19 pandemic in 2020. Methods and results We collected data on all newborns with PPHN born between 2018 and 2020. We excluded premature infants (<34+0 weeks) and infants with other significant pathology or genetic syndromes. Compared to 5 cases of PPHN of 22930 live births in 2018, and 6 cases of PPHN of 22270 live births in 2019 (2-year average 0.02%, 95% CI 0.013%-0.043%), there were 16 PPHN cases from 22323 live births in 2020 (0.07%, 95% CI 0.044%-0.12%), a 3 fold increase (p<0.01). We report 5 cases of term and near-term neonates born to mothers who had highly suspected (2) and PCR proven (3) COVID-19 infection during the third trimester of pregnancy, who presented with PPHN during COVID-19 pandemic in 2020. All had otherwise unexplained pulmonary hypertension, right ventricular hypertrophy (RVH) and dilatation. Two patients needed endotracheal intubation, one was supported by nasal continuous positive airway pressure (CPAP) without intubation, two needed O2 support by nasal cannula only ant two newborns (one of them was intubated) needed Nitric oxide (NO) as pulmonary vasodilator therapy. No patient required Extracorporeal membrane oxygenation (ECMO) or died, and no prolonged residual cardiovascular or pulmonary morbidity was recorded during a median follow up of 4.8 months (range 4–6 months). Conclusions The increase in the incidence of PPHN during the COVID-19 pandemic, and the cases presented, suggest an intrauterine effect of maternal COVID-19 infection on the fetal pulmonary circulation. It is possible that the maternal infection affected the fetal pulmonary vascular resistance, or altered the normal decline in the resistance after birth. The right ventricular hypertrophy and dilatation with reduced function may be secondary to this hypothetical increased afterload or a direct effect of the infection. Further studies are warranted to elucidate the pathogenesis and clinical implications of this phenomenon. FUNDunding Acknowledgement Type of funding sources: None.

Acute Hemodynamic Effect of Acetazolamide in Patients With Pulmonary Hypertension Whilst Breathing Normoxic and Hypoxic Gas: A Randomized Cross-Over Trial

Aims: To test the acute hemodynamic effect of acetazolamide in patients with pulmonary hypertension (PH) under ambient air and hypoxia.Methods: Patients with pulmonary arterial or chronic thromboembolic PH (PAH/CTEPH) undergoing right heart catheterization were included in this randomized, placebo-controlled, double-blinded, crossover trial. The main outcome, pulmonary vascular resistance (PVR), further hemodynamics, blood- and cerebral oxygenation were measured 1 h after intravenous administration of 500 mg acetazolamide or placebo-saline on ambient air (normoxia) and at the end of breathing hypoxic gas (FIO2 0.15, hypoxia) for 15 min.Results: 24 PH-patients, 71% men, mean ± SD age 59 ± 14 years, BMI 28 ± 5 kg/m2, PVR 4.7 ± 2.1 WU participated. Mean PVR after acetazolamide vs. placebo was 5.5 ± 3.0 vs. 5.3 ± 3.0 WU; mean difference (95% CI) 0.2 (−0.2–0.6, p = 0.341). Heart rate was higher after acetazolamide (79 ± 12 vs. 77 ± 11 bpm, p = 0.026), pH was lower (7.40 ± 0.02 vs. 7.42 ± 0.03, p = 0.002) but PaCO2 and PaO2 remained unchanged while cerebral tissue oxygenation increased (71 ± 6 vs. 69 ± 6%, p = 0.017). In acute hypoxia, acetazolamide decreased PVR by 0.4 WU (0.0–0.9, p = 0.046) while PaO2 and PaCO2 were not changed. No adverse effects occurred.Conclusions: In patients with PAH/CTEPH, i.v. acetazolamide did not change pulmonary hemodynamics compared to placebo after 1 hour in normoxia but it reduced PVR after subsequent acute exposure to hypoxia. Our findings in normoxia do not suggest a direct acute pulmonary vasodilator effect of acetazolamide. The reduction of PVR during hypoxia requires further corroboration. Whether acetazolamide improves PH when given over a prolonged period by stimulating ventilation, increasing oxygenation, and/or altering vascular inflammation and remodeling remains to be investigated.