Challenges for Emergent Combined Cesarean Delivery and Type A Aortic Dissection Repair Including Bleeding Management in the Setting of Full Heparinization: A Case Report.

Type A aortic dissection is rare in young females; however, it is associated with a high mortality rate. This case report describes a 30-year-old female at 38 weeks of gestation who presented with acute onset chest pain and hypotension responsive to intravenous fluid therapy. Transthoracic echocardiogram and chest computed tomography angiography confirmed a type A aortic dissection. The patient was transported urgently to the operating room for a Cesarean section and aortic dissection repair. Following induction of general anesthesia, the baby was delivered, oxytocin infusion was started, and a Bakri balloon was placed in the uterus. On cardiopulmonary bypass with circulatory arrest, the ascending aorta and aortic valve were repaired. Multiple uterotonic agents were required intraoperatively to manage persistent uterine bleeding in the setting of full heparinization. Both mother and baby survived without major complications. Preoperative management should focus on maternal hemodynamic control while completing a diagnostic evaluation. Intraoperative considerations include minimizing fetal exposure to medication, maintaining hemodynamic stability, and managing intraoperative blood loss in the setting of full anticoagulation.

Hypercapnia in diving: a review of CO2 retention in submersed exercise at depth.

Carbon dioxide (CO2) retention, or hypercapnia, is a known risk of diving that can cause mental and physical impairments leading to life-threatening accidents. Often, such accidents occur due to elevated inspired carbon dioxide. For instance, in cases of CO2 elimination system failures during rebreather dives, elevated inspired partial pressure of carbon dioxide (PCO2) can rapidly lead to dangerous levels of hypercapnia. Elevations in PaCO2 (arterial pressure of PCO2) can also occur in divers without a change in inspired PCO2. In such cases, hypercapnia occurs due to alveolar hypoventilation. Several factors of the dive environment contribute to this effect through changes in minute ventilation and dead space. Predominantly, minute ventilation is reduced in diving due to changes in respiratory load and associated changes in respiratory control. Minute ventilation is further reduced by hyperoxic attenuation of chemosensitivity. Physiologic dead space is also increased due to elevated breathing gas density and to hyperoxia. The Haldane effect, a reduction in CO2 solubility in blood due to hyperoxia, may contribute indirectly to hypercapnia through an increase in mixed venous PCO2. In some individuals, low ventilatory response to hypercapnia may also contribute to carbon dioxide retention. This review outlines what is currently known about hypercapnia in diving, including its measurement, cause, mental and physical effects, and areas for future study.

Sildenafil: Possible Prophylaxis against Swimming-induced Pulmonary Edema.

Swimming-induced pulmonary edema (SIPE) occurs during swimming and scuba diving, usually in cold water, in susceptible healthy individuals, especially military recruits and triathletes. We have previously demonstrated that pulmonary artery (PA) pressure and PA wedge pressure are higher during immersed exercise in SIPE-susceptible individuals versus controls, confirming that SIPE is a form of hemodynamic pulmonary edema. Oral sildenafil 50 mg 1 h before immersed exercise reduced PA pressure and PA wedge pressure, suggesting that sildenafil may prevent SIPE. We present a case of a 46-yr-old female ultratriathlete with a history of at least five SIPE episodes. During a study of an exercise submerged in 20°C water, physiological parameters before and after sildenafil 50 mg orally were as follows: O2 consumption 1.75, 1.76 L·min; HR 129, 135 bpm; arterial pressure 189/88 (mean 121.5), 172/85 (mean 114.3) mm Hg; mean PA pressure 35.3, 28.8 mm Hg; and PA wedge pressure 25.3, 19.7 mm Hg. She has had no recurrences during 20 subsequent triathlons while taking 50 mg sildenafil before each swim. This case supports sildenafil as an effective prophylactic agent against SIPE during competitive surface swimming.

Deaths in triathletes: immersion pulmonary oedema as a possible cause.

BACKGROUND/AIM: To address the question as to whether immersion pulmonary oedema (IPO) may be a common cause of death in triathlons, markers of swimming-induced pulmonary oedema (SIPO) susceptibility were sought in triathletes' postmortem examinations. METHODS: Deaths while training for or during triathlon events in the USA and Canada from October 2008 to November 2015 were identified, and postmortem reports requested. We assessed obvious causes of death; the prevalence of left ventricular hypertrophy (LVH); comparison with healthy triathletes. RESULTS: We identified 58 deaths during the time period of the review, 42 (72.4%) of which occurred during a swim. Of these, 23 postmortem reports were obtained. Five individuals had significant (≥70%) coronary artery narrowing; one each had coronary stents; retroperitoneal haemorrhage; or aortic dissection. 9 of 20 (45%) with reported heart mass exceeded 95th centile values. LV free wall and septal thickness were reported in 14 and 9 cases, respectively; of these, 6 (42.9%) and 4 (44.4%) cases exceeded normal values. 6 of 15 individuals (40%) without an obvious cause of death had excessive heart mass. The proportion of individuals with LVH exceeded the prevalence in the general triathlete population. CONCLUSIONS: LVH-a marker of SIPO susceptibility-was present in a greater than the expected proportion of triathletes who died during the swim portion. We propose that IPO may be a significant aetiology of death during the swimming phase in triathletes. The importance of testing for LVH in triathletes as a predictor of adverse outcomes should be explored further.

Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil.

BACKGROUND: Swimming-induced pulmonary edema (SIPE) occurs during swimming or scuba diving, often in young individuals with no predisposing conditions, and its pathophysiology is poorly understood. This study tested the hypothesis that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susceptible individuals during submerged exercise than in the general population and are reduced by sildenafil. METHODS AND RESULTS: Ten study subjects with a history of SIPE (mean age, 41.6 years) and 20 control subjects (mean age, 36.2 years) were instrumented with radial artery and pulmonary artery catheters and performed moderate cycle ergometer exercise for 6 to 7 minutes while submersed in 20°C water. SIPE-susceptible subjects repeated the exercise 150 minutes after oral administration of 50 mg sildenafil. Work rate and mean arterial pressure during exercise were similar in controls and SIPE-susceptible subjects. Average o2 and cardiac output in controls and SIPE-susceptible subjects were: o2 2.42 L·min(-1) versus 1.95 L·min(-1), P=0.2; and cardiac output 17.9 L·min(-1) versus 13.8 L·min(-1), P=0.01. Accounting for differences in cardiac output between groups, mean pulmonary artery pressure at cardiac output=13.8 L·min(-1) was 22.5 mm Hg in controls versus 34.0 mm Hg in SIPE-susceptible subjects (P=0.004), and the corresponding pulmonary artery wedge pressure was 11.0 mm Hg versus 18.8 mm Hg (P=0.028). After sildenafil, there were no statistically significant differences in mean pulmonary artery pressure or pulmonary artery wedge pressure between SIPE-susceptible subjects and controls. CONCLUSIONS: These observations confirm that SIPE is a form of hemodynamic pulmonary edema. The reduction in pulmonary vascular pressures after sildenafil with no adverse effect on exercise hemodynamics suggests that it may be useful in SIPE prevention. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00815646.

Failure rate and complications associated with the use of spinal catheters for the management of inadvertent dural puncture in the parturient: a retrospective comparison with re-sited epidural catheters.

Objective To report on the failure rate of spinal catheters placed following inadvertent dural puncture (IDP) compared with re-sited epidural catheters in the obstetric population. Research design and methods Patients who experienced IDP during epidural or combined spinal epidural placement with 17 or 18 gauge Tuohy needles for labor analgesia between 2003 and 2014 were identified using our post-dural puncture headache (PDPH) database. Patients were categorized into two groups: those who had spinal catheters inserted and those who had epidural catheters re-sited. Main outcome measure Failure rate associated with spinal or re-sited epidural catheters (defined as need for repeat block or alternative analgesic modality). Secondary outcomes were incidence of PDPH, need for epidural blood patch (EBP), and adverse events. Results A total of 109 patients were included in the final analysis; 79 ultimately had spinal catheters and 30 ultimately had re-sited epidural catheters. There were no differences between spinal catheters and re-sited epidural catheters in failure rate (22% vs. 13%, P = 0.33), incidence of PDPH (73% vs. 60%, P = 0.24), need for EBP (42% vs. 30%, P = 0.28), number of headache days, or maximum headache scores. There was also no difference in the rate of adverse events including high block levels, hypotension, and fetal bradycardia (9% vs. 7%, P = 1.0) between the two groups. Conclusions There were no differences in failure rates, PDPH outcomes, or adverse events between spinal catheters and re-sited epidural catheters following IDP in parturients receiving labor analgesia. Limitations of the study include its single-center retrospective non-randomized design, and the uneven number of patients in the two groups with a relatively small number in the re-sited epidural catheter group.

The HO-1/CO system regulates mitochondrial-capillary density relationships in human skeletal muscle.

The heme oxygenase-1 (HO-1)/carbon monoxide (CO) system induces mitochondrial biogenesis, but its biological impact in human skeletal muscle is uncertain. The enzyme system generates CO, which stimulates mitochondrial proliferation in normal muscle. Here we examined whether CO breathing can be used to produce a coordinated metabolic and vascular response in human skeletal muscle. In 19 healthy subjects, we performed vastus lateralis muscle biopsies and tested one-legged maximal O2 uptake (V̇o2max) before and after breathing air or CO (200 ppm) for 1 h daily for 5 days. In response to CO, there was robust HO-1 induction along with increased mRNA levels for nuclear-encoded mitochondrial transcription factor A (Tfam), cytochrome c, cytochrome oxidase subunit IV (COX IV), and mitochondrial-encoded COX I and NADH dehydrogenase subunit 1 (NDI). CO breathing did not increase V̇o2max (1.96 ± 0.51 pre-CO, 1.87 ± 0.50 post-CO l/min; P = not significant) but did increase muscle citrate synthase, mitochondrial density (139.0 ± 34.9 pre-CO, 219.0 ± 36.2 post-CO; no. of mitochondrial profiles/field), myoglobin content and glucose transporter (GLUT4) protein level and led to GLUT4 localization to the myocyte membrane, all consistent with expansion of the tissue O2 transport system. These responses were attended by increased cluster of differentiation 31 (CD31)-positive muscle capillaries (1.78 ± 0.16 pre-CO, 2.37 ± 0.59 post-CO; capillaries/muscle fiber), implying the enrichment of microvascular O2 reserve. The findings support that induction of the HO-1/CO system by CO not only improves muscle mitochondrial density, but regulates myoglobin content, GLUT4 localization, and capillarity in accordance with current concepts of skeletal muscle plasticity.

Immersion pulmonary edema and comorbidities: case series and updated review.

PURPOSE: Immersion pulmonary edema (IPE) occurs in swimmers (especially triathletes) and scuba divers. Its pathophysiology and risk factors are incompletely understood. This study was designed to establish the prevalence of preexisting comorbidities in individuals who experience IPE. METHODS: From 2008 to May 2010, individuals who had experienced IPE were identified via recruitment for a physiological study. Past medical history and subject characteristics were compared with those available in the current body of literature. RESULTS: At Duke University Medical Center, Durham, NC, 36 subjects were identified (mean age = 50.11 ± 10.8 yr), of whom 72.2% had one or more significant medical conditions at the time of IPE incident (e.g., hypertension, cardiac dysrhythmias or structural abnormality or dysfunction, asthma, diabetes mellitus, overweight or obesity, obstructive sleep apnea, hypothyroidism). Forty-five articles were included, containing 292 cases of IPE, of which 24.0% had identifiable cardiopulmonary risk factors. Within the recreational population, cases with identifiable risk factors comprised 44.9%. Mean age was 47.8 ± 11.3 yr in recreational divers/swimmers and 23.3 ± 6.4 yr in military divers/swimmers. CONCLUSIONS: Cardiopulmonary disease may be a common predisposing factor in IPE in the recreational swimming/diving population, whereas pulmonary hypertension due to extreme exertion may be more important in military cases. Individuals with past history of IPE in our case series had a greater proportion of comorbidities compared to published cases. The role of underlying cardiopulmonary dysfunction may be underestimated, especially in older swimmers and divers. We conclude that an episode of IPE should prompt the evaluation of cardiac and pulmonary function.

Effects of hyperoxia on ventilation and pulmonary hemodynamics during immersed prone exercise at 4.7 ATA: possible implications for immersion pulmonary edema.

Immersion pulmonary edema (IPE) can occur in otherwise healthy swimmers and divers, likely because of stress failure of pulmonary capillaries secondary to increased pulmonary vascular pressures. Prior studies have revealed progressive increase in ventilation [minute ventilation (Ve)] during prolonged immersed exercise. We hypothesized that this increase occurs because of development of metabolic acidosis with concomitant rise in mean pulmonary artery pressure (MPAP) and that hyperoxia attenuates this increase. Ten subjects were studied at rest and during 16 min of exercise submersed at 1 atm absolute (ATA) breathing air and at 4.7 ATA in normoxia and hyperoxia [inspired P(O(2)) (Pi(O(2))) 1.75 ATA]. Ve increased from early (E, 6th minute) to late (L, 16th minute) exercise at 1 ATA (64.1 +/- 8.6 to 71.7 +/- 10.9 l/min BTPS; P < 0.001), with no change in arterial pH or Pco(2). MPAP decreased from E to L at 1 ATA (26.7 +/- 5.8 to 22.7 +/- 5.2 mmHg; P = 0.003). Ve and MPAP did not change from E to L at 4.7 ATA. Hyperoxia reduced Ve (62.6 +/- 10.5 to 53.1 +/- 6.1 l/min BTPS; P < 0.0001) and MPAP (29.7 +/- 7.4 to 25.1 +/- 5.7 mmHg, P = 0.002). Variability in MPAP among subjects was wide (range 14.1-42.1 mmHg during surface and depth exercise). Alveolar-arterial Po(2) difference increased from E to L in normoxia, consistent with increased lung water. We conclude that increased Ve at 1 ATA is not due to acidosis and is more consistent with respiratory muscle fatigue and that progressive pulmonary vascular hypertension does not occur during prolonged immersed exercise. Wide variation in MPAP among healthy subjects is consistent with variable individual susceptibility to IPE.