scholarly journals In-Flight Hypoxemia in a Tracheostomy-Dependent Infant

2017 ◽  
Vol 2017 ◽  
pp. 1-5
Author(s):  
Jason Quevreaux ◽  
Christopher Cropsey
Keyword(s):  
Sea Level ◽  
Healthcare Providers ◽  
Barometric Pressure ◽  
Federal Aviation Administration ◽  
Anesthesia Resident ◽  
Cardiac Pathology ◽  
Mechanically Ventilated ◽  
Good Samaritan ◽  
Medical Supplies ◽  
Commercial Flight

Millions of passengers board commercial flights every year. Healthcare providers are often called upon to treat other passengers during in-flight emergencies. The case presented involves an anesthesia resident treating a tracheostomy-dependent infant who developed hypoxemia on a domestic flight. The patient had an underlying congenital muscular disorder and was mechanically ventilated while at altitude. Although pressurized, cabin barometric pressure while at altitude is less than at sea level. Due to this environment patients with underlying pulmonary or cardiac pathology might not be able to tolerate commercial flight. The Federal Aviation Administration (FAA) has mandated a specific set of medical supplies be present on all domestic flights in addition to legislature protecting “Good Samaritan” providers.

Chest Compression Duration May Be Improved When Rescuers Breathe Supplemental Oxygen

2020 ◽  
Vol 91 (12) ◽  
pp. 918-922
Author(s):  
Anna Clebone ◽  
Katherine Reis ◽  
Avery Tung ◽  
Michael OConnor ◽  
Keith J. Ruskin
Keyword(s):  
Sea Level ◽  
Chest Compression ◽  
Hypoxic Condition ◽  
Barometric Pressure ◽  
Supplemental Oxygen ◽  
Normoxic Condition ◽  
Chest Compressions ◽  
Commercial Airline ◽  
Commercial Flight

BACKGROUND: At sea level, performing chest compressions is a demanding physical exercise. On a commercial flight at cruise altitude, the barometric pressure in the cabin is approximately equal to an altitude of 2438 m. This results in a Po2 equivalent to breathing an FIo2 of 15% at sea level, a condition under which both the duration and quality of cardiopulmonary resuscitation (CPR) may deteriorate. We hypothesized that rescuers will be able to perform fewer rounds of high-quality CPR at an FIo2 of 15%.METHODS: In this crossover simulation trial, 16 healthy volunteers participated in 2 separate sessions and performed up to 14 2-min rounds of chest compressions at an FIo2 of either 0.15 or 0.21 in randomized order. Subjects were stopped if their Spo2 was below 80%, if chest compression rate or depth was not achieved for 2/3 of compressions, or if they felt fatigued or dyspneic.RESULTS: Fewer rounds of chest compressions were successfully completed in the hypoxic than in the normoxic condition, (median [IQR] 4.5 [3,8.5]) vs. 5 [4,14]). The decline in arterial Spo2 while performing chest compressions was greater in the hypoxic condition than in the normoxic condition [mean (SD), 6.19% (4.1) vs. 2% (1.66)].DISCUSSION: Our findings suggest that the ability of rescuers to perform chest compressions in a commercial airline cabin at cruising altitude may be limited due to hypoxia. One possible solution is supplemental oxygen for rescuers who perform chest compressions for in-flight cardiac arrest.Clebone A, Reis K, Tung A, OConnor M, Ruskin KJ. Chest compression duration may be improved when rescuers breathe supplemental oxygen. Aerosp Med Hum Perform. 2020; 91(12):918922.

Improvement in lung diffusion by endothelin A receptor blockade at high altitude

2012 ◽  
Vol 112 (1) ◽  
pp. 20-25 ◽  
Author(s):  
Claire de Bisschop ◽  
Jean-Benoit Martinot ◽  
Gil Leurquin-Sterk ◽  
Vitalie Faoro ◽  
Hervé Guénard ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Exercise Capacity ◽  
Barometric Pressure ◽  
Membrane Component ◽  
Alveolar Volume ◽  
Double Blind ◽  
Lung Diffusion ◽  
Endothelin A Receptor ◽  
Endothelin A

Lung diffusing capacity has been reported variably in high-altitude newcomers and may be in relation to different pulmonary vascular resistance (PVR). Twenty-two healthy volunteers were investigated at sea level and at 5,050 m before and after random double-blind intake of the endothelin A receptor blocker sitaxsentan (100 mg/day) vs. a placebo during 1 wk. PVR was estimated by Doppler echocardiography, and exercise capacity by maximal oxygen uptake (V̇o2 max). The diffusing capacities for nitric oxide (DLNO) and carbon monoxide (DLCO) were measured using a single-breath method before and 30 min after maximal exercise. The membrane component of DLCO (Dm) and capillary volume (Vc) was calculated with corrections for hemoglobin, alveolar volume, and barometric pressure. Altitude exposure was associated with unchanged DLCO, DLNO, and Dm but a slight decrease in Vc. Exercise at altitude decreased DLNO and Dm. Sitaxsentan intake improved V̇o2 max together with an increase in resting and postexercise DLNO and Dm. Sitaxsentan-induced decrease in PVR was inversely correlated to DLNO. Both DLCO and DLNO were correlated to V̇o2 max at sea level ( r = 0.41–0.42, P < 0.1) and more so at altitude ( r = 0.56–0.59, P < 0.05). Pharmacological pulmonary vasodilation improves the membrane component of lung diffusion in high-altitude newcomers, which may contribute to exercise capacity.

Oxygen transport to exercising leg in chronic hypoxia

1988 ◽  
Vol 65 (6) ◽  
pp. 2592-2597 ◽  
Author(s):  
P. R. Bender ◽  
B. M. Groves ◽  
R. E. McCullough ◽  
R. G. McCullough ◽  
S. Y. Huang ◽  
...  
Keyword(s):  
Blood Flow ◽  
Sea Level ◽  
Chronic Hypoxia ◽  
Peripheral Resistance ◽  
Hemoglobin Concentration ◽  
Barometric Pressure ◽  
Ambient Air ◽  
Leg Blood Flow ◽  
State Cycle ◽  
O2 Delivery

Residence at high altitude could be accompanied by adaptations that alter the mechanisms of O2 delivery to exercising muscle. Seven sea level resident males, aged 22 +/- 1 yr, performed moderate to near-maximal steady-state cycle exercise at sea level in normoxia [inspired PO2 (PIO2) 150 Torr] and acute hypobaric hypoxia (barometric pressure, 445 Torr; PIO2, 83 Torr), and after 18 days' residence on Pikes Peak (4,300 m) while breathing ambient air (PIO2, 86 Torr) and air similar to that at sea level (35% O2, PIO2, 144 Torr). In both hypoxia and normoxia, after acclimatization the femoral arterial-iliac venous O2 content difference, hemoglobin concentration, and arterial O2 content, were higher than before acclimatization, but the venous PO2 (PVO2) was unchanged. Thermodilution leg blood flow was lower but calculated arterial O2 delivery and leg VO2 similar in hypoxia after vs. before acclimatization. Mean arterial pressure (MAP) and total peripheral resistance in hypoxia were greater after, than before, acclimatization. We concluded that acclimatization did not increase O2 delivery but rather maintained delivery via increased arterial oxygenation and decreased leg blood flow. The maintenance of PVO2 and the higher MAP after acclimatization suggested matching of O2 delivery to tissue O2 demands, with vasoconstriction possibly contributing to the decreased flow.

Cardiovascular adaptations in Andean natives after 6 wk of exposure to sea level

1991 ◽  
Vol 70 (6) ◽  
pp. 2650-2655 ◽  
Author(s):  
D. C. McKenzie ◽  
L. S. Goodman ◽  
C. Nath ◽  
B. Davidson ◽  
G. O. Matheson ◽  
...  
Keyword(s):  
Sea Level ◽  
Barometric Pressure ◽  
Cycle Ergometer ◽  
Left Ventricular ◽  
Structure And Function ◽  
Left Ventricular Ejection ◽  
Noninvasive Methods ◽  
Functional Changes ◽  
And Function ◽  
Quechua Indians

Six male Quechua Indians (34.0 +/- 1.1 yr, 159.5 +/- 2.1 cm, 60.5 +/- 1.6 kg), life-long residents of La Raya, Peru (4,350-m altitude with an average barometric pressure of 460 Torr), were studied using noninvasive methods to determine the structural and functional changes in the cardiovascular system in response to a 6-wk deacclimation period at sea level. Cardiac output, stroke volume, and left ventricular ejection fractions were determined using radionuclide angiographic techniques at rest and during exercise on a cycle ergometer at 40, 60, and 90% of a previously determined maximal O2 consumption. Subjects at rest were subjected to two-dimensional and M-mode echocardiograms and a standard 12-lead electrocardiogram. Hemoglobin and hematocrit were measured on arrival at sea level by use of a Coulter Stacker S+ analyzer. After a 6-wk deacclimation period, all variables were remeasured using the identical methodology. Hemoglobin values decreased significantly over the deacclimation period (15.7 +/- 1.1 to 13.5 +/- 1.2 g/dl; P less than 0.01). The results indicate that the removal of these high-altitude-adapted natives from 4,300 m to sea level for 6 wk results in only minor changes to the cardiac structure and function as measured by these noninvasive techniques.

scholarly journals Nurses on the Frontline against the COVID-19 Pandemic: An Integrative Review

2020 ◽  
Vol 3 (3) ◽  
pp. 87-92
Author(s):  
Abdullelah Al Thobaity ◽  
Farhan Alshammari
Keyword(s):  
Nursing Staff ◽  
Personal Protective Equipment ◽  
Critical Line ◽  
Healthcare Providers ◽  
Healthcare Systems ◽  
Integrative Review ◽  
Protective Equipment ◽  
Crisis Plans ◽  
Medical Supplies ◽  
The World

COVID-19 has affected the life and health of more than 1 million people across the world. This overwhelms many countries’ healthcare systems, and, of course, affects healthcare providers such as nurses fighting on the frontlines to safeguard the lives of everyone affected. Exploring the issues that nurses face during their battle will help support them and develop protocols and plans to improve their preparedness. Thus, this integrative review will explore the issues facing nurses during their response to the COVID-19 crisis. The major issues facing nurses in this situation are the critical shortage of nurses, beds, and medical supplies, including personal protective equipment and, as reviews indicate, psychological changes and fears of infection among nursing staff. The implications of these findings might help to provide support and identify the needs of nurses in all affected countries to ensure that they can work and respond to this crisis with more confidence. Moreover, this will help enhance preparedness for pandemics and consider issues when drawing up crisis plans. The recommendation is to support the nurses, since they are a critical line of defense. Indeed, more research must be conducted in the field of pandemics regarding nursing.

Time course of augmentation and depression of hypoxic ventilatory responses at altitude

1994 ◽  
Vol 77 (1) ◽  
pp. 313-316 ◽  
Author(s):  
M. Sato ◽  
J. W. Severinghaus ◽  
P. Bickler
Keyword(s):  
Pulse Oximetry ◽  
Sea Level ◽  
Time Course ◽  
Ventilatory Response ◽  
Barometric Pressure ◽  
Hypoxic Ventilatory Response ◽  
Set Point ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Arterial O2 Saturation

Hypoxic ventilatory response (HVR) and hypoxic ventilatory depression (HVD) were measured in six subjects before, during, and after 12 days at 3,810-m altitude (barometric pressure approximately 488 Torr) with and without 15 min of preoxygenation. HVR was tested by 5-min isocapnic steps to 75% arterial O2 saturation measured by pulse oximetry (Spo2) at an isocapnic PCO2 (P*CO2) chosen to set hyperoxic resting ventilation to 140 ml.kg-1.min-1. Hypercapnic ventilatory response (HCVR, 1.min-1.Torr-1) was tested at ambient and high SPO2 6–8 min after a 6- to 10-Torr step increase of end-tidal PCO2 (PETCO2) above P*CO2. HCVR was independent of preoxygenation and was not significantly increased at altitude (when corrected to delta logPCO2). Preoxygenated HVR rose from -1.13 +/- 0.23 (SE) l.min-1.%SPO2(-1) at sea level to -2.17 +/- 0.13 by altitude day 12, without reaching a plateau, and returned to control after return to sea level for 4 days. Ambient HVR was measured at P*CO2 by step reduction of SPO2 from its ambient value (86–91%) to approximately 75%. Ambient HVR slope was not significantly less, but ventilation at equal levels of SPO2 and PCO2 was lower by 13.3 +/- 2.4 l/min on day 2 (SPO2 = 86.2 +/- 2.3) and by 5.9 +/- 3.5 l/min on day 12 (SPO2 = 91.0 +/- 1.5; P < 0.05). This lower ventilation was estimated (from HCVR) to be equivalent to an elevation of the central chemoreceptor PCO2 set point of 9.2 +/- 2.1 Torr on day 2 and 4.5 +/- 1.3 on day 12.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of beta-adrenoceptor blockade on renin-aldosterone and alpha-ANF during exercise at altitude

1989 ◽  
Vol 67 (1) ◽  
pp. 141-146 ◽  
Author(s):  
P. Bouissou ◽  
J. P. Richalet ◽  
F. X. Galen ◽  
M. Lartigue ◽  
P. Larmignat ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Acute Mountain Sickness ◽  
Plasma Renin ◽  
Barometric Pressure ◽  
Suppressive Effect ◽  
Beta Blockade ◽  
Plasma Norepinephrine ◽  
Plasma Aldosterone Concentration ◽  
Ergometer Exercise

The renin-aldosterone system may be depressed in subjects exercising at high altitude, thereby preventing excessive angiotensin I (ANG I) and aldosterone levels, which could favor the onset of acute mountain sickness. The role of beta-adrenoceptors in hormonal responses to hypoxia was investigated in 12 subjects treated with a nonselective beta-blocker, pindolol. The subjects performed a standardized maximal bicycle ergometer exercise with (P) and without (C) acute pindolol treatment (15 mg/day) at sea level, as well as during a 5-day period at high altitude (4,350 m, barometric pressure 450 mmHg). During sea-level exercise, pindolol caused a reduction in plasma renin activity (PRA, 2.83 +/- 0.35 vs. 5.13 +/- 0.7 ng ANG I.ml-1.h-1, P less than 0.01), an increase in plasma alpha-atrial natriuretic factor (alpha-ANF) level (23.1 +/- 2.9 (P) vs. 10.4 +/- 1.5 (C) pmol/1, P less than 0.01), and no change in plasma aldosterone concentration [0.50 +/- 0.04 (P) vs. 0.53 +/- 0.03 (C) nmol/1]. Compared with sea-level values, PRA (3.45 +/- 0.7 ng ANG I.ml-1.h-1) and PA (0.39 +/- 0.03 nmol/1) were significantly lower (P less than 0.05) during exercise at high altitude. alpha-ANF was not affected by hypoxia. When beta-blockade was achieved at high altitude, exercise-induced elevation in PRA was completely abolished, but no additional decline in PA occurred. Plasma norepinephrine and epinephrine concentrations tended to be lower during maximal exercise at altitude; however, these differences were not statistically significant. Our results provide further evidence that hypoxia has a suppressive effect on the renin-aldosterone system. However, beta-adrenergic mechanisms do not appear to be responsible for inhibition of renin secretion at high altitude.

Measurement of factors impairing gas exchange in man with hyperbaric pressure

1964 ◽  
Vol 19 (2) ◽  
pp. 189-194 ◽  
Author(s):  
C. Lenfant
Keyword(s):  
Sea Level ◽  
Venous Blood ◽  
Barometric Pressure ◽  
Bimodal Distribution ◽  
Arterial Oxygen ◽  
Dissociation Curve ◽  
Group Of Units ◽  
Hyperbaric Pressure ◽  
Oxygen Difference ◽  
Made In

Alveoli with very low ventilation/perfusion ratios (Va/Q) contribute capillary blood with venous saturation to the mixed arterial stream. The portion of the alveolar arterial oxygen difference (A-a Do2) due to these units with very low Va/Q ratios cannot be differentiated from that due to an anatomical shunt at ambient pressures. By raising the barometric pressure to such a level that venous blood is saturated, the O2 dissociation curve no longer affects the A-a Do2 measurement, and the differentiation can be made. In the present experiments 75% O2 was inspired at sea level and at a depth equivalent to 2.6 atm. The A-aD was measured for O2, CO2 and N2. In seven out of eight subjects A-a Do2 and A-a Dn2 varied when the barometric pressure was increased. A theoretical analysis showed that the results can be interpreted on the basis of a bimodal distribution of Va/Q composed of a large group of well-ventilated alveoli and of a small group of units having an undeterminable Va/Q. The shunt calculated from the total A-a Do2 at sea level was 3.47% of the total cardiac output. When the A-a Do2 due to Va/Q (i.e., A-a Dco2 + A-a Dn2) was subtracted from the total A-a Do2 the shunt was 1.78%. At 2.6 atm that part of the total A-a Do2 found to be due to shunt was 0.8%, or 25% of the shunt estimated at sea level from the pure O2 technique. pulmonary shunts; ventilation/perfusion distribution; diving; hyperbarism Submitted on June 24, 1963

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