Academic literature on the topic 'Acute arterial hypoxemia'
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Journal articles on the topic "Acute arterial hypoxemia"
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Dalinghaus, M., J. W. Gratama, W. G. Zijlstra, and J. R. Kuipers. "Cardiovascular adjustments to acute hypoxemia superimposed on chronic hypoxemia in lambs." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 3 (March 1, 1995): H974—H979. http://dx.doi.org/10.1152/ajpheart.1995.268.3.h974.
Full textAbstract:
Cardiovascular responses to acute hypoxemia are in part mediated through adrenergic and chemoreceptor stimulation. In chronic hypoxemia the response to these stimuli may be blunted. Therefore, we determined whether the cardiovascular responses to acute hypoxemia superimposed on 3–4 wk of chronic hypoxemia were blunted in lambs with an experimental cardiac right-to-left shunt (combination of atrial septal defect and variable pulmonary stenosis). Cardiovascular variables and regional blood flows were determined during chronic hypoxemia and after acutely reducing the arterial oxygen saturation by increasing the cardiac right-to-left shunt. Arterial oxygen saturation decreased (65 +/- 7 to 40 +/- 7%, P < 0.001) and systemic blood flow increased (164 +/- 63 to 233 +/- 100 ml.min-1.kg-1, P < 0.01), maintaining systemic oxygen supply and oxygen uptake. Blood flow to the myocardium (P < 0.01), the adrenals (P < 0.05), and the brain (0.05 < P < 0.10) increased, and oxygen supply to these organs was maintained. Conversely, blood flow to the kidneys and the gastrointestinal tract was unaltered, so that oxygen supply to these organs was decreased. The responses to acute hypoxemia in chronically hypoxemic lambs were similar to those previously reported in normoxemic lambs. We conclude that the cardiovascular responses to acute hypoxemia in chronically hypoxemic lambs are not blunted.
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Todd, M. M., B. Wu, M. Maktabi, B. J. Hindman, and D. S. Warner. "Cerebral blood flow and oxygen delivery during hypoxemia and hemodilution: role of arterial oxygen content." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 5 (November 1, 1994): H2025—H2031. http://dx.doi.org/10.1152/ajpheart.1994.267.5.h2025.
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To determine the role of arterial O2 content (CaO2) in the cerebral blood flow (CBF) responses to hypoxemia and hemodilution, CaO2 was progressively reduced from approximately 18 to approximately 6 ml O2/dl in normocapnic, normothermic, pentobarbital-anesthetized rabbits. This was done either by reducing PaO2 (hypoxemia, minimum PaO2 approximately 26 mmHg) or arterial hematocrit (isovolemic hemodilution with hetastarch, minimum hematocrit approximately 14%) while CBF was measured with radioactive microspheres. As CaO2 decreased, CBF increased in both groups but was greater in hypoxemic animals at CaO2 values < or = 9 ml O2/dl. For example, at a CaO2 approximately 6 ml O2/dl, CBF in hypoxemic animals was 110 +/- 38 ml.100 g-1.min-1 (means +/- SD) compared with 82 +/- 22 ml.100 g-1.min-1 in hemodiluted animals (means +/- SD). While calculated cerebral O2 delivery (cerebral DO2) was well maintained in hypoxemic animals, it decreased significantly during hemodilution (from 7.95 +/- 2.92 baseline to 5.08 +/- 1.10 ml O2/dl.100 g-1.min-1 at the lowest CaO2 value). This decrease in cerebral DO2 was offset by an increase in oxygen extraction ratio during hemodilution. By contrast, the small increase in oxygen extraction ratio seen with hypoxemia did not achieve significance. These results suggest that there are different adaptive responses to acute hypoxemia or hemodilution . They also imply that at similar CBF and CaO2 values, tissue O2 availability may be greater during hemodilution than during hypoxemia.
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Baertschi, A. J., J. M. Adams, and M. P. Sullivan. "Acute hypoxemia stimulates atrial natriuretic factor secretion in vivo." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 2 (August 1, 1988): H295—H300. http://dx.doi.org/10.1152/ajpheart.1988.255.2.h295.
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The hypothesis was tested that acute hypoxemia may be a physiological stimulus for atrial natriuretic factor (ANF) secretion in anesthetized, spontaneously breathing rabbits. Base-line plasma ANF (range from 29.8 to 219 pg/ml; mean +/- SE = 87.0 +/- 14.1 pg/ml; n = 16 rabbits) was negatively correlated with base-line arterial PO2 (r = -0.759; P less than 0.01) but not with PCO2, pH, mean arterial blood pressure, central venous pressure (CVP), minute ventilation, heart rate, or type of anesthetics used. Acute hypoxemia (arterial PO2 22.3-44.3 mmHg) lasting 10 min increased plasma ANF levels over base line by 69.2 +/- 47.7 (SE) pg/ml at 6 min and 87.5 +/- 46.8 (SE) pg/ml at 9 min (P less than 0.01; n = 9). The increase in arterial pH and minute ventilation and the decrease of arterial PCO2 paralleled the changes in plasma ANF. Mean arterial blood pressure, CVP, and heart rate did not change significantly. ANF responses to hypoxemia (range from 4.4 to 423 pg/ml) correlated with base-line CVP (r = 0.761; P less than 0.01) and base-line ANF (r = 0.523; P less than 0.05) but with no other measured variable. Although the mediators of hypoxemia-induced release of ANF need to be explored further, this study raises the possibility that ANF might be involved in the adaptation to hypoxemia.
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Perez, R., M. Espinoza, R. Riquelme, J. T. Parer, and A. J. Llanos. "Arginine vasopressin mediates cardiovascular responses to hypoxemia in fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 5 (May 1, 1989): R1011—R1018. http://dx.doi.org/10.1152/ajpregu.1989.256.5.r1011.
Full textAbstract:
Acute hypoxemia results in hypertension, bradycardia, and cardiac output redistribution in fetal sheep. The blood flow redistribution is produced by differential changes in vascular resistance of various fetal organs. alpha-Adrenergic activity is one of the few vasoconstrictor mechanisms thus far identified in the hypoxemic fetal sheep. Arginine vasopressin (AVP) is a potent vasoconstrictor in adults. Since AVP administration to the normoxic fetus mimics some of the fetal cardiovascular responses to hypoxemia and fetal plasma AVP levels increase with hypoxemia, we examined the hypothesis that AVP modifies the fetal cardiovascular response to hypoxemia by changing the vascular resistance of some fetal vascular beds. To test this we determined fetal systemic arterial pressure and fetal cardiac output and its distribution during hypoxemia with and without the V1 AVP antagonist d(CH2)5-Tyr(Me)AVP. Fourteen fetal sheep (0.79-0.90 of gestation) were chronically catheterized. Five days after surgery fetal hypoxemia was induced by introducing a mixture of 95% N2-5% CO2 (10-20 l/min) into a maternal tracheal catheter. The hypoxemia was maintained for 40 min. Fetal heart rate, systemic arterial blood pressure, and combined ventricular output and its distribution (radiolabeled microspheres) were measured before hypoxemia, at 20 min of hypoxemia alone, and at 20 min of hypoxemia plus either AVP antagonist (n = 5) or NaCl 0.9% (n = 5, controls). Fetal hypertension and bradycardia were partially reversed after the AVP antagonist administration during hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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Reller, M. D., M. A. Burson, J. L. Lohr, M. J. Morton, and K. L. Thornburg. "Nitric oxide is an important determinant of coronary flow at rest and during hypoxemic stress in fetal lambs." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 6 (December 1, 1995): H2074—H2081. http://dx.doi.org/10.1152/ajpheart.1995.269.6.h2074.
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Fourteen fetal lambs were instrumented with atrial, coronary sinus, and arterial catheters and a proximal left circumflex coronary artery Doppler probe and were studied at a mean gestational age of 130 +/- 3 (SD) days, 7 +/- 2 days after surgery. Myocardial blood flow was assessed using 15-microns microspheres and Doppler flow velocities. In 11 fetuses, the maximal myocardial flow response to left atrial adenosine infusion was 802 +/- 215 ml.min-1x 100 g-1, 3.5-fold greater than baseline flow. Acute fetal hypoxemia in six fetuses to an arterial PO2 of 8.8 +/- 0.8 mmHg and an arterial O2 content (CaO2) of 1.7 +/- 0.2 ml/dl was not associated with significant change in coronary perfusion pressure; yet left ventricular myocardial flow increased to 1,020 +/- 198 ml.min-1 x 100 g-1, a value significantly greater than that seen with adenosine (P < 0.05). Left atrial N omega-nitro-L-arginine (L-NNA), a competitive inhibitor of nitric oxide synthase (NOS), was infused at a dosage of approximately 1 mg.kg-1.min-1 for 60 min in 10 fetuses. Although L-NNA was associated with a significant increase in arterial pressure, left ventricular myocardial flow decreased (162 +/- 79 ml.min-1 x 100 g-1) as did myocardial O2 consumption (P < 0.05). Acute hypoxemia in five fetuses that received L-NNA was associated with significant further increases in systemic arterial pressure; however, left ventricular myocardial flow was only 771 +/- 237 ml.min-1 x 100 g-1, a value similar to that seen with adenosine and approximately 75% of that seen with acute hypoxemia alone. We conclude that nitric oxide plays an important role in the regulation of fetal myocardial flow during basal conditions as well as in the exuberant vasodilatory response associated with acute hypoxemic stress.
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Franchini, K. G., I. A. Cestari, and E. M. Krieger. "Restoration of arterial blood oxygen tension increases arterial pressure in sinoaortic-denervated rats." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 3 (March 1, 1994): H1055—H1061. http://dx.doi.org/10.1152/ajpheart.1994.266.3.h1055.
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The objective of the present study was to analyze whether the hypoxemia produced by chemoreceptor elimination influences the arterial pressure level after sinoaortic denervation (SAD) in rats. Hypoxemia and hypercapnia were observed in acute (1 day) and chronic (20 days) SAD rats [arterial PO2 (PaO2) = 65 +2- 1.6 and 71 +2- 2.2 mmHg and arterial PCO2 (PaCO2) = 46 +/- 1.3 and 37 +/- 1.8 mmHg, respectively] compared with control rats (PaO2 = 85 +/- 1.6 mmHg, PaCO2 = 31 +/- 1.07 mmHg). Increasing inspired PO2 (PIO2) from 138 mmHg (room air) to 155 mmHg restored the PaO2 of SAD rats to control levels (acute = 81 +/- 2.21 mmHg, chronic = 85 +/- 2.35 mmHg). PaO2. restoration produced pronounced elevation of mean arterial pressure (MAP) of acute (from 121 +/- 4 to 147 +/- 3.5 mmHg) and chronic (from 121 +/- 3 to 134 +/- 3.5 mmHg) SAD rats. Progressive stepwise increase of PIO2 (from 138 to 175, 210, and 235 mmHg) produced no additional elevation of MAP of acute (113 +/- 4, 137 +/- 5, 143 +/- 5, and 147 +/- 5 mmHg) and chronic (111 +/- 3.6, 131 +/- 7.4, 130 +/- 8.7, and 130 +/- 7 mmHg) SAD rats. Otherwise, the arterial pressure of control rats remained unchanged to progressive stepwise increase of PIO2 (118 +/- 5, 117 +/- 4, 118 +/- 4, 116 +/- 4 mmHg). These data suggest that the elimination of chemoreceptors in SAD rats produces hypoxemia responsible for hypotensive influences that counteract the pressor effects produced by baroreceptor elimination.
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Ruijtenbeek, K., C. G. A. Kessels, E. Villamor, C. E. Blanco, and J. G. R. De Mey. "Direct effects of acute hypoxia on the reactivity of peripheral arteries of the chicken embryo." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 2 (August 1, 2002): R331—R338. http://dx.doi.org/10.1152/ajpregu.00675.2001.
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In the chicken embryo, acute hypoxemia results in cardiovascular responses, including an increased peripheral resistance. We investigated whether local direct effects of decreased oxygen tension might participate in the arterial response to hypoxemia in the chicken embryo. Femoral arteries of chicken embryos were isolated at 0.9 of incubation time, and the effects of acute hypoxia on contraction and relaxation were determined in vitro. While hypoxia reduced contraction induced by high K+ to a small extent (−21.8 ± 5.7%), contractile responses to exogenous norepinephrine (NE) were markedly reduced (−51.1 ± 3.2%) in 80% of the arterial segments. This effect of hypoxia was not altered by removal of the endothelium, inhibition of NO synthase or cyclooxygenase, or by depolarization plus Ca2+ channel blockade. When arteries were simultaneously exposed to NE and ACh, hypoxia resulted in contraction (+49.8 ± 9.3%). Also, relaxing responses to ACh were abolished during acute hypoxia, while the vessels became more sensitive to the relaxing effect of the NO donor sodium nitroprusside (pD2: 5.81 ± 0.21 vs. 5.31 ± 0.27). Thus, in chicken embryo femoral arteries, acute hypoxia blunts agonist-induced contraction of the smooth muscle and inhibits stimulated endothelium-derived relaxation factor release. The consequences of this for in vivo fetal hemodynamics during acute hypoxemia depend on the balance between vasomotor influences of circulating catecholamines and those of the endothelium.
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Gagnon, R., J. Murotsuki, J. R. Challis, L. Fraher, and B. S. Richardson. "Fetal sheep endocrine responses to sustained hypoxemic stress after chronic fetal placental embolization." American Journal of Physiology-Endocrinology and Metabolism 272, no. 5 (May 1, 1997): E817—E823. http://dx.doi.org/10.1152/ajpendo.1997.272.5.e817.
Full textAbstract:
The purpose of this study was to determine the endocrine and circulatory responses of the ovine fetus, near term, to sustained hypoxemic stress superimposed on chronic hypoxemia. Fetal sheep were chronically embolized (n = 7) for 10 days between 0.84 and 0.91 of gestation via the descending aorta until arterial oxygen content was decreased by approximately 30%. Control animals (n = 8) received saline only. On experimental day 10, both groups were embolized over a 6-h period until fetal arterial pH decreased to approximately 7.00. Regional distribution of lower body blood flows was measured on day 10, before and at the end of acute embolization. On day 10, the chronically embolized group had lower arterial oxygen content (P < 0.05), Po2 (P < 0.01), and placental blood flow (P < 0.05) than controls and higher prostaglandin E2 (PGE2) and norepinephrine plasma concentrations (both P < 0.05). In response to a superimposed sustained hypoxemic stress, there was a twofold greater increase in PGE2 in the chronically embolized group than in the control group (P < 0.05). However, the increase in fetal plasma cortisol in response to superimposed hypoxemic stress was similar in both groups, despite significantly lower adrenocorticotropic hormone and adrenal cortex blood flow responses in the chronically hypoxemic group (both P < 0.05). We conclude that PGE2 response to a sustained superimposed reduction in placental blood flow, leading to metabolic acidosis, is enhanced under conditions of chronic hypoxemia and may play an important role for the maintenance of the fetal cortisol response to an episode of superimposed acute stress.
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Rose, C. E., N. V. Ragsdale, and R. M. Carey. "Role of vasopressin in renal vascular changes with hypoxemia and hypercapnic acidosis in conscious dogs." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 259, no. 4 (October 1, 1990): R690—R702. http://dx.doi.org/10.1152/ajpregu.1990.259.4.r690.
Full textAbstract:
To evaluate the role of vasopressin in the renal changes during combined acute hypoxemia and acute hypercapnic acidosis, eight conscious female mongrel dogs prepared with controlled sodium intake at 80 meq/24 h for 4 days were studied in one of the following six protocols: acute hypoxemia (80 min, arterial PO2 34 +/- 1 mmHg) followed by combined acute hypoxemia and hypercapnic acidosis (40 min, arterial PO2 35 +/- 1 mmHg, arterial PCO2 58 +/- 1 mmHg, pH = 7.20 +/- 0.01) during 1) intrarenal vehicle at 0.5 ml/min (N = 8); or 2) intrarenal infusion of vasopressin V1-receptor antagonist [d(CH2)5Tyr(Me)]AVP at 5 ng.kg-1.min-1 (N = 5); and with normal gas exchange during 3) intrarenal vasopressin at 0.05 mU.kg-1.min-1 (N = 8); 4) simultaneous infusion of intrarenal vasopressin and [d(CH2)5Tyr(Me)]AVP, 5 ng.kg-1.min-1 (N = 4); 5) intrarenal [d(CH2)5Tyr(Me)]AVP, 5 ng.kg-1.min-1 (N =4); and 6) intrarenal vehicle at 0.5 ml/min (N = 7). Intrarenal infusion of a subpressor dose of vasopressin resulted in a transient decrease in glomerular filtration rate and effective renal plasma flow over the first 20 min of infusion, suggesting that vasopressin induced nonsustained vasoconstriction of the renal vasculature. Intrarenal administration of [d(CH2)5Tyr-(Me)]AVP failed to block the fall in glomerular filtration rate or effective renal plasma flow when renal arterial blood vasopressin levels were elevated by intrarenal administration of exogenous vasopressin or by elevated systemic arterial endogenous circulating vasopressin during combined acute hypoxemia and hypercapnic acidosis. These data suggest that vasopressin (V1-receptor stimulation) does not play an important role in the renal vasoconstriction during combined acute hypoxemia and hypercapnic acidosis in conscious dogs.
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Kamitomo, M., L. D. Longo, and R. D. Gilbert. "Cardiac function in fetal sheep during two weeks of hypoxemia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 266, no. 6 (June 1, 1994): R1778—R1785. http://dx.doi.org/10.1152/ajpregu.1994.266.6.r1778.
Full textAbstract:
Although several studies have examined fetal cardiac responses to acute hypoxemia, relatively little is known of the response to prolonged hypoxemia. To determine the effects of long-term hypoxemia on ovine fetal cardiac function, we measured right (QRV) and left ventricular outputs (QLV) and determined the effects of increasing preload (ventricular function curve) and afterload (arterial pressure sensitivity curve) on the left ventricle. Six days after fetal surgical instrumentation with catheters and electromagnetic flow probes (approximately 123 days gestation), we administered N2 into the maternal trachea for 14 days to reduce maternal PO2 to approximately 55 Torr (hypoxemic group, Hyp, n = 6). Normoxic animals were used as controls (Cont, n = 6). With the onset of hypoxemia, fetal arterial PO2 was reduced from approximately 27 to approximately 18 Torr. Fetal heart rate in Hyp fetuses decreased approximately 22% on day 14 compared with Cont (P < 0.05). Mean arterial pressure in the Hyp group was higher than that of Cont but not significantly so. Right and left atrial pressures were not affected by hypoxemia. QRV in Hyp fetuses was maintained on day 1 but decreased significantly by day 3 (approximately 19%) and further decreased on days 7 (approximately 28%) and 14 (approximately 34%). QLV was not depressed until day 7 (approximately 20%), with a further decrease on day 14 (approximately 38%). In association with the decreased QLV the plateau of the ventricular function curve in Hyp fetuses was depressed significantly on days 7 and 14. In contrast, the slope of the arterial pressure sensitivity curve in the Hyp group did not differ from Cont.(ABSTRACT TRUNCATED AT 250 WORDS)
Dissertations / Theses on the topic "Acute arterial hypoxemia"
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Zavorsky, Gerald Stanley. "The acute effects of volume infusion on mechanisms and severity of exercise-induced arterial hypoxemia." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ61211.pdf.
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Rodriguez-Anderson, Ramón F. "The Influence of Respiratory Muscle Work on Locomotor and Respiratory Muscle Oxygenation Trends in Repeated-Sprint Exercise." Thesis, 2018. https://vuir.vu.edu.au/37831/.
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This thesis investigated the role respiratory muscle work has on locomotor and respiratory muscle oxygen (O2) utilisation during multiple sprint work. To measure O2 delivery and uptake in real time, near-infrared spectroscopy (NIRS) can be used. However, there are inconsistent methods of smoothing and determining peaks and nadirs from the NIRS signal. Therefore, the aim of study 1 was to examine the effects of different methodologies commonly used in the literature on the determination of peaks and nadirs in the vastus lateralis deoxyhaemoglobin (HHbVL) signal. Means derived from predetermined windows, irrespective of length and data smoothing, underestimated the magnitude of peak and nadir [HHbVL] compared to a rolling mean approach. Based on the results, we suggest using a digital filter to smooth NIRS data, rather than an arithmetic mean, and a rolling approach to determine peaks and nadirs for accurate interpretation of muscle oxygenation trends.
In the second study, the effects of heightened inspiratory muscle work on [HHbVL] and respiratory muscle deoxyhaemoglobin ([HHbRM]) trends were examined. In response to the heightened inspiratory muscle work, HHbRM was elevated across the sprint series. There were no clear differences in HHbVL trends between exercise conditions. The lack of difference in HHbVL between trials implies respiratory muscle O2 uptake does not limit locomotor oxygenation trends.
Study 3 investigated the role of arterial hypoxemia on respiratory muscle oxygenation trends, and its implications on locomotor oxygenation. While exercising in hypoxia (14.5% O2), HHbVL was higher during the sprint and recovery phases of the repeated-sprint protocol compared to normoxia (21% O2). There were no clear differences in respiratory muscle oxygenation trends between conditions. The clear reduction in locomotor muscle O2 delivery (inferred from HHbVL) while respiratory muscle oxygenation was maintained, suggests preferential blood flow distribution to the respiratory muscle to compensate for arterial hypoxemia, which may explain in part compromise locomotor O2 delivery.
The aim of the final study was to examine the role of respiratory muscle strength on locomotor and respiratory muscle oxygenation trends in repeated-sprint exercise. Inspiratory muscle training (IMT) was used to reduce the relative intensity of exercise hyperpnoea by strengthening the respiratory muscles. Repeat-sprint ability was again assessed in normoxia and hypoxia. After 4 weeks of training, there was a 35% increase of inspiratory muscle pressure in the IMT beyond the control group. Despite the substantial change in respiratory muscle strength, oxygenation trends were not affected in either normoxia or hypoxia.
The findings of this thesis do not support the work of breathing as being a limiting factor in locomotor muscle oxygenation in normoxia. The intermittent nature of repeated-sprint activity is likely a key mediating factor for which O2 delivery can be maintained to both the locomotor and respiratory muscles. However, under conditions of arterial hypoxemia, locomotor muscle oxygenation may be compromised by preferential O2 delivery to the respiratory muscles.
Books on the topic "Acute arterial hypoxemia"
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Kreit, John W. Respiratory Failure and the Indications for Mechanical Ventilation. Edited by John W. Kreit. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.003.0007.
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Respiratory failure occurs when a disease process significantly interferes with the respiratory system’s vital functions and causes arterial hypoxemia, hypercapnia, or both. Typically, respiratory failure is divided into three categories based on the underlying pathophysiology: ventilation failure, oxygenation failure, and oxygenation-ventilation failure. With severe disturbances in gas exchange, mechanical ventilation is often needed to assist the respiratory system and restore the PaCO2, PaO2, or both, to normal. Respiratory Failure and the Indications for Mechanical Ventilation defines and describes the three types of respiratory failure and reviews the four indications for intubation and mechanical ventilation—acute or acute-on-chronic hypercapnia, refractory hypoxemia, inability to protect the lower airway, and upper airway obstruction.
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Gattinon, Luciano, and Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0064.
Full textAbstract:
Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.
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Gattinon, Luciano, and Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0064_update_001.
Full textAbstract:
Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.
Book chapters on the topic "Acute arterial hypoxemia"
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Gattinoni, Luciano, Mattia Busana, and Eleonora Carlesso. "Acute respiratory failure and acute respiratory distress syndrome." In The ESC Textbook of Intensive and Acute Cardiovascular Care, edited by Marco Tubaro, Pascal Vranckx, Eric Bonnefoy-Cudraz, Susanna Price, and Christiaan Vrints, 863–79. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198849346.003.0065.
Full textAbstract:
Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.