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PubMed2001

Feto-placental hypoxemia regulates the release of fetal activin A and prostaglandin E(2).

The evaluation of the role of critical hypoxia in unexplained fetal death in utero has been hampered by the lack of a physiological marker. Here we report the novel observation that feto-placental hypoxemia is an acute trigger for increased activin secretion from the feto-placental unit in late pregnancy. Hypoxemia was induced in chronically cannulated late pregnant fetal sheep by restricting blood flow through the maternal uterine arteries. Using maternal and fetal blood samples and amniotic fluid obtained via chronically implanted catheters, fetal blood gas parameters, plasma and amniotic fluid concentrations of activin A, prostaglandin (PG) E(2) and PGFM, the circulating metabolite of PGF(2alpha), were determined before, during and after a ten hour period of fetal hypoxemia. Hypoxemia acutely increased activin A and PGE(2) levels in both amniotic fluid and the fetal circulation with values rapidly returning to baseline with normoxemia. PGFM also increased in both compartments with a relatively delayed time frame compared to that of activin A and PGE(2). The increase in activin A and PGE(2) induced by hypoxemia may be a mechanism to regulate feto-placental blood flow during fetal compromise and also offers the possibility that activin A represents a useful marker of feto-placental hypoxemia.

Activins↗

PubMed1998

Gestational age-dependent changes in the levels of mRNAs encoding cortisol biosynthetic enzymes and IGF-II in the adrenal gland of fetal sheep during prolonged hypoxemia.

Hypoxemia represents a major stress for the fetus, and is associated with alterations and adaptations in cardiovascular, metabolic and endocrine responses, which in turn may affect tissue growth and differentiation. To determine the effects of hypoxemia on fetal adrenal activity and growth, we subjected sheep fetuses at days 126-130 and 134-136 (term 145 days) to reduced PaO2 by reducing the maternal fraction of oxygen for 48 h (mean reduction of 6.8 mmHg), without change in arterial pH or PaCO2. This stimulus resulted in similar increases in the plasma immunoreactiveACTH response at both ages. Among adrenal steroids, plasma cortisol (C21Delta4) rose in both groups of animals, but plasma androstenedione (C19Delta4) declined marginally, resulting in a pronounced increase in the cortisol:androstenedione ratio in the plasma that was greater and more sustained in the older fetuses. In the younger fetuses, after 48 h of hypoxemia, there were no significant changes in mRNAs encoding steroidogenic enzymes in the fetal adrenal gland. However, in the older fetuses, hypoxemia resulted in significantly increased levels of mRNAs encoding P450scc, P450C21 and 3beta-hydroxysteroid dehydrogenase, but not for P450C17, in the fetal adrenal gland. Levels of IGF-II mRNA in the fetal adrenal gland fell in both groups of fetuses, and this response was greater at the later gestational age. We conclude that sustained hypoxemia is a potent stimulus which activates adrenal steroidogenesis in the late gestation fetal sheep. The resultant increase in cortisol synthesis is associated with decreased expression of adrenal IGF-II mRNA. We speculate that this relationship might influence patterns of fetal organ growth and differentiative function in response to fetal stress such as hypoxemia.

3-Hydroxysteroid Dehydrogenases↗

PubMed1994

Role of angiotensin II in renal vasoconstriction with acute hypoxemia and hypercapnic acidosis in conscious dogs.

To evaluate the role of renin-angiotensin in the renal vasoconstriction with combined acute hypoxemia and hypercapnic acidosis preceded by acute hypoxemia, we studied eight conscious mongrel uninephrectomized dogs with chronic renal catheters and controlled sodium intake (80 mEq/24 h x 4 days). The animals were studied during combined acute hypoxemia and hypercapnic acidosis (PaO2 34 +/- 1 mm Hg, PaCo2 57 +/- 1 mm Hg, pH 7.20 +/- 0.01) preceded by 80 min of acute hypoxemia (PaO2 34 +/- 1 mm Hg) during: (a) intrarenal infusion of vehicle (n = 8); or (b) intrarenal administration of the angiotensin II antagonist [Sar1,Ala8]-AII, 70 ng kg-1 min-1 (n = 8). The combination of acute hypoxemia and hypercapnic acidosis resulted in diminished effective renal plasma flow and increased renal vascular resistance during intrarenal vehicle infusion. Intrarenal [Sar1,Ala8]-AII did not abolish the renal vasoconstriction in the initial 20 min of this combined blood gas derangement but resulted in a more prompt return of the renal vascular variables toward control levels with continuation of the blood gas derangement for an additional 20 min, suggesting a role for angiotensin in renal vasoconstriction. These observations suggest that while renin-angiotensin may not mediate the initial renal vasoconstriction in the first 20 min of combined acute hypoxemia and hypercapnic acidosis, in uninephrectomized conscious dogs, it attenuates the spontaneous recovery of renal hemodynamic variables to baseline as the blood gas derangement continues.

Acidosis, Respiratory↗

PubMed2002

Risk factors for hypoxemia and respiratory failure in respiratory syncytial virus bronchiolitis.

Respiratory syncytial virus (RSV) bronchiolitis is a common infection in young children and may result in hospitalization. We examined the incidence of, and risk factors associated with, hypoxemia and respiratory failure in 216 children aged < 24 months admitted consecutively for proven RSV bronchiolitis. Hypoxemia was defined as SpO2 < 90% in room air and severe RSV bronchiolitis requiring intubation and ventilation was categorized as respiratory failure. Corrected age at admission was used for premature children (gestation < 37 weeks). Hypoxemia was suffered by 31 (14.3%) children. It was more likely to occur in children who were Malay (OR 2.56, 95%CI 1.05-6.23, p=0.03) or premature (OR 6.72, 95%CI 2.69-16.78, p<0.01). Hypoxemia was also more likely to develop in children with failure to thrive (OR 2.96, 95%CI 1.28-6.82, p<0.01). The seven (3.2%) children who were both premature (OR 11.94, 95%CI 2.50-56.99, p<0.01) and failure to thrive (OR 6.41, 95%CI 1.37-29.87, p=0.02) were more likely to develop respiratory failure. Prematurity was the only significant risk factor for hypoxemia and respiratory failure by logistic regression analysis (OR 1.17, 95%CI 1.06-1.55, p<0.01 and OR 1.14 95%CI 1.02-2.07, p=0.02 respectively). Prematurity was the single most important risk factor for both hypoxemia and respiratory failure in RSV bronchiolitis.

Analysis of Variance↗

PubMed1992

[The effects due to reduced coronary inflow and hypoxemia during myocardial ischemia].

The events associated to myocardial ischemia result from 2 overlapping phenomena due to reduced blood flow (ischemia) and reduced O2 supply (hypoxemia). To distinguish these effects, 2 groups of isolated rat hearts were perfused through the aorta (Langendorff's method) with Krebs-Henseleit buffer, and were exposed for 20 min to hypoxemia or ischemia, matched in terms of the O2 supply (10% of baseline), with continuous monitoring of cardiac contractility, O2 uptake and lactate production. The developed pressure and the O2 uptake were similar in hypoxemic and ischemic hearts; heart rate, end-diastolic pressure and lactate production rate were higher in hypoxemia than in ischemia; the recovery from hypoxemia was less than that from ischemia, despite the same O2 supplies; treatment with superoxide dismutase and catalase, scavengers of the O2 derived free radicals, during hypoxemia, allowed hypoxemic hearts to recover as ischemic hearts. Therefore, the main determinant of the reperfusion injury is to be attributed to the low O2 supply rather than to the low coronary flow; part of the injury is due to free radicals; a substantial portion is mediated by the energy demand during the stress which was higher in hypoxemia than in ischemia.

Animals↗

PubMed1992

Combined acute hypoxemia and hypercapnic acidosis increases atrial natriuretic polypeptide in conscious dogs.

To evaluate the changes in atrial natriuretic polypeptide during acute hypoxemia and acute hypercapnic acidosis, conscious mongrel dogs with controlled sodium intake were evaluated in four protocols: (1) 80 min of acute hypoxemia (PaO2 = 34 +/- 1 mm Hg) followed by 40 min of combined hypoxemia and hypercapnic acidosis (PaO2 = 38 +/- 1 mm Hg, PaCO2 = 60 +/- 3 mm Hg, pH = 7.15 +/- 0.03) (n = 7); (2) 40 min of combined acute hypoxemia and hypercapnic acidosis (PaO2 = 36 +/- 1 mm Hg, PaCO2 = 56 +/- 2 mm Hg, pH = 7.20 +/- 0.03) induced immediately following control measurements (n = 5); (3) 120 min of acute hypercapnic acidosis (PaCO2 = 58 +/- 1 mm Hg, pH = 7.20 +/- 0.01) (n = 5), and (4) 120 min of normoxemia and normocapnia (n = 7). These studies did not observe any association between urinary sodium excretion and circulating atrial natriuretic polypeptide during acute blood gas derangements in conscious dogs. The natriuresis with acute hypoxemia or acute hypercapnic acidosis was unaccompanied by change in plasma atrial natriuretic polypeptide concentrations. Conversely, the rise in circulating atrial natriuretic polypeptide during combined acute hypoxemia and hypercapnic acidosis was not associated with an increase in urinary sodium excretion. These observations do not exclude a role for atrial natriuretic polypeptide in altering sodium excretion during acute blood gas derangements, since the effects of this autacoid on renal sodium excretion may have been offset by other counterregulatory mechanisms of sodium excretion activated during the acute blood gas derangement.

Acidosis↗

PubMedDate not supplied

Benzodiazepine premedication causes hypoxemia during spinal anesthesia in geriatric patients.

BACKGROUND AND OBJECTIVES: The use of sedatives during regional anesthesia can lead to life-threatening hypoxemia. Older patients particularly are prone to enhanced effects of these drugs. We studies whether oral premedication with benzodiazepines produced hypoxemia during spinal anesthesia in elderly patients. METHODS: In a prospective, double-blind, and randomized study, we evaluated the effect of oral benzodiazepine premedication on the incidence of hypoxemia measured by pulse oximetry (arterial oxygen saturation less than 90% for 30 seconds or longer) during surgery under spinal anesthesia in 80 geriatric patients divided into four equal groups: 1, control, no premedication; 2, 1 mg flunitrazepam; 3, 1 mg lorazepam; and 4, 7.5 mg midazolam. RESULTS: The incidence of hypoxemia in the four groups was: 1, 15%; 2, 45%; 3, 20%; and 4, 60% (p = 0.0078); overall incidence was 42% in premedicated patients versus 15% in unpremedicated controls (p = 0.0304). Seventy-four percent of patients who presented drowsiness and anesthetic level above T7 had desaturation compared to only 7% of those who were awake and had lower level (p less than 0.0005). No association between hypoxemia and other factors (age, weight, ASA physical status, and position during surgery) was found. All the episodes of desaturation were easily corrected with low supplemental oxygen concentrations. CONCLUSIONS: Premedication with oral benzodiazepines may produce hypoxemia during spinal anesthesia in elderly patients. Lorazepam appeared safer than flunitrazepam and midazolam. Monitoring of arterial blood oxygen saturation and/or supplemental oxygen is mandatory in geriatric patients with high spinal anesthetic level and/or drowsiness during surgery.

Administration, Oral↗

PubMed1991

Effects of acute hypoxemia on responses to dopamine and dobutamine in neonatal swine.

The effects of acute hypoxemia on cardiovascular responses to dopamine (DA) and dobutamine (DB) were studied in 2-4 day (n = 21) and 13-17 day (n = 27) old swine under sodium pentobarbital anesthesia. Sequential 10-min infusions of 2, 5 and 15 mu/kg/min of DA or DB or normal saline were administered under conditions of normoxemia and repeated during hypoxemia. Data are presented as mean percent of baseline value +/- SE. During normoxemia, DA increased aortic pressure, cardiac output, heart rate, LV dP/dt max and renal resistance and decreased mesenteric resistance in both ages, while DB increased heart rate, LV dP/dt max and cardiac output in both age groups and decreased total arterial resistance and renal resistance in the youngest. Increases in LV dP/dt max were larger with DA as compared to DB (p less than 0.05) with the highest dose in younger (152 +/- 5% vs. 124 +/- 4%) and older (201 +/- 29% vs. 157 +/- 9%) animals. Hypoxemia reduced heart rate responses to DA and DB in older piglets, contractility responses to DB in older animals, aortic pressure responses to DA in all animals and renal resistance responses to DA in older animals. Hypoxemia had little or no effect on cardiac output and total arterial, mesenteric and carotid resistance responses to DA and DB. Thus, in the newborn: 1) DA is a stronger inotropic agent during normoxemia and hypoxemia while the chronotropic effects of the two drugs did not differ. 2) Changes in cardiac output with both drugs did not differ significantly during normoxemia and were not affected by hypoxemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMed1975

Effect of hypoxemia on responses to norepinephrine and angiotensin in coronary and muscular vessels.

The purpose of this study was to determine the relative effects of acute hypoxemia on constrictor responses to norepinephrine and angiotensin in two vascular beds, the coronary and skeletal muscle. The left circumflex coronary and gracilis muscle arteries of anesthetized dogs were perfused at constant flow. Practolol or propranolol was administered to block indirect myocardial effects of norepinephrine on coronary resistance. When Po2 of arterial blood perfusing the coronary and muscle beds was reduced from 101 to 44 mm while systemic Pco2 remained normal, constrictor responses to both norepinephrine and angiotensin were inhibited in coronary vessels but not in muscle vessels. When local Po2 was reduced to 27 mm Hg, inhibition of responses was again observed in the coronary circulation with both drugs; in the muscle, responses to angiotensin but not to norepinephrine were depressed significantly. Since intracoronary infusion of adenosine increased, rather than inhibited, vasoconstrictor responses to angiotensin, it is unlikely that release of adenosine during hypoxemia accounts for inhibition of vasoconstriction in the coronary circulation. Indomethacin did not alter the inhibition of coronary vasoconstrictor responses to angiotensin during hypoxemia, which suggests that releease of prostglandins during htpoxemia is not the primary mechanism for inhibition of coronary vascular responses. When contractions in the gracilis muscle were produced by electrical stimulation, vasconstrictor responses to norepinnephrine were inhibited during hypoxemia. We conclude that depression of constrictor responses by hypoxemia is more pronounced in the coronay circulation than in resting muscle, but when muscle is contracting, vasoconstrictor responses are impaired during hypoxemia.

Adenosine↗

PubMed1979

Leukopenia and hypoxemia. Unrelated effects of hemodialysis.

Hemodialysis-induced hypoxemia has been attributed to membrane-related complement activation leading to pulmonary leukostasis and to hypoventilation secondary to carbon dioxide losses via the dialyzer. We have separately assessed the role of membrane- and dialysis-related factors by using different dialyzers and sequential ultrafiltration and hemodialysis with first-use cellulose dialyzers produced both leukopenia and hypoxemia. With reused cellulose and polyacrylonitrile dialyzers, hypoxemia still occurred, but without leukopenia. Ultrafiltration produced leukopenia and no changes in Pao2; during the subsequent hemodialysis, hypoxemia developed as the leukocyte count increased by 50%. Our data indicate that leukopenia and hypoxemia are unrelated effects of hemodialysis, and favor hypoventilation as the major determinant of hypoxemia during hemodialysis.

Adult↗

PubMed1982

[Exercise-induced asthma and arterial hypoxemia].

40 young asthmatic patients performed submaximal work on a treadmill ergometer for 6 minutes. In 20 cases the PaO2 was found to be below 77.5 mm Hg (arterial hypoxemia) at the 10th or the 20th minute of post-exercise recovery time. A first subgroup A of 9 asthmatics presented hypoxemia together with a fall of FEV1 below 90% of control at the first to the 20th minute post-exercise recovery phase. A second subgroup B of 11 asthmatics showed hypoxemia with FEV1's higher than 90%, often higher than 100% of the control value. The following features of the recovery period were observed: 1. 10 minutes delay of onset of hypoxemia in relation to the FEV1 drop in group A. 2. Progressive hypoxemia despite a clear return of FEV1 versus the control value during the late recovery phase of group A. 3. Appearance of arterial hypoxemia despite unchanged normal FEV1's in group B. These three observations suggest that there are 2 kinds of post-exercise bronchoconstrictions. The first may be situated in the large bronchi (FEV1-drop), the second in the small peripheral airways (PaO2-drop), from the first to the 20th and from the 20th to the 40th minute respectively after the end of submaximal work load. It is concluded that there must be 2 sequential bronchoconstrictions due to cooling of the airways and these constrictions may guarantee alveolar homeostasis for body temperature and full saturation with water vapour. However, the first barrier in the large airways can be abolished by high blood levels of adrenaline. In such cases the second barrier in the small airways becomes important and may protect the alveoli from cooling and dry air.

Adult↗

PubMed1994

Arterial hypoxemia and performance during intense exercise.

In order to determine the level of hypoxemia which is sufficient to impair maximal performance, seven well-trained male cyclists [maximum oxygen consumption (VO2max) > or = 5 l.min-1 or 60 ml.kg-1.min-1] performed a 5-min performance cycle test to exhaustion at maximal intensity as controlled by the subject, under three experimental conditions: normoxemia [percentage of arterial oxyhemoglobin saturation (%SaO2) > 94%], and artificially induced mild (%SaO2 = 90 +/- 1%) and moderate (% SaO2 = 87 +/- 1%) hypoxemia. Performance, evaluated as the total work output (Worktot) performed in the 5-min cycle test, progressively decreased with decreasing % SaO2 [mean (SE) Worktot = 107.40 (4.5) kJ, 104.07 (5.6) kJ, and 102.52 (4.7) kJ, under normoxemia, mild, and moderate hypoxemia, respectively]. However, only performance in the moderate hypoxemia condition was significantly different than in normoxemia (P = 0.02). Mean oxygen consumption and heart rate were similar in the three conditions (P = 0.18 and P = 0.95, respectively). End-tidal partial pressure of CO2 was significantly lower (P = 0.005) during moderate hypoxemia compared with normoxemia, and ventilatory equivalent of CO2 was significantly higher (P = 0.005) in both hypoxemic conditions when compared with normoxemia. It is concluded that maximal performance capacity is significantly impaired in highly trained cyclists working under an % SaO2 level of 87% but not under a milder desaturation level of 90%.

Adult↗

PubMedDate not supplied

Prolonged repolarization during hypoxemia in epicardial electrogram: difference from ischemia and a competitive action of cyclic AMP.

The effects of regional hypoxemia and ischemia on epicardial electrogram were studied in anesthetized, open-chest dogs. The left circumflex artery (LCx) was cannulated and perfused with either arterial blood or hypoxic solution. A contact electrode for recording monophasic action potential (MAP) was applied to the epicardial site of the LCx area. Epicardial electrograms and MAP in the LCx perfusion territory were recorded 1) just before and at the end of a 2-min coronary occlusion (ischemia) and 2) just before and at the end of a 2-min perfusion of hypoxic solution (hypoxemia). The activation-recovery interval (ARI), defined as an interval from the minimum derivative of the QRS complex to the maximum derivative of the T-wave in the unipolar electrogram, changed linearly with MAP duration during above interventions. The ARI decreased by 29% from 189 +/- 14 to 134 +/- 30 ms during ischemia (p < .001), and it increased by 39% from 183 +/- 11 to 254 +/- 31 ms during hypoxemia (p < .001). Hypoxemia produced a giant negative T-wave whose pattern was not modified by pretreatments with autonomic nerve blockers (propranolol and atropine), a Ca2+ channel blocker (verapamil), an ATP-sensitive K+ channel (KATP blocker (5-hydroxydecanoate or transient outward K+ current (I(to) blocker (4-aminopyridine). Isoproterenol, forskolin or aminophylline inhibited both the appearances of giant negative T and the ARI prolongation. Accordingly, unlike ischemia, hypoxemia prolongs repolarization process and this prolongation is inhibited by the augmentation of intracellular cyclic AMP.

Action Potentials↗

PubMed2006

Which clinical signs and symptoms predict hypoxemia in acute childhood asthma?

OBJECTIVE: To find the clinical signs that are the best predictors of hypoxemia (SpO2 =92%) in acute asthma in children. METHODS: Color of skin, dyspnea (by single breath counting), alertness, respiratory rate, presence of audible wheeze, wheezing on auscultation, accessory muscle use, nasal flaring, pulse rate, systolic and diastolic blood pressure, pulsus paradoxus and oxygen saturation at room air (by pulse oximetry) were recorded at the time of presentation and one hour after presentation after completion of 3 doses of nebulized salbutamol and budesonide. RESULTS: Hypoxemia (SpO2 92% pounds sterling) was seen in 45% children at presentation and 14(28.6%) after one hour. The clinical signs that correlated significantly with hypoxemia at both time points were dyspnea assessed by single breath count (OR 3.3, 95% CI 0.9-12.9), accessory muscle use score > or = 3 (OR 3.0, 95% CI 0.9-15.4) and pulsus paradoxus> 10 (OR 3.0, 95% CI 0.7-13.6). In a multiple logistic regression model accessory muscle score > or = 3 and pulsus paradoxus> 10 were identified as independent predictors of hypoxemia (sensitivity 64.3%, specificity 91%). CONCLUSION: Physical assessment in a child with acute exacerbation of asthma should at least include accessory muscle use and pulsus paradoxus, since these predict hypoxemia the best.

Acute Disease↗

PubMed2003

Preservation of electrocortical brain activity during hypoxemia in preterm lambs.

Adequate cerebral perfusion is necessary to preserve cerebral O(2) supply in order to maintain brain cell function. Our aim was to assess the influence of gestational age on the response of cerebral hemodynamics to hypoxemia and to determine thresholds of cerebral O(2) supply for preservation of brain cell function in preterm born lambs. Lambs were delivered by hysterotomy at 141 (n=5), 134 (n=5) or 127 (n=7) days of gestation. Decreases in arterial oxygen content (CaO(2)) were induced by stepwise reduction of the fraction of O(2) in inspired air (FiO(2)). Mean arterial blood pressure (MABP), carotid artery blood flow (Qcar), and electrocortical brain activity as a measure of brain cell function, were continuously recorded. Cerebral arterial blood gases were analyzed at the end of each hypoxemic level to calculate CaO(2) and cerebral O(2) supply. In contrast to 141-day lambs, MABP could not be maintained in 134-day and 127-day lambs at levels of severe hypoxemia. Increases in Qcar were observed at levels of moderate hypoxemia in all gestational age-groups. Albeit Qcar increased further at levels of severe hypoxemia in the 141-day lambs, Qcar declined under these conditions in the 134-day and 127-day lambs. The threshold of cerebral O(2) supply for the preservation of brain cell function was however similar in all gestational age-groups (1.7 ml/min). It is concluded that the ability to maintain cerebral function during hypoxemia depends upon the ability to preserve cerebral O(2) supply by means of cerebral hemodynamic compensatory mechanisms, which are not fully matured until 96% of gestation.

Animals↗

PubMed1998

Bradykinin and hypoxemia-induced renal changes in the newborn rabbit.

Acute hypoxemia causes a decrease in glomerular filtration rate (GFR) and renal blood flow (RBF) in newborns. These changes are partly mediated by local-acting vasoactive factors. We have previously shown that bradykinin (BK) has a vasodilatory role in the basic regulation of neonatal hemodynamics. The purpose of the present study was to evaluate whether BK can modulate the severe renal vasoconstriction associated with hypoxemia in the newborn rabbit. The effect of systemic hypoxemia (PaO2 approximately 40 mmHg) on renal function was investigated in 9 newborn rabbits (controls) and in 8 animals in which BK-B2 receptors were blocked by Hoe 140 (300 microg/kg subcutaneously), given prior to the induction of hypoxemia. The studies were performed under pentobarbital anesthesia at the age of 5-9 days. In control animals, acute hypoxemia caused a significant decrease in GFR and RBF and an increase in renal vascular resistance. Similar glomerular hemodynamic changes were observed in BK-B2 receptor-blocked newborn rabbits. These results indicate that BK does not play a significant role in the renal vascular changes of the hypoxemic-stressed newborn.

Animals↗

PubMed1994

The incidence and effect on outcome of hypoxemia in hospitalized medical patients.

The effect on survival of episodic hypoxemia was prospectively studied in 100 patients hospitalized on general medicine services of a large, tertiary care, university hospital. Pulse oximetry monitoring (POM) was initiated within 24 hours of admission and was maintained for approximately 24 hours independent of patient management. Hypoxemia lasting for at least 5 consecutive minutes and resulting in an arterial oxygen saturation of less than 90% occurred in 26 of the 100 patients. No clinical characteristics were found that could reliably distinguish those patients who did develop hypoxemia from those who did not, though the small number of patients in many categories precludes drawing firm conclusions. However, severe desaturation was unlikely to occur in patients with normal chest roentgenograms. During the following 4 to 7 months, 8 patients (32%) suffering episodic hypoxemia died, while only 7 individuals (10%) without hypoxemia died, an increase in mortality that remained significant after adjustment for severity of illness. The relative risk of death associated with desaturation was 3.3 (95% CI 1.41 to 8.2). The severity of hemoglobin oxygen desaturation, expressed as the saturation-time index, correlated inversely with survival time.

Adult↗

PubMed1984

Responses of the growth-retarded fetus to acute hypoxemia.

Growth retardation in the human fetus associated with maternal cardiovascular disease is frequently accompanied by birth asphyxia and perinatal mortality. We have investigated the cardiovascular responses to acute hypoxemia in the fetal lamb with growth retardation secondary to embolization of the uteroplacental vascular bed. In the basal period, fetal arterial P02 and umbilical perfusion were significantly lower, and perfusion of the adrenal glands, brain, and heart was significantly higher, in embolized than in control fetal lambs. During imposed acute hypoxemia there was preferential perfusion of vital organs, the adrenal glands, brain, and heart in control and embolized fetuses. This preferential perfusion to the vital organs during hypoxemia was significantly more pronounced in embolized animals. Because of the increased compensation during acute hypoxemia, as reflected by the increased preferential perfusion of vital organs, the growth-retarded fetuses would probably decompensate sooner if the hypoxemia was prolonged.

Acute Disease↗