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PubMed1984

Antidiuresis and vasopressin release with hypoxemia and hypercapnia in conscious dogs.

To determine the effects of acute blood gas derangements on renal water and solute excretion and vasopressin secretion, six unanesthetized mongrel dogs were studied during 1) combined acute hypoxemia and hypercapnic acidosis [arterial O2 partial pressure (PaO2) 36 +/- 1 Torr, arterial CO2 partial pressure (PaCO2) 54 +/- 2 Torr, pH 7.18 +/- 0.01], 2) acute hypoxemia (PaO2 33 +/- 2 Torr, PaCO2 33 +/- 1 Torr, pH 7.34 +/- 0.01), and 3) acute hypercapnic acidosis (PaO2 83 +/- 3 Torr, PaCO2 53 +/- 1 Torr, pH 7.19 +/- 0.02). Combined acute hypoxemia and hypercapnic acidosis increased (P less than 0.05) mean arterial pressure, but renal hemodynamic function deteriorated with decreased (P less than 0.05) glomerular filtration rate and increased (P less than 0.05) renal vascular resistance. Moreover free water clearance became more negative (P less than 0.05) and urine osmolality increased (P less than 0.05). During acute hypoxemia or acute hypercapnic acidosis alone, mean arterial pressure and renal hemodynamic function were unchanged but free water clearance became more negative (P less than 0.05). During acute hypoxemia, urine osmolality increased (P less than 0.05) comparably with values observed during combined acute hypoxemia and hypercapnic acidosis. Plasma vasopressin concentrations increased profoundly (P less than 0.05) during combined hypoxemia and hypercapnic acidosis and during acute hypoxemia alone and were significantly elevated (P less than 0.05) above the increased plasma vasopressin concentrations observed during acute hypercapnic acidosis. We conclude that acute hypoxemia and hypercapnic acidosis result in impairment of renal water excretion, probably mediated through vasopressin secretion.

Animals↗

PubMed1984

Hypoxemia increases plasma catecholamine concentrations in exercising humans.

To determine whether plasma catecholamine concentrations (a measure of sympathetic nervous activity [SNA]) rise above normoxic levels during exercise with hypoxemia, we exercised seven men for 15 min at three loads that required from 40 to 88% of maximal O2 uptake (VO2max). Subjects breathed room air on one day and 11-12% O2 on another with relative work loads corrected for the 24% fall in VO2max during hypoxemia. Hypoxemia caused large increments in norepinephrine (NE) concentration (radioenzyme technique) to 1.21 +/- 0.20 ng/ml (mean +/- SE), 2.79 +/- 0.38, and up to 5.90 +/- 0.75 (hypoxemia) compared with 0.89 +/- 0.06, 1.66 +/- 0.16, and 3.95 +/- 0.39 in normoxia at the three loads, respectively (P less than 0.001). Epinephrine (E) concentration approximately doubled (P less than 0.001) in hypoxemia at each load when compared with normoxic levels (i.e., 0.10 +/- 0.01 ng/ml, 0.23 +/- 0.03, and 0.46 +/- 0.06 in normoxia). However, hypoxemia did not significantly alter linear relationships between log plasma NE concentration and either heart rate (HR) or percent VO2max utilized, or between HR and percent VO2max. Thus NE concentration, like HR, appeared to reflect relative severity of exercise and overall SNA in both hypoxemia and normoxia. Above 40% VO2max during hypoxemia, circulating NE and E far exceeded levels known to have direct vasoconstrictor and metabolic effects in normoxic humans, but hypoxemia may blunt vasoconstriction in some regions.

Adult↗

PubMed1986

Extracellular fluid volume during pneumothorax and hypoxemia in rabbits.

This study was designed to test the hypothesis that persistent pneumothorax of greater than or equal to 6 days duration causes a decrease of extracellular fluid volume (ECF). Such changes are of interest as they may be causally related to persistent hypotension that has occurred in humans following pneumothorax evacuation. Experiments were done in rabbits to determine the effect on ECF of persistent pneumothorax with or without systemic hypoxemia. Animals were divided into four treatment groups: 1) pneumothorax with hypoxemia [fractional concentration of O2 in inspired gas (FIO2) = 0.21, n = 30], 2) pneumothorax without hypoxemia (FIO2 = 0.40, n = 25), 3) hypoxemia alone (FIO2 = 0.14, n = 11), and 4) normal controls (FIO2 = 0.21, n = 15). Measurements of ECF were made in the base-line control state and after 6 days of treatment using the dilution volume of thiocyanate sodium as an estimate of ECF volume. We found a reduction of ECF in 53% of animals with pneumothorax plus hypoxemia (range -47% to +13%) and in 54% of animals with hypoxemia alone (range -26% to +25%). ECF declined in only 7% of normal controls and 20% of animals with pneumothorax without hypoxemia. Arterial O2 tensions after 6 days of treatment were 58 +/- 12.6, 141 +/- 28, 60 +/- 5.1, and 97 +/- 9.3 Torr (mean +/- SD) in groups 1-4, respectively. The results suggest that pneumothorax with hypoxemia or hypoxemia alone may contribute to depletion of ECF, but this response is variable and unpredictable in individual animals.

Animals↗

PubMed1995

Effect of theophylline on metabolic and ventilatory response to hypoxemia during quiet sleep in piglets.

Theophylline, a drug frequently used in newborns, stimulates respiration and increases the metabolic rate in a sustained fashion; hypoxemia, on the other hand, decreases metabolic rate and increases ventilation slightly and, at times, only transiently. This study looked at the effect of theophylline on the metabolic and ventilatory response to hypoxemia in piglets. We studied two groups of piglets during normoxia and hypoxemia: first during a baseline period; and second, after the infusion of either theophylline or a placebo. All studies were done in quiet sleep, 2 d after instrumentation was performed to place vascular catheters and electroencephalographic electrodes. O2 consumption (VO2) and CO2 production (VCO2) were measured in a metabolic chamber, and alveolar ventilation (VA) was then derived from VCO2 and PaCO2. We found that theophylline did not abolish the small decrease in oxygen consumption brought about by hypoxemia. Nor did theophylline augment the ventilatory response to hypoxemia. In fact, the percent change in alveolar ventilation decreased slightly: going from 17 +/- 8% during the baseline period to 9 +/- 6% (p < 0.005) after theophylline administration. We found a significant increase in respiratory exchange ratio (R) in response to hypoxemia (from 0.87 +/- 0.05 to 0.97 +/- 0.04, p < 0.001). However, after the administration of theophylline, additional exposure to hypoxemia did not result in a change in R. In summary, our results show that, in sleeping newborn piglets, theophylline does not abolish the decrease in oxygen consumption observed in response to hypoxemia; nor does it enhance the ventilatory response to a moderate degree of hypoxemia.

Animals↗

PubMed1996

Differential regulation of proopiomelanocortin messenger ribonucleic acid in the pars distalis and pars intermedia of the pituitary gland after prolonged hypoxemia in fetal sheep.

POMC messenger RNA (mRNA) is synthesized and translated to form ACTH in the pars distalis and ACTH-related peptides in the pars intermedia of the pituitary in fetuses of species such as sheep. In the fetal sheep, maturation of hypothalamo-pituitary-adrenal (HPA) function occurs during late pregnancy accompanied by increased levels of POMC mRNA in the pars distalis, and contributes to the stimulus for birth. Activation of fetal HPA function also occurs with short term hypoxemia. However, the effects of more prolonged fetal hypoxemia, which may predispose to premature parturition, on POMC mRNA levels in the pars distalis and pars intermedia are not known. We studied the effects of sustained hypoxemia (48 h) in the absence of acidosis on fetal HPA responses at two times in late gestation, days 126-130 and days 134-136 (term = approximately 145 days). Hypoxemia was induced by lowering the fraction of oxygen in the maternal inspired gas mixture. Fetal arterial oxygen tension fell by 6-8 mm Hg, without a change in fetal arterial pH or carbon dioxide tension. Pituitary POMC mRNA was localized and quantified by in situ hybridization. At both gestational ages, hypoxemia caused a transient elevation in fetal plasma ACTH, with a maximum response at +2 h, and a sustained elevation in circulating cortisol. Cortisol responses were greater in the older fetuses. Changes in plasma cortisol were not associated with alterations in the plasma corticosteroid-binding capacity or in levels of hepatic corticosteroid-binding globulin mRNA. Pituitary POMC mRNA showed a regional distribution in the pars distalis, and mean levels increased with gestational age. After 48 h of hypoxemia, POMC mRNA levels had increased in the pars distalis. The regional distribution was unaffected by the hypoxemic insult. In contrast, POMC mRNA levels in the pars intermedia decreased after hypoxemia, and the reduction was greater in the older fetuses. We conclude that in response to prolonged hypoxemia, there is differential regulation of POMC mRNA levels in the pars distalis and pars intermedia of the pituitary in fetal sheep. The magnitude of these responses also changes with gestational age. The increase in POMC mRNA levels in the pars distalis at 48 h of hypoxemia, despite a rise in plasma cortisol and without a change in corticosteroid-binding globulin, suggests altered regulation of HPA function at this time.

Adrenal Cortex Hormones↗

PubMed2005

The effect of thoracic epidural analgesia on the occurrence of late postoperative hypoxemia in patients undergoing elective coronary bypass surgery: a randomized controlled trial.

STUDY OBJECTIVES: To evaluate the effect of perioperative thoracic epidural analgesia followed by postoperative epidural analgesia compared with conventional IV anesthesia on the occurrence of late postoperative hypoxemia in patients undergoing elective coronary bypass graft (CABG) surgery. DESIGN: Randomized controlled trial. SETTING: Cardiac surgery unit at a university hospital. PATIENTS: A total of 50 patients undergoing elective CABG surgery. INTERVENTION: Patients were randomly assigned to receive either conventional IV anesthesia (CON) or general anesthesia combined with thoracic epidural anesthesia followed by postoperative epidural analgesia (TEA) with bupivacaine. Postoperatively, the patients were monitored in the surgical ward with a pulse oximeter for a total of two postoperative nights (the second and third postoperative nights). MEASUREMENTS AND RESULTS: The overall incidence of episodic hypoxemia was 56% (28 of 50 patients) on the second postoperative night and 89% (41 of 46 patients) on the third postoperative night. More than 30 episodes of hypoxemia developed on the second night in 22% of patients (11 of 50 patients), and on the third night in 30% of patients (14 of 46 patients). Despite oxygen therapy, 7% of patients (3 of 46 patients) experienced constant hypoxemia on the third night. In general, hypoxemia seemed to be slightly worse on the third postoperative night compared with the second postoperative night. Significantly more patients in the TEA group (25 of 25 patients) experienced episodic hypoxemia on the third postoperative night compared with the CON group (16 of 21 patients; p < 0.05). Otherwise, there were no significant differences between the two regimens. CONCLUSIONS: Both episodic and constant hypoxemia were common in the late postoperative period in patients on the ward after CABG surgery with no clinically significant intergroup differences. Thus, perioperative epidural anesthesia/analgesia combined with postoperative epidural anesthesia/analgesia was not protective against hypoxemia, and therapy with opioids did not seem to be of importance for the occurrence of late postoperative hypoxemia on nights 2 and 3 after CABG surgery.

Aged↗

PubMed2006

Hypoxemia in children with pneumonia and its clinical predictors.

OBJECTIVES: To assess the prevalence of hypoxemia in children, 2 months to 5 years of age, with pneumonia and to identify its clinical predictors. METHODS: Children between 2-60 months of age presenting with a complaint of cough or difficulty breathing were assessed. Hypoxemia was defined as an arterial oxygen saturation of < 90% recorded by a portable pulse oximeter. Patients were categorized into groups: cough and cold, pneumonia, severe pneumonia and very severe pneumonia. RESULTS: The prevalence of hypoxemia (SpO2 of < 90%) in 150 children with pneumonia was 38.7%. Of them 100% of very severe pneumonia, 80% of severe and 17% of pneumonia patients were hypoxic. Number of infants with respiratory illness (p value = 0.03) and hypoxemia (Odds ratio = 2.21, 95% CI 1.03, 4.76) was significantly higher. Clinical predictors significantly associated with hypoxemia on univariate analysis were lethargy, grunting, nasal flaring, cyanosis, and complaint of inability to breastfeed/drink. Chest indrawing with 68.9% sensitivity and 82.6% specificity was the best predictor of hypoxemia. CONCLUSION: The prevalence and clinical predictors of hypoxemia identified validate the WHO classification of pneumonia based on severity. Age < 1 year in children with ARI is an important risk factor for hypoxemia.

Child, Preschool↗

PubMed2006

Nocturnal episodic hypoxemia after ambulatory breast cancer surgery: comparison of sevoflurane and propofol-fentanyl anesthesia.

PURPOSE: To study the incidence and severity of nocturnal episodic hypoxemia after ambulatory breast cancer surgery and its differences with sevoflurane and propofol anesthesia. METHODS: Sixty-one adult female patients (ASA PS I-II; age, 32-77 years) without an apparent history of sleep apnea and respiratory disease undergoing major breast cancer surgery on an outpatient basis and with planned overnight admission were randomized to one of two anesthesia maintenance groups: sevoflurane anesthesia (SEV, n = 31) or intravenous propofol, fentanyl, and vecuronium anesthesia (TIVA, n = 30). All patients were administered propofol 2 mg x kg(-1) intravenously for anesthesia induction, had a laryngeal mask airway placed, and received rectal diclofenac and local infiltration anesthesia for pain relief. No opioid analgesic or oxygen was administered after discharge from the postanesthesia care unit (PACU). Oxygen saturation (Sp(O) (2)) was recorded continuously during the first postoperative night. Sp(O) (2) <90% that lasted >10 s was regarded as hypoxemia, and the percentage of effective recording time with Sp(O) (2) <90% (%time with Sp(O) (2) <90) was evaluated. RESULTS: Six patients (SEV3/TIVA3) had >1% of %time with Sp(O) (2) <90 (S-hypoxemia group), 17 (SEV7/TIVA10) had >0% and <or=1% (M-Hypoxemia group), and 38 (SEV21/TIVA17) had 0% (no-hypoxemia group). There were no statistical differences in age, ASA PS, anesthesia technique, and duration of anesthesia among groups. The S-hypoxemia group had higher body mass index (BMI) and incidence of oxygen supplementation in the PACU than the no-hypoxemia group. No patient had major complications. CONCLUSION: Nocturnal episodic hypoxemia occurs frequently after ambulatory breast cancer surgery. The incidence was not different between SEV and TIVA. Hypoxic patients had a higher BMI and needed oxygen therapy in PACU more frequently.

Adult↗

PubMed1987

Acute hypoxemia does not increase blood fibrinolytic activity in man.

The influence of acute hypoxemia on blood fibrinolytic activity was investigated in 12 healthy males. Physiologically significant hypoxemia was produced by inspiration of 13% oxygen for 30 min. Six healthy males were exposed to hypoxemia at rest and 6 males to hypoxemia during exhaustive physical exercise on an ergocyclometer. During control experiments both groups of health males inspired 21% oxygen. In 5 patients with manifest respiratory insufficiency the effect of hypoxemia at rest was studied during withdrawal of oxygen treatment for up to 2.5 hours. No increase in fibrinolytic activity (measured with euglobulin clot lysis and fibrin plates) due to hypoxemia was observed either in resting healthy males or in patients. In healthy males the increase in fibrinolytic activity after physical exercise at 13% oxygen was even somewhat lower compared to 21% oxygen. No changes in other hemostatic parameters (activated partial thromboplastin time, factor VIII-related antigen, fibrinogen, plasminogen, alpha-2-antiplasmin, fibrin(ogen) degradation products) that could be attributed to hypoxemia, were observed in any group tested. It was concluded that short-term acute hypoxemia does not increase blood fibrinolytic activity in man.

Acute Disease↗

PubMed1996

Role of hypoxemia in sleep apnea-induced sympathoexcitation.

The importance of hypoxemia in determining sympathoexcitation during obstructive sleep apnea was examined by comparing changes in efferent sympathetic nerve activity (SNA) during spontaneous obstructive apneas with hypoxemia alone of similar magnitude and duration induced by 1-4 breaths of 100% nitrogen in six patients with obstructive sleep apnea and with spontaneous apneas while breathing 100% oxygen (apnea without hypoxemia) in three patients. In addition, eight control subjects were studied during induced hypoxemia. The magnitude of sympathoexcitation during spontaneous apneas (103 +/- 15%) was more than twice that observed during induced hypoxemia (47 +/- 14%) during episodes in which the nadir of oxygen desaturation (78 +/- 2 and 75 +/- 2%, respectively) and duration of hypoxemia (27 +/- 3 and 33 +/- 3 s, respectively) were the same (P > 0.20). Similarly, in three patients SNA increased 115% during normoxic spontaneous obstructive apneas, but increased only 43% during hyperoxic spontaneous obstructive apneas in which oxygen saturation did not decrease significantly. Sympathetic neural responses to induced hypoxemia in control subjects (17 +/- 7%) were significantly less than that of the sleep apnea patients. We conclude that hypoxemia contributes importantly, but is not the sole determinant of the sympathoexcitation provoked during episodes of obstructive sleep apnea.

Adult↗

PubMed2004

Postoperative hypoxemia exacerbates potential brain injury after deep hypothermic circulatory arrest.

BACKGROUND: Deep hypothermic circulatory arrest (DHCA) is often used in infants undergoing the Norwood procedure. These infants are hypoxic after surgery. Previous investigations into the cerebral metabolic response and oxygen utilization after DHCA examined animals with normal arterial oxygenation. This study reports the cerebral metabolic consequences if hypoxemic conditions are present after DHCA. METHODS: Eighteen neonatal piglets were randomly assigned to three groups. The control group was ventilated; the cardiopulmonary bypass group underwent 60 minutes of normothermic cardiopulmonary bypass, and the DHCA group underwent cardiopulmonary bypass and 60 minutes of DHCA (16 degrees to 18 degrees C) followed by rewarming. Hemodynamic and cerebral perfusion data were measured at an arterial partial pressure of oxygen (PaO2) of 150 to 250 mm Hg, and then at moderate hypoxemia (PaO2, 50 to 60 mm Hg) and severe hypoxemia (PaO2, 25 to 35 mm Hg). RESULTS: Cerebral oxygen delivery decreased by 44% from PaO2 150 to 250 mm Hg to severe hypoxemia (p < 0.001). Cerebral oxygen extraction increased from moderate hypoxemia to severe hypoxemia in the control (57.9% +/- 3.7% to 71.8% +/- 3.8%; p = 0.002) and cardiopulmonary bypass groups (61.2% +/- 2.6% to 70.6% +/- 1.2%; p = 0.035); however, the cerebral oxygen extraction of the DHCA group did not increase under these conditions (82.8% +/- 1.8% to 77.9% +/- 4.3%; p = 0.32). The cerebral metabolic rate of oxygen consumption of the DHCA group decreased from PaO2 150 to 250 mm Hg to severe hypoxemia (1.86 +/- 0.20 to 0.99 +/- 0.24 mL O2 x 100 g(-1) x min(-1); p = 0.02), whereas the cerebral metabolic rate of oxygen consumption did not change under these conditions in the control and cardiopulmonary bypass groups. CONCLUSIONS: Under hypoxemic conditions cerebral metabolic rate of oxygen consumption deteriorates after DHCA. Infants exposed to DHCA may be at greater risk of brain injury when postoperative hypoxemia is present. Because maximal cerebral oxygen extraction after DHCA occurs at moderate hypoxemia, techniques that increase cerebral oxygen delivery may reduce the risk of hypoxic brain injury.

Animals↗

PubMed1999

Alteration of fetal oxygenation and responses to acute hypoxemia by increased myometrial contracture frequency produced by pulse administration of oxytocin to the pregnant ewe from 96 to 131 days' gestation.

OBJECTIVES: This study examined the effects of increased myometrial contracture frequency from 96 to 131 days' gestation on ovine fetal oxygen transport and physiologic response to acute hypoxemia. STUDY DESIGN: Ten pregnant ewes received either saline solution (control, n = 5) or long-term administration of oxytocin (600 microU. kg-1. min-1) in 5-minute pulses every 20 minutes to the maternal jugular vein beginning at 96 days' gestation (n = 5). Maternal tracheal tubes, fetal carotid artery and jugular vein catheters, and electrocorticographic and electromyographic electrodes were placed with the animals under halothane general anesthesia at 122 days' gestation. At 131 days' gestation fetal hypoxemia was induced for 1 hour. Maternal and fetal arterial blood gas samples were obtained at 60, 15, and 5 minutes before the start of hypoxemia and at 5, 10, 20, 30, 40, 60, and 120 minutes after the start of hypoxemia. RESULTS: Baseline PO2 before hypoxemia was significantly lower and oxygen content was significantly higher in fetuses in the long-term oxytocin group than in control fetuses. At the end of hypoxemia the fetal pH, oxygen saturation, and oxygen content were significantly higher in the long-term oxytocin group than in the control group, although PO2 did not differ between groups. The fetal blood oxygen dissociation curve was shifted to the left in the long-term oxytocin group. During hypoxemia the absolute fetal blood pH was higher and the blood pH variation was lower in long-term oxytocin group than in the control group. Lower baseline and hypoxia-induced fetal plasma cortisol concentrations were observed in fetuses in the long-term oxytocin group than in fetuses of control ewes. CONCLUSION: Increased contracture frequency during a period of 35 days shifts the fetal oxygen dissociation curve toward the left and alters fetal response to acute hypoxemia.

Adrenocorticotropic Hormone↗

PubMed2002

Cardiovascular response to acute hypoxemia in adult rats hypoxemic neonatally.

OBJECTIVE: To determine the effects of chronic hypoxemia neonatally on the cardiovascular response to acute hypoxemia in adulthood. METHODS: Experiments were conducted on adult rats (82+/-2 days) which had been made chronically hypoxemic (hypobaric hypoxia equivalent to FiO(2)=0.14) during the first ten days of life but raised in room air (Neonatally Hypoxemia) as well as on adult rats never previously hypoxemic (Control). The animals were instrumented with catheters in the right common carotid artery and superior vena cava for measurements of mean systemic arterial pressure (MAP), central venous pressure, heart rate (HR), arterial blood gases, and arterial as well as mixed venous O(2) saturation. Oxygen consumption (VO(2)) was measured allowing calculation of cardiac index (CI), stroke volume index (SVI) and systemic vascular resistance index (SVRI). The rats were made acutely hypoxemic by exposure to FiO(2)=0.10 for 20 min. RESULTS: HR increased and MAP decreased to similar extents in both groups during acute hypoxemia. However, SVI and CI increased significantly (P<0.05) during acute hypoxemia in the Neonatally Hypoxemic group (24+/-6%, 41+/-8%) but respectively decreased and did not change in the Control animals (-13+/-6%, 2+/-6%). SVRI fell significantly more during hypoxemia in the Neonatally Hypoxemic animals than in the Control group (36+/-4% vs. 14+/-5%). CONCLUSIONS: Hypoxemia experienced in early life has long-term effects on the cardiovascular response to acute hypoxemia at maturity. This may have important implications for individuals hypoxemic in early life due to congenital cyanotic heart defects or pulmonary disease secondary to prematurity.

Animals↗

PubMed1991

Prevalence and prediction of hypoxemia in children with respiratory infections in the Peruvian Andes.

To determine the effect of respiratory infections on oxyhemoglobin saturation in a high-altitude population, we recorded clinical signs, oxyhemoglobin saturation determined by pulse oximetry, and findings on radiographs of the chest of 423 children with acute respiratory infections; the children were living at an altitude of 3750 m in the Peruvian Andes. We defined hypoxemia as an oxyhemoglobin saturation value greater than 2 SD below the mean value for 153 well children in this population. Eighty-three percent of children with clinical bronchopneumonia, but only 10% of children with upper respiratory tract infection, had hypoxemia (p less than 0.001). Compared with previous studies of children living at lower altitudes, the presence of tachypnea was relatively nonspecific as a predictor of radiographically determined pneumonia or of hypoxemia, especially in infants. A history of rapid breathing was 74% sensitive and 64% specific in the prediction of hypoxemia, and performed as well as a standard World Health Organization case management algorithm in the prediction of radiographic pneumonia or hypoxemia. Radiographic pneumonia was not a sensitive predictor of hypoxemia or clinically severe illness. In contrast, the presence of hypoxemia was a useful predictor of radiographic pneumonia, with both sensitivity and specificity of 75% in infants. We conclude that acute lower respiratory tract infection in children living at high altitude is frequently associated with hypoxemia, and that oxygen should be administered to children with a diagnosis of pneumonia in these regions. Case management algorithms developed in low-altitude regions may have to be modified for high-altitude settings. In this setting, pulse oximetry is a good predictor of pneumonia. Because pulse oximetry is more objective and cheaper than radiography, its role as a clinical and investigative tool merits further exploration.

Acute Disease↗

PubMedDate not supplied

Periodic fetal heart rate decelerations during 6 hours' hypoxemia induced in goats.

OBJECTIVE: To determine if fetal heart rate (FHR) decelerations periodically occur with uterine contractures during 6 hours' induced hypoxemia in goats. METHODS: In five chronically catheterized goat fetuses at 125-130 days' gestation, incidence of FHR decelerations was compared between 6 hours' control time and 6 hours' induced hypoxemia with two-way ANOVA and Duncan's multiple range test. Three other fetuses were used as controls for circadian rhythm. RESULTS: Fetal PaO2 was significantly decreased from 26.1 to 16.3 mmHg without acidemia. During hypoxemia, 42 decelerations were induced along with 5 initial decelerations during the acute phase hypoxemia. Incidence of decelerations increased significantly from 0.07 +/- 0.15 per hour in 6-hour controls to 1.40 +/- 0.28 per hour during 6 hours' induced hypoxemia. Short-term variability and long-term variability of the 42 decelerations were significantly increased. These variabilities were also increased during the 5 initial decelerations. Frequency of uterine contractures did not change during hypoxemia. There was an observable association of FHR decelerations with uterine contractures during hypoxemia. CONCLUSION: Fetal heart rate decelerations occurred periodically in association with uterine contractures during induced 6 hours' hypoxemia, which were characterized by slow onset and recovery with increases in variability.

Animals↗

PubMed1996

The influence of acute hypoxemia and hypovolemic hypotension of neuronal brain activity measured by the cerebral function monitor in newborn piglets.

Little is known about the cerebral electrical response to short periods of hypoxemia, hypotension and their combination. These conditions occur frequently in critically ill newborn infants; their cerebral electrical activity can be registrated easily with the Cerebral Function Monitor (CFM). Therefore we recorded on-line cortical electrical activity during hypoxemia and hypotension in 11 newborn piglets aged 13-18 days. Hypoxemia was induced by reducing inspired oxygen fraction. Hypotension was induced by withdrawal of blood. The experimental groups were: Group I: arterial oxygen saturation (SaO2) 45-85%, group II: SaO2 < 45%, group III: mean arterial pressure (MAP) 50-75 mmHg, group IV: MAP < 50 mmHG, group V: SAO2 < 85% and MAP 50-75 mmHg and group VI: SaO2 < 85% and MAP < 50 mmHg. CFM registrated normal cortical electrical activity during periods of moderate or severe hypoxemia (group I and II) and during isolated moderate hypotension (group III). The cortical activity decreased significantly due to severe hypotension alone (group IV) and combined hypotension and hypoxemia (group V and VI). Hypotension has a more potent effect on cortical electrical activity than hypoxemia in the newborn piglet. Cerebral electrical activity does not change during severe hypoxemia and moderate hypotension possibly due to cerebral flow regulation. CFM recorded decreased cerebral electrical activity during severe hypotension and hypotension with hypoxemia. CFM could provide invaluable data in severely ill newborns.

Animals↗

PubMed1990

Sympathetic blockade by epidural anesthesia attenuates the cardiovascular response to severe hypoxemia.

Blood pressure is usually well maintained during epidural or spinal anesthesia even in the presence of extensive sympathetic blockade. The authors investigated whether hormonal systems support arterial pressure and how the circulation copes with a hypoxic challenge when activation of the sympathetic nervous system is selectively impaired by neural blockade. Accordingly, the effects of high epidural anesthesia alone and combined with hypoxia were evaluated in seven awake trained dogs. On different days, either bupivacaine 0.5% (8-12 ml) or saline (placebo) were randomly injected epidurally and the effects evaluated on cardiovascular (arterial pressure, heart rate) and respiratory (blood gases, oxygen consumption) variables, as well as on hormone plasma concentrations (vasopressin, norepinephrine, epinephrine, renin) during both normoxia and hypoxia. During epidural anesthesia alone, vasopressin increased tenfold (1.7 pg/ml +/- 1.0 SD to 16.8 +/- 13.8, P less than 0.05), norepinephrine decreased (90 pg/ml +/- 31 to 61 +/- 28, P less than 0.05) while epinephrine and renin concentrations remained unchanged. Mean arterial and pulse pressure decreased by 13 mmHg and 23 mmHg (P less than 0.05), respectively. In dogs without sympathetic blockade (saline group), hypoxemia (PaO2: 31 +/- 4 mmHg) evoked an increase in mean blood pressure by 37 mmHg +/- 8 and heart rate by 50 beats per min +/- 17. In contrast, in the presence of sympathetic blockade but with a similar degree of hypoxemia, blood pressure failed to increase (+ 1 mmHg +/- 14) and heart rate rose by only 15 beats per min +/- 11. These differences between groups were statistically significant (P less than 0.001). Hypoxemia induced a similar hypocarbia (PaCO2:25 mmHg) in both groups, indicating that the ventilatory response to hypoxemia was preserved after epidural blockade. During hypoxemia vasopressin concentrations increased 35-fold to 64 pg/ml +/- 38 (P less than 0.0001) compared to base line only during epidural anesthesia, but not after epidural saline (2 pg/ml +/- 2), while other hormones showed no significant differences. The authors conclude that high epidural anesthesia in awake unsedated dogs: 1) almost completely abolishes the normal cardiovascular response to hypoxemia while promoting vasopressin secretion; 2) preserves the ventilatory response to hypoxemia; and 3) is associated with increased vasopressin concentrations, most likely to compensate for decreased cardiac filling and/or arterial blood pressure when sympathoadrenal responses are impaired. Thus, the changes in cardiovascular vital signs in response to severe hypoxemia are markedly blunted when spinal sympathetic outflow is selectively eliminated by epidural anesthesia.

Anesthesia, Epidural↗

PubMed1992

Effects of hypoxemia on regional blood flows during anesthesia with halothane, enflurane, or isoflurane.

Hypoxemia during anesthesia can cause severe morbidity and mortality. To determine how the volatile anesthetics alter the normal hemodynamic compensation for hypoxemia, we investigated the effects of various anesthetics on regional blood flows during normoxemia and during normocapnic hypoxemia (FIO2 0.12 for 20 min) in rats. Using the radioactive microsphere method, organ blood flows were determined in animals anesthetized with 1 MAC of halothane, enflurane, or isoflurane and in awake animals. Brain blood flow increased significantly with hypoxemia in awake animals. However, brain blood flow decreased in all anesthetized animals that were hypoxemic. Coronary blood flow also increased significantly with hypoxemia in awake animals. In the presence of volatile anesthetics, coronary blood flow decreased, a decrease that was unchanged with hypoxemia. Thus, there was a large difference in brain and coronary blood flows between awake hypoxemic and anesthetized hypoxemic animals. Hypoxemia did not alter the magnitude of renal, gastrointestinal tract, or total hepatic blood flows in awake animals. However, all three blood flows decreased significantly in anesthetized hypoxemic animals. We conclude that volatile anesthetics modify the compensatory responses to hypoxemia that occur in awake animals, resulting in decreased blood flow to vital organs.

Anesthesia, Inhalation↗