Umbilical cord occlusion stimulates breathing independent of blood gases and pH

1991 ◽  
Vol 70 (4) ◽  
pp. 1796-1809 ◽  
Author(s):  
S. L. Adamson ◽  
I. M. Kuipers ◽  
D. M. Olson
Keyword(s):  
Prostaglandin E2 ◽  
Umbilical Cord ◽  
Blood Gases ◽  
High Frequency Oscillation ◽  
Breathing Rate ◽  
Fetal Sheep ◽  
Arterial Pco2 ◽  
Arterial Blood Gas ◽  
Arterial Blood

The role of umbilical cord occlusion in the initiation of breathing at birth was investigated by use of 16 unanesthetized fetal sheep near full term. Artificial ventilation with high-frequency oscillation was used to control fetal arterial blood gas tensions. At baseline, PCO2 was maintained at control fetal values and PO2 was elevated to between 25 and 50 Torr. In the first study on six intact and four vagotomized fetuses, arterial PCO2 and PO2 were maintained constant during two 30-min periods of umbilical cord occlusion. Nevertheless, the mean fetal breathing rate increased significantly when the umbilical cord was occluded. In the second study on six intact fetuses, hypercapnia (68 Torr) was imposed by adding CO2 to the ventilation gas. When the umbilical cord was occluded, there was a significantly greater stimulation of breathing (rate, incidence, and amplitude) in response to hypercapnia than in response to hypercapnia alone. During cord occlusion, plasma prostaglandin E2 concentration decreased significantly. Results indicate that cord occlusion stimulates breathing possibly by causing the removal of a placentally produced respiratory inhibitor such as prostaglandin E2 from the circulation.

The adrenocorticotropic hormone and arginine vasopressin responses to hypercapnia in fetal and maternal sheep

1993 ◽  
Vol 264 (2) ◽  
pp. R324-R330 ◽  
Author(s):  
H. G. Chen ◽  
C. E. Wood
Keyword(s):  
Arginine Vasopressin ◽  
Adrenocorticotropic Hormone ◽  
Fetal Sheep ◽  
Arterial Pco2 ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Bilateral Vagotomy ◽  
Pregnant Ewe

Previous studies have demonstrated that fetal adrenocorticotropic hormone (ACTH) and arginine vasopressin (AVP) are increased during periods of acidemia produced by infusion of acid intravenously or by acidemia secondary to hypovolemia. The purpose of this study was to quantify ACTH and AVP responses to hypercapnic acidemia and to test the role of the peripheral chemoreceptors in the control of these responses. Chronically catheterized fetal sheep were subjected to carotid sinus denervation and bilateral vagotomy or were studied intact. At least 5 days after surgery, fetuses were exposed to a 60-min period of normocapnia or hypercapnia, delivered via a polyethylene bag containing 5-8% CO2 in 21% O2 fitted over the head of the pregnant ewe. Hypercapnia significantly increased fetal arterial PCO2 to 55.2 +/- 1.8 and 55.9 +/- 2.2 mmHg and decreased arterial pH to 7.257 +/- 0.011 and 7.281 +/- 0.010 in intact and denervated fetuses, respectively. Fetal mean arterial blood pressure was decreased slightly in the denervated fetuses during hypercapnia. Fetal plasma AVP was increased in both groups equally, and plasma ACTH and cortisol were increased in the denervated fetuses only. Fetal heart rate was increased significantly in intact but not denervated fetuses. We conclude that respiratory acidemia is a mild stimulus to AVP secretion and that this response is not attenuated by peripheral chemodenervation.

scholarly journals Roles of parasympathetic outflow and sympathetic outflow in the cardiovascular response to brief umbilical cord occlusion in fetal sheep

PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0254155
Author(s):  
Morgan Recher ◽  
Arthur Lauriot Dit Prevost ◽  
Dyuti Sharma ◽  
Julien De Jonckheere ◽  
Charles Garabedian ◽  
...  
Keyword(s):  
Umbilical Cord ◽  
Early Stage ◽  
Cardiovascular Response ◽  
Blood Gases ◽  
Cord Compression ◽  
Fetal Sheep ◽  
Uterine Contractions ◽  
Baseline Values ◽  
To Receive

Fetal heart rate (FHR) deceleration is the most common change seen during labor. The role of the autonomic nervous system in regulating the fetal cardiovascular response during multiple uterine contractions has been well-established. However, the mechanism underlying the hemodynamic response remains unclear and the specific reflex that mediates the cardiovascular modifications is still controversial. This study aimed to determine the role of the sympathetic and parasympathetic systems on fetal hemodynamics in complete cord occlusion. Chronically instrumented fetal sheep were randomized to receive an intravenous injection of atropine 2.5 mg (n = 8), propranolol 5 mg (n = 7), atropine and propranolol (n = 7), or a control protocol (n = 9), followed by three episodes of 1-minute umbilical cord occlusion repeated every 5 minutes. Cord compression induces a rapid decrease in the FHR and a rapid increase in MAP. The decrease in FHR is caused by an increase in parasympathetic activity, (atropine and atropine-propranolol abolish the FHR response to the occlusion). The change in FHR during occlusion was not modified by propranolol injection, showing no effect of sympathetic tone. The increase in MAP during occlusion was similar in the four protocols. After releasing occlusion, the FHR was still lower than that at baseline due to a sustained parasympathetic tone. Suppression of the parasympathetic output to the cardiovascular system unmasks an increase in the FHR above baseline values. The lower FHR with the propranolol protocol further supports an increase in myocardial β-adrenoceptor stimulation after cord release. The increase in MAP after cord release was similar in the four protocols, except after the early stage of interocclusion period in atropine protocol. Four minutes after cord release, the FHR returned to baseline irrespective of the drugs that were infused, thereby showing recovery of ANS control. Blood gases (pH, PaCO2, PaO2) and plasma lactate concentrations was similar between the four protocols at the end of three applications of UCO. Complete cord compression-induced deceleration is likely due to acute activation of parasympathetic output. β-adrenoceptor activity is involved in the increase in FHR after cord release. Understanding the reflexes involved in FHR deceleration may help us understand the mechanisms underlying fetal autonomic adaptation during cord occlusion.

Inspiratory airway CO2 loading in the pony

1984 ◽  
Vol 57 (4) ◽  
pp. 1097-1103 ◽  
Author(s):  
H. W. Shirer ◽  
J. A. Orr ◽  
J. L. Loker
Keyword(s):  
Tidal Volume ◽  
Dead Space ◽  
Blood Gases ◽  
Minute Volume ◽  
Arterial Pco2 ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Airway Dead Space ◽  
Arterial Po2 ◽  
Stimulation Of

To determine if CO2-sensitive airway receptors are important in the control of breathing, CO2 was preferentially loaded into the respiratory airways in conscious ponies. The technique involved adding small amounts of 100% CO2 to either the latter one-third or latter two-thirds of the inspiratory air in an attempt to raise CO2 concentrations in the airway dead space independent of the arterial blood. Arterial blood gas tensions (PCO2 and PO2) and pH, as well as respiratory output (minute volume, tidal volume, and respiratory rate), were measured in a series of 20 experiments on 5 awake ponies. Elevation of airway CO2 to approximately 12% by addition of CO2 to the latter portion of the inspiratory tidal volume did not alter either ventilation or arterial blood gases. When CO2 was added earlier in the inspiratory phase to fill more of the airway dead space, a small but significant increase in minute volume (2.1 l X min-1 X m-2) and tidal volume (0.1 l X m-2) was accompanied by an increase in arterial PCO2, arterial PO2, and a fall in pH (0.96 Torr, 10.5 Torr, 0.007 units, respectively). A second series of 12 experiments on 6 awake ponies using radiolabeled 14CO2 determined that the increases in breathing were minimal when compared with the large increase that occurred when these animals inhaled 6% 14CO2 (12.7 l X min-1 X m-2). Also, stimulation of systemic arterial or central nervous system chemoreceptors cannot be eliminated from the response since significant amounts of 14CO2 were present in the arterial blood when this marker gas was added to the latter two-thirds of the inspiratory tidal volume. The results, therefore, provide no evidence for CO2-sensitive airway receptors that can increase breathing when stimulated during the latter part of the inspiratory cycle.

Role of hilar nerve afferents in hyperpnea of exercise

1985 ◽  
Vol 59 (3) ◽  
pp. 798-806 ◽  
Author(s):  
C. Flynn ◽  
H. V. Forster ◽  
L. G. Pan ◽  
G. E. Bisgard
Keyword(s):  
Minute Ventilation ◽  
Blood Gases ◽  
Vagal Afferents ◽  
Vagus Nerves ◽  
Inspiratory Time ◽  
Arterial Pco2 ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Cervical Vagotomy

The objective of this study was to determine the role of hilar nerve (lung vagal) afferents in the hyperpnea of exercise. Ten ponies were studied before and 2–4 wk and 3–12 mo after sectioning only the hilar branches of the vagus nerves (HND). After HND, lung volume feedback to the medullary centers was attenuated as indicated in the anesthetized state by 1) attenuation or absence of the Hering-Breuer inflation reflex (P less than 0.01) and 2) attenuation of the lengthened inspiratory time (TI) when the airway was occluded at end expiration (P less than 0.01). Moreover, after HND in the awake state, there was an increase in the ratio of TI to total cycle time (P less than 0.01). These changes verify a compromise in lung innervation comparable to cervical vagotomy. Resting arterial PCO2, PO2, and pH were not altered following HND (P greater than 0.10). Moreover, at three levels of mild and moderate treadmill exercise, no difference in either the temporal pattern or the absolute levels of arterial blood gases and arterial pH was found between pre- and post-HND studies (P greater than 0.10). In addition, minute ventilation (VE) at rest and during exercise was not altered by HND (P greater than 0.10). However, 2–4 wk after HND the increase in breathing frequency (f) during exercise was less, whereas the increase in tidal volume during exercise was greater than pre-HND (P less than 0.05). The reduced f was due to an increase in TI with no change in expiratory time. We conclude that lung afferents via the hilar nerves influence the pattern of breathing at rest and during exercise in ponies.

scholarly journals Prehospital Diagnosis of Shortness of Breath Caused by Profound Metformin-Associated Metabolic Acidosis

Healthcare ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 74
Author(s):  
Pietro Elias Fubini ◽  
Laurent Suppan
Keyword(s):  
Metabolic Acidosis ◽  
Hospital Setting ◽  
Blood Gases ◽  
Shortness Of Breath ◽  
Potential Harm ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Common Causes ◽  
Prehospital Diagnosis ◽  
Gas Measurement

Shortness of breath is a common complaint among patients in emergency medicine. While most common causes are usually promptly identified, less frequent aetiologies might be challenging to diagnose, especially in the pre-hospital setting. We report a case of prehospital dyspnoea initially ascribed to pulmonary oedema which turned out to be the result of profound metformin-associated metabolic acidosis. This diagnosis was already made during the prehospital phase by virtue of arterial blood gas measurement. Pre-hospital measurement of arterial blood gases is therefore feasible and can improve diagnostic accuracy in the field, thus avoiding unnecessary delay and potential harm to the patient before initiating the appropriate therapeutic actions.

Role of tracheal and bronchial circulation in respiratory heat exchange

1985 ◽  
Vol 58 (1) ◽  
pp. 217-222 ◽  
Author(s):  
E. M. Baile ◽  
R. W. Dahlby ◽  
B. R. Wiggs ◽  
P. D. Pare
Keyword(s):  
Blood Flow ◽  
Blood Gases ◽  
Lung Parenchyma ◽  
Arterial Blood ◽  
Respiratory Heat Loss ◽  
Reference Flow ◽  
Pulmonary Arterial ◽  
End Tidal ◽  
Humidified Air

Due to their anatomic configuration, the vessels supplying the central airways may be ideally suited for regulation of respiratory heat loss. We have measured blood flow to the trachea, bronchi, and lung parenchyma in 10 anesthetized supine open-chest dogs. They were hyperventilated (frequency, 40; tidal volume 30–35 ml/kg) for 30 min or 1) warm humidified air, 2) cold (-20 degrees C dry air, and 3) warm humidified air. End-tidal CO2 was kept constant by adding CO2 to the inspired ventilator line. Five minutes before the end of each period of hyperventilation, measurements of vascular pressures (pulmonary arterial, left atrial, and systemic), cardiac output (CO), arterial blood gases, and inspired, expired, and tracheal gas temperatures were made. Then, using a modification of the reference flow technique, 113Sn-, 153Gd-, and 103Ru-labeled microspheres were injected into the left atrium to make separate measurements of airway blood flow at each intervention. After the last measurements had been made, the dogs were killed and the lungs, including the trachea, were excised. Blood flow to the trachea, bronchi, and lung parenchyma was calculated. Results showed that there was no change in parenchymal blood flow, but there was an increase in tracheal and bronchial blood flow in all dogs (P less than 0.01) from 4.48 +/- 0.69 ml/min (0.22 +/- 0.01% CO) during warm air hyperventilation to 7.06 +/- 0.97 ml/min (0.37 +/- 0.05% CO) during cold air hyperventilation.

Arterial blood gases

2007 ◽  
pp. 319-326
Keyword(s):  
Decision Making ◽  
Pulse Oximetry ◽  
Respiratory Rate ◽  
Management Strategy ◽  
Blood Gases ◽  
Capillary Blood ◽  
Blood Gas ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Gas Measurements

Arterial blood gas (ABGs) analysis forms the cornerstone of emergency respiratory investigation. In many situations values obtained dictate management strategy and facilitate decision-making. It is an uncomfortable procedure for the patients and if repeated ABGs are required, consider whether less invasive measures, such as respiratory rate, pulse oximetry or capillary blood gas measurements could be used....

Comparison of SVO2, SpO2, and clinical parameters with arterial blood gases during ventilatory weaning after cardiac surgery

1994 ◽  
Vol 3 (5) ◽  
pp. 353-355 ◽  
Author(s):  
ML Noll ◽  
JF Byers
Keyword(s):  
Oxygen Saturation ◽  
Respiratory Rate ◽  
Artery Bypass ◽  
Arterial Oxygen Saturation ◽  
Bypass Graft ◽  
Blood Gases ◽  
Arterial Oxygen ◽  
Arterial Blood Gases ◽  
Arterial Blood Gas ◽  
Arterial Blood

Correlations of mixed venous and arterial oxygen saturation, heart rate, respiratory rate, and mean arterial pressure with arterial blood gas variables were computed for 57 sets of data obtained from 30 postoperative coronary artery bypass graft patients who were being weaned from mechanical ventilation. Arterial oxygen saturation and respiratory rate correlated significantly, although moderately, with blood gases.

Successful Treatment of Experimental Neonatal Respiratory Failure Using Extracorporeal Membrane Lung Assist

1986 ◽  
Vol 9 (6) ◽  
pp. 427-432 ◽  
Author(s):  
R. Fumagalli ◽  
T. Kolobow ◽  
P. Arosio ◽  
V. Chen ◽  
D.K. Buckhold ◽  
...  
Keyword(s):  
Respiratory Failure ◽  
Pulmonary Ventilation ◽  
Blood Gases ◽  
Blood Gas ◽  
Arterial Blood Gases ◽  
Arterial Blood Gas ◽  
Membrane Lung ◽  
Arterial Blood ◽  
Long Term Survivors

A total of 44 preterm fetal lambs at great risk of developing respiratory failure were delivered by Cesarean section, and were then managed on conventional mechanical pulmonary ventilation. Fifteen animals initially fared well, and 14 of these were long term survivors. Twenty-nine other lambs showed a progressive deterioration in arterial blood gases within 30 minutes of delivery, of which 10 lambs were continued on mechanical pulmonary ventilation (20% survival), while the remaining 19 lambs were placed on an extracorporeal membrane lung respiratory assist (79% survival). Extracorporeal membrane lung bypass rapidly corrected arterial blood gas values, and permitted the use of high levels of CPAP instead of the continuation of mechanical pulmonary ventilation at high peak airway pressures. Improvement in lung function was gradual, and predictable. Early institution of extracorporeal respiratory assist using a membrane artificial lung rapidly corrected arterial blood gas values and significantly improved on neonate survival.

Arterial blood gas tensions during breath-hold diving in the Korean ama

1993 ◽  
Vol 75 (1) ◽  
pp. 285-293 ◽  
Author(s):  
J. Qvist ◽  
W. E. Hurford ◽  
Y. S. Park ◽  
P. Radermacher ◽  
K. J. Falke ◽  
...  
Keyword(s):  
Radial Artery ◽  
Breath Hold ◽  
Blood Gas ◽  
Arterial Pco2 ◽  
Blood Samples ◽  
Arterial Blood Gas ◽  
Time Limits ◽  
Arterial Blood ◽  
Normal Ranges ◽  
Arterial Po2

Korean female unassisted divers (cachido ama) breath-hold dive > 100 times to depths of 3–7 m during a work day. We sought to determine the extent of arterial hypoxemia during normal working dives and reasonable time limits for breath-hold diving by measuring radial artery blood gas tensions and pH in five cachido ama who dove to a fixed depth of 4–5 m and then continued to breath hold for various times after their return to the surface. Eighty-two blood samples were withdrawn from indwelling radial artery catheters during 37 ocean dives. We measured compression hyperoxia [arterial PO2 = 141 +/- 24 (SD) Torr] and hypercapnia (arterial PCO2 = 46.6 +/- 2.4 Torr) at depth. Mean arterial PO2 near the end of breath-hold dives lasting 32–95 s (62 +/- 14 s) was decreased (62.6 +/- 13.5 Torr). Mean arterial PCO2 reached 49.9 +/- 5.4 Torr. Complete return of these values to their baseline did not occur until 15–20 s after breathing was resumed. In dives of usual working duration (< 30 s), blood gas tensions remained within normal ranges. Detailed analysis of hemoglobin components and intrinsic oxygenation properties revealed no evidence for adaptive changes that could increase the tolerance of the ama to hypoxic or hypothermic conditions associated with repetitive diving.

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