Consultation with the Specialist

1992 ◽  
Vol 13 (10) ◽  
pp. 379-380
Author(s):  
William B. Strong
Keyword(s):  
Cardiac Output ◽  
Oxygen Saturation ◽  
Carrying Capacity ◽  
Hemoglobin Concentration ◽  
Cyanotic Congenital Heart Disease ◽  
Compensatory Mechanism ◽  
Peripheral Tissues ◽  
Arterial Blood ◽  
Infant And Young Child ◽  
Oxygen Carrying Capacity

What is the likely pathophysiology of this event? What are the more common complications of hypoxemia in the older infant and young child? This clinical scenario is uncommon, but it represents one of the two feared central nervous system complications of cyanotic congenital heart disease, (ie, cerebrovascular accident and brain abscess). A uniform response to hypoxemia of cardiac etiology is the production of erythropoietin to produce more red blood cells. This is a compensatory mechanism to maintain oxygen delivery to the peripheral tissues. Normally, hemoglobin is about 96% saturated with oxygen. Therefore, the oxygen-carrying capacity of blood with a normal hemoglobin concentration of 15 g/dL is approximately 20.3 mL of oxygen per 100 mL of blood (ie, 15 g of hemoglobin x 1.35 mL of O2 per g of hemoglobin = 20.3). The oxygen content of blood equals the oxygen-carrying capacity multiplied by the oxygen saturation. At a normal oxygen saturation of 96%, the O2 content of arterial blood (Hgb 15 g/dL) equals 19.5 mL/dL (96% x 20.3 mm3/dL) or 195 mL per liter of cardiac output. The arterial O2 content of this child, assuming an average arterial saturation of 85%, will be 11.1 mL/dL. Therefore, every liter (10 dL) of cardiac output will carry 111 mL of O2 or 84 mL of O2 less than the child with a 15 g/dL hemoglobin level.

Effects of acute prolonged hypoxia on cardiovascular dynamics in dogs

1977 ◽  
Vol 43 (5) ◽  
pp. 784-789 ◽  
Author(s):  
J. F. Borgia ◽  
S. M. Horvath
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cardiac Index ◽  
Carrying Capacity ◽  
Hemoglobin Concentration ◽  
Severe Hypoxia ◽  
Systemic Hypertension ◽  
Anesthetized Dogs ◽  
Oxygen Tensions ◽  
Oxygen Carrying Capacity

Intact anesthetized dogs were exposed for 75 min to either 5.75, 9.0, or 12.0% oxygen in nitrogen. Although pulmonary artery pressures were significantly elevated in all hypoxic exposures, systemic hypertension occurred only at the onset of severe hypoxia(5.75% O2). Coronary blood flow increased from an average of 130 during normoxia to a peak of 400 ml/100 g per min during inhalation of 5.75% O2, and coronary sinus oxygen tensions of 8 Torr and oxygen contents of 1.1 ml/100 ml were sustained for 75 min without biochemical, functional, or electrophysiological evidence of myocardial ischemia. Cardiac index (CI) increased significantly only during severe hypoxia (5.75% O2) with the greatest elevation after 30 min. Subsequently, CI decreased concomitantly with a 27% elevation in arterial hemoglobin concentration and oxygen-carrying capacity. It is concluded that the hypoxic threshold for significant elevations of cardiac output is between 6.0 and 9.0% O2.

scholarly journals BIOCHEMICAL STUDIES ON SHOCK

1944 ◽  
Vol 79 (1) ◽  
pp. 9-22 ◽  
Author(s):  
Frank L. Engel ◽  
Helen C. Harrison ◽  
C. N. H. Long
Keyword(s):  
Blood Pressure ◽  
Amino Acids ◽  
Oxygen Saturation ◽  
Hepatic Artery ◽  
Arterial Oxygen Saturation ◽  
Amino Nitrogen ◽  
Arterial Oxygen ◽  
High Positive Correlation ◽  
Peripheral Tissues ◽  
Arterial Blood

1. In a series of rats subjected to hemorrhage and shock a high negative correlation was found between the portal and peripheral venous oxygen saturations and the arterial blood pressure on the one hand, and the blood amino nitrogen levels on the other, and a high positive correlation between the portal and the peripheral oxygen saturations and between each of these and the blood pressure. 2. In five cats subjected to hemorrhage and shock the rise in plasma amino nitrogen and the fall in peripheral and portal venous oxygen saturations were confirmed. Further it was shown that the hepatic vein oxygen saturation falls early in shock while the arterial oxygen saturation showed no alteration except terminally, when it may fall also. 3. Ligation of the hepatic artery in rats did not affect the liver's ability to deaminate amino acids. Hemorrhage in a series of hepatic artery ligated rats did not produce any greater rise in the blood amino nitrogen than a similar hemorrhage in normal rats. The hepatic artery probably cannot compensate to any degree for the decrease in portal blood flow in shock. 4. An operation was devised whereby the viscera and portal circulation of the rat were eliminated and the liver maintained only on its arterial circulation. The ability of such a liver to metabolize amino acids was found to be less than either the normal or the hepatic artery ligated liver and to have very little reserve. 5. On complete occlusion of the circulation to the rat liver this organ was found to resist anoxia up to 45 minutes. With further anoxia irreversible damage to this organ's ability to handle amino acids occurred. 6. It is concluded that the blood amino nitrogen rise during shock results from an increased breakdown of protein in the peripheral tissues, the products of which accumulate either because they do not circulate through the liver at a sufficiently rapid rate or because with continued anoxia intrinsic damage may occur to the hepatic parenchyma so that it cannot dispose of amino acids.

The Influence of Nutritional State on the Circulatory and Respiratory Physiology of the Shore Crab, Carcinus Maenas

1985 ◽  
Vol 65 (1) ◽  
pp. 69-78 ◽  
Author(s):  
M. H. Depledge
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Salinity Stress ◽  
Carrying Capacity ◽  
Carcinus Maenas ◽  
Nutritional State ◽  
Respiratory Physiology ◽  
Shore Crab ◽  
Decapod Crustaceans ◽  
Oxygen Carrying Capacity

The oxygen-carrying capacity of the blood of decapod crustaceans fluctuates widely. Salinity stress results in doubling of haemocyanin concentration within 24–48 h in Carcinus maenas (Boone & Schoeffeniels, 1979) while in the lobster, Homarus gammarus respiratory pigment levels are very low prior to and following moulting (Spoek, 1974). In general, however, the most important factor regulating haemocyanin concentration is nutritional state. Following starvation low values are recorded (Wieser, 1965; Uglow, 1969; Djangmah, 1970) and there are concomitant reductions in ventilation, oxygen consumption and cardiac output (Ansell, 1973; Marsden, Newell & Ahsanullah, 1973; Wallace, 1973). The interrelationships between these events are poorly understood.

Chronic hypoxia and the cerebral circulation

2006 ◽  
Vol 100 (2) ◽  
pp. 725-730 ◽  
Author(s):  
Kui Xu ◽  
Joseph C. LaManna
Keyword(s):  
Blood Flow ◽  
Carrying Capacity ◽  
Hemoglobin Concentration ◽  
Capillary Density ◽  
Hypoxic Exposure ◽  
Blood Oxygen ◽  
Brain Capillary ◽  
Blood Flow Increase ◽  
Time Courses ◽  
Oxygen Carrying Capacity

Exposure to mild hypoxia elicits a characteristic cerebrovascular response in mammals, including humans. Initially, cerebral blood flow (CBF) increases as much as twofold. The blood flow increase is blunted somewhat by a decreasing arterial Pco2 as a result of the hypoxia-induced hyperventilatory response. After a few days, CBF begins to fall back toward baseline levels as the blood oxygen-carrying capacity is increasing due to increasing hemoglobin concentration and packed red cell volume as a result of erythropoietin upregulation. By the end of 2 wk of hypoxic exposure, brain capillary density has increased with resultant decreased intercapillary distances. The relative time courses of these changes suggest that they are adjusted by different control signals and mechanisms. The CBF response appears linked to the blood oxygen-carrying capacity, whereas the hypoxia-induced brain angiogenesis appears to be in response to tissue hypoxia.

scholarly journals Reduction of Oxygen-Carrying Capacity Weakens the Effects of Increased Plasma Viscosity on Cardiac Performance in Anesthetized Hemodilution Model

2012 ◽  
Vol 2012 ◽  
pp. 1-9
Author(s):  
Surapong Chatpun ◽  
Pedro Cabrales
Keyword(s):  
Cardiac Output ◽  
Carrying Capacity ◽  
Oxygen Delivery ◽  
Maximum Rate ◽  
Systolic Pressure ◽  
Pressure Change ◽  
Plasma Viscosity ◽  
Cardiac Performance ◽  
Dextran 70 ◽  
Oxygen Carrying Capacity

We investigated the effects of reduced oxygen-carrying capacity on cardiac function during acute hemodilution, while the plasma viscosity was increased in anesthetized animals. Two levels of oxygen-carrying capacity were created by 1-step and 2-step hemodilution in male golden Syrian hamsters. In the 1-step hemodilution (1-HD), 40% of the animals' blood volume (BV) was exchanged with 6% dextran 70 kDa (Dx70) or dextran 2000 kDa (Dx2M). In the 2-step hemodilution (2-HD), 25% of the animals' BV was exchanged with Dx70 followed by 40% BV exchanged with Dx70 or Dx2M after 30 minutes of first hemodilution. Oxygen delivery in the 2-HD group consequently decreased by 17% and 38% compared to that in the 1-HD group hemodiluted with Dx70 and Dx2M, respectively. End-systolic pressure and maximum rate of pressure change in the 2-HD group significantly lowered compared with that in the 1-HD group for both Dx70 and Dx2M. Cardiac output in the 2-HD group hemodiluted with Dx2M was significantly higher compared with that hemodiluted with Dx70. In conclusion, increasing plasma viscosity associated with lowering oxygen-carrying capacity should be considerably balanced to maintain the cardiac performance, especially in the state of anesthesia.

Integrated Evaluation of Neonatal Hemodynamics, Part 2: Systematic Bedside Assessment

2016 ◽  
Vol 35 (4) ◽  
pp. 192-203 ◽  
Author(s):  
Yasser N. Elsayed ◽  
Debbie Fraser
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Oxygen Uptake ◽  
Carrying Capacity ◽  
Clinical Markers ◽  
Organ Function ◽  
Term Infants ◽  
Routine Monitoring ◽  
Oxygen Carrying Capacity ◽  
Sufficient Oxygen

AbstractIntact hemodynamics results when there is adequate oxygen uptake by the respiratory system, normal cardiac output, sufficient oxygen-carrying capacity of blood, and intact autoregulatory mechanisms to maintain enough oxygenation for normal end-organ function. The current routine monitoring of cardiovascular dynamics in sick preterm and term infants has been based on incomplete evaluation and relies on nonspecific and sometimes misleading clinical markers such as blood pressure. A thorough understanding of perinatal and neonatal cardiovascular, respiratory, oxygen, and other specific end-organ physiology is also mandatory for proper targeted interpretation.

scholarly journals Hydrogen Sulfide Is a Regulator of Hemoglobin Oxygen-Carrying Capacity via Controlling 2,3-BPG Production in Erythrocytes

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Gang Wang ◽  
Yan Huang ◽  
Ningning Zhang ◽  
Wenhu Liu ◽  
Changnan Wang ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Binding Affinity ◽  
Carrying Capacity ◽  
Inhibitory Effect ◽  
Peripheral Tissues ◽  
Metabolomic Profiling ◽  
Wide Range ◽  
Mammalian Tissues ◽  
Oxygen Carrying Capacity ◽  
O2 Binding

Hydrogen sulfide (H2S) is naturally synthesized in a wide range of mammalian tissues. Whether H2S is involved in the regulation of erythrocyte functions remains unknown. Using mice with a genetic deficiency in a H2S natural synthesis enzyme cystathionine-γ-lyase (CSE) and high-throughput metabolomic profiling, we found that levels of erythrocyte 2,3-bisphosphoglycerate (2,3-BPG), an erythroid-specific metabolite negatively regulating hemoglobin- (Hb-) oxygen (O2) binding affinity, were increased in CSE knockout (Cse-/-) mice under normoxia. Consistently, the 50% oxygen saturation (P50) value was increased in erythrocytes of Cse-/- mice. These effects were reversed by treatment with H2S donor GYY4137. In the models of cultured mouse and human erythrocytes, we found that H2S directly acts on erythrocytes to decrease 2,3-BPG production, thereby enhancing Hb-O2 binding affinity. Mouse genetic studies showed that H2S produced by peripheral tissues has a tonic inhibitory effect on 2,3-BPG production and consequently maintains Hb-O2 binding affinity in erythrocytes. We further revealed that H2S promotes Hb release from the membrane to the cytosol and consequently enhances bisphosphoglycerate mutase (BPGM) anchoring to the membrane. These processes might be associated with S-sulfhydration of Hb. Moreover, hypoxia decreased the circulatory H2S level and increased the erythrocyte 2,3-BPG content in mice, which could be reversed by GYY4137 treatment. Altogether, our study revealed a novel signaling pathway that regulates oxygen-carrying capacity in erythrocytes and highlights a previously unrecognized role of H2S in erythrocyte 2,3-BPG production.

Effects of protoveratrine on coronary blood flow of the renal hypertensive dog

1963 ◽  
Vol 204 (5) ◽  
pp. 895-898 ◽  
Author(s):  
James W. West ◽  
Elwood L. Foltz
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Saturation ◽  
Coronary Blood Flow ◽  
Arterial Oxygen Saturation ◽  
Renal Hypertension ◽  
Peripheral Resistance ◽  
Arterial Oxygen ◽  
Arterial Blood ◽  
Venous Oxygen Saturation

In renal hypertension, protoveratrine decreased coronary blood flow, cardiac oxygen consumption, arterial and venous oxygen saturation, coronary arteriovenous oxygen difference, mean arterial blood pressure, cardiac output, cardiac work, cardiac efficiency, cardiac rate, total peripheral resistance, coronary resistance, respiratory rate, and minute volume. The decrease was significant in all functions except coronary blood flow, coronary venous oxygen saturation, and cardiac output. The results of these experiments indicate that in the renal hypertensive animal, a therapeutically beneficial effect was derived from protoveratrine on the circulation by its ability to decrease the work of the heart (lowering the elevated mean arterial pressure) and the coronary vascular resistance while maintaining coronary blood flow and cardiac output within normal levels. The less advantageous effect of protoveratrine on circulation resulted from its respiratory inhibiting effect which reduced the arterial blood oxygen saturation. Although a small decline in coronary venous oxygen saturation was noted, the coronary flow and oxygen delivery in face of the reduced arterial oxygen saturation was apparently adequate to maintain a normal cardiac activity.

scholarly journals Relationship Between Arterial Oxygen Saturation and Hematocrit, and Effect of Slow Deep Breathing on Oxygen Saturation in Himalayan High Altitude Populations

2013 ◽  
Vol 10 (3) ◽  
pp. 30-34 ◽  
Author(s):  
Ojashwi Nepal ◽  
BR Pokharel ◽  
K Khanal ◽  
SL Mallik ◽  
BK Kapoor ◽  
...  
Keyword(s):  
Oxygen Saturation ◽  
High Altitude ◽  
Carrying Capacity ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
P Value ◽  
Deep Breathing ◽  
Cross Sectional ◽  
Lower Altitude ◽  
Oxygen Carrying Capacity

Background The oxygen saturation of haemoglobin is reduced in high altitude-living organisms. Increase in the hematocrit is responsible for rise in the hemoglobin concentration so that the oxygen carrying capacity in the hypobaric hypoxic subject is elevated. Objectives To compare two different high altitude populations, in order to study the relationship between arterial oxygen saturation and hematocrit. Methods lIn the cross-sectional study of two populations residing at altitude of 2800 m and 3760 m are compared for the difference in hematocrit. The oxygen carrying capacity of arterial haemoglobin (SaO2) is determined by pulse oximetry. The sample is drawn from the natives of two small villages, Thini at Jomsom (2800 m) and Jharkot (3760 m) in Mustang district of Nepal. The natives at 2800 m are termed as lower high altitude population and local residents at 3760 m are said to be higher altitude population in this study. The sample blood was drawn by venipuncture and packed cell volume was determined by Wintrobe’s method. Results The hematocrit obtained from 3760 m altitude population and the lower high altitude population at altitude of 2800 m differ significantly with the p value < 0.0001and the SaO2 in both the population fails to show any difference with p value > 0.05. Deep breathing exercise in these populations however increased SaO2 significantly. Conclusion The higher altitude natives have greater arterial oxygen saturation than lower altitude population which is due to rise in red cell concentration. The slow deep breathing raises oxygen saturation irrespective of altitude. Kathmandu University Medical Journal | VOL.10 | NO. 3 | ISSUE 39 | JUL- SEP 2012 | Page 30-34 DOI: http://dx.doi.org/10.3126/kumj.v10i3.8014

Sign in / Sign up

Export Citation Format

Share Document