scholarly journals Stewart analysis unmasks acidifying and alkalizing effects of ionic shifts during acute severe respiratory alkalosis

2021 ◽  
Vol 66 ◽  
pp. 1-5
Author(s):  
Paul Brussee ◽  
Jelle Zwaag ◽  
Lucas van Eijk ◽  
Johannes G. van der Hoeven ◽  
Miriam A. Moviat ◽  
...  
Author(s):  
C. Meyer ◽  
R. Gerber ◽  
A.J. Guthrie

A 4-year-old Thoroughbred gelding racehorse was referred to the Onderstepoort Veterinary Academic Hospital (OVAH) with a history of post-race distress and collapse. In the absence of any obvious abnormalities in the preceding diagnostic work-up, a standard exercise test was performed to determine an underlying cause for the post-race distress reported. In this particular case oxygen desaturation became evident at speeds as slow as 6 m/s, where PO2 was measured at 82.3 mm Hg. Similarly at a blood pH of 7.28, PCO2 had dropped to 30.0mm Hg indicating a combined metabolic acidosis and respiratory alkalosis. The cause of the distress was attributed to a severe hypoxia, with an associated hypocapnoea, confirmed on blood gas analyses, where PO2 levels obtained were as low as 56.6 mm Hg with a mean PCO2 level of 25.4 mm Hg during strenuous exercise. Arterial oxygenation returned to normal immediately after cessation of exercise to 106.44 mm Hg, while the hypocapnoeic alkalosis, PCO2 25.67 mm Hg, persisted until the animal's breathing normalized. The results obtained were indicative of a dynamic cardiac insufficiency present during exercise. The combination of an aortic stenosis and a mitral valve insufficiency may have resulted in a condition similar to that described as high-altitude pulmonary oedema, with respiratory changes and compensation as for acute altitude disease. The results obtained were indicative of a dynamic cardiac insufficiency present during exercise and substantiate the fact that an extensive diagnostic regime may be required to establish a cause for poor performance and that the standard exercise test remains an integral part of this work-up.


2020 ◽  
Vol 98 (Supplement_3) ◽  
pp. 7-7
Author(s):  
Betty R McConn ◽  
Alan W Duttlinger ◽  
Kouassi R Kpodo ◽  
Jacob M Maskal ◽  
Brianna N Gaskill ◽  
...  

Abstract Pregnant sows, especially during late-gestation, may be susceptible to heat stress due to increased metabolic heat production and body mass. Therefore, the study objective was to determine the thermoregulatory and physiological responses of sows exposed to increasing ambient temperature (TA) at 3 reproductive stages. In 3 repetitions, 27 multiparous sows (parity 3.22±0.89) were individually housed and had jugular catheters placed 5.0±1.0 d prior to the experiment. To differentiate between reproductive stages, sows were categorized as open (not pregnant, n=9), mid-gestation (59.7±9.6 days pregnant, n=9), or late-gestation (99.0±4.8 days pregnant, n=9). During the experiment, sows were exposed to 6 consecutive 1 h periods of increasing TA (period 1, 14.39±2.14°C; period 2, 16.20±1.39°C; period 3, 22.09±1.87°C; period 4, 26.34±1.39°C; period 5, 30.56±0.81°C; period 6, 35.07±0.96°C), with 1 h transition phases in between each period. Respiration rate (RR), heart rate (HR), skin temperature, and vaginal temperature (TV) were measured every 20 min and the mean was calculated for each period. At the end of each period, blood gases, leukocytes, and red blood cell counts were measured. Overall, RR and HR were greater (P≤0.04; 45.6% and 12.9%, respectively) in late-gestation versus mid-gestation sows. Compared to mid-gestation and open sows, TV tended to be greater (P=0.06) during period 4 (0.18°C and 0.29°C, respectively) and period 5 (0.14°C and 0.18°C, respectively) in late-gestation sows. Blood O2 increased (P< 0.01; 18.1%) for all sows with advancing period, regardless of reproductive stage. Late-gestation sows had reduced (P=0.02; 16.1%) blood CO2 compared to mid-gestation sows, regardless of period. In summary, late-gestation sows appear to be more sensitive to increasing TA as indicated by increased RR, HR, TV, and blood O2, and reduced blood CO2 when compared to mid-gestation or open sows. This change in O2 and CO2, due to increasing RR and heat stress sensitivity of late-gestation sows, may suggest an alteration to the acid-base balance, leading to respiratory alkalosis.


1956 ◽  
Vol 9 (3) ◽  
pp. 367-370 ◽  
Author(s):  
Kathleen E. Roberts ◽  
F. Gregg Thompson ◽  
J. William Poppell ◽  
Parker Vanamee

1994 ◽  
Vol 8 (1) ◽  
pp. 110-112
Author(s):  
Arifumi Kohyama ◽  
Masaaki Uno ◽  
Toshihiko Doi ◽  
Takao Saito

1970 ◽  
Vol 33 (5) ◽  
pp. 498-505 ◽  
Author(s):  
R. Zupping

✓ Acid-base and gas parameters of CSF, jugular venous and arterial blood were measured in 45 patients with brain injury in the first 12 days after trauma or operation. CSF metabolic acidosis together with respiratory alkalosis and hypoxemia in the cerebral venous and arterial blood were the most characteristic findings. A close correlation between the severity of brain damage and the intensity of the CSF metabolic acidosis and arterial hypocapnia was revealed. It was concluded that brain hypoxia and acidosis play an important role in the development of cerebral edema and permanent brain damage.


1979 ◽  
Vol 26 (6) ◽  
pp. 687-692 ◽  
Author(s):  
Hassan Rastegar ◽  
Monty Woods ◽  
Alden H. Harken

2017 ◽  
Author(s):  
Horacio J Adrogué ◽  
Nicolaos E Madias

Respiratory acid-base disorders are those disturbances in acid-base equilibrium that are expressed by a primary change in CO2 tension (Pco2) and reflect primary changes in the body’s CO2 stores (i.e., carbonic acid). A primary increase in Pco2 (and a primary increase in the body’s CO2 stores) defines respiratory acidosis or primary hypercapnia and is characterized by acidification of the body fluids. By contrast, a primary decrease in Pco2 (and a primary decrease in the body’s CO2 stores) defines respiratory alkalosis or primary hypocapnia and is characterized by alkalinization of the body fluids. Primary changes in Pco2 elicit secondary physiologic changes in plasma [HCO3ˉ] that are directional and proportional to the primary changes and tend to minimize the impact on acidity. This review presents the pathophysiology, secondary physiologic response, causes, clinical manifestations, diagnosis, and therapeutic principles of respiratory acidosis and respiratory alkalosis.  This review contains 4 figures, 3 tables, and 59 references. Key words: Respiratory acidosis, respiratory alkalosis, primary hypercapnia, primary hypocapnia, hypoxemia, pseudorespiratory alkalosis


1978 ◽  
Vol 44 (4) ◽  
pp. 534-537 ◽  
Author(s):  
M. Maskrey ◽  
P. P. Hoppe ◽  
O. S. Bamford

Five adult male dik-dik (Madoqua kirkii) were exposed in a climatic chamber to an air temperature of 45 degrees C. Measurements were made of rectal temperature (Tre) and respiratory frequency (f) and arterial blood samples taken before and during heat exposure were analyzed for pH, PCO2 and PO2. During exposure, Tre and f increased in all animals. In the first 80 min dik-dik displayed thermal tachypnea and minor changes in blood gases. Continued exposure lead to hyperpnea accompanied by a fall in PaCO2 and a rise in pH. PaCO2 at first fell and then increased toward or above control levels. The dik-dik did not display second phase breathing. This observation confirms that second phase breathing is not essential to the development of respiratory alkalosis. The main conclusion of the study is that the dik-dik, unlike another heat-adapted antelope, the wildebeest (Taylor, Robertshaw, and Hoffmann. Am. J. Physiol. 217:907–910, 1969), is unable to resist alkalosis during heat stress.


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