scholarly journals Management of Metabolic Acidosis in the Post-Cardiac Surgical Patient

2020 ◽  
pp. 12-15
Author(s):  
Jeevan Francis ◽  
Sneha Prothasis ◽  
Richard Varghese ◽  
Midhuna Jomon ◽  
Rexy Roy ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Blood Gases ◽  
Cellular Level ◽  
Base Deficit ◽  
Active Management ◽  
Surgical Patient ◽  
Arterial Blood ◽  
A Value ◽  
Circulatory Physiology ◽  
Not At Risk

The base deficit is the best way to evaluate severity of Metabolic Acidosis (MA). It indicates a value corresponding to the number of mmol/L below 24 of the measured bicarbonate concentration. Base deficit between 0 and 5 mmol/L indicates that the patient is not at risk of immediate harm. Arterial blood gases are typically measured every 2-4 hours following cardiac surgery and there is always a trend in base deficit changes to consider. Where the base deficit is diminishing, this indicates that the patient is improving, whereas when it is worsening, the opposite is true. Base deficits between 5 and 10 indicate that a serious problem is present which requires urgent correction. Where the base deficit is greater than 10, cardiac arrest may occur, and such patients require constant supervision by a doctor if active management is being pursued. Where the base deficit is persistently greater than 15, survival is extremely unlikely. This degree of acidosis is associated with widespread disruption of mitochondria at cellular level. The mitochondria often do not recover even if the precipitating cause of the MA is corrected, in which case the patient develops fatal multisystem organ failure. The management of MA in post-cardiac surgical patients is indivisibly bound up in optimizing circulatory physiology. We have not expounded on how this foundational knowledge should be applied but without it the management of MA in this patient population will be severely hampered.

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.

Arterial blood acid-base regulation during exercise in rats

1984 ◽  
Vol 57 (2) ◽  
pp. 396-402 ◽  
Author(s):  
R. F. Fregosi ◽  
J. A. Dempsey
Keyword(s):  
Metabolic Acidosis ◽  
Lactate Concentration ◽  
Blood Gases ◽  
Fold Increase ◽  
Respiratory Alkalosis ◽  
Male Rats ◽  
Co2 Production ◽  
Acid Base ◽  
Arterial Blood ◽  
Exercise Induced

For the first time in the rat, we described the effects of exercise on arterial acid-base status and examined the role of chemical stimuli as determinants of the hyperventilatory response in this species. O2 consumption (VO2), CO2 production (VCO2), arterial blood gases, arterial lactate concentration ([LA-]a), and rectal temperature (Tre) were measured in non-trained male rats at rest and during 10 min of treadmill exercise at various intensities. During mild exercise (2.5-fold increase in VCO2), PaCO2 fell 5.5 +/- 0.6 Torr, and despite a small but significant increase in [LA-]a, respiratory alkalosis prevailed [change in arterial pH (delta pHa) = 0.034 +/- 0.006]. Arterial PO2 (PaO2) increased 4.1 +/- 1.5 Torr and Tre increased 0.6 +/- 0.1 degrees C. A progressive hyperventilation occurred from mild to heavy exercise. This response was not attributable to arterial hypoxemia or acidosis and it was not affected by preventing the exercise-induced increase in body temperature. During maximal exercise, VO2 increased 3.4-fold (72 +/- 1.50 ml X kg-1 X min-1) and VCO2 increased 4.5-fold (74 +/- 1.90 ml X kg-1 X min-1), resulting in a 9-fold increase in [LA-]a and a severe metabolic acidosis (pHa 7.31 +/- 0.02). A marked hyperventilation [arterial PCO2 (PaCO2) 28.5 +/- 1.4 Torr] resulted in partial compensation of pHa, but almost all of this hyperventilation occurred before the onset of metabolic acidosis, [i.e., at less than 65% maximum VO2 (VO2max)], and the increased [H+]a with further elevations in VO2 produced no further hypocapnia.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Can Venous Blood Gases Replace Arterial Blood Gases in Diabetic Ketoacidosis/Renal Failure Induced Metabolic Acidosis?

2015 ◽  
Vol 3 (3) ◽  
pp. 65-69
Author(s):  
Naveen Mohan ◽  
Gireesh Kumar K. P ◽  
Sreekrishnan T. P ◽  
Ajith Kumar J ◽  
Ajith V. ◽  
...  
Keyword(s):  
Renal Failure ◽  
Metabolic Acidosis ◽  
Diabetic Ketoacidosis ◽  
Venous Blood ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Arterial Blood

The Correlation of Near-Infrared Spectroscopy with Changes in Oxygen Delivery in a Controlled Model of Altered Perfusion

2007 ◽  
Vol 73 (10) ◽  
pp. 1017-1022 ◽  
Author(s):  
Brant Putnam ◽  
Scott Bricker ◽  
Peter Fedorka ◽  
Juliette Zelada ◽  
Saad Shebrain ◽  
...  
Keyword(s):  
Infrared Spectroscopy ◽  
Standard Deviation ◽  
Near Infrared Spectroscopy ◽  
Oxygen Delivery ◽  
Near Infrared ◽  
Blood Gases ◽  
Tissue Perfusion ◽  
Base Deficit ◽  
Arterial Blood ◽  
Noninvasive Monitor

Alterations in regional tissue perfusion may precede global indications of shock. This study compared regional tissue oxygenation saturation (StO2) using near-infrared spectroscopy with standard hemodynamic and biochemical variables in 40 patients undergoing cardiopulmonary bypass (CPB). Mean arterial pressure, cardiac output, oxygen delivery, arterial blood gases, and lactate were recorded at specific intervals during surgery. Data were organized by stage of procedure, and the relationship of StO2 to established parameters was investigated. With initiation of CPB, StO2 declined by 12.9 per cent (standard deviation ± 14.75%) with a delayed increase in lactate from 0.9 (interquartile range [IQR], 0.6–1.5) mmol/L to 2.3 (IQR, 1.8–2.5) mmol/L. The minimum StO2 value preceded the maximum lactate level by an average time of 93.9 (standard deviation ± 86.3) minutes. Additionally, a decrease in StO2 corresponded with an increase in base deficit of 4.84 (standard deviation ± 2.37) mEq/L over the same period. Calculated oxygen delivery decreased from a baseline value of 754 (IQR, 560–950) mL/min to 472 (IQR, 396–600) mL/min with initiation and maintenance of CPB. For patients undergoing CPB, StO2 is a reliable, noninvasive monitor of perfusion, which correlates well with oxygen delivery and identifies perfusion deficits earlier than lactate or base deficit.

Respiratory acidosis in carbonic anhydrase II-deficient mice

1998 ◽  
Vol 274 (2) ◽  
pp. L301-L304 ◽  
Author(s):  
Yeong-Hau H. Lien ◽  
Li-Wen Lai
Keyword(s):  
Metabolic Acidosis ◽  
Carbonic Anhydrase ◽  
Respiratory Acidosis ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Arterial Blood ◽  
Blood Ph ◽  
Type Ii Pneumocytes ◽  
Deficient Mice

To investigate the role of carbonic anhydrase (CA) II on pulmonary CO2 exchange, we analyzed arterial blood gases from CA II-deficient and normal control mice. CA II-deficient mice had a low arterial blood pH (7.18 ± 0.06) and[Formula: see text] concentration ([[Formula: see text]]; 17.5 ± 1.9 meq/l) and a high [Formula: see text](47.4 ± 5.3 mmHg), consistent with mixed respiratory and metabolic acidosis. To eliminate the influence of metabolic acidosis on arterial blood gases, NaHCO3 (4 mmol/kg body weight) was given intraperitoneally, and arterial blood gases were analyzed 4 h later. Normal mice had a small increase in pH and were able to maintain [Formula: see text] and [[Formula: see text]]. The metabolic acidosis in CA II-deficient mice was corrected ([[Formula: see text]], 22.9 ± 2.4 meq/l), and respiratory acidosis became more profound ([Formula: see text], 50.4 ± 2.4 mmHg). These results indicate that CA II-deficient mice have a partial respiratory compensation for metabolic acidosis. We conclude that CA II-deficient mice have a mixed respiratory and metabolic acidosis. It is most likely that CO2 retention in these animals is due to CA II deficiency in both red blood cells and type II pneumocytes.

scholarly journals Exertional dyspnea in mitochondrial myopathy: clinical features and physiological mechanisms

2011 ◽  
Vol 301 (4) ◽  
pp. R873-R884 ◽  
Author(s):  
Katja Heinicke ◽  
Tanja Taivassalo ◽  
Phil Wyrick ◽  
Helen Wood ◽  
Tony G. Babb ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Clinical Features ◽  
Mitochondrial Myopathy ◽  
Blood Gases ◽  
Underlying Mechanism ◽  
Exertional Dyspnea ◽  
Arterial Blood ◽  
Exercise Ventilation ◽  
Mitochondrial Defects ◽  
Breathing Effort

Exertional dyspnea limits exercise in some mitochondrial myopathy (MM) patients, but the clinical features of this syndrome are poorly defined, and its underlying mechanism is unknown. We evaluated ventilation and arterial blood gases during cycle exercise and recovery in five MM patients with exertional dyspnea and genetically defined mitochondrial defects, and in four control subjects (C). Patient ventilation was normal at rest. During exercise, MM patients had low V̇o2peak (28 ± 9% of predicted) and exaggerated systemic O2 delivery relative to O2 utilization (i.e., a hyperkinetic circulation). High perceived breathing effort in patients was associated with exaggerated ventilation relative to metabolic rate with high V̇e/V̇o2peak, (MM = 104 ± 18; C = 42 ± 8, P ≤ 0.001), and V̇e/V̇co2peak, (MM = 54 ± 9; C = 34 ± 7, P ≤ 0.01); a steeper slope of increase in ΔV̇e/ΔV̇co2 (MM = 50.0 ± 6.9; C = 32.2 ± 6.6, P ≤ 0.01); and elevated peak respiratory exchange ratio (RER), (MM = 1.95 ± 0.31, C = 1.25 ± 0.03, P ≤ 0.01). Arterial lactate was higher in MM patients, and evidence for ventilatory compensation to metabolic acidosis included lower PaCO2 and standard bicarbonate. However, during 5 min of recovery, despite a further fall in arterial pH and lactate elevation, ventilation in MM rapidly normalized. These data indicate that exertional dyspnea in MM is attributable to mitochondrial defects that severely impair muscle oxidative phosphorylation and result in a hyperkinetic circulation in exercise. Exaggerated exercise ventilation is indicated by markedly elevated V̇e/V̇o2, V̇e/V̇co2, and RER. While lactic acidosis likely contributes to exercise hyperventilation, the fact that ventilation normalizes during recovery from exercise despite increasing metabolic acidosis strongly indicates that additional, exercise-specific mechanisms are responsible for this distinctive pattern of exercise ventilation.

scholarly journals The frequency and severity of metabolic acidosis related to topiramate

2016 ◽  
Vol 44 (6) ◽  
pp. 1376-1380 ◽  
Author(s):  
Hatice Türe ◽  
Özgül Keskin ◽  
Ülkem Çakır ◽  
Canan Aykut Bingöl ◽  
Uğur Türe
Keyword(s):  
Metabolic Acidosis ◽  
Blood Gases ◽  
Blood Gas Analysis ◽  
Blood Chemistry ◽  
Gas Analysis ◽  
Blood Gas ◽  
High Respiratory Rate ◽  
Cross Sectional ◽  
Arterial Blood ◽  
Sectional Analysis

Objective We planned a cross-sectional analysis to determine the frequency and severity of metabolic acidosis in patients taking topiramate while awaiting craniotomy. Methods Eighty patients (18 – 65 years) taking topiramate to control seizures while awaiting elective craniotomy were enrolled. Any signs of metabolic acidosis or topiramate-related side effects were investigated. Blood chemistry levels and arterial blood gases, including lactate, were obtained. The severity of metabolic acidosis was defined according to base excess levels as mild or moderate. Results Blood gas analysis showed that 71% ( n = 57) of patients had metabolic acidosis. The frequency of moderate metabolic acidosis was 56% ( n = 45), while that of mild metabolic acidosis was 15% ( n = 12). A high respiratory rate was reported in only 10% of moderately acidotic patients. Conclusions In patients receiving topiramate, baseline blood gas analysis should be performed preoperatively to determine the presence and severity of metabolic acidosis.

scholarly journals Subdiaphragmatic venous stasis and tissular hypoperfusion as sources of metabolic acidosis during passive portal-jugular and caval-jugular bypasses in dogs

2000 ◽  
Vol 15 (2) ◽  
pp. 94-101 ◽  
Author(s):  
Antônio Roberto de Barros Coelho ◽  
Álvaro Antônio Bandeira Ferraz ◽  
Renato Dornelas Câmara Neto ◽  
Ayrton Ponce de Souza ◽  
Edmundo Machado Ferraz
Keyword(s):  
Carbon Dioxide ◽  
Liver Transplantation ◽  
Metabolic Acidosis ◽  
Venous Blood ◽  
Blood Stasis ◽  
Carbon Dioxide Tension ◽  
Base Deficit ◽  
Venous Stasis ◽  
Acid Base ◽  
Arterial Blood

Subdiafragmatic venous decompression during anhepatic stage of canine orthotopic liver transplantation attenuates portal and caval blood stasis and minimize hipoperfusion and metabolic acidosis observed with occlusion of portal and caval veins. During two hours, six dogs submitted to portal-jugular and caval-jugular passive shunts, with maintenance of arterial hepatic flow, were evaluated for pH, carbon dioxide tension (PCO2), base deficit (BD) and oxygen tension (PO2) in portal, caval and systemic arterial blood, as well as for increments of BD (DBD) in portal and caval blood. With a confidence level of 95%, the results showed that: 1. There were not changes of pH anDBD in portal and systemic arterial blood in the majority of studied times; 2. There was metabolic acidosis in caval blood; 3. The negative increments of BD (DBD) were higher in caval blood than in splancnic venous blood at T10, T30 and T105; and, 4. Deoxigenation of portal and caval blood were detected. Acid-base metabolism and oxigenation monitoring of subdiaphramatic venous blood can constitute an effective way to evaluate experimental passive portal-jugular and caval-jugular bypass in dogs.

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