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What Is The Compensation For Respiratory Acidosis?

Respiratory Acidosis

Respiratory Acidosis

DEFINITION Respiratory acidosis = a primary acid-base disorder in which arterial pCO2 rises to an abnormally high level. PATHOPHYSIOLOGY arterial pCO2 is normally maintained at a level of about 40 mmHg by a balance between production of CO2 by the body and its removal by alveolar ventilation. PaCO2 is proportional to VCO2/VA VCO2 = CO2 production by the body VA = alveolar ventilation an increase in arterial pCO2 can occur by one of three possible mechanisms: presence of excess CO2 in the inspired gas decreased alveolar ventilation increased production of CO2 by the body CAUSES Inadequate Alveolar Ventilation central respiratory depression drug depression of respiratory centre (eg by opiates, sedatives, anaesthetics) neuromuscular disorders lung or chest wall defects airway obstruction inadequate mechanical ventilation Over-production of CO2 -> hypercatabolic disorders Malignant hyperthermia Thyroid storm Phaeochromocytoma Early sepsis Liver failure Increased Intake of Carbon Dioxide Rebreathing of CO2-containing expired gas Addition of CO2 to inspired gas Insufflation of CO2 into body cavity (eg for laparoscopic surgery) EFFECTS CO2 is lipid soluble -> depressing effects on intracellular metabolism RESP increased minute ventilation via both central and peripheral chemoreceptors CVS increased sympathetic tone peripheral vasodilation by direct effect on vessels acutely the acidosis will cause a right shift of the oxygen dissociation curve if the acidosis persists, a decrease in red cell 2,3 DPG occurs which shifts the curve back to the left CNS cerebral vasodilation increasing cerebral blood flow and intracranial pressure central depression at very high levels of pCO2 potent stimulation of ventilation this can result in dyspnoea, disorientation, acute confusion, headache, Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

What is respiratory acidosis? Respiratory acidosis is a condition that occurs when the lungs can’t remove enough of the carbon dioxide (CO2) produced by the body. Excess CO2 causes the pH of blood and other bodily fluids to decrease, making them too acidic. Normally, the body is able to balance the ions that control acidity. This balance is measured on a pH scale from 0 to 14. Acidosis occurs when the pH of the blood falls below 7.35 (normal blood pH is between 7.35 and 7.45). Respiratory acidosis is typically caused by an underlying disease or condition. This is also called respiratory failure or ventilatory failure. Normally, the lungs take in oxygen and exhale CO2. Oxygen passes from the lungs into the blood. CO2 passes from the blood into the lungs. However, sometimes the lungs can’t remove enough CO2. This may be due to a decrease in respiratory rate or decrease in air movement due to an underlying condition such as: There are two forms of respiratory acidosis: acute and chronic. Acute respiratory acidosis occurs quickly. It’s a medical emergency. Left untreated, symptoms will get progressively worse. It can become life-threatening. Chronic respiratory acidosis develops over time. It doesn’t cause symptoms. Instead, the body adapts to the increased acidity. For example, the kidneys produce more bicarbonate to help maintain balance. Chronic respiratory acidosis may not cause symptoms. Developing another illness may cause chronic respiratory acidosis to worsen and become acute respiratory acidosis. Initial signs of acute respiratory acidosis include: headache anxiety blurred vision restlessness confusion Without treatment, other symptoms may occur. These include: sleepiness or fatigue lethargy delirium or confusion shortness of breath coma The chronic form of Continue reading >>

Compensated Respiratory Acidosis

Compensated Respiratory Acidosis

Definition In a compensated respiratory acidosis, although the PCO2 is high, the pH is within normal range. The kidneys compensate for a respiratory acidosis by tubular cells reabsorbing more HCO3 from the tubular fluid, collecting duct cells secreting more H+ and generating more HCO3, and ammoniagenesis leading to increased formation of the NH3 buffer. Compensated respiratory acidosis is typically the result of a chronic condition, the slow nature of onset giving the kidneys time to compensate. Common causes of respiratory acidosis include hypoventilation due to: Respiratory depression (sedatives, narcotics, CVA, etc.) Respiratory muscle paralysis (spinal cord injury, Guillan-Barre, residual paralytics). Chest wall disorders (flail chest, pneumothorax) Lung parenchyma disorders (ARDS, pneumonia, COPD, CHF, aspiration) Abdominal distension (laporoscopic surgery, ascites, obesity, etc.). Subspecialty Keyword history Similar Keyword: Respiratory acidosis: Compensation Sources Miller’s Anesthesia, 7th ed. Ch. 49. PubMed Continue reading >>

Respiratory Compensation

Respiratory Compensation

Metabolic Acidosis Respiratory compensation for metabolic disorders is quite fast (within minutes) and reaches maximal values within 24 hours. A decrease in Pco2 of 1 to 1.5 mm Hg should be observed for each mEq/L decrease of in metabolic acidosis.27 A simple rule for deciding whether the fall in Pco2 is appropriate for the degree of metabolic acidosis is that the Pco2 should be equal to the last two digits of the pH. For example, compensation is adequate if the Pco2 decreases to 28 when the pH is 7.28. Alternatively, the Pco2 can be predicted by adding 15 to the observed (down to a value of 12). Although reduction in Pco2 plays an important role in correcting any metabolic acidosis, evidence suggests that it may in some respects be counterproductive because it inhibits renal acid excretion. Fetoplacental Elimination of Metabolic Acid Load Fetal respiratory and renal compensation in response to changes in fetal pH is limited by the level of maturity and the surrounding maternal environment. However, although the placentomaternal unit performs most compensatory functions,3 the fetal kidneys have some, although limited, ability to contribute to the maintenance of fetal acid–base balance. The most frequent cause of fetal metabolic acidosis is fetal hypoxemia owing to abnormalities of uteroplacental function or blood flow (or both). Primary maternal hypoxemia or maternal metabolic acidosis secondary to maternal diabetes mellitus, sepsis, or renal tubular abnormalities is an unusual cause of fetal metabolic acidosis. Pregnant women, at least in late gestation, maintain a somewhat more alkaline plasma environment compared with that of nonpregnant control participants. This pattern of acid–base regulation in pregnant women is present during both resting and after maximal e Continue reading >>

[kinetics Of The Compensation Of Respiratory Acidosis Induced By Experimentalchronic Hypercapnia In Man (author's Transl)].

[kinetics Of The Compensation Of Respiratory Acidosis Induced By Experimentalchronic Hypercapnia In Man (author's Transl)].

1. Bull Eur Physiopathol Respir. 1976 Jan-Feb;12(1):87-101. [Kinetics of the compensation of respiratory acidosis induced by experimentalchronic hypercapnia in man (author's transl)]. Radziszewski E, Guillerm R, Badre R, Abran C. Four groups of male volunteers have been exposed in a tight climatical chamber toPICO2 of 14, 21, 28 and 32 torr; exposure periods varied from two to 30 days,between two reference periods in normal air. The results deal with the evolution of arterial blood acid-base equilibrium and that of renal response in relation toPICO2. In all exposures, the carbon dioxide alveolar overload increases byseveral torr during the first 24 hours on account of attenuation of the initialhyperventilation. Kinetics of the respiratory acidosis compensation differsaccording to hypercapnia which is moderate (PICO2 of 14 and 21 torr) orrelatively severe (PICO2 of 28 and 32 torr). The decrease in arterial pH lessens as early as the 24th hour at PICO2 28 and 32 torr, and only after two days atPICO2 14 and 21 torr. The renal response is characterized by a significantincrease in aciduria during the first 24 hours at PICO2 28 and 32 torr; thechanges are smaller and start latter at PICO2 14 torr. Continue reading >>

Renal Compensation

Renal Compensation

Chronic Carbon Dioxide Retainer Renal compensation of respiratory acidosis is by increased urinary excretion of hydrogen ions and resorption of HCO3−. This relatively slow process occurs over several days. Slowly, pH reaches low normal values, but HCO3− levels and BE are increased. This is the situation of the patient with chronic respiratory failure. Pulmonary patients usually have chronic obstructive pulmonary disease or restrictive pulmonary disease, or they are morbidly obese. Increased Co2 stores are the rule, and the normal respiratory drive to Paco2 is obtunded. This group of patients is sensitive to O2 supplementation because respiratory drive is predominantly determined by hypoxemia. Patients with a Pao2 in the mid-50s and a Paco2 at the same level usually receive home O2 treatment, initially at night to reduce pulmonary hypertension and to relieve dyspnea. When the chronic Co2 retainer develops an acute respiratory problem and pH levels fall to less than 7.20, noninvasive ventilatory assistance is usually indicated. Fetoplacental Elimination of Metabolic Acid Load Fetal respiratory and renal compensation in response to changes in fetal pH is limited by the level of maturity and the surrounding maternal environment. However, although the placentomaternal unit performs most compensatory functions,3 the fetal kidneys have some, although limited, ability to contribute to the maintenance of fetal acid–base balance. The most frequent cause of fetal metabolic acidosis is fetal hypoxemia owing to abnormalities of uteroplacental function or blood flow (or both). Primary maternal hypoxemia or maternal metabolic acidosis secondary to maternal diabetes mellitus, sepsis, or renal tubular abnormalities is an unusual cause of fetal metabolic acidosis. Pregnant women, a Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory acidosis is a medical emergency in which decreased ventilation (hypoventilation) increases the concentration of carbon dioxide in the blood and decreases the blood's pH (a condition generally called acidosis). Carbon dioxide is produced continuously as the body's cells respire, and this CO2 will accumulate rapidly if the lungs do not adequately expel it through alveolar ventilation. Alveolar hypoventilation thus leads to an increased PaCO2 (a condition called hypercapnia). The increase in PaCO2 in turn decreases the HCO3−/PaCO2 ratio and decreases pH. Terminology[edit] Acidosis refers to disorders that lower cell/tissue pH to < 7.35. Acidemia refers to an arterial pH < 7.36.[1] Types of respiratory acidosis[edit] Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH <7.36). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (HCO3− >30 mm Hg). Causes[edit] Acute[edit] Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, inability to ventilate adequately due to neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis, Guillain–Barré syndrome, muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation. Chronic[edit] Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

LABORATORY TESTS The following lab tests can be used to interpret and explain acidosis and alkalosis conditions. All are measured on blood samples. 1. pH: This measures hydrogen ions - Normal pH = 7.35-7.45 2. pCO2= Partial Pressure of Carbon Dioxide: Although this is a pressure measurement, it relates to the concentration of GASEOUS CO2 in the blood. A high pCO2 may indicate acidosis. A low pCO2 may indicate alkalosis. 3. HCO3- = Bicarbonate: This measures the concentration of HCO3- ion only. High values may indicate alkalosis since bicarbonate is a base. Low values may indicate acidosis. 4. CO2 = Carbon Dioxide Content: This is a measure of ALL CO2 liberated on adding acid to blood plasma. This measure both carbon dioxide dissolved and bicarbonate ions and is an older test. Do not confuse with pCO2 Typically, dissolved carbon dioxide = l.2-2.0 mmoles/L and HCO3- = 22-28 mmoles/L Therefore, although it is listed as CO2 content, the lab test really reflects HCO3- concentration. Respiratory Acidosis .ABNORMAL pH IN THE BODY: ACIDOSIS AND ALKALOSIS: INTRODUCTION: Normal blood pH is maintained between 7.35 and 7.45 by the regulatory systems. The lungs regulate the amount of carbon dioxide in the blood and the kidneys regulate the bicarbonate. When the pH decreases to below 7.35 an acidosis condition is present. Acidosis means that the hydrogen ions are increased and that pH and bicarbonate ions are decreased. A greater number of hydrogen ions are present in the blood than can be absorbed by the buffer systems. Alkalosis results when the pH is above 7.45. This condition results when the buffer base (bicarbonate ions) is greater than normal and the concentration of hydrogen ions are decreased. Both acidosis and alkalosis can be of two different types: respiratory and metabol Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Practice Essentials Respiratory acidosis is an acid-base balance disturbance due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly and failure of ventilation promptly increases the partial pressure of arterial carbon dioxide (PaCO2). [1] The normal reference range for PaCO2 is 35-45 mm Hg. Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2, in turn, decreases the bicarbonate (HCO3–)/PaCO2 ratio, thereby decreasing the pH. Hypercapnia and respiratory acidosis ensue when impairment in ventilation occurs and the removal of carbon dioxide by the respiratory system is less than the production of carbon dioxide in the tissues. Lung diseases that cause abnormalities in alveolar gas exchange do not typically result in alveolar hypoventilation. Often these diseases stimulate ventilation and hypocapnia due to reflex receptors and hypoxia. Hypercapnia typically occurs late in the disease process with severe pulmonary disease or when respiratory muscles fatigue. (See also Pediatric Respiratory Acidosis, Metabolic Acidosis, and Pediatric Metabolic Acidosis.) Acute vs chronic respiratory acidosis Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (ie, >45 mm Hg) with an accompanying acidemia (ie, pH < 7.35). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate levels (ie, >30 mEq/L). Acute respiratory acidosis is present when an abrupt failure of ventilation occurs. This failure in ventilation may result from depression of the central respiratory center by one or another of the foll Continue reading >>

Assessment Of Compensation In Acute Respiratory Acidosis - Deranged Physiology

Assessment Of Compensation In Acute Respiratory Acidosis - Deranged Physiology

Assessment of Compensation in Acute Respiratory Acidosis Mechanisms and classification of metabolic acidosis This chapter is concerned with the changes in pH and serum bicarbonate which result from acute fluctuations in dissolved CO2, as a consequence of acute changes in ventilation. It is a more detailed look at the wayCO2interacts with the human body fluid, and the resulting changes which develop in theserum bicarbonate concentration and pH. The discussion which follows builds upon and benefits from someof thebackground knowledgeoffered in otherchapters: Let us consider the favoured model of acute respiratory acidosis, the patient who has stopped breathing. Conventional wisdom dictates that so long as the oxygen supply continues to mass-transfer its way into the patient, then the patient will continue to produce CO2, and as a result of this metabolic activity the PaCO2will rise at a rate of around 3mmHg every minute. This technique of "apnoeic anaesthesia" is well known to anaesthetists, and has enjoyed a fluctuating level of interest since the sixties. With a high PEEP and a sufficient attention to detail one may go through the entire hour-long case without any breaths being taken by the patient. But, let us consider a situation where the airway isnotpatent, and a constant supply of oxygen is not available. The patient has stopped exhaling CO2. What will happen? Well, the PaCO2will rise by about 12mmHg over the first minute, and by about 3.4 mmHg per minute for every minute after that. How do we know this? Because in 1989, 14 volunteers consented to having their tube clamped during an anaesthetic. The clamps were released after 5 minutes, or if the patients became dangerously hypoxic. Magnitude of pH change due to pCO2increase Knowing the change in PaCO2,one can att Continue reading >>

Uncompensated, Partially Compensated, Or Combined Abg Problems

Uncompensated, Partially Compensated, Or Combined Abg Problems

Arterial Blood Gas (ABG) analysis requires in-depth expertise. If the results are not understood right, or are wrongly interpreted, it can result in wrong diagnosis and end up in an inappropriate management of the patient. ABG analysis is carried out when the patient is dealing with the following conditions: • Breathing problems • Lung diseases (asthma, cystic fibrosis, COPD) • Heart failure • Kidney failure ABG reports help in answering the following questions: 1. Is there acidosis or alkalosis? 2. If acidosis is present, whether it is in an uncompensated state, partially compensated state, or in fully compensated state? 3. Whether acidosis is respiratory or metabolic? ABG reports provide the following descriptions: PaCO2 (partial pressure of dissolved CO2 in the blood) and PaO2 (partial pressure of dissolved O2 in the blood) describe the efficiency of exchange of gas in the alveolar level into the blood. Any change in these levels causes changes in the pH. HCO3 (bicarbonate in the blood) maintains the pH of the blood within normal range by compensatory mechanisms, which is either by retaining or increasing HCO3 excretion by the kidney. When PaCO2 increases, HCO3 decreases to compensate the pH. The following table summarizes the changes: ABG can be interpreted using the following analysis points: Finding acidosis or alkalosis: • If pH is more it is acidosis, if pH is less it is alkalosis. Finding compensated, partially compensated, or uncompensated ABG problems: • When PaCO2 is high, but pH is normal instead of being acidic, and if HCO3 levels are also increased, then it means that the compensatory mechanism has retained more HCO3 to maintain the pH. • When PaCO2 and HCO3 values are high but pH is acidic, then it indicates partial compensation. It means t Continue reading >>

Acid Base Disorders

Acid Base Disorders

Arterial blood gas analysis is used to determine the adequacy of oxygenation and ventilation, assess respiratory function and determine the acid–base balance. These data provide information regarding potential primary and compensatory processes that affect the body’s acid–base buffering system. Interpret the ABGs in a stepwise manner: Determine the adequacy of oxygenation (PaO2) Normal range: 80–100 mmHg (10.6–13.3 kPa) Determine pH status Normal pH range: 7.35–7.45 (H+ 35–45 nmol/L) pH <7.35: Acidosis is an abnormal process that increases the serum hydrogen ion concentration, lowers the pH and results in acidaemia. pH >7.45: Alkalosis is an abnormal process that decreases the hydrogen ion concentration and results in alkalaemia. Determine the respiratory component (PaCO2) Primary respiratory acidosis (hypoventilation) if pH <7.35 and HCO3– normal. Normal range: PaCO2 35–45 mmHg (4.7–6.0 kPa) PaCO2 >45 mmHg (> 6.0 kPa): Respiratory compensation for metabolic alkalosis if pH >7.45 and HCO3– (increased). PaCO2 <35 mmHg (4.7 kPa): Primary respiratory alkalosis (hyperventilation) if pH >7.45 and HCO3– normal. Respiratory compensation for metabolic acidosis if pH <7.35 and HCO3– (decreased). Determine the metabolic component (HCO3–) Normal HCO3– range 22–26 mmol/L HCO3 <22 mmol/L: Primary metabolic acidosis if pH <7.35. Renal compensation for respiratory alkalosis if pH >7.45. HCO3 >26 mmol/L: Primary metabolic alkalosis if pH >7.45. Renal compensation for respiratory acidosis if pH <7.35. Additional definitions Osmolar Gap Use: Screening test for detecting abnormal low MW solutes (e.g. ethanol, methanol & ethylene glycol [Reference]) An elevated osmolar gap (>10) provides indirect evidence for the presence of an abnormal solute which is prese Continue reading >>

Intro To Arterial Blood Gases, Part 2

Intro To Arterial Blood Gases, Part 2

Arterial Blood Gas Analysis, Part 2 Introduction Acute vs. Chronic Respiratory Disturbances Primary Metabolic Disturbances Anion Gap Mixed Disorders Compensatory Mechanisms Steps in ABG Analysis, Part II Summary Compensatory Mechanisms Compensation refers to the body's natural mechanisms of counteracting a primary acid-base disorder in an attempt to maintain homeostasis. As you learned in Acute vs. Chronic Respiratory Disturbances, the kidneys can compensate for chronic respiratory disorders by either holding on to or dumping bicarbonate. With Chronic respiratory acidosis: Chronic respiratory alkalosis: the kidneys hold on to bicarbonate the kidneys dump bicarbonate With primary metabolic disturbances, the respiratory system compensates for the acid-base disorder. The lungs can either blow off excess acid (via CO2) to compensate for metabolic acidosis, or to a lesser extent, hold on to acid (via CO2) to compensate for metabolic alkalosis. With Metabolic acidosis: Metabolic alkalosis: ventilation increases to blow off CO2 ventilation decreases to hold on to CO2 The body's response to metabolic acidosis is predictable. With metabolic acidosis, respiration will increase to blow off CO2, thereby decreasing the amount of acid in the blood. Recall that with metabolic acidosis, central chemoreceptors are triggered by the low pH and increase the drive to breathe. For now, it is only important to learn (qualitatively) that there is a predictable compensatory response to metabolic acidosis. Later, during your 3rd or 4th year rotations, you might learn how to (quantitatively) determine if the compensatory response to metabolic acidosis is appropriate by using the Winter's Formula. The body's response to metabolic alkalosis is not as complete. This is because we would need to hypov Continue reading >>

Acute Renal Response To Rapid Onset Respiratory Acidosis

Acute Renal Response To Rapid Onset Respiratory Acidosis

Acute Renal Response to Rapid Onset Respiratory Acidosis Jayanth Ramadoss , Randolph H. Stewart , and Timothy A. Cudd Department of Veterinary Physiology and Pharmacology and Michael E. DeBakey Institute, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, Texas, 77843, USA Send correspondence to: Timothy A. Cudd, DVM, PhD, Department of Veterinary Physiology and Pharmacology, Hwy 60, Building VMA, Rm 332, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843-4466 Fax: 979-845-6544 [email protected] The publisher's final edited version of this article is available at Can J Physiol Pharmacol See other articles in PMC that cite the published article. Renal strong ion compensation to chronic respiratory acidosis has been established but the nature of the response to acute respiratory acidosis is not well defined. We hypothesized that the response to acute respiratory acidosis in sheep is a rapid increase in the difference in renal fractional excretions of chloride and sodium (FeCl-FeNa). Inspired CO2 concentrations were increased for one hour to alter significantly PaCO2 and pHa from 32 1 mm Hg and 7.52 0.02 to 74 2 mm Hg and 7.22 0.02, respectively. FeCl-FeNa increased significantly from 0.372 0.206 to 1.240 0.217 % and returned to baseline at two hours when PaCO2 and pHa were 37 0.6 mm Hg and 7.49 0.01, respectively. Arterial pH and FeCl-FeNa were significantly correlated. We conclude that the kidney responds rapidly to acute respiratory acidosis, within 30 mins of onset, by differential reabsorption of sodium and chloride. Disturbances of acid-base balance are common in patients admitted to intensive care units; causes include acute respiratory failure, diabetic ketoacidosis a Continue reading >>

Respiratory Compensation

Respiratory Compensation

Publisher Summary This chapter elaborates the bicarbonate buffer system and respiratory compensation. The plasma pH is defined as –log [H+], and when [H+] increases, the pH decreases. The condition of high plasma pH is called alkalosis and low plasma pH is acidosis. The body has three lines of defense against departures from normal plasma pH—the chemical buffers, the respiratory system, and the renal system. The chemical buffers passively resist changes in pH by absorbing excess H+ when pH falls or by releasing H+ ions when pH rises. Chemical buffers include proteins, phosphate, and bicarbonate buffers. All of these equilibrate with a single [H+], and so the buffer systems are linked. This is the isohydric principle, and because of this link, adjustment of the bicarbonate buffer system controls all buffer systems. The bicarbonate buffer system has two components that include plasma [CO2] and [HCO3−]. The respiratory system controls plasma pH by adjusting the [CO2]. The equilibrium between dissolved CO2 and H2CO3 is accelerated by carbonic anhydrase. Respiratory alkalosis results from hyperventilation as the primary disturbance. Hyperventilation also forms the respiratory compensation of metabolic acidosis. It is found that complete compensation of pH disturbances requires the kidney to change plasma [HCO3−]. Increased Carbon Dioxide: Respiratory Acidosis Respiratory acidosis may result from a primary respiratory disorder or it can be a physiologic respiratory compensation for a metabolic alkalosis. An increase in HCO3− of 1 mEq/L should result in an increase in PCO2 of 0.7 mm Hg in both dogs and cats.1,3 Pathologic respiratory acidosis results from an imbalance in CO2 production via metabolism and excretion via the lung. Common causes include large airway obst Continue reading >>

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