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Respiratory alkalosis, or primary hypocapnia, occurs when alveolar ventilation exceeds that required to eliminate the carbon dioxide produced by tissues. Concurrent decreases in Paco 2 , increases in pH, and compensatory decreases in blood HCO 3 - levels are associated with respiratory alkalosis. Respiratory alkalosis can be acute or chronic, with metabolic compensation initially consisting of cellular uptake of HCO 3 - and buffering by intracellular phosphates and proteins. Chronic respiratory alkalosis results in longer-lasting decreases in renal reabsorption of HCO 3 - ; the arterial pH can approach near-normal values., (Copyright © 2016 Elsevier Inc. All rights reserved.)

The incidence of respiratory acid-base abnormalities in the critical care unit (CCU) is unknown, although respiratory alkalosis is suspected to be common in this population. Abnormal carbon dioxide tension can have many physiologic effects, and changes in Pco 2 may have a significant impact on outcome. Monitoring Pco 2 in CCU patients is an important aspect of critical patient assessment, and identification of respiratory acid-base abnormalities can be valuable as a diagnostic tool. Treatment of respiratory acid-base disorders is largely focused on resolution of the primary disease, although mechanical ventilation may be indicated in cases with severe respiratory acidosis., (Published by Elsevier Inc.)

Objective: To determine whether Labrador Retrievers participating in field trials develop respiratory alkalosis and hypocapnia primarily in conditions of high ambient temperatures., Animals: 16 Labrador Retrievers., Procedures: At each of 5 field trials, 5 to 10 dogs were monitored during a test (retrieval of birds over a variable distance on land [1,076 to 2,200 m]; 36 assessments); ambient temperatures ranged from 2.2 degrees to 29.4 degrees C. For each dog, rectal temperature was measured and a venous blood sample was collected in a heparinized syringe within 5 minutes of test completion. Blood samples were analyzed on site for Hct; pH; sodium, potassium, ionized calcium, glucose, lactate, bicarbonate, and total CO2 concentrations; and values of PvO2 and PvCO2. Scatterplots of each variable versus ambient temperature were reviewed. Regression analysis was used to evaluate the effect of ambient temperature (< or = 21 degrees C and > 21 degrees C) on each variable., Results: Compared with findings at ambient temperatures < or = 21 degrees C, venous blood pH was increased (mean, 7.521 vs 7.349) and PvCO2 was decreased (mean, 17.8 vs 29.3 mm Hg) at temperatures > 21 degrees C; rectal temperature did not differ. Two dogs developed signs of heat stress in 1 test at an ambient temperature of 29 degrees C; their rectal temperatures were higher and PvCO2 values were lower than findings in other dogs., Conclusions and Clinical Relevance: When running distances frequently encountered at field trials, healthy Labrador Retrievers developed hyperthermia regardless of ambient temperature. Dogs developed respiratory alkalosis and hypocapnia at ambient temperatures > 21 degrees C.

This article serves as a quick reference for respiratory alkalosis. Guidelines for analysis and causes, signs, and a stepwise approach are presented.

Respiratory acid-base disorders, although infrequently diagnosed in veterinary medicine, can cause or contribute to adverse clinical outcomes. Recognition of the mechanisms and causes of respiratory acidosis and alkalosis can prompt clinical detection of the acid-base derangement, allowing for appropriate intervention.

The use of arterial blood gas analysis, pulse oximetry, and capnography has become commonplace in the assessment of veterinary patients. Blood gas analysis allows for the qualitative and quantitative assessment of both metabolic and respiratory acid-base problems, including the interrelationships between ventilation, oxygenation, and metabolic conditions. Blood gas analysis is a useful adjunct to clinical patient assessment and other diagnostics in determining appropriate therapy for specific and complex conditions. Both pulse oximetry and capnography are useful monitoring tools. However, they have technical limitations and cannot comprehensively evaluate patient oxygenation and ventilation. Pulse oximetry and capnography are not replacements for arterial blood gas analysis, but rather serve as adjunctive monitoring tools.

Detection of alkaline urine traditionally sends an alert to the clinician to consider the presence of a urease-producing bacterial urinary tract infection, postprandial alkaline tide, or the ingestion of a diet that is nonacidifying. In the cat of this report, acid urine was produced while the cat was in the home environment, but alkaline urine was produced following the stress of a long trip to the veterinarian's office. Stress-induced respiratory alkalosis was highly suspected as the cause for the alkaline urine. If traditional causes for alkaline urine are not apparent for cats that produce alkaline urine at the veterinary clinic, we suggest that urinary pH be determined on samples collected in the home.

Exposure to heat stress lowered partial pressure of arterial blood carbon dioxide (paCO2), arterial blood bicarbonate ion (HCO3-), but increased arterial blood pH (pHa) and plasma lactate (LA). Increasing ambient carbon dioxide (CO2) to 1.5% increased paCO2 from hypocapnic levels to normocapnic levels, raised HCO3-, lowered pHa and plasma LA to pre-heat stress levels. Following CO2 treatment, respiratory alkalosis conditions returned. It was evident in this study that increasing ambient chamber CO2 to 1.5% was effective in ameliorating acid-base disturbances and reducing elevated levels of plasma LA which normally develops when laying hens are subjected to an acute heat stress exposure.

1. During hyperthermia-induced thermal panting, there was a progressive development of alkalosis, hypocapnia, hypocalcemia and plasma lactate accumulation in both mature and immature domestic fowl. 2. The results of this study further demonstrate that hypocalcemia is a general consequence of respiratory alkalosis in animals. 3. The significant (P less than 0.05) regression analysis of plasma lactate vs arterial blood pH, suggest a relationship between these two variables. 4. Plasma lactate accumulation may therefore play an important role as an extrarenal buffering component in the normal defense against severe alkalosis.

Alterations in acid-base status and blood-gas dynamics were studied during induced progressive hyperkalaemia in neonatal calves. The hyperkalaemia was associated initially with respiratory alkalosis in arterial blood when plasma K+ was increased to 6.08 +/- 1.02 mmol litre-1. The rise of plasma K+ above 6.08 +/- 1.02 mmol litre-1 led to the development of metabolic acidosis in arterial and venous blood. There was partial respiratory compensation. Plasma K+ concentrations at or above 11.03 +/- 0.34 mmol litre-1 were associated with a decrease in arterial oxygen tension and arterial oxygen saturation. The oxygen extraction ratio was increased during hyperkalaemia.

Alkalemia (pH greater than 7.50) was measured in 20 dogs admitted over a 3-year period for various clinical disorders. Alkalemia was detected in only 2.08% of all dogs in which blood pH and blood-gas estimations were made. Thirteen dogs had metabolic alkalosis (HCO3- greater than 24 mEq/L, PCO2 greater than 30 mm of Hg), of which 8 had uncompensated metabolic alkalosis, and of which 5 had partially compensated metabolic alkalosis. Seven dogs had respiratory alkalosis (PCO2 less than 30 mm of Hg, HCO3- less than 24 mEq/L); 4 of these had uncompensated respiratory alkalosis and 3 had partially compensated respiratory alkalosis. Ten dogs had double or triple acid-base abnormalities. Dogs with metabolic alkalosis had a preponderance of clinical signs associated with gastrointestinal disorders (10 dogs). Overzealous administration of sodium bicarbonate or diuretics, in addition to anorexia, polyuria, or hyperbilirubinemia may have contributed to metabolic alkalosis in 8 of the dogs. Most of the dogs in this group had low serum K+ and Cl- values. Two dogs with metabolic alkalosis had PCO2 values greater than 60 mm of Hg, and 1 of these had arterial hypoxemia (PaO2 less than 80 mm of Hg). Treatments included replacement of fluid and electrolytes (Na+, K+, and Cl-), and surgery as indicated (8 dogs). Six dogs with respiratory alkalosis had a variety of airway, pulmonary, or cardiac disorders, and 3 of these had arterial hypoxemia. Two other dogs were excessively ventilated during surgery, and 1 dog had apparent postoperative pain that may have contributed to the respiratory alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)

The occurrence of respiratory alkalosis and potential benefit derived from treatment were examined in thermostressed 4-week-old broiler chicks. Blood pH was greater (P less than .05) in heat-stressed (32 C) panting birds (7.395) than either nonpanting (7.28) or birds raised at 24 C (7.28). Acute thermostress, obtained by elevating ambient temperature from 32 to 41 C over a 20-min period further elevated (P less than .05) blood pH to 7.521. Chronic heat-stressed broiler chicks suffer from intermittent respiratory alkalosis during panting; with acute heat stress, chicks pant continuously and suffer from alkalosis. Including .5% sodium bicarbonate (NaHCO3) in the diet of birds subjected to chronic heat stress enhanced body weight gain by 9% even though it tended (P less than .10) to increase blood pH in nonpanting birds. Adding .3 or 1% ammonium chloride (NH4Cl) to diets decreased blood pH (P less than .01) to 7.194 and increased (P less than .05) body weight gains by 9.5 and 25%, respectively. Effects appeared linear with NH4Cl dose to 1% NH4Cl, but 3% NH4Cl elevated weight gains by only 8% and precipitated blood acidosis (pH 7.09) in nonpanting birds. Supplementing the 1% NH4Cl diet with .5% NaHCO3 increased weight gains an additional 9%. Manipulating sodium: chloride ratios by addition of calcium chloride increased body weight gain 8% and slightly reduced severity of alkalosis. Data indicate that blood alkalosis limits growth rate of broiler chicks reared under chronic thermostress and that the respiratory alkalosis and weight gain depressions attributed to thermostress can be partially alleviated dietarily.

The body regulates pH closely to maintain homeostasis. The pH of blood can be represented by the Henderson-Hasselbalch equation: pH = pK + log [HCO3-]/PCO2 Thus, pH is a function of the ratio between bicarbonate ion concentration [HCO3-] and carbon dioxide tension (PCO2). There are four simple acid base disorders: (1) Metabolic acidosis, (2) respiratory acidosis, (3) metabolic alkalosis, and (4) respiratory alkalosis. Metabolic acidosis is the most common disorder encountered in clinical practice. The respiratory contribution to a change in pH can be determined by measuring PCO2 and the metabolic component by measuring the base excess. Unless it is desirable to know the oxygenation status of a patient, venous blood samples will usually be sufficient. Metabolic acidosis can result from an increase of acid in the body or by excess loss of bicarbonate. Measurement of the "anion-gap" [(Na+ + K+) - (Cl- + HCO3-)], may help to diagnose the cause of the metabolic acidosis. Treatment of all acid-base disorders must be aimed at diagnosis and correction of the underlying disease process. Specific treatment may be required when changes in pH are severe (pH less than 7.2 or pH greater than 7.6). Treatment of severe metabolic acidosis requires the use of sodium bicarbonate, but blood pH and gases should be monitored closely to avoid an "overshoot" alkalosis. Changes in pH may be accompanied by alterations in plasma potassium concentrations, and it is recommended that plasma potassium be monitored closely during treatment of acid-base disturbances.

Mixed acid-base disturbances are combinations of two or more primary acid-base disturbances. Mixed acid-base disturbances may be suspected on the basis of findings obtained from the medical history, physical examination, serum electrolytes and chemistries, and anion gap. The history, physical examination, and serum biochemical profile may reveal disease processes commonly associated with acid-base disturbances. Changes in serum total CO2, serum potassium and chloride concentrations, or increased anion gap may provide clues to the existence of acid-base disorders. Blood gas analysis is usually required to confirm mixed acid-base disorders. To identify mixed acid-base disorders, blood gas analysis is used to identify primary acid-base disturbance and determine if an appropriate compensatory response has developed. Inappropriate compensatory responses (inadequate or excessive) are evidence of a mixed respiratory and metabolic disorder. The anion gap is also of value in detecting mixed acid-base disturbances. In high anion gap metabolic acidosis, the change in the anion gap should approximate the change in serum bicarbonate. Absence of this relationship should prompt consideration of a mixed metabolic acid-base disorder. Finding an elevated anion gap, regardless of serum bicarbonate concentration, suggests metabolic acidosis. In some instances, elevated anion gap is the only evidence of metabolic acidosis. In patients with hyperchloremic metabolic acidosis, increases in the serum chloride concentration should approximate the reduction in the serum bicarbonate concentration. Significant alterations from this relationship also indicate that a mixed metabolic disorder may be present. In treatment of mixed acid-base disorders, careful consideration should be given to the potential impact of therapeutically altering one acid-base disorder without correcting others.

An experiment was conducted to determine the change with time in the blood ionized calcium concentration of hens exposed to an acute heat stress. Five hens were surgically fitted with carotid artery cannulae and placed in cages inside a temperature-controlled chamber. Blood samples were drawn before (23 C), during (35 C), and after (23 C), a 3-hr heat-stress exposure. Whole blood ionized calcium, blood gas, plasma pyruvate, and lactate were determined. Respiratory alkalosis developed 1 hr after the start of heat exposure (35 C). Approximately 1 hr later, there was a concomitant decline in blood pH as plasma lactate and pyruvate concentration increased (P less than .05). In addition, the blood ionized calcium level was reduced (P less than .05) by 19% and was negatively correlated (P less than .05) with plasma pyruvate (-.77) and lactate (-.81). These results suggest that changes in acid-base balance during heat stress reduce the blood ionized calcium level, which may in turn limit the availability of calcium for egg shell formation.

An understanding of acid-base disturbances depends on the interpretation of changes in blood pH, P-co-2, and bicarbonate concentration and a comprehension of the physiologic mechanisms that control them. The physiologic relationships between Pco-2 and bicarbonate can be visualized by means of the balance nomogram and this visualization facilitates determination of any excess or deficit for both respiratory and metabolic factors.

Hyperhydrated goats were exposed to an environmental temperature of 45 degrees C (relative humidity 70%) for 120 min. After 90 min, rectal temperature and respiratory frequency reached plateau levels of 40.5 degrees C and 280 respirations min-1, respectively. Measurements of arterial and venous blood acid-base parameters revealed that respiratory alkalosis had started to develop after 60 min, and had become obvious at the end of the heat exposure period. Renal compensation (evidenced by gradual increases in urinary pH and renal Na excretion) developed in parallel with the respiratory alkalosis. The heat exposure elicited a moderate, temporary inhibition of the water diuresis, but no obvious increase in the renal excretion of arginine vasopressin (antidiuretic hormone, ADH). Preliminary determinations of plasma aldosterone did not show any change during the actual heat exposure period, but a 50% temporary decrease in plasma aldosterone 30 min thereafter. The study confirms the susceptibility of goats to develop respiratory alkalosis during thermoregulatory panting, and shows that this is not to any appreciable extent diminished during hyperhydration. It can further be concluded that a heat-induced rise in body temperature to 40.5 degrees C is no powerful stimulus for vasopressin release in the hyperhydrated goat. The determinations of plasma aldosterone suggest that reduced liberation of the hormone does not contribute to the immediate renal compensation of respiratory alkalosis, but that respiratory alkalosis reaching a certain intensity inhibits aldosterone secretion.

1. Changes in respiratory rate (f), rectal temperature (Tr) and blood acid-base values were measured in laying hens exposed to ambient temperatures (Ta) of 32, 35, 38 or 41 degrees C. 2. At Ta 32 degrees C there was no panting. At Ta 35 degrees C panting occurred without any increase in Tr but there was a slight alkalosis (pH 7.55). 3. At Ta 38 degrees C Tr increased and panting was accompanied by moderate alkalosis (pH 7.58). 4. At Ta 41 degrees C Tr increased considerably and severe alkalosis developed (pH 7.65). 5. From the relation between Tr, f and pH it is concluded that some degree of alkalosis is a normal response to panting in the laying hen.