History and physical examination

Signalment (age, sex, breed), past medical history, drug therapy, noted alterations in drinking, urination, defecation, vomiting, weight loss, respiratory changes, behavior and mentation, and possible toxic exposures are all important when collecting a history. Historical information may provide insight into the nature of the acid–base disturbance.

A list of physical examination findings associated with acidemia and alkalemia is provided in Table 7.4 and covers the entire spectrum of serious illness. It is important to remember that this association does not imply that the acidemia or alkalemia is the direct biochemical cause of these signs. Continuous monitoring of physical parameters such as temperature, pulse rate, pulse quality, heart rate and rhythm, respiratory rate, respiratory effort, mentation, mucous membrane color, and capillary refill time is essential for early detection of problems resulting from or causing changes in acid–base balance.

Point of care testing

The minimum database consists of packed cell volume (PCV), total proteins (TP), blood glucose, blood urea nitrogen (BUN), electrolytes, and blood gas analysis. The PCV is important in determining the contribution that hemoglobin makes to the assessment of pH. The remainder of the database will contribute to the SQAB profile (see Box 7.4). A complete blood count, serum biochemistry, and urinalysis provide important data for identifying factors potentially contributing to acid–base disorders.

There are no analyzers that will assay all of the necessary SQAB analytes from one sample. Therefore, an important step for SQAB analysis is to equip the ICU with the point of care (POC) analyzers (blood gas, electrolyte, biochemistry) that can provide SQAB profile results rapidly and efficiently. Point of care analyzers should be selected that use minimal sample size and provide rapid sample processing. It is important to use a brand of analyzer that has been validated in animals and for which reference ranges for the species being studied have been provided.

Data is only useful if it is free from errors in sampling or laboratory technique, and if it is obtained often enough to reflect important changes in a patient’s condition. The frequency of testing intervals should be based on the severity of illness, the presence of unstable trends in monitored parameters, and the presence of known or anticipated etiologies that cause rapid changes in acid–base status. It is important to: (1) draw blood samples only in the frequency and quantity needed, to prevent significant patient blood loss, (2) use lyophilized or minimal volume of anticoagulant to prevent dilution of the sample, and (3) run the tests with minimal delay from time of sample collection.

Diagnostic imaging

Diagnostic imaging will typically include plain thoracic and abdominal radiographs. Assessment of the lungs and pulmonary vasculature can aid in the assessment of respiratory acid–base changes. Should the lungs appear normal, changes in PCO₂ may reflect physiological compensation for metabolic acid–base disturbances. Normal lungs also suggest that the patient will probably be able to expire any additional CO₂ that is produced (such as after bicarbonate administration). Imaging of the heart may support the presence of heart disease, which could be a contributor to the acid–base disturbance or to a lack of response to therapy. A small vena cava and cardiac silhouette may indicate a hypovolemic state.

Ultrasound is used in evaluation of the heart, vessels, gastrointestinal tract, pancreas, spleen, liver, kidneys, and bladder. Abnormalities could support an underlying cause or demonstrate a serious consequence of an acid–base disorder.

Equipment‐based monitoring

In seriously ill patients, change in acid–base balance can be continuous and dynamic. The life‐threatening potential of the causes and effects of acid–base disorders necessitates POC testing and intensive monitoring. Monitoring intensity can be decreased when: (1) response to therapy is predictable and appropriate, (2) repeated results stabilize into favorable trends, and (3) the patient’s overall condition (not just acid–base status) is improving.

Blood pressure is monitored to detect alterations in cardiac output and peripheral vascular resistance, each potentially a cause or result of acid–base disturbances (see Chapter 3). End‐tidal CO₂ monitoring (ETCO₂) provides a continuous reflection of the PCO₂ in the blood (see Chapter 8). This can provide a direct indication of respiratory acidosis or alkalosis, whether it is physiological (compensatory) or pathological. During early recovery from cardiopulmonary arrest, a rise in ETCO₂ helps to confirm return to spontaneous circulation, restoration of oxidative metabolism, and clearance of acidity in the tissues as CO₂ is transported to the lungs for excretion.

Pulse oximetry (see Chapter 8) measures the oxygen saturation of hemoglobin (SpO₂), a major component of oxygen delivery (DO₂) and of the maintenance of oxidative metabolism. A significant decrease in SpO₂ and DO₂ can lead directly to anaerobic metabolism and severe lactic acidosis. It can also lead indirectly to a full spectrum of acid–base changes due to complete disruption of cellular physiology. Continuous electrocardiographic monitoring (see Chapter 11) can demonstrate changes in heart rate, rhythm, and electrical activity, which could cause acid–base abnormalities or result from changes in acid–base status. If a dysrhythmia disrupts cardiac output, the alteration in DO₂ can create global problems down to the cellular level.

The ability to continuously monitor many of the parameters of acid–base analysis (PO₂, PCO₂, glucose, electrolytes, lactate) is under development using subcutaneous probes that measure these analytes in interstitial fluid or intravascular probes that analyze blood. The technology is costly and of limited use at this time since many of the important parameters needed for complete acid–base analysis are not reported. Currently, the most useful continuous monitoring is ETCO₂ during anesthesia, ventilator therapy, or during treatment and recovery of cardiopulmonary arrest.

Disorders of pH, HCO₃⁻, and BE

As in all systems of acid–base analysis, pH is the final summation of all acid–base disturbances, metabolic and respiratory. Base excess and [HCO₃⁻] are parameters that sum the effects of all metabolic disturbances. Using the SQAB method, the standard BE is compared with the sum of the individual metabolic effects to unmask acid–base effects from unmeasured anions or cations. Since it is not a causative agent of acid–base change, [HCO₃⁻] is of little importance. It is included to compare the SQAB profile to HH analysis.

The plasma [H⁺] in dogs and cats is approximately 40 nmol/L, with cats normally slightly more acidic than dogs. In comparison, K⁺ is 100 000 times more concentrated than H⁺ in plasma; Na⁺ and Cl⁻ are 3 000 000 times more concentrated. One of the variables that alters hydrogen ion activity, and therefore pH, is temperature. Aqueous solutions are neutral when hydrogen ion equals hydroxyl ion, H⁺ = OH⁻. This occurs at pH = 7.0 when the temperature of the solution is 25 °C. However, at body temperature (37 °C), neutral pH = 6.8. Hydrogen ion activity increases with increased temperature and the pH is lower [1,15].

The pH range compatible with life (6.8–7.8; see Table 7.1) represents a 10‐fold difference in H⁺, a wider range than is tolerated with other important ionic species. However, because normal [H⁺] is so small (40 nmol/L), this range represents a change in H⁺ of only 0.000143 mEq/L. It is remarkable that the body can sense and adjust to such minute changes in H⁺ and that clinicians can successfully intervene, without doing more harm than good, when homeostatic mechanisms are overwhelmed by illness or injury.

There is accumulating evidence that increased extracellular H⁺ may be well tolerated and may even have a protective effect in some clinical situations. Permissive hypercapnia in the management of acute respiratory distress syndrome (ARDS) is a ventilator strategy that is considered to be beneficial to the patient when compared to the damage to the lung that may occur with greater tidal volumes and inspiratory pressures [16]. Acidemia may improve outcomes in ARDS patients and there is evidence that buffering respiratory acidosis may exacerbate the condition.

Animal studies have demonstrated that acidemia can protect myocardial and hepatic cells during hypoxia [17]. A lower pH increases the release of oxygen from hemoglobin, thereby increasing oxygen extraction by the tissues. In exercising athletes (with lactic acidosis and pH as low as 7.0), this mechanism can account for up to 60% of the oxygen available to the tissues. Experimental levels of arterial PCO₂ up to 1 atmosphere (750 mmHg) and intracellular brain pH of 6.2 have been tolerated in rats for 15 minutes without neurological impairment [17–19]. Acidemia has been found to attenuate inflammatory processes, including leukocyte superoxide formation, apoptosis of nerve cells, phospholipase A2 activity, expression of cell adhesion complexes, and xanthine oxidase activity [16,20,21].

Studies have shown, however, that the body reacts differently depending on the source of substances creating the acidemia. Cardiac myocytes show a faster increase in intracellular [H⁺] caused by increased PCO₂ compared to hydrochloric acid (HCl), a fixed acid. This increased acidity does decrease myocardial contractility, but it also decreases myocardial oxygen consumption that may have a short‐term protective effect. When brain acidosis is a result of CO₂ rather than HCl, there is less free radical production and less lipid peroxidation. Acidosis caused by CO₂, compared to acidosis from HCl, has an inhibitory effect on lactate production in the tissues [16,18,20,21].

At this early stage of our understanding of alkalemia and acidemia, the take‐home message is that alkalemia may be far more harmful than a comparable acidemia, and that a change in H⁺ activity is almost always less important than the underlying cause of the change.

Disorders of CO₂

An increase in PCO₂ >44 mmHg (hypercapnia) is also termed hypoventilation and creates a respiratory acidosis, with low pH, high H⁺, and a compensatory increase in HCO₃⁻. The development of respiratory acidosis can be classified as acute or chronic, which will subsequently influence the degree of metabolic compensation that has been demonstrated in dogs and cats (see Table 7.3) [22].

Respiratory acidosis may result from any disease process that can affect neuromuscular control of ventilation, loss of small or large airway integrity, or alveolar gas exchange. Common causes include large airway obstruction, respiratory center depression, increased CO₂ production, impaired alveolar ventilation, restrictive extrapulmonary disorders, parenchymal and small airway diseases, improper mechanical ventilation, and obesity. Clinical signs of respiratory acidosis may be more indicative of the underlying disease process than of the hypercapnia itself. These are typically more severe in patients with acute disorders (such as congestive heart failure, pneumonia) than in those with chronic, compensated respiratory disorders. Hypercapnia can also trigger cardiovascular changes such as tachycardia and vasodilation. Vasodilation can be of clinical significance in patients with intracranial disease; the increase in intracranial volume can cause a dramatic increase in intracranial pressure. Altered mentation is known to occur when PCO₂ is significantly elevated.

Treatment of respiratory acidosis is aimed at the underlying cause. Oxygen therapy is indicated in the treatment of hypoxemia caused by hypoventilation. In cases of airway obstruction, sedation, oxygen therapy, and airway management may be necessary to allow adequate ventilation. In some instances, mechanical ventilation may be required until the underlying disease process is corrected. Treatment with sodium bicarbonate or other alkalizing agents should be undertaken with extreme caution because, without mechanical ventilation, the patient may not be able to remove the CO₂ that is produced when these agents are metabolized [3,23–25].

A decrease in PCO₂ <36 mmHg (hypocapnia) is also termed hyperventilation and creates a respiratory alkalosis, with high pH, low H⁺ and a compensatory decrease in HCO₃⁻. The development of respiratory alkalosis can be classified as acute or chronic, which will subsequently influence the degree of metabolic compensation that may be expected (see Table 7.3) [24]. Respiratory alkalosis may result from any disease process that can increase alveolar ventilation above what is necessary to expire the CO₂ produced through normal metabolic processes. Common causes include hypoxemia, pulmonary parenchymal disease independent of hypoxemia, centrally mediated hyperventilation, overzealous mechanical ventilation, or situations that induce pain, fear, or anxiety. Treatment is aimed at addressing the underlying cause, and may include sedation, pain medications, and diuretics. Oxygen should be provided when hypoxemia contributes to respiratory alkalosis [24–26].

Disorders of Na⁺ or free water

Sodium is the major extracellular cation and exists in the ionic form in body fluids at any pH. The contribution that Na⁺ makes to the SQAB analysis is expressed in the formulas shown in Box 7.5.