INTRODUCTION

Perhaps Rawson and Quinlan said it best when they asserted that, “the interpretation of blood gas analysis may be very difficult because it requires an understanding of not only the physiology of acids and bases, but also the physiology of ventilation and gas exchange, the dynamics of electrolyte and water movement, plasma composition, and the renal mechanisms of hydrogen ion, electrolyte and water excretion.”¹ Blood gas analysis is, however, an invaluable tool for assessing the physiologic status of critically ill patients. It is necessary, therefore, to develop a method for efficiently and effectively evaluating this information to treat the patient appropriately.

Although a thorough description of acid-base regulation and blood gas analysis is beyond the scope of this chapter (the reader is directed to several excellent references for a more detailed description of these subjects^2-9), what follows is a brief overview of acid-base physiology and a practical method of interpreting blood gases (see Chapter 59, Acid-Base Disturbances).

HYDROGEN IONS

The proton is one of the basic chemical units of matter. The term proton has become synonymous with the term hydrogen ion or H⁺ in medical physiology. This electrolyte is the end product of many metabolic processes within the body and the normal H⁺ concentration ([H⁺]) in the extracellular fluid is maintained at around 40 nanoequivalents per liter. Comparatively, the normal concentrations of most physiologically important electrolytes (e.g., Na⁺, K⁺, Ca²⁺, Mg²⁺, Cl⁻, ) are present in the body in the range of milliequivalents per liter.

Although hydrogen ion concentration [H⁺] is one millionth the concentration of other electrolytes in the body, its regulation is of paramount importance to normal homeostasis. Hydrogen ions are highly reactive and therefore readily interact with dissociable moieties on proteins. Because proteins play a major role in all biologic functions, alterations in protein structure or function as a result of changes in [H⁺] within the body can have catastrophic effects on biologic homeostasis.

HENDERSON-HASSELBACH

In the early 1900s, L.J. Henderson revolutionized the study of acid-base physiology by noting that CO₂ (a primary end product of cellular metabolism) combines with H₂O in the presence of carbonic anhydrase to form H₂CO₃ (carbonic acid). This acid will then further dissociate into its conjugate base, bicarbonate (), and H⁺:

By applying the laws of mass action and because H₂CO₃ exists in equilibrium with dissolved CO₂, Henderson substituted the value of dissolved CO₂ in his equation. Thus:

This equation had major implications because it not only described one of the first known buffer pairs (H₂CO₃ and ), but also illuminated a process by which the body could buffer changes in H⁺ load, namely ventilation. Later Hasselbach would add further utility to the equation by substituting the partial pressure of CO₂ in blood (PCO₂) for dissolved CO₂ and applying Sorenson’s concept of pH (the negative logarithm of [H⁺]) by putting the equation in logarithmic notation:

where pKa = the logarithm of the ionization constant K_a for H₂CO₃, and SC = the solubility coefficient of CO₂ in blood (0.03).

This is the classic Henderson-Hasselbach equation.

Regulation of pH

On a daily basis, pH changes within the body are opposed by multiple complex processes which, for the sake of simplicity, can be presented as (1) the actions of intracellular and extracellular buffering systems (chemical buffering), (2) modulation of ventilation (physiologic buffering), and (3) renal clearance. All body fluids contain buffer systems. Of these systems, hemoglobin, phosphate, protein (predominately intracellular buffers), bone, and (predominately extracellular buffer), the system is of utmost importance. The reasons are twofold. Not only is the buffering system capable of responding to an acute change in [H⁺] within seconds of an acid load, but its role in the equilibrium equation allows changes in pH to be further modulated by changes in ventilation. This “open system” greatly enhances the buffering capacity of the system and is capable of buffering changes in pH within minutes of an acid or alkali load. Finally, the kidneys play a major role in maintaining pH by increasing or decreasing acid elimination in the urine. This system takes hours to days to reach completion, but is the most capable of all the processes for returning the body’s pH to normal.

BLOOD GAS ANALYSIS: GETTING STARTED

Although blood gas analysis may be performed on venous blood (see Venous Blood Gases later in this chapter), arterial blood gas analysis yields information about oxygenation as well as ventilation and acid-base disorders and is preferentially performed, when possible. There are several potential sites for arterial puncture (the dorsopedal artery, the digital artery in the front paw, the auricular artery, the lingual artery, the femoral artery). However, the dorsopedal artery is chosen most often because of its size, superficial location, and ease of ensuring adequate hemostasis.

A small amount of local anesthetic such as 0.05 to 0.1 ml of 2% lidocaine injected subdermally 2 to 3 minutes before sampling may aid in restraint. An arterial catheter may allow for repeated blood gas sampling with less stress for the patient. Blood should be drawn into a syringe coated with sodium or lithium heparin (1000 U/ml), keeping in mind that heparin is acidic and excessive amounts in the syringe may have a detrimental effect on blood gas values.¹⁰ Any air bubbles should be expelled from the sample, and the sample corked or attached to a stopper to prevent further exposure to room air, which could decrease the sample’s PCO₂ to zero and sample partial pressure of oxygen (PO₂) level to that of room air (150 mmHg at sea level).¹⁰ The sample should be analyzed immediately or held in an ice- water bath at 4° C (up to 2 hours) to minimize the effects of cellular metabolism on sample pH, PCO₂, and PO₂.¹¹

Temperature Correction

Whether or not to correct blood gas values for temperature remains a controversial subject in both human and veterinary medicine. The issue centers around the hypothesis that as temperature changes, blood gas solubility also changes, and blood gas values may be altered as well. The pH-stat strategy suggests correcting blood gas values for patient temperature and maintaining the corrected values within accepted norms for pH and PCO₂. The α-stat strategy assumes that hemoglobin’s buffering capacity, which is related to the ionization of the imidazole group of histidine residues, is not affected by temperature changes. Under these circumstances there would be no need to temperature correct blood gas values.

According to the literature, most attempts at critically applying one strategy over the other have been performed in the context of providing improved neurologic outcomes in human patients after coronary artery bypass surgery and have shown differing and confounding results.^12,13 There is no clear indication that routine temperature correction in the clinical setting is necessary. It is up to the clinician, therefore, to decide which strategy seems most reasonable and apply that strategy consistently to serial sampling.

Step-by-Step Acid-Base Analysis

Table 208-1 shows normal arterial blood gas values in dogs and cats.^14,15 As pH varies inversely with [H⁺], any process that increases H⁺ load will decrease pH and produce acidosis. Conversely, any process that decreases [H⁺] will tend to increase pH and produce alkalosis. The terms alkalemia and acidemia imply that blood pH is outside the normal range, which may or may not be true depending on the nature of the acid-base disorder and the effectiveness of organism’s compensatory mechanisms.

Table 208-1 Normal Arterial Blood Gas Values for Dogs and Cats^14,15

	Dog	Cat
Parameter	Value	Value
pH	7.39 ± 0.03	7.39 ± 0.08
PaCO₂ (mm Hg)	37 ± 3	31 ± 6
PaO₂ (mm Hg)	102 ± 7	107 ± 12
(mEq/L)	21 ± 2	18 ± 4
Base excess (mEq/L)	−2 ± 2	−2 ± 2