Using blood gases in practice (Proceedings)

Blood gas, electrolyte and lactate analysis are very useful in management of the ill or injured dog or cat. Knowledge of normal values and what they indicate can help improve patient care and understanding of the pathophysiological changes accompanying critical illness.

Blood gas analysis

Blood gas analysis is a specialized method of evaluating the acid base and oxygenation indices in the blood stream. Blood gas analysis helps the clinician to better care for the individual patient through careful titration of fluids and supplemental oxygen AND imparts a better knowledge of underlying pathophysiology accompanying various diseases. Blood gases can be measured on venous or arterial blood. In fact, gas concentrations can be evaluated in any fluid that is run through a blood gas analyzer.

Historically, blood gas analysis has only been available at large referral or university hospitals, but in the last decade a variety of portable point-of care (POC) machines have become affordable and available in practices. The ISTAT (Heska-Fort Collins CO) model has been widely used and is generally considered accurate and user-friendly; the IRMA (ITC, Edison, NJ) is also popular. These devices (and other similar products) are able to measure blood gas values and other chemistries on small volumes of blood. Disposable cartridges make each test relatively economical and the turn-around time is excellent. Larger veterinary hospitals often used the Nova Biomedical Analyzer ( Nova- Waltham, MA). Other alternatives may include local human hospital or regional veterinary laboratories.

However, practically the only way an individual practitioner (or hospital)will be able to gain comfort in interpretation of blood gases is through frequent analysis of samples from a variety of patients. This is much less likely to be done if a machine is not available in-house. Most practice managers and clinicians rapidly determine that despite the initial purchase cost, the benefits of better patient care and improved revenue are quickly realized. Additionally, patient care is often optimized and there appears to be improved job satisfaction!

Blood gas samples can be either from a central vein (or rarely the pulmonary artery) or a peripheral vein. Arterial samples are typically collected from the dorsal pedal artery or the femoral artery. Samples may also be collected from indwelling arterial or venous catheters. In healthy pets, there is little variation from samples collected from various venous sites, but in patients with cardiovascular compromise the differences can be outstanding (eg. And clinically significant!) . (due to differences in oxygen extraction).

Arterial samples will "gush" from the catheter!

Using blood gas analysis

The first area in which blood gases are useful are in the assessment of acid-base balance. The following guidelines have been adapted from the references and serve as the recommendation for interpretation from the American College of Veterinary Emergency and Critical Care.

Normal values

pH= 7.36-7.44

PC02= 36-40mmHg

HCO3=20-24 mEq/l

BE = ± 4

PO2= 90-100 mmHg

Disturbance                              Clinical guidelines for compensation

Metabolic Acidosis                      Each 1 mEq/L decrease in HCO3 will decrease PCO2 by 0.7 mmHg

Metabolic Alkalosis                      Each 1 mEq/L increase in HCO3 will increase PCO2 by 0.7 mmHg

Respiratory ccidosis

Acute: Each 1 mmHg increase in PCO2 will increase HCO3 by 0.15 mEq/l

      Chronic: Each 1 mmHg increase in PCO2 will increase HCO3 by 0.35 mEq/l

Respiratory alkalosis

Acute: Each 1 mmHg decrease in PCO2 will decrease HCO3 by 0.25 mEq/l

      Chronic: Each 1 mmHg decrease in PCO2 will decrease HCO3 by 0.55 mEq/l

When a patient has a simple disorder with appropriate compensation it is described with the following terms. The implication is that the phrase conveys that compensation is occurring. For example, in a dog with a HCO3 of 14 mEq/l if the PCO2 is 33mmHg, the acid-base disorder may be described as simply "metabolic acidosis". If the appropriate compensation has not occurred, this suggests the presence of a mixed acid base-disturbance.

Typical metabolic changes that are commonly observed common disease in veterinary patients include metabolic acidosis- renal, hypoperfusion (lactate), diabetic ketoacidosis

Metabolic alkalosis- high gi obstruction, profound hypokalemia

Respiratory acidosis- loss of central drive, airway obstruction

Respiratory alkalosis- fever, anxiety, pleural space disease

Blood gases are also useful for evaluation of oxygenation. Oxygen levels should always be interpreted in light of the PCO2 level and also the inspired oxygen concentration. It is also important to remember that even though an arterial blood gas analysis may reveal normal PaO2 levels, this does not imply normal oxygen delivery to tissues. The PaO2 is an indicator of arterial oxygen tension. Adequate oxygen delivery is dependant on normal cardiac function, normal hemoglobin concentrations and the affinity which exists between oxygen and hemoglobin.

Oxygen content of blood is calculated by the following equation

O2 content (ml O2/100ml blood) = (1.34 x Hb x Sat/100) + 0.003 PO2

Where Hb is hemoglobin concentration in gm/100ml, Sat is the percentage saturation of hemoglobin, and PO2 is in mmHg.

Respiratory failure may be associated with diseases such as pneumonia, pulmonary edema, pulmonary thromboembolism, and acute respiratory distress syndrome. These diseases cause impairments in ventilation and gas exchange and it is important to assess these before establishing a therapeutic course. Failure of gas exchange typically causes hypoxemia (lowered arterial oxygen tension) with blood CO2 levels often within normal limits. The patient's response to hypoxemia may be to hyperventilate, thus decreasing the PaCO2. Hypoventilation results in carbon dioxide retention and hypoxemia.

Blood gases are neither sensitive nor specific to changes in the efficiency of gas exchange because they are influenced by changes in ventilation and by extra-pulmonary factors such as perfusion abnormalities that alter mixed venous O2 and CO2 tensions. The alveolar-arterial oxygen gradient is a derived calculation which may be used to negate the effect of nonpulmonary factors on evaluation of the efficiency of gas exchange using PaO2 values.

The alveolar-arterial O2 gradient will increase with pulmonary pathology. A normal alveolar-arterial O2 gradient (0 – 10mmHg) exists due to a degree of ventilation/perfusion mismatch and shunting in normal individuals. A significantly increased alveolar-arterial O2 gradient (>30mm Hg) may be consistent with severe disease and Adult Respiratory Distress syndrome, and implies increased morbidity and mortality. The alveolar-arterial O2 gradient is unreliable in evaluation of gas exchange efficacy in the presence of oxygen supplementation.

The alveolar-arterial oxygen gradient may be calculated to detect ventilation-perfusion mismatch by the following formula:

A-a gradient = (150-pCO2/0.8) – PaO2

This equation is accurate at sea level with 21% inspired oxygen)

The calculation of the ratio of PaO2/ FiO2 is useful in assigning severity of lung injury/disease. A normal value is greater than 350, while a value of less than 200 is considered supportive of acute respiratory distress syndrome (ARDS) and a value of less than 300 is considered supportive of acute lung injury (ALI).

      Electrolytes

Electrolytes disturbances are very common in critical care, and typically reflect either the primary underlying disease or the body's response to that disease. Patients developing hypernatremia in the hospital have a worse prognosis that those with normonatremia. Specific electrolytes that are important in medicine include sodium, potassium and chloride. I would strongly encourage any e/cc clinician to read Rose's Clinical Physiology of Acid Base and Electrolyte Disturbances. I think this one of the best books written – good style, good example etc and even fun for recreational reading.

Sodium

Sodium levels are perhaps one of the most underutilized tools in veterinary medicine. Sodium is the principal determinate of plasma osmolarity, with hypernatremia and hyponatremia almost invariably associated with hyper and hypo-osmolarity. It is essential to remember that changes in sodium levels reflect changes in water balance (with the exception of the salt poisoned pig!). The kidneys play a vital role in excreting dilute or concentrated urine. Thus, the development of hyper or hyponatremia requires answering both the questions "Why did this occur in the first place" and "Why has abnormality been maintained?"

Common differentials for hyponatremia include 1) decreased effective circulating volume 2) diuretics and 3)renal failure, although other causes may potentially exist as well. Decreased effective circulating volume (DECV) is probably the most important and most common cause of hyponatremia in the E/CC setting. DECV can represent either true or perceived hypovolemia. True hypovolemia may accompany severe volume losses (eg pu/pd, including diabetes, vomiting and diarrhea) or relative hypovolemia (decreased perfusion to tissues-eg pericardial effusion, ascites, CHF). DECV predisposes a pet to the development of hyponatremia primarily by stimulating ADH to appropriately trigger water retention in an attempt to improve perfusion. Additionally, decreasing GFR and increasing proximal tubular sodium and water reabsorption decreasing the amount of fluid delivered to the diluted segment of the nephron. This is likely of less significance. Hyponatremia is a marker of a relatively serious disease as osmolarity is tightly controlled. Syndrome of Inappropriate ADH secretion (SIADH) is syndrome that is widespread in people and likely animals. However, it has rarely been reported in companion animals. (Brofman PJ, Knostman KA, DiBartola SP. Granulomatous amebic meningoencephalitis causing the syndrome of inappropriate secretion of antidiuretic hormone in a dog. J Vet Intern Med. 2003 Mar-Apr;17(2):230-4) SIADH is characterized by the non-physiological release of ADH and the impaired water excretion with normal sodium excretion. It is characterized by low sodium and hypo-osmolarity, high urine osmolarity with a urine sodium of > 40 meq/L, normovolemia with normal acid-base balance, renal, adrenal and thyroid function.

Treatment of hyponatremia is directed at the underlying cause. Fluid therapy, paracentesis, therapy for CHF and rarely with hypertonic solutions are all potentially indicated based upon the underlying cause. While uncommon, it is also important to exclude pseudohyponatremia which may occur as a result of severe hyperlipidemia, hyperproteinemia, or hyperglycemia.

Hypernatremia is also frequently seen in the e/cc setting. Hypernatremia almost invariably represents the lack of free water rather than too much salt. Causes for hypernatremia include excessive water losses and the inability to drink and to adequately concentrate the urine. Thus, on hot day, a dog may lose a large volume of water through panting, but is easily able to replace those losses if permitted free access to water. Recently, paintball ingestion which results in marked osmotic diarrhea has been reported as a cause of significant (> 165 meq/l) hypernatremia. The development of hypernatremia has been associated with a negative outcome in cats and dogs. (Waldrop J.et al. Hypernatremia in Cats and Dogs, IVECCS 2003) Other clinically significant causes for the development of hypernatremia include 1)lack of access to water, particularly in a dog with a prior history of PU/PD- 2x main fluid problem 2) Lactulose therapy in a presumed HE dog- massive water losses, inadequate "ins" and 3) Chronic therapy with a replacement fluid (eg LRS, plasmalyte A) in a pet with renal failure (inability to secrete a non-isothenuric urine coupled with obligate free water losses. Hypernatremia that develops rapidly should be corrected rapidly. However, during long-standing hypernatremia there is a formation of osmolytes (aka idiogenic osmoles) such as inositol, taurine, glutamine and glutamate that act to buffer the brain against volume depletion. Therefore, if long-standing hypernatremia is corrected too rapidly, cerebral edema may result. Proposed time frame for correction of chronic hypernatremia in on order of 0.5 meq/l/hr.

Lactate analysis has been promoted as a marker of global hypoperfusion as an indicator of anaerobic metabolism. As you may recall from biochemistry, lactate is produced as a by-product of anaerobic metabolism from glycolysis. Anaerobic metabolism is much less efficient at the generation of ATP than is aerobic metabolism. It is important to recall some distinctions in definitions and that lactate and lactic acid are not the same thing. Elevated blood lactate is called hyperlactatemia and may or may not be associated with lactic academia. (Blood pH < 7.35 in the presence of hyperlactatemia).

Elevated blood lactate occurs when the rate of lactate production exceed that of lactate clearance. The most clinically important cause of elevated lactate in dogs is hypoperfusion. However, dogs (and cats) may also develop hyperlactatemia from moderate to strenuous exercise, seizures or struggling from relative tissue hypoxia. In some cases, elevated lactate (referred to as Type B) may result from other conditions not related to hypoperfusion such as diabetes, lymphoma or certain drugs.

In our hospital, we use lactate measurements as an objective form of support for clinical examination. Most, if not all, dogs that look hypoperfused have elevated lactates. The rate of fall of lactate values seems to correlate with reversal of hypoxic conditions. Lactate assessments can also help provide security for newer technicians or clinicians as high lactates should prompt rapid assessment, while normal lactate levels may provide some assurance of adequate oxygen delivery. However, animals can still worsen and die despite normal lactates, so staff members should be counseled that vital signs and careful monitoring are still vital to good patient outcome.