Blood Gas Interpretation & Acid-Base Balance

• Blood gas interpretation is critical for assessing a patient's respiratory and acid-base status.

Learning Objectives

• Understand the physiology behind acid-base balance
• Describe the pathology of acidosis and alkalosis
• Know why and what a blood gas sample determines
• Explain how to obtain an arterial sample in different species
• Interpret primary blood gas disturbances using normal value ranges
• List factors affecting the accuracy of arterial samples
• Calculate the arterial oxygen content using the appropriate equation

Homeostasis

• Maintaining constant internal body conditions through dynamic equilibrium.
• Lungs, kidneys, and liver/GI regulate homeostasis
• Individual differences in CO2 and H+ production vary by species, diet, metabolic rate, protein levels, strong ions, and body temperature.
• Carnivores produce CO2 and H+ precursors.
• Herbivores produce CO2 and HCO3- precursors.

Mechanisms to Buffer H+

• Chemical buffers like bicarbonate act extracellularly within seconds.
• Phosphate, hemoglobin, and proteins are intracellular buffers, working within 2-4 hours.
• The respiratory system adjusts the respiratory pattern based on H+ and pCO2 levels within minutes to hours, via chemoreceptors.
• Renal system eliminates H+ through urine excretion, taking hours to days.

Henderson-Hasselbalch Equation

• pH = pKa + log([HCO3-] / [0.0301 * pCO2]).
• 7.4 = 6.1 + log([24] / [0.0301 * 40]).
• The equation relates pH to the bicarbonate buffer system components.
• Acid-base disturbances instantly reflect in buffer components and their ratio.
• The ideal HCO3-:pCO2 ratio is 20:1.
• Diagnosis and treatment approaches for acid-base disorders rely on this equation.

Primary Disturbances and Compensation

• Metabolic acidosis involves decreased pH and HCO3-, with compensatory decrease in CO2.
• Metabolic alkalosis involves increased pH and HCO3-, with compensatory increase in CO2.
• Respiratory acidosis involves decreased pH and increased CO2, with compensatory increase in HCO3-.
• Respiratory alkalosis involves increased pH and decreased CO2, with compensatory decrease in HCO3-.
• Red arrows indicate the primary disturbance.

Mixed Disturbances

• Mixed disturbances involve two separate primary disorders occurring simultaneously.
• pCO2 and HCO3- change in opposite directions.
• Normal pH can occur with abnormal pCO2 and/or HCO3-.
• pH change goes in the opposite direction of what is predicted for the primary disorder.
• Disorders can have neutralizing or additive effects on pH.
• A triple disorder can include metabolic acidosis, metabolic alkalosis, and either respiratory acidosis or alkalosis.

Alternative Diagnostic Methods

• Stewart's approach uses "independent variables."
• Independent Variables include PCO2, strong ion difference (SID), and total concentration of nonvolatile weak acids (ATOT).
• Strong ion difference (SID) involves Na+, K+, Cl-, Ca+2, Mg+2.
• Stewart's approach is informative if mixed acid-base disorders and electrolyte imbalances co-exist.

Causes of Respiratory Acidosis

• Pleural space disease, pneumothorax, severe pulmonary disease.
• Upper airway obstruction
• Neurologic disease (central or peripheral)
• Anesthetic drugs and equipment dead space.
• Decreased functional residual capacity.
• Examples are: pregnancy or full stomach/rumen.
• Malignant hyperthermia
• Cardiopulmonary arrest

Causes of Respiratory Alkalosis

• Pain, fear, anxiety, stress.
• Hypotension, low cardiac output.
• Sepsis or SIRS.
• Pulmonary thromboembolism.
• Overzealous IPPV.
• Respiratory disease.
• Hypoxemia.
• Fever/hyperthermia.
• Severe anemia.

Metabolic Acidosis Causes

• Vomiting, diarrhea
• Renal loss of HCO3- or H+ retention
• IV nutrition
• Dilutional acidosis
• Ammonium chloride
• Hypomineralocorticism

Causes of Metabolic Alkalosis

• Vomiting due to pyloric obstruction
• Hypochloremia and hypokalemia
• Furosemide
• Hypermineralocorticism
• Contraction alkalosis

Consequences of Acidosis

• Impaired cardiac contractility and response to catecholamines.
• Decreased cardiac output, renal, and hepatic blood flow results.
• Ventricular arrhythmias or fibrillation may occur.
• Arterial vasodilation and venous constriction centralize blood that causes pulmonary congestion volume.
• Shifts the oxygen-hemoglobin curve to the right with delivery of O2 to tissue.
• Insulin resistance occurs, impairing glucose uptake.
• Hyperkalemia occurs with transcellular shift.
• Increased iCa2+
• CNS depression and coma
• Osteodystrophy and hypercalciuria

Consequences of Alkalosis

• CNS signs like agitation, disorientation, stupor, coma.
• Seizures or tetany due to hypocalcemia (rare)
• Hypokalemia from transcellular shifting causing muscle weakness, cardiac arrhythmias, GI motility disturbances, and altered renal function.
• Shifts the oxygen-hemoglobin curve to the left, which impairs oxygen release from hemoglobin initially.

The need for blood gas analysis

• Excellent for monitoring respiratory and acid-base status, as well as electrolytes and lactate.
• Treatment can be quickly tailored to blood gas results.
• Can be performed on awake and anesthetized patients using arterial or venous samples.
• Equipment is becoming affordable for general practitioners.

Arterial vs Venous Blood Gas

• Arterial samples evaluate respiratory gas exchange.
• Venous samples are useful in determining acid-base status.
• Venous blood pH is slightly lower and pCO2 is higher than arterial blood due to local tissue metabolism.

Arterial Sample Identification

• PaO2 approximately 80-110 mmHg on room air or ~500 mmHg on 100% O2.
• SaO2 > 88%.
• Bright cherry red color.
• Pulsatile flow, with arterial waveform if a catheter is the source.

Venous Sample Characteristics

• PvO2 ~ 35-45 mmHg regardless of FiO2.
• SvO2 65-75%
• Darker color of red.
• No pulsatile flow, and no arterial waveform present.

Obtaining a Blood Sample

• Clip and clean the site.
• Use a dry lithium heparin syringe or heparinize a 1-3 mL syringe with a 22-25 g needle.
• Aspirate air and rapidly expel a few times before filling with ~1 mL of blood.
• Get rid of any air bubbles quickly and analyze the sample immediately (30 minutes.
• Apply pressure to the sampling site to prevent hematoma formation.

Arterial Blood Gas Measurements

• Analyzers directly measure pH, oxygen partial pressure(PO2), and carbon dioxide partial pressure (PCO2).
• Analyzers calculate HCO3-, BE, and SaO2.

Blood Gas Values

• pH reflects the balance between acid/base in the body and H+ concentration.
• The equation for blood pH is pH = log (1/[H+]).
• One unit change in pH causes a 10-fold increase or decrease in [H+].
• The pH of 6.8-7.8 is compatible with life
• PaO2 indicates oxygen molecules dissolved.
• They are dissolved in the plasma phase of an arterial sample (i.e. not bound to Hb), depends on FiO2 and barometric pressure.
• PaCO2 reflects the respiratory component of acid-base balance and identifies if the patient is hypocapnic, hypercapnic, or eucapnic.
• PaCO2 is inversely related to alveolar ventilation.

Bicarbonate (HCO3-)

• It is part of the bicarbonate-carbonic acid buffering system.
• Bicarbonate is responsible for regulating the pH of body fluids.
• Acts as an immediate buffer when fixed acids enter the blood.
• It facilitates carbon dioxide transport from body tissues to the lungs.
• Changes in respiration rate will alter the bicarbonate-carbonic acid ratio and pH.
• Bicarbonate assessment reflects the metabolic component of acid-base status.

Total Carbon Dioxide (TCO2)

• Measure of carbon dioxide gas in the plasma.
• TCO2 Consists of 85% bicarbonate, 10% carbonic acid, and 5% dissolved CO2.

Base Excess (BE)

• The amount of strong acid or alkali needed to titrate 1L of blood.
• The blood needs to measure at a pH of l7.4 at 37°C, partial pressure of CO2 is constant at 40 mmHg.
• Base excess/deficit value does not change in venous or arterial blood sample.
• Base excess indicates metabolic alkalosis.
• Base deficit indicates metabolic acidosis.
• Used in the bicarbonate therapy calculation: mEq to infuse = base deficit x kg of BW x 0.3
• Infuse 1/3 of the total volume over 20 minutes before reassessing acid-base status.
• Bicarbonate therapy is controversial due to side effects such as paradoxical cerebral acidosis.
• Mild BE = ± 5
• Moderate BE = ± 10-15
• Severe BE = > 15

Oxygen Saturation (SaO2)

• The percentage of heme-binding sites saturated with oxygen.
• SaO2 is a calculated value based on the oxygen hemoglobin dissociation curve and PaO2 from an arterial sample.

Normal Arterial Blood Values

• pH is 7.35-7.45 (~7.4)
• PaCO2 is 35-45 mmHg (~40)
• PaO2 is 80-110 mmHg (room air) (~104)
• HCO3- is 15-25 mmol/L (carnivore) or 20-28 mmol/L (herbivore) (~24 ± 4)
• BE is 0 ± 4 mmol/L
• SaO2 is 95-100% (= ≥95%)
• Lactate is < 2.0 mmol/L; increasing values indicate a perfusion issue

Blood Gas Interpretation Steps

• Determine if the sample is arterial or venous.
• SaO2 > 88% suggests arterial, SaO2 < 88% suggests mixed sample, venous sample, or pulmonary disease.
• Determine the acid/base status.
• Normal pH is 7.35-7.45.
• Acidemia is pH < 7.35.
• Alkalemia is pH > 7.45.
• Assess ventilatory status using PaCO2 which assesses ventilation.
• Hypoventilation = increased PaCO2.
• Hyperventilation = decreased PaCO2.
• Assess oxygenation by the Alveolar-arterial (A-a) O2 gradient.
• A-a gradient = [(barometric pressure - 47)0.21] - (P2CO2/0.8) - PaO2
• PaO2:FiO2 ratio use: patient is on an FiO2 > 0.21. Use to compare arterial samples when the PaCO2 is stable.
• Determine the Anion Gap by using the equation AG = (Na+ + K+) – (HCO3¯ + Cl-) = UA- - UC
• AG is composed of phosphate, sulfate, plasma proteins, and organic acid anions.
• Normal AG varies based on the animal (dogs 12 to cats 27), can also increase the change of developing metabolic acidosis.

A-a O2 Gradient

• Normal = 0-10
• Probably Normal = 11-20
• ARDS? = 21-30.
• ARDS = >30

PaO2:FiO2 Ratio Interpretation

• Greater than 400 is normal pulmonary function
• 200-400 is due to decreased pulmonary function
• often V/Q mismatch under anesthesia
• Less than 200 is severe pulmonary dysfunction/ARDS

Anion Gap

• Normal is 12-24 mEQ/L for dogs
• Normal is 13-27 mEq/L for cats
• Increased AG points identifying the cause of metabolic acidosis.

Accuracy of Blood Sample

• Air bubbles in blood sample increase PaO2 and decrease PaCO2.
• Excess heparin in blood sample decreases pH.
• Use specialized syringes like lithium heparin, if electrolytes are checked.
• <0.1 ml is needed for use with 2ml of blood.
• Delaying analysis decreases PaO2, increases PaCO2, and decreases pH.
• Blood clots in a blood sample will result in hemolysis
• Syringe Type- glass preferred over plastic when analyzing a blood sample.
• Temperature and barometric pressure impact the test.
• Hyperthermia brings lower values of PaO2 and PaCO2.
• Hypothermia elevates values of PaO2 and PaCO2.

Hypoxemia vs Hypoxia

• Hypoxemia is the decrease of of PaO2, SaO2, hemoglobin content.
• If PaO2 is < 60 mmHg and/or SpO2 < 90% .
• Hypoxia = general term for impairment of oxygen delivery to the tissue.
• Hypoxemia is one type of Hypoxia.

Causes of Hypoxemia

• Ventilation/perfusion (V/Q) mismatch which is the more common cause.
• Hypoventilation
• Low FiO2
• Right to left shunt
• Diffusion impairment

V/Q Mismatch

• Neoplasia
• Pulmonary edema
• Pneumonia