GASP! OXYGENATION, VENTILATION, AND BLOOD GAS MANAGEMENT IN ANESTHETIZED PATIENTS Kim Spelts, BS, CVT, VTS

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1 GASP! OXYGENATION, VENTILATION, AND BLOOD GAS MANAGEMENT IN ANESTHETIZED PATIENTS Kim Spelts, BS, CVT, VTS ANESTHESIA Providing adequate oxygen delivery and maintaining tissue perfusion is key in maintaining homeostasis in anesthetized patients. Oxygen delivery is not directly measureable, and it is a function of cardiac output and arterial oxygen content: DO 2= CO x C ao 2. Therefore, to improve oxygen delivery, one must increase the patient s cardiac output and/or increase the arterial oxygen content. Arterial oxygen content is a function of the patient s total hemoglobin, hemoglobin saturation, and the partial pressure of oxygen dissolved in arterial blood: C ao 2= (Hb x 1.34 x S ao 2) + (P ao 2 x 0.003). Cardiac output is a function of heart rate (HR) and stroke volume (SV), which in turn is a function of preload, afterload, and cardiac contractility: CO = HR x SV. Prior to induction, the anesthetist must set up a properly functioning machine and breathing circuit and gather the tools necessary to adequately manage the patient s airway. This includes a rebreathing or nonrebreathing circuit, a reservoir bag, endotracheal tubes, a laryngoscope, and a mask for providing preoxygenation. Size selection of the equipment should be based on the goal of minimizing resistance and dead space while also being able to achieve an adequate seal in the trachea. Preoxygenation for three to five minutes prior to the administration of induction drugs helps to replace nitrogen in the lungs with oxygen, which greatly reduces the risk of hypoxemia that can result from the respiratory depressive effect of most induction drugs. Rapid control of the airway is best achieved with proper patient positioning and restraint as well as the use of a laryngoscope. The laryngoscope assists the anesthetist in visualizing the airway, reducing the risk of esophageal intubation, as well as reducing the risk of laryngeal irritation and damage. Once endotracheal (ET) intubation is achieved, confirm the placement of the tube by using another ET tube to measure from the patient s thoracic inlet (~ point of the manubrium) to the canine teeth. A tube that is placed too far in may result in one-stem bronchial ventilation, atelectasis, and hypoxemia. A tube that is not placed in far enough results in increased dead space and breathing resistance. Secure the tube and place enough air in the cuff to create a seal that does not leak until cmh 2O pressure is reached on the anesthesia machine s pressure gauge during the administration of a manual breath. Keep the oxygen flow rate high immediately after induction to increase the rate of change of inhalant level in the circuit and the patient; this allows for a more rapid achievement of adequate anesthetic plane. Once homeostasis is achieved, oxygen flow should be administered at ~ 30 ml/kg/min on a circle (rebreathing) circuit or 200 ml/kg/min on a nonrebreathing circuit. Keep in mind that these rates are much higher than the actual metabolic requirement of oxygen (4 6 ml/kg/min). An oxygen flow rate that is too high increases anesthetic waste (which increases the cost), and greatly contributes to the development of hypothermia. An oxygen flow rate that is too low results in a slower change of anesthetic plane when the vaporizer setting is changed, and may result in rebreathing of carbon dioxide on nonrebreathing circuits. Respiratory Monitoring Complications arising from a patient s inability to ventilate adequately are common and are not always evident by simply observing the movements of a patient s chest and abdominal wall. Capnometry and pulse oximetry are two methods available to help assess the quality of a patient s ventilation. Capnometry Capnometry is the measurement of a patient s exhaled carbon dioxide (end-tidal CO 2, or ETCO 2). A capnogram can give the anesthetist valuable information related to a patient s ability to exchange oxygen and carbon dioxide during ventilation. A sudden, rapid decrease in exhaled CO 2 can indicate pulmonary embolism and/or cardiac arrest. Changes in the baseline, upstroke, plateau, and/or downstroke of the capnogram are indicators of a variety of mechanical and physiological problems, such as inadequate oxygen flow, kinked or inadequately sealed ET tube, bronchospasm, and bronchial secretions.

2 Elevated ETCO 2 is common under anesthesia. Anesthetic agents depress the respiratory center in the central nervous system (CNS), so patients often hypoventilate even in the presence of elevated levels of CO 2 in the blood. Some patients may not be able to fully expand their chests due to surgical positioning, body conformation, or obesity. Elevated ETCO 2 may also be caused by an inability to fully expand the lungs due to atelectasis, diaphragmatic hernia, or underlying pulmonary disease. Decreased ETCO 2 may be caused by hyperventilation, usually the result of a light plane of anesthesia. It may also be an indicator of decreased cardiac output, which could cause a decrease in gas exchange in the lungs. Increased dead space (gas flow, but no gas exchange) can also result in a decrease in expired CO 2. Pulse Oximetry Pulse oximetry is a measurement of the percentage of hemoglobin saturated with oxygen (SpO 2). SpO 2 can give an indication of the partial pressure of oxygen in arterial blood (P ao 2), although under anesthesia a normal SpO 2 may not necessarily indicate adequate ventilation given the fact that the patient is on 100% oxygen (according to the oxygen-hemoglobin dissociation curve, an SpO 2 >95% only indicates a P ao 2 >80 mmhg). Hypoxemia (SpO2 <90% and/or P ao 2 <60 mmhg) can result from the following conditions: Low inspired oxygen This is generally not a problem under anesthesia, since patients are usually intubated and receiving 100% oxygen. Hypoventilation Again, hypoventilation under anesthesia does not normally result in hypoxemia. However, hypoventilation can become dangerous during the recovery period if a patient is breathing room air (21% oxygen). RL shunt The shunting of unoxygenated blood into systemic circulation is not something that can be controlled under anesthesia, and unfortunately it is not remedied by increasing the inspired oxygen content. Diffusion impairment Some disease processes (such as pulmonary edema) impair the diffusion of gases across the capillary-alveolar membrane. Ventilation-perfusion (V/Q) mismatch This is the most common cause of hypoxemia during the perianesthetic period. Common causes include decreased cardiac output (poor perfusion), atelectasis (poor ventilation), positioning (weight of viscera in dorsal recumbency my impede chest expansion), and patient conformation (deep chest, obese, etc.). In some cases, the administration of intermittent positive pressure ventilation (IPPV) may be indicated to correct abnormalities in ventilation and oxygenation (e.g., hypoventilation, increased ETCO 2 and PaCO 2, V/Q mismatch). If utilizing a mechanical ventilator, calculate a tidal volume (V T) ml/kg. Adjust the tidal volume and ventilation rate to achieve a peak inspiratory pressure (PIP) of cmh 2O and an ETCO 2 of mmhg. Some patients may require a higher PIP in order to adequately overcome a V/Q mismatch and improve their oxygenation. Keep in mind that the introduction of positive pressure into the thorax decreases venous return to the heart and therefore may decrease cardiac output, which in turn can make the V/Q mismatch worse. Proper management of a patient s hemodynamic status is crucial in this case. Blood Gas Management In anesthetized patients, especially those who are critically ill, maintaining proper acid-base and electrolyte balances is crucial in order to optimize the body s functions while compromised under anesthesia, ensure adequate ventilation, and ensure effective enzymatic function throughout the perianesthetic period. Blood Gas Parameters ph: ph is the inverse logarithmic measurement of hydrogen ions (H + ) circulating in the blood. Normal ph is Efficient and effective enzymatic and biomechanical functions in the body occur between ph of ~ PCO 2: PCO 2 is the partial pressure of carbon dioxide dissolved in blood. The partial pressure of arterial CO 2 (P aco 2) indicates the respiratory component of the patient s acid-base status. Normal P aco 2 at sea level is mmhg. An increase in P aco 2 of 20 mmhg will decrease the ph by 0.1.

3 P ao 2: P ao 2 is the partial pressure of oxygen dissolved in arterial blood. This value is used to evaluate the functional efficiency of the lung s ability to move oxygen from the alveoli to the blood. Normal P ao 2 at sea level is mmhg. HCO - 3 : Bicarbonate (HCO - 3 ) is a weak base and an important blood buffer and is generated by renal tubular cells. This value can be an indicator of the metabolic component of a patient s acid-base status. Normal - - HCO 3 at sea level is mmhg. Extracellular buffering of the blood by HCO 3 is immediate, and buffering of blood via the respiratory system by PCO 2 occurs in minutes to hours. The kidneys take hours - - to days to markedly change the HCO 3 concentration. HCO 3 and CO 2 are interrelated by the carbon dioxide hydration equation: CO 2+H 2O H 2CO 3 H + - +HCO 3 BE: Base excess (or deficit) is the amount of base that needs to be added or subtracted in order to normalize the ph when the P aco 2 is normal. This value gives an indication of the metabolic component of acid-base status independent of CO 2. Normal BE is between 3 and +3. Under anesthesia, base excess is a more valuable indicator of the metabolic component of a patient s acid-base status because it is not affected by constant changes in carbon dioxide concentrations. A-a Gradient: The alveolar-arterial oxygen gradient helps determine the effectiveness of the patient s oxygenation. It is evaluated by comparing the measured P ao 2 from the calculated partial pressure of oxygen in the alveoli, P AO 2: P AO 2 = [(P bar P H2O) x F IO 2] (P aco 2 / 0.8), where P bar = barometric pressure = 760 mmhg at sea level, P H2O = water vapor pressure = 47 mmhg, and F IO 2 = fraction of inspired oxygen (%). Stepwise Evaluation of Arterial Blood Gases 1. Is the patient acidemic, alkalemic, or normal? ph <7.35 = acidemic ph >7.45 = alkalemic 7.35< ph <7.45 = normal 2. What is the respiratory component? P ACO 2 (hypoventilation) P ACO 2 (hyperventilation) ph = respiratory acidosis ph = respiratory alkalosis 3. What is the metabolic component? BE < 3 = metabolic acidosis BE >+3 = metabolic alkalosis 4. Is the patient appropriately and efficiently oxygenated? P ao 2 / P AO 2 >0.8 (i.e., P ao 2 no more than 10-20% less than P AO 2) = appropriate oxygenation P ao 2 / P AO 2 <0.8 (P ao 2 more than 20% less than P AO 2) = inappropriate oxygenation P ao 2 <80 mmhg at sea level = hypoxemia Treatment of Acid-Base Abnormalities Respiratory acidosis is the most common acid-base disturbance seen under anesthesia and is generally resolved with the application of intermittent positive pressure ventilation (IPPV) with a tidal volume of ml/kg and peak inspiratory pressure of cm H 2O. If there is a concurrent metabolic acidosis, always treat the respiratory component first (because of the CO 2 hydration equation, administration of sodium bicarbonate will drive the CO 2 even higher). Respiratory alkalosis is generally resolved by treating the underlying cause. Under anesthesia, the most common causes of respiratory alkalosis are a light plane of anesthesia, inadequate oxygenation, hyperthermia, or a compensation for metabolic alkalosis. If a patient is exhibiting metabolic acidosis, IV sodium bicarbonate may be administered. The full calculated dose of NaHCO 3 is: NaHCO 3 = 0.3 x body weight (kg) x BE. Administer 1/3 1/2 of the calculated amount over 20 minutes and recheck the blood gas. Consider placing the patient on IPPV even if the P aco 2 is normal to avoid the development of a respiratory acidosis.

4 Metabolic alkalosis is rarely seen as an anesthetic complication; rather, it can develop with chronic vomiting and/or diarrhea, and with certain electrolyte abnormalities. The causes of hypoxemia and/or inadequate oxygenation are described above. Electrolyte Management Maintaining adequate electrolyte balances under anesthesia is critical to preserving myocardial function, muscle function, and tissue perfusion that is dependent on electrolyte homeostasis. The longer the anesthetic procedure and the more critical the patient, the higher the likelihood the patient will experience electrolyte abnormalities. While it is important to maintain a balance in sodium, potassium, chloride, calcium, and magnesium, the two most anesthetically significant electrolytes are potassium and calcium. Potassium (K + ) is the primary intracellular cation, and it plays an integral role in neuromuscular function and electrical conduction. Normal serum potassium in dogs is meq/l, and in cats it is meq/l. There is a shift of potassium to the extracellular space in the presence of acidemia, which leads to a decrease in intracellular K + concentration even if the serum value is normal. If a patient is acidemic and the potassium value is low to normal, there is a high likelihood that potassium supplementation will be required as the academia is resolved. Caution must be taken when administering potassium to avoid inducing acute hyperkalemia. Do not administer potassium chloride (KCl) any faster than 0.5 meq/kg/hr, and recheck the potassium every 30 minutes. Hyperkalemia can be a life-threatening condition. A patient with K + >6.5 meq/l should not be anesthetized unless some other disease process is immediately threatening the patient s life. Hyperkalemia often occurs as the result of renal failure, urethral obstruction, and hypoadrenocorticism (Addison s Disease). Clinical signs include bradycardia and a decrease in myocardial contractility. An ECG may show tall, tented T waves as well as a decrease in P wave amplitude. Concentrations in excess of 8 meq/l result in a prolonged PR interval, and the P wave may be absent altogether. As the potassium level increases, the QRS complex widens, AV disassociation occurs, and eventually asystole or ventricular fibrillation ensues. Rapid resolution of moderate to severe hyperkalemia may be accomplished with administration of the following: Sodium bicarbonate 1 2 meq/kg IV over 20 minutes. This will increase the ph and move K + to the intracellular space in exchange for H +. Hyperventilation to induce respiratory alkalosis, increase the ph, and drive potassium from the extracellular space to the intracellular space. Dextrose 1.5 g/kg IV bolus. This stimulates insulin release, which promotes the movement of K + to the intracellular space. 10% calcium chloride or calcium gluconate at mg/kg IV over minutes. This dose of calcium should be used in an emergency situation only (K + >8.0 meq/l), and an ECG should be monitored during administration. This will help antagonize the cardiotoxic effects of K +. Calcium (Ca ++ ) plays a major role in neuromuscular function, cell membrane permeability, muscle contraction (especially cardiac muscle), and hemostasis. ~ 40% of calcium is in the ionized form. Ionized calcium (ica ++ ) is biologically active, and it increases with acidemia and decreases with alkalemia. Hypercalcemia (serum calcium >12 mg/dl in dogs and >11 mg/dl in cats) is rarely seen as an anesthetic complication. It can result from hyperparathyroidism or some tumors in small animals. A rapid overdose of supplemental calcium may result in vagal stimulation and severe bradycardia. Less rapid increases may result in ventricular dysrhythmias. Hypocalcemia (serum calcium <7 mg/dl or ica ++ <1.0 meq/l) can occur as a result of hypoparathyroidism or eclampsia. Intraoperatively, the most common cause of hypocalcemia is the administration of blood products that contain citrate as an anticoagulant (the citrate binds with ica ++ ). Treatment for this iatrogenic hypocalcemia is IV 10% calcium chloride or calcium gluconate, 10 mg/kg. This dose can be administered slowly (over minutes), but it can also be administered over 5 10 minutes in patients who are doing poorly (decreased cardiac output and blood pressure). Supplemental calcium can also work as a positive inotrope.

5 Suggested Reading Bryant S. Anesthesia for Veterinary Technicians. Ames: Wiley-Blackwell, Muir W, Hubbell J. Handbook of Veterinary Anesthesia. 3 rd ed. St. Louis: Mosby, Inc., Thurmon J, Tranquilli W, Benson GJ. Essentials of Small Animal Anesthesia & Analgesia. Baltimore: Lippincott Williams & Wilkins, 1999.

Capnography in the Veterinary Technician Toolbox. Katie Pinner BS, LVT Bush Advanced Veterinary Imaging Richmond, VA

Capnography in the Veterinary Technician Toolbox Katie Pinner BS, LVT Bush Advanced Veterinary Imaging Richmond, VA What are Respiration and Ventilation? Respiration includes all those chemical and physical