Monitoring and management of perioperative problems (Proceedings)


All commercially available sedatives and anesthetics are safe when properly administered to normal animals.

All commercially available sedatives and anesthetics are safe when properly administered to normal animals. Physiologically compromised patients, however, are predisposed to complications, and the risks are increased when the pharmacodynamic effects of the anesthetic conflict with the physiologic compromise of the patient. Although there are no absolute contra-indications to any specific anesthetic drug, it is preferable to implement an anesthetic plan which best complements the physiologic compromise of the patient.

The organ systems about which we are most concerned in the critically ill patient are the cardiovascular, respiratory, central nervous system, and visceral. Pre-existing dehydration or hypovolemia, anesthesia-induced vasodilation, or intra-operative blood loss or plasma exudation may contribute to perioperative hypovolemia. Myocardial contractility can be reduced by pre-existing myocardial disease and many anesthetic drugs. Stroke volume can be decreased by incompetent atrioventricular valves, stenotic outflow valves, and by ventricular arrhythmias. Excessive bradycardia can be caused by anesthetic drugs or high vagal tone, and can diminish cardiac output. Excessive hypotension diminishes cerebral and coronary perfusion. Excessive vasodilation causes hypotension; excessive vasoconstriction reduces visceral organ perfusion. Anemia diminishes oxygen content and oxygen delivery; hypoxemia diminishes the partial pressure gradients between the plasma and the mitochondria.

Cardiovascular evaluation always begins with an evaluation of venous return and preload pressure; adequate diastolic filling is a prerequisite to an adequate stroke volume. The most common cause of poor venous return is hypovolemia. Once the heart is properly filled, it must then contract with sufficient force to create a useful stroke volume. Most anesthetic drugs are generally considered to decrease preload and afterload independent myocardial contractility. The inhalational anesthetics, as a class group of drugs appear to be more depressant than are the injectables, at all dosages. Of the inhalants, the least depressant appears to be desflurane followed by sevoflurane and isoflurane followed by halothane; enflurane appears to be the most depressant. Of the injectable anestheics, propofol is notably depressant while the barbiturates, opioids, etomidate, and ketamine have minimal effects but could decrease myocardial contractility at high dosages or at normal dosages in patients with debilitated hearts.

Alterations in heart rate would cause a linear change in cardiac output if stroke volume remained unchanged. Stroke volume, however, increases at slower heart rates and vice versa which offsets heart rate-induced changes in cardiac output or oxygen delivery. Animals also compensate for bradycardia-induced decreases in cardiac output with systemic vasoconstriction so as to maintain arterial blood pressure. The administration of atropine increases heart rate in bradycardic patients and increases arterial blood pressure, cardiac index, oxygen delivery, and venous partial pressure of oxygen (PvO2) from a low to a high normal value, and decreases systemic vascular resistance and oxygen extraction. Heart rate is decreased by anesthetic dosages of alpha2-agonists (xylazine, metdetomidine, and romifidine) in a dose-related manner and opioids. Benzodiazepines and phenothizines generally minimally increase heart rate although if the benzodiazepine or opioid cause CNS excitation, the heart rate will increase. The cyclohexanones and inhalational anesthetics generally increase heart rate. The barbiturates, etomidate and propofol generally increase heart rate slightly. Tachycardia can impair stroke volume by limiting the amount of time available for diastolic filling and ventricular arrhythmias can impair stroke volume by causing an uncoordinated myocardial contraction.

Cardiac output is the product of preload, contractility, and heart rate, and is an important systemic forward flow parameter. Cardiac output is generally decreased by the alpha2-agonists in a dose-related manner. Benzodiazepines and phenothiazines generally have minimal, but variable, effects on cardiac output. Anesthetic dosages of opioids appear to decrease cardiac output. The cyclohexanones generally increase cardiac output although very high dosages can decrease cardiac output. Cardiac output is generally well maintained during inhalational anesthesia, although there is a gradual decrease with increasing dosages. The barbiturates and propofol are generally associated with a decrease in cardiac output.

Arterial blood pressure is primarily determined by the balance between cardiac output and systemic vascular resistance with the latter being the most potent determinant. Blood pressure is important to cerebral and coronary perfusion. The alpha2-agonists typically, initially increase blood pressure in a dose-related manner, and subsequently decrease blood pressure. Benzodiazepines generally have minimal effects on blood pressure although if the benzodiazepine causes CNS excitation, blood pressure may increase. Phenothiazines tend to decrease arterial blood pressure. Anesthetic dosages of opioids have variable effects; oxymorphone was associated with an increase, morphine with no change after a transient decrease. The cyclohexanones are generally associated with an increase in arterial blood pressure, although large dosages may cause a decrease. The barbiturates are generally associated with an increased arterial blood pressure (after a very transient initial decrease). Etomidate may be associated with no change to a slight increase while propofol usually causes a significant decrease in arterial blood pressure. The inhalational anesthetics are associated with a dose-dependent decrease in arterial blood pressure.

Systemic vascular resistance is important for two reasons: 1) regulation of arterial blood pressure (vasodilation causes hypotension), and 2) regulation of peripheral tissue perfusion (vasoconstriction impairs visceral perfusion). The alpha2-agonists typically cause an initial vasoconstriction. Benzodiazepines generally have minimal effects on systemic vascular resistance. Phenothiazines exhibited no vasodilation in one study of normal dogs but can be potent vasodilators in some critically ill animals. Anesthetic dosages of opioids have variable effects on arterial blood pressure; oxymorphone was associated with vasoconstriction while meperidine was associated with an initial, transient vasodilation. The cyclohexanones are generally associated with a decrease while the barbiturates are generally associated with an increase in systemic vascular resistance. Propofol usually causes vasodilation The inhalational anesthetics are generally associated with a dose-dependent decrease in systemic vascular resistance.

Oxygen delivery is the product of cardiac index and blood oxygen content and represents the effectiveness of cardiopulmonary performance with regard to systemic oxygen flow. In general, since oxygen content does not change during the induction process, oxygen delivery mirrors the changes in cardiac output in most studies. Oxygen delivery has been reported to decrease with zylazine and acepromazine premedication and to increase with the administration of ketamine. Over the course of a surgical procedure, however, changes in hemoglobin concentration, blood oxygenation, preload, and body temperature, in addition to variations in anesthetic depth, can have a dramatic impact oxygen delivery. When oxygen delivery declines, for any reason, tissue oxygenation is maintained by an immediate increase in oxygen extraction. Eventually compensatory processes reach their limit and any further decrease in oxygen delivery causes a decrease in oxygen consumption. Oxygen delivery needs to be adequate to meet the metabolic (oxygen) requirements of the patient. The adequacy of the oxygen delivery must, therefore, be defined in the context of tissue oxygen requirements and the balance between oxygen delivery and oxygen consumption. Oxygen consumption is highly variable in the unanesthetized state, depending upon whether the animal is asleep, awake but relaxed, or awake and excited. Anesthetics generally decrease oxygen consumption from the awake, baseline state, the notable exceptions are ketamine and ether. Any sedative or anesthetic which increases excitation (as sometimes occurs with benzodiazepines, opioids) will increase oxygen consumption. At a comparable anesthetic dosage, the best critical oxygen delivery seems to be associated with pentobarbital = ketamine > alfentanil > etomidate = propofol > inhalational anesthetics.

When oxygen delivery decreases, extraction increases and venous oxygen decreases. When these compensatory mechanisms reach their limit, tissue oxygenation becomes inadequate and lactic acidosis develops. Oxygen extraction and venous oxygen provide an ongoing index to the oxygen delivery/consumption ratio. Ketamine alone was reported to increase oxygen delivery and oxygen extraction, with essentially no change in venous oxygen or base deficit. Xylazine premedication decreased oxygen delivery and venous oxygen, while markedly increasing oxygen extraction; base deficit increased slightly.


A functional hypovolemia is assumed to be present if there is evidence or history of blood or fluid loss, if the patient is dehydrated, or if the preload parameters (collapsed jugular veins, low central venous pressure, or low end-diastolic diameter [cardiac ultrasound]). Poor peripheral tissue perfusion (vasoconstriction [pale mucous membrane color, prolonged capillary refill time, cool appendages], oliguria, lactic acidosis may be due to any cause of poor cardiac output (hypovolemia or heart disease). Hypotension may be caused by hypovolemia, heart disease, or vasodilation. If an absolute or a relative (due to vasodilation) hypovolemia is thought to be present, fluids should be administered.

The usual crystalloid fluids of choice for acute blood volume restoration are those with electrolyte concentrations close to plasma with regard to sodium, potassium, chloride, and a "bicarbonate-like" anion (bicarbonate, lactate, gluconate, or acetate); such as lactated Ringer's, Plasmalyte 148® , or Normosol R® . These solutions are economical, readily available, and can be safely administered in large volumes to normal animals.

Because polyionic, isotonic, crystalloid fluids are highly redistributed to the interstitial fluid compartment, they often need to be administered in large volumes to achieve blood volume restoration goals: dogs 20-40-60-80-100 ml/kg may be required; cats have a smaller blood volume (50 to 60 ml/kg vs 80-90 ml/kg in the dog) and so fluid volume should be more conservative (10-20-30-40-50-60 ml/kg).

Isotonic crystalloid fluids, are substantially redistributed to the interstitial fluid compartment. This is an advantage if the animal has an interstitial fluid deficit but eventually predisposes to interstitial edema, pulmonary edema, and cerebral edema . Hemodilution of blood constituents that are not in the crystalloid fluid may be a problem: 1) anemia; 2) hypoproteinemia (low colloid oncotic pressure); 3) hypo-coagulopathy. If any of these abnormalities occur during the administration of crystalloid fluids, red cells, colloids, or coagulation factors, respectively, must be added to the fluid therapy regimen.

Colloid fluids (Dextran 70 in saline, Hetastarch in saline, and Hextend® in a polyionic, isotonic solution) are more effective blood volume expanders than are crystalloid fluids because they are redistributed to a much lesser extent to the interstitial fluid compartment. Artificial colloids could be used routinely but should be considered when the circulating volume does not appear to be responding appropriately to a crystalloid fluid infusion or if edema develops prior to adequate blood volume restoration. A small to a large loading dose of a any colloid (artificial colloid, plasma, or whole blood) is 10 to 30 ml/kg for the dog (5 to 15 ml/kg for the cat).


Plasma could be used to augment circulating blood volume in administered volumes of 10 to 30 ml/kg. It is, however, quite costly to used for this purpose compared to artificial colloids. Plasma is primarily used to treat coagulopathies. The ability of plasma to increase the albumin concentration in a patient in any meaningful way, is, however, very disappointing. Twenty-five% human plasma concentrate is available and is much more effective in this regard, but has been reported to be associated with serious transfusion reactions in some instances.

Plasma contains different coagulation factors, depending upon how it is stored. Fresh (within 6 hours of collection) plasma has everything and therefore is good for the treatment of all coagulation disorders. Freezing destroys the platelets and therefore fresh frozen plasma would not be good for the treatment of thrombocytopenia or disseminated intravascular coagulation. Refrigerator storage is associated with the loss of both platelets and labile coagulation factors V, VIII, and vonWillebrand's and therefore would not be good for the treatment of these diseases but could still be used for the stabile factors for vitamin K-antagonist rodenticide-induced bleeding.

Heart rate and rhythm

Heart rate is too slow when it is associated with low cardiac output, hypotension or poor tissue perfusion. In lieu of this kind of evidence or a reasonable cause for the bradycardia, values of 60 for the dog, 90 for the cat are common triggers for treatment. Verify that the problem is truly bradycardia as opposed to a slow pulse rate, which could be caused by ventricular arrhythmias. Excessive vagal tone can be caused by pharyngeal, laryngeal or tracheal stimulation; pressure on the eyeball or rectus muscles; or by visceral inflammation, distention, or traction.

Causes of perioperative bradycardia

Sinus tachycardia is primarily a sign of an underlying problem. It only becomes a problem for the patient when there is not enough time for diastolic filling; cardiac output decreases. In people, because of coronary artery disease, sinus tachycardia is feared because the increased myocardial oxygen consumption may exceed oxygen delivery capabilities. In lieu of cardiac output information, the trigger level for specific treatment of sinus tachycardia may be somewhere in the low 200's for dogs and high 200's for cats.

Causes and treatment of tachycardia

Ventricular arrhythmias, in an animal that did not have them prior to anesthesia, are primarily a sign of an anesthetic-induced complication. Make sure that the ECG abnormality is truly of ventricular origin as opposed to a right bundle branch block which appears similar to a ventricular rhythm except that it is preceded by a P wave. Ventricular arrhythmias may also be due to intrinsic myocardial disease or arrhythmogenic factors released from various debilitated abdominal organs. Ventricular arrhythmias become a problem for the patient when they interfere with cardiac output, arterial blood pressure and tissue perfusion, or when they threaten to convert to ventricular fibrillation. Ventricular arrhythmias should be treated when: 1) the minute-rate equivalent approaches the trigger point for treating sinus tachycardia; 2) they are multiform; 3) the ectopic beat over-rides the T-wave of the preceding depolarization. Total elimination of the ventricular arrhythmia is not necessarily the goal of therapy since large dosages of anti-arrhythmic drugs have deleterious cardiovascular and neurologic effects. A simple decrease in the rate or severity of the arrhythmia may be a suitable end-point to the titration of the anti-arrhythmic drugs.

Causes of ventricular ectopic pacemaker activity

  • Endogenous release of catecholamines or sympathomimetic therapy

  • Hypoxia or hypercapnia

  • Hypovolemia or hypotension

  • Myocardial inflammation, disease or stimulation (intracardiac catheters, pleural tubes)

  • Thoracic and nonthoracic trauma

  • Certain anesthetics lower the threshold to endogenous or exogenous catecholamines (halothane, xylazine, thiamylal, thiopental)

  • Hypokalemia (potentiated by respiratory or metabolic alkalosis, glucose or insulin therapy)

  • Hyperkalemia (potentiated by acidosis, hypocalcemia, succinylcholine or may be iatrogenic)

  • Visceral organ disease (gastric volvulus/torsion)

  • Intracranial disorders (increased pressure, hypoxia)

  • Digitalis toxicity (potentiated by hypokalemia and hypercalcemia)

Ventricular arrythmias can be caused by several mechanisms and these are not readily apparent from the ECG appearance of the arrhythmia. A given anti-arrhythmic may be effective in one mechanism and be ineffective, or even worsen, another. Anti-arrhythmic therapy is always a bit of a clinical trial. Lidocaine is a first choice anti-arrhythmic because it selectively effects abnormal cells without affecting automaticity or conduction in normal cells.

Antiarrhythmic drugs


Hypotension is caused by hypovolemia, poor cardiac output, and systemic vasodilation. Systemic vasodilation and hypotension may be caused by administration of anesthetic drugs (particularly with inhalational anesthetics and propofol, and phenothiazines and alpha2-agonists). Vasoconstrictors should be administered if fluid therapy alone has failed to restore ABP. Poor cardiac output can be caused by impaired stroke volume or heart rate/rhythm problems. Contractility can be reduced by intrinsic myocardial disease or extrinsic myocardial depressants (cytokines in systemic sepsis or SIRS; electrolyte abnormalities; hypoxemia and hypoxia; anesthetic drugs). There are many causes of poor cardiac output but when preload/afterload independent contractility is thought to be poor, positive inotropes are indicated. In general, hypotension should be treated when it decreases below about 60 mmHg mean, or about 80 mmHg systolic.

Summary of receptor activity of common sympathomimetics

Dose:response relationship, notwithstanding, these designations indicate the approximate relative ability of the drug to have the designated effect: INC = very potent tendency to increase (+++) INC = marked tendency to increase (+++); Inc = moderate tendency to increase (++); inc = slight tendency to increase (+); var = variable ; 0 = no effect; dec = slight tendency to decrease; Dec = moderate tendency to decrease; DEC = marked tendency to decrease; DEC = very potent tendency to decrease.

Cardiotonic and vaso-active drugs

Catecholamines are endogenous chemical compounds derived from tyrosine and include epinephrine, norepinephrine, and dopamine. Epinephrine and dopamine act as neurotransmitters in the central nervous system and as hormones in the systemic circulation. Norepinephrine acts primarily as a neurotransmitter in the peripheral sympathetic nervous system but also as a hormone in the systemic circulation. Sympathomimetics are compounds that, when administered to a patient, approximately mimic the effect of endogenous catecholamine release and include drugs like isoproterenol, dobutamine, ephedrine, phenylephrine. Catecholamines and sympathomimetics operate via alpha and beta membrane receptors. There are other agents which could reasonably be classified as sympathomimetics because they either increase heart rate or contractility, and have vascular effects which generally increase arterial blood pressure: phosphodiesterase inhibitors (caffeine/aminophylline/theophylline, amrinone/milrinone, pimobendan), vasopressin, angiotensin, and calcium. The effects of these drugs are not alpha or beta receptor-mediated and they are not typically classified as a sympathomimetics.

The choices for cardiovscular support in the generic critically ill patient are dopamine or dobutamine. Isoproterenol and dopexamine are considered too vasodilatory, and epinephrine, norepinephrine, and neosynephrine are too vasoconstrictive, for routine use in critically ill patients. Dopamine causes somewhat more vasoconstriction compared to dobutamine which is more often associated with slight vasodilation and is preferred when arterial blood pressure augmentation is desired; dopamine is considered the "pressure" drug of these 2 choices. Dobutamine is more often associated with minimal changes in blood pressure and better improvement in cardiac output and tissue perfusion. Dosing typically starts at 5 mcg/kg/min and is increased in 5 mcg/kg/min increments until a desirable endpoint, or 20 mcg/kg/min, has been reached. If dosages of 20 mcg/kg/min fail to achieve acceptable results, other drugs should be employed. To augment arterial blood pressure, a norepinephrine or phenylephrine infusion can be added. To augment arterial blood pressure and myocardial contractility, an epinephrine infusion can be substituted. All sympathomimetics may be associated with sinus tachycardia and ventricular arrhythmias and appropriate monitoring for these adverse effects is necessary.

Ephedrine is an indirect-acting sympathomimetic, which causes the release of norepinephrine from the sympathetic nerve endings. Prolonged use can deplete the stores of norepinephrine resulting in tachyphylaxis. Ephedrine is a general cardiovascular stimulant, a bronchodilator, and a relaxant of the urethral sphincter. It crosses the blood-brain barrier and has a mild analeptic effect. Ephedrine could be used as a first line therapy in cardiovascular support instead of dopamine or dobutamine. It can be administered intermittently (or as a CRI) since it has a longer duration of action, but it is not usually considered to be as effective as dopamine and dobutamine.

Inhibition of phosphodiesterase increases the concentration of cAMP within the cell. In the heart, increased cAMP increases calcium transients and contractility. In vascular smooth muscle, increased cAMP inhibits myosin light chain kinase (myosin phosphorylation) and promotes vasodilation. The phosphodiesterase inhibitors are not as effective inotropic agents as are the sympathomimetics. Pimobendan and levosimendan, in addition to being phosphodiesterase inhibitors, sensitize the myofilament to calcium, and have been reported to somewhat more effective than amrinone and milrinone, but neither is yet available for clinical use in the United States. Aminophylline is a weak inotropic agent.

Norepinephrine and phenylephrine are primarily alpha-receptor agonists (table 2) which are associated with arteriolar and venous constriction. Both are short duration drugs and must be administered as a CRI. Vasopressin activates phospholipase C resulting in the release of IP3 and DAG from membrane phospholipids, both of which increase in cytoplasmic calcium.


Vasoconstriction may be caused by hypovolemia, poor cardiac output, hypothermia, administration of vasoconstrictor drugs, pain or excitement postoperatively. The underlying cause must be identified so that the appropriate therapy can be instituted.


Whether or not animals are anemic prior to the operative procedure, hemoglobin concentrations can be decreased intraoperatively by anesthetic-induced vasodilation and splenic dilation, non-hemoglobin-containing fluid administration, and blood loss. In humans, the trigger for a hemoglobin transfusion has traditionally been a hemoglobin concentration of 10 g/dL (a packed cell volume [PCV] of 30%), however recent studies suggest that a more relaxed trigger of 7 g/dL (PCV = 21%) might represent a better benefit:risk ratio. In veterinary medicine, a packed cell volume of 20% has been a common trigger for blood transfusion, however, given the complexities of cardiac output and oxygen-extraction compensatory mechanisms, it is not possible to precisely define a minimum hemoglobin concentration. Anesthetic agents decrease myocardial contractility and cardiac output and it would be predicted that anesthetized patients require a relatively higher hemoglobin concentration (7-8g/dl). Metabolic markers of poor tissue oxygenation, such as a low PvO2 or a metabolic (lactic) acidosis, may help guide the need for hemoglobin transfusions.

Whole blood may need to be administered in volumes of 10 to 30 ml/kg, depending on the magnitude of anemia and hypovolemia (cats: 5 to 15 ml/kg). These volumes should be halved if packed red blood cell products are used. The rate of administration depends upon the magnitude of the hypovolemia. The amount of blood to administer can also be calculated: (desired PCV - current PCV) x body weight (kg) x 2 ml whole blood (assumes a PCV of about 40%) (or 1 ml packed red blood cells [assumes a PCV of about 80%]).

Although many canine erythrocyte antigens have been identified, only 6 (DEA 1.1, 1.2, 3, 4, 5, and 7) are commonly tested. Dog erythrocyte antigen 1.1 and 1.2 are the most antigenic and are present in approximately 62% of the canine population. Fortunately naturally-occurring isoantibodies to DEA 1.1 and 1.2 do not exist and, in this regard, first-time transfusions are relatively safe. Donors and recipients should be DEA 1.1 and 1.2 typed to assure that recipients receive type-similar blood. DEA 1.1 and 1.2 negative recipients should not receive type-positive blood because it would prime them from a second-time transfusion reaction. The other four canine blood groups are weak antigens as are any naturally-occurring isoantibodies and transfusion reactions are mild if they occur at all. In vitro cross matching would help sort out potentially incompatible transfusion from any cause and may be important for sequential transfusions and in immune-mediated hemolytic anemia.

There are primarily two commonly identified red cell antigens in the domestic cat — A and B (a third type, AB, is rare). The domestic "mongrel" cats, Siamese, Burmese, and Russian Blue breeds are typically Type A . Type B blood types occur in up to 10% of Maine Coon cats, up to 20% in Abyssinian, Birman, Persian, Somali, Spinx, and Scottish Fold cats, and up to 45% in British Shorthair, and Cornish and British Rex cats. Type A cats have low titers of naturally occurring anti-B antibodies. Type B cats have high titers of strong, naturally occurring anti-A antibodies. Matched transfusions were associated with a mean survival time of labeled red cells of 29 to 39 days. Transfusion to Type B blood into Type A cats was associated with a mean red blood cell survival time of 2 days and minor transfusion reactions, while transfusion of Type A blood into Type B cats was associated with a mean red blood cell survival time of 1 hour and marked transfusion reactions. Feline blood transfusions should by type-matched, either by blood typing of both donor and recipient or by in vitro cross-matching.

Breathing Rate, Rhythm, Nature, and Effort

The breathing rate can vary widely, and except for extreme values is of limited value as a respiratory monitor. A change in breathing rate, however, is a sensitive indicator of an underlying change in the status of the patient. Bradypnea may be a sign of deep anesthesia or hypothermia. There are many cause of tachypnea and it is important not to default to the conclusion that its occurrence represents too light a level of anesthesia . Arrhythmic breathing patterns are indicative of a problem with the central pattern generator in the medulla. A Cheyne-Stokes breathing pattern (cycling between hyperventilation and hypoventilation) may be seen in otherwise healthy anesthetized horses and an apneustic breathing pattern (inspiratory hold) may be seen in otherwise healthy dogs and cats anesthetized with ketamine.

Cause of tachypnea

  • Too lightly anesthetized

  • Too deeply anesthetized

  • Agonal "gasps"

  • Hypoxemia

  • Hypercapnia

  • Hyperthermia

  • Hypotension

  • Sepsis

  • Atelectasis

  • Postoperative recovery phase

  • Postoperative pain

  • Drug-induced (opioids)

  • Individual variation


Hypoxemia may be due to: 1) a low inspired oxygen any time an animal is attached to a mechanical apparatus (anesthetic machine, ventilator, nonrebreathing circuit); 2) hypoventilation when an animal is breathing room air (if the animal is attached to a 100% oxygen source (an operating anesthetic machine) hypoxemia cannot occur; 3) venous admixture (aka "lung disease" or "impaired lung function"). The treatment for dysfunction of the anesthetic apparatus is, of course, to fix it. The treatment for hypoventilation is to provide positive pressure ventilation support until the underlying disease can be effectively treated. The treatment for venous admixture is first to increase the inspired oxygen concentration (one of the common causes of hypoxemia in pulmonary parenchymal disease is responsive to oxygen therapy). When oxygen therapy is ineffective (the other common cause of hypoxemia in pulmonary parenchymal disease) positive pressure ventilation must be employed to re-expand collapsed small airways and alveoli.

The general guidelines for positive pressure ventilation of animals with relatively normal lungs(regardless of the method or brand of ventilator utilized) are: 1) a peak proximal airway pressure of 10 to 20 cm H20; 2) a tidal volume of 10 ml/kg; 3) an inspiratory time of about 1 second (or just long enough to achieve a full tidal volume); 4) a ventilatory rate of about 15 times per minute; 5) a minute ventilation of about 150 to 250 ml/kg/minute; and 6) a 0 to +2 end-expiratory pressure. Some ventilated patients should receive a deep breath (a sigh) at an airway pressure of 30 cm H20 at regular intervals (30 minutes) to minimize small airway and alveolar collapse.

Diseased lungs are stiffer (less compliant) than normal lungs, and are therefore much more difficult to ventilate. It is a common finding that the above recommended guidelines are insufficient to adequately oxygenate or ventilate a patient with diffuse pulmonary parenchymal disease. Whenever ventilator settings do not seem to meet the needs of the patient or the aforementioned goals: 1) make sure that the ventilator settings are indeed what you had planned (including the inspired oxygen); 2) make sure that there is patient synchrony; and 3) make sure that other untoward events are not present (hyperthermia, pneumothorax). After these conditions are met, adjust ventilator settings. There is no particular order in which ventilator settings should be adjusted. To improve ventilation: 1) the proximal airway pressure could be increased in a step-wise fashion up to 60 cm H20 (or to the limit of the ventilator); 2) the tidal volume should probably not be increased in an animal with diffuse lung disease. Pulmonary disease is associated with a reduced vital capacity due to a reduced inspiratory and expiratory reserve volume. What would be a normal tidal volume for a normal lung could easily over-distend the reduced number of remaining lung units, contributing to volutrauma. Protective lung strategies currently aim for very small tidal volumes, e.g. 5 ml/kg; 3) the ventilatory cycle rate could be increased in a step-wise fashion up to 60 breaths per minute; 4) the inspiratory time or the inspiratory plateau could be increased. The inspiratory/expiratory [I/E] ratio must allow sufficient time for exhalation of all of the last breath, otherwise air trapping and auto-PEEP will occur; and 5) the PEEP can be increased. Lung units are easier to ventilate when they are kept open after the last breath rather than having to start from a collapsed position.

If oxygenation must be improved: 1) all of the above techniques to improve ventilation will also improve oxygenation; 2) the inspired oxygen could be increased up to 100% for short periods of time or up to 60% for prolonged periods of time; or 3) the end-expiratory pressure could be increased up to 20 cm H20. PEEP increases transpulmonary pressure and functional residual capacity, and keeps small airways and alveoli open during the expiratory phase and improves ventilation and oxygenation. PEEP also minimizes the repetitive collapse and re-opening of small airways, a process which contributes to ventilator-induced injury.


Hypothermia during anesthesia may be associated with anesthetic drug depression of muscular activity, metabolism and hypothalamic thermostatic mechanisms. Heat loss may be augmented by evaporation of surgical scrub solutions from the skin surface, by the infusion of room temperature fluids, by contact with cold, un-insulated surfaces, and by evaporation of surface fluid from an exposed body cavity. Core temperature can be measured with either esophageal or rectal thermistors attached to a continuously displayed thermometer.

Core body temperatures down to 36 °C (96 °F) are not associated with detrimental effects to the patient. Nonshivering thermogenesis will increase and there may be some shivering thermogenesis during recovery. Recovery should not be prolonged in any noticeable way. Body temperatures of 32-34 °C (90-94 °F) are associated with reduced anesthetic requirements; recovery should be noticeably prolonged. Shivering will occur if it is possible for the animal but some animals will not shiver and will have to be artificially rewarmed. Body temperatures of 28-30 °C (82-86 °F) have a marked CNS depressant effect and usually no anesthetic agent is required. Shivering thermogenesis will not occur and the animal will have to be rewarmed artificially. Atrial arrhythmias may occur. Oxygen consumption is reduced to about 50% of normal; heart rate and cardiac output to about 35-40% of normal; and arterial blood pressure to about 60% of normal. Cerebral metabolism is about 25% of normal. These decreases in hemodynamic parameters are secondary to cold-induced hypometabolism. Measurements must be interpreted in this context rather than in comparison to normothermic values. Body temperatures of 25-26 °C (77-80 °F) are associated with prolongation of the PR interval and widened QRS complexes, increased myocardial automaticity, decreased tissue oxygen delivery out of proportion to decreases in oxygen requirement resulting in anaerobic metabolism, lactic acidosis and rewarming acidemia. Blood viscosity is about 200% of normal. Body temperatures of 22-23 °C (72-74 °F) are usually associated with ventricular fibrillation.

Intra-operative hypothermia is usually mild to moderate and, as long as appropriate safeguards are exercised, is seldom detrimental to the patient. The largest problem with intra-operative hypothermia is the non-recognition of it. The continued administration of normothermic amounts of anesthetic to a hypothermic patient results in an anesthetic overdosage.

Passive rewarming (minimizes further heat loss and allows the patient to warm themselves metabolically) is usually effective in mild hypothermia (above 34 °C [94 °F]) when the patient is capable of metabolic or shivering thermogenesis. Intra-operative heat loss can be minimized by warm room temperatures, insulating barriers between the patient and table surfaces, administering warmed fluids. Active rewarming can be achieved by circulating warm water or air blankets, infrared heat lamps (optimal distance 75 cm or radiant heat warmers, hot water bottles placed under the drapes (avoid contact with skin if the water temperature exceeds 42 °C), flushing the abdominal cavity or colon with warm, sterile, isotonic, polyionic fluids, or by extracorporeal techniques.

Aggressive surface rewarming should be avoided in very cold patients(82-84) because peripheral vasodilation may induce excessive hypotension in the face of a cold-depressed heart. Ischemic peripheral tissues may have accumulated various metabolites which may have deleterious cardiovascular effects when large quantities are washed into the central circulation. The rewarming rate should be limited to about 1 °C per hour.


Fever is a reset thermostat and is caused by the release of endogenous pyrogens (interleukin-I) from monocytes in response to infections, tissue damage, antigen-antibody reactions. Interleukin-I stimulates prostaglandin synthesis in the hypothalamic thermoregulatory center. Hyperthermia, without a reset thermostat, is pathologic. It not uncommonly occurs in large dogs which are cacooned on the operating table with many layers of drapes. Hyperthermia may be potentiated by surface vasoconstriction, light levels of anesthesia, and ketamine.

Mild degrees of hyperthermia are not, per se, harmful to the patient and may represent an appropriate response to an underlying disease (fever of infection). Mild hyperthermia (less than 40 °C or 104 °F) does not normally require treatment, per se. Cell damage starts to occur at body temperatures above 42 °C (108 °F) when oxygen delivery can no longer keep pace with the racing metabolic activity and increased oxygen consumption. Severe hyperthermia causes multiple organ dysfunction and failure: renal; hepatic; gastrointestinal failure; myocardial and skeletal muscle; cerebral edema, disseminated intravascular coagulation, hypoxemia, metabolic acidosis, and hyperkalemia. Malignant hyperthermia is a rapidly, relentlessly, progressive increase in body temperature associated with the metabolic heat production of disturbed intracellular calcium recycling at the sarcoplasmic reticulum. Muscle hypertonicity may or may not occur, depending upon the calcium concentration in the sarcoplasm. Dantrolene is the specific and often effective treatment for this syndrome; 2.5 to 10 mg/kg, intravenously.

Surface cooling techniques are most effective with room temperature fluids; it is the evaporation of the water from the skin surface that causes the cooling. Ice water causes vasoconstriction which impedes heat loss from the core until skin temperature is <10 °C, at which time vessel paralysis and vasodilation occur, and core temperatures decrease precipitously. Convective heat loss can be enhanced with fans. Conductive heat loss can be enhanced with ice packs. Large volumes of cold crystalloid fluids intravenously, per colon or stomach, or into a body cavity are effective internal cooling techniques. Antipyretic drugs (antiprostaglandins, dipyrone, aminopyrine) are generally effective for fever but are not effective for pathologic hyperthermia.

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