HuiChu Lin Department of Clinical Sciences, College of Veterinary Medicine, Auburn University, Auburn, AL, USA Anesthetized animals should be monitored closely and continuously throughout the anesthesia period. Routine variables to be monitored include heart rate and rhythm, pulse strength, respiratory rate and depth, arterial blood pressures, palpebral and corneal reflexes, eyeball rotation, capillary refill time, and mucous membrane color. Accurate assessment of the physical condition of an anesthetized patient and the depth of anesthesia of that patient are best accomplished using a combination of several parameters rather than relying on a single parameter. Presence of palpebral reflex, position of the eyeballs, and change in respiratory rate, heart rate, and arterial blood pressure are the most useful parameters and reliable indicators of the depth of anesthesia. These parameters should be evaluated, and their values recorded periodically throughout the duration of anesthesia. Following induction of anesthesia, peripheral pulse should be palpable, and an electrocardiogram (ECG), if available, should be used at all times. Position of the eyeballs in anesthetized large ruminants correlates well with the depth of anesthesia. During the surgical plane of anesthesia, eyeballs rotate ventromedially, with the cornea partially obscured by the lower eyelids. Palpebral reflex should be sluggish or just absent. As anesthetic depth deepens, eyeballs rotate to the central position with no palpebral reflex, diminished corneal reflex, and dilated cornea (Figure 7.1). Reducing the concentration of injectable or inhalation anesthetic delivered to the patient at this time may be warranted to avoid unnecessarily deepening the plane of anesthesia of the patient. If eyeballs are at the center position with strong palpebral and corneal reflexes, the depth of anesthesia may be inadequate and patients may be too light for surgical manipulation, and an increase in the anesthetic(s) concentration delivered is required. Eyeball rotation or position is not as reliable in small ruminants, camelids, and pigs as an indicator of anesthetic depth as it is in large ruminants. Changes in heart rate, respiratory rate, arterial blood pressures, and palpebral and corneal reflexes can be used to assess the depth of anesthesia in these animals. As a general rule, decrease in heart rate, respiratory rate, and arterial blood pressures, and absence of palpebral and corneal reflexes are more likely indicators of deep anesthesia. Maintaining normal heart rate and stroke volume is the most important factor in maintaining normal cardiac output (cardiac output = heart rate × stroke volume) and normal arterial blood pressure (mean arterial blood pressure = cardiac output × systemic vascular resistance). ECG can be used to monitor heart rate and cardiac rhythm continuously throughout anesthesia. Abnormal cardiac rhythm and significant changes in heart rate have the potential to impact stroke volume, cardiac output, and thus O2 delivery to the tissues. The most common method for ECG monitoring of ruminant patients requires placement of electrodes at the left forelimb (LA), right forelimb (RA), and left hind limb (LL) of the patient. This simple technique generates three bipolar limb leads for evaluation of the cardiac rhythm. Lead I indicates the voltage difference between the RA and LA electrodes, lead II the voltage difference between the RA and LL electrodes, and lead III the voltage difference between the LA and LL electrodes. These electrodes are attached to a main cable that interfaces with a simple ECG monitor or a multiparameter monitor. The monitor then displays a real‐time tracing of cardiac electrical activity using any one of the three leads, most commonly for cardiac rhythm analysis is lead II, but the lead with largest amplitude should be used. The characteristic normal waveform composition includes a distinct P wave, QRS complex, and T wave [1]. Most ECG monitors also display heart rate. Tachycardia, bradycardia, and ventricular dysrhythmias such as premature ventricular contraction and ventricular tachycardia are the most commonly observed cardiac arrhythmias in farm animals undergoing anesthesia. Sinus tachycardia and atrial fibrillation, though rarely, have also been observed in these animals. The ECG only shows the electrical activity of the myocardium; it does not provide information on the arterial blood pressure or pulse strength. Digital palpation of a peripheral artery for pulse strength should always be incorporated with the data from the ECG rhythm. Arterial blood pressure can be measured by either indirect or direct methods. Indirect arterial blood pressures can be measured using an oscillometric blood pressure machine with an inflatable blood pressure cuff placed on the coccygeal or dorsal metatarsal artery. The cuff is inflated automatically to a suprasystolic pressure, and the air is gradually released until the characteristic arterial oscillation is detected by an electronic sensor. The computer then interprets the oscillation and displays measured values of systolic, mean, and diastolic blood pressures. For accurate measurement, the width of the cuff should be approximately 40% of the circumference of the extremity around which the cuff is placed. Too small a cuff tends to overestimate the blood pressure, whereas too big a cuff tends to underestimate it. Direct arterial blood pressure measurement is achieved using a catheter placed in a superficial artery such as auricular artery or metatarsal artery. The catheter is connected to an electronic resistance‐type transducer via a semirigid saline‐filled arterial blood pressure tubing. The transducer is then connected to a cable that interfaces with a simple sphygmomanometer or a multiparameter monitor. A sphygmomanometer provides mean arterial blood pressure, whereas a multiparameter monitor displays systolic, mean, and diastolic arterial blood pressures as well as heart rate. Both indirect and direct methods provide continuous monitoring and reading of the arterial blood pressures. Changes in arterial blood pressures can be detected immediately and treatment can be instituted if needed [1, 2]. Sophisticated multiparameter monitor may not be practical in field settings; simple auscultation of the heart and lung, continuous recording of the heart rate and respiratory rate, digital palpation of the pulse strength, and close monitoring of the eye reflexes should be sufficient for routine patient monitoring during field anesthesia. Significant changes in heart rate, cardiac rhythm, respiratory rate, and breathing pattern should provide sufficient information regarding the depth of anesthesia and the condition of the patient. The use of capnogram and pulse oximetry to evaluate end‐tidal partial pressure of carbon dioxide (ETCO2) and arterial O2 saturation via a pulse oximeter (SpO2), respectively, has become part of the routine monitoring accessories to ensure adequate ventilation, efficient gas exchange, and appropriate oxygenation of an anesthetized patient (Figure 7.2). The alveolar ventilation (V A) to eliminate overall systemically produced CO2 determines the arterial partial pressure of CO2 (PaCO2). While CO2 production remains stable under normal conditions, PaCO2 varies inversely with the changes in V A. The ability of the lung to remove PaCO2 indicates the effectiveness of ventilation. When an anesthetized patient is healthy and has no preexisting diffusion disturbance in the pulmonary tissues, ETCO2 is usually closely related to alveolar CO2 and PaCO2. Therefore, ETCO2 can be used to estimate PaCO2 and to assess the adequacy of ventilation. Capnography allows continuous monitoring of the adequacy of ventilation during anesthesia. The amount of alveolar CO2 and thus ETCO2 measured in the exhaled gas at the end of expiration is determined by infrared absorption. Samples for measurement of ETCO2 are collected directly at the connecting point between the Y piece of the breathing system of an anesthesia machine and the end of an endotracheal tube (Figure 7.2). In awake, unsedated cattle, normal PaCO2 is reported to be between 38 and 43 mmHg [3]. ETCO2 is usually lower than PaCO2 by 10–15 mmHg in large animal species due to a slight degree of ventilation/perfusion (V/Q) mismatch even in the awake state [4]. Most anesthetics depress respiratory function, resulting in hypoventilation and a significant increase in PaCO2 with subsequent respiratory acidosis [5–12]. Severe hypoventilation with PaCO2 greater than 60 mmHg is common in anesthetized, recumbent farm animals, particularly in adult cattle. Furthermore, a greater difference between ETCO2 and PaCO2 is also expected because of the increased V/Q mismatch in anesthetized, recumbent large animals, with the greatest difference occurring during dorsal recumbency (Figure 7.3) [13]. In halothane‐anesthetized horses, a significantly greater difference between ETCO2 and PaCO2 occurred when they were anesthetized longer than 90 minutes as compared to that recorded at 60 minutes or less. But this increased difference with time between ETCO2 and PaCO2 did not occur in isoflurane‐anesthetized horses [14]. Though there is no similar study reported in farm animals, increase in the difference between ETCO2 and PaCO2 as a result of prolonged duration of isoflurane anesthesia has not been observed in anesthetized adult cattle. The measurement of ETCO2 does not reflect the true value of PaCO2; clinical experience shows that monitoring of ETCO2 can be used as an indicator to predict the direction of the change of PaCO2 during anesthesia. However, it is important to remember that the difference between ETCO2 and PaCO2 is affected by the efficiency of the ventilation during anesthesia and the position of the patient required for surgery [4]. Adequate tissue oxygenation is essential for patient survival following anesthesia. Tissue O2 delivery is determined by the blood flow and arterial blood O2 content (CaO2) in that tissue. When O2 diffuses into the blood, 98% of that is bound to hemoglobin and only 1–2% is dissolved in the plasma. The O2‐bound hemoglobin is represented by the measurement of O2 saturation (SaO2), and the amount dissolved in the plasma is represented as the partial pressure of arterial O2 (PaO2). Although PaO2 only constitutes a small fraction of total CaO2, its well‐defined relationship with SaO2 in the arterial blood is demonstrated by the O2 dissociation curve. Therefore, SaO2 can be used to estimate PaO2. A pulse oximeter uses the difference in the ability to absorb infrared light of saturated and desaturated hemoglobin to calculate the amount of O2 bound to the hemoglobin (SpO2) [15]. This technique is noninvasive with the sensor clip or probe placed on a superficial pulsating artery on the lingual artery in the tongue, on the auricular artery in light‐colored ears, or occasionally on the mucous membrane of the rectum of the animal (Figure 7.2). In normal, healthy patients, SpO2 readings are reliable estimates of SaO2, ranging from 80% to 100% [16]. Normal hemoglobin SaO2 should always be near 98–100%, which correlates to a PaO2 of 95–100 mmHg when breathing room air with 21% O2. During anesthesia, when a patient is breathing 100% O2, PaO2 can range from 60 to 500 mmHg. Using the O2 dissociation curve, PaO2 can be estimated by subtracting 30 from the SpO2 value when the SpO2 is in the range of 60–90%. For example, PaO2 is estimated to be 60 mmHg when the SpO2 reading is 90% [17]. Factors that alter the pulse strength of a peripheral artery, such as hypotension, hypothermia, and vasoconstriction, affect the ability of a pulse oximeter to accurately estimate the SpO2 [1, 4]. Increased ETCO2 and decreased SpO2 imply inadequate ventilation and severe V/Q mismatch, which are often the result of abnormal positioning of the animal and deep anesthesia. Decrease delivery of anesthetics and assisted or controlled ventilation should be instituted immediately to improve ventilation. Measurements of ETCO2 and SpO2 require appropriate pulmonary perfusion and pulsating peripheral arterial blood flow from adequate myocardial contractility and cardiac output. A sudden dramatic decrease in ETCO2 and SpO2 is the first indication of impending cardiac arrest. Gradual and persistent increase in ETCO2 may indicate the beginning of a malignant hyperthermia episode. Tables 7.1–7.6 provide normal values of commonly monitored physiological parameters (body temperature, heart rate, respiratory rate, and systolic, mean, and diastolic arterial blood pressures), hematology, and blood chemistry for cattle, goats, sheep, camelids, and pigs. Table 7.1 The body temperature, heart rate, respiratory rate, and arterial blood pressures for farm animals. SAP, systolic arterial pressure; MAP, mean arterial pressure; DAP, diastolic arterial pressure. a Lin, H.C. Clinical observation. Table 7.2 Normal values for hematology and blood chemistry of cattle. a Reference data from Clinical Pathology Laboratory, Auburn University. Table 7.3 Normal values for hematology and blood chemistry of goats. Table 7.4 Normal values of hematology and blood chemistry of sheep. Table 7.5 Normal values for hematology and blood chemistry of camelids.
7
Perioperative Monitoring and Management of Complications
7.1 Perioperative Monitoring
Species
Temperature (°F)
Heart rate (beats/minute)
Respiratory rate (breaths/minute)
Arterial blood pressure (mmHg)
Cattle [18]
101–103
70–90
20–30
SAP: 120–150
MAP: 90–120
DAP: 80–110
Camelids [19]
100–102
60–80
10–30
SAP: 60–135
MAP: 70–100
DAP: 45–95
Goats [20]
102–104
70–95
15–30
SAP: 80–120
MAP: 75–100
DAP: 60–80
Sheep [20]
102–104
70–80
20–30
SAP: 80–120
MAP: 75–100
DAP: 60–80
Pigs [21] (adult)
101–104
70–110
20–30
SAP: 95–126
MAP: 68–83
DAP: 44–77
Pigs [21] (weaning)
102
80–100
25–30
SAP: 83–114a
MAP: 58–76a
DAP: 40–51a
Hematologya
Blood chemistrya
Hematocrit (%)
24–46
Blood urea nitrogen (mg/dl)
7–17
Hemoglobin (g/dl)
8–15
Creatinine (mg/dl)
1–3
Red blood cells (106/μl)
5–10
Total protein (g/dl)
5.8–8.5
Mean corpuscular hemoglobin (pg)
14–19
Albumin (g/dl)
3–4.8
Mean corpuscular hemoglobin concentration (g/dl)
30–36
Bilirubin(mg/dl)
0.2–4
Mean corpuscular volume (fl)
40–65
Glucose (mg/dl)
48–70
White blood cells (103/μl)
5–17
Calcium (mg/dl)
8.5–10.3
Segamental neutrophils (103/μl)
0.6–4
Phosphorus (mg/dl)
2.4–7.9
Band neutrophils (103/μl)
0–0.1
Sodium (mEq/l)
137–151
Lymphocytes (103/μl)
2.5–7.5
Potassium (mEq/l)
2.5–5.9
Basophils (103/μl)
0–0.1
Chloride (mEq/l)
98–107
Monocytes (103/μl)
0.025–0.85
Magnesium (mg/dl)
1.9–2.7
Eosinophil (103/μl)
0–1.6
Bicarbonate (mmol/l)
16–40
Reticulocytes (103/μl)
0.001–0.008
Anion gap (mmol/l)
10–27
Platelets (103/μl)
0.1–0.8
Osmolality (mmol/kg)
270–350
Fibrinogen (mg/dl)
100–600
Creatine kinase (U/l)
40–264
Aspartate aminotransferase (U/l)
69–112
γ‐Glutamyl transferase (U/l)
3.7–31
Sorbitol dehydrogenase (U/l)
4.5–18
Hematologya
Blood chemistrya
Hematocrit (%)
22–38
Blood urea nitrogen (mg/dl)
10–20
Hemoglobin (g/dl)
8–12
Creatinine (mg/dl)
1–1.82
Red blood cells (106/μl)
8–18
Total protein (g/dl)
6.4–7
Mean corpuscular hemoglobin (pg)
5.2–8
Albumin (g/dl)
2.7–3.9
Mean corpuscular hemoglobin concentration (g/dl)
30–36
Bilirubin (mg/dl)
0.10–1.71
Mean corpuscular volume (fl)
16–25
Glucose (mg/dl)
50–75
White blood cells (103/μl)
4–13
Calcium (mg/dl)
8.9–11.7
Seg. neutrophils (103/μl)
1.2–7.2
Phosphorus (mg/dl)
4.2–9.1
Band neutrophils (103/μl)
0
Sodium (mEq/l)
142–155
Lymphocytes (103/μl)
2–9
Potassium (mEq/l)
3.5–6.7
Basophils (103/μl)
0–0.3
Chloride (mEq/l)
99–110.3
Monocytes (103/μl)
0–0.05
Magnesium (mg/dl)
2.8–3.6
Eosinophil (103/μl)
0.05–0.65
Bicarbonate (mmol/l)
N/A
Platelets (103/μl)
0.3–0.6
Anion gap (mmol/l)
N/A
Fibrinogen (g/l)
100–400
Creatine kinase (U/l)
0.8–9
Aspartate aminotransferase (U/l)
167–513
γ‐Glutamyl transferase (U/l)
20–56
Sorbitol dehydrogenase (U/l)
14–23.6
Hematologya
Blood chemistrya
Hematocrit (%)
27–45
Blood urea nitrogen (mg/dl)
8–20
Hemoglobin (g/dl)
9–15
Creatinine (mg/dl)
1.2–1.9
Red blood cells (10/μl)6
9–15
Total protein (g/dl)
6–7.5
Mean corpuscular hemoglobin (pg)
8–12
Albumin (g/dl)
2.4–3
Mean corpuscular hemoglobin concentration (g/dl)
31–34
Bilirubin (mg/dl)
0.1–0.5
Mean corpuscular volume (fl)
28–40
Glucose (mg/dl)
50–80
White blood cells (103/μl)
4–12
Calcium (mg/dl)
11.5–12.8
Seg. neutrophils (103/μl)
0.7–6
Phosphorus (mg/dl)
5–7.3
Band neutrophils (103/μl)
0
Sodium (mEq/l)
139–152
Lymphocytes (103/μl)
2–9
Potassium (mEq/l)
3.9–5.4
Basophils (103/μl)
0–0.3
Chloride (mEq/l)
95–103
Monocytes (103/μl)
0–0.75
Magnesium (mg/dl)
2.2–2.8
Eosinophil (103/μl)
0–1
Bicarbonate (mmol/l)
20–25
Platelets (103/μl)
0.21–0.71
Creatine kinase (U/l)
8–13
Fibrinogen (mg/dl)
100–500
Aspartate aminotransferase (U/l)
60–280
γ‐Glutamyl transferase (U/l)
20–52
Sorbitol dehydrogenase (U/l)
5.8–27.9
Hematologya
Blood chemistrya
Hematocrit (%)
34 ± 4.0
Blood urea nitrogen (mg/dl)
29.0 ± 6.1
25–46
9–34
Hemoglobin (g/dl)
15.3 ± 1.7
Creatinine (mg/dl)
2.5 ± 0.5
11.5–19.5
1.4–3.2
Red blood cell (106/μl)
10.88 ± 1.1
Total protein (g/dl)
5.9 ± 0.5
9.9–17.7
5.1–7.8
Mean corpuscular hemoglobin (pg)
11.2
Albumin (g/dl)
3.6 ± 0.6
9.8–12.7
3.1–5.2
Mean corpuscular hemoglobin concentration (g/dl)
43.3
Bilirubin (mg/dl)
0.2 ± 0.2
37.7–49
0–0.2
Mean corpuscular volume (fl)
26
Glucose (mg/dl)
134.2 ± 36.0
22–30.1
74–154
White blood cell (103/μl)
8.0–23.3
Calcium (mg/dl)
9.0 ± 0.7
7.5–20.0
7.4–10.4
Seg. neutrophils (103/μl)
4.18–14.87
Phosphorus (mg/dl)
5.8 ± 2.2
2.6–7.3
Band neutrophils (103/μl)
0–0.13
Sodium (mEq/l)
149.4 ± 5.4
0–169
148–158
Lymphocytes (103/μl)
0.96–7.64
Potassium (mEq/l)
3.8 ± 0.9
0.7–4.9
3.7–6.1
Basophils (103/μl)
0–0.3
Chloride (mEq/l)
115.9 ± 4.8
102–120
Monocytes (103/μl)
0.0–1.34
Magnesium (mg/dl)
1.9 ± 0.3
0.0–1.0
Eosinophil (103/μl)
0.07–5.83
Bicarbonate (mmol/l)
N/A
0.16–4.5
Total CO2 (mm/l)
13–31
Reticulocytes (103/μl)
12–79
Creatine kinase (U/l)
81.8 ± 110
8–77
Platelets (103/μl)
200–600
Aspartate aminotransferase (U/l)
216–378
166–447
Fibrinogen (g/l)
300 ± 114
γ‐Glutamyl transferase (U/l)
7–29
100–500
9–27
Sorbitol dehydrogenase (U/l)
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