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Veterinarian Technician July 2013 (Vol 34, No 7)

Equine Essentials: Blood Pressure Management in Equine Anesthesia

by Samantha Rowland, LVT, VTS (Anesthesia)

    CETEST This course is approved for 1.0 CE credits

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    Expect the best, plan for the worst, and prepare to be surprised.
    —D. Wholey

    Anesthesia is a complex science in which many factors, both physiologic and external, play a role in the overall result. A diligent anesthetist and proper monitoring are necessary for a successful anesthesia experience for the patient and the veterinary team. Monitoring arterial blood pressure (BP) is considered a minimum standard of care for safe anesthetic management.1 In equine anesthesia, accurate and consistent BP monitoring is vital for helping to ensure a positive outcome.

    Physiology and Components of Blood Pressure

    Arterial BP is measured using the systolic and diastolic pressures and the mean arterial pressure (MAP), which are expressed as millimeters of mercury (mm Hg). BP is the driving force of blood flow and, therefore, tissue perfusion. BP refers to the pressure of the blood within the arteries (i.e., arterial BP).1

    The primary factors that determine BP include cardiac output (CO), systemic vascular resistance (SVR), and stroke volume:

    BP = CO × SVR

    CO is determined by stroke volume and heart rate:

    CO = stroke volume × heart rate

    CO is defined as the volume of blood pumped by the ventricles in 1 minute. Stroke volume is the volume of blood pumped from one ventricle during each contraction and is determined by contractility, preload, afterload, and heart rate. In a healthy patient with normal cardiac function, the volume of blood being delivered from the heart should equal the amount being returned to the heart (venous return).2

    Preload is the force that acts on a muscle before contraction. Afterload is the resistance that the ventricles must contract against to expel blood (ventricular wall stress).2 Vasoconstriction or vasodilation affects the afterload of the heart, which affects the stroke volume, thereby increasing or decreasing CO and BP.

    SVR is the resistance to blood flow caused by the peripheral vasculature. This resistance must be overcome to push blood through the circulatory system. The determinants of SVR are MAP and CO:3

    SVR = MAP ÷CO

    MAP = ⅓(systolic – diastolic) + diastolic

    What does all of this mean to an anesthetist? If any one of these factors is affected, BP will be altered.

    Why Is Blood Pressure Monitored?

    Arterial BP measurement is one of the key elements of providing safe anesthetic management; it is a window into the patient’s cardiovascular status. During general anesthesia, horses have a greater risk of morbidity and mortality than dogs, cats, and humans.4 Studies on anesthesia have shown that equine patients have a 1% mortality rate compared with 0.1% for human patients; the equine mortality rate increases to 10% if emergency patients (e.g., those with colic or receiving obstetrical care) are included.4 It is hoped that a greater understanding of all aspects of anesthesia, including BP abnormalities during anesthesia, by anesthetists will help decrease patient mortality.

    Anesthetic Agents and Adjunctive Drugs

    Anesthetic agents and many adjunctive drugs have a direct impact on cardiovascular function. They can affect heart rate, BP, CO, and respiratory function; the associated changes are typically dose-dependent. α2-Adrenergic agonists are commonly used for sedating horses in the preanesthetic and recovery periods and for standing surgical procedures. These agents produce sedation, muscle relaxation, and somatic and visceral analgesia as well as allow a decrease in the minimum alveolar concentration (MAC) of inhalants.5

    Although α2-adrenergic agonists have many benefits, adverse effects can include decreased CO, respiratory depression, increased vagal tone and SVR, and bradycardia with a transient second-degree heart block.5 The bradycardia is in response to the transient initial hypertension due to vasoconstriction—a compensatory reaction.6 This is a biphasic event; after the initial vasoconstrictive effects subside,7 vasodilation and, therefore, hypotension can result.

    Acepromazine (a phenothiazine tranquilizer) is commonly used in combination with an α2-adrenergic agonist for preanesthetic sedation. Phenothiazines block α1-adrenergic receptors, which can cause hypotension and inhibit platelet function. Therefore, phenothiazines are contraindicated in horses in shock or with bleeding disorders or blood loss.8 The benefits of acepromazine are tranquilization and calming effects, which are especially useful in excitable breeds and in racehorses, as well as significant MAC reduction.5 The combination of an α2-adrenergic agonist and phenothiazine is beneficial for the recovery period as well. However, due to the potentially negative effects of phenothiazines, anesthetists must use care when administering them to high-risk patients or should consider using a different medication.

    Opioids and synthetic opioid agonist-antagonists are used as analgesics and do not have the significant cardiovascular effects that α2-adrenergic agonists do; however, opioids and opioid agonist-antagonists can cause excitement in awake horses and do not reduce MAC. The analgesic effect of opioids can enhance the stability of general anesthesia.5 Inhalants such as isoflurane cause dose-dependent vasodilation, which decreases CO, thereby decreasing BP. Inhalant anesthetics provide little to no analgesia, so adjunctive agents should be used to provide adequate pain control.9

    Certain medications can be given by constant-rate infusion (CRI) to provide consistent analgesia and reduce inhalant MAC. Use of these drugs in combination with anesthetics is called multimodal anesthesia/analgesia. Drugs commonly administered by CRI include ketamine, lidocaine, opioids, and α2-adrenergic agonists. It is typically recommended to stop the CRI approximately 20 to 30 minutes before the end of anesthesia to reduce the risk of ataxia and a prolonged recovery time.10

    How Is Blood Pressure Measured?

    Arterial BP can be monitored by Doppler ultrasound, DINAMAP (device for indirect, noninvasive, automatic mean arterial pressure) oscillometric monitoring, or invasive direct monitoring. Compared with the direct method, indirect monitoring devices have proven to be less accurate and to have more variable results in horses.

    The noninvasive methods can be performed using an inflatable cuff on the base of the tail in adults and foals or on a distal limb in foals. The Doppler system provides systolic BP readings; however, the readings can be inaccurate if the cuff size is not correct or the horse is in dorsal or lateral recumbency.11 Like the Doppler system, DINAMAP monitoring uses an inflatable cuff placed in the same location as a Doppler cuff would be placed. These monitors deliver systolic, diastolic, and MAP values, along with the heart rate. They are useful for monitoring trends but become significantly inaccurate if the patient is hypotensive, is moving, or has bradycardia or arrhythmias.9

    The gold standard for measuring arterial BP is direct monitoring using an indwelling arterial catheter connected to short, noncompliant tubing (FIGURE 1); a pressurized transducer (FIGURE 2); and a monitor. This setup allows an anesthetist to examine trends for systolic, diastolic, and MAP values, along with a waveform. The direct arterial BP waveform helps the anesthetist to evaluate cardiac function, specifically relating to left ventricular ejection, and also helps the anesthetist decide whether pulse deficits are becoming detrimental and arrhythmias are causing a low BP.1 Direct BP monitoring can also be used to assess inotropic and vasopressor therapy, fluid resuscitation efforts, and arterial blood gas readings (FIGURE 3). The latter is used to assess ventilation and acid-base status, both of which can also affect CO and BP.1 This monitoring method is consistent with every heartbeat and is the most accurate way to monitor trends that can provide important clues to help avoid anesthetic crises.

    CO, stroke volume, vessel wall compliance, peripheral vascular resistance, and heart rate affect the BP waveform. To form a more complete picture of the horse’s cardiovascular status, the waveform should be analyzed along with the BP, pulses, mucous membrane color, and capillary refill time. Horses that are mechanically ventilated under anesthesia have BP waveform changes consistent with the respiratory cycle. The peak of inspiration is typically synchronized with the highest systolic pressure; the lowest systolic pressure occurs after peak inspiration.9

    When BP is monitored directly through an indwelling arterial catheter, the BP waveform depicted on the monitor needs to be continually assessed. The anesthetist should see (1) waveform peak changes that may be associated with the respiratory cycle of the ventilator and (2) flattening (dampening) of the waveform when the systolic and diastolic readings are close in numeric value or when the catheter needs to be flushed. Arterial lines need to be periodically flushed with heparinized saline. Equipment maintenance is very important for ensuring reliability of BP measurements. Some machines have more maintenance requirements than others, so obtaining experience using different types of equipment can help troubleshoot problems.

    By palpating multiple arteries, the anesthetist can consistently assess pulse quality/strength, heart rate and rhythm, and pulse deficits. Pulse palpation allows a qualitative assessment of pressure; however, pulse palpation is not a good indicator of arterial BP, anesthetic depth, or tissue perfusion. Pulse pressure/strength is essentially the difference between the systolic and diastolic arterial pressures.11 Inhalant anesthetics cause vasodilation, which results in a decrease in vascular tone (tension on the vessel wall), an increase in pulse pressure, and a decrease in perfusion.11 Vasodilation causes the vessel wall to be closer to the skin surface, which makes the artery easier to palpate and may therefore deceive an anesthetist into thinking that a horse has good blood pressure. Vasoconstriction causes a vessel to shrink away from the skin surface and become difficult to palpate, which is also deceiving. Therefore, pulse palpation should be used to verify that the heart rate and rhythm and the electrocardiogram are accurate; however, pulse palpation should not be relied on for assessing BPs.

    Normal blood pressure values in an anesthetized horse are as follows10:

    Systolic: 90 to 120 mm Hg

    Diastolic: 40 to 70 mm Hg

    MAP: 60 to 85 mm Hg (goal: 70 to 80 mm Hg)


    Although hypertension can compromise an anesthetized patient, it is not as prevalent as hypotension in horses. Because of risks associated with hypertension, it must be addressed. Potential causes of intraoperative hypertension include inadequate anesthetic depth, inadequate analgesia, hypoxemia, hypercarbia, and hyperthermia.12 α2-Adrenergic agonists can cause hypertension from initial vasoconstriction with compensatory bradycardia, followed by hypotension. Cyclohexamines, such as ketamine, cause an increase in BP through direct stimulation of the sympathetic nervous system, which increases heart rate, BP, and CO.13 Hypertension can occur from the overuse of vasopressors or positive inotropes when correcting hypotension. Patients may also have hypertension due to an underlying disease, a medication that causes secondary hypertension, or an increase in intracranial pressure.14 Risks associated with hypertension include retinal detachment, increased hemorrhage, increased intracranial pressure, and an increase in cardiac afterload.15 To see these effects in horses, the MAP would typically have to be quite high (>120 mm Hg). Hypertension can also cause bradyarrhythmias, increase bleeding at a surgical site, and increase the difficulty of maintaining anesthesia.12

    Treatment of hypertension is aimed at correcting the underlying cause. If the horse is not adequately anesthetized, take steps to remedy this, such as increasing the inhalant concentration. The inhalant concentration is controllable and reversible, if necessary. If the horse seems to be adequately anesthetized but responds to pain during a procedure, address the analgesic therapy. α2-Adrenergic agonists can be reversed if necessary, but this is generally not needed. Acepromazine can be administered at 0.01 mg/kg IV in normovolemic patients to obtain normotension without inducing hypotension.12 Acepromazine also decreases the MAC requirement of the inhalant.

    For procedures such as assisted vaginal delivery during dystocia or procedures involving abdominal laparoscopy, the horse must be placed in the Trendelenburg position: dorsal recumbency with the hind end elevated 30° to 45° above the head to enhance access to the pelvic organs by using gravity to “move” the gastrointestinal tract out of the way. This position causes noticeable hypertension; therefore, the time spent in this position should be as short as possible to avoid complications.


    Hypotension negatively affects tissue perfusion and oxygenation as well as distribution of anesthetic agents and other medications. Patients with a MAP of ≤60 mm Hg are considered to be hypotensive and must be treated immediately. The vital organs (i.e., the heart, brain, and kidneys) have mechanisms that allow them to maintain consistent blood flow despite changes in BP; this is known as autoregulation. The kidneys are less able to autoregulate than the heart and the brain. Hypotension affects autoregulation when the MAP drops below 80 mm Hg. When the MAP falls below 50 mm Hg, blood flow to the myocardium (heart muscle) decreases.16

    Among the major complications for horses undergoing general anesthesia are the development of postoperative myopathies and neuropathies. These can result from hypotension, hypoxemia, improper positioning, inadequate padding, and poor perfusion; any of which can also cause rhabdomyolysis (“tying up”). Myopathies are more common in larger and/or heavily muscled horses; the dependent muscle groups (the side the horse was lying on) are affected more than the nondependent groups. The affected muscles become hard, painful, and swollen; the horse can be either mildly lame after recovery or unable to stand altogether. Postoperative myopathies in the horse can be compared with compartmental syndrome in people: the muscles are underperfused/hypoxic, which causes a chain of events including ischemia, cell damage, and increased pressure and swelling.17 A MAP of ≥70 mm Hg must be maintained to adequately perfuse the muscles and other organs6; however, these complications may still occur even if the horse was padded and positioned properly and had no anesthetic complications.

    Hypotension has many causes, including a deep anesthetic plane, vasodilation secondary to inhalant and injectable anesthetic agents, decreased CO, hypovolemia, dehydration, endotoxemia, positive-pressure ventilation, vena cava compression, preexisting diseases, some concurrent medications, significant blood loss, gastric distention, poor cardiac function, tachycardia, arrhythmias, and bradycardia.12 In horses, the primary causes of hypotension during anesthesia are significant vasodilation from injectable and inhalant anesthetics, a prolonged duration of anesthesia/surgery, inadequate intravenous fluid therapy/circulating volume, and positive-pressure ventilation.

    Positive-pressure (controlled mechanical) ventilation has negative effects on a horse’s cardiovascular system, largely due to a change in intrathoracic pressure. Patients that are breathing spontaneously, whether awake or anesthetized, have a decreased intrathoracic pressure on inspiration. This pressure gradient increases blood flow to the thorax and right atrium during inspiration, which in turn increases preload in the right ventricle and increases stroke volume in a normal heart (this is called the Starling effect).18 Positive-pressure ventilation causes increased intrathoracic pressure, which compresses the vena cava and decreases preload and stroke volume; this can cause decreased CO and BP.18 However, the inhalant causes respiratory depression, so a horse in lateral or dorsal recumbency would not adequately ventilate spontaneously and would quickly become hypercarbic and hypoxemic. Therefore, it is almost always necessary to provide mechanical ventilation during anesthesia of adult horses.

    Hypovolemia and endotoxemia can be major causes of hypotension in horses undergoing colic surgery. Colicky horses can have profound dehydration, electrolyte/metabolic derangements, shock, and significant pain. To prevent severe hypotension, it is best to treat these abnormalities before induction of anesthesia; however, depending on the situation, treatment may not be possible. Endotoxemia needs to be addressed immediately to avoid cardiovascular collapse. Common therapies include administration of flunixin meglumine, preoperatively if possible, or a polypeptide microbial such as polymyxin B.19

    It is ideal to use the least amount of inhalant possible to achieve an adequate surgical anesthetic plane. Typically, this is accomplished through multimodal anesthesia/analgesia. Aside from decreasing the amount of inhalant used, the most common way to prevent and treat hypotension is through proper intravenous fluid therapy and vasopressor support. An average adult horse should receive approximately 5 L of crystalloid fluids per hour (10 mL/kg/h) while anesthetized. The fluid plan should be adjusted based on the physical status of the horse and its response to fluid therapy. Horses that experience significant hypovolemia have higher fluid requirements, which most likely involve the placement of a second large-bore IV catheter to deliver a higher fluid volume. The type and amount of fluid is based on several factors, including the packed cell volume, total protein level, blood lactate level, acid-base status, and electrolyte concentrations.20

    Dobutamine—a β1-adrenergic agonist—is the standard “go to” positive inotropic agent for treating equine hypotension. This drug acts on the myocardium to increase the strength of contraction. This causes the heart to eject a greater blood volume during each beat (increase in stroke volume), which increases CO.15 Dobutamine has a very short half-life and must be given by CRI. It takes effect quickly, which is necessary when treating anesthetic hypotension. If the horse is hypovolemic, the use of dobutamine may cause tachycardia with no improvement in BP, which causes the heart to work harder and increase oxygen consumption. If there is not enough blood to pump, increasing the force of contraction will not help. However, in healthy patients undergoing elective procedures, dobutamine is generally the drug of choice and works very well.

    Calcium gluconate is another positive inotrope that can be used to treat perianesthetic hypotension; calcium plays a significant role in cardiac function, specifically triggering contraction by entering the cells of the myocardium (heart muscle). Changes in the serum calcium level can affect repolarization of the heart.3 If the patient is hypocalcemic or likely to be, calcium gluconate can be administered at 10 to 20 mg/kg IV.5 Calcium gluconate comes in a 23% solution in 500-mL bottles, which is the most common formulation used in horses.

    Phenylephrine—an α1-adrenergic agonist and a vasopressor—causes vasoconstriction by stimulating the α1receptors in the peripheral circulation. The drug can increase diastolic pressure and preload by increasing vasomotor tone.21 The drug does not increase CO or blood flow to muscles and can have adverse effects, such as reflex vagal bradycardia, which must be considered; therefore, it is not recommended if a horse is already bradycardic (<24 bpm). This drug has a rapid onset and short duration of action and is generally given by CRI.

    Colloids are intravenous fluid solutions used to correct hypotension due to hypovolemia. The large molecules in these fluids help maintain or increase intravascular volume by slowing redistribution of these fluids; crystalloids have smaller molecules than colloids and therefore redistribute more quickly. Hetastarch (6%) is a commonly used colloid that typically comes in 500-mL bags. The standard dose is 5 mL/kg/d; for managing intraoperative hypotension, the dose ranges from 2 to 5 mL/kg/d.

    Hypertonic saline (7.2%) can be administered when patients have severe hypotension and/or hypovolemia and the administration of hetastarch will take too much time to achieve quick volume expansion. Hypertonic saline can act as a “Band-Aid” to quickly restore intravascular volume and overall hemodynamics. Each liter of hypertonic saline can increase intravascular volume by 3 to 4 L, resulting in rapid and significant increases in BP, perfusion, and CO. The effects of hypertonic saline last approximately 30 to 90 minutes. During a crisis in which a horse requires immediate anesthetic induction (e.g., severely painful colic), hypertonic saline can adequately increase BP for a relatively safe induction period until the horse can be given additional fluid therapy during surgery. Hypertonic saline brings fluid from the intracellular and interstitial spaces back into the vasculature; this fluid needs to be replaced with crystalloid fluid to avoid severe dehydration and electrolyte derangements. Combining hypertonic saline and hetastarch can have more prolonged and marked beneficial effects on a horse’s hemodynamics than either solution could on its own.18

    Less common vasopressors include ephedrine, vasopressin, norepinephrine, and epinephrine. Ephedrine increases BP through vasoconstriction caused by stimulation of the α1-adrenergic receptors. Administration as a CRI can cause tachycardia, so ephedrine is commonly given as a single bolus at a dose of 0.03 to 0.06 mg/kg IV. Vasopressin is the most potent vasoconstrictor in use and is classified as a nonadrenergic endogenous stress hormone. Vasopressin increases BP, improves tissue perfusion, and improves cardiac contractility. At a dose of 0.4 to 0.6 µg/kg IV, the drug stimulates the release of catecholamines; therefore, repeat doses are not necessary. Epinephrine is an endogenous catecholamine that is typically reserved for cardiopulmonary resuscitation (CPR). The drug acts as a positive inotrope and as a chronotrope, so it increases contractility and heart rate. At a dose of 1 to 3 µg/kg/min, the drug is administered as a bolus during CPR or as a CRI for severely hypotensive horses that are not responding well to other agents.15 Norepinephrine is a sympathomimetic agent that acts as a peripheral vasoconstrictor by acting on the αreceptors. It also acts as an inotrope on the heart and dilates coronary arteries by acting on the β receptors. The drug is used to treat acute hypotension and is used as a secondary agent during cardiac arrest.22 Norepinephrine increases heart rate and arterial BP, increases the potential for arrhythmias,12 and is contraindicated in hypovolemic patients.22 At a dose of 0.2 to 2 µg/kg/min, this drug can increase vasomotor tone, helping to increase tissue perfusion.15

    Anticholinergics such as atropine and glycopyrrolate can be used to increase BP if a horse has bradycardia (<24 bpm). Glycopyrrolate is dosed at 0.0025 to 0.005 mg/kg IV,21 typically takes longer than atropine to take effect, and has a longer duration of action than atropine; unlike atropine, glycopyrrolate does not cross the blood-brain barrier.23 Atropine has a quick onset and short duration of action and is generally used during CPR. Adverse effects of atropine include tachycardia and ileus, which must be considered before the drug is used. Anticholinergic administration is contraindicated in horses with bradycardia due to α2-adrenergic agonist administration because anticholinergics can trigger arrhythmias and bradycardia is the body’s natural response to the vasoconstrictive action of α2-adrenergic agonists.


    Horses can be challenging anesthetic patients, even when they are healthy. BP is an essential monitoring parameter during equine anesthesia. For success, anesthetists must know how to correct anesthetic abnormalities and have a thorough understanding of cardiovascular and respiratory physiology as well as pharmacology.

    Downloadable PDF

    1. Reuss-Lamky H. Monitoring blood pressure and end-tidal CO2 in the anesthetized patient. In: Bryant S, ed. Anesthesia for Veterinary Technicians. Ames, IA: Wiley-Blackwell Publishing; 2010:105-122.

    2. Doherty T, Valverde A, et al. The cardiovascular system. In: Manual of Equine Anesthesia and Analgesia. Ames, IA: Blackwell Publishing Professional; 2006:11-26.

    3. Muir W, Hubbell J, et al. The cardiovascular system. In: Muir W, Hubbell J, eds. Equine Anesthesia Monitoring and Emergency Therapy. 2nd ed.St. Louis, MO: Saunders Elsevier; 2009:37-50.

    4. Muir W, Hubbell J. History of equine anesthesia.In: Muir W, Hubbell J, eds. Equine Anesthesia Monitoring and Emergency Therapy. 2nd ed.St. Louis, MO: Saunders Elsevier;2009:8-10.

    5. Doherty T, Valverde A, et al.Pharmacology of drugs in equine anesthesia. In: Manual of Equine Anesthesia and Analgesia. Ames, IA: Blackwell Publishing Professional; 2006:128-174.

    6. Nann L. Equine anesthesia. In: Bryant S, ed. Anesthesia for Veterinary Technicians. Ames, IA: Wiley-Blackwell Publishing; 2010:357-373.

    7. Palmer DL. Canine and feline pharmacology: inter- and intra-species differences in drug pharmacokinetics & pharmacodynamics. VSPN continuing education. www.vspn.org. Accessed 2009.

    8. Hubbell J. Horses. In: Tranquilli W, Thurmon J, Grimm K, eds. Lumb & Jones’ Veterinary Anesthesia & Analgesia. Ames, IA: Blackwell Publishing Professional; 2007:717-729.

    9. Fornes S. Inhalant anesthetics. In: Bryant S, ed. Anesthesia for Veterinary Technicians. Ames, IA: Wiley-Blackwell Publishing; 2010:153-159.

    10. Muir W, Yamashita K. Intravenous anesthetic and analgesic adjuncts to inhalation anesthesia. In: Muir W, Hubbell J, eds. Equine Anesthesia Monitoring and Emergency Therapy. 2nd ed. St. Louis, MO: Saunders Elsevier; 2009:260-274.

    11. Hubbell J, Muir W. Monitoring anesthesia. In: Muir W, Hubbell J, eds. Equine Anesthesia Monitoring and Emergency Therapy. 2nd ed. St. Louis, MO: Saunders Elsevier; 2009:149-170.

    12. Muir W, Hubbell J. Anesthetic-associated complications. In: Muir W, Hubbell J, eds. Equine Anesthesia Monitoring & Emergency Therapy. 2nd ed. St. Louis, MO: Saunders Elsevier; 2009:397-417.

    13. McNally E, Pablo L. Equine anesthesia. In: Reeder D, et al, eds. AAEVT’s Equine Manual for Veterinary Technicians. Ames, IA: Wiley-Blackwell Publishing; 2009:217-249.

    14. McMillan S. Anesthetic complications and emergencies. In: Bryant S. Anesthesia for Veterinary Technicians. Ames, IA: Wiley-Blackwell; 2010:167-187.

    15. Haskins S. Monitoring anesthetized patients. In: Tranquilli W, Thurmon J, Grimm K, eds. Lumb & Jones’ Veterinary Anesthesia and Analgesia. Ames, IA: Blackwell Publishing; 2007:533-560.

    16. Guedes A. Support. In: Carroll G, ed. Small Animal Anesthesia & Analgesia. Ames, IA: Blackwell Publishing; 2008:259-279.

    17. Taylor PM, Clarke KW. Anesthetic problems. In: Handbook of Equine Anesthesia. St. Louis, MO: WB Saunders; 1999:95-145.

    18. Kerr C, McDonell W. Oxygen supplementation and ventilator support. In: Muir W, Hubbell J, eds. Equine Anesthesia Monitoring & Emergency Therapy. 2nd ed. St. Louis, MO: Saunders Elsevier; 2009:332-353.

    19. Kelmer G. Equine endotoxemia: any new therapies in the horse. Proc Am Coll Vet Surg 2012.

    20. Hardy J. Venous and arterial catheterization and fluid therapy. In: Muir W, Hubbell J, eds. Equine Anesthesia Monitoring & Emergency Therapy. 2nd ed.St. Louis, MO: Saunders Elsevier; 2009:131-147.

    21. Papich M. Saunders Handbook of Veterinary Drugs. 2nd ed. St. Louis, MO: Saunders Elsevier; 2007.

    22. US National Library of Medicine. http://www.nlm.nih.gov. Accessed April 2013.

    23. Systemic therapy of airway disease: systemic pharmacotherapeutics of the respiratory system. In: The Merck Manual for Veterinary Professionals. http://www.merckmanuals.com/vet/pharmacology/systemic_pharmacotherapeutics_of_the_respiratory_system/systemic_therapy_of_airway_disease.html?qt=glycopyrrolate&alt=sh. Accessed April 2013.

    References »

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