Welcome to the all-new Vetlearn

  • Vetlearn is becoming part of NAVC VetFolio.
    Starting in January 2015, Compendium and
    Veterinary Technician articles will be available on
    NAVC VetFolio. VetFolio subscribers will have
    access to not only the journals, but also:
  • Over 500 hours of CE
  • Community forums to discuss tough cases
    and networking with your peers
  • Three years of select NAVC Conference
  • Free webinars for the entire healthcare team

To access Vetlearn, you must first sign in or register.


  Sign up now for:
Become a Member

Veterinarian Technician November 2009 (Vol 30, No 11)

Peer Reviewed — Perioperative Hypotension

by Christopher Norkus, BS, CVT, VTS (ECC), VTS (Anesthesia)

    Hypotension is a frequent phenomenon observed during human and veterinary anesthesia.1-3 Unfortunately, in the past, blood pressure (BP) was not routinely monitored in veterinary patients under anesthesia, and the presence of perioperative hypotension was likely overlooked.4 In 1995, the American College of Veterinary Anesthesiologists (ACVA) published recommendations for regular monitoring of multiple physiologic parameters, including BP, in patients undergoing general anesthesia.5 Additionally, with the increasing availability of BP monitoring devices and education regarding their use, veterinarians and veterinary technicians are now more aware of the risk of perioperative hypotension and, therefore, seek effective strategies for treating it.

    Components of Blood Pressure

    BP is the pressure exerted by circulating blood on the walls of blood vessels and is composed of systolic and diastolic pressures. The systolic pressure occurs at the end of the cardiac cycle when the ventricles are contracting and represents a peak pressure in the arteries. Diastolic pressure is the minimum pressure in the arteries, occurring at the beginning of each cardiac cycle when the ventricles are completely filled with blood.

    Arterial BP is the mathematical product of systemic vascular resistance (SVR) and cardiac output (CO)6:

    BP = SVR × CO

    SVR refers to the degree of dilation (vasodilation) or constriction (vasoconstriction) of systemic blood vessels. CO is the volume of blood being pumped by the heart in a given minute. CO is the product of stroke volume (SV) and heart rate (HR).6 SV is the volume of blood being pumped from the heart, whereas HR is the number of times the heart pumps per minute:

    CO = SV × HR

    SV is composed of cardiac preload, cardiac contractility, and cardiac afterload.6 Cardiac preload is the blood volume returning to the heart, whereas afterload is the resistance the heart pumps against for blood to leave the heart. Factors that increase afterload typically decrease SV. Cardiac contractility is the strength of the heart's contraction (Figure 1).

    What Constitutes Perioperative Hypotension?

    Methods for measuring BP currently include indirect means via ultrasonic Doppler and oscillometric techniques as well as direct means via arterial catheterization. In dogs and cats, hypotension is defined as a systolic BP <80 mm Hg or a mean arterial pressure (MAP) <60 mm Hg.7 MAP is commonly estimated using the following formula:

    MAP = Diastolic pressure + 1/3 × (Systolic pressure - Diastolic pressure)

    The Doppler method tends to underestimate systolic BP in cats by about 10 to 14 mm Hg.8

    Why Measure Blood Pressure During Anesthesia?

    Innumerable reasons exist for measuring BP during the perioperative period. First, most anesthetic agents have negative cardiovascular effects.9-14 With this in mind, insufficient monitoring of physiologic status introduces unsettling guesswork into the use of anesthesia. For example, because pulse strength is merely the difference between the systolic and diastolic pressures, patients can have strong pulses and appear clinically normal but still have perioperative hypotension.15 Renal autoregulation and splanchnic perfusion are compromised if MAP <60 mm Hg.16 Decreased delivery of oxygen to tissue due to perioperative hypotension can easily result in necrosis and organ failure after anesthesia. In more severe cases in which cardiac and cerebral perfusion is compromised, acute cardiac arrest and death can rapidly ensue. It is well documented that the occurrence of hypotension is correlated with mortality in the intensive care unit, perioperatively and postoperatively.17-19 In humans undergoing non-cardiac surgery, a perioperative hypotension episode was a significant predictor of 1-year mortality, suggesting that hypotensive episodes may affect outcomes over longer time periods than previously appreciated.19


    Factors affecting any of the components of circulation can lead to changes in BP and, in turn, hypotension. The causes of hypotension are generally broken into three categories: decreased preload, decreased cardiac function, and decreased vascular resistance. Common causes of decreased preload include hypovolemia and decreased venous return. Hemorrhage, gastrointestinal losses and dehydration, polyuria, hypoadrenocorticism, effusion or third spacing of fluid, burns, heatstroke, and the use of many prescription drugs (e.g., diuretics, ACE inhibitors) are all recognized causes of hypovolemia.20 Causes of decreased venous return include patient positioning, pericardial tamponade, severe pneumothorax, positive pressure ventilation, gastric dilatation and volvulus, and caval syndrome of heartworm disease.20 The numerous causes of decreased cardiac function include cardiomyopathy, valvular disease, bradyarrhythmias, tachyarrhythmias, electrolyte and acid-base abnormalities, severe hypoxia, and the use of many prescription drugs and anesthetic agents (e.g., β blockers, inhalant anesthetics).20 Patients presenting with decreased vascular tone commonly have sepsis or systemic inflammatory response syndrome (SIRS), anaphylaxis, dramatic neurogenic insult, electrolyte and acid-base abnormalities, or severe hypoxia or are receiving prescription drugs or anesthetic agents (e.g., β blockers, calcium channel blockers, acepromazine, propofol).20


    Treatment of perioperative hypotension is as much of an art as it is a science. However, treatment generally includes initial minimization of the causes of hypotension (e.g., stopping blood loss, minimizing or discontinuing hypotensive drugs) and then management of the hypotension itself (e.g., administering fluids and drugs). If a hypotensive reading occurs while monitoring BP, the anesthetist should recognize this as an anesthetic emergency and address it immediately. The anesthetist should quickly confirm that hypotension exists and that the reading is not false. This may include changing Doppler locations, ensuring proper cuff size, or evaluating other physiologic parameters, such as mucous membrane color, capillary refill time, HR, electrocardiogram rhythm, the end tidal carbon dioxide (ETCO2) level, saturation of peripheral oxygen (Spo2), blood gas levels, and plasma lactate level. After confirming the presence of perioperative hypotension, the anesthetist should evaluate the patient's ventilation and temperature and ensure that they are adequate. Simultaneously, the anesthetist should begin to reduce the use of drugs that may cause hypotension. In many incidences, this means immediate reduction of the inhalant anesthetic. In some cases of severe hypotension, it may be necessary to discontinue the use of the inhalant until safer BP readings are obtained. However, if the hypotension is not severe and surgery will begin momentarily, a patient's BP will sometimes improve once surgical stimulation begins.

    If the above steps fail to correct hypotension by the next measurement, further steps must be initiated. If the patient has bradycardia and hypotension, the decrease in HR may be affecting CO enough to also decrease BP. Therefore, patients with bradycardia can be treated with either atropine (0.02-0.04 mg/kg IV) or glycopyrrolate (0.005-0.01 mg/kg IV) until the HR returns to normal.21 Because of the slower onset of glycopyrrolate, it is inappropriate for use in life-threatening emergencies. One exception to this is if the patient was given an α2 adrenergic agonist (e.g., dexmedetomidine) as part of the anesthesia. In these cases, rather than giving the patient an anticholinergic, the most effective strategy is drug reversal with atipamezole. This should resolve the problem by improving CO, if the cause of hypotension was bradycardia. If these steps are not effective or only partially improve the problem, the anesthetist should proceed to the next treatment.

    At this point, an intravenous fluid bolus is given to correct potential hypovolemia and to maximize cardiac preload. This step aims to correct problems such as subclinical dehydration and decreases in venous return resulting from patient position or the use of anesthetic drugs. A bolus of a balanced crystalloid (e.g., 0.9% sodium chloride, lactated Ringer's solution, Normosol-R) is typically administered rapidly at 5-10 mL/kg IV. If this fails to improve BP, cardiac preload has not fully been restored to normal or the problem is not due to decreased cardiac preload. At this point, some anesthetists administer a second crystalloid bolus (5-10 mL/kg IV) or a colloid (e.g., hetastarch) at 2.5-5 mL/kg IV in cats and 5-10 mL/kg IV in dogs. Another option is to slowly administer 7% hypertonic saline at 4 mL/kg IV over 5-15 minutes.22 This technique is very useful for rapidly correcting hypovolemia specifically due to surgical hemorrhage once surgical homeostasis has been obtained. Patients experiencing significant intraoperative hemorrhage will likely require intraoperative administration of blood products.

    Patients that have not responded to treatment of their abnormal HR and to maximization of cardiac preload likely have inadequate SVR, cardiac contractility, or both. Some routine patients, many geriatric patients, and most critically ill patients do not tolerate the vasodilatory and negative inotropic properties of inhalant anesthetics. Therefore, the anesthetist may choose to further decrease or to eliminate the use oftheinhalant drug.

    The minimum alveolar concentration (MAC) of an anesthetic agent is the lowest administered end tidal concentration of drug that produces no gross motor response in 50% of the patients exposed to a painful stimulus.23 Anesthetists should remember that the MAC of sevoflurane in oxygen is 2.36% in dogs and 2.58% in cats.24,25 The MAC of isoflurane in oxygen is 1.28% in dogs and 1.6% in cats.26

    Inhalation requirements can be dramatically reduced by cardiovascular-sparing options such as a bolus or a constant-rate infusion (CRI) of an opioid (e.g., fentanyl, hydromorphone) alone or in conjunction with a benzodiazepine (e.g., diazepam, midazolam) or with ketamine.27-30 Combinations of morphine, lidocaine, and ketamine (MLK) have been widely used and can significantly decrease MAC and improve analgesia during inhalant anesthesia.30 To reduce MAC, the author generally prefers to administer intermittent intravenous boluses of hydromorphone (0.1 mg/kg IV) as needed with or without midazolam (0.1 mg/kg IV) as needed or fentanyl (0.003-0.04 mg/kg/h CRI) with or without midazolam (0.1-0.5 mg/kg/h CRI). In some cases, anesthesia can be maintained in critically ill patients with little or no inhalant. In very unstable cases, the use of nondepolarizing muscle relaxants (e.g., atracurium, pancuronium, vecuronium) along with opioid administration may help to avoid the use of an inhalant.

    In most patients with perioperative hypotension, the above techniques can improve BP. Patients that do not respond to these techniques likely have a significant decrease in cardiac function and/or a decrease in vascular tone. In these cases, a pharmacologic aid is used to improve SVR and inotropy (see Pharmacologic Management of Systemic Vascular Resistance).


    Prevention of perioperative hypotension involves initial stabilization of a patient's disease state as much as possible before administration of anesthesia. Patient monitoring is crucial to preventing perioperative hypotension. All patients undergoing anesthesia, regardless of age, the procedure, or health status, should have their BP monitored at regular intervals. In these patients, an IV catheter should be placed and a balanced crystalloid administered perioperatively.

    For healthy patients under anesthesia that are not at risk for volume overload (e.g., heart failure, anuria), fluid rates are typically 10-20 mL/kg/h for the first hour and 10 mL/kg/h thereafter. In patients that are at risk for fluid overload, a central venous catheter should be placed (e.g., in the jugular vein) and central venous pressure (CVP) monitored during anesthesia to assess cardiac preload status and to direct fluid therapy. A starting fluid rate for these cases is often 2.5-5 ml/kg/h but should be adjusted according to individual needs.

    A balanced anesthesia technique allows the use of multiple drugs in small quantities to avoid large doses of a single agent. This helps avoid adverse effects seen with the dependence on a single drug, especially limiting the pronounced cardiac depression that can be observed with the use of inhalant anesthetics.31

    1. Redondo JI, Rubio M, Soler G, et al. Normal values and incidence of cardiorespiratory complications in dogs during general anesthesia. A review of 1281 cases. J Vet Med A Physiol Pathol Clin Med 2007;54(9):470-477.

    2. Bijker J, van Klei W, Kappen TH, et al. Incidence of intraoperative hypotension as a function of the chosen definition: literature definitions applied to a retrospective cohort using automated data collection. Anesthesiology 2007;107(2):213-220.

    3. Gaynor JS, Dunlop CI, Wagner AE, et al. Complications and mortality associated with anesthesia in dogs and cats. JAAHA 1999;35:13-17.

    4. Wagner AE, Hellyer PW. Observations of private veterinary practices in Colorado, with an emphasis on anesthesia. J Vet Med Educ 2002;29:176-182.

    5. Diplomates of the ACVA. Suggestions for monitoring anesthetized veterinary patients. JAVMA 1995;206(7):936-937.

    6. Tranquilli WJ, Thurmon JC, Grimm KA. In: Lumb & Jones' Veterinary Anesthesia & Analgesia. 4th ed. Ames, IA: Blackwell-Wiley; 2007: 79-81.

    7. Ettinger SJ, Feldman EC. In: Textbook of Veterinary Internal Medicine. 6th ed. St. Louis: Elsevier Saunders; 2005;480.

    8. Grandy JL, Dunlop CI, Hodgson DS, et al. Evaluation of the Doppler ultrasonic method of measuring systolic arterial blood pressure in cats. Am J Vet Res 1992;53:1166-1169.

    9. Todd MM, Drummond JC. A comparison of the cerebrovascular and metabolic effects of halothane and isoflurane in the cat. Anesthesiology 1984;60:276-282.

    10. Mutoh T, Nishimura R, Kim HY, et al. Cardiopulmonary effects of sevoflurane, compared with halothane, enflurane and isoflurane, in dogs. Am J Vet Res 1997;58:885-890.

    11. Ebert TJ, Harkin CP, Muzi M. Cardiovascular response to sevoflurane: a review. Anesth Analg 1995;81(Suppl):11-22.

    12. Coulter DB, Whelan SC, Wilson RC, et al. Determination of blood pressure by indirect methods in dogs given acetylpromazine maleate. Cornell Vet 1981;71:75-84.

    13. Doi M, Ikeda K. Respiratory effects of sevoflurane. Anesth Analg 1987;66:241.

    14. Ilkiw JE, Pascoe PJ, Haskins SC, Patz JD. Cardiovascular and respiratory effects of propofol administration in hypovolemic dogs. Am J Vet Res 1992;53:2323-2327.

    15. Cole S, Otto C, Hughes D. Cardiopulmonary cerebral resuscitation in small animals—a clinical practice review. Part II. JVECC 2003;3(1):13-23.

    16. Stoelting RK. Kidneys. In: Pharmacology and Physiology in Anesthetic Practice. Philadelphia: JB Lippincott; 1987:761-799.

    17. Silverstein DC, Wininger FA, Shofer FS, et al. Relationship between Doppler blood pressure and survival or response to treatment in critically ill cats: 83 cases (2003-2004). JAVMA 2008;232(6):893-897.

    18. Simpson KE, McCann TM, Bommer NX, et al. Retrospective analysis of selected predictors of mortality within a veterinary intensive care unit. J Feline Med Surg 2007;9(5):364-368.

    19. Monk TG, Saini V, Weldon BC, et al. Anesthetic management and one-year mortality after noncardiac surgery. Anesth Analg 2005;100(1):4-10.

    20. Ettinger SJ, Feldman EC. In: Textbook of Veterinary Internal Medicine. 6th ed. St. Louis: Elsevier Saunders; 2005:482.

    21. Tranquilli WJ, Thurmon JC, Grimm KA. In: Lumb & Jones' Veterinary Anesthesia & Analgesia. 4th ed. Ames, IA: Blackwell Wiley; 2007:205-206.

    22. Tranquilli WJ, Thurmon JC, Grimm KA. In: Lumb & Jones' Veterinary Anesthesia & Analgesia. 4th ed. Ames, IA: Blackwell Wiley; 2007:971.

    23. Tranquilli WJ, Thurmon JC, Grimm KA. In: Lumb & Jones' Veterinary Anesthesia & Analgesia. 4th ed. Ames, IA: Blackwell Wiley; 2007:13.

    24. Kazama T, Ikeda K. Comparison of MAC and the rate of rise of alveolar concentration of sevoflurane with halothane and isoflurane in the dog. Anesthesiology 1988;68:435.

    25. Doi M, Yunoki H, Ikeda K. The minimum alveolar concentration of sevoflurane in cats. J Anesthesia 1988;2:113.

    26. Steffey EP, Howland D. Isoflurane potency in the dogs and cat. Am J Vet Res 1977;38:1833-1836.

    27. Hellyer PW, Mama KR, Shafford HL, et al. Effects of diazepam and flumazenil on minimum alveolar concentrations for dogs anesthetized with isoflurane or a combination of isoflurane and fentanyl. Am J Vet Res 2001;62(4):555-560.

    28. Mednes GM, Selmi AL. Use of a combination of propofol and fentanyl, alfentanil, or sufentanil for total intravenous anesthesia in cats. JAVMA 2003;223(11):1608-1613.

    29. Liehmann L, Mosing M, Auer U. A comparison of cardiorespiratory variables during isoflurane-fentanyl and propofol-fentanyl anesthesia for surgery in injured cats. Vet Anaesth Analg 2006;33(3):158-168.

    30. Muir WW, Wiese AJ, March PA. Effects of morphine, lidocaine, and ketamine on MAC in isoflurane dogs. Am J Vet Res 2003;64:1155-1160.

    31. Norkus C. Balancing act: combining inhalant anesthetics and injectable drugs. Vet Tech 2006;12:770-780.

    32. Monteiro ER, Teixeira Neto FJ, Castro VB, et al. Effects of acepromazine on the cardiovascular actions of dopamine in anesthetized dogs. Vet Anaesth Analg 2007;(2):312-21.

    33. Tranquilli WJ, Thurmon JC, Grimm KA. Lumb & Jones' Veterinary Anesthesia & Analgesia. 4th ed. Ames, IA: Blackwell Wiley; 2007:975.

    34. Chen HC, Sinclair MD, Dyson DH. Use of ephedrine and dopamine in dogs for the management of hypotension in routine clinical cases under isoflurane anesthesia. Vet Anaesth Analg 2007;34(5):301-311.

    35. Rosati M, Dyson DH, Sinclair MD, et al. Response of hypotensive dogs to dopamine hydrochloride and dobutamine hydrochloride during deep isoflurane anesthesia. Am J Vet Res 2007;68(5):483-494.

    36. Dyson DH, Sinclair MD. Impact of dopamine or dobutamine infusions on cardiovascular variables after rapid blood loss and volume replacement during isoflurane-induced anesthesia in dogs. Am J Vet Res 2006;67(7):1121-1130.

    37. Hofmeister EH, Keenan K, Egger CM. Dobutamine-induced bradycardia in a dog. Vet Anaesth Analg 2005;32(2):107-111.

    38. Tranquilli WJ, Thurmon JC, Grimm KA. In: Lumb & Jones' Veterinary Anesthesia & Analgesia. 4th ed. Ames, IA: Blackwell Wiley; 2007:973.

    39. Wheeler AH, Turchiano J, Tobias JD. A case of refractory intraoperative hypotension treated with vasopressin infusion. J Clin Anesth 2008;20(2):139-142.

    40. Tranquilli WJ, Thurmon JC, Grimm KA. In: Lumb & Jones' Veterinary Anesthesia & Analgesia. 4th ed. Ames, IA: Blackwell Wiley. 2007:982.

    References »

    NEXT: PetSmart Expands Recall on Pet Carousel, Inc. Products


    Did you know... A hyperbaric oxygen therapy session is called a “dive.” Read More

    These Care Guides are written to help your clients understand common conditions. They are formatted to print and give to your clients for their information.

    Stay on top of all our latest content — sign up for the Vetlearn newsletters.
    • More