By definition, blood pressure (BP) is the force that the flow of blood exerts on the walls of the vessels and what drives tissue perfusion. It is believed that a mean arterial blood pressure of 70 mm Hg is required for adequate perfusion of vital organs such as the brain, heart and kidneys. Blood pressure is directly affected by cardiac output and systemic vascular resistance (BP = CO x SVR). Because cardiac output is dependent on the heart rate and stroke volume, the latter two components will affect blood pressure. In addition, stroke volume is affected by preload, afterload and cardiac contractility. Therefore, hypotension is normally a result of a combination of factors such as bradycardia, vasodilation (decreases in systemic vascular resistance), and decreases in cardiac contractility which in turn will reduce stroke volume and cardiac output.¹

Blood pressure is measured either indirectly (oscillometric sphygmomanometry or Doppler ultrasonography) or directly when a catheter is placed in an artery and connected to a pressure transducer that allows constant and continuous evaluation of systolic, mean and diastolic blood pressure. In fact, invasive blood pressure is widely used for accurate BP monitoring of critical patients or during general anesthesia where arterial blood sampling is required.^2,3 Cardiac output may be evaluated noninvasively in client-owned animals; however, such techniques are most commonly applied in research.⁴

Within physiological conditions, neural, hormonal and local mediators control systemic blood pressure. These strict mechanisms might be affected during disease and anesthesia, and hypotension inevitably occurs. Common causes of hypotension include hypovolemia (hemorrhage, fluid deficits, relative hypovolemia due to vasodilation), vasodilation (anesthetic drug-induced, severe metabolic or respiratory acidosis, severe hypoxemia, endotoxemia, septicemia, anaphylactic reactions), myocardial depression (decreased contractility - drug-induced such as inhalant anesthetics, hypoxemia, acid-base disturbances, electrolyte imbalances, cardiomyopathy, catecholamine depletion), cardiac arrhythmias (bradycardia, bradyarrhythmias, atrial fibrillation, ventricular tachycardia), obstruction of venous return (mechanical ventilation, gastric-dilatation volvulus, pericardial effusion, tumors, surgery packing), vagal stimulation (drug-induced - opioids, excessive traction of abdominal organs, pressure on the eye) and sympathetic blockade (loco-regional anesthesia), among others. It is crucial to understand the possible causes of hypotension for adequate treatment.

A stepwise approach to the treatment of hypotension is recommended.

 Diagnose and identify the underlying cause(s) of hypotension based on physical examination (heart rate, mucous membrane colours, capillary refill time, pulse quality, evident blood loss, arrhythmias on auscultation, behavioral changes), blood work (PCV, TP, blood gas, CBC, electrolyte imbalance, lactate), drugs that were administered (anesthetics, opioids, epidural administration of local anesthetics)⁶, monitoring (ECG and arrhythmias) and diagnostic tools (radiology, ultrasonography and echocardiography for tumours, GDV, pericardial effusion, peritonitis, etc.). It is also important to identify technical errors such as cuff size and position, transducer calibration and height and inaccuracy of the monitor before triggering the treatment for hypotension.

 Fluid therapy is administered only when primary cardiogenic disease has been excluded. In this case, positive inotropes (dobutamine 1–5 mcg/kg/min IV - an agonist of beta-adrenergic receptors) and diuretics are administered depending on the cardiomyopathy.

 Fluid therapy aims to correct fluid deficits and ameliorate preload, stroke volume, and cardiac output. Fluid therapy will correct ongoing losses, and balanced, isotonic crystalloids are the first option to increase intravascular volume (10–20 mL/kg over 15 min or so-called "fluid challenge").⁷ This is usually not attempted in patients with oliguria or anuria, and heart disease. Colloids (3–5 mL/kg over 20 minutes) are administered in combination or not with crystalloids especially in hypoalbuminemia. Hypertonic saline (saline 7.5%) is administered (3–4 mL/kg in 5–10 minutes) also if excessive hypotension is observed. These therapies are better used in combination in high-risk cases such as GDV. Blood pressure is closely monitored for observation of "endpoints." Fluid therapy may produce adverse-effects which are discussed in the course of the lecture. Current trends indicate pulse-pressure variation as means of monitoring the effectiveness of fluid therapy.

 Hypoxemia, hypercapnia and electrolyte disturbances should be corrected.

 Doses of anesthetics and other cardiovascular depressant drugs should be reduced or adjusted in cases where hypotension is hypothetically caused by bradycardia and vasodilation. In these cases, fluid therapy will most likely have no effect unless if dehydration and hypovolemia are concomitantly present. For example, it is important to adjust the depth of anesthesia during surgery according to the surgical stimulus and vital parameters (surgical depth of anesthesia). Inhalant anesthetics, propofol and barbiturates are well-known for decreasing myocardial contractility and systemic vascular resistance (vasodilation). Balanced anesthesia aims to administer additional analgesics or sedatives with anesthetic-sparing effects.⁸ Ventilation is adjusted in order to reduce peak airway pressure and positive end-expiratory pressure without affecting gas alveolar change.

 Hypotension is commonly associated with bradycardia or bradyarrhythmias (2nd degree AV block or ventricular escape beats). The cause of bradycardia is identified and treatment with an anticholinergic (atropine or glycopyrrolate) is recommended especially in opioid-vagal induced bradycardia. Hypothermia is another common cause of bradycardia which pharmacotherapy may not be effective. On the other hand, dexmedetomidine-induced bradycardia associated with hypertension should not treated.

 Tachycardia may affect diastolic filling and reduce coronary perfusion which will consequently affect stroke volume and cardiac output. It increases myocardial oxygen consumption and work. Tachycardia is treated with fluid bolus (in cases of hypovolemia and dehydration, and reflex tachycardia) or antagonists of beta-adrenergic receptors ("beta-blockers") in case of excessive sympathetic stimulation.

 Sympathetic support is recommended when positive inotropism, chronotropism and vasoconstriction are desired, especially in normovolemia. Drugs such as dopamine (5–20 mcg/kg/min, an agonist of D1, D2, beta and alpha receptors depending on the dose) and ephedrine (0.2 mg/kg, IV, an agonist of beta and alpha receptors) are administered during anesthesia.⁹ In cases of severe vasodilation during sepsis and endotoxemia, norepinephrine (0.05–2 µg/kg/min; an agonist of alpha receptors) that provides arterial vasoconstriction, and/or arginine vasopressin (0.5–2 mU/kg/min, IV) that causes arterial and venoconstriction and increase venous return, are administered.

It is important to understand the physiologic, humoral and tissue mechanisms that regulate blood pressure. Hypotension is only treated appropriately when the underlying causes are properly identified. Ultimately, the therapy will aim to correct fluid deficits while maximizing cardiac output (heart rate and stroke volume, myocardial contractility) and systemic vascular resistance.

References

1.  Klein BG. Cunningham's Textbook of Veterinary Physiology. 5th ed. London, UK: Elsevier Health Sciences; 2013.

2.  Monteiro ER, Campagnol D, Bajotto GC, Simões CR, Rassele AC. Effects of 8 hemodynamic conditions on direct blood pressure values obtained simultaneously from the carotid, femoral and dorsal pedal arteries in dogs. J Vet Cardiol. 2013;15:263–270.

3.  Bosiack AP, Mann FA, Dodam JR, Wagner-Mann CC, Branson KR. Comparison of ultrasonic Doppler flow monitor, oscillometric, and direct arterial blood pressure measurements in ill dogs. J Vet Emerg Crit Care. 2010;20:207–215.

4.  Shih A, Maisenbacher HW, Bandt C, et al. Assessment of cardiac output measurement in dogs by transpulmonary pulse contour analysis. J Vet Emerg Crit Care. 2011;21:321–327.

5.  Petit AM, Gouni V, Tissier R, et al. Systolic arterial blood pressure in small-breed dogs with degenerative mitral valve disease: a prospective study of 103 cases (2007–2012). Vet J. 2013;197:830–835.

6.  Iizuka T, Kamata M, Yanagawa M, Nishimura R. Incidence of intraoperative hypotension during isoflurane-fentanyl and propofol-fentanyl anaesthesia in dogs. Vet J. 2013;198:289–291.

7.  Silverstein DC, Kleiner J, Drobatz KJ. Effectiveness of intravenous fluid resuscitation in the emergency room for treatment of hypotension in dogs: 35 cases (2000–2010). J Vet Emerg Crit Care. 2012;22:666–673.

8.  Steagall PV, Teixeira Neto FJ, Minto BW, Campagnol D, Corrêa MA. Evaluation of the isoflurane-sparing effects of lidocaine and fentanyl during surgery in dogs. J Am Vet Med Assoc. 2006;229:522–527.

9.  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;34:301–311.