Hypotension....what to do? (Proceedings)
Why treat hypotension?
Mean arterial pressure (MAP) is the driving force for blood flow (perfusion) through capillaries that supply oxygen to organs and tissue beds of the body. Thus, when speaking of hypotension it is most important to focus on the MAP. In small animals, MAP < 60 mm of Hg result in compromised perfusion of visceral organs and peripheral tissues, potentially leading to whole organ or regional ischemia. In large animals perfusion of skeletal muscle (especially skeletal muscle in recumbent areas of the body) is compromised at MAP < 70 mm of Hg. In all species, MAP < 40 mm of Hg are associated with inadequate perfusion of vessel-rich organs such as the heart, lungs, and CNS. Clinically significant hypotension (i.e. mean arterial pressure less than 60 mm of Hg) can lead to renal failure, reduced hepatic metabolism of drugs, worsening of ventilation/perfusion mismatch and hypoxemia, delayed recovery from anesthesia, neuromuscular complications during recovery (especially large animals), and CNS abnormalities including blindness after anesthesia that may or may not resolve with time. Untreated, severe hypotension can lead to cardiac and respiratory arrest.
Estimation of MAPMean arterial pressure = diastolic pressure + 1/3(systolic pressure - diastolic pressure). Most indirect blood pressure monitors provide data for systolic pressure (e.g. doppler method) or systolic, diastolic, and mean arterial pressure (e.g. oscillometric devices). Roughly, the mean arterial pressure is 20 - 30 mm of Hg less than the measured systolic pressure on a doppler in most species. Thus, a doppler reading of 80 to 90 mm of Hg correlates with a mean arterial pressure that would be considered hypotensive. The exception to this rule is cats < 4 - 5 kg (and likely other small mammals) in which the doppler reading correlates most closely with mean arterial pressure.
What determines blood pressure?
Mean arterial pressure = cardiac output x systemic vascular resistance. In thinking about causes of hypotension, it is useful to break this equation down into its various components and then assess the effects of anesthetic drugs or the animal's physiologic state on each component. Cardiac output = heart rate x stroke volume. For example, a drug that reduces contractility (e.g. isoflurane) will lower stroke volume and can then contribute to a lower cardiac output, which may result in low mean arterial pressure if systemic vascular resistance has not increased.
Systemic vascular resistance
A reduction in systemic vascular resistance (SVR) will decrease mean arterial pressure. Many of the drugs commonly used for anesthesia will reduce systemic vascular resistance. These drugs include: acepromazine, thiobarbiturates, propofol, and, most importantly, inhalants. All of the above listed drugs decrease systemic vascular resistance in a dose-dependent fashion. Preexisting physiologic factors in a patient that presents for anesthesia (e.g. dehydration), or events that may occur as a result of surgical intervention (e.g. blood loss), will also decrease SVR. When possible, preexisting causes of reduced SVR should be corrected prior to general anesthesia. Examples include: hemorrhage, inadequate volume administration or replacement, dehydration, endotoxemic shock, overwhelming sepsis, cardiogenic shock, neurogenic shock, anaphylaxis, histamine release, severe hypercapnia.
A reduction in heart rate may or may not affect mean arterial pressure. If heart rate is low in the face of good contractility, then often the increase in end-diastolic ventricular volume (and associated increase in ejected stroke volume) will help to maintain cardiac output and therefore mean arterial pressure. If contractility is poor, however, as is often the case in patients receiving inhalant anesthetics, then stroke volume may not increase in response to a longer diastolic filling time and measured mean arterial pressure will be reduced. The following is a list of drugs or pre-existing conditions that may reduce heart rate: physiologic (athletic) bradycardia, hypothermia, increased vagal tone, high cervical cord compression, intracranial disease, electrolyte imbalances, opioids, alpha-2 agonists, inhalants, acetylcholinesterase inhibitors, anticholinesterases (transient, paradoxical; increase in heart rate usually follows; e.g. glycopyrrolate).