Treating Anesthetic Hypotension – Beyond the Fluid Bolus

By Becca Reader, DVM, DACVAA
angell.org/anesthesia
anesthesia@angell.org
617-541-5048

March 2025

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Introduction

Photo courtesy Phil Zeltzman

Many of the commonly used anesthetic agents produce dose-dependent vasodilation, and hypotension is frequently observed in patients placed under general anesthesia. Left untreated, anesthesia-related hypotension can have significant consequences. As a result, it is important to recognize and treat hypotension when it occurs. One of the most commonly utilized treatments for hypotension under anesthesia is the administration of an intravenous fluid bolus. However, several other factors may be contributing to low blood pressure. This article will discuss additional contributors to anesthesia-related hypotension and provide a visual algorithm to help determine which factors are likely contributing to low blood pressure and how to treat them.

Hypotension: Definitions

Traditionally, hypotension under anesthesia has been defined as a mean arterial blood pressure (MAP) below 60 mmHg.¹ This is considered the minimum pressure required to provide adequate blood flow to the kidneys. In addition to maintaining a MAP > 60 mmHg under anesthesia, one should also aim to maintain a systolic blood pressure (SAP) > 90 mmHg and a diastolic blood pressure (DAP) > 40 mmHg. At pressures lower than this, there is a risk of causing acute kidney injury secondary to hypoperfusion.

Many would argue that the lower limit for an acceptable MAP should actually be slightly higher than 60 mmHg. Recall that autoregulatory mechanisms allow for maintaining constant blood flow between MAPs of 60 to 160 mmHg. However, autoregulatory mechanisms rely on input from the sympathetic nervous system, which is depressed under general anesthesia. Additionally, if a MAP of 60 mmHg is considered the minimal acceptable blood pressure, patients may not be assessed as hypotensive, and treatments may not be initiated until the patient is outside the zone of autoregulation.² As a result, it is likely more appropriate to set a MAP of 70 mmHg as the lower limit for acceptable blood pressure under anesthesia.

Mean arterial blood pressure is determined by the product of the patient’s cardiac output (CO) and systemic vascular resistance (SVR). This can be represented by the equation MAP = CO x SVR.² Cardiac output can be further broken down into the product of heart rate (HR) and stroke volume (SV). Rewritten with the expanded definitions, MAP is determined by the product of HR x SV x SVR. Derangements in any one of these components may result in a low MAP.

Anesthesia-Associated Hypotension: Rationale Behind the Fluid Bolus

As mentioned above, many of the commonly used anesthetic drugs produce dose-dependent vasodilation. It is also important to note that of these drugs, inhalant anesthetics (e.g., isoflurane) cause vasodilation at clinically relevant concentrations.³ In addition to causing arterial vasodilation, anesthetic drugs also cause venodilation. This venodilation effectively increases venous capacitance, making it appear that the venous circulation can hold a larger blood volume.³ Because the animal’s blood volume has not actually changed, this results in a “relative” hypovolemia manifesting clinically as hypotension.³ Since the underlying cause of this hypotension is dose-dependent vasodilation secondary to anesthetic agents, the first action steps should be to decrease the concentration of inhalant being delivered to the patient, if feasible.

An intravenous fluid bolus is also considered an appropriate intervention for treating anesthesia-associated hypotension. However, the fluid bolus is not directly intended to correct the “relative” hypovolemia. Instead, the administration of an IV fluid bolus takes advantage of the impact that preload has on the strength of cardiac contraction (or stroke volume). Up to a certain point, the strength of ventricular contraction is proportional to the amount of blood returning to the right side of the heart. An IV fluid bolus will increase the amount of blood returning to the heart, resulting in an increased “stretch” of cardiac myocytes, increasing stroke volume and improving cardiac output.³ Recall the equation, MAP = HR x SV x SVR; in this situation, an IV fluid bolus increases the cardiac stroke volume to improve MAP.

Figure 1 – A visual algorithm illustrating the various potential contributors to hypotension under anesthesia. Mean arterial pressure (MAP) is determined by the product of heart rate x stroke volume x systemic vascular resistance. Derangements in any one of these components may result in a low MAP, and treatments should be aimed at the most likely contributing factor to the patient’s low blood pressure.

Other Contributors to Hypotension

Looking closely at the components of MAP (HR x SV x SVR), it is clear that several factors may contribute to hypotension under anesthesia, and intravenous fluids will only address a few of these factors. Derangements in heart rate, particularly bradycardia, may result in decreased cardiac output and contribute to hypotension under anesthesia. In this circumstance, an IV fluid bolus would be unlikely to improve the patient’s blood pressure, and interventions should instead be aimed at increasing the patient’s heart rate. Likewise, many anesthetic agents – and sometimes underlying disease – can decrease a patient’s cardiac contractility. In this circumstance, efforts should be made to reduce the concentration of anesthetic agent delivered to the patient or improve cardiac contractility using a positive inotrope. Finally, as discussed previously, most anesthetic drugs reduce systemic vascular resistance through dose-dependent vasodilation. Every effort should be made to decrease the concentration of these agents administered to the patient, and under specific circumstances, an IV fluid bolus may be an appropriate intervention. However, if an IV fluid bolus fails to improve the patient’s blood pressure, subsequent interventions should improve vascular tone using vasopressors.

Inotropes and Vasopressors

Inotropes (e.g., dobutamine) increase myocardial contractility, whereas the administration of vasopressors (e.g., norepinephrine, phenylephrine, vasopressin) causes vasoconstriction and increased systemic vascular resistance. Dopamine has dose-dependent effects and doesn’t tend to fit nicely into one category or another (see below for more detail). The decision of which inotrope or vasopressor to use and when requires a fundamental understanding of the mechanism of action of each agent, as well as a clinical interpretation of the pathophysiology behind the low blood pressure.

As mentioned above, dopamine is an endogenous catecholamine with dose-dependent effects. The typical dose rates used for dopamine are 1 to 15 mcg/kg/min.^1,2  At low doses (1–5 mcg/kg/min), dopamine’s main sites of action are at the dopamine 1 and 2 (DA1 and DA2) receptors, resulting in renal vasodilation and increased blood flow to the kidneys.² Mid- to high-range doses (5–10 mcg/kg/min) activate beta-1 receptors, increasing heart rate and contractility.² Doses greater than 10 mcg/kg/min activate alpha-1 receptors, resulting in peripheral vasoconstriction.² The recommended dose for dopamine for improvement of cardiac output is 7 mcg/kg/min, but ultimately, the CRI should be dosed to effect based on response (or lack thereof). This author typically uses dopamine as a first-line agent to treat anesthesia-associated hypotension refractory to the IV fluid bolus.

Norepinephrine is an endogenous catecholamine with primary effects at both alpha-1 and beta-adrenergic receptors, with effects at the alpha-1 receptors predominating.² The typical dose rates used for norepinephrine are 0.05 to 2.0 mcg/kg/min.^1,2 At low to mid-range doses, norepinephrine activates primarily alpha-1 receptors, resulting in peripheral vasoconstriction and increased systemic vascular resistance.² At high doses, norepinephrine will activate beta-1 receptors, increasing heart rate and contractility.² Norepinephrine is best used to treat septic shock or other disease states that result in systemic vasodilation.

Dobutamine is a synthetic catecholamine with primary effects at beta-1 and beta-2 receptors.² The typical dose rates used for dobutamine are 1 to 10 mcg/kg/min.^1,2 At lower dose ranges (1–5 mcg/kg/min), dobutamine activates primarily beta-1 receptors, increasing cardiac contractility and heart rate.²  At higher doses, dobutamine may activate beta-2 receptors and will induce a decrease in systemic vascular resistance due to beta-2-mediated vasodilation.² Dobutamine is typically used in patients with known cardiac disease that is associated with decreased contractility or in clinical situations where either drugs or disease are known to impact cardiac contractility negatively.

Conclusion

Intravenous fluids are important in treating anesthesia-associated hypotension, but an IV fluid bolus may not always be the most appropriate intervention. It is important to evaluate all contributors to MAP (MAP = HR x SV x SVR) and target interventions at the component of the MAP equation most likely to be causing the patient’s low blood pressure.

References

1. Grubb T, Sager J, Gaynor JS et al. 2020 AAHA anesthesia and monitoring guidelines for dogs and cats. J Am Anim Hosp Assoc. 2020;56(2): 59-82.
2. Congdon J. Cardiovascular Disease. In: Snyder LBC, Johnson RA, eds. Canine and Feline Anesthesia and Co-Existing Disease. Wiley-Blackwell; 2022:1-85.
3. Noel-Morgan J and William W. Muir. Anesthesia-associated relative hypovolemia: mechanisms, monitoring, and treatment considerations. Front Vet Sci. 2018;16(5):53.