Happy Medium: Blood Pressure Goals in the OR

Sustained intraoperative hypotension is associated with end-organ injury. Postoperative acute kidney injury (AKI), for example, is a common complication in major noncardiac surgery. The incidence of AKI has been reported to be as high as 12% in certain surgical populations and has been repeatedly associated with increased long-term morbidity, including the development of chronic kidney disease, increased length of hospital stay, and death (Anesthesiology 2021;134:250-61; JAMA Netw Open 2019;2:e1916921). The pathophysiology of AKI is multifactorial; however, intraoperative hypotension has been implicated as a modifiable risk factor in large observational studies and randomized clinical trials (RCTs) (Nat Rev Nephrol 2021;17:605-18). These studies have shown that AKI is associated with the severity and duration of hypotensive episodes.

Myocardial injury is another frequent complication after major noncardiac surgery. Multiple observational studies have reported an incidence of postoperative cardiac injury between 8%-10% but as high as 18% in high-risk patients. While most patients with myocardial injury have underlying coronary artery disease, acute thrombosis is rarely the cause of ischemia in the perioperative setting. Hypotension and consequently oxygen supply-demand mismatch have been identified as a predominant factor (Anesthesiology 2021;134:250-61). Postoperative myocardial injury after noncardiac surgery is associated with postoperative congestive heart failure, nonfatal cardiac arrest, stroke, and 30-day mortality (Anesthesiology 2014;120:564-78).

Intraoperative hypotension has also been linked to postoperative neurologic complications. In a recent retrospective trial, a mean arterial pressure (MAP) <55 mmHg was associated with a duration-dependent increase in odds of delirium within 30 postoperative days (Anesth Analg 2022;134:822-33). A case-control study from 2012 found an association between the duration of MAPs below 30% from baseline and the occurrence of postoperative ischemic strokes (Anesthesiology 2012;116:658-64).

In patients without traumatic injury, induced hypotension is no longer recommended as a routine strategy to decrease intraoperative blood loss due to the risk of compromising organ perfusion and should only be used after discussing risks and benefits with the surgical team (Anesthesiology 2019;130:12-30).

Intraoperative hypertension is thought to increase the risk for cardiac events, vascular injury, neurologic complications, and surgical blood loss (J Patient Saf 2021;17:e758-e64; Vasc Health Risk Manag 2008;4:615-27; Hypertension 2018;72:806-17). But literature on adverse effects of perioperative hypertension in noncardiac surgery remains controversial. In a retrospective study of 55,563 normotensive patients, major adverse cardiac events were associated with intraoperative systolic blood pressures (SBPs) ≥50 mmHg from baseline (J Hypertens 2021;39:1982-90). However, a larger retrospective analysis of 76,042 adults found no meaningful relationship between intraoperative SBPs ranging from 120-200 mmHg and AKI or the composite of myocardial injury and mortality (Eur J Anaesthesiol 2022;39:315-23). Literature about hypertension during cardiac surgery seems less ambiguous. In a prospective multicenter epidemiological study of 2,417 patients undergoing CABG surgery, isolated hypertension increased the risk of a composite outcome, including left ventricular dysfunction, cerebrovascular events, renal insufficiency, and all-cause mortality, by 30% (Anesth Analg 2002;94:1079-84). Evidence between surgical blood loss and blood pressure remains vague. While blood loss is associated with blood pressure in certain types of surgery, there is no clear association between blood pressure peaks and blood loss in cardiac surgery (J Neurosurg 2017;127:1025-40; J Orthop Surg Res 2020;15:350; Intensive Crit Care Nurs 2017;42:122-6).

Not surprisingly, postoperative complications have a significant impact on health care costs (J Gen Intern Med 2006;21:177-80). In 2018, Keuffel and colleagues estimated annual cost reductions of $1.19 million-$4.58 million by avoiding intraoperative hypotension and related AKI and myocardial injury for a hospital system with 10,000 noncardiac cases a year (J Med Econ 2019;22:645-51). Nanji et al. estimated that postoperative complications associated with intraoperative hypotension and hypertension led to costs of $1.7 billion to the U.S. health system, with stroke after intraoperative hypertension being the most expensive adverse outcome (J Patient Saf 2021;17:e758-e64).

There remains little consensus on defining hypotension or hypertension in the OR. Many clinical trials use a threshold of MAP <60 mmHg to characterize intraoperative hypotension, while multiple national societies define perioperative hypertension as a blood pressure ≥160/90 mmHg (Br J Anaesth 2018;121:706-21; Hypertension 2018;72:806-17; Hypertension 2018;71:1269-324). However, standardized blood pressure goals might be insufficient, as individual physiologic or surgical demands differ (Br J Anaesth 2018;121:706-21; Anesth Analg 2002;95:273-7; Hypertension 2018;72:806-17).

Patient factors such as age and comorbidities affect intraoperative blood pressure thresholds. In an RCT of chronically hypertensive patients undergoing gastrointestinal surgery, a targeted MAP ≥80 mmHg led to a lower incidence of postoperative AKI compared to a MAP goal ≥65 mmHg (J Clin Anesth 2017;43:77-83). Similarly, different retrospective trials have found an association between reductions in intraoperative blood pressure from the preoperative baseline and MI, ischemic strokes, and mortality in noncardiac surgery (Anesthesiology 2012;116:658-64; Anesthesiology 2016;124:35-44; Anesthesiology 2015;123:307-19). While these findings were based on prolonged or extreme blood pressure variations, a multicenter RCT showed that restricting fluctuations to 10% from the patient’s systolic baseline improved a composite outcome of postoperative organ function, including renal, cardiovascular, respiratory, coagulation, and cerebral dysfunction (JAMA 2017;318:1346-57).

Surgical factors such as positioning, surgery type, and choice of anesthesia also influence intraoperative blood pressure goals. For surgeries in the sitting position, for example, it is common practice to consider the hydrostatic pressure gradient between the brain and heart when defining an intraoperative blood pressure target (Anesthesiology 2021;134:250-61). During cross-clamping in carotid endarterectomies, MAPs are often kept above the patient’s baseline to improve collateral flow. Evidence to support these practices, however, is limited. It further remains unclear if different anesthetic techniques, which allow for neurologic assessments such as neuraxial anesthesia or conscious sedation, require the same blood pressure goals as general anesthetics (Hypertension 2018;72:806-17).

A similar debate about absolute or relative thresholds exists for perioperative hypertension. In a large retrospective study, major adverse cardiac events were associated with a relative increase in intraoperative SBP ≥50 mmHg from preoperative baseline. However, only patients with SBP ≤140 mmHg at baseline were included, limiting the generalizability of the results (J Hypertens 2021;39:1982-90). For neurosurgical patients, many institutions choose SBP goals of ≤140 mmHg given the concern for intracranial hematoma formation or expansion. But more recent evidence suggests an association between intensive blood pressure control and brain tissue hypoxia or AKI in patients with spontaneous intracranial hemorrhage (J Neurosurg 2021;135:1656-65; Anesthesiology 2017;126:47-65). Some societies, therefore, acknowledge the concern for end-organ ischemia in chronically hypertensive patients and define perioperative hypertension as an SBP elevation ≥20% of the preoperative value (Hypertension 2018;71:1269-324).

Overall, many retrospective trials found associations between relative or absolute thresholds and worse outcomes, highlighting the need for more RCTs (Anesth Analg 2002;95:273-7; J Hypertens 2021;39:1982-90; Anesthesiology 2015;123:307-19; N Engl J Med 2016;375:1033-43). Future work should also investigate how the duration of intraoperative hypotensive and hypertensive episodes impacts clinical outcomes (JAMA Neurol 2020;77:622-31).

Due to a complex array of patient-individualized aspects, surgery-customized factors, and anesthetic actions, we often find ourselves controlling extremes in blood pressure.

Innocuous forms of hypotension could result from our anesthetic actions, such as positive pressure ventilation and drugs. More severe reductions could be from hypovolemia due to blood loss or long case times with sparse fluid administration (Anesthesiology 2021;134:250-61). It is essential, though, to properly evaluate and diagnose cardiogenic, distributive, or obstructive causes (Anesthesiology 2020;132:908-16).

Noninvasive and invasive hemodynamic monitoring can provide important information on volume responsiveness and cardiac output, which, along with more traditional methods of end-organ monitoring such as urine output and telemetry, can help drive decision-making (Br J Anaesth 2018;121:706-21; Anesthesiology 2021;134:250-61). Lately, echocardiography has been advocated to provide real-time information to differentiate volume responsiveness from more sinister causes (Anesthesiology 2020;132:908-16). Other types of end-organ monitoring, such as intraoperative neurophysiologic and tissue oxygenation monitoring, allow adjusting blood pressure goals to effect organ function (Hypertension 2018;72:806-17; Clin Neurophysiol 2013;124:2291-316). Significant reductions in evoked potentials, for example, may be due to a disruption in the perfusion of the spinal cord or central nervous system. Increasing perfusion pressure and monitoring the effect on responses may reverse hypoperfusion-related injuries (Clin Neurophysiol 2013;124:2291-316). Regardless, it is imperative that risks and benefits are discussed with the surgical team.

Overall, timely treatment of hypotension with goal-directed fluid management and vasoactive drugs is critical in preventing end-organ injury (Anesthesiology 2021;134:250-61). Vasoconstricting agents, including catecholaminergic drugs, vasopressin, or novel agents such as angiotensin II, increase perfusion pressure, while inotropic agents improve cardiac output (N Engl J Med 2017;377:419-30). Controversy exists regarding which agent best enhances end-organ perfusion while causing minimal adverse effects, and additional research by our specialty is required (Anesthesiology 2021;134:250-61).

Hypertension also requires the anesthesiologist’s attention. Initial management often involves deepening the anesthetic and treating pain, but the primary cause of hypertension should be identified and addressed. For example, patients with underlying uncontrolled primary hypertension may require treatment with antihypertensive agents, while secondary etiologies such as endocrine emergencies may also involve causal therapy. Short-acting beta and calcium channel blockers are often preferred in the OR. Calcium channel blockers or nitrodilators are readily available as continuous drip. Ultra-short-acting agents such as clevidipine have been shown to effectively treat hypertensive emergencies while avoiding iatrogenic hypotension and should be the focus of clinical outcomes research (Vasc Health Risk Manag 2008;4:615-27).

Overall, the blood pressure should be kept at the acceptable upper range when the possibility of organ ischemia is substantial; if hypertension-related risks are significant, it should be held at the lower accepted limit. Regardless, targets should always be defined based on an interdisciplinary benefit-risk discussion.

In conclusion, the anesthesiology community significantly impacts perioperative clinical outcomes and health care costs through cause-related and goal-directed treatment of intraoperative hypotension and hypertension. Our community should lead the effort for more RCTs proving the benefits of optimized end-organ perfusion on perioperative outcomes.