Intraoperative hypotension—defined as a decrease in blood pressure during surgery—is a common and potentially serious complication. Recognizing intraoperative hypotension is crucial. Effective treatment is vital to prevent adverse outcomes such as organ hypoperfusion, myocardial ischemia, and postoperative morbidity. But what constitutes intraoperative hypotension? When is a “good” BP bad?
Case
I was returning from a Chief’s meeting. I decided to walk through the post anesthesia care unit (PACU) to check on progress. One of the nurses approached me concerned that she had a patient who remained unresponsive after 30 minutes. The patient was a 70-year-old woman who had a history of chronic hypertension. She had undergone a total abdominal hysterectomy for cancer under general anesthesia.
Her anesthesiologist was busy with another surgery, so I checked her medical records. Normally, she took hydrochlorothiazide and metoprolol, but she skipped them that morning. Her preoperative BP was 175/90, attributed to “nerves”. Yet, when I reviewed her prior history, I noticed her systolic arterial pressure (SAP) was often above 180. Her blood pressure seemed poorly controlled. Her pulse was typically in the 80s. In prior office visits, they had attributed her hypertensive numbers to “white coat” syndrome. This syndrome is the fear of visiting the doctor causing a rise in BP.
During surgery her anesthesiologist had used fairly high concentrations of isoflurane. This was done to lower her blood pressure to reduce blood loss during the operation. Additionally, he gave her several 5 mg doses of labetalol. Intraoperatively, her SAP ran 100s, MAP 73, pulse of 60. Surgery lasted 2 hours.
Evaluation
Evaluating unfamiliar patients in PACU can be difficult. Anesthesia providers should include all pertinent details in the preoperative assessment and intraoperative course to help others diagnose complications. Consider what information you’d want to know if asked to assess someone else’s patient urgently.
Delayed emergence can occur for a wide variety of reasons, including:
- lingering anesthesia
- hypoglycemia
- electrolyte imbalances
- hypoxia
- hypercarbia
- neurological problems like increased intracranial pressure or stroke.
Time is of the essence in such a workup because minutes can translate into brain and organ damage.
The patient was still unresponsive with vital signs: BP 120/80, P 60, RR 12, O2Sat 96% on 40% face mask. Point of care tests showed normal blood glucose, Hct, and electrolytes; blood gas was normal. Bedside EKG was normal. She had received 5 mg of morphine intraoperatively 45 minutes before. She had not received any narcotic in PACU. Nonetheless, I did give several small, titrated 0.1 mg doses of Narcan anyway. It had no effect.
I called a code stroke.
The stroke team came quickly and transported her for a stat MRI which showed damage from an ischemic stroke. Follow up workup did not reveal any heart or carotid artery pathology. The ICU eventually concluded that an SAP of 100 had been too low for this poorly controlled chronic hypertensive. It was considered a “good” BP, but inappropriate for her condition. They believed that poor perfusion resulting from the lower BP had caused the stroke.
The patient never recovered consciousness.
What Is Intraoperative Hypotension?
Surprisingly, there isn’t a uniform definition of intraoperative hypotension. And there isn’t a uniform approach to managing it. One systematic review identified 140 definitions of intraoperative hypotension in 130 studies (Bijker). Typical fixed formulas rely on systolic arterial pressure (SAP), mean arterial pressure (MAP), or a combination of the two.
A few of the various definitions include:
- SAP less than 80 mmHg
- Decrease in SAP greater than 20%, or 30%, or 40%
- SAP less than 100 and a decrease of 30% below baseline
- MAP less than 55-65 mmHg, where MAP= (2 x diastolic BP + systolic BP)/3
Fixed formulas are a good place to start, but they overlook individual risk factors. For example, a patient in the beach chair position will need higher SAPs/MAPs. This is to guarantee adequate cerebral blood flow because of the effects of gravity. There is also a difference in MAP due to the position of the cuff below the head. A patient undergoing carotid endarterectomy will need higher MAP to compensate for obstructed flow and clamping. Or like our case patient, a poorly controlled hypertensive may have different autoregulation thresholds. This makes them vulnerable to ischemia at blood pressures typically deemed safe.
What is Cerebral Autoregulation?
The brain is a closed system containing parenchyma, cerebrospinal fluid, and blood sealed inside the skull. An uncompensated increase in any component raises intracranial pressure, while reduced blood flow can cause ischemia. Autoregulation also ensures that cerebral perfusion pressure (CPP) is closely regulated according to metabolic needs.
Cerebral perfusion pressure (CPP) = MAP – Intracranial pressure (ICP)
Raising MAP increases CPP. Lowering MAP decreases CPP. Raising ICP lowers CPP.
Cerebral autoregulation keeps blood flow stable despite changes in systemic blood pressure, mainly by altering cerebral vessel diameter. This process is active between a MAP of 60–150 mmHg mean arterial pressure. It involves myogenic, neurogenic, endothelial, and metabolic mechanisms to prevent damage. This helps manage excessive or insufficient blood flow. Below 60, or above 150 autoregulation starts to fail.

Factors like chronic hypertension, recent brain injury, and anesthesia can shift both the MAP curve and range of autoregulation. This means that this MAP autoregulatory range is not universal. It must be individualized to the patient and the circumstances.
Before starting any anesthetic, I always advised my students to decide on an acceptable SAP/MAP range. They had to consider the patient’s preoperative blood pressures, medical history, and surgical context. If the optimal SAP/MAP was considered higher than the default range, I instructed them to change the monitor settings. This ensured it would alarm at a higher reading.
MAP, CPP and the Beach Chair Position
Understanding the relationship between MAP and CPP is especially important when the patient is in a head up position. For example, the beach chair position is often used for orthopedic shoulder surgeries. It’s also utilized for some neurosurgical access. The beach chair also decreases the risk of certain injuries, like brachial plexus palsy.
Sitting alters hemodynamics. When upright, CPP only drops by about 15% because wake patients increase systemic vascular resistance by 50–80% to compensate. This keeps MAP stable or higher, so SAP stays steady. Without this response (e.g., orthostatic hypotension), standing quickly can cause dizziness or fainting from falling CPP.
Under anesthesia, vasoconstriction is impaired, so head-up positioning significantly lowers MAP and CPP.
Also consider BP cuff placement. When lying down, arm and brain BP are equal. When sitting, brain MAP is lower than arm MAP. MAP at the brain base is 15–20 mmHg less than at the arm. It can be another 9 mmHg lower at the top of the cerebral cortex. If you don’t take this into account your patient’s brain may experience poor perfusion despite a seemingly normal cuff pressure.
It’s recommended to keep MAP between 70–93 to keep CPP while in a sitting position, especially for high-risk patients. This sometimes brings you into conflict with a surgeon concerned about blood loss. Be prepared to negotiate, educate, and even compromise. But stand your ground on safety in the high-risk patient.
What Is Intraoperative Hypotension in a Child?
Neonates, infants and small children normally have lower blood pressures than older children and adults. However, providers who rarely do children may tolerate hypotensive pressures in young children — they fail to recognize abnormal. To spot abnormal, you must know what normal is.

The most common causes of intraoperative hypotension in children are hypovolemia and bradycardia. Pediatric hemodynamics is too broad to cover here. For more information see:
Pediatric Hypotension: Think Hypovolemia
Pathophysiology and Causes of Intraoperative Hypotension
Hypotension during anesthesia can result from multiple factors, including anesthetic drug effects, fluid shifts, blood loss, and underlying patient comorbidities. Common causes include:
- Vasodilation due to anesthetic agents (e.g., propofol, volatile anesthetics)
- Myocardial depression from drugs or pre-existing cardiac conditions
- Hypovolemia resulting from bleeding or inadequate fluid replacement
- Positional changes (e.g., Trendelenburg or sitting positions)
- Neurogenic causes (e.g., spinal or epidural anesthesia)
- Changes to the amount of surgical stimulation
Many of these changes are predictable — and preventable. Anesthesia providers should anticipate and manage blood pressure shifts proactively, not just reactively.
Post-induction Hypotension
Not all hypotension occurs during surgery. I find that managing anesthesia after induction, before incision, is one of the most difficult parts of the case. Patients must stay anesthetized with little stimulation. Usually, a lighter anesthetic is needed, timed to get deeper right before incision. If positioning, prepping, or draping takes a long time, keeping SAP stable is harder. Encourage efficiency in your OR team, and occasionally your surgeon, to speed prep.
Regional Anesthesia and Intraoperative Hypotension
Regional blockade can complicate general anesthesia. If the block is effective, incisions often cause no response. Older shoulder surgery patients with a strong interscalene block in the beach chair position may experience hypotension. Lack of stimulus plus anesthesia can rapidly lower SAP. The patient may need vasopressor treatment to maintain a higher MAP to guarantee cerebral perfusion.
I have observed that anesthesia providers sometimes tolerate lower blood pressures in patients under spinal or epidural anesthesia. This occurs because these patients are more on “autopilot”. MAP is MAP. Consider SAP support if below your acceptable optimal range.
Recognition of Intraoperative Hypotension
- Early recognition of hypotension is essential for effective management. Key strategies include:
- Continuous non-invasive blood pressure (NIBP) or invasive arterial line monitoring
- Trend analysis of vital signs (heart rate, oxygen saturation, end-tidal CO2)
- Clinical assessment: observing skin perfusion, urine output, and mental status
- Evaluating for signs of bleeding or fluid loss in the surgical field
All of these are active not passive modalities. Providing anesthesia demands constant focus on both the patient and procedure. Anesthesia is said to be long hours of tedium interspersed with moments of sheer terror. During the tedium, the monotony can lead some providers to seek distractions from cellphones, newspapers, and conversations. They rely on default alarms, resulting in an increased tendency to function on autopilot.
An anesthesia provider is like a lifeguard. A lifeguard who stops watching the water will miss the drowning child. Prompt recognition is critical. Prolonged hypotension can lead to ischemic injury in organs like the brain, heart, and kidneys.
Treatment Approaches
Treatment of intraoperative hypotension aims to restore adequate tissue perfusion and address underlying causes. Management strategies include:
- Anticipating surgical periods to prevent, not just treat, hypotension
- Adjusting Anesthetic Depth: Reducing the dose of anesthetic drugs if excessive vasodilation or cardiac depression is suspected.
- Fluids: Administering intravenous crystalloids or colloids to correct hypovolemia.
- Vasopressors: Using agents like phenylephrine, ephedrine, or norepinephrine to increase vascular tone and blood pressure.
- Inotropes: In cases of myocardial depression, drugs like dobutamine or epinephrine can be used to enhance cardiac output.
- Blood Products: Transfusing blood or plasma if significant hemorrhage is identified.
- Addressing Specific Causes: Treating arrhythmias, correcting electrolyte imbalances, or reversing neuraxial blockade if necessary.
- Don’t forget to plan for potential PACU changes.
Prevention and Risk Mitigation
Preoperative assessment and preparation, intraoperative vigilance, and postop planning are key to preventing hypotension. Strategies include:
- Identifying patients at risk (elderly, cardiac disease, hypovolemia)
- Tailoring anesthetic plans and drug choices suitably
- Ensuring adequate preoperative hydration
- Using appropriate monitoring and maintaining readiness to intervene rapidly
Don’t Forget Postoperative Hypotension
The anesthesia provider must think ahead to potential causes of postoperative hypotension. Rewarming hypotension is a good example. If a patient becomes significantly hypothermic intraoperatively, vasoconstriction will often mask hypovolemia. Once the patient rewarms in PACU, vasodilation takes place and hypotension can begin. Discussion of all causes of postoperative hypotension is beyond the scope of this article.
Conclusion
Anesthesia is not a one-size-fits-all procedure. It requires a carefully developed plan suited to each patient’s unique needs. The plan must also consider important events during surgery. For patients at higher risk, establish in advance an appropriate range for SAP/MAP.
Anesthetic recognition and treatment of intraoperative hypotension are fundamental to safe surgical care. Anesthesiologists can reduce complications by understanding the underlying mechanisms. They also enhance patient outcomes by utilizing effective monitoring techniques and implementing prompt, targeted interventions. Ongoing education and protocol development are essential to further improve the management of intraoperative hypotension.



