Chapter 24
Reacting to Common Intraoperative Events

Hypotension

Hypotension refers to abnormally low blood pressure. In the operating room, this is a common event and usually due to anesthetic-induced vasodilation, but may co-exist with other etiologies such as hypovolemia. Shock is a clinical syndrome characterized by inadequate perfusion of oxygenated blood to end-organs, leading to tissue ischemia. Perioperative ischemia is to be avoided, as it is clearly associated with stroke, acute kidney injury, metabolic acidosis, delirium, myocardial infarction, and prolonged hospital stay. Shock will result if hypotension is prolonged.

Hypotension in the OR demands simultaneous diagnosis and treatment. Treat it while you are working up the etiology. As you gain experience, you’ll develop an intuitive “feel” for the likely cause, allowing you to manage both fronts in parallel. Approach hypotension methodically.

The Core Framework for Intraoperative Hypotension

Use the following structure to build your differential:

Rhythm: Is the heart beating too fast or irregularly producing adequate cardiac output?
Afterload: Is there vasodilation from anesthetics, sepsis, or anaphylaxis?
Preload: Is the patient hypovolemic?
Contractility: Is there impaired myocardial function?
Obstruction: Is there tamponade, tension pneumothorax, or pulmonary embolism? Is the surgeon pushing on a major vascular structure?

With this differential in mind, here is a real-life thought process:

Anesthetic Causes

Vasodilation from anesthetic agents is the most common cause of intraoperative hypotension, but it should still be considered a diagnosis of exclusion. While you assess other causes, take control of the patient and get the blood pressure back up with vasoconstrictors. Lower your volatile agent if you can safely do so. This minimizes time spent in a low perfusion state, stabilizes your anesthetic plane, and reduces the risk of compounding events.

Volatile agents alone rarely cause significant hypotension. Hypotension usually arises when there is a second physiologic factor (hypovolemia) or when they are combined with boluses of opioids, induction agents, or neuraxial blockade. Hypotension from vasodilation is common after induction since volatile agent working alongside propofol, fentanyl, midazolam, etc.
Anesthetics blunt sympathetic tone, suppressing endogenous catecholamines. Catecholamines such as epinephrine and norepinephrine are often elevated in acutely or critically ill patients. Induction blunts sympathetic outflow, often resulting in a dramatic drop in BP after induction. Most ICUs have protocols to mitigate this effect, which include empiric norepinephrine infusions and fluid boluses in the peri-intubation period.
Epidural anesthesia causes hypotension via sympathectomy from blunting of cardiac accelerator fibers in the spinal cord.
Young patients can compensate for anesthetic-induced vasodilation with an increase in heart rate and vascular smooth muscle tone. Elderly patients, or those on beta-blockers, compensate poorly.
Patients with chronic hypertension, especially those with left ventricular hypertrophy (LVH), are susceptible to hypotension during hypovolemia. This is due to blunted baroreceptor reflexes and limited ventricular compliance.
There is unclear evidence surrounding ACE-inhibitor (ACEI) and angiotensin receptor block (ARB) therapy and potentiation of anesthetic vasodilation. It is confounded by the fact that these patients have underlying hypertension and other factors that may contribute to a higher risk of intraoperative hypotension.

Surgical Causes

After addressing anesthetic contributors, turn your attention to the surgical field.

Bleeding is sometimes obvious, and sometimes subtle and cumulative. There are cases where bleeding is obvious and rapid. But more commonly, cases will bleed via a slow, continuous oozing. Examples include prolonged spine exposure, bleeding from a raw liver edge, or continuous leaking from femoral access sites during a noninvasive endovascular procedure.
Other surgical causes of hypotension are as follows:
- Vagal responses from peritoneal stretching, an especially common phenomenon in young patients.
- IVC compression from retraction or surgical compression.
- Oculocardiac reflex during surgery in and around the eyeball.
- Steep reverse Trendelenburg, decreasing venous return.
- Drainage of large ascites or pleural effusions, which may not be intuitive since this involves the removal of extravascular fluid. However, ascites drainage reduces abdominal pressure and induces splanchnic vasodilation, which triggers a reduction in systemic vascular resistance. Pleural fluid removal reduces intrathoracic pressure and can decrease preload, resulting in hypotension.
- Pneumothorax from laparoscopic dissection. If significant enough to induce hypotension, it will be accompanied by rising airway pressures.
- Air embolism, though rare, should be considered in high-risk cases (e.g., craniotomy in sitting position, transurethral resection, robotic bronchoscopy). This typically presents with severe hypotension accompanied by a sudden drop-off in ETCO₂.

Patient-related Factors

Once anesthetic and surgical factors are addressed, assess the underlying patient physiology.

Hypovolemia

This is the most common patient-related cause. Many patients are volume-depleted due to:

poor oral intake (e.g., illness, cancer, long NPO times);
increased losses (fever, drains, wounds, diuretics); and
ERAS protocols, which promote fluid restriction for faster recovery.

ERAS-guided fluid-sparing techniques are beneficial when things go smoothly. Fluid restriction is associated with early ambulation, fewer GI complications, less pain, and overall decreased length of stay. ERAS is great for a short to medium-length case with no complications, and it is certainly beneficial for the postoperative recovery period on the floor. However, it is my experience that fluid restriction can be overdone in cases that exceed the normal length of time or experience an undue complication. When surgery is prolonged, complicated, or involves bleeding, use clinical judgment, not ERAS protocols, to guide fluid resuscitation. Consider estimated blood loss, urine output, systolic pressure variation, and insensible loss estimates.

Other Considerations

Time in the OR: Prolonged exposure, prolonged open body cavities, and prolonged instrumentation increase inflammation and capillary leak, resulting in vasodilation.
Hypothermia and anemia can contribute to vasodilation.
Massive transfusion can lead to vasodilation from inflammatory and hemodilutional effects.
Metabolic acidosis can occur due to poor perfusion and leads to vasodilation. This can be obvious, such as during an aortic cross clamp, or more subtle and gradual, such as during open esophagectomy in steep reverse Trendelenburg.
Anaphylaxis, either due to an intravenous drug or surgical materials: chlorhexidine, latex, etc.