• Hypertension:
  • Systolic BP >140 mm Hg
  • Diastolic BP >90 mm Hg
• Hypertensive crisis or emergency:
  • Systolic BP >180 mm Hg
  • Diastolic BP >120 mm Hg
  • Accompanied by end-organ dysfunction such as hypertensive encephalopathy, intracerebral hemorrhage, subarachnoid hemorrhage, acute stroke, unstable angina, acute myocardial infarction, congestive heart failure, acute renal dysfunction, and acute aortic dissection.
• Hypertensive urgency is defined as a severe elevation in BP without progressive end-organ dysfunction.

• Primary hypertension: Sedentary lifestyle, stress, obesity (in particular visceral), hypokalemia, salt sensitivity, alcohol intake, vitamin D deficiency, aging, family history. Other correlating factors include elevated renin, sympathetic nervous system overactivity, insulin resistance (Syndrome X or metabolic syndrome), and low birth weight.
• Secondary hypertension: Conditions that affect the kidneys, arteries, heart, or endocrine systems such as renal stenosis, coarctation of the aorta, pheochromocytoma, preeclampsia, and Cushing's disease.

• Systolic BP
  • Within the heart, it refers to the pressure during a cardiac contraction and requires invasive monitoring.
  • In the periphery, it can be measured with a non-invasive BP cuff. It measures the resultant pulsatile pressure against the peripheral vasculature from the blood ejected during cardiac systole.
  • Systole accounts for 1/3^rd of the systole–diastole cycle.
• Diastolic BP
  • Within the heart, it refers to the pressure of the relaxed ventricles.
  • In the peripheral vasculature, it refers to the tone of the arteries.
• Mean arterial pressure is the average pressure in the heart and vasculature. It is calculated as follows, MAP = (diastolic pressure) + (systolic pressure).
• Primary hypertension is not well understood.
  • During the early stages, there is increased cardiac output and normal total peripheral resistance.
  • With time, the cardiac output drops to normal levels, but the total peripheral resistance increases.
  • Theories include the inability of the kidneys to excrete sodium, causes natriuretic factor to increase (excretes sodium, but side effect is increased total peripheral resistance); overactive renin–angiotensin system causing vasoconstriction and retention of sodium and water (increased blood volume causes hypertension); and overactive sympathetic nervous system leading to increased stress response.
  • The end result is reduced intravascular volume and increased total peripheral resistance.
  • With time, this can lead to hemodynamic instability perioperatively (see below) and end-organ damage.
    • Central nervous system (CNS)
    • Cardiac
    • Renal
    • Retina
    • Metabolic
• Preoperatively: Patients can present with anxiety about the procedure/anesthesia or without taking their scheduled morning antihypertensive.
• Intraoperatively: Induction often produces an exaggerated drop in BP attributed to the sympatholysis from induction medications combined with the intravascular hypovolemia from abnormal fluid regulation with hypertension (sympatholytics unmask the relative hypovolemia). Laryngoscopy often demonstrates an exaggerated increase in BP likely due to an exaggerated sympathetic response. Hypotension during maintenance often occurs from direct vascular dilation or sympatholysis.
• Postoperative: The early post-anesthesia period is associated with pain-induced sympathetic stimulation, hypothermia, hypoxia, and intravascular volume overload. In addition, fluid mobilization 24–48 hours postoperatively results in intravascular hypervolemia.

• Preoperative evaluation to allay fears and concerns as well as advise about BP medications.
  • Preoperative clinic may allow the opportunity, if identified early enough, to optimize poorly controlled hypertension with the primary care physician
  • A phone call the night prior to surgery (along with proper instructions for antihypertensive medications on the morning of surgery), meeting preoperatively to discuss the operative course thoroughly, and home anxiolysis can aid in BP control.
• Induction and laryngoscopy: Anticipate instability. These events occur back to back with widely different hemodynamic responses.
  • Propofol decreases preload, afterload, and contractility, hypotension may be avoided with slower and smaller doses.
  • Etomidate may provide more stable hemodynamics. A balanced induction with etomidate and propofol can avoid hypotension and hypertension.
  • Large narcotic doses can reduce induction medications and may blunt the sympathetic response to laryngoscopy. Although it preserves cardiac contractility, it may blunt sympathetic drive with resultant bradycardia and vasodilation.
  • Administration of vasopressors as appropriate; performing a laryngoscopy and intubation to "treat" hypotension prior to readiness is a poor practice.
  • Lidocaine IV or topical may blunt sympathetic response to laryngoscopy.
  • Volatile agents during bag mask ventilation can blunt sympathetic response.
  • Airway instrumentation should be performed quickly and effectively.
  • Preoperative placement of an arterial line or frequent BP cuff measurements (change frequency) may improve appropriate titration of medications.
• Intraoperatively: Periods of low stimulation may be met with hypotension or a BP that precludes adequate perfusion of vital organs.
  • Assessment of volume status: NPO, maintenance, insensible and blood loss, other causes such as sepsis or anaphylaxis. Volume replacement should be performed; avoid overhydration which can result in postoperative fluid shifting.
  • Titrate narcotics and epidural boluses slowly to assess effects and have the opportunity to treat hypotension.
  • Heart rate, and rhythm should be optimized.
  • Reduction of volatile or TIVA while maintaining unconsciousness.
  • Nitrous oxide can maintain hemodynamics to a greater extent than volatile agents; additionally, it allows for "titrating down" volatile agents.
  • During stimulation, hypertensives may have an exaggerated response. Consider titrating short-acting medications, particularly if it is felt that the stimulation will be short lived (e.g., propofol, volatile agents, esmolol, nitroglycerine, calcium channel blockers).
• Emergence: Consider titrating longer-acting antihypertensives if the patient's BP starts increasing. Choices include metoprolol, labetalol, and hydralazine.
• Postoperative: Orders for antihypertensive medications should identify titration parameters and appropriate dosing. If ineffective, consider alternative medications, telemetry, or ICU admission. Appropriate pain management should be provided (consider regional blocks, PCA, local infiltration, as appropriate). Pain, anxiety, delirium, hypoxia, and hypercarbia can result in hypertension and should be appropriately managed.

• Incorrect reading from poor technique, such as small cuff, or inappropriate placement.
• Cushing's response from increased intracranial pressure (an adaptive measure that increases the mean arterial pressure in order to preserve adequate cerebral perfusion; classically accompanied by bradycardia and irregular respirations).

Not investigated

• Hypertension
• Intraoperative Myocardial Ischemia

• 401.9 Unspecified essential hypertension
• 405.99 Other unspecified secondary hypertension

• I10 Essential (primary) hypertension
• I15.9 Secondary hypertension, unspecified

Cameron J. Ricks , MD

Nina Singh-Radcliff , MD