DBP, Diastolic blood pressure; SBP, systolic blood pressure;.
From U.S. Department of Health and Human Services, National Heart Lung and Blood Institute. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Bethesda, MD: NIH publication No. 04-5230; 2004. Available at www.nhlbi.nih.gov/guidelines/hypertension/jnc7full.pdf.
The risk of cardiovascular disease doubles with each increment of 20/10 mmHg above 115/75 mmHg. It is estimated that the implementation of antihypertensive therapy is associated with a 25% decrease in cardiovascular complications and a 38% decrease in stroke.
Pathophysiology
Systemic blood pressure is regulated by interactive feedback mechanisms involving the sympathoadrenal axis and baroreceptors in the heart and great vessels. It is accepted that some degree of sympathetic dysfunction is responsible for essential hypertension. Dysfunction of the SNS leads to a state of chronic vasoconstriction. In an attempt to maintain normal intravascular volume, the renal juxtaglomerular apparatus secretes renin. All of the vascular and hormonal effects of renin are caused by its conversion of angiotensin I to angiotensin II. Angiotensin II is the major stimulus for the secretion of aldosterone by the adrenal cortex.
Deposition of collagen and metalloproteinases within the intima of arteries leads to vascular stiffness, and this occurs normally as part of the aging process. Narrowing of the vascular lumen and endothelial dysfunction causing inability of complete vasodilation decreases blood flow, especially within the microvasculature. Furthermore, vascular stiffness increases afterload and myocardial oxygen demand and can cause LV hypertrophy, myocardial ischemia or infarction, and CHF.
Treatment
When the diastolic blood pressure (DBP) is greater than 90 mmHg, drug treatment is usually used, although isolated systolic hypertension may respond to diet modification and weight loss. Patients with borderline hypertension can decrease their blood pressure with exercise and weight loss. If the DBP exceeds 105 mmHg, aggressive treatment is needed to decrease morbidity and mortality from MI, CHF, cerebrovascular accident, and renal failure.
Drugs used to treat patients with hypertension include diuretics, ACE inhibitors, calcium antagonists, β-blockers, and vasodilators. A combination of two antihypertensives is often used to minimize the undesirable physiologic responses to any one particular drug (e.g., a compensatory increase in renin activity). Serum potassium levels should be monitored because hypokalemia or hyperkalemia may be a side effect.
Anesthetic considerations
Preoperative
The most important issues to be addressed in the preoperative evaluation are the identification and the adequacy of treatment. If the perioperative DBP is maintained below 110 mmHg, the risk of perioperative cardiac morbidity does not increase significantly. Reviewing the patient’s medication and determining adequacy of blood pressure control are essential.
An individualized anesthetic plan must be created by taking into account the type and extent of cardiac pathophysiology, other disease states, and the surgical procedure. To maintain a stable intraoperative course, administration of antihypertensive medications should be continued on schedule until the time of surgery. Tachycardia, hypertension, angina, and MI can result from interruption of therapy with β-blockers and calcium channel–blocking agents. These drugs should be discontinued with caution and only after utmost discretionary review of the patient’s physiologic status.
Determining whether to proceed with elective surgery in a patient in whom hypertension is untreated or poorly controlled remains controversial. Patients who have DBPs greater than 110 mmHg have a significantly increased risk of perioperative cardiac morbidity. This caveat may be modified in patients with hypertension in whom DBPs greater than 110 mmHg occur frequently despite aggressive antihypertensive drug therapy (e.g., patients with end-stage renal disease).
Preoperative sedation may be indicated for patients with hypertension to attenuate sympathetic responsiveness. Establishing control of the blood pressure before induction should result in a more stable hemodynamic course during the induction, maintenance, and emergence from anesthesia. A fluid bolus and incremental titration of anesthetic induction agents may help to decrease the degree and duration of hypotension.
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