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Example Of Case Study On Hypertension

Ms. C is a 42-year-old black American woman with a 7-year history of hypertension first diagnosed during her last pregnancy. Her family history is positive for hypertension, with her mother dying at 56 years of age from hypertension-related cardiovascular disease (CVD). In addition, both her maternal and paternal grandparents had CVD.

At physician visit one, Ms. C presented with complaints of headache and general weakness. She reported that she has been taking many medications for her hypertension in the past, but stopped taking them because of the side effects. She could not recall the names of the medications. Currently she is taking 100 mg/day atenolol and 12.5 mg/day hydrochlorothiazide (HCTZ), which she admits to taking irregularly because “... they bother me, and I forget to renew my prescription.” Despite this antihypertensive regimen, her blood pressure remains elevated, ranging from 150 to 155/110 to 114 mm Hg. In addition, Ms. C admits that she has found it difficult to exercise, stop smoking, and change her eating habits. Findings from a complete history and physical assessment are unremarkable except for the presence of moderate obesity (5 ft 6 in., 150 lbs), minimal retinopathy, and a 25-year history of smoking approximately one pack of cigarettes per day. Initial laboratory data revealed serum sodium 138 mEq/L (135 to 147 mEq/L); potassium 3.4 mEq/L (3.5 to 5 mEq/L); blood urea nitrogen (BUN) 19 mg/dL (10 to 20 mg/dL); creatinine 0.9 mg/dL (0.35 to 0.93 mg/dL); calcium 9.8 mg/dL (8.8 to 10 mg/dL); total cholesterol 268 mg/dL (< 245 mg/dL); triglycerides 230 mg/dL (< 160 mg/dL); and fasting glucose 105 mg/dL (70 to 110 mg/dL). The patient refused a 24-h urine test.

Clinical Management and Treatment Decisions

Taking into account the past history of compliance irregularities and the need to take immediate action to lower this patient’s blood pressure, Ms. C’s pharmacologic regimen was changed to a trial of the angiotensin-converting enzyme (ACE) inhibitor enalapril, 5 mg/day; her HCTZ was discontinued. In addition, recommendations for smoking cessation, weight reduction, and diet modification were reviewed as recommended by the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI).1

After a 3-month trial of this treatment plan with escalation of the enalapril dose to 20 mg/day, the patient’s blood pressure remained uncontrolled. The patient’s medical status was reviewed, without notation of significant changes, and her antihypertensive therapy was modified. The ACE inhibitor was discontinued, and the patient was started on the angiotensin-II receptor blocker (ARB) losartan, 50 mg/day.

After 2 months of therapy with the ARB the patient experienced a modest, yet encouraging, reduction in blood pressure (140/100 mm Hg). Serum electrolyte laboratory values were within normal limits, and the physical assessment remained unchanged. The treatment plan was to continue the ARB and reevaluate the patient in 1 month. At that time, if blood pressure control remained marginal, low-dose HCTZ (12.5 mg/day) was to be added to the regimen.

Hypertension in Black Americans

Hypertension remains a significant health problem in the United States (US) despite recent advances in antihypertensive therapy. The role of hypertension as a risk factor for cardiovascular morbidity and mortality is well established.2–7 The age-adjusted prevalence of hypertension in non-Hispanic black Americans is approximately 40% higher than in non-Hispanic whites.8 Black Americans have an earlier onset of hypertension and greater incidence of stage 3 hypertension than whites, thereby raising the risk for hypertension-related target organ damage.1,8 For example, hypertensive black Americans have a 320% greater incidence of hypertension-related end-stage renal disease (ESRD), 80% higher stroke mortality rate, and 50% higher CVD mortality rate, compared with that of the general population.1,9 In addition, aging is associated with increases in the prevalence and severity of hypertension.8

Pharmacologic Treatment of Hypertension in Black Americans

Research findings suggest that risk factors for coronary heart disease (CHD) and stroke, particularly the role of blood pressure, may be different for black American and white individuals.10–12 Some studies indicate that effective treatment of hypertension in black Americans results in a decrease in the incidence of CVD to a level that is similar to that of nonblack American hypertensives.13,14

Data also reveal differences between black American and white individuals in responsiveness to antihypertensive therapy. For instance, studies have shown that diuretics15,16 and the calcium channel blocker diltiazem16,17 are effective in lowering blood pressure in black American patients, whereas β-adrenergic receptor blockers and ACE inhibitors appear less effective.15,16 In addition, recent studies indicate that ARB may also be effective in this patient population.

Angiotensin-II receptor blockers are a relatively new class of agents that are approved for the treatment of hypertension. Currently, four ARB have been approved by the US Food and Drug Administration (FDA): eprosartan, irbesartan, losartan, and valsartan. Recently, a 528-patient, 26-week study compared the efficacy of eprosartan (200 to 300 mg/twice daily) versus enalapril (5 to 20 mg/daily) in patients with essential hypertension (baseline sitting diastolic blood pressure [DBP] 95 to 114 mm Hg). After 3 to 5 weeks of placebo, patients were randomized to receive either eprosartan or enalapril. After 12 weeks of therapy within the titration phase, patients were supplemented with HCTZ as needed. In a prospectively defined subset analysis, black American patients in the eprosartan group (n = 21) achieved comparable reductions in DBP (−13.3 mm Hg with eprosartan; −12.4 mm Hg with enalapril) and greater reductions in systolic blood pressure (SBP) (−23.1 with eprosartan; −13.2 with enalapril), compared with black American patients in the enalapril group (n = 19) (Fig. 1).18 Additional trials enrolling more patients are clearly necessary, but this early experience with an ARB in black American patients is encouraging.

Efficacy of the angiotensin II receptor blocker eprosartan in black American with mild to moderate hypertension (baseline sitting DBP 95 to 114 mm Hg) in a 26-week study. Eprosartan, 200 to 300 mg twice daily (n = 21, solid bar), enalapril 5 to 20 mg daily (n = 19, diagonal bar). †10 of 21 eprosartan patients and seven of 19 enalapril patients also received HCTZ. Adapted from data in Levine: Subgroup analysis of black hypertensive patients treated with eprosartan or enalapril: results of a 26-week study, in Programs and abstracts from the 1st International Symposium on Angiotensin-II Antagonism, September 28–October 1, 1997, London, UK.

Approximately 30% of all deaths in hypertensive black American men and 20% of all deaths in hypertensive black American women are attributable to high blood pressure. Black Americans develop high blood pressure at an earlier age, and hypertension is more severe in every decade of life, compared with whites. As a result, black Americans have a 1.3 times greater rate of nonfatal stroke, a 1.8 times greater rate of fatal stroke, a 1.5 times greater rate of heart disease deaths, and a 5 times greater rate of ESRD when compared with whites.19 Therefore, there is a need for aggressive antihypertensive treatment in this group. Newer, better tolerated antihypertensive drugs, which have the advantages of fewer adverse effects combined with greater antihypertensive efficacy, may be of great benefit to this patient population.

References

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Joint National Committee

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© 1998 by the American Journal of Hypertension, Ltd.

American Journal of Hypertension, Ltd.

CASE 14: Hypertension

Fun-Sun F. Yao

Chee-Yueh A. Ho

Related Links in other Resources

A 70-year-old man with cholelithiasis was scheduled for a cholecystectomy. His blood pressure (BP) was 230/120 mm Hg; pulse 60 beats/minute. Hematocrit was 38%; serum sodium, 140 mEq/L; and serum potassium, 2.7 mEq/L. His medications included propranolol and hydrochlorothiazide.

  1. Medical Disease and Differential Diagnosis
    1. Define hypertension and classify its severity.

    2. What is the prevalence of hypertension?

    3. What is the general classification of hypertension? Enumerate the causes of each type of hypertension.

    4. What are the usually clinical patterns of hypertension encountered?

    5. What is the pathophysiology of essential hypertension?

    6. What are the end-organ damages caused by longstanding hypertension?

    7. Are hypertensive patients at an increased risk of perioperative cardiac morbidity?

    8. Are hypertensive patients at increased risk for perioperative cerebral and renal complications? Why?

    9. Would you employ a controlled hypotensive technique for hypertensive patients? How much would you safely lower the blood pressure (BP)?

    10. What is the mechanism of action of antihypertensive drugs?

    11. Does the choice of antihypertensive therapy influence hemodynamic responses to induction, laryngoscopy, and intubation?

    12. Does chronic angiotensin-converting enzyme (ACE) inhibition influence anesthetic induction?



  2. Preoperative Evaluation and Preparation
    1. How would you evaluate this patient preoperatively?

    2. Would you postpone the surgery? Why? What BP would you like the patient to achieve before surgery?

    3. Should all or any of the chronic medications be discontinued before the operation?

    4. Should hypokalemia be treated before anesthesia? Why?

    5. Should hypomagnesemia be treated before anesthesia? Why?

    6. Does an asymptomatic carotid bruit increase the risk in these patients?

    7. The surgery was postponed for 6 weeks. The patient has been on propranolol, captopril, hydrochlorothiazide, and KCl. His BP was 160/95 mm Hg and potassium 4.0 mEq/L. How would you premedicate this patient?

    8. If the patient is an untreated hypertensive patient with BP 170/100 mm Hg, would you pretreat the patient preoperatively with an antihypertensive agent?



  3. Intraoperative Management
    1. How would you monitor this patient?

    2. What are the anesthetic goals for hypertensive patients?

    3. How would you induce anesthesia for the hypertensive patient?

    4. How does tracheal intubation produce hypertension?

    5. What happens to the left ventricular ejection fraction during and immediately following intubation?

    6. What other measures can prevent hypertension and tachycardia at the time of intubation?

    7. After induction and intubation, the BP went down to 70/40 mm Hg. What would you do?

    8. What is your choice of agents for maintenance of anesthesia? Why?

    9. How would you manage fluid therapy for hypertensive patients?

    10. During the surgery, BP went up to 220/120 mm Hg. How would you treat the hypertension?

    11. What could you do to prevent hypertension during extubation and emergence?

    12. Would you consider regional anesthesia for this patient?



  4. Postoperative Management
    1. The patient developed hypertension BP 210/110 mm Hg in the postanesthesia care unit. What would you do?



A. Medical Disease and Differential Diagnosis

Back to Quick Links

A.1. Define hypertension and classify its severity.

True systemic hypertension can be diagnosed when there is an increase in arterial pressure above accepted normal pressure for age, sex, and race. The accepted upper limits of normal BP are as follows:

Adult
140/90 mm Hg
Adolescent
100/75 mm Hg
Early childhood
85/55 mm Hg
Infant
70/45 mm Hg

The accepted upper limit of normal pressure in the adult was chosen as 140/90 mm Hg rather than 160/95 mm Hg (World Health Organization criteria) because systolic BP levels above 140 mm Hg and diastolic levels above 90 mm Hg are associated with increased risk for eventual cardiovascular disease.

The classification of severity of hypertension is shown in Table 14.1.

Back to Quick Links

Braunwald E, Heart disease6th ed. Philadelphia: WB Saunders, 2001:942–945.

Braunwald E, Isselbacher KJ, Fauci AS, et al,, Harrison's principles of internal medicine15th ed. New York: McGraw-Hill, 2001:212–213.

A.2. What is the prevalence of hypertension?

The prevalence of hypertension depends on both the racial composition of the population and the criteria used to define hypertension. In a white suburban population like that in the Framingham Study, nearly one fifth have BPs greater than 160/95 mm Hg, and almost one half have BPs greater than 140/90 mm Hg. A higher prevalence has been found in the nonwhite population. The frequency increases with the age of the population. The number of hypertensive persons in the United States in 1983 was estimated to be 57.7 million—more than double the estimate made in 1960 to 1962.

Back to Quick Links

Braunwald E, Heart disease6th ed. Philadelphia: WB Saunders, 2001:945–946.

Braunwald E, Isselbacher KJ, Fauci AS, et al., Harrison's principles of internal medicine15th ed. New York: McGraw-Hill, 2001:1414.

A.3. What is the general classification of hypertension? Enumerate the causes of each type of hypertension.

The classification is outlined in Table 14.2.

Systolic and Diastolic Hypertension

  • Essential hypertension

    Unknown etiology

  • Renal

    Acute and chronic glomerulonephritis, chronic pyelonephritis, polycystic kidney, diabetic nephropathy, hydronephrosis, renovascular stenosis, renin-producing tumors, primary sodium retention

  • Endocrine

    Adrenal: Cushing's syndrome, primary aldosteronism, congenital adrenal hyperplasia, pheochromocytoma, acromegaly, hypothyroidism, carcinoid, hyperthyroidism, oral contraceptives, corticosteroids

  • Neurogenic

    Psychogenic, increased intracranial pressure, spinal cord section, familial dysautonomia, lead poisoning, Guillain–Barré syndrome, sleep apnea

  • Miscellaneous

    Coarctation of aorta, increased intravascular volume, pregnancy-induced hypertension, polyarteritis nodosa, acute porphyria, hypercalcemia, alcohol and drug use, acute stress including surgery

Systolic Hypertension with Wide Pulse Pressure

  • Arteriosclerosis, rigidity of aorta

  • Increased cardiac output

Arteriovenous fistula, thyrotoxicosis, patent ductus arteriosus, beriberi heart, fever, aortic valvular insufficiency

Back to Quick Links

Braunwald E, Heart disease6th ed. Philadelphia: WB Saunders, 2001:946.

Braunwald E, Isselbacher KJ, Fauci AS, et al., Harrison's principles of internal medicine15th ed. New York: McGraw-Hill, 2001:1414.

A.4. What are the usually clinical patterns of hypertension encountered?

  • "Vasoconstricted" hypertension—in medical patient with chronic renovascular hypertension, characterized by diastolic hypertension and systemic vascular resistant with normal or even decreased cardiac output and heart rate.

  • "Hyperdynamic" hypertension—in postoperative surgical patient, characterized by acute systolic hypertension; widened pulse pressure; and increased cardiac output, heart rate, and systemic vascular resistant.

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Sladen RN. Perioperative hypertension. IARS Review Course Lectures Cleveland; OH: International Anesthesia Research Society, 2002:100–114.

A.5. What is the pathophysiology of essential hypertension?

The underlying mechanism of essential hypertension is unknown. A variety of abnormalities including heredity, fetal undernutrition, abnormal sympathetic nervous system (SNS) activity, cell membrane defects, renal retention of excess salt, microcirculatory alterations, endothelial cell dysfunction, hyperinsulinemia secondary to insulin resistance, vascular hypertrophy, and altered renin-angiotensin system regulation are implicated. There is increasing evidence that "local renin-angiotensin" paracrine factors may be involved in the development of hypertension. However, characteristic hemodynamic changes are present as follows:

  • Increased systemic vascular resistance (SVR) with normal cardiac output

  • Markedly increased sympathetic response to stress such as endotracheal intubation

  • A greater increase in BP with vasoconstriction and a greater decrease in BP with vasodilation because of the increased thickening of arterial wall and high ratio of wall thickness to internal diameter

The higher the level of BP, the more likely that various cardiovascular diseases will develop prematurely through acceleration of atherosclerosis. If untreated, about 50% of hypertensive patients die of coronary heart disease or congestive heart failure (CHF), about 33% of stroke, and 10% to 15% of renal failure.

Back to Quick Links

Braunwald E, Heart disease6th ed. Philadelphia: WB Saunders, 2001:950–955.

Braunwald E, Isselbacher KJ, Fauci AS, et al., Harrison's principles of internal medicine15th ed. New York: McGraw-Hill, 2001:1414–1417.

Murray MJ, Perioperative hypertension. ASA Annual Refresher Course Lectures Park Ridge, IL: American Society of Anesthesiologists, 2002:512.

A.6. What are the end-organ damages caused by longstanding hypertension?

The end-organ damages caused by longstanding hypertension are as follows:

Cardiac involvement:

Left ventricular hypertrophy (LVH)

Angina or myocardial infarction

Arrhythmias

Congestive failure

Eye involvement:

Vascular changes in the fundus reflect hypertensive retinopathy and arteriosclerotic retinopathy

Renal involvement:

Nephropathy

Cerebral involvement:

Stroke or transient ischemic attack (TIA)

Complications of hypertension to vascular disease probably involve three interrelated processes: pulsatile flow, endothelial cell dysfunction, and smooth muscle cell hypertrophy. These three interrelated processes are probably responsible for the arteriolar and arterial sclerosis that is the usual consequence of longstanding hypertension. Large vessels such as the aorta may be directly affected and be at risk for aneurysms and dissection.

Back to Quick Links

Braunwald E, Heart disease6th ed. Philadelphia: WB Saunders, 2001:950–955.

A.7. Are hypertensive patients at an increased risk for perioperative cardiac morbidity?

Hypertensive patients are at increased risk for coronary artery disease, silent myocardial ischemia, CHF, and stroke. However, whether preoperative hypertension is predictive of perioperative major cardiac morbidity remains controversial. Some investigators have shown that patients with untreated, poorly controlled, or labile preoperative hypertension are at increased risk for perioperative BP lability, dysrhythmias, myocardial ischemia, and transient neurologic complications. Some suggested that preoperative hypertension predicted perioperative myocardial infarction. However, Goldman and Caldera demonstrated that mild-to-moderate hypertension did not increase the risk of major morbid events. Instead, preoperative hypertension may predict several intermediates of outcome, such as BP lability and myocardial ischemia. The controversy may be due to the wide variability in the hypertensive population. Hypertension may affect perioperative morbidity through the extent of end-organ damage and not the manifestation of the disease itself. LVH, which signifies longstanding poorly controlled hypertension, can increase the risk of myocardial ischemia from imbalances of myocardial oxygen supply and demand regardless of the presence or absence of coronary artery disease.

Isolated systolic hypertension (systolic BP greater than 160 mm Hg and diastolic BP less than 90 mm Hg) has been identified as a risk factor for cardiovascular complications in the general population and treatment reduces the future risk of stroke.

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Allman KG. Muir A. Howell SJ, et al.Resistant hypertension and preoperative silent myocardial ischaemia in surgical patients. Br J Anaesth 1994:73:574–578.

Fleisher LA. Preoperative evaluation of the patient with hypertension. JAMA 2002:287:2043–2046.

Foëx P. Prys-Roberts C. Anaesthesia and the hypertensive patient. Br J Anaesth 1974:46:575.

Goldman L. Cardiac risk in noncardiac surgery: an update. Anesth Analg 1995:80:810–820.

Goldman L. Caldera DL. Risks of general anesthesia and elective operation in the hypertensive patient. Anesthesiology 1979:50:285–292.

Hollenberg M. Mangano DT. Browner WS, et al.Predictors of postoperative myocardial ischemia in patient undergoing noncardiac surgery. JAMA 1992:268:205–209.

Mangano DT. Perioperative cardiac morbidity. Anesthesiology 1990:72:153–184.

A.8. Are hypertensive patients at increased risk for perioperative cerebral and renal complications? Why?

Hypertensive patients are at increased risk for perioperative cerebrovascular accidents (CVAs) and acute renal failure. Most anesthetic agents produce a dose-related depression of myocardial contractility with a fall in cardiac output and a decreased blood flow to brain and kidneys. Because autoregulation may be impaired in these patients, there is a greater susceptibility of the brain and kidney to sudden changes in pressure. In hypertensive patients, autoregulation of cerebral blood flow is reset to a higher range than normal, and although it protects the brain against sudden increases in pressure, it makes it more vulnerable to hypotension. Thus, when BP is lowered acutely, hypertensive patients will show signs of cerebral ischemia at a higher level of BP than normotensive patients.

Hypertension may accelerate cognitive decline with age. Hypertension, particularly systolic, is a major risk factor for initial and recurrent stroke and for transient ischemia attacks caused by extracranial atherosclerosis.

Chronic renal insufficiency is a common sequela of hypertension. Patients with hypertension should have a measurement of baseline serum creatinine. In the original Cardiac Risk Index, an elevated serum creatinine level [greater than 3.0 mg/dL (greater than 265.2 mol/L)] was one of the independent risk factors for perioperative cardiovascular morbidity and mortality. This has been confirmed in the revised Cardiac Risk Index, in which a preoperative serum creatinine level greater than 2.0 mg/dL [176.8 mol/L] was one of six independent factors that predicted increased cardiovascular risk.

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Davis BR. Vogt T. Frost PH, et al.Risk factors for stroke and type of stroke in persons with isolated systolic hypertension. Stroke 1998:29:1333.

Finnerty FA. Witkin L. Fazekas JF. Cerebral hemodynamics during cerebral ischemia induced by acute hypotension. J Clin Invest 1955:34:1227.

Fleisher LA. Preoperative evaluation of the patient with hypertension. JAMA 2002:287:2043–2046.

Goldman L. Caldera DL. Risks of general anesthesia and elective operation in the hypertensive patient. Anesthesiology 1979:50:285.

Goldman L. Caldera DL. Nussbaum SR, et al.Multifactorial index of cardiac risk in noncardiac surgical procedures. N Engl J Med 1977:297:845–850.

Lee TH. Marcantonio ER. Mangione CM, et al.Derivation and prospective validation of a simple index for prediction of cardiac risk of major noncardiac surgery. Circulation 1999:100:1043–1049.

Matthews DM. Miller ED. Mechanism and treatment of perioperative hypertension. ASA Refresher Courses in Anesthesiology Park Ridge, IL: American Society of Anesthesiologists, 1990:18:237–250.

Strangaard S. Olsen J. Skinhof E, et al.Autoregulation of brain circulation in severe arterial hypertension. Br Med J 1973:3:507.

Yao FSF. Tseng CC. Boyd WC, et al.Frontal lobe dysfunction following cardiac surgery is associated with cerebral oxygen desaturation. Ann Thorac Surg 1999:68:1464.

A.9. Would you employ a controlled hypotensive technique for hypertensive patients? How much would you safely lower the blood pressure (BP)?

Uncontrolled or untreated severe hypertension is a contraindication to controlled hypotension. However, controlled hypotension may be used with caution in treated hypertensive patients. Because cerebral autoregulation is shifted to the right with chronic hypertension, the lower limit of controlled hypotension should be higher for hypertensive patients. However, with long-term treatment, the autoregulation curve shifts leftward to approach that in normals. Strangaard found that the lower limit of autoregulation was 113 mm Hg in severe untreated or uncontrolled hypertensives; 96 mm Hg in formerly severe, now-treated hypertensives; and 73 mm Hg in normotensive patients. The lowest level of mean BP tolerated without symptoms of hypoperfusion was 65 mm Hg in severe hypertensives, 53 mm Hg in treated hypertensives, and 43 mm Hg in normal patients. However, although the autoregulation may shift toward normal with treatment, in many patients the autoregulation did not shift toward normal even after 12 months of treatment. Because one cannot measure patients' autoregulation, a useful clinical guide is that a 25% decrease in mean arterial pressure (MAP) reaches the lower limit of autoregulation and a 55% decrease in MAP reaches symptomatic cerebral hypoperfusion. Another suggested rule is that the systolic pressure of controlled hypotension should not be lower than the diastolic pressure of the patient's usual pressure.

Recently, noninvasive cerebral oximeter using near-infrared spectroscopy may be used to monitor the oxygen saturations of cerebral cortex. The values of cerebral oxygen saturations correspond with those of a mixture of 85% jugular venous O2 saturation and 15% of arterial O2 saturation. It reflects the balance between cerebral O2 delivery and O2 demand. In a steady state of anesthesia, the cerebral O2 demand does not change significantly. Therefore, cerebral O2 saturations will not decrease until the BP falls below its autoregulation range. Thus, the cerebral oximeter may be employed to determine the lower limit of autoregulation and to ensure adequate cerebral oxygenation.

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Lindop MJ. Complications and morbidity of controlled hypotension. Br J Anaesth 1975:47:799.

Murray MJ. Perioperative hypertension. ASA Annual Refresher Course Lectures Park Ridge, IL: American Society of Anesthesiologists, 2002:512.

Strangaard S. Autoregulation of cerebral blood flow in hypertension patients. Circulation 1976:53:720–727.

A.10. What is the mechanism of action of antihypertensive drugs?

Antihypertensive drugs are categorized by their mechanism of action as follows.

Diuretics

They include thiazides (e.g., hydrochlorothiazide), loop diuretics (e.g., furosemide, ethacrynic acid), and potassium-sparing agents (e.g., spironolactone, triamterene). All diuretics initially lower the BP by increasing urinary sodium excretion and by reducing plasma volume, extracellular fluid volume, and cardiac output. Within 6 to 8 weeks the cardiac output returned to normal. The lowered BP is related to a fall in peripheral resistance. Diuretics may cause hypokalemia, hypomagnesemia, hyperuricemia, hyperlipidemia, hypercalcemia, and hyperglycemia. For patients with ST-segment changes and evidence of pulmonary edema and hypertension or with increased intracranial cerebral pressure and hypertension, intravenous furosemide may be appropriate.

Antiadrenergic Agents

  • Centrally acting drugs—clonidine, methyldopa, guanfacine, guanabenz, and mivazerol. These drugs and their metabolites are primarily –2 receptor agonists. Stimulation of –2 receptors in the vasomotor centers of the brain reduces sympathetic outflow.

  • Peripherally acting drugs—reserpine, guanethidine, guanadrel, and bethanidine. These drugs inhibit the release of norepinephrine from peripheral adrenergic neurons, each in a different manner.

    • –Receptor blockers

      • –1 and –2 Receptors—phenoxybenzamine (Dibenzyline), phentolamine (Regitine)

      • –1 Receptor—prazosin (Minipress), doxazosin (Cardura)

        By blocking –mediated vasoconstriction, these drugs induce a fall in peripheral resistance with both arteriolar and venous dilation.

  • –Receptor blockers—atenolol (Tenormin), metoprolol (Lopressor), nadol (Corgard), pindolol (Visken), propranolol (Inderal), esmolol (Brevibloc). These drugs lower the BP by decreasing heart rate, contractility, cardiac output, and renin levels. BP is decreased without reflex tachycardia or widening of the pulse pressure. They also have antiarrhythmic activity and suppress both ventricular and supraventricular ectopic rhythms.

  • – and –Receptor blockers—labetalol (Trandate)

Direct Vasodilators

They include hydralazine, diazoxide, minoxidil, nitroprusside, and nitroglycerin. These drugs directly relax the smooth muscle of resistance and capacitance vessels to different degrees.

Dopaminergic Agonists (DA)

Classified into DA1 and DA2 subtypes.

Stimulation of DA1 receptors causes vasodilation, and inhibition of active sodium transport in the proximal tubule, leading to natriuresis.

Stimulation of DA2 receptors inhibits norepinephrine release and promotes peripheral vasodilation.

Fenoldopam—dopamine receptor (DA1 selective) agonist, a systemic and renal vasodilator, offers significant advantages as a parenterally administered agent for the management of BP in hypertensive emergencies and in the perioperative setting. Parenteral fenoldopam has a rapid onset and offset of effect, with an elimination half-time of approximately 10 minutes. Prepared in concentration of 10 mg in 250 mL (40 g/mL), the recommended starting dose is 0.05 g/kg/minute. This should be titrated to effect by 0.025 g/kg/minute every 10 to 15 minutes, to a maximum dose of 0.5 to 0.8 g/kg/minute. The drug should not be administered in boluses; the incidence of reflex tachycardia is related to rapidity of upward titration. Unlike dopamine, it has no – or –adrenergic activity and increasing doses result in increasing vasodilation without tachycardia or tachyarrhythmias.

Calcium Channel Blockers

The cardiovascular effects of calcium antagonists are listed in Table 14.3. These drugs decrease BP mainly by peripheral vasodilation. Renin and aldosterone secretion may be reduced as well.

Angiotensin–Converting Enzyme (ACE) Inhibitors

They include captopril, enalapril, lisinopril, quinapril, and ramipril. The renin-angiotensin system may be inhibited in four ways as shown in Fig. 14.1. These drugs inhibit the conversion of the inactive decapeptide angiotensin I to the active octapeptide angiotensin II. Lower levels of angiotensin II may decrease BP by reducing angiotensin II-induced vasoconstriction and by decreasing aldosterone synthesis. ACE inhibitors also retard the degradation of a potent vasodilator (bradykinin), alter prostaglandin production (most notably with captopril), and can modify the activity of the adrenergic nervous system.

Figure 14.1. The renin-angiotensin system and the mechanism of action of antihypertensive drugs.


ACE inhibitors provide predominantly arterial vasodilation and have become primary therapy for the treatment of CHF by afterload reduction. Cardiac output is increased without excessive decrease in preload, with a favorable effect on survival.

Other Vasodilators

They include endothelin receptor antagonists and agents that inhibit both ACE and neutral endopeptides, thereby increasing atrial natriuretic hormone. In the distant future, gene therapy may be applied.

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Barash PG, Cullen BF, Stoelting RK, Clinical anesthesia4th ed. Philadelphia: Lippincott Williams & Wilkins, 2001:309–319.

Benigni A. Remuzzi G. Endothelin antagonists. Lancet 1999:353:133.

Braunwald E, Heart disease6th ed. Philadelphia: WB Saunders, 2001:978–989.

Braunwald E, Isselbacher KJ, Fauci AS, et al., Harrison's principles of internal medicine15th ed. New York: McGraw-Hill, 2001:1420–1426.

Murray MJ. Perioperative hypertension. ASA Annual Refresher Course Lectures Park Ridge, IL: American Society of Anesthesiologists, 2002:512.

Oparil S. Aronson S. Deeb GM, at al. Fenoldopam: a new parenteral antihypertensive: consensus roundtable on the management of perioperative hypertension and hypertensive crisis. Am J Hypertens 1999:12:653–664.

Rousso P. Buclin T. Nussberger J, et al.Effects of a dual inhibitor of angiotensin-converting enzyme and neutral endopeptides, MDL 100240 on endocrine and renal functions in healthy volunteers. J Hypertens 1999:17:427.

Sladen RN. Perioperative hypertension. IARS Review Course Lectures Cleveland, OH: International Anesthesia Research Society, 2002:100–114.

A.11. Does the choice of antihypertensive therapy influence hemodynamic responses to induction, laryngoscopy, and intubation?

The pressor responses to induction, laryngoscopy, and intubation differ little whether patients with mild to moderate hypertension receive a –blocker, a calcium channel blocker, an ACE inhibitor, or a diuretic. Even changes of a similar magnitude are also observed in untreated hypertensive patients.

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Sear JW. Jewkes C. Teller JC, et al.Does the choice of antihypertensive therapy influence haemodynamic responses to induction, laryngoscopy and intubation?. Br J Anaesth 1994:73:303–308.

A.12. Does chronic angiotensin-converting enzyme (ACE) inhibition influence anesthetic induction?

Coriat et al. reported that, in hypertensive patients chronically treated with ACE inhibitors, therapy until the day of surgery is a major factor influencing BP responsiveness to anesthetic induction for vascular surgery. If enalapril (a long–acting ACE inhibitor) treatment is continued, a very low plasma–converting enzyme activity will be observed and an exaggerated hypotensive response may occur at induction. If captopril (a short–acting ACE inhibitor) treatment is continued, the magnitude of the decrease in BP in response to induction, although lower than with enalapril, is enhanced compared with that noted in patients in whom captopril had been stopped. All of the hypotensive episodes in patients who received ACE inhibitors until the day of surgery were easily corrected by ephedrine infusion. The temporary withdrawal of these two ACE inhibitors attenuated the hypotensive response to induction but did not lead to an abnormal BP response to induction and intubation. However, recently Ryckwaert and Colson reported that ACE inhibitor treatment in patients with infarction-induced myocardial dysfunction does not increase the incidence of severe hypotension after induction of anesthesia.

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Coriat P. Richter C. Douraki T, et al.Influence of chronic angiotensin–converting enzyme inhibition on anesthetic induction. Anesthesiology 1994:81:299–307.

Ryckwaert F. Colson P. Hemodynamic effects of anesthesia in patients with ischemic heart failure chronically treated with angiotensin–converting enzyme inhibitors. Anesth Analg 1997:84:945–949.

B. Preoperative Evaluation and Preparation

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B.1. How would you evaluate this patient preoperatively?

In addition to the routine systemic preoperative physical and history, special attention should be paid to the following: etiology and severity of hypertension, current therapy, and the end-organ damage by chronic hypertension.

The underlying cause of hypertension should be clear. Surgical mortality is relatively high in patients with renovascular hypertension. Moreover, failure to diagnose a pheochromocytoma preoperatively may prove fatal, because anesthetic agents are well known to precipitate a crisis in such patients. Meanwhile, the severity of hypertension alters anesthetic risk.

Antihypertensive drugs have different anesthetic implications. Diuretics frequently cause chronic hypokalemia and hypomagnesemia, which may increase the risk of arrhythmia. Therefore, serum electrolytes should be checked preoperatively.

The presence of target-organ damage in the brain, heart, and kidney signifies longstanding, poorly controlled hypertension.

For cardiac evaluation, electrocardiogram (ECG) and chest x-ray film serve as minimal tests. The echocardiogram will be helpful. LVH can increase the risk of perioperative myocardial ischemia from imbalances of myocardial oxygen supply and demand regardless of the presence or absence of coronary artery disease. Some authorities believe that hypertensive patients without evidence of LVH or other risk factors are at a lower perioperative cardiac risk and do not require further evaluation for most operations. Patients with severe hypertension are also at increased risk for CHF and pulmonary edema.

For renal evaluation, urinalysis, serum creatinine, and blood urea nitrogen should be measured to define the presence and extent of renal parenchymal disease. If chronic renal failure exists, hyperkalemia and elevated plasma volume should be considered.

For cerebrovascular evaluation, a history of CVAs and TIAs and the presence of hypertensive retinopathy should be looked for.

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Barash PG, Cullen BF, Stoelting RK, Clinical anesthesia4th ed. Philadelphia: Lippincott, Williams & Wilkins, 2001:476.

Fleisher LA. Preoperative evaluation of the patient with hypertension. JAMA 2002:287:2043–2046.

Fleisher LA. Barash PH. Preoperative cardiac evaluation for noncardiac surgery. Anesth Analg 1992:74:586–598.

Murray MJ. Perioperative hypertension. ASA Annual Refresher Course Lectures Park Ridge, IL: American Society of Anesthesiologists, 2002:512.

Tubau JF. Szlachcic J. Meyer L, et al.Left ventricular hypertrophy increases the risk of postoperative myocardial ischemia. Circulation 1990:82:11–163(abst).

Yurenev AP. Dequattro V. Devereux RB. Hypertensive heart disease: relationship of silent ischemia to coronary artery disease and left ventricular hypertrophy. Am Heart J 1990:120:928–933.

B.2. Would you postpone the surgery? Why? What BP would you like the patient to achieve before surgery?

Yes. I would postpone the elective surgery because the BP was 230/120 mm Hg. In general, elective surgery should be delayed for patients with severe hypertension (diastolic BP greater than 115 mm Hg) or with severe isolated systolic hypertension (systolic BP greater than 200 mm Hg) until the BP is below 180/110 mm Hg. If time permits, the BP should be lowered over 6 to 8 weeks to 140/90 mm Hg. Acute control within several hours is inadvisable before elective surgery, because this practice may put the cerebral or other circulations at risk for ischemia.

In moderate hypertensive patients with severe end-organ involvement, preoperative BP should be normalized as much as possible, although in asymptomatic patients with mild to moderate hypertension (diastolic BP less than 110 mm Hg), elective surgery may proceed without increased cardiovascular risks.

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Fleisher LA. Preoperative evaluation of the patient with hypertension. JAMA 2002:287:2043–2046.

Fleisher LA. Barash PH. Preoperative cardiac evaluation for noncardiac surgery. Anesth Analg 1992:74:586–598.

Murray MJ. Perioperative hypertension. ASA Annual Refresher Course Lectures Park Ridge, IL: American Society of Anesthesiologists, 2002:512.

B.3. Should all or any of the chronic medications be discontinued before the operation?

Current opinion generally favors continuation of antihypertensive medications, especially –blockers, up to the time of surgery. There is concern that acute withdrawal of these medications may precipitate ischemic myocardial events. Because –blockade does not impair the hemodynamic response to hemorrhage and does not adversely affect responses to hypoxia, the medications should be continued. The withdrawal syndrome is characterized by an enhanced sensitivity to sympathetic stimulation and has been attributed to various factors, including sympathetic overactivity and increased triiodothyronine levels, but most probably it is a result of increased –receptor density.

The safety of –blockers and their benefits (prevention of hypertensive responses, dysrhythmias, and myocardial ischemia) have been long established. Similarly, treatment with calcium channel blockers, ACE inhibitors, and diuretics can be maintained. Indeed, the responses to induction of anesthesia, laryngoscopy, and intubation differ little whether patients receive a –blocker, a calcium channel blocker, an ACE inhibitor, or a diuretic. However, Coriat et al. reported that maintenance of ACE inhibitor therapy until the day of surgery might increase the probability of hypotension at induction and that the hypotensive episodes were easily corrected by ephedrine infusion.

Withdrawal of clonidine has been associated with rebound hypertension.

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Barash PG, Cullen BF, Stoelting RK, Clinical anesthesia4th ed. Philadelphia: Lippincott–Raven, 2001:1103–1104.

Coriat P. Richters C. Douraki T, et al.Influence of chronic angiotensin-converting enzyme inhibition on anesthetic induction. Anesthesiology 1994:81:299–307.

Fleisher LA. Preoperative evaluation of the patient with hypertension. JAMA 2002:287:2043–2046.

Mangano DT, Preoperative cardiac assessment Philadelphia: JB Lippincott, 1990:141–163.

Prichard BWC, et al.The syndrome associated with the withdrawal of beta-adrenergic receptor blocking drugs. Br J Clin Pharm 1982:13:337.

Sear JW. Jewkes C. Tellez JC, et al.Does the choice of antihypertensive therapy influence haemodynamic responses to induction, laryngoscopy and intubation?. Br J Anaesth 1994:73:303–308.

Sladen RN. Perioperative hypertension. IARS Review Course Lectures Cleveland, OH: International Anesthesia Research Society, 2002:100–114.

Stoelting RK, Diedorf SF, Anesthesia and co-existing disease4th ed. New York: Churchill Livingstone, 2002:99–103.

B.4. Should hypokalemia be treated before anesthesia? Why?

Hypokalemia is a frequent finding in hypertensive patients treated with the diuretic thiazides. It is important to maintain normal electrolyte balance in patients with heart or coronary artery disease. A low value of potassium (3.0 to 3.5 mEq/L) in these patients may cause arrhythmias, increase sensitivity to digitalis, and depress neuromuscular function. In patients without risk of cardiac complications of surgery and anesthesia, this modest reduction (3.0 to 3.5 mEq/L) should not prompt postponement of surgery or immediate potassium replacement. Patients with more severe potassium depletion (2.9 mEq/L or lower) should be treated. For those patients, at least 1 week before surgery supplemental potassium should be given if renal function is not impaired. In surgical emergencies, potassium may be given at a rate not to exceed 0.5 mEq/kg of body weight per hour. Administration should be stopped during surgery and restarted postoperatively, depending on serial potassium determinations. Vitez et al. concluded that chronic hypokalemia per se is not associated with a higher incidence of intraoperative arrhythmia.

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Barash PG, Cullen BF, Stoelting RK, Clinical anesthesia4th ed. Philadelphia: Lippincott Williams & Wilkins, 2001:186–187.

McGovern B. Hypokalemia and cardiac arrhythmias [Editorial]. Anesthesiology 1985:63:127.

Schwartz SI, Shires GT, Spencer FC, Principles of surgery7th ed. New York: McGraw-Hill, 1999:63–64.

Stoelting RK, Diedorf SF, Anesthesia and co-existing disease4th ed. New York: Churchill Livingstone, 2002:99–103.

Vitez TS. Soper LE. Wong KC, et al.Chronic hypokalemia and intraoperative dysrhythmias. Anesthesiology 1985:63:130–133.

B.5. Should hypomagnesemia be treated before anesthesia? Why?

The normal level of magnesium is between 1.5 and 2.5 mEq/L. Magnesium ion is essential for the proper function of most enzyme systems. Depletion is characterized by neuromuscular and central nervous system hyperexcitability. These signs are similar to those of calcium deficiency. Cardiovascular abnormalities include coronary artery spasm, cardiac failure, and dysrhythmias. When severe, hypomagnesemia may induce seizures, confusion, and coma. Replacement should be done only in cases of severe depletion. Magnesium should not be given to the oliguric patient and should be given very carefully to patients with renal insufficiency. Small intravenous doses should be used, with careful observation for toxicity (lethargy, weakness, and loss of deep tendon reflexes).

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Barash PG, Cullen BF, Stoelting RK, Clinical anesthesia4th ed. Philadelphia: Lippincott Williams & Wilkins, 2001:194–195.

Schwartz SI, Shires GT, Spencer FC, Principles of surgery7th ed. New York: McGraw-Hill, 1999:65.

B.6. Does an asymptomatic carotid bruit increase the risk in these patients?

Yes. The incidence of stroke is increased in such patients, although the stroke may not be thrombotic or related to the carotid artery in which the bruit was heard. Bruits are general predictors of vascular disease and may be predictors of perioperative strokes.

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Wolf P. Kannel WB. Sorlie P, et al.Asymptomatic carotid bruit and the risk of stroke: the Framingham Study. JAMA 1981:245:1442.

Yatsu FM. Hart RG. Asymptomatic carotid bruit and stenosis: a reappraisal. Curr Concepts Cerebrovascular Dis 1982:17:21.

B.7. The surgery was postponed for 6 weeks. The patient has been on propranolol, captopril, hydrochlorothiazide, and KCl. His BP was 160/95 mm Hg and potassium was 4.0 mEq/L. How would you premedicate this patient?

Because most hypertensive patients still have elevated BPs despite treatment, the anesthesiologist should determine the anxiety level of the patient. With this knowledge, the premedication with diazepam, lorazepam, or midazolam can be regulated to have the patient arrive in the operating room sedated. This will help to prevent a starting BP well above the optimal level. Glycopyrrolate is the preferred anticholinergic because it produces less tachycardia than atropine. All the antihypertensive medications are continued up to the day of surgery with the possible exception of ACE inhibitors, which may be discontinued the evening before surgery. Coriat et al. reported that the incidence of induction-induced hypotension was significantly less when enalapril or captopril has been discontinued. If ACE inhibitors are maintained until the day of surgery, phenylephrine or ephedrine should be ready to treat the possible induction-induced hypotension.

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Coriat P. Richters C. Douraki T, et al.Influence of chronic angiotensin-converting enzyme inhibition on anesthetic induction. Anesthesiology 1994:81:299–307.

B.8. If the patient is an untreated hypertensive patient with BP 170/100 mm Hg, would you pretreat the patient preoperatively with an antihypertensive agent?

Yes. The preoperative administration of clonidine, –blockers, or ACE inhibitors has been advocated to reduce the intraoperative hemodynamic lability and myocardial ischemia in hypertensive patients. Clonidine, a central –2 agonist, decreases sympathetic outflow and reduces plasma catecholamines, aldosterone levels, and renin activity. A single dose of clonidine, 5 g/kg orally, 2 hours before surgery significantly decreases anesthetic requirements and hemodynamic lability in patients with mild to moderate hypertension. However, preoperative clonidine did not decrease BP lability during aortic operation.

The best treatment may be cardioselective –blocker therapy. A single small oral dose of a –adrenergic blocking agent such as labetalol, atenolol, or oxprenolol given preoperatively to untreated, asymptomatic, mildly hypertensive patients effectively attenuated tachycardia with tracheal intubation and emergence. The incidence of myocardial ischemia was reduced from 28% in the control group to 2% in the –blocker groups. An oral-dose ACE inhibitor such as enalapril given preoperatively also attenuates the hemodynamic responses to intubation and surgical stimulation.

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Engelman E, et al.Effects of clonidine on anesthetic drug requirements and hemodynamic response during aortic surgery. Anesthesiology 1989:71:178–187.

Fleisher LA. Preoperative evaluation of the patient with hypertension. JAMA 2002:287:2043–2046.

Ghignone M, et al.Anesthesia and hypertension: the effect of clonidine on perioperative hemodynamics and isoflurane requirements. Anesthesiology 1987:67:3–10.

Stone JG, et al.Myocardial ischemia in untreated hypertensive patients: effect of a single small oral dose of a beta-adrenergic blocking agent. Anesthesiology 1988:68:495–500.

Yeates AP. Anaesthesia and angiotensin-converting enzyme inhibitors. Anaesthesia 1988:43:935–939.

C. Intraoperative Management

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C.1. How would you monitor this patient?

  • ECG—Simultaneous leads V5 and II, multiple lead ST analysis, if possible, are essential because hypertensive patients are at increased risk for myocardial ischemia regardless of the presence or absence of coronary disease.

  • BP—A continuous monitoring of BP is essential because of lability of BP in these patients. Direct intraarterial measurement of BP permits beat-to-beat observation. However, noninvasive automatic sphygmomanometric techniques are usually sufficient.

  • Swan–Ganz catheter—Only for those hypertensive patients with a history of CHF or a recent myocardial infarction, a Swan–Ganz catheter may be extremely helpful in managing fluid replacement and monitoring ventricular function.

  • Pulse oximeter—This should be used to monitor peripheral blood flow and oxygenation.

  • End-tidal CO2 analyzer—This monitor will help maintain normocarbia.

  • Temperature

C.2. What are the anesthetic goals for hypertensive patients?

The anesthetic goal is to minimize wide lability of BP in response to anesthetic and surgical stimuli to prevent

  • Myocardial ischemia from either hypertension or, less commonly, hypotension

  • Cerebral hypoperfusion from hypotension

  • Cerebral hemorrhage and hypertensive encephalopathy resulting from hypertension

  • Renal failure from renal hypoperfusion

Careful control of the hemodynamic responses to noxious stimuli such as endotracheal intubation, surgical incision and manipulation, and emergence from anesthesia is essential in the hypertensive patient.

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Stoelting RK, Diedorf SF, Anesthesia and co-existing disease4th ed. New York: Churchill Livingstone, 2002:99–103.

Thomas S, Manual of cardiac anesthesia2nd ed. New York: Churchill Livingstone, 1993:259.

C.3. How would you induce anesthesia for the hypertensive patient?

Before induction of anesthesia, I would like to hydrate the patient with at least 200 mL of lactated Ringer's solution. While the patient is being preoxygenated, fentanyl, 7 to 8 g/kg, is given slowly to achieve drowsiness. Then, either thiopental in 50-mg increments or midazolam in 1-mg increments is titrated to produce unconsciousness, followed by succinylcholine, 1 mg/kg, or nondepolarizing muscle relaxants to facilitate tracheal intubation.

All anesthetic agents are acceptable with the possible exception of ketamine, which may produce significant hypertension and tachycardia. However, deeper anesthesia with potent inhalation agents to attenuate tachycardia and hypertension is not recommended because of higher incidence of hypotension because of both vasodilation and cardiac depression.

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Martin DE. Rosenberg H. Aukburg SJ, et al.Low-dose fentanyl blunts circulatory responses to tracheal intubation. Anesth Analg 1982:61:680.

C.4. How does tracheal intubation produce hypertension?

Translaryngeal intubation of the trachea stimulates laryngeal and tracheal receptors, resulting in marked increase in the elaboration of sympathomimetic amines. This sympathetic stimulation results in tachycardia and a rise in BP. In normotensive patients, this rise is approximately 20 to 25 mm Hg; it is much greater in hypertensive patients. This increase in BP results from vasoconstriction, because of unopposed alpha stimulation in hypertensive patients taking –blocking drugs.

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Prys-Roberts C. Greene LT. Meloche R, et al.Studies of anaesthesia in relation to hypertension. II: haemodynamic consequences of induction and endotracheal intubation. Br J Anaesth 1971:43:531.

C.5. What happens to the left ventricular ejection fraction during and immediately following intubation?

During and immediately following intubation associated with tachycardia and hypertension, there is a decrease in the left ventricular ejection fraction. This is particularly marked in patients with coronary artery disease.

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Giles RW. Berger JH. Barash PG, et al.Continuous monitoring of left ventricular performance with the computerized nuclear probe during laryngoscopy and intubation before coronary artery bypass surgery. Am J Cardiol 1982:50:735.

C.6. What other measures can prevent hypertension and tachycardia at the time of intubation?

The rise in BP and heart rate occurs about 14 seconds after the start of laryngoscopy and becomes maximal after 30 to 45 seconds of direct laryngoscopy. If possible, laryngoscopy time should be 15 seconds or less to minimize BP elevation. Simultaneous administration of fentanyl 7 to 8 g/kg with the induction dose of thiopental can blunt the cardiovascular response to tracheal intubation. Other measures are described as follows:

  • Lidocaine 1.5 mg/kg is given 2 minutes before intubation.

  • Sodium nitroprusside 1 to 2 g/kg has been recommended.

  • Esmolol, up to 2 mg/kg, appears to be especially effective in providing consistent and reliable protection against hypertension and tachycardia with intubation. It is easy to titrate and does not exacerbate postintubation hypotension because of its short duration of action.

  • Labetalol 0.15 to 0.45 mg/kg is comparable to esmolol 1.5 to 4.5 mg/kg in attenuating hemodynamic effects. However, the half-lives of intravenous esmolol and labetalol are 9 minutes and 5 hours, respectively.

  • Diltiazem, 0.1 or 0.2 mg/kg, given 2 minutes before extubation was of value in attenuating the cardiovascular responses occurring in association with tracheal extubation and emergence of anesthesia. This alleviative effect of diltiazem was equal or superior to that of intravenous lidocaine, 1 mg/kg.

  • Verapamil, 0.1 mg/kg, given 2 minutes before tracheal extubation is a more effective prophylactic for attenuating the cardiovascular responses associated with extubation than is diltiazem, 0.2 mg/kg.

  • Nicardipine, 1 mg intravenously 2 minutes before tracheal intubation maintained hemodynamic stability during the intraoperative period. Both doses of 0.015 and 0.03 mg/kg attenuated BP but not heart rate responses during emergence and extubation. Greater BP control occurred with the larger nicardipine dose of 0.03 mg/kg.

It is important to remember that all the previously mentioned doses are used with a single agent only. If a combination of different agents or anesthetics is used, doses should be decreased accordingly. Otherwise, severe hypotension may ensue.

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Anthony LK. Cindy M. Carol JT, et al.Comparison of nicardipine versus placebo to control hemodynamic responses during emergence and extubation. J Cardiothorac Vasc Anesth 2001:15:704–709.

Barash PG, Cullen BF, Stoelting RK, Clinical anesthesia4th ed. Philadelphia: Lippincott-Raven, 2001:459, 1187.

Cucchiara RF, et al.Evaluation of esmolol in controlling increases in heart rate and blood pressure during endotracheal intubation in patients undergoing carotid endarterectomy. Anesthesiology 1986:65:528–531.

Gold MI, et al.Use of esmolol during anesthesia to treat tachycardia and hypertension. Anesth Analg 1989:68:101–104.

Helfman SM, et al.Which drug prevents tachycardia and hypertension associated with tracheal intubation: lidocaine, fentanyl, or esmolol?. Anesth Analg 1991:72:482–486.

Kapnoudhis P. Vaghadia H. Jenkins LC, et al.Esmolol versus fentanyl for preventing haemodynamic response to intubation in cardiovascular disease. Can J Anaesth 1990:37:S145.

Martin DE. Rosenberg H. Aukburg SJ, et al.Low-dose fentanyl blunts circulatory responses to tracheal intubation. Anesth Analg 1982:61:680.

Mikawa K. Nishina K. Maekawa N, et al.Attenuation of cardiovascular responses to tracheal extubation: verapamil versus diltiazem. Anesth Analg 1996:82:1205–1210.

Nishina K, et al.Attenuation of cardiovascular responses to tracheal extubation with diltiazem. Anesth Analg 1995:80:1217–1222.

Sladen RN. Perioperative hypertension. IARS Review Course Lectures Cleveland, OH: International Anesthesia Research Society, 2002:100–114.

Song D. Singh H. White PF, et al.Optimal dose of nicardipine for maintenance of hemodynamic stability after tracheal intubation and skin incision. Anesth Analg 1997:85:1247–1511.

Stoelting RK. Blood pressure and heart rate changes during short-duration laryngoscopy for tracheal intubation: influence of viscous or intravenous lidocaine. Anesth Analg 1978:57:197.

Stoelting RK. Attenuation of blood pressure response to laryngoscopy and tracheal intubation with sodium nitroprusside. Anesth Analg 1979:58:116.

Stoelting RK, Diedorf SF, Anesthesia and co-existing disease4th ed. New York: Churchill Livingstone, 2002:99–103.

C.7. After induction and intubation, the BP went down to 70/40 mm Hg. What would you do?

Hypotension after induction of anesthesia is usually due to combination of vasodilation, hypovolemia, and cardiac depression. Vasodilation can be caused by inducing agents such as thiopental, diazepam, or midazolam; moderate to high doses of narcotics; and potent inhalation agents. Hypertensive patients are in relative hypovolemia because of chronic vasoconstriction and/or diuretic therapy. Preoperative bowel preparation and nothing by mouth further contribute to hypovolemia. Barbiturates, benzodiazepines, and inhalation agents can cause a mild to moderate degree of cardiac depression.

Hypotension after induction of anesthesia usually can be easily corrected by volume replacement and simultaneous titration of vasopressors such as ephedrine 5 to 10 mg or phenylephrine in 0.1-mg increments.

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Coriat P. Richters C. Douraki T, et al.Influence of chronic angiotensin-converting enzyme inhibition on anesthetic induction. Anesthesiology 1994:81:299–307.

C.8. What is your choice of agents for maintenance of anesthesia? Why?

I would use nitrous oxide and low to moderate doses of fentanyl and isoflurane for maintenance of anesthesia. No particular anesthetic technique or specific drug combinations have been demonstrated to be superior to others in hypertensive patients. Potent inhalation anesthetics or narcotics should be titrated to the desired level of central nervous system depression while the BP is monitored continuously.

Narcotics and nitrous oxide provide an anesthetic with less overall lability of BP, but commonly intraoperative hypertension is difficult to control by moderate doses of narcotics. High doses of narcotics are not suitable for early extubation.

Potent inhalation agents provide greater control of hypertension but seem to produce less stability. Isoflurane, desflurane, and sevoflurane possess the advantage of more peripheral vasodilation and less cardiac depression. Enflurane may be least useful in patients receiving –blockers because of the potential for greater cardiac depression than is observed with halothane or isoflurane. The combination of nitrous oxide and low to moderate doses of narcotics and potent inhalation agents may provide the most stable intraoperative course.

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Kaplan JA, Cardiac anesthesia4th ed. Philadelphia: WB Saunders, 2001:167–168.

Stoelting RK, Diedorf SF, Anesthesia and co-existing disease4th ed. New York: Churchill Livingstone, 2002:99–103.

C.9. How would you manage fluid therapy for hypertensive patients?

Patients with essential hypertension are usually hypovolemic because of vasoconstriction and diuretic therapy. Hydration of the hypertensive patient should be started before induction of anesthesia to minimize the "roller-coaster" often seen with hypertension. However, overhydration should be avoided because it may contribute to postoperative hypertension when the vasodilating effects of anesthetics are gone. Therefore, careful estimation of fluid intake and output is essential. Foley catheter and central venous pressure monitor are indicated for major surgery with extensive fluid exchange.

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Murray MJ, Perioperative hypertension. ASA Annual Refresher Course Lectures Park Ridge, IL: American Society of Anesthesiologists, 2002:512.

C.10. During the surgery, BP went up to 220/120 mm Hg. How would you treat the hypertension?

Intraoperative control of hypertension is outlined in Table 14.4. Severe hypertension that occurs during a surgical procedure is most frequently due to inadequate anesthesia. Inadequate blockade of sensory input from the surgical procedure stimulates the elaboration of sympathomimetic amines, resulting in hypertension and tachycardia. If a potent inhalation anesthetic is being used, the level of anesthesia should be deepened by increasing the inspired concentration of the anesthetic. A narcotic may not control the rise in BP, and it may be necessary to switch to a potent inhalation anesthetic.

Droperidol, 2.5-mg increments up to 10 mg, may be titrated to control hypertension because it not only deepens anesthesia but also dilates peripheral vessels from its –blocking effect.

Hydralazine, 5-mg increments, may be titrated to decrease BP safely with little chance of excessive reduction. The onset of action is in 10 to 15 minutes with 1 to 2 hours duration.

Phentolamine, 5-mg increments, may be titrated to control hypertension, especially for patients with pheochromocytoma.

Labetalol, 5- to 10-mg increments, is very useful in controlling hypertension and tachycardia.

Rarely, continuous infusion of trimethaphan, a ganglionic blocker, or nitroprusside, 1 to 2 g/kg/minute, a direct arteriolar vasodilator, is needed to control hypertension during anesthesia. It is necessary to monitor BP by an intraarterial catheter.

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Matthews DM. Miller ED. Mechanism and treatment of perioperative hypertension. ASA Refresher Courses in Anesthesiology Park Ridge, IL: American Society of Anesthesiologists, 1990:18:237–250.

Sladen RN. Perioperative hypertension. IARS Review Course Lectures Cleveland, OH: International Anesthesia Research Society, 2002:100–114.

Stoelting RK, Diedorf SF, Anesthesia and co-existing disease4th ed. New York: Churchill Livingstone, 2002:99–103.

C.11. What could you do to prevent hypertension during extubation and emergence?

Intraoperative hypertension can be controlled either by adequate anesthesia with moderate to high doses of narcotics or inhalation agents or by antihypertensive agents listed in question A.8. It is logical to use anesthetic agents to prevent hypertension during induction and intubation and to use antihypertensive agents during extubation and emergence, because the patient has to be awakened at the end of surgery. The alternative measures listed in question C.7 may be applied to prevent hypertension. I prefer to give lower doses of preventive medications such as 1 mg/kg of lidocaine or esmolol or 0.1 mg/kg of labetalol, diltiazem, or verapamil 2 minutes before extubation. If BP goes over desired levels after extubation, additional doses may be titrated to control BP.

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Mikawa K. Nishina K. Maekawa N, et al.Attenuation of cardiovascular responses to tracheal extubation: verapamil versus diltiazem. Anesth Analg 1996:82:1205–1210.

Nishina K, et al.Attenuation of cardiovascular responses to tracheal extubation with diltiazem. Anesth Analg 1995:80:1217–1222.

C.12. Would you consider regional anesthesia for this patient?

Certainly, regional anesthesia can avoid marked increases in sympathetic tone and hemodynamic changes that occur with intubation and extubation. Spinal or epidural anesthesia may be used for lower abdominal surgery. For cholecystectomy, higher levels of regional anesthesia are needed and may compromise respiratory function. Meanwhile, prolonged surgery can cause anxiety and irritability that may induce hypertension and tachycardia.

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Stoelting RK, Diedorf SF, Anesthesia and co-existing disease4th ed. New York: Churchill Livingstone, 2002:99–103.

D. Postoperative Management

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D.1. The patient developed hypertension BP 210/110 mm Hg in the postanesthesia care unit. What would you do?

The management of postoperative hypertension depends on the etiology of the hypertension, the clinical scenario, and the level of hypertension. First, the cause of hypertension should be determined and treated accordingly. Hypertension per se should also be treated by an antihypertensive agent. The causes of postoperative hypertension include pain, emergence excitement, hypoxemia, hypercarbia, reaction to endotracheal tube, full bladder, hypothermia, relative hypervolemia from intraoperative administration of excess fluid, and chronic medication and withdrawal. The most common cause of postoperative hypertension is incisional pain. As the patient awakens, pain triggers an outpouring of catecholamines. The extreme lability of BP in many hypertensive patients makes this rapid increase critical to control. Depending on the cause of hypertension, intravenous analgesics and antihypertensives or diuretics should be titrated to control hypertension. If both tachycardia and hypertension occurred postoperatively, calcium channel blockers such as verapamil, diltiazem, or nicardipine and –blocking agents such as propranolol, esmolol, labetalol, or metoprolol are preferred agents.

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Barash PG, Cullen BF, Stoelting RK, Clinical anesthesia4th ed. Philadelphia: Lippincott, Williams & Wilkins, 2001:310–315, 1378.

Davis RF. Acute postoperative hypertension. ASA Refresher Courses in Anesthesiology Park Ridge, IL: American Society of Anesthesiologists, 1989:17:59–70.

Gal TJ. Cooperman LH. Hypertension in the immediate postoperative period. Br J Anesth 1975:47:70.

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