Hypertension



Hypertension


Cindy Wang

Fun-Sun F. Yao





A. Medical Disease and Differential Diagnosis



  • Define hypertension and classify its severity.


  • What is the prevalence of hypertension?


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


  • What are the clinical patterns of hypertension encountered?


  • What is the pathophysiology of essential hypertension?


  • What is the pathophysiology of isolated systolic hypertension (ISH) and of pulse pressure hypertension (PPH)?


  • What are the end-organ damages caused by long-standing hypertension?


  • Are hypertensive patients at an increased risk for perioperative cardiac morbidity?


  • Perioperative cerebral and renal complications are mostly associated with which subtype of hypertension?


  • Would you employ a controlled hypotensive technique for hypertensive patients? How much would you safely lower the BP?


  • What are BP goals for patients with hypertension and when should antihypertensive drugs be initiated?


  • What is the mechanism of action of antihypertensive drugs?


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


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


B. Preoperative Evaluation and Preparation



  • How would you evaluate this patient preoperatively?


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


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


  • Should hypokalemia be treated before anesthesia? Why?


  • Should hypomagnesemia be treated before anesthesia? Why?


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



  • The surgery was postponed for 6 weeks. The patient was on metoprolol, aspirin, atorvastatin, captopril, hydrochlorothiazide, and potassium chloride. His BP was 160/60 mm Hg and potassium 4.0 mEq per L. How would you premedicate this patient?


  • If the patient is an untreated hypertensive patient with BP 170/70 mm Hg, would you treat the patient preoperatively with an antihypertensive agent?


C. Intraoperative Management



  • How would you monitor this patient?


  • What are the anesthetic goals for hypertensive patients?


  • How would you induce anesthesia for the hypertensive patient?


  • How does tracheal intubation produce hypertension?


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


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


  • After induction and intubation, the BP decreased to 70/40 mm Hg. What would you do?


  • What is your choice of agents for maintenance of anesthesia? Why?


  • How would you manage fluid therapy for hypertensive patients?


  • During the surgery, BP increased to 220/120 mm Hg. How would you treat the hypertension?


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


  • Would you consider regional anesthesia for this patient?


D. Postoperative Management



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


A. Medical Disease and Differential Diagnosis


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. According to the seventh report on classification and characterization of BP by the Joint National Committee (JNC) on Evaluation, Detection, and Prevention of High Blood Pressure in 2003, a normal BP for adults 18 years or older is less than 120 mm Hg systolic with a diastolic of less than 80 mm Hg. Table 11.1 shows the classification of BP for adults by the JNC 7 report: normal, prehypertension, stage 1 hypertension, and stage 2 hypertension.








TABLE 11.1 Classification of Blood Pressure for Adults





























JNC 7 CATEGORY


SBP


DBP


Normal


<120


<80


Prehypertension


120-139


80-89


Hypertension


≥140


≥90


Stage 1


140-159


90-99


Stage 2


≥160


≥100


Adults, 18 years or older; DBP, diastolic blood pressure; JNC, Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; SBP, systolic blood pressure.


From Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the Joint National Committee On Prevention, Detection, Evaluation, And Treatment Of High Blood Pressure: the JNC 7. JAMA. 2003;289:2560-2572.



Hypertension in children and adolescents is defined as BP at the 95th percentile or greater. Prehypertension is defined as BP between the 90th and 95th percentile. The fourth report on high BP in children and adolescents by the National High Blood Pressure Education Program provides BP tables with percentiles based on gender, age, and height.

It is important to note that the classification of hypertension defines and specifies hypertension according to systolic and/or diastolic limits, each representing different pathophysiologic processes. Systolic hypertension is a marker of macrovascular disease and large arterial stiffening (atherosclerosis), and diastolic hypertension is a consequence of microvascular disease involving typically vessels less than 1 mm in size.

Uncontrolled hypertension can escalate to a hypertensive crisis defined as systolic BP greater than 180 mm Hg or diastolic BP greater than 120 mm Hg and categorized as urgent and emergent. According to the JNC 7 Report, hypertensive emergency is defined as elevated BP (usually ≥180/120 mm Hg) complicated by evidence of impending or progressive end-organ damage, whereas hypertensive urgency is severe elevation of BP without progressive end-organ damage.



Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7. JAMA. 2003;289(19):2560-2572.

Longo DL, Fauci AS, Kasper DL, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012:2042-2059.

Mann DL, Zipes DP, Libby P, et al, eds. Braunwald’s Heart Disease. 10th ed. Philadelphia, PA: Elsevier; 2015:934-952.

National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and

Adolescents. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Pediatrics. 2004;114:555-576.

Rodriguez MA, Kumar SK, De Caro M. Hypertensive crisis. Cardiol Rev. 2010;18:102-107.


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 has a BP greater than 160/95 mm Hg and almost one-half has a BP greater than 140/90 mm Hg. A higher prevalence of hypertension has been found in the non-white population. The frequency increases with the age of the population with nearly two-thirds of hypertensive patients being older than 50 years, and by the age of 75 years, almost 90% will have hypertension. The subtype of hypertension is also influenced by age. Younger individuals suffer from diastolic hypertension and combined systolic and diastolic hypertension, whereas older persons predominantly experience systolic hypertension. 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. Currently, approximately 70 million Americans suffer from hypertension.



Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289(19):2560-2572.

Franklin SS, Larson MG, Khan SA, et al. Does the relation of blood pressure to coronary heart disease risk change with aging? The Framingham Heart Study. Circulation. 2001;103:1245-1249.

Longo DL, Fauci AS, Kasper DL, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012:2042-2059.

Mann DL, Zipes DP, Libby P, et al, eds. Braunwald’s Heart Disease. 10th ed. Philadelphia, PA: Elsevier; 2015:934-952.


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

Hypertension is classified according to its subtypes: systolic, diastolic, and pulse pressure (Table 11.2). Historically, only diastolic hypertension—essential hypertension—was recognized, but more recently, there has been increasing emphasis and recognition of systolic hypertension, namely, isolated systolic hypertension (ISH). ISH is the most common subtype of hypertension affecting predominantly individuals older than 60 years of age. In fact, approximately 70% of hypertensive patients have ISH with approximately half of these individuals having very wide pulse pressure (>65 mm Hg) or pulse pressure hypertension (PPH). Isolated diastolic hypertension is most prevalent in individuals younger than 50 years and is an important marker of coronary heart disease and mortality in this age group. Some hypertensive
patients have both systolic and diastolic hypertension categorized as combined systolic and diastolic hypertension. The ranges of systolic, diastolic, and pulse pressure that define each subtype of hypertension are presented in Table 11.1.








TABLE 11.2 Classification of Hypertension




























Systolic and diastolic hypertension



• Essential



• Renal



• Endocrine



• Neurogenic



• Miscellaneous


Systolic hypertension with wide pulse pressure



• Increased cardiac output



• Rigidity of aorta



Etiology of 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 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



Longo DL, Fauci AS, Kasper DL, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012:2042-2059.

Mann DL, Zipes DP, Libby P, et al, eds. Braunwald’s Heart Disease. 10th ed. Philadelphia, PA: Elsevier; 2015:934-952.

Sesso HD, Stampfer MJ, Rosner B, et al. Systolic and diastolic blood pressure, pulse pressure, and mean arterial pressure as predictors of cardiovascular disease risk in men. Hypertension. 2000;36:801-807.


A.4. What are the 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



Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7. JAMA. 2003;289(19):2560-2572.

Mann DL, Zipes DP, Libby P, et al, eds. Braunwald’s Heart Disease. 10th ed. Philadelphia, PA: Elsevier; 2015:934-952.


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 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 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 arteriosclerosis. If untreated, approximately 50% of hypertensive patients die of coronary heart disease or congestive heart failure (CHF), approximately 33% of stroke, and 10% to 15% of renal failure.



Longo DL, Fauci AS, Kasper DL, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012:2042-2059.

Mann DL, Zipes DP, Libby P, et al, eds. Braunwald’s Heart Disease. 10th ed. Philadelphia, PA: Elsevier; 2015:934-952.


A.6. What is the pathophysiology of isolated systolic hypertension (ISH) and of pulse pressure hypertension (PPH)?

ISH is a manifestation of atherosclerotic disease involving predominantly the aorta and its major branches. Both ISH and PPH reflect arterial stiffening and represent the pulsatile component of BP, whereas the mean arterial pressure (MAP) represent the static state. Systole, then, is directly influenced by the ventricular contractile state, the ejected volume, heart rate, and, importantly, compliance of the aorta and pulse wave velocity. With increasing age and factors such as diabetes, smoking, increased cholesterol as well as some genetic factors, compliance of the aorta diminishes markedly (Fig. 11.1). The net result is stiffening of the arterial
tree and inability to absorb the pulsatile load, causing the systolic pressure to rise sharply. Pulse wave velocity has gained much attention lately because it may be a richer substrate for characterizing the physiology of blood flow and pressure. Under normal physiologic conditions, the ejected blood volume is transmitted peripherally as a propagated wave. After reaching the periphery, in particular, at the bifurcation sites, a reflected wave or a retrograde wave is generated from the encountered impedance. Under normal conditions, wave reflection arrival coincides with the beginning of diastole, thereby augmenting the diastolic pressure. However, with stiffening of the aorta as occurs with aging, both the propagated and the reflected waves travel much more rapidly, and early return of the reflected arterial wave during late systole augments the systolic component, effectively increasing afterload. The ensuing loss of diastolic augmentation results in a disproportionate increase in the systolic BP and lower diastolic BP—a hallmark of ISH and of PPH.






FIGURE 11.1 Change in amplitude and contour of the upper limb (A) and ascending aortic (B) pressure wave with age, as recorded in three female members of a family: at age 18 (left), at age 48 (center), and at age 97 years (right). Upper limb pulse pressure was just more than twice as high in the old compared with the young subject (102 vs. 46 mm Hg), whereas aortic pulse pressure was more than three times higher (104 vs. 27 mm Hg). (From O’Rourke MF, Nichols WW. Aortic diameter, aortic stiffness, and wave reflection increase with age and isolated systolic hypertension. Hypertension. 2005;45[4]:652-658, with permission.)

Mechanistically, pulse pressure is also an index of the stiffness of conduit vessels and the rate of pressure wave propagation and reflection within the arterial tree. Approximately half of patients with ISH also have wide pulse pressure; however, both individuals who are normotensive (systolic, <140 mm Hg) with a low diastolic pressure or persons with combined systolic and diastolic hypertension (systolic >140 mm Hg and diastolic >90 mm Hg) can have wide pulse pressure (normal values being ≤40 mm Hg).



Dart AM, Kingwell BA. Pulse pressure—a review of mechanism and clinical relevance. J Am Coll Cardiol. 2001;37:975-984.

O’Rourke MF, Nichols WW. Aortic diameter, aortic stiffness, and wave reflection increase with age and isolated systolic hypertension. Hypertension. 2005;45(4):652-658.

Schiffrin EL. Vascular stiffening and arterial compliance. Implications for systolic blood pressure. Am J Hypertens. 2004;17:39S-48S.


A.7. What are the end-organ damages caused by long-standing hypertension?

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


Cardiac involvement

Left ventricular hypertrophy (LVH)

Angina or myocardial infarction (MI)

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

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 long-standing hypertension. Large vessels such as the aorta may be directly affected and be at risk for aneurysms and dissection. As discussed previously, the consequences of long-standing hypertension need be addressed according to the subtypes of hypertension; for the associated risks for cerebral, cardiac, and renal vascular complications differ according to systolic, diastolic, and PPH. For example, diastolic hypertension being a better predictor of coronary heart disease in younger patients, whereas systolic and pulse pressure hypertension being associated with greater risk of stroke, coronary heart disease, and mortality in persons older than 60 years.



Aronson S, Fontes ML. Hypertension: a new look at an old problem. Curr Opin Anesthesiol. 2006;19:59-64.

Mann DL, Zipes DP, Libby P, et al, eds. Braunwald’s Heart Disease. 10th ed. Philadelphia, PA: Elsevier; 2015:934-952.



A.8. 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 MI. 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 long-standing 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.

ISH (systolic BP >140 mm Hg and diastolic BP <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. Aronson et al. and Fontes et al. found that among the various components of BP, preoperative pulse pressure hypertension was independently and significantly associated with postoperative stroke, renal failure, and mortality in patients undergoing coronary artery bypass. Neither ISH nor isolated diastolic hypertension were predictive of vascular complications. This finding is consistent with results of longitudinal studies finding that increase in pulse pressure is a better predictor of major vascular complications than increase in either systolic or diastolic BP. Interestingly, rises in pulse pressure as few as 10 mm Hg in both normotensive and hypertensive individuals is associated with 20% or more increase risk of renal, coronary, and cerebral events.



Aboyans V, Frank M, Nubret K, et al. Heart rate and pulse pressure at rest are major prognostic markers of early postoperative complications after coronary bypass surgery. Eur J Cardiothorac Surg. 2008;33:971-976.

Aronson S, Fontes ML, Miao Y, et al; for the Investigators of the Multicenter Study of Perioperative Ischemia Research Group and the Ischemia Research and Education Foundation. Risk index for perioperative renal dysfunction/failure: critical dependence on pulse pressure hypertension. Circulation. 2007;115(6):733-742.

Casadei B, Abuzeid H. Is there a strong rationale for deferring elective surgery in patients with poorly controlled hypertension? J Hypertens. 2005;23(1):19-22.

Fontes ML, Aronson S, Mathew JP, et al; for the Multicenter Study of Perioperative Ischemia (McSPI) Research Group and the Ischemia Research and Education Foundation (IREF) Investigators. Pulse pressure and risk of adverse outcome in coronary bypass surgery. Anesth Analg. 2008;107:1122-1129.

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


A.9. Perioperative cerebral and renal complications are mostly associated with which subtype of hypertension?

Both systolic hypertension and high pulse pressure are strongly associated with risk for perioperative cerebrovascular accidents and acute renal failure. The brain and the kidneys as well as the heart differ from most organs in that they receive large amount of blood flow and have very low resistance. As such, the pulsatile load (pulse pressure) tends to be very high. Over a period of many years of poorly or untreated hypertension, endothelial injury and vascular remodeling changes can promote both arteriosclerosis and atherosclerosis, which are known risk factors for cerebral and renal vascular complications. The pulsatile stress also can cause dislodgment of plaques from the aorta and its major branches, resulting in embolic stroke.

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. Therefore, 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 (gt;3.0 mg per dL [>265.2 mmol per 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 per dL (176.8 mmol per L) was one of six independent factors that predicted increased cardiovascular risk.



Aronson S, Fontes ML, Miao Y, et al; for the Investigators of the Multicenter Study of Perioperative Ischemia Research Group and the Ischemia Research and Education Foundation. Risk index for perioperative renal dysfunction/failure: critical dependence on pulse pressure hypertension. Circulation. 2007;115(6):733-742.

Benjo A, Thompson RE, Fine D, et al. Pulse pressure is an age-independent predictor of stroke development after cardiac surgery. Hypertension. 2007;50:630-635.

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Mar 18, 2021 | Posted by in ANESTHESIA | Comments Off on Hypertension

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