Management of Complicated Hypertension
The goals of antihypertensive therapy, to lower the blood pressure to a safe level, reduce LV hypertrophy, and improve other cardiovascular risk factors without adversely affecting other organ systems or risk factors, become more difficult to attain in the presence of concomitant disease of the heart, lungs, or kidneys. In tailoring antihypertensive therapy to the individual patient, it is best to simplify therapy by using medications that will improve the hypertension as well as (or at least not exacerbate) any coexisting condition (Table Recommended Initial Agent in Patients with Concomitant Disease).
Table: Recommended Initial Agent in Patients with Concomitant Disease
| Disease | Initial Agent | Additional Agent |
|---|---|---|
| CAD | β-Blocker | ACEI, ARB, calcium channel blocker, diuretic |
| CHF | ACE inhibitor (ACEI) | β-Blockers, ARB, diuretic |
| CRI | Calcium channel blocker, -blockers | Diuretic* |
| Diabetes | ACEI | β-Blocker, ARB, diuretic |
* If CRI is due to decreased cardiac output, ACEI/ARB may be used with caution.
ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; CAD, coronary artery disease; CHF, congestive heart failure; CRI, chronic renal insufficiency.
Coronary Artery Disease
In hypertensive patients with concomitant coronary artery disease manifested by angina, lowering blood pressure alone may improve anginal symptoms by decreasing myocardial oxygen demand. Beneficial agents include the non-ISA β-blockers, ACE inhibitors, ARBs, and calcium channel blockers. Care should be taken to avoid sudden drops in blood pressure to hypotensive levels. Patients with an acute coronary syndrome, unstable angina or non–ST-segment elevation myocardial infarction and hypertension should receive standard therapy for acute coronary syndrome (ie, intravenous heparin or low-molecular-weight heparin and nitroglycerin, aspirin, and β-blockers). This will usually lower blood pressure to a safe level. In patients with acute ST-segment elevation myocardial infarction complicated by hypertension, -blockers are the mainstay of therapy. Blood pressure should be reduced to < 140/90 mm Hg. Drastic reductions should be avoided because coronary perfusion pressure is directly related to mean arterial pressure; coronary vascular reserve is exhausted in the peri-infarction area, and further ischemia or infarction could result. β-Blockers have been clearly demonstrated to decrease postmyocardial infarction mortality and ischemic event rates. In several large meta-analyses, calcium channel blockers have been shown to be highly effective in lowering blood pressure but have a 25% excess incidence of acute myocardial infarction and heart failure in patients with acute coronary syndromes. The mechanisms are as yet to be delineated.
Heart Failure
In patients with reduced LV systolic function (from any cause), elevated blood pressure may contribute to further signs and symptoms of heart failure. Even normal levels of blood pressure may be too high in patients with moderate-to-severe LV systolic dysfunction. The goal of therapy should be to lower systolic blood pressure as low as possible without symptoms (< 110 mm Hg and lower if tolerated). ACEIs have proved very useful in reducing blood pressure and symptoms of heart failure and improving survival rates in such patients (see Table 13–3). Diuretics augment the antihypertensive effects of ACEI and are useful additions for the hypertensive patient with or without congestive heart failure. When starting an ACEI in a patient who is already taking a diuretic, the dose of the ACEI should be reduced and the diuretic should be withheld or given at a reduced dose that day to avoid hypotension. ARBs may be substituted in ACEI-intolerant patients.
β-Blockade has been definitively shown to improve symptoms, LV systolic function, and longevity in patients with heart failure when added to ACEI or alone. Metoprolol, bisoprolol, and carvedilol are the agents that have been used in the major heart failure trials.
It is not yet clear as to the most beneficial way to treat patients with preserved systolic function heart failure. The cornerstone of therapy is to reduce the invariably present hypertension to the usual target levels. These patients respond similarly to other hypertensive patients. Clinicians should be careful to not reduce preload too much with diuretics.
Cerebrovascular Disease
Patients with symptomatic or otherwise evident cerebrovascular disease coexistent with hypertension should receive antihypertensive therapy. Such patients tend to be older and therefore respond similarly to other older patients. Acute cerebrovascular accidents are frequently accompanied by hypertension, which is sometimes severe. Rapid reduction of blood pressure in patients with acute stroke is associated with increased morbidity and mortality and should be avoided during the acute phase. In fact, unless the diastolic blood pressure is greater than 115 mm Hg, treatment should either be withheld or instituted slowly and with great caution until the patient has stabilized. Because cerebrovascular disease and coronary artery disease frequently coexist, antihypertensive therapy should be instituted judiciously in patients with stroke and evidence of ischemia or heart failure.
Renal Insufficiency
Effective antihypertensive therapy will halt or slow the progression of renal insufficiency in most hypertensive patients (see Table Recommended Initial Agent in Patients with Concomitant Disease). In patients with established renal insufficiency, ACEI therapy may be very effective and improve renal function but should be used carefully, with frequent monitoring of renal function and serum potassium during initiation and titration of therapy. Patients with renovascular hypertension may have rapid worsening of renal function when treated with ACE inhibitors. Such patients must be monitored carefully during initiation of antihypertensive therapy for worsening of renal function or the development of hyperkalemia. Potassium supplementation or potassium-sparing diuretics should be avoided in patients with even moderate renal insufficiency. Even a modest decrease in renal function could cause serious or fatal hyperkalemia. Most patients with renal insufficiency and hypertension respond well to all types of antihypertensive therapy, however. Such patients tend to have volume-dependent hypertension and respond well to loop diuretics, although higher doses must be used as renal function deteriorates.
Diabetes Mellitus
Diabetic patients are known for their almost universal incidence of vascular disease and increased susceptibility to cardiovascular complications. The coexistence of diabetes and hypertension markedly increases the risk of coronary artery disease, stroke, and renal failure. If dyslipidemia is also present, the risk is even greater. Hypertension should be treated aggressively in diabetic patients, using agents that are renal-protective and do not further aggravate glucose intolerance or adversely affect lipids (see Table Recommended Initial Agent in Patients with Concomitant Disease). ACE inhibitors, β-blockers, and ARBs are extremely useful in both controlling blood pressure and preventing or slowing the onset of proteinuria and renal failure in diabetic patients. The Hypertension Optimal Treatment Trial (HOT) established that lowering diastolic blood pressure in diabetic patients to levels below 80 mm Hg decreases the risk of major cardiovascular events and mortality compared with lowering diastolic blood pressure to “normal” (< 90 mm Hg) levels. The goal for systolic blood pressure is < 130 mm Hg. β-Blockers, ACEI, and ARBs, which are effective in diabetic patients, are glucose- and lipid-beneficial or neutral. It is recommended that an ACEI be used as the first agent in all diabetic patients. ARBs appear to have the same renal protective effects in diabetic patients as ACE inhibitors. No clear-cut superiority of ACEI compared with ARBs in diabetic patients has been demonstrated. Due to the much higher cost of ARBs and the proven efficacy of ACE inhibitors, diabetic patients should start on an ACEI and ACEI-intolerant patients should use ARBs.
Hypertensive Emergencies
Patients with severe hypertension (> 220/120 mm Hg) and signs and symptoms of encephalopathy, acute myocardial ischemic syndromes, stroke, pulmonary edema, or aortic dissection should be treated emergently to achieve rapid reduction of their blood pressure (Table Antihypertensive Therapy for Hypertensive Emergencies). Because of its rapid onset and short duration of therapy, which allow for smoother titration of blood pressure, intravenous sodium nitroprusside is the treatment of choice. Patients should be admitted to the intensive care unit and monitored closely during therapy. The aim is to reduce blood pressure very quickly within the first hour or two after presentation but to avoid hypotension. Patients must be monitored for thiocyanate toxicity if therapy is prolonged. An alternative is intravenous fenoldopam, a selective dopamine-1 receptor agonist. It has a similar antihypertensive profile to nitroprusside with a rapid predictable onset of action, short half-life (9.8 min), and few side effects at effective doses. There is a linear correlation between fenoldopam infusion rate and blood pressure lowering. Its use still requires monitoring in the intensive care unit.
Table: Antihypertensive Therapy for Hypertensive Emergencies
| Drug | Dose | Comments |
|---|---|---|
| Nitroprusside | 0.25–10 mcg/kg/min | Treatment of choice |
| Fenoldopam | 0.1 mcg/kg/min, increased by 0.05 mcg/kg/min | Does not require thiocyanate monitoring |
| Labetalol | 20–40 mg IV q10 min to 300 mg | Commonly used after surgery |
| Esmolol | 500 mcg/kg over 1 min, then 25–200 mcg/kg/min | Can aggravate heart failure |
| Clonidine | 0.1–0.2 mg PO, 0.05–0.1 mg qh until 0.8 mg | Sedation possible |
| Captopril | 6.25–50 mg PO q 6–8 h | Excessive hypotension possible |
If aortic dissection is present, a short-acting β-blocker such as esmolol should be added to decrease shear forces in the aorta. Intravenous labetalol is highly effective and can also be used. Oral immediate-release clonidine and ACEI are effective in rapidly reducing blood pressure and can be added orally. Oral immediate-release nifedipine may cause unpredictable hypotension and should not be used.
Hypertensive urgencies (defined as patients who have severe hypertension but with minimal or no symptoms) may be treated more slowly, achieving a significant reduction in blood pressure within the first 24 hours. Intravenous labetalol is particularly useful in these patients.
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