ENSAYOS PREVIOS

Certain disease processes are discussed in greater detail in other sections of this handbook. However, treatment with respect to blood pressure control is discussed here.

Table 2A.1. JNC-VI classification of blood pressure in adults

Category Systolic BP Diastolic BP

Optimal <120 <80

Normal <130 <85

High-Normal 130-139 85-89

Hypertension

Stage 1 140-159 90-99

Stage 2 160-179 100-109

Stage 3 >180 >110

Table 2A.2. Hypertensive emergencies Hypertensive encephalopathy

Stroke (ischemic or hemorrhagic) Myocardial infarction or unstable angina Pulmonary edema/congestive heart failure Aortic dissection

Acute renal failure Preeclampsia/eclampsia

Microangiopathic hemolytic anemia Catecholamine excess

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Hypertensive Encephalopathy

• When the acutely elevated blood pressure exceeds the CNS’s ability for autoregulation, uncontrolled cerebral blood flow occurs. This results in vasospasm, vascular damage and leakage, and potential cerebral hemorrhage, ischemia, and/or edema.

• Patient complaints include headache, vomiting, drowsiness, confusion, visual changes, or focal neurologic changes. Papilledema is present and severe retinopathy is often present.

• Untreated, patients will progress to coma and death.

• Treatment involves the acute lowering of blood pressure with titratable IV medica-tions. By definition, patients with hypertensive encephalopathy lack cerebral auto-regulation. Precipitous lowering of the systemic blood pressure may cause a dangerous fall in cerebral perfusion pressure, leading to further cerebral ischemia. Therefore, careful monitoring of patients is necessary to evaluate for neurologic deterioration.

Systemic blood pressure reduction should be done slowly with published guidelines of approximately 15-20% reduction in diastolic pressure within 1 h or a diastolic pres-sure of 110 mm Hg as therapeutic goals.

Hypertensive Stroke

• Severe, uncontrolled hypertension is frequently an etiologic factor in patients with strokes. Patients with this degree of hypertension have cerebral autoregulatory set points changed to accommodate the degree of chronic hypertension. Therefore, overaggres-sive lowering of blood pressure may cause a dangerous lowering of cerebral perfusion pressure and extend ischemic zones of the brain.

• Patients with hemorrhagic infarctions may present with severe hypertension as a re-sponse to the bleed, as well as an etiology of the infarction. This may resolve without treatment.

• With the above considerations, there is debate in the literature regarding the appropri-ate management of severe hypertension in stroke. Many authors recommend lowering for diastolic pressures >120, while others recommend that blood pressure never needs acute lowering in the emergency setting.

Hypertension with Ischemic Coronary Syndromes

• Severe hypertension is an etiologic factor in atherosclerotic heart disease. Many pa-tients presenting with acute coronary syndromes (myocardial infarction or unstable angina) have chronic hypertension which may be severe or uncontrolled. Acute eleva-tions in blood pressure may exacerbate coronary ischemia by increasing ventricular strain and myocardial oxygen demand.

• Decreasing afterload with the use of IV nitrates decreases myocardial work. IV β-blockers also decrease myocardial work by decreasing blood pressure and heart rate.

• The use of direct vasodilators, which may cause a reflex tachycardia, is contraindicated in the setting of ischemia.

Hypertension with Pulmonary Edema or Congestive Heart Failure

• Severe hypertension is an etiologic factor for congestive heart failure but may also be secondary to the catecholamine response to pulmonary edema.

• Treatment for these patients includes nitroglycerin and diuretics but may also require the addition of morphine sulfate and nitroprusside. The use of morphine sulfate is effective in decreasing the catecholamine response to heart failure. Both nitroglycerin and nitroprusside produce vasodilatation in the capacitance vessels thus improving cardiac hemodynamics. Nitroprusside has a more pronounced effect on arterioles, thus reducing afterload. However, a reflexive tachycardia and increased inotropy may counteract the decrease in afterload and even lead to an increase in cardiac workload.

Nitroprusside may also cause coronary steal in patients with coronary artery disease. It is therefore not the first line drug in cardiac failure with severe hypertension.

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Aortic Dissection

• The control of hypertension is essential in the emergency stabilization of a patient with an aortic dissection.

• The use of both β-blockers and nitroprusside is recommended to both decrease the sys-temic blood pressure and to decrease the shearing force of the systolic pulse on the weak-ened aortic wall. Standard medications used are nitroprusside plus labetolol or esmolol.

• Blood pressure should be decreased to the lowest possible level without exacerbating ischemic symptoms.

Hypertension and Acute Renal Failure

• Patients with long-standing uncontrolled hypertension often develop renal failure.

Acute elevations in blood pressure may lead to intrarenal vascular injury, glomerular ischemia, and subsequent hematuria, proteinuria and loss of renal function.

• The management of acute renal failure secondary to acute hypertension is focused on maintaining normal volume status, renal perfusion, and minimizing secondary complications.

• IV β-blockers or calcium channel blockers are the drugs of choice. They must be used with caution, and euvolemia must be maintained in order to not decrease renal perfu-sion to a level which exacerbates instead of alleviating renal damage. The use of diuret-ics may be either beneficial, if used in hypervolemic or euvolemic patients to increase GFR, or problematic if used in hypovolemic patients. Nitroprusside, while effective for decreasing blood pressure, is problematic in patients with renal dysfunction because the thiocyanate metabolite of the drug may accumulate, leading to cyanide toxicity.

• Dialysis may be needed in severely symptomatic or hypertensive patients.

Preeclampsia/Eclampsia

• Preeclampsia and eclampsia represent diffuse end-organ damage secondary to preg-nancy induced hypertension.

• Most patients with preeclampsia/eclampsia are vasoconstricted and hypovolemic.

• Hydralazine is the standard antihypertensive used in preeclampsia. However, IV β-blockers or calcium channel blockers may also be used.

• Careful management of volume status is important as these patients have renal and often cerebral vascular injury and are therefore prone to develop edema with overaggressive hydration. The treatment for preeclampsia/eclampsia is delivery of the fetus and pla-centa and close communication with an obstetric specialist is required.

Microangiopathic Hemolytic Anemia

• The endovascular damage associated with hypertensive crises results in fibrin deposi-tion in arterioles and ultimately fibrinoid necrosis. This fibrin deposideposi-tion may lead to a hemolytic anemia which is diagnosed by the presence of schistocytes on peripheral blood smear. This anemia is rarely seen in isolation in hypertensive emergencies and management is based on end-organ damage in other organ systems.

Catecholamine Excess

• Excess catecholamines may lead to hypertensive emergencies. Causes include pheo-chromocytomas; ingestions of stimulant medications or drugs, such as cocaine or am-phetamines; withdrawal syndromes as seen in the rebound hypertension with clonidine withdrawal; or the ingestion of tyramine rich foods while taking MAOIs. These con-ditions all result in an increased α-adrenergic tone.

• Treatment requires α blockade with phentolamine. B-blockade alone is contraindi-cated as it leads to unopposed α stimulation. In the case of stimulant drug ingestions, anxiolytics such as lorazepam or valium may be effective in lowering blood pressure as well as treating associated hyperactivity.

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Medications Used to Treat Hypertensive Emergencies