What Causes Emergency Hypertension

What Causes Emergency Hypertension

Emergency hypertension can result from several disorders, drugs, and procedures. Be alert for any of the following in your patient’s history.

Cardiovascular Disorders

acute left ventricular failure

acute myocardial infarction

dissecting aortic aneurysm

unstable angina pectoris

worsening of chronic hypertension

Neurologic Disorders

cerebrovascular accident

head trauma

hypertensive encephalopathy

intracranial hemorrhage

spinal cord disease

subarachnoid hemorrhage

Renal Disorders

acute glomerulonephritis

renal parenchymatous disease

renovascular hypertension

Other Disorders

eclampsia

necrotizing vasculitis

pheochromocytoma

preeclampsia

scleroderma crisis

vasculitis

Drugs

amphetamines

clonidine (withdrawal syndrome)

cocaine

lysergic acid diethylamide

monoamine oxidase inhibitors taken with

foods containing tyramine

oral contraceptives

phencyclidine

sympathomimetic drugs

Medical and Surgical Procedures

carotid artery manipulation

coronary artery bypass surgery

Diagnostic Tests for Cad

A physician uses certain tests to assess the patient’s risk of CAD, others to indicate whether he has CAD, and still others to determine if he has had an MI-a serious complication of CAD.

Blood Tests

A physician typically orders a serum lipid profile to assess the patient’s risk of CAD. A total blood cholesterol level below 200 mg/dl indicates a relatively low risk of CAD. A level of 200 to 239 mg/dl indicates a moderate risk; one that exceeds 239 mg/dl indicates a serious risk of CAD.

High-density lipoprotein (HDL) and LDL cholesterollevels may help predict the risk of CAD more accurately than total cholesterol levels. An elevated LDL cholesterol level indicates an increased risk of CAD, but a high HDL cholesterol level indicates a lower risk.

A series of cardiac serum enzyme assays can confirm an MI. Total creatine kinase (CK) levels rise within 6 hours after the start of an Ml and peak in 12 to 24 hours after cardiac tissue death. When cardiac tissue dies, CK-MB isoenzymes, which are found only in myocardial cells, enter the blood­stream. Measuring their level can help determine the amount of myocardial damage. Cardiac troponin levels may be better indicators of myocardial damage than CK levels .

The lactate dehydrogenase (LD) level also can indicate an MI. The blood’s LD level rises 24 to 48 hours after an MI and peaks in 3 to 6 days. Two of the five isoenzymes that make up LD-LD1 and LD2-appear primarily in the heart. Normally, the LD2 level is higher than the LD1 level. But when a patient has had an MI, the LD1 level is higher.

Other blood tests, such as aspartate aminotransferase and myoglobin protein levels, also may be used to detect an ML However, because these tests are not specific for MI, they aren’t commonly used. With an MI, the level of serum aspartate aminotransferase, formerly called serum glutamic-oxaloacetic transaminase, rises. But because serum aspartate aminotransferase doesn’t contain any heart-specific isoenzymes, the results aren’t definitive. The myoglobin protein level is highly sensitive to myocardial injury, but an elevated level doesn’t confirm an MI because trauma, inflammation, and ischemia also can increase the myoglobin protein level.