1. Can hypertension be an emergency by Hossam Ahmed Mowafi
2. Hypertensive Crisis
3. Systemic hypertension
4. It is estimated that 50 million persons in the United States have systemic , hypertension.many of whom are inadequately treated
5. Between 1% and 2% of the 50 million have primary hypertension that progresses to a crisis phaseaccounting for more than 50% of all cases .of hypertensive crisis
6. Uncontrolled or suboptimally controlled hypertensioncauses high rates of mortality from ,premature cardiac, vascular . and renal disease
7. In most instances, end-organ damage occurs after decades .of elevated blood pressure
8. Hypertensive crisis
9. In rare instances, hypertension may become acutely life threatening. This emergency situation, occurs when an abrupt, marked increase in blood pressure “relative to the patients baseline” causes acute or rapidly progressing end-organ damage.
10. Unless promptly recognized and treated, hypertensive crisis can lead to cardiovascular, renal, and central nervous system complications and death.Effective and prompt anti-hypertensive treatment improves the prognosis.
11. Hypertensive crisis can manifest de novo, but most patients have a history ofchronically elevated blood pressure that has been poorly controlled or untreated.
12. Public health campaignsaimed at educating and treating patients with hypertension have markedly decreased . the incidence of hypertensive crisis
13. Nevertheless, it continues to represent a large portion of .emergency department visits
14. Because the cardiovascular system is , imminently threatened cardiologistsare called on to provide expert management of these emergencies, and patients withsevere elevations in blood pressure often . go to a cardiologist for initial care
15. The cardiologist must be able to differentiate an emergency from urgency or a pseudoemergency; understand the underlying pathophysio- logic mechanisms, potential complications, and treatment options; and guide the evaluation.
16. Overzealous treatment can cause severe morbidity and even death. A working knowledge of the pharmacologic characteristics and side effects of the various .therapeutic agents is essential
18. Hypertensive crisis traditionally has been classified as ,emergency or urgency depending on the presence of acute or progressive . end-organ damage
19. , This distinction , although not absoluteaids in formulating an effective and .safe treatment plan
20. Hypertensive emergencies include conditions characterized byrapid decompensation of vital organ function caused by inappropriate . elevations in blood pressure
21. Treatment requires immediate reduction in blood pressure and parenteral medication, usually in an intensive care .unit Delay may cause.irreversible organ damage and death
22. Several clinical syndromes can manifest as .hypertensive emergencies
23. Accelerated or malignant hypertension andhypertensive encephalopathy are the prototypical hypertensive emergencies.
24. Accelerated or malignant hypertension is a systemic disease characterized by:.• An extreme elevation in blood pressure (mean arterial blood pressure [MAP] greater than 120 mm Hg).• Bilateral retinal hemorrhage.• Exudates.• Papilledema. This hypertensive emergency demands emergency treatment and close follow-up care.
25. HYPERTENSIVE EMERGENCIES 16– In general, diastolic blood pressure exceeds 120 mm Hg.– Malignant hypertension with papilledema.– Hypertensive encephalopathy.– Severe hypertension in the setting of stroke.– Subarachnoid hemorrhage.– Head trauma
26. – Acute aortic dissection.– Hypertension and left ventricular failure.– Hypertension and myocardial ischemia and infarction.– Hypertension after coronary artery bypass operation.– Pheochromocytoma crisis.– Food or drug interactions with monoamine oxidase inhibitors.
27. – Cocaine abuse.– Rebound hypertension after sudden drug withdrawal (clonidine).– Idiosyncratic drug reactions (atropine).– Eclampsia.
28. Exceptions include cardiovascular dysfunction in which low blood pressure may represent an emergency.
29. "Considered emergencies when associated with end-organ damage; otherwise treated as urgencies.
30. Hypertensive encephalopathy causes , headache, irritability and altered state of consciousnessfrom a sudden marked increase in blood . pressure
31. Hypertensive encephalopathy occurs when cerebral edema is induced by markedly elevated blood pressures that overwhelm the auto-regulatory capabilities . of the brain
32. This condition tends to affect a person withpreviously normal blood pressure who has . a rapid rise in blood pressure
33. Persons with chronic hypertension are relatively resistant to encephalopathy because their autoregulatory systems have adapted to.the chronically elevated blood pressure
34. When persons with chronic hypertension do haveencephalopathy, it is usually in the setting of markedly elevated blood pressure diastolic blood pressures higher . than 150 mm Hg
35. Mental status reverts to normal with the . lowering of blood pressure
36. Hypertensive urgenciesmanifest as marked elevations in blood pressure diastolic blood pressure higher than 120mm Hg withoutevidence of acute or progressive target organ damage and minimal or no . symptoms
37. .The risk for tissue damage is not immediate
38. Blood pressure can be lowered . over a period of hours to daysPatients usually can be treated with oral .medication, often as outpatients
39. Pseudoemergencies must be differentiated from truehypertensive emergencies because the treatments . differ markedly
40. The increase in blood pressure in a pseudoemergency is caused by massive sympathetic outflow as the result of pain, hypoxia, hypercarbia, hypoglycemia, anxiety, or the . postictal stateTreatment is directed at the underlying .cause
41. HYPERTENSIVE URGENCIESDiastolic blood pressure exceeds 120 mm Hg, but patients have no symptoms, and there are no signs of tissue damage
42. Clinical presentation.If an emergency is suspected, appropriate arrangements for ICU admissionand parenteral treatment are made without waiting for the results of further tests.
43. – Chest pain.– shortness of breath.– Headache.– Blurred vision.– signs of altered mental status.– Focal neurologic signs.– Grade III or IV retinopathy.– Rales.– Gallop.– Pulse deficits.
44. – Chest pain.– shortness of breath.– Headache.– Blurred vision.– signs of altered mental status.– Focal neurologic signs.– Grade III or IV retinopathy.– Rales,– Gallop.– Pulse deficits. all point toward an emergency.
45. Severe hypertension in the presence of chronic organ damage without associated symptoms does not . constitute an emergencyPseudoemergencies must be ruled .out
46. Signs and symptoms.The following history is elicited from patients withincreased blood pressure.
47. – Nausea.– Vomiting, weight loss.– Anorexia.– Shortness of breath, chest pain.– Headache.– Blurred vision.– Abdominal pain.– Patients with accelerated or malignant hypertension often have oliguria.
48. Chronology of symptoms . is important
49. . History of hypertensionMost patients with accelerated or malignanthypertension have an underlying history of ,chronic essential hypertension although a significant percentage of patients have secondary forms of . hypertension A search for correctable causes is .indicated
51. Use of recreational drugs, cocaine, amphetamines.
52. Smoking history. Smokers are at increased risk for progression to malignant hypertension.
53. Physical findings
54. . Vital signsBlood pressure is measured in both upper . and lower extremities
55. Severe hypertension is confirmed with twoblood pressure measurements separated . by 15 to 30 minutes
56. No absolute level of blood pressure differentiates an emergency from an .urgency
57. The distinction is based on a thorough . clinical evaluation
58. Optic fundi are examined for signs of retinopathy, including exudates, hemorrhages, or papilledema.
59. The CNS is examined for– Mental status.– Focal neurologic signs.– Patients with hypertensive encephalopathy may manifest focal neurologic signs, confusion, or seizure activity.
60. Heartand lungs are examined for presence of edema, S3, or S4. Vascular system is examined for pulses and bruits.
61. Patients with chronic hypertension usually progress to an accelerated or malignant phase or have severe blood pressure elevationsand progressive end-organ damage and . aortic dissection
62. A thorough search for secondary causes and precipitants isindicated in the evaluation of all patients . with hypertensive crisis
63. Between 20% and 56% of patients have an identifiable underlyingcause, compared with less than 5% of those .with uncomplicated hypertension
64. CONDITIONS THAT MAYPRECIPITATE A HYPERTENSIVE CRISIS– Essential hypertension.– Renovascular hypertension.– Parenchymal renal diseases.– Drug-induced causes.– Head injuries.– Central nervous system events.– Vasculitis Collagen vascular disease.
65. HYPERTENSIVE CRISISA common situation is that a patient has been. – Inadequately treated. – Has been noncompliant with a medical regimen.
66. Risk factors for progression to hypertensive crisis include. – Male sex. – Black race. – Cigarette smoking. – Tobacco abuse. – Oral contraceptive use. – Low socioeco-nomic status.
67. Unlike essential hypertension, the incidence of which increases with age, the peak incidenceof hypertensive crisis occurs among persons 40 to 50 years old.
68. Underlying diseases that can precipitate hypertensive crisis include – Renal parenchymal disease. – Renovascular hypertension. – Collagen vascular disease. – Pheochromocytoma. – Vasculitis. – Preeclampsia. – Burns – Head trauma.
69. A number of medications can cause marked elevations in systemic blood pressure.The most common offenders are – Oral contraceptives. – Sympathomimetic agents. – Cold remedies. – Nonsteroidal antiinflammatory drugs. – Cocaine. – Tricyclic antidepressants. – Mono-amine oxidase inhibitors.
70. In rare instances, a hypertensive crisis is the first manifestation of disease. These patients tend to have secondary forms of hypertension, most commonly: – Renovascular. – Renal parenchymal disease. – Reaction to medications.
71. Left ventricular failure or pulmonary . edema
72. Elevated blood pressure poses an enormous workload on a failing heart.Even patients with normal systolic functioncan have pulmonary edema in the setting of markedly elevated blood pressures .afterload mismatch
73. Hypertensive crisis associated with . hypercatecholaminemia
74. A hypercatecholamine state can cause severeelevations in blood pressure that threaten tissue function and necessitate . parenteral treatment
75. Hypercatecholamine commonly are induced by the exaggerated effects of medication , drugs or . food-drug interactions
76. . Postoperative hypertension
77. Severe hypertension can complicatethe postoperative course after coronary and . peripheral vascular procedures The elevated pressure threatens suture. lines and promotes excessive bleeding
79. Pathophysiology Although the exact pathophysiologicmechanism is unknown, it is believed that hypertensive emergencies are triggeredby an abrupt increase in systemic vascular resistance caused by increases in circulating vasoconsictors, norepinephrine, angiotensin II.
80. The resulting increase in blood pressure leads to:Arteriolar fibrinoid necrosis characterized by – Endothelial damage. – Fibrin deposition. – Loss of autoregulatory function.
81. Ischemia and dysfunction in the target organ cause further release of vasoactive substances, producing – A cycle of increasing SVR. – Elevated systemic blood pressure. – Decreased cardiac output. – Vascular injury. – Tissue damage.
82. An alternative explanation is that elevated blood pressure complicates a Primary disease process and . accelerates tissue injuryThe specific organ system affected defines the hypertensive crisis – Aortic dissection. – Acute left ventricular failure. – Stroke.
84. The kidney, brain, and heart all possess autoregulatory mechanisms that maintain blood flow at near constantlevels despite fluctuations in blood pressure.
85. Because the brain is encased in a definit space and because it maximally extracts , oxygen at baselineit is most vulnerable when its autoregulatory . systems fail
87. Cerebral blood flow normally is maintainedat a near-constant level despite variations .in cerebral perfusion pressure
88. An elevated MAP causes an increase in CPP, whereas a decreasing MAP causes decreased CPP. Despite changes in CPP, cerebralautoregulatory mechanisms maintain CBF; as MAP rises, vasoconstriction occurs, and as MAP .decreases, vasodilatation occurs .CPP: Eerebral perfusion pressure
89. This system has upper and lower limits beyond .which CBF can no longer be controlled
90. When CPP decreases below the lower limits of autoregulation, brain hypoxia ensues, and symptoms of hypoperfusion manifest: – Headache. – Nausea. – Dizziness. – Altered sensorium. – Lethargy.
91. If unconnected or extreme,this may ultimately cause infarction.
92. When MAP exceeds autoregulatory capabilities, hyperperfusionoccurs, leading to an increase in ICP,cerebral edema, and progressive organ dysfunction.
93. Most persons with normal blood pressuremaintain autoregulation of MAP between , 50 and 150 mm Hg . although this is highly variable
94. These values generally increase among .patients with chronic hypertension
95. These patients consequently may havecerebral hypoperfusion at an MAP that is . considered normal
96. – Elderly persons.– Cerebrovascular accidents.– Subarachnoid hemorrhage.– Hypertensive encephalopathy.– Accelerated or malignant hypertension have altered autoregulation.
97. Treatment must be tempered by the fact thatoverzealous blood pressure reduction can lead to permanent neurologic . damage
98. – Cerebrovascular accidents.– Blindness-piaralysis.– Coma.– MI.– Death have been reported sequences of aggressive blood pressure reduction.
100. The prognosis of a patient who hasundergone hypertensive crisis and not been treated is poor.
101. Before the introduction of effective antihypertensive agents, more than 90%of patients with accelerated malignant hypertension died within 1 year of diagnosis.
102. Modern pharmacotherapy and theavailability of dialysis have substantially , increased survival rates with studies reporting survival rates of more than 70% .at 5-year follow-up
103. Laboratory examination and diagnostic . testing
104. The diagnostic evaluation must be brief because . time to treatment is crucialDiagnostic imaging if clinically indicated can be performed after treatment has been .instituted
105. Azotemia and hemolysis indicate an emergency.
106. Blood chemistries to rule out uremia.
107. Urinalysis to look for– Proteinuria.– Hematuria.– casts. Hematuria and moderate to severe proteinuria indicate an emergency.
108. Finger-stick glucose test can rule out hypoglycemia as a cause of changes in mental status.
109. Ischemic changes on theelectrocardiogram indicate an emergency.
110. Pulmonary edema on chest radiography indicates an emergency.
111. Computed tomography may beneeded in the setting of a possible cerebrovascular accident.
113. The presence of acute or rapidly progressive end-organ damage, not the absolute blood pressure reading, determines whether the situation is an emergency or urgency.
114. This determination dictates the type of treatment – Parenteral. – Oral. – ICU. – Ward. – outpatient.
115. For example, a blood pressure of 120/80 mm Hg may represent a hypertensive emergencyfor a patient with aortic dissection, whereas a blood pressure of 200/120 mm Hg for a person with asymptomatic chronic hypertension usually does not necessitate emergency therapy.
116. The appropriate diagnostic evaluation and therapeutic plan also are dictated by the specific disease.
117. For example, the specific pharmacologic regimen for a pregnant womanwith preeclampsia differs from that for anelderly man who has had a stroke.
118. Regardless of drug regimen, the goal of treatment is– Break the cycle of increasing blood pressure.– Preserve cardiac output.– Renal blood flow.– Limit end-organ damage.
119. Neurologic emergencies
120. Patients with neurologic findings and severe hypertension present a particular challenge.
121. Neurologic emergencies can result from hypertensive emergencies or may themselves cause markedly elevatedblood pressures, which may exacerbate neurologic damage.
122. The key differentiating point is thatneurologic alterations caused by elevatedblood pressure are reversed when blood pressure is controlled, whereas primary neurologic disorders are not.
123. The insidious progression of symptoms in hypertensive encephalopathy aids in differentiating hypertensive encephalopathy from cerebrovascular accidents, which usually manifest abruptly.
124. Nevertheless, the diagnosis is one of exclusion because other hypertensive emergencies. – Cerebrovascular accident. – Subarachnoid hemorrhage. – Intraparenchymal bleeding. – Primary seizure disorder. Share many symptoms and signs.
125. Evaluation oftennecessitates further diagnostic imaging, such as CT, and consultation with a neurologist.
126. Hypertensive emergencies
127. The goal of therapy is immediate, controlled reduction in blood pressure.toxic side effects of antihypertensive agents must be understood and anticipated.
128. Patients are treated in an ICU, where clinical status and vital signs canbe constantly monitored with the aid of an arterial line.
129. Attention is focused on the status of airway, breathing, and circulation(ABCs). Ancillary measures such as intubation and dialysis are instituted if necessary.
130. Blood pressure is reduced in acontrolled, predictable manner.
131. The lower limit of autoregulation among persons with normal blood pressure and those with hypertension is approximately 25% of MAP.
132. It is recommended that blood pressure initially be reduced by no more than 25% of MAP over minutes to hours and that further reductions occur over days to weeks toallow the autoregulatory mechanisms to reset.
133. Exceptions include. – Aortic dissection. – Left ventricular failure. – Pulmonary edema. which demand more aggressive blood pressure reduction to limit tissue damage.
134. Specific antihypertensive therapy is tailored to the underlying disease as aortic dissection angina
135. Diagnosis and treatment are reassessed if the clinical condition, especially neurologic status, deteriorates with reduction of blood pressure.
136. Medical therapy.
137. A number of parenteral antihypertensive medications are available to manage hypertensive emergencies.
138. The specific clinical scenario dictates the agents used.
139. Characteristics of an ideal agent include – Rapid onset. – Cessation of action. – A predictable dose-response curve – Minimal side effects.
140. Patients with hypertensive emergencies have– Excessive elevations in SVR.– Decreased cardiac output.– Decreased renal blood flow.– Volume depletion.
141. The most useful agents are vasodilating agents such as nitroprusside. Diuretics and beta-blockers are avoided unless the patient has– Aortic dissection.– MI.– Pulmonary edema.
142. For hypertensive encephalopathy, cerebrovascular accidents,or other conditions in which mental status must be monitored, agents that have prominent CNS side effects as sedation are avoided.
143. For conditions associated with elevated ICP, such as – Cerebrovascular accident. – Subarachnoid hemorrhage. – Hypertensive encephalopathy.Agents that directly increase CBF are avoided.
144. The agent selected has the most favorable hemodynamic and side effect profile on the basis of the specific hypertensive emergency.
145. The drug of choice for most hypertensive crises is sodium nitroprusside. Effective alternatives include labetalol in certain circumstances, nitroglycerin or hydralazine may be preferred.
146. Sodium nitroprusside is the drug of choice for most hypertensive emergencies.
147. – The favorable hemodynamic profile.– Rapid onset.– Rapid cessation of action of sodium nitroprusside. Make it the preferred parenteral agent for most emergencies.
148. A potent, direct vascular smooth musclerelaxant, sodium nitroprusside decreases afterload and preload by dilating arterioles and increasing venous capacitance.
149. Hemodynamic effects include a decrease in– MAP.– Afterload– Preload an increase or no change in– Cardiac output– Increased– Renal blood flow– Glomerular filtration rate.
150. Although the direct action of sodiumnitroprusside on the cerebral vasculaturemay cause increased cerebral perfusion, this is counteracted by a potent effect on MAP.
151. Most patients with neurologic crisis who need blood pressure control toleratesodium nitroprusside without a worsening of neurologic status.
152. However, the possibility of an increase in ICP and further clinical deterioration despite a decrease in MAP must be kept in mindas a potential side effect in patients with severely increased ICP.
154. Sodium nitroprusside must be administered by means of constant intravenous infusion in an intensive care setting with constant monitoring of arterial blood pressure.
155. It has a rapid onset of action, and its effect ceases within 1 to 5 minutes of cessation of infusion.
156. Side effects.
157. Red blood cells and muscle cells Metabolize sodium nitroprusside to cyanide which is converted to thiocyanatein the liver and excreted in the urine.
158. Thiocyanate levels rise in patients with renal insufficiency, and cyanide accumulates in patients with hepatic disease.
160. Monitoring for signs and symptoms oftoxicity and maintaining thiocyanate levels less than 12 mg/dL allow safe use of sodium nitroprusside.
161. Labetalolis useful in most hypertensive crises. The main disadvantage is its relatively long duration of action.
162. Labetalol is an alpha-blocker andNonselective beta-blocker with partial B2 agonist activity.
163. When given through continuous intravenous infusion, the relative beta- to alpha- blocking Effect of labetalol is 7 : 1.
164. The hemodynamic effects of labetalol include decrease in– SVE.– MAP.– Heart rate. a decrease or no change in– Cardiac output.
165. Labetalol has little direct effect on cerebral vasculature, does not increase ICP and is considered by some to be the drug of choice in situations characterized by markedly elevated ICP.
166. Labetalol begins to lower blood pressure within 5 minutes, and its effects can last1 to 3 hours after cessation of the infusion.
168. Labetalol is contraindicated for patients with– Congestive heart failure.– Bradycardia.– Heart block more than first degree.– Reactive airway disease.
169. Nitroglycerin is considered the drug of choice for managing hypertension in the setting of – Myocardial ischemia. – Acute MI. – Pulmonary edema. – After coronary artery bypass grafting.
170. The role of intravenous nitroglycerin therapy is limited to hypertension complicating – Myocardial ischemia. – MI. – Congestive heart failure.
171. Nitroglycerin is primarily a venodilator and has modest effects on afterload at high doses.
172. The decrease in preload and afterload decreases myocardial oxygen demand.
173. Nitroglycerin also– Dilates the epicardial coronary arteries.– Inhibits vasospasm.– Favorably redistributes blood flow to the endocardium.
174. Nitroglycerin directly increases CBF and is not used in situations characterized by high ICP.
175. Fenoldopam Is a selective peripheral dopamine-1- receptor agonist approved forthe management of severe hypertension. Fenoldopam is an arterial vasodilator with a rapid onset of action and a relatively short half-life when administered intravenously.
176. It may be of particular benefit in patients with renal insufficiencyas it has been shown to improve renal perfusion.
177. Fenoldopam may cause a reflex tachycardia, which can be blunted by theconcomitant use of a beta-blocker.
178. Fenoldopam is contraindicated in patients with glaucomabecause it can increase intraocular pressure.
179. HydralazineThe role of intravenous hydralazine is limited to the treatment of pregnant women with preeclampsia.
180. Hydralazine is a direct arterial vasodilator with no effect on venous capacitance. Itcrosses the uteroplacental barrier but has minimal effects on the fetus.
181. It is usually administered in boluses of 10 to 20 mg and has a long duration of action. – Hydralazine decreases SVR. – Induces compensatory tachycardia. – Increases ICP.
182. It can exacerbate angina and is contraindicated in the care of patients with– Ongoing coronary ischemia.– Aortic dissection.– Increased ICP.
183. Management of specific emergencies
184. Accelerated or malignant hypertension
185. In the acute phase, the pharmacologic agent of choice is sodium nitroprusside. Labetalol is an effective alternative.
186. Because patients usually have markedelevations of SVR and volume depletion, diuretics are contraindicated.
187. Hypertensive encephalopathy
188. The treatment of choice is sodium nitroprusside or labetalol.Agents that depress the sensorium or increase ICP are avoided.
189. Most patients with hypertensive encephalopathy improve within hours of blood pressure reduction
190. If there is no improvement despite a decrease in blood pressure, thediagnosis must be reconsidered.
192. Extreme cautionMust be exercised when lowering evenmarkedly elevated blood pressures in the setting of a cerebrovascular accident.
193. Elevated ICP caused by cerebral edema or intraparenchymal hemorrhage increases the MAP needed to adequately perfuse the brain CPP = MAP - ICP.
194. Subarachnoid hemorrhage is characterized by intense vasospasm at and adjacent to the site of rupture. Reduction of blood pressure in these circumstances may cause globalor in the case of subarachnoid hemorrhage focal hypoperfusion.
195. Markedly elevated blood pressures, however, may increase risk forrebleeding in subarachnoid hemorrhage or extend a hemorrhagic infarct.
196. Lesions that are potentially surgically correctable such as sub-arachnoid hemorrhage and neoplasms must be identified.
197. Management of markedly elevated bloodpressure in the setting of cerebrovascular accident or subarachnoid hemorrhage is tempered by concerns about further reducing blood flow to underperfused areas of the brain.
198. The followingguidelines are suggested.
199. When blood pressure is less than 180/105 mm Hg, no treatment is recommended.
200. When blood pressure is 180/105 to 230/120 mm Hg for longer than 60 minutes, treatment is started.
201. When treatment is indicated, it must beclosely monitored, often with direct ICP monitor.
202. Target blood pressures are160/100 to 175/110 mm Hg for patients who had normal blood pressure and180/110 to 185/120 mm Hg for persons with chronic hypertension.
203. The drug of choice is labetalol or sodium nitroprusside.
204. NimodipineA calcium channel blocker with modest antihypertensive effect, has been beneficial in the management of subarachnoid hemorrhage.
205. If blood pressure remains higher thandesired despite use of nimodipine, therapy sodium nitroprusside or labetalol may be considered.
206. Agents that directly increase CPP and therefore ICP are avoided.
207. Aortic dissection is an emergency.
208. Blood pressure must be lowered immediately.
209. Patients with type A dissection have a mortality rate of 1% per hour in the first 48 hours unless medical therapyis instituted and the patient is referred for emergency surgical intervention.
210. Antihypertensive therapy is the treatment of choice for type B dissection.
211. Labetalol or the combination of sodium nitroprusside with a beta-blocker is the treatment of choice.
212. Aggressive blood pressure reduction is indicated even for patients with normal blood pressure because shear force and afterloadmust be reduced to limit tissue damage.
213. A reasonable goal is a MAP of approximately 70 mm Hg.
214. Drugs that decrease afterload and induce compensatory tachycardia are contraindicated.
215. Left ventricular failure or pulmonary edema.
216. Treatment is best accomplished with sodium nitroprusside and small doses of diuretics.
217. Nitroglycerin is an effective alternative, especially if ischemia is present.
218. Sodium nitroprusside and nitroglycerin often are used concomitantly.
219. Beta-Blockers and calcium channel blockers must be avoided in the decompensated state.
220. Myocardial ischemia.
221. Blood pressure reduction with nitrates and beta-blockers is the treatment of choice.
222. Sodium nitroprusside is added if further blood pressure reduction is required. Reperfusion and antithrombotictherapy are the mainstays of management of acute MI and unstable angina.
223. Hypertensive crisis associated with hypercatecholaminemia.
224. The pharmacologic agents of choice include sodium nitroprusside, labetalol, or calcium channel blockers.
225. Phentolamine can be useful in cases of pheochromocytoma.
226. Beta-Blockers must be avoided, because they can cause a paradoxical increase in blood pressure because of the effects of unopposed alpha-receptor stimulation.
227. Postoperative hypertension.
228. Parenteral treatment with sodium nitroprusside or labetalol is preferred.
229. After coronary bypass grafting,nitroglycerin is considered the initial drug of choice.
230. Hypertensive urgencies.
231. Most patients diagnosed with hypertensive urgency actually have severe hypertension and are notin any immediate danger of progressing to hypertensive emergency.
232. They are often persons with chronic hypertension who aresuboptimally treated or noncompliant.
233. Priority of therapy
234. Hypertensive urgencies usually can be managed with oral medication without admission to the hospital.
235. End-organ damage is not imminent, andblood pressure can be modestly lowered over a period of hours as long as adequate follow-up care is ensured.
236. The great danger lies in overtreating these patients and inciting a hypotensive crisis.
237. Sometimes, placing the patient in a quiet, calm environment can decrease blood pressure to a less alarming level.
238. If the blood pressure is still markedlyelevated, reinstitution or enhancement of prior therapy often is effective.
239. MAP is not decreased more than 15% to 20%.
240. Lower initial doses of antihypertensivemedications are used to treat patients with cerebrovascular disease or coronary artery disease who are taking antihypertensive drugs or who are volume depleted.
241. These patients tend to have exaggerated responses to drug therapy. They also are especially vulnerable to hypotension.
242. Lower doses of medications must be used. Monitoring for 4 to 6 hours is necessary to judge treatment effect and look for complications.
243. Urgent follow-up care is mandatory within 24 hours.
244. Evaluation for secondary causes of hypertension is indicated.
245. Drug therapy.
246. Oral agents used to manage hypertensive urgencies.
247. The drugs of choice include– Captopril.– Clonidine– Oral labetalol.
248. CaptoprilConsidered by some to be the drug of choice, captopril is the fastest-acting oral angiotensin-converting enzyme inhibitor.
249. At small doses, it rarely causes markedhypotension, although this potential exists in patients who are markedly volume depleted or who have renal artery stenosis.
250. Captopril begins to work within 15 to 30 minutes of ingestion and has a 4- to 6- hour duration of activity.
251. Caution is advised in the treatment ofpatients with marked renal insufficiency or volume depletion.
252. Clonidineacts through central alpha-agonist activity.
253. It has been administered in repeated hourly doses and safely lowers blood pressure over a period of hours.
254. Untoward effects, include sedation and rebound hypertension.
255. Clonidine is not administered to anyone with altered sensorium or who may not comply with treatment.
256. Labetalol “A combined alpha- and beta-blocker”, labetalol taken orally has a relative beta- to alpha-blocking effect of approximately 3:1. Dosage begins at 100 mg (taken orally twice daily) and is titrated to the desired response.The onset of action is 30 minutes to 2 hours after administration; the duration of action is 8 to 12 hours.
257. Nifedipine.The use of sublingual nifedipine has been reported to cause – Hypotension. – Syncope. – Transient ischemic attacks. – Cerebrovascular accidents. – Myocardial ischemia. – Infarction.
258. Sublingual nifedipine should not be usedin the treatment of patients with hypertension.