201111180335高血壓危象 嚴重高血壓 的評估與處置 hypertensive crisis emergency urgency management

2017-04-11 編輯. 

自發性腦出血.如果初始血壓 150-200沒有IICP現象. 可將血壓控制在 140 以下. 

一開始血壓如果非常高. 給予持續性靜脈滴注降壓藥物. 每五分鐘監測血壓
http://blog.xuite.net/ymmcc/twblog/114385954

2016-12-11 from 張志華醫師 
http://www.emnote.org/

腦出血可以使用靜脈注射藥物降血壓. 


2016-06-12 修改

http://jerryljw.blogspot.tw/2016/06/drug-therapy-of-hypertensive-crisis.html

(1) Esmolol:號稱作用最快的乙型阻斷劑,作用起始時間只有2分鐘,連泡麵都還沒泡開,但來的快去得也快,大約10分鐘排除一半 (半衰期)。

乙型阻斷劑的優點就是劑量與反應曲線很好,劑量上去,血壓下來、心跳變慢,但缺點就是氣喘、心臟收縮功能不全 (例如收縮性心衰竭 HFrEF) 就不太適合。

(2) Labetalol:20mg IV drip 2min, then 40-80mg q10min. LABETALOL (NORMODYNE, TRANDATE) Onset & Duration Onset: Within 5 min
Duration: 3-6 hr...  著名的甲型 (alpha) 與乙型 (beta) 阻斷劑,避免傳統甲型阻斷劑擴張血管後的"反射性心搏過速 (reflex tachycardia)",這點在心肌缺血病人十分好用,心肌缺血時,再讓心跳增加,絕對是雪上加霜。

雖然這個藥品的速度與反應並不是那麼出色,但目前仍然常用於心臟或腦血管事件重症病人。

(3) Nicardipine:最常用於高血壓危像的鈣離子阻斷劑 (calcium channel blockers),透過擴張血管平滑肌快速降低血管阻力,降低血壓。要注意的是,如果病人已經因為心臟衰竭正在使用乙型阻斷劑,儘量避免併用這兩種藥品,可能會導致嚴重的低血壓。

(4) Nitroprusside:這絕對是降血壓藥品、血管擴張劑界的王牌,作用快速、效果超強,但因為結構的關係,大量、長期使用可能導致氰化物中毒 (cyanide toxicity),不經酵素代謝就可以直接釋放"cyanide",也可已經由肝臟代謝為"thiocyanate"。

氰化物中毒可能有:乳酸中毒 (lactic acidosis)、意識改變及嚴重低血壓。

曾經使用"維生素B12 (Hydroxocobalamin)"預防nirtoprusside引起的氰化物中毒。

 

 

2016-01-28 編輯

HYPERTENSIVE EMERGENCY  TREATMENT 高血壓急症/危象 治療目標

http://emedicine.medscape.com/article/1952052-overview#a2

高血壓腦病變 八小時內, 降壓 MAP 25% (MAP= DBP + 高低壓力差/3), 可使用  Labetalol, nicardipine, esmolol, 避免使用 nitroprusside and hydralazine

缺血性腦中風, 使用  labetalol and nicardipine , 血壓如果超過 220/120 才使用降壓藥物. 

腦出血, 使用  labetalol, nicardipine, and esmolol; 避免 nitroprusside and hydralazine. 前 24 小時, 如果有顱內壓上升跡象, 控制MAP < 130. 或 SBP < 180, 如果沒有顱內壓上升跡象, 控制血壓 MAP < 110 或 SBP < 160

腦出血, 最初六小時, 血壓控制在 SBP < 140 連續七天. 可減少血塊擴大. 

在SAH 病患, 可使用  labetalol, and esmolol , 避免使用   nitroprusside and hydralazine, 治療目標 SBP < 160 直到動脈瘤治療完畢, 或出現腦血管孿縮現象, 口服 NIMODIPINE 可以避免腦缺血後遺症, 但不可用在急性高血壓.  

Neurologic emergencies

Rapid BP reduction is indicated in neurologic emergencies, such as hypertensive encephalopathy, acute ischemic stroke, acute intracerebral hemorrhage, andsubarachnoid hemorrhage.

In hypertensive encephalopathy, the treatment guidelines are to reduce the MAP 25% over 8 hours.[11] Labetalol, nicardipine, esmolol are the preferred medications; nitroprusside and hydralazine should be avoided.

For acute ischemic stroke, the preferred medications are labetalol and nicardipine. Withhold antihypertensive medications unless the SBP is >220 mm Hg or the DBP is >120 mm Hg, UNLESS the patient is receiving IV or intra-arterial (IA) fibrinolysis; then, the goal BP is an SBP of < 185 mm Hg and DBP < 110 mm Hg. After treatment with fibrinolysis, the SBP should be maintained < 180 mm Hg and the DBP at < 105 mm Hg for 24 hours.[11]

For acute intracerebral hemorrhage, the preferred medications are labetalol, nicardipine, and esmolol; avoid nitroprusside and hydralazine. The treatment is based on clinical/radiographic evidence of increased intracranial pressure (ICP). If there are signs of increased ICP, maintain the MAP just below 130 mm Hg (or SBP < 180 mm Hg) for the first 24 hours after onset. In patients without increased ICP, maintain the MAP < 110 mm Hg (or SBP < 160 mm Hg) for the first 24 hours after symptom onset.[11]  

Recent evidence shows that in cases of acute intracerebral hemorrhage, early intensive BP control is well tolerated and can reduce hematoma growth in patients treated within 6 hours after the onset of intracerebral hemorrhage.[12, 13] The target systolic pressure for these studies was 140 mm Hg and routine IV medications were used. The target SBP was maintained over 7 days.[12, 13]

In subarachnoid hemorrhage, nicardipine, labetalol, and esmolol are also the preferred agents; again, nitroprusside and hydralazine should be avoided. Maintain the SBP < 160 mm Hg until the aneurysm is treated or cerebral vasospasm occurs. Although oral nimodipine is used to prevent delayed ischemic neurologic deficits, it is NOT indicated for treating acute hypertension.[11] 

主動脈剝離, 可使用 labetalol, nicardipine, nitroprusside (with beta-blocker), esmolol, and morphine sulfate. 但有主動脈瓣膜逆流或心包膜填塞病患避免使用 beta-blockers, 維持 SBP <110, 除非出現低血壓, 可以用 CCB 替代 beta-blockers

急性冠心症 ACS, 可使用 beta blockers and nitroglycerin , 如果血壓SBP > 160 或 DBP> 100 可以開始用藥, 血壓降低原先的 20-30 %, 血壓如果超過 185/100 不可使用血栓溶解劑. 

急性心衰竭, 可使用  IV nitroglycerin or sublingual nitroglycerin and IV enalaprilat. 治療至血壓 SBP = 140

 

Cardiovascular emergencies 

Rapid BP reduction is also indicated in cardiovascular emergencies, such as aortic dissection, acute coronary syndrome, and acute heart failure.

In aortic dissection, the preferred medications are labetalol, nicardipine, nitroprusside (with beta-blocker), esmolol, and morphine sulfate. However, avoid beta-blockers if there is aortic valvular regurgitation or suspected cardiac tamponade. Maintain the SBP at < 110 mm Hg, unless signs of end-organ hypoperfusion are present. The preferred treatment includes a combination of narcotic analgesics (morphine sulfate), beta blockers (labetalol, esmolol), and vasodilators (nicardipine, nitroprusside). Calcium channel blockers (verapamil,diltiazem) are an alternative to beta blockers.[14]

For acute coronary syndrome, beta blockers and nitroglycerin are the preferred drugs. Treatment is indicated if the SBP is >160 mm Hg and/or the DBP is >100 mm Hg. Reduce the BP by 20-30% of baseline. Note that thrombolytics are contraindicated if the BP is >185/100 mm Hg.[15]

In acute heart failure, the preferred medications are IV nitroglycerin or sublingual nitroglycerin and IV enalaprilat. Treat with vasodilators (in addition to diuretics) for a SBP =140 mm Hg.[15] 

 

古柯鹼中毒可使用 Diazepam, phentolamine, and nitroglycerin/nitroprusside 避免使用 beta-adrenergic antagonists

病患可能出現 血壓高 心跳快  可使用 Alpha-adrenergic antagonists (phentolamine) 治療古柯鹼引起的急性冠心症 

Cocaine toxicity/pheochromocytoma

Diazepamphentolamine, and nitroglycerin/nitroprusside are the preferred drugs. However, avoid beta-adrenergic antagonists before administering phentolamine.

Hypertension and tachycardia from cocaine toxicity rarely require specific treatment. Alpha-adrenergic antagonists (phentolamine) are the preferred agents for cocaine-associated acute coronary syndromes.[16] Pheochromocytoma treatment guidelines are similar to that of cocaine toxicity. Only after alpha blockade can beta blockers be added for BP control. 

 

子癲症 子癲前症, 可使用  hydralazine, labetalol, and nifedipine.

避免使用  Nitroprusside, ACEI , esmolol, 治療目標 SBP < 160 AND DBP < 110

如果血小板小於十萬, 血壓要降更低 150/100. 使用 MgSO4 避免癲癇.  

Preeclampsia/eclampsia 

The preferred medications are hydralazine, labetalol, and nifedipine. Avoid - Nitroprusside, angiotensin-converting enzyme inhibitors, esmolol. In women with eclampsia or preeclampsia, the SBP should be < 160 mm Hg and the DBP should be < 110 mm Hg in the antepartum and intrapartum periods. If the platelet count is less than 100,000 cells mm3, the BP should be maintained below 150/100 mm Hg. Patients with eclampsia or preeclampsia should also be treated with IV magnesium sulfate to avoid seizures.[17]

 

 

 

Perioperative hypertension 

Nitroprusside, nitroglycerin, and esmolol are preferred. Target the perioperative BP to within 20% of the patient's baseline pressure, except if there is the potential for life-threatening arterial bleeding. Perioperative beta blockers are the first choice in patients undergoing vascular procedures or in patients with an intermediate or high risk of cardiac complications.[14]

END 

===============================================================

 

 

From Rosen

HTN present in ED in the following four general ways:

1. HTN emergency or HTN crisis with acute end-organ damage

2. HTN urgency or significantly elevated blood pressure with nonspecific symptoms

3. mild HTN without end-organ damage

4. transient HTN related to anxiety or the primary complaint

 

Clinical Presentation of hypertensive emergencies

1. hypertensive encephalopathy

2. Malignant hypertension

3. stroke syndromes

4. pulmonary edema

5. cardiac ischemia

6. renal failure

7. pregnancy

8. aortic dissection

 

 

HTN encephalopathy

1. MAP > 160mmHg, autoregulation may not be able to control cerebral blood flow

2. Marked vasospasm may occur, with ischemia, increased vascular permeability, punctate hemorrhages, resultant brain edema.

3. Immediate reduction of BP by 30-40% will reverse the vasospasm.

4. excessive reduction of blood pressure must be avoided to prevent the increased cerebral ischemia that results if the pressure falls below the lower level of cerebral autoregulation. In normal humans, this is set at an MAP of about 60 mmHg. In patients with uncontrolled HTN, the level of autoregulation is elevated, and cerebral ischemia may occur at a much higher MAP. BP below this level will result in cerebral ischemia

5. HTN encephalopathy is

(1) acute in onset

(2) reversible

6. Patients often present with severe headaches, vomiting, drowsiness, and confusion. Seizures, blindness, focal neurologic deficits, or coma may occur.

7. Papilledema is usually present, along with significant hypertensive retinopathy.

8. DD: all types of strokes, ICH, meningoencephalitis, brain tumors, and metabolic coma.

9. focal deficits secondary to HTN encephalopathy usually do not follow a singular anatomic pattern.

10. systemic signs of infection associated with meningitis are absent.

11. CT usually normal

12. CSF: clear, with a increased opening pressure, normal or increased protein.

13. treatment: IV nitroprusside--> reduction of MAP by 25% over an hour.

oral or nontitratable agent may result in an excessive reduction of BP and irreversible cerebral ischemia.

14. other treatment: fenoldopam mesylate, labetalol, nicardipine and enalaprilat. 

(Fenoldopam is a rapid-acting vasodilator. It is an agonist for D1-like dopamine receptors and binds with moderate affinity to α2-adrenoceptors. It has no significant affinity for D2-like receptors, α1 and β adrenoceptors, 5HT1 and 5HT2 receptors, or muscarinic receptors. )

15 fast-acting nifedipine: uncontrolled hypotension and sympathetic release--> controindicated for acute HTN

16. admission and invasive BP monitoring

 

Malignant HTN

1. Diastolic BP is usually> 130mmHg. Readings below this level are seldom associated with either malignant HTN or HTN encephalopathy.(但極少數會發生在DBP

2. Most patient with diastolic pressures aboves 130mmHg do not develop either of these clinical syndromes.

3. Malignant HTN only effects 1% of HTN population.

4. Fibrinoid necrosis of small arterioles:

    rapid, sustained rise in BP--> overwhelms the high-pressure of autoregulation--> small arterioles dilate--> pressure in the proximal capillary beds increases--> fluid leak  into the tissues.

   arterioles rupture and leak plasma and blood--> fibrin deposition into their walls.

   Fibrinoid necrosis= necrosis of myofibrils in smooth muscle cells + leaking of plasma + fibrin deposition in the walls of arterioles.

5. retina: linear hemorrhages dissecting along nerve fibers. cotton-wool spot that consists of swollen, ishcemic axons.

 

 圖:cotton wool spots, yellow white spots in the retina

   cytoid body: the aggregation of materials within the ischemic axons produces a nuclear-like structure. 細胞樣體

6. patients with malignant HTN appear ill and ofter present with complaints of severe headache, blurred vision, dyspnea, chest pain or with symptoms of uremia.

7. malignant HTN is a medical emergency, if untreated, it may result in acute renal failure, severe cardiac decompensation, MI, HTN cerebral hemorrhage, or HTN encephalopathy.

8. In addition to elevated BP, patients with malignant HTN must demonstrate evidence of acute end-organ damage as a result of the hypertension.

9. PE: enlarged LV, rales at the lung bases. Marked retina finding are ofter present(linear hemorrhage, cotton wool patches).

10. acute elevation of BUN and Cr or hematuria(involves of the kidneys)

11. ECG: LVH and strained.

12. CXR: cardiomegaly and congestive heart failure

13. treatment: lowering the MAP to 25% of the pretreatment levels over the initial minutes to hours of treatment. then toward 160/100 over 2-6 hours. avoiding excessive falls in pressure that may precipitate renal, cerebral, coronary ischemia.(最常用nitroprusside,以免過度降壓)

14. all patients should be hospitalized and invasive BP monitoring may be preferable.

 

 

Stroke syndromes

1. careful anti-HTN treatment for patients with persistent extreme elevation of BP after a stroke(例如:DBP>140mmHg, MAP>130mmHg)

2. patients with persistent pressures > 185/110 should not receive thrombolytic therapy.

3. modest reduction in BP after ICH (20% reduction of MAP) have not been clearly associated with a worse outcome.

4. Should not use NTG or nitroprusside.

5. Labetalol is probably the agent of choice.

 

 

Pulmonary edema

1.多數CHF病患有某些程度的周邊血管阻力上升PVR=peripheral vesicular resistance,導致血壓上升,這是正常反應

2. 這種血壓上升的程度是中度的而非醫療急症

3. 控制不良的時候,長時間的高血壓導致myocardial hypertrophy, 當心肌肥大再也無法克服上升的PVR時,左心室開始衰竭 + 擴張

4. 肺水腫造成壓力==> 分泌catecholamines上升--> PVR上升--> HTN

5. 少數病患,突然嚴重上升的血壓促使左心室急性衰竭,導致肺水腫

6. NTG是第一線用藥,如果無效,應使用 ITROPRUSSIDE

7. ACEI輔助治療肺水腫的效果也不錯

8. 治療肺水腫如果血壓降太低可能導致中風症狀

 

Cardiac ischemia

1. HTN and angina are ofter found together.

2. 嚴重高血壓合併ANGINA,需要立即降血壓,以免導致心肌受損。多數病患適合用NTG,但是有極端高血壓的病患,單獨用NTG可能不夠,需加上BETA BLOCKER

3. ACEI也是有用的輔助藥物,可降低MI死亡率

4. CCB在無法使用BETA BLOCKER的病患是不錯的替代藥物

5. NITROPRUSSIDE會導致反射性心博過速,在心肌缺血病患需小心使用

6. 使用血栓溶解劑治療MI時,需比照中風使用條件,嚴格控制血壓

 

 

Renal failure

1. CRF最重要的心血管併發症是高血壓

2. Uncontrolled HTN會加速心血管問題的發展,是洗腎及腎臟移植病患的最常見死因

3. HTN在ARF的任何階段都可能出現,且發生在80%的advanced renal failure病患上

4. 沒有高血壓時,CRF的惡化會變慢,有高血壓但控制良好時,CRF的進展會延緩

5. 因為malignant HTN導致腎功能惡化的病患,在開始治療期間常出現腎功能惡化,但過一段時間,腎功能會改善。

6. CRF病患的高血壓原因是因為NA滯留和RENIN-ANGIOTENSION SYSTEM的活化

7. 腎衰竭+高血壓的第一線治療:DIURETICS + ACEI + CCB

8. Severe elevation of BP may lead to acute renal failure or may exacerbate CRF. This requires immediate reduction of BP. Nitroprusside  is the drug of choice, although the IV CCB nicardipinie is a resonable alternative.

 

 

Pregnancy

1. 高血壓是妊娠常見的併發症,5-10%的懷孕婦女在妊娠某些時期會發生

2. Women with pre-eclampsia or eclampsia represent HTN emergencies and can occur without an extreme elevation of BP.

3. Any acute elevation of diastolic BP > 100mmHg in the pregnant patient represents a true HTN emergencies.

4. treatment: reduction of BP, control of seizures, early obstetric consultation. IV hydralazine.

5. 替代藥物:labetalol, nicardipine, nitroprusside (但nitroprusside會在子宮產生cyanide,所以只用在其他藥物無效時)

 

Aortic dissection

1. aortic dissection is associated with a history of HTN

2. medical therapy: reducing BP to limit the extent of the dissection.

3. Goal: systolic level of 100-120 mmHg. reduce the ejection force of the heart.

4. 不能單獨使用血管擴張劑

5. 藥物選擇:Beta blocker=控制tachycardia  + vasodilator(nicardipine, nitroprusside, fenoldopam).

6. ganglionic blocker trimethaphan camsylate(arfonad) and the combined alpha/beta-blocker labetalol have been used successfully in these patients.

 

 

HTN urgencies Rosen 5ed P 1166

1. elevated BP without evidence of progressive end-organ involvement rarely mandates urgent antihypertensive therapy.

2. It is unnecessary to lower BP acutely in patient with so-called HTN urgencies.

3. Initial:未曾被檢查過的病患

   history and PE to cardiovascular, funduscopic, and neurologic systems.

   UA: renal function

   BUN, Cr, electrolytes

   CXR + ECG: if patient with chest pain of symptoms.

4. initial evaluation fails to show any acute end-organ damage=> the patient may be prompt referred.

5. It is not generally necessary to document an acute change in BP before discharge.

 

特殊情況:sympathomimetic overdose, clonidine or B-blocker withdrawal, postoperative HTN, extremely elevated BP

1. urgent therapy for patients without end-organ ischemia== Clonidine 0.1-0.2mg po stat , 最大效果 60分鐘出現, 如果需要可以每小時給予 0.1mg clonidine 直到DBP降低20%或

2. 當開始給予口服藥物急速降壓,在給予其他治療或出院前,要觀察病患至最大效果出現為止。

3. 不要給予短效的dyhydropyridine CCB

4. 如果出現任何 progressive end-organ disease,HTN病患要當成emetgent,且住院治療

============================= 

 

底下是舊的文章

高血壓急症 血壓控制目標值 

定義: 嚴重高血壓 BP > 180/120 mmHg 以上(但有些高血壓急症的血壓在此之下就會有醫療急迫性) 

重點:

1. 先區分是否為HYPERTENSIVE EMERGENCY

2. 如果不是HYPERTENSIVE EMERGENCY. 則可能是下列第 2.3.4

3. 如果沒有任何症狀, MAP > 160 mmHg DBP> 130 mmHg, 建議急診留觀, 可考慮降壓藥物

4. 如果觀察過程出現 END-ORGAN ISCHEMIA症狀, 回到 HYPERTENSIVE EMERGENCY 流程 

HTN present in ED in the following four general ways:

1. HTN emergency or HTN crisis with acute end-organ damage

2. HTN urgency or significantly elevated blood pressure with nonspecific symptoms

3. mild HTN without end-organ damage

4. transient HTN related to anxiety or the primary complaint

 

Clinical Presentation of hypertensive emergencies

1. hypertensive encephalopathy

2. Malignant hypertension

3. stroke syndromes

4. pulmonary edema

5. cardiac ischemia

6. renal failure

7. pregnancy

8. aortic dissection

 HTN encephalopathy

1. MAP > 160mmHg, autoregulation may not be able to control cerebral blood flow

2. Marked vasospasm may occur, with ischemia, increased vascular permeability, punctate hemorrhages, resultant brain edema.

3. Immediate reduction of BP by 30-40% will reverse the vasospasm.

4. excessive reduction of blood pressure must be avoided to prevent the increased cerebral ischemia that results if the pressure falls below the lower level of cerebral autoregulation. In normal humans, this is set at an MAP of about 60 mmHg. In patients with uncontrolled HTN, the level of autoregulation is elevated, and cerebral ischemia may occur at a much higher MAP. BP below this level will result in cerebral ischemia

5. HTN encephalopathy is

(1) acute in onset

(2) reversible

6. Patients often present with severe headaches, vomiting, drowsiness, and confusion. Seizures, blindness, focal neurologic deficits, or coma may occur.

7. Papilledema is usually present, along with significant hypertensive retinopathy.

8. DD: all types of strokes, ICH, meningoencephalitis, brain tumors, and metabolic coma.

9. focal deficits secondary to HTN encephalopathy usually do not follow a singular anatomic pattern.

10. systemic signs of infection associated with meningitis are absent.

11. CT usually normal

12. CSF: clear, with a increased opening pressure, normal or increased protein.

13. treatment: IV nitroprusside--> reduction of MAP by 25% over an hour.

oral or nontitratable agent may result in an excessive reduction of BP and irreversible cerebral ischemia.

14. other treatment: fenoldopam mesylate, labetalol, nicardipine and enalaprilat.

15 fast-acting nifedipine: uncontrolled hypotension and sympathetic release--> controindicated for acute HTN

16. admission and invasive BP monitoring 

Malignant HTN

1. Diastolic BP is usually> 130mmHg. Readings below this level are seldom associated with either malignant HTN or HTN encephalopathy.(但極少數會發生在DBP<110 mmHg)

2. Most patient with diastolic pressures aboves 130mmHg do not develop either of these clinical syndromes.

3. Malignant HTN only effects 1% of HTN population.

4. Fibrinoid necrosis of small arterioles:

    rapid, sustained rise in BP--> overwhelms the high-pressure of autoregulation--> small arterioles dilate--> pressure in the proximal capillary beds increases--> fluid leak  into the tissues.

   arterioles rupture and leak plasma and blood--> fibrin deposition into their walls.

   Fibrinoid necrosis= necrosis of myofibrils in smooth muscle cells + leaking of plasma + fibrin deposition in the walls of arterioles.

5. retina: linear hemorrhages dissecting along nerve fibers. cotton-wool spot that consists of swollen, ishcemic axons.

   cytoid body: the aggregation of materials within the ischemic axons produces a nuclear-like structure. 細胞樣體

6. patients with malignant HTN appear ill and ofter present with complaints of severe headache, blurred vision, dyspnea, chest pain or with symptoms of uremia.

7. malignant HTN is a medical emergency, if untreated, it may result in acute renal failure, severe cardiac decompensation, MI, HTN cerebral hemorrhage, or HTN encephalopathy.

8. In addition to elevated BP, patients with malignant HTN must demonstrate evidence of acute end-organ damage as a result of the hypertension.

9. PE: enlarged LV, rales at the lung bases. Marked retina finding are ofter present(linear hemorrhage, cotton wool patches).

10. acute elevation of BUN and Cr or hematuria(involves of the kidneys)

11. ECG: LVH and strained.

12. CXR: cardiomegaly and congestive heart failure

13. treatment: lowering the MAP to 25% of the pretreatment levels over the initial minutes to hours of treatment. then toward 160/100 over 2-6 hours. avoiding excessive falls in pressure that may precipitate renal, cerebral, coronary ischemia.(最常用nitroprusside,以免過度降壓)

14. all patients should be hospitalized and invasive BP monitoring may be preferable.  

Stroke syndromes

1. careful anti-HTN treatment for patients with persistent extreme elevation of BP after a stroke(例如:DBP>140mmHg, MAP>130mmHg)

2. patients with persistent pressures > 185/110 should not receive thrombolytic therapy.

3. modest reduction in BP after ICH (20% reduction of MAP) have not been clearly associated with a worse outcome.

4. Should not use NTG or nitroprusside.

5. Labetalol is probably the agent of choice. 

 

Pulmonary edema

1.多數CHF病患有某些程度的周邊血管阻力上升PVR=peripheral vesicular resistance,導致血壓上升,這是正常反應

2. 這種血壓上升的程度是中度的而非醫療急症

3. 控制不良的時候,長時間的高血壓導致myocardial hypertrophy, 當心肌肥大再也無法克服上升的PVR時,左心室開始衰竭 + 擴張

4. 肺水腫造成壓力==> 分泌catecholamines上升--> PVR上升--> HTN

5. 少數病患,突然嚴重上升的血壓促使左心室急性衰竭,導致肺水腫

6. NTG是第一線用藥,如果無效,應使用NITROPRUSSIDE

7. ACEI輔助治療肺水腫的效果也不錯

8. 治療肺水腫如果血壓降太低可能導致中風症狀

 

 Cardiac ischemia

1. HTN and angina are ofter found together.

2. 嚴重高血壓合併ANGINA,需要立即降血壓,以免導致心肌受損。多數病患適合用NTG,但是有極端高血壓的病患,單獨用NTG可能不夠,需加上BETA BLOCKER

3. ACEI也是有用的輔助藥物,可降低MI死亡率

4. CCB在無法使用BETA BLOCKER的病患是不錯的替代藥物

5. NITROPRUSSIDE會導致反射性心博過速,在心肌缺血病患需小心使用

6. 使用血栓溶解劑治療MI時,需比照中風使用條件,嚴格控制血壓 

Renal failure

1. CRF最重要的心血管併發症是高血壓

2. Uncontrolled HTN會加速心血管問題的發展,是洗腎及腎臟移植病患的最常見死因

3. HTNARF的任何階段都可能出現,且發生在80%的advanced renal failure病患上

4. 沒有高血壓時,CRF的惡化會變慢,有高血壓但控制良好時,CRF的進展會延緩

5. 因為malignant HTN導致腎功能惡化的病患,在開始治療期間常出現腎功能惡化,但過一段時間,腎功能會改善。

6. CRF病患的高血壓原因是因為NA滯留和RENIN-ANGIOTENSION SYSTEM的活化

7. 腎衰竭+高血壓的第一線治療:DIURETICS + ACEI + CCB

8. Severe elevation of BP may lead to acute renal failure or may exacerbate CRF. This requires immediate reduction of BP. Nitroprusside  is the drug of choice, although the IV CCB nicardipinie is a resonable alternative. 

 

 Pregnancy

1. 高血壓是妊娠常見的併發症,5-10%的懷孕婦女在妊娠某些時期會發生

2. Women with pre-eclampsia or eclampsia represent HTN emergencies and can occur without an extreme elevation of BP.

3. Any acute elevation of diastolic BP > 100mmHg in the pregnant patient represents a true HTN emergencies.

4. treatment: reduction of BP, control of seizures, early obstetric consultation. IV hydralazine.

5. 替代藥物:labetalol, nicardipine, nitroprusside (nitroprusside會在子宮產生cyanide,所以只用在其他藥物無效時) 

Aortic dissection

1. aortic dissection is associated with a history of HTN

2. medical therapy: reducing BP to limit the extent of the dissection.

3. Goal: systolic level of 100-120 mmHg. reduce the ejection force of the heart.

4. 不能單獨使用血管擴張劑

5. 藥物選擇:Beta blocker=控制tachycardia  + vasodilator(nicardipine, nitroprusside, fenoldopam).

6. ganglionic blocker trimethaphan camsylate(arfonad) and the combined alpha/beta-blocker labetalol have been used successfully in these patients.  

HTN urgencies Rosen 5ed P 1166

1. elevated BP without evidence of progressive end-organ involvement rarely mandates urgent antihypertensive therapy.

2. It is unnecessary to lower BP acutely in patient with so-called HTN urgencies.

3. Initial:未曾被檢查過的病患

   history and PE to cardiovascular, funduscopic, and neurologic systems.

   UA: renal function

   BUN, Cr, electrolytes

   CXR + ECG: if patient with chest pain of symptoms.

4. initial evaluation fails to show any acute end-organ damage=> the patient may be prompt referred.

5. It is not generally necessary to document an acute change in BP before discharge. 

特殊情況:sympathomimetic overdose, clonidine or B-blocker withdrawal, postoperative HTN, extremely elevated BP

1. urgent therapy for patients without end-organ ischemia== Clonidine 0.1-0.2mg po stat , 最大效果 60分鐘出現, 如果需要可以每小時給予 0.1mg clonidine 直到DBP降低20%或<110 mmHg.

2. 當開始給予口服藥物急速降壓,在給予其他治療或出院前,要觀察病患至最大效果出現為止。

3. 不要給予短效的dyhydropyridine CCB

4. 如果出現任何 progressive end-organ diseaseHTN病患要當成emetgent,且住院治療

 


2012-11-13 更新. 下面是2007年的文章
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