½²«Tº_¡]¬K¤Ñ¡^¶E©Ò -- Arterial hypertension
 
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Arterial hypertension

( §ó·s¤é´Á¡G2007-01-29 )

¡EÁöµM¤j³¡¥÷ªºhypertension ¯f¤H¤£·|¦³»{¦ó¯gª¬¡A¦ýºC©Êªº°ª¦åÀ£¡A«o·|Åý¤H¿©±w¤@¨Ç«á¿ò¯g¡A¥]¬Acongestive heart failure ¡Bmyocardial infarction ¡Bcerebrovascular accident¡A and renal insufficiency¡C
¡Edefinition and epidemiology
diastolic BP(blood pressure) > 90mmHg §YºÙ hypertension¡C ¥i¨Ìdiastolic BP ªºlevel ¤À¬°mild¡B moderate & severe hypertension¡C ¦ý­Ydiastolic BP < 90mmHg, ¦Ósystolic BP > 160mmHg¡A¥çÄÝhypertension¡AºÙ¬°isolated sysotolic hypertension¡C
°·±d¤p«Ä& pregnant women ¤@¯ë·|¦³¸û§CªºBP¡A ­YBP > 120/80¡A «hBP ¤wÄݵy°ª¡C
¡Erisk factor of hypertension
1. age¡C
2. heredity¡J ¬ù80% ªºhypertension ¯f¤H¦³family history ¡C
3. obesity¡C
4. dietary intake of sodium¡C
 
the pathophysiology of hypertension
¡E·ícardic contraction ®É¡A»s³y¤Fmaximal pressureºÙ¬°systolic BP¡C·ícardiac relaxation ®É¡A³y¦¨BP ­°¦Ü³Ì§CÂI¡AºÙdiastolic BP¡C
¡Emean arterial pressure (MAP) ³B©ósystolic & diastolic BP ¤§¶¡¡A¬Ocardiac output »Psystemic vascular resistance ªº­¼¿n¡C
¡E¥i¥H¼vÅTcardiac output »Psystemic vascular resistanceªºmechanism¡A ¬Ò¥i¥H¼vÅTBP ªºcontrol¡J
1. baroreceptor reflex
·íBP ¦³ÅܰʮɡA¦ì©óÀV³¡ªºcarotid sinus §Y·|µo¥X«H¸¹¨ìbrain stem¡A  brain stem §Y·|³z¹Ladrenergic outflow¡A ª½±µ¼vÅT heart rate¡B cardiac contractility  & systemic vascular resistance  ¥H§ïÅÜBP ¨ì¤w³]©wªºBP ­È¡C
2. renin-angiotensin system
renin (from kidney ) ¡X¡r angiotensin£L(lung)¡X¡r angiotensin£S
„³ ¡X raise SVR
   ¡X aldosterone (at adrenal gland, a mineralocorticoid hormone )¡÷   resorption of sodium & water by kidney

«Ü¦h¦]¯À·|¼vÅT renin ªº¤Àªc, ¥]¬A renal perfusion pressure ªº§ïÅÜ¡B distal renal tubule³B¯ÇÂ÷¤lªº§ïÅÜ¡B£]-adrenergic ªº¨ë¿E¡B ¤Îprostaglandinsªº¼vÅT¡C
3. the extracellular fluid volume
kidney ¯à±±¨îÊ^¤º¦³¾A·í¦a extracellular fluid volume¡A¥H«K¦³adequate tissue perfusion¡C
°²¦p¦bextracellular fluid volume ¯Ê¤Öªºª¬ªp¡Akidney ªºrenal tubules ·|«P¶ireabsorption of sodium & water¡C
¬Û¤Ï¦a¡A°²¦p¥Ñ©ó  extracellular fluid volume ¤Ó¦h¡A¤Þ°_BP ªº¤W¤É¡A¨º»òkidney ´N·|¥[±jÅ餺Na ªº±Æªn¡A¥ç§Y·|´î¤Öreabsorption of sodium & water¡C

clinical aspects of hypertension
¡E 90-95% ªºhypertension¯f¤H¡A¥L­ÌªºHP(hypertension) ¬O¨S¦³¯f¦]ªº¡AºÙ¤§¬°primary hypertension or essential hypertension¡C
¡EÁöµM essential hypertension ³Ì±`¦b¤¤¦~ªº®É­Ô³Qµo²{¡A¦ý¨Æ¹ê¤W¥¦¥i¯à¤w¦b§ó¦~»´®É¤wº¥º¥¦b§Î¦¨¡CHP¥i¯à·|¦]¬°¤@ª½³£¨S¤°»ò¯gª¬¦Ó¤£³Qµo²{¡A­Y¤@ª½³£¨S¥[¥HªvÀø¡A¨º»òHP ´N·|²£¥Í¦UºØmorbidity & mortality ¡C
¡Emorbidity & mortality (M&M) ªº­ì¦]¡J
ÁöµM¤W¤ÉªºBP ¥»¨­·|³y¦¨vascular injury & end-organ damage¡A ¦ý¥t¤è­±atherosclerosis (°Ê¯ßµ°ª¬µw¤Æ)¡A¦]HP ªº¦s¦b¦Ó´c¤Æ¡A¤]¬O³y¦¨M & M ªº­ì¦]¡C
¡EHP ³y¦¨ªºcomplication ³Ì±`involved ªºtarget organ ¬Obrain¡B heart & kidney ¡F¦Ó¦º¦]±`¬Omyocardiac infarction & cerebrovascular accident¡C
¡E ¹ï©óHP ªºseverity ¤§µû¦ôÀ³¸Ó¥]¬A
optic fundus: grade 3 retinopathy (hemorrhage & exudates)¡A or grade 4 retinopathy(papilledema)¡Aªí¥Üsevere HP ¡C
¹ï©ó­è³Qµo²{¦³°ª¦åÀ£ªº¯f¤H¡AÀ³¸Ó§@ªºroutine lab. studies ¥]¬A¡JEKG ¡BCBC ¡BU/A¡B blood chemistries (serum electrolytes¡B Cr¡B glucose¡B triglycerides¡B cholesterol ¡Buric acid)
¡Emalignant hypertension ¡J ³o¬O¤@ºØÄY­«¦Ó«æ¶·³B²zªºHP ¡A¯S¼x¬O«Ü°ªªºBP (diastolic BP > 120mmHg ) & widespread end-organ dysfunction¡C
°²¦p¨S¦³treatment (Tx)¡A ¥i¯à·|²£¥Ídiffuse fibrinoid necrosis of arterioles¡C
¯f¤H±`·|©ê«èheadache¡B blurred vision ¡B& dyspnea¡C optic fundus ¥i¨£papilledema ¡C¦Óencephalopathy ¡B congestive heart failure¡B & renal function impairment ³£¥i¯àµo¥Í¡C

secondary hypertension
¡E¹ï©ó(1) young patients with severe HP
      (2) the individual whose BP is poorly controlled on antihypertensive therapy
      (3) ·íinitial screen evaluation ®É§YÃhºÃ¦³underlying disease ªÌ
¬Ò¸û¦³¥i¯à·|¦³secondary HP¡C
¡E ¬ù¥u¦³5%-10%ªºHP ¯f¤H¬OÄÝ©ósecondary HP¡A ¥u­nTx ¨äunderlying
dz.¡A³oºØHP ¬O¦³±æ³Qªv¡ªº¡C

¡Esecondary HP ªºcause
1. renovascular HP
ƒÞ ¥Ñ©ó¤@Ãä©Î¤GÃ䪺renal arteries ²£¥Ístenotic lesion¡A ¦Ó¤Þ°_renal   ischemia ¡A¶i¦Ó²£¥Ístimulation of the renin ¡V angiotensin system¡C
ƒÞ in the initial phase
    HP ¬O¥Ñ©órenin ªº¤j¶q¤Àªc³y¦¨angiotensin £S & aldosterone ªº¤Àªc¼W¥[¡A¦Ó³y¦¨vasocontriction & volume expansion¡C
³o¬q´Á¶¡¥u­nrepair of the vascular stenosis ¡A©Îµ¹¤©ACEI ´N·|¨ÏBP ¤U­°¡C¦ý­Y in the chronic or late phase ¡A¥Ñ©ó¹ï°¼ªºrenal parenchymal dz ªºµo®i¡A¨äHP ªº­ì¦]¤£¬O¦]renin ¤j¶q¤Àªc³y¦¨ªº¡A©Ò¥H¨Ï¥Î¤W­zªº¤è¦¡¤]¤£¯à¨ÏBP ¤U­°¡C
ƒÞ the stenotic renal vascular lesion ¦³¤GºØ«¬ºA¡J
(1) fibromuscular dysplasia¡V ¤D¥Ñ©óproliferation of the vascular
   media¡C ³Ì±`µo¥Í©ó¦~»´¦Ó¨ä¥L¤è­±¬Ò¥¿±`ªº¤k«Ä¤l¡C    
(2) atheromatous plaque(°Ê¯ßµ°ª¬´³¶ô)¡V ³o¬O³Ì±`¨£ªº«¬ºA¡A±` 
   µo²{©óproximal renal artery ¡C older individuals with widespread atherosclerotic dz ªº¤H³Ì©ö±o¨ì¡C
ƒÞ §@physical examination (P.E.)®É¥iÅ¥¨ìabdominal bruit¡C §@lab. routine ®É¡A¥iµo²{hypokalemic metabolic alkalosis (¦]chronic stimulation of aldosterone )¡A¤]¥iµo²{serum Cr. ¤W¤É(¦]renal dysfunction)¡C
ƒÞ ­n§@definitive diagnosis ¶·°µrenal arteriogram ¡A¦P®É´úlesion °¼ªºrenal renin ­È¡F­Y¬Ounilateral renal artery stenosis ¡A«h¦P°¼ªºvenous rennin level ·|¤W¤É¡A¦Ó¹ï°¼ªº·|¤U­°¡C
ƒÞ ¦¹¥~¦³¤@ºØÂ²«K¡B¥i«H¥ô¡B¦Ó¤Snoninvasive ªº¤è¦¡¡A¥Hscreen ¥X renovascular dz ¡A§Ycaptopril challenge test ¡C
ƒÞ Tx ¡J
¾A©y°Ê¤â³NªÌ ¡A¥i¬I¥Hsurgical revascularization or transluminal angioplasty of the stenotic lesion ¡C
¤£¾A©y°Ê¤â³NªÌ¡A¦p«Ü¦Ñªº¯f¤H©Î¦³¨ä¥Lcomplication ªÌ¡A¥i¨Ï¥ÎACEI ¡C
2. parenchymal renal disease
ƒÞ hypervolemia ¬O³y¦¨HP ªº¥D¦]¡C
ƒÞ ÁöµM¤j³¡¤Àªºchronic renal dz ¬O¨S¿ìªkªv¡ªº¡A¦ý­Y¯à¾A·í¦a±±¨îHP¡A «h¥i¥H´î½wrenal insufficiency ªº³t«×¡A¤]¥i­°§C¨ä¥Lmorbidity ªºrisk ¡C
3. pheochromocytoma
ƒÞ ¬O¤@Ïúchromaffin cell ªºtumor ¡A¥i¥H¤j¶q¤Àªcnorepinephrine (NE) & epinephrine(Epi)¡A ±`ªø¦badrenal medulla ¤º¡C
ƒÞ ¯f¤H·|¦³¨ä¥LªºS/S¡A ¦pparoxysmal sweating¡B flushing¡B palpitation ¡A·íµM°¸¥ç¦³¨Ç¯f¤H¤£ªí²{³o¨Çclassic finding¡C
ƒÞ diagnosis¡J (1) urine catecholamine ¡BVMA ¡B& metanephrine ·|
¤W¤É¡C(2) CT scan ¡C
ƒÞ Tx¡J
 ¶}¤M¡A¦ýpreoperative control of the blood pressure & extracellular fluid volume is critically important ¡C
 
4. mineralcorticoid excess (primary aldosteronism )
±`¬O¥Ñ©óbenign adrenal adenoma ³y¦¨aldosterone ªº¤j¶q¤Àªc¡C HP ¬O¥Ñ©ókidney ªºreabsorption of sodium & water ªº¼W¥[¦Ó¤Þ°_volume expansion¡C ·|¦³hypokalemic metabolic alkalosis¡C
Dx¡J ¨Ì¾Ú¬O(1) plasma or urine ªºaldosterone ¤W¤É¡A¦ýrenin level «o¤U­°(2) CT scan
Tx¡J (1) surgical removal
     (2) ­Y¤£¯àsurgical intervation ¡A«h±Ämedication¡J aldosterone antagonist such as spironolactone + other antihypertensive drugs ¡C
5. coarctation of the aorta
ƒÞ aorta ªºnarrow ³B±`¬O¦ì¦b distal to the left subclavian artery¡C
ƒÞ ¥Ñ©ómechanical impairment of blood flow to the kidney results in stimulation of the renin ¡V angiotensin axis
ƒÞ ±`¦b¤pªB¤Íªº¶¥¬q§Y³Qµo²{¡C
ƒÞ ¶qBP ¥iµo²{arm ªºBP ¤W¤É¡A¦Óleg ªºBP ¤U­°¡C
ƒÞ Tx¡J surgical repair of the vascular narrowing ¡C

Treatment of essential HP
¡E¥Øªº¬Oreduce the risk of M&M due to cerebrovascular¡B cardiovascular¡B & renal dz ¡C
¡Ediastolic BP > 95 mm Hg ¥H¤W§Y¶·±µ¨üTx (¥]¬Adrug & nonpharmcological intervention )¡A ¥H¨ÏBP ­°¨ì90 mmHg¥H¤U¡F ·ídiastolic BP 90-95 mmHg «h¥u¶·nonpharmcological intervention ¡A¦ý­Y¦³other risk factors , ex.  Diabetis, hyperlipidemia «hÀ³±µ¨üdrug Tx¡C

¡E nonpharmacologic Tx¡J: dietary sodium restriction ¡Bexercise ¡Bweight loss ¡Bbehavior modification¡B & limitation of heavy alcohol or tobacco consumption¡C

.¡Edrug Tx:
ƒÞ initial therapy ¥]¬A
(1) diuretics.
(2) B-adrenergic blockers.
(3) Ca. channel blocker.
(4) ACEI.
(5) (1)+(2), or (1)+(3), or (1)+(4).
ƒÞ ­Ypoor control to initial therapy
«h¥i¥H¥H¤UÃþ§Îªºantihypertensive drug ¥[¥H²Õ¦X¡J
a diuretic ¡Óa vasodilator ¡Óadrenergic inhibitor

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