¼±Åà - È­»ìǥŰ/¿£ÅÍŰ ´Ý±â - ESC

 

Acute Myocardial Infarction

1. °³¿ä

»ç¸Á·üÀÌ ´ë·« 30% Á¤µµ µÇ¸ç, ÀÌÁß ¹ÝÀÌ»óÀÌ º´¿ø¿¡ µµÂøÇϱâ Àü¿¡ »ç¸ÁÇÑ´Ù. Áö³­ 20³â°£

ÀÔ¿øÈÄ »ç¸Á·üÀÌ 30%Á¤µµ °¨¼ÒÇÏ¿´À¸³ª º´¿ø¿¡¼­ »ýÁ¸ÇÑ 25¸íÁß ÇѸí²Ã·Î ù 1³â³» »ç¸Á

ÇÑ´Ù.

2. º´Å»ý¸® : Role of acute plaque rupture

slowly developing, high-grade coronary a. stenosis´Â ½Ã°£ÀÌ Áö³ª¸é¼­ dzºÎÇÑ collateral

networkÀÌ »ý±â¹Ç·Î AMI¸¦ Ã˹߽ÃŰÁö ¾Ê´Â´Ù. ´ë½Å vascular injury site¿¡ coronary a.

thrombus°¡ »¡¸® Çü¼ºµÉ ¶§ AMI°¡ ¹ß»ýÇÑ´Ù. ÀÌ·¯ÇÑ vascular injury´Â cigarette smoking,

hypertension, lipid accumulation°ú °°Àº ÀÎÀڵ鿡 ÀÇÇØ »ý±â°Å³ª ÃËÁøµÈ´Ù.

´ëºÎºÐÀÇ infarctionÀº atherosclerotic plaque fissure, rupture or ulceration¶§ »ý±ä´Ù.

(-> rupture site¿¡ mural thrombusÇü¼º -> coronary a. occlusion)

ruptured plaque¿¡ initial platelet monolayer°¡ Çü¼ºµÈÈÄ ¿©·¯ °¡Áö agonist(collagen, ADP,

epinephrine, serotonin)°¡ Ç÷¼ÒÆÇÀ» Ȱ¼ºÈ­½ÃŲ´Ù.

-> Ç÷¼ÒÆÇÀÌ thromboxane A2(potent local vasoconstrictor) release

-> further plt activation : thrombolysis¿¡ potential resistance

µå¹°°Ô, AMI´Â coronary emboli, congenital anomaly, coronary spasm, ´Ù¾çÇÑ systemic

(ƯÈ÷ inflammatory) ds¿¡ ÀÇÇÑ coronary a. occlusionÀ¸·Î ¹ß»ýÇÒ¼öµµ ÀÖ´Ù.

coronary occlusion¿¡ ÀÇÇÑ ½É±Ù¼Õ»óÁ¤µµ´Â ´ÙÀ½°ú °°Àº ¿ä¼Ò¿¡ ´Þ·Á ÀÖ´Ù.

i) ¼Õ»óÇ÷°ü¿¡¼­ °ø±Þ¹Þ´Â ¿µ¿ª(territory)

ii) ¿ÏÀüÆó¼â¿©ºÎ

iii) ±â°£

iv) collateral vsÁ¤µµ

v) »ê¼Ò¿ä±¸·®

vi) spontaneous lysis¸¦ ÀÏÀ¸Å³¼ö ÀÖ´Â native factors

vii) flow°¡ ȸº¹µÇ¾úÀ» ¶§ infarct zone¿¡¼­ myocardial perfusion adequacy

* AMI risk°¡ ³ôÀº °æ¿ì : multiple coronary risk factor°¡ ÀÖ´Â °æ¿ì

unstable angina or Prinzmetal's variant angina

* Less common : hypercoagulability, collagen vascular ds, cocaine abuse, intracardiac

thrombi or mass

3. ÀÓ»ó¹ßÇö

¹Ý¼ö°¡±îÀÌ AMI°¡ »ý±â±âÀü À¯¹ßÀÎÀÚ°¡ ÀÖ´Ù.

¿¹> vigorous physical exercise, emotional stress or medical or surgical illness

³·, ¹ã ¸ðµÎ »ý±æ¼ö ÀÖÁö¸¸ À̸¥ ¾ÆÄ§(±ú°í³­ÈÄ ¸î½Ã°£³»)¿¡ Àß »ý±ä´Ù. À̸¥ ¾ÆÄ§¿¡ Àß

»ý±â´Â ÀÌÀ¯´Â 6AM - 12 noon»çÀÌ¿¡

i) sympathetic tone¡è

ii) thrombosis tendency¡èÀ̱⠶§¹®.

pain : mc presenting complaint

´À²¸º» °Í Áß °¡Àå ½ÉÇϴٴ ǥÇöÀ» ÇÔ.

deep or visceral(heavy, squeezing & crushing), °¡²û stabbing or burning

AP¶§ÀÇ discomfort¿Í À¯»çÇϳª ´õ ½ÉÇϰí,´õ¿À·¡ Áö¼ÓµÈ´Ù.

µ¿¹ÝÁõ»ó : weakness, sweating, N/V, anxiety, a sense of impending doom

¿îµ¿½Ã ÅëÁõÀÌ ½ÃÀÛÇÏÁö¸¸ Áß´ÜÈÄ¿¡µµ ¾ø¾îÁöÁö ¾Ê´Â´Ù.

painless AMI : DM, old age¿¡¼­ Áõ°¡

³ëÀε鿡¼­ sudden-onset breathlessness(-> pul edema·Î ÁøÇà)fh ¹ßÇöµÇ±âµµ ÇÑ´Ù.

other less presentations c/s pain

sudden loss of consciousness, confusional state, profound weakness,

arrhythmia, peripheral embolism, unexpalined drop in arterial pr.

DDx) acute pericarditis, pul embolism, acute aortic dissection, costochondritis, GI

disorders

*Physical Findings

´ëºÎºÐ anxious & restless, ÀÚ¼¼º¯°æ µîÀ¸·Î ÅëÁõÀÌ ¼Ò½ÇµÇÁö ¾Ê´Â´Ù.

â¹é, ¹ßÇÑ, »çÁö ³Ã°¨ÀÌ ÈçÇÏ´Ù.

substernal chest pain(>30min) + diaphoresis = AMI°­·ÂÈ÷ ½Ã»ç

¸¹Àº ȯÀÚ°¡ ù 1½Ã°£³»¿¡´Â normal PR & BP¸¦ º¸ÀÌÁö¸¸,

ant. infarctÀÇ 1/4¿¡¼­´Â sympathetic n. system hyperactivity°¡ ³ªÅ¸³ª°í

(tachycardia and/or hypertnesion)

inf. infarctÀÇ 1/2¿¡¼­´Â parasympathetic n. system hyperactivity°¡ ³ªÅ¸³­´Ù.

(bradycardia and/or hypotension)

*other physical signs of ventridular dysfunction

S4, S3

paradoxical splitting of S2

(midsystolic or late systolic) transiant apical systolic murmur

pericardial friction rub : transmural AMIȯÀÚ¿¡¼­

JV distention with clear lung field: RV infarction

38¡É±îÁöÀÇ ¹Ì¿­Àº °üÂû°¡´ÉÇϳª 38¡ÉÀ϶© ´Ù¸¥ ¿øÀÎÀ» ã¾Æ¾ß ÇÑ´Ù.

arterial pr.´Â ´Ù¾çÇÏ´Ù: tranmural infarctionÀÇ ¸¹Àº ȯÀÚ¿¡¼­ systolic BP´Â Àüº¸´Ù

10--15mmHg±îÁö ¶³¾îÁø´Ù.

4. Lab

MIÁø»ý¼ø¼­ acute stage(¼ö½Ã°£-7ÀÏ)

healing stage(7-28ÀÏ)

healed stage(29ÀÏ- )

È®ÁøÀ» À§ÇÑ lab test·Î ´ÙÀ½ÀÇ 4 groupsÀ» µé¼ö ÀÖ´Ù.

1) ECG 2) Serum cardiac markers 3) Cardiac imaging

4) nonspecific indexes of tissue necrosis & inflammation

1) ECG

ST segment elevation : ´ëºÎºÐ Q wave(+), ¼Ò¼ö¿¡¼­ non-Q wave MI

non-ST segment elevation MI(NSTEMI) : ´ëºÎºÐ non-Q wave MI, ¼Ò¼ö¿¡¼­ QMI

acute coronary syndromeÀÇ spectrum

: unstable angina - non-Q MI - Q-MI

2) Serum cardiac markers

¨ç CK : 4-8½Ã°£ ³»¿¡ »ó½ÂÇÏ¿© 48-72½Ã°£±îÁö Á¤»óÈ­µÈ´Ù.

IM injectionÈÄ¿¡µµ 2-3¹è Áõ°¡Çϸç, AMI¿¡ ´ëÇØ ƯÀ̵µ°¡ ³·´Ù.

* other origins

i) skeletal muscular disease(muscular dystrophy, myopathy, polymyositis)

ii) electrical cardioversion

iii) hypothyroidism

iv) stroke

v) surgery

vi) skeletal muscle damage : trauma, convulsion, prolonged immobilization

* CK-MB isoenzyme : more specific but cardiac surgery, myocarditis,

electrical cardioversion½Ã¿¡µµ Áõ°¡ÇÔ.

CKMB2/CKMB1 > 1.5 => highly sensitive for the diagnosis of AMI

¨è Cardiac-specific troponin T(cTnT) & cTnI

°Ç°­Àο¡¼­´Â Áõ°¡ÇÏÁö ¾Ê°í, AMIȯÀÚ¿¡¼­´Â 20¹èÀÌ»ó Áõ°¡ÇÑ´Ù.

»ó´çÇÑ Áø´ÜÀû À¯¿ë¼ºÀÌ ÀÖÀ¸¸ç ÇöÀç MIÁø´ÜÀ» À§ÇÑ biochemical marker·Î ¼±È£µÈ´Ù.

CK & CKMB°¡ Á¤»ó¼öÄ¡¸¦ º¸À̳ª skeletal m. injury³ª small MI¸¦ ÀǽÉÇÒ ¶§ ƯÈ÷ À¯¿ë

ÇÏ´Ù.

cTnI´Â 7-10Àϰ£ Áõ°¡ÇØ ÀÖÀ¸¸ç, cTnT´Â 10-14Àϰ£ Áõ°¡ÇØ ÀÖ´Ù.

MI¸¦ ÀǽÉÇϴ ȯÀÚ¿¡¼­ sx onsetÈÄ 24-48½Ã°£ÀÌ»ó Áö³µÀ» ¶§ LDH & isoenzyme¸¦ ´ë½Å

ÇÏ¿© »ç¿ëÇÑ´Ù.

¨é myoglobin

AMI onsetÈÄ ¼ö½Ã°£³»¿¡ Ç÷ÁßÀ¸·Î À¯¸®µÈ´Ù.

1st serum cardiac markerÁß ÇϳªÁö¸¸ ƯÀ̵µ°¡ ¾ø°í, ºü¸£°Ô ¼Òº¯À¸·Î ¹è¼³µÇ¹Ç·Î 24

½Ã°£³»¿¡ Á¤»ó¼öÄ¡°¡ µÈ´Ù.

- À¯¸®µÈ protein ÃÑ·®Àº infarct size¿Í »ó°ü°ü°è°¡ ÀÖÀ¸³ª peak protein concentrationÀº

infarct size¿Í »ó°ü°ü°è°¡ ¾àÇÏ´Ù.

- Á¶±â¿¡ coronary a. recanalizationÇϸé serum cardiac marker´Â Á¶±â¿¡ ´õ ³ôÀº peak¸¦

º¸ÀδÙ.

(´ë·« reperfusionÈÄ 8-12½Ã°£)

- CK & CKMB levelÀº unstable angina¿¡¼± Áõ°¡ÇÏÁö ¾ÊÀ¸³ª unstable angina¶ó°í »ý°¢µÇ´Â

ȯÀÚ ÀÇ 1/3ÀÌ CK or CKMBÁõ°¡°¡ ¾øÀÌ cTnT or cTnIÀÇ Áõ°¡¸¦ º¸À̴µ¥ ÀÌ´Â

microinfarctionÀÌ Á¸ÀçÇÔÀ» ÀǹÌÇÑ´Ù.

- ºñ·Ï CK & CKMB¼öÄ¡°¡ Á¤»óÀÌÁö¸¸ cardiac-specific troponin levelÀÇ Áõ°¡´Â adverse

progosis¸¦ ³ªÅ¸³½´Ù. ±×·± ȯÀÚ´Â sustained MI¸¦ °¡Áú°ÍÀ¸·Î »ý°¢ÇØ¾ß ÇÏ¸ç ´ÙÀ½°ú °°ÀÌ

manageÇØ¾ß ÇÑ´Ù.

: MIÁø´Ü¸ñÀûÀ¸·Î serum cardiac marker¸¦ ÀÔ¿ø½Ã, ÀÔ¿øÈÄ 6-9½Ã°£, 12-24½Ã°£¿¡ ÃøÁ¤ÇÑ´Ù.

¨ê nonspecific reaction

i) polymorphonuclear leukocytosis

¼ö½Ã°£³» ¹ß»ýÇÏ¿© 3-7Àϰ£ Áö¼Ó

12,000-15,000 /mL

ii) ESR : WBCº¸´Ù õõÈ÷ »ó½ÂÇÏ¿© ùÁÖ¿¡ peak¿¡ µµ´Þ, ±×ÈÄ 1-2ÁÖµ¿¾È »ó½ÂÇØ ÀÖ´Ù.

3) Cardiac imaging

¨ç 2D-echo : most frequently employed imaging modality

- AMI¿¡¼­´Â wall motion abnormality°¡ °ÅÀÇ Ç×»ó Á¸ÀçÇϸç

ST segment elevationÀÌ ¾ø´õ¶óµµ wall motion abnormality¸¦ °üÂûÇÒ¼ö ÀÖ´Ù.

- old myocardial scar¿Í acute severe ischemia´Â ±¸º°ÇÒ¼ö ¾øÁö¸¸ ¾ÈÀüÇÏ°í °Ë»ç°¡

½¬¿ì¹Ç·Î screening tool·Î´Â À¯¿ëÇÏ´Ù.


- ÀÀ±Þ½Ç¿¡¼­ Á¶±â¿¡ wall motion abnormalityÀÇ Á¸ÀçÀ¯¹«¸¦ ÆÄ¾ÇÇϸé Ä¡·á°áÁ¤

(¿¹, thrombolysis or PCI)¿¡ Å« µµ¿òÀÌ µÈ´Ù.

- LV function ÃøÁ¤ÀÌ °¡´ÉÇÏ¸ç ¿¹ÈÄ ÆÇÁ¤¿¡ Áß¿äÇÏ´Ù.

; LV functionÀúÇÏ -> ACE inhibitor »ç¿ëÀÇ ÀûÀÀÀÌ µÊ.

- RV infarction, ventricular aneurysm, pericardial effusion, LV thrombusÈ®Àεµ °¡´ÉÇÏ´Ù.

- Doppler Echo : VSD & MRÀ» ¹ß°ßÇϰí Á¤·®È­Çϴµ¥ À¯¿ëÇÏ´Ù.

¨è Radionuclide imaging technique

°Ë»ç°¡ ¹ø°Å·Ó°í, ÀÓ»ó¿¡¼­ ¹Î°¨µµ, ƯÀ̵µ°¡ ¶³¾îÁö¹Ç·Î Echoº¸´Ù ´ú »ç¿ëµÈ´Ù.

i) 201Tl or 99mTc-sestamibi¸¦ ÀÌ¿ëÇÑ myocardial perfusion imaging

-> myocardial blood flow¿¡ ºñ·ÊÇÏ¿© ºÐÆ÷µÇ°í, viable myocardium¿¡ ³óÃàµÇ¾î

defect¸¦ ³ªÅ¸³½´Ù("cold spot"): transmural infarct¹ß»ýÈÄ Ã¹ ¼ö½Ã°£µ¿¾È ´ëºÎºÐÀÇ È¯ÀÚ

¿¡¼­.

±×·¯³ª perfusion scanningÀÌ ¾ÆÁÖ ¹Î°¨ÇÒÁö¶óµµ acute infarct°ú chronic scar¸¦ ±¸º°ÇÒ

¼ö´Â ¾øÀ¸¹Ç·Î acute MIÁø´Ü¿¡ ƯÀÌÇÏÁö´Â ¾Ê´Ù.

ii) 99mTc-labeled RBC¸¦ ÀÌ¿ëÇÑ RI ventriculography

wall motion disorder, ventricular EF°¨¼Ò¸¦ º¼¼ö ÀÖ´Ù.

RV EFÀÌ °¨¼ÒÇÒ ¶§ RV infarctionÁø´Ü¿¡µµ µµ¿òÀÌ µÇÁö¸¸ MIÀÌ¿ÜÀÇ ´Ù¸¥ ¸¹Àº cardiac

abnormality°¡ RI ventriculogramÀ» º¯È­½ÃŰ¹Ç·Î ¿ª½Ã ºñƯÀÌÀûÀÌ´Ù.

5. Ä¡·á

1) Prehospital care

AMI ¿¹ÈÄ¿Í °ü·ÃÇÑ ÀϹÝÀûÀÎ 2°¡Áö complicationÀº

i) electrical complication(arrhythmia)

ii) mechanical problems(pump failure)

´ëºÎºÐÀÇ ¿ø¿Ü»ç¸ÁÀº °©ÀÛ½º·´°Ô ¹ß»ýÇÑ VF ¶§¹®ÀÌ´Ù.

´ëºÎºÐ ù 24½Ã°£³»¿¡ ¹ß»ýÇϰí, ±×Áß ¹ÝÀº ù 1½Ã°£³»¿¡ ÀϾ´Ù.

prehospital careÀÇ °¡Àå Áß¿äÇÑ ¿ä¼Ò´Â

i) ȯÀÚ°¡ ÀÚ½ÅÀÇ Áõ»óÀ» ÀÎÁöÇϰí, Áï°¢ ÀÇ·áÁøÀ» ã´Â °Í

ii) defibrillation°ú °°Àº ¼Ò»ý¼úÀ» ½ÃÇàÇÒ¼ö ÀÖ´Â ÀÇ·áÁøÀÇ Ã⵿

iii) ȯÀÚ¸¦ º´¿øÀ¸·Î »¡¸® ÈļÛ

iv) reperfusion tx¸¦ »¡¸® ½ÃÇàÇÏ´Â °ÍÀÌ´Ù.

°¡Àå Å« Áö¿¬Àº º´¿ø±îÁöÀÇ ÈļÛÀÌ ¾Æ´Ï¶ó ȯÀÚ°¡ µµ¿òÀ» ¿äûÇϱâ±îÁö °áÁ¤ÀÇ Áö¿¬ÀÌ´Ù.

ÀÌ·± Áö¿¬Àº º¸°ÇÀü¹®°¡°¡ °øÁßÀÇ ±³À°À» ÅëÇØ °¨¼Ò½Ãų¼ö ÀÖ´Ù.

2) ER¿¡¼­ÀÇ initial management

¨ç ÀÀ±Þ½Ç¿¡¼­ AMI·Î ÀǽɵǴ ȯÀÚ¸¦ Ä¡·áÇÒ¶§ÀÇ ¸ñÇ¥´Â

i) cardiac pain control

ii) urgent thrombolytic tx´ë»óÀÌ µÇ´ÂÁö »¡¸® ÀÎÁö

iii) lower-risk pt¸¦ ¼±Á¤ÇÏ¿© º´¿øÀÇ ÀûÀýÇÑ °÷À¸·Î ¹èÄ¡

iv) ºÎÀûÀýÇÑ Åð¿øÀÇ ¹æÁöÀÌ´Ù.

¨è Aspirin : ÀÀ±Þ½Ç¿¡¼­ ÇʼöÀûÀÎ Ä¡·á·Î 165-325mgÀ» Åõ¿©ÇÑ´Ù.

¨é Oxygen : LV failure & intrinsic pul disease·Î ventilation-perfusion abnormality°¡

»ý±æ¼ö ÀÖ°í ÀÌ·Î ÀÎÇØ 2Â÷ÀûÀ¸·Î hypoxemia°¡ »ý±æ¼ö ÀÖÀ¸¹Ç·Î routineÀ¸·Î »ê¼Ò¸¦

Åõ¿©ÇØ ¿Ô´Ù. SaO2°¡ Á¤»óÀΠȯÀÚ¿¡¼­ »ê¼Ò°ø±ÞÀº ÀÓ»óÀû À̵æÀÌ Á¦ÇѵǹǷΠcost

effectiveÇÏÁö ¾Ê´Ù. ±×·¯³ª hypoxemia°¡ ÀÖÀ»¶§´Â »ê¼Ò¸¦ Åõ¿©ÇÑ´Ù.

: nasal prongs or fase mak(2-4 L/min ¡¿ 6-12hr after infarction)

3) Pain control

¨ç Morphine : very effective analgesics

i) sympathetically medated arteriolar & venous constriction¡é

-> venous pooling -> C.O¡é, arterial pressure¡é

: venous pooling°ú °ü·ÃÇÑ hypotensionÀº leg elevationÀ¸·Î ¹Ù·Î ±³Á¤µÇÁö¸¸ ÀϺÎȯÀÚ

´Â IV salineÀ¸·Î volume expansionÀÌ ÇÊ¿äÇÒ¼ö ÀÖ´Ù.

ii) vagotonic effect -> bradycardia & advanced degree of heart block

ƯÈ÷, posteroinferior infarctionȯÀÚ¿¡¼­ Àß »ý±â¸ç, atropine(0.5mg IV)¿¡ Àß ¹ÝÀÀÇÑ´Ù.

morphine ¼Ò·®À» 5ºÐ°£°ÝÀ¸·Î ¹Ýº¹ÀûÀ¸·Î IVÇÏ´Â °ÍÀÌ °ú·® SCÇϴ°ͺ¸´Ù ³ªÀºµ¥ SC´Â

¼öÁ¤µµ¸¦ ¿¹ÃøÇÒ¼ö ¾ø±â ¶§¹®ÀÌ´Ù.

¨è Nitroglycerine : morphineÅõ¿©Àü NTG SLÅõ¿©ÇÒ¼ö ÀÖ´Ù.

0.4mgÀ» 5ºÐ°£°ÝÀ¸·Î ¼¼ ¹ø Åõ¿©ÇÑ´Ù.

chest discomfort°¨¼Ò¿Ü¿¡ NTG´Â myocardial oxygen demand¸¦ °¨¼Ò½Ã۰í(by

lowering preload) myocardial oxygen supply¸¦ Áõ°¡½ÃŲ´Ù(by dilating infarct-related

coronary vs or collateral vs).

óÀ½¿£ Àß ¹ÝÀÀÇÏ¿´´Ù°¡ chest painÀÌ ´Ù½Ã ³ªÅ¸³ª¸é IV nitroglycerinÀ» Åõ¿©ÇÏ¿©¾ß ÇÑ´Ù.

* ±Ý±â i) low systolic pressure(<100mmHg)

ii) RV infarctionÀǽÉ(EKG»ó inf. infarction, JVP¡è, clear lung & hypotension)

iii) phosphodiesterase 5 inhibitor sildenafilÀ» Åõ¿©¹Þ°í Àִ ȯÀÚ)

¨é IV ¥â-blockers : pain control¿¡ À¯¿ë, in-hospital mortality°¨¼Ò,

metoprolol 5mg IV q 2-5min(total 3ȸ)

HR >60ȸ, SBP>100mg, PR interval < 0.24sec

diaphragm 10cm À̻󿡼­ raleÀÌ µé¸®Áö ¾ÊÀ» ¶§ »ç¿ë°¡´É

¸¶Áö¸· IV 15ºÐÈÄ oral regimenÀ» ½ÃÀÛ : 50mg q 6hr ¡¿ 48hr -> 100mg q 12hr

¨ê Ca antagonist ; little value

short-acting dihidropyridineÀº »ç¸ÁÀ§ÇèÀ» Áõ°¡½ÃŰ´Â °ÍÀ¸·Î ÀÔÁõµÇ¾ú´Ù.

4) Management strategies(Fig 243-2, 243-3)

¿¬¼Ó 2°³ ÀÌ»óÀÇ lead¿¡¼­ ST elevationÀ» º¸ÀÏ ¶§ reperfusiont txÀÇ ´ë»óÀÌ µÈ´Ù.

(V1-3´Â 2mmÀÌ»ó, ´Ù¸¥ lead¿¡¼± 1mm)

ST segment elevationÀÌ ¾øÀ»¶§´Â pharmacotherapy

: cardiac pain control, aspirin, antithrombin tx(LMWH), NTG infusion

high risk pt : glycoprotein IIb/IIIa inhibitor IV infusion°í·Á

5) Limitation of infarct size

glucocorticoid & NSAID´Â AMI¿¡¼­ »ç¿ëÇÏ¸é ¾ÈµÈ´Ù.

¡ñ i) infarct healing¿¡ Àå¾Ö¸¦ ÃÊ·¡ÇÏ¿© myocardial ruptureÀ§ÇèÀÌ Áõ°¡Çϸç

larger infarct scar¸¦ ³²±è.

ii) coronary vascular resistance¡è

-> ischemic myocardiumÀ¸·ÎÀÇ flow¡é

6) Thrombolysis

- FDA °øÀξ๰ : tPA, streptokinase, APSAC(Anisoylated plasminogen streptokinase

activator complex). reteplase(rPA)

¸ðµÎ´Ù plasmingen -> plasminÀ¸·Î ÀüȯÀ» ÃËÁø½ÃÄÑ fibrin thrombi¸¦ ³ìÀÓ

fibrin-specific agent : tPA

non-fibrin-specific agent : streptokinase, urokinase, ASPAC, reteplase(rPA)

- ÁÖ¸ñÀûÀº Áï°¢ÀûÀÎ coronary a. patency¸¦ ȸº¹ÇÏ´Â °Í.

- thrombolysisÈÄ coronary a. flow¸¦ angiographically assess = TIMI grading

grade 0 : complete occlusion

grade 1 : some penetration without distal coronary a. bed perfusion

grade 2 : distal bed±îÁö perfusionµÇ³ª delayed flow

grade 3 : full perfusion

- Ãʱ⿣ patency category¿¡ grade 2,3¸¦ À̾߱âÇÏ¿´À¸³ª ÇöÀç´Â reperfusion txÀÇ ¸ñÇ¥´Â

grade 3ÀÌ´Ù. ¿Ö³ÄÇϸé, infarct-related coronary a.ÀÇ full perfusionÀÌ

i) infarct size°¨¼Ò

ii) LV functionÀ¯Áö

iii) both short & long-term mortality rate°¨¼Ò¿¡ À־ ÁÁÀº °á°ú¸¦ °¡Á®¿À±â ¶§¹®ÀÌ´Ù.

- AMI sx onset 1½Ã°£³»¿¡ thrombolytic tx¸¦ Çϸé in-hospital death risk¸¦ 50%±îÁö °¨¼Ò

½Ãų¼ö ÀÖÀ¸¸ç ÀÌ·¯ÇÑ µæÀº ÃÖ¼Ò 10³âÀÌ»ó Áö¼ÓÇÒ¼ö ÀÖ´Ù.

ÀûÀýÈ÷ »ç¿ëµÈ thrombolytic tx´Â ´ÙÀ½°ú °°Àº À̵æÀÌ ÀÖ´Ù.

i) infarct size°¨¼Ò

ii) LV dysfunctionÀ» ÃÖ¼ÒÈ­

iii) serious complication°¨¼Ò(septal rupture, cardiogenic shock, malignant ventricular

arrhthmia°°Àº)

- ºñ°¡¿ªÀûÀ¸·Î ¼Õ»óµÇ±â Àü¿¡ ½É±ÙÀ» ±¸ÇÒ¼ö ÀÖ´Â °¡Àå Áß¿äÇÑ ÀÎÀÚ´Â reperfusion tx

timingÀÌ´Ù.

1-3½Ã°£ ³» : most benefit

3-6½Ã°£ : benefit

12½Ã°£ ³» : some benefit -> ƯÈ÷ chest discomfort°¡ ¿©ÀüÇÏ°í »õ·Î¿î Q wave¾øÀÌ

ST segment elevationÀÌ °è¼ÓµÉ ¶§

- early tx°¡´É¼º ¿Ü¿¡ thrombolytic tx¸¦ ¿ì¼±ÇÏ´Â °ÍÀÌ ÁÁÀº clinical factors·Î´Â

: ant. wall injury, hemodynamically complicated infarction,

widespread ECG evidence of myocardial jeapardy

- late coronary reperfusionÈÄ¿¡µµ LV fx°³¼±, mortality rate°¡ °¨¼ÒµÉ¼Ò ÀÖ´Ù. ÀÌ´Â infarct

size°¡ °¨¼ÒµÇ±â ¶§¹®ÀÌ ¾Æ´Ï¶ó

i) infarct zoneÀÇ tissue healingÃËÁø

ii) infarct expansion¹æÁö

iii) collateral flow¡è

iv) myocardial contractile performanceÇâ»ó

v) electrical instability°æÇâ °¨¼Ò¿¡ ÀÇÇÑ °ÍÀÌ´Ù.

vi) ±×¿Ü, hibernating myocardium

* hibernating myocardium : poorly contractile myocardium in a zone that is supplied by

a stenotic infarct-related coronary a. with slow antegrade perfusion.

-> angioplastyÈÄ contraction Çâ»ó

- tPA°¡ streptokinaseº¸´Ù ´õ È¿°úÀûÀ̸ç ÇöÀç tPA recommendationÀº ´ÙÀ½°ú °°´Ù.

15mg bolus IV -> 50mg IV over the first 30min

-> 35mg IV over the next 60min

- New pharmacologic regimens

: IV glycoprotein IIb/IIIa inhibitor + thrombolytic agent °¨·®

- Contraindication

¨ç clear CIx i) cerebrovascular hemorrhage Hx(+)

ii) ÃÖ±Ù 1³â³» nonhemorrhagic stroke or other cerebrovascular event

iii) marked hypertension(systolic >180 mmHg and/or diastolic>110 mmHg)

iv) suspicious of aortic dissection

v) active internal bleeding(excluding menses)

¨è relative CIx : µæ½Ç °í·Á

i) current use of anticoagulant(INR ¡Ã2)

ii) recent(<2wk) invasive or surgical procedure

iii) prolonged(>10min) CPR

iv) known bleeding diathesis

v) pregnancy

vi) hemorrhagic ophthalmic condition(hemorrhagic diabetic retinopathy)

vii) active peptic ulcer disease

viii) severe hypertension Hx(+), currently adequately controlled

- Complication

Hemorrage - most frequent & serious

hemorrhagic stroke : most serious Cx(0.5-0.9%)

³ªÀ̰¡ ¸¹À»¼ö·Ï ºóµµ°¡ Áõ°¡Çϸç 70¼¼ ÀÌ»óÀº ´ë·« 2¹èÁ¤µµ.

- thrombolysisÈÄ routine angiography´Â ÃßõµÇÁö ¾Ê´Â´Ù. thrombolytic txÈÄ cardiac cath &

coronary angiography°¡ ÇÊ¿äÇÑ °æ¿ì

i) reperfusion failure(persistent chest pain & ST segment elevation beyond 90 min)

-> rescue PCI°í·Á

ii) coronary a. reocclusion(ST segment reelevation and/or recurrent chest pain)

iii) the development of recurrent ischemia(recurrent angina in the early hospital

course or a positive exercise stress test before discharge)

-> elective PCI°í·Á

7) Primary PCI

thrombolytic tx¿¡ CIxÀÌ ÀÖÁö¸¸ reperfusionÀ» ½ÃÇàÇØ¾ß ÇÒ ¶§ PCI ½ÃÇà

°æÇèÀÖ´Â operator°¡ ½ÃÇàÇÒ ¶§´Â ´õ È¿°úÀûÀϼöµµ ÀÖÁö¸¸ ºñ¿ëÀÌ ºñ½Î°í,

½Ã¼³, Àåºñ¹®Á¦·Î ¼Ò¼öº´¿ø¿¡¼­¸¸ ½ÃÇà°¡´ÉÇÏ´Ù.

6. Hospital phase management

1) CCU - continuous monitoring

* stay±â°£

AMI°¡ ¹èÁ¦µÇ°í(8-12½Ã°£³») oral tx·Î Áõ»óÀÌ Á¶ÀýµÇ¸é CCU¹ÛÀ¸·Î transfer°¡´É

AMI·Î Áø´ÜµÇ¾úÀ¸³ª low riskÀÎ °æ¿ì 24-36½Ã°£¸¸¿¡ CCU¹ÛÀ¸·Î transfer°¡´É

¨ç Anxiety : ½ÉÀåÀÇ ÀÏÀ» Áõ°¡½Ã۸é infact size°¡ Ä¿Áú¼ö ÀÖÀ¸¹Ç·Î ù 12½Ã°£Àº

bed restÇϵµ·Ï ÇÑ´Ù. ´Ù¸¥ ÇÕº´ÁõÀÌ ¾ø´Ù¸é ù 24½Ã°£³»¿¡ chair sitting

°¡´ÉÇÏ´Ù.

ÀúÇ÷¾Ð ¹× ´Ù¸¥ ÇÕº´ÁõÀÌ ¾ø´Ù¸é 2-3Àϰ room ambulation°¡´ÉÇÏ´Ù.

3-4Àϰ ambulationÀ» Áõ°¡½ÃÄÑ ÇÏ·ç ¼¼ ¹ø 600ft±îÁö ´Ã¸±¼ö ÀÖ´Ù.

¨è Diet : emesis & aspiration risk·Î ÀÎÇÏ¿© ù 4-12½Ã°£Àº ±Ý½Ä ³»Áö´Â clear liquid¸¸

ÁÖµµ·Ï ÇÑ´Ù.

typical CCU¿¡¼­´Â fat - total calorieÀÇ 30%¹Ì¸¸(cholesterol content¡Â300 mg/d)

complex carbohydrate : 50-55% of total cal

NaÁ¦ÇÑ

DM & hypertriglyceridemia : concentrated sweatÁ¦ÇÑ

¨é Bowels : bed rest & narcotics·Î ÀÎÇÏ¿© º¯ºñ°¡ À¯¹ßµÈ´Ù.

bulking diet & routine stool softener°¡ ÃßõµÈ´Ù(dioctyl sodium sulfosuccinate 200

mg/d)

°è¼Ó º¯ºñ°¡ ÀÖÀ¸¸é laxative»ç¿ë

¨ê sedation : ¸¹Àº ȯÀÚ¿¡¼­ sedationÇÊ¿ä

diazepam(5mg), oxazepam(15-30mg), lorazepam(0.5-2mg) ÇÏ·ç 3-4ȸ

CCU¿¡¼­ »ç¿ëÇÏ´Â ¸¹Àº ¾à(atropine, H2 blocker, narcotics)ÀÌ deliriumÀ» À¯¹ß(ƯÈ÷ ³ëÀÎ

¿¡¼­)

À̰ÍÀ» agitationÀ¸·Î È¥µ¿Çؼ­´Â ¾ÈµÇ¸ç anxiolytics¸¦ »ç¿ëÇϱâ Àü¿¡ ȯÀÚÀÇ medication

À» Àß »ìÆìº¸¾Æ¾ß ÇÑ´Ù.

7. Pharmacotherapy

1) Antithrombotic agents

1Â÷Àû ¸ñÇ¥´Â infarct-related a.ÀÇ patency¸¦ À¯ÁöÇÏ´Â °Í

2Â÷Àû ¸ñÇ¥´Â thrombosis°æÇâÀ» °¨¼Ò½ÃÄÑ mural thrombus formation or DVT·Î ÀÎÇÑ

pul. embolism°¡´É¼ºÀ» ÁÙÀÌ´Â °Í.

¨ç Aspirin : standard antiplatelet agent, »ç¸Á·üÀ» °¨¼Ò½ÃÅ´.

¨è glycoprotein IIb/IIIa receptor inhibitor

platelet-rich thrombi°¡ platelet-poor thrombiº¸´Ù thrombolytic agent¿¡ ´õ resistantÇϸç

¼º°øÀûÀÎ thrombolysisÈÄ reocclusion¿¡ ÀÖ¾î Ç÷¼ÒÆÇÀÌ Áß¿äÇÑ ¿ªÇÒÀ» ÇϹǷÎ

glycoprotein IIa/IIIa receptor¸¦ inhibition½Ã۸é thrombolysis¸¦ ÃËÁøÇϰí reperfused vsÀÇ

reocclusion rate¸¦ °¨¼Ò½ÃŲ´Ù.

ÀÌ ¾àÀº PCI(percutaneous coronary intervention)À» ½ÃÇàÇÑ AMIȯÀÚ¿¡¼­ thrombotic cx

À» ¿¹¹æÇϴµ¥ À¯¿ëÇÏ¸ç »ç¸Á·üÀ» °¨¼Ò½Ã۰í, ¹ßÇö´ç½Ã ST segment elevationÀÌ ¾ø´ø

ȯÀÚ¿¡¼­ recurrent AMIºóµµ¸¦ °¨¼Ò½ÃŲ´Ù.

¨é Heparin

i) UFH(unfractionated heparin)

È®½ÇÈ÷ Áõ¸íµÇÁö´Â ¾Ê¾ÒÀ¸³ª aspirin°ú tPA¸¦ ÇÔ²² Åõ¿©ÇÏ¿©

thrombolysis¸¦ ÃËÁøÇϰí infarct-related a. patency¸¦ À¯ÁöÇÑ´Ù.

aPTT¸¦ control valueÀÇ 1.5-2.0¹è À¯ÁöÅä·Ï ÇÑ´Ù.

ii) LMWH(Low-molecular weight heparin)

more stable anticoagulant effect

bioavailability¡è ¡Å SCÅõ¿©°¡´É

stable anticoagulant effect¶§¹®¿¡ hematologic test monitoring(aPTT°°Àº)À» ÇÒ Çʿ䰡

¾ø´Ù.

Á¾·ù> nadroparin & dalteparin(fragmin) - UFH¿Í À¯»ç

enoxaparin(clexane)(1mg/kg Sc q 12hr) - ST elevation¾ø´Â AMIȯÀÚ¿¡¼­

mortality rate°¨¼Ò ¹× cardiac ischemic event°¨¼Ò¿¡ ÀÖ¾î UFHº¸´Ù ³´´Ù.

¨ê Warfarin

´ë»ó : ant. infarction, severe LV dysfunction, CHF, embolism Hx(+),

mural thrombus(+), AF

ÀÌ·± ȯÀÚµéÀº systemic or pul. thromboembolismÀ§ÇèÀÌ ³ô¾Æ

ÀÔ¿ø±â°£Áß full therapeutic levelÀÇ antithrombic tx(UFH or LMWH)¸¦ ¹Þ°í

±×ÈÄ ÃÖ¼Ò 3°³¿ù ÀÌ»ó warfarin tx¸¦ ÇØ¾ß ÇÑ´Ù.

2) ¥â-blockers

acute IV ¥â-blocker : myocardial oxygen supply-demand relationshipÀ» °³¼±ÇÏ¿©

ÅëÁõ°ú infarct size, serious ventricular arrhythmia ºóµµ¸¦ °¨¼Ò½ÃŲ´Ù.

: mortality, nonfatal reinfarction, nonfatal cardiac arrest¸¦ °¨¼Ò½ÃŲ´Ù(15%).

chest pain onsetÈÄ Áï½Ã thrombolysis¸¦ ½ÃÇàÇÑ È¯ÀÚ¿¡¼­´Â mortality rate°¨¼Ò°¡ ¾øÁö¸¸

recurrent ischemia & reinfarctionÀ» °¨¼Ò½ÃŲ´Ù.

AMIÈÄ ¥â-blocker´Â ÀϺΠ±Ý±âȯÀÚ¸¦ Á¦¿ÜÇϰí´Â ´ëºÎºÐ À¯¿ëÇÏ´Ù.

* CIx : heart failure or severely compromised LV fx

heart block, orthostatic hypotension, asthma Hx(+)

°á·Ð : cardiovascular mortality & reinfarction rate¡é

long-term survival¡è

3) ACE inhibitor - AMIÈÄ mortality°¨¼Ò

aspirin & ¥â-blocker¿Í ÇÔ²² mortality benefitÀÌ ÀÖ´Ù.

³ëÀÎ or ant. infarction, prior infarction and/or globally depressed LV fx°ú °°Àº high risk

pt¿¡¼­ ÃÖ´ëÀ̵æÀÌ ÀÖÁö¸¸ hemodynamically stable pt(SBP>100 mmHg)¸ðµÎ¿¡¼­µµ

short-term benefitÀÌ ÀÖ´Ù.

recurrent infarction rate¶ÇÇÑ °¨¼Ò½ÃŲ´Ù.

AMI ¸ðµç ȯÀÚ & overt CHF¿¡¼­ 24½Ã°£³»¿¡ Åõ¿©Çϰí Åð¿øÀü¿¡ LV functionÀ» Æò°¡ÇÏ¿©

clinically evident CHF, global LV dysfunction, large RWMA or hypertensive pt¿¡¼­´Â

°è¼Ó »ç¿ëÇÏ¿©¾ß ÇÑ´Ù.

4) other agents

¨ç nitrates(IV or oral) pain relief¿¡ À¯¿ë

ischemic process & ventricular remodeling¿¡ favorable effect

¸¹Àº ÀÇ»çµéÀÌ infarction onset 24-48½Ã°£µ¿¾È IV nitroglycerinÀ» routineÀ¸·Î »ç¿ëÇÑ´Ù.

¨è Ca antagonist : routineÀ¸·Î »ç¿ëÇÏ´Â °ÍÀº ÃßõµÇÁö ¾Ê´Â´Ù.

¨é BST control : DMȯÀÚ¿¡¼­ Ç÷´çÀ» ¾ö°ÝÈ÷ Á¶ÀýÇÏ¸é »ç¸Á·üÀ» °¨¼Ò½ÃŰ´Â °ÍÀ¸·Î ¾Ë·ÁÁ®

ÀÖ´Ù.

¨ê Mg : AMI¶§ intracellular Mg levelÀÌ ÈçÈ÷ °¨¼ÒµÈ´Ù.

ÀÔ¿ø´ç½Ã serum MgÀ» ÃøÁ¤ÇÏ¿© ºÎÁ·ÇÏ¸é ±³Á¤ÇØ¾ß ÇÑ´Ù(arrhythmiaÀ§ÇèÀ» ÃÖ¼ÒÈ­Çϱâ

À§ÇÏ¿©)

±×·¯³ª ´Ù¼Ò ½Ã°£ÀÌ Áö³­ÈÄ(>6hr) routineÀ¸·Î »ç¿ëÇÏ´Â °ÍÀº À̵æÀÌ ¾ø´Ù.

8. Complication & their treatment

1) Ventricular dysfunction

AMIÈÄ LV´Â ÀÏ·ÃÀÇ infarcted & noninfarcted segment¿¡¼­ shape, size & thickness°¡ º¯È­

ÇÏ´Â °úÁ¤À» °Þ´Â´Ù. ÀÌ °úÁ¤À» "ventricular remodeling"À̶ó ÇÏ¸ç °æ»öÈÄ ¼ö°³¿ù¿¡¼­ ¼ö³â

¿¡ °ÉÃÄ CHF ¹ß»ý¿¡ ¼±ÇàÇÑ´Ù.

acutely : infarct expansion¿¡ ÀÇÇØ(slippage of m. bundles, normal myocardial cell

disruption, necrotic zoneÀÇ tissue loss¿¡ ÀÇÇØ) -> disproportionate thinning &

infarct zone elongation

later : noninfarcted segment lengthening

overall chamber enlargment : infarct size & location°ú °ü·Ã

apex infarct¶§ ´õ È®ÀåµÇ¾î º¸´Ù ½ÉÇÑ hemodynamic impairment,

º¸´Ù ÈçÇÑ heart failure¸¦ ¾ß±âÇÑ´Ù.

ACE inhibitor & other vasodilator(nitrates) Ä¡·á·Î ÀÌ °úÁ¤À» °³¼±ÇÒ¼ö ÀÖ´Ù. µû¶ó¼­

EF<40%

ȯÀÚ´Â heart failureÀ¯¹«¿¡ »ó°ü¾øÀÌ ACE inhibitor¸¦ »ç¿ëÇØ¾ß ÇÑ´Ù.

(1) Hemodynamic assessmnet

* pump failure : AMI·Î ÀÎÇÑ ¿ø³»»ç¸ÁÀÇ 1Â÷Àû ¿øÀÎ

ischemic necrosisÁ¤µµ¿Í pump failure & mortality »çÀÌ¿¡ »ó°ü°ü°è°¡ ÀÖ´Ù.

mc clinical signs : pul rales & S3, S4 gallop rhythms

CXR : pul. congestion

characteristic hemodynamic findings

elevated LV filling pressure & elevated pul. a. pr

=> ventricular compliance°¨¼Ò·Î ¹ß»ý(diastolic failure)

and/or secondary cardiac dilatationÀ» µ¿¹ÝÇÏ´Â stroke volume°¨¼Ò·Î ¹ß»ý(systolic

failure)

* Killip classification - 4 groups (»ç¸Á·ü)

class I : no signs of pul. or venous congestion(0-5%)

class II : moderate heart failure - lung base rale, S3 gallop, tachypnea

or Rt side heart failure signs(venous & hepatic congestion) (10-20%)

class III : severe heart failure, pul. edema (35-45%)

class IV : shock with systolic pr<90 mmHg

peripheral vasoconstriction evidence(+)

peripheral cyanosis(+)

mental confusion, oliguria (85-95%)

Ä¡·á¸¦ Àû±ØÀûÀ¸·Î Çϸ鼭 »ç¸Á·üÀÌ 1/3-1/2Á¤µµ·Î °¨¼ÒÇÏ¿´´Ù.

LV contractionÀÇ 20-25%Á¤µµ ¼Õ»óµÉ¶§ abnormal LV functionÀÇ hemodynamic findingÀ»

°üÂûÇÒ¼ö ÀÖÀ¸¸ç 40%ÀÌ»óÀÇ infarction½Ã cardiogenic shockÀÌ »ý±ä´Ù.

LV filling pr¡è(>22 mmHg) & normal cardiac index(>2.6 & 3.6 L/min/m2) - diuresis tx

low LV filling pr(<15mmg) & C.O¡é - volume expansion(colloid) tx

(2) Hypovolemia

optimal LV filling or pul a. wedge pr´Â ȯÀÚ¸¶´Ù ´Ù¾çÇÏ´Ù.

°¢ ȯÀÚÀÇ ideal level(ÀϹÝÀûÀ¸·Î ¡­20mmHg)À» À¯ÁöÇϱâ À§ÇØ Á¶½É½º·´°Ô fluid¸¦ Åõ¿©

ÇÑ´Ù.

(3) Ä¡·á

AMI¿Í °ü·ÃÇÑ CHFÀÇ Ä¡·á´Â ´Ù¸¥ ¿øÀο¡ ÀÇÇÑ heart fallure¿Í µ¿ÀÏÇÏ´Ù.

: hypoxemiaÇÇÇÒ °Í, diuresis, afterload¡é, inotropic support

(´Ù¸¸ digitalisÈ¿°ú´Â unimpressive.)

Nitrates : preload¡é, congestive sx¡é, ventricular compliance°³¼±

ACEI : AMIÈÄ ventricular dysfunctionÄ¡·á¿¡ ÀÌ»óÀûÀÎ ¾àÀÌ´Ù. ƯÈ÷ long termÀ¸·Î ¾µ¶§.

2) Cardiogenic shock

ÃÖ±Ù infarct size¸¦ ÁÙÀÌ·Á´Â ³ë·Â°ú ongoing ischemia¸¦ Áï°¢ Ä¡·áÇÔÀ¸·Î½á cardiogenic

shockÀÇ ºóµµ°¡ 20%¿¡¼­ 7%·Î °¨¼ÒÇÏ¿´´Ù. cardiogenic shockÁß 10%¸¸ÀÌ ÀÔ¿ø´ç½Ã¿¡

°ÜÀÖ°í ³ª¸ÓÁö 90%´Â ÀÔ¿øÁß¿¡ ¹ß»ýÇÑ´Ù. ÀüÇüÀûÀ¸·Î cardiogenic shockÀÌ »ý±â´Â ȯÀÚ´Â

original infarct zone¿¡¼­ ¹ÛÀ¸·Î »¸¾î³ª°¡´Â "piecemeal" necrosis¸¦ º¸ÀÌ´Â severe

multivessel coronary a. disease¸¦ °¡Áö°í ÀÖ´Ù.

Cardiogenic shockÀº severe LV failureÀÇ ÇÑ ÇüÅ·Π»ý°¢ÇØ¾ß ÇÑ´Ù.

marked hypotension(SBP<80 mmHg)

cardiac index¡é(<1.8L/min/m2)

LV filling pressure(PCWP)¡è(>18mmHg)

hypovolemic hypotension°ú´Â ´Þ¸® cardiogenic shockÀº »ç¸Á·üÀÌ 70%ÀÌ»óÀÌ´Ù. ±×·¯³ª

ÃÖ±Ù angioplasy or surgical revascularizationÀ¸·Î perfusionÀ» ȸº¹ÇÏ·Á´Â ³ë·Â¿¡ ÈûÀÔ¾î

»ç¸Á·üÀ» ¹ÝÁ¤µµ·Î ³·Ãâ¼ö ÀÖ¾ú´Ù.

* Shock¹ß»ýÀÇ risk factors

i) advanced age

ii) depressed LVEF on admission

iii) large infarct

iv) previous MI

v) DM Hx(+)

¢¼Ä¡·á

pain relief- Áß¿ä

: pain -> vasodepressor reflex activity¸¦ À¯¹ß

±×·¯³ª narcotic´Â Á¶½É½º·´°Ô »ç¿ëÇØ¾ß ÇÑ´Ù(¡ñBP¸¦ ¶³¾î¶ß¸®¹Ç·Î)

Ä¡·áÀÇ ¸ñÇ¥´Â vasopressor, IABP, ÀûÁ¤ LV filling pr(¡­20mmHg)¸¦ À¯ÁöÇÒ¼ö ÀÖ´Â blood

volume manipulationÀ¸·Î arterial BP¸¦ ¿Ã¸²À¸·Î½á coronary perfusionÀ» À¯ÁöÇÏ´Â °ÍÀÌ

´Ù. ÈÄÀÚÀÇ °æ¿ì¿¡ À־´Â crystalloid infusion or diuresis°¡ ÇÊ¿äÇÏ´Ù.

¨ç Vasopressors

i) isoproterenol : sympathomimetic amineÀ¸·Î Áö±ÝÀº °ÅÀÇ »ç¿ëÇÏÁö ¾Ê´Â´Ù.

contractility¡è, peripheral vasodilation, HR¡è

=> »ê¼Ò¿ä±¸·®¡è, coronary perfusion pr¡é

ii) norepinephrine : potent ¥á-adrenergic agonist with powerful vasoconstrictor

properties

¥â-adrenergic activity -> contractility¡è

=> afterload¡è, contractility¡è => »ê¼Ò¿ä±¸·®¡è

iii) Dopamine : severe power failureÀÇ ¸¹Àº ȯÀÚ¿¡¼­ À¯¿ëÇÏ´Ù.

low dose(2-10 ug/kg/min) : ¥â receptorÀÚ±Ø -> positive chronotropic & inotropic

effect

high dose : ¥á receptor ÀÚ±Ø -> vasoconstrictor effect

lower dose(¡Â2 ug/kg/min) : renal & splanchnic vascular bedÈ®ÀåÈ¿°ú

myocardial oxygen consumption¿¡´Â °ÅÀÇ ¿µÇâ¡¿

¿ë¹ý> 2-5 ug/kg/min¿¡¼­ ½ÃÀÛÇÏ¿© ¸Å 2-5ºÐ¸¶´Ù Áõ°¡½ÃÄÑ ÃÖ´ë

20-50 ug/kg/min±îÁö.

systolic BP´Â ¡­90 mmHg·Î À¯ÁöÇØ¾ß ÇÑ´Ù.

iv) Dobutamine : synthetic sympathomimetic amine

positive inotropic action & minimal positive chronotropic or

peripheral vasoconstrictive activity(Åë»ó¿ë·® 2.5-10 ug/kg/min¿¡¼­)

vasoconstrictor effect°¡ ÇÊ¿äÇÒ¶© »ç¿ëÇÏÁö ¾Ê°í

positive chronotropy¸¦ ÇÇÇØ¾ß ÇÒ¶§´Â ¾ÆÁÖ À¯¿ëÇÏ´Ù.

v) Amrinone & milrinone : positive inotropic agent without catecholamine structure

or activity

cholinesterase inhibitor

dobutamine°ú À¯»çÇÑ ¾à¸®ÀÛ¿ë

¿ë¹ý> Amrinone : 0.75mg/kg loading(2-3ºÐ) -> 5-10 ug/kg/min(ÃÖ´ë 15 ug/kg/min)

Milrinone : 50 ug/kg loading(10ºÐÀÌ»ó) -> 0.375-0.75 ug/kg/min

¨è Aortic counterpulsation

IABP -> diastolic pr & CO µÑ´Ù ÁõÆø

early diastole¶§ ÀÚµ¿À¸·Î inflationµÇ¾î coronary blood flow¸¦ Áõ°¡½Ã۰í

early systole¶§ collapseµÇ¾î afterload¸¦ °¨¼Ò½ÃÅ´À¸·Î½á

hemodynamic status°¡ °³¼±µÈ´Ù.

early revascularization¾øÀÌ´Â long-term survivalÀ» ±â´ëÇÒ¼ö ¾øÀ¸¹Ç·Î

mechanical(surgical or angioplastic) intervention(¿¹, ischemiaÁö¼Ó, VSD or MR¿¡¼­)À»

½ÃÇàÇÑ È¯ÀÚ¿¡¼­ ¼º°øÀûÀ¸·Î IABP°¡ ½ÃÇàµÇ¾úÀ» ¶§ cardiogenic shockÀ» µÇµ¹¸±¼ö

ÀÖ´Ù.

*CIx : AR or aortic dissection

3) RV infarction

- inferoposterior infarctionȯÀÚÀÇ 1/3ÀÌ ÃÖ¼ÒÇÑ ¾à°£ÀÇ RV necrosis¸¦ µ¿¹ÝÇÑ´Ù.

- °£È¤ inferoposterior LV infarctionȯÀÚ°¡ extensive RV infarctionÀ» µ¿¹ÝÇϸç,

µå¹°°Ô´Â ÀÏÂ÷ÀûÀ¸·Î RV¿¡ ±¹ÇѵDZ⵵ ÇÑ´Ù.

- ÀÓ»óÀûÀ¸·Î Áß¿äÇÑ RV infarctionÀº ½ÉÇÑ RV failure signÀ» ³ªÅ¸³½´Ù.

: Jugular venous distention, Kussmaul's sign, hepatomegaly

c/s hypotension

- Rt-sided precordial ECGÀÇ ST elevation(ƯÈ÷ V4R)ÀÌ RV infarction ù 24½Ã°£³»¿¡

ÈçÈ÷ ³ªÅ¸³­´Ù.

- 2D echo°¡ RV dysfunctionÁ¤µµ¸¦ º¸´Âµ¥ µµ¿òÀÌ µÈ´Ù.

- Rt side heart catheterizationÀ» ½ÃÇàÇϸé cardiac tamponade or constrictive pericarditis

¿Í À¯»çÇÑ hemodynamic patternÀ» º¸ÀδÙ.

: steep RA "y" descent and an early diastolic dip & plateau in RV wave forms

- Ä¡·á : RV preload¸¦ À¯ÁöÇϱâ À§ÇØ volume expansion

& PCWP & pul. a. pressure¸¦ °¨¼Ò½ÃÅ´À¸·Î½á LV performance¸¦ °³¼±Çϱâ À§ÇÑ ³ë·Â

4) Mechanical causes of heart failure

(1) Free wall rupture : ù 1ÁÖ¿¡ Àß ¹ß»ý

* °íÀ§Ç豺 : 1st infarction, Hypertension Hx(+), no history of AP

relatively large Q-wave infarct

- ÀÓ»ó¹ßÇö : sudden loss of pulse, BP, consciousness

- ECG : sinus rhythm(EMD or pulseless electrical activity)

- ¿¹ÈÄ : °ÅÀÇ fatal

(2) VSD

- º´ÀÎÀº free wall rupture¿Í À¯»ç. ±×·¯³ª VSD´Â Ä¡·á°¡´É¼ºÀÌ ³ô´Ù.

- sudden, severe LV failure, pansystolic murmur(Á¾Á¾ parasternal thrillµ¿¹Ý)

- papillary m. rupture¿¡ ÀÇÇÑ MR°ú ±¸º°Çϱ⠺Ұ¡´ÉÇÏ´Ù.

- Áø´Ü : i) cardiac cath : Lt to Rt shunt·Î ÀÎÇÑ O2 step-up of the RV

ii) Color flow Doppler echo

=> ¿À·¡ Áö¼ÓµÇ¸é end-organ damage & other Cx¾ß±âÇϹǷÎ

early interventionÀÌ ÇÊ¿äÇÏ´Ù(Nitroprusside infusion & IABP)

- acute MRÀÇ º´Å»ý¸®´Â acute VSD¿Í À¯»çÇѵ¥ VSD¿¡¼± LV outputÀÇ ÀϺΰ¡ RV·Î

ºÐÃâµÇ°í MRó·³ mechanical(IABP) and/or pharmacologic means(nitroglycerin

or nitroprusside)À¸·Î aortic systolic pr¸¦ ³·ÃãÀ¸·Î½á perforation¿¡ ÀÇÇÑ hemodynamic

compromise¸¦ °¨¼Ò½Ãų¼ö ÀÖ´Ù.

(3) MR : ù ¸îÀϵ¿¾È¿¡ ¹ß»ý(10-50%)

- ±×·¯³ª acute hemodynamic compromise¸¦ ÀÏÀ¸Å°´Â °æ¿ì´Â ¼Ò¼öÀ̸ç, late CHF ¹×

»ýÁ¸·ü °¨¼ÒÀÇ À§ÇèÀÎÀÚ°¡ µÈ´Ù.

- ¿øÀÎ

i) ischemia & infarctionÀ¸·Î ÀÎÇÑ mitral valve dysfx(mc cause)

ii) LV size & shapeÀÇ º¯È­·Î ÀÎÇÑ LV dilatation

(¼öÃà·Â Àå¾Ö ȤÀº aneurysm formationÀ¸·Î ÀÎÇÑ)

-> papillary m. contractionÀå¾Ö ¹× MV leaflet coaptation failure

iii) papillary m. rupture(ÁÖ·Î head)(rare)

- IABP´Â aortic systolic pr¸¦ ±â°èÀûÀ¸·Î ³·Ãß°í nitroglycerin or sodium nitroprusside

infusionÀº systemic vascular resistance¸¦ °¨¼Ò½ÃÅ´À¸·Î½á AMIÀÇ severe MRȯÀÚÀÇ

Àӽà ġ·á¿¡ ¼º°øÀûÀ¸·Î ½ÃÇàÇÒ¼ö ÀÖ´Ù.

ÀÌ»óÀûÀ¸·Î´Â definite op tx¸¦ pul. congestionÀÌ ±ú²ýÇØÁö°í infarctÀÌ healingµÉ¶§±îÁö

¿¬±âÇØ¾ß ÇÑ´Ù.

±×·¯³ª ȯÀÚÀÇ hemodynamic and/or clinical conditionÀÌ È£ÀüµÇ°Å³ª ¾ÈÁ¤µÇÁö ¾ÊÀ¸¸é

acute stage¶§¶óµµ ¼ö¼úÀ» ½ÃÇàÇØ¾ß ÇÑ´Ù.

5) Arrhythmia

ºóµµ´Â Áõ»ó ¹ß»ýÈÄ Ãʱ⿡ ³ô´Ù.

Infarction-related arrhythmia¹ß»ý±âÀü

: autonomic nervous system imbalance, electrolyted disturbance, ischemia,

slowed conduction in zones of ischemic myocardium

´ëºÎºÐÀÇ »ç¸ÁÀº °æ»öÈÄ ¼ö½Ã°£³»¿¡ ¹ß»ýÇϹǷΠġ·áÀÇ È¿°ú´Â ȯÀÚ°¡ ¾ó¸¶³ª º´¿ø¿¡ »¡¸®

¿À´À³Ä¿Í Á÷Á¢ÀûÀ¸·Î »ó°üÀÖ´Ù.

(1) VPB

- infrequent, sporadic VPB : Ä¡·áÇÒ ÇÊ¿ä ¾ø´Ù.

- past, frequent, multifocal or early diastolic ventricular extrasystole(¼ÒÀ§ warning

arrhythmia)

: VT & VF risk¸¦ °¨¼Ò½Ã۱â À§ÇØ Ä¡·á°¡ ÇÊ¿äÇÏ´Ù.

- VPB¿¡¼­ prophylactic antiarrhythmic tx(lidocaine)´Â ±Ý±â ->»ç¸Á·üÀ» Áõ°¡½ÃŲ´Ù.

- ¥â-blocker : AMI¿¡¼­ ventricular ectopic activity¸¦ ¾ø¾Ö°í VF¸¦ ¿¹¹æÇϴµ¥ È¿°úÀûÀ̹ǷÎ

±Ý±â°¡ ¾ø´Ù¸é routineÀ¸·Î »ç¿ëÇØ¾ß ÇÑ´Ù.

- hypokalemia & hypomagnesemia°¡ VFÀÇ risk factorÀ̹ǷÎ

K>4.5 mmol/L, Mg>2.0 mmol/L¸¦ À¯ÁöÇØ¾ß ÇÑ´Ù.

(2) VT & VF

- ù 24½Ã°£³»¿¡ warning arrhythmia¾øÀÌ ¹ß»ýÇÒ¼ö ÀÖ´Ù.

- prophylactic lidocaineÅõ¿©·Î VF¹ß»ýÀ» °¨¼Ò½Ãų¼ö´Â ÀÖÀ¸³ª AMI·Î ÀÎÇÑ Àüü »ç¸Á·üÀ»

°¨¼Ò½ÃŰÁö´Â ¸øÇÑ´Ù. lidocaineÀº noncardiac cxÀ» ÀÏÀ¸Å°´Â ¿Ü¿¡ bradycardia &

asystoleÀÇ À§ÇèÀ» Áõ°¡½ÃŲ´Ù. ÀÌ·± ÀÌÀ¯·Î ÇØ¼­ active ischemiaÀÇ ÃʱâÄ¡·á¶§ routine

prophylactic antiarrhythmic drug tx´Â ´õ ÀÌ»ó ÃßõµÇÁö ¾Ê´Â´Ù.

- sustained VT¹ß»ý½Ã

hemodynamically stableÇÏ´Ù¸é: IV lidocaine, procainamide, amiodarone

-> IVÈÄ Áï½Ã ¾ø¾îÁöÁö ¾ÊÀ¸¸é electroversionÀ» ½ÃÇàÇØ¾ß ÇÑ´Ù.

VF ¹× hemodynamic deteriorationÀ» ÀÏÀ¸Å°´Â VT¿¡ ´ëÇØ¼­´Â

-> unsynchronized discharge(200-300J defibrillation)¸¦ Áï½Ã ½ÃÇàÇØ¾ß ÇÑ´Ù.

- electroshock¿¡ ¹ÝÀÀÇÏÁö ¾Ê´Â VT or VF´Â ´ÙÀ½°ú °°Àº ¾à¹°Ä¡·áÈÄ¿¡ ´õ Àß ¹ÝÀÀÇÒ¼ö

ÀÖ´Ù.

: epinephrine 1mg IV or 10 mL via intracardiac route

bretylium 5mg/kg bolus, amiodarone 75 - 150 mg bolus

- torsade de points°°Àº unusual VT°¡ AMIȯÀÚ¿¡¼­ ÀϾ ¼ö ÀÖ´Ù. À̶§´Â ´Ù¸¥ µ¿¹Ý¹®Á¦

(hypoxia, hypokalemia or other electrolyte disturbance µî)ÀÇ °á°ú·Î ÀϾ°Å³ª,

digoxin or quinidine°°Àº ¾àÁ¦ÀÇ toxic effect·Î ÀÎÇØ ¹ß»ýÇϹǷΠÀÌ·¯ÇÑ ¹®Á¦°¡ ¾ø´ÂÁö

Àß »ìÆìº¸¾Æ¾ß ÇÑ´Ù.

- primary VFÈÄ¿¡ in-hospital mortality´Â Áõ°¡ÇÏÁö¸¸ Åð¿ø½Ã »ýÁ¸ÇÑ È¯ÀÚ¿¡¼­ÀÇ long-term

survivalÀº ÁÁ´Ù.

* primary VF : acute ischemia¿¡ ´ëÇÑ primary response·Î¼­ÀÇ VF

Áï, CHF, shock, BBB or ventricular aneurysm°ú °°Àº ¼±ÇàÀÎÀÚ°¡ ¾ø´Â °æ¿ì

- severe pump failure·Î ÀÎÇØ 2Â÷ÀûÀ¸·Î ¹ß»ýÇÑ VF´Â ¿¹Èİ¡ ÁÁÁö ¾Ê´Ù.

- ÀÔ¿øÈÄ ´Ê°Ô(>48½Ã°£) VT or VF°¡ ¹ß»ýÇÑ È¯ÀÚ¿¡¼­ÀÇ »ç¸Á·üÀº in-hospital & long-term

follow-up µ¿¾È Áõ°¡ÇÑ´Ù. ±×·± ȯÀÚ´Â EPS¸¦ °í·ÁÇØ¾ß ÇÑ´Ù.

(3) AIVR(Accelerated idioventricular rhythm) = "slow ventricular tachycardia"

AMIÀÇ 25%¿¡¼­ ¹ß»ýÇϸç 60-100 ȸ/ºÐÀ¸·Î sinus rhythm°ú ºñ½ÁÇÑ rate¸¦ º¸ÀδÙ.

thrombolytic tx¶§ reperfusionµÇ´Â ½ÃÁ¡¿¡ ÀϽÃÀûÀ¸·Î ¹ß»ýÇÑ´Ù.

´ëºÎºÐ ¾ç¼ºÀ¸·Î classic VT·Î ÁøÇàÇÏÁö ¾Ê°í Àß °üÂûÇÏ¸é Æ¯º°ÇÑ Ä¡·á°¡ ÇÊ¿ä¾ø´Ù.

½ÉÇÑ ºÎÁ¤¸ÆÀ¸·ÎÀÇ ÁøÇàÀº µå¹°°í ¸¸¾à »ý±ä´Ù¸é sinus rate¸¦ ¿Ã¸®´Â ¾à(atropine)À¸·Î

½±°Ô Ä¡·áµÈ´Ù.

(4) Supraventricular arrhythmia

¨ç sinus tachycardia : most common

i) ´Ù¸¥ ¿øÀο¡ ÀÇÇØ 2Â÷ÀûÀ¸·Î ¹ß»ýÇß´Ù¸é ¿øÀÎÀ» ±³Á¤ÇÏ¿©¾ß ÇÑ´Ù.

¿¹> anemia, fever, heart failure or metabolic derangement

ii) sympathetic overstimulation¶§¹®À̶ó¸é ¥â-blocker·Î Ä¡·áÇÑ´Ù.

¨è Atrial flutter & fibrillation : LV failure¿¡ ÀÇÇØ 2Â÷ÀûÀ¸·Î ¹ß»ý

heart failure(+) : digoxinÀÌ drug of choice

heart failure(-) : ¥â-blocker, verapamil or diltiazemÀ¸·Î ventricular rateÁ¶Àý.

¨é 120ȸ/ºÐ ÀÌ»óÀÇ ºñÁ¤»ó¸®µëÀÌ 2½Ã°£ ÀÌ»ó Áö¼ÓÇϰųª, tachycardia°¡ heart failure,

shock or ischemia¸¦ À¯¹ßÇϸé synchronized electroshock(100-200J)À» ½ÃÇàÇØ¾ß

ÇÑ´Ù.

(5) Sinus bradycardia

ÀϹÝÀûÀ¸·Î Ä¡·á°¡ ÇÊ¿ä¾øÀ¸¸ç atropine»ç¿ë¿¡µµ ºÒ±¸Çϰí persistent bradycardia

(<40bpm)°¡ ÀÖ´Ù¸é electrical pacingÀÌ ÇÊ¿äÇÏ´Ù. IsoproterenolÀº ÇÇÇϵµ·Ï ÇÑ´Ù.

(6) Atrioventricular & Intraventricular conduction

complete AV blockȯÀÚ¿¡¼­ÀÇ in-hospital & post-discharge mortality rate´Â

ant. infarctionÀÌ inf. infarctionº¸´Ù ÈξÀ ³ô´Ù.

*ÀÌÀ¯

inf. infarction : vagal toneÁõ°¡ and/or adenosineÀ¯¸®·Î ÀÎÇØ ¹ß»ýÇϹǷΠÀϽÃÀûÀÌ´Ù.

ant. infarction : conduction systemÀÇ ischemic malfunction°ú °ü·ÃÀÖÀ¸¸ç ÈçÈ÷

extensive myocardial necrosis¿Í µ¿¹ÝµÈ´Ù.

ant. wall MIÀÇ complete AV block¶§ ¿¹ÈÄ¿Í °ü·ÃÈù ÁÖ ÀÎÀÚ´Â infarct sizeÀÌ´Ù.

inferopost. infarctȯÀÚ¿¡¼­ heart failure, hypotension, marked bradycardia, significant

ventricular ectopic activity¸¦ µ¿¹ÝÇÑ complete AV blockÀ» °¡Áú ¶§ pacingÀº À¯¿ëÇÏ´Ù.

ÀÌ·± ȯÀÚÁß ÀϺÎ(RV infarctionµ¿¹Ý)´Â ventricular pacing¿¡ Àß ¹ÝÀÀÇÏÁö ¾Ê´Âµ¥ ÀÌ´Â

ventricular filling¿¡ ±â¿©ÇÏ´Â atrial pacingÀÌ ¾ø±â ¶§¹®ÀÌ´Ù. ÀÌ·± ȯÀÚ¿¡¼­´Â

dual-chamber AV sequential pacingÀÌ ÇÊ¿äÇÏ´Ù.

6) Other complications

(1) Recurrent chest discomfort

recurrent angina(¡­25%)

successful thrombolysis¸¦ ½ÃÇàÇÑ È¯ÀÚ¿¡¼­ ´õ ³ô´Ù.

ÀÌ·± ȯÀÚµéÀº repeat thrombolysis or prompt CAG & mechanical revascularizationÀ»

°í·ÁÇØ¾ß ÇÑ´Ù.

(2) Pericarditis

pericardial friction rubs and/or pericardial pain : transmural AMIȯÀÚ¿¡¼­ ÈçÇÏ´Ù.

Ä¡·á: aspirin 650 mg qid

recurrent ischemic pain and/or infarct extensionÀ¸·Î ¿ÀÁøÇÏ¿© ºÎÀûÀýÇϰÔ

anticoagulant, nitrate, ¥â-blocker or CAG¸¦ ½ÃÇàÇÏ´Â °æ¿ì°¡ ÀÖÀ¸¹Ç·Î Á¤È®ÇÑ Áø´ÜÀÌ

ÇÊ¿äÇÏ´Ù.

anticoagulant´Â tamponade¸¦ À¯¹ßÇÒ¼ö ÀÖÀ¸¹Ç·Î ÀûÀýÇÑ IxÀÌ ¾ø´Ù¸é »ç¿ëÇÏÁö ¸»¾Æ¾ß

ÇÑ´Ù.

(3) thromboembolism

clinically apparent(¡­10%)

necropsyÀÇ 20% : often clincally silent

ÀÔ¿øÈÄ »ç¸ÁÀÇ 25%

arterial emboli : LV mural thrombi

pul. emboli : ´ëºÎºÐ leg vein¿¡¼­ ±â¿ø

large infarct(ƯÈ÷ ant), CHF & LV thrombus¿Í °ü·ÃÀÖ´Ù.

2D echo : LV thrombi(ant. infarctÀÇ 1/3¿¡¼­, inf. & post infarctÀº ¼Ò¼ö)

CIxÀÌ ¾ø´Ù¸é anticoagulantÇÊ¿ä

Ä¡·á±â°£Àº Àß ¾Ë·ÁÁ® ÀÖÁö ¾ÊÀ¸³ª 3-6°³¿ùÀÌ ÇÕ´çÇÏ´Ù.

(4) LV aneurysm

¨ç true aneurysm : scar tissue·Î ÀÌ·ç¾îÁö¸ç cardiac rupture¿Í °ü·Ã¾ø´Ù.

complication(CHF, arterial embolism, ventricular arrhythmia)Àº ¼öÁÖ-¼ö°³¿ùµ¿¾È ¹ß»ý

ÇÏÁö ¾ÊÀ¸¸ç apical aneurysmÀÌ °¡Àå ÈçÇÏ°í ½±°Ô detectµÈ´Ù.

mural thrombus°¡ ¹ß°ßµÉ¼ö ÀÖ´Ù.

¨è pseudoaneurysm

LV cavity¿Í narrow neckÀ» ÅëÇØ ¿¬°áµÇ¾î ÀÖÀ¸¸ç spontaneous rupture°¡´É¼º ¶§¹®¿¡

¼ö¼úÇØ¾ß ÇÑ´Ù.

9. Postinfarction risk stratification & management

¨ç AMI ȸº¹ÈÄ cardiovascular risk Áõ°¡¿Í °ü·ÃÇÑ most important factors

i) persistent ischemia(spontaneous or provoked)

ii) depressed LVEF(<40%)

iii) lung base rales or CXR»ó congestion

iv) symptomatic ventricular arrhythmia

¨è Other factors

i) previous MI Hx(+)

ii) 70¼¼ ÀÌ»ó

iii) DM, Hypertension

iv) prolonged sinus tachycardia

v) St segment change at rest without angina(silent ischemia)

vi) abnormal signal-averaged ECG

vii) infarct-related coronary a.ÀÇ nonpatency

viii) persistent advanced heart block

ix) new intraventricular conduction abnormality on ECG

- ¾ÈÁ¤µÈ ȯÀÚ´Â Åð¿øÀü submaximal exercise stress test¸¦ ½ÃÇàÇÑ´Ù.

¸ñÀû i) residual ischemia & ventricular ectopy¹ß°ß

ii) early recovery period¿¡ exercise guidelineÁ¦°ø

- maximal(sx-limited) exercise stress test´Â 4-6ÁÖÈÄ¿¡ ½ÃÇàÇÑ´Ù.

- LV fxÀÇ Æò°¡µµ ÇÊ¿äÇѵ¥ Echo³ª Radionuclide ventriculogram»ó LVEF°¡ °¨¼ÒÇÑ °æ¿ì¿£

ACEI¸¦ Åõ¿©Çϵµ·Ï ÇÑ´Ù.

- Perfusion scan»ó large reversible defect or depressed EF, symptomatic ventricular

arrhythmia

= high risk for recurrent MI or death

=> cardiac cath with CAG and/or invasive EPSÇÊ¿ä

- predischarge stress test : ȯÀÚ¿¡°Ô Áß¿äÇÑ ½É¸®Àû À̵æÀÌ ÀÖ´Ù.

2ÁÖµ¿¾È ȯÀÚ´Â activity¸¦ Áõ°¡½Ãų¼ö ÀÖÀ¸¸ç normal sexual activityµµ À̶§ Àç°³ÇÒ¼ö

ÀÖ´Ù. ´ëºÎºÐÀÇ È¯ÀÚ´Â 2-4ÁÖÈÄ ÀÛ¾÷ÀåÀ¸·Î º¹±ÍÇÒ¼ö ÀÖ´Ù.

10. Secondary prevention of infarction

¨ç long-term antiplatelet agent(Aspirin)

recurrent infarction, stroke, cerebrovascular mortality¸¦ 25%°¨¼Ò½ÃÅ´

aspirin¿¡ intolerantÇÒ ¶§ clipidogrel(75mg/day)»ç¿ë = ADP receptor antagonist

¨è ACE inhibitor

¨é ¥â-blocker : ÃÖ¼Ò 2³â

¨ê Ca antagonist : ÃßõµÇÁö ¾ÊÀ½

¨ë Warfarin : embolism risk°¡ ³ôÀº ȯÀÚ¿¡¼­

¨ì Atherosclerosis risk factorÁ¶Àý

i) smoking Áß´Ü

ii) hypertension & hyperlipidemia control(LDL <100 mg/dL)

iii) regular physical activity

iv) emotional stress¡é

v) HRT : controversial Ãʱ⿣ À§ÇèÀ» Áõ°¡½Ã۰í Èı⿣ °¨¼Ò½ÃŲ´Ù.