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¤»óȵȴÙ.
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¿¡ ÀÖ¾î¼ 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 ÇÏ¸é¼ »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־ 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.