ARDS(Acute Respiratory Distress Syndrome)
alveolar-capillary membranes permeabilityÁõ°¡, diffuse alveolar damage, protenaceous
pul. edema accumulationÀ» Ư¡À¸·Î Çϸç óÀ½¿£ NRDS¿Í ±¸º°Çϱâ À§ÇØ adult RDS¶ó
ÇÏ¿´À¸³ª ¸ðµç ³ªÀÌ¿¡ ´Ù »ý±â¹Ç·Î "A"´Â ÇöÀç Acute"·Î ¹Ù²î¾ú´Ù.
ARDS¸¦ Á¤ÀÇÇϱâ À§ÇØ Áö³ 30³âµ¿¾È Áø´Ü±âÁØÀÌ º¯ÇÏ¿´´Ù. ¿ø·¡ ¼¼°¡Áö ÀϹÝÀû criteria´Â
i) severe hypoxemia ii) decreased pul. compliance iii) CXR»ó diffuse pul. infiltrates¿´´Ù.
ÇöÀç pulmonary artery catheter»ç¿ëÀÌ Áõ°¡ÇÔ¿¡ µû¶ó ARDS´Â "noncardiogenic" form of
pulmonary edema·Î ÀνĵǾú´Ù. ±×°á°ú, pulmonary artery occlusion pressure°¡ Áø´Ü¿¡
ÇÊ¿äÇÏ°Ô µÇ¾î ÇöÀç ³Î¸® »ç¿ëµÇ´Â ARDSÀÇ Á¤ÀÇ´Â Tab 265-1°ú °°´Ù(Tab 265-1 ALI¿Í
ARDSÀÇ criteria).
* ARDS: acute onset, PaO2/FiO2 ¡Â 200 mmHg, CXR»ó bilateral infiltrates, PCWP ¡Â18
cmH2O
1. ÀÓ»óƯ¡
mc risky condition : severe sepsis, major trauma, gastric content aspiration
À̵éÁß Àû¾îµµ ÇѰ¡Áö¸¦ °¡Áö´Â ȯÀÚÁß 30-40%°¡ °á±¹ ARDS·Î ÁøÇàÇϸç chronic alcohol
abuse history°¡ Àִ ȯÀÚ´Â ARDSÀ§ÇèÀÌ ´õ Áõ°¡ÇÑ´Ù.
initial at-risk diagnosisÈÄ 5Àϳ» ÁÖ·Î ¹ß»ýÇϸç, 50%´Â ù 24½Ã°£³» ¹ß»ýÇÑ´Ù.
earliest clinical signÀº respiratory frequencyÀÇ Áõ°¡(followed by dyspnea)ÀÌ´Ù.
2. º´Å»ý¸®
inflammatory cascade : 3 overlapping phases
initiation, amplification, injury
¨ç initiation(precipitating event)
¿¹) sepsis : immune or nonimmune cells -> ´Ù¾çÇÑ mediator, cytokines(TNF- , IL-1)
ºÐºñ
¨è amplification
neutrophil°ú °°Àº effector cellÀÌ È°¼ºÈµÇ¾î lungÀ» Æ÷ÇÔÇÑ Æ¯Á¤Àå±â¿¡ ¸ðÀÓ.
moncyte¿Í ´Ù¸¥ ¼¼Æ÷¿¡¼ IL-8ºÐºñ.
* IL-8 : neutrophil activation¿¡ Áß¿äÇÑ ¿ªÇÒÀ» ÇÔ. ¨é injury phase
effector cell¿¡ lung¿¡ ¸ðÀ̸é reactive oxygen metabolite¿Í protease¸¦ ºÐºñÇÏ¿©
cellular damage¸¦ ¾ß±âÇÑ´Ù. ÀÌ·¯ÇÑ inflammatory cascade°¡ Á¡Â÷ÀûÀ¸·Î ÀϾ¼
¸¹Àº Àå±âÀÇ ±â´ÉÀå¾Ö¸¦ À¯¹ßÇϴµ¥ À̸¦ multiple organ dysfunction syndromeÀ̶ó ÇÑ´Ù.
* Pathophysiologic hallmark: protein¿¡ ´ëÇÑ vascular permeability
-> pul. capillary pre°¡ ¾à°£¸¸ Áõ°¡(IV liquid administration and/or myocardial depression)
ÇØµµ interstitial & alveolar edema°¡ Å©°Ô ¹ß»ýÇÑ´Ù.
- type II pneumocyte¼Õ»ó¿¡ µû¸¥ surfactant Ȱ¼º°¨¼Ò·Î ÀÎÇØ alveolar damage´Â
´õ °¡¼ÓȵȴÙ.
- atelectatic & liquid-filled region¿¡¼± lung compliance°¡ ¶³¾îÁöÁö¸¸
nondependent lungÀÇ »ó´ç
ºÎºÐÀº ºñ±³Àû normal mechanical & gas-exchanging property¸¦ °¡Áø´Ù.
±×·¯³ª pul. compliance°¨¼Ò·Î ÀÎÇÏ¿© ¸¹Àº inspiratory pressure°¡ ÇÊ¿äÇÏ°Ô µÇ´Âµ¥
ÀÌ·ÎÀÎÇØ work of breathingÀÌ Áõ°¡ÇÏ°Ô µÈ´Ù.
cf. Work of breathing(È£ÈíÀÏ)
W = TV [Pd - 0.5Ps] ´ÜÀ§: J
Pd ; peak dynamic airway pressure
Ps ; static plateau pressure obtained during airway occlusion at the inspiration
ºñ·Ï ARDS°¡ airway disease´Â ¾Æ´ÏÁö¸¸ bronchial wall edema, cytokine-mediated
bronchospasm ¿¡ ÀÇÇØ airway resistance°¡ Áõ°¡ÇÏ°Ô µÈ´Ù.
pul. vascular smooth m. toneÀÇ Áõ°¡, perivascular edema, microvascular thrombosis,
LT, TXA2
°°Àº humoral factor(direct vasoconstriction¾ß±â)¿¡ ÀÇÇØ pul. vascular resistance¿Í
pulmonary artery pressure¶ÇÇÑ Áõ°¡µÉ¼ö ÀÖ´Ù.
3. º´¸®
¨ç initial exudative phase : lung injuryÈÄ ¼öÀÏ
i) type I pneumocyteÀÇ ±¤¹üÀ§ÇÑ ±«»ç, basement membrane¼Ò½Ç·Î ÀÎÇØ epithelial cell
¼Õ»ó
ii) endothelial cell swelling with the widening of intercellular junctions
iii) hyaline membrane formation
iv) neutrophilic inflammation
¨è 2nd pathologic phase
cell proliferation, neutrophilic inflammation resolution
ARDS »ýÁ¸ÀÚ¿¡¼ ÈçÈ÷ architectural restorationÀÌ °üÂûµÇÁö¸¸ lung parenchymaÀÇ
interstitial fibrosis & extensive restructuringÀ¸·Î ÀϺÎȯÀÚ¿¡¼ cystic & honeycomb
change°¡ ÀϾ ¼ö ÀÖ´Ù. ±× °á°ú chronic pul. dysfunction ȤÀº »ç¸ÁÇÒ¼ö ÀÖ´Ù.
4. Ä¡·á
1) Mechanical ventilatory support
mechanical ventilationÀÇ ÁÖ¿äÇÑ ÇÕº´ÁõÀº oxygen toxicity¿Í barotraumaÀε¥ ¿©±â¿£
pneumothorax, pneumomediastinum, subcutaneous emphysema»Ó¸¸ ¾Æ´Ï¶ó primary
alveolar damageµµ Æ÷ÇԵȴÙ.
¸¹Àº alveoli°¡ liquid-filled or atelectatic state·Î ÀÖÁö¸¸ nondependent regionÀº ¹æ»ç¼±
ÇÐÀûÀ¸·Î ħ¹üµÇÁö ¾ÊÀº ä·Î ÀÖ¾î ¸¹Àº ¾çÀÇ tidal volumeÀ» ¼ö¿ëÇÒ Á¤µµ·Î Å« compliance
¸¦ °®°í ÀÖ´Ù.
large TV(10-12 mL/kg)ÀÌ ÀÌ·± ÀϺΠÁö¿ª¿¡ ¸ô¸®¸é epithelial & endothelial damage°¡ ¾ß±â
µÈ´Ù. ÀÌ·± ¼Õ»óÀÇ ÈÄÀ¯ÁõÀ¸·Î lung liquid balance¿¡ º¯È°¡ »ý±â°í permeability°¡ Áõ°¡
µÇ°í, severe alveolar damage°¡ ¹ß»ýÇÑ´Ù.
ÇöÀç ÃßõµÇ´Â ventilatory strategy´Â normal PaCO2¿¡ µµ´ÞÇÏ´Â °ÍÀÌ ¾Æ´Ï¶ó maximum
inflation pressure°¡ 30-35 cmH2O¸¦ ³ÑÁö¾Ê°Ô ÇÏ´Â °ÍÀÌ´Ù.
overall lung complianceÀÇ °¨¼Ò·Î ÀÎÇÏ¿© low tidal volume( 6 mL/kg)°¡ ÇÊ¿äÇÏ´Ù.
minute ventilationÀÇ °¨¼Ò´Â hypercapnia, resp. acidosis¸¦ À¯¹ßÇÏ°Ô µÇ´Âµ¥ ÀÌ·¯ÇÑ È¯±â
Àü·«Àº transpulmonary pressure¸¦ Á¦ÇÑÇÔÀ¸·Î½á hypercapnia»óŸ¦ Çã¿ëÇϴµ¥ À̸¦
permissive hypercapnia"¶ó ÇÑ´Ù.
PaO2´Â ´ë·« 60 mmHg·Î À¯ÁöÅä·Ï Çϰí FiO2 0.6¿¡¼ PaO2°¡ 60 mmHg·Î À¯ÁöµÇÁö ¾Ê´Â´Ù
¸é PEEPÀ» Ãß°¡Åä·Ï ÇÑ´Ù. PEEPÀº 5 cmH2O¿¡¼ ½ÃÀÛÇØ¼ 3-5 cmH2O¾¿ Áõ°¡½Ã۴µ¥
ÃÖ´ë 20-24 cmH2O±îÁö Áõ°¡½Ãų¼ö ÀÖ´Ù.
low tidal volume + adequate PEEPÀ» combinationÇÏ´Â ventilatory strategy¸¦
lung-protective strategy¶ó ÇÑ´Ù.
oxygenationÀ» °³¼±Çϱâ À§ÇØ prone positionÀ» °í·ÁÇØº¼¼ö ÀÖÀ¸³ª ÀÚ¼¼º¯°æÀº ¹«¸®°¡
µû¸£¸ç inverse ratio ventilationÀº dynamic hyperinflation & end-exp. pressure Áõ°¡¸¦ ¾ß±â
ÇÑ´Ù(=auto-PEEP).
2) Pharmacologic treatment
steroid : no benefit
surfactant-replacement therapy : no significant effect
NO : ventilation-perfusion mismatch¸¦ °³¼±Çϰí, oxygenation°³¼±½Ã۸ç mortality rate¸¦
°¨¼Ò½ÃŲ´Ù.
5. ¿¹ÈÄ
mortality rate : 50-70%
65¼¼ ÀÌ»ó, sepsis, other organ dysfunctionÀÌ ÀÖÀ» ¶§ »ç¸Á·üÀÌ Áõ°¡ÇÑ´Ù.
* »ç¸ÁÇÏ´Â °æ¿ì
early(3Àϳ») - original presenting illness or injury
late(3ÀÏÈÄ) - 2nd infection & sepsis, persistent respiratory failure, multiple organ
dysfunction
* survivor - PFTÀÌ»óÀº 3°³¿ù±îÁö »ó´çÈ÷ È£ÀüµÇ¸ç 6°³¿ù±îÁö maximum level·Î ±³Á¤µÈ´Ù.
50%À̻󿡼± abnormality°¡ Áö¼ÓµÇ´Âµ¥ À̶§ restrictive impairment or diffusion capacity
°¨¼Ò¸¦ º¸ÀδÙ.
severe ARDS´Â mild ARDS°æ¿ìº¸´Ù extreme hypoxemia, longer duration of illness¸¦
º¸ÀÌ°í °á±¹ more pulmonary dysfunctionÀ» º¸ÀδÙ.