¼±Åà - È­»ìǥŰ/¿£ÅÍŰ ´Ý±â - ESC

 

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 °¡¼ÓÈ­µÈ´Ù.

- 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.