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Pemicu 2B
Kegawatdaruratan
Clara Petrisiela
405100063
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SHOCK (INTRODUCTION)
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Shockis the clinical syndrome that resultsfrom inadequate tissue erfusion!
"he hyoerfusion#induced im$alance
$etween the deli%ery of and requirementsfor o&ygen and su$strate leads to cellulardysfunction!
'eads to a vicious cycle (((
Harrison's principles of internal
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Harrison's principles of internal
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Pathogenesis ) *rgan+esonses
1! ,icrocirculation
2! Cellular resonses
3! -euroendocrine resonses
4! Cardio%ascular resonses
5! Pulmonary resonses
6! +enal resonses
.! ,eta$olic dearangements
/! namatory resonses
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"reatment Principle
Monitoring
+equire care in an C
ssessment of the hysiologic status
,onitoring arterial ressure indwelling line7ulse7 and resiratory rate !
8oley catheter urin ow
,ental status assessment
9edated atients should $e awa:en daily;drug holiday;assess neurologic status )to shorten duration of %entilator suort!
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HYPOO!"MIC SHOCK
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Nor#%l p&ysiologic response
,aintain erfusion of the $rain and heartto restorean e@ecti%e circulating $lood %olume!
9igns=
symathetic acti%ity A
hyer%entilation7
collase of %enous caacitance %essels7
stress hormones A
an attemt to relace the loss of intra%ascular%olume
recruitment of interstitial and intracellular uid
$y reduction of urine outut!
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iagnosis
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Plasma losses hemoconcentration
8ree water loss hyernatremia
+educed cardiac outut Comensatory symathetic
tachycardia ) ele%ated systemic
%ascular resistance!
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"reatments
nitial resuscitation7 !D line
"he raid infusion of either isotonic saline7 or
Balanced salt solution = +ingerEs lactate
nfusion of 2F3 ' of salt solution o%er 20F30min!
cute $lood loss ' 10g>d'initiate $lood transfusion!
dds! fresh#froGen lasma 88P and lateletsaroaching a 1=1 ratio of P+BC>88P imro%e sur%i%al!
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Inotropic suort noreinehrine7%asoressin7 or doamine maintainadequate %entricular erformance but only
after $lood %olume has $een restored7 toa%oid tissue loss and organ failure!
9ulemental o&ygen (
Hndotracheal intu$ation to maintainarterial o&ygenation!
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N"URO'"NIC SHOCK
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-eurogenic 9hoc:
nterrution of symathetic %asomotorinut!
H!c>
high cer%ical sinal cord inIury
inad%ertent cehalad migration of sinalanesthesia
de%astating head inIury
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rteriolar dilation ) %enodilation
ooling in the %enous system%enousreturn and cardiac outut J!
T&e etre#ities %re o$ten %r#7 incontrast to the usual symathetic
%asoconstriction#induced coolness inhyo%olemic > cardiogenic shoc:!
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"reatment
9imultaneous aroach to therelati%e hyo%olemia and to the lossof %asomotor tone!
H&cessi%e %olumes of uid!
+ule out hemorragenoreinehrineor a ure #adrenergic agenthenylehrineto maintain ,P!
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C*RDIO'"NIC SHOCK
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eidemiology
,ost causes= ,#'osing a large amount of myocardium $ynecrosis
2!L= unsta$le angina ectoris
2!1L= non#9" ele%ation ,
"he median time to rogression of shoc:= .6#4hours7 4/ hours commonest
,ore often seen as a comlication of , with 9"ele%ation than other tyes of acute coronarysyndromes
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deMnition
isrution caused $y a decrease in cardiac oututsystemic intra%ascular %olume sucientcondition7 and can lead to tissue hyo&ia!
Primary diagnosis of systemic hyotension 9ystolic $lood ressure N0 mm
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"he clinical manifestationsfound signs of systemichyoerfusion include mental status changes7 colds:in7 and oliguria
Cardiogenic shoc:
#systolic BP N0 mm
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comonents cardiogenicshoc:
maired %entricular function
H%idence of organ failure due toreduced tissue erfusion
"he a$sence of hyo%olemia or othercauses
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etiology
cute myocardial infarction
Dentricular setal ruture
+uture or aillary muscledysfunction
myocardial ruture
+ight %entricular myocardialinfarction or without left %entriculardysfunction
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+is: factors
,yocardial ischemia >infarction
nemia= tachycardia >$radycardia
nfections=endocarditis7myocarditis7 or heartinfections outside
ulmonary em$olism
H&cess uid or salt
,yocardialsuressi%e drugssuch as $eta $loc:ers
*ther= regnancy7thyroto&icosis7anemia7 stresshysical or
emotional7 acutehyertension
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iagnosis of cardiogenicshoc:
,ain comlaint Cardiogenic 9hoc:
*liguric urine N20 m' > hour!
"here may $e a relationshi with ,acute myocardial infarction!
9u$sternal ain as ,!
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iagnosis of cardiogenicshoc:
mortant 9igns =
"ension dros N/0#0mm
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H&amination
HC?
Chest rays
Hchocardiograhy hemodynamic monitoring
o&ygen saturation
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TR*UM*TIC SHOCK
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9hoc: following trauma due tohemorrhage!
H%en when hemorrhage has $een controlled7
atients can continue to su@er loss of lasma%olume into the interstitium of inIured tissues!
na$ility of the atient to maintain a systolic
$lood ressure 0 mm
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"hese uid losses inIury#inducedinammatory resonses contri$ute tothe secondary microcirculatory inIury!
Proinammatory mediators are induced $y,Ps released from inIured tissue recogniGed $y the highly conser%edmem$rane recetors of the "'+ family!
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+ecetors on cells= the circulatingmonocyte7 tissue#M&ed macrohage7 anddendritic cell otent acti%ators of an
e&cessi%e roinammatory henotye inresonse to cellular inIury =
causes secondary tissue inIury andmaldistri$ution of $lood ow7
intensifying tissue ischemia
leading to multile organ system failure!
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"reatment
"he initial management = ;BCs; ofresuscitation
Control of ongoing hemorrhage
Harly sta$iliGation of fractures
e$ridement of de%italiGed orcontaminated tissues
H%acuation of hematomas 9ulementation of deleted
endogenous antio&idants
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S"PTIC SHOCK
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Sepsis
9+9 that has a ro%en or susectedmicro$ial etiology
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Syste#ic in+%##%toryresponse syn,ro#e (SIRS)
"wo or more of the following conditions=
1fe%er oral temerature O3/SC
or hyothermia N36SC
2 tachynea O24 $reaths>min
3 tachycardia heart rate O0 $eats>min
4 leu:ocytosis O127000>'7 leucoenia
N47000>'or O10L $ands may ha%e a noninfectiousetiology!
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Septic s&oc-
9esis with hyotension arterial $loodressure N0 mm
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9etic shoc: causes three maIor e@ects thatmust $e addressed during resuscitation=
hyo%olemia7
cardio%ascular deression7 induction of systemic inammation!
causes a$solute hyo%olemia fromgastrointestinal %olume losses7 tachynea7sweating7 and decreased a$ility to drin:during de%eloment of the illness!
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Htiology
n fact7 $lood cultures yield $acteria orfungi in only F20F40L of cases of se%eresesis and 40F.0L of cases of setic
shoc:! ndi%idual gram#negati%e or gram#ositi%e
$acteria account for F.0L of theseisolates the remainder are fungi or a
mi&ture of microorganisms
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Pathohysiology
,ost cases of se%ere sesis are triggered$y $acteria or fungi that do not ordinarilycause systemic disease in
immunocometent hosts ! "o sur%i%e within the human $ody7 these
micro$es often e&loit deMciencies in hostdefenses7 indwelling catheters or other
foreign matter7 or o$structed uiddrainage conduits!
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,icro$ial athogens7 in contrast7 cancircum%ent innate defenses $ecause they=
1 lac: molecules that can $e recogniGed
$y host recetors see $elow or 2 ela$orate to&ins or other %irulencefactors!
9o the $ody can mount a %igorousinammatory reaction se%ere sesis yetfails to :ill the in%aders!!
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Clinical ,anifestations
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Cellulitis7 ustules7 $ullae7 or hemorrhagiclesionshematogenous $acteria or fungi!
Bacterial to&ins distri$uted hematogenouslyand elicit di@use cutaneous reactions!
cutaneous etechiae or ururainfection N.meningitidisor7 less commonly7 H. inuenzae
etechial lesions and +oc:y ,ountain sotted
fe%er $itten $y a tic: while in an endemicarea!
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ecthyma gangrenosum7 almost e&clusi%elyin neutroenic atients caused $y P.aeruginosa!
?eneraliGed erythroderma in a seticatient suggests the to&ic shoc: syndromedue to S. aureusor S. pyogenes!
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?astrointestinal manifestations = nausea7%omiting7 diarrhea7 and ileus
Cholestatic Iaundice= ele%ated le%els of
serum $iliru$in and al:aline hoshatase Blood lactate le%els rise early increased
glycolysis as well as imaired clearance ofthe resulting lactate and yru%ate $y the
li%er and :idneys $lood glucose concentration often
increases!
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iagnosis
fe%er or hyothermia7 tachynea7tachycardia7 and leu:ocytosis or leu:oenia
acutely altered mental status7throm$ocytoenia7 an ele%ated $lood lactate
le%el7 or hyotension $lood cultures
?ramEs staining and culture of material fromthe rimary site of infection or from infected
cutaneous lesions PC+ dentiMcation of micro$ial - in
eriheral#$lood
Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed
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"reatments
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+emo%al or drainage of a focal source ofinfection
dequate organ erfusion
nitial management of hyotension administration of D uids with 1F2 ' ofnormal saline o%er 1F2 h!
Patients w>setic shoc:7 lasma%asoressin le%els increase transiently $utthen decrease dramatically!
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Dentilator for rogressi%e hyo&emia7hyercania7 neurologic deterioration7 orresiratory muscle failure!
Hrythrocyte transfusion recommendedfor $lood d'7 with a targetle%el of g>d' in adults!
Bicar$onate for se%ere meta$olicacidosis arterial < N.!2!
C should $e treated with transfusionof fresh#froGen lasma and latelets!
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*n%p&yl%ctic S&oc-
+esults from an gH#mediated systemicresonse to an allergen!
"he mast cella central role!
gH causes mast cells to release histamine7which results in %ascular smooth musclerela&ation7 $ronchial smooth muscleconstriction7 and caillary lea: of lasma
into interstitial saces!
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Plateletssecreting latelet#acti%atingfactor P87 deri%ed from mem$ranehosholiid!
P8 eriheral %asodilation7
$ronchial constriction7
ulmonary arterial and coronary%asoconstriction!
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ntagonists to P8 can re%erse thenegati%e inotroy and %asodilation !
s such7 P8 may $e an imortant
mediator of anahyla&is that is refractoryto antihistamine treatments!
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"heray
ggressi%e %olume resuscitation withisotonic uid
Hinehrine e@ecti%ely counteracts the%asoderession7 $ronchoconstriction7 uid
transudation7 and reduced cardiac functionin anahyla&is!
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"pinep&rine intra%enously in atientswith hyotension7 e%en in the resence ofcoronary artery disease!
nitially7 1 m' of 1=107000 einehrine100 #g can $e inIected slowly and theresonse monitored!
fterward7 5 mg of einehrine can $e
diluted in 500 m' of saline7 with a startinginfusion rate of 10 m'>hr a$out 0!02 #g>:g>mintitrated to maintain erfusion!
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Corticosteroi,s are integral to arrestingsynthesis and release of anahyla&ismediators!
inhi$it hosholiase 2 and decreaserostanoid7 leu:otriene7 and P8 synthesis7quench "#cell and mast cell triggering andreduce late#hase $ronchial inammation!
:g !D ormethylrednisolone 1!5#2 mg>:g !D
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Hist%#ine receptor %nt%gonists (H.%n, H/)re%ent urticaria7 aid in reducing$ronchoconstriction7 reduce uid transudation7and may imro%e myocardial function!
ihenhydramine 0!5 mg>:g D and cimetidine2#5 mg>:g D
Ne0uli1e, p/2%gonists hel reduce
$ronchosasm!
Ket%#ineis a logical agent to use for sedationduring raid sequence intu$ation withsuccinylcholine!
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Whipple's triad
1 symtoms consistent withhyoglycemia7 2 a low lasmaglucose concentration measured with
a recise method not a glucosemonitor
3 relief of those symtoms after the
lasma glucose le%el is raised!
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Clinical ,anifestations
-euroglycoenic symtoms C-9 glucosederi%ation= $eha%ioral changes7 confusion7 fatigue7seiGure7 loss of consciousness7 and death!
-eurogenic or autonomic symtomsthe ercetion
of hysiologic changes caused $y the C-9#mediatedsymathoadrenal discharge =
drenergic syms= alitations7 tremor7 and an&iety!
Colinergic syms = sweating7 hunger7 andaresthesias!
iahoresis and allor
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Con%entional +is: 8actors
1 insulin or insulin secretagogue doses aree&cessi%e7 ill#timed7 or of the wrong tye
2 the inu& of e&ogenous glucose is reducede!g!7 during an o%ernight fast or following missed
meals or snac:s 3 insulin#indeendent glucose utiliGation is
increased e!g!7 during e&ercise
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4 sensiti%ity to insulin is increased e!g!7 withimro%ed glycemic control7 in the middle of thenight7 late after e&ercise7 or with increased Mtnessor weight loss
5 endogenous glucose roduction is reduced e!g!7following alcohol ingestion and
6 insulin clearance is reduced e!g!7 in renalfailure!
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rgent "reatment
*ral treatment with glucose ta$lets orglucose#containing uids7 candy7 or food!
initial dose is 20 g of glucose!
-euroglycoenia ntra%enous glucose 25 g ) followed $y a
glucose infusion guided $y serial lasmaglucose measurements!
su$cutaneous or intramuscular glucagon1!0 mg in adults