Pemcu 2B

Kegawatdaruratan
Cara Petrsea
405100063
SHOCK (INTRODUCTION)

Shock s the cnca syndrome that resuts

from nadequate tssue perfuson.

The hypoperfuson-nduced mbaance

between the devery of and requrements
for oxygen and substrate eads to ceuar
dysfuncton.

Leads to a vicious cycle !!!

Harrison's principles of internal
medicine. 8
th
Ed.
Harrison's principles of internal
medicine. 8
th
Ed.
Pathogeness & Organ
Responses
1. Mcrocrcuaton
2. Ceuar responses
3. Neuroendocrne responses
4. Cardovascuar responses
5. Pumonary responses
6. Rena responses
7. Metaboc dearangements
8. Inamatory responses
Treatment (Principle)
Monitoring

Requre care n an ICU

Assessment of the physoogc status

Montorng artera pressure; ndweng ne,

puse, and respratory rate .

A Foey catheter (urn ow)

Menta status assessment

Sedated patents shoud be awaken day

("drug hoday") assess neuroogc status &
to shorten duraton of ventator support.
HYPOO!"MIC SHOCK
Hypovoemc shock

Ths #ost co##on $or# of shock.

Resuts from :

the oss of red bood ce mass and

pasma from hemorrhage

the oss of pasma voume aone due to

extravascuar ud sequestraton/GI,
urnary, and nsensbe osses.
Nor#%l p&ysiologic response

Mantan perfuson of the bran and heart to restore

an ehectve crcuatng bood voume.

Sgns:

sympathetc actvty

hyperventaton,

coapse of venous capactance vesses,

stress hormones

an attempt to repace the oss of ntravascuar

voume
recrutment of nterstta and ntraceuar ud
by reducton of urne output.
Dagnoss

Hemodynamc nstabty and the source of

voume oss s obvous.

Perfuson of the CNS s we mantaned

unt shock becomes severe.

More dmcut when the source of bood

oss s occut, as nto the GIT/when pasma
voume aone s depeted.

Hb and Ht vaues do not change unt

compensatory ud shfts have occurred or
exogenous ud s admnstered.

Pasma osses hemoconcentraton

Free water oss hypernatrema

Reduced cardac output

Compensatory sympathetc
tachycarda & eevated systemc
vascuar resstance.
Treatments

Inta resusctaton, I.V ne

The rapd nfuson of ether sotonc sane, or

Baanced sat souton : Rnger's actate

Infuson of 2-3 L of sat souton over 20-30

mn.

Acute bood oss; Hb decne to 100 g/L (10

g/dL) ntate bood transfuson.

Adds. fresh-frozen pasma (FFP) and pateets

approachng a 1:1 rato of PRBC/FFP
mprove survva.

Inotropic support; norepnephrne,

vasopressn, or dopamne mantan
adequate ventrcuar performance but only
after bood voume has been restored, to
avod tssue oss and organ faure.

Suppementa oxygen !

Endotrachea ntubaton to mantan

artera oxygenaton.
N"URO'"NIC SHOCK
Neurogenc Shock

Interrupton of sympathetc vasomotor

nput.

E.c/

hgh cervca spna cord n|ury

nadvertent cephaad mgraton of spna

anesthesa

devastatng head n|ury

Arteroar daton & venodaton

poong n the venous system venous
return and cardac output J.

T&e e(tre#ities %re o$ten )%r#, n

contrast to the usua sympathetc
vasoconstrcton-nduced cooness n
hypovoemc / cardogenc shock.
Treatment

Smutaneous approach to the

reatve hypovoema and to the oss
of vasomotor tone.

Excessve voumes of ud.

Rue out hemorrage norepnephrne

or a pure -adrenergc agent
(phenyephrne) to mantan MAP.
C*RDIO'"NIC SHOCK
epdemoogy

Most causes: AMI

-Losng a arge amount of myocardum by
necross

2.9%: unstabe angna pectors

2.1%: non-ST eevaton AMI

The medan tme to progresson of shock: 76-94

hours, 48 hours commonest

More often seen as a compcaton of AMI wth ST

eevaton than other types of acute coronary
syndromes
denton

Dsrupton caused by a decrease n cardac output

systemc ntravascuar voume sumcent
condton, and can ead to tssue hypoxa.

Prmary dagnoss of systemc hypotenson

Systoc bood pressure <90 mmHg ncrease
catechoamnes constrct the arteres and
vens of systemc

The cnca manfestatons found sgns of systemc

hypoperfuson ncude menta status changes, cod
skn, and ogura

Cardogenc shock
-systoc BP <90 mm Hg for> 1 hour where:
-Not responsve to ud admnstraton aone
-Secondary to cardac dysfuncton, or,
-Assocated wth sgns of hypoperfuson or cardac
ndex |<2.2 (L/mn)/m
2
| and pumonary --capary
wedge pressure> 18 mmHg
components cardogenc
shock

Impared ventrcuar functon

Evdence of organ faure due to

reduced tssue perfuson

The absence of hypovoema or other

causes
etoogy

Acute myocarda nfarcton

Ventrcuar septa rupture

Rupture or papary musce

dysfuncton

myocarda rupture

Rght ventrcuar myocarda

nfarcton or wthout eft ventrcuar
dysfuncton
Rsk factors

Myocarda schema /
nfarcton

Anema: tachycarda /
bradycarda

Infectons:
endocardts,
myocardts, or heart
nfectons outsde

pumonary embosm

Excess ud or sat

Myocarda
suppressve drugs
such as beta bockers

Other: pregnancy,
thyrotoxcoss,
anema, stress
(physca or
emotona), acute
hypertenson
Dagnoss of cardogenc
shock
Man compant Cardogenc Shock

Ogurc (urne <20 mL / hour).

There may be a reatonshp wth IMA

(acute myocarda nfarcton).

Substerna pan as IMA.

Dagnoss of cardogenc
shock
Important Sgns :

Tenson drops <80-90

mmHg.

Takpneu and deep.

Tachycarda.

Rapd puse, uness

there are bocks A-V.

Sgns of ung dam: wet

crackes n both basa
ung.

The sound of the

heart s very weak,
the thrd heart
sound s often
heard.

Cyanoss.

Daphoress
(sweatng).

Cod extremtes.

Menta changes.
Examnaton

ECG

Chest x-rays

Echocardography

hemodynamc montorng

oxygen saturaton
TR*UM*TIC SHOCK

Shock foowng trauma due to

hemorrhage.

Even when hemorrhage has been controed,

patents can contnue to suher oss of pasma
voume nto the ntersttum of n|ured tssues.

Inabty of the patent to mantan a systoc

bood pressure90 mmHg after trauma-
nduced hypovoema s assocated wth a
mortaty rate up to 50%.

These ud osses n|ury-nduced

nammatory responses contrbute to
the secondary mcrocrcuatory n|ury.

Pronammatory medators are nduced by

DAMPs reeased from n|ured tssue
recognzed by the hghy conserved
membrane receptors of the TLR famy.
Receptors on ces: the crcuatng
monocyte, tssue-xed macrophage, and
dendrtc ce potent actvators of an
excessve pronammatory phenotype n
response to ceuar n|ury :
causes secondary tssue n|ury and
madstrbuton of bood ow,

ntensfyng tssue schema

eadng to mutpe organ system faure.

Treatment

The nta management : "ABCs" of

resusctaton

Contro of ongong hemorrhage

Eary stabzaton of fractures

Debrdement of devtazed or
contamnated tssues

Evacuaton of hematomas

Suppementaton of depeted
endogenous antoxdants
S"PTIC SHOCK
Sepsis

SIRS that has a proven or suspected

mcroba etoogy
Syste#ic in+%##%tory
response syn,ro#e (SIRS)
Two or more of the foowng condtons:
(1)fever (ora temperature >38C)
or hypotherma (<36C)
(2) tachypnea (>24 breaths/mn)
(3) tachycarda (heart rate >90 beats/mn)
(4) eukocytoss (>12,000/L), eucopena
(<4,000/L)
or >10% bands; may have a nonnfectous
etoogy.
Septic s&oc-

Sepss wth hypotenson (artera bood

pressure <90 mmHg systoc, or 40 mmHg
ess than patent's norma bood pressure)
for at east 1 h despte adequate ud
resusctaton.

Need for vasopressors to mantan systoc

bood pressure 90 mmHg or mean artera
pressure 70 mmHg.

Septc shock causes three ma|or ehects that

must be addressed durng resusctaton:

hypovoema,

cardovascuar depresson,

nducton of systemc nammaton.

causes absoute hypovoema from

gastrontestna voume osses, tachypnea,
sweatng, and decreased abty to drnk
durng deveopment of the ness.
Etoogy

In fact, bood cutures yed bactera or

fung n ony -20-40% of cases of severe
sepss and 40-70% of cases of septc
shock.

Indvdua gram-negatve or gram-postve

bactera account for -70% of these
soates; the remander are fung or a
mxture of mcroorgansms
Epdemoogy

Invasve bactera nfectons are promnent

causes of death around the word,
partcuary among young chdren.

Nontyphoda Salmonella speces,

Streptococcus pneumoniae, Haemophilus
infuenzae, and Escherichia coli were the
most commony soated bactera.

Bacteremc chdren often had HIV

nfecton or were severey manourshed.
Pathophysoogy

Most cases of severe sepss are trggered

by bactera or fung that do not ordnary
cause systemc dsease n
mmunocompetent hosts .

To survve wthn the human body, these

mcrobes often expot decences n host
defenses, ndweng catheters or other
foregn matter, or obstructed ud
dranage conduts.

Mcroba pathogens, n contrast, can

crcumvent nnate defenses because they:
(1) ack moecues that can be recognzed
by host receptors (see beow) or
(2) eaborate toxns or other vruence
factors.

So the body can mount a vgorous

nammatory reacton severe sepss yet
fas to k the nvaders..
Cnca Manfestatons

Hyperventaton

Dsorentaton, confuson, and other

manfestatons of encephaopathy,
partcuary n the edery and n ndvduas
wth preexstng neuroogc mparment.

Foca neuroogc sgns f has preexstng

foca dects .

Hypotenson

DIC acrocyanoss and schemc necross of

perphera tssues

Ceuts, pustues, buae, or hemorrhagc

esons hematogenous bactera or fung.

Bactera toxns dstrbuted hematogenousy

and ect dhuse cutaneous reactons.

cutaneous petechae or purpura nfecton N.

meningitidis (or, ess commony, H. infuenzae)

petecha esons and Rocky Mountan spotted

fever btten by a tck whe n an endemc
area.

ecthyma gangrenosum, amost excusvey

n neutropenc patents caused by P.
aeruginosa.

Generazed erythroderma n a septc

patent suggests the toxc shock syndrome
due to S. aureus or S. pyogenes.

Gastrontestna manfestatons : nausea,

vomtng, darrhea, and eus

Choestatc |aundce: eevated eves of

serum brubn and akane phosphatase

Bood actate eves rse eary ncreased

gycoyss as we as mpared cearance of
the resutng actate and pyruvate by the
ver and kdneys

bood gucose concentraton often

ncreases.
Dagnoss

fever or hypotherma, tachypnea,

tachycarda, and eukocytoss or eukopena

acutey atered menta status,

thrombocytopena, an eevated bood actate
eve, or hypotenson

bood cutures

Gram's stanng and cuture of matera from

the prmary ste of nfecton or from nfected
cutaneous esons

PCR Identcaton of mcroba DNA n

perphera-bood
Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed
Treatments

Remova or dranage of a foca source of

nfecton

Adequate organ perfuson

Inta management of hypotenson

admnstraton of IV uds wth 1-2 L of
norma sane over 1-2 h.

Patents w/septc shock, pasma

vasopressn eves ncrease transenty but
then decrease dramatcay.

Ventator for progressve hypoxema,

hypercapna, neuroogc deteroraton, or
respratory musce faure.

Erythrocyte transfuson recommended

for bood Hb eve < 7 g/dL, wth a target
eve of 9 g/dL n aduts.

Bcarbonate for severe metaboc

acdoss (artera pH <7.2).

DIC shoud be treated wth transfuson

of fresh-frozen pasma and pateets.
Genera supports

Entera devery route (NGT)

Nutrtona suppementaton

Prophyactc heparnzaton to prevent DVT.

If heparn s contrandcated
compresson stockngs /an ntermttent
compresson devce.
*n%p&yl%ctic S&oc-

Resuts from an IgE-medated systemc

response to an aergen.

The mast ce a centra roe.

IgE causes mast ces to reease hstamne,

whch resuts n vascuar smooth musce
reaxaton, broncha smooth musce
constrcton, and capary eak of pasma
nto nterstta spaces.

Pateets secretng pateet-actvatng

factor (PAF), derved from membrane
phosphopd.

PAF

perphera vasodaton,

broncha constrcton,

pumonary artera and coronary

vasoconstrcton.

Antagonsts to PAF can reverse the

negatve notropy and vasodaton .

As such, PAF may be an mportant

medator of anaphyaxs that s refractory
to anthstamne treatments.
Therapy

Aggressve voume resusctaton wth

sotonc ud

Epnephrne ehectvey counteracts the

vasodepresson, bronchoconstrcton, ud
transudaton, and reduced cardac functon
n anaphyaxs.

"pinep&rine ntravenousy n patents

wth hypotenson, even n the presence of
coronary artery dsease.

Intay, 1 mL of 1:10,000 epnephrne

(100 p-g) can be n|ected sowy and the
response montored.

Afterward, 5 mg of epnephrne can be

duted n 500 mL of sane, wth a startng
nfuson rate of 10 mL/hr (about 0.02 p-
g/kg/mn) ttrated to mantan perfuson.

Corticosteroi,s are ntegra to arrestng

synthess and reease of anaphyaxs
medators.
nhbt phosphopase A
2
and decrease
prostanod, eukotrene, and PAF synthess,
quench T-ce and mast ce trggerng and
reduce ate-phase broncha nammaton.

Hydrocortsone (5-10 mg/kg I.V ) or

methyprednsoone (1.5-2 mg/kg I.V)
Hist%#ine receptor %nt%gonists (H
.
%n, H
/
)
prevent urtcara, ad n reducng
bronchoconstrcton, reduce ud transudaton,
and may mprove myocarda functon.

Dphenhydramne (0.5 mg/kg IV) and cmetdne

(2-5 mg/kg IV)
Ne0uli1e, p
/
2%gonists hep reduce
bronchospasm.

Ket%#ine s a ogca agent to use for sedaton

durng rapd sequence ntubaton wth
succnychone.
Hypogycema

Most commony caused by drugs used to treat dabetes

metus or by exposure to other drugs, ncudng acoho.

Can cause serous morbdty; f severe and proonged

fata.
It shoud be consdered n any patent wth epsodes of
confuson, an atered eve of conscousness, or a sezure.
Hosptazed patents, serous nesses such as rena,
hepatc, or cardac faure, sepss, and nanton are
second ony to drugs as causes of hypogycema.
Whipple's triad
(1) symptoms consstent wth
hypogycema, (2) a ow pasma
gucose concentraton measured wth
a precse method (not a gucose
montor)
(3) reef of those symptoms after the
pasma gucose eve s rased.
Cnca Manfestatons

Neurogycopenc symptoms (CNS) gucose

deprvaton: behavora changes, confuson, fatgue,
sezure, oss of conscousness, and death.

Neurogenc (or autonomc) symptomsthe percepton

of physoogc changes caused by the CNS-medated
sympathoadrena dscharge :

Adrenergc symps: paptatons, tremor, and anxety.

Conergc symps : sweatng, hunger, and

paresthesas.

Daphoress and paor

Heart rate and systoc bood pressure are typcay

ncreased.
Hypogycema n Dabetes

Hypogycema s a fact of fe for peope wth

T1DM.

They suher an average of two epsodes of

symptomatc hypogycema per week and at east
one epsode of severe, at east temporary
dsabng, hypogycema each year.

An estmated 6-10% of peope wth T1DM de as a

resut of hypogycema.

Hypogycema occurs ess frequenty n T2DM.

Conventona Rsk Factors
(1) nsun (or nsun secretagogue) doses are
excessve, -tmed, or of the wrong type;
(2) the nux of exogenous gucose s reduced
(e.g., durng an overnght fast or foowng mssed
meas or snacks);
(3) nsun-ndependent gucose utzaton s
ncreased (e.g., durng exercse);

(4) senstvty to nsun s ncreased (e.g., wth
mproved gycemc contro, n the mdde of the
nght, ate after exercse, or wth ncreased tness
or weght oss);
(5) endogenous gucose producton s reduced (e.g.,
foowng acoho ngeston); and
(6) nsun cearance s reduced (e.g., n rena
faure). However, these conventona rsk factors
aone expan a mnorty of epsodes; other factors
are typcay nvoved.
Urgent Treatment

Ora treatment wth gucose tabets or

gucose-contanng uds, candy, or food.

nta dose s 20 g of gucose.

Neurogycopena

Intravenous gucose (25 g) & foowed by a

gucose nfuson guded by sera pasma
gucose measurements.

subcutaneous or ntramuscuar gucagon

(1.0 mg n aduts)