Download - Emd166 Slide Shock-1
-
7/31/2019 Emd166 Slide Shock-1
1/53
SHOCK
Hasanul Arifin
Departemen Anestesiologi dan Reanimasi
Fakultas Kedokteran USU
-
7/31/2019 Emd166 Slide Shock-1
2/53
26/08/2010 2
-
7/31/2019 Emd166 Slide Shock-1
3/53
glucose oksigen
38 Mol ATP
-
7/31/2019 Emd166 Slide Shock-1
4/53
glucose oksigen
2 Mol ATP
+
36 Mol Lactate
-
7/31/2019 Emd166 Slide Shock-1
5/53
Definition of Shock
Reduced perfusion of vital organs leading to
inadequate oxygen and nutrients necessaryfor normal tissue and cellular function.
2 2
Cellular level:
Reduction of mitochondrial oxygen Anaerobic glycolysis of ATP
Accumulation of pyruvate lactate Lactic Acidosis
-
7/31/2019 Emd166 Slide Shock-1
6/53
SHOCKSHOCKSHOCKSHOCK
26/08/2010 6
IT IS HYPOPERFUSION..
-
7/31/2019 Emd166 Slide Shock-1
7/53
B1B1, nafasnafas sesaksesak, RR ,, RR , cupingcuping hidunghidung
B2,B2, HR ,HR , nadinadi halushalus cepatcepat, TD. N/, TD. N/PulsePulse--press ,press , perfusiperfusi dingindingin,, pucatpucat,, basahbasah,,
capill.refillcapill.refill > 2 det., lactic> 2 det., lactic--acidacid
SHOCKSHOCKSHOCKSHOCKSHOCKSHOCKSHOCKSHOCK
26/08/2010 7
B3B3,,
B4B4,,
anxious, confused, lethargyanxious, confused, lethargy
urine outurine out--put ,
-
7/31/2019 Emd166 Slide Shock-1
8/53
Shock in Trauma
-
7/31/2019 Emd166 Slide Shock-1
9/53
Clinical differentiation
1. Hemorrhagic Shock
2. Non Hemorrhagic Shock
Cardiogenic
ens on pneumot orax Neurogenic
Septic
Anaphylactic
-
7/31/2019 Emd166 Slide Shock-1
10/53
BASIC CARDIACBASIC CARDIACBASIC CARDIACBASIC CARDIACBASIC CARDIACBASIC CARDIACBASIC CARDIACBASIC CARDIAC
-
7/31/2019 Emd166 Slide Shock-1
11/53
PREPRE--LOADLOAD CONTRACTILITYCONTRACTILITY AFTERAFTER--LOADLOAD
STROKE VOLUMESTROKE VOLUME HEARTHEART--RATERATE
26/08/2010 11
CARDIAC OUTPUTCARDIAC OUTPUT TOTAL PERIPHERALTOTAL PERIPHERAL
RESISTANCERESISTANCE
BLOOD PRESSUREBLOOD PRESSURE
HasanulHasanul,, 20092009
TissueTissue PerfusionPerfusion
-
7/31/2019 Emd166 Slide Shock-1
12/53
Pathophysiology
The human body responds to acute
hemorrhage by activating the following majorphysiologic systems:
,
cardiovascular,
renal, and
neuroendocrine systems.
-
7/31/2019 Emd166 Slide Shock-1
13/53
The hematologic systemThe hematologic system activating the coagulation cascade and
contracting the bleeding vessels (by means oflocal thromboxane A2 release). platelets are activated (also by means of local
thromboxane A2 release) and form an immature
clot on the bleeding source. The damaged vessel exposes collagen, which
subsequently causes fibrin deposition andstabilization of the clot.
Approximately 24 hours are needed forcomplete clot fibrination and mature formation.
-
7/31/2019 Emd166 Slide Shock-1
14/53
The cardiovascular system initially responds to hypovolemic shock by increasing
the heart rate, increasing myocardial contractility,
constricting peripheral blood vessels.
s response occurs secon ary to an ncrease re ease o
norepinephrine and decreased baseline vagal tone(regulated by the baroreceptors in the carotid arch, aorticarch, left atrium, and pulmonary vessels).
The cardiovascular system also responds byredistributing blood to the brain, heart, and kidneysand away from skin, muscle, and GI tract.
-
7/31/2019 Emd166 Slide Shock-1
15/53
The renal systemThe renal system increase in renin secretion from the
juxtaglomerular apparatus. Renin converts angiotensinogen to angiotensin I,which subsequently is converted to angiotensin II
.
Angiotensin II has 2 main effects, both of whichhelp to reverse hemorrhagic shock :vasoconstriction of arteriolar smooth muscle,
stimulation of aldosterone secretion by the adrenalcortex. Aldosterone is responsible for active sodiumreabsorption and subsequent water conservation
-
7/31/2019 Emd166 Slide Shock-1
16/53
TheThe neuroendocrineneuroendocrine systemsystem increase in circulating antidiuretic hormone
(ADH). ADH is released from the posterior pituitary gland
in response to :
decrease in BP (as detected by baroreceptors)decrease in the sodium concentration (as detected by
osmoreceptors).
ADH indirectly leads to an increased reabsorptionof water and salt (NaCl) by the distal tubule, thecollecting ducts, and the loop of Henle.
-
7/31/2019 Emd166 Slide Shock-1
17/53
HEMORRHAGEHEMORRHAGE
HYPOVOLEMIAHYPOVOLEMIA
BaroreceptorBaroreceptor reflex (arterial & cardiopulmonary)reflex (arterial & cardiopulmonary) Circulating vasoconstrictorsCirculating vasoconstrictors
Chemoreceptor reflexesChemoreceptor reflexes RenalRenal reabsorptionreabsorption of Na+ and waterof Na+ and water Cerebral ischemiaCerebral ischemia
Increased SVR and Cardiac OutputIncreased SVR and Cardiac Output
Shunting blood to vital organsShunting blood to vital organs
-
7/31/2019 Emd166 Slide Shock-1
18/53
VolumeVolume losslossAutonomic tone
Catecholamine release
Fluid shifts from
extracellular to
intravascular
Partial restoration of
intravascular volumesurvivalsurvival
Intervention / stabilization
PathophysiologyPathophysiology ofof HypovolemicHypovolemic ShockShock
Venous capacitance
Heart rate
26/08/2010 18
Maintenance of perfusion
Continued volume loss
Blood flow shunted to vital
organs (heart,lung,brain)
Cellular hypoxia / anaerobicCellular hypoxia / anaerobic
metabolismmetabolism
ATP production / lactic acidosis
Survival / delayed morbidity / mortality
Intervention / stabilization
-
7/31/2019 Emd166 Slide Shock-1
19/53
ATP production / lactic acidosis
Survival / delayed morbidity /Survival / delayed morbidity /
mortalitymortality
Intervention / stabilization
Cellular functionCellular function
impairedimpaired
Cellular hypoxia /Cellular hypoxia /
anaerobic metabolismanaerobic metabolism
PATHOPHYSIO, CONTNPATHOPHYSIO, CONTN
26/08/2010 19
Continued volume loss
Membrane porosity
Movement of fluid
from intravascular to
interstitial spaces
Lysozymal leakage
Cellular autodigestion
IrreversibleIrreversible
shockshockintervention
DEATHDEATHNo. intervention
-
7/31/2019 Emd166 Slide Shock-1
20/53
CELL MEMBRANE FAILURE:
DIRECTEndotoxinComplement
INDIRECTFailure to maintain normal Na+, K+ or Ca2+ gradientDecreased oxidative phosphorylation
EFEK SHOCK PADA TINGKATAN SELEFEK SHOCK PADA TINGKATAN SEL
26/08/2010 20
OSMOTICGRADIENT
Water entryinto cell
CELLULAREDEMA
IMPAIREDINTRACELLULAR
METABOLISM
Na+ entryinto cell
-
7/31/2019 Emd166 Slide Shock-1
21/53
STAGES OF SHOCK
21
-
7/31/2019 Emd166 Slide Shock-1
22/53
COMPENSATED SHOCK
Body defense mechanisms attempt to preserve
major organsPrecapillary sphincters close, blood is shunted
Increased heart rate and stren th of contractions
22
Increased respiratory function, bronchodilation
-
7/31/2019 Emd166 Slide Shock-1
23/53
COMPENSATED SHOCK
Will continue until problem solved or shock
progresses to next stage Can be difficult to detect with subtle indicators
Tach cardia
23
Decreased skin perfusion
Alterations in mental status
Some medications such as propranolol can hide signsand symptoms
-
7/31/2019 Emd166 Slide Shock-1
24/53
UNCOMPENSATED SHOCK
Physiological response
Precapillary sphincters open, blood pressure fallsCardiac output falls
24
,
stagnates
Red cells stack up in rouleaux
-
7/31/2019 Emd166 Slide Shock-1
25/53
UNCOMPENSATED SHOCK
Easier to detect than compensated shock
Prolonged capillary refill timeMarked increase in heart rate
25
Agitation, restlessness, confusion
-
7/31/2019 Emd166 Slide Shock-1
26/53
IRREVERSIBLE SHOCK
Compensatory mechanisms fail, cell death begins,
vital organs falter Patient may be resusitated but will die later of (ARDS,
renal and liver failure, sepsis)
26
-
7/31/2019 Emd166 Slide Shock-1
27/53
Decompensation
-
7/31/2019 Emd166 Slide Shock-1
28/53
Initial assessmentInitial assessmentAirway , Breathing ok?Airway , Breathing ok?
CirculationCirculation
w t n norma m t
Pulse pressure WNL
Warm, Pink, Dry
NO SHOCKNO SHOCKNO SHOCKNO SHOCK
-
7/31/2019 Emd166 Slide Shock-1
29/53
Initial assessmentInitial assessmentAirway , Breathing ok?Airway , Breathing ok?
CirculationCirculation
ac ycar a
Cutaneous vasoconstriction
Pulse pressure
Calmy
SHOCKSHOCKSHOCKSHOCK
-
7/31/2019 Emd166 Slide Shock-1
30/53
Classes of acute hemorrhage*Class I Class II Class III Class IV
Bloodloss < 750 cc0-15% 750-150015-30% 1500-200030-40% >2000cc>40%
HR Normal
PP Normal
BP Normal Normal
UOP Normal Normal Decreased Negligible
Mental Normal Anxious Confused Lethargic
Fluid Crystalloid Crystalloid Crys+blood Crys+blood
*ATLS; 2004. 70kg male
-
7/31/2019 Emd166 Slide Shock-1
31/53
Clinical differentiation1. Hemorrhagic Shock
2. Non Hemorrhagic Shock
Cardiogenic
ens on pneumot orax
Neurogenic
Septic
Anaphylactic
-
7/31/2019 Emd166 Slide Shock-1
32/53
Picture of isreali military or war
-
7/31/2019 Emd166 Slide Shock-1
33/53
Non Hemorrhagic ShockNon Hemorrhagic Shock
-
7/31/2019 Emd166 Slide Shock-1
34/53
Cardiogenic Shock Myocardial dysfunction
Blunt cardiac trauma Cardiac tamponade
Air embolism
TachycardiaBlowing heart sound
Venectasia regio colliHypotension
Valve rupture
ECG monitoring
Isoenzynme-CPK
Echocardiography
-
7/31/2019 Emd166 Slide Shock-1
35/53
Ventil mechanism/flap-valve
Sesak nafas , RR > Emphysema subcutan
Perkusi hypersonor
Tension Pneumothorax
Suara paru menghilang pada ipsilateral
Trakhea terdorong kontralateral
Tachycardia
Hypotension
-
7/31/2019 Emd166 Slide Shock-1
36/53
Neurogenic Shock,
Spinal Shock Cedera tulang belakang
Cedera medulla spinalis Sympathetic denervasi
Vasodilatasi, gambaran hypovolemia
No tachycardia,
No vasokonstriksi
-
7/31/2019 Emd166 Slide Shock-1
37/53
Septic Shock Jarang terjadi segera setelah trauma
Dapat terjadi pada kasus trauma yangterlantar
,
Shock septik pada periode awal : Tachycardia
Perifer hangat
Systolik bisa normal Pulse pressure lebar
-
7/31/2019 Emd166 Slide Shock-1
38/53
-
7/31/2019 Emd166 Slide Shock-1
39/53
ShockShock padapada TraumaTrauma
26/08/2010 39
PerdarahanPerdarahan
HasanulHasanul,, 20092009
PneumothoraxPneumothorax
HematothoraxHematothoraxCardiacCardiac TamponadeTamponade
Spinal ShockSpinal Shock
MyocardialMyocardial
ContussionContussion
-
7/31/2019 Emd166 Slide Shock-1
40/53
Hemorrhagic Shock
Perdarahan ( Hemorrhage)
Kehilangan akut volume sirkulasi darah
( hilang volume, hilang RBC )
-
7/31/2019 Emd166 Slide Shock-1
41/53
Volume Darah
(EBV, Estimated Blood Volume)
Dewasa : 70 mL k
Anak anak : 80 90 mL/kg
-
7/31/2019 Emd166 Slide Shock-1
42/53
Resusistasi cairan harus segera dimulai bilatanda tanda dan gejala kehilangan darah
tampak atau diduga, JANGAN menunggu s/dtanda tanda shock jelas.
-
7/31/2019 Emd166 Slide Shock-1
43/53
KlassifikasiKlassifikasiKlassifikasiKlassifikasiKlassifikasiKlassifikasiKlassifikasiKlassifikasi PerdarahanPerdarahanPerdarahanPerdarahanPerdarahanPerdarahanPerdarahanPerdarahan
-
7/31/2019 Emd166 Slide Shock-1
44/53
Perdarahan kelas I
( s/d 15 % EBV)
Klinis minimal
Pada penderita sehat, tidak perlu diganti
Dalam 24 jam akan ada kompensasi Bila ada kehilangan cairan tubuh oleh sebab
lain, ganti kehilangan cairan primer
-
7/31/2019 Emd166 Slide Shock-1
45/53
Perdarahan kelas II
( 15 s/d 30% EBV)
tachycardia
tachypnoe
Pulse pressure menyempit ( diastolik naik, okkatekolamine )
Gelisah ringan
Hampir selalu membutuhkan transfusi
-
7/31/2019 Emd166 Slide Shock-1
46/53
Perdarahan kelas III
( 30 s/d 40% EBV)
tanda perfusi inadekwat
tachycardia
ac ypnoe
Pulse pressure menyempit ( diastolik naik, okkatekolamine )
Systolik menurun
Produksi urine menurun, pekat Gelisah dan cofuse
-
7/31/2019 Emd166 Slide Shock-1
47/53
Perdarahan kelas IV
( >40% EBV)
tanda perfusi inadekwat sangat jelas tachycardia
Pulse pressure sanagt menyempit atau diastolikyang tdk terukur
Produksi urine sangat menurun s/d negatif, pekat Penurunan kesadaran Kulit dingin , pucat, basah Memerlukan transfusi dan tindakan bedah segera
-
7/31/2019 Emd166 Slide Shock-1
48/53
Class IClass I Class IIClass II Class IIIClass III Class IVClass IV
BloodBlood--Loss[ml]Loss[ml] -->750>750 750750--15001500 15001500--20002000 >2000>2000
BloodBlood--loss [%BV]loss [%BV] -->15%>15% 1515--30%30% 3030--40%40% >40%>40%
PulsePulse--Rate [x/min.]Rate [x/min.] 100 >120>120 >140>140
BloodBlood--PressurePressure NormalNormal NormalNormal DecreasedDecreased DecreasedDecreased
Estimated Fluid and Blood Losses Based onEstimated Fluid and Blood Losses Based on
Patients Initial PresentationPatients Initial Presentation
26/08/2010 48
PulsePulse--PressurePressure N orN orincreasedincreased DecreasedDecreased DecreasedDecreased DecreasedDecreased
Respiratory RateRespiratory Rate 1414--2020 2020--3030 3030--3535 >35>35
Urine outUrine out--putput[ml/hour][ml/hour]
>30>30 2020--3030 55--1515 NegligibleNegligible
Mental status/CNSMental status/CNS SlightlySlightlyanxiousanxious
MidlyMidlyanxiousanxious
AnxiousAnxiousandandconfusedconfused
ConfusedConfusedandandlethargiclethargic
EEBVBV = 70 ml/kg= 70 ml/kg
Ke naan Klinis
-
7/31/2019 Emd166 Slide Shock-1
49/53
Kegunaan Klinis
Tabel Prakiraan Kehilangan Darah Dengan menyesuaikan tanda dan gejala dari penderita pada
tabel, dapat diperkirakan berapa kehilangan darah yang sdh
terjadi. Kemudian kita dapat memperhitungkan berapa jumlah cairan
yang harus diberikan untuk resusitasi
Bila post resisitasi belum ada tanda perbaikan, makakemungkinan :
Ongoing loss
Prakiraan ada kesalahan (BB tidak sesuai, kurang jeli menilai tanda dangejala
Ada tambahan kehilangan cairan lain selain perdarahan Shock bukan ok. perdarahan
-
7/31/2019 Emd166 Slide Shock-1
50/53
Sources of HemorrhageFemur fracture ( 1500 mL)
ChestAbdomen (liver, spleen)
-
Muscle compartments
-
7/31/2019 Emd166 Slide Shock-1
51/53
Thank you for listeningThank you for listeningThank you for listeningThank you for listeningThank you for listeningThank you for listeningThank you for listeningThank you for listening
8/26/2010 51
an o e con n uean o e con n uean o e con n uean o e con n uean o e con n uean o e con n uean o e con n uean o e con n ue
-
7/31/2019 Emd166 Slide Shock-1
52/53
-
7/31/2019 Emd166 Slide Shock-1
53/53