emd166 slide shock-1

7/31/2019 Emd166 Slide Shock-1

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SHOCK

Hasanul Arifin

Departemen Anestesiologi dan Reanimasi

Fakultas Kedokteran USU


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glucose oksigen

38 Mol ATP


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glucose oksigen

2 Mol ATP

+

36 Mol Lactate


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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


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SHOCKSHOCKSHOCKSHOCK

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IT IS HYPOPERFUSION..


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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

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B3B3,,

B4B4,,

anxious, confused, lethargyanxious, confused, lethargy

urine outurine out--put ,


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Shock in Trauma


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Clinical differentiation

1. Hemorrhagic Shock

2. Non Hemorrhagic Shock

Cardiogenic

ens on pneumot orax Neurogenic

Septic

Anaphylactic


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BASIC CARDIACBASIC CARDIACBASIC CARDIACBASIC CARDIACBASIC CARDIACBASIC CARDIACBASIC CARDIACBASIC CARDIAC


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PREPRE--LOADLOAD CONTRACTILITYCONTRACTILITY AFTERAFTER--LOADLOAD

STROKE VOLUMESTROKE VOLUME HEARTHEART--RATERATE

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CARDIAC OUTPUTCARDIAC OUTPUT TOTAL PERIPHERALTOTAL PERIPHERAL

RESISTANCERESISTANCE

BLOOD PRESSUREBLOOD PRESSURE

HasanulHasanul,, 20092009

TissueTissue PerfusionPerfusion


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Pathophysiology

The human body responds to acute

hemorrhage by activating the following majorphysiologic systems:

,

cardiovascular,

renal, and

neuroendocrine systems.


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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.


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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.


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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


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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.


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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


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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

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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



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ATP production / lactic acidosis

Survival / delayed morbidity /Survival / delayed morbidity /

mortalitymortality


Cellular functionCellular function

impairedimpaired

Cellular hypoxia /Cellular hypoxia /

anaerobic metabolismanaerobic metabolism

PATHOPHYSIO, CONTNPATHOPHYSIO, CONTN

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Continued volume loss

Membrane porosity

Movement of fluid

from intravascular to

interstitial spaces

Lysozymal leakage

Cellular autodigestion

IrreversibleIrreversible

shockshockintervention

DEATHDEATHNo. intervention


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CELL MEMBRANE FAILURE:

DIRECTEndotoxinComplement

INDIRECTFailure to maintain normal Na+, K+ or Ca2+ gradientDecreased oxidative phosphorylation

EFEK SHOCK PADA TINGKATAN SELEFEK SHOCK PADA TINGKATAN SEL

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OSMOTICGRADIENT

Water entryinto cell

CELLULAREDEMA

IMPAIREDINTRACELLULAR

METABOLISM

Na+ entryinto cell


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STAGES OF SHOCK

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COMPENSATED SHOCK

Body defense mechanisms attempt to preserve

major organsPrecapillary sphincters close, blood is shunted

Increased heart rate and stren th of contractions

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Increased respiratory function, bronchodilation


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COMPENSATED SHOCK

Will continue until problem solved or shock

progresses to next stage Can be difficult to detect with subtle indicators

Tach cardia

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Decreased skin perfusion

Alterations in mental status

Some medications such as propranolol can hide signsand symptoms


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UNCOMPENSATED SHOCK

Physiological response

Precapillary sphincters open, blood pressure fallsCardiac output falls

24

,

stagnates

Red cells stack up in rouleaux


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UNCOMPENSATED SHOCK

Easier to detect than compensated shock

Prolonged capillary refill timeMarked increase in heart rate

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Agitation, restlessness, confusion


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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


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Decompensation


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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


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Initial assessmentInitial assessmentAirway , Breathing ok?Airway , Breathing ok?

CirculationCirculation

ac ycar a

Cutaneous vasoconstriction

Pulse pressure

Calmy

SHOCKSHOCKSHOCKSHOCK


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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


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Clinical differentiation1. Hemorrhagic Shock

2. Non Hemorrhagic Shock

Cardiogenic

ens on pneumot orax

Neurogenic

Septic

Anaphylactic


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Picture of isreali military or war


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Non Hemorrhagic ShockNon Hemorrhagic Shock


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Cardiogenic Shock Myocardial dysfunction

Blunt cardiac trauma Cardiac tamponade

Air embolism

TachycardiaBlowing heart sound

Venectasia regio colliHypotension

Valve rupture

ECG monitoring

Isoenzynme-CPK

Echocardiography


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Ventil mechanism/flap-valve

Sesak nafas , RR > Emphysema subcutan

Perkusi hypersonor

Tension Pneumothorax

Suara paru menghilang pada ipsilateral

Trakhea terdorong kontralateral

Tachycardia

Hypotension


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Neurogenic Shock,

Spinal Shock Cedera tulang belakang

Cedera medulla spinalis Sympathetic denervasi

Vasodilatasi, gambaran hypovolemia

No tachycardia,

No vasokonstriksi


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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


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ShockShock padapada TraumaTrauma

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PerdarahanPerdarahan

HasanulHasanul,, 20092009

PneumothoraxPneumothorax

HematothoraxHematothoraxCardiacCardiac TamponadeTamponade

Spinal ShockSpinal Shock

MyocardialMyocardial

ContussionContussion


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Hemorrhagic Shock

Perdarahan ( Hemorrhage)

Kehilangan akut volume sirkulasi darah

( hilang volume, hilang RBC )


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Volume Darah

(EBV, Estimated Blood Volume)

Dewasa : 70 mL k

Anak anak : 80 90 mL/kg


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Resusistasi cairan harus segera dimulai bilatanda tanda dan gejala kehilangan darah

tampak atau diduga, JANGAN menunggu s/dtanda tanda shock jelas.


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KlassifikasiKlassifikasiKlassifikasiKlassifikasiKlassifikasiKlassifikasiKlassifikasiKlassifikasi PerdarahanPerdarahanPerdarahanPerdarahanPerdarahanPerdarahanPerdarahanPerdarahan


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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


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Perdarahan kelas II

( 15 s/d 30% EBV)

tachycardia

tachypnoe

Pulse pressure menyempit ( diastolik naik, okkatekolamine )

Gelisah ringan

Hampir selalu membutuhkan transfusi


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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


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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


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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

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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


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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


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Sources of HemorrhageFemur fracture ( 1500 mL)

ChestAbdomen (liver, spleen)

-

Muscle compartments


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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

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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


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emd166 slide shock-1

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