SHOCK

Hasanul Arifin

Departemen Anestesiologi dan Reanimasi

Fakultas Kedokteran USU

26/08/2010 2

glucose oksigen

38 Mol ATP

glucose oksigen

2 Mol ATP

+

36 Mol Lactate

Definition of Shock

• Reduced perfusion of vital organs leading to

inadequate oxygen and nutrients necessary

for normal tissue and cellular function.

• DO < VO• DO2 < VO2

• Cellular level:

– Reduction of mitochondrial oxygen

– Anaerobic glycolysis of ATP

– Accumulation of pyruvate � lactate � Lactic Acidosis

IT IS NOT LOW BLOOD PRESSURE !!!

SHOCKSHOCKSHOCKSHOCK

26/08/2010 6

IT IS NOT LOW BLOOD PRESSURE !!!

IT IS HYPOPERFUSION…..

•• 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 , <0.5 ml/kg/jam, pekatput , <0.5 ml/kg/jam, pekat

Hasanul, 2003Hasanul, 2003

Shock in Trauma

Clinical differentiation

1. Hemorrhagic Shock

2. Non Hemorrhagic Shock

� Cardiogenic

� Tension pneumothorax� Tension pneumothorax

� Neurogenic

� Septic

� Anaphylactic

BASIC CARDIAC BASIC CARDIAC BASIC CARDIAC BASIC CARDIAC BASIC CARDIAC BASIC CARDIAC BASIC CARDIAC BASIC CARDIAC

PHYSIOLOGY PHYSIOLOGY PHYSIOLOGY PHYSIOLOGY PHYSIOLOGY PHYSIOLOGY PHYSIOLOGY PHYSIOLOGY PHYSIOLOGY PHYSIOLOGY PHYSIOLOGY PHYSIOLOGY PHYSIOLOGY PHYSIOLOGY PHYSIOLOGY PHYSIOLOGY

PREPRE--LOADLOAD CONTRACTILITYCONTRACTILITY AFTERAFTER--LOADLOAD

STROKE VOLUMESTROKE VOLUME HEARTHEART--RATERATE

26/08/2010 11

CARDIAC OUTPUTCARDIAC OUTPUT TOTAL PERIPHERAL TOTAL PERIPHERAL

RESISTANCERESISTANCE

BLOOD PRESSUREBLOOD PRESSURE

HasanulHasanul, , 20092009

Tissue Tissue PerfusionPerfusion

Pathophysiology

• The human body responds to acute

hemorrhage by activating the following major

physiologic systems:

� the hematologic, � the hematologic,

� cardiovascular,

� renal, and

� neuroendocrine systems.

The hematologic system The hematologic system

• activating the coagulation cascade and contracting the bleeding vessels (by means of local thromboxane A2 release).

• platelets are activated (also by means of local thromboxane A2 release) and form an immature clot on the bleeding source. thromboxane A2 release) and form an immature clot on the bleeding source.

• The damaged vessel exposes collagen, which subsequently causes fibrin deposition and stabilization of the clot.

• Approximately 24 hours are needed for complete clot fibrination and mature formation.

The cardiovascular system

• initially responds to hypovolemic shock by increasing the heart rate,

• increasing myocardial contractility,

• constricting peripheral blood vessels.

– This response occurs secondary to an increased release of – This response occurs secondary to an increased release of norepinephrine and decreased baseline vagal tone (regulated by the baroreceptors in the carotid arch, aortic arch, left atrium, and pulmonary vessels).

• The cardiovascular system also responds by redistributing blood to the brain, heart, and kidneys and away from skin, muscle, and GI tract.

The renal system The renal system

• increase in renin secretion from the juxtaglomerular apparatus.

• Renin converts angiotensinogen to angiotensin I, which subsequently is converted to angiotensin II by the lungs and liver. by the lungs and liver.

• Angiotensin II has 2 main effects, both of which help to reverse hemorrhagic shock : – vasoconstriction of arteriolar smooth muscle,

– stimulation of aldosterone secretion by the adrenal cortex. Aldosterone is responsible for active sodium reabsorption and subsequent water conservation

The The neuroendocrineneuroendocrine system system

• 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 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, the collecting ducts, and the loop of Henle.

HEMORRHAGEHEMORRHAGE

HYPOVOLEMIAHYPOVOLEMIA

•• BaroreceptorBaroreceptor reflex (arterial & cardiopulmonary)reflex (arterial & cardiopulmonary)

•• Circulating vasoconstrictors Circulating vasoconstrictors

•• Chemoreceptor reflexesChemoreceptor reflexes•• Chemoreceptor reflexesChemoreceptor reflexes

•• Renal Renal 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

VolumeVolume lossloss����Autonomic tone

Catecholamine release

Fluid shifts from

extracellular to

intravascular

Partial restoration of

intravascular volumesurvivalsurvival

Intervention / stabilization

Maintenance of perfusion

PathophysiologyPathophysiology of of 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 / anaerobic Cellular hypoxia / anaerobic

metabolismmetabolism

����ATP production / lactic acidosis

Survival / delayed morbidity / mortality

Intervention / stabilization

����ATP production / lactic acidosis

Survival / delayed morbidity / Survival / delayed morbidity /

mortalitymortality

Intervention / stabilization

Cellular function Cellular function

impairedimpaired

Cellular hypoxia / Cellular hypoxia /

anaerobic metabolismanaerobic metabolism

PATHOPHYSIO, CONT’NPATHOPHYSIO, CONT’N

26/08/2010 19

Continued volume loss

����Membrane porosity

Movement of fluid

from intravascular to

interstitial spaces

Lysozymal leakage

Cellular autodigestion

Irreversible Irreversible

shockshockintervention

DEATHDEATHNo. intervention

CELL MEMBRANE FAILURE:

• DIRECT EndotoxinComplement

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

EFEK SHOCK PADA TINGKATAN SELEFEK SHOCK PADA TINGKATAN SEL

26/08/2010 20

OSMOTIC GRADIENT

Water entry into cell

CELLULAR EDEMA

IMPAIRED INTRACELLULAR

METABOLISM

Na+ entry into cell

STAGES OF SHOCK

21

COMPENSATED SHOCK

• Body defense mechanisms attempt to preserve

major organs

– Precapillary sphincters close, blood is shunted

– Increased heart rate and strength of contractions

22

– Increased heart rate and strength of contractions

– Increased respiratory function, bronchodilation

COMPENSATED SHOCK

• Will continue until problem solved or shock

progresses to next stage

• Can be difficult to detect with subtle indicators

– Tachycardia

23

– Tachycardia

– Decreased skin perfusion

– Alterations in mental status

• Some medications such as propranolol can hide signs

and symptoms

UNCOMPENSATED SHOCK

• Physiological response

– Precapillary sphincters open, blood pressure falls

– Cardiac output falls

– Blood surges into tissue beds, blood flow

24

– Blood surges into tissue beds, blood flow

stagnates

– Red cells stack up in rouleaux

UNCOMPENSATED SHOCK

• Easier to detect than compensated shock

– Prolonged capillary refill time

– Marked increase in heart rate

– Rapid thready pulse

25

– Rapid thready pulse

– Agitation, restlessness, confusion

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

Decompensation

Initial assessmentInitial assessment

Airway , Breathing ok?Airway , Breathing ok?

CirculationCirculation

• HR within normal limit• HR within normal limit

• Pulse pressure WNL

• Warm, Pink, Dry

NO SHOCKNO SHOCKNO SHOCKNO SHOCK

Initial assessmentInitial assessment

Airway , Breathing ok?Airway , Breathing ok?

CirculationCirculation

• Tachycardia• Tachycardia

• Cutaneous vasoconstriction

• Pulse pressure

• Calmy

SHOCKSHOCKSHOCKSHOCK

Classes of acute hemorrhage*

Class I Class II Class III Class IV

Blood

loss

< 750 cc 0-15%

750-1500 15-30%

1500-200030-40%

>2000cc>40%

HR Normal

PPPP 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

Clinical differentiation

1. Hemorrhagic Shock

2. Non Hemorrhagic Shock

� Cardiogenic

� Tension pneumothorax� Tension pneumothorax

� Neurogenic

� Septic

� Anaphylactic

• Picture of isreali military or war

Non Hemorrhagic ShockNon Hemorrhagic Shock

Cardiogenic Shock

• Myocardial dysfunction

• Blunt cardiac trauma

• Cardiac tamponade

• Air embolism

• Valve rupture

•Tachycardia

•Blowing heart sound

•Venectasia regio colli

•Hypotension

• Valve rupture

• ECG monitoring

• Isoenzynme-CPK

• Echocardiography

• Ventil mechanism/flap-valve

• Sesak nafas , RR >

• Emphysema subcutan

• Perkusi hypersonor

• Suara paru menghilang pada ipsilateral

Tension Pneumothorax

• Suara paru menghilang pada ipsilateral

• Trakhea terdorong kontralateral

• Tachycardia

• Hypotension

Neurogenic Shock,

Spinal Shock

• Cedera tulang belakang

• Cedera medulla spinalis

• Sympathetic denervasi

• Vasodilatasi, � gambaran hypovolemia

• No tachycardia, • No tachycardia,

• No vasokonstriksi

Septic Shock

• Jarang terjadi segera setelah trauma

• Dapat terjadi pada kasus trauma yang terlantar

• Luka tembus abdomen, perforasi• Luka tembus abdomen, perforasi

• Shock septik pada periode awal :• Tachycardia

• Perifer hangat

• Systolik bisa normal

• Pulse pressure lebar

Shock Shock padapada TraumaTrauma

26/08/2010 39

PerdarahanPerdarahan

HasanulHasanul, , 20092009

PneumothoraxPneumothorax

HematothoraxHematothorax

Cardiac Cardiac TamponadeTamponade

Spinal ShockSpinal Shock

Myocardial Myocardial

ContussionContussion

Hemorrhagic Shock

• Perdarahan ( Hemorrhage)

• Kehilangan akut volume sirkulasi darah

( hilang volume, hilang RBC )

Volume Darah

(EBV, Estimated Blood Volume)

• Dewasa : 70 mL/kg• Dewasa : 70 mL/kg

• Anak anak : 80 – 90 mL/kg

• Resusistasi cairan harus segera dimulai bila

tanda tanda dan gejala kehilangan darah

tampak atau diduga, JANGAN menunggu s/d tampak atau diduga, JANGAN menunggu s/d

tanda tanda shock jelas.

KlassifikasiKlassifikasiKlassifikasiKlassifikasiKlassifikasiKlassifikasiKlassifikasiKlassifikasi PerdarahanPerdarahanPerdarahanPerdarahanPerdarahanPerdarahanPerdarahanPerdarahan

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

Perdarahan kelas – II

( 15 s/d 30% EBV)

• tachycardia

• tachypnoe

• Pulse pressure menyempit ( diastolik naik, ok

katekolamine )

• Gelisah ringan

• Hampir selalu membutuhkan transfusi

Perdarahan kelas – III

( 30 s/d 40% EBV)

• tanda perfusi inadekwat

• tachycardia

• tachypnoe• tachypnoe

• Pulse pressure menyempit ( diastolik naik, ok katekolamine )

• Systolik menurun

• Produksi urine menurun, pekat

• Gelisah dan cofuse

Perdarahan kelas – IV

( >40% EBV)

• tanda perfusi inadekwat sangat jelas

• tachycardia

• tachypnoe• tachypnoe

• 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

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<100 >100>100 >120>120 >140>140

BloodBlood--PressurePressure NormalNormal NormalNormal DecreasedDecreased DecreasedDecreased

Estimated Fluid and Blood Losses Based on Estimated Fluid and Blood Losses Based on

Patient’s Initial PresentationPatient’s Initial Presentation

26/08/2010 48

PulsePulse--PressurePressure N or N or increasedincreased

DecreasedDecreased DecreasedDecreased DecreasedDecreased

Respiratory RateRespiratory Rate 1414--2020 2020--3030 3030--3535 >35>35

Urine outUrine out--put put [ml/hour][ml/hour]

>30>30 2020--3030 55--1515 NegligibleNegligible

Mental status/CNSMental status/CNS Slightly Slightly anxiousanxious

Midly Midly anxiousanxious

Anxious Anxious and and confusedconfused

Confused Confused and and lethargiclethargic

EEBV BV = 70 ml/kg= 70 ml/kg

Kegunaan Klinis

Tabel Prakiraan Kehilangan Darah• Dengan menyesuaikan tanda dan gejala dari penderita pada

tabel, dapat diperkirakan berapa kehilangan darah yang sdhterjadi.

• Kemudian kita dapat memperhitungkan berapa jumlah cairanyang harus diberikan untuk resusitasi

• Bila post resisitasi belum ada tanda perbaikan, maka• 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

Sources of Hemorrhage

– Femur fracture ( 1500 mL)

– Chest

– Abdomen (liver, spleen)

– Retroperitoneal ( 2-4 L)– Retroperitoneal ( 2-4 L)

– Muscle compartments

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

and to be continuedand to be continuedand to be continuedand to be continuedand to be continuedand to be continuedand to be continuedand to be continued

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and to be continuedand to be continuedand to be continuedand to be continuedand to be continuedand to be continuedand to be continuedand to be continued