SHOCK

Hasanul Arifin

Departemen Anestesiologi dan Reanimasi Fakultas Kedokteran USU

26/08/2010

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. DO2 < VO2
Cellular level:

Reduction of mitochondrial oxygen Anaerobic glycolysis of ATP Accumulation of pyruvate lactate

Lactic Acidosis

SHOCK
IT IS NOT LOW BLOOD PRESSURE !!!

IT IS HYPOPERFUSION..

26/08/2010

SHOCK
B1 nafas sesak,, RR , cuping hidung B1, sesak B2, HR , nadi halus cepat,, TD. N/ cepat
PulsePulse-press , perfusi dingin, pucat, basah, dingin, pucat, basah, capill.refill > 2 det., lactic-acid lactic-

B3, B3, B4, B4,

anxious, confused, lethargy urine out-put , <0.5 ml/kg/jam, pekat out-

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Hasanul, 2003

Shock in Trauma

Clinical differentiation
1. Hemorrhagic Shock 2. Non Hemorrhagic Shock
Cardiogenic Tension pneumothorax Neurogenic Septic Anaphylactic

BASIC CARDIAC PHYSIOLOGY

PREPRE-LOAD

CONTRACTILITY

AFTER-LOAD AFTER-

STROKE VOLUME

HEART-RATE HEART-

CARDIAC OUTPUT

TOTAL PERIPHERAL RESISTANCE

BLOOD PRESSURE
26/08/2010 Hasanul, Hasanul, 2009

Tissue Perfusion
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Pathophysiology
The human body responds to acute hemorrhage by activating the following major physiologic systems:
the hematologic, cardiovascular, renal, and neuroendocrine systems.

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. 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 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

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. 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 neuroendocrine 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 the sodium concentration (as detected by osmoreceptors).

ADH indirectly leads to an increased reabsorption of water and salt (NaCl) by the distal tubule, the collecting ducts, and the loop of Henle.

HEMORRHAGE HYPOVOLEMIA
Baroreceptor reflex (arterial & cardiopulmonary) Circulating vasoconstrictors Chemoreceptor reflexes Renal reabsorption of Na+ and water Cerebral ischemia

Increased SVR and Cardiac Output Shunting blood to vital organs

Pathophysiology of Hypovolemic Shock Volume loss

Autonomic tone Catecholamine release Fluid shifts from extracellular to intravascular Partial restoration of intravascular volume

survival
Intervention / stabilization

Venous capacitance Heart rate

Maintenance of perfusion Blood flow shunted to vital organs (heart,lung,brain) Continued volume loss Cellular hypoxia / anaerobic metabolism

Survival / delayed morbidity / mortality ATP production / lactic acidosis

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PATHOPHYSIO, CONTN

Cellular hypoxia / anaerobic metabolism

Survival / delayed morbidity / mortality

ATP production / lactic acidosis

Intervention / stabilization

Cellular function impaired

Continued volume loss Membrane porosity Lysozymal leakage Movement of fluid from intravascular to interstitial spaces Cellular autodigestion

Irreversible shock
intervention No. intervention

DEATH
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EFEK SHOCK PADA TINGKATAN SEL

CELL MEMBRANE FAILURE: DIRECT Endotoxin Complement INDIRECT Failure to maintain normal Na+, K+ or Ca2+ gradient Decreased oxidative phosphorylation OSMOTIC GRADIENT

Na+ entry into cell

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Water entry into cell

CELLULAR EDEMA

IMPAIRED INTRACELLULAR METABOLISM

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STAGES OF SHOCK

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COMPENSATED SHOCK
Body defense mechanisms attempt to preserve major organs Precapillary sphincters close, blood is shunted Increased heart rate and strength of contractions 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 Tachycardia Decreased skin perfusion Alterations in mental status Some medications such as propranolol can hide signs and symptoms

23

UNCOMPENSATED SHOCK
Physiological response Precapillary sphincters open, blood pressure falls Cardiac output falls Blood surges into tissue beds, blood flow stagnates Red cells stack up in rouleaux

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UNCOMPENSATED SHOCK
Easier to detect than compensated shock Prolonged capillary refill time Marked increase in heart rate Rapid thready pulse 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)

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Decompensation

Initial assessment
Airway , Breathing ok?

Circulation
HR within normal limit Pulse pressure WNL Warm, Pink, Dry

NO SHOCK

Initial assessment
Airway , Breathing ok?

Circulation
Tachycardia Cutaneous vasoconstriction Pulse pressure Calmy

SHOCK

Classes of acute hemorrhage*

Class I Blood loss HR PP BP UOP Mental Fluid < 750 cc 0-15% Normal Normal Normal Normal Normal Crystalloid Normal Normal Anxious Crystalloid Decreased Confused Crys+blood Negligible Lethargic Crys+blood Class II 750-1500 15-30% Class III 1500-2000 30-40% Class IV >2000cc >40%

*ATLS; 2004. 70kg male

Clinical differentiation
1. Hemorrhagic Shock 2. Non Hemorrhagic Shock
Cardiogenic Tension pneumothorax Neurogenic Septic Anaphylactic

 Picture of isreali military or war

Non Hemorrhagic Shock

Cardiogenic Shock
Myocardial dysfunction Blunt cardiac trauma Cardiac tamponade Air embolism Valve rupture ECG monitoring Isoenzynme-CPK Echocardiography
Tachycardia Blowing heart sound Venectasia regio colli Hypotension

Tension Pneumothorax
Ventil mechanism/flap-valve Sesak nafas , RR > Emphysema subcutan Perkusi hypersonor 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 vasokonstriksi

Septic Shock
Jarang terjadi segera setelah trauma Dapat terjadi pada kasus trauma yang terlantar Luka tembus abdomen, perforasi Shock septik pada periode awal :
Tachycardia Perifer hangat Systolik bisa normal Pulse pressure lebar

Shock pada Trauma Perdarahan

Cardiac Tamponade
Hasanul, Hasanul, 2009

Pneumothorax

Myocardial Contussion

Hematothorax

Spinal Shock

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Hemorrhagic Shock
Perdarahan ( Hemorrhage)

Kehilangan akut volume sirkulasi darah ( hilang volume, hilang RBC )

Volume Darah (EBV, Estimated Blood Volume) 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 tanda tanda shock jelas.

Klassifikasi Perdarahan

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 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 Pulse pressure sanagt menyempit atau diastolik yang tdk terukur Produksi urine sangat menurun s/d negatif, pekat Penurunan kesadaran Kulit dingin , pucat, basah Memerlukan transfusi dan tindakan bedah segera

Estimated Fluid and Blood Losses Based on Patients Initial Presentation

Class I
BloodBlood-Loss[ml] BloodBlood-loss [%BV] PulsePulse-Rate [x/min.] BloodBlood-Pressure PulsePulse-Pressure Respiratory Rate Urine out-put out[ml/hour] Mental status/CNS ->750 ->15% <100 Normal N or increased 14-20 14>30 Slightly anxious

Class II
750-1500 75015-30% 15>100 Normal Decreased 20-30 2020-30 20Midly anxious

Class III Class IV

1500-2000 150030-40% 30>120 Decreased Decreased 30-35 305-15 Anxious and confused >2000 >40% >140 Decreased Decreased >35 Negligible Confused and lethargic

EBV = 70 ml/kg
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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, maka kemungkinan :
Ongoing loss Prakiraan ada kesalahan (BB tidak sesuai, kurang jeli menilai tanda dan gejala 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) Muscle compartments

Thank you for listening and to be continued

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