KELOMPOK 6 PRABEDAH DASAR

Shock Shock

Cellular injury Reversible or Irreversible

•Inadequate delivery of oxygen •Nutrient requirements are not filled•Toxic metabolites not removed

Clinical manifestations are the results of :Symphatethic and neuroendocrine stress

responsesInadequate O2 deliveryEnd-organ dysfunction

Management of patient is empiric: securing airway, restoration of vascular volume and tissue perfussion; prior to definitive diagnosis

Forms of shock Hypovolemic Cardiogenic Septic Neurogenic

Stage of shock Initial stage :

Tissue perfusion Aerobic metabolism to anaerobic metabolism

lactic acid injures cells cell death Fluid moves from interstitial to capillary to increase

volume Problem not solved compensatory stage.

Stage of shock Compensatory stage

Release of renin; ADH; Aldosterone; epinephrine; norepinephrine

Body will alter its hemodynamic functions to compensate for poor tissue perfusion

Heart rate will increase, the vessels will begin constricting and the body will begin to retain sodium and water

Blood glucose levels will begin to rise and the respiratory rate will increase in an attempt to blow off the effects of lactic acidosis.

Stage of shock Progressive stage

Characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic imbalances

Tissue hypoxia has worsenedFluids moves from vascular to interstitial

spaceAnaerobic metabolism does not produce

enough energy to sustain cellular life and cells begin to die.

Stage of shock Irreversible stage

Body has incurred cellular and tissue injury so severe that even if the hemodynamic defects are corrected, survival is not possible

Cellular ischemia and necrosis leads to organ failure

Hypovolemic shock The most common cause of shock Inadequate circulating blood volume Loss of whole blood, plasma, interstitial

fluid or combination

Loss of blood (hemorrhagic)External bleeding (wound to the outside or

gastrointestinal)Internal bleeding (hematoma, hemothorax,

hemopertitoneum) Loss of plasma

Burns Loss of fluids and electrolytes

External (vomiting, diarrhea, excessive sweating)Internal ( “third spacing” = pancreatitis, ascitis, bowl

obstruction )Excessive sweating

Physiologic mechanismsReduced intravascular volume primarily

affects cardiovascular system. Decreased preload Decreased cardiac output Reduced mean arterial blood pressure Diminished baroreceptor stimulation

Inhibit parasymphatic Activate sympathetic outflow →

norepinephrine release

Physiologic mechanismsEpinephrine and norepinephrine → Increase heart rate and myocardial

contractility →Constriction of arterioles and venules

Compensate decreased preload and myocardial contractility

maintain adequate perfusion pressure

Physiologic mechanisms O2 ↓& CO2 ↑ → acidosis →

chemoreceptors stimulant → respiratory changes & vasoconstriction

Vasoconstriction → selective ↓ blood flow to skin, muscle, and splanchnic circulation. (Brain, heart and kidneys spared)

Fluid shift: extracellular → intravascular to restore blod volume →hematocrit level↓

Physiologic mechanisms The kidney affected by adrenegic

response & blood flow diverted away from kidney & towards the heart & Brain

The Sympathetic discharge kidney perfusion result of renal artery constriction reduces GFR urine output

MEKANISME FISIOLOGIS DANRESPON KOMPENSASI SYOK

HIPOVOLEMIK•Mekanisme fisiologis syok hipovolemik yang paling utama dan penting adalah menurunnya volume intravaskuler mempengaruhi sistem kardiovaskuler preload tekanan arteri rata-rata dan stimulasi baroreseptor dan kemoreseptor stimulasi aktivitas pusat kardiovaskular dan aktivitas simpatis pelepasan epinephrine dan norepinephrin vasokonstriksi periferal dan terjadi ke curah jantung.

Clinical manifestationsDepend on several factors: Degree of hypovolemia Rate of blood loss Ability of body to compensate

Clinical manifestationsClinical signs: Hypotension Weak or absent peripheral pulse Cold clammy skin Tachycardia Oliguria Agitated / mental status changes

ClassificationClass I Volume loss <15% Decrease in perfusion to organs

designed to tolerate some ischemia without profound consequences.

Like a donation of a single unit of blood Slightly anxious

ClassificationClass II 15-30% loss of blood Pulse pressure decrease Kidneys: vasoconstriction, retain sodium,

decreased urine output. Mild anxious & Tachycardia Adrenergic discharge constriction of

blood vessels in the skin pale, cool extremities

ClassificationClass III 30% - 40% blood loss Leads classic finding of haemorragic

shock Tachycardia, tachypnea, significant

alterations in mental status & fall blood pressure

The least amount of blood loss that consistently causes a drop in systolic blood pressure

ClassificationClass IV >40% blood volume deficit Decreased perfusion to heart and brain Classic signs: cold, oliguria, tachycardia,

hypotension, narrowed pulse pressure, deep and rapid respiration.

Depressed mental status Late intervention : death.

ClassificationBlood loss (%)

Blood loss (ml)

BP HR RR

Class I

15 750 Normal <100 14 -20

Class II

15-30 750 - 1500

Normal >100 20 - 30

Class III

20-40 1500-2000

Decreased >120 30 - 40

Class IV

>40 >2000 Decreased >140 >35

ClassificationPulse

PressureUrine output

( ml )Mental status

changes

Class I normal >30 Slight anxious

Class II decreased 20 - 30 Mild anxious

Class III decreased 5 - 15 Anxious,confused

Class IV decreased negligible Confused, lethargic

Diagnosis Search for the cause of hypotension Shock in trauma and postoperative

patient should be presumed as hemorrhage until proven otherwise.

Treatment Primary goals:

Re-expand circulating blood volumeIntervention to control ongoing blood loss

Appropriate priorities:Secure the airwayControl the source of blood lossIntravenous volume rescucitation

Intravenous access Two IV-line access (16-gauge or larger) Access :

Peripheral vein catheterizationCutdowns on basilic, greater sapheous, or

cephalic veins.Percutaneous central venous access via

subclavian, internal jugular or femoral venous puncture.

(~ experience, skill, patient’s conditions)

Choice of fluid for volume rescucitation Most efficacious & effective: rapid

infusion of isotonic saline or balanced salt solution

2-3 L crystalloid over 10-30 minutes Hemorrhagic shock: crystalloid required

at least 3x estimated blood loss. Further should include simultaneous

blood transfusion (either full crossmatched, type-specific, O+, or O- packed cells)