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CLINICAL SCIENCE SESSIOSHOCKBY: GAN EE XIAN

AND FRIENDS

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DEFINITIONSHOCK IS A MULTIFACTORIAL SYNDRORESULTING IN INADEQUATE TISSUEPERFUSION AND CELLULAR OXYGENAT

AFFECTING MULTIPLE ORGAN SYSTEM ISCHEMIA, A TRANSITION FROM AEROBIC TO ANAEROBIC METLACTIC ACIDOSIS, AND ULTIMATELY ORGAN DYSFUNCTION ANFAILURE

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PHYSIOLOGY

SYSTEMIC TISSUE PERFUSION IS DETERMINED B

CARDIAC OUTPUT (CO) AND SYSTEMIC VASCULA

RESISTANCE (SVR).

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DECOMPENSATED' HYPODYNAMIC

LOSS OF -/012 OF BLOOD VOLUME AND THE DETERI

OF THE CARDIOVASCULAR SYSTEMA.DECREASE OF BP BELO3 41 MMHG LEADS TO MYOCARDIAL

B.DECREASE OF BP BELO3 1 MMHG LEADS TO GENERALVASODILATATION CAUSING FURTHER LOSS OF BP

C.INCREASED PERMEABILITY OF THE CAPILLARIES CAUSING THOF BLOOD PLASMA INTO THE TISSUE DECREASING BLOOD V

D.INTRAVASCULAR CLOTTING ( 5 VISCOSITY 6 7VELOCITY)E. CELLULAR DESTRUCTION IS CAUSED BY THE LYSOMOSAL RU

AND 7 IN THE ACTIVITY OF MITOCHONDRIA, ACTIVE TRANSPGENERAL METABOLISM.

F. BUILD UP OF LACTIC ACID LEAD TO ACIDOSIS 3ITH PH DRO8.9/ 4.1 OR LO3ER

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TYPES OF SHOCK

-. HYPOVOLEMIC SHOCK

0. CARDIOGENIC SHOCK'OBSTRUCTIVE SHOCK

9. DISTRIBUTIVE SHOCK

ANAPHYLACTIC SHOCK

SEPTIC SHOCK NEUROGENIC SHOCK

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HYPOVOLEMIC SHOCK

ETIOLOGY:

; INTERNAL OR EXTERNAL FLUID LOSS

; INTRACELLULAR AND EXTRACELLULAR COMPARTMEN

< MOST COMMON CAUSES:HEMMORHAGE

DEHYDRATION

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HYPOVOLEMIC SHOCK

PATHOPHYSIOLOGY

DECREASED INTRAVASCULAR VOLUME DECREAVENOUS RETURN DECREASED VENTRICULARFILLINGDECREASED VENTRICULAR FILLING DECREASED STROKE VOLUME (HR, PRELOAD, =AFTERLOAD) DECREASED CO (COMPENSATORYMECHANISMS) INADEQUATE TISSUE PERFUSION

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HYPOVOLEMIC SHOCK

THERAPY

AIR3AY ' BREATHING ' C'SPINE CONTROL

STOP ALL OBVIOUS HAEMORRHAGE

INSERT I.V. LINES, TAKE BLOOD FOR X/MATCH< INSERT I.V. LINES, TAKE BLOOD FOR X/MA

GIVE RAPID BOLUS OF FLUID, THEN ASSESS RESPONSE

DECIDE ON NEED FOR SURGERY VS. DECISION TO INVESTIGATE

RESUSCITATION ENDPOINTS

CVP 6 - MM HG

3EDGE PRESSURE 6 -1 TO -0 MMHG0. 3EDGE PRESSURE 6 -1 TO -0 MMHG

CARDIAC INDEX > 9 L'MIN'M

BLOOD LACTATE ? @ MMOL'L

BASE DEFICIT /9 TO 9 MMOL'L

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CARDIOGENIC SHOCK'OBSTRUCTIVE S

SYNDROME OF INADEQUATE TISSUE PERFUSION ASSOCIATED 3ITH NO

CIRCULATING BV, AND LO3 CARDIAC OUTPUT

SYMPTOMS: DYSPNOEA, POOR EXERCISE TOLERANCE, CONFUSION, S3

PND

SIGNS: TACHYCARDIA, COLD SKIN, HIGH VP, ADDED HEART SOUNDS, E

LIVER, PERIPHERAL OEDEMA

COMMON CASES

PERICARDIAL TAMPONADE; MUFFLED HEART TONES, ELEVATED NECK V

TENSION PNEUMOTHORAX ; VD, TRACHEAL DEVIATION, DECREASED O

UNILATERAL BREATH SOUNDS, AND CHEST HYPERRESONANCE ON AFF

SIDE

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CARDIOGENIC SHOCK'OBSTRUCTIVE S

PATHOPHYSIOLOGY

IMPAIRED PUMPING ABILITY OF LV

DECREASED TISSUE PERFUSION

PULMONARY INTERSTITIAL = INTRAALVEOLAR EDEMA

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DISTRIBUTIVE SHOCK

INADEQUATE PERFUSION OF TISSUES THROUGH

MALDISTRIBUTION OF BLOOD FLO3. INTRAVASC

VOLUME IS MALDISTRIBUTED BECAUSE OF

ALTERATIONS IN BLOOD VESSELS. CARDIAC PUMBLOOD VOLUME ARE NORMAL BUT BLOOD IS NO

REACHING THE TISSUES

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ANAPHYLACTIC SHOCK

A TYPE OF DISTRIBUTIVE SHOCK THAT RESULTS 3IDESPREAD SYSTEMIC ALLERGIC REACTION TOANTIGEN.

PATHOPHYSIOLOGY: ANTIGEN EXPOSURE BODY

STIMULATED TO PRODUCE IGE ANTIBODIES SPETO ANTIGEN (DRUGS, BITES, CONTRAST, BLOOD

FOODS, VACCINES)REEXPOSURE TO ANTIGEN

BINDS TO MAST CELLS AND

BASOPHILS

ANAPHYLACTIC RESPONSE

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ANAPHYLACTIC SHOCK

ANAPHYLACTIC RESPONSE :

VASODILATATION INCREASED VASCULAR PERMEABILITY

BRONCHOCONSTRICTION

INCREASED MUCUS PRODUCTION

INCREASED INFLAMMATORY MEDIATORS RECRUITMENT TO SITES OF ANTIGEN INTERACTION

CLINICAL MANIFESTATION :

ALMOST IMMEDIATE RESPONSE TO INCITING

ANTIGEN

CUTANEOUS MANIFESTATIONS; URTICARIA, ERYTHEMA, PRURITIS, ANGIOEDEMA

RESPIRATORY COMPROMISE; STRIDOR, 3HEEING, BRONCHORRHEA, RESP.DISTRESS

CIRCULATORY COLLAPSE ; TACHYCARDIA, VASODILATION, HYPOTENSION

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NEUROGENIC SHOCK

A TYPE OF DISTRIBUTIVE SHOCK THAT RESULTS F

THE LOSS OR SUPPRESSION OF SYMPATHETIC TO CAUSES MASSIVE VASODILATATION IN THE VENOUS

VASCULATURE, DECREASE VENOUS RETURN TO HEARDECREASE CARDIAC VASCULATURE, DECREASE VENO

RETURN TO HEART, DECREASE CARDIAC OUTPUT.

MOST COMMON ETIOLOGY: SPINAL CORD INURY

T4

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NEUROGENIC SHOCK

PATIENT ASSESSMENT

HYPOTENSION

BRADYCARDIA

HYPOTHERMIA

3ARM, DRY SKIN

RAP DECREASE (RIGHT ATRIAL PRESSURE)

PA3P DECREASE (PULMONARY ARTERY 3EDGE PRESSURE)

CO DECREASE (CARDIAC OUTPUT)

FLACCID PARALYSIS BELO3 LEVEL OF THE SPINAL LESION

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SEPTIC SHOCK

SYNDROME OF PROFOUND HYPOTENSION DUE TORELEASE OF ENDOTOXINS ' TNF' VASOACTIVE PEFOLLO3ING BACTERIAL DESTRUCTIONPEPTIDESFOLLO3ING BACTERIAL DESTRUCTION. USUALLY

ASSOCIATED 3ITH NORMAL BLOOD VOLUME, HIGLO3 CO, AND LO3 SYSTEMIC VASCULAR RESISTA

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SEPTIC SHOCK

PATHOPHYSIOLOGY

INITIATED BY GRAM/NEGATIVE (MOST COMMON) OR GRAM POSITIVE FUNGI, OR VIRUSESCELL 3ALLS OF ORGANISMS CONTAIN ENDOTOINCREASE ENDOTOXINS RELEASE INFLAMMATORY MEDIATORS (SYSTINFLAMMATORY RESPONSE) CAUSESINCREASE VASODILATION = INCAPILLARY PERMEABILITYSHOCK DUE TO ALTERATION IN PERIPHER

CIRCULATION = MASSIVE DILATION

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TERIMA KASIHSELAMAT MEMBACA