PATHOPHYSIOLOGY OF SHOCK - M56BOOKSTORE -BY TAHER & MANOJ - JOIN US THANKS

1. PATHOPHSIOLOGY OF SHOCK
M56BOOKSTORE
BY MOHAMMED TAHER
MOHAMMED IBRAHIM
MANOJ

2. OBJECTIVE
DEFINITION
REVIEW BASIC PHYSIOLOGY ASPECTS OF SHOCK
DIFFERENT CATEGORIES WITH ETIOLOGY AND
CLINICAL FEATURES
MANAGEMENT ASPECTS

3. DEFINITION
• SHOCK IS A PHYSIOLOGICAL STATE CHARACTERIZED BY
SYSTEMIC REDUCTION IN TISSUE PERFUSION RESULTING
IN DECREASED TISSUE OXYGEN DELIVERY
• BY DECREASING CARDIAC OUTPUT

5. STAGES OF SHOCK
SHOCK HAS TWO STAGES
REVERSIBLE STAGE
IRREVERSIBLE STAGE
REVERSIBLE STAGE :
IN THIS STAGE WITH ACTIVATION OF COMPENSTAORY
MECHANISM STARTS AND THE PATIENT IMPROVES.COMPESNSATORY
REACTIONS ARE DIVIDED INTO 2 TYPES
• RAPID COMPENSATORY OR SHORT TERM MECHANISM
• LONG TERM MECHANISMS

6. RAPID COMPENSATORY MECHANISM
THESE ARE PRIMARILY NEURAL AND VASCULAR THOUGH
HORMONAL MECHANISM ALSO ROLE PLAY
OCCURS MOSTLY DUE TO STIMULATION OF SYMPATHETIC
SYSTEM
SYMPATHETIC ACTIVATION OCCURS MAINLY BY
DECREASED STIMULATION OF BARORECEPTORS AND
HYPOXIA
BUT IN SEVER SHOCK CHEMORECEPTORS AND CUSHINGS
EFFECT IS ACTIVATED

7. LONG TERM COMPENSATORY MECHANISM
IT MAINLY INTENDS TO INCREASE THE RED CELL MASS OF THE
BODY,OXYGEN CARRYING CAPACITY OF BLOOD INCREASE WHICH
ARE
INCREASED SYNTHESIS OF ERYTHROPOIETIN:ERYTHROPOIETIN
SECRETION INCREASES FROMM KIDNEY INCREASED WITIN 48
HOURS,RBC CELL PRODUCTION RETURNS TO NORMAL IN 4-5
WEEKS
INCREASED PLASMA PROTEIN SYNTHESIS: SYNTHESIS OF PROTIEN
BY LIVER WITHIN 2-4 DAYS,INCREASES HEMOGLOBIN SYNTHESIS

8. IRREVERSIBLE STAGE
COMPENSATORY MECHANISM FAIL TO IMPROVE BODY FUNCTIONS
INSPITE OF COMPENSATORY MECHANISM SHOCK PROGRESSES
AND LEADS TO CARDIOVASCULAR RESPONSES TO FAIL
CARDIAC OUTPUT AND BLOOD PRESSURE DECREASE DESPITE OF
THE NORMAL BLOOD VOLUME THIS IS ALSO CALLED AS
REFRACROTY SHOCK OR IRREVERSIBLE SHOCK
USUALLY PATIENT DIES IRRESPECTIVE OF TREATMENT

9. TYPES OF SHOCKS
IT IS DIVIDED INTO FOUR CATEGORIES
HYPOVOLEMIC SHOCK :
DUE TO DECREASED VOLUME OF FLUID IN THE VASCULAR SYSTEM CAUSES INADEQUATE
CARDIAC OUTPUT,MOST COMMON OF ALL SHOCKS . OCCURS DUE TO
 ACUTE HEMORRHAGE OR HEMORRHAGIC SHOCK
 INJURY OR TRAUMATIC SHOCK
 BLOOD LOSS DURING SURGERY OR SURGICAL SHOCK
 METABOLIC DISEASES AS ADRENAZL INSUFFICIENCY,DIABETIC KETOACIDOSIS
 SEVERE DIARRHEA OR VOMITING

10. HEMORRHAGICSHOCK
 MOST COMMON HYPOVOLEMIC SHOCK AND MOST COMMON IN ALL SHOCKS
 ACUTE HEMORRHAGE OF MORE THAN 15 ML/KG BODY WEIGHT RESULTS IN SHOC
FEATURES
• TACHYCARDIA
• HYPOTENSION
• COLD AND PALE SKIN (COLD SHOCK)
• INTENSE THRIST
TRAUMATIC SHOCK
• OCCURES DUE TO SEVERE INJURY ESPECIALLY WHEN MUSCLES OR BONES ARE SEVERLY DAMAGED,MOST
COMMONLY IN ROAD ACCIDENTS
MECHANISM OF TRAUMATIC SHOCK
1. BLEEDING INTO INJURED MUSCLES MAIN CAUSE OF SHOC
 MOST PART IS INTERNAL BLEEDING
2. RHABDOMYOLYSIS : DUE TO SKELETAL MUSCLE CRUSHING ANOTHER CAUSE OF SHOCK

11. SURGICAL SHOCK
 IT OCCURS DUE TO IMPROPER HEMOSTASIS DURING SURGICAL PROCESS OR PROLONGED
SURGRIES
 MAY BE DUE TO INTERNAL OR EXTERNAL HEMORRHAGE OR BOTH
BURN SHOCK
 IN BURNS PLASMA IS LOST FROM THE BURNED SURFACE AD EXUDATE
 EXUDTE IS RICH IN PLASMA PROTIENS ANS FLUIDS DOES NOT CONTAIN RBC,RESULTS IN
HEMOCONCENTRATION
 HEMATOCRIT IS HIGH IN BURN
 HEMOLYTIC ANMEIA ALSO COMPLICATES THE BURN CONDITION

12. THE NEUROHORMANAL MECHANISM THAT COMPENSATE
HYPOVOLEMIC SHOCK ARE :
• 1.TACHYCARDIA : LOSS OF BLOOD DECREASES BLOOD VOLUME AND BLOOD PRESSURE THAT DECREASES
STIMULATION OF BARORECEPTOR AND RESULTS IN SYMPATHETIC ACTIVATION AND INCREASED HEART RATE
• 2. VASO CONSTRICTION : OCUURS DUE TO DECREASED STIMULATION OF BARPRECEPTORS THAT ACTIVATES
SYMPATHETIC SYSTEM
• DUE TO NO VASOCONSTRICTION IN CERBRAL AND CORONARY ARTERIES THEIR BLOOD FLOW MAINTAINED IN
SHOCK
• SKIN BECOMES PALE AND COLD DUE TO INTENSE CUTANEOUS VASOCONSTRICTION THEREFORE CALLED AS
COLD SHOCK
• 3.INCREASED VENOUS RETURM
• 4.INCREASED THORACIC PUMPING
• 5.INCREASED SKELETAL PUMPING
• 6.CAPILLARY FLUID SHIFT : SHIFT OF BLOOD FROM INTERSTITIAL FLUID COMPARTEMENT TO CAPILLARIES

13.  7.ACTIVATION OF CHEMORECEPTOR REFLEX ; BLOOD LOSS SEVERE TO CAUSE HYPOXIA CHEMORECEPTORS ARE
STIMULATED
8.ACTIVATION OF CUSHINGS REFLEX : HYPOTENSION SEVERE AND PERSISTENT CEREBRAL HYPOXIA STIMULATES
VASOMOTOR CENTER RESULTS IN INTENSE VASOCONSTRICTION AND TRIES TO MAINTAIN BLOOD PRESSURE
• 9.INCREASED SECRETIONS OF CATECHOLAMINES :STIMULATES HEART AND MAINTAINS
VASOCONSTRICTION
• 10.INCREASED SECRETION OF VASOPRESSIN : DECREASED BLOOD VOLUME STIMULATES SECRETION OF
ADH WHICH INCREASES REABSORPTION OF WATER FROM COLLECTING DUCT OF KIDNEY RESTORES
BLOOD VOLUME
• 11.ACTIVATION OF RENIN ANGIOTENSIN SYSTEM :HYPOVOLEMIA AND SYMPATHETIC STIMULATION
INCREASES SECRETION OF RENIN FROM JUXTAGLOMERULAR CELLS
• RENIN CONVERTS ANGIOTENSIN TO ANGIOTENSIN I WHICH FURTHERS CONVERTS INTO ANGIOTENSIN II
• ANGIOTENSIN II RESTORES BLOOD VOLUME AND BLOOD PRESSURE
• INCREASES VASOCONSTRICTION
• INSCREASES RELASE OF ALDOSTERONE

14. DISTRIBUTIVE SHOCK :
IN THIS BLOOD VOLUME IS NORMAL BUT BLOOD PRESSURE DECREASES DUE TO SUDDEN
INCREASE IN CAPACITY OF THE VASCULAR COMPARTMENT DUE TO ACUTE MARKED
VASODILATION
CARDIAC OUTPUT ALSO DECREASES IN RESPONSE TO DECREASED VENOUS RETURN
 THIS ALSO CALLED WARM SHOCK AS SKIN BLOOD FLOW INCREASES DUE TO VASODILATION
 EXAMPLES : ANAPHYLATIC SHOCK,SEPTIC SHOCK,ENDOTOXIC SHOCK,NEUROGENIC SHOCK
 ANAPHYLATIC SHOCK :
 SEEN IN ACUTE SYSTEMIC ALLERGY
 ANTIGEN ANTIBODY COMPLEX RELEASES HISTAMINE FROM MAST CELLS CAUSES SEVERE HYPOTENSION
DUE TO VASODILATION AND ACUTE HYPOVOLEMIA
 ANAPHYLATIC SHOCK IS BOTH DISTRIBUTIVE AND HYPOVOLEMIC IN NATURE
SEPTIC SHOCK :
 SEEN IN SYSTEMIC SEPSIS OR BACTERIAL INFECTION
 BACTERIA TOXIN CAUSED VASODILATION SUPRESS MYOCARDIAL CONTRACTILITY
 SEPTIC SHOCK IS COMBINATION OF HYPOVOLEMIC CARDIOGENIC AND DISTRIBUTIVE SHOCK

15.  ENDOTOXIC SHOCK :
IT IS SPECIAL VARETY OF SEPTIC SHOCK OCCURS DUE TO INFECTION BY GRAM
NEGATIVE BACTERIA
THIS BACTERIA RELEASE ENDOTOXIN THAT PRODUCE VASODILATION
CELL WALL OF THESE ORGANISMS CONTAINS LIPOPOLYSACCHARIDES STIMULATE
MACROPHAGES TO RELEASE CYTOKINES
NEUROGENIC SHOCK
 SUDDEN VASODILATION OCCURS DUE TO ACTIVATION OF AUTONOMIC RESPONSES
 CAUSES PERIPHERAL POOLING OF BLOOD DUE TO VASODILATION
 FREQUENTLY SEEN IN EMOTIONAL OUTBURST OVEREXCITEMENT SEVERE GRIEF OR FEAR
 FAINTING OR SYNCOPE OCCURS IN NEUROGENIC SHOCK
CARDIOGENIC SHOCK :
 OCCURS DUE TO DECREASED MYOCARDIAL CONTRACTILITY
 MAY OCCUR DUE TO EXTENSIVE MYOCARDIAL DAMAGE AS IN ACUTE MYOCARDIAL INFARCTION
OR HEART FAILURE
 CARDIAC OUTPUT DECREASES DUE TO DECREASED PUMPING OF BLOOD BY HEART

16.  OBSTRUCTIVE SHOCK :
DUE TO OBSTRUCTION TO THE OUTFLOW OF BLOOD FROM THE HEAR(AORTIC STENOSIS)
OR OBSTRUCTION TO EXPANSION OF HEART
CARDIAC TAMPONADE VENTRICULAR MUSCLES CANNOT RELAX IN DIASTOLE DUE TO EXTERNAL
PRESSURE THAT DECREASES END DIASTOLIC VOLUME THEREFORE DECREASES CARDIAC OUTPUT
TREATMENT OF SHOCK
 BLOOD TRANSFUSION: REQUIRED IN HEMORRHAGIC SHOCK TO INCREASES BLOOD VOLUME
 PLASMA TRANSFUSION : NEEDED IN BURN SHOCK TO INCREASE PLASMA VOLUME
 EPINEPHRINE:INJECTED IN ANAPHYLATIC SHOCK INCREASES BLOOD PRESSURE BY CAUSING
VASOCONSTRICRION AND BY INCREASING CARDIAC OUTPUT
 DOPAMINE:IS DRUG OF CHOICE IN TRAUMATIC AND CARDIOGENIC SHOCK PRODUCES RENAL
VASODILATION THAT MAINTAINS KIDNEY FUNCTION
 HAS POSITIVE INOTROPIC EFFECT THAT INCREASES CARDIA OUTPUT