shock defination: shock is defined as an acute clinical syndrome characterized by hypoperfusion and severe disfunction of vital organs. types of shock: hypovolaemic cardiogenic obstructive distructive neurogenic anaphylactic septic pathophysiology causes treatment clinical features

1. DEFINITION
CLASSIFICATION AND
PATHOPHISIOLOGY
By: Dr. kajal sachdeva
Dr. Prabhjot

2. DEFINITION:
 Shock is defined as an acute clinical syndrome
characterized by hypoperfusion and severe disfunction
of vital organs.
 There is failure of the circulatory system to supply
blood in sufficient quantities.

3. CLASSIFICATION OF SHOCK:
SHOCK
HYPOVOLAEMIC
CARDIOGENIC
OBSTRUCTIVE
DISTRIBUTIVE
1)NEUROGENIC
2)ANAPHYLACTIC
3)SEPTIC

4. HYPOVOLAEMIC SHOCK:
 LOSS OF BLOOD – HAEMRRAGHIC SHOCK.
 LOSS OF PLASMA – AS IN BURNS SHOCK.
 LOSS OF FLUID – DEHYDRATION.

5. LOSS OF
BLOOD
DECREASE
FILLING OF
RIGHT HEART
DECREASE
FILLING OF
PILMONARY
VASCULATURE
DECREASE
FILLING OF
LEFT ATRIUM
AND
VENTRICLE
DECREASE
LEFT
VENTRICULAR
STROKE
VOLUME
THIS CAUSES
DROP IN
ARTERIAL
BLOOD
PRESSURE

6. SIGNS :
 Compensatory events take place :
1) Tachycardia.
2) Peripheral vasoconstriction.
3) hypotension,.

7. TREATMENT:
1) Primary goal is to return the blood volume,tissue
perfusion and oxygenationyo normal.
2) CRYSTALLOIDS : 2-3 times the volume of blood lost
must be replaced with isotonic saline or ringer
lactate.
3) COLLOIDS : 1-1.5 times the blood lost can be
replaced with colloids instead of crystalloids.
4) BLOOD TRANSFUSION :

9. CARDIGENIC SHOCK:
DEFINITION
INCIDENCE
CAUSES
CLASSIFICATION SYMPTOMS
PATHOPHYSIOLOGY
DIAGNOSIS
PREVENTIONS TREATMENTS

11. DEFINITION:
Cardiogenic shock is
acondition in which
your heart suddenly
cant pump enough
blood to meet your
body needs.

12. INCIDENCE:
Cardiogenic
shock occurs as a
serious
complications in
5% to 10% of
patienys
hospitalized with
acute myocardial
infarction
Historically
morality for
cardiogenic
shock had been
80% to 90%

13. CAUSES:
 MYOCARDIAL ISCHEMIA:
Compensatory mechanisms may initially stablizes the
patient but later on would cause deterioration with the
rising demands of oxygen of the already
Compromised myocardium.
 MYOCARDIAL INFARCTION:
 INFLAMMATION OF THE HEART MUSCLES:
 INFECTION OF HEART VALVES:
 WEAKENED HEART:
 DRUG OVERDOSES:

14. CLASSIFICATION:
CORONARY
SHOCK
NON
CORONARY
SHOCK

16. CORONARY SHOCK:
 IT IS MORE
COMMON IN
THAN NON
CORONARY
SHOCK AND IS
SEEN IN
MYOCARDIAL
INFECTED
PATEIENT.

17. NON CORONARY SHOCK:
NON CORONARY SHOCK IS
RELATED TO CONDITIONS
LIKE STRESS THE
MYOCARDIUM AS WELL
AS CONDITIONS THAT
RESULT IN AN INFECTIVE
MYOCARDIAL FUNCTION.

18. SYMPTOMS:
CLAMMY
SKIN
DECREASED
SYSTOLIC
BLOOD
PRESSURE
TACHYCARDIA
RAPIDRESPIRATINS
OLIGURIA

19. OTHER SYMPTOMS ARE:
RAPID BREATHING
SEVERE SHORTNESS OF BREATHE
SUDDEN RAPID HEART BEAT
LOSS OF CONSCIOUSNESS
WEAK PULSE
URINATING LESS THAN NORMAL

20. PATHOPHYSIOLOGY:
INADEQUATE PERFUSION
CELL HYPOXIA
ENERGYB DEFICIT
LACTIC ACID ACCUMULATION
METABOLIC ACIDOSIS
DYSFUNCTION AND FAILURE OF SODIUM PUMP
DIGESTIVE ENZYMES APPEARANCE
TOXIC SUBSTANCES IN TO CIRCULATION
CAPPILARY ENDOTHELIAL DAMAGED

21. PREVENTION:
DONT SMOKE
EAT HEALTHY
DIET
EAT LESS
CHOLESTEROL
LIMIT ADDED
SUGAR AND
ALCOHOL
EXCERCISE
REGULARLY

22. TREATMENT:
MEDICATIONS:
INOTROPIC AGENTS : TO IMPROVE HEART FUNCTIONS SUCH AS
NOREPINEPHRINE OR DOPAMINE
ASPIRIN:
TO REDUCE BLOOD CLOTTING AND KEEP THE BLOOD FLOWING
THROMBOLYTIC DRUGS:
ARE A GROUP USED TO DISSOLVE CERTAIN TYPE OF CLOTS LIKE
STREPTOKINASE ANDG UROKINASE

23. ANTIPLATELET MEDICATIONS:
THESE DRUGS ARE SIMILar to aspirin and help to
prevent new clots

25. CARDIAC CATHETRIZATION

26. Angioplasty:

28. BALLON PUMP:

29. SURGERY:

30. HEART TRANSPLANT:

31. VENTRICULAR ASSIT DEVICE:

32. DIS TRIBUTIVE SHOCK :
 THIS OCCURS WHEN THE AFTERLOAD IS
EXCESSIVELY REDUCED.
 SITUATIONS ARE :
I. SEPTIC SHOCK
II. ANAPHYLACTIC SHOCK
III. ACUTE RENAL INSUFFICIENY
IV. NEUROGENIC SHOCK

33. SEPTIC SHOCK:
 INTRODUCTION
 AETIOLOGY
 CLINICAL FEARTERES
 INVESTIGATIONS
 TREATMENT

34. SEPTIC SHOCK:
The most common of all distributive shocks
The leading cause of death in icu in the us
Increasing in occurence
Increases life support fo high ill patients

35. PREDISDPOSING FACTORS ARE:
 Extended hospitalization
 Advanced age
 Debilitating illness
 Immunodeficiency disorder
 Disseminated malignancy

36. AETIOLOGY:
 BACTERIAL INFECTION : GRAM NEGATIVE
 BACTERIODES
 SERRATIA
 PROTEUSD

38. PATHOGENESIS:
 ANTI INFLAMMATORY OR IMMUNESUPPRESSION
CYTOKINES IL-4 INHIBITS THE ACTIVITY OF
PROINFLAMMATORY CYTOKINES TO LIMIT
DAMAGE.

40. PATHOGENISIS:

41. CLINICAL FEATURES:
 LOW SYSTEMIC VASCULAR RESISTANCE
 GENEALIZED TISSUE HYPOPERFUSION
 EARLY STAGE:
1. FEBRILE
2. SHIVERING
3. HOT FLUSHY SKIN

42. LATE STAGE:
1. FEEBLE
2. OLIGURIA
3. JAUNDICE
4. ALTERED SENOSORIUM

43. TREATMENT:
1) removal of septic shockis essential process
2) Antibiotics
3) Oxygenation
4) Intravenous fluids
5) Vasoactice

44. ANAPHYLACTIC SHOCK:
 INTRODUCTION
 CLINICAL FEATURES
 TREATMENT

46. ANAPHYLACTIC:
 it is the type of distributive shock
 Occurs by the exposure of allergans the patient is
sensitive too
 It may be pollen and food stuff
 The anaphylactic shock tha occur in the hopital is
usually due to some drufgs
 Example is penicillin allergy

47. FEATURES ARE:
 Reaction may shows rash with bronchospasm or
without bronchospasm
 Generalized edema
 Bronchospam
 Hypotension

49. TREATMENT:
 PRIMARY : oxygenation if necessary
 Endotracheal intubation
 Ventilation
 Adrenaline
 Interavenous fluids
 Leg and elevation of bed
 SECONDARY: chlorpheniramine meleate
 Hydrocortisone

50. NEUROGENIC SHOCK:
 INTRODUCTION
 CAUSES
 CLINICAL FEATURES
 TREATMENT

51. INTRODUCTION:
 Rare shock

52. CAUSES:
 High spinal cord injury
 Vagolytic shock
 Trauma

53. CLINICAL FEATURES:
 Hypotension without tachycardia may deteriorate to
produce shock and cardiac arrest

54. TREATMENT:
 Interavenous fluids
 Inotropes
 Vagolytics