Shock is defined as inadequate tissue perfusion resulting from reduced blood flow or oxygen delivery. There are four main types of shock: hypovolemic, cardiogenic, distributive, and obstructive. The management of shock involves treating the underlying cause, restoring circulating volume with intravenous fluids, and providing supportive care such as oxygen supplementation. Goals are to improve oxygen delivery and prevent end organ damage. Early recognition and treatment are important for successful management.

1. MANAGEMENT OF
SHOCK
SuamePrecious

2. OBJECTIVES
 Define shock and its different categories.
 Review basic physiologic aspects of shock.
 Describe the management of shock.

3. Definition of Shock
Shock is an abnormal physiological state resulting
from wide-spread and serious reduction of tissue
perfusion that if prolonged will lead to generalized
impairment of cellular function.
Inadequate tissue perfusion to meet tissue demands
Usually as a result of inadequate blood flow and/or
oxygen delivery.

4. Classification and Causes of Shock
(1) HYPOVOLEMIC SHOCK (DECREASE IN BLOOD
VOLUME):
Hemorrhagic
Cutaneous shock: burns
(external fluid loss)
Gastrointestinal
(vomiting&diarrhea)
 Diabetic shock
 Diabetes insipidus.
 Excessive use of diuretics.
 Internal sequestration
(fractures,
hemothorax,ascites)

5. 2) CARDIOGENIC (DECREASED CARDIAC OUTPUT)
 Myocardial infarction
 Arrhythmias
 Pump failure

6. (3)
DISTRIBUTIVE/NEUROGENIC
SHOCK:
 Sepsis
 Anaphylactic
-Insulin shock
-Barbiturate injection
-Anaesthesia (spinal)
 Spinal cord injury
(4) OBSTRUCTIVE
 Massive Pulmonary
embolism
 Tension pneumothorax
 Cardiac tamponade
 Constrictive pericarditis
 Aortic stenosis.

7. Classification according to degree:
 Compensated: Organ perfusion is maintained.
 Uncompensated: Circulatory failure with end
organ dysfunction.
 Irreversible: Irreparable loss of essential
organs.

8. CLINICAL ALTERATIONS IN SHOCK
Restlessness.
Apathy & confusion.
Unconsciousness.
Rapid thready pulse
followed by weak
pulse.
Increased respiratory
rate, shallow
respiration.
Decreased BP
Subnormal
temperature
Cold & clammy skin
Decreased urinary output
Cyanosis
Decreased/absence
bowel sound

9. PATHOPHYSIOLOGY
Initial stage
Compensatory stage
Progressive stage
Refractory stage

10. Initial stage
• Hypo-perfusion leads to hypoxia.
• lactic acid begins to accumulate,
leading to lactic acidosis.

11. compensatory stage
 Physiologic response to hypovolemia is directed at preservation of
perfusion to vital organs.
 Stimulation of renin angiotensin system in order to increase cardiac
contractility & peripheral vascular tone
 Release of Anti-Diuretic Hormone (ADH) to conserve salt and water.
 Change in local micro circulation to regulate regional blood flow.
 Victim begins to Hyperventilate
 Mediation via Baro & chemo receptors which stimulates ANS & HPA
axis to Release of epinephrine & norepinephrine.

12. Compensatory (Hormonal response)
HyperglycemiaLypolysisGluconeogenesisGlycogenolysis
Cortisol
ACTH
CRH
HYPOTHALAMUS

13. Progressive stage
•Compensatory mechanism begins to fail.
•Anaerobic metabolism progresses, increasing
metabolic acidosis.

14. Refractory stage
•There is organ failure.
•Shock is irreversible.
•Brain damages and cells die.
•Death occurs imminently.

15. MANAGEMENT OF SHOCK:
GENERAL Principles of shock management
The overall goal of shock management is to improve oxygen
delivery/utilization in order to prevent cellular and organ injury.
Effective therapy requires treatment of the underlying etiology.
Restoration of adequate perfusion, monitoring and comprehensive
supportive care.
Interventions to restore perfusion center on achieving an adequate B.P
increasing cardiac output and optimizing oxygen content of the blood
Oxygen demand should also be reduced.

16. Initial Treatment in Shock
-Assess airway and breathing Airway and begin CPR if necessary.
-Lay the person down.
-Elevate feet unless head, neck, hip or leg is injured.
-Turn patient to his side if vomiting or bleeding from the mouth.
-Keep patient warm.
-Administer oxygen if available.
-Treat obvious injuries.
-Administer volume expansions (usually Normal Saline).

17. Restoration of Circulation
VOLUME- FLUID CHOICES:
CRYSTALLOIDS VS COLLOIDS
Crystalloids: for initial resuscitation
IVF 0.9% Normal Saline is the fluid of choice. Give
2-3 liters over 15-30 min.
 Ringers lactate may also be used.

18. Colloids: to replace blood loss
Albumin
Dextran
Blood
•They are great volume expanders used
for major haemorrhage

19. DIAGNOSTIC INVESTIGATIONS
 Blood test
• Fasting Blood Sugar (FBS)
• Random Blood Sugar (RBS)
• Microscopic Culture and Sensitivity test (MCS)
 X- ray
 Electrocardiogram (ECG)
 Echocardiogram (ECHO)
 Pulmonary artery catheterization

20. DRUGS USED IN SHOCK MANAGEMENT
Inotropes –cardiac support
Vasopressins (pitressin)
Steroids

21. Inotropes
Agent Site of Action Dose
Mcg/kg/min
Effects
Dopamine Dopaminergic
Beta
Alpha < Beta
1-3
5-10
11-20
Renal vasodilation
Inotrope/vasoconstriction in order to increase BP
Increase peripheral. Vascular resistance
Dobutamine Beta 1 & 2 1-20 Inotrope
Vasodilation
Epineprhine Beta < alpha 0.05 – 1.0 Inotrope, vasoconstriction
Tachycardia
Norepinephrine Alpha < beta 0.05 – 1.0 Profound vasoconstriction
inotrope
Nitroprusside Vasodilator
(arterial < venous)
0.5 – 1.0 Vasodilation
Milranone Phosphodiesterase inhibitor 0.5 – 0.75 Inotrope
vasodilation

22. Vasopressin (pitressin)
 Initiates reabsorption of water by the kidney
 Also causes constriction of blood vessels.
 Blood flow diversion from non-vital to vital
organs
 Dosage 0.01 – 0.04U/min up to 0.08U/min IV

23. Steroids
Glucocorticoid function
-Maintain homeostasis.
-Increases BP.
-Modulate inflammatory response.
-Normalize vascular reactivity.
-Boosts blood glucose level.
Dosage: Hydrocortisone 200 mg IV

24. Hypovolemic shock
• It occur when the intra vascular volume is depleted relative to
the vascular capacity.
Mild (<20%) Moderate(20-40%) Severe(<40%)
-Cold
extremities
-Decreased CRT
-Diaphoresis
-Anxiety
Same +
-Tachycardia
-Tachypnoea
-Oliguria
-Postural
hypotension
Same +
-Hypotension
-Mental status
deterioration

25. MANAGEMENT OF Hypovolemic shock
 I.V. fluid normal saline 2-3 liters over 15-30 min.
 If hemodynamic instability persist then start blood transfusion
& control on going heamorrhage.
 Give Inotropes:
Dopamine 5-10microgms/Kg/min
Dobutamine 2-20microgms/Kg/min

26. Cardiogenic shock
• Circulatory pump failure
• Sustained hypotension SBP < 90 mm
Hg for at least 30 minutes.
MANIFESTATIONS
• Chest pain
• Hypotension
• Arrhythmias
MANAGEMENT:
 Conformation of diagnosis by ECG,
ECHO & X-RAY.
 Intubation & mechanical
ventilation often required.
 Avoid fluid overload.
 Inotropic support preferably
Dobutamine 2-20microgms/Kg/min.
 USG guided pericardiocentesis.

27. Neurogenic shock
• DECRESED tissue perfusion as a
result of loss of vasomotor tone to
peripheral arterial beds
• Secondary to spinal cord injury
from vertebral
• Hypotension with bradycardia
• Warm extremities
• Motor and sensory deficit
MANAGEMENT
• Restoration of intravascular
volume by crystalloids
• Administer vasoconstrictors:
Dopamine <10mcg/kg/min

28. OBSTRUCTIVE SHOCK
• Blood flow is stopped as a
result of cardiac (or pericardiac)
tamponade (the build-up of
fluid in the pericardium) that
compresses the heart and stops
it from beating properly , or
pulmonary embolism ( a blood
clot in the pulmonary artery,
blocking the flow of blood to
the lungs)
MANAGEMENT
• Removing the obstruction ,
for example,surgery or clot-
dissolving medication
(heparin 3000-5000units IV)
to remove a clot in the
pulmonary artery.

29. Septic shock
-Manifestation of excessive &
inflammatory response of
endogenous immune
mechanism
MANAGEMENT
 Culture of body fluids
 Infuse BSS 500 cc/15min monitor
SBP/CVP
 If hemodynamic instability persists
start vasopressor preferably
Norepinephrine 0.02-
0.25microgms/Kg/min
 Administer broad spectrum antibiotic

30. Case scenario
1) A 25 year old trainee with no prior history of any chronic disease
presented to the emergency clinic complaining of weakness and had
been stooling for the past 24 hours.
Temp:35.80C, pulse:129b/min, R.R: 27c/min, BP:100/58mmHg
While still in the clinic, he rushed to the toilet. Coming out from the
toilet, he was restless, and showing apathy. Again V/S quickly recorded
BP:95/56mmHg, PR:49b/min (weak), RR: 27c/min, and patient is
becoming more disoriented as V/S been checked.
• a) What information do you need to determine if this client is in shock?
• b) what would be your goal of management for this client?
• c) What initial interventions are needed to stabilize that Pt.?

31. 2) A 50 year old trainer (a known diabetic) was rushed into the
emergency clinic with a history of sudden collapse while in the
workshop.
On examination, he is unresponsive.
BP:110/60mmHg, pulse:67c/m, RR: 30b/m, temp: 36.9OC
• How can you ascertain that the client is in shock?
• What type of shock is he in if:
 RBS is 25mg/dl
 RBS is 358mg/dl
c) What are the probable etiologies of each type of shock
d) How will you manage this client?

32. CONCLUSION
Early recognition of warning signs and diagnosis in the initial
stage is important for successful management of shock.
Hypovolemia and sepsis account for majority of shock.
Principles of initial resuscitation same irrespective of type of
shock.
Ultimate treatment of underlying cause forms cornerstone of
management.

33. Abbreviations
HPA----Hypothalamic Pituitary
Adrenal
CRH----Corticotropin-Releasing
Hormone
ACTH---AdrenoCorticotropic
Hormone
ADH----Anti Diuretic Hormone
ATP-----Adenosine TriPhosphate
BP ------Blood Pressure
CRT-----Capillary Refill Time
SBP-----Systolic Blood Pressure
ECG-----Electrocardiogram
ECHO---Echocardiogram
USG-----Ultrasonography
SIRS ----Sepsis Inflammatory
Response Syndrome
BSS------Balanced Salt Solution (eg
Ringers Lactate )
CVP-----Cell Volume Profile