SHOCK

DR. BASANT KUMAR

DEPARTMENT OF SURGERY
ISRA UNIVERSITY
HYDERABAD
 SHOCK

Shock is a systemic state of low tissue

perfusion, which is inadequate for normal
cellular respiration
SHOCK
Pathophysiology

A Cellular

B Micro vascular

C Systemic

D Ischemic-reperfusion syndrome
 PATHOPHYSIOLOGY

A. CELLULAR
 tissue perfusion

 0
2

Cell Metabolism from

- Aerobic to anaerobic

- Lactic acid accumulation

- Systemic metabolic acidosis

 PATHOPHYSIOLOGY

B. MICROVASCULAR
Tissue ischemia leads to

-Activation of immune & Coagulation system

-Hypoxia + Acidosis leads to
Complement and neutrophils activation 
Oxygen free radicals and cytokine release .
leads to -injury of capillary endothelial cells
-fluid leaks
-tissue oedema
 PATHOPHYSIOLOGY
C. SYSTEMIC
C.V.S
 Preload and after load baroreceptor  sympathetic activity
and release of catecholamine  tachycardia and
vasoconstriction
Respiratory
• Metabolic acidosis  respiration rate
Renal
Perfusion Filtration  urine output
Endocrine
Activation of adrenal
Activation of Rein angiotensin
Activation of ADH
Release of Cortisol
 PATHOPHYSIOLOGY
D. ISCHEMIC-REPERFUSION SYNDROME

 Hypoperfusion O2Cellular damage + local

activation of inflammation.
 Further injury when normal circulation is restored.
 Cellular and humoral elements flushed back into
circulation endothelial injury to organs
-lungs & kidneys.
 Classification of Shock

A. Hypovolumic Shock
B. Cardiogenic Shock
C. Obstructive Shock
D. Distributive Shock
E. Endocrine Shock
 A. Hypovolumic Shock
 Circulatory volume
Causes
Haemorrhage
Poor fluid intake
Excessive fluid loss
Vomiting
Diarrhea
Polyuria
Burn
Third space loss (Int obs + Pancreatitis)
 B. Cardiogenic shock
Cardiac pump failure
Causes
M.I
Dysrhythmias
Vascular disease
Cardiomyopathy
Blunt myocardial injury
 C. Obstructive shock
Reduction in preload leads to obstruction in
cardiac filling
Causes
Cardiac tamponade
Tension pneumothorax
Massive pulmonary embolism
Air embolism
 D. Distributive shock
It describes Pattern of Cardio Vascular responses
characterising a variety of conditions
including:
Septic shock
Anaphylaxis
Spinal cord injury
 E. Endocrine shock
Present as combination of hypovolumic,
cardiogenic and distributive shock
Causes
Hypothyroidism = HR &  COP
Hyperthyroidism = COP failure
Adrenal insufficiency= Addison disease
 Hypovolumic Cardiogenic Obstructive
Distributive


COP  


VASCULAR  

RESISTENCE

 
VENOUS 
PRESSURE

MIXED 
 
VENOUS O2 
SATURATION

 
BASE DEFICIT 
 CLINICAL FEATURES
OF
SHOCK
Compensated Mild Moderate Severe
Lactic acidosis + ++ ++ +++

Urine output Normal Normal Reduced Anuric

Level of consciousness Normal Mild anxiety Drowsy Comatose

Respiratory rate Normal Increased Increased Laboured

Pulse rate Mild increased Increased Increased Increased

Blood pressure Normal Normal Mild Hypotension Sever Hypotension

 SEVERITY OF SHOCK
&
CLINICAL FEATURES
COMPENSATED SHOCK

C.V.S + endocrine compensatory response

flow to non essential organs (skin, muscle, GIT)
Maintain flow to kidney, lung and brain

Cool periphery + HR

 SEVERITY OF SHOCK
&
CLINICAL FEATURES

MILD SHOCK
Tachycardia, tachypnoea and urine output
Mild anxiety
BP maintained
Periphery cool + sweaty
 SEVERITY OF SHOCK
&
CLINICAL FEATURES
MODERATE SHOCK
Urine output  (<0.5ml/kg/h)
BP - 
Patient is drowsy
SEVERE SHOCK
 Tachycardia
 Hypotension

Anuria
Patient unconscious
Respiration laboured
 Consequences
Unresuscitatable shock
Long period of shock  unresuscitable
Cellular ischemia  cell death

Myocardial depression

 loss of vascular resistance

No response to vasopressor agents

Death results
 Multiorgan Failure
Period of shock is limited, intervention is timely then
patient recover.
Results of prolonged systemic ischemia and reperfusion
injury is end organ damage and multiorgan failure
(MOF)
MOF in defined as two or more failed organs.
Lung – Acute respiration distress syndrome
Kidney – Acute renal insufficiency
Liver – Acute liver insufficiency
Clotting – Coagulopathy
Cardiac – Cardiovascular failure
Resuscitation:
A. Airway
B. Breathing

C. Circulation

Examination and Find Causes

Bleeding – Stop
Assume as hypovolumic
I/V fluid
Type of fluid
Crystalloids – Normal Saline, Hartman's solution, Ringer Lactate
Colloids – Albumin
Blood
DYNAMIC FLUID RESPONSE
200 – 500 cc in 5-10 min
Check HR, BP, CVP
A. Responder – Sustained improvement.

B. Transient responder – transient improvement moderate blood

loss.
C. Non responder – no improvement
Severe volume depletion
Major ongoing loss /persistent uncontrolled haemorrhage
Vasopressor and Inotropic support

Vasopresor – phenylephrine, Nor adrenaline

(Sepsis, neurogenic shock)
Inotropic – dobutamine
(Cardiogenic shocks )
MONITORING FOR PATIENTS IN SHOCK

Minimum
ECG
Pulse Oximetry
Blood pressure
Urine output

Additional modalities
CVP
Invasive BP
Cardiac output
Base deficit and serum lactate
 Endpoints of Resuscitation
Traditionally – pulse, BP, urine output.
OCCULT HYPOPERFUSION
State of normal vital signs and occult
underperfusion
manifested by :-
- Persistant lactic acidosis
 Mixed venous oxygen saturation level
Thanks