SHOCK

Gross-1850
“Rude unhinging of machinery
of life”

Hardway - 1990
“Inadequate capillary perfusion”
 SHOCK has a haemodynamic
component, which is the initial focus
of resuscitation

BUT
SHOCK also has systemic
inflammatory component, that leads
to multiple organ failure.
 Container Concept

2L
5L
3L
3L

2L
7L
5L
 Capillary Cellular
Relationship in Shock
Stage I - Volume loss 15%
• Vasoconstriction
Decreased O2, Substrate delivery
Anaerobic metabolism
Lactic acidosis, ↑H ions

• Increased capillary permeability

• AV shunt opens in skin, kidney, GIT
• Increased Sympathetic stimulation
 Contd...Capillary Cellular
Relationship in Shock
Stage II - Volume loss 15-25%
• Capillaries and venules open
• Pre Cap.Sphincter relaxes
• Pooling, sludging, stagnation
• Expansion of vascular space
• Increase in ventilation
Contd... Capillary Cellular
Relationship in Shock
Stage III - Volume loss 25-35%

• DIC, Lactic acidosis

Stage IV - Volume loss 35-40%

• Multiple Organ Failure

 Since 1996….2003
• Focus on Microcirculation “ Sludge”
• Endothelium dysfunction
• Coagulation cascade and microthrombi
• Platelets and neutrophils plug vessels
• Trap bacteria , enhance growth
• Vascular permeability and edema
• Hypoperfusion, Lactic acidosis/MSOF
(Review: CCM: Hinshaw:
1996:1072)
 Septic Shock
Nidus of Infection - Exotoxins, Endotoxins
• Release of endogenous mediators,
Arachidonic acid metabolites, Kinins
MYOCARDIAL DEPRESSANT SUBSTANCE
• Myocardial depression, Vasodilation
• Organ dysfunction, Coagulopathy
• Refractory hypotension, MOF
Sepsis Pathophysiology
 Microcirculation in
Sepsis: AJRCCM: Backer

July 1 2002
 “Shock is recognized at the
bedside when haemodynamic
instability leads to hypoperfusion
of several organ systems.

SHOCK IS A CLINICAL
DIAGNOSIS”
Holmes, Walley. Clinics in chestmedicine, Dec. 2003
 Diagnosis
Recognized by hypoperfusion of
several organ systems.
• Altered level of consciousness
• Decreased urine output
• Mottled skin
• Haemodynamic instability
 Hypovolaemic
Shock
Inadequate venous return due

to haemorrhage or

dehydration.
 Vasodilatory Shock
Inadequate venous return due to
vasoplegia, or lack of vascular
tone.

Sepsis, Anaphylaxis, poisoning,

Ischaemic reperfusion syndrome
 Cardiogenic Shock
Pump failure due to
• Loss of contractility (MI)
• Impaired diastolic filling
• Abnormal rate/rhythm
• Obstruction to flow - Valvular,

pulm.embolism, tamponade
 Working diagnosis for cause of
Shock
High output Cardiogenic
Vasodilatory Hypovolaemic
Cardiac output ? Raised Reduced
Pulse pressure Wide Narrow
Diastolic Very low Low
Extremities Warm Cool
Capillary Rapid Slow
Heart soundCrisp Muffled
Temperature High/low Normal
WBC High/low Normal
Infection Present Absent
 Contd...
Cardiogenic Hypovolaemic
Clinical Angina, Abnormal Blood loss,
ECG Vol.loss

JVP High Low

Rhythm Gallop Tachy

Lungs Crepts Normal

X’Ray Cardiomegally,

Pulm oedema Normal

Laboratory Investigation
Mainly to know the response to Rx.

Hb, Haematocrit, WBC, Serum

Electrolytes, Bl.Urea, Creatinine,

Bl.Sugar, ABG, Serum Lactate,

ECG, Chest X’Ray, etc, etc..

 Primary Survey
• Assess and Establish Airway

• Evaluate Breathing

• Consider ventilatory support

• Resuscitate inadequate circulation

 Airway and Breathing
• Recognize Weak airway reflexes

• Recognize Ventilatory Failure

• Respiratory muscle fatigue

• Severe metabolic acidosis, mental

obtundation, sedatives

• Early intervention, even before ABG

 Airway and Breathing
• Initially high FIO2

• Protect airway - ET intubation

• Increased VO2 by respiratory

muscle - Mechanical ventilation

 Circulation
Rx according to working diagnosis

• Haemorrhagic shock - Haemostasis,

infusion of warmed blood substitutes

• Dehydration - Rapid boluses of

crystalloid - 1L. Hypertonic solutions

• Cardiogenic Shock

Smaller volume challenge - 250 ml. cryst.

• Vasodilatory Shock

Large vols. of crystalloid- 6-10L / Colloid

Alderson, Cochrane Database 2000

 Circulation
Adequacy of volume expansion to be
titrated to an easily observable end
point.
Benefit - ↑BP, ↓HR, ↑PP, ↑Urine

Harm - Pulm.oedema, Rt. Heart dysfunction.

Absence of either response - Volume challenge

inadequate
 Circulation
“Time is Tissue”
Early Goal directed treatment reduces
mortality.
Goal Directed Therapies -
• Kern, Shoemaker, 2000 (Meta analysis)
Invasive monitoring - ↑CI, ↑DO2, PA occlusion
press < 18 mmHg.
• Rivers et al - 2001
CVP 8-12, MAP > 65, SCVO2 > 70%
 Vasoactive Therapy
Low Cardiac Output with High Cardiac
filling pressure - Inotropic support.
Hypotension with high Cardiac Output
- Pressure support.
CO is more important than BP
Distribution of flow needs adequate BP
 Vasoactive Therapy
• Use a vasoactive agent which you are
familiar

• Titrate dose to Systolic or MAP to

restore autoregulation

Adequacy of CO measuring CO, SCVO2,

Lactate, Acid Base

 Vasoactive Agents
Beta agonists - Cardiac Contractility

Alpha agonist - Perfusion pressure

Beta agonist receptor down regulation

- Amrinone

Alpha agonist receptor down

regulation - Vasopressin
Common Vasoactive Agents
• Dopamine - 2-3, 3-10, 10-20 µ g/kg/min

• Dobutamine - 2.20 µ g/kg/min

• Adrenaline - 2 µ g/kg/min

• Nor Ad - 1 µ g/kg/min

• Milnirone- 50 µ g/kg bolus over 10 min

Followed by 0.5 µ g/kg/min
 Secondary Survey
Search for Definitive Cause
Inadequate Organ perfusion - ↓Pump
action, ↓Venous return with normal
pump.
High CO hypotension - ↓Vascular
tone, abnormal flow distribution
Look for Unique causes of shock
Definitive Management
After establishing working

hypothesis and rapid

stabilization - Plan

Definitive Management
 Definitive Management
Haemorrhagic Shock
Goals-
• To restore oxygen perfusion to the
tissues
• To stop haemorrhage - surgical
etc.
 Definitive Management
Haemorrhagic Shock
Aggressive Resuscitation ?
• Classic Approach - Am.Col.Surg ATLS
programme 93
• Current animal model - Bickel et al ‘91
• Kawaseki et al ‘91 - Aggressive fluid before
control of bleeding does not improve outcome
• Bicket et al ‘94 - Group with delayed fluid
resuscitation had better survival
• Seigell et al ‘98, Orlinsky 2001, Smail ‘98
 Definitive Therapy
Cardiogenic Shock
Mortality 50-80%
Initial approach - Fluids if no
Pulm.Oedema, Vasoactive Therapy, Urgent
Echo., Thrombolytics,
Consider urgent revascularization -
Lower mortality than Thrombolytic with
IABP
 Septic Shock
Surviving Sepsis Campaign Guidelines
Crit.Care Med -2004
Early resuscitation goals -

CVP - 8-12, MAP 65, Urine 0.5 ml/kg/hr

SCVP > 70%

If <70%, RBC transfusion, HCl 30%,

Dobutamine 20 Mg/kg/mi
 Septic Shock
Diagnosis
• Appropriate Culture before antimicrobials
• I.V. antibiotic therapy - Emperical
• Broadest Spectrum Therapy
• Remember Renal, Hepatic status
• Reassess after 72 hours
• Continue Specific therapy for 7-10 days
• Mostly cultures come negative
 Septic Shock
Source Control

• Drainage of abscess

• Debridement of necrotic tissue

• Removal of a device
 Septic Shock
Fluid and Vasopressor
• Colloids/Crystalloid - no evidence base
• Fluid Challenge - Crystalloid 500-1000
• Colloid 300-500 ml over 30 mins
• Input output ratio is of no Utility
• Norepinephrine or Dopamin is the first choice
• NO LOW DOSE DOPAMIN
 Septic Shock
Ionotropic Therapy

In patients with low CO despite fluids.

Dobutamine - drug of choice with

vasopressor
 Septic Shock
• Steroid

• Vasopressin

• Sodium bicarbonate

• Recombinant Human activated Protein

 Septic Shock
• Glucose control

• DVT prophylaxis

• Stress ulcer prophylaxis

 Septic Shock
Open Lung Policy

Mechanical Ventilation for ALI/ARDS

Low VT, End inspiratory plateau

pressure<30, Permissive Hypercapnea,

Minimum PEEP, Recruitment maneuvers