SHOCK

“A rude unhinging
of the machinery of
life”

- Gross -: RAJAN
 Definition
 Shock is a systemic state of low
tissue perfusion, which is
inadequate for normal cellular
respiration. With insufficient
delivery of oxygen and glucose,
cells switch from aerobic to
anaerobic metabolism. If
perfusion is not restored in a
timely fashion, cell death ensues.
 Pathophysiology
 Physiologic response to hypovolemia
directed at preservation of
perfusion to vital organs

-Increase cardiac contractility &

peripheral vascular tone via
ANS
-Hormonal response to preserve
salt & water
-Change in local micro circulation to
 Cellular response
 Inadequate delivery of oxygen &
substrates leads to in oxidative
phosphorylation & ATP
generation.

 Anaerobic respiration leads to

lactic acidosis.
 Cellular response
 Na+,K+ ATP ase activity
decrease leading to
accumulation of Na+ & leak of
K+
 Intracellular lysosomes release
autodigestive enzymes & cell
lysis ensues leading to release of
K+ into bloodstream.
 Microvascular
Progressive tissue ischemia

Change in local milieu

(hypoxia & acidosis)

Activation of immune & coagulation

system
(compliment & prime neutrophils)
Contd.

O2 free radical & cytokine

Injury of capillary endothelial cells

(becomes ‘leaky’)

Tissue oedema

Cellular hypoxia
 Systemic
 Cardiovascular
in preload & afterload

Compensatory baroreceptor activation

Sympathetic activity

Tachycardia & systemic

vasoconstriction
Arterial Baroreceptors
Autonomic Responses to
Baroreceptor Activity
 Arterial
baroreceptor firing
inhibits
sympathetic
outflow and
stimulates
parasympathetic
outflow
 Therefore, reduced
firing, which occurs
during
hemorrhage, leads
to sympathetic
 Cardiopulmonary
Baroreceptors
• Location: Venoatrial Junction
– Tonically active
• Receptor firing decreases ADH
(vasopressin) release leading to diuresis
and vasodilation
• Hemorrhage → increase ADH (reduced
urine formation and increased
vasoconstriction)
• Location: Atria and Ventricles
– Tonically active
• affect vagal and sympathetic outflow
similar to arterial baroreceptors
Baroreceptor Reflexes
Chemoreceptor Reflexes
 Peripheral chemoreceptors
– Carotid bodies
– Aortic bodies

 Central chemoreceptors
– Medulla (associated with
cardiovascular control “centers”)
Contd.
 Increasingly important when mean
arterial pressure falls below 60
mmHg (i.e., when arterial
baroreceptor firing rate is at
minimum)
 Acidosis resulting from decreased
organ perfusion stimulates central
and peripheral chemoreceptors →
sympathetic activation
 Stagnant hypoxia in carotid bodies
enhances peripheral vasoconstriction
 Respiratory

Metabolic acidosis & sympathetic

response

R.Rate & MV
(excretion of Co2)

Compensatory respiratory
alkalosis
 Renal
 Endocrine
 Vasopressin (ADH) released from
hypothalamus in response to
preload vasoconstriction &
reabsorption of water in collecting
system.

 Cortisol released from adrenal cortex

Na+ & H2O reabsorption and
sensitising the cells to
catecholamines.
 Hormonal response

Hypothalamus

CRH

ACTH

Cortisol

Glycogenolysis Gluconeogenesis Lypolysis Hyperglycemia

 Ischaemia-reperfusion
syndrome
 During the period of systemic
hypoperfusion, cellular and organ
damage progresses because of direct
effects of hypoxia & local activation
of inflammation.
 Further injury occurs once normal
circulation is restored to these
tissues.
 The acid & K+ load can lead to

-direct myocardial depression

Ischaemia-reperfusion
syndrome
Hypoxia

Cellular & humoral components

Flushed back into circulation

Endothelial injury(lungs,kidney)
 Ischaemia-reperfusion
syndrome

Acute lung,kidney injury,

multi organ failure & death

 This injury can be attenuated by

reducing the extent and duration of
tissue hypoperfusion
 Classification
 Hypovolaemic

 Cardiogenic

 Obstructive

 Distributive

 Endocrine
 Types

Hypovolaemic shock
-Due to reduced circulating volume.
3. Haemorrhagic

4. Non-Haemorrhagic
 Causes of non-haemorrhagic shock

-Dehydration,
diarrhoea,vomiting,evaporation,3rd
space loss, bowel obstruction or
pancreatitis.
 Types

Cardiogenic shock
 Primary failure of the heart to pump.

 Causes
-MI, cardiac dysrhytmias, valvular
heart disease,blunt myocardial
injury,cardiomyopathy.
-d/t endogenous factors (in sepsis)
-d/t exogenous factors (drugs)
 Types

Obstructive shock
 Reduction in preload due to
mechanical obstruction of
cardiac filling.
 Causes

- cardiac tamponade, tension

pneumothorax, massive
pulmonary embolus, air embolus.
 Types

Distributive shock
 Inadequate organ perfusion
accompanied by
3. Vascular dilatation with
hypotension
4. Low SVR
5. Inadequate afterload
6. Abnormally high cardiac output
 Types
 Causes

-Septic shock
-Anaphylaxis
-Spinal cord injury
 Types

Endocrine shock
 Combination of hypovolaemic,
cardiogenic & distributive shock.
 Causes

-Hypo- & hyperthyroidism

-Adrenal insufficiency
 Cardiovascular & metabolic
characteristics
hypovolae cardioge obstructi distributi
mia nic ve ve
Cardiac low low low High
output
Vascula high high high low
r
resistan
Venous Low High high Low
ce
pressur
e
Base high high high high
deficit
 Severity of shock
 Compensated shock
 Decompensation

 Mild shock

 Moderate shock

 Severe shock
 Clinical features
compensa mild moderat severe
ted e
Lactic + ++ ++ +++
acidosis
UOP normal normal oliguric Anuric
Level of Normal Mild drowsy Comat
consciou anxiety ose
sness
R.Rate Normal Increased Increase Labour
d ed
Pulse Mild increased increase increas
increase d ed
B.P. normal normal Mild low Severe
low
 Clinical Markers
 Brachial systolic blood
pressure: <110mmHg
 Sinus tachycardia: >90
beats/min
 Respiratory rate: <7 or >29
breaths/min
 Urine Output: <0.5cc/kg/hr

 Metabolic acidemia:
 Contd.

 Hypoxemia: 0-50yr: <90mmHg;

51-70yr: <80mmHg; >71yo;
<70mmHg;
 Cutaneous vasoconstriction vs.
vasodilation.
 Mental Changes: anxiousness,
agitation, indifference, lethargy,
obtundation
 Prolonged capillary refill time
 Pitfalls
 Capillary refill
-prolonged
-not a specific marker. (varies in
adults)
-if short then may be early stage of
shock
-in septic shock:- BRISK despite
of profound shock
 Contd.

 Tachycardia
- Not always accompany shock
- Who on β-blocker or have implanted
pacemakers unable to mount
tachycardia
- A pulse rate of 80 in a fit young adult
who normally has a pulse of 50 is
abnormal
 Contd.

 Blood pressure
- Hypotension is one of the last sign
- Children & fit young adults are able
to maintain B.P. until the final stages
(compensatory mechanism lead to
in SV & peripheral vasoconstriction)
- Elderly hypertensive pts may present
with ‘normal’ BP but be hypovolemic
& hypotensive
-
 Consequences
 Unresuscitable shock
- Profound shock for a prolonged
period of time
- Cell death follows from cellular
ischemia
- Ability to compensate lost
- Myocardial depression
- Non responsive to fluid or ionotropes
- Peripherally loss of ability to maintain
SVR
 Contd.

 Multiple organ failure

- Defined as 2 or more failed organ
systems
- No specific treatment
- Supporting organ systems with
ventilation, cardiovascular support &
dialysis until there is recovery of
function
- Mortality rate 60%
- Prevention by early aggressive
Effects of organ failure
Lung ARDS

Kidney Acute renal

insufficiency
Liver Acute liver
insufficiency
Clotting Coagulopathy

Cardiac Cardiovascular failure

 Resuscitation
A – airway
 B – breathing i.e.
oxygenation & ventilation
 C – circulation
(cardiovascular
resuscitation)
 Contd.

 Conduct of resuscitation
- Should not be delayed
- Timing & nature of resuscitation
depend on type of shock and timing
& severity of insult
- Rapid examination to make a
diagnosis & detect the source
- If there is doubt about cause it is
safer to assume the cause is
hypovolemia. Begin with fluid
 Contd.

 The pts who are actively bleeding it

is counterproductive to institute high
volume fluid therapy
 Operative hemorrhage control should
not be delayed & resuscitation
should proceed in parallel with
surgery
 A pt with bowel obstruction &
hypovolemic shock must be
adequately resuscitated before
 Contd.

 Fluid therapy
- Hypovolemia & inadequate preload
must be addressed 1st
- First-line therapy is IV access and
administration of IV fluids
- Short wide bore catheters preferred
- Central venous catheters are more
appropriate for monitoring
 Contd.
 Type of fluid
- There is no ideal resuscitation fluid
- It is more important to understand
how & when to administer them
- Crystalloid vs Colloid
- Their O2 carrying capacity zero
- Blood should be replaced with blood
- Hypotonic solution like dextrose
should not be used unless the deficit
is free water loss(DI) or Na+ overload
 Contd.

 Dynamic fluid response

- Shock status can be determined by
the cardiovascular response to the
rapid administration of a fluid bolus
- Interpretation
4. Responders
5. Transient responders
6. Non-responders
 Contd.

 Vasopressor and inotropic

support
- Not indicated as 1st line therapy in
hypovolemia
- Vasopressor agents (phenylepherine,
nor-adrenaline) used in distributive
shock state
- If vasodilation is resistant to
catecholamines, vasopressin may be
 Monitoring
 Minimum  Additional
- ECG modalities
- Pulse oximetry
- Central venous
pressure
- Blood pressure
- Invasive Blood
- Urine output
pressure
- Cardiac output
- Base deficit and
serum lactate
Cardiovascular
monitoring
 Central venous pressure
- There is no ‘normal’ CVP for a
shocked pt.
- It varies patient to patient
- Ventricular compliance can change
rapidly
- It is a poor reflection of preload
- Measurement during fluid challenge
test
 Contd.

 Cardiac output
- Asseses
3. Cardiac function
4. Systemic vascular resistance
5. Preload (end-diastolic volume)
6. Blood volume
 Systemic & organ
perfusion
 Goal of t/t is to restore cellular &
organ perfusion
 UOP is the best monitor
 Level of consciousness – marker of
cerebral perfusion
 Clinical indicators of perfusion of GIT
& muscular beds are lactate & base
deficit and the mixed venous oxygen
saturation
 Clinical Investigationa
l
System Base deficit; lactate;
ic mixed venous O2 sat.
perfusi
Organ
on
perfusi
on
Muscle - Near infrared
spectroscopy
Gut - Sublingual
capnometry;p
H;flowmetry
Kidney UOP -
Brain Level of consciousness Near infrared
spectroscopy
Base deficit and lactate

 Sensitive tool for both diagnosis and

monitoring
 >6mmol/l have higher morbidity &
mortality
 Occult hypoperfusion- state of
normal vital signs and continued
underperfusion manifested by ed
base deficit
 ABG measurement
Mixed venous oxygen
saturation
 % saturation of oxygen returning to
heart from body
 Measure of O2 delivery & extraction
by tissues
 measurement ;- sample from rt
atrium
 50-70% normal
 <50% indicate inadequate O2
delivery & ed O2 extraction by cells
 Contd.

 >70% in sepsis
 Disordered utilisation of O2 at
cellular level
 Arteriovenous shunting of blood
 Rapid correction required with
- Fluid therapy
- Inotropes
 Endpoints of
resuscitation
 Resuscitation complete when
oxygen debt repaid,tissue acidosis
corrected & aerobic metabolism
restored
 Systemic Parameters
 Lactate
 Base deficit
 Tissue Parameters
 Gastric tonometery
 Sepsis in a
surgical patient
 Shock associated with sepsis is
found to be major cause of death
in surgical intensive care

 Incidence of sepsis has increased

steadily over time

 Cause of this is
- widespread use of
antimicrobials, steroids,
indwelling catheters &
 What is sepsis?
 Sepsis can be response to any class
of micro organism that may spread
beyond invaded tissue

 Microbial bloodstream invasion not

essential

 Fever or hypothermia, tachypnea,

tachycardia herald onset

 When counter regulatory

mechanisms overwhelmed,
 Definitions in sepsis
 Bacteremia – presence of bacteria in
blood with +ve blood cultures

 Septicemia – presence of bacteria +

toxins in blood

 Systemic inflammatory response

syndrome (SIRS) – may have infectious
or noninfectious aetiology
2 or more of following conditions
- fever or hypothermia
- tachycardia
- tachypnea
Contd.

 Sepsis – SIRS with a documented

INFECTION

 Severe Sepsis or Sepsis

Syndrome – Sepsis with evidence of
one or more organ failures
[respiratory (ARDS), cardiovascular
(compromise of cardiac function & in
PVR ), renal (ATN), hepatic, blood
coagulation system or CNS]
SUSPECT SEVERE SEPSIS
IF
 systolic BP <90 mm Hg or > 40 mm
Hg fall from pts normal BP
 hypoxemia
 lactic acidemia
 oliguria
 acute encephalopathy
 Hypotension unresponsive to fluid
resuscitation denotes septic shock
 OMINOUS SIGNS
 Septic shock lasts for > 1 hr and
does not respond to fluid or pressor
administration : Refractory septic
shock

 Dysfunction of > 1 organ requiring

intervention to maintain
homeostasis: Multiple organ
dysfunction syndrome –
 Organisms causing
sepsis
 Gram +ve
- staph. Aureus
- enterococcus,
- coagulase –ve staph
 Gram –ve
- E. coli
- Klebsiella
- Pseudomonas
 Pathophysiology

Septic insult
Complement activation Macrophage activation
TNF, IL – 1,6
Neutrophil Endothelial cell
activation Up regulation
Arachidonic
bradykinin coagulation metabolites
N2O Oxygen radicals

Tissue
Capillary leak microthrombosis vasodilation vasodilation
destruction

Organ injury
 Complications of sepsis
 Cardiopulmonary – ARDS, arteriolar
vasodilatation, myocardial
dysfunction

 Renal – acute tubular necrosis

 Coagulation – thrombocytopenia,
disseminated intravascular
coagulation
 Initial Resuscitation

 Should begin as soon as

severe sepsis or sepsis
induced tissue hypoperfusion
recognized
 Elevated Serum lactate
identifies tissue
hypoperfusion in patients not
 Initial Resuscitation

 Goals of therapy within first

6 hours
- Central Venous Pressure 8-12
mm Hg (12-15 in ventilator pts)
- Mean arterial pressure > 65 mm
Hg
- Urine output > 0.5 mL/kg/hr
-
 Initial Resuscitation
- if not achieved with fluid
resuscitation during first 6
hours:

- Transfuse RCC to hematocrit

> 30%
 Diagnosis
 Before the initiation of
antimicrobial, at least two blood
cultures should be obtained
- At least one drawn
percutaneously
- At least one drawn through
each vascular access device if
inserted longer than 48 hours
 Diagnosis
 Cultures such as urine,
cerebrospinal fluid, wounds,
respiratory secretions obtained
as clinical situation dictates
 Imaging and sampling performed
promptly to determine source
and causative organism
 may be limited by patient stability
 Source Control
 Evaluate patients for focus of
infection amenable to source
control measures
 Drainage of an abscess or local focus
of infection
 Debridement of infected necrotic
tissue
 Removal of a potentially infected
device
 Definitive control of a source of
 Antibiotic Therapy
 Start i.v. antibiotics within 1st hr
of recognition of severe sepsis
after obtaining cultures
 Antibiotic Therapy
 Empirical choice of
antimicrobials should include 1
or more drugs with activity
against likely pathogens,
bacterial & fungal
1. Penetrate presumed source of
infection
2. Guided by susceptibility patterns
in hospital
 Antibiotic Therapy
 Reassess after 48-72 hours to
narrow spectrum of therapy

 Duration of therapy should be 7-

10 days and guided by clinical
response
 Antibiotic Therapy
 Some experts prefer combination
therapy for Pseudomonas
infections or neutropenic
patients

 Stop antimicrobials promptly if

clinical syndrome is determined
to be noninfectious
Fluid Therapy: Choice of
Fluid
 Fluid resuscitation consists of natural
or artificial colloids or crystalloids

 No evidenced-based support for one

type of fluid over another
- Crystalloids have much larger volume
of distribution compared to colloids
- Crystalloid resuscitation requires
more fluid to achieve same endpoints
as colloid
-
 Fluid Therapy: Fluid
Challenge
 Fluid challenge in patients with
suspected hypovolemia may be
given
 500 - 1000 mL of crystalloids over 30
mins
 300 - 500 mL of colloids over 30 mins

 Repeat based on response and

tolerance
 Input is greater than output due to
venodilation and capillary leak

 Vasopressor
 Initiate vasopressor therapy if
fluid challenge fails to restore
adequate blood pressure and
organ perfusion

 Vasopressor therapy used

transiently in face of life-
threatening hypotension, even
when fluid challenge is in
 Vasopressor
 Norepinephrine or dopamine
first line agents to correct
hypotension in septic shock
 Norepinephrine more potent
than dopamine and more
effective at reversing
hypotension
 Dopamine particularly useful in
patients with compromised
systolic function but causes more
 Vasopressor
 Low dose dopamine should not be
used for renal protection in
severe sepsis
 An arterial catheter placed as soon
as practical in all patients requiring
vasopressors
 Arterial catheters provide more
accurate and reproducible
measurement of arterial pressure in
shock states compared to a cuff
 Vasopressin considered in refractory
shock patients refractory to fluid
 Inotropic Therapy
 In patients with low cardiac output
despite adequate fluid resuscitation,
dobutamine may be used to
increase cardiac output
 Combined with vasopressor therapy
in hypotension
 Steroids
 I.V corticosteroids recommended in
patients with septic shock requiring
vasopressors to maintain blood
pressure
 Administer i.v. hydrocortisone 200-
300 mg/day for 7 days in 3 or 4
divided doses or by continuous
infusion
 Reduces mortality rate in patients
with relative adrenal insufficiency
 Blood Product
Administration
 Blood transfusion when
hemoglobin decreases to < 7
g/dL
- Once tissue hypo-perfusion has
resolved and in the absence of
significant coronary artery
disease, acute hemorrhage or
lactic acidosis
 Blood Product
Administration
Erythropoietin not recommended
for treatment of anemia
associated with severe sepsis
- Unless septic patients have
other accepted reasons for
administration of erythropoietin
 Blood Product
Administration
 Routine use of fresh frozen
plasma to correct laboratory
clotting abnormalities in absence
of bleeding
 Platelets administered when platelet
counts are <5000/mm3 regardless of
apparent bleeding
 Platelet transfusion when counts
are 5000 - 30,000/mm3 and
significant risk of bleeding
3
 Glucose Control
 Following initial stabilization of
patients, maintain blood glucose
to < 150 mg/dL

 Best results when blood glucose

maintained between 80 and 110
mg/dl
 Glucose Control
 Glycemic control strategy includes a
nutrition protocol with preferential
use of the enteral route
 Risk of hypoglycemia minimized
by providing a continuous supply
of glucose substrate
 Accomplished by 5% or 10%
dextrose IV infusion ,followed by
initiation of feeding preferably by
enteral route
 Renal Replacement
 Continuous venovenous
hemofiltration and intermittent
hemodialysis considered equivalent
in acute renal failure (in absence of
hemodynamic instability)
 Continuous hemofiltration offers
easier management of fluid balance
in hemodynamically unstable
patients
 Bicarbonate Therapy
 Bicarbonate not recommended
for improving hemodynamics or
reducing vasopressor requirements
for hypoperfusion induced lactic
acidemia with pH ≥ 7.15
 No difference in vasopressor
requirements or hemodynamic
variables between bicarbonate
and normal saline for treating
hypoperfusion-induced acidemia
 DVT prophylaxis
 DVT prophylaxis with low-dose
unfractionated heparin or low
molecular weight heparin
Use mechanical prophylactic
device or intermittent
compression in patients with
contraindications to heparin
Use a combination of
pharmacological and
mechanical therapy in very
Stress ulcer prophylaxis
 Stress ulcer prophylaxis given to all
patients with severe sepsis
H2 receptor blockers more
efficacious than sucralfate
and are preferred agents

Proton pump inhibitors

 Basics of management
 Suspect sepsis if clinical signs
present
 Resuscitation should be started
immediately (fluids/pressors/steroid
as indicated)
 Identify source if possible
 Baseline investigations and blood
culture
 Start empirical antibiotics according
to center policy
 Conclusion
 Sepsis is a widespread problem in a
surgical set up
 Sepsis is reversible in early stages
 Hence early detection and prompt
treatment necessary
 High index of suspicion, active
resuscitation and judicious use of
antibiotics, pressors etc are
cornerstones of therapy
 Antibiotic choice dictated by culture