Shock

Dr. Naser El-Hammuri

Head of the Department of
Surgery
Hashemite University

Shock

Definition
Pathophysiology
Ischemic reperfusion syndrome
Classification of shock
Severity of shock
Consequences of shock
Resuscitation & Monitoring
End point of resuscitation
Conclusion

Shock
Definition:
Shock is a systemic state of
low tissue perfusion, which is
inadequate for normal cellular
respiration

Shock
Definition
Inadequate delivery of oxygen
and nutrients to maintain normal
tissue and cellular function
The resultant cellular injury is initially
reversible
If the hypo-perfusion is severe enough and
prolonged, the cellular injury becomes
irreversible

Shock
The clinical manifestations of shock are
result of stimulation of the
- Sympathetic & Neuroendocrine stress response
- Inadequate oxygen response
- End organ dysfunction

Blood pressure alone is an insensitive

measure of shock
Significant hypoperfusion and cellular
death may be ongoing, despite normal
blood pressure

Shock / Pathophysiology
Tissue hypoperfusion that is insufficient to
maintain normal aerobic metabolism
This represents an imbalance between
substrate delivery (Supply) and cellular
substrate requirements (Demand)
The initial insult, whether hemorrhage, injury, or
infection, initiates both neuroendocrine and
inflammatory mediator response
The magnitude of physiologic response is
proportional to both the degree and the
duration of shock

Shock / Pathophysiology
While the quantitative nature of the
physiologic response to shock will vary with
etiology of shock, the qualitative nature of
the response to shock is similar, with
common pathways in all types of shock.
Persistent hypoperfusion will result in
hemodynamic derangements, end organ
dysfunction, cell death, and death of the
patient if treated late or inadequately

Shock / Neuroendocrine
Response
The goal of the neuroendocrine
response to hemorrhage is maintain
perfusion to the heart and the brain,
even at the expense of other organ
system
- Peripheral
vasoconstriction
- Inhibition of fluid
excretion

Shock / Neuroendocrine
Response
The mechanism include
(1) Autonomic control of peripheral
vascular tone and contractility.
(2) Hormonal response to stress and
volume depletion
(3) Local microcirculatory
mechanisms that are organ specific
and regulate regional blood flow

Shock
Tissue hypoperfusion results in:
Insufficient delivery of O2 and
glucose to tissue
Cells switches from aerobic to
anaerobic metabolism
If perfusion not restored, cell
death

Shock / Pathophysiology
Pathophysiology (1) Cellular
Accumulation of Lactic Acid results in systemic
metabolic acidosis
Glucose get within cells get exhausted, anaerobic
respiration ceases
Failure of Na/K pump in cell membrane and
intracellular organelles
Intracellular lysosomes release autodigestive
enzymes and cell lysis ensues
Intracellular content including K are released in
bloodstream

Shock / Pathophysiology
Pathophysiology (2) Micro-vascular
Tissue ischemia result in activation of immune and
coagulation system
Hypoxia and acidosis activate complement, prime
Neutrophils, resulting in generation of O2 free
radicals and release of cytokine
This result in injury of capillary endothelial cells
which will further activate the immune and
coagulation systems
Endothelial cells losses integrity and becomes leaky
Results in tissue edema

Shock / Pathophysiology
Pathophysiology (3) Systemic
Cardiovascular
Preload and after load decrease
Compensatory Baroreceptor response
Increased sympathetic
activity
& Release of Catecholamine

Tachycardia & Systemic

vasoconstriction (except in sepsis)

Shock / Pathophysiology
Pathophysiology (3) Systemic
Respiratory
The metabolic acidosis and increased
sympathetic response result in increased
respiratory rate and minute ventilation to
increase excretion of CO2

Shock / Pathophysiology
Pathophysiology (3) Systemic
Renal
Decreased perfusion pressure

Decrease glomerular filtration &

urine out put

Stimulation of Renin
Angiotensin Aldosterone axis

More vasoconstriction and Na &

H2O reabsorption

Shock / Pathophysiology
Pathophysiology (3) Systemic
Endocrine
Release of Antidiuretic hormone from
hypothalamus
Release of cortisol from adrenal cortex

Vasoconstriction
Reabsorption of Na & H2O

Shock / Pathophysiology
Ischemia Reperfusion Syndrome
Hypoperfusion
Further injury occurs once normal circulation is
restored to these tissue:

The acid and K load that has build can lead

to myocardial depression , vascular dilatation and
further hypotension

The cellular and humoral elements activated

by the hypoxia (complement, neutrophils and
microvascular thrombi are flushed back in the
circulation where they cause further endothelial injury
to organs such as lungs and kidneys

Shock
Ischemia Reperfusion Syndrome
(continue)

This leads to acute lung injury,

acute renal injury, MOF and death
Reperfusion
injury
can
currently only be attenuated by
reducing
the
extent
and
duration
of
tissue
hypoperfusion

Classification of Shock
Hypovolemic Shock
(1) Hemorrhagic
(2) Non-Hemorrhagic
Poor fluid intake Dehydration
Excessive fluid loss

Hypovolemia is probably the most

common form of shock and to some
degree a component of all other
forms of shock

Classification of Shock
Cardiogenic Shock
Primary failure of the heart to pump
blood
forward
to
tissue
and
subsequent tissue hypoxia
MI
Cardiac dysrhythmias
Valvular heart disease
Blunt myocardial injury
Cardiomyopathy

Classification of Shock
Obstructive Shock
Reduction in preload because of mechanical
obstruction of cardiac filling
Cardiac temponade
Tension pneumothorax
Massive pulmonary embolus
Air embolus

Reduced filling of left &/or right

sides of the heart leading to reduced
preload and fall in cardiac output

Classification of Shock
Distributive Shock
Describes the pattern of
cardiovascular responses
characterizing a variety of conditions
Septic shock
Anaphylaxis
Spinal cord injury

Classification of Shock
Distributive Shock
Inadequate organ perfusion is
accompanied by vascular dilatation with
hypotension,
low
systemic
vascular
resistance, inadequate afterload and
resulting in abnormally high cardiac
output

In later phases of septic shock there is

hypovolemia from fluid loss into the intestinal
spaces and there may be concomitant
myocardial depression

Classification of Shock
Endocrine Shock
May be present as a combination of
hypovolaemic,
Cardiogenic
and
distributive shock

Hypo and hyperthyroidism

Adrenal insufficiency

Severity of Shock
Compensated shock
Reduce blood flow to non-essential organs to reserve
preload and flow to lungs and brain
Adequate compensation to maintain central blood
volume and pressure flow to kidneys, lungs and brain
Apart from tachycardia cool peripheries there may be
no other clinical signs of hypovolemia

Occult systemic metabolic acidosis, and

activation of humoral and cellular elements
within the underperfused organs
If
prolonged MOF & Death

Severity of Shock
Decompensated

Compensat
ed

Severe

Moderate

Mild

+++

++

++

Lactic
Acidosis

Anuric

Reduced

Normal

Normal

Urine output

Comatose

Drowsy

Mild Anxiety

Normal

Loss of
Consciousne
ss

Laboured

Increased

Increased

Normal

Respiratory
Rate

Increased

Increased

Increased

Mild
increase

Pulse Rate

Severe

Mild

Normal

Normal

Blood

Shock
Remember
Capillary refill
Early shock normal
Septic shock
Tachycardia
-blockers
Pacemakers
Adult with normal pulse around 50/min
Hypotension
Late sign of shock in young
Hypertensive patients

Consequences of Shock
Patients in profound shock for prolonged
period of time become unresuscitable
Cell death follows from cellular ischemia
Ability of the body to compensate is lost
Myocardial depression and loss of responsiveness to fluid
or inotropic therapy
Peripherally there is loss of the ability to maintain
systemic vascular resistance and further hypotension
ensues
The peripheries no longer respond to vasopressor agents

Death is inevitable result

Consequences of Shock

Multiple Organ Failure: Failure of

two or more organ systems
Lung
Acute respiratory distress
syndrome
Kidney
Acute renal insufficiency
Liver
Acute liver insufficiency
Clotting Coagulopathy
Cardiac Cardiovascular failure

Consequences of Shock

Intervention
be timely

must

and
period
of
shock
must be limited

Resuscitation
Should not be delayed
If in doubt about cause of shock, assume
hypovolaemic
Stop bleeding
Resuscitate before surgery (bowel
obstruction)
Fluid therapy
Initially no inotropes or chronotropes
Fluid through short wide-bore access

Resuscitation
Type of fluids
No ideal resuscitation fluid
Crystalloids vs. Colloids
Hypotonic solutions are poor volume
expander
If blood is lost, use blood

Resuscitation
Dynamic fluid response
Rapid administration of fluid bolus
250 500 cc given rapidly over 5
10 min, and the cardiovascular
responses (HR, BP, CVP) are
observed:
Responder
Transient responder
Non-Responder

Resuscitation
Vasopressor and Inotropic support
Not used initially
Indicated in Distributive shock
Cardiogenic shock

Monitoring
Monitoring of patient in shock
Minimum
ECG
Pulse oximetry
BP
Urine output

Additional modalities
CVP
Invasive BP
Cardiac out put
Base deficit and serum lactate

End Point of Resuscitation

End point of resuscitation is not by having
normal pulse, BP, and Urine output
The goal in the treatment of shock is
restoration of adequate organ perfusion
and tissue oxygenation
Resuscitation is complete when oxygen
dept is repaid, tissue acidosis is
corrected, and aerobic metabolism
restored
Occult Hypoperfusion

End Point of Resuscitation

Endpoints in resuscitation can be divided into
Systemic or global parameters
- Vital signs
-

Cardiac output
Pulmonary artery wedge pressure
Oxygen delivery and consumption
Lactate

- Base deficit
Tissue specific parameters
Cellular parameters

End Point of Resuscitation

Lactate is generated by conversion of pyruvate to
lactate by pyruvate dehydrogenase in the setting of
insufficient oxygen.
Lactate is released in the circulation and
predominantly taken up and metabolized by the
liver and kidneys
Elevated serum lactate is an indirect measure of the
oxygen dept, an therefore an approximation of the
magnitude and duration of the severity of shock
Normalization of serum lactate is considered
prognostic factor of outcome

End Point of Resuscitation

Base deficit is the amount of base in
millimoles that is required to titrate 1 L of
whole blood to a pH of 7.4 with the sample fully
saturated with O2 at 37 C and PaCO2 of 40
mmHg.
It is usually measured by arterial blood gasses
analysis
The mortality of trauma patients can be
stratified according to the magnitude of base
deficit measured in the first 24 hours after
admission

Conclusion
State of tissue hypoperfusion
Cellular injury ends up by death
Physiologic response to shock happens at cell, microvascular and systemic levels.
Multiple neuroendocrine and hormonal responses
Common pathways in response to all types of shock
Severity of shock is stratified by level of lactate and
base deficit
Outcome depends on degree, duration of shock and the
prompt response.
Endpoint of resuscitation determined by normalization
of serum lactate / base deficit