Shock

Shock ,Principles &
Management
Dr. Abdallah Alabadla

General Surgery specialist
Nasser Medical Complex
Definition
A physiological state that results in inadequate
organ perfusion and tissue oxygenation
Imbalance between substrate supply &

demand leads to decreased tissue
Oxygenation and anaerobic metabolism
Ultimate Effects of Anaerobic Metabolism
perfusion
Energy production anaerobic Lactic acid

metabolism Production
Metabolic CELL Metabolic

Failure DEATH Acidosis
Cardiac Output = HR x Stroke Volume
Stroke Volume is a function

Preload, Afterload, Myocardial Contractility
MAP: (Systolic BP + 2(Diastolic BP))/3

Pulse P = SBP - DBP
Symptoms & signs
low blood pressure

decreased urine output
Weakness, Confusion
Tachycardia
Dry mucous membrane, reduced skin turgor
Prolonged capillary refill time
weak peripheral pulses and cold extremities
Stages of shock
1. Compensated ( nonprogressive) shock
2. Uncompensated (progressive) shock
3. Irreversible (refractory) shock

Compensated shock
“Reversiblestage during which
compensatory mechanisms are effective
and homeostasis is maintained”
Clinical presentation begins to reflect the

body’s response to the imbalance of
oxygen supply and demand
Compensated shock
At first, blood pressure will decrease, which
happens because of the decrease in cardiac
output (CO) and a narrowing of the pulse
pressure.
The baroreceptors in the carotid and aortic

bodies immediately respond by activating the
sympathetic nervous system (SNS). The SNS
stimulates vasoconstriction and release of
epinephrine and norepinephrine
Compensated shock
 Bloodflow to the vital organs, such as the heart and brain, are
maintained
 Bloodflow to non-vital organs, the kidneys, liver, skin, GI tract is

shunted.
 Decreased blood flow to the kidneys activates the renin-

angiotensin system.
 Reninis released, which activates angiotensinogen to produce

angiotensin I, which is then converted to antiotesnsin II.
 AngiotensinII causes vasoconstriction in both the arteries and

venous system
Compensated shock
At this stage, the body is able to compensate
for the changes in tissue perfusion. If the
underlying cause is corrected, the patient will
recover with little to no residual effects.
Ifthe body is unable to compensate the body

will enter the progressive stage of shock
Uncompensated Shock
Thisstage of shock begins when the body’s

compensatory mechanisms fail
Aggressive interventions are need to prevent

the development of multiple organ dysfunction
syndrome (MODS)
Continued decreased cellular perfusion and

resulting alerted capillary permeability
Uncompensated shock
Altered capillary permiability allows leakage of fluid
and protein out of the vascular space into the
surrounding interstitial space causing a decrease in
circulating volume and an increase in systemic
interstitial edema.
This fluid leak from the vascular space also affects

the solid organs, liver, spleen, GI tract, lungs, and
peripheral tissues by further decreasing oxygen
perfusion
Irreversible Shock
Final stage of shock
Decreased perfusion from peripheral VC and

decreased cardiac output exacerbate anaerobic
metabolism
Lactic acid accumulates and contributes to an

increased capillary permeability and dilation of the
capillaries
Increased capillary permeability allows for fluid and

plasma to leave the vascular space and move to the
interstitial space
Irreversible Shock
Blood pools in the capillary beds secondary to
constricted veins and dilated arteries
Loss of intravascular volume leads to worsening

of hypotension and tachycardia resulting in a
decrease in coronary blood flow
Decreased coronary blood flow results in

decreased cardiac output
Cerebral blood flow cannot be maintained and

cerebral ischemia results
Hypovolemicshock
most common type
 Causes
insufficientcirculating volume
Hemorrhage (internal or external)
vomiting and diarrhea
Burns
excess urine loss due to DKA or D.I.
Hemorrhagic Shock
Treatment
Cardiogenic shock
Failure of the heart to pump effectively
 Causes
damage to the heart muscle,
myocardial infarction
Dysrhythmias
cardiomyopathy/myocarditis
CHF
myocardial contusion
valvular heart disease problems.
Obstructive shock
Physical obstruction of great vessels of the

systemic or pulmonary circulation
 Causes
 Cardiac tamponade
 Constrictive pericarditis
 Tension pneumothorax
 Pulmonary embolism
 Aortic stenosis
 Abdominal compartment syndrome
Distributive Shock
Distributive shock is low blood pressure
due to a dilation of blood vessels within
the body.

systemic infection (septic shock)
severe allergic reaction (anaphylaxis)
spinal cord injury (neurogenic shock)

SIRS
Systemic Inflammatory Response Syndrome
◦ Defined by the presence of two or more of the

following:
 Body temp < 36 °C (97 °F) or > 38 °C (100 °F)

 Heart Rate > 90 bpm
 RR > 20 bpm
 WBC < 4,000 cells/mm3 or > 12,000 cells/mm3 (<
4 × 109 or > 12 × 109 cells/L), or greater than 10% band
Sepsis and Septic Shock
Sepsis-Defined as SIRS in response to a

confirmed infectious process.
Septic shock- Defined as sepsis with

refractory arterial hypotension or
hypoperfusion abnormalities in spite of
adequate fluid resuscitation.
Ghana Emergency Medicine Collaborative

Advanced Emergency Trauma Course
Treatment
Fluid administration
Monitor VS
Antibiotics: broad spectrum until source
is identified
Vasopressors
Anaphylactic Shock
 An IgE mediated event that triggers massive release of immune
response mediators
 Results in widespread peripheral vasodilation, bronchial smooth
muscle contraction, and local vascular dilatation
 Treatment:
 Airway management
 Epi 0.3mg SQ or IM to vastus lateralis
 BLS/ACLS
Neurogenic Shock
 Result of spinal cord injury
 Loss of sympathetic tone
 Decreased vasomotor tone
 Resultsin hypotension and

bradycardia
 Patientsmay remain alert, warm,

and dry despite the hypotension
Ghana Emergency Medicine Collaborative
Advanced Emergency Trauma Course

Shock

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Shock ,Principles &

Dr. Abdallah Alabadla

Imbalance between substrate supply &

Energy production anaerobic Lactic acid

Metabolic CELL Metabolic

Stroke Volume is a function

MAP: (Systolic BP + 2(Diastolic BP))/3

low blood pressure

2. Uncompensated (progressive) shock

3. Irreversible (refractory) shock

Clinical presentation begins to reflect the

The baroreceptors in the carotid and aortic

 Bloodflow to non-vital organs, the kidneys, liver, skin, GI tract is

 Decreased blood flow to the kidneys activates the renin-

 Reninis released, which activates angiotensinogen to produce

 AngiotensinII causes vasoconstriction in both the arteries and

Ifthe body is unable to compensate the body

Thisstage of shock begins when the body’s

Aggressive interventions are need to prevent

Continued decreased cellular perfusion and

This fluid leak from the vascular space also affects

Decreased perfusion from peripheral VC and

Lactic acid accumulates and contributes to an

Increased capillary permeability allows for fluid and

Loss of intravascular volume leads to worsening

Decreased coronary blood flow results in

Cerebral blood flow cannot be maintained and

Failure of the heart to pump effectively

Physical obstruction of great vessels of the

severe allergic reaction (anaphylaxis)

spinal cord injury (neurogenic shock)

◦ Defined by the presence of two or more of the

 Body temp < 36 °C (97 °F) or > 38 °C (100 °F)

Sepsis-Defined as SIRS in response to a

Septic shock- Defined as sepsis with

Ghana Emergency Medicine Collaborative

 Result of spinal cord injury

 Loss of sympathetic tone

 Decreased vasomotor tone

 Resultsin hypotension and

 Patientsmay remain alert, warm,

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