Physiology of Shock

Martin Bailey
 Outcomes
1. Discuss the factors contributing to the
development of shock

2. Differentiate between the types of shock

3. Appreciate the effects of shock on the

systems of the body

4. Identify the complications of shock

 Definition
……..a syndrome characterised by
hypoperfusion of the body tissues
Long et al 1996

A pathological condition characterised by

inadequate tissue and oxygen perfusion,
which, seriously reduces the delivery of
oxygen and other essential nutrients to a level
below that required for normal cellular
activities. Cellular injury and destruction
may occur and tissue and organ functions
deteriorate.
Watson 1980
 Mechanism of Shock
- Widespread vasoconstriction and vasodilation
altering the peripheral vascular tone and resistance

- Reduction in the intravascular volume

- Inadequate Cardiac output

Whatever the cause of shock, the body responds in

a similar way
 THREE stages of SHOCK:

1. Compensation stage
2. Progressive stage

3. Irreversible stage
 Compensation
The body is able to compensate and maintain the CVS
dynamics by:

Neurogenic means

Hormonal means

Chemical means
 Neurogenic Compensation

By:

Responding to the decrease in blood pressure the SNS

releases ADRENALINE / NORADRENALINE to raise
the BP and maintain flow to vital organs
 Hormonal Compensation

By:

Responding to the drop in renal blood flow causing

Angiotensin 1 & 11 to be released. Then Aldosterone and
ADH released.
 Chemical Compensation

By:

Responding to the ventilation / perfusion imbalance

caused by the decrease in pulmonary blood flow.
Chemoreceptors activate an increase in the respiratory
rate and depth. Increasing CO2 leads to alkalosis (which
causes cerebral hypoxia).
 Chemical Compensation
Decreased Pulmonary Blood Flow and pressure

Decreased PO2 concentration: Increased PCO2

Activation of Chemoreceptors
(carotid bodies and aortic arch)
Increased Rate
and Depth of Stimulation of
Respirations the SNS

Decreased PCO2 Respiratory Alkalosis

Vasoconstriction

Cerebral Hypoxia
 Hormonal Compensation
Decreased in Renal Blood Flow

Release of RENIN and ANGIOTENSIN

ANGIOTENSIN 1
ANGIOTENSIN 11
Vasoconstriction Aldosterone and ADH

Increased Blood Pressure and Reabsorption of

venous return to the heart Sodium and
Water
 Neurogenic Compensation
Decreased Blood Pressure
Increased rate and Increased sweat
depth of respirations SNS stimulation gland activity
Pupils dilate Moist, clammy
Catecholamine release skin
(Adrenaline/Noradrenaline)
Vasoconstriction in
Increased rate and
skin, lungs, GI tract,
force of cardiac
kidneys Increased Venous contractions
return
Maintenance of Increased cardiac output
blood flow to the Increased blood pressure
heart and brain
 Progressive
Compensation mechanisms fails to maintain adequate
CO. This leads to:
Ischaemia and hypoxia
Anaerobic metabolism and production of lactic
acid, pyruvate and CO2 (causing pH to fall)
Venous constriction
Causing oedema, erythrocyte and platelet
clumping
These inhibit the circulation and lead to…………..
 Irreversible
This stage CANNOT be reversed.

It occurs mainly due to:

- decreased coronary blood supply

- metabolic acidosis
- presence of toxins from injured cells

DEATH follows
 Types of shock

Hypovolaemic
Cardiogenic
Septic / bacteraemic / endogenic
Anaphylactic / neurogenic
 Hypovolaemic
Decrease in circulating fluid volume

Can be caused by haemorrhage,

diarrhoea, vomiting, dehydration,
burns etc
 Decrease in blood volume

Pain Catecholamines
released Reduction in venous return

tachycardia
Peripheral Arterial hypotension
vasoconstriction
Reduced tissue perfusion
Increased cardiac
contractability
Anaerobic metabolism

Increased myocardial O2
Acidosis
demand
Myocardial failure
Multi-organ failure
Signs and Symptoms of
Hypovolaemic Shock
General Weakness
Anxiety Thirst
Skin Pallor
Tachycardia
Hypotension
Confusion
Tachypnoea
Cyanosed nail beds
Decreased urine output
Oedema
Complications
ARDS

DIC
Renal Failure

o DEATH…….
 Cardiogenic Shock

This is PUMP failure

Often happens post MI, Post PE, after cardiac

surgery, stab wounds to the chest, Asthmatics at
risk and those with Tension Pneumothorax

There is increase in the intrathoracic pressure - this

reduces the PUMP effect in the chest
 What Happens?
- Tissue oxygenation falls and lactic acid accumulates

- As CO2 decreases, hypotension and vasoconstriction

occur
- Vasoconstriction increases the resistance to the
outflow of blood from the heart and increases left
ventricular workload

- Increased release of Aldosterone causing Na+ and H2O

reabsorption, thus increasing circulating blood volume
 Signs and Symptoms
- Pallor and feeling cold

- Cyanosed nail beds

- Cardiac Arrest
- Cardiac Arrhythmias
- Poor or no cardiac output
- Hypotension (BP below 90mmHg)
- Oliguria
Signs and Symptoms (cont’d)
- Arterial vasoconstriction (hypoperfusion of
vital organs and peripheries)

- Rapid and Shallow respiratory rate

- Tachycardia
- Restless, anxious, stupor / unconsciousness
- Increased Multi-Organ Failure
Septic / Bacteraemic / Endotoxic
(endogenic) SHOCK
Most often occurs when there is infection of the:

GUT
RESPIRATORY TRACT
URINARY TRACT
OBSTRUCTIONS
Surgical Intervention / invasive
procedures (IPPV etc)

Usually GRAM NEGATIVE and consequently have a rapid

onset
Presenting Signs and Symptoms
Initially warm and flushed skin

Restless and anxious

Tachycardia
Tachypnoea
Fever
Thirst
Hypotension (associated with vasodilation)
Although often have a good urine output
Mortality is 50%
Continued………
 BUT…….

Can be cold and shivery

Have a pyrexia or be hypothermic

May have Diarrhoea and Vomiting

May be jaundiced
 Anaphylaxis

An extreme reaction to an allergen

Bee stings, peanuts, drugs, chemicals etc

Histamine is released
Signs and Symptoms
Pale
Feeling faint and collapsing
Swollen face and neck
Tachycardia / Tachypnoea
Respiratory Distress / Stridor
Sudden collapse and loss of consciousness
Hypotension
Local Inflammation
Pain in the lower back