Shock

 

A state with significant reduction in systemic tissue perfusion, resulting in decreased delivery of oxygen and reduced removal of waste products, leading to tissue injury.

 

Blood pressure = cardiac output x peripheral resistance

 

Cardiac output is dependent on venous return

 

Cardiac output = heart rate x stroke volume

 

Clinical forms of shock

 

Hypovolaemic shock

Haemorrhage

Burns

Dehydration

Oedema

Third spacing

 

Cardiogenic shock

Myocardial infarction

Valve dysfunction

Dysrhythmias

Cardiomyopathy

Cardiac failure

 

Obstructive shock

Obstruction within veins

Compression of heart

Pressure on vessels

 

Distributive forms of shock

 

Septic shock

Uncomplicated sepsis

Severe sepsis

Septic shock

 

Allergic shock

Anaphylaxis

 

Neurogenic shock

Sympathetic decrease

Parasympathetic increase

Spinal shock

Vasovagal syncope

Psychogenic

 

 

Patient assessment

Airway and C spine control

Breathing and ventilation - aim for 95% O2 sats

Circulation and haemorrhage control

Disability – neurological examination

Exposure – complete examination

 

 

Recognise if shock is present

Early features;

Tachycardia

Cutaneous vasoconstriction

 

Any injured patient who is cool and tachycardic is considered to be in shock until proved otherwise.

 

Haemodynamic collapse

Inadequate perfusion of;

Skin

Kidneys

CNS

 

Respiratory rate

Narrowed pulse pressure

 

Identify the cause of the shock state

Patient history

Treat simultaneously

 

After trauma

Hamorrhagic or nonhaemorrhagic

 

General management principles

The Golden Hour

Establish and maintain a clear airway

Ensure adequate ventilation

Oxygen to keep sats above 95%

Adequate intravenous access

Continuous cardiac monitoring

Urinary catheter

Recording of fluid balance

Central venous monitoring

Physiologically desirable position

Maintain optimum temperature

Blood gases

Acid / base balance assessment

Psychological and family support.

Observation of response to treatment

Inotropes and vasoconstricting drugs

Treatment of underlying disorder

 

Specific management measures

 

Hypovolaemic shock

Arrest bleeding

Intravenous fluids

Assess response

Oral rehydration

Treat underlying causes

 

Diarrhoea and Vomiting in Children

Continue breast feeding

Encourage fluid intake

No fizzy drinks or fruit juice

Oral Rehydration Salts

Consider nasogastric ORS

IVIs for shock or deterioration

Eg. 0.9% saline or saline with 5% glucose

Check Na, K, urea, creatinine, glucose

After rehydration give normal food and milk

 

Cardiogenic shock

Early thrombolysis

Valve replacement surgery

Correct dysrhythmias

Medications

 

 

 

Obstructive shock

Heparin

Thrombolysis

Pericardiocentesis

Chest decompression

Chest drainage

 

Septic shock

Initial resuscitation

Cultures

Antibiotics

Correct cause

Vasopressors

Inotropic therapy

 

Allergic shock

Epinephrine

Adrenaline

Chlorphenamine

Hydrocortisone

Bronchodilators

Oxygen

Fluids

Prevention

 

Neurogenic shock

Spinal shock

Vasovagal syncope

Psychogenic

Inotropes

Vasopressors

Treat cause

Position

 

Stages of shock

 

Compensated shock

Non-progressive

Neurological compensations

Endocrine compensations

Increased absorption of fluids

 

Blood pressure maintained

Circulatory system protected

 

Progressive shock

Decompensated

Condition deteriorates

Blood pressure starts to fall

Hypoperfusion of;

kidneys

gut

myocardium

medulla oblongata

Last window of opportunity for curative treatment

 

Irreversible shock

Still alive, but die

Transient increase in BP

Treat shock before this stage

 

The Golden Hour 

Treatment ASAP, or within one improves survival

Stop the bleeding, treat injuries and restore blood pressure within one hour

The ‘Golden Hour’ begins at the time of trauma

 

Physiological response

 

Neurological response

When a baroreceptor is stretched it is stimulated and produces nerve impulses

Sensory nerves travel from the baroreceptors to the medulla oblongata

Here they influence the activity of the vasomotor and cardiac centres

Impulses from the baroreceptors inhibit the sympathetic outflow from these centres

When blood pressure falls there is a reduced firing rate from the baroreceptors

Reduced inhibitory effect on the sympathetic outflow

This results in increased sympathetic outflow from the medulla

There will also be inhibition of the parasympathetic vagal outflow

 

Endocrine response

Catecholamines

Renin - Angiotensin - Angiotensinogen - Aldosterone

Antidiuretic Hormone, Vasopressin

 

Clinical features of classical shock

Arterial vasoconstriction

Venous vasoconstriction

Pallor / cyanosis

Cold and clammy

Tachycardia

Pulse

Tachypnoea

Thirst

Oliguria / anuria 

Jugular venous pressure

Hyperglycaemia

Lactic acidosis

Coronary and cerebral circulation

End organ damage

Vascular damage

 

In cardiogenic shock

Pulmonary oedema

 

In distributive shock

Initially warm / red peripheries

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Special groups

 

Shock and athletes

Athletes have increased blood volume, cardiac output, stroke volume but reduced pulse rate

Are brilliant compensators

 

Shock and the elderly

Unable to increase heart rate and efficiency of myocardial contraction

Atherosclerosis means even slight reductions in tissue perfusion may lead to early end organ injury

Reduce pulmonary compliance results in early hypoxic injury

Kidneys are less able to preserve blood volume

Kidneys sensitive to reduced blood flow

Therefore mortality and morbidity increases with age

Therefore give aggressive resuscitation and monitor carefully

Young adults are much better compensators than older adults

 

Shock and children

Child blood volume 80ml / Kg

Excellent compensators

Systolic BP maintained until 30% of blood volume is lost

 

Look out for;

Poor skin perfusion

Tachycardia

Progressive weakening of peripheral pulses

Skin mottling (as opposed to clammy)

Cool extremities

Prolonged capillary refill

Anxious, irritable, confused

Reduced organ perfusion and oliguira are late signs

 

No progressive development of hypotension

Sudden decompensation

Past 30 % blood loss BP and CO fall rapidly

Bradycardia may replace tachycardia

Give early crystalloid fluid resuscitation

Get early assessment by a surgeon

 

Management in children

In suspected shock give 20ml / Kg warmed isotonic crystalloid

3 for 1 rule applies

Repeated 2 more times to a total of 60ml / Kg

Consider PRBCs at 10ml / Kg

 

Peripheral vein

Central line

Intraosseous, anterior tibial bone marrow

 

Urine output and specific gravity is a good titration aid for fluid resuscitation

 

Hypothermia may render the child refractory to treatment

 

 

 

 

 

 

 

 

 

 

 

 

Sepsis

 

 

Screening, any 2 of the following

 

Fever > 38oC or <36oC

Heart rate >90

Tachypnoea >20

Leucocytosis >12,000 or <4,000

Altered mental status

Hyperglycaemia >6.6 mmol / L (unless diabetic)

 

 

also

 

>10% immature forms

Increased C-reactive protein

SBP < 90 mmHg

Oedema or positive fluid balance

 

 

 

Any history of,

 

Pneumonia

UTI

Abdominal pain, diarrhoea, distension

Meningitis

Cellulitis, septic arthritis, fasciitis, wound infection

Endocarditis

Catheter infection

 

 

 

Severe sepsis care pathway – sepsis 6

 

Oxygen, high flow rate, aim for >94%

Blood culture, before antibiotics, also cultures

IV antibiotics

Fluid resuscitation, if hypotensive give 20ml/Kg bolus

Serum lactate, grey top bottle on ice

Catheterise, hourly fluid balance

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Questions

What are the 3 stages of shock

Give 4 possible causes of hypovolaemia

Describe the surface area of the body in the rule of 9

Give 4 causes of cardiogenic shock

Give 3 causes of obstructive shock

 

What receptors detect blood pressure in the carotid sinus

What part of the brain contains the vasomotor centre

What is the initial dose of adrenalin used in anaphylaxis

List 5 places where blood may be lost

List 5 possible clinical features of septic shock

 

Which statement is true of the Golden Hour

It begins at the time of the trauma

It begins when the patient arrives in A and E