SHOCK

Failure of adequate O2 delivery to tissues can be due to:

- decreased blood perfusion of tissues.
- inadequate O2 sats.
- increased O2 demand.
BMJ best practice (2019) Shock. https://bestpractice.bmj.com/topics/en- gb/1013/pdf/1013.pdf

 restless
 CVS - tachycardia (↑HR), hypotensive (↓BP)
 reduced sensory impairment - slow, drowsy
 cool, moist skin
 rapid, shallow breathing
 cyanosis, pale
 oliguria - reduced urine output
 reduced consciousness

PATHOPHYSIOLOGY OF SHOCK
Peate I., Nair M., Hemming L. and Wild, K. (2012) Adult nursing, acute and ongoing care. Harlow,
Essex: Pearson Education Limited.

EARLY STAGE
 drop in mean arterial pressure (MAP) causing compromised tissue perfusion - lack of
oxygenated blood flow resulting in inadequate tissue function.
 cellular hypoxia (↓O2) - anaerobic respiration (breaks down glucose instead), but because
there’s no O2, the liver can’t remove the lactic acid which is produced, causing build up.
Lactic acid can cause muscle fatigue, cramps, increase in respiration.
 compensation - although there’s low blood volume, the body can maintain BP and organ
perfusion by increasing HR and constricting blood vessels.

PROGRESSIVE STAGE
 compensatory mechanism of early-stage shock begin to fail.
 MAP is no longer sufficient in maintaining adequate tissue perfusion of vital organs.
 continued decreased cellular perfusion resulting in altered capillary permeability - allows
leakage of fluid out of vascular space into interstitial space causing decrease in circulating
volume and increase in systemic interstitial oedema.
 lactic acid accumulates and contributes to increased capillary permeability and dilation of
capillaries.
 patient urgently requires fluids and vasopressors (to raise BP)

COMPENSATORY MECHANISMS OF SHOCK –

- TACHYCARDIA – response to hypotension,
hypoxemia, and to prevent tissue hypoxia. HR
increases to maintain cardiac output band
deliver O2.
- TACHYPNOEA – response to increase CO2
removal and O2 intake.

TYPES OF SHOCK
 1. Distributive
2. Cardiogenic
3. Hypovolaemic
4. Obstructive

1. DISTRIBUTIVE – problem with blood distribution (blood and fluids in the wrong place).
- Excessive vasodilation (arteries open) and a lack of systemic vascular resistance (decrease in
BP) and so there’s less blood going to organs.
- Includes sepsis, anaphylaxis and neurogenic shock.

ANAPHYLAXIS – Systemic IgE mediated hypersensitivity reaction – when in contact with an antigen,
IgE antibodies attach to surface of mast cells in the tissues and basophils in blood. Continuous
exposure to the same antigen results in IgE-mediated release of histamine, causing vasodilation and
capillary fluid leakage.
National library of medicine (2023) Distributive shock.
https://www.ncbi.nlm.nih.gov/books/NBK470316/

 Hypotension – vasodilation and increased permeability (fluid leaves blood and goes to
tissues) causing BP to drop.
 Oedema and swelling – increased vascular permeability leading to fluid leakage from vessels
into surrounding tissue.
 Low SpO2 – increased secretion of mucus in airways causing bronchoconstriction causing
wheezing and dyspnoea (difficult breathing)
Treatment –
- IM adrenaline 500mcg (1:1000 concentration).
- High flow O2 therapy, 15L via non-rebreathe mask.
- IV antihistamines – reduce production of histamine, which causes dilation of blood vessels
leading to swelling (not first line).
- IV steroid such as hydrocortisone to reduce asthma symptoms (not first line).
Resuscitation council UK (2021) https://www.resus.org.uk/sites/default/files/2021-05/Emergency
%20Treatment%20of%20Anaphylaxis%20May%202021_0.pdf#page24
(Print pages 24-39 for treatment of anaphylaxis and refractory anaphylaxis)
Ring, J. Klimek, L. & Worm, M. (2018). Adrenaline in the Acute Treatment of Anaphylaxis. Deutsches
Arzteblatt international. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6131363/ Also includes
symptoms of anaphylaxis.

NEUROGENIC – Stimulates parasympathetic activity or inhibits sympathetic activity of vascular

smooth muscles, causing vasodilation.
 Loss of sympathetic tone – spinal cord is responsible for autonomic control of CV system. In
trauma (spinal cord injuries), especially to the upper segment, there is a disruption in the
sympathetic tone.
 Hypotension – vasodilation causes reduced systemic vascular resistance, decreases venous
return to the heart.
 Bradycardia - nerves damaged in spine, can't tell the brain to tell the heart to pump faster, so
HR can't increase.
Dave S et al. (2023) Neurogenic shock. National library of medicine.
https://www.ncbi.nlm.nih.gov/books/NBK459361/#:~:text=Neurogenic%20shock%20is%20a
%20combination,heart%20rate%2C%20and%20temperature%20regulation.

SEPTIC SHOCK – Response to infection.

 2. CARDIOGENIC – heart is unable to pump enough blood to the rest of the body.
Causes –
 Myocardial infarction (heart attack) – blood vessels blocked, so blood can’t reach heart.
Chest pain, SOB, dizzy, sweating.
 Cardiac trauma – blunt injury – a blow to the chest that bruises heart muscles, ruptures
heart walls, or damages heart valve.
 Valve problem – stenosis (narrowing).
 Arrhythmias – irregular heartbeat.
 Inflammation/ infection – myocarditis (inflammation of heart muscles) /endocarditis
(infection of inner lining of heart).
 Tachycardia – HR increases, but there is not enough time for ventricles to fill with blood.
 Bradycardia – decrease in cardiac output.

Symptoms –
 Acute hypo-perfusion – reduced blood flow.
 Hypotension – heart can't maintain BP.
 Low SpO2, hypoxia – inadequate O2 supply to tissues.
 Cold, clammy hands – reduced blood flow.
 Pale, cyanosis skin (bluish skin) – high CO2, low O2
 Confusion, agitation, drowsiness – reduced blood flow to brain, metabolic disturbances.
 Oliguria or anuria – reduced urine output due to decreased renal perfusion.
 Pulmonary congestion – fluid backing up into lungs, coughing up sputum.
Early recognition –
- NEWS2 – 5 or above
- Cool peripheries
- Pulmonary oedema
- BP under 90mmHg
- MAP under 60mmHg
- Pulse pressure under 20mmHg
- HR over 100 or under 60bpm

Investigations –
- ECG
- Blood gas: lactate, pH, base excess
- Focused cardiac ultrasound: assess for LV, RV and biventricular dysfunction and exclude
tamponade.
- Bloods: FBC, U&E, LFT, coagulation, troponin
 3. HYPOVOLAEMIA – inadequate organ perfusion caused by loss of intravascular volume,
usually acute. Insufficient amounts of blood/fluid inside the body so heart can't pump
enough blood.
Causes –
- Traumatic injury
- GI bleed
- Abdominal aortic aneurysm rupture – sudden severe pain in abdomen, back or lower back.
Caused by bulging, weakened area in vessel walls, resulting in widening of vessels.
- Burns – inflammation of muscle cells result in leakage of fluid to extra vascular space.
- Severe vomiting or diarrhoea
- Bowel obstruction
- Pancreatitis – pancreatic fluid and blood can leak into abdominal cavity, decreasing blood
volume and blood pressure.
- DKA – lack of insulin to take up glucose from blood.

Symptoms –
 Hypotension – loss of blood volume causes low venous return and low cardiac output.
 Hypoxemia (low SpO2) due to low cardiac output.
 Cells switch to anaerobic metabolism, resulting in lactic acidosis.
 Oliguria
 Tachycardia and tachypnoea – compensatory response to hypoxemia.

Treatment –
- Control ongoing fluid loss
- IV fluids to restore fluid volume, replace lost fluids.
- Prevent hypothermia.
- Blood transfusion – if patient has lost a large volume of blood.
- Crystalloids to help with hypotension.

Taghavi, S. et al (2023). HYpovolaemic shock. National library of medicine.

https://www.ncbi.nlm.nih.gov/books/NBK513297/

https://www.britishjournalofnursing.com/content/at-a-glance/hypovolaemic-shock

4. OBSTRUCTIVE –
- Tension pneumothorax – lungs can’t expand so can’t exchange gas and so can’t bring in O2 or
take out CO2.
- Cardiac tamponade – heart cant expand or fill up with blood and so there’s no blood to travel
around the body.
- Pulmonary embolism – blood clot in major artery (blood backs up to rest of bloody) or vein
(fluid backs up into lungs).