Shock and trauma Flashcards
Why do shock states occur?
There is cellular ischaemia from decreased perfusion and impaired metabolism.
When there is an imbalance between oxygen demand and oxygen supply.
General pathophysiology of impaired O2 (in shock states)
- impaired oxygen delivery to cell
- anaerobic metabolism (lactic acid produced)
- decreased production of ATP
- loss of cell membrane permeability (Na+/K+ pump lost)
- fluid shifts
- lysosomal enzymes released
- cellular death and organ failure
Functional states of shock:
- Hypovolaemic: impaired oxygenation due to inadequate cardiac output as a result of intravascular volume (absolute volume loss)
- Distributive: impaired oxygenation because of inadequate cardiac output as a result of widespread vasodilation and decreased peripheral resistance
- Obstructive: impaired oxygenation because of a mechanical barrier to blood flow
- Cardiogenic: impaired oxygenation because the heart fails to function as a pump to deliver oxygenated blood
Examples of causes of hypovolaemic shock
- third spacing
- haemorrhage
- severe dehydration
- severe vomiting/diarrhoea
- burns
- renal losses
Explain how hypovolaemic shock works:
- decrease in venous blood return to the heart (preload) = decreased ventricular filling = decreased stroke volume, CO = decreased BP
Interventions for hypovolaemic shock:
- fluid resuscitation is the primary intervention (choice of fluid is dependent upon the cause)
Name three types of distributive shock:
- Septic shock
- Anaphylactic shock
- Neurogenic shock
Describe septic shock
- systemic response to microorganisms
- release of endotoxins invade bloodstream and stimulate release of cytokines
- causes vasodilation and increases capillary permeability
- venous return reduced and maldistribution of blood volume
- decreased cellular oxygen supply, decreased tissue perfusion, impaired cellular metabolism
Describe anaphylactic shock:
- exposure to allergen results in activation of mast cells
- these release massive amounts of vasoactive substances that cause vasodilation and increase capillary permeability
- this results in a shift of fluid from the intravascular to interstitial spaces
- this causes oedema, swelling (around the neck and face), and decreases venous return
- this decreases CO and hence, oxygen delivery
Most common causative agent of septic shock
- gram-negative bacteria
What are the sepsis six??
steps in the first hour of sepsis recognition to decrease mortality rate:
- Give high-flow oxygen
- take blood cultures
- give IV antibiotics
- give a fluid challenge
- measure lactate
- measure urine output
Stage 1: Initial stage of shock
May not be clinically apparent, no outward signs of decreased tissue perfusion.
- hypoperfusion begins
- imbalance between demand and supply
- anaerobic metabolism begins (lactic acid production)
- cellular acidosis developing
- MAP decreases 10mmHg from baseline
- effective compensation
- O2 goes to vital organs
- increased HR
Stage 2: compensatory stage of shock
Body activates compensatory mechanisms in attempts to maintain homeostasis
- decreased blood flow to kidneys, flow to brain and heart maintained
- decreased CO stimulates baroreceptors and chemoreceptors
- if corrected patient can recover
- MAP decreased (hypotension)
- increased renin and ADH
- vasoconstriction
- decreased pulse pressure
- tachycardia
- decreased pH
- tachypnoea
- cool, clammy skin
- increased thirst
- hyperglycaemia
- decreased urine output
- restless
- apprehensive
Stage 3: progressive stage of shock
Compensatory mechanisms fail, decreased cellular perfusion and altered capillary permeability
- myocardial hypoxia
- tissue ischaemia
- MAP decrease 20mmHg from baseline (hypotension)
- tissue/organ hypoxia
- oliguria
- weak, rapid pulse (tachycardia)
- arrhythmias
- decreased pH
- delirium, anxiety
- tachypnoea, increased WOB, crackles
- peripheral oedema
- cyanosis, jaundice
Stage 4: irreversible phase
Decreased perfusion and cardiac output exacerbates anaerobic metabolism
- compensatory mechanisms are overwhelmed
- build up of toxins
- multi-organ failure
- recovery unlikely
- decreased cellular perfusion
- altered capillary permeability
- severe metabolic acidosis
- continuous vasoconstriction
- blood pooling
- peripheral oedema
- profound hypoxaemia
- worsening myocardial functioning
refractory stage:
* cerebral ischaemia (unconscious)
* respiratory failure
* oliguria to anuria
* coagulation altered
Principles of management of shock: diagnostics
- no single test
- identify type of shock
- history and physical examination
- ABGs (pH, base deficit, lactate)
- 12 lead ECG
- chest x-ray
- arterial pressure, central venous pressure
- blood cultures, FBC (Hb and WCC), UECs
Multidisciplinary care for shock:
- emergency care
- medications
- oxygen therapy
- fluid replacement (crystalloid/colloid, blood and blood products)
Principles of management:
Early recognition and prompt intervention
1. Treat underlying cause
2. increase arterial oxygenation
3. improve tissue perfusion
Management of hypovolaemic shock:
- emergency care (DRSABCDE)
- fluid replacement (large bore IVC or CVC, crystalloid/colloid, blood and blood products)
- oxygen therapy
Management of septic shock
- emergency care (DRSABCDE)
- sepsis 6
- fluid replacement (crystalloid/colloid, blood and blood products)
- medications (antibiotics - blood cultures, wound swab, urine, faeces, sputum, noradrenaline)
- oxygen therapy
Management of anaphylactic shock
- emergency care (DRSABCDE)
- maintain patent airway
- medications (adrenaline - IV and nebulised, antihistamines, corticosteroids)
- oxygen therapy
- fluid replacement (colloids)
ongoing monitoring for shock
- vital signs
- pulse oximetry
- capillary refill
- peripheral pulses
- level of consciousness
- ECG/cardiac monitors
- urine output (hourly) - 0.5-1mL/kg/hr
- ABGs (PaO2 > 80mmHg)
Lactate is a byproduct of:
anaerobic metabolism
If a cervical spine (c-spine) injury is suspected, how can you check the airway of an unconscious patient in DRSABCDE?
Jaw thrust only
Clinical manifestations of anaphylactic shock?
- breathing difficulties
- wheezing
- tacycardia
- clammy skin
- light-headed
- confusion and anxiety
- losing consciousness
- rash
Explain the mechanisms of action of adrenaline in relation to anaphylactic shock:
- alpha-adrenergic receptor stimulation causes vasoconstriction, reducing oedema and increasing BP
- beta-adrenergic receptor stimulation causes increased vascular smooth muscle contraction to reduce oedema, and cause bronchodilation, increased cardiac contraction and increased HR.
Why would someone who has had an anaphylactic shock require IV normal saline?
- Due to the massive vasodilation caused by anaphylaxis, much fluid is lost from the circulatory system
- this means the patient is likely to be hypotensive and go into shock
- normal saline reverses the hypovolaemia
