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NUR5002 > Shock and trauma > Flashcards

Shock and trauma Flashcards

1
Q

Why do shock states occur?

A

There is cellular ischaemia from decreased perfusion and impaired metabolism.

When there is an imbalance between oxygen demand and oxygen supply.

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2
Q

General pathophysiology of impaired O2 (in shock states)

A
  • 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
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3
Q

Functional states of shock:

A
  1. Hypovolaemic: impaired oxygenation due to inadequate cardiac output as a result of intravascular volume (absolute volume loss)
  2. Distributive: impaired oxygenation because of inadequate cardiac output as a result of widespread vasodilation and decreased peripheral resistance
  3. Obstructive: impaired oxygenation because of a mechanical barrier to blood flow
  4. Cardiogenic: impaired oxygenation because the heart fails to function as a pump to deliver oxygenated blood
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4
Q

Examples of causes of hypovolaemic shock

A
  • third spacing
  • haemorrhage
  • severe dehydration
  • severe vomiting/diarrhoea
  • burns
  • renal losses
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5
Q

Explain how hypovolaemic shock works:

A
  • decrease in venous blood return to the heart (preload) = decreased ventricular filling = decreased stroke volume, CO = decreased BP
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6
Q

Interventions for hypovolaemic shock:

A
  • fluid resuscitation is the primary intervention (choice of fluid is dependent upon the cause)
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7
Q

Name three types of distributive shock:

A
  1. Septic shock
  2. Anaphylactic shock
  3. Neurogenic shock
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8
Q

Describe septic shock

A
  • 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
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9
Q

Describe anaphylactic shock:

A
  • 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
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10
Q

Most common causative agent of septic shock

A
  • gram-negative bacteria
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11
Q

What are the sepsis six??
steps in the first hour of sepsis recognition to decrease mortality rate:

A
  1. Give high-flow oxygen
  2. take blood cultures
  3. give IV antibiotics
  4. give a fluid challenge
  5. measure lactate
  6. measure urine output
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12
Q

Stage 1: Initial stage of shock

A

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
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13
Q

Stage 2: compensatory stage of shock

A

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
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13
Q

Stage 3: progressive stage of shock

A

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
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14
Q

Stage 4: irreversible phase

A

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

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15
Q

Principles of management of shock: diagnostics

A
  • 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
16
Q

Multidisciplinary care for shock:

A
  • emergency care
  • medications
  • oxygen therapy
  • fluid replacement (crystalloid/colloid, blood and blood products)
17
Q

Principles of management:

A

Early recognition and prompt intervention
1. Treat underlying cause
2. increase arterial oxygenation
3. improve tissue perfusion

18
Q

Management of hypovolaemic shock:

A
  • emergency care (DRSABCDE)
  • fluid replacement (large bore IVC or CVC, crystalloid/colloid, blood and blood products)
  • oxygen therapy
19
Q

Management of septic shock

A
  • 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
20
Q

Management of anaphylactic shock

A
  • emergency care (DRSABCDE)
  • maintain patent airway
  • medications (adrenaline - IV and nebulised, antihistamines, corticosteroids)
  • oxygen therapy
  • fluid replacement (colloids)
21
Q

ongoing monitoring for shock

A
  • 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)
22
Q

Lactate is a byproduct of:

A

anaerobic metabolism

23
Q

If a cervical spine (c-spine) injury is suspected, how can you check the airway of an unconscious patient in DRSABCDE?

A

Jaw thrust only

24
Q

Clinical manifestations of anaphylactic shock?

A
  • breathing difficulties
  • wheezing
  • tacycardia
  • clammy skin
  • light-headed
  • confusion and anxiety
  • losing consciousness
  • rash
25
Q

Explain the mechanisms of action of adrenaline in relation to anaphylactic shock:

A
  • 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.
26
Q

Why would someone who has had an anaphylactic shock require IV normal saline?

A
  • 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

NUR5002 (10 decks)

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