Shock Flashcards

1
Q

What is shock?

A

A syndrome characterised by decreased tissue perfusion resulting in impaired cellular metabolism

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2
Q

When does shock occur?

A

When tissue oxygen supply does not meet the oxygen demand

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3
Q

Pathophysiology of shock

A
  1. Impaired oxygen delivery to cell
  2. Anaerobic metabolism (lactic acid)
  3. Decreased production of ATP
  4. Loss of cell membrane permeability - Na+K+ pump lost
  5. Fluid shifts
  6. Lysosomal enzymes released
  7. Cellular death and organ failure
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4
Q

What are the 4 shock states?

A
  1. Initial
  2. Compensatory
  3. Progressive
  4. Irreversible
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5
Q

What occurs during the initial state of shock?

A

Hypoperfusion resulting in an imbalance between supply and demand.
Anaerobic metabolism begins which produces lactic acid.
Cellular acidosis develops

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6
Q

Clinical manifestations of initial state of shock

A

May not be clinically apparent, no outward signs of decreased tissue perfusion

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7
Q

What happens during the compensatory shock state?

A

Compensatory mechanisms are activated in attempt to maintain homeostasis.
- Decreased cardiac output stimulates baroreceptors and chemoreceptors resulting in adrenaline and noradrenaline being released to vasoconstriction and increase BP to maintain blood flow to brain and heart
- Decreased blood flow to kidneys activates the renin-angiotensin-aldosterone system and ADH release is stimulated to increase blood volume and therefore BP

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8
Q

Clinical manifestations of the compensatory state of shock

A

Tachycardia
Hypotension
Tachypnoea due to hypoxia
Cool, clammy skin
Decreased urine output
Increased thirst due to activation of RAAS
Altered level of consciousness
Hyperglycaemia

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9
Q

What happens during the progressive state of shock?

A

Compensatory mechanisms fail resulting in decreased cellular perfusion, hypoxia of vital organs, decreased cardiac output and tissue ischaemia.
Low oxygen leads to increased lactic acid production and failure of Na+K+ pump, therefore altering electrolytes. Altered cell membrane permeability leads to release of lysosomes causing increased risk of gastric ulcers and gastric bleeding and increased risk of developing DIC.
Acute renal failure occurs leading to metabolic acidosis.

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10
Q

Clinical manifestations of the progressive state of shock

A

Hypoxia
Tachypnoea, deep respirations, increased WOB, crackles
Tachycardia, arrhythmias, hypotension, weak peripheral pulses
Peripheral oedema, peripheral cyanosis
Decreased urine output
Delirium, anxiety
Jaundice

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11
Q

What happens during the irreversible stage of shock?

A

Compensatory mechanisms overwhelmed
Severe hypoxia with ischaemia, necrosis and cell death
Altered capillary permeability
Severe metabolic acidosis
Continuous vasoconstriction
Build up of toxins
Multi-organ failure

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12
Q

Clinical manifestations of the irreversible stage of shock?

A

Blood pooling
Peripheral oedema
Profound hypotension
Profound hypoxemia
Worsening myocardial functioning
Cerebral ischaemia
Respiratory failure
Oliguria and anuria
Coagulation altered

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13
Q

What are the 4 functional states of shock?

A
  1. Hypovolemic
  2. Distributive
  3. Obstructive
  4. Cardiogenic
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14
Q

What causes impaired oxygenation in hypovolemic shock?

A

Inadequate cardiac output as a result of decreased intravascular volume
Decreased blood volume leads to decreased venous return (preload), the ventricular filling decreases resulting in decreased stroke volume, cardiac output and BP

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15
Q

What causes impaired oxygenation in distributive shock?

A

Inadequate cardiac output as a result of widespread vasodilation and decreased peripheral resistance

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16
Q

What are the 3 types of distributive shock?

A
  1. Septic shock
  2. Anaphylactic shock
  3. Neurogenic shock
17
Q

What causes impaired oxygenation in obstructive shock?

A

A mechanical barrier to blod flow

18
Q

What causes impaired oxygenation in cardiogenic shock?

A

The heart fails to function as a pump to deliver oxygenated blood

19
Q

Causes of hypovolemic shock

A

Dehydration
Haemorrhage
Burns
Third spacing
Renal losses

20
Q

What is the treatment for hypovolemic shock?

A

Fluid resuscitation. The choice of fluid is dependent on the cause of hypovolemia

21
Q

What causes widespread vasodilation in the 3 types of distributive shock?

A

Septic shock - endotoxin release
Anaphylactic shock - histamine release
Neurogenic shock - sympathetic tone

22
Q

Distributive shock treatment

A
  • Fluid resuscitation to increase preload and cardiac output
  • Administer vasopressors like noradrenaline to increase the systemic vascular resistance (SVR)
23
Q

What occurs during septic shock?

A

Endotoxin release into the bloodstream stimulates the release of cytokines causing vasodilation and increased capillary permeability.
Results in reduced venous return and maldistribution of blood volume

24
Q

What is the sepsis six?

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
25
Q

What occurs during anaphylactic shock?

A

Massive amounts of vasoactive substances released from mast cells causing vasodilation and increased capillary permeability.
Increased size of compartment and fluid shifts from intravascular to interstitial spaces.
Combined vasodilation and increased capillary permeability decrease venous return, cardiac output and oxygen delivery

26
Q

What occurs during neurogenic shock?

A

Parasympathetic overstimulation and sympathetic under stimulation causes an imbalance of vascular smooth muscle stimulation resulting in vasodilation.
Results in decreased venous return and decreased cardiac output.

27
Q

Examples of obstructive shock causes

A

Pulmonary embolism
Tension pneumothorax
Cardiac tamponade

28
Q

Examples of cardiogenic shock causes

A

Myocardial infarction
Dysrhythmias

29
Q

Shock diagnostics

A

No single test. The following can help identify the type of shock and assess the patient’s status:
- History and physical examination
- ABGs (pH, base deficit, lactate)
- 12 lead ECG
- Chest X-ray
- Arterial pressure, central venous pressure
- Blood cultures, UECs, FBC (Hb, WCC)

30
Q

Shock nursing care

A

Emergency care
Medications
Oxygen treatment
Fluid replacement
Blood products

31
Q

Shock management aims

A

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

32
Q

Hypovolemic shock care

A

Emergency care (DRSABCDE)
Oxygen therapy
Fluid replacement
- Large bore IVC or CVC
- Crystalloid, colloid, blood and blood products

33
Q

Septic shock care

A

Emergency care (DRSABCDE)
Sepsis 6
Fluid replacement (crystalloid, colloid, blood and blood products)
Medications (antibiotics and noradrenaline)
Take blood cultures, wound swabs, urine, faeces and sputum samples

34
Q

Anaphylactic shock care

A

Emergency care (DRSABCDE)
Maintain patent airway
Oxygen therapy
Fluid replacement (colloids)
Medications (adrenaline, antihistamine, corticosteroids)

35
Q

Ongoing monitoring for shock

A

Vital signs
Pulse oximetry
Capillary refill
Peripheral pulses
Level of consciousness
ECG / cardiac monitor
Urine output (hourly): 0.5-1.0ml/kg/hr
ABGs (PaO2>80mmHg)