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shock Flashcards

1
Q

define clinical shock

A

acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in cellular hypoxia

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2
Q

how does cellular hypoxia lead to cell death?

A

• Cells switch from aerobic to anaerobic metabolism  lactic acid production  cell function ceases and swells  membrane becomes more permeable  electrolytes and fluids seep in and out of cell  Na+/K+ pump impaired  cells swell-mitochondria damage  cell death

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3
Q

what are the normal values for CO, systolic BP, MAP?

A

o C/O. ~ 5 l/min
o Systolic B.P. ~120 mm Hg
o Mean arterial pressure (MAP) ~100 mmHg

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4
Q

what makes a shock diagnosis more likely?

A

• Shock diagnosis is likely if MAP <60 mmHg + clinical signs of hypo-perfusion of vital organs inc. tachycardia, tachypnea, mental confusion, pallor

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5
Q

what can cause a low BP?

A

o Low CO
o Low systemic vascular resistance
o Or both

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6
Q

what are the causes of shock due to decreased CO?

A

decreased preload

decreased myocardial contractility

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7
Q

what are causes of reduced preload?

A

tension pneumothorax, pulmonary embolism, reduced venous return due to haemorrhage

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8
Q

what are causes of decreased myocardial contractility?

A

cardiac disease, hypoxia/hypercapnia, pH or electrolyte disturbance, drugs (e.g. beta blockers, calcium channel blockers)

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9
Q

what maintains SVR?

A

balance between vasoconstrictor factors and vasodilator factors

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10
Q

what part of the body do vasoconstrictors act on?

A

arterioles in end organs

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11
Q

how does noradrenaline work as a vasoconstrictor?

A
  1. SNS releases noradrenaline locally on alpha receptors on the outside of arterioles
    • Circulating adrenaline is relatively ineffective vasoconstrictor bc it cant easily pass through the endothelium to the a receptors
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12
Q

how does angiotensin 2 act as a vasoconstrictor?

A

Angiotensin II in the plasma acts on angiotensin AT1 receptors on the endothelium lining arterioles  stimulates contraction of underlying smooth muscle

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13
Q

why is circulating adrenaline an ineffective vasoconstrictor?

A

bc it cant easily pass through the endothelium to the a receptors

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14
Q

name vasoconstrictors

A

noradrenaline, angiotensin 2, endothelin, 5-HT

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15
Q

name vasodilators

A

prostacyclin
nitric oxide
adenosine

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16
Q

how are prostacyclins made?

A

produced in endothelial cells from arachidonic acid

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17
Q

how do prostacyclins work?

A

Ca2+ entry into smooth muscle cells around the endothelium –> reduces contractility

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18
Q

how is nitric oxide made in the body?

A

produced in endothelial cells from arginine

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19
Q

how does nitric oxide work?

A

Diffuses into smooth muscle and stimulates cAMP formation  decreases Ca2+ entry and relaxes muscle.
o Continuously produced in healthy arterioles by the blood moving on glycoproteins on the endothelium membrane

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20
Q

when is adenosine released and from where?

A

released from endothelial cells and smooth muscle during activity

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21
Q

what causes shock due to low SVR?

A
  • Often caused by pathogens in the blood releasing toxins – act on vascular smooth muscle  force it to relax
  • Toxins block the actions of noradrenaline, angiotensin etc  prevent vasoconstriction
  • Excess NO made by immune cells helps w loss of vasoconstrictor tone
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22
Q

what happens in the early stages of shock?

A

•Either SVR isn’t maintained (arterioles don’t constrict effectively) or CO decreases (loss of blood volume or obstruction to flow) –> activates homeostatic mechanisms

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23
Q

what is the initial stage of shock called?

A

compensation/compensated shock

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24
Q

what is decompensation?

A

later stage where arterioles can’t maintain constriction, or the blood preload reduction is too great. End organs aren’t perfused with oxygenated blood –> fail

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25
Q

how does BP get restored in sepsis?

A

Sepsis/anaphylaxis produces a pathological vasodilation in one or more end organs –> prevents normal arteriolar constriction –> SVR can’t be maintained –> BP falls –> detected by baroreceptors –> HR increased as compensation –> increased CO –> blood pressure restored

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26
Q

when does decompensation occur?

A

occurs if vasodilation is excessive and BP doesn’t recover despite max increase in HR

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27
Q

why can someone die in decompensation?

A

Low BP inadequate to perfuse end organs  end organ failure  person will die unless brought back to a state of compensation

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28
Q

what is obstructive shock? give examples

A

physical obstruction to the vessels entering/leaving the heart.
o E.g. pulmonary embolism, pneumothorax, cardiac tamponade

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29
Q

what is distributive shock? give examples

A

loss of vasoconstriction in one or more end organs – producing excess blood flow in this system and poor perfusion of other organs
o E.g. sepsis, anaphylaxis, neurogenic

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30
Q

what is hypovolaemic/haemorrhagic shock? give examples

A

due to haemorrhage

o E.g. haemorrhage, burns, surgery/trauma, loss of fluid/electrolytes from gut

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31
Q

what is cardiogenic shock? give examples

A

failure of heart to pump efficiently and supply blood to body
o E.g. MI, heart failure, arrhythmias, ventricular septal rupture, ischaemic cardiomyopathy, valvular disease etc

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32
Q

what is cardiopulmonary obstructive shock?

A

Cardiogenic and Obstructive shock often grouped together as cardiopulmonary obstructive shock

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33
Q

what is septic shock?

A

a type of distributive shock bc of sepsis

34
Q

what is neurogenic shock?

A

type of distributive shock. Results in low BP, sometimes with slow HR. Caused by disruption of the autonomic pathways in the spinal cord. Can occur after damage to the CNS e.g. spinal cord injury

35
Q

what are the classic signs of hypovolaemic shock?

A

confusion / anxiety, cold, clammy skin, low BP, high heart rate, slow capillary refill, greyish pallor, oliguria, absent bowel sounds

36
Q

what is hypovolaemic shock secondary to?

A

secondary to external blood loss is obvious + easily diagnosed

37
Q

why isnt internal bleeding obvious in hypovolaemic shock?

A

• Internal bleeding isn’t as obvious bc patients may only present with weakness, lethargy or a change in mental status

38
Q

what should you ask about in patients with suspected GI bleeding in hypovolaemic shock?

A

find out about hematemesis, melena, alcohol drinking history, excessive nonsteroidal anti-inflammatory drug use, and coagulopathies

39
Q

how do patients with cardiogenic shock present?

A

present with symptoms of acute cardiac ischaemia e.g. chest pain, shortness of breath, diaphoresis, nausea, vomiting

May also present with; pulmonary edema, acute circulatory collapse, and presyncopal or syncopal symptoms

40
Q

what are signs of cardiogenic shock?

A

o ECG shows the pattern of AMI or acute coronary insufficiency
o Systolic BP < 80 mm Hg *
o Pulse rate is 100 per min or faster
o The urinary output is low, 30 ml or less per hour
o There are clinical signs of peripheral circulatory collapse

41
Q

what is the treatment for cardiogenic shock?

A

expand circulating BV with IV fluids using central venous pressure as a basic guide

42
Q

what is the mortality rate of people with cardiogenic shock?

A

80% or higher

43
Q

what are signs of septic shock?

A

low BP

tachycardia

44
Q

what are symptoms of septic shock?

A

nonspecific and include fever, chills, rigors, fatigue, malaise, nausea, vomiting, difficulty breathing, anxiety, or confusion
o Fever is common but may be absent in elderly/immunosuppressed patients

45
Q

how does obstructive shock present?

A

• Tachycardia, anxiety, chest pain, breath sounds are absent on the affected hemiothorax, trachea deviates away from the affected side

  • • Classic presentation of pulmonary embolism – abrupt onset of pleuritic chest pain, shortness of breath and hypoxia
    o Symptoms can also be present for weeks
46
Q

what are the causes of obstructive shock?

A

Can be caused by a tension pneumothorax or pulmonary embolism

47
Q

what body systems act in the physiological response to hypovolaemic shock?

A

haematologic
cardiovascular
renal
neuroendocrine

48
Q

what is the haematologic system response to hypovolaemic shock?

A

activates clotting cascade.
o Contracts bleeding vessels via local thromboxane A2 release
o Local TXA2 activates platelets to form an immature clot on bleeding source

49
Q

what is the cardiovascular system response to hypovolaemic shock?

A

activates SNS  Increases HR, increases myocardial contractility and constricts peripheral BVs in skin, muscle and GI tract  redistributes blood to the brain, heart and kidneys

50
Q

what is the renal system response to hypovolaemic shock?

A

increases renin secretion  angiotensin II (has 2 effects;)
o Vasoconstriction of arteriolar smooth muscle in skin, muscle and GI tract
o Stimulation of aldosterone secretion by the adrenal cortex  increases Na+ reabsorption  increases water reabsorption
 Reverses haemorrhagic shock

51
Q

what is the neuroendocrine system’s response to shock?

A

releases ADH from posterior pituitary gland bc of decreased BP (detected by baroreceptors) and decreased plasma Na+ conc (detected by osmoreceptors)

52
Q

what is the amount of total body water, intracellular and extracellular fluid we have in our bodies?

A
  • Total body water ~ 45 litres
  • Intracellular 27 litres
  • Extracellular 18 litres
53
Q

how much blood loss is life threatening?

A

• Acute loss of >40% of blood volume (>2 litres) is immediately life threatening

54
Q

what are the immediate compensatory mechanisms in a venous haemorrhage?

A
  • Drop in venous return (preload) reduces SV and CO  decreased BP detected by baroreceptors  compensate by increasing sympathetic outflow increases HR and contractility
  • SNS constricts large veins – moves blood from venous reservoir and restores preload
55
Q

what are the immediate compensatory mechanisms in an arterial haemorrhage?

A
  • Arterial bleed – similar response to venous
  • Vasomotor centre in medulla signals to hypothalamus to release vasopressin (ADH)
  • Reduced preload reduces release of ANP  urine flow and Na+ excretion decreases
56
Q

for which classes of hypovolaemic shock will immediate compensatory mechanisms completely compensate?

A

class I and II

57
Q

what is the aim of long term compensatory mechanisms?

A

Na+, water, plasma proteins and RBCs are brought back to normal levels

58
Q

how is circulating blood volume restored by long term compensatory responses?

A
  • Increased renin is released from the kidney
  • Aldosterone released from adrenal cortex by angiotensin II – increases Na+ retention + increases thirst (receptors in subfornical organ above hypothalamus stimulated)
  • Na+ and water retention are increased to restore the circulating blood volume
59
Q

how is plasma protein synthesis increased by long term compensatory mechanisms?

A

•Stimulation of albumin and other plasma protein synthesis in the liver – unknown mechanism

60
Q

how are haematocrit levels restored by long term compensatory responses?

A

• Fibroblasts in the extracellular space around the kidney tubules (peritubular cells) are sensitive to hypoxia – release more EPO to restore haematocrit levels

61
Q

how does hypovolaemic shock present clinically?

A

tachycardia, pale, shut down, sweaty, clammy, oliguria (pass urine less than usual), confusion

62
Q

what is class I hypovolaemic shock?

A

When there’s loss of <15% blood volume

63
Q

what causes class I hypovolaemic shock?

A

• Occurs after blood donation or a minor injury

64
Q

how is class i hypovolaemic shock compensated?

A

• Normally fully compensated by immediate compensatory responses

65
Q

how does class I hypovolaemic shock present?

A

•Patient feels normal or may be slightly fatigued

66
Q

what is class 2 hypovolaemic shock?

A

• Loss of 15-30% of blood

67
Q

what are the clinical symptoms of class 2 hypovolaemic shock?

A

tachycardia (rate >100bpm), tachypnea, decrease in pulse pressure, cool clammy skin, delayed capillary refill and slight anxiety

68
Q

how will patients with class 2 hypovolaemic shock recover?

A

Patients will compensate for the blood loss – will fully recover without intervention

69
Q

what is class 3 hypovolaemic shock?

A

Loss of >30% of blood – will normally produce a persistent drop in BP

70
Q

how do people with class 3 shock present?

A

Patient will be anxious and/or confused

71
Q

how is class 3 hypovolaemic shock treated?

A

Most patients will require plasma volume expanders or a blood transfusion – may have end organ damage, especially to the kidneys

72
Q

what is class 4 hypovolaemic shock?

A

Occurs when there’s loss of >40% of blood volume

73
Q

how does a patient with class 4 hypovolaemic shock present?

A

• Patient is confused/unconscious with marked tachycardia, no urine output and severely decreased systolic pressure

74
Q

how should class 4 hypovolaemic shock be treated and why?

A

Immediately life-threatening - blood transfusion should be initiated immediately

75
Q

what is sepsis?

A

a systemic response to the presence of pathogens in the blood or other organs

76
Q

what is septic shock manifested by?

A 
•	Manifested by ≥ 2 of:
o	Temp > 38oC or < 36oC
o	HR > 90 bpm
o	RR > 20 bpm or PaCO2 < 32 mmHg
o	WBC > 12 x 109/L, or >10% band form
77
Q

what causes sepsis and septic shock?

A

bacterial toxins and/or host response leads to microvascular damage in one or more end organs

Bacterial infection –> excessive immune response* –> microvascular (endothelial) damage –> reduced systemic vascular resistance –> low BP –> septic shock

78
Q

how do bacteria reduce vascular resistance in affected organs in sepsis?

A

Lipopolysaccharide (LPS) in G-ve bacterial cell walls stimulates neutrophils and monocytes to release cytokines  damage endothelium and prevent normal vasoconstriction  reduces vascular resistance in affected organs – may be severe enough to cause shock

79
Q

why do you make a shock patient lie down?

A

to maintain cerebral perfusion

80
Q

how do you treat a patient if hypovolaemia is the cause of shock

A

restore circulating BV with IV colloids (gelatins, dextrans, hydroxyethyl starches, or 4% or 20% albumin) or crystalloids (isotonic or hypertonic saline, or Ringer lactate solution) – will restore preload and CO
• Use standard vasopressor drugs (dopamine, noradrenaline, phenylephrine, ADH) to restore blood pressure

81
Q

how do you treat a patient if the cause of shock is sepsis?

A

use appropriate antimicrobials

82
Q

what are the therapeutic goals of treating shock

A
  • Central venous pressure: 8 – 12 mmHg
  • Mean arterial pressure: ≥ 65 mmHg
  • Urine output: 0.5 mL/kg/h
  • Central venous (SVC) or mixed venous oxygen saturation: ≥ 70%

c2 (37 decks)

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