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Unit 1 > Shock > Flashcards

Shock Flashcards

1
Q

Define aerobic respiration

A

The process of producing cellular energy involving oxygen

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2
Q

Define anaerobic respiration

A

The process of producing cell energy when there is not enough oxygen for aerobic respiration. Glucose -> lactic acid (+energy released)

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3
Q

Define metabolic acidosis

A

A pH imbalance where too much acid is accumulated in the body or too much alkali (bicarbonate) has been lost from the body

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4
Q

Define respiratory acidosis

A

Results of hypoventilation and accumulation of CO2

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5
Q

Define stroke volume

A

The volume of blood pumped out of the left ventricle with every heart beat

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6
Q

Define blood pressure

A

The pressure of blood on the walls of the arteries

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7
Q

Define systolic blood pressure

A

The force exerted on the walls of the arteries as blood is pumped from the ventricles

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8
Q

Define diastolic blood pressure

A

The force of blood on the walls of the arteries when the ventricles are relaxed (filling)

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9
Q

Define shock

A

Situation where oxygen delivery to cells/tissues is insufficient for demand

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10
Q

What does SIRS stand for?

A

Systemic inflammatory response syndrome

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11
Q

Define bacteraemia

A

Presence of viable bacteria in the blood

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12
Q

Define sepsis

A

Clinical manifestations of SIRS secondary to an infectious cause

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13
Q

When is sepsis considered severe?

A

Evidence of dysfunction of at least one organ

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14
Q

Definer septic shock

A

Severe sepsis association with hypotension that is unresponsive to appropriate fluid resuscitation

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15
Q

What does MODS stand for?

A

Multiple organ dysfunction syndrome

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16
Q

Define MODS

A

Dysfunction of the endothelial, cardiopulmonary, renal, nervous, endrocrine and gastrointestinal systems associated with the progression of system inflammation

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17
Q

What does DIC stand for?

A

Disseminated intravascular coagulation

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18
Q

What is a crystalloid?

A

Solutions of electrolyte and/or glucose in water

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19
Q

Define a colloid

A

Macromolecules in solution. Because of their size, they are retained intravascularly and exert colloid osmotic pressure

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20
Q

What does anaerobic metabolism produce?

A

Lactic acid accumulation -> metabolism acidosis

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21
Q

What substances are produced by ongoing anaerobic respiration that are harmful to cells?

A

Cytokines
lactate
Nitric oxide

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22
Q

What are the four categories of shock?

A

Hypovolaemic
Distributive
Obstructive
Cardiogenic

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23
Q

Define hypovolaemic shock

A

Due to loss of intravascular volume which leads to decreased venous cardiac return/cardiac preload i.e. blood loss

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24
Q

Define distributive shock

A

Maldistribution of blood and is generally associated with sepsis, SIRS or anaphylaxis. Widespread vasodilation, ‘leaky’ vessels and activation of the coagulation cascade

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25
Q

Define obstructive shock

A

Associated with physical impediment to blood flow i.e. GDV

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26
Q

Define cardiogenic shock

A

Caused by severe cardiac dysfunction which results in markedly decreased cardiac output despite normal blood volume i..e ventricular tachycardia

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27
Q

What are the most common causes of shock?

A

Hypovolaemic and septic

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28
Q

What are some common causes of hypovolaemic shock

A

Haemorrhage (trauma, surgical, coagulopathy)
Gastrointestinal losses (vomiting secondary to gastrointestinal foreign body)

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29
Q

What are common causes of septic shock?

A

Septic peritonitis
Pyometra
Pyothorax

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30
Q

What are causes of obstructive shock?

A

Pericardial effusion
GDV
Pulmonary thromboembolism

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31
Q

Give an example of a patient with obstructive shock where hypovolaemia may also be present

A

GDV

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32
Q

What are common causes of cardiogenic shock?

A

End-stage DCM
Severe arrhythmias

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33
Q

What is blood pressure affected by?

A

Cardiac output
Total peripheral resistance (vasodilation/construction)
Blood viscosity

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34
Q

What are compensatory mechanisms mediated by?

A

HPA axis - also known as the sympatho-adrenal response

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35
Q

What is the aim of compensatory mechanisms?

A

Increase cardiac output and blood vessel tone to increase cell perfusion

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36
Q

Define acute compensatory mechanisms

A

Focused on increased venous return to the heart and increasing blood supply to the myocardium

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37
Q

What triggers the acute compensatory response?

A

Sympathetic nervous system

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38
Q

What stimulates the sympathetic nervous system during decreased blood volume?

A

Decreased baroreceptor impulses

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39
Q

What is the acute compensatory response during decreased blood volume?

A

Increased sympathetic activity and catecholamine release leads to peripheral vasoconstriction, tachycardia and increase in cardiac contractility

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40
Q

How is hypoxaemia detected?

A

Chemoreceptors in the aorta and carotid artery

41
Q

Define RAAS

A

Decreased renal perfusion results in stimulation of baroreceptors in the kidney

This stimulates RENIN release with converts angiotensinogen into angiotension I and angiotension II

Immediate response of angiotension II = peripheral vasoconstriction (and reabsorbs some salt and water)

Delayed response of angiotension II - aldosterone release from the adrenal cortex -> increased sodium, chloride and water reabsorption from distal convoluted tubules in the kidney -> increased blood volume

42
Q

What is the aim of the neurohormonal response (RAAS) in moderate compensatory mechanisms?

A

Retain more fluid at the kidney aiming to restore normal intravascular volume and increase cardiac perload/venous return

42
Q

What happens if short-term compensatory vasoconstriction occurs for a prolonged period?

A

Cellular hypoxia and death due to decreased perfusion

43
Q

Why is the gastrointestinal tract a concern during prolonged compensatory vasoconstriction?

A

During ‘shock’, the blood flow to the GIT is reduced by up to 70% which can lead to GI complications such as vomiting and diarrhoea, therefore worsening hypovolaemia

44
Q

What is released from the posterior pituitary gland when blood osmolarity increases and blood volume decreases?

A

Vasopression (ADH)

45
Q

What is an immediate effect of vasopressin (ADH) during hypovolaemia?

A

Binds to V1 receptors in peripheral arterioles causes peripheral vasoconstruction (which angiotensin II and catecholamines also do)

46
Q

Define chronic compensatory mechanisms

A

Responses to hypovolaemia after acute responses have been actioned. They take longer to have an effect and are aimed at increasing/restoring blood volume

47
Q

What happens during chronic compensatory mechanisms?

A

Aldosterone/adh act on nephrons to reabsorb sodium, chloride and water.

48
Q

What does ADH bind to and where?

A

V2 receptors in the distal convoluted tubules to reabsorb water

49
Q

What is an underlying abnormality with distributive shock?

A

Vasoplegia

50
Q

Define vasoplegia

A

Paralysis of blood vessels - they cannot constrict which causes low systemic vascular resistance and pooling of blood

51
Q

What is the difference between sepsis and SIRS?

A

Both involve vasodilation and poor perfusion due to widespread inflammation but SIRS happens without infection, whereas sepsis is when there is an identifiable infectious cause

52
Q

What might be seen on an ultrasound that would be highly suggestive of anaphylaxis?

A

Oedema in the wall of the gall bladder (halo sign)

53
Q

How can SIRS/sepsis lead to shock?

A

Inflammatory chemicals are released into the blood stream leading to vasodilation, decreased perfusion of organs and hypotension

54
Q

What are the early signs of distributive shock?

A

Pyrexia
Brick-red mucous membranes
Bounding pulses
Rapid CRT

55
Q

Why might patients in distributive shock initially have normal arterial blood pressure?

A

Due to the hyper-dynamic response

56
Q

What is obstructive shock sometimes categorized as?

A

Hypovolaemic shock but with a different aetiology

56
Q

Cats with sepsis are not likely to have a…

A

hyperdyanmic response

57
Q

Shock is not a…

A

primary disease

58
Q

Define compensated shock

A

Early phase of shock
Compensatory mechanisms can maintain adequate perfusion of the brain and vital organs
Likely to have normal blood pressure as cardiac output is being maintained

59
Q

Define and describe decompensated shock

A

When compensatory mechanisms are not able to manage/fix the underlying problem
Patient becomes increasingly stuprous/comatose, mm become grey/brown and increasing hypotension

60
Q

Describe irreversible shock

A

There has been too much cell damage
Can lead to SIRS, DIC, MOD and death

61
Q

What does AKI stand for?

A

Acute kidney injury

62
Q

What does ALI stand for?

A

Acute lung injury

63
Q

What does ARDS stand for?

A

Acute respiratory distress syndrome

64
Q

Many of the clinical signs of shock are due to…

A

compensatory mechanisms i.e. peripheral vasoconstriction leads mm to appear pale with prolonged CRT and hypovolaemia results in catecholamine release which causes tachycardia

65
Q

What are some clinical signs of shock

A

Impaired mentation
Tachycardia (cats may be brady or normocardic)
Tachypneoa
Pale mucous membranes
Prolonged CRT
Weak/absent peripheral pulses
Cold extremities
Decreased temperature

66
Q

Weak central pulses in a shock patient suggest…

A

Compensatory mechanisms are failing and the patient is progressing to irreversible shock

67
Q

What signs may a dog with early septic shock display that are outside of the normal clinical signs of shock?

A

Red mucous membranes due to vasoplegia and pooling of RBC in the capillaries
Rapid CRT
Normal to increased body temperature

68
Q

Why might the cranium and axillary region provide more reliable information regarding hydration status than the scruff, especially in overweight or elderly patients?

A

Subcutaneous fat provides greater lubrication than lean tissue and the amount of subcutaneous fat decreased with advancing age

69
Q

How can the nictitating membrane indicate dehydration in cats?

A

In normal hydration, retropulsion of the eye will result in the nictitating membrane immediately returning to it’s normal position. In dehydrated cats, this return will be delayed and more likely to stick to the globe and then slowly slide back

70
Q

What type of patients are more likely to have a high PCV?

A

Sighthounds

71
Q

What type of patients are more likely to have a low PCV and why?

A

Animals less than 6 months old due to larger amounts of free water present

72
Q

How can dehydration lead to hypovolaemia?

A

As cells and interstitial fluid become progressively dehydrated, fluid will be drawn from the intravascular space due to osmosis

73
Q

What are some infectious causes of sepsis?

A

Septic abdomen
Bite wounds
Pyothorax
Parvoviral enteritis
Pyometra

74
Q

What are some non-infectious causes of SIRS?

A

Trauma/burns
Pancreatitis
Surgery
Immune-mediated disease
Neoplasia

75
Q

Define inflammation

A

Increased blood supply to the area
Increased capillary permeability
Fluid exudate
Leucocyte delivery

76
Q

What is the impact of SIRS on the patient?

A

Loss of effective circulating volume (due to increased capillary permability) and vasoplegia caused by inflammatory mediators
Decreased tissue perfusion (due to loss of circulating blood volume)
Interference with cell energy production by mitochondria

77
Q

Why can SIRS lead to immunosuppression and immunoparalysis when SIRS is an inflammatory immune response?

A

The body’s compensatory anti-inflammatory response can often also be excessive. The above leads to cell death which further encourages the SIRS until leading to serious conditions such as DIC and MOD.

78
Q

What increases the chance of a patient developing SIRS?

A

The severity and duration of the inciting cause

79
Q

What is the key component of the cell wall of gram-negative bacteria?

A

Lipopolysaccharide (LPS)

80
Q

What are the most common sources of gram-negative bacteria?

A

Gastrointestinal and urogenital

81
Q

What can cause leakage of GI contents into the abdomen?

A

Secondary to ingestion of penetrating foreign body’s
Entertomoy/biopsy dehiscence
GI neoplasia
Perforated ulcers

82
Q

What does the cell wall of gram-positive bacteria contain?

A

Peptidoglycan
Lopoteichoic acid

83
Q

What are potential sources of gram-positive sepsis?

A

Wounds and intravenous catheters

84
Q

Name an example of a gram-positive bacteria

A

Streptococcus canis

85
Q

What can a streptococcus canius infection result in?

A

Toxic shock syndrome and necrotizing fasciitis

86
Q

Septic shock is an example of…

A

Distributive shock

87
Q

What type of shock will a patient remain hypotensive despite IVFT?

A

Septic shock

88
Q

How can SIRS/septic shock cause vascular dysfunction?

A
  • Vasodilation
    Leads to hypotension and decreased organ perfusion
  • Vasoplegia
    Loss of vasoconstrictor response to catecholamines/sympathomimetics
  • Increased vascular permeability
    Leads to intersitital oedema (loss of fluid and albumin into the interstitium) and decreased plasma volume and hypoalbuminaemia
89
Q

How can SIRS/septic shock cause renal dysfunction?

A
  • Prolonged hypotension may result in renal failure
  • Dogs with MOF commonly develop acute kidney injuries and azotaemia which worsen over a short timescale
90
Q

How can SIRS/septic shock cause pulmonary dysfunction?

A

ALI/ARDS
Leads to loss of pulmonary surfactent and accumulation of protein rich fluids in the lungs

91
Q

How can SIRS/septic shock cause cardiac dysfunction?

A

Septic animals may have altered/decreased cardiac contractility and are predisposed to arrhytmias

92
Q

How can SIRS/septic shock cause gastrointestinal dysfunction?

A

The body does not consider the GIT to be a vital organ and is therefore vasoconstriction and reduced perfusion

Increased epithileal permeability, secondary to GI hypoperfusion, can result in bacterial translocation into the lymphatics and blood stream

Hypoalbuminaemia can result in bowel oedema

GI signs such as vomiting, diarrhoea, haematochezia and ileus are common due to decreased perfusion

93
Q

What can be measured in dogs as a marker for systemic inflammation?

A

C-reactive proteins (CRP)

94
Q

What are C-reactive proteins?

A

Proteins released by hepatocytes in response to tissue injury

95
Q

What is a normal lactate level?

A

<2.5mmol/L

96
Q

What two levels can be monitored and indicative of sepsis?

A

Low blood glucose
Increased blood lactate

Unit 1 (6 decks)

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