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ECC > Shock, vascular access and fluid therapy 1.2 > Flashcards

Shock, vascular access and fluid therapy 1.2 Flashcards

1
Q

Define respiratory acidosis

A

The result of hypoventilation and accumulation of CO2

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2
Q

Define stroke volume

A

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

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3
Q

Define systolic blood pressure

A

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

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4
Q

Define diastolic blood pressure

A

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

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5
Q

Provide multiple definitions of shock

A
  1. Where oxygen delivery to cells/tissues is insufficient for demand
  2. Inadequate cellular energy production or decreased cellular oxygen utilisation related to decreased blood flow that leads to cell death and organ failure
  3. Failure of circulatory system to maintain effective circulation, resulting in decreased oxygen delivery to cells
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6
Q

Define bacteraemia

A

The presence of viable bacteria in the blood

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7
Q

Define septic shock

A

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

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8
Q

Define multiple organ dysfunction syndrome (MODS)

A

Dysfunction of the endothelial, cardiopulmonary, renal, nervous, endocrine and gastrointestinal systems associated with the progression of systemic inflammation

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9
Q

Define crystalloids

A

Solutions of electrolytes and/or glucose in water

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10
Q

Define colloids

A

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

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11
Q

Why is anaerobic metabolism considered a temporary fix during low oxygen delivery?

A

Results in lactate accumulation and metabolic acidosis

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12
Q

How can a reduced DO2 lead to death?

A

Forced to utilise anaerobic metabolism
Insufficient energy produced = cells unable to function normally
Abnormal cell function = cell death = Organ dysfunction = organ failure = death

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13
Q

What are potential causes of hypovolaemic shock?

A

Haemorrhage
GI losses

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14
Q

What are potential causes of distributive/septic shock?

A

Septic peritonitis
Pyometra
Pyothorax

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15
Q

What are potential causes of obstructive shock?

A

Pericardial effusion (could also be considered cardiogenic)
GDV
Pulmonary thromboembolism

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16
Q

What are potential causes of cardiogenic shock?

A

End stage cardiomyopathy
Severe arrhythmias

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17
Q

What impacts blood pressure?

A

Cardiac output
Total peripheral resistance
Blood viscosity

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18
Q

In sequence, describe how haemorrhage impacts stroke volume

A

Haemorrhage -> decreased blood volume -> decreased venous return/cardiac preload to right atrium -> decreased volume from left ventricle (stroke volume)

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19
Q

Neuroendocrine compensatory mechanisms are mediated by what?

A

HPA axis - Sympatho-adrenal response

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20
Q

What are the aims of compensatory mechanisms during shock?

A

Increase cardiac output and blood vessel tone to increase cell perfusion

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21
Q

Describe/define acute compensatory mechanisms for shock

A

Immediate onset
Focus on increasing venous return and blood supply to myocardium -> allows to function effectively under increased demands
Triggered by sympathetic nervous system
If reliance if prolonged, mechanisms fail = decompensated shock

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22
Q

Explain how decrease blood volume leads to acute compensatory mechanisms being activated and what are these?

A

Decreased blood volume = decreased baroreceptor impulses
Stimulates SNS = increased activity
Catecholamine release
Peripheral vasoconstriction
tachycardia
Increased cardiac contractility

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23
Q

Explain how hypoxaemia leads to acute compensatory mechanisms being activated and what are these?

A

Hypoxaemia detected by chemoreceptors -> aorta and carotid artery
Increase in SNS activity and catecholamine release
Also cortisol release
Cortisol provides immediate glucose source

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24
Q

What are the vital roles of cortisol, including during shock?

A

Normal maintenance of vascular tone and endothelial integrity
Regulation of fluid within extravascular compartments
Potentiates impact of catecholamines on vasoconstriction

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25
Q

Describe the chronological sequence of RAAS

A

Decreased real perfusion stimulates baroreceptors in kidney
Stimalates RENIN release
RENIN converts Angiotensinogen to Angiotension I and II
Immediate response of angiotensin II = peripheral vasoconstruction & reabsorption of some salts and water
Delayed response of angiotensin II - Aldosterone release from adrenal cortex = increase sodium, chloride and water reabsorption from distal convoluted tubules in the kidney (v2 receptors) = increased blood volume

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26
Q

Where/when is ADH released during hypovolaemia and what is it’s role?

A

Released from posterior pituitary gland when osmolarity of blood increases and volume decreases
Binds to V1 receptors on peripheral arterioles = peripheral vasoconstriction

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27
Q

Define cardiogenic shock

A

Major failure of forward flow such that CO is insufficient to allow perfusion of the whole body

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28
Q

Briefly, how can DCM lead to cardiogenic shock?

A

Thin myocardial walls
Insufficient contractile strength
Inadequate stroke volume

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29
Q

Define distributive shock

A

Abnormal distribution of blood due to peripheral vasodilation
Blood pools in peripheral vessels and capillaries
Decreased CIRCULATING blood

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30
Q

During treatment, how may hypovolaemic and distributive shock respond differently?

A

Hypovolaemic = lack of circulating volume = Clinical signs improve with IVFT
Distributive = Inadequate circulation, not a volume issue = no response to IVFT

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31
Q

What abnormality causes peripheral vasodilation in distributive shock?

A

Vasoplegia due to exaggerated inflammatory response (inflammatory mediators)

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32
Q

What is the most common cause of sepsis?

A

Bacteria - E.coli

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33
Q

What diagnostic is highly suggestive of anaphylaxis?

A

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

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34
Q

What are the initial clinical signs of distributive shock

A

Pyrexia
Brick-red mucous membranes
Bounding pulses
Rapid CRT
Due to vasoplegia, peripheral vasodilation and initial hyperdynamic response (dogs)

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35
Q

What causes distributive shock to later mimic hypovolaemic shock in its clinical signs?

A

Ongoing cell death
Fluid loss

36
Q

How might cats present differently with sepsis?

A

Not likely to have a hyperdynamic response
Will present similarly to hypovolaemic, alongside icterus and abdominal pain

37
Q

How can pericardial effusion lead to obstructive shock?

A

Fluid in pericardial sac = insuffcient pre-load = reduced CO (aka tamponade)

38
Q

Give examples of clinical signs associated with decompensated shock

A

Increasingly stuporous/comatose
Mucous membranes grey/brown
Increasing hypotension
Bradycardia
Ventricular arrhythmias

39
Q

List 9 clinical signs associated with shock (not including early distributive)

A

Impaired mentation - decreased oxygen delivery to neurons
Tachycardia (cats may have normal HR or be bradycardic)
Tachypnoea
Pale MM
Prolonged CRT
Weak/absent peripheral pulses
Cold extremities
Decreased peripheral temperature
Decreased rectal/core temperature

40
Q

Why do skin tents occur?

A

Loss of interstitial fluid leads to loss of tissue pliability and lubrication

40
Q

Why might retropulsion of the eye be used to assess feline dehydration and what would the findings be?

A

In normal hydration, nicitating membrane should immediately reduce to normal position following retropulsion
When dehydrated, nicitating membrane more likely to stick to the globe and slowly slide back

40
Q

Which area of a patient is the best to assess skin tenting and why?

A

Subcutaneous fat provides greater lubrication than lean tissue
Cranium and axillary region

41
Q

Why can PCV allow for assess of dehydration?

A

PCV & TP increased due to overall loss of free water leading to haemoconcentration

42
Q

Why do sighthounds usually have a higher PCV?

A

Large muscle mass
Low body fat

43
Q

Why do young animals (<6 months) have a lower PCV?

A

Larger amount of free water present

44
Q

How can severe dehydration lead to hypovolaemia?

A

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

45
Q

Briefly explain the pathogenesis of SIRS

A

Excessive response to inciting insult
Normal response causes localised pro-inflammatory response
If insult severe enough, systemic pro-inflammatory response develops

46
Q

Describe what happens during inflammation

A

Increased blood supply to the area (vasodilation)
increased capillary permability
Fluid exudate
Leucocyte delivery

47
Q

Aside from an excessive inflammatory response, what else is excessive during SIRS? and what does this cause?

A

Anti-inflammatory response
Immunosuppression
Immunoparalysis

48
Q

What factors affect the likelihood of SIRS developing?

A

The severity and duration of the insult

49
Q

What is LPS and what is it’s role in distributive shock?

A

Lipopolysaccharide
Key component of cell wall of gram-negative bacteria
Potent initiator of septic inflammatory cascade

50
Q

What are common sources of gram-negative bacteria in sepsis? Give examples of how these may occur

A

GI and urogenital
GI leakage into abdomen i.e. penetrating FB, GI neoplasia, perforated ulcers

51
Q

What components of the cell wall of gram-positive bacteria can activate the inflammatory cascade? and explain potential sources

A

peptidoglycan
lipoteichoic acid
Wounds and IV catheters

52
Q

Give two examples that a Streptococcus Canis infection can cause?

A

Toxic shock syndrome
Necrotizing fasciitis

53
Q

How can vasodilation lead to MODS?

A

Hypotension and decreased organ perfusion

54
Q

Define vasoplegia

A

Loss of vasoconstrictor response to catecholamines

55
Q

Describe how increased vascular permeability can lead to MODS/MOF

A

Leads to interstitial oedema and decreased plasma volume and hypoalbuminaemia

56
Q

What other disease process is commonly associated with SIRS?

A

DIC

57
Q

Describe covert DIC

A

Inflammation leads to activation of haemostatic mechanisms inducing a prothombotic state - hypercoagulable

58
Q

What issue does covert DIC pose?

A

Micro-thombi in organs - widespread clot formation, organ ischaemia due to flow being reduced

59
Q

Describe over DIC

A

Consumption of coagulation factors and platelets - hypocoagulable state, leads to bleeding tendencies

60
Q

Explain why SIRS can lead to renal dysfunction

A

Prolonged hypotension

61
Q

Which pulmonary dysfunctions are associated with SIRS and why do they happen?

A

Acute lung injury (ALI)
Acute Respiratory Distress Syndrome
Secdonary to systemic inflammation leads to loss of normal pulmonary surfactant and accumulation of protein-rich fluids in the lungs

62
Q

Which large organ system is not considered vital during shock and what impact does this have?

A

GIT - Vasoconstriction = reduced perfusion

63
Q

List GIT complications associated with SIRS and what clinical signs may be seen

A

Hypotension, micro thombi and deregulation of rregional blood flow impact GI perfusion

Increased epithelial permeability, due to hypoperfusion, can result in bacterial translocation into the lymphatics and blood stream

Bowel oedema due to hypoalbuminaemia

Vomiting, diarrhoea, haematochezia and ileus

64
Q

List clinical signs associated with SIRS

A

Depression
Fever (dogs) Hypothermia (cats and late stage dogs)
Red mm/Rapid CRT
Bounding pulses (dogs only)
Tachycardia (dogs) Bradycardia (cats)
Tachypnoea
V/D

65
Q

Define C-reactive proteins (CRP)

A

Released by hepatocytes in response to tissue injury
Measured in dogs as marker for systemic inflammation
Can be used to identify improvement/deterioration

66
Q

Describe the role of lactate measurements in shock patients

A

Expected increased lactate due to anaerobic metabolism (normal <2.5mmol/L)
Best to use as a trend rather than evaluating one-off value which is snapshot of that moment

67
Q

Why are septic patients often hypoglycaemic?

A

Increased glucose utilisation

68
Q

What are two parameters to measure which would be highly indicative of sepsis?

A

Low BG
Increased lactate

69
Q

Why might patients with SIRS become hypoalbuminaemic?

A

Associated vasculitis leads to protein loss from vasculature

70
Q

What may be seen regarding the leukocytes in a septic patient?

A

Leucocytosis or leucopaenia

71
Q

What unique change may a septic cat show on bloods?

A

Hyperbilirubinaemia - Alongside clinically icteric

72
Q

Describe/list monitoring requirements for a SIRS patient

A

Frequent assessment of perfusion parameters
Frequent assessment for complications i.e. petechiation, prolonged bleeding
Serial BP reading
Monitoring delivery/response to IVFT
Collecting samples for BG, electrolytes, PCV, WBC, platelets, lactate, clotting times, urinalysis
Monitor ECG for arrhythmias
Monitoring urine output - ongoing oliguria/anuria is significant
Pain scoring/monitoring - monitor response/need for analgesia
Pulse oximetry

73
Q

Describe/list nursing care requirements for a SIRS patient

A

Maintain vascular access/delivery of IVFT
Pain assessment, administer analgesia, decreased stress/pain
Deliver medication
Nutritional management - feeding tubes
Oxygen provisions - ensure correct, not distressing

74
Q

Describe/list nursing care requirements for recumbent patients

A

Bladder/urinary cath care
Regular turning (q2-4h) to prevent decutis ulcers
Prevention of aspiration pneumonia
oral/ocular care
Prevent of soiling - management of rectal foley systems
PROM/massage/coupage/physio

75
Q

Name three things an IV catheter can be placed/used for

A

Infusion of fluids (inc blood products)
Sampling
Medication administration

76
Q

List reasons a central venous catheter may be placed

A

> 5 days IVFT administration
Hypertonic medications/fluids
Multiple necessary medications
Serial sampling
total parenteral nutrition
Measuring CVP

77
Q

List unique properties of catheters that make them safe for use

A

Most made of silicone/polyurethane
Inert so less likely to stimulate inflammatory reaction/clot formation
Flexibility useful for IV/central lines
Radiopaque

78
Q

What type of catheter is best suited for large volume of fluids for a hypovolaemic patient

A

Short length
Wide gauge

79
Q

List different types of IV catheters

A

Over-the-needle
Through-the-needle
Butterfly/winged
Peel-away
Over-the-wire/guide wire

80
Q

What is the most commonly type of catheter used?

A

Over the needle

81
Q

What type of catheters are often used for central lines and what makes them different?

A

Through the needle

Longer and wider bore
Multi-lumen option - bloods/meds/fluids

82
Q

What is the main vein which central catheters are placed and what other alternative placements are there?

A

Jugular - Main

Medial saphenous - cats
Lateral/medial saphenous - dogs
Known as PICC line - peripherally inserted central catheter

83
Q

How often should syringe drivers and infusion pumps be serviced and calibrated?

A

Yearly

84
Q
A

ECC (3 decks)

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