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

Shock, vascular access and fluid therapy 1.2 Flashcards

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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
Describe the chronological sequence of RAAS
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
26
Where/when is ADH released during hypovolaemia and what is it's role?
Released from posterior pituitary gland when osmolarity of blood increases and volume decreases Binds to V1 receptors on peripheral arterioles = peripheral vasoconstriction
27
Define cardiogenic shock
Major failure of forward flow such that CO is insufficient to allow perfusion of the whole body
28
Briefly, how can DCM lead to cardiogenic shock?
Thin myocardial walls Insufficient contractile strength Inadequate stroke volume
29
Define distributive shock
Abnormal distribution of blood due to peripheral vasodilation Blood pools in peripheral vessels and capillaries Decreased CIRCULATING blood
30
During treatment, how may hypovolaemic and distributive shock respond differently?
Hypovolaemic = lack of circulating volume = Clinical signs improve with IVFT Distributive = Inadequate circulation, not a volume issue = no response to IVFT
31
What abnormality causes peripheral vasodilation in distributive shock?
Vasoplegia due to exaggerated inflammatory response (inflammatory mediators)
32
What is the most common cause of sepsis?
Bacteria - E.coli
33
What diagnostic is highly suggestive of anaphylaxis?
Oedema in the wall of the gall bladder (halo sign) on ultrasound
34
What are the initial clinical signs of distributive shock
Pyrexia Brick-red mucous membranes Bounding pulses Rapid CRT Due to vasoplegia, peripheral vasodilation and initial hyperdynamic response (dogs)
35
What causes distributive shock to later mimic hypovolaemic shock in its clinical signs?
Ongoing cell death Fluid loss
36
How might cats present differently with sepsis?
Not likely to have a hyperdynamic response Will present similarly to hypovolaemic, alongside icterus and abdominal pain
37
How can pericardial effusion lead to obstructive shock?
Fluid in pericardial sac = insuffcient pre-load = reduced CO (aka tamponade)
38
Give examples of clinical signs associated with decompensated shock
Increasingly stuporous/comatose Mucous membranes grey/brown Increasing hypotension Bradycardia Ventricular arrhythmias
39
List 9 clinical signs associated with shock (not including early distributive)
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
Why do skin tents occur?
Loss of interstitial fluid leads to loss of tissue pliability and lubrication
40
Why might retropulsion of the eye be used to assess feline dehydration and what would the findings be?
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
Which area of a patient is the best to assess skin tenting and why?
Subcutaneous fat provides greater lubrication than lean tissue Cranium and axillary region
41
Why can PCV allow for assess of dehydration?
PCV & TP increased due to overall loss of free water leading to haemoconcentration
42
Why do sighthounds usually have a higher PCV?
Large muscle mass Low body fat
43
Why do young animals (<6 months) have a lower PCV?
Larger amount of free water present
44
How can severe dehydration lead to hypovolaemia?
As cells and interstitial spaces become progressively dehydrated, fluid is drawn from the intravascular space due to osmosis
45
Briefly explain the pathogenesis of SIRS
Excessive response to inciting insult Normal response causes localised pro-inflammatory response If insult severe enough, systemic pro-inflammatory response develops
46
Describe what happens during inflammation
Increased blood supply to the area (vasodilation) increased capillary permability Fluid exudate Leucocyte delivery
47
Aside from an excessive inflammatory response, what else is excessive during SIRS? and what does this cause?
Anti-inflammatory response Immunosuppression Immunoparalysis
48
What factors affect the likelihood of SIRS developing?
The severity and duration of the insult
49
What is LPS and what is it's role in distributive shock?
Lipopolysaccharide Key component of cell wall of gram-negative bacteria Potent initiator of septic inflammatory cascade
50
What are common sources of gram-negative bacteria in sepsis? Give examples of how these may occur
GI and urogenital GI leakage into abdomen i.e. penetrating FB, GI neoplasia, perforated ulcers
51
What components of the cell wall of gram-positive bacteria can activate the inflammatory cascade? and explain potential sources
peptidoglycan lipoteichoic acid Wounds and IV catheters
52
Give two examples that a Streptococcus Canis infection can cause?
Toxic shock syndrome Necrotizing fasciitis
53
How can vasodilation lead to MODS?
Hypotension and decreased organ perfusion
54
Define vasoplegia
Loss of vasoconstrictor response to catecholamines
55
Describe how increased vascular permeability can lead to MODS/MOF
Leads to interstitial oedema and decreased plasma volume and hypoalbuminaemia
56
What other disease process is commonly associated with SIRS?
DIC
57
Describe covert DIC
Inflammation leads to activation of haemostatic mechanisms inducing a prothombotic state - hypercoagulable
58
What issue does covert DIC pose?
Micro-thombi in organs - widespread clot formation, organ ischaemia due to flow being reduced
59
Describe over DIC
Consumption of coagulation factors and platelets - hypocoagulable state, leads to bleeding tendencies
60
Explain why SIRS can lead to renal dysfunction
Prolonged hypotension
61
Which pulmonary dysfunctions are associated with SIRS and why do they happen?
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
Which large organ system is not considered vital during shock and what impact does this have?
GIT - Vasoconstriction = reduced perfusion
63
List GIT complications associated with SIRS and what clinical signs may be seen
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
List clinical signs associated with SIRS
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
Define C-reactive proteins (CRP)
Released by hepatocytes in response to tissue injury Measured in dogs as marker for systemic inflammation Can be used to identify improvement/deterioration
66
Describe the role of lactate measurements in shock patients
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
Why are septic patients often hypoglycaemic?
Increased glucose utilisation
68
What are two parameters to measure which would be highly indicative of sepsis?
Low BG Increased lactate
69
Why might patients with SIRS become hypoalbuminaemic?
Associated vasculitis leads to protein loss from vasculature
70
What may be seen regarding the leukocytes in a septic patient?
Leucocytosis or leucopaenia
71
What unique change may a septic cat show on bloods?
Hyperbilirubinaemia - Alongside clinically icteric
72
Describe/list monitoring requirements for a SIRS patient
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
Describe/list nursing care requirements for a SIRS patient
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
Describe/list nursing care requirements for recumbent patients
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
Name three things an IV catheter can be placed/used for
Infusion of fluids (inc blood products) Sampling Medication administration
76
List reasons a central venous catheter may be placed
>5 days IVFT administration Hypertonic medications/fluids Multiple necessary medications Serial sampling total parenteral nutrition Measuring CVP
77
List unique properties of catheters that make them safe for use
Most made of silicone/polyurethane Inert so less likely to stimulate inflammatory reaction/clot formation Flexibility useful for IV/central lines Radiopaque
78
What type of catheter is best suited for large volume of fluids for a hypovolaemic patient
Short length Wide gauge
79
List different types of IV catheters
Over-the-needle Through-the-needle Butterfly/winged Peel-away Over-the-wire/guide wire
80
What is the most commonly type of catheter used?
Over the needle
81
What type of catheters are often used for central lines and what makes them different?
Through the needle Longer and wider bore Multi-lumen option - bloods/meds/fluids
82
What is the main vein which central catheters are placed and what other alternative placements are there?
Jugular - Main Medial saphenous - cats Lateral/medial saphenous - dogs Known as PICC line - peripherally inserted central catheter
83
How often should syringe drivers and infusion pumps be serviced and calibrated?
Yearly
84

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