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ECC Flashcards

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1
Q

what does CPCR stand for?

A

cardiopulmonary cerebral rescusitation

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2
Q

what is the aim of CPR?

A

perfusion of the heart, lungs and brain
ROSC

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3
Q

why is it essential that the heart, lungs and brain are perfused?

A

require the most oxygen and glucose

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4
Q

what is respiratory arrest?

A

apnoea

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5
Q

what is caused by apnoea?

A

hypoxia
hypercapnia

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6
Q

what can respiratory arrest lead to?

A

cardiac arrest

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7
Q

what happens in the heart during cardiac arrest?

A

the patient has no cardiac output

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8
Q

will patients in cardia arrest be breathing?

A

no

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9
Q

what patients are at high risk of arrest?

A

trauma
systemically unwell
paediatric
geriatrics
iatrogenic causes like anaesthetic overdose
recently arrested

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10
Q

when should CPR start?

A

as soon as we think a patient has arrested

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11
Q

how long should you check for a heartbeat if a patient is not breathing?

A

no more than 2 seconds

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12
Q

what will respiratory arrest rapidly lead to?

A

cardiac arrest

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13
Q

who can help with CPR?

A

anyone
no schedule 3 procedures
ideally people with CPR training

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14
Q

how can we best prepare for CPR?

A

regular training
have crash kit/box/trolley
crash alarm (or call for help)

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15
Q

what is involved in BLS?

A

CPR cycle
oxygen therapy (including intubation)

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16
Q

what is involved in ALS?

A

drug therapy
fluid therapy
cardioversion

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17
Q

are BLS and ALS schedule 3 procedures?

A

BLS is not but ALS is and needs vet direction

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18
Q

what position should patients be in ideally for CPR?

A

right lateral recumbancy

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19
Q

where should the compressor be located in relation to the patient?

A

dorsal side

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20
Q

what is the correct rate of cardiac compressions?

A

100-120 compressions per minute

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21
Q

how deep should cardiac compressions be?

A

50% to 2/3 the width/depth of the thorax

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22
Q

what should be felt for every cardiac compression?

A

femoral pulse

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23
Q

what should be allowed for between each compression?

A

full elastic recoil of the chest

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24
Q

what animals are cardiac pump compressions used on?

A

cats
small dogs
keel chest dogs

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25
Q

what animals are thoracic pump compressions used on?

A

medium to large breed dogs

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26
Q

if one cardiac compression technique isn’t producing output what can be done?

A

change compression technique

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27
Q

what happens during cardiac pump compressions?

A

compression of the thorax directly over the heart

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28
Q

in what patient position are thoracic pump compressions performed?

A

lateral
dorsal

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29
Q

how are lateral thoracic pump compressions performed?

A

over the widest part of the thorax

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30
Q

how are dorsal thoracic pump compressions performed?

A

either over the caudal thorax or the xiphisternum

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31
Q

can nurses perform direct internal cardiac compressions?

A

yes but they cannot open the chest

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32
Q

in what animals may direct internal cardiac compressions be performed?

A

large breed dogs

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33
Q

when may direct internal cardiac compressions be performed?

A

if thoracotomy or laparotomy already being performed
if external compressions have not been effective

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34
Q

what rate should IPPV be given during CPR?

A

10-12 breaths per minute

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35
Q

how often should breaths be given during CPR?

A

every 6 seconds

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36
Q

when should ventilation start?

A

as soon as respiratory arrest suspected

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37
Q

how much should the chest be inflated by during CPR?

A

‘normal amout”
guided by CO2 levels

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38
Q

what should patients be ventilated with?

A

ambubag on 100% O2
room air if no O2

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39
Q

what should be done if anything in the crash trolley is changed?

A

explain changes in training sessions

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40
Q

when should the crash trolley be checked and restocked?

A

checked monthly
restocked ASAP after every crash

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41
Q

what equipment is needed for airway access?

A

ET tubes (cuffed, whole sizes)
laryngoscope
ET tube tie
cuff puff
guide wire
plain swabs
intubeaze
u cath

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42
Q

what equipment is needed for IV access?

A

various size IV catheters
IV/IO connectors - primed
tape
scissors
cut down kit
no 11 scalpel blade

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43
Q

what equipment is needed for ventilation?

A

paediatric ambubag with capnograph connector and flow regulator
adult ambubag with capnograph connector and flow regulator
in line capnograph

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44
Q

what is the benefit of an inline capnograph?

A

doesn’t need to calibrate
instant reading

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45
Q

what are the main first line drugs in a crash trolley?

A

low dose adrenaline (0.1mg/ml)
high dose adrenaline (1mg/ml)
atropine
saline (pre drawn)
pre prepared needles and syringes
ECG pads

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46
Q

why is an ECG necessary for CPR?

A

ECG will dictate drugs and whether defibrillation used

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47
Q

what is the mg/ml of high dose adrenaline?

A

1mg/ml

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48
Q

what is the mg/ml of low dose adrenaline?

A

0.1 mg/ml

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49
Q

when is adrenaline given during CPR?

A

asystole

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50
Q

what environment is adrenaline less effective in?

A

acidic

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51
Q

why is it significant that adrenaline is less effective in acidic environments?

A

acidic environment seen in CPA

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52
Q

what does adrenaline do?

A

positive inotrope
positive chronotrope
potent vasopressor
profound vasoconstriction
increase SVR
increase MAP

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53
Q

what does a positive inotrope do?

A

increase cardiac contractility

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54
Q

what does a positive chronotrope do?

A

increase heart rate

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55
Q

what is the benefit of a vasopressor in CPA?

A

vessels have no tone so no SVR

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56
Q

when is low dose adrenaline given?

A

initial dose unless anaphylaxis

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57
Q

when is high dose adrenaline given?

A

second line if low dose non effective
anaphylaxis

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58
Q

how can adrenaline be administered?

A

IV
IO
intratracheal

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59
Q

how should adrenaline not be administered?

A

intra-cardiac

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60
Q

how should drugs be dosed intra-tracheally?

A

double dose
fill syringe with 100% more air

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61
Q

when is atropine given?

A

profound brady cardia
peri-arrest
PEA

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62
Q

what is the role of atropine?

A

positive chronotrope

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63
Q

how should atropine be given?

A

IV (ideally central line)
IO
intra-tracheal

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64
Q

via what route should atropine not be administered?

A

intra-cardiac

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65
Q

how often can atropine be given?

A

only once

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66
Q

what other drug types may be in the crash trolley?

A

antagonists
propofol
glucose

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67
Q

what can be used to antagonise opioids?

A

naloxone

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68
Q

what can be used to antagonise benzodiazepines?

A

flumazenil

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69
Q

what can be used to antagonise dexmedetomidine?

A

atipamezole

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70
Q

what is the role of amiodarone?

A

antidysrhythmic through Na channel blocking

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71
Q

when is amiodarone used?

A

second line for prolonged VT or VF
if unable to cardiovert

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72
Q

how should amiodarone be given?

A

IV (ideally central)
IO

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73
Q

how should amiodarone not be given?

A

intra-cardiac

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74
Q

what is a risk when giving amiodarone?

A

anaphylaxis

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75
Q

what bolus dose of dextrose can be given if patient is tanking?

A

0.5 ml/kg of 50% dextrose

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76
Q

what is a risk when giving neat dextrose?

A

phlebitis

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77
Q

what is propofol?

A

phenol as lipid IV anaesthetic agent

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78
Q

when is propofol given?

A

respiratory distress that may lead to arrest if airway not controlled

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79
Q

how can propofol be given?

A

IV
IO
(not intra cardiac)

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80
Q

what equipment is needed for thoracotomy during CPR?

A

long sleeved surgical gown
gloves (6.5 and 7.5)
drape (150x180cm)
small and large chloraprep
thoracoctomy kit
no 11 blade
small radioopaque swabs
lap swabs
small and large finochietto retractors
internal defibrillator paddles
100ml 0.9% NaCl

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81
Q

what additional equipment is necessary for CPR?

A

capnography
suction
crash chart
ECG
defib and gel
IO drill

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82
Q

what monitoring equipment is less crucial during CPR?

A

pulse ox
NIBP
invasive BP

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83
Q

what is capnography a representation of?

A

ventilation

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84
Q

why is capnography important for CPR?

A

show perfusion and gas exchange which then indicates if metabolism is occurring

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85
Q

what EtCO2 indicates that compressions are adequate?

A

12 mmHg

86
Q

what EtCo2 indicates ROSC?

A

> 24 mmHg

87
Q

what is the benefit of having suction during a crash?

A

removal of airway secretions
improve visualisation of the larynx
reduce risk of aspiration

88
Q

what is the purpose of a crash chart?

A

clear record of what happened
timings and drugs
used for clinical governance

89
Q

if a crash record cannot be completed at the time what should be done?

A

asap afterwards
its not always possible to record at the time

90
Q

what is ECG used for?

A

shows if there is electrical impulse or conduction in the heart
shows whether cardioversion or drugs are necessary

91
Q

does ECG show perfusion?

A

no

92
Q

is defibrillation a schedule 3 procedure?

A

no - anyone can perform

93
Q

when is defibrillation used?

A

non-perfusing rhythms
VF
pulseless ventricular tachycardia

94
Q

what method other than defibrillation can be used for VF?

A

precordial thump

95
Q

what is VF?

A

disorganised and random depolarisation all over the heart

96
Q

what is VT in CPA?

A

Hr >180 with ventricular complexes

97
Q

how much should the voltage be increased by each round of defibrillation?

A

50% each time

98
Q

who is responsible for ensuring staff safety during defibrillation?

A

user

99
Q

when should defibrillation not be used?

A

if the patient is very wet
if lots of spirit used

100
Q

what is the go to for drug access?

A

IO

101
Q

would IVFT be used during a crash?

A

unlikely - makes CO harder to acchieve

102
Q

what must you be aware of following a crash?

A

patient may rearrest

103
Q

what is involved in a CPR debrief?

A

what happened (facts)
what went well
what went less well
suggested improvements
no blame culture
be kind

104
Q

what is type 1 decision making?

A

These are irreversible decisions that cannot be changed once executed. Therefore, they require careful thought

105
Q

what are type 2 decisions?

A

These are reversible decisions. Even after executing them, you can change them if you like. Therefore, you must act on such decisions quickly

106
Q

what is a risk with seizures?

A

hyperthermia

107
Q

what is ARDS?

A

distributive shock within the lungs

108
Q

what is involved in tracheostomy management?

A

minimal handling
keep clean
no water in kennel
nebulisation - 20mins QID
change SID or if causing an issue

109
Q

what is the benefit of high flow oxygen?

A

comfort for patient as warmed / humidified
lung recruitment increased due to high pressure
less aggressive than ventilation

110
Q

what is CPAP?

A

provision of positive pressure (PEEP) to airway while patient breathes to keep airway open (prevents collapse)

111
Q

what areas of the body can be used for IO access?

A

greater tubercle of the humerus
trochanteric fossa
flat medial surface of te proximal tibia
tibial tuberosity
wing of ilium

112
Q

what are the preferred IO access points?

A

greater tubercle of the humerus
flat medial surface of the proximal tibia
wing of ilium

113
Q

via what route should glucose be given?

A

IV ideally central catheter

114
Q

how can a 5% dextrose solution be made up?

A

0.5ml neat 50% dextrose to 9.5ml 0.9NaCl
gives 10ml of 5% solution

115
Q

what is the rescue dose of dextrose?

A

0.5ml/kg of 5% dextrose

116
Q

how is invasive blood pressure measured?

A

through arterial catheter and transducer to a monitor

117
Q

how is central venous pressure measured?

A

via central line

118
Q

what patients is CVP used in?

A

those at risk of volume overload

119
Q

what lactate level is considered normal?

A

<2.4 mmols

120
Q

what needs to be carried out before a blood transfusion?

A

cross matching

121
Q

what is pH a measure of?

A

hydrogen ions present

122
Q

what is base excess?

A

H ions needed to return the pH back to normal

123
Q

what is the anion gap?

A

unmeasured ions in the blood (e.g. ketones, uric acid) that may be contributing to acidaemia

124
Q

when is an elevated anion gap seen?

A

end stage renal failure

125
Q

what is normal pH?

A

7.35-7.45

126
Q

what is normal PaO2?

A

80-100 mmHg

127
Q

what is normal PaCO2?

A

35-45 mmHg

128
Q

what is normal bicarbonate?

A

21-24

129
Q

what is normal base excess?

A

+2 - -2 mEq

130
Q

what is the normal anion gap in cats?

A

12-24 mEq/L

131
Q

what is the normal anion gap in cats?

A

13-27 mEq/L

132
Q

what is the effect of respiratory acidosis on RR?

A

hyperventilation to blow off CO2

133
Q

what is the effect of respiratory alkalalosis on RR?

A

hypoventilation to retain CO2

134
Q

what are the effects of compensatory mechanisms in metabolic acidosis?

A

pH WNL
HCO3 very low
PaCO2 low

135
Q

what are the effects of compensatory mechanisms in metabolic alkalosis?

A

pH WNL
HCO3 very high
PaCO2 high

136
Q

what effect can lactate have on acid base?

A

cause metabolic acidosis

137
Q

what can cause metabolic acidosis?

A

diarrhoea
DKA
renal failure
Addisons
lactic acidosis (sepsis)

138
Q

what can cause metabolic alkalosis?

A

vomiting (loss of H+)
hypoalbuminaemia
upper GI obstruction

139
Q

why does albumin affect acid base?

A

weak acid

140
Q

what is Kirbys rule of 20?

A

lists critical parameters to be checked in critical care patients

141
Q

what determines stroke volume?

A

preload
afterload
contractility

142
Q

what drugs may be used to increase BP?

A

vasopressors
inotropes

143
Q

what determines cardiac output?

A

HR
SV

144
Q

what are the sections within Kirbys rule of 20?

A

fluid balance
oncotic pull (albumin)
glucose
acid base and electrolytes
oxygenation and ventilation
demenour/mentation
BP
HR and rhythm
temp
coagulation
RBC and Hb
renal function
immune status
GI motility
drug metabolism
nutrition
Pain
mobilisation
wounds
TLC

145
Q

what reflex may be stimulated in head trauma patients?

A

cuchings (hypertension, reflex bradycardia)

146
Q

what electrolyte derangement may be seen with head trauma?

A

hyperglycaemia (mechanism unknown)

147
Q

what basic function may be affected by head trauma?

A

ventilation

148
Q

why is ventilation affected by head trauma?

A

altered drive

149
Q

why is it important to elevate raised ICP patients 30 degrees?

A

reduce CSF flow in brain
regurge risk

150
Q

will mannitol be given to all head trauma patients?

A

potential to worsen haemorrhage
hypertonic saline instead

151
Q

what assisted feeding tube could be used for head trauma patients?

A

O or PEG
NO is contraindicated due to ICP risk

152
Q

what may be given to manage hyperfibrinolysis?

A

TXA

153
Q

why may TXA be contraindicated in head trauma patients?

A

induces emesis - raising ICP
(dilute and give slow)

154
Q

how can oral care reduce aspiration pneumonia risk?

A

removal of bacteria / saliva and secretions which can reduce incidence and severity of AP

155
Q

what are the main considerations for patients on high flow O2?

A

lots of ongoign losses even though air is warmed and humidified
eye care crucial

156
Q

what effect can reduction of pyrexia have on AP?

A

may make AP worse

157
Q

why may TPN be needed in AP cases?

A

to prevent further regurge and allow lungs to rest

158
Q

what is a preferable option to ventilation?

A

HFO2

159
Q

what is needed before moving tetanus patients?

A

propofol / muscle relaxant bolus to facilitate movement

160
Q

what is involved in the nursing care of the ventilator patient?

A

eye care
oral care
airway management (suction)
humidifcation
cleaning of tubes and lines
physio
positioning
U+/F+ managed
drugs needed
treat underlying disease
communication with team and owners
records
acid base/BG/electrolytes

161
Q

what is the intervention value for GCPS?

A

6/24
5/20

162
Q

what drop in MGCS should clinicians be notified about?

A

2 or more

163
Q

what is most body heat produced by?

A

muscular activity (seizures / exercise)

164
Q

where are thermoreceptors located?

A

peripherally
centrally

165
Q

where is the thermoregulation centre located in the body?

A

anterior hypothalamus

166
Q

what is indicated by thermoreceptors?

A

when temperature is above or below the set point

167
Q

what does temperature above the set point trigger?

A

heat dissipation

168
Q

what does temperature below the set point trigger?

A

heat conservation and production

169
Q

define hyperthermia

A

increased body temperature (>39.2)

170
Q

what are the causes of hyperthermia?

A

pyrexia
increased heat production due to increased muscular activity (seizures/exercise)
heat stroke

171
Q

what are the 2 types of heat stroke?

A

classic
exertional

172
Q

what is classic heat stroke caused by?

A

reduced heat loss

173
Q

what is exertional heat stroke caused by?

A

overheating due to exercise in high temperatures

174
Q

what is heat stroke caused by?

A

failure of heat dissipation

175
Q

what factors may cause failure of heat dissipation?

A

Upper respiratory obstruction
Increased environmental temperature/humidity
Poor environmental ventilation
Circulatory compromise
Obesity
Breed predisposition

176
Q

at what temperature is the patient at risk of permanent organ damage or failure?

A

> 41.6

177
Q

why are organs at risk at temperatures >41.6?

A

cell death and increased oxygen demand leads to DIC

178
Q

what are the main clinical signs of heat stroke?

A

Stress
Hyperthermia
Tachycardia
Hypovolaemia
Hyperdynamic pulses
Peripheral vasodilation
Collapse
Hyperaemic MM (bright red) with rapid CRT

179
Q

what temperature may patients be if heat stroke is advanced?

A

normothermic

180
Q

why may patients with advanced heat stroke be normothermic?

A

due to impaired peripheral perfusion leading to colder extremities but hyperthermic core

181
Q

what may be seen in advanced heat stroke?

A

Hypovolaemia
GI losses
Vasodilation
Increased intestinal mucosal permeability and impaired GI perfusion
Tachypnoea
Secondary respiratory complications

182
Q

what can cause hypovolaemia in heatstroke patients?

A

GI losses
vasodilation and so relative hypovolaemia due to systemic compromise

183
Q

what can increased GI mucosal permeability ad reduced perfusion lead to?

A

endotoxin translocation = sepsis

184
Q

what may patients with severe GI compromise require?

A

mucosal protectants (omeprazole)
IV antibiotics

185
Q

what secondary respiratory complications may be seen with heatstroke?

A

AP
pulmonary oedema
pulmonary haemorrhage (DIC)
obstruction risk

186
Q

why do secondary respiratory complications occur?

A

panting
DIC

187
Q

what are secondary complications of heat stroke?

A

impaired renal perfusion leading to AKI
CNS compromise
coagulopathies - DIC

188
Q

why is impaired renal perfusion seen?

A

distributive shock
vasodilation to loose heat
hypovolaemia due to losses

189
Q

how can heatstroke lead to CNS compromise?

A

direct thermal damage
secondary effects e.g. hypoglycaemia

190
Q

what are the signs seen on blood work that indicate heatstroke?

A

Hypoglycaemia
Hyperbilirubinemia
Epithelial desquamation
Thrombosis
Myopathy
Electrolyte derangements

191
Q

where is most heat lost when body temperature increases?

A

body surface
then panting

192
Q

what does heat loss through the body surface lead to?

A

increase in peripheral circulation through vasodilation and so increase in cardiac output
results in overall decreased perfusion

193
Q

at what temperature should patients be actively cooled?

A

> 41 degrees C

194
Q

when should active cooling end?

A

39.4 degrees C

195
Q

why should active cooling end at 39.4 degrees C?

A

prevent hypothermia

196
Q

how often should patients temperature be taken if they have heat stroke?

A

every 5 mins minimum

197
Q

what is involved in emergency management of heatstroke patients?

A

active cooling
O2
maintain patent airway
IVFT
bloods
consider raised ICP

198
Q

how can patients be actively cooled?

A

lukewarm water
run over the body
wipe over with cloths
DO NOT USE TOWELS LAID OVER

199
Q

why is oxygen supplementation needed?

A

ventilation may be inadequate due to panting

200
Q

what bloods may be required for heatstroke patients?

A

PCV
TP
glucose
electrolytes
coags
ABG

201
Q

how may coagulation be affected by hyperthermia?

A

increase clotting time

202
Q

why can heat stroke case increased ICP?

A

cerebral vasodilation due to peripheral vasodilation leading to raised ICP

203
Q

should pyrexic patients be actively cooled?

A

no - it is beneficial

204
Q

why should pyrexic patients not be actively cooled?

A

slows replication of pathogens
increases function of WBC

205
Q

what are examples of antipyretic drugs?

A

paracetamol
NSAIDs

206
Q

when may antipyretic drugs be given to patients?

A

patients with
cancer and immune compromise

207
Q

should antipyretic drugs be given to all pyrexic patients?

A

no - pyrexia is of benefit to the patient

208
Q

what can cause pyrexia?

A

Inflammatory disease
Neoplastic disease
Other causes

209
Q

what types of inflammatory disease may cause pyrexia?

A

infectious
immune mediated

210
Q

what are some causes of pyrexia other than inflammatory or neoplastic disease?

A

opioids
hepatic encephalopathy
transfusion reaction

211
Q

what type of transfusion is particularly likely to lead to pyrexia?

A

xenotransfusion

Advanced Clinical Nursing Theory (36 decks)

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