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ISVPS Ncert Anaesthesia & Analgesia > CPR, Accidents and Emergencies > Flashcards

CPR, Accidents and Emergencies Flashcards

1
Q

Define respiratory arrest

A

‘Sudden or complete cessation of respiratory movement’

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2
Q

Define cardiac arrest

A

‘Sudden and often unexpected stoppage effective heart action’
There may be some electrical activity but it wont be effective at pumping blood round the body.

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3
Q

What is CPA?

A

Cardiopulmonary arrest when both spontaneous circulation and breathing cease.

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4
Q

What would indicate cardiac arrest?

A
  • no palpable pulse
  • no heart sounds
  • ECG shows asystole or arrythmia
  • Blood intraop stops flowing freely and is thick and dark
  • MM colour change and drying of gums
  • Prolonged CRT
  • No cranial nerve reflexes.
  • eye position
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5
Q

Why does respiratory arrest lead to cardiac arrest?

A

Starts as the brain an heart receive inadequate amounts of oxygen.
Could also be due to co2 accumulation and acidosis

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6
Q

What is the reason for cardiac arrest that has the best resucitation success? Why?

A

Drug overdose/associated with anaesthesia.

  • often correctable
  • no delay with placing IV/ETT as already there?
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7
Q

Describe the mechanism of spontaneous ventilation

A

-Diaphragm contracts, flattening
- Abdominal contents pushed caudally and abdomen moves outwards
- Intercostal muscles contract, pulling the ribs up and out creating negative pressure in the thoracic cavity.
- This causes air to be drawn into the trachea and to the lungs.
- muscles relax and normal positioning of muscles and ribs is restored, gas is exhaled.

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8
Q

What nerve supplies the diaphragm?

A

Phrenic

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9
Q

What indicated to the brain that a breath needs to be taken?

A

Chemoreceptors detecting a build up of carbon dioxide in the blood.

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10
Q

Where does the initial signal to start a breath come from

A

Brain stem

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11
Q

List the 5 groups of respiratory complications that can lead to respiratory arrest

A
  • Ventilatory Drive
  • Mechanical ability to breathe
  • Obstruction
  • Restriction
  • Absorption of oxygen
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12
Q

What can affect ventilatory drive under GA?

A
  • Hyperventilation , reduced CO2 reduces drive
  • Overzealous IPPV causing hyperventilation
  • Drugs affecting sensitivity of chemoreceptors allowing more co2 to build up than normal
  • Hypothermia
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13
Q

What can affect the physical ability to breathe

A
  • Interference to the nervous system or respiratory muscles
  • cervical spine damage may affect teh phrenic nerve
  • muscular or neuromuscular disease may affect the muscles controlling rib movement.
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14
Q

What are the causes of upper respiratory tract obstruction?

A
  • breed disposition (brachys)
  • phargeal tissue or tongue relaxation
  • head position (increased risk if flexed head)
  • Bandaging
  • Congestion - can happen is head is positioned lower than body, gravity causes fluid to build up
  • Inflammation of airway from trauma
  • laryngeal paralysis (nerve controlling opening of glottis is damaged) No active opening of larynx on inspection.
  • Tumours, blood clots etc
  • ETT obstruction
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15
Q

What is the difference between a stertor and a stridor?

A

Stertor - a low pitched snore cause by pharyngeal/nasal obstruction.
Stridor - a high-pitched sound more likley to be cause by laryngeal obstruction

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16
Q

What is paradoxial ventilation ?

A

When there is a blockage stopping air being sucked into the lungs so when the negative pressure builds up the ribcage is sucked in on inspiration and the abdomen moves out.

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17
Q

How can we treat suspected airway obstruction

A
  • pull tongue out
  • straighten head and neck position
  • Remove the cause if a bandage or FB
  • Suction use to clear any liquid secretions
  • Intubate or tracheostomy tube.
  • drugs to reduce swelling e.g. steroids
  • sedative if short sharp stressed breathing (creating a dynamic obstruction as soft tissues are sucked in) to slow respiration. CARE with sedation.
  • ## check temp if able as usually hyperthermic
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18
Q

What can cause lower airway obstruction ?

A

Bronchoconstriction due to to manipulation of airways (bronchoscopy) or disease.
Narrowed lower airways as seen in feline asthma (would see as ‘resistance’ on a capno or feel less compliance when using reservoir bag, less movement of thorax between inspo and expiraion and could affect SPO2)

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19
Q

What would restrict tidal volume in an anaesthetised patient?

A
  • restriction of thorax to expand from equipment or positioning, dilated abdomens, pneumothorax, diaphragmatic rupture.
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20
Q

What physiological effects would hypercapnia have under GA?

A

A small-mod increase in CO2 causes increased sympathetic stimulation, HR and BP. A large increase in CO2 will cause vasodilation, decreased BP, red MM and deeping anaesthesia due to depression of CNS.
Hypercapnia can increase the risk of cardiac dysrhythmias (VPCs), can alter blod pH and may even lead to seizures/arrest.

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21
Q

What can cause hypoventilation under GA

A
  • Deep anaesthesia (depression of ventilatory centres)
  • Drugs (decreased sensitivity centres to CO2 in the brain)
  • Physical limitations on expansion of chest or lungs.
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22
Q

What is rebreathing

A

When there is a significant amount of inhalaed fraction of CO2 (anything over 3mmHg)

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23
Q

What are the formulas for BP and CO

A

BP = CO x systemic vascular resistance (SVR)
SVR is affected by vasodilation and vasoconstriction

CO = HR x SV

Stroke volume is affected by pre-load, afterload and contractility

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24
Q

What is normal MAP under GA

A

70-90mmHg

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25
Q

What parameters can we check to identify hypotension?

A
  • BP
  • pulse quality
  • CRT
  • ETCO2 (indicates problem with circualtion)
  • Urine output
  • Any H+?
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26
Q

What is the circulating blood volume of a dog and cat?

A

Dog 88mls/kg
Cat 56mls/kg

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27
Q

What compensating may a patient do for hypovoleamia?

A

vasocontriction and an increase in HR and reading a normal BP because of it.

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28
Q

Describe what crystalloids are and when they would be used?

A

0.9% saline, Ringers or Hartmanns solution
They are isotonic
Good choice to replace water or electrolytes.
They stay in circulationfor a short period then distribute to the tissues to replace losses.

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29
Q

When would colloids be more applicable to use and why

A

They contain larger molecules which stay in the circulation for longer so are good for hypovoleamia without dehydration affecting other fluid compartments. E.g. Gelofusin

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30
Q

Name common blood products

A

Whole Blood
Packed RBCs (PRBCs)
Fresh frozen Plasma (FFP)

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31
Q

Why would you use whole blood over PRBCs?

A

PRBCs lack the clotted factors in whole blood even though they will help with the oxygen carrying capacity

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32
Q

What percentage blood loss should be replaced by what fluid/product?

A

10% by crystalloids
10-20% by colloids
and over 20% with blood products

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33
Q

What can affect pre-load volume?

A

Poor flow of blood in vena cava - compression or occulsion.

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34
Q

What physiological measurements taken under GA would indicate vasodilation?

A
  • Red MMs
  • Low diastolic pressure
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35
Q

List the actions of adrenoreceptors alpha 1 & 2 and beta 1&2

A

alpha 1 - vasocontriction
alpha 2 - central vasodilation and peripheral vasoconstriction

beta 1 - positive inotropy and chronotropy
beta 2 - vasodilation and bronchodilation

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36
Q

What does an inotrope do?

A

Alters the strength of heart muscle contraction. A negative inotrope weakens the contraction; a positive strenghtens.

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37
Q

What does a chronotrope do?

A

Changes teh heart rate. Negative decreases and positive increases HR

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38
Q

What does a vasopressor do?

A

Causes vasoconstriction

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39
Q

When can atropine or glyco be used to treat hypotension?

A

Only if the hypotension is associated with a low HR

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40
Q

What class of drug are atropine and glyco and how do they work?

A

Parasympatholytics or Antimuscarinics or Anticholinergics

  • block parasympathetic input (vagal input) to the heart (which usually slows the heart rate) at the SA node (pacemaker) and therefore these drugs will increase the HR.
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41
Q

What does ephedrine do?

A

Causes the release of endogenous stores of catecholamines. It can be used as a vasopressor (vasoconstrictor) and positive inotrope.

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42
Q

What type of drug is dopamine

A

Positive inotrope and chronotrope and a vasopressor.
Acts on cardiac beta adrenoreceptors to increase cardiac output. Care with lower doses and undesired effects.

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43
Q

What type of drug is dobutamine?

A

Positive inotrope
Acts on beta adrenoreceptors

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44
Q

What type of drug is noradrenaline?

A

Positive inotrope and vasopressor
Produces vasoconstriction via alpha adrenoreceptor action (with some beta action). Useful in vasodilated patients. .e. those with sepsis.

45
Q

What type of drug is phenylephrine

A

Vasopressor and acts on alpha adrenoreceptors. Can have a profound effect and the increase in SVR can cause a relfex bradycardia.

46
Q

What is definition of hypertension?

A

Abnormally high blood pressure over 100-120mmHg mean

47
Q

Why is hypertension bad?

A

Excessive BP can reduce tissue perfusion and cause damage to organs

48
Q

What are causes of hypertension?

A
  • Pain
  • Inadequate depth of anaesthesia
  • CO2
  • Increase ICP
49
Q

What are the signs of raised ICP or ‘the cushings triad’?

A
  • hypertension
  • bradycardia
  • irregular ventilation
50
Q

Why would you check ventilation if there was hypertension present?

A

Because hypoventilation can increase CO2 which can increase BP

51
Q

What is the definition of tachycardia in dogs and cats?

A

Excessively high HR
Dogs: over 160-180bpm
Cats: over 200-210bpm

52
Q

Why are we worried about tachycardia?

A
  • Increased HR, increases cardiac workload and with it the energy and oxygen requirements.
  • Coronary vessels can only deliver oxygen to the heart during diastole as squeezed shut during systole. Increased HR will disproportionately affect diastolic time.
    So during tachycardia there is an increased myocardial oxygen demand and a reduced delivery of oxygen to the myocardium. Patient can become myocardially hypoxic even if not hypoxaemic.
  • Tachycardia also reduces filling time and reduces stroke volume and therefore BP
53
Q

How can we identify myocardial hypoxia?

A

On an ECG you can get ST segment depression where it doesnt return to the previos level or ST coving where it bends up like a reverse shark fin.

54
Q

What are the causes of tachycardia?

A
  • Hypovoleamia or hypotension (in an effort to maintain CO)
  • Hypoxia (in an effort to deliver oxygen tot the tissues)
  • Sympathetic stimulation - usually due to inadequate depth or analgesia
  • Hypercapnia
  • Hyperglycaemia
55
Q

What should you do if the patietn is tachycardic?

A
  • Check depth +/- increase
  • Check BP and ETCO2 to determine cause
  • Fluid bolus
  • Analgesia/positioning/surgery stage
  • Chek for myocardial hypoxia (ST segment depression)
  • Check for hypoxia (SPO2) and ensure enough oxygen is given.
56
Q

Define bradycardia

A

Usually less than 60bpm for a dog and 100-110 bpm for a cat.

57
Q

What can cause bradycardia under GA?

A
  • depth
  • drugs (resp depression or reflex bradycardia due to vasoconstriction)
  • hypoxia (more long-term)
  • electrolyte abnormalities (hyperkalaemia)
  • vagally mediated reflexes (causes increase in parasympathetic outflow reducing heart rate - e.g. pressure on the eye, pulling ovary)
  • Hypothermia (metabolic demand decreases)
  • Hypoglycaemic
  • Raised ICP or cushings triad
58
Q

What effect can hyperkalaemia have on an ECG?

A

Tall, spikey T waves.

59
Q

Why may you treat hyperkaelaemia with glucose?

A

It wncourages the uptake of potassium into the cells. It may be severe enough to also require insulin alongside to encourage uptake of potasium.

60
Q

What cases would you commonly see hyperkalaemia?

A

Urinary obstruction or rupture

61
Q

What should you do if your patient is bradycardic?

A
  • Check BP
  • Check ECG
  • feel pulses
  • Consider the patient history ( any neuro signs that would indicate raised ICP?)
62
Q

What can you do if raised ICP is suspected as cause of bradycardia whilst drugs (usually mannitol) are being prepared?

A

IPPV to reduce co2 - aim for slight hypocapnia of 30mmHg

63
Q

Describe what 2nd degree AV block is?

A

when some p waves are not conducted down through the AV node so they have no associated QRS complex therefore no ventricular contraction occurs.
It is commonly seen with alpha 2 adrenoreceptor agonists and a low HR

64
Q

Describe a 1st degree AV block

A

Elongation of the PR interval
(unlikely to need any intervention)

65
Q

Describe 3rd degree AV block

A

Complete failure of the AV node to conduct an electrical impulse to the ventricles

There are p waves at regular intervals and QRS at regular different intervals but no links between them. Both atria and ventricles are conducting at their own rates.

Intervention can be tried e.g. atropine but likely to ineffective and indicates heart disease and possibly needs a pacemaker.

66
Q

What is a VPC?

A

Its a complex that arrives early (premature) anf originates in the ventricle instead of the atrium.

67
Q

What is the difference between a VPC and an escape complex?

A

VPCs are often early and on a normal ECG whereas an escape ventricular complex tends to come when there has been a long gap in beats and it contracts as a safety mechanism.

68
Q

What can cause VPCs?

A
  • sympathetic stimulation (check depth and analgesia)
  • elevated CO2
  • hypoxia
69
Q

When are VPCs a concern?

A
  • When there is a run of them i.e. ventricular tachycardia (more than 4 in a row)
  • When there are lots of different VPCs instead of one look (polymorphic VPCs)
  • They form a pattern instead of being isolated or random. This is called ventricular bigeminy when the complexes alternate between normal and abnormal.
  • R on T. When the VPC looks to start before the T wave (or depolarisation/reset) ends - this is may lead to dangerous arrthmyias
70
Q

What should be checked if we start to seee VPCs?

A
  • is the pulse affected?
  • can you feel a pulse for every complex?
  • BP
  • is there a lot of sympathetic stimulation? e.g. light or painful
  • is ventilation and oxygenation adequate?
71
Q

What can be used to treat VPCs?

A

Lidocaine can be used to block some sodium channels in the heart
(ENSURE they are first VPCs and not escape complexes!!)

72
Q

What causes histamine release under GA?

A
  • anaphylaxis
  • Mast cell tumour degranulation
73
Q

What can cause delayed recovery from anaesthesia?

A
  • hypothermia
  • hypoglycaemia
  • electrolyte disturbance
  • impaired circulation (slower delivery to elimination organ)
  • impaired ventilation (struggle to eliminate volatile agent)
  • drugs
  • medical (e.g. poor organ function)
74
Q

Define hypothermia

A

core body temp of less than 37 degrees

75
Q

What can hypothermia cause in a patient?

A

-increased risk of bradycardia and arrthymias
- clotting dysfunciton (hypothermia makes blood more viscous
- decreased enzyme activity
- decreased biotransformation of drugs
- decreased renal blood flow
- left shift of oxyhaemaglobin dissociation curve

76
Q

What is malignant hyperthermia and what causes it?

A

Very rare cause of increased body temp. Its caused by a genetic mutation in a very specific part of the muscle. It can be triggered by stress or volatile agents. When its triggered it causes persistent muscle contraction.

77
Q

Why are the signs of malignant hyperthermia?

A

Under GA it can be seen as rigidity and poor relaxation under GA. Can pull ears back and splay toes.
The persistant muscles contraction uses more oxygen and produces more co2 - so an early sign may be increased ETCO2.

78
Q

How can malignant hyperthermia be rectifed?

A
  • active cooling of body temp
  • can leave under GA and change to TIVA whilst cooling
  • can be treated with dantrolene
79
Q

What is neuropraxia? when might it happen?

A

Temporary paralysis due to pressure on a nerve during GA due to positioning

80
Q

What can cause blindness in cats under GA

A

extreme opening of the mouth can cause compression of the maxillary artey and starve brain of oxygen causing blindness

81
Q

What can regurgitation during sedation/GA cause?

A

Regurgitated material could be aspirated, can lead to an immediate pysical obstruction of the airway, bronchoconstrictive inflammatory response to the acidic contents, and eventually pneumonia.

82
Q

What can we do to prevent aspiration pneumonia/regurgitation?

A
  • induce GA in sternal, elevated head. Inflate cuff before head dropped down
  • If regurge occurs in surgery, drop head down to allow contents to drain. Use suction. May want to flush oesophagus to reduce acidity
  • Drug treatments e.g. omeprazole for treatment or pre-treatment.
83
Q

What is reflux oesophagitus?

A

When stomach contents are released and sit in the oesophagus without visible regurgitation. Acidic damage over time can lead to stricture formation

84
Q

What does the A-F stand for in terms of resucitation?

A

Airway
Breathing
Circulation
Drugs
ECG/ electrical defib
Follow up

85
Q

Describe the cardiac pump technique

A

lateral recumbency
compress over the 3-6th intercostal space (where you (should) can feel the heart)
Compress 100-120bpm
Compress thorax at least 1/3rd depth
Allow recoil
Perform with patients back to compressors body to stop falling off table.

86
Q

What is the difference between cardiac and throacic pump techniques for CPR?

A

Exact same except postion of compressors hands. In thoracic pump, hands are places on highest point of the dogs chest when the dog is in lateral.

87
Q

How can we evaluate the efficiency of compressions?

A
  • Capno (is a circulation being generated?) Aiming for over 15-18mmHg
  • palpable pulse?
  • Can use probe on cornea to hear circulation
88
Q

How is internal cardiac massage performed?

A

Milking the ventricles into the arteries.
Rapid clip over 3-6th intercostal space, incise 5th intercostal space on expiration
Open pleura and pericardium, continue ventilation!!
Most suitable technique during surgery

89
Q

How much flush should follow emergency IV drugs in a cat, small dog, large dog?

A

Cat 3-5mls, 5-10mls in small med dogs and 10-15mls in giant breeds.

90
Q

If IV drugs during CPA is not an option how can drugs be administered?

A

Transtracheal. Pass a urinary catheter downt he ETT to sit at the carina (the level of the 6th rib). Deposit drugs here - doses will need to be 2-3x IV dose - usually adrenaline and atropine given this way. Dilute the drugs to make 5-10mls using sterile water and follow with a few breaths to distribute

91
Q

What vein should be used for IV drugs during arrest ideally?

A

Jugular vein

92
Q

When is adrenaline used and how does it work?

A

Adrenaline is used in asystole. Its main action is to increase SVR and return blood to central circulation. It also increases the force of contraction.

93
Q

When is atropine used and how does it work?

A

Used where bradycardia preceeded arrest. Also used when AV block present.

94
Q

What is the dose of adrenaline, atropine and lidocaine?

A

Adrenaline 0.01mg/kg IV
Atropine 0.04mg/kg IV
Lidocaine 1-4mg/kg IV (bolus and then CRI)

95
Q

When is lidocaine used and how does it work?

A

Used to treat ventricular arrthymias e.g. VFib.

96
Q

Describe asystole on an ECG

A

Flatline

97
Q

Describe ventricular fibrilation on an ECG

A

Irregular electrical activity. No clear defined waves or baseline. Can be coarse and have large zig-zags or ‘fine’ when zig-zags are erally small.

98
Q

Describe ventricular tachycardia on an ECG

A

Large wave sall together. Considered an arrest rhythm when combined with no pulses.

99
Q

What is pulseless electrical activity (PEA) and describe it?

A

ECG looks normal, or maybe just slightly wider but still has PQRST. Over time may become increasingly abnormal. No pulses and no audible heartbeat.

100
Q

What info about the heart does an ECG not tell us?

A

THe cardiac output

101
Q

Describe how you’d defib something?

A

Charge device, apply gel., one paddle on each side of thorax and current applied across chest.
1-5 joules/kg. (0.1-0.5 if direct contact with heart during surgery)

102
Q

What is ROSC?

A

Return of spontaneous circulation i.e. when the patient has pulses and CO itself.

103
Q

What signs would show our CPR worked and the patient starts recovering?

A
  • improved MM colour
  • ECG more normal
  • lacrimation
  • pupils constrict
  • return of cranial nerve reflexes
  • return of spontaneous ventilation
104
Q

Describe a crash scenario from when the patietn is found and the order of events.

A
  • Arrest observed
  • Shout CRASH. Note the time
  • Check for pulse/respiration (no more than 10s)
  • Start compressions. Note time
  • If pulse, check airway
  • Intubate patient and start lung ventilation
  • Attach ECG
  • Administer adrenaline. Note time.
    Continue CPR cycles as per recover guidleines.
  • Swap staff on compressions every 2 minutes.
105
Q

Describe the main roles for CPR

A
  1. Director - making decisions and assessing patient
  2. Ventilation
  3. Compressions
  4. Drawing up drugs, attaching monitoring, keeping records
106
Q

List the items in a well-stocked crash box

A
  • ETTs of different sizes
  • Laryngoscope
  • IV catheter stuff
    -ECG pads
  • Defib
  • Rigid dog urinary catheter
  • adrenaline, atropine, lidocaine
  • saline, giving set
  • flow chart/calculations dose chart
  • clippers
  • contact gel
  • doppler
  • stopwatch
  • note-taking stuff
  • bandage material (ETT tie)
  • ambu bag
107
Q

What percentage of dogs that have arrested will arrest again?

A

50%

108
Q
A

ISVPS Ncert Anaesthesia & Analgesia (8 decks)

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