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Michaelmas 5th year > Critical care, sepsis and CPR > Flashcards

Critical care, sepsis and CPR Flashcards

1
Q

How long do we feel for pulse to assess circulation in an emergency

A

If no pulse after 10 seconds, assume the worst

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2
Q

How to triage a patient

A

ABC of airway, breathing, circulation
Major body systems assessmet
brief history

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3
Q

How does heart rate change in shock in dogs

A

Dogs become tachycardic in shock i.e 160-200bpm

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4
Q

How does heart rate change in shock in cats

A

Cats become bradycardic ~100-140bpm

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5
Q

Normal dog and cat heart rates

A

Dog = 60-120bpm
Cat = 160-200bpm

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6
Q

How does pulse quality change as shock progresses

A

Initially: feel stronger, shorter pulses = ‘hyperdynamic’/’bounding’ due to drop in diastolic pressure first

Then as systolic pressure falls, pulse gets weaker and weaker

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7
Q

What are dark MMs with very fast CRT a sign of

A

Severe congestion i.e in sepsis

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8
Q

Where to listen for lung in the thorax

A

Middle 1/3 of thorax

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9
Q

What does it mean if we can hear respiratory noise without a stethoscope

A

It is upper airway

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10
Q

Respiratory pattern in upper airway disease

A

High inspiratory effort

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11
Q

Respiratory pattern/sound in lower airway disease

A

High expiratory effort
Hear wheezes

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12
Q

Respiratory pattern/sound in pulmonary disease

A

Variable resp effort
Hear harsh sounds or crackles

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13
Q

Resp pattern and auscultation in pleural space disease

A

Shallow beathing
Dull and distant sounding heart and lung sounds

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14
Q

Why can we get obtundation in shock

A

Due to blood not reaching the brain with major cardiovascular compromise

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15
Q

Definition of shock

A

Systemic failure of ATP production

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16
Q

Ways in which ATP production can fail

A
  • Oxygen delivery to capillary bed
    –> Including cardiac output, arterial oxygen concentration
  • Oxygen delivery to the cell; = microcirculatory flow
  • Actual ATP production by mitochondrial function
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17
Q

4 types of circulatory shock and what are their mechanisms

A

Hypovolaemic; decreased blood volume
Distributive; vasodilation
Cardiogenic; failure of forward flow
Obstructive; mechanical obstruction to venous return

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18
Q

WHat is the most common type of shock

A

Circulatory; 90% of shock cases seen

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19
Q

What type of shock might we get in pericardial effusion

A

Obstructive; mechanical obstruction of venous return

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20
Q

What type of shock might we get in sepsis

A

Distributive; vasodilation

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21
Q

What type of shock might we get with severe dehydration

A

Hypovolaemic

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22
Q

What type of shock might we get with GDV

A

Obstructive; mechanical obstruction of venous return

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23
Q

How does distributive shock work

A

Get siginficant vasodilation due to cytokines or other vasoactive substances
Blood pools in the periphery and lose ability to normally vasoconstrict

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24
Q

3 causes of hypovolaemic shock

A

Haemorrhage
Massive ascites
Severe dehydration

All cause a depletion in the intravascular volume

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25
Q

What are signs of shock compensation

A

Increase in heart rate
Vasoconstriction; pale MMs, reduced CRT, cold extremities
(dogs)

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26
Q

What are signs of non-compensated shock

A

Obtundation due to insufficient oxygen delivery to the brain
Can be non-ambulatory

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27
Q

Bolusing isotonic crystalloids to treat shock what amount and what type

A

Hartmann’s

Give 10m/kg over 15 mins

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28
Q

WHen might we choose to bolus lower quantities of isotonic crystalloids in shock cases

A

Cats vs dogs
Patients with known cardiac or pulmonary disease

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29
Q

What is MM colour and CRT like in mild vs moderate shock

A

Mild = <1sec and normal to more pink than normal
Moderate shock = pale pink MMs and normal CRT

Severe shock = slow or absent CRT, grey/white/muddy MMs

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30
Q

Treatment of distributive shock

A

Bolus fluids to increase cardiac output; but not too much as still normovolaemic

Vasopressors

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31
Q

What are the end points of resuscitation

A

Normal major body systems assessment = HR, CRT, MM colour etc

32
Q

What is popping the clot

A

When fluid boluses given to patients following a bleed can increase hydrostatic pressure and destroy a soft clot therefore exacerbating bleeding

Should be cautious with fluid volues given to bleeding patients; just get them stable

33
Q

What is the difference between SIRS and sepsis

A

Sepsis inflammation is due to infection

34
Q

SIRS criteria roughly

A

High or low temp
High respiratory rate
High heart rate (high or low in cats)
High or low white blood cells

= very sensitive but poorly specific

35
Q

Treating distributive shock e.g in sepsis

A

Start with fluid boluses but not TOO much
If hypotension persists after a few boluses then add in vasopressors e.g noradrenaline, dopamine

Control source of infection and remove if possible
Broad spectrum IV antibiotics

36
Q

What is the key thing to remember in the approach to a dyspnoeic patient

A

do not stress them; they are on a physiological knife edge

37
Q

What to do next in upper airway localised resp distress

A

Bypass the obstruction
Usually sedation enough
May have to intubate

38
Q

What to do next in lower airway source respiratory distress

A

Bronchodilator

39
Q

What to do next with pulmonary sources of respiratory distress

A

Not much can do except give oxygen
Look for underlying cause and treat

40
Q

What to do next with pleural space causes of respiratory distress

A

Thoracocentesis to empty pleural space

41
Q

What is the glide sign on thoracic ultrasound

A

= when there is a sense of movement along the pleural line (bright white line) like beads moving along it
This is as the two pleural layers glide over each other

42
Q

Why do we assess the pleural line/glide sign on a thoracic POCUS

A

To look for pneumothorax; will have no sense of movement with breathing if this is the case

43
Q

How does pleural fluid look on POCUS

A

Black

44
Q

What are B lines and what do lots of them suggest

A

= shimmering lines that extend from the pleural line
Having lots of them suggests abnormal pulmonary parenchyma e.g fluid in alveoli or interstitium (congestive heart failure, aspiration pneumonia)

45
Q

Why do we look at left atrium to aorta ratio in resp distress to POCUS

A

Look very quickly to rule in or out congestive heart failure as the cause of respiratory distress

46
Q

Two ways to get direct oxygen flow to the airways

A

Nasal prongs: quick and easy but less secure
Nasal cannulae = long and need suturing in but more secure and better O2 delivery

47
Q

When might we place a chest tube

A

If worried about ongoing large accumulation of fluid or air
e.g air keeps on coming, can’t empty space

Or have done thoracocentesis 3 times less than 24 hours apart and still rapidly re=filling

48
Q

Difference between seldinger and trocar chest tubes

A

Trocar tubes are wide diameter; patient must be GA or deeply sedated
Seldinger = narrow diameter, thread in via a wire and can just use mild sedatino

49
Q

Where in relation to the rib do we insert a catheter for thoracocentesis

A

Cranial to rib
(Vessels run caudally)

50
Q

What rate of chest compressions to do and how much of the chest width to compress

A

100-120/min
Compress 1/3 to 1/2 of chest width

51
Q

How long must a chest compressor do compressions for before switching over

A

2 mins minimum
Then check for pulse/look at ECG for 3-5 secs at changeover

52
Q

What is the cardiac pump theory and which animals is it applicable for

A

Direct compression of the heart forces blood out the ventricle into aorta and pulmonary artery

Good in cats, small dogs, keel chested dogs because the chest is more compliant

53
Q

What is the thoracic pump theory

A

Where chest compressions raise the intrathoracic pressure which pushes blood forward from the ventricles into the systemic circulation

Then during recoil, negative pressure pulls blood into the heart

This is main thing in barrel chested dogs, round chested dogs

54
Q

How to do mouth to snout ventilation

A

30 chest compressions then 2 breaths
Cover mouth so only nostrils clear and blow into nostrils

55
Q

What is the reversal agent for opioids

A

Naloxone

56
Q

What is the reversal agent for alpha-2 agonists

A

Atipamezole

57
Q

WHat is the reversal agent for benzodiazepines

A

flumazenil

58
Q

Why do we start with the low dose of adrenaline during CPR

A

Because the higher dose is associated with lower survivl to discharge in humans
+ neurological deterioration

59
Q

What is favourable between vasopressin and adrenaline to cause vasoconstriction during CPA event

A

Vasopressin
But more expensive

60
Q

What might we use amiodarone for

A

Anti-arrhythmic e.g
refractory ventricular fibrillation/pulseless ventricular tachycardia

61
Q

If amiodarone not available as an anti-arrhythmic

A

Lidocaine

62
Q

Which CPA heart rhythms are shockable

A

Ventricular fibrillation

Pulseless ventricular tachycardia

63
Q

How does defibrillation work

A

Re-sets normal heart rhythm by depolarising the heart muscle to synchronise the cells in the refractory period

64
Q

Which rhythms are non-shockable

A

Asystole
Pulseless electrical activity

65
Q

What is the difference between monophasic and biphasic defibrillation

A

Monophasic is higher current just from one electrode to another
4-6J/kg

Biphasic is from one electrode to another and back and is lower energy; 2-4J/kg

66
Q

When might we do open chest CPR

A

if arrest occurs during an operation
If external compression might not be effective e.g pheumothorax, cardiac tamponade, diaphragmatic hernia, XXL dogs

67
Q

What do we need to be aware of after open chest CPR

A

risk of bleeding and worsening of condition if an animal has coagulopathy or thrombocytopaenia

68
Q

What biochem changes might we see after CPA event

A

Metabolic acidosis
Hyperkalaemic
Hypocalcaemia

69
Q

What end tidal CO2 is it good to raise amove during CPR for better change of resuscitation

A

Above 15mmHg

70
Q

Post-CPR care

A

Want slight hypothermia
Only give fluids if they are hypovolaemic/haemorrhaged
Consider analgesia since pain from chest compression
May do vasopressors

O2 maintenance

71
Q

CPA ischemia phases

A

Electrical phase = first 4 mins; ischaemic damage limited due to energy stores available - should shock immediately
Circulatory phase = 4-10 mins; reversible ichaemic damage but ATP depresion; do CPR cycle first then shock
–> THis is when most defibrillation is done

Metabolic phase = >10 mins; irreversible ischaemic damage; CPR round then shock

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Q
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Michaelmas 5th year (41 decks)

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