A B C Flashcards

1
Q

how can you assess a patients airway?

A

if conscious and speaking in full sentences = reassuring
if unconscious - get down to level of mouth listen for breath sounds, feel for breath on your cheeks and view chest for any movement.

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2
Q

what are the features suggestive of a:

a) completely obstructed airway
b) partly obstructed airway

A

a) silent chest, unable to talk, cough or breathe

b) stridor - partial obstruction at the level of or above larynx
wheeze - partial obstruction of lower airways
gurgling - vomit, blood or secretions.

other features:
reduced level of consciousness, respiratory distress , make look distress e.g. if choking

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3
Q

what are the signs of respiratory distress?

A
tachypnoea
use of accessory muscles - intercostal recession, tracheal tugging, sea saw pattern of chest wall and abdomen. 
cyanosis 
grunting
apnoea 
tachycardia
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4
Q

what can airway obstruction lead to?

A

cardiac arrest.

complete obstruction leads to rapid cardiac arrest
partial obstruction leads to pulmonary oedema, cerebral oedema, hypoxia, exhaustion, apnoea and eventually cardiac arrest.

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5
Q

give examples of causes of airway obstruction

A

reduced conscious level (head injury, intoxication, hypoglycaemia) - loss of protective reflexes so tongue and epiglottis can occlude upper airway.

foreign body - more common in children

secretions - (blood, vomit) - e.g. intoxication and reduced level of consciousness can result in aspiration

swellings:
anaphylaxis - oedema of larynx and upper airways
infection - tonsillitis, quinsy, epiglottitis, supraglottitis
external compression - goitre, tumour, haematoma (after thyroid surgery)

other laryngospasm, bronchospasm, blocked tracheostomy

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6
Q

what manoeuvres are available to secure an airway?

A

head tilt chin lift - assuming no c spine injury

jaw thrust - when C spine injury suspected

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7
Q

what different adjuvants can be used to help maintain an airway. briefly compare the use of each one

A

Oropharyngeal (Guedel)

nasopharyngeal - can be better tolerated in semi conscious patients (therefore if cant tolerate guedel use this instead)

laryngeal mask / I gel - needs to be fully unconscious to be tolerate. more secure than the above two. reduces risk of gastric inflation and thus aspiration.

endotracheal tube - the most secure airway, needs skilled anaesthetist to set up, needs to be fully unconscious to be tolerated. reduces risk of gastric inflation/aspiration

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8
Q

how is the size of oropharyngeal airway measured?

A

from midpoint of incisor to angle of jaw

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9
Q

how is the size of the nasopharyngeal airway measured?

A

from nose to tragus.

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10
Q

when should a nasopharyngeal airway be avoided?

A

basal skull injury

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11
Q

what happens if a nasopharyngeal airway is too big?

A

bleeding, gagging, vomitting

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12
Q

what size of laryngeal airway is used for most men/women?

A

most men - size 5

most women - size 4

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13
Q

how do laryngeal airways and I gels differ?

A

laryngeal mask airways - require inflation of cuff when in larynx

I gel is covered in jelly and thus no inflation is required. - easier to use in CPR

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14
Q

what is bag valve mask ventilation?

A

allows us to manually ventilate patients who are either fully unconscious or have a reduced respiratory drive.

2 person technique: the mask is held tightly over the mouth and the other person squeezes the bag to deliver air.

if someone has 0 respirations then give one breath every 5 seconds = 12 breaths/ min
if someone has a reduced respiratory rate e.g. of 6, then give a breath in between each of their own.

can be used along side adjuvants:

  • laryngeal airways and endotracheal can actually be attached to the bag and the mask bit can be removed
  • if no adjuvant is present then whilst holding the mask over the face, a head tilt chin lift/ jaw thrust needs to be maintained.

high flow oxygen can be attached to reservoir bag (gives around 85% oxygenation)

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15
Q

what should be considered if there is resistance against ventilation by bag valve mask ?

A

airway obstruction e.g. foreign body

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16
Q

what is a risk of mechanical ventilation? what contributes to this problem?

A

over inflation and gastric inflation.
gastric inflation can lead to aspiration of stomach contents

this occurs if breaths are being given too quickly and not enough time for adequate expiration.
also can occur if there is airway obstruction
also partly due to relaxed oesophageal sphincter in those who are unconscious

the risk is reduced in laryngeal / endotracheal airway is used.

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17
Q

how can the airway be additionally protected in those who are at risk of aspirating?

A

recovery position
suction if gurgling heard
consider NGT to empty stomach contents.

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18
Q

what are the signs of choking?

A

occurs during eating and patient will suddenly grab their neck and become distressed.

mild: they can speak but struggling, coughing
severe: unable to speak or cough, quickly turns blue

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19
Q

how is a choking patient managed?

A

if mild - encourage coughing

if severe:

  • give 5 blows to back whilst patient is leant forward (use blade of hand and give sharp blows between scapula).
  • if not successful give 5 abdominal thrusts (wrap arms around patient and make a fist below xiphisternum and pull sharply inwards and upwards) .
    - continue to alternate between these two manoeuvres
    - if still not successful, get resuscitation team and someone with skills to use a laryngoscope and Magills foreceps to remove obstructed foreign body.
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20
Q

where is the pharynx positioned and what parts does it consist of?

A

pharynx extends from cranial base to the inferior border of cricoid cartilage (anteriorly) and inferior border of C6 (posteriorly)

consists of nasopharynx, oropharynx and laryngopharynx

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21
Q

what is included in a breathing assessment?

A

look: deformity, wounds, cyanosis, chest expansion, resp rate
feel: chest expansion, tracheal, surgical emphysema, percuss
listen
extras: oxygen sats, ABG, CXR

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22
Q

what is respiratory failure and how can it be categorised?

A

respiratory failure is the failure of adequate gas exchange which results in hypoxia. defined as a pO2 <8kpa and can be divided into:

type 1: PCO2 normal or low
type 2: PCO2 >6kpa

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23
Q

list the causes of type 1 respiratory failure

A

COPD, asthma, pulmonary fibrosis, pulmonary HTN, pneumonia, ARDS, pneumothorax, P.E, pulmonary oedema, bronchiectasis

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24
Q

list the causes of type 2 respiratory failure

A

pulmonary disease: severe COPD/ asthma, pneumonia, end stage fibrosis, obstructive sleep apnoea

reduced respiratory drive: head injury, brain tumour, CNS depressants, hypothyroidism

neuromuscular: MS, myasthenia, guillian barre, cord lesion

chest wall: kyphoscoliosis, flail chest

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25
Q

how can a fractured rib result in respiratory failure? (assume no pneumothorax)

A

pain - reduced breathing and coughing
eventually exhaustion from breathing
results in depressed respiratory drive overall.

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26
Q

what are the signs of symptoms of respiratory failure?

A

hypoxia: reduced sats, dyspnoea, tachycardia/ arrhythmia, confusion, agitation, central cyanosis (late sign)
hypercapnia: peripheral vasodilation, bounding pulse, tachycardia, flapping tremor, headache, papilledema, confusion, drowsiness, coma

others: tachypnoea (>25) - useful and simple indicator
signs and symptoms relating to specific cause

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27
Q

what are the consequences of long standing hypoxaemia?

A

polycythemia
pulmonary HTN
cor pulmonale

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28
Q

what are the complications of respiratory failure?

A
arrhythmias
GI bleed
stress ulceration (duodenal) 
organ failure (due to lack of O2) - AKI and can lead to cardiac arrest 
neurological damage from hypoxia 
complications of mechanical ventilation
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29
Q

why is acute respiratory failure so dangerous?

A

no time for compensatory mechanisms (renal bicarb, polycythaemia ) to develop. So become quickly acidotic and unwell.

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30
Q

what is the normal respiratory rate?

A

12 - 20 breaths / min

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31
Q

what are the causes of tachypnoea?

A

exertion, anxiety, pain
pneumothorax, P.E, pleural effusion , pneumonia, asthma
sepsis, DKA,

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32
Q

what are the causes of bradypnoea?

A

raised ICP, intoxication (opiate overdose), obstructive sleep apnoea, exhaustion after airway obstruction, sedation, hypothyroid.

33
Q

what are the different types of hypoxaemia ?

A

hypoxemia is defined as low arterial oxygenation (can be measured by oxygen saturations.

ischaemia hypoxaemia - thrombus/ embolus/ shock
hypoxic hypoxaemia - poor oxygenation at lungs i.e. any cause of respiratory failure. also CO poisoning due to binding to Hb more tightly than O2

anaemic hypoxaemia - not enough Hb

cellular hypoxaemia - e.g. cyanide poisoning blocks oxidative phosphorylation

34
Q

how can we investigate hypoxaemia?

A
O2 sats 
FBC - anaemia, polycythemia 
BP - shock (ischaemic hypoxaemia)
CXR - respiratory cause 
other tests : TFT (hypothyroid), U&amp;E (electrolytes can disturb respiratory muscles and heart) 

more specific tests:
spirometry, ECHO, ECG, Ddimer/CTPA, toxological screen , CT head (trauma)

35
Q

how is acute respiratory failure managed?

A

A TO E
airways - secure it? treat obstruction e.g. nebulisers

breathing - assess and treat - high flow oxygen (unless CO2 retainer) , may require non invasive ventilation (if exhausted)/ mechanical ventilation/ ECMO if severe. check if on morphine (may need naloxone and alternative pain management if resp rate low)

Circulation - fluid resus if BP low to improve tissue oxygenation
D - look for other causes of respiratory failure e.g. signs of head trauma.
E - any wounds to chest etc

treat underlying cause e.g. salbutamol nebuliser, EpiPen, Abx for pneumonia

36
Q

what is ECMO?

A

extracorporeal membrane oxygenation

37
Q

list the differentials for respiratory acidosis?

A

respiratory centre depression (decreased resp rate): drugs, raised ICP, encephalitis, stroke, central apnoea, excess o2 in CO2 retainer

neuromuscular disorders (decreased vital capacity): Myasthenia gravis, guillian barre, polio, ALS, muscular dystrophy

parenchymal disease: COPD, pulmonary oedema, pneumothorax, pneumonia, interstitial lung disease, ARDS

airway obstruction - COPD, Asthma, foreign body

inadequate mechanical ventilation

38
Q

list the differentials for respiratory alkalosis?

A

hypoxaemia:
leads to hyperventilation and lowers CO2 (better diffusion than O2). e.g. severe anaemia, heart failure, high altitude, type 1 resp failure

resp centre stimulation:
CNS disorder, hepatic failure, gram negative sepsis, anxiety, pregnany, pain, drugs (catecholamines, theophylline)

excess mechanical ventilation

39
Q

what is the cause of respiratory acidosis? respiratory alkalosis?

A

acidosis: raised CO2 secondary to poor ventilation/ gas exchange
alkalosis: low CO2 due to hyperventilation

40
Q

how can the effectiveness of oxygenation/ ventilation be assessed?

A

O2 sats - should respond to oxygen

ABG

41
Q

when is ABG indicated as well as O2 pulse oximetry ?

A

ABG indicated in any CO2 retainers (and repeat in 30 mins)
critically ill patients (although O2 sats may be fine may have high CO2)
anyone with sats below 92

42
Q

what may it indicate if pulse oximetry not pick up a value?

A

shock - poor peripheral perfusion and thus no sats measured.

43
Q

what situations is pulse oximetry unreliable?

A
shock 
hypothermia (vasoconstriction)
methamoglobinaemia 
CO poisoning 
sickle cell disease 
surgical dye (methylene blue) - falsely low sats
nail varnish 

(not affected by jaundice or anaemia)

44
Q

what oxygen saturations should we aim for?

A

non CO2 retainer - 94-98%

CO2 retainer - 88-92%

45
Q

what should you ensure before mechanical ventilation of a patient?

A

no tension pneumothorax

46
Q

when is high flow/ concentration of oxygen via non-rebreathe mask used?

A

critically ill patient / hypoxic - that isn’t a long term CO2 retainer.
type 1 respiratory failure?
after return of spontaneous circulation after arrest

47
Q

what % oxygen does:

a) high flow oxygen via non-rebreathe mask?
b) nasal cannulae?
c) Hudson mask?
d) venturi mask?

A

a) 85% to 100%
b) 24-30% oxygen delivery (flow rate 1-4 L / min)
c) 24-60% (flow rate 5-10L)
d) venturi:
blue - 24% (2-4L/min)
white - 28% (4-6 L/min)
yellow - 35% (8-10L/min)
red - 40% (10-12 L/min)
green - 60% (12-15 L/ min

48
Q

why should we not keep high flow oxygen on for a long period? (oxygen delivery)

A

need to aim for sats of 94-98%.

there is evidence that high blood oxygenation after cardiac arrest/ MI can be harmful

49
Q

when is a simple face mask used? (oxygen delivery)

A

mild hypoxia without chronic lung disease

could also use nasal cannulae here

50
Q

how is safe oxygen delivery achieved in to those with long standing CO2 retention or acute type II respiratory failure?

A

any CO2 retention - acute or long standing need to give 24% venture mask and aim for sats of 88-92%

keep reassessing ABG and alter % O2 accordingly

51
Q

what things should be documented when prescribing oxygen?

A

oxygen mask type
flow rate
target sats

52
Q

what are the different types of mechanical ventilation?

A

positive pressure - increases airway pressure to deliver oxygen. Negative pressure - reduces pressure in alveoli to create sub atmospheric pressure in chest and draw air in (not used anymore)

controlled vs patient initiated:
- controlled initiates ventilation automatically. patient sensored initiates when it senses patients effort and then adds to this to aid ventilation.

invasive vs non invasive:

  • invasive: endotracheal tube and tracheostomy
  • non invasive: nose mask or full face mask (CPAP/ BiPAP)
53
Q

when is invasive ventilation used over non-invasive?

A

generally intubate people with GCS = 8 i.e. invasive ventilation used. (endotracheal tube)
however if the cause of respiratory depression is unknown then intubate at GCS 9 too.

for non invasive ventilation patient should have patent protective airway reflexes and be alert/responsive

54
Q

how deep is an endotracheal tube inserted in men and women?

A

23cm in men
21 cm in women.
CXR to confirm correct placement
need to monitor endotracheal cuff pressure periodically to prevent its migration

55
Q

give examples of ventilation associated trauma?

A

pneumothorax
pneumomediastinum
subcutaneous emphysema
alveolar wall stress

56
Q

compare CPAP and BiPAP?

A

CPAP - continuous positive airway pressure

  • high pressure oxygen with tight fitted mask
  • continuous positive pressure to help keep aiways open
  • good for acute pulmonary oedema and sleep apnoea

BiPAP

  • bilevel positive airway pressure
  • high positive pressure on inspiration and lower level positive pressure on expiration
  • good for COPD and ARDS
57
Q

what is the modified WELLS score?

A

clinical signs and symptoms of DVT - 3 points
alternative diagnosis less likely - 3 point
HR >100 - 1.5 points
immbolisation (>3 days)/ surgery in last 4 weeks - 1.5
previous history of VTE - 1.5
haemoptysis - 1 point
active cancer in last 6 months - 1 point

low risk <2
moderate risk 2-6
high risk >6

58
Q

how can we identify circulation failure/ shock?

A

arterial hypotension

  • systolic BP <90 or MAP <65
  • tachycardia

poor perfusion:

  • long cap refil, cold, pale, clammy, mottling
  • oliguria (<0.5ml/kg/hr)/ anuria
  • neurological - syncope , low GCS

hyperlactataemia:
- high lactate due to anaerobic respiration
- tachypnoea (due to acidosis)

59
Q

what is circulation failure/ shock?

A

failure of the circulatory system to provide adequate delivery of oxygen and nutrients to tissues (inadequate organ perfusion

60
Q

what are the causes of shock?

A

hypovolaemic shock

  • blood loss - AAA, GI bleed, trauma, splenic rupture, ectopic pregnancy
  • fluid loss - pancreatitis, diarrhoea/ vomiting, burns

cardiogenic shock:

  • primary - arrhythmia, MI, valve problems, myocarditis
  • secondary - tension pneumothorax, tamponade, P.E

distributive shock

  • anaphylaxis/ sepsis
  • neurogenic shock - reduced vascular resistance.
61
Q

what are the ways to differentiate distributive, cardiogenic and hypovolaemic shock?

A

hypovolaemic - cold, clammy, low JVP
cardiogenic - cold clammy, raised JVP
distributive - warm, well perfused, bounding pulse, low JVP

62
Q

what are the causes of ventricular fibrillation?

A
MI/ ACS 
hypertensive heart disease
valve disease 
acidosis
hyper K, Mg or Ca
hypothermia 
long QT
drugs - antiarrhythmics, TCA, digoxin 
electrocution
63
Q

what is the most common cause of cardiac arrest?

A

arrhythmia post MI

64
Q

how is shock managed?

A

A to E

  • airways, oxygenation
  • raise foot of bed
  • IV access (2 wide bore cannulas)
    • take bloods from these
  • ECG
  • 500ml 0.9% saline STAT (unless cardiogenic cause and be cautious if AAA is the cause)

treat specific cause of shock

65
Q

what are the causes of tachycardia?

A

sinus tachycardia - pain, anxiety, sepsis, shock, hyperthyroid, drugs, anaemia , P.E

atrial flutter, AF, re-entry loop tachycardia, junctional tachycardia, VF, VT

66
Q

what are the causes of bradycardia?

A

sinus brady - high resting vasal tone in athletes
drugs - B blockers, amiodarone, verapamil, CaCB
hypothyroid, hypothermia, hypoxia
cushings reflex/ triad
sick sinus syndrome, heart block, inferior MI

67
Q

what are the causes of oliguria?

A
dehydration 
vascular collapse/ shock
nephritic syndrome 
AKI / acute tubular necrosis 
post renal obstruction - tumour, stone, catheter
68
Q

what are the causes of hypotension?

A

shock
acutely may be neurogenic e.g. epidural;/ drugs
orthostatic hypotension - aortic stenosis, arrhythmias, diabetes, dumping syndrome, vasovagal faints, parkinsons.

69
Q

what are the causes of electrolyte imbalance?

A

diuretics, AKI, SiADH, dehydration , vomiting, diarrhoea, iatrogenic from incorrect fluids.

70
Q

what is bleeding diathesis?

A

the susceptibility to bleed mostly due to hypercoagulability

71
Q

what are the causes of bleeding diathesis?

A

vascular defects
- connective tissue disorder e.g. ehlers danlos, berry aneurysms in PCKD1

platelet disorders

  • poor production - aplastic anaemia, marrow suppression (cytotoxic drugs, cancer infiltration, radiation)
  • destruction - splenic sequestration (hypersplenism), immune (immunothrombocytopenic purpura and SLE), DIC
    - defective - NSAIDs, increased urea, myeloproliferative disease

coagulation defects

  • congenital - haemophilia (A/B)
  • acquired - liver disease, vit K deficiency, warfarin, DIC
72
Q

how does bleeding diathesis present?

A

petechial rash - non blanching, non palpable, red pin point due to capillary inflammation and haemorrhage
ecchymosis (bruise) - collection of blood under skin due to extravastion (leakage) of nearby vessel.
bleeding gums, epistaxis, menorrhagia
prolonged bleeding after injury
haematoma
massive haemorrhage - GI, stroke

73
Q

what investigations should be ordered if someone presents with bleeding diathesis?

A

prothrombin time (PT) - tests for abnormalities in factor I, II, V, VII and X. can be converted to INR. altered with warfarin, liver disease, DIC, vit K deficiency

activated partial thromboplastin time (APTT) - looks at factors I, II, V, VIII, IX, X, XI, XII. normally 35-45s. prolonged by heparin, haemophilia, DIC and liver disease

thrombin time - measures how well fibrinogen is working. normally 10-15s. prolonged by heparin/ DIC

other things:

  • platelet levels - if low could be due to chemotherapy or massive blood transfusion , coeliacs, leukaemia
  • factor V assay - low in liver disease, DIC
  • fibrinogen levels - If low may suggest haemorrhage, fibrinolysis or placental abruption
74
Q

how is bleeding diathesis managed?

A

if shocked - resuscitate with fluids
discuss need for FFP and platelets or specific factor replacement e.g. prothrombin complex concentrate

treat cause of coagulopathy e.g. ITP - steroid and Ig
stop anticoagulation and reverse effects - e.g. vit K

75
Q

how is the drip rate of an infusion calculated?

A

20 x ml in the bag
divided by time to run in minutes

use a clock and count the drips to make sure it is correct rate e.g. count drips over 10 seconds and times by 6

76
Q

how can we clinically assess cardiac output?

A

CO = HR x SV
SV can be assessed with ECHO and LVOT

however easier way = pulse pressure x1.75 is an estimate of SV.

otherwise cardiac output can be assessed based on clinical signs: perfusion of peripheries, strength of pulse, urine output.

barely palpable central pulse suggests low CO

77
Q

how is epistaxis managed?

A

if haemodynamically unstable: A+E, resuscitate, use first aid measures to control bleed in meantime.

if patient is stable: first aid measures:

  - get the patient to lean forward and open their mouth. (leaning forward reduces blood flow through nasopharynx and minimises swallowing of blood)
 - pinch cartilaginous (soft part of nose) firmly and hold for 10-15 mins whilst they breathe through mouth
 - ice pack on bridge of nose

if bleeding stops:

  • inspect nose with nasal canulae
  • consider applying topical antiseptic to reduce crusting and vestibulitis. Prescribe Naseptin (chlorhexidine and neomycin) cream for nostrils 4x daily for 10 days)

if bleeding does not stop:

  • if bleeding from posterior area of nose suspected (bleeding profusely from both nostrils and cant identify source with speculum exam) - admit to hospital
  • consider nasal cautery (silver nitrate or electical wire used to cauterise the site of bleed) or nasal packing ( can add adrenaline too)
78
Q

when should secondary care for a nose bleed be considered?

A

haemodynamic instability
<2 yrs old
underlying reason e.g. haemophilia, leukaemia
if there is comorbidity e.g. severe HTN, coronary artery disease.