Foundation Exam Flashcards

1
Q

What are the 6 principles of high performance CPR?

A

Continuous high quality compressions, correct pad placement, early airway management, refined pharmacological prioritisation, emphasis on non-technical skills, clinical case review and debrief.

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2
Q

What are the 8 patient cohorts that require consult within 15 minutes of commencing CPR?

A

a. Patients >18 years of age
b. Hypothermia, temp >32 degrees
c. Suspected toxicology/toxinology cause
d. Post QAS fibrinolysis administration
e. Pregnancy (clinically apparent)
f. STEMI diagnosed by 12 lead prior to arrest
g. Suspected PE
h. Evidence of CPR induced consciousness

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3
Q

Why is optimal pad positioning important?

A

Optimal defib pad positioning ensures transmyocardial current density is maximised and has been proven to improve shock efficacy

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4
Q

What is the correct placement of Antero lateral pads?

A

a. Anterior pad should be placed to the right of the sternum below the clavicle
b. The lateral pad should be placed at the level of 5th intercostal space on the mid axilla line (where V6 electrode would be places.

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5
Q

What is the stepwise approach to airway management in cardiac arrest?

A

a. Being with basic adjuncts such as BVM, OPA/NPA or i-Gel insertion.
b. I-Gel should be used early if the patient presents with a patent airway clear of any soilage or vomitus
c. If the patient is able to be ventilated effectively with an i-Gel it should not be removed.
d. Escalation to intubation should only occur if the i-Gel is not effective at providing adequate ventilation.

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6
Q

In regards to pharmacological prioritisation in resuscitation, when should adrenaline and amiodarone be used?

A

a. Adrenaline should be prioritised in patients that present with non-shockable rhythms. This should not be prioritised over high quality compressions and defibrillation.
b. Amiodarone should be prioritised over adrenaline in patients with shockable rhythms that are refractory to 3 defibrillation attempts.
c. When the patient is in a shockable rhythm and they are refractory to the defibrillations they are in a refractory shockable rhythm. Amiodarone should be prioritised over adrenaline.

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7
Q

How much sodium chloride should be used to flush medications in cardiac arrest?

A

10-20mL sodium chloride.

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8
Q

What are the 5H’s and 4T’s of cardiac arrest?

A

a. The Hs and Ts are the reversible causes of sudden cardiac arrest
b. Hypoxia
c. Hypothermia
d. Hypovolaemea
e. Hyper and hypokalaemia
f. Hydrogen Ions (acidosis)
g. Tension Pneumothorax
h. Toxins
i. Tamponade
j. Thrombus

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9
Q
  1. What are the two categories of bradycardia?
A

a. Cardiogenic and non cardiogenic
b. Cardiac = diseased conduction system
c. Non-cardiac = environmental conditions (hypothermia), metabolic and endocrine disorders, and toxicology causes

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10
Q

What are the 6 ECG changes to differentiate other broad complex tachycardias with VT? (Wellen’s Criteria)

A

a. AV dissociation
b. Left axis deviation or extreme axis deviation
c. QRS >0.14 seconds
d. Fusion or capture beats present
e. Precordial QRS concordance – both positive and negative QRS concordance
f. R’SR pattern in V1, or monophasic QS in V6

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11
Q

What are the signs of haemodynamic compromise from broad complex tachycardia?

A

ALOC, hypotension, chest pain, and heart failure

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12
Q

How do you treat hemodynamically stable broad complex tachycardia and hemodynamically unstable?

A

a. stable – amiodarone or magnesium sulphate if torsades des pointes
b. unstable – electrical cardioversion

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13
Q

Why should patients with AF of >24 hour duration not be cardioverted?

A

Due to risk of thrombus formation

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14
Q

What are the 4 signs of shoulder dystocia?

A

a. Prolonged or difficult birth of the face and chin
b. The head is birthed but remains tightly applied to the vulva
c. Turtle sign – after birth of head, chin retracts into perineum when the birthing parent stops pushing
d. The foetal head fails to undergo restitution

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15
Q

What are the manoeuvres in shoulder dystocia designed to do?

A

a. Increase the functional size of the pelvis
b. Change relationship of the biacromial diameter within the bony pelvis by rotating the foetus into the wider oblique diameter
c. Decrease the bisacromial diameter of the foetus

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16
Q

What are 3 first line external manoeuvres for shoulder dystocia?

A

a. Mcroberts
b. Supra pubic pressure
c. All fours

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17
Q

What are the three types of uterine inversion?

A

a. Incomplete – the fundus reaches the cervix but does not pass through it
b. Complete – the fundus passes through the cervix
c. Prolapsed – the fundus extends through the vaginal opening

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18
Q

What is the management for cord prolapse?

A

a. Ask mother to replace exposed cord inti the vagina using a dry towel or pad
b. If cord is not pulsating attempt to push the presenting part off the cord
c. Transport in the exaggerated sims position – left lateral with pillow under hip

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19
Q

What is the very brief pathophys of anticholinergic toxidrome?

A

Competitive antagonism at the muscarinic receptor.

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20
Q

What types of drugs have anticholinergic effects?

A

a. Antispasmodics
b. Antihistamines
c. Antipsychotics
d. Tricyclic antidepressants
e. Anti-Parkinson agents
f. Belladonna alkaloids (atropine, nightshage

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21
Q

What are the effects of anticholinergic syndrome?

A

a. Dilated pupils
b. Tachycardia
c. Dry, flushed skin
d. Urinary retention
e. Hyperthermia
f. Hallucinations,
g. Agitation and delirium
h. Seizures
i. Coma

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22
Q

How do benzodiazepines work?

A

Benzodiazepines work by potentiating the effects of inhibitory neurotransmitter GABA within the CNS there by causing sedation

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23
Q

What does profound coma suggest in the context of benzodiazepine overdose?

A

Co-ingestion with another CNS depressing agent such as alcohol

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24
Q

What are the symptoms of benzo overdose?

A

a. Drowsiness
b. Ataxia
c. Slurred speech
d. Decrease level of consciousness
e. Hypotension and bradycardia (only in large ingestions)

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25
Q

What are the symptoms of beta-blocker overdose?

A

a. Bradycardia
b. Hypotension
c. Heart block
d. Cariogenic shock
e. Hypo and hyperglycaemia
f. Pulmonary oedema
g. Seizures, coma

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26
Q

What are the two particularly toxic beta blockers and why?

A

a. Propranolol – sodium channel blocker that crosses the blood brain barrier. Causes seizure, coma, and QAS widening due to sodium channel blockade
b. Sotalol – potassium channel blocker that causes long QT and torsades
c. P propranolol is opposite of sotalol – P should be potassium blocker but is sodium blocker. S should be sodium blocker but is potassium blocker.

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27
Q

What do calcium channel blockers cause in overdose?

A

a. CCB cause hypotension and vasodilatory (distributive) shock in overdose
b. Seizures
c. Coma
d. Hyperglycaemia
e. Metabolic acidosis

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28
Q

What are the two most toxic CCBs?

A

a. Diltiazem and verapamil
b. Diltiazem and verapamil act on CCBs in the myocardium causing slow heart rate and decreased myocardial contractility. This results in combination of the vasodilation and hypotension plus bradycardia and cardiogenic shock.

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29
Q

What is the treatment for calcium channel toxicity?

A

Calcium gluconate

30
Q

How does amiodarone work?

A

Amiodarone prolongs the duration of the action potential and therefore the refractory period of atrial, nodal, and ventricular tissues.
It also reduces conduction across all cardiac tissue including myocardial and conduction system cells.

31
Q

What class of anti-arrhythmic drug is amiodarone?

A

Amiodarone is an anti-arrhythmic drug that specifically is a Class 3 anti-arrhythmic but also demonstrates electrophysiology across all Vaughan-Williams class groups.

32
Q

Amiodarone can cause QT prolongation which can result in what? And what is the treatment?

A

Amiodarone can cause QT prolongation which can result in torsades des pointes.
To treat this magnesium sulphate should be administered.

33
Q

If a patient is taking oral amiodarone can IV amiodarone still be administered in cardiac arrest?

A

Yes in cardiac arrest but not in patients with sustained conscious VT.

34
Q

What class of drug is atropine?

A

Anticholinergic/antimuscarinic

35
Q

How does atropine work?

A

Atropine works by inhibiting the action of the parasympathetic nervous system allowing an uncalled sympathetic response.
Atropine blocks the action of the vagus nerve on the heart which increases the rate of SA node and of conduction through the AV node.
Atropine also blocks exocrine gland activity thereby reducing secretions.

36
Q

What class of drug is ketamine? (2 classes)

A

Anaesthetic
Analgaesic

37
Q

What receptor does ketamine work on and in what way?

A

Ketamine is an NMDA receptor antagonist

38
Q

What does ketamine do at low doses?

A

At low doses ketamine produces significant analgaesic properties while preserving the airway reflexes and respiratory drive.

39
Q

What does ketamine do at high doses?

A

At high doses ketamine can be used as an induction gent for anaethesia

40
Q

What is the benefit of ketamine as an induction agent?

A

Unlike other induction agents, ketamine produces only minimal haemodynamic compromise since it acts as a sympathomimetic agent.

41
Q

What type of drug is midazolam?

A

Midazolam is a benzodiazepine

42
Q

What effect does midazolam have?

A

Midazolam is a short acting CNS depressant that induces amnesia, anaesthesia, hypnosis, and sedation.

43
Q

How does midazolam work?

A

Midazolam binds to a specific site on the GABA receptors, enhancing binding of GABA and increasing the activity of the receptor.

44
Q

What drug class is ticagrelor?

A

Ticagrelor is an anti-platelet.

45
Q

How does ticagrelor work?

A

Ticagrelor is a reversibly binding, direct-acting adenosine diphosphate ADP receptor antagonist that inhibits platelet activation and aggregation.

46
Q

What drug class is clopidogrel?

A

Clopidogrel is an antiplatelet

47
Q

How does clopidogrel work>?

A

Clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet receptor thereby inhibiting platelet aggregation

48
Q

What drug class is Tenecteplase?

A

Tenecteplase is a fibrinolytic

49
Q

How does tenecteplase work?

A

Tenecteplase combines with the fibrin component of the thrombus and converts thrombus bound plasminogen into plasmin. This degrades the fibrin matrix of the thrombus.

50
Q

Airway position: what is the goal of airway positioning?

A

To align the oral, pharyngeal, and laryngeal axes.
This is achieved by aligning the auditory meatus with the sternal notch

51
Q

How do you align the airway axes in infant, small child, and older child/adult?

A

Infant - slight elevation of shoulders
Small child - slight extension of head
Olderchild/adult - extension of hear (elevation of head may also be necessary)

52
Q

What are the 5 complications of direct laryngoscopy?

A

Laryngospasm
Hypoxia due to delays in oxygenation while performing the procedure
Trauma to the mouth or upper airway
Exacerbation of underlying c-spine injuries
Vomiting/regurgitation

53
Q

How do you measure an orogastric tube?

A

From the tip of nose to the earlobe then to the xiphisternum then mark the length with a pieve of tape.

53
Q

What are the 5 complications of SGA or iGel?

A

Failure to provide adequate airway or ventilation
Patient intolerance
Hypoxia
Can precipitate vomiting and aspiration in a patient with intact airway reflexes
Oropharyngeal trauma

54
Q

What are the four reversible causes of traumatic cardiac arrest?

A

Hypovolaemia
Hypoxaemi
Tension pneumothorax
Tamponade
(HOTT)

55
Q

What are the standard post-ROSC cares?

A

Support ABC, maintain cerebral perfusion, manage dysrhythmias

12 lead ECG
Maintain spo2 >94%
Maintain BP >100 for adults and >80 for paediatric
Maintain ETCO@ 30-40mmHG

56
Q

Briefly explain V/Q mismatch.

A

V/Q mismatch is when a part of your lung receives oxygen but there is no blood flow or when there is blood flow to the lung but no oxygen.

57
Q

What is the V/Q ratio?

A

The V/Q ratio is is the amount of air entering lungs vs amount of blood flow through pulmonary capillaries.
Normally 4 litres of air and 5 litres of blood which equals a ratio of 0.8

58
Q

In VQ mismatch, what is shunt?

A

Shunt is when there is blood flow to the alveoli but no ventilation

59
Q

In VQ mismatch what is dead space?

A

Dead space is when the alveoli are well ventilated but there is now blood flow to the alveoli. This means these alveoli are not participating in gas exchange.

60
Q

What are the three types of dead space?

A

Anatomical - conducting zones like bronchioles, bronchi, trachea
Physiological - asthma, pneumonia, COPD, shock, PE

61
Q

Does ventilation equipment contribute to dead space or shunting?

A

Dead space

62
Q

What are the 9 components of the respiratory status assessment?

A

Conscious state
General appearance
Speech
Ventilatory rate
Ventilatory rhythm
Ventilatory effort
Skin
Pulse rate
Breath sounds

63
Q

What are the 4 components of the perfusion status assessment?

A

Skin
Pulse
BP
Consciousness

64
Q

What are the 5 components of the neurological status assessment?

A

Level of consciousness
Pupils
Motor function
Sensory function
Vital signs

65
Q

During a neurological status assessment, what would widening pulse pressure and slowing heart rate signify?

A

Rising ICP

66
Q

Does calcium reduce serum potassium in hyperkalaeima?

A

No, it only stabilises the myocardium

67
Q

Does sodium bicarb reduce serum potassium levels in hyperkalaemia?

A

Yes it reduces serum potassium levels by 0.5-1.0mmol

68
Q

Does salbutamol reduce serum potassium levels in hyperkalaemia?

A

Yes with continuous nebulisation over 30 minutes it will reduce serum potassium levels by 0.5-1.0mmol

69
Q

What is considered normal tidal volume?

A

7mL/kg

70
Q
A