1st random 100 Flashcards

1
Q

In TBI what is associated with poor outcomes?

A

Hypotension
Hypoxia
Poor jugular vein drainage
Spiking ICP
Hypertension

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2
Q

In capnography what do the angles represent and how might the change in a COPD patient?
alpha:
Beta:

A

Alpha: This represents the transition from dead space emptying to alveolar gas. This is often less pronounced in COPD due to uneven alveoli emptying and increased ETCO2.
Beta: This represents the transition from expiration to inspiration and often hyper angulated in COPD due to the increase in ETCO2 and the high levels that we see.

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3
Q

What are the strengths and weaknesses of Video laryngoscope?

A

Strengths:
- Ability to perform both DL and VL.
- Ability to audit.
- Others can see where you are at with obtaining a view (ELM).
- Great teaching aid

Weaknesses:
- Visual obstructions with white/pink out.
- May become obstructed in soiled airways.
- May forget to charge.
- Temperamental in extraem temperatures.

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4
Q

What presentations are we likely going to see with adrenal insufficiency?

A

Hypotension, Hyperpigmentation, Fatigue, Weight loss, Salt craving, Gastrointestinal, Abdo pain.
Will also see evidence of decreased aldosterone (hypoNa+ and hyperK+)

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5
Q

Anaerobic respiration is characterised by:

A
  • absent beta oxygenation
  • inability to access the citric acid cycle (Krebs cycle)
  • low production of ATP
  • over production of private which is converted to lactate.
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6
Q

What are the indications, contraindications and precautions of shoulder relocation?

A

Indications:
anterior Glenn-humeral dislocation, low energy.
Contraindications:
posterior Glenn-humeral dislocation, high energy injury, suspected clavicular or humeral #, acromio-clavicular dislocation.
Precautions:
large muscle masses, elderly, paediatrics, degenerative bone disease.

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7
Q

What is the dose of MgSO4 in pre-eclampsia?

A

20mmol

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8
Q

What is the MOA for fexofenadine and what is its primary role in allergies/anaphylaxis?

A

H1 (histamie)receptor antagonist which doesn’t cross the BBB.

It primarily has effects of preventing or treating urticria.

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9
Q

What are the length and weights for each IO needle?
Red)
Bleu)
Yellow)

A

Red) 3-39kg/15mm
Bleu) >20kg/25mm
Yellow) >40kg/45mm

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10
Q

when considering who would benefit from hospitalisation from a black spider bite?

A

≥ 4 hrs ago and no signs of funnel web sider bite, are unlikely to benefit from hospitalisation

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11
Q

what benefits does hydrocortisone have over prednisolone in adrenal insufficiency ?

A

hydrocortisone has greater minerocorticoid effects (increased K+ excretion). hydrocortisone was associated with less effects the liver but reduced control of oedema.

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12
Q

What is the risk of over oxygenation is some COPD patients?

A

increasing PAO2 is some aspects of diseased lung has the potential reverse hypoxic pulmonary vasoconstrictions. The vessels around these alveoli are filled with CO2 which would normally trickle into the vasculature. When the hypoxic vasoconstriction is reversed CO2 pools into the vasculature overwhelming gas exchange.

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13
Q

What is the significance of saturation on the R) hand in new borns?

A

Pre-ductal (before the ductus arteriosus) saturation give a fast reliable way of assessing lung function as blood travels straight from the left chamber to the R) subclavian

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14
Q

What is the risk of insulin therapy in DKA patients?

A

These patients often have a relative hyperK+ in the vasculature with a reduced k+ levels in the tissues. These patients have over the time of their disease progression excreted large amount of k+ through urine. The introduction of insulin will likely drive k+ into tissues with significant and rapid drop in k+ causing hypok+.

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15
Q

What is the MOA for benzodiazapines?

A

Potentates the effects of GABA increasing the influx of cl- ions hyperpolarising neurons.

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16
Q

What are the benifits/risks of fluid regiemes in trauma?

A

Prevention of coagulopathies through:
Maintaining perfusion
Haemodilution
Hypothermia
Hypercholoremic acidosis

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17
Q

why is it important to be overly cautious in reducing inferior shoulder dislocations with neuromuscular complications?

A

high likelihood of inferior dislocations (60% with axillary nerve impingement).

…..

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18
Q

Why is posterior glena-humeral shoulder dislocation reduced in hospital?

A

Injuries associated with Posterior dislocations include:
# tuberosity and humeral neck fractures, reverse Hill-Sachs lesions, and injuries to the labrum and rotator cuff.
Reduction in hospitable is important due to the forces that are likely required to reduce the shoulder.

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19
Q

What’s the risk of normal saline in the hypotensive pt with liver failure?

A

These patients have a large degree of hypoalbuminemia meaning that there is a significant reduction in oncotic pressure. Normal saline in these patients results in large fluid shifts as Na crosses into the tissue and fluid follows. These patients become oedematous quickly.

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20
Q

what are the considerations for prednisolone over hydrocortisone in Asthma?

A

Prednisolone has greater potency with high bioavailability when delivered orally. It also has an increased duration of action but is required to be taken orally.

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21
Q

You have a spinal patient who is presenting with hypertension and stroke like symptoms, what are your considerations?

A

this presents a difficult patient as GTN is contraindicated even if the cause of the stroke is from autonomic dysreflexia. Likewise the presentation of autonomic dysreflexia may present with similar signs of stroke.

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22
Q

What is the benefit of prednisolone over hydrocortisone in COPD?

A

The bioavaliability of prednisolone is 100% making it a more potent and effective gluccocortcoid steroid. It is also longer acting hence only the need to give it if patient haven’t had prednisolone within the last 24hrs.

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23
Q

Why might Ketamine be appropriate in prolonged seizures?

A

as seizures are prolonged GABA receptors/Cl- channels migrate within the cells meaning there is little action to be had. In the absence of being able to affect the resting membrane potential directly Ketamine may be able to reduce the excretory nature of the rapid depolarisation.

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24
Q

What is the starting Adrenaline dose for paediatrics in sepsis?

A

0.5microg/kg/min
ie 18kg pt would get 9 microg/min

adjusted dose is 0.1 microg/kg/min
ie 18kg pt would receive 1.8 microg/min

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25
Q

What is the MOA for atropine?

A

Muscirenic (ach) receptor antagonist => inhabiting of parasympathetic innervation at the sites of the SA and AV node.

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26
Q

What is the MOA in Droperidol for both nausea and agitation.

A

Nausea: D2 receptor antagonist acting in the CTZ to reduce stimulus.

Agitation: D2receptor antagonist in the brain, midbrain and brain stem. MOA is largely unknown.

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27
Q

What is the benefit of bougie and stylets in ETT?

A

Stylet:
- able to be bent to shape of airway.
- may be good in a low resource setting.
- able to be used in the heat when bougie/tube is floppy.
- able to be used in ETT < size 5.

Bougie:
- supported by literature.
- everyone is trained in this as a standard approach.
- able to oxygenate through it if stuck.

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28
Q

What is an adult IM dose of midazolam in agitation?

A

50 microg/kg up to a single Max dose 5 mg repeat up to a total max dose of 10mg.

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29
Q

What are your treatment options and considerations for each patient in wide comple tachycardia?

A

Fluid resuscitation

Amioderone (stable patient)
- caution in torsade due to risk of r on t.
- caution inhyperK+ and tricyclic overdose (qrs >200ms) due to Na+ channel effects of combined treatment.

Cardioversion (+/- midazolam)

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30
Q

what is the dose and considerations for Ketamine for sedations?

A

Dose: 25-50mg

Considerations:
Setting up for potential over (partial) sedation.
Team is prepped and roles allocated.
Patient is briefed about the process.
Patient is briefed about the potential dreams.

therapeutic dose and use of Midazolam/Fentanyl should also be considered. Pt’s will likely be traveling through multiple therapeutic ranges (disassociated, emergent and analgesic) during their time with you.

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31
Q

What is the MOA for ipratropium in bronchospasm?

A

Muscarenic (Ach) 3 receptor antagonist => inhibits intracellular messaging that contributes to mucus production and bronchospasm.

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32
Q

how often and to what extent do we see hypotension with paracetamol?

A

Most commonly seen in the septic patients and/or patient with large surface area’s (paeds), in these groups a drop of 5-15mmHg SBP may be seen in up to 20% of patients. This is thought to be related to the dulling of thermoregulation in these disease processes.

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33
Q

What is the MOA for adrenaline in the peripheral vasculature?

A

a1 receptor agonise => cAMP => increased intracellular Ca+ => increased myosin/actin interaction => peripheral vasoconstriction.

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34
Q

What are our checks for conformation of ETT placement?

A
  • Visualisation
  • Positive ETCO2
  • Rise and fall of the chest
  • Auscultation
  • Misting in the tube
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35
Q

What is Neuroleptic malignant syndrome and pheochromocytoma and their relevance to practise?

A

Both are contraindications for the Droperidol administration.

Neuroleptic malignant syndrome: caused by antipsychotic agents and characterised by mental status change, rigidity, fever, and dysautonomia.

Pheochromocytoma (paradoxyal HTN):
adrenal gland tumour in the medulla characterised in fluctuating catecholamine release causing head aches, HTN and diaphoresis.

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36
Q

What is the role of bicarbonate?

A

H2O + CO2 = H2CO3 = HCO3 + H.

a constant state of flux occurs where carbon dioxide and free hydrogen ions are able to be buffered to ensure that pH is maintained.

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37
Q

What are the key components that cause a R) ward shift on the oxygen-haemaglobin disassociation curve? and what is it’s significance?

A

Factors:
increased temp
increased DGP
increased CO2
decreased pH

This results in reduced affinity for oxygen to haemoglobin (SpO2 drops faster and harder to re-establish)

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38
Q

In the dialysis renal patient, what piece of information may help drive your fluid regime?

A

These patients will likely know their urine out put and pre/post dialysis weight.

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39
Q

what are the preferred sites for IO access and what are two alternate sites which may be considered.

A

Primary sites:
proximal tibia and humeral head.

Alternate sites:
distal tibia and distal femur.

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40
Q

What is the likely occurrence and cause of a posterior Glenn-humeral dislocation and what will is look like?

A

Occurrence:<5%
Causes:
Seizures, outstretched arm with inward rotation forward falls.
Presentations:
bilateral dislocations, patient holds the arm in adduction and internal rotation, prominent coracoid process.

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41
Q

Why in newborn cardiac arrest do we focus on ventilation initially as opposed to oxygenation?

A

Patients transitioning from interuterine life to extra uterine life haven’t previously had to rely on oxygen from their lungs. In these patients they have significant hypoxic pulmonary vasoconstriction due to collapsed and mucused filled alveoli. This must fist be reversed prior before gas exchange may occur.

42
Q

What should a normal QTc be?

A

Males: 440ms
Females: 460ms

43
Q

GTN is contraindicated with use of PDE-5 inhibitors. What drugs are in this drug class? And why

A

24hrs:
Sildenafil
Verdenafil
Avanafil

48hrs:
Tardalafil

Due to the inhibition of metabolism.

44
Q

What is the MOA for hydrocortisone in adrenal insufficiency?

A

Hydrocortisone has synergistic effects with adrenaline/nor-adrenaline on adrenoceptors

45
Q

What are the risks of treating Opioid overdose with naloxone?

A
  • pt’s may be aggressive on waking up.
  • pt’s may leave the scene uninformed of naloxone half-life risk.
  • patient’s may experience negative pulmonary oedema in the case of rapid introduction naloxone.
  • Naloxone induced withdrawal.
46
Q

What methods are used for the reduction of anterior Glenn-humeral shoulder dislocations?

A

Cunningham Method
Scapular manipulation
Stimson method

47
Q

What are the precautions and contraindications for Droperidol?

A

Precautions:
age <16 or >65yo
15-20min onset time

Contraindications:
parkinsons
allergies
Neuroleptic malignant syndrome
Phaeochromocytoma

48
Q

What is the MOA for Aspirin in ACS?

A

Aspirin inhibits COX-1 → inhibition to form prostaglandins → decreased release of Thromboxane A2 by activated platelets → inability to further build clot.

49
Q

What are the three qSOFA principles for identifying sepsis in patients?

A

Hypotension - SBP <100mmHg
Altered mental status
Tachypnoea - RR >22

50
Q

What are some contraindications for the insertion of an IO?

A
  • Fracture to the bone.
  • Infection of the site of insertion.
  • Prosthetic limb
  • IO in last 48hrs
  • ## Previous Orthopaedic surgery to the site.
51
Q

What is the MOA for MgSO4 in Pre-eclampsia?

A

Theory:
1) stabilises and increase threshold potential in CNS through its effects on NMDA receptors.

2) opposes Ca+ dependent vasoconstriction off cerebral vasculature stabilising BBB.

52
Q

What is the mechanism by which normal saline 0.9% may cause acidosis?

A

in measuring the anion gap we recognise that Cl- and HCO3- are the most prevalent anions. By introducing large amounts of Cl- ions the bicarbonate must move else where. It does this by moving into the tissues. The overall effect is the net loss of bicarbonate.

53
Q

What is the MOA for amioderone

A

Amioderone is primarily a class 3 antiarrhythmic which prolongs the efflux of k+. This then increases the absolute refactory period and reduces the time in which myocytes can’t be depolarised.

54
Q

How does Ketamine affect blood pressure and how might this change in different patients?

A

Ketamine has synergetic adrenergic effects. This means that it will potentiate already circulating catecholamines such as nor-adrenaline. In instances of prolonged shock these patients are likely to be catecholamine fatigued where ketamine will probably induce some level of further shock.

55
Q

What changes are you going to make for a paediatric cardiac arrest including drug doses?

A
  • Focus on hypoxia and hypovolaemia.
  • Cardioversion 4J/kg
  • Adrenaline 10 microg/min
  • Amioderone 5mg/kg
56
Q

Cyanide poisoning causes what to happen to aerobic respiration?

A

An inability to access beta oxygenation in The mitochondria.

57
Q

Which of these is likely appropriate for shoulder relocation in the pre-hospital setting?
a. sub corticoid
b. sub clavicular
c. intra thoracic
d.sub glenoid

A

a. subcorticoid

58
Q

what characteristics are cause for non-initiation of CPR?

A

-ADC
- Pt made their wishes known to family
-Rigor mortis
- Morbid lividity (blood pooling)
- Injuries incompatible with life
- > 30 mins with no CPR prior to SAAS arrival

59
Q

What two different ketamine regimes may be used and what is the indication of either?

A

25-50mg bolus:
this may be repeated once and is for planed extrication. Prep and consideration to ongoing care is important in these cases.

10.5-18mg/hr infusion either through a manual infusion or driver for analgesia.

60
Q

What is your treatment options for a narrow come tachycardia? What are your considerations for irregular rhythms?

A

We want to consider origin (ie if it’s a re entry circut that is dependent on the av node or independent of the av node). This may be indicated by the regularity, morphology or presence of a p wave.
- Fluid administration to increase ventricular filling.
- modified valsalva
- adenosine
- cardioversion

61
Q

How does the CNS contribute to retention of CO2 in COPD?

A

The blood brain barrier is an independent compartment within the body. CO2 can cross the membrane H2CO3 can not => chemoreceptors within the BBB become dulled to these high levels of H2CO3 resulting in a decrease in sensitivity and reduced expiration of CO2 from vasculature.

62
Q

What is the MOA of Ketamine?

A

Largely a glutamate receptor antagonist with both NMDA and AMPA receptor effects. This affects our ability to perceive pain. It may also have effects on opioid receptors.

63
Q

What is the MOA for Naloxone in overdose patients?

A

competitive opioid antagonist

64
Q

What is the drug dose for:
1) Amioderone cardiac arrest 4yo:
2) MgSo4 12yo:
3) Cardioversion 8yo:
4) Amioderone conscious vt 6yo:

A

1) 5mg/kg = 80mg/1.6ml
2) 0.1mmol/kg=4.3mmol/2.2ml
3) 1J/kg =35J
4) 5mg/kg = 125mg/2.5ml

65
Q

What is the IV Midazolam dose for patient with Traumatic brain injury, hypoxic brain injury and post-ictal agitation with SBP >110mmHg.

A

14 to 64 yrs - up to 1 mg
≤ 65 yrs - up to 0.5 mg

slow push over ≥ 1 min
repeat every 5 mins prn
reassess after each dose
total max dose 5 mg

66
Q

What is the MOA for TXA?

A

TXA competitively and reversibly inhibits the activation of plasminogen → plasminogen + fibrin = fibrinolysis

67
Q

What modification in hypothermic cardiac arrest from normal practice?

A

tympanic temperature < 30°C:
max 3 defibrillations
withhold cardiac arrest drugs

tympanic temperature 30 - 35°C:
double drug administration intervals
otherwise normal resuscitation

68
Q

What are the differential diagnosis for bradycardia?

A

Cardiac disease
Hypoxia
Electrolytes disturbance (hyperK+)
Medications
Toxins
Hypothermia
Hypothyroid
Raised ICP
Infections
Physiological (vagal stimuli)

69
Q

What does MR SOPA stand for?

A

Mask
Reposition

Suction
Open mouth
Pressure
Airway

70
Q

What are the primary and secondary causes of adrenal insufficiency ?

A

Primary: Addison’s disease (TB was the likely cause which has been overtaken by autoimmune)
Secondary causes – autoimmune, genetic, TBI, stress, infection

71
Q

What are the main neurotransmitters responsible for mental instability?

A

Dopamine
Serotonin
Nor-adrenaline
Glutamate

72
Q

What is the MOA for Paracetamol in pain?

A

It is thought to be an indirect COX inhibitor which doesn’t affect the peripheral tissue, this means that it does not exhibit anti-inflammatory effects.

Other theories include:
central substance P inhibition and canabanoid receptor stimulation.

73
Q

What is the MOA for GTN in ACPO?

A

Nitric oxide →increased cGMP → Ca+ efflux → decreased myosin actin filament constriction → peripheral Vasodilation → increased venous pooling → deceased preload → decreased R) SV → pulmonary hydrostatic pressure.

74
Q

What is the MAP for the following blood pressures:
1) 120/50
2) 105/40
3) 160/50
4) 85/40

A

1) 73
2) 61
3) 86
4) 55

75
Q

What is the MOA for MgSO4 in bronchospasm?

A

magnesium disrupts Ca2+ influx through voltage-gated ion channels, resulting in less Ca2+ available for muscle contraction.

76
Q

What is the MOA for Adenosine?

A

Adenosine 1 receptor antagonist → Inhibits activation of Adenylate cyclase and reduces cAMP →increasing K+ efflux → hyperpolarise AV node → decreased AV nodal conduction

77
Q

What is the MOA for MgSO4 in Torsades de pointes?

A

In Torsades de Pointes (TdP), magnesium suppresses early after-depolarisations by reducing Ca2+ influx into cardiomyocytes.

78
Q

What role does oxygen play in the heart failure?

A
  • Oxygenation optimises both the diastolic and systolic dysfunction of the heart.
  • Reliant on aerobic respiration the heart depends on constant perfusion for ATP production, essential for myosin-actin filament contraction and relaxation
79
Q

What is the MOA of Levetiracetam in seizure Patients?

A

Mechanisms mainly unknown:
binds to the synaptic vesicle protein SV2A on the pre-synaptic => decreased exocytosis.

May also potentiate GABA

80
Q

What is the MOA of glucocorticoid steroids in inflammatory process?

A

binding to DNA → transcription or regulation of specific mRNA’s → induction or repression of particular genes → increased or decreased synthesis of specific proteins → generation or suppression of inflammatory mediators

81
Q

What is the aetiology of toxic effects from paracetamol overdose?

A

metabolism of paracetamol occurs naturally with minimal effect due to its binding with glutathione. In excess where glutathione and sulphate pathways have been exhausted paracetamol is metabolised through the CYP2E1 pathway. This results in hepatic and renal tubular necroses. N-acetylcysteine (NAC) assists in the metabolism of unchanged drug.

82
Q

In relation to COPD why is the CNS sensitive to respiratory acidosis as opposed to metabolic acidosis?

A

CO2 is able to diffuse across the BBB where as H+ ions are not. This results in CNS being sensitive to CO2 as opposed to metabolic acidosis.

83
Q

What is the benefits of lorazopam over midazolan in agitated patients?

A

Lorazamap has a longer duration when compare to that of midazolam meaning that will have both a positive and negative effect in different patiet groups. The main difference coming from the empowerment of patients having a say in their on treatment pathways. This includes benefits such as:
Shared decision-making.
Better future engagement.
Reduced “drop out” from care.
Better understanding of care.

84
Q

What is the MOA for Ondansetron?

A

5-HT3 receptor antagonist preventing the transmission of vagal stimulation to the CNS for nausea and vomiting.

85
Q

What are the indications for TXA? and what are some of the practical essentials?

A

Significant trauma with a SBP < 90mmHg and or HR >120
PPH defined as 500ml blood loss within 24hours of delivery.

Ideally this is delivered over 2-3min within 3 hours of injury. Best success is seen when delivered in the first 15 min.

86
Q

In assessing PPH what is the main considerations?

A

Temperature management
Assess fundus
Assess external labia and perineum
Encourage patient to empty bladder
Facilitate skin to skin contact

87
Q

What is the MOA for adrenaline in cardiac tissues?

A

B1 receptor agonise = increased cAMP => increased Ca+ => resting membrane potential and myosin/actin binging due to displaced tropariosin => increased FOC/HR/conduction (ie. Chronatropic, dromatropic, ionotropic effects)

88
Q

Explain the difference between diastolic and systolic dysfunction in ACPO

A

Diastolic dysfunction is seen an inability to muscle to relax. This may be due to an inability to relax the muscle as in anoxia or physical obstruction such as hypertrophic myopathy.
Systolic disfunction relates to an inability to overcome the after load to sufficiently empty the ventricle (ie increased systemic vascular resistance, anoxia or cardiomyopathy relating to dilation.

89
Q

What occurs at each phase of the pacemaker action potential?
Phase 4:
Phase 0:
Phase 3:

A

Phase 4: Initial phase of inflection with slow Na+/Ca+ influx
Phase 0: Threshold is met with depolarisation and rapid Ca+ influx
Phase 3: Depolarisation K+ efflux

90
Q

What is the MOA for salbutamol and adrenaline in bronchospasm?

A

B2 receptor agonise => cAMP => Ca+ secured to the sarcoplasmic reticulum (unavailable for intracellular processes) => myosin actin filaments unable to interact => smooth muscle relaxation in the bronchiols

91
Q

What are the considerations for IV GTN in ACPO patients and what adjustments might you make based of blood pressure values?

A
  • contraindicated in PDE-5 inhibitors.
  • SL GTN dose and serum levels don’t always outweigh IV GTN (ie higher indication in CPAP)
  • Only begin if SBP above 120mmHg
  • If SBP drops below 110mmHg stop wait for SPB to rise and begin at half initial dose.
  • May increase by 5 microg/5min
92
Q

What is the pathophysiology of torsadas de point?

A
  • prolonged qt reflects prolonged repol due to ion channel malfunction.
  • prolonged repol = early after depol.
93
Q

At what dose does GTN begin to affect systemic vascular resistance?

A

100micrograms/min

94
Q

In traumatic brain injuries what is our goal in regards to BP.

A

MAP ≥ 90 mmHg or SBP ≥ 110 mmHg.

95
Q

what length black spiders pose a risk to humans?

A

> 2cm

96
Q

In adrenal insufficiency what metabolic disorders may we see?

A

Hyperglycaemia
HypoNa-
HyperK+

97
Q

What are the four T’s of PPH?

A

Tone
Trauma
Tissue
Thrombin

98
Q

What is the focus of care from blue ringed octopus bites?

A

focus on airway and ventilation due to paralysing effects of venom.

99
Q

What are the potential negative effects of adrenaline?

A

Increased preload/afterload increasing ATP demand in the myocardial tissue.

Ionotropic effects may lead adrenaline to increase automaticity/conduction leading to it being a pro arrhythmic drug.

100
Q

What are the four H’s and T’s?

A

Hypoxia
Hypovolaemia
Hyper/hypokalemia hypoglycaemia/calcaemia
Hypothermia

Thrombus
Tension pneumothorax
Tamponade
Toxin

101
Q

What do each of the phases of capnography represent?
Phase 1:
Phase 2:
Phase 3:
Phase 0:

A

Phase 1: inspiration/inspiratory pause.
Phase 2: initiation of expiration with dead space slowly increasing.
Phase 3: plateau phase with alveoli emptying sustained.
Phase 0: start of inspiration.