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Module 7 > Knowledge Questions > Flashcards

Knowledge Questions Flashcards

1
Q

What is the difference between primary and secondary PPH?

A

Primary within 24 hours from birth, secondary within 24 hours - 6 weeks post birth

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2
Q

List patients that are high risk for PPH

A

Multiple pregnancy, more than 4 pregnancies, phx of PPH, phx of APH, large baby

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3
Q

Define PPH

A

Blood loss greater than 500mL in the first 24 hours from birth

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4
Q

Describe the four T’s

A

Tone - atonic uterus not contracting causing haemorrhage, can be due to polyhydramnios, multigravida, prolonged labour or rapid delivery, Trauma (to genital structures) - can be due to placenta previa (placenta covers cervix) or placental abruption (placenta detached from the wall of the uterus), Tissue (retention of placenta or membranes causing atony), Thrombin (coagulopathy) - fibrin deposit at maternal blood vessels causing endothelial damage, decreases maternal coagulation

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5
Q

What is the goal of fundal massage and how does it work?

A

Fundal massage is thought to promote uterine contraction through local prostaglandin release which can cause the uterus to contract to reduce bleeding (bleeding commonly occurs after the placenta has detached from the uterus and is birthed and the vessels that were connecting it remain uncontracted and bleed).

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6
Q

How does oxytocin assist PPH? (Mechanim of action)

A

Oxytocin is a synthetic pituitary gland hormone that stimulates uterine muscle contraction which aids PPPH as uterine atony is the most common cause

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7
Q

Why do we provide O2 to this patient? Under which specific guideline?

A

Hypoxia is one of the leading causes of uterine atony and increases oxygenenation through inhaled 100% O2 can promote uterine contraction in the haemorrhaging patient. High flow O2 is indicated under the oxygen therapy guideline.

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8
Q

What symptoms would we see in this patient? Why? (patho -hypovoloaemic shock)

A

Dizzy, nauseous, pale, altered conscious state, weak, abdominal pain, abdominal distention, PV bleeding

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9
Q

What is Cushing’s triad and why does it happen?

A

Hypertension (widened pulse pressure) due to detection of poor CPP due to haemorrhage body compensations by inducing a sympathetic response to increase blood pressure and therefore perfusion to the brain, baroreceptors detect a sudden rise in BP and create a parasympathetic response resulting in bradycardia, irregular respirations occur due to pressure on the brain stem which controls breathing

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10
Q

What is Cushing’s triad and why does it happen?

A

Hypertension (widened pulse pressure) due to detection of poor CPP due to haemorrhage body compensations by inducing a sympathetic response to increase blood pressure and therefore perfusion to the brain, baroreceptors detect a sudden rise in BP and create a parasympathetic response resulting in bradycardia, irregular respirations occur due to pressure on the brain stem which controls breathing

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11
Q

Define concussion

A

When the brain shakes within the skull due to mild-moderate force causing shearing of neurons without structural damage - can cause confusion, LOC, drowsiness and visual disturbances

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12
Q

What is the formula for CPP?

A

CPP = MAP - ICP

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13
Q

What is normal ICP range?

A

5-15mmHg

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14
Q

List the three priorities under care objectives for head injury

A

Optimize ventilation, oxygen and cerebral perfusion - in order to prevent secondary brain injury A B C

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15
Q

What is a secondary head injury?

A

Occurs after the initial insult due to ongoing ischaemia, oedema and haemorrhage

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16
Q

Occurs after the initial insult due to ongoing ischaemia, oedema and haemorrhage

A

“Damage to brain and skull through trauma
Shearing / tearing of neurons or vessels
Blood leaves intravascular space causing oedema
Swelling in fixed cranium increases ICP
Detected by body, increases MAP to improve cerebral perfusion
Bleeding and oedema worsens, ICP increases
Baroreceptors detect HTN and parasympathetic response causes bradycardia
Pressure on brain stem causes coning and irregular respirations
Cerebral herniation, papilloedema, vision problems, nausea vomiting, ALOC, cerebral ischaemia”

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17
Q

Why do we avoid NPA or OPA?

A

Has the potential to induce gag reflex therefore vomiting which will further raise ICP

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18
Q

What are our target vitals for managing TBI?

A

SPO2>95%, EtCO2 30-35, ventilate at 6-7mls/kg, BP>120

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19
Q

Why do we withold midazolam in the combative head injured patient?

A

Hypoxia is one of the “H’s” causes of secondary brain injury. Midazolam may cause respiratory depression which could worsen cerebral hypoxia, therefore copious pain relief or ketamine is the preferred method of sedation.

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20
Q

What is the recommended on scene time for major trauma?

A

20 minutes for non-trapped major trauma patient

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21
Q

When to consider respiratory tract burns?

A

Burns to upper face, neck and torso, airway oedema, singed facial hair, sooty sputum, hypoxia, enclosed space, respiratory distress (BOSSHER)

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22
Q

Why do electrical burns put kidney function at risk?

A

During electrocution when organs such as the kidneys come in the circuit of the current it can cause significant cellular damage. Additionally, electrical injury to muscles can cause leaking of myoglobin through rhabdomyolysis which can cause renal failure from renal vasoconstriction and direct myoglobin toxicity.

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23
Q

What are the major burns services in Victoria?

A

Alfred or RCH - transport here if within 60 minutes

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24
Q

Describe pathophysiology of burns

A

“Exposure to heat causing cell damage / death
Release of inflammatory mediators
Increased vascular permeability and vasodilation to allow recruitment of mediators
Fluid shift from intravascular to interstitial space (relative fluid loss)
Hypotension, compensatory tachycardia
Hypothermia due to inability to retain heat through skin and fluid loss
Large TBSA can cause SIRS = tissue hypoperfusion, MODS and death”

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25
Q

Type of fluid loss associated with burns

A

Relative and Actual

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26
Q

Describe the 5 H’s of secondary brain injury

A
  1. Hypoxia
    • Neurons need oxygen to maintain aerobic respiration and function normally
  2. Hypotension
    • Neurons need adequate CBF in order to maintain oxygenation status
  3. Hypoglycemia
    • Neurons need adequate glucose supply to function normally
  4. Hypercapnia
    • Increased CO2 levels in the blood cause vasodilation & increased bleeding
  5. Hypocapnia
    Decreased CO2 levels in the blood cause vasoconstriction & reduced CBF
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27
Q

Define SVT

A

Tachydysrhythmia arising from above the ventricles (bundle of His)

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28
Q

What is the difference between AVNRT and AVRT?

A

AVNRT (more common) is often triggerred by a PAC that arrives while an impulse is travelling down the slow pathway as the fast pathway is still refractory, then as that refractory period ends it travels retrogradely up the fast pathway and gets stuck in a circuit between the two pathways in the bundle of HIS. AVRT is due to an accessory pathway that exists, e.g. in patients with WPW; with a PAC the accessory pathway can form a re-entry circuit between it and the AV node

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29
Q

List other types of narrow complex tachycardias

A

Atrial tachycardia, rapid AF, atrial flutter, sinus tachycardia

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30
Q

How do we detect SVT?

A

Regular, narrow QRS, no P waves (hidden in QRS), rate>100 (usually faster), may have rate-related ST depression

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31
Q

How do you perform valsalva?

A

Patient either semi-recumbent or supine, to blow forcefully for 15 seconds into 10mL syringe then lay semi-recumbent pt supine with legs at 45 degrees for 15 seconds x3

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32
Q

Why do we aim for a large cannula in the AC when cannulating an SVT patient?

A

Adenosine requires a large vein close to the heart to work best

33
Q

Why does valsalva work?

A

Purpose is to induce vagal firing from the cardiovascular control centre in the medulla to slow the heart rate and interrupt the rapid SVT. Bearing down causes an increase in intrathoracic pressure, in turn the heart rate and blood pressure inevitably increase, the sudden cessation period of the action stimulates a vagal response due to detection of changes by baroreceptors prompting a period of transient hypotension and bradycardia. Allowing for a “reset” of the SVT circuit.

34
Q

List the different nodes from top to bottom anatomically

A

Sinoarial node, AV node, Bundle of His, right and left bundle branches, purkinje fibres

35
Q

Describe the pathophysiology of APO

A

APO is the accumulation of excess fluid within the alveolar walls and alveolar space of the lungs. Cardiogenic APO is secondary to problems with heart function. The volume of blood entering the left ventricle exceeds the amount ejected causing backflow through the left atrium and pulmonary circuit. This causes an increase in pressure which then causes the fluid to shift from the capillaries into the alveolar space. (fluid shift > surfactant washout > dry crackly and inefficient alveoli

36
Q

Describe the pathophysiology of APO

A

APO is the accumulation of excess fluid within the alveolar walls and alveolar space of the lungs. Cardiogenic APO is secondary to problems with heart function. The volume of blood entering the left ventricle exceeds the amount ejected causing backflow through the left atrium and pulmonary circuit. This causes an increase in pressure which then causes the fluid to shift from the capillaries into the alveolar space. (fluid shift > surfactant washout > dry crackly and inefficient alveoli

37
Q

What is the difference between cardiogenic and non-cardiogenic APO?

A

Cardiogenic is secondary to LVF or CCF. Left ventricle weakened and enlarged therefore unable to pump blood effectively causing backflow into the lungs. Non-cardiogenic e.g. smoke / toxic gas inhalation, aspiration and anaphylaxis - pulmonary oedema likely a result of altered permeability from surfactant loss and should be treated with supplemental oxygen and assisted ventilation

38
Q

Why is GTN beneficial for APO?

A

GTN is an organic nitrate that is a vascular smooth muscle relaxant which causes vasodilation allowing the fluid to re-enter systemic circulation (promotes pooling reducing preload and reduces SVR). This reduces preload/afterload > svr/co > metabolic demand > sbp/db/pp

39
Q

List the contraindications of CPAP

A

(A)Airway - (B)Breathing - (C)Circulation - (O)Other. (A) - Inability to manage own airway (vomiting, secretions, altered conscious), Upper airway obstruction. (B) - Hypoventilating, TPT. (C) - Hypotension, Life threatening arrythmias. (O) Injuries preventing the mask.

40
Q

Why would salbutamol be detrimental in APO?

A

Salbutamol causes vasodilation which leads to tachycardia and hypotension- both detrimental to a heart that’s already failing to pump.

41
Q

List some reasons why we attempt to avoid opioids for headache

A

If the patient has an ICH opioids may cause deterioration in conscious state, morphine may make migraines worse and delay recovery, opioids do not treat the cause and may worsen symptoms in the future, opioids are drugs of addiction

42
Q

List signs and symptoms of possible ICH

A

Thunderclap headache, nausea, vomiting, ALOC, CNS depression, headache intensity increases within seconds to minutes of onset, atypical aura, seizure, fever, neck stiffness, bradycardia, hypertension

43
Q

List the stages of migraine

A

Prodrome, aura, headache, resolution, hangover

44
Q

Define cluster headache

A

Rarer than other types, occur in clusters with each attack lasting 1-3 hours. Cluster periods followed by remissions that may last months or years. Symptoms: sudden pain generally behind the eye, pain peaks in 10-15 minutes, restlessness, red or watering eyes, nasal congestion, sweating forehead, eyelid drooping or swelling.

45
Q

Define migraine

A

Recurrent episodic attacks of head pain associated with nausea and sensitivity to light sound or head movement. Often throbbing and unilateral.

46
Q

List metro neurosurgical facilities

A

Alfred, RMH, SVH, Austin, MMC

47
Q

What is the risk of adminstering nebulized salbutamol to paediatric patients?

A

Profound lactic acidosis

48
Q

What are the three main characteristics of asthma pathophysiology?

A

Airway oedema, mucous plugging, bronchospasm

49
Q

List common asthma triggers

A

Dust, exercise, medications, pollen

50
Q

How does salbutamol treat asthma?

A

Adrenegic B2 receptor agonist causes bronchodilation

51
Q

Why do we do gentle lateral chest pressure when ventilating a paediatric asthma patient?

A

Gas trapping occurs due to bronchospasm, lateral chest wall pressure assists expiration and maximises air expelled during each effort.

52
Q

What is the minimum mL required to run nebulizer?

A

5mL

53
Q

What is the minimum mL required to run nebulizer?

A

5mL

54
Q

What is the preferred IM adrenaline injection site?

A

Anterolateral mid-thigh

55
Q

Why do all anaphylaxis patients need transport and 4 hour monitoring?

A

Potential bi-phasic reaction in 20% of patients, which is return of symptoms after initial resolution

56
Q

What is food protein induced enterocolitis?

A

Non-immunoglobulin E mediated paediatric allergy that presents with nausa, vomiting, collapse, confusion or ALOC, patient will usually have careplan

57
Q

What is hereditary angioedema?

A

Non-allergic angioedema - similar presentation however will not respond to adrenaline, follow treatment plan and use patients only medication

58
Q

Define anaphylaxis

A

Severe, potentially life-threatening systemic hypersensitivity reaction

59
Q

List six risk factors for severe anaphylaxis

A

Phx of severe, asthma, medication as trigger, hypotensive, respiratory distress, no response to initial IM adrenaline

60
Q

List signs and symptoms or adrenaline toxicity

A

Nausea, vomiting, shaking, tachycardia, arrhythmias

61
Q

What is the minimum paediatric dose of adrenaline?

A

100mcg (0.1mL) for a 10kg child

62
Q

How do we assess for anaphylaxis?

A

Sudden onset of symptoms with two or more of RASH, OR isolation hypotension after exposure to known antigen OR isolated respiratory distress following exposure

63
Q

How do we position anaphylaxis patients and why?

A

Do not sit or walk, have them supine or sitting with legs out flat - reduces risk of postural hypotension

64
Q

How do we position anaphylaxis patients and why?

A

Do not sit or walk, have them supine or sitting with legs out flat - reduces risk of postural hypotension

65
Q

What is the paediatric dose of adrenaline?

A

10mcg/kg IM max of 500mcg repeating at 5 minute intervals

66
Q

How does adrenaline treat airway oedema / stridor?

A

alpha-1 effects: peripheral vasoconstriction to increase blood pressure, beta-1 effects: increases blood pressure by causing increased myocardial contractility, irritibility, conduction velocity and SA firing rate, beta-2 effects: bronchodilation

67
Q

How does salbutamol treat bronchospasm?

A

Beta-2 agonist causing bronchodilation

68
Q

How does ipratropium bromide treat bronchospasm?

A

Anticholinergic bronchodilator - inhibits cholinergic bronchomotor tone / blocks vagal reflexes which mediate bronchoconstriction

69
Q

How does dexamethasone treat bronchospasm?

A

Corticosteroid secreted by the adrenal cortex, steroids relieve inflammatory reactions through immunosuppression

70
Q

What is the paediatric dose of dexamethasone?

A

600mcg/kg IV / oral max 12mg

71
Q

When MUST we request MICA for an anaphylactic patient?

A

If the patient has risk factors or is non-responsive to 1x dose of adrenaline. Risk factors: Expected clinical course (e.g hx of ICU), SBP <90mmHg, medication is the cause of the reaction, respiratory symptoms/distress, hx asthma or multiple comorbidities/medications.

72
Q

What is the difference between DKA and HHS?

A

HS differs to DKA as enough insulin may be present to prevent fat metabolism (→ no ketogenesis and subsequent acidosis), therefore no kussmals breathing, no increase in ketones and no acetone smell breath. HHS more common in T2DM with a marked increase of BGL 35+. DKA more common in T1DM particularly in first presentation hyperglycaemia in teenagers.

73
Q

What is the paediatric management of nausea and vomiting?

A

2mg ODT ondansetron for a small child, 4mg for a medium child]

74
Q

What hormones are activated by the body to produce glucose when it detects unavailable sugar?

A

Adrenaline, glucacon, growth hormone, cortisol

75
Q

List common symptoms of hyperglycaemia

A

Tachypnoea, dehydration, confusion, kussmaul’s, polyuria, polydipsia, polyphagia

76
Q

Why don’t we give insulin to hyperglycaemic patients pre-hospitally?

A

Insulin titration, especially in acutely hyperglycemic patients, is incredibly complicated. Insulin affects glucose and potassium metabolism, along with a few other electrolytes. Basically, in order to use insulin safely and effectively in these settings, you need a working lab to adequately assess the patient’s various physiologic factors. Using insulin in things like DKA can go very wrong very fast, and in a pre-hospital setting

77
Q

What are AV prehospital goals for fractures?

A

Adequate analgesia, good splinting technique, control major haemorrhage, manage neurovascular and neurological compromise

78
Q

Signs and symptoms of compartment syndrome

A

○ Pain (more than expected)
○ Paresis (partial loss of movement)
○ Paraesthesia (altered sensation, pins and needles)
○ Pallor
Pulselessness

Module 7 (3 decks)

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