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CSB339 > Paediatric CVS, endocrine, CNS, and respiratory emergencies > Flashcards

Paediatric CVS, endocrine, CNS, and respiratory emergencies Flashcards

1
Q

What are the most common causes of ALOC in paeds?

A
  • Hypoxaemia
  • Shock with hypovolaemia
  • Hypoglycaemia
  • Drug intoxications
  • Head trauma
  • Sepsis
  • Seizures
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2
Q

What are the points of the GHOST acronym and what is it used for?

A

G - glucose

H - head trauma

O - oxygen deficiency/overdose

S - shock/seizures

T - temperature

Used to determine the cause of ALOC in paeds.

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3
Q

What are the points of the AEIOUTIPS acronym?

A

A - alcohol, abuse

E - epilepsy, electrolyte disorders, encephalopathy, endocrine

I - insulin, intussusception, intoxication

O - overdose, oxygen

U - uraemia (and other metabolic causes)

T - trauma, temperature, tumours

I - infections

P - psychiatric

S - shock, space-occupying lesion, subarachnoid haemorrhage, shunt-related problems if in situ

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4
Q

When obtaining a hx of an ALOC paed, it’s important to ask if they have any hx of…

A
  • Head trauma
  • Neck stiffness
  • Seizures
  • Poisoning (or potential for overdose/poisoning)
  • Infection with fever and/or rashes
  • Shunts/brain tumour
  • Diabetes (including parental hx)
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5
Q

What is the definition of syncope?

A

Sudden loss of consciousness and postural tone with spontaneous and complete recovery after a brief duration.

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6
Q

What is pre-syncope?

A

The feeling that one is about to pass out but remains conscious with a transient loss of postural tone.

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7
Q

What is the common pathophysiologic pathway syncope follows?

A

Cerebral perfusion is compromised by a transient decrease in cardiac output caused by vasomotor changes decreasing venous return, a primary dysrhythmia, or impairment of vascular tone.

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8
Q

True or false: most common causes of syncope in paeds are not immediately life-threatening.

A
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9
Q

What are some common causes of syncope in paeds?

A
  • Breath-holding episode
  • Vagal stimulation
  • Sudden fear or panic
  • Hyperventilation
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10
Q

What are some rare but potentially life-threatening causes of syncope in paeds?

A
  • Cardiac dysrhythmia
  • MI
  • Significant congenital heart disease
  • Drug intoxication
  • Hypoglycaemia
  • Hypoxia
  • Head trauma
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11
Q

What are some additional situations/observations that would alert paramedics to more serious aetiology of syncope in paeds?

A
  • Evidence of injury, especially head trauma
  • Continuing ALOC, especially >5 minutes
  • Recurrent episodes
  • Hx of cardiac conditions/surgery
  • Associated chest pain or palpitations
  • Significant persistent abnormalities in VS
  • The syncopal episode was exercise related or occurred in the recumbent position
  • Family hx of sudden death, deafness, cardiac disease
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12
Q

List the types of seizures.

A
  • Generalised seizures
    • Tonic-clonic
    • Absence
  • Focal seizures
    • Simple partial (no change to mental state/awareness)
    • Complex partial (changes to mental state/awareness)
  • Febrile seizures
    • Usually between 6 months and 6 years
  • Impact seizures
    • Immediately post injury (less serious)
    • Minutes - hours post injury (more significant; due to ICP or brain injury)
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13
Q

Can partial seizures become generalised seizures?

A
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14
Q

What is the operational definition of SE?

A

Generalised, convulsive SE in adults and older children (>5) refers to >/= 5 minutes of a) continuous seizures or b) two or more discreet seizures between which there is incomplete recovery of consciousness.

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15
Q

List the issues with prolonged convulsion.

A
  • Injury
  • Acidosis and other electrolyte imbalances
  • Hypoxia/hypercarbia
  • Hypoglycaemia
  • Hyperthermia
  • Permanent neuronal injury
  • Cardiovascular collapse
  • Difficult to control the longer it lasts
  • Increases morbidity and mortality
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16
Q

Describe the mx of seizures.

A
  • Protect from injury
  • Posture laterally
  • Maintain oxygenation
  • Rapid hx to identify cause and rx if possible
    • Check glucose
  • Cessation of convulsion
    • Midazolam
  • Secondary survey and more comprehensive hx
    • Anything that injures the brain can ause seizures (AEIOUTIPS)
    • Do not assume seizures are due to idiopathic epilepsy until proven otherwise
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17
Q

What kind of drug is Midazolam?

A

Benzodiazepine.

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18
Q

Benzodiazepines enhance the effect of the ____ ____ ____ on the ____ ____.

A

Inhibitory neurotransmitter GABA; GABA receptors.

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19
Q

Benzodiazepines potentiate the effects of GABA by increasing the frequency of ____ ____ ____.

A

Chloride channel opening.

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20
Q

Benzodiazepines increase the activity of ____.

A

GABA

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21
Q

What is the dosage of midazolam for paeds?

A

200microg/kg as a single initial dose (not to exceed 5mg); may repeat at half the initial dose at 10 minute intervals (not to exceed 2.5mg)

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22
Q

When is midazolam indicated?

A

Generalised seizure or pt with complex partial seizure with ALOC.

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23
Q

What is a febrile seizure?

A

A seizure in response to rise in temperature due to fever without evidence of intracranial infection, intracranial abnormality, or toxins or endotoxins

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24
Q

Febrile seizures occur in ____-____% of children.

A

2 - 5%

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25
Q

Between what ages do febrile seizures usually occur?

A

6 months and 5 years.

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26
Q

What must be ruled out when determining the cause of a febrile seizure?

A

Meningitis, encephalitis, and sepsis.

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27
Q

True or false: most febrile seizures are not self-limiting.

A
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28
Q

Describe the mx for febrile seizures.

A
  • Reassurance
  • Manage ABCs and check BGL
  • Cooling with tepid water/removal of clothing
  • Manage prolonged seizures with midazolam if indicated
  • When indicated administer paracetamol (controversial)
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29
Q

What diabetic emergencies might present in paeds?

A
  • Hypoglycaemia
  • Hyperglycaemia
  • Diabetic ketoacidosis (DKA)
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30
Q

True or false: first presentation of diabetes may be development of DKA.

A
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31
Q

Can children without diabetes develop hypoglycaemia?

A
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32
Q

Children can develop ____ ____ in response to infections and other medical conditions.

A

“Stress” hyperglycaemia.

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33
Q

Hypoglycaemia is defined as BGL…

A

< 4mmol/L

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34
Q

The BGL of young children may be normal at BGL levels of…

A

>/= 3mmol/L

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35
Q

The BGL of a neonate may be normal at what level?

A

>/= 2.6mmol/L

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36
Q

What should guide clinicians with assessing hypoglycaemia in paeds?

A

Mental state (clinical picture)

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37
Q

Why is early detection of hypoglycaemia critical in paeds?

A

Permanent brain damage may begin shorty after symptoms develop, particularly in newborns and infants.

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38
Q

Describe the mx of hypoglycaemia.

A
  • Mx ABCs
  • Oxygenation
  • IV access if required
  • Mx other presentations as necessary (seizures etc)
  • Goal of mx is to restore normal BGL rapidly.
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39
Q

What is the dosage of PO glucose gel for paeds?

A
  • > 2 years
  • Oral single dose of 15g
  • May be repeated after 15 minutes until BGL is = 4.0mmol/L
  • Total max dose = 30g
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40
Q

What is the dosage of glucagon for >25kg paeds?

A

1mg in 1mL of water for injection

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41
Q

Edit is glitching - end of Q is “for paeds =25kg”.

What is the dosage of glucagon for paeds

A

0.5mg (reconstitute 1mg in 2mL water for injection and administer 1mL)

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42
Q

What is the initial bolus dosage of gluose 10%?

A

2.5mL/kg

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43
Q

What should be done after administering the initial bolus of glucose 10%?

A

Retake the BGL; if <4.0mmol/L, give a further 1mL/kg bolus. Continue until BGL >4.0mmol/L.

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44
Q

The pathophysiology of DKA can be condensed to a blend of ____ ____ and ____ during physiologic stress with the actions of counterregulatory hormones.

A

Insulin deficiency; antagonism.

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45
Q

Describe the pathophysiology of hyperglycaemia.

A

Increased glucose production from glycogenolysis and gluconeogenesis coupled with the incapacity to use glucose leads to hyperglycaemia, osmotic diuresis, loss of electrolytes, hyperosmolarity, and dehydration.

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46
Q

Describe the progression of hyperglycaemia and DKA.

A

Low insulin levels - glucose cannot enter cells to be used for energy

↓

High blood glucose - body increases glucose production due to lack of glucose in cells, raising BGL

↓

Polyuria - High BGL cause water and glucose to be lost in urine

↓

Polydipsia - loss of water in urine causes dehydration and thirst

↓

Fatigue - not enough glucose in cells for energy results in fatigue

↓

Severe dehydration, shock, and acidosis - unless sufficient fluid is consumed, severe dehydration leading to shock and lactic acidosis can occur.

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47
Q

What is the greatest risk of hyperglycaemia?

A

Dehydration secondary to the resulting urinary loss of glucose and osmotic diuresis. The hyperosolarity and osmotic shifts can increase the risk of cerebral oedema due to brain cell dehydration, dilation of capillaries, and an inability to autoregulate cerebral blood pressure.

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48
Q

What is the dosage for fluid boluses in mx of hyperglycaemia?

A

10 to 20mL/kg boluses to a maximum of 60mL/kg.

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49
Q

What is the primary goal in initial mx of DKA?

A

To restore intravascular volume and improve tissue perfusion.

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50
Q

How does restoring intravascular volume and improving tissue perfusion help mx DKA?

A

It will decrease insulin counter-regulatory hormones (glucagon, catecholamines, cortisol, and GH) levels, hyperosmolarity, and glucose concentration.

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51
Q

Fluid replacement alone may decrease serum glucose concentration by as much as 23% through what two mechanisms?

A

Increased renal perfusion and loss of glucose in the urine.

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52
Q

What is the defining BGL range of DKA, and what is it accompanied by?

A

>11-15mmol/L with ketones.

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53
Q

In which form of diabetes does DKA usually occur?

A

Type I (IDDM), though it can occur in type II (NIDDM).

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54
Q

DKA is usually associated with BGL in the range of ____ to ____mmol/L.

A

11 - 34mmol/L

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55
Q

In DKA, more ____ than ____ are lost.

A

Water; electrolytes.

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56
Q

In DKA, the increase in osmolarity draws more water ____ of the cells.

A

Out.

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57
Q

Drawing of water out of cells by an increase in osmolarity is a mechanism that helps preserve….

A

Intravascular volume which makes decompensated shock unusual in DKA.

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58
Q

True or false: DKA pts tend to appear less dehydrated than they actually are.

A
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59
Q

DKA results from the absence of ____.

A

Insulin.

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60
Q

In simple terms, how does absence of insulin lead to DKA?

A

Prevents glucose from entering cells → glucose accumulates in the blood → body releases more glucose.

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61
Q

Why is DKA dangerous? (pathophysiological reasons)

A

Cells become starved for glucose and begin to use other energy sources (primarily fats) → fat metabolism generates fatty acids → these are further metabolised into ketoacids (ketone bodies).

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62
Q

What is the renal threshold for reabsorption?

A

>10mmol/L BGL

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63
Q

How does DKA cause osmotic diuresis?

A

BGL rises above renal threshold (>10mmol/L) → glucose spills into urine → loss of glucose in urine causes osmotic diuresis.

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64
Q

DKA results in what three basic things?

A
  • Dehydration
  • Metabolic acidosis
  • Electrolyte imbalances (especially K+)
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65
Q

Describe the progression of ketone production.

A

Excess fat metabolism → increased ketone production and ketoacidosis → emesis and abdominal pain → ALOC

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66
Q

What is the most common precipitating factor in DKA in paeds?

A

Ignorance and new onset diabetes followed by infection.

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67
Q

List the six I’s of DKA precipitants.

A
  • Infection
  • Infarction (brain)
  • Ignorance
  • Ischaemia (AMI)
  • Intoxication
  • Implantation (pregnancy conditions)
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68
Q

True or false: DKA on its own generally does not cause significant hypotension.

A
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69
Q

What is the definitive rx for DKA?

A

Insulin therapy, secondary to intravenous fluid replacement and should be withhold in pts with hypotension and hypoglycaemia.

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70
Q

Cerebral oedema associated with DKA has a high mortality rate of ____ to ____%.

A

40 to 90%

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71
Q

Cerebral oedema associated with DKA is more likely in those with what conditions?

A
  • Severe DKA
  • New-onset IDDM
  • Younger age
  • Longer duration of symptoms
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72
Q

What are some possible contributing factors to the mechanism of cerebral oedema associated with DKA?

A
  • Hypoxia
  • Osmotically driven movement of water into the CNS when plasma osmolarity declines too rapidly during the rx of DKA with aggressive fluid management
  • The direct effect of insulin on the plasma membrane of brain cells, which may promote cellular oedema
  • Greater risk for cerebral oedema owing to the immaturity of autoregulatory mechanisms
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73
Q

In what time range does cerebral oedema associated with DKA usually begin?

A

4 - 12 hours after rx.

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74
Q

What are inborn errors of metabolism (IEM)?

A

Hereditary disorers involving gene mutations, usually of a single enzyme or transport system, causing significant blocks in metabolic pathways and accumulation or deficiency of a particular metabolite.

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75
Q

IEMs may lead to permanent ____ ____ and ____ if specific rx is not initiated.

A

Neurologic sequelae; death.

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76
Q

True or false: IEM should not be considered in a previously normal neonate with acute clinical deterioration.

A
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77
Q

What are the most common emergent clinical manifestations of IEMs in the neonatal period?

A
  • Vomiting
  • Neurologic abnormalities
  • Metabolic acidosis
  • Hypoglycaemia
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78
Q

True or false: buccal mucosa/lips are good indicators of paed hydration.

A
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79
Q

Laryngotracheobronchitis is more commonly known as ____.

A

Croup.

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80
Q

What is the most common upper respiratory obstruction in paeds between 6 months and 6 years of age?

A

Croup

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81
Q

____% of croup cases are mild.

A

80%

82
Q

Croup accounts for ____% of all respiratory illnesses.

A

15%

83
Q

List the characteristics of croup.

A
  • Seasonal (mainly winter)
  • Inflammation of upper airway as well as larynx, trachea, and bronchi
  • Barking cough
  • Hoarse voice
  • Inspiratory stridor (significant obstruction)
84
Q

In cases of croup, is inspiratory stridor more significant when active or when at rest?

A

At rest.

85
Q

List some viruses that cause Croup.

A
  • Parainfluenza
  • Influenza A
  • Rhinovirus
  • Adenovirus
  • Enterovirus
86
Q

What should be administered in cases of Croup with stridor at rest?

A

Oxygen and nebulised adrenaline.

87
Q

What is epiglottitis?

A

Inflammation of the lining of the cartilaginous tissue that protects the airway during swallowing.

88
Q

Epiglottitis is usually caused by ____ ____.

A

Bacterial infection.

89
Q

What are the clinical features of epiglottitis?

A
  • High fever
  • Sore throat/difficulty swallowing
  • Stridor/respiratory distress
  • Drooling
  • Hoarse voice
90
Q

Describe the mx of epiglottitis.

A
  • Put nothing in their mouth
  • Consider pain relief
  • Maximise oxygenation
  • Don’t lie the child down
  • Keep child calm (even if it means keeping away)
91
Q

What is ‘reactive airways’?

A

Wheeze in children under 5 years old.

92
Q

What causes reactive airways?

A

Often viral, however numerous environmental stimuli induce an allergen-antibody interaction causing release of mediators that create airway inflammation.

93
Q

True or false: reactive airways predisposes the child to asthma.

A
94
Q

Does reactive airways always respond to Beta2-agonists?

A
95
Q

Describe the rx for reactive airways.

A
  • High flow nasal cannula if SPO2 <93% (high pressure, can be done on RA)
  • Oral fluid/NGA
  • Burst and stretch attempted - salbutamol/atrovent
96
Q

What is the definition of asthma?

A

Chronic inflammatory disease of the airways characterised by reversible airways and bronchospasm.

97
Q

Asthma exacerbations in children are often precipitated by ____ ____.

A

Viral infection.

98
Q

What should be considered in paeds <12 months with a wheeze?

A

Bronchiolitis.

99
Q

True or false: wheeze in preschoolers tends not to respond well to bronchodilators and steroids may be less effective.

A
100
Q

List the four criteria that should be met to dx asthma.

A
  • At least 5 years of age
  • Episodic symptoms of airflow obstruction/airway hyperresponsiveness
  • Reversible airflow obstruction of at least 10% of predicted FEV in one minute after use of short-acting beta2-agonist (i.e. salbutamol)
  • Alternative dx have been excluded
101
Q

What additional parts of pt hx should be obtained when assessing paeds with asthma?

A
  • Duration and nature of symptoms (paeds tire a lot faster)
  • Rx used (relievers, preventers, compliance?)
  • Trigger factors
  • Hx of ICU admission
102
Q

True or false: wheeze is a good marker of asthma exacerbation severity independently of other symptoms.

A
103
Q

Note: regarding pt presentation.

When assessing severity of an asthma exacerbation, what should be taken into account?

A
  • Wheeze
  • Appearance
  • Mental state
  • WOB
  • SPO2
104
Q

O2 should be given for anything in paeds with SPO2 <____%

A

<92%

105
Q

What are the three overarching complications of asthma?

A
  • Respiratory compromise
  • Haemodynamic instability
  • Electrolyte abnormalities
106
Q

What is bronchiolitis?

A

Inflammation and oedema of the lower airway (viral bronchiolitis).

107
Q

Bronchiolitis has a presentation similar to ____.

A

Asthma.

108
Q

What is the most common respiratory tract infection in infants?

A

Bronchiolitis.

109
Q

What are the causes of bronchiolitis?

A
  • Parainfluenza
  • Influenza
  • Rhinovirus
  • Adenovirus
110
Q

What are the three categories of bronchiolitis?

A

Mild, moderate, and severe.

111
Q

What is the common name of pertussis?

A

Whooping cough.

112
Q

Name the three stages of pertussis.

A
  • Catarrheal
  • Paroxysmal
  • Convalescent
113
Q

Describe the catarrheal stage of pertussis.

A
  • Rhinorrhoea
  • Conjunctivitis
  • Low grade fever
  • Malaise
114
Q

Describe the paroxysmal stage of pertussis.

A

Coughing phase.

115
Q

How long does the paroxysmal phase of pertussis last?

A

2 - 6 weeks.

116
Q

Describe the convalescent stage of pertussis.

A

Intensity of cough decreases over many weeks.

117
Q

Which stage of pertussis is the most infectious?

A

Catarrheal (first stage)

118
Q

Why is pertussis dangerous to infants?

A
  • Become quickly exhausted
  • Feeding is impacted
  • Dehydration is common
119
Q

True or false: pertussis in paeds is usually more severe than in infants and is easily diagnosed.

A
120
Q

True or false: chest pain in paeds is rarely due to a life-threatening cause.

A
121
Q

What are some common causes of paed chest pain that are usually benign?

A
  • Muscoluskeletal
  • Emotional
  • Minor trauma
  • Gastritis/reflux
122
Q

What are some less common causes of paed chest pain that are potentially life threatening?

A
  • Asthma
  • Pneumonia
  • Oesophageal foreign body
  • Tracheobronchial foreign body
123
Q

What are some rare causes of paed chest pain that are generally life threatening?

A
  • Significant trauma
  • Cardiac problems
  • Pneumothorax
  • Pulmonary embolism
124
Q

Myocarditis in paeds is often preceded by ____ ____ ____.

A

Viral respiratory illness.

125
Q

What is the presentation of paed myocarditis?

A
  • Respiratory distress
  • Fever
  • Tachypnoea
  • Tachycardia
  • Generalised malaise
  • ECG may show widespread ST segment changes
126
Q

Myocarditis may predispose pt to developing ____.

A

Cardiomyopathy.

127
Q

Pulmonary embolus in paeds is rare but may occur in what four circumstances?

A
  • Adolescent girls with hx of:
    • Recent termination of pregnancy
    • Use of birth control pill (increases coagulopathy)
  • Recent long bone #
  • Recent surgery
  • Recent period of being immobile/non-ambulatory
128
Q

What is Kawasaki disease?

A

Inflammation of blood vessels including coronary arteries, which can cause saccular dilations or aneurysms.

129
Q

What is the danger of aneurysms in Kawasaki disease?

A

Aneurysms can become obstructed by a thrombus, causing an infarction.

130
Q

List the key dx criteria of Kawasaki disease.

A
  • Conjuntivitis
  • Mucousitis (strawberry tongue and fissured lips)
  • Persistent fever >39.5 that is not very responsive to normal rx
  • Rash
  • Lymph node enlargement
  • Spindle-shaped swelling of digits followed by desquamation
131
Q

What is Marfan Syndrome?

A

Abnormality of connective tissue that causes weakened blood vessels.

132
Q

Marfan syndrome pts usually have dilation of the ____.

A

Aorta.

133
Q

Describe the typical presentation of Marfan syndrome.

A
  • Tall and thin
  • Long arms and fingers
  • May have vision disturbances
134
Q

Chest/back pain in pts with Marfan syndrome may be indicative of what two things?

A
  • Aortic dissection
  • Ruptured aortic aneurysm
135
Q

Most paed cases, bradycardia is associated with ____.

A

Hypoxia.

136
Q

Bradycardia in paeds is ____.

A

Pre-terminal.

137
Q

Bradycardia in paeds is usually caused by ____ and ____.

A

Hypoxaemia; acidosis.

138
Q

Primary causes of bradycardia in paeds are rare. What two conditions might include primary bradycardia?

A

Sick sinus syndrome and atrioventricular block.

TL;DR: usually in paeds with congenital heart issues.

139
Q

Describe the rx for paed bradyarrhythmias.

A
  • Ensure appropriate oxygenation (IPPV)
  • Consider cardiac compressions as appropriate
  • Consider causes
  • IV access
  • CCP backup
  • Time critical tx
    • One of the few circumstances you’d tx during arrest mx
140
Q

True or false: tachyarrhythmias can cause non-specific signs and sympoms, and will differ with the age of the pt.

A
141
Q

List three tachyarrhythmias.

A
  • Sinus tachycardia
  • Supraventricular tachycardia
  • Ventricular tachycardia (perfusing)
142
Q

Pts with congenital heart disease may present with what two cardiac rhythms?

A

Atrial flutter and atrial fibrillation.

143
Q

Differentiate between ST, SVT, and VT: in which are P waves present/normal?

A

ST

144
Q

Differentiate between ST, SVT, and VT: in which are P waves absent/abnormal?

A

SVT

145
Q

Differentiate between ST, SVT, and VT: in which may there be dissociated P waves?

A

VT

146
Q

Differentiate between ST, SVT, and VT: in which are there abrupt rate changes?

A

SVT

147
Q

Differentiate between ST, SVT, and VT: which is often regular?

A

VT

148
Q

Differentiate between ST, SVT, and VT: which has a variable R-R with constant PR?

A

ST

149
Q

Differentiate between ST, SVT, and VT: which two are more likely to have hx of congenital heart disease?

A

SVT and VT

150
Q

Differentiate between ST, SVT, and VT: which has a narrow QRS (<0.8 seconds)?

A

All three.

151
Q

Differentiate between ST, SVT, and VT: in which is the HR usually <220bpm in infants and <180bpm in children?

A

ST

152
Q

Differentiate between ST, SVT, and VT: in which is HR usually >220bpm in infants and >180bpm in children?

A

SVT

153
Q

Differentiate between ST, SVT, and VT: in which is HR usually >150bpm?

A

VT

154
Q

Differentiate between ST, SVT, and VT: in which does HR often vary with activity?

A

ST

155
Q

Differentiate between ST, SVT, and VT: in which two does HR often not change with activity?

A

SVT and VT

156
Q

Children augment cardiac output by increasing ____ ____ rather than ____ ____.

A

Heart rate; stroke volume.

157
Q

Sinus tachycardia in paeds should be considered a sign of what?

A

An underlying process rather than an intrinsic cardiac problem.

158
Q

For every 1 degree C increase in body temperature, the pulse rate increases by an average of ____bpm.

A

9.6bpm

159
Q

What is the overall mx for ST?

A

Address the underlying cause.

160
Q

What are the three types of SVT?

A
  • AV reentrant tachycardia phenomonon
  • AV nodal, or junctional tachycardia
  • Ectopic atrial tachycardia (rare)
161
Q

Name an example of AV reentrant tachycardia phenomenon.

A

Wolff-Parkinson-White syndrome

162
Q

What kind of pattern is AV nodal or junctional tachycardia?

A

Cyclical reentrant pattern.

163
Q

Ectopic atrial tachycardia is caused by the…

A

Rapid firing of a single ectopic focus in the atrium.

164
Q

SVT can be well tolerated initially but will eventually lead to…

A

Ineffective ventricular filling and decreased cardiac output.

165
Q

SVT can lead to what two life-threatening conditions in the long term?

A

Congestive heart failure and cardiogenic shock

166
Q

Describe the rx for SVT.

A
  • Valsalva manoeuvre (if able to understand)
  • Brief application of an ice towel to the face (may stimulate a vagal response)
  • CCPs (cardioversion)
167
Q

List some causes of VT.

A
  • Underlying congenital heart disease
  • Intentional or inadvertent drug overdose
  • Myocarditis
  • Cardiomyopathy
  • LQTS
168
Q

True or false: the QRS interval will be dependent on age.

A
169
Q

What is the most common ECG finding in paed pulseless arrest?

A

Asystole

170
Q

Asystole is a terminal rhythm often associated with deterioration from what two rhythms?

A

Symptomatic bradycardia or PEA.

171
Q

Asystole usually arises as the end result of ____ ____ ____.

A

Untreated respiratory failure.

172
Q

Describe the pathophysiological events leading to asystole.

A
  • Prolonged ineffective ventilation
  • Severe hypoxaemia and acidosis
  • Slows the heart rate
  • Decreases perfusion and exacerbates cellular hypoxia and acidosis
  • Hypoxic damage
  • Cardiac arrest
173
Q

List some precipitating factors/circumstances for VF and pulseless VT.

A
  • Hx of congenital heart disease
  • Hyperkalaemia (renal failure)
  • Hypomagnaesemia
  • Commotio cordis (sudden blunt trauma to chest causing cardiac dysrhythmias)
  • Respiratory failure leading to severe hypoxaemia
  • Drug overdose (TCAs, beta-agonists in asthmatic paeds)
  • Electrocution
  • Re-entry tachycardias (WPW)
174
Q

What is pulseless electrical activity (PEA)?

A

A paradoxical phenomenon in which the ventricles contract, but little or no blood is pumped.

175
Q

List possible causes of PEA.

A
  • Tension pneumothorax
  • Cardiac tamponade
  • Severe hypovolaemia
  • Severe acidosis
  • Hypoxia
  • Hypothermia
  • Hypoglycaemia
176
Q

In general terms, what is the rx for PEA?

A

CPR and adrenaline.

177
Q

5 H’s and 5 T’s

List the reversible causes of cardiac arrest.

A
  • Hypovolaemia
  • Hypoxia
  • Hydrogen ion (acidosis)
  • Hypo/hyperkalaemia
  • Hypothermia
  • Tension pneumothorax
  • Tamponade (cardiac)
  • Toxins
  • Thrombosis (pulmonary)
  • Thrombosis (coronary)
178
Q

What is long QT syndrome (LQTS)?

A

Prolongation of ventricular repolarisation secondary to impaired ion channels in the myocardium.

179
Q

Describe the pathophysiology of LQTS.

A

Multiple genetic mutations lead to dysfunction of potassium, sodium, and/or calcium ion channels which in turn leads to an overabundance of cations within the myocardium.

180
Q

LQTS puts the heart at risk of what two dysrhythmias?

A

Torsades de Pointes and VF.

181
Q

LQTS in paeds is most likely caused by…

A

Consumption of TCAs

182
Q

What is the characteristic manifestation of LQTS?

A

Sudden loss of consciousness during exercise or an emotional/stressful experience.

183
Q

When is the typical onset of LQTS?

A

Late childhood/adolescence.

184
Q

What may be evident during the syncope period in LQTS?

A

Various arrhythmias, particularly VF.

185
Q

What are the possible causes of LQTS?

A
  • Due to acquired heart disease
    • Myocarditis
    • Mitral valve prolapse
    • Electrolyte abnormalities
    • Drug induced
  • Congenital forms
    • Autosomal recessive treat associated with deafness (Jervell and Lange-Nielsen syndrome)
    • Autosomal dominant trait (Romano-Ward syndrome)
186
Q

What is commotio cordis?

A

A life-threatening dysrhythmia caused by a direct, non-penetrating blow to the chest that may be confused with syncope.

187
Q

Which rhythm is typically seen in commotio cordis?

A

VF

188
Q

Most paed cases of heart failure are due to ____ ____ ____.

A

Structural heart disease.

189
Q

List four possible reasons for heart failure.

A
  • LV volume overload or excessive pulmonary blood flow
  • Left heart obstruction
  • Primary ‘pump’ failure
  • Dysrhythmia
190
Q

List some presentations of heart failure in paeds.

A
  • Breathlessness
  • Cyanosis
  • Signs of cardiogenic shock
  • Failure to thrive
  • Refusal to feed
  • Persistent irritability
  • Poor toleration of respiratory illnesses
  • Crackles/heart murmurs
191
Q

What is the meaning of duct-dependent congenital heart disease?

A

The ductus arteriosis has to stay open to allow oxygenation of the rest of the body.

192
Q

List some examples of duct-dependent congenital heart disease.

A
  • Pulmonary atresia
  • Critical pulmonary valve stenosis
  • Tricuspid atresia
  • Severe Tetralogy of Fallot
  • Transposition of the Great Vessels
  • Hypoplastic left heart syndrome
  • Critical aortic stenosis
193
Q

In general terms, describe Transposition of the Great Vessels.

A

The aorta and pulmonary veins are on the wrong sides (will be fixed in surgery).

194
Q

What is the most common cause of right-to-left shunt?

A

Tetralogy of Fallot.

195
Q

Describe the pathophysiology of Tetralogy of Fallot.

A
  • Pulmonary stenosis
    • Narrowing of the pulmonary valve and outflow tract, obstructing blood flow from the RV to the pulmonary artery
  • Overriding aorta
    • Aortic valve is enlarged and appears to arise from both the LV and RV (instead of the normal LV)
  • Ventricular septal defect
    • Abnormal hole between the ventricles
  • Right ventricular hypertrophy
    • Thickening of the muscular walls of the RV as a result of increased workload
196
Q

What are hypercyanotic attacks (Tet spells)?

A
  • Pts with Tetralogy of Fallot have spells where they suddenly turn a blue colour due to low O2 in the bloodstream
  • Decreased blood flow through the lungs due to elevated resistance in the pulmonary blood vessels
    • Caused by much of the blood going directly from RV (less oxygenated) to LV through defects
197
Q

What is the immediate rx for hypercyanotic attacks? Give the reasoning for this rx.

A

Putting pt in the lateral position with knees to chest or squatting; this mechanism attempts to increase systemic vascular resistance to overcome the pulmonary resistance.

198
Q

When does the ductus arteriosus usually close?

A

Within the first 24 hours.

199
Q

What is the role of the ductus arteriosus before birth?

A

To avoid blood flow to the foetus’ fluid filled/under developed lungs

200
Q

What signs and symptoms may occur if the ductus arteriosus fails to close, causing a right to left shunt?

A
  • Heart failure
  • Cardiogenic shock
  • Cyanosis
201
Q

What urgent rx may be given to babies born with transposition of vessels to maintain patency of the ductus arteriosus until urgent surgical intervention?

A

Prostaglandin infusion.

CSB339 (7 decks)

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