Cardio + resp Flashcards
(105 cards)
1
Q
Define apnoea
A
cessation of breathing for 20 seconds or shorter if there is bradycardia, cyanosis, pallor or hypotonia
2
Q
Give 3 central and 3 obstructive causes of apnoea (in a child)
A
central: - apnoea of prematurity - head trauma - toxins - seizures - breath holding spells - arrhythmias - congential hydrocephalus obstructive: - adenotonsillar hypertrophy - reflux - foreign body - anatomical obstruction - LRTI or URTI
3
Q
What is apnoea of prematurity and how is it treated?
A
decreased responsiveness to hypercapnia due to immaturity of system- treat with caffeine
4
Q
What are breath holding spells and how are they managed?
A
When an infant cries and they hold their breath, it can lead them to become pale/ blue and even faint.
They are benign and self limiting and the parent just needs reassurance that theyll grow out of them
5
Q
Describe the clinical features of a child with asthma
A
- recurrent symptoms (wheeze, cough, SOB) which occur between exacerbations (differentiates from viral induced wheeze)
- variable symptoms (worse at night, with certain triggers, at different times of year)
- history of atopy (eczema, hay fever, allergy)
- variable PEF
- Age >2 (generally >5)
6
Q
How is a diagnosis of asthma and decision to treat made in a child?
A
- high probability based on symptoms: start 6 weeks ICS, good response then diagnose as asthma
- mid probability: spirometry and reversibility, FeNO, blood eosinophils, IgE testing
- too young for spirometry (generally <5yrs): watchful waiting if asymptomatic and monitored treatment if symptomatic
7
Q
Name 2 long acting beta agonists and 3 corticosteroids used to treat asthma?
A
LABA: salmeterol (MDI, accuhaler), fometerol (turbohaler)
ICS: beclomethasone (MDI, clickhaler, easibreathe, easihaler), fluticasone (MDI, accuhaler), budesonide (MDI, easihaler, turbohaler)
8
Q
Name 2 combination inhalers and the drugs that are in them
A
Seretide (fluticasone + salmeterol)- MDI or accuhaler
Symbicort (budesonide +fometerol)- turbohaler
9
Q
What is the first line therapy for asthma if >5 and <5yrs
A
if >5yrs very low dose ICS
if <5yrs can use leukotriene receptor antagonists (monteleukast)
+ SABA for symptom relief
10
Q
What are the 2nd, 3rd and 4th line therapies for asthma in children
A
2nd= add LABA if >5 and LRTA if <5yrs 3rd= increase ICS dose, consider adding LTRA. stop LABA if no help, continue if some help 4th= increase ICS again, consider adding 4th agent eg theophyline and refer to specialist 5th= specialist use of oral steroids, monoclonal antibodies etc
11
Q
Why may a childs asthma be poorly controlled?
A
- poor inhaler technique
- parental smoking
- unidentified triggers/ lack of avoidance
- poor adherence with steroid therapy
- inadequate dose of ICS
- damp/ mould
- developed allergic rhinitis
- chest infection
- wrong diagnosis
12
Q
give 5 features of well controlled asthma
A
- SABA use <3 times per week (<1 inhaler per month)
- no daytime symptoms
- no night time wakening
- no rescue med use
- no attacks
- no limits on physical activity
- normal lung function tests
- minimal side effects
- on lowest possible dose of ICS
13
Q
Describe the features of a moderate and severe asthma attack
A
Moderate: sats>92%, able to talk, PEFR >50% best/ predicted. HR <25 (or 140 if <5yrs), RR < 30 (<40 if <5yrs)
Severe: <92%, cant talk, accessory muscle use, PERF 33-50%, HR >125//140 RR>30//40
14
Q
Describe the features of a life threatening asthma attack
A
Sats <92% + any of:
- poor resp effort
- exhaustion
- agitation
- altered consciousness
- cyanosis
- silent chest
- PEFR <33% best/ predicted
15
Q
how is a moderate- severe asthma attack managed initially and what do you do if good and poor response?
A
Salbutamol 6 puffs via inhaler + pred 1-2mg/kg up to 40mg. Give 8L O2 and consider salbutamol as neb (2.5-5mg)if severe.
If good response (PEFR >75%) after 15 mins, continue spacer as needed but if needs >4hrly manage as poor response. continue pred for 3 days and arrange F/U
Poor response: repeat salbutamol 1-2 times. If still poor, send to hospital if not already and manage as life threatening
16
Q
How is a life threatening asthma attack managed?
A
Oxygen Salbutamol neb 2.5-5 mg back to back PO Prednisolone (1-2mg up to 40mg) / IV hydrocortisone (4mg/kg up to 100mg) Ipratropium bromide neb (0.25mg) Consider Theophylline IV Consider anaphylaxis dose adrenaline ITU support
17
Q
Describe the 7 safe discharge criteria for asthma attacks
A
- PEFR >75%
- stopped nebs for 24hrs
- inpt asthma nurse r/v
- PEFR meter and written asthma action plan given
- 5 days oral pred given
- GP follow up in 2 working days
- resp clinic follow up within 4 weeks
18
Q
Describe the pathophysiology of bronchiolitis
A
- viral infection (respiratory syncytial virus- RSV)- often picked up from a sibling going to nursery
- causes excess mucus production, IgE mediated type 1 allergic reaction (infalmmation), bronchiolar constriction, infiltration of lymphocytes (submucosal odema) in the bronchioles
- this leads to a ball valve effect which causes hyperinflation, increased airway resistance, atelectasis (lung collapse) and a V/Q mismatch
19
Q
What age does bronchiolitis affect? Give 3 risk factors
A
- children <2yrs, generally <1 yr
RFs: breast feeding for <2 months, parental smoking, siblings are nursery, chronic lung disease due to prematurity
20
Q
Describe the clinical features of bronchiolitis
A
- usually starts off as cold like symptoms for 2-5 days
- Over 6-12 hrs they begin to get wheezy, have feeding difficulty, may have low grade fever
- tachypnoea, grunting, nasal flaring, inter/ subcostal or subclavicular recessions, inspiratory crackles and expiratory wheeze, hyperinflated chest, cyanosis or pallor may be seen on examination
21
Q
How should bronchiolitis be investigated? and what are cxr signs (4)
A
- nasopharyngeal aspirate/ throat swabs for RVS rapid testing and viral cultures to confirm diagnosis
- blood and urine sample if pyrexic for sepsis screen
- fbc, crp and cap blood gas to check not in resp failure
- CXR if diagnostic uncertainty or atypical course (findings: hyperinflation, focal atelectasis, air trapping, flattened diaphragm)
22
Q
How should bronchiolitis be managed in hosp?
A
- O2 if sats <92%
- NG fluids if reduced oral intake
- CPAP if resp failure
- upper airway suctioning if secretions are causing apnoeas
- no role for abx, steroids or bronchodilators (NICE) but bronchodilators in particular are often given anyway
23
Q
When can a bronchiolitis baby be discharged? (3)
A
- clinically stable
- adequate oral fluids
- sats >92% for 4 hrs
24
Q
give 4 complications of bronchiolitis?
A
- hypoxia
- dehydration
- fatigue
- resp failure
- persistent cough or wheeze for several weeks
- bronchiolitis obliterates- permanent damage due to inflammation and fibrosis (rare)
25
How is cystic fibrosis diagnosed?
- one or more characteristic phenotypical features AND
- a history of CF in a sibling
- or +ve newborn screening rest AND increase sweat chloride concentration
- or two CF mutations identified on genotyping
- or demonstration of abnormal nasal epithelial ion transport (nasal potential difference)
26
What 4 ways does cystic fibrosis tend to present?
1. meconium ileus (intestinal obstruction shortly after birth- bilious vomiting, abdo distension, delay meconium)
2. intestinal malabsorbtion -> failure to thrive (deficiency in pancreatic enzymes is main cause)
3. recurrent chest infections
4. newborn screening (heel prick test)
27
Give 4 common complications of cystic fibrosis, briefly describe their management
1. resp infections- aggressive chest physio and abx, prophylactic abx and other prevention measures
2. low body weight- give pancreatic enzyme replacement therapy + high calorie diet, NG or PEG feeding
3. distal intestinal obstruction syndrome (DIOS)- usually due to insufficiency of pancreatic enzyme replacement, salt deficiency or hot weather. Manage w/ AXR to diagnose, gastrogaffin to treat and dietician r/v and movicol on d/c
4. diabetes- as normal
28
What lifestyle advice should be given to a pt with cystic fibrosis?
- no smoking
- avoid other cf pts
- avoid hot tubs
- clean and dry nebs well
- avoid ppl with colds/ infections
- avoid stables and compossts
- get flu jabs
- NaCl tablets in hot weather and exercise
29
What are the 3 types of LRTI?
- bronchiolitis
- bronchitis
- pneumonia
- viral induced wheeze
30
What are the common and atypical causes of LRTIs?
60% bacterial: strep pneumonia, h influenza, staph a, klebsiella pneumonia, e coli
45% viral: influenza virus, RSV, VZV
atypical: mycoplasma pneumonia, legionella pneumophila, chlamydia pneumoniae
31
Describe the normal resp rates for children of different ages
<60 for 0-5 months
<50 for 6-12 months
<40 for >12 months
<30 for >24 months
32
give 6 signs of resp distress in children/ babies
- cyanosis
- grunting
- nasal flaring (<12 months)
- tachypnoea
- chest indrawing
- recessions (intercostal, subcostal, supraclavicular)
- seesaw breathing
- tripod positioning
- low sats
- crackles/ wheeze on auscultation
33
give 4 differentials for LRTI in children
- asthma attack
- inhaled foreign body (usually stridor but may be small and gone lower)
- pneumothorax
- cardiac failure (think congenital defects and check liver size)
- pneumonitis from other causes (smoke, aspiration of reflux, extrinsic allergic alveolitis)
- URTI (no tachypnoea)
34
How should an LRTI be investigated?
- fbc, crp, cap blood gas
- sputum and blood cultures
- cxr- poor at differentiating viral from bacterial but may pick up pleural effusions, empyemas and diagnosing pneumonia
- tuberculin skin testing if ?TB
- drainage and culture if pleural effusions
35
What abx are used for pneumonia?
If no recessions- mild- oral amoxicillin +/- erythromycin
If recessions, no cyanosis- moderate- Iv cefuroxime +/- PO erythromycin
If recessions + cyanosis- severe- Iv cefuroxime +/- PO erythromycin and consider others
36
What causes croup and who gets it?
- laryngotracheobronchitis usually caused by parainfluenza virus, can be caused by RSV, adenovirus, rhinovirus
- common infection affecting 6months- 3 yr olds.
- affects M>F, commonest in autumn and spring
37
Describe the clinical features of croup?
- 1-4 day history of non specific cold like symptoms
- cough starts and progresses to become barking and hoarse
- symptoms worse at night
- O/E: stridor, chest sounds decreased (severe airflow limitation), tachypnoea and recessions if severe
- concerning features: lethargy/ drowsiness, cyanosis, laboured breathing, tachycardia
38
Describe the differences between mild, mod and severe croup
mid: ocassional barking cough, no stridor, no recession, eats and plays
mod: frequent cough, stridor, recession, not distressed
severe: cough, prominent stridor, recessions, agitated/ distressed, tachycardia
39
Give 3 differentials for croup? (stridor)
- epiglottitis
- inhaled foreign body
- acute anyphalxis
- peritonsilar abscess
40
Describe how epiglottitis is different from croup?
- onset over hrs
- no coryza
- drooling saliva
- marked fever
- soft rather than rasping stridor
- doesn't eat/ drink
- weak or silent rather than hoarse voice
- it is much rarer due to Hib vaccine
41
How should croup be investigated?
clinical diagnosis
- can do cxr if ?foreign body
- direct or infirect laryngoscopy not usually performed unless illness is atypical or ? another cause
- pulse oximetry to monitor sats
42
How should croup be managed?
- single dose oral dexamethasone (0.15mg/kg) or oral pred
- adrenaline neb can provide temporary relief but may distress baby so only if needed
- keep child calm- play specialist, keep with mum, quiet surroundings etc
- oxygen
- ENT/ anaesthetist referral if need airway support
43
When does a child with croup need to be admitted?
- <6 months old
- Immunocompromised
- Inadequate fluid intake
- Poor response to initial treatment
- Uncertain diagnosis
- Significant parental anxiety
- Moderate- severe croup or resp failure signs need urgent admission
44
What is the peak age for a child to inhale a foreign body?
1-2 yrs
45
How should an inhaled foreign body be managed? (3 scenarios)
Conscious + effective cough: encourage child to cough and monitor
Conscious but cough ineffective: infant= 5 back blows then chest thrusts// child= 5 back blows then abdo thrusts
Unconscious: call for help, finger sweep, life support with 5 rescue breaths and compressions. once help arrives then can do laryngoscopy, cricothyroidotomy etc
46
Describe the common aetiology of pleural effusion in children
- usually secondary to acute bacterial pneumonia (parapneumonic)
- less likely bacterial causes: TB, abscess, bronchiectasis)
- malignancy (rare)
- CHD, renal disease, CT disorders (bilateral, transudative)
- trauma
47
How should pleural effusions be investigated?
- CXR
- USS chest
- blood and sputum culture
- FBC, u&E, serum albumin, CRP, dipstick
- small volume diagnostic tap for cytology if suggestion that it may not be infective
- biochemical analysis of aspirated effusion rarely needed as most are parapneumonic
48
how should a parapneumonic pleural effusion be managed?
- O2, fluid, IV abx, analgesia, antipyretics, refer to resp paediatrician
- most will get chest drain initially, if loculated or empyema on USS then intrapleural fibrinolytics (urokinase) can be given
- If this fails then they may get surgery- minithoracotomy or VATS procedure
- abx continued for 1-4 weeks after chest drain removed
- follow up after 4 weeks
49
How may TB manifest in a child?
- pleural effusion
- lymphadenopathy
- progressive primary TB(presents similar to pneumonia)
- reactivation TB (weightloss, night sweats, cough, fever)
- TB meningitis (younger kids, 3-6 months after exposure, meningism develops over a couple of weeks)
- milliary TB (fever, weightloss, malaise, cough)
- bone/ joint TB
50
How is TB investigated and managed in children?
- TST +/- interferon gamma test
- specimen collection via sputum, gastric, bronchoalveolar levage, lung tissue, CSF, urine, stool, lymph node FNA for ZN stain and cultures
- treatment is same as adult: 6 months I and R, 2 months P and E
51
What causes whooping cough?
- bordetella pertussis
a gram neg bacillus which releases a toxin which paralyse cilia and promote inflammation. due to vaccine made in 1950s, its now very rare
52
Describe the clinical features of whooping cough
- rhinitis, conjunctivitis, irritability, sore throat and low fever for 1-2 weeks
then development of whooping cough for 2-8 weeks
53
How should whooping cough be diagnosed?
- if <2 weeks cough: nasopharyngeal aspirate + cultures
- if > 2weeks - anti pertussis toxin IgG serology if age >5yrs and anti pertussis toxin detection in oral fluid if 5-17
- vaccination within a year will produce a false positive
54
How should whooping cough be managed?
admit if <6 months and acutely unwell, breathing difficulties, feeding difficulties or complications such as pneumonia or seizures
- give abx (clarithromycin) if cough <21 days
- warn about secondary bacterial pneumonia (in 20%), seizures ans encephalopathy
55
How does chronic lung disease of prematurity/ bronchopulmonary dysplasia develop?
In infants who need ventilation in the early days of life. It is thought to be due to irritation and scarring of airways due to high pressures of ventilation and high concentration of oxygen
56
How is risk of bronchopulmonary dysplasia reduced?
- gentle ventilation
- permissive hypercapnia
- budesonide and surfactant inhalation
- caffeine
- vit a
- nitric oxide
57
Give 4 common causes of cyanotic heart disease?
- tetralogy of fallot
- tricuspid atresia
- transposition of great arteries
- total anomalous pulmonary venous return
- preductal coarctation
58
Give 4 causes of acyanotic heart disease?
- atrial +/- ventricular septal defects
- PDA
- aortic stenosis
- pulmonary valve stenosis
- coarctation of the aorta
59
Give 6 differentials for a blue baby
central: CO poisioning, sepsis, polycythameia, congenital heart disease
resp: penumonia, pneumonthorax, ARDS, pulmonary atresia, foreign body inhalation
Neuro: asphyxia, seizures, sedatives
60
What could cause a systolic murmer in a child? (4)
- non pathological, innocent murmur
- VSD
- outflow tract obstruction
- mitral regurg
- PDA
61
Describe the features of an innocent murmur?
- grade 1/2 (barely audible/ quiet)
- change with position or respiration
- short duration
- no clicks of gallops
- limited to small area
- systolic
- soft
- not harsh
62
what could cause a diastolic murmur in a child? (3)
- venous hum (non pathological)
- Aortic regurg
- Atrial septal defect
63
What is tetralogy of fallot?
- VSD + pulmonary stenosis
- leads to ventricular hypertrophy and overriding aorta
- blood flows mostly into aorta and baby relies on PDA to get blood to lungs
64
How will a child with a mild ("pink") TOF present?
- asymptomatic at birth as plenty blood can still get out pulmonary artery
- heart failure will progress as they grow and the heart cannt meet demands
- usually presents age 1-3 with odema, SOB, fatigue, failure to thrive, basal crackles, hepatomegaly, murmur
65
how may a moderate- severe TOF present?
- moderate presents with resp distress or cyanosis in first few weeks as the ductus arteriosus starts to close
- severe TOFs with pulmonary atresia is usually detected antenatally, if not theyll present with resp distress/ cyanosis within the first few hrs of life
66
Describe the medical management of TOF?
- squatting/ knees to chest to increase venous return
- prostaglandin infusion to help keep PDA open
- beta blockers to slow HR and increase venous return
- morphine- reduced resp drive and so reduced hypercapnia
- saline bolus: volume expander so increases pulmonary flow (caution if congestive heart failure)
67
What are the side effects of prostaglandin infusions?
- apnoeas
- bradycardia
- hypotension
68
describe the surgical management of a TOF
- transcatheter RV outflow tract stents and modified blalock taussig shunts (PDA mimics) buy time for 3-4 months till child can grow
- then definitive repair with RV outflow tract stenosis resection and augmentation and VSD patch closure. PV can be repaired or spared depending on degree of PS
69
Describe the complications of TOF with and without corrective surgery
No surg: polycythamia, cerebreal abscess, stroke, IE, heart failure, death
Post Surg: pulmonary valve regurg, arrhythmias, exercise intolerance, sudden death
- need regular ECGs, echos and exercise testing
70
Describe the pathophys of dextro and levo transposition of the great arteries
Dextro: aorta arises from RV, PA from the LV. blood leaves RV and goes to body, then comes back to RA- RV and then back to body. Deoxygenated blood leaves LV and goes to lungs before coming back to LV. Needs PDA, ASD or VSD to allow blood to mix.
Levo: RV and LV swapped , which would be fine but RV and tricuspid not made for high pressures of left side of heart so get hypertrophy, tricuspid regurg and heart failure over time
71
How does dextro TGA present?
Cyanosis within 24 if not mixing at atrial level or resp distress after 2-3 weeks as PDA closes. If large septal defect, may only be cyanosis when crying and then signs of heart failure after 3-6 weeks.
Rv heaves, systolic murmur and no signs of resp distress may be found on examination
72
How is TGA managed?
- prostaglandin infusion
- correct metabolic acidosis
- emergency ballon septostomy to allow mixing
- surgical correction with arterial switch operation at 4 weeks of age
- long term follow up and counselling in future if female pts want to have kids
73
Give 3 complications of TGA?
- neopulmonary stenosis, regurg or root dilation can occur post op
- coronary artery disease
- sudden cardiac death
74
What is hypoplastic left heart syndrome and how does it present?
- left side of heart doesnt develop properly so blood flows from RV to lungs and body via PDA, blood from lungs flow from LA to RA via foramen ovale
- this allows adequate mixing to sustain life
- if smaller atrial septal defect theyll decompensate sooner
- associated with trisomies and other genetic defects
75
How does hypoplastic left heart present
resp distress, cyanosis, acidosis and poor feeding etc when PDA closes (first few weeks of life)
hepatomegaly
no murmur usually
76
What procedure is used to treat hypoplastic left heart?
norwood procedure in first few days of life, then fontan- makes RV pump blood around body and lets passive venous pressure pass deoxygenated blood through lungs - low oxygen air used to increase pulmonary vascular resistance and improve blood flow around body
77
What is total anomalous venous return?
where all the pulmonary veins drain into the systemic venous system such as into the RA or SVC rather than LA. PDA, PFO or ASD much be present to allow mixing and sustain life, but surgery is needed to correct as these close
78
give 3 risk factors for a VSD/ ASD
- maternal diabetes
- maternal rubella
- foetal alcohol syndrome
- downs and other trisomies
- fhx
79
Which portion of the septum is a VSD most likely to occur
perimembranous (upper) portion
80
Describe how a moderate or large VSD may present
Moderate: excessive sweating, easily fatigues, tachypnoea (usually only on feeding), symptoms develop by 2-3 months as pulmonary resistance increases and L-R shunting increases
Large: congestive heart failure, eisenmegers syndrome
Sytolic murmur on left lower stanl boarder, holostolic or early systolic
81
what is eisenmengers syndrome?
When VSD/ ASD is diagnosed late and RV pressure > LV pressure due to hypertrophy, causing shunt reversal and so deoxygenated blood enters systemic circulation so they become cyanotic
82
How should VSD be investigated?
- ECG (LVH or bilateral VH)
- septic screen for non cardiac cause of collapse/ deterioration
- U&E before diuretics or ACEi
- microarray/ karyotype if genetic syndrome suspected
- CXR normal or cardiomegaly but helps rule out resp causes
- Echo for diagnosis and evaluation
- Cardiac CT angio with ECG gating to help visualise lesion and make 3D models
- cardiac catheterisation often used to determine relative pressure, pulmonary resistance etc
83
How are VSDs managed?
Small: no specific, good oral hygiene to avoid IE
Medical: calorie dense feeds, diuretics, ACEi to reduce arterial pressure so more blood through valves and less through defect.
Surgical: if medium- large or when pulmonary/ systemic flow is >2 or more in adults. repaid is with patch or stitch via catheter and a mesh
Lifelong f/u, no activity restriction
84
Give 3 complications of VSD (treated and untreated)
Untreated: growth failure, heart failure, aortic valve regurg, eisenmengers, chest infections, IE, arrhythmias, sudden death
Treated: heart block, wound infection, reoperation
85
Describe the clinical features of ASD
- usually asymptomatic and picked up on screening
- rarely present with tachypnoea, poor weight gain, recurrent chest infections
- subtle SOB with exercise or palpitations between age 10-20
- adults with large ASD may get fatigue, reduced ET, palpitations, syncope, SOB, peripheral odema
- eisenmengers syndrome develops in 5-10%
- soft systolic ejection murmur in pulmonary areas
86
How are ASD managed?
most dont need any treatment
none need exercise restriction
some may need diuretics if develop heart failure
haemodynamically significant ASDs get elective surgical closure at 4-5 yrs of age via open surg or catheter (if <4cm)
no endocarditis prophylaxis needed
87
if pregnancy safe with an ASD?
yes if isolated ASD. slightly higher risk of pre eclampsia, fetal loss and low birth weight. if ASD + pulmonary HTN pregnancy should be avoided as high risk of maternal complications
88
When does the ductus arteriosus normally close?
12-18 hrs after birth functionally and anatomically after 2-3 weeks. it is classes as patent if still open after 3 months for prem baby and 1 yr in term baby
89
Describe the clinical features of PDA
- usually asymptomatic
- large shunts may cause frequent LRTIs, failure to thrive, feeding difficulties etc due to heart failure
- O/E: hepatomegaly, tachycardia, tachypnoea, hyperactive precordium, systolic thrill, machinery murmur
90
How is PDA managed in term babies
If asymptomatic and well, wait till 1 yr with regular echo evaluation for spontaneous closure, if still patent at 1yr close with endovascular occlusion. If symptomatic then close earlier
91
How is PDA managed in prem babies?
extremely common and should be suspected if resp distress does not improve or worsens after initial improvement and baby cannot be weaned off vent. treatments include surgical ligation, echo guided catheter closure or can just give diuretics and fluid restrict while you wait for it to close on its own. in ELBW babies (<1000g) prophylactic NSAIDS can be given to aid closure.
92
What is coarctation?
narrowing of aorta, if before ductus arteriorsus= pre ductal= infantile type. If after ductus arteriosis= post ductal= adult type
93
Describe the clinical features of preductal/ infantile coarctation
If minor or postductal, may be asymptomatic or present with with poor feeding, failure to thrive or later in life with differences in upper and lower limb BP or HTN.
If more severe presents acutely w/ breathing difficulties and heart failure, acidosis and oliguria within 2-3 weeks of life (as PDA closes/ they decompensate).
Absent/ reduced femoral pulses is the give away- always check. .
Sats in the legs may be lower than right arm as blood supply to legs will come through ductus arteriosus and so have some deoxygenated blood from the pulmonary arteries- >3% difference in pre and post ductal SpO2
94
How is coarctation diagnosed and managed?
- most need MRI angio as echo isnt always diagnostic
- if symptomatic or arterial HTN they will get surgical resection of angioplasty
- often need f/u due to risk of reoccurrence and late HTN
95
What is a tet spell?
acute hypoxaemic attacks with low sats and cyanosis. Most are caused by tetralogy of fallot and are precipitated by crying, defecation, feeding fevers, dehdyration, tachycardia becauses these increase venous return, increasing L to R shunting so decrease pulmonary blood flow
96
How should tet spells be managed?
knee- chest position (increases venous return), calm child, oxygen, morphine. Saline bolus, ketamine, betablockers, phenylephrine can be used if this isnt working
97
other than congenital heart defects, what could cause heart failure in a child?
- inherited or aquired cardiomyopathies (dilated- barths, cartinine deficiency, myocarditis or hypertrophic- pompes, noonan, HOCM)
- arrhythmias (channelopathies, AVNRT, AVRT, ectopic atrial tachy)
- infection (sepsis induced myocardial dysfunction)
- high output states (thyrotoxicosis, systemic AV fistula, severe anaemia)
98
describe management options for paediatric heart failure
- nutrition support
- vent support
- diuretics, ACEi, BB, inotropes (digoxin), dopamine
- device therapy- implantable defib, LVSassist devises, resychronisation therapy)
- surgery for congenital disorders
- transplants
99
Give 3 indications and contraindications of heart transplants
indications:
- end stage HR
- severe limitation to activity
- life threatening arrhythmias
- cardiomyopathies with previously repaired CHDs
contra:
- recent or recurrent malignancy
- active or recent infection
- significant systemic diseases
- genetic or metabolic disease with poor long term prognosis
- renal or hepatic dysfunction not explained by HR
- pharmacologically reversible pulmonary HTN
100
How should viral induced wheeze be managed?
```
nutrition and hdyration
oxygen
salbutamol nebs
ipratropium nebs
NOT Steroids
```
101
How can viral induced wheeze be differentiated from pneumonia?
PNEUMONIA: any age, unilateral signs usually of creps, dullness, CXR changes (pleuritic pain), abrupt onset, high temp >39 + rigors, resp distress, others at home usually fine
VIRAL INDUCED WHEEZE: age 1-7, bilateral signs usually of wheeze +/- creps, slow onset, low temp <39. not usually resp distress unless severe, coryza rash, myalgia before, others unwell at home
102
How do you distinguish between acute asthma attack and a viral induced wheeze?
ASTHMA: no fever, history of atopy, cough, night symptoms, symptoms between episodes, usually a trigger (got to be AT LEAST 2, usually >5)
VIW: low fever, tight cough, others at home usually, unwell, coryza, age >2 (<2 more likely bronciolitis)
103
what are requirements for sweat test to be +ve?
need 100mcg sweat
cl conc >60mmol/l is positive
in infants, a conc of >30 is suggestive
104
what changes may be seen on cystic fibrosis CXRs over time?
- bronchial wall thickening
- progressive air trapping w/ bronchiestasis
- pulmonary nodules from abscesses
- atelectasis
- hyperinflation
- pulmonary artery dilation and RV hypertrophy associated w/ cor- pulmonale may be masked by hyperinflation
105
What is a hyperoxia test and what is it used to determine?
- 100% oxygen given for 10 mins, do ABG before and after
| - if cyanosis is due to lung problem, SpO2 will increase, if heart or circulation problem, it wont
