Skillnader i andningsfysiologi mellan barn och vuxna

En presentation över ämnet: "Skillnader i andningsfysiologi mellan barn och vuxna"— Presentationens avskrift:

1 Skillnader i andningsfysiologi mellan barn och vuxna
Ingrid Didriksson, Överläkare Kliniken för Intensivvård och Perioperativ medicin SUS Malmö

2 Respirations utveckling

3 Vid förlossningen Första andetaget
Krävs cm H2O för att övervinna ytspänning i alveoler samt att fylla luft i vätskefyllda alveoler Surfactant behövs Ökat PaO2 ger minskat motstånd i lungkretsloppet, foramen ovale sluts fysiologiskt First breath(s) up to 40 (to 80 cmH2O needed to overcome high surface forces to introduce air into liquid-filled lungs adequate surfactant essential for smooth transition Elevated PaO2 Markedly increased pulmonary blood flow -> increased left atrial pressure with closure of foramen ovale Neonatal breathing is a continuation of fetal breathing Clamping umbilical cord is important stimulus to rhythmic breathing Relative hyperoxia of air augments and maintains rhythmicity Independent of PaCO2; unaffected by carotid denervation Hypoxia depresses or abolishes coninuous breathing

4 Respiratorisk och cirkulatorisk anpassning efter förlossning
Neonatal breathing is a continuation of fetal breathing Clamping umbilical cord is important stimulus to rhythmic breathing Relative hyperoxia of air augments and maintains rhythmicity Independent of PaCO2; unaffected by carotid denervation Hypoxia depresses or abolishes coninuous breathing

5 Lungans utveckling Surfactant bildas i Pneumocyter typ II from v 24-26
Adaptation postpartum pågår til gestationsvecka 44 Respiratorisk kontroll utvecklas fram till v 60 Alveoli bildas tom 18 månader Lungelasticitet och collagen fibrer utvecklas tom 10 års åldern Dynamic FRC in awake, spontaneously ventilating infants is maintained near values seen in older children and adults because of 1. continued diaphragmatic activity in early expiratory phase 2. intrinsic PEEP (relative tachypnea with start of inspiration before end of preceding expiration) 3. *sustained tonic activity of inspiratory muscles (probably most important) By 1 year of age, relaxed end-expiratory volume predominates Infants and toddlers to age 2 years: VT preferentially distributed to uppermost part of lung

6 Problem i neonatalperioden
IRDS pga surfactant brist PPHN om acidos, hypoxi, kall… (Kongenitala hjärtvitier) Mekonium aspiration Apné Central apnea apnea > 15 seconds or briefer but associated with bradycardia (HR<100) cyanosis or pallor rare in full term majority of prematures

7 0-1 månad Låg lung compliance
Hög bröstkorgs compliance/svag andningsmuskulatur Mer benägen till atelektaser, svårt behålla FRC. AutoPEEP för att motverka atelektas mha grunting, hög andningsfrekvens Näsandare Neonate Lung compliance high elastic fiber development occurs postnatally static elastic recoil pressure is low Chest wall compliance is high cartilaginous ribs limited thoracic muscle mass More prone to atalectasis and respiratory insufficiency especially under general anesthesia Infancy and childhood static recoil pressure steadily increases compliance, normalized for size, decreases By 9-12 months CW = CL Dynamic FRC in awake, spontaneously ventilating infants is maintained near values seen in older children and adults because of 1. continued diaphragmatic activity in early expiratory phase 2. intrinsic PEEP (relative tachypnea with start of inspiration before end of preceding expiration) 3. *sustained tonic activity of inspiratory muscles (probably most important) By 1 year of age, relaxed end-expiratory volume predominates Infants and toddlers to age 2 years: VT preferentially distributed to uppermost part of lung

8 Barn 1-12 månader Lungvolymen är låg i förhållande till kroppsstorleken VO2/kg = Dubbelt så stor som hos vuxen => Fördubblat krav på respirationen! Mindre reserver, snabbare desaturering vid apné.

9 Lung volymer = 60 ml/kg 0-12 månader 90 ml/kg hos 5-åring 50% av TLC Ca 15% av TLC om generell anestesi och muskelrelaxantia

10 0-6 år Mindre luftvägsdiameter gör dem mer känsliga för övre och nedre luftvägsobstruktion Inflammation, ödem och sekret kan leda till obstruktion Sämre immunförsvar-ÖLI, pneumoni Främmande kropp i luftvägarna en risk.

11 http://www. youtube. com/watch

12 Är luftvägen fri? Titta-bröstkorgsrörelser mot stängd luftväg?
Lyssna-stridor? Känn-känns andetagen mot din hand? Chin lift Jaw thrust Svalgtub Intubation Airway – look, listen, feel Chin lift Jaw thrust Oral airway - size? Intubation – tube size? Surgical airway – cricothyroidotomy

13 Intubation - anatomi Larynx anterior och cephalad Lång epiglottis
Stor tunga Crichoid brosket minsta diametern Kort avstånd I trachea. Stor risk för accidentell extubation eller bronkintubation Larynx cephalad and anterior in children Long epiglottis Large tongue Narrowest point = cricoid cartilage You may need to be lower than patient and look up! If possible nasal intubation. If not, reintubate nasally after stabilization.

14 Ventilation Effort-RR, indragningar, stridor
Efficacy-Bröstkorgsrörelser, andningsljud, SpO2 Effect –cirkulationssvikt, påverkat medvetande

15 Undersökningsfynd Stridor  övre luftvägs obstruktion
Rhonki  nedre luftvägs obstruktion Feber  pneumoni? Rassel  Hjärtsvikt? Urticaria  anafylaxi? Key features give a first clue as to the emergency treatment needed Be prepared to consider other causes if poor response to a treatment option

16 Tecken till försämring
Ökande indragningar Ökande RR Ökande HR Utmattning Sjunkande medvetande Cyanos

17 Initial resuscitering
Fria luftvägar Ge O2 högflöde Maskventilation

18 Stridor Sekret– dålig hostkraft? Snarkning – sänkt medvetandegrad?
Ljudlig stridor/hosta – Falsk krupp? Främmande kropp Plötslig debut – Främmande kropp Tyst stridor/allmänpåverkan – tracheit? Epiglottit? With secretions, suction (unless evidence of upper airway pathology i.e. croup, FB, epiglottitis) If snoring, airway opening manoevre/oro- or naso-pharyngeal airway (unless evidence of upper airway pathology i.e. croup, FB, epiglottitis) Further conditions-next slides

19 Stridor Falsk krupp-behandling
Syrgas Adrenalininhalation Betapred Högläge Dose of dexamethasone is 150mcg/kg and budesonide, 2mg for all.

20 Stridor Bakteriell tracheit
Syrgas Ofta intubation och Ventilatorbehandling IV antibiotika

21 Stridor Epiglottit akut behandling
Syrgas ÖNH läk/anestesiolog-intubation IV antibiotika Undvik att stressa barnet

22 Stridor :Främmande kropp i luftvägar
Stel bronkoskopi med jet ventilation Ryggdunk etc Direkt laryngoscopi Kirurgisk luftväg??? Which intervention is used depends on the individual child’s predicament If there is sufficient airway patent to maintain reasonable oxygenation, do not jeopardise it but get an anaesthetist and if available an ENT surgeon with a view to the controlled removal of the FB after gaseous induction of anaesthesia If the child is in extremis then attempt the “choking child” manoevre and if unsuccessful attempt direct laryngoscopy and removal with Magill’s forceps. If unsuccessful attempt cricothyroidotomy or surgical airway

23 Rhonki Bronchiolit – Oftast under ett år Astma – oftast över ett år
Have a brief discussion of the difficulties of diagnosing/treating asthma in the under one age group, poor response to bronchodilator therapy Many children with recurrent viral induced wheeze between 1 and 4y are treated with and respond to asthma therapy. Most will grow out of this tendency to wheezy bronchitis – those with interval symptoms and strong personal or family histories of atopy are more likely to have asthma, and be treated with preventer inhalers (eg beclomethasone or budesonide).

24 Svårt /livshotande astmaanfall
Svårt att prata eller amma pga andnöd RR >30 >5 år > år Puls >120 >5 år > år Livshotande Utmattad Dåliga andningsrörelser Tysta andningsljud Hypotensiv Sänkt medvetandegrad Features of severe and life-threatening episodes of acute asthma. Wheeze is not on here, as it decreases with increasing airways obstruction. Recession and use of accessory muscles will occur in severe and life-threatening attacks. Some children with acute severe asthma do not appear distressed. Consider whether this could be anaphylaxis – see section 9.10 of APLS 5e for further details. Svår Too breathless to talk or feed Resp >30 >5 years > years Pulse >120 >5 years > years Livshotande Exhaustion Poor respiratory effort Silent chest Hypotension Conscious level depressed/agitated

25 Svårt astmaanfall Syrgas högflöde ß-agonist och ipratropium inhalation
ß-agonist systemiskt IV steroider Teofyllin Mg Mekanisk ventilation RtgPulm In severe asthma, the child is not in extremis but may become so if bronchospasm is not reversed promptly. If the initial dose of nebulised salbutamol and ipratropium has not produced any significant improvement, go straight onto a second and possibly a third dose of nebulised salbutamol. Ipratroprium can be nebulised every minutes (BTS-SIGN guidelines, 2004). In the younger child who may have poor inhalation of nebulised medication, consider moving on to intravenous therapy earlier. The patient needs continued monitoring and frequent reassessment. If there is improvement then continue with frequent or even continuous nebulised salbutamol, monitoring and reassessing the child frequently. Failure to respond to continuous nebulised salbutamol means that I.V. treatment is needed and either aminophylline or salbutamol can be used. We do not know which of these two drugs is the best to use in this circumstance yet but both have been shown to be helpful in severe cases – salbutamol has less serious side-effects (BTS-SIGN Guidelines, 2004). Both need ECG monitoring. The earlier steroids are given the better. The IV route will be necessary in this instance. A portable chest radiograph should be obtained. It is rarely helpful but occasionally may show a clinically unsuspected pneumothorax which can then be treated. There is not yet sufficient evidence for the routine use of magnesium sulphate in acute severe asthma in children, although some clinicians are using this.

26 Bronchiolit Spädbarn Oftast prematura Hosta Rhonki Apné

27 Pneumoni Syrgas Antibiotika Pleuradrän? Respirator/NIV
Cefuroxime for common bacterial pathogens, cefotaxime if there appears to be sepsis, flucloxacillin if staph aureus is a possibility, and a macrolide antibiotic for possible pertussis or atypical pneumonias. Large pleural effusions that may be causing respiratory distress should be drained under ultrasound guidance; specimens should be collected for bacteriology, virology and histopathology. Intra-pleural urokinase is commonly instilled via the intercostal drain to help break down loculations.

28 Hjärtsvikt Hjärtförstoring Leverförstoring ± blåsljud ± Cyanos
Inkompensation på Rtg Pulm Cardiac enlargement detected clinically or on CXR suggests a possible cardiac cause for respiratory failure. The liver may be pushed down by over-inflated lungs or congested due to heart failure. In the latter situation, the liver size may change in line with jugular venous pressure measurements. Not all children with CHD have a murmur The cyanosis is pulmonary if it improves with oxygen. If it does not then the child has a right to left shunt (but these children usually present with cyanosis rather than dyspnoea)

29 Hjärtsvikt Som kan se ut som andningsproblem…
Vä->Hö tex VSD Vä kammar obstruktion tex aorta stenos Nedsatt EF tex myocardit Arrytmier tex SVT The reduction of pulmonary vascular resistance over the first days of life will cause an increased left to right shunt in babies with a large VSD, PDA etc. This will produce pulmonary congestion and dyspnea, tachypnea, tachycardia, sweating and poor feeding. Myocarditis is very rare and will present similarly. Heart failure from left to right shunts almost always presents in infancy.

30 Hjärtsvikt /akut behandling
Syrgas Diuretika Prostaglandin till Dc beroende hjärtfel

31 Syrgasdissociationskurvan
If SpO2 = 91 then = PaO2 = Adult 6 months 66 6 weeks 6 hours

32 Sammanfattning Immunologiskt omogen Liten luftvägsdiameter
Svårare luftvägshantering Låg bröstkorgscompliance Svaga accessoriska andningsmuskler Omogen respirationskontroll