Clinical Practice Guidelines – Respiratory

Respiratory• Acutepulmonaryoedema(OPA)

• Airwayobstruction(foreignbody)

• Asthma

• COPD

• Croup/epiglottis

• Dyspnoea

• Hyperventilation

Version 1.0 – September 2011

Clinical practice guidelines Acute pulmonary oedema

Clinical features (continued)

• Pink,frothysputummaybepresentinpatientswithseveredisease.

• Tachypnoeaandtachycardia

• Hypertensionisoftenpresentbecauseofthehyperadrenergicstate.

• HypotensionindicatessevereLVdysfunctionandcardiogenicshock.

• Patientsusuallyappearanxiousanddiaphoretic.

• Cyanosis(latesign)

Risk assessment

Precipitants of acute pulmonary oedema (APO)Primary cardiogenic causes:

• LVfailure:

- ACS- Arrhythmia- Pericarditis,myocarditisorendocarditis- Valvedysfunction(e.g.Aorticstenosis,mitralregurgitation)

• Increasedintravascularvolume:

- Fluidoverload- Non-compliancewithfluidrestrictionordiuretics- Renalfailure

• Pulmonaryvenousoutflowobstruction:

- mitralvalvestenosis

Acutepulmonaryoedema(APO)referstotherapidbuildupoffluidinthealveoliandlunginterstitiumthathasextravasatedoutofthepulmonarycirculation.Asthefluidaccumulates,itimpairsgasexchangeanddecreaseslungcompliance,producingdyspnoeaandhypoxia.[1]Thepathophyisiologicalmechanismsaretraditionallycategorisedintotwoprimarycauses:

Cardiogenic ThisformofAPOoccurswhencardiacoutputdropsdespiteanincreasedsystemicresistance,sothatbloodreturningtotheleftatriumexceedsthatleavingtheleftventricle(LV).Asaresult,pulmonaryvenouspressureincreases,causingthecapillaryhydrostaticpressureinthelungstoexceedtheoncoticpressureoftheblood,leadingtoanetfiltrationoffluidoutofthecapillaries.[2]

Non-cardiogenicPathologicalprocessesactingeitherdirectlyorindirectlyonthepulmonaryvascularpermeabilityarethoughttocausethisformofAPO.Asaresult,proteinsleakfromthecapillaries,increasingtheinterstitialoncoticpressure,sothatitexceedsthatofthebloodandfluidissubsequentlydrawnfromthecapillaries.[2]

Clinical features

• Suddenonsetofextremebreathlessness,anxiety,andthefeelingofdrowning

• Profusediaphoresis

• Cracklesareusuallyheardatthebasesfirst;astheconditionworsens,theyprogresstotheapices.

• CoughisafrequentcomplaintthatsuggestsworseningpulmonaryoedemainpatientswithchronicLVdysfunction.

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Risk assessment (continued)

Non-cardiogenic causes:

• Highoutputstates:

- Septicaemia- Anaemia- Thyrotoxicosis

• Systemicincreasevascularpermeability

- Pancreatitis- Eclampsia- DIC- Burns

• Toxins/environmental

- Immersion/submersion- Toxicinhalation- Highaltitudes(HAPE)&decompressionillness

• Other

- HeadInjury/intracranialhaemorrhage- Drugs(e.g.NSAIDs,calciumchannelblockersandnaloxone)

- Pulmonaryembolus

Additional information

• Cardiogenicpulmonaryoedemapatientsoftenhaveahistoryofcardiachypertrophy/AMI/LVF.[3]

• Theprimarygoalinthetreatmentofcardiogenicpulmonaryoedemaisreductioninpreloadandafterloadwithnitrates.

• AllpatientswithAPOshouldbegivensupplementaloxygentomeettheirphysiologicalneedsandreducehypoxia.

• APOpatientswhoarehypotensiveareincardiogenicshockandrequireICPsupportwhereavailable.Thesepatientsmayhaveafluiddeficitandthereforecautiousfluidbolus(250–500mLmaximum)resuscitationshouldbetitratedagainsthaemodynamicsandclinicaleffect.Inotropicsupportmayberequiredtoincreasecardiacoutput.

• Non-cardiogenicAPOrequiresrespiratorysupportandtreatmentoftheunderlyingcause.

Acutepulmonaryoedema–Page2of4

Version 1.0 – September 2011

Clinical practice guidelines Acute pulmonary oedema

Standard Cares

Appropriateposturing

Determinecauseofoedema

Cardiogenic? Non-cardiogenic?

Consider:• Oxygen• Aspirin• GTN• 12-LeadECG• IPPV• PEEP• CPAP

Consider:• Oxygen• 12-LeadECG• IPPV• PEEP• CPAP

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Transporttohospital

Pre-notifyasappropriate

ManageasperCPG:

• Relevantdysrrhythmia

• ACS

ManageasperCPG:

• Burns• Postsubmersion• Headinjury• Spinalinjury• Toxicology

Isthepatienthypotensive?

ManageasperCPG:

• Cardiogenicshock

Acutepulmonaryoedema–Page4of4

Version 1.0 – September 2011

Clinical practice guidelines Airway obstruction (foreign body)

• Aninfantmaybeplacedinaheaddownpositionbeforedeliveringthebackblows(i.e.acrossthelap).[2]

Chest thrusts:

• Ifbackblowsareunsuccessful,performuptofivechestthrusts.

• Checktoseeifeachchestthrusthasrelievedtheairwayobstruction.Theaimistorelievetheobstructionwitheachchestthrustratherthengiveallfive.

• Toperformchestthrusts,identifythesamecompressionpointforCPRandgiveuptofivechestthrusts.Theyaresimilartoachestcompression,butsharperanddeliveredataslowerrate.

• Iftheobstructionisnotrelieved,repeatthebackblowsandchestthrusts.

Aforeignbodyairwayobstructionisalifethreateningemergency,mostoftenoccurringwheneating.[1]

Itisimportantparamedicsrecogniseanairwayobstructionasitcanbereadilytreatedpre-hospital.

Clinical features

• History:

- suddendyspnoea,gaggingorcoughing

• Examination:

- respiratorydistresswithstridor,accessorymuscleuseandrecession

- restlessnessandcyanosis

- unconsciousnessandbradycardia(periarrest)

Risk assessment

• Notapplicable

Additional information

Back blows:

• Performuptofivesharpbackblowswiththeheelofonehandinthemiddleofthebackbetweentheshoulderblades.

• Checktoseeifeachbackblowhasrelievedtheairwayobstruction.Theaimistorelievetheobstructionwitheachbackblowratherthengiveallfive.

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Standard Cares

Severeairwayobstruction

Transporttohospital

Pre-notifyasappropriate

Effectivecough?

Conscious?

Mild airway obstruction

• Encouragecoughing• Provideongoingreassurance• Providesupportivecares

Consider:• Removingobstructionunderdirectvisualisation

• Oxygen• GentleIPPV• LMA/ETT• AppropriateresuscitationCPG

Consider: • Uptofivesharpbackblows• Uptofivechestthrusts• Repeatifrequired• Ensureongoingassessmentofairwayandconsciousstate

Note: OfficersareonlytoperformproceduresforwhichtheyhavereceivedspecifictrainingandauthorisationbytheQAS.

Airwayobstruction(foreignbody)–Page2of2

Version 1.0 – September 2011

Clinical practice guidelines Asthma

Clinical features (continued)

Mild Moderate Severe Life-threatening

Alert Alert Agitated Confused/drowsy

Nilaccessorymuscleuse

Mildaccessorymuscleuse

Moderateaccessorymuscleuse

Severeaccessorymuscleuseorminimalduetotiring

Notachypnoea Mildtachypnoea

Somephysicalexhaustion

Physicalexhaustion

Notachycardia Mildtachycardia

Markedtachypnoea

Markedtachypnoea

Variablewheeze

Variablewheeze

Markedtachycardia

Hypotension/bradycardia

Talksinsentences

Talksinphrases

Variablewheeze

Oftensilentchest

Saturation>94%roomair

Saturations90–94%roomair

Talksinwords Unabletotalk

Nocyanosis Nocyanosis Saturations<90%roomair

Saturations<90%roomair

Cyanosis/sweating

Cyanosis/sweating

Patientseatedupright,unabletoliesupine,pursedlipbreathing

Patientseatedupright,unabletoliesupine,pursedlipbreathing

Prolongedexpiratoryphase

Prolongedexpiratoryphase

Hyperinflatedthorax

Hyperinflatedthorax

Asthmaisapotentiallylifethreateningcondition.Itisachronicinflammatory,obstructivedisorderofthelowerairways,characterisedbyepisodesofreversiblepartiallowerairwayobstruction.Episodesofasthmacommonlycausewheezing,coughing,chesttightnessandbreathlessness.[1]

Obstruction of the lower airways results from a combination of:• bronchospasm

• inflammationandoedemaofairways

• mucousplugging

• airwaysmoothmusclehyperplasiaandhypertrophy.

Theaboveresultinincreasedairwayresistance,increasedworkofbreathing,alterationsinpulmonarybloodflowandmismatchesbetweenventilationandperfusion,eventuallycausinghypoxia.[2]

Treatment of asthma has two key concepts:

• Relievingthebronchospasm(relievers)

• Reducingtheinflammation(steroids).Steroidstakeseveralhourstoworkandsoearlieradministrationmeansearlieronsetofaction.

Clinical features

Asthmacanbeclassifiedasmild,moderate,severeornear-fatal(life-threatening).Near-fatalisacuteasthmaassociatedwithrespiratoryarrestorsignificanthypercarbia.[2]Therearetwobroadcategories:

• Gradualonsetoverdaysorweeksinpatientswithpoorlycontrolledasthma.Thisformisslowtorespondtotherapy.Thisisthemostcommonform,responsiblefor80–85%ofallfatalevents.[2]Thispatternrespondsslowlytotreatment.

• Rapidonsetandrespondsquicklytotreatment.

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Risk assessment (continued)

• Wheezingisanunreliablesignofseverity,assevereasthmamaybeassociatedwithaninabilitytomoveairduetophysicalexhaustion,resultinginasilentchest.[4]

• Notallpatientswithwheezehaveasthma–considerdifferentialdiagnoses(e.g.smokeinhalation,COPD,foreignbody,APO).[5]

Asthma attacks are not generally characterised by hypoxia until late in the episode. Beware the patient with normal SpO2.

Additional information

Important points in patient history:

• Previousasthmahistory–ageofonset,frequencyandseverityofsymptoms,numberofhospitalpresentationsinlast12months,ICUadmissions,previousintubation

• Co-existingmedicalconditions

• Allergies

• Asthmatriggersifknown

• Causeofcurrentepisodeifknown

• Durationofsymptoms–prolongedepisodesincreasepossibilityofphysicalexhaustion

• Medications.(reliever,preventer,steroids,compliance)

• Howtheyhavebeenmanagingcurrentepisode

Clinical features (continued)

Complications of asthmaRespiratory compromise• Gastrappingwithincreasedworkofbreathing,reducedventilation

• Hypoxia(late)duetoventilation-perfusionmismatch

• Hypercarbia–associatedwithexhaustion,alteredlevelofconsciousness(late)

• Barotrauma–particularlyinventilatedpatients[3]

- pneumothorax/tensionpneumothorax- pneumomediastinum/pneumopericardium.

• Pneumonia• Respiratoryarrest

Haemodynamic instability• Bradycardia/cardiacarrest–usuallysecondarytohypoxia

• Cardiacarrhythmias• Hypotension

Electrolyte abnormalities • Lacticacidosis,hypokalaemia,hypomagnesaemia

Risk assessment

Risk Factors for life-threatening disease• PriorICUadmissionsandpriorintubation• Threeormorehospitaladmissionsoverthelast12months

• Currentlytakingsteroidsforasthmaorchronicsteroiduse

• Poorcompliancewithmedications

Asthma–Page2of4

Version 1.0 – September 2011

Clinical practice guidelines Asthma

Standard Cares

Assessseverityandconsiderdifferentialdiagnosis

Life-threatening/imminentarrest

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Consider:• Adrenaline(early)IV/IM• IPPVwithprolongedexpiratoryphase

- adult:4–6b/m- largechild:8–10b/m- smallchild:10–15b/m- infant:15–20b/m

• Monitorforbarotrauma• Magnesiumsulphate• Hydrocortisone• Intubation

Consider:• SalbutamolandipratropiumNeb

• SalbutamolIV• AdrenalineIV/IM• IVfluid• Hydrocortisone• Magnesiumsulphate

Severe

Moderate/mild

Consider:• SalbutamolandipratropiumNeb

• IVaccess• Hydrocortisone

Transporttohospital

Pre-notifyasappropriate

Asthma–Page4of4

Version 1.0 – September 2011

Clinical practice guidelines Chronic 0bstructive pulmonary disease

Clinical features

An‘acuteexacerbation’ofCOPDusuallyfollowsinfection,althoughinsomecasesnoclearprecipitantisapparent.Clinicalfeaturesofanacuteexacerbationinclude:

• History:

- URTIsymptoms- Increaseddyspnoea,difficultyinspeaking,reducedexercisetolerance,fatigue

- Increasedsputumvolumeandpurulence- Chesttightnessandwheeze- Increasedcough- Anxiety- Increasedmedicationusewithminimalornoeffect

• Examination:

- Respiratorydistress- Intercostalorsuprasternalrecession- Accessorymuscleuse- Fever/sepsis- Cyanosis- Wheeze,crackle,reducedairentryonauscultation

- Tachycardia

Chronicobstructivepulmonarydisease(COPD)describesanumberofpulmonarydiseasesthatarecharacterisedbychronicairflowlimitationthatisnotfullyreversible.COPDincludes:

Chronic bronchitis –isdefinedasdailysputumproductionforatleastthreemonthsovertwoormoreconsecutiveyears.[1]Classicalpresentation:

• Cyanosed• Oftenoverweight• Oedematous• Chroniccough• Chronicsputumproduction• Corpulmonale(latesign)

Emphysema –ischaracterisedbydilatationanddestructionofalveoli.Thelossofelasticityandenlargementoftheseairspacesleadstohyperinflationofthelungsandincreasedworkofbreathing.[1]Classicalpresentation:

• Thin• Barrelchest• Dyspnoea• Tachypnoea• Pursedlipwhilebreathing• Intercostalorsuprasternalrecession• Tripodposture

Bothpresentationscansharesymptomsofdyspnoea,coughandsputumproduction,withchesttightness,airwayirritabilityandwheezesalsocommon.ThenaturalcourseofCOPDischaracterisedbyepisodesofacuteexacerbationwheretheabovesymptomsworsen.[2]

Note:COPDisaspectrumofdiseaseandmanypatientshavefeaturesofbothchronicbronchitisandemphysema.

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Risk assessment

COPDexacerbationmaymaskotherpathology,makingdiagnosisandmanagementdifficult.Thefollowingconditionsarecommondifferentialdiagnoses:[2]

• CardiogenicAPO/CCF/AMI

• Asthma

• Pneumonia/pleuraleffusion

• Upperairwayobstruction

• Pulmonaryembolism

• Pneumothorax

• Lungcancer

Additional information

Hypoxic drive

Theaimofoxygentherapyistopreventlife-threateninghypoxia;attemptsshouldbemadetotitratesupplementaloxygentoachieveSpO2readingsbetween88%and92%.[2]SomeCOPDpatientsrelyonhypoxiatodriverespirationratherthanhypercapniaduetochronicallyraisedCO2levels.Thusuncontrolledoxygentherapycanresultinsuppressionofrespiratorydrive,carbondioxidenarcosisandultimatelyrespiratoryarrest.[3]

If the patient is hypoxic high dosages of oxygen therapy are indicated, with a view to de-escalate oxygen concentration where appropriate; the lowest dosage of O2 possible should be used.

Standard Cares

Consider:

• SalbutamolNeb• IpratropiumbromideNeb

• SalbutamolIV• Hydrocortisone• Adrenaline• IPPV

Severerespiratorydistress?

Consider:

• MaintainSpO2at88–92%• SalbutamolNeb• IpratropiumbromideNeb• Hydrocortisone

Transporttohospital

Pre-notifyasappropriate

Chronicobstructivepulmonarydisease–Page2of2

Version 1.0 – September 2011

Clinical practice guidelines Croup or epiglottitis

Clinical features (continued)

• Highfever,septicaemia

• Maypresentinatripodposition,mouthbreathingwithtongueandjawprotrusion

• Stridororrespiratorydistress:

- snoringorstridor

- dyspnoea

- intercostalorsuprasternalretractions

- cyanosis

Distinguishing between croup and epiglottitis• Age

• Onset

• Typeofcough

• Degreeofrespiratorydistress

• Usually,croupoccursinyoungerchildrenandisproceededbyacoldorotherviralinfectionandthechildrarelyappearstoxic.

Risk assessment

• Notapplicable

CroupCroup(laryngotracheitis)isanillnessofinfantsandyoungerchildrenwithapeakincidencebetweensevenmonthsandthreeyearsofage.[1]

ItismostcommonlyassociatedwithaviralURTIincoldermonthsandisoftenworseatnight.[2]

EpiglottitisEpiglottitisisanacuteinflammationinvolvingtheepiglottis,vallecula,aryepiglotticfolds,andarytenoidsoccurringinbothadultsandchildren.Itoccursmostofteninadultsintheir40sand50sandchildrenbetweentwotofiveyearsofage.[3]

Itisanuncommon(duetovaccinationforHiB),butdangerouscauseofairwayobstruction.[4]

Clinical features

Croup• URTIsymptoms

• Fever

• Croupy(sealbark)cough

• Stridor(thismaybeabsentinseverecroup)

• Respiratorydistress:

- suprasternal,intercostalorsubcostalretractions

- cyanosis,pale/‘dusky’appearance

- agitation/distress

Epiglottitis• Rapidonset

• Muffledorhoarsevoice

• Sorethroat,painonswallowinganddrooling

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Standard Cares

• Calmpatient• Allowpatienttoassumeapositionofcomfort

• Consideraetiology

Patientpresentationconsistentwithcroup?

Patientpresentationconsistentwithepiglottitis?

• Managesymptomatically

Consider:• AdrenalineNeb• Oxygen(allowadequateexpiratorytime)

• Monitorfordeterioration

• Managesymptomatically• Donotvisualisetheairway• Monitorfordeterioration

Transporttohospital

Pre-notifyasappropriate

Additional information

• Avoidagitatingpatientswithcrouporepiglottitis.Letthepatientassumeapositioninwhichtheyfeelcomfortable.

• Directvisualisationoftheepiglottisshouldnotbeperformed.

• Loudnessofstridorisnotagoodindicatorofseverity.[1]

• ETIwillbeextremelydifficultduetoinflamationoftheairway.

• Mist,humidified,orcoldairhasnotbeendemonstratedtobeaneffectivetreatmentforcroup.[1]

• Allcrouporepiglottitispatientsshouldbetransportedtohospital,irrespectiveofpatient’sconditionpostinitialmanagement.Nebulisedadrenalineforcroupisatemporisingmeasureonlyandcliniciansmustbeawarethatsymptomsmayreturn.

Crouporepiglottitis–Page2of2

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Clinical practice guidelines Dyspnoea

Dyspnoeaisasubjectivefeeling,describedas‘shortnessofbreath’,butitalsoimpliesasenseofdiscomfort,withbreathinghavingbecomeaconsciouseffort.[1]

Therearefourmaincausesofdyspnoea:

• airwayobstruction• respiratoryfailure• cardiovascularfailure• thoracicmusculoskeletalcompromise.

Wheneverpossible,determineandtreatthecauseofthedypnoea.

Clinical features

General• Abnormalrespiratoryrateorpattern• Difficultyinspeakingorachangeintone• Diminishedairentryorabnormalrespiratorysounds• Flaringnostrils,accessorymuscleuse,trachealtug,intercostalorsupraclavicularrecession

• Restlessnessorposturalchanges(tripoding)

Obstruction• Inspiratorystridor(FBortissueoedema)• Snoringduetosofttissuecollapse• Gurglingduetofluidsinupperairway• Drooling,oradifficulty/inabilitytoswallowduetosofttissueoedema

Signs• Expiratory(orinspiratory)wheeze,crackles• Pursingoflips• Hyperinflatedchest• Silentchest

Risk assessment

• Acutecoronarysyndrome(ACS)canmanifestasdyspnoeaandmaybetheonlyindicationofanAMI,thereforetheneedfora12-LeadECGshouldbeconsidered.[1]

• Oedematousupperairwayobstructionsofrapidonsetandanyairwayobstructionduetonecktraumahaveahighpotentialtoevolveintocompleteairwayobstruction.[2]Necktraumacancauserapidoedemaandcompleteairwayobstruction,thereforerapidtransporttodefinitivecareisessential.

• Partialupperairwayobstructionmayprogresstocompleteobstruction.Limitinterventionstoonlythoseessentialtomaintainadequateoxygenation,calmthepatientandtransportrapidlytomoreskilledcare;alwaysprepareforthemanagementofacompleteobstruction.

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Standard Cares

ManageasperCPG:

• Airwayobstruction(foreignbody)

Airwayobstruction?

Foreignbody?Cardiovascular:• Acutecoronarysyndrome

• Acutepulmonaryoedema

• Pulmonaryembolism• Shock&sepsis• Dysrrhythmias• Specifictoxidromes

Respiratory:• Asthma• Anaphylaxisorallergies

• COPD• Inhalationinjury• Specifictoxidromes

Neurological:• Headinjury• Spinalinjury• CVA/TIA• Seizure• Pain• Hyperventilation• Metabolicacidosis• Toxidromes

Musculoskeletal:• Chestinjuries• Spinalinjury• Burns

ManageasperCPG:

• Croup/epiglotitis• Anaphylaxisorallergies

• Inhalationinjury

Transporttohospital

Pre-notifyasappropriate

Treat cause

Dyspnoea–Page2of2

Version 1.0 – September 2011

Clinical practice guidelines Hyperventilation

Clinical features

• Respiratoryratewilldependonageandunderlyingcomorbidities.

• Hypocapniaasaresultofhyperventilationmayleadtoparaesthesia(pinsandneedles)aroundthemouth,handsandfeet,restlessness,dyspnoea,pain,vertigo,carpopedalspasmandeventuallyunconsciousness.[3]

• RapidbreathingduetohypoxaemiawillusuallybereflectedinlowSpO2readings,withthenotableexceptionofcarbonmonoxidepoisoning.

Risk assessment

• Hyperventilationduetoemotionalstressisrareinchildrenandsothefocusshouldbeonfindingaphysicalcauseforanyrapidrespiratoryrate.[4]

• Theuseofapaperbagtotreathyperventilationhasbeendiscouragedforsometime.Thisisduetothetechniquefailingtoreversehypocapniaandactuallycausingmildhypoxia,whichhashadfatalconsequenceswhencasesofrespiratorydisease,PEandAMIhavebeenmisdiagnosed.[5]

• Anofteneffectivemethodofbreathingcontrolisencouragingthepatienttoreadapassageoftextoutloud.Thisdistractiontechniquealsoforcesthepatienttomodulatetheirbreathinginordertospeak.

Hyperventilationisanextremeformoftachypnearesultinginsignificanthypocapniaandsubsequentrespiratoryalkalosis.[1]Intheabsenceofbloodlevels,ifapatienthasarapidrespiratoryrateitisessentialtoruleoutpotentiallylife-threateningconditions,suchas:

• Lungpathology:

- pulmonaryembolism- pneumothorax- asthma- pneumonia

• Brainpathology:

- hypoxia- brainsteminjury

• Systemicillness:

- heatstroke- anaphylaxis- toxidromes(e.g.tricyclicsoraspirin)- metabolicacidosis(e.g.diabeticketoacidosis)- sepsis

Hyperventilation syndrome (rapid breathing caused solely by emotional disturbance) should always be considered a diagnosis of exclusion. [2]

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Isthereanyevidenceoflungorbrainpathologyorsystemicillness?

Isapsychologicalcauselikely?

Calmpatientandencourageadecreasedrespiratoryrate

ManageasperCPG:• specifictopathology

Reconsiderothercauses

Standard Cares

Transporttohospital

Pre-notifyasappropriate

Hyperventilation–Page2of2