Respiratory Terminology•Dyspnoea •Difficulty in breathing•Orthopnoea •Dyspnoea necessitating an upright, sitting position for its relief•Tachypnoea •Abnormally rapid rate of breathing (>20)•Bradypnoea •Abnormally slow rate of breathing (<12)•Hypoxia •Inadequate o2 at cellular level•Hypoxaemia •Low o2 levels in blood•Anoxia •Lack or oxygen, local or systemic
Assessing the Respiratory PatientA-F approach:• assess Airway and treat if needed• assess Breathing & treat if needed• assess Circulation & treat if needed• assess Disability& treat if needed• Expose & examine patient fully once A.B.C.D are stable.• Full set of vital signs!
The Respiratory ExamGeneral:Level of consciousness:• Agitation/anxiety• Speech – Sentences/phrases/words/unable to speak – Quality (hoarness)Skin colour:• Pallor/cyanosis• Exercise tolernace/bodyposition
The Respiratory ExamHead and neck:• Nasal flaring• Pursed-lip breathing• Mouth vs nose breathing• Evidence of trauma: deformity, bruising, wounds, swelling, burns• Tracheal position• Tracheal plug
The Respiratory ExamThorax:• Symmetry of chest wall movement• Accessory muscle use, recession• Rate, rhythm, pattern of breathing• Evidence of trauma, wounds, deformity, flail, bruising, scars• Anterposterior vs transverse diameter of chest• Alignment of spine, presence of kyphosis, scoliosis
The Respiratory ExamExtremities:• Clubbing• Oedema• Peripheral cyanosis
Breath Sounds1. Crackles •Caused by opening of collapsed alveoli, or from fluid in smaller airways. (pneumonia)2. Wheezes •Air moves through narrowed/tight airways. (FB, bronchoconstriction, sputum). Continuous musical sound.3. Rhonchi •Caused by secretions in large airways.4. Pleural rub •Heard on inspiration, grating or crackling sound.5. Stridor •High-pitched crowing-type noise-louder during inspiration. Indicates obstruction.
Investigating & Monitoring the Respiratory Patient• Physical assessment can be further informed by appropriate use of investigations in the ED such as: • Pulse oximetry • Capnography • Blood Gases • Radiographs • Peak Flow • Spirometry
The Humble Respiratory Rate• The neglected vital sign• Done poorly by nurses• Pulse oximetry is not a replacement• Average adult RR ?10-18• Recent study showed RR >27 was the most important predictor of cardiac arrest in ward patients. • (Cretikos, A. Et al. (2008) Medical Journal Australia)
Pulse Oximetry •Pulse oximetry provides non-invasive (almost) real-time measurement of oxygen saturation.• Amount of oxygenated haemaglobin being transferred• Normal range 95-99%• Accuracy decrease when Spo2 <70%• Poor perfusion and shock states will result inaccurate readings• Finger, ear, forehead devices available.
Capnography• End-tidal carbon dioxide monitoring (EtCO2)• Gold standard for ET placement, and procedural sedation• Correlates similarly to PaC02• Demonstrates adequacy of ventilation• Superior to pulse oximetry (real time)• More accurate than nurse’s at taking RR.• Normal range 35-45mmHg
The Blood GasProvides information regarding respiratory function:• Acid-base balance• Oxygenation• Ventilation• Tissue perfusion & compensation
Blood Gas ValuesValue ABG VBGpH 7.35-7.45 7.35-7.38PaCO2 35-45mmHg 44-48mmHgPaO2 80-100mmHg 40mmHgHCO3 22-26mmol/L 21-22mmlol/LBase Excess (-)2-2mmol/L (-)2-2mmol/L • Most info that was traditionally gained from an ABG can now be gained from a VBG!!!
5 steps to interpreting the Blood GasStep 1• Look at Pa02 level “does the Pao2 show hypoxaemia?”Step 2• Look at the pH level “Is the pH on the acid /alkaline side of 7.40Step 3• Look at PaCO2 level “does it show resp acidosis/alkalosis or normalcy?”Step 4• Look at HC03 level “does it show metabolic acidosis/alkalosis or normalcy?”Step 5• Go back to the pH level does it show a compensated or uncompensated condition?
Interpreting the CXRAppearance •Chest view (AP, lateral, PA), airway, addition apparatus- (ETT, trachy, ECG leads, NGT), Lung fieldsBones •FracturesCardiac shadow •Cardiac & costophrenic angles, aortic arch & width of mediastinumDiaphragm •Shape, breadth, depth (8th rib viewed) in lung field.Exposure •Are the posterior spinous process visible?Fine lines •Fine lines (Normal lung markings out to edge of lung field), fat line (congested fluid volume), fuzzy lines (infection).Gastric bubble •Gastric bubbleHylus markings •Hylus markingsIdentification •Named, URM
PEFM & Spirometry• Both assess for airway limitations & obstructionPEFM – used to assess “Peak Expiratory Flow” – Monitors effectiveness of asthma therapySpirometry – More sensitive info gathered – Forced vital capacity – Forced expiratory capacity – (FEV1:FVC) <80% = airflow limitations
Respiratory Failure is the Enemy •Respiratory failure occurs when either function of gas exchange- the exchange of oxygen and of carbon dioxide between the lungs and the atmosphere fails.Occurs when:• Pa02 fall < 60 mmHg (Type 1 – hypoxaemia)• PaC02 rises > 50mmHg (Type 2- hypercapnia) – Can be acute or chronic!
Causes of HypoxiaMechanism Common clinical causesDecrease in Fi02 •High altitude •Low O2 concentration of gas mixture •SuffocationHypoventilation of the alveoli •Lack of neurological stimulation of the respiratory centre (medulla) •Defects in chest wall mechanics •Large airway obstruction •Increased work of breathingVentilation-perfusion mismatch •Asthma •Chronic bronchitis •Pneumonia •Atelectasis •Pulmonary embolus •ARDSAlveolocapillary diffusion abnormality •Oedema •Fibrosis •EmphysemaDecreased pulmonary capillary •Intracardic defectsperfusion •Intrapulmonary ateriovenous malformations
Case Study• 69 male• Presents with 3/7 hx of cough, SOB, and feversPMHx: MI, CVA, COPD, DM TYPE 2Meds: Home O2, spiriva, aspirin, ISMN.O/A: Sitting tripod position, pursed lip breathing, mildly agitated.O/E: Audible wheeze, using full accessory muscles, talking in words.Vitals: HR 123, RR44, Spo2 88, BP 179/94, T 38.4An ABG and CXR are done:
Blood Gas and CXR• An ABG shows the following: – pH 7.20mmHg – PaC02 69mmHg – Pa02 70mmHg – HC03 25 mmol/L
The Result’s• pH is acidotic• PaC02 is acidotic (High)• HC03 is normal (no compensation)• Pa02 is low – hypoxaemic – Respiratory acidosis• The chest X-ray shows: – Dynamic hyperinflation – RU Lobe pneumonia
COPD “COPD- pulmonary disease characterised by airflow limitation that is not fully reversible”Combination: – Chronic bronchitis – EmphysemaNarrowing of the airway = decrease airflow (FEV1)Poor gas exchange results hypercapnea & hypoxaemia• Chronic condition with acute exacerbations• Infective Vs Non-infective
Non-Invasive Ventilation• Used a lot in ED• NIV= delivery of O2 by positive pressure mask.Two modalities: – CPAP = fixed pressure through-out. – BiPAP = 2 different pressure IPAP & EPAP through- out cycle.• Most effective in COPD, ACPE, asthma!
Case Study• 19 y.o. male• Playing Basket ball• Sudden onset SOB and R sided inspiratory chest pain.Vitals: RR 28, SPO2 93% RA, BP 105/62, P 110,O/E: Sitting high fowlers, talk in words, moderate use of accessory musclesO/A: Decreased Air Entry R side, ∧resonance on percussion
Pneumothorax “PTX is a collection of gas in the pleural cavity of the chest between the lung and chest wall.”• Primary PTX- occurs in healthy-no lung disease, tall patients.• Secondary PTX- occurs in chronic lung disease, (smokers high risk)• PTX – from blunt & penetrating trauma• Tension PTX – haemodynamic collapse –medical emergency
Pneumothorax Management• Small <2cm, with no lung disease .D/C home GP F/U. (No flying 1/52, Never SCUBA dive)Moderate –Large PTX (2cm or more/50% lung volume lost)1. Needle aspiration2. Intercoastal catheter – ICC – Pigtail• Resp admit, serial CXR, encourage smoking cessation.• Tension = Needle Decompression – (14g canula 2nd intercostal space –midclavicular line)
Case Study• 44 female• P1 from SJA, severe SOB, wheezing, becoming more agitatedPMHx: Asthma x2 ICU admits, depressionMeds: Ventolin, Prednisolone, AvanzaO/A: Nebs insitu, talking in words, wheeze audible,O/E: Using accessory muscles, restless, tremulousVitals: RR36, spo2 97, HR 142, temp 35.9, BP 143/89
Asthma •Asthma characterised by bronchial hyper-responsiveness and inflammation that cause episodic reversible bronchospasm and increased mucus and oedema production.• Leads to widespread but variable airway obstruction that’s reversible either spontaneously or with treatment.• Activated by an allergic/inflammatory cascade.• Long term – develop irreversible lung function impairment.
Asthma AssessmentLook for:• Dyspnea > tachypnoea• Wheezing, chest tightness, cough• Prolonged expiration, ability to speak• Past asthma hxDeteriorating:• Inability to talk• Silent or quiet chest• Agitation, decreased level of consciousness
Asthma Investigations“Test’s provide little information over clinical assessment”• P.E.F.M.• Spirometry• CXR• Blood gas
Asthma ManagementManagement determined by severity.Mild > Moderate:Oxygen: Keep spo2 >95%Bronchodilators: Salbutamol 5mg MDI (prefered) or NebsAntichoinergics: Ipratropium bromide 500mcg MDI or NebSteriods: Prednisolone PO or Hydrocortisone IV• AB’s only if infective process present
Asthma Management• Severe:• Goal is to prevent intubation but maximising therapy.• Ventilation: Trial NIV – Intubation if fails.• Magnesium - causes smooth muscle relaxation > bronchodilation• Adrenaline –Alpha effect > airway oedema, Beta effect > bronchodilation
Case Study• 38 y.o. female• C/O increasing SOB and inspiratory chest pain.PMHx: Recent DVT – post flight from LondonMeds: Warfrin, OCPVitals: RR 24, Spo2 96 2l O2, BP 139/88, Temp 37.3, P 124O/A: Talking in sentences, no accessory muscle use,0/E: Good A:E bilaterally, no adventious sounds
Pulmonary Embolus •PE is blockage of the main artery of the lung or one of its branches by a substance that has traveled elsewhere in the body through the bloodstream.• Usually results from DVT• Risk Factors (Vircow’s Triad) – Hypercoaguability – Venous stasis – Endothelial damage• Impact of PE- dependent on size & blood flow compromise.
Case Study• 23 female• C/O SOB, wheezing, productive cough, runny nose. Currently 20/40.PMHx: Nil.Meds: OCP.O/A: Severe SOB, blue lips,O/E: Agitated, using all accessory muscles, talk in wordsVitals: RR42, SPO2 85%NRBM, BP 90/55, TEMP 37,5, GCS 14
Influenza Like IllnessCharacterised:• Temp >37.8°C• Cough• Sore throat• Absence of a KNOWN cause other than influenza •Generally benign clinical course
H1N1• Influenza A virus is quadruple reassortant virus – genes from avian strain, 2 swine strains, 2 human strains.• Full extent of virus unknown• 2009-10 left huge strain on ICU beds• High mortality in young patients• Relative lack of humoral immunity!!
@ Risk Groups for Critical H1N1• Children <5 y.o.• Adults > 65 y.o• Pregnant women• PT’s with – CHRONIC pulmonary, cardiovascular, hepatic, haematologic, neuro or metabolic disorders.• PT’s with immune defficency– (HIV , CHEMO)• Residents of NH
Influenza Like Illness Management• PPE-Droplet Precautions• Majority of cases are the humble FLU!• Swabs – supportive/respiratory care.• Commence antiviral: – Tamiflu 75-150mg BD – RelenzaDeteriorating:• Admit Resp or ICU• Early ventilatory support• ECMO
Take Home Points• You will see lots of different respiratory conditions during your ED period.• Most are chronic.• Assessment is important – reassessment is paramount.• Respiratory rate – do it properly• Enjoy the learning – NIV, mechanical ventilation – “skills for a lifetime”