Approach to dyspnoea

DYSPNOEA IS DEFINED AS THE UNDUE AWARENESS OF UNPLEASANT BREATHING.WHEN THERE IS AMIS MATCH BETWEEN THE AFFERENT VENTILATORY SIGNALS AND THE EFFERENT RESPIRATORY SIGNALS IN THE BRAIN WE MAY GET AN UNIGNORABLE FEELING FOR NEED OF MORE AND MORE OXYGEN.

1. “ I CANNOT BREATH VERY WELL ” DR.RISHIKESAN K.V SPECIALIST PHYSICIAN VENNIYIL MEDICAL CENTRE, SHARJAH

2. AIMS AND LEARNING OBJECTIVE DEFINITION OF DYSPNOEA AND DISCUSSION OF PATHOPHYSIOLOGY AETIOLOGY, DIFFERENTIAL DIAGNOSIS, EVALUATION OF BREATHLESS PATIENTS APPROACH TO THE PATIENTS WITH DYSPNOEA CASE STUDY UNDERSTANDING THE INTERPRETATION OF PULSE OXIMETRY, AND SPIROMETRY.

3. DEFINITION DYSPNEA, ALSO KNOWN AS SHORTNESS OF BREATH OR BREATHLESSNESS, IS A SUBJECTIVE SENSATION OF BREATHING DISCOMFORT. IT IS AN UN IGNORABLE FEELING OF NEEDING OXYGEN THE SENSATIONS ARE SIMILAR TO THAT OF THIRST OR HUNGER ACTIVATION OF SEVERAL PATHWAYS CAN LEAD TO THE SENSATION OF BREATHLESSNESS. 

4. DEFINITION BY MY PROFESSOR DYSPNOEA IS DEFINED AS UNDUE AWARENESS OF UNPLEASANT BREATHING

5. PATHOPHYSIOLOGY THE PATHOPHYSIOLOGY OF DYSPNOEA IS COMPLEX. IT INVOLVES THE ACTIVATION OF SEVERAL PATHWAYS AS WELL AS, STIMULATION OF THE RECEPTORS OF THE UPPER OR LOWER AIRWAY, LUNG PARENCHYMA, CHEST WALL, CENTRAL AND PERIPHERAL CHEMORECEPTORS. ACTIVATION OF THESE PATHWAYS IS RELAYED TO THE CNS VIA RESPIRATORY MUSCLE AND VAGAL AFFERENTS, WHICH ARE CONSEQUENTLY INTERPRETED BY THE INDIVIDUAL IN THE CONTEXT OF THE AFFECTIVE STATE, ATTENTION, AND PRIOR EXPERIENCE, RESULTING IN THE AWARENESS OF BREATHING . The pathophysiology, aetiology, clinical presentation and management of dyspnoea are reviewed. S Afr Med J 2016;106(1):32-36. DOI:10.7196/SAMJ.2016.v106i1.10324

6. AETIOLOGY CAREFUL HISTORY-TAKING IS THE MOST USEFUL FIRST STEP IN ELUCIDATING THE ETIOLOGY OF DYSPNEA. THE ETIOLOGY OF DYSPNEA COVERS A BROAD RANGE OF PATHOLOGIES FROM MILD, SELF-LIMITED PROCESSES TO LIFE-THREATENING CONDITIONS. THE MOST COMMON ETIOLOGIES ARE DISEASES OF CARDIOVASCULAR, PULMONARY, AND NEUROMUSCULAR SYSTEMS

7. DYSPNOEA SEVERAL FACTORS NEED TO BE ADDRESSED IN THE CLINICAL HISTORY WHEN CONSTRUCTING THE INITIAL DIFFERENTIAL DIAGNOSIS THE EVALUATION AND MANAGEMENT OF DYSPNOEA IS DIRECTED BY THE CLINICAL PRESENTATION, FINDINGS FROM THE HISTORY AND PHYSICAL EXAM, THE PRELIMINARY INVESTIGATION RESULTS.

8. USEFUL APPROACH IN THE DIAGNOSIS…. IS TO ENVISION THE ETIOLOGIES AND DIAGNOSTIC WORK-UP AS A CHECK LIST OF THE PHYSIOLOGIC PROCESS THAT MOVE OXYGEN FROM THE ATMOSPHERE INTO THE MITOCHONDRIA. RESPIRATORY CAUSES OF DYSPNOEA MAY AFFECT ANY LEVEL OF THE RESPIRATORY TRACT FROM THE NARES AND MOUTH TO THE PULMONARY ALVEOLI WE HAVE THE RESPIRATORY PUMP (1.NEURO MUSCULO SKELETAL DISEASES) TO GENERATE NEGATIVE PLEURAL PRESSURE (2.PLEURAL DISEASES) SO AS TO EXPAND THE COMPLIANT LUNG PARENCHYMA (3.PARENCHYMAL LUNG DISEASES) SO THAT AN OPEN CONDUCTING AIRWAY SYSTEM (4.LARYNGEAL AND TRACHEOBRONCHIAL DISEASES) CAN ADEQUATELY MOVE THE OXYGENATED AMBIENT AIR (5.HIGH ALTITUDE) FOR THE EXTRACTION OF OXYGEN

9. RESPIRATORY CAUSES OF DYSPNOEA

10. THE DISTRIBUTORY CIRCULATORY SYSTEM THE DISTRIBUTORY CIRCULATORY SYSTEM REQUIRES AN ADEQUATE AMOUNT OF OXYGEN CARRIERS (6.ANAEMIA AND HAEMOGLOBINOPATHY) AND AN INTACT SERIES OF UNIDIRECTIONAL PRIMING (7.ATRIAL AND VALVULAR DISEASES) AND PUMPS (8.DIASTOLIC AND SYSTOLIC DYSFUNCTION) AS WELL AS AN OPEN VASCULAR DISTRIBUTORY NETWORK (9.PULMONARY AND SYSTEMIC VASCULAR DISEASES) TO DELIVER THE OXYGEN TO THE LUNGS (10.PULMONARY EMBOLISM AND PULMONARY HYPERTENSION) AND TO THE END USERS SUCH AS MUSCLES AND VITAL ORGANS.

11. THE DISTRIBUTORY CIRCULATORY SYSTEM….. THE HEART HAS TO EXPAND TO RECEIVE AND SEND BLOOD INTO THE LUNGS AND DISTRIBUTE IT INTO AERATED EXCHANGE UNITS (11.V/Q MISMATCH AND SHUNTS) BEFORE IT IS RECEIVED INTO LEFT ATRIUM (12.PULMONARY VENO OCCLUSIVE DISEASES). THE LEFT HEART THEN DELIVER THIS BLOOD TO THE SYSTEMIC CIRCULATION THROUGH A SERIES OF VASCULAR CONDUITS (13.ATHEROSCLEROSIS AND OTHER OBSTRUCTIVE VASCULOPATHY) . THE OXYGEN FINALLY DIFFUSES FROM THE CAPILLARIES TO MITOCHONDRIA .

12. INITIAL ASSESSMENT OF PATIENTS WITH DYSPNOEA: STARTING WITH ABC ASSESSS A IRWAY PATENCY AND LISTEN TO THE LUNGS OBSERVE B REATHING PATTERN, INCLUDING USE OF ACCESSORY MUSCLES MONITOR C ARDIAC RHYTHM MEASURE VITAL SIGNS AND PULSE OXIMETRY OBTAIN ANY HISTORY OF CARDIAC , PULMONARY DISEASE OR TRAUMA EVALUATE MENTAL STATUS

13. RED FLAGS FOR SERIOUS FORMS OF DYSPNOEA HYPOTENSION RESPIRATORY RATE >40 ALTERED MENTAL STATUS HYPOXIA CYANOSIS STRIDOR BREATHING EFFORT WITHOUT AIR MOVEMENT TRACHEAL DEVIATION WITH UNILATERAL BREATH SOUNDS UNSTABLE ARRHYTHMIA

14. DIFFERENTIAL DIAGNOSIS CARDIAC : CCF, CAD , ARRHYTHMIAS, VALVULAR HEART DISEAS, ACUTE MI , PERICARDITIS AND CARDIAC TAMPONADE PULMONARY : COPD , ASTHMA, PNEUMONIA, PNEUMOTHORAX, PUL EMBOLISM, PLEURAL EFFUSION, METASTATIC DISEASE,GERD WITH ASPIRATION, RESTRICTIVE LUNG DISEASE PSYCHOGENIC : PANIC ATTACKS, HYPERVENTILATION, PAIN AND ANXIETY UPPER AIRWAY OBSTRUCTION : EPIGLOTTITIS, CROUP, FOREIGN BODY, EBV ENDOCRINE : METABOLIC ACIDOSIS, MEDICATIONS CNS DISEASES, NEUROMUSCULAR DISORDERS PAEDIATRIC : BRONCHIOLITIS,CROUP, FOREIGN BODY, MYOCARDITIS

15. ACUTE DYSPNOEA ACUTE DYSPNOEA APPEARS SUDDENLY OR IN A MATTER OF MINUTES IT TYPICALLY INDICATES ACUTE AND SEVERE CONDITIONS THAT MAY BE LIFE THREATENING ACUTE PUL.EMBOLISM MYOCARDIAL INFARCTION ACUTE VALVULAR INSUFFICIENCY FLASH PULMONARY EDEMA PNEUMOTHORAX ANAPHYLAXIS FB ASPIRATION CARDIAC TAMPONADE

16. SUBACUTE DYSPNOEA SUB ACUTE DYSPNOEA DEVELOPS OVER HOURS TO DAYS COMMON CAUSES INCLUDE : ACUTE ASTHMA EXACERBATION OF COPD PULMONARY EDEMA LESS COMMON CAUSES INCLUDE : MYOCARDITIS SVC SYNDROME ACUTE EOSINOPHILIC PNEUMONIA CARDIAC TAMPONADE

17. CHRONIC DYSPNOEA DEVELOPS OVER WEEKS TO MONTHS IT IS ASSOCIATED WITH CHRONIC PATHOLOGY 5 MAIN AETIOLOGICAL CATEGORIES ACCOUNT FOR MOST CASES OF CHRONIC DYSPNOEA : CARDIOVASCULAR DISEASE PULMONARY DISEASE RESPIRATORY MUSCLE DYSFUNCTION PSYCHOGENIC DYSPNOEA DECONDITIONING/OBESITY leads to chronic dyspnoea and may result from immobilisation after medical illness, surgery, trauma, a sedentary lifestyle

18. TIME COURSE OF DYSPNOEA ACUTE DYSPNOEA: appears suddenly or in a matter of minutes SUBACUTE : develops over hours to days CHRONIC: develops over weeks to months RECURRENT : dyspnoea occurs in paroxysm ACUTE PULMONARY EMBOLISM ACUTE ASTHMA CCF PAROXYSMAL TACHYARRHYTHMIAS MYOCARDIAL INFARCTION COPD EXACERBATION COPD INTERMITTENT CHB ACUTE VALVULAR INSUFFICIENCY PULMONARY EDEMA CARDIOMYOPATHY PNEUMOTHORAX MYOCARDITIS PHT ANAPHYLAXIS SVC SYNDROME VALVULAR HD FB ASPIRATION ACUTE EOS.PNEUMONIA ANEMIA PULMONARY EDEMA CARD.TAMPONADE MUSCULAR DYSTROPHIES

19. ASSOCIATED SYMPTOMS FEVER,COUGH PNEUMONIA, BRONCHITIS, LARYNGITIS CHEST PAIN CAD, PUL.EMB; PTX, PNEUMOMEDIASTINUM, PNEUMONIA, PLEURO PERICARDIAL DISEASES PALPITATION PUL.EMB; TACHYARRHYTHMIAS,VALVULAR HD, ANXIETY ATTACKS SYNCOPE TACHYARRHYTHMIAS, PUL.EMBOLISM WHEEZING ASTHMA,COPD, PUL.EDEMA, BRONCHIOLITIS, FB ASPIRATION CHANGE IN VOICE PNEUMOMEDIASTINUM, AORTIC ANEURYSM, GERD HEMOPTYSIS BRONCHITIS, BRONCHIECTASIS, CHEST MALIGNANCY,VASCULITIS, TB, PE DYSPHAGIA PNEUMOMEDIASTINUM, FB ASPIRATION, TETANUS MUSCLE WEAKNESS MYALGIA DECONDITIONG, MUSCULAR DYSTROPHIES, AML, GBS, ARBOVIRAL DISEASE, LEPTOSPIROSIS BONE PAIN SCD WITH ACUTE CHEST SYNDROME, FAT EMBOLISM WITH LONG BONE# ANXIETY PANIC ATTACKS, HYPERVENTILATION, TAKOTSUBO CMP

20. CLUES TO THE DIAGNOSIS FROM SYMPTOMS COUGH ASTHMA, PNEUMONIA SEVERE SORE THROAT EPIGLOTTITIS PLEURITIC CHEST PAIN PERICARDITIS, PUL.EMBOLISM, PNEUMONIA, PNEUMOTHORAX ORTHOPNOEA,PND,EDEMA CCF TOBACCO USE COPD,CCF, PUL.EMBOLISM INDIGESTION,DYSPHAGIA GERD,ASPIRATION BARKING COUGH CROUP

21. WHEEZING AND STRIDOR WHEEZING IS EXPIRATORY IN NATURE AND ASSOCIATED WITH LOWER AIRWAY DISEASE LIKE ASTHMA, AND BRONCHIOLITIS STRIDOR IS INSPIRATORY IN NATURE AND IS ASSOCIATED WITH OBSTRUCTION/ NARROWING AT OR ABOVE THE LEVEL OF THE VOCAL CORDS IN THE ROUTINE MANAGEMENT OF THE PATIENT WHO CARRIES A DIAGNOSIS OF ASTHMA AND PRESENTS WITH WHEEZING, IMAGING IS USUALLY NOT INDICATED IN A PATIENT WITH NO H/O ASTHMA ( AKA “FIRST TIME WHEEZERS”) IN MY OPINION IMAGING IS STRONGLY ENCOURAGED

22. ORGANISE YOUR THOUGHTS IS DYSPNOEA…….. A NEW PROBLEM ? EXACERBATION OF OLD PROBLEM? A COMBINATION? IS DYSPNOEA……. CARDIAC? PULMONARY? NEITHER? IS DYSPNOEA ONE OF THE DEADLY BUT SUBTLE DIAGNOSIS I SHOULD THINK OF EVERY TIME?

23. IS THE DYSPNOEA ? A NEW PROBLEM : MYOCARDIAL INFARCTION PULMONARY EMBOLISM PNEUMONIA TRAUMA ANAPHYLAXIS ARRHYTHMIA KEYS TO DIAGNOSIS: NO PAST H/O CARDIOPULMONARY DISEASES ATYPICAL OF OTHER DISEASE PRESENTATIONS NEW RISK FACTORS Eg. RECENT SURGERY

24. IS THE DYSPNOEA AN EXACERBATION OF….? CONDITIONS DIAGNOSTIC CLUES COPD/EMPHYSEMA/ASTHMA PAST MEDICAL HISTORY CCF TYPICAL OR ATYPICAL OF PRIOR PRESENTATIONS INTERSTITIAL LUNG DISEASE PRECIPITATING OR EXACERBATING FACTORS CARDIAC ARRHYTHMIA Eg. AF WITH FVR PHYSICAL EXAMINATION FINDINGS ANEMIA LABS AND TESTING NEUROMUSCULAR DISEASE PLEURAL/PERICARDIAL DISEASE

25. IS IT A COMBO OF NEW & CHRONIC PROBLEM ? RECURRENT DISEASE MYOCARDIAL DISEASE PULMONARY EMBOLISM ARRHYTHMIA MULTIPLE DISEASE CONSPIRING TOGETHER INFECTION EXACERBATING HEART FAILURE ARRHYTHMIAS EXACERBATING HEART FAILURE PNEUMONIA COMPLICATING COPD ANEMIA WORSENING CARDIAC ISCHAEMIA

26. Which of the following exams is most useful in differentiating copd from asthma? CHEST X RAY BNP PFT PULMONARY AUSCULTATION SPIROMETRY WITH BRONCHODILATOR

27. IS DYSPNOEA CARDIAC ? MYOCARDIAL ISCHAEMIA LEFT HEART DISEASE : ACUTE VALVULAR INSUFFICIENCY, LVF TACHYARRHYTMIAS, PHT, SLEEP APNOEA PERICARDIAL EFFUSION, CARDIAC TAMPONADE KEYS TO DIAGNOSIS MURMERS ECG BED SIDE ECHO

28. IS THE DYSPNOEA PULMONARY? ASTHMA,COPD/EMPHYSEMA ANAPHYLAXIS TRACHEAL DISEASE MUCUS PLUGGING PNEUMONIA PULMONARY EMBOLISM PNEUMOTHORAX KEY TO DIAGNOSIS ABNORMAL BREATH SOUNDS, STRIDOR , I/E RATIO CHEST X RAY

29. IS DYSPNOEA SOMETHING ELSE ENTIRELY? NEUROMUSCULAR DISEASES ANEMIA ENDOCRINE DISEASES METABOLIC DISORDERS PSYCHOGENIC OBESITY/DECONDITIONING TRAUMA TOXIC EXPOSURE ABDOMINAL DISTENTION (ASCITES, LIVER DISEASES )

30. ANXIETY AS A CAUSE OF DYSPNOEA THE MOST DANGEROUS DIFFERENTIAL DIAGNOSTIC CONSIDERATION DOESN’T REQUIRE CONFIRMATORY LAB OR IMAGING CAN’T BE DEFINITIVELY EXCLUDED BY ANY DEGREE OF TESTING “GARBAGE CAN” DIAGNOSIS BELONGS AT THE BOTTOM OF ANY PATIENT WORK UP ANY CLINICAL CONDITION THAT CAUSES DISTRESS CAN ALSO CAUSES ANXIETY BE VERY, VERY CAREFUL ATTRIBUTING PATIENT SYMPTOMS TO ANXIETY A THERAPEUTIC RESPONSE TO AN ANXIOLYTIC SUGGESTS ONLY THAT THERE IS AN ANXIETY COMPONENT; IT DOESN’T R/O ANYTHING

31. ANXIETY ANY CLINICAL CONDITION THAT CAUSES PHYSICAL DISCOMFORT WILL CONTRIBUTE TO DYSPNOEA WHAT CAME FIRST? ANXIETY OR PHYSICAL SYMPTOMS IF ANXIETY FIRST… IT MAY BE A COMPONENT IF PHYSICAL SX. FIRST… LOOK FIRST TO A PATHOLOGIC EXPLANATION EVEN IF YOU SUSPECT DIAGNOSIS KEEP IT IN THE BACKYARD OF YOUR MIND ADVISE THE PATIENT TO RETURN IF WORSE, NO BETTER, NEW SX, OR UNEXPECTED PROBLEMS Weinstock, M. Risk Management Monthly Emergency Medicine.Vol.11,No.6.June2017

32. DIAGNOSES TO CONSIDER EVERYTIME MYOCARDIAL ISCHAEMIA PULMONARY EMBOLISM INFECTION SEPSIS ARRHYTHMIAS CARDIAC TAMPONADE DIAGNOSTIC TEST TO CONSIDER: CXR, ECHO, ECG PULSE OXIMETRY

33. PULMONARY EMBOLUS IN PATIENTS WITH COPD PULMONARY EMBOLUS SHOULD BE CONSIDERED IN DIFFERENTIAL DIAGNOSIS FOR PATIENTS PRESENTING WITH COPD EXACERBATION ONE STUDY HIGH LIGHTED THAT UPTO 25% OF PATIENTS HOSPITALISED WITH COPD EXACERBATION HAD CONCOMITANT PULMONARY EMBOLISM BE SURE TO KEEP YOUR DIFFERENTIAL DIAGNOSIS BROAD

34. DIAGNOSTIC WORKUP CBC BASIC CHEMISTRY PANEL BLOOD GAS/PULSE OXIMETRY SPIROMETRY WITH BRONCHODILATOR PEAK FLOW CARDIAC TROPONIN, ECG CXR, CHEST CT BED SIDE ULTRA SOUND/ECHO D-DIMER BNP OR NT- BNP

35. BLOOD GAS ANALYSIS VENOUS BLOOD GAS IS PREFERRED OVER ABG IN THE EMERGENCY ROOM ABG EVALUATES OXYGENATION VENOUS BLOOD GAS EVALUATES VENTILATION VENOUS BLOOD GAS CORRELATES CLOSELY TO ABG. WE WILL GET FAIRLY GOOD IDEA REGARDING THE OXYGENATION FROM PULSE OXIMETRY

36. INTERPRETING BLOOD GAS IN ASTHMA & COPD A NORMALISED BLOOD GAS ( pH 7.4/ PCO2 40) SHOULD BE CONCERNING IN PATIENTS WITH MODERATE TO SEVERE ASTHMA EXACERBATION THIS MAY INDICATE THAT THE PATIENT IS TIRING OUT AND IN NEED OF VENTILATOR SUPPORT PATIENTS WITH COPD GENERALLY CHRONICALLY RETAIN CO2 AND MAY HAVE NORMAL pH ALTHOUGH THEY HAVE AN ELEVATED CO2 LEVEL . IT MAY BE IN THE RANGE OF 60s or 70S

37. BASIC OFFICE SPIROMETRY TWO QUESTIONS/STEPS PROVIDE INITIAL GUIDANCE: STEP1: IS THE FEV1/FVC RATIO NORMAL ( >/= 70% ) OR LOW (<70%) STEP2: IS THE FVC NORMAL (>/= 80% PREDICTED) OR LOW <80% PREDICTED FEV1 MEASURES HOW MUCH AIR CAN BE EXHALED IN THE FIRST SECOND FVC MEASURES HOW MUCH TOTAL AIR CAN BE EXHALED, FROM MAXIMAL INSPIRATION TO MAXIMAL EXPIRATION

38. BASIC SPIROMETRY : A CASE ILLUSTRATED 68 YEAR OLD ,OBESE MALE WITH PROGRESSIVELY WORSENING DOE FOR 6-7 YEARS HAS GOT SIG. ACTIVITY LIMITATION OVER 6 MONTHS HAS GOT PRODUCTIVE COUGH MOST MORNINGS. USED TO GET 4-5 EPISODES OF URI EVERY YEAR OVER THE PAST COUPLE OF YEARS, TREATED WITH SHORT COURSES OF ORAL STEROIDS AND ANTIBIOTICS BY THE FAMILY PHYSICIAN SMOKER 1.5 PACKS/DAY CAD S/P 3V CABG 4 YEARS AGO, HTN, DLP, BPH AND WELL CONTROLLED T2D

39. PHYSICAL EXAM OBESE, RUDDY FACED GETS VISIBLY SOB WHEN WALKING APPROX. 30 FT AFEBRILE, BP 162/90 , HR 112 REGULAR, MILDLY RAISED JVP, HS NORMAL LUNGS: INCREASED AP DIAMETER, DIMINISHED BREATH SOUNDS THROUGHOUT NO ADDED SOUNDS ABDOMEN : OBESE, EXTREMITIES : 1+ PEDAL EDEMA B/L NEURO INTACT

40. LABS ,CXR, AND PFT ROUTINE BLOOD TEST , LFT, BUN AND SERUM CREAT. AS WELL AS ELECTROLYTES : NORMAL CXR PA/LATERAL : EMPHYSEMATOUS , HEART SIZE RELATIVELY SMALL PUL. FUNCTION TEST : FLOW VOLUME CURVE: NORMAL INSPIRATORY CURVE BUT VERY PROLONGED EXPIRATORY CURVE FEV1 = .88 (38% PREDICTED) FVC = 1.38 (69% PREDICTED) FEV1/FVC = 64%

41. WHAT DO YOU THINK THE MOST LIKELY DIAGNOSIS ? A PURELY OBSTRUCTIVE PATTERN A PURELY RESTRICTIVE PATTERN A MIX.OF OBSTRUCTION AND RESTRICTION WITH A PREDOMINANT OBSTRUCTION A MIX. OF BOTH WITH PREDOMINANT RESTRICTION

42. SPIROMETRY (Cont.) STEP 1: CALCULATE FEV1/FVC RATIO : DEFINES OBSTRUCTION IF LOW (< 70% ) OBSTRUCTIVE LUNG DISEASE (OBSTRUCTION DURING EXHALATION E.g. COPD) IF NORMAL >70% NO OBSTRUCTION STEP2: CALCULATE FVC : SUGGESTS RESTRICTION; TLC IS NECESSARY FOR CONFIRMATION IF LOW <80% LIKELY RESTRICTIVE DISEASE (RESTRICTED BREATHING DURING INHALATION) IF NORMAL > 80% UNLIKELY RESTRICTIVE DISEASE

43. DIFFUSING CAPACITY FOR CO(DLCO) IS THE DLCO LOW <80% PREDICTED OR NORMAL (>/= 80%) IT DEFINES HOW FAST GAS DIFFUSES FROM LUNG ALVEOLI INTO BLOOD STREAM LOW DLCO : ALVEOLAR DISEASES ( EMPHYSEMA AND PULMONARY FIBROSIS) NORMAL DLCO : CHRONIC BRONCHITIS AS IT IS A DISEASE OF AIRWAYS DLCO IS USEFUL IN DIFFERENTIATING EMPHYSEMA FROM CHRONIC BRONCHITIS DLCO ALSO HELPS TO IDENTIFY IF RESTRICTION IS INSIDE THE LUNG (PULMONARY FIBROSIS) OR OUTSIDE THE LUNG ( OBESITY,CHEST WALL DEFORMITIES,NEUROMUSCULAR DISEASES etc.) NORMAL DLCO SEEN IN EXTRA PULMONARY RESTRICTION

44. PULSE OXIMETRY/S a O2 interpretation ONLY PATIENTS WITH FULLY FUNCTIONAL CARDIOVASCULAR/PULMONARY SYSTEMS SHOULD HAVE AN SaO2 ~ 100% ON ROOM AIR OUR PATIENT HAD COPD AND ONGOING TOBACCO USE WE DON’T EXPECT A PRETTY WELL SaO2 IN THIS PATIENT Hb LEVELS WILL AFFECT SaO2 Hb(ANEMIA) THE EASIER IT IS TO SATURATE Hb THE SaO2 MAY BE HIGH, BUT TOTAL O2 CONTENT WILL BE LOW Hb(POLYCYTHAEMIA) DIFFICULT TO SATURATE THE EXTRA MOLECULES OF Hb WITH O2 PSEUDO HYPOXAEMIA ---WHEN THE PATIENT’S O2 CONTENT MAY WELL BE NORMAL Carroll P. RT: For Decision Makers in Respiratory Care.2007

45. S a O2 INTERPRETATION AND TEMPERATURE PATIENT’S TEMPERATURE WILL ALSO AFFECT SaO2 READINGS HYPOTHERMIA TIGHTER Hb- O2 BOND WITH OXYGEN DELIVERY HYPERTHERMIA LOOSER Hb- O2 BOND WITH OXYGEN DELIVERY Shipsey P. Emergency Medicine Reviews and Perspectives.2012

46. CYANOSIS BLUE DISCOLORATION OF SKIN AND OR MUCUS MEMBRANE SECONDARY TO DEOXYGENATED Hb IN THE BLOOD , OFTEN FIRST VISUALISED IN THE TONGUE CENTRAL ( FACE, LIPS ,TONGUE etc ) PERIPHERAL (FINGERS OR TOES) CENTRAL CYANOSIS USUALLY SEEN > 5G/dL DESATURATED Hb DUE TO INADEQUATE BLOOD OXYGENATION FROM CARDIAC OR PULMONARY DISEASE. USUALLY APPARENT WITH SaO2 <85% OR < 75% ANEMIC PATIENT IS EXTREMELY UNLIKELY TO BE CYANOTIC AS THEY DO NOT HAVE ENOUGH Hb TO BE DEOXYGENATED POLYCYTHAEMIC CAN MORE SHOW CYANOSIS Lundsgard C , et al.Medicine.1923;2(1):1-76

47. Which of the following test is most useful in initially differentiating copd exacerbation from heart failure? CALF DIAMETER MEASUREMENTS CXR SPIROMETRY WITH BRONCHODILATOR BNP BMP

48. CONGESTIVE HEART FAILURE INABILITY OF THE HEART TO ADEQUATELY PUMP NECESSARY BLOOD REQUIRED TO MAINTAIN HOMOEOSTASIS DIASTOLIC HF : INABILITY OF THE HEART TO RELAX AND ADEQUATELY FILL RESULTING IN DECREASED SV SYSTOLIC HF :INABILITY OF THE HEART TO PUMP BLOOD FORWARDLEADING TO INADEQUATE ORGAN PERFUSION AND LUNG CONGESTION ECHOCARDIOGRAPHY IS THE KEY TO UNDERSTANDING THE CAUSE OF PULMONARY EDEMA AND IF SO WHICH TYPE

49. D-DIMER NEGATIVE D-DIMER TEST CAN HELP EXCLUDE PULMONARY EMBOLISM. SPIRAL CT HAS GOT A DEFINITE ROLE IN THE DIAGNOSTIC WORK UP OF PUL.EMBOLISM IT MAY EVENTUALLY REPLACE PULMONARY ANGIOGRAM

50. 5 CAUSES OF DYSPNOEA 1 AIR PROBLEM EMPTY TANK 2 NEUROMUSCULOSKELETAL OR VENTILATION PROBLEM GUILLAIN-BARRE, UNILATERAL DIAPHRAGMATIC PARALYSIS,RIB FRACTURES , MEDIASTINAL MASS etc 3 LUNG PROBLEM PNEUMONIA, PUL EMBOLISM, TUMOR, PLEURAL EFFUSION, PTX, PULMONARY CONTUSSION etc 4 HEART PROBLEM MI,VALVULAR HEART DISEASE, CARDIAC TAMPONADE etc 5 BLOOD PROBLEM ANEMIA, CARBOXY HAEMOGLOBINAEMIA, METHEMOGLOBINAEMIA, SC DISEASE etc Wahls SA. Am Fam Physician.2012 Jul15;86(2): 173-180

51. SUMMARY DYSPNOEA IS A SUBJECTIVE SENSATION OF BREATHING DISCOMFORT ACTIVATION OF SEVERAL PATHWAYS CAN LEAD TO THE SENSATION OF BREATHLESSNESS THE EVALUATION AND MANAGEMENT OF DYSPNOEA IS DIRECTED BY THE CLINICAL PRESENTATION, FINDINGS FROM THE HISTORY , PHYSICAL EXAM AND PRELIMINARY INVESTIGATION RESULT THE ETIOLOGY COVERS A BROAD RANGE OF PATHOLOGIES DISEASES OF HEART, LUNG AND NEUROMUSCULAR SYSTEMS ARE THE MOST COMMON ETIOLOGIES

52. REFERENCES 1 . The pathophysiology, aetiology, clinical presentation and management of dyspnoea are reviewed. S Afr Med J 2016;106(1):32-36. DOI:10.7196/SAMJ.2016.v106i1.10324 2.Weinstock, M. Risk Management Monthly Emergency Medicine.Vol.11,No.6.June2017 3.Carroll P. RT: For Decision Makers in Respiratory Care.2007 4.Shipsey P. Emergency Medicine Reviews and Perspectives.2012 5.Lundsgard C , et al.Medicine.1923;2(1):1-76 6.Swadron, S. National Emergency Medicine Board Review. August 17,2015 7.Wahls SA. Am Fam Physician.2012 Jul15;86(2): 173-180 8.William Hampton. Quantia MD. Topics: Case: Pulmonology 2017 October. 9.Christopher Kabrhel , MD . Approach to the patient with dyspnea 10.My BMJ Best Practice/monograph

53. TAKE HOME MESSAGE IF YOU FIND SOMETHING ANOTHER CLINICIAN MAY HAVE MISSED, DON’T POINT FINGERS EXPLAIN THAT THE LAST PHYSICIAN TO SEE A PATIENT FOR A PARTICULAR COMPLAINT ONLY APPEARS TO BE SMARTER BECAUSE SHE OR HE HAS EVERYONE ELSE’S KNOWLEDGE TO BUILD UPON. THANK YOU FOR HAVING ME