Acute dyspnea Vicken Y. Totten MD MS, FACEP FAAFP

1. Acute dyspneaVicken Y. Totten MD MS, FACEP FAAFP

2. Definition • Dyspnea: Subjective sensation of abnormal / insufficient respiration. • Unpleasant, concomitant with excessive respiratory effort

3. Goals of this presentation • Initial evaluation of selected causes of dyspnea: severe asthmapneumothoraxpulmonary embolismacute pulmonary edema. • Initial pediatric assessment

4. Tools to evaluate dyspnea • index of suspicion • Stethoscope / Physical Exam • Possibly CO & CO2 monitors • pulse oximeter • peak flow meter • chest radiograph • Ultrasound

5. Subjective vs Objective evidence

6. PNEUMOTHORAXCHIEF COMPLAINT • 28 yo man. 2 d SOB1 ppdsings in church denies asthma or trauma, malaise, fever or URI symptomspain is right-sided and respirophasicCLINICAL MANIFESTATIONSTall, slender, alert and a bit anxious. Palpation does not reproduce the pain. auscultation suggests decreased breath sounds on Rno wheezes, rales or ronchipulse oximetry reading is 93%.Scratch test + (What is this?)Scratch TestPlace stethoscope on mediastinum, gently scratch the anterior chest wall alternate sides, equidistantEPIDEMIOLOGYunilateral respirophasic chest pain & dyspnea.incidence 1.7 to 18 per 100,000more common in males, especially tall, slender young men, half < 4080% are smokersif over 50, COPDRecurrence1/3 develop a second episodeif 2 episodes, 1/2 suffer a third episodeClassificationby etiology: spontaneous vs traumaticby severity: ‘small’, ‘medium’ or ‘large.’Spontaneous: primary (idiopathic) or secondarySecondary minimal barotraumachanges in ambient air pressurecommercial air travel.prolonged breath holding: Straining, valsalvastraining at stoolemesisliftingcocaine or marijuanaInfectionsnecrotizing infections streptococcal pneumonia or tuberculosisDue to underlying defectsRupture of weak pulmonary connective tissue Marfan’s syndromesarcoidosis pulmonary fibrosisoccasionally neoplasmsRISK FACTORS smoking, asthma, barotraumapositive pressure breathingbreath holding, strainingnecrotizing infections, tuberculosisAIDS (especially in association with pneumocystis carinii pneumonia)Catamenial pneumothorax (exceedingly rare).PATHOLOGY -1elastic recoil of pulmonary tissue counteracted by the ‘vacuum effect’ of visceral and parietal pleurapleurae approximatedPleural space violatedfrom without (communicating pneumothorax) from pulmonary leak (simple pneumothorax)air enters the pleural spacepulmonary elastic recoil contracts the lung until the tensions again balanceTENSION PNEUMOTHORAXflap or ball-valve effect permits air entrance, prevents air escape thoracic structures displaced awaycompromises blood return to the heart and air exchange in the undamaged lungUntreated tension pneumothorax can be rapidly fatalDIAGNOSISsuspected by clinical maneuversbreath sounds unilaterally decreased lack of tactile fremituspulse ox unexpectedly lowincreased A-a gradientabnormal EKG (normalizes in the standing position)If no immediate life threatassess the degree of dyspneathe work of breathingoxygenationconfirm radiographicallyDIAGNOSISradiographic AP CXR expiratory or lateral decubitus filmUltrasound “waves on the beach”CT scanSuspect tension pneumothorax severe respiratory distress severely diminished or absent breath sounds bulging neck veinsdeviation of the trachea (late sign)mediastinal shiftAbsence of these signs does not exclude a tension pneumothorax.Needle thoracostomyconverts closed tension pneumothorax into a simple open pneumothorax. The lung does NOT expand spontaneously. What normally keeps the lungs from collapsing? Treatment depends on size of the pneumothoraxavailable resourcesskill of practitionerTube thoracostomy traditionalmoderate to large pneumothoraxtension or increasing sizeif ventilator support neededif air evacuation is contemplatedSmall pneumothorax optionsBreathing 100% oxygen hastens resolutionobservationneedle thoracostomy with daily radiographs until resolutionlater tube thoracostomy if continuing air leakNeedle thoracostomy and repeated aspirationregained favor since modern catheter-over-needle intravenous catheters has diminished the risk of further lung injury during pleural space aspirationNeedle Thoracostomy SetupHigh flow Oxygen with a Non-Rebreather Face MaskBuffered local anesthetic16-18 g catheter-over-needleThree-way stopcock20-60 mL Luer-lock tipped syringeNeedle Thoracostomy Techniquebe prepared for all complicationshigh-flow oxygenbag-valve-mask equipmentchest radiographycapability to intubate Prepare the patientOxygenateCleanse and anesthetize the skinAnesthetize the intra-costal muscles and pleurumWater – filled syringe; catheter over needleTechniqueInsert needle into the 2nd to 3d intercostal space, mid clavicular line, on affected sideRemove needle as soon as the pleural space is penetrated. Aspirate through stopcock, empty through other port> 2 L air is indication for tube thoracostomy Tension pneumothorax “hear a psst” – usually doesn’t happenconvert the open port of the stopcock to a one-way ‘flutter’ valve by cutting a flap in the finger of an exam glove and attaching it to the hub of the catheter with rubber-bandprepare the patient for definitive tube thoracostomy.COMPLICATIONSRe-expansion pulmonary edema remove no more than 1 liter of air at a timerisk for a recurrence monitor frequently in the first few months, less as months passACUTE PULMONARY EDEMAcircadian rhythm: suddenly in the very early morningED presentation at change of shiftafternoon presentation likely to be associated with MICHIEF COMPLAINT68 year old woman, severely SOBshe has a HX of CHF, hypertension, diabetes, MIothers may occasionally have CRF on Dialysis or ongoing MINon-cardiogenic APE unable to adequately excrete fluids (renal failure)toxic gas inhalationacute volume overload from transfusions over hydration with crystaloidssalicylate or narcotic abuse and toxicityPATHOLOGYcapillary hydrostatic pressure > intra-alveolar pressure.LV dysfunction +  PVRCapillary pressure  when LV pumps against resistance catecholamine release -> SVR  ; BP  Many not acutely fluid overloadedTreatment goal:  PVR &  intra-alveolar pressure NOT: diurese, sedate, intubate or restrain!Pathologyacute MI precipitant?circadian onset of APE precedes that of MI by 4 hoursif APE presents in afternoon hours AMI more likely Clinical manifestations of APE acute, severe hypertension tachycardia ->  LV filling time, & impairs outflowlung compliance  , work of breathing  Gas exchange impaired with rales, ronchi, or wheezes. Clinical manifestationshypoxia -> tachypnea, dyspnea, anxietycatacholamine release -> diaphoretic, mottled, JVD, variable gallop rhythms and edema Blood tinged frothy sputum is pathognomonic, but is not required to make the diagnosisDiagnostic testsbest test is therapeutic responseAPE responds as quickly as it starts when it is appropriately treatedDD OF CARDIOGENIC APECHF or non-cardiogenic pulmonary edemasarcoid, TB, asthmamyocardial infarction with cardiogenic shockhypertensive urgencymassive pulmonary embolismdissecting thoracic aortaModern MANAGEMENTbased on  LV after-load and  alveolar air pressureOutmoded treatments Bloodletting, rotating tourniquets -> thrombosis and embolismMorphine  intubation and LOS (vasodilatation 2° histamine release)diuretics  heart rate &  pulmonary capillary wedge pressure50% of APE patients euvolemic, diuresis is of no benefit to them Physiologic management of APEincrease oxygenationreduce vascular resistancereduce the work of breathingthus improve LV functionNoninvasive respiratory support via bag-valve mask or BiPAPraises pulmonary alveolar pressure decreases the work of breathingimprove cardiac functionMedications3-5 SL nitroglycerine q 5 min2” ointment AFTER diaphoresis and mottling abatedCrush & moisten 25 mg tab of Capoten SLVasotec (enalapril) 1.25 - 2.5 mg IVWhy ACE inhibitors?ACE-inhibitors reduce pulmonary capillary wedge pressure within 10 minutesdyspnea improves within 15 minutesACE inhibitors cause relaxation of the left ventricle and peripheral vasodilatationAs peripheral vascular resistance falls, more blood returns to the heart from the pulmonary bedPATIENT EDUCATION risk of another episodecompliance with medicationrisks of airplane travel educate about calling 911 ASTHMAdefinition = recurrent bronchospasmalso a chronic immune-mediated disease characterized airway hyper-responsiveness causing reversible obstruction, and by airway inflammation manifested by secretion and edemaDiagnosis straightforward, or remarkably obscurechronic or seasonal coughnocturnal cough or post-tussive vomitingchest tightness or dyspnea Pulmonary function studies peak-flow monitoringtherapeutic trial CHIEF COMPLAINTChest tightness and dyspnea. A 32 year old woman presents with a 3 week history of gradually increasing dyspnea, dry cough, and mild, respirophasic chest pain. She has a 10 pack-year history of smoking, and a family history of asthma. She says she outgrew her childhood asthma which her pediatrician used to treat with ‘shots.’CLINICAL MANIFESTATIONSSigns and symptoms: comfortable at resttalks in short sentencescoughing fits & gags Children -> post tussive vomitingNocturnal coughing jags 2°  airway diameter StudiesPulse oximetry is 94%, PEF 150A quiet chest is more ominous than a ‘calliope’infants  RR then suddenly become apneicadults usually become hostile and agitated before developing apneaPATHOLOGY responsiveness of respiratory tree to irritantssmooth muscles contract ->  airway diameterleukotrienes signal mast cell degranulationSecretions  , become thicker and more tenaciousInflammationinvolves terminal bronchioles & alveolimucosa thickens from inflammationdistance gas travels  air flow  , secretions insipate and block the smallest airwaysCough predisposes to airway hypersensitivitytriggered when respiratory cilia are bent Air travels in excess of 150 kilometers per second during a coughcan denude respiratory epitheliumexposed basement membranes stimulate future antigenic responseTreatment“beta-agonists treat the symptoms, steroids treat the disease.”cromones and leukotriene inhibitors DIFFERENTIAL DIAGNOSIS in children:tracheomalaciaaspirated foreign bodybroncho-pulmonary dysplasiacroup or URIbronchitis or pneumoniaDD in adults:CHF or impending pulmonary edemaemphysema or COPDforeign body aspirationbronchial neoplasmsfungal, viral or bacterial infections of the airwaysDiagnostic testsPEF simple, non-invasive and can be performed at home after age 5commence treatment if 20%  in PEFPulse oximetry -> no patient cooperationuseful for diagnosis, less for dispostionABG only in potentially life threatening asthmaChest radiography (CXR)seldom helpfulmay show other abnormalities which have been mis-diagnosed as asthma(heart failure, anomalous great vessels, unilateral pulmonary atresia)only if complication like pneumonia or pneumothorax is suspectedThree Step Treatment 1° = attacks less than once a month-> inhaled beta-agonists PRN2° = attacks about once a week if untreated -> prophylaxis with inhaled steroids, or cromones. Consider ipratropium if COPD3° = attacks almost daily -> inhaled beta agonists PRN, inhaled prophylaxis & oral leukotriene inhibitorsMANAGEMENTevaluate potential for life threatsymptoms have worsened gradually --> greatest risk because insipated secretions and mucosal edema cannot easily be reversedfalling pulse oximetry reading near 90% -- > consider respiratory failureMedications Beta agonists: albuterol, salmeterol, isoetharine ,etcSteroids: inhaled, oral or parenteralCromones: cromolyn & nedocromyl leukotriene inhibitors: zafirkulast, montekulastanticholinergics: ipratropium bromideDYSPNEA AND THE THROMO-EMBOLIC DISEASES Acute pulmonary embolism (PE) dyspnea unexplained tachycardialarge PE can be rapidly lethalsmall PE can leave residual pulmonary damagediagnosis can be as important as it is difficultCHIEF COMPLAINT:34 yo woman, sudden SOB day after return from other coastmild respirophasic chest painBCP & smokes no history of asthmaAlso exertional palpitations, chest pain with or without dyspnea, or syncopeCLINICAL MANIFESTATIONStachypneic @ 22, pulse oximeter 93% on room airtachycardic @ 102, sinusHeart RRR, no RMGLungs clear without rales or wheezesno pedal edemanegative Homan’s signPATHOLOGY embolization blocks blood flow to a discrete area blood shunted through already deoxygenated alveolilower PaO2 & higher PaCO2 respiratory rate, but not usually enough to normalize the ABGChest radiography (CXR) usually normalinsufficient, but can exclude pneumothorax, aortic dissection, pneumoniasometimes pleural effusions, sub-segmental atelectasis, pulmonary infiltrates or an elevated hemi-diaphragm“Hampton's Hump” exceedingly rare.ECGusually sinus tachycardiaexcluding pericarditis, or myocardial infarctionnew onset atrial fibrillation or right heart strain (S1Q3T3, right axis deviation)Arterial Blood Gases (ABG) If abnormal, ABG can be helpful, but a normal ABG does not exclude the diagnosis15% of patients have a normal A-a gradientPulse oximetry, likewise, is insensitivePaO2 is > 80 mm Hg in up to 26% of patientsEchocardiographycan detect the right ventricular strain rarely, a skilled echocardiographer can detect a thrombus in the pulmonary artery.transesophagyl echocardiogram (TEE) is > 90% sensitive for large clots, very specificTEE excludes aortic dissection, cardiac tamponade, acute valvular lesionVentilation / Perfusion Scanning (V/Q Scan)combined with clinical suspicioninitial diagnostic test of choice sensitivity is 85 - 90%positive predictive value is 96% when combined with a high clinical suspicionPulmonary arteriography replaced by helical CT scanning CT more rapid, safer, detects other potential causes of dyspnea with better accuracyOther treatment modalities surgical resection of the clot, (especially in massive pulmonary embolus) Thrombolyticstheoretically interesting to reduce vascular pruning BUT not FDA approved problems: time of development of the thrombus is seldom knownunclear if embolus young or organizing risk of pulmonary necrosis with subsequent hemorrhageSummarythe end