SHORTHNESS OF BREATH

SHORTHNESS OF BREATH Objectives 1. Develop priorities in the work-up of patients with shortness of breath 2. Distinguish between the causes of shortness of breath based on history, physical findings and the use of lab tests, EKGs, ABGs and CXRs. 3. Determine interventions based on the cause of shortness of breath Copyright UC Regents 1

SHORTNESS OF BREATH Introduction Shortness of breath, or dyspnea, is a very common problem in the Emergency Department. It is a sensation of breathlessness that is both unanticipated and unpleasant. It is fundamentally important to understand how respiration is controlled. As background for this talk you should understand the following factors that control respiration: Medulla controls involuntary respirations Pons controls switching from inspiration to expiration Cerebral Cortex controls voluntary respiration Central Chemoreceptors located in the Pons, respond to increased pco2, acid, ASA, progesterone, fever Peripheral Chemoreceptors located in the Carotid Bodies, respond to decreased po2 Peripheral Mechanoreceptors located in the chest and abdominal wall, respond to stretch Pulmonary Receptors (irritant, stretch and C fiber) respond to edema, change in compliance and irritants The following may adversely impair the above respiratory regulators and thereby cause dyspnea: Hypoxia Hypercarbia Pulmonary edema and other alveolar filling (pneumonia) Reduced pulmonary compliance Damage to the chest wall Inhaled irritants and ingested drugs Pregnancy Copyright UC Regents 2

Remember the following terms and use them precisely when discussing patients with dyspnea: Dyspnea Shortness of breath The sensation of having difficulty breathing beyond that which is expected This is a symptom related by the patient Tachypnea Higher than normal respiratory rate This is a sign observed by the examiner Bradypnea Lower than normal respiratory rate This is a sign observed by the examiner Ventilation The degree to which gas is moved in and out of the alveoli This is assessed by measurement of arterial CO2 Hyperventilation Minute ventilation increased above normal so that CO2 is removed more rapidly than CO2 is produced, resulting in a pco2 <35. Minute ventilation may be increased by a rapid respiratory rate, increased tidal volume of each breath, or both Hypoventilation Minute ventilation decreased below normal so that CO2 is removed less rapidly than CO2 is produced, resulting in a pco2 > 45 Minute ventilation may be decreased by a slow respiratory rate, decreased tidal volume of each breath, or both Respiratory Distress Severe dyspnea The subjective observation that a patient is having significant problems breathing Oxygenation The degree to which oxygen is delivered to the pulmonary capillaries This is measured as arterial po2 Respiratory Failure Acute inability to either adequately ventilate or oxygenate Typically defined as a pco2 > 50, and/or a po2 < 50 Copyright UC Regents 3

SHORTHNESS OF BREATH CASE 1 40 year old woman c/o SOB and DOE x 1 day Sore throat, dry cough, fever, chills x 7 days Myalgias and fatigue x 2 days No orthopnea or PND No sputum or chest pain No leg trauma or swelling No travel or immobilization No hx asthma, COPD, CHF No smoking, alcohol, drugs, medications RR 32, P 120, BP 124/76, T 37, sat 88% RA What do you want to do? IV, O2, Monitor CXR AP portable if patient is hypoxic on room air or is unstable PA and lateral in radiology suite if patient is stable ABG room air EKG Patient appears fatigued and sleepy Chest nontender, decreased breath sounds bilaterally, no wheezes, rhonchi or rales Heart no JVD, no gallop, rub, or murmur Abd soft, nontender, no mass Ext no edema or rash, no calf tenderness Neuro A + O x 3, PERL, moving all extremities Results WBC 12,500, Hct 36, platelets 125,000 Chem 7 WNL ABG on RA ph 7.26 / pco2 60 / po2 60 CXR WNL ABG interpretation Hypoventilation, acute Respiratory acidosis A-a gradient = 150-(1.25XCO2) O2 (measured on ABG) This patient=150 (1.25x60) - 60 = 15 A-a gradient at sea level, on room air= 10 + age of patient/10 = 14 What s going on? clear CXR minimally increased A-a gradient diagnosis- acute hypoventilation with increased RR low tidal volumes why? Copyright UC Regents 4

Acute and subacute causes of low tidal volumes: Splinting (rib fxts, pleurisy, abdominal pain) Displacement of lung (pneumo or hemothorax) Ruptured diaphragm, flail chest Weakness Guillain-Barre ascending, no reflexes Botulism bulbar findings Myasthenia Gravis bulbar, improves with rest Organophosphate poisoning bradycardia, SLUDGE Spinal cord injury sensory and motor levels CASE 2 32 year old man c/o SOB x 1 day Fatigue x 3 days No chest pain No fever, chills, sweats No cough, sore throat, coryza No travel, trauma, leg pain No hx asthma, COPD, CHF No smoking, alcohol, drugs or medications RR 30, P 132, BP 102/64, T 37, sat 99% RA What do you do now? IV, O2, monitor Labs? ABG? CXR? Wide awake, labored breathing Chest clear, good breath sounds bilateral Cor no JVD, I/IV SEM, no gallop or rub Abd soft, nontender, no mass Ext no edema Neuro A + Ox3, MAE, PERL Results WBC 15,500, Hct 48, Platelets 325,000 Electrolytes: Na+ 128 Cl 92 HCO2 48 K+ 4.7 BUN 16 Creatinine 3.6 ABG RA 7.26 / 24 / 106 EKG sinus tachycardia, otherwise WNL CXR WNL ABG interpretation Hyperventilation Metabolic Acidosis A-a gradient = 150 (1.25x 24) 106 = 14 Copyright UC Regents 5

What s going on? Tachypnea Hyperventilation Normal A-a gradient Clear CXR Anion gap metabolic acidosis Did you forget to check the glucose? Causes of anion gap metabolic acidosis MUDPILES Methanol, Metformin Uremia DKA, AKA Paraldehyde Iron, Isoniazid Lactic acid ( COHb, methb, cyanide ) Ethylene glycol Salicylates CASE 3 37 year old man c/o SOB x 2 hours Left pleuritic chest pain x 2 hours Lightheaded and weak x 1 hour No trauma, travel, leg pain No cough, coryza, sore throat No fever, chills, sweats No hx COPD, CHF, asthma Smokes marijuana No cigarettes, other drugs, alcohol, medications RR 36, P 132, BP 92/60, T 37, sat 90% RA What do you do now? IV, O2, monitor Do not get ABG, bloods or CXR Focused physical exam Listen to chest JVD? Tracheal deviation? Copyright UC Regents 6

Tension Pneumothorax! Duck Theory Looks, walks and sounds like a duck it s a duck However, classical presentations not common Do not expect all patients to have read the textbooks Many presentations are atypical Sutton s Law Go where the money is In EM treat before all is information available What else could this be? Acute, chest pain, SOB, low BP, low O2 sat Pulmonary embolus - does not cause tracheal deviation Myocardial infarction - does not cause tracheal dev Pleurodynia - does not cause tracheal deviation, low BP or SOB Herpes zoster - does not cause tracheal deviation, low BP or SOB Acute anxiety may cause tingling fingertips Copyright UC Regents 7

CASE 4 45 year old man c/o SOB x 6 days Gradually increasing DOE x 6 days Diffuse pleuritic chest pain x 4 days Nonproductive cough x 4 days No sore throat, coryza No fever, chill, sweats No trauma, leg pain, long trips No hx asthma, COPD, CHF No smoking, drugs, alcohol, medications RR 26, P 116, BP 160/92, T 38, sat 95% RA What do you do now? IV, O2, monitor CXR? ABG? Labs? Pleasant man, NAD Chest nontender, diffuse mild end expiratory wheezing R>L Cor no JVD, I/IV SEM LUSB Abd soft, nontender, no mass Ext 1+ bilateral pedal edema Neuro A + Ox3, MAE, PERL Results WBC 11,200, Hct 42, platelets 315,000 Chem 7 WNL ABG RA 7.42 / 32 / 74 EKG sinus tachycardia CXR WNL ABG interpretation Hyperventilation Mild respiratory alkalosis A-a gradient = 150 (1.25x32) 74 = 36 What s going on? Wheezing Low grade fever Pleuritic chest pain Hyperventilation Increased A-a gradient Clear CXR Pulmonary embolus Dyspnea, tachypnea or pleuritic chest pain Must R/O if most likely dx 35% will have temp > 38 65% will have wheezing or rales ABG variable - hypoxia or A-a gradient not necessary Copyright UC Regents 8

CXR variable - often normal Low Probability R/I or R/O with V/Q scan or CT High Probability R/I with V/Q scan or CT R/O with angiography CASE 5 65 year old man c/o SOB x 1 day No chest pain, cough, coryza No trauma, leg pain or swelling No fever, chills, sweats Hx COPD and CHF Meds furosemide, NTG, digoxin, KCl, albuterol, Atrovent, prednisone 120 pack years, bourbon 1 liter/day, no drugs RR 16, P132, BP 194/112, T 36, sat 75% NRM What do you do now? IV, O2 (already maximum), monitor Set up for endotracheal intubation Look for reversible causes of respiratory failure Pneumothorax Narcotic OD Myasthenia Gravis Indications for endotracheal intubation Hypoventilation Hypoxia Failure to protect airway Any of the above impending Trauma going to CT or OR Tiring borderline patient Behavioral control Copyright UC Regents 9

Selected Causes of Dyspnea Pulmonary Embolus Entertain the diagnosis if the patient has dyspnea, chest pain, tachypnea or deep venous thrombosis. PE may be a cause of worsening dyspnea in patients with CHF or COPD. Many patients will not have classic risk factors. Remember, low risk patients can be ruled out with V/Q or CT. High risk can only be ruled out with pulmonary angiography. Asthma Ask 4 questions: 1. Ever been in the ICU? 2. Ever been intubated? 3. Are you as bad as when you were intubated? If yes, may need intubation now. 4. Is this the worst you have ever been? When patients get progressively tighter, breath sounds change from: End expiratory wheezing, to Diffuse expiratory wheezing, to Inspiratory and expiratory wheezing, to High pitched, barely audible wheezing with diminished breath sounds As before, all that wheezes is not asthma. Think of: CHF Pulmonary embolus Foreign body Pneumonia Pneumonia Consider if the patient has fever, chills, is elderly, immunosuppressed, or has an infiltrate on CXR. Admit for: po2 less than 60-65 Inability to keep down pills Empyema (new pleural effusion should be tapped) Very young and very old (less than 1 and over 70) Severe underlying disease (DM, COPD, splenectomy, alcoholism, dialysis) Unreliable or has a poor social situation (e.g. is homeless) Any 2 of the following: - RR>30 - DBP<60, SBP<90 - T>101 (38.3) - WBC<4,000 or >30,000, PMNs<1,000 - pco2>50 - Hct<30 - Cr>1.2, BUN>20 Copyright UC Regents 10

- multilobe or cavity, pleural effusion on CXR - metabolic acidosis - coagulopathy Pleural Effusion May, or may not cause chest pain. May be difficult to diagnose on physical exam. Pleural effusion is one reason to always get a CXR when patients are dyspneic. May be the presenting finding in lung or breast cancer. Cardiogenic Pulmonary Edema Classically progresses from dyspnea on exertion, to paroxysmal nocturnal dyspnea, to orthopnea, to dyspnea at rest. But may occur suddenly with myocardial infarction or as an angina equivalent. Angina equivalent dyspnea is shortness of breath secondary to ischemia and decreased ventricular compliance causing acute pulmonary edema rather than typical chest pain. For this reason, dyspnea of unknown etiology should prompt an EKG and cardiac evaluation, especially in the elderly, women and diabetics. COPD Be wary of interpreting hypercapnia in COPD patients. If the ph is close to normal, hypercapnia is probably chronic. These patients must be watched for CO2 narcosis if given high flow oxygen. They may be dependent on hypoxia to drive them to breathe since their medulla may have become tolerant to chronically elevated pco2. Without hypoxia their respiratory drive may be decreased, causing the pco2 to increase which may result in somnolence, which decreases respiratory drive even further, resulting in a viscous cycle. If the ph is decreased, hypercapnia is probably acute. If the patient is sleepy, immediate intubation may be necessary. BIPAP, however may be effective in some patients. If awake, the patient should be treated aggressively and followed carefully. If there is no improvement, intubation may be necessary. Hyperventilation Syndrome Hyperventilation syndrome is often associated with anxiety, although the patient may not volunteer this information. Patients are often diaphoretic, tachypneic, and may have a tingling sensation around their mouth or fingertips. Carpal pedal spasm may occur due to respiratory alkalosis which causes increased binding of calcium on albumin and a reduction in serum ionized calcium (total serum calcium remains unchanged). Even if not present, carpal spasm may be elicited using Trousseau s sign. Trousseau s sign is carpal spasm (extension of MCP 1-3, flexion of MCP 4-5) brought on by leaving a BP cuff on the arm 20 mm above systolic for 3 minutes. Some patients with anxiety may have Globus hystericus ; a full sensation in the neck feeling like a large object is blocking the flow of air (and sometimes blocking the ability to swallow). Make sure there is no real local pathology in the neck or otherwise before treating their hyperventilation. Copyright UC Regents 11

Treatment involves increasing the alveolar pco2 by rebreathing through a facemask (paper bag at home) attached to oxygen at a LOW flow rate (1-2 liter/min). Sedation with benzodiazepines may be necessary. Pearls Always address the ABCs first IV, O2, monitor IV, O2, monitor IV, O2, monitor If a patient needs one of the above, consider all 3 Tachypnea is not hyperventilation Get ABG on RA if possible Is there hyperventilation of hypoventilation? For an increase of pco2 of 10, ph should drop by 0.08 Is the change in ph accounted for by the change in pco2? If so, pure respiratory acidosis/alkalosis If not, metabolic component to ph abnormality Estimate the A-a gradient A-a gradient (room air) = 150 (1.25x pco2) po2 A-a gradient (normal) = 10 + age of pt/10 Correlate vital signs with ABG Dyspnea is not always due to hypoxia, consider: Hypoxia Hypercarbia Metabolic acidosis Lung receptors - stretch, C (vascular), irritant Always think of pulmonary embolus All that wheezes is not asthma, consider: Pulmonary embolus CHF Foreign body Pneumonia Think of non-pulmonary diseases causing SOB Predict the need for endotracheal intubation Copyright UC Regents 12

SHORTNESS OF BREATH Bibliography 1. Williams, J et al: Dyspnea. In Rosen, P et al (ed): Emergency Medicine, St. Louis, 1998, Mosby. 2. Goldhaber, S: Pulmonary Embolism, NEJM 339:93-104, 1998. Malas, O et al: Cardiac of Pulmonary Dyspnea in Patients Admitted to the Emergency Department, Respir Med 97(12):1277-81, 2003. 3. Stein, P et al: Clinical Characteristics of Patients with Acute Pulmonary Embolus Stratified According to Their Presenting Syndromes, Chest 112:974-9, 1997. 4. Hamlin, M et al: Blood Gases: Pathophysiology and Interpretation. In Tintinalli, J et al (ed): Emergency Medicine, New York, 2000, McGraw-Hill. Copyright UC Regents 13