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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.

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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

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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

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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?

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• 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

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• 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?

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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

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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

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• 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

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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

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- 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.

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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

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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,

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