Alan Gelb, MD

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

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Alan Gelb, MD

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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Alan Gelb, MD
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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Alan Gelb, MD

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
Whats going on?
clear CXR
minimally increased A-a gradient
diagnosis- acute hypoventilation with increased RR
low tidal volumes why?

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Alan Gelb, MD

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

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Alan Gelb, MD

Whats 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?

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Alan Gelb, MD

Tension Pneumothorax!

Duck Theory
Looks, walks and sounds like a duck its a duck
However, classical presentations not common
Do not expect all patients to have read the textbooks
Many presentations are atypical
Suttons 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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Alan Gelb, MD
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
Whats 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

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Alan Gelb, MD

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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Alan Gelb, MD
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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Alan Gelb, MD
- 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 Trousseaus sign. Trousseaus 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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Alan Gelb, MD
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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Alan Gelb, MD

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.

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