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Diagnosis of Dyspnea

Vicken Y. Totten MD MS, FACEP

Associate Professor
Emergency Medicine
University Hospitals
Case Medical Center


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Dyspnea from Latin dyspnoea
Dyspnea (also SOB, air hunger)
subjective symptom of breathlessness.
normal in heavy exertion
pathological if it occurs in unexpected

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Dyspnea: unpleasant, subjective
sensation of abnormal respiration.
Labored breathing - physical
presentation of respiratory distress/
Many causes

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Descriptors of Dyspnea
Dyspnea on Exertion (DoE)
Dyspnea after Eating (PPD)
Nocturnal Dyspnea
Paroxysmal nocturnal dyspnea
Dyspnea in Pregnancy
(hormonal, mechanical)

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What is respiratory distress?
Vague term meaning not breathing well.
A constellation of signs including:
using accessory muscles of respiration
Sometimes, also confusion (hypoxemia)
Somnolence (hypercarbia)

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Respiratory Definitions
Eupnea - normal breathing
Bradypnea - decreased breathing rate
Tachypnea breathing very fast. Pt not
always aware of it.
Apnea not breathing at all
Hyperpnea - faster and/or deeper
Hyperventilation - rapid breathing with
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Goals of this presentation
Discuss dyspnea & its
differential diagnosis
Discuss pathophysiology
Discuss diagnostic tests
for dyspnea

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My Philosophy of teaching:
Me: make it as simple as you can. No
You: Interact, ask questions. You will stay
awake ;).
No question is dumb, and the answer will
be just in front of you.

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Principles of Emergency Medicine
Air goes in and out.
Blood goes round and
All bleeding stops
All else is details.
Butthe devil is in the
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What is NOT Dyspnea?
Not the O2 saturation of Hemoglobin
Not the total amount of O2 attached to
Not the amount of O2 in solution in the
blood (the PaO2)
Not the respiratory rate, (not all
tachypnea is dyspnea)
But: a subjective sensation of air hunger.
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Case 1
47 y/o man c/o dyspnea. SOB, worse on
Also admits to mild left sided CP, maybe
Onset 5-7 days ago. Getting slightly worse
What else do you want to know?
Whats your current differential?
Admit or Discharge?
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Case 1 additional history
PMHx: none. No asthma
SHx: Tobacco Smoker. Social drinker.
Occasional MJ. Married. No Children. Likes
to jog, last 5 mi run yest. Works at a desk.
ROS: needs to see a dentist. No
palpitations. No edema. No PND, nor
orthopnea. Otherwise negative.
What else do you want to know?

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Case 1
V/S: T=36.9; P=85; RR=20; BP 128/79
CHEST: WD, nl excursion, lungs hard to
hear, but no rales, ronchi, wheezes.
Cor: RRR w/o RMG.
Abd: soft & NT, well muscled.
Extr/MS/Neuro/Skin: all wnl.
How will you approach this?

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Approach to the patient with
shortness of breath, or
respiratory distress: the
emergency approach.

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1: Degree of urgency
Is the patient going to live long enough to
give you a history?
If not, intervene.
If yes, try to make a diagnosis.

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2. Assess patient.
Is the patient actively trying to breath?
look for mechanical obstruction. Correct it.
Is patient hypoxic? If yes, increase
Is the patient not able to breathe
adequately? If no, supplement
respiratory efforts.

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3. Locate the problem
Causes of air hunger:

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4. Correct it
Topic for another lecture
After the (correct) diagnosis is made,
treatment is (relatively) simple

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You dont have to know all the diagnoses,
but you do have to evaluate threat to life
Know when & how to intervene.
Understand your tools.
Understand your available interventions.
Know when to get help

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Ask (yourself) questions.
Can the chest wall support breathing?
Are there barriers preventing the air
getting through the airway to the blood?
Are there metabolic reasons to increase
respiratory rate?
Is enough blood, of good quality, going
round and round? if not, assist

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What is the purpose of
Gas exchange
To assist in balancing blood (body) pH
Lesser extent: temperature regulation /
cooling the body
Cellular respiration vs Organism

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Abnormal atmosphere
CO: even small amounts of CO can bind
with hemoglobin in place of O2 and
prevent O2 binding (competitive
inhibition) 300 times more tightly than O2
Methemoglobinemia occasionally causes
dyspnea; usually just tachypnea
Heliox: helium instead of nitrogen as the
inert gas. Helium molecules are smaller
than nitrogen, slicker, less turbulent flow.
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Other substances
can injure the airways directly
Noxious / toxic gases work in many
different ways and levels.
Allergens immune system modulated
Particulates smothering
Irritants cause bronchospasm

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Mechanical Airway Obstruction
External: gagging, strangulation,
Internal: food bolus, other mechanical
airway obstructions: peanuts, beads,
Internal growths: tumors, infections,
Encroachment on the airway
Internal substances: pus, blood, mucus,
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Muscular / Chest Wall system
Chest wall muscles
Accessory muscles such as
supraclaviculars, neck muscles.
Myesthenia, paralysis other muscular
Increased muscle tension.

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Air to blood interface:
Mechanical filling of alveoli
Lack of surfactant: alveoli collapse with
Abnormalities (thickening) of alveolar
Interstitium (tissues between the alveolus
and the capillary endothelium)
Capillary endothelium
Blood: enough of it, flowing well enough
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Causes of dyspnea
Any others?

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Tools to evaluate dyspnea
Suspicion / Clinical knowledge. If
you dont think of it, you will never
find it.
PE including
Vital Signs, pulse ox, PEF
Formal Studies

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What other tools?
Other blood tests

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Additional items of history
Temporal relationship What does that
Circadian variations

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What good is a cough?
What bad is a cough?
Central & peripheral triggers
Air travels in excess of 150 kilometers per
second during a cough
can denude respiratory epithelium
exposed basement membranes stimulate
future antigenic response
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Coughing till you vomit is bronchospasm
till proven otherwise. Consider cardiac.
Vomiting AND THEN coughing -> think

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Vital Signs
What are the VS?
Normal vs Stable
How do they change over time?
What does this tell you?

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Vital Signs
The meaning of each value depends on its
A slowing respiratory rate in a bad
asthmatic may mean he is about to die.
A slowing respiratory rate in an anxious
bystander may mean he is getting better.

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Vital Signs:
Respiratory rate: Do it yourself!
Temp. Dont trust the Triage Temps.
HR, BP. What do they tell you about the

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Pulse Ox
What is a dangerous level? Why?
When is the pulse ox normal and the
patient about to die? Why?
When is the pulse ox bad and the patient
is fine? Why?

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VS - Combinations:
High RR, HR, BP
Low RR, HR, BP
High RR, HR, low BP

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Focused exam
Accessory muscles
Facial expression, color.
Chest wall, lungs, heart, abd & extr.

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Physical Exam
Auscultation with and without a
stethoscope. Where?
Palpation what & where & why?
Scratch test
The REST of the exam habitus, edema,
muscle wasting, lots more.

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Scratch Test
Place stethoscope on
mediastinum, gently scratch
the anterior chest wall
alternate sides, equidistant
from the stethoscope. One
side may not transmit sounds
as well as the other.
What would the scratch test
tell you?
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chemoreceptors, mechanoreceptors, lung
3 components that contribute to dyspnea:
afferent signals, efferent signals, and
central information processing.
brain compares the afferent and efferent
signals, and a "mismatch" results in the
sensation of dyspnea.

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Afferent neurons
carotid bodies, Various brain organs,
juxtacapillary (J) receptors,
chest wall and its musclesMuscle spindles
sense stretch
Lung parenchymal tissues,

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Efferent signals
motor neurons of respiratory muscles.
Diaphragm, intercostal, abdominal
muscles, accessory muscles.

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Central Processing
Objective data
Subjective data
Psychiatric is a diagnosis of exclusion

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MRC Breathlessness Scale
Degree of dyspnea

0 no dyspnea except with strenuous exercise

1 Only when walking up incline or hurryingl
2 Slow on level, or stops after 15 minutes
3 stops few minutes of walking on the level
4 minimal activity such as getting dressed,
too dyspneic to leave the house
The Modified Borg Scale

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Causes of dyspnea
4 general categories:
mixed cardiac or pulmonary,
Non-cardiac, non-pulmonary

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Common specific disease entities
Asthma Pericardial effusion
Pneumonia Cardiac ischemia
Pleural effusion CHF
Pneumothorax Dysrhythmia
Interstitial Lung Mechanical
disease obstruction
COPD Anemia

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Blood tests
Vidas d-Dimer
Basic Metabolic Panel
Cardiac Enzymes
What else, and why?

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Chest radiography (CXR)
Insufficient by itself
Do your own read: the radiologist may not
know what you are looking for and may
overlook the most important clue.
Look for pneumothorax, aortic dissection,
pneumonia, pleural effusions, sub-
segmental atelectasis, pulmonary
infiltrates or an elevated hemi-diaphragm
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Lots of clues as to cause of dyspnea
Look for pericarditis (S1Q3T3, right axis
myocardial infarction, ST segment
new onset atrial fibrillation or right heart

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EKGs (TB Inserted)

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Arterial Blood Gases (ABG)
Must be interpreted in context.
Complete ABG includes lactate
VBG sometimes very useful.
When? Why?

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ABG and Acid base balance.
(This could easily be a few hours
3 important components
pH, CO2 and O2
pH changes because of both metabolic
and respiratory causes. Each tries to
compensate for abnormalities in the other.

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pH should be 7.4.
If lower acidotic.
If higher basic.

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should be 40, +/-
If lower, breathing too much.
If higher, not breathing enough.
CO2 / HCO3 is the end product of
oxidative metabolism

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O2 % (Pulse Ox) = saturation.
Should be 85 -100.
If lower hypoxic.
If higher than 100 getting more than
21% or over-breathing seriously.
PaO2 is a measure of oxygen carriage.
Oxygen carrying capacity is a function of
amount of carrier, and carrier saturation.
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Respiratory Acidosis and Alkalosis
Low pH = acidosis
Lo pH, high CO2 respiratory acidosis
Lo ph, low CO2 metabolic alkalosis
High pH = alkalosis
Hi pH, low CO2 respiratory alkalosis
Hi pH, high CO2 metabolic alkalosis

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Ventilation / Perfusion Scanning
(V/Q Scan)
combined with clinical suspicion
sensitivity is 85 - 90%
positive predictive value depends on
clinical suspicion
More radiation than a CT-PE study.

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CT Scan of the Chest
2 kinds: rapid helical without contrast.
Usual speed, with contrast.
CT more rapid, safer, detects other
potential causes of dyspnea with better
accuracy than VQ
helical CT scanning no contrast needed
Regular PE protocol requires normal Cr or
GFR. Why?
Always consider Metformin. Why?
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Ultrasonography &
Next lecture
TEE = transesophagyl echocardiogram
(TEE) is > 90% sensitive for large clots,
very specific. This, we cant do yet.
TTE = TransThoracic echocardiogram:
aortic dissection, cardiac tamponade,
acute valvular lesion. This, we can do.

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Specific entities:
Acute Pulmonary Edema
Pulmonary Embolism
Pneumo / hemothorax
Carbon Monoxide (CO)
Cyanide poisoning

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Reversible bronchoconstrictuion
Air blocked between the large airways to
the alveoli.
Alveoli may collapse.
Treatment: open the airways, prevent
stacking (time enough for exhalation).
Keep O2 high enough to keep patients
brain alive.
Consider steroids, permissive hypercarbia.
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Pulmonary edema:
Basic problem: Heart stretches so far it cant
contract well. (Falls off Frank Starling Curve)
Cardiac oxygen demand exceeds availability.
Air cant cross the air-blood interface.
Fluid seeps from the blood into the alveoli.
Surfactant gets diluted.
Caused by cardiac and vascular derangements.
Vicious cycle.

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Pulmonary edema:
Sudden onset; respiratory distress,
Rales, ronchi. Foamy sputum. Sometimes
blood tinged.
Blood pressure high (vasoconstriction)
usually 240/120.
If onset between 4 pm and 8 pm, likely to
be associated with acute MI.
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Pulmonary edema
Treatment: increase airway pressure, to
force fluids back into the vascular system,
(BVM with patient effort, CPAP or
intubation) increase FiO2, dilate blood
vessels and reduce systemic blood
pressure (which reduces the work of the
heart and reduces oxygen demand). Get
excess fluid off via kidneys (if working),
via bleeding (bloodletting) or sequester
fluid (tourniquets).
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Diabetic KetoAcidosis DKA
Tachypnea often without Air hunger
metabolic derangement: blood is too acid.
Respiratory system tries to compensate,
gets overwhelmed.

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Pneumo / hemo thorax.
Stuff gets between the inside of the chest
wall and the lung. Air cant get in well,
and blood cant go round and round well
Treatment: mechanically remove the stuff
that keeps the lung collapsed. Needle,
needle with flutter valve, or chest tube.
Intubation or BVM may make things
worse, if there is a flap.
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Infection in the lower airway. Consolidation
(fluid in alveoli)
often only one part of a lung.
Generally SICK. Upper, middle and lower
airways clogged by mucus, often tenacious.
Fever increases metabolic demand for O2.
Antibiotics if bacterial (Abx)
thin the mucus
mechanical ventilation if needed.

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Pulmonary Embolism
A blood clot in the pulmonary circulation (often
from the systemic venous circulation) blocks.
Blood cant go round and round, so there is lack
of oxygen in the circulating blood.
Diagnosis: hypoxemia, tachycardia, tachypnea,
sometimes chest pain.
Treatment: anticoagulation and o2
supplementation. CO2 usually normal.
Why is CO2 normal?

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Not enough lung tissue. That is, a paucity
of the blood/air interface.
Optimize all functioning tissue.
Treatment: new lungs.

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CO poisoning:
competitive inhibition of O2 binding at
hemoglobin site.
Treatment: overwhelm the CO with 100%
If not good enough, use hyperbaric O2.

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Cyanide poisoning:
Mechanism: inhibition of O2 utilization at
the cellular level. There can be plenty of
O2 in the air, and in the blood, but the
cells cant use it.
Treatment: inactivate the cyanide using
BAL British Anti-Lewisite.
Time is of the essence

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Dyspnea is a subjective
Think systematically
Multiple causes / multiple tools to
diagnose the problem
When you cant breathe, not much else

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