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Diagnosis of Dyspnea

Vicken Y. Totten MD MS, FACEP


FAAFP

Associate Professor
Emergency Medicine
University Hospitals
Case Medical Center

2010-11
Dyspnea
DyspneaDyspnea

Dyspnea from Latin dyspnoea

Dyspnea (also SOB, air hunger)


subjective symptom of
breathlessness.
normal in heavy exertion
pathological if it occurs in
unexpected situations.

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Definition

Dyspnea: unpleasant, subjective


sensation of abnormal
respiration.
Labored breathing - physical
presentation of respiratory
distress/ dyspnea
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


tachypnea
Gasping
Panting
restlessness
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
breathing
Hyperventilation - rapid breathing
with hypocarbia
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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


simpler.
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 round.
All bleeding stops
eventually.
All else is details.
Butthe devil is in
the details.
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What is NOT Dyspnea?

Not the O2 saturation of Hemoglobin


Not the total amount of O2 attached to
Hemoglobin
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


exertion
Also admits to mild left sided CP, maybe
respirophasic.
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


HEENT: nl
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
FiO2
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:


mechanical,
metabolic,
cerebral,
Psychological

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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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Suspicion

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
circulation
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What is the purpose of


respiration:

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

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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,


smothering
Internal: food bolus, other mechanical
airway obstructions: peanuts, beads,
Internal growths: tumors, infections,
abscesses
Encroachment on the airway
Internal substances: pus, blood,
mucus, transudates
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Muscular / Chest Wall system

Diaphragm
Chest wall muscles
Accessory muscles such as
supraclaviculars, neck muscles.
Myesthenia, paralysis other muscular
causes
Increased muscle tension.
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Air to blood interface:

Mechanical filling of alveoli


Lack of surfactant: alveoli collapse with
exhalation
Abnormalities (thickening) of alveolar
membranes,
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

Psychogenic
Hypoxic
Metabolic
Pulmonary
Cardiogenic
Hematologic
Any others?
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Tools to evaluate dyspnea

Suspicion / Clinical knowledge.


If you dont think of it, you will
never find it.
History
PE including

Vital Signs, pulse ox, PEF

Formal Studies
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What other tools?

PEF
ABG
Other blood tests
CXR
EKG
CT
UltraSound
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Additional items of history

Cough
Vomiting
Temporal relationship What does
that mean?
Circadian variations

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Cough

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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Aphorism

Coughing till you vomit is


bronchospasm till proven otherwise.
Consider cardiac.
Vomiting AND THEN coughing ->
think aspiration

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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 context.
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 RR?

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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


Discussion
Low RR, HR, BP
Discussion
High RR, HR, low BP
Discussion

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Focused exam

Accessory muscles
Facial expression, color.
Chest wall, lungs, heart, abd & extr.
(Discussion)

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Physical Exam

Observation
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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Pathophysiology

chemoreceptors, mechanoreceptors,
lung receptors
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

chemoreceptors
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

Grade

1
2
3
4

Degree of dyspnea

no dyspnea except with strenuous exercise


Only when walking up incline or hurryingl
Slow on level, or stops after 15 minutes
stops few minutes of walking on the level
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:
cardiac,
pulmonary,
mixed cardiac or pulmonary,
Non-cardiac, non-pulmonary

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Common specific disease entities

Asthma
Pneumonia
Pleural effusion
Pneumothorax
Interstitial Lung
disease
COPD
Psychogenic

Pericardial effusion
Cardiac ischemia
CHF
Dysrhythmia
Mechanical
obstruction
Anemia

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Blood tests

ABG
Vidas d-Dimer
BNP
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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CXR 1

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CXR 2

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CXR 3

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ECG

Lots of clues as to cause of dyspnea


Look for pericarditis (S1Q3T3, right
axis deviation),
myocardial infarction, ST segment
elevation
new onset atrial fibrillation or right
heart strain
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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


lecture.)
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

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

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PaCO2

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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PaO2

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 &
Echocardiography

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:

Asthma
Pneumonia
Acute Pulmonary Edema
Pulmonary Embolism
Emphysema
Pneumo / hemothorax
Carbon Monoxide (CO)
Cyanide poisoning
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Asthma:

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:

Symptoms:
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
enough.
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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Pneumonia

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.
Treatment:

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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Emphysema

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% O2.
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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Summary:

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

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