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Associate Professor
Emergency Medicine
University Hospitals
Case Medical Center
2010-11
Dyspnea
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Definition
April, 99
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Descriptors of Dyspnea
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Respiratory Definitions
My Philosophy of teaching:
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Case 1
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Case 1
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1: Degree of urgency
If not, intervene.
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2. Assess patient.
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4. Correct it
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Suspicion
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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
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Other substances
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Diaphragm
Chest wall muscles
Accessory muscles such as
supraclaviculars, neck muscles.
Myesthenia, paralysis other muscular
causes
Increased muscle tension.
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Causes of dyspnea
Psychogenic
Hypoxic
Metabolic
Pulmonary
Cardiogenic
Hematologic
Any others?
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Formal Studies
April, 99
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PEF
ABG
Other blood tests
CXR
EKG
CT
UltraSound
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Cough
Vomiting
Temporal relationship What does
that mean?
Circadian variations
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Cough
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Aphorism
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Vital Signs
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Vital Signs
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Vital Signs:
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Pulse Ox
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VS - Combinations:
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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
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Central Processing
Objective data
Subjective data
Psychiatric is a diagnosis of exclusion
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Grade
1
2
3
4
Degree of dyspnea
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Causes of dyspnea
4 general categories:
cardiac,
pulmonary,
mixed cardiac or pulmonary,
Non-cardiac, non-pulmonary
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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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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
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pH
pH should be 7.4.
If lower acidotic.
If higher basic.
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PaCO2
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PaO2
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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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April, 99
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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:
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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
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Pneumonia
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Pulmonary Embolism
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Emphysema
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CO poisoning:
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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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REFERENCES
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