2. outline
• Definition of dyspnea
• Mechanism of dyspnea
• Assesing dyspnea
• DDx
• approach
Berhanu s. 2
3. Dyspnea
dyspnea as a "subjective experience of breathing discomfort that
consists of qualitatively distinct sensations that vary in intensity.
The experience derives from interactions among multiple physiological,
psychological, social, and environmental factors “
.
Dyspnea is distinct from labored breathing, which is rather a common
physical presentation of respiratory distress.
Berhanu s. 3
4. ORTHOPNEA
It is dyspnea occur at lying and improving at sitting position
Patient require extra pillow to sleep
PND (PAROXISMA NOCTURNAL DYSPNEA)
Episode of sudden dyspnea & orthopnea that awakens patients from sleep
That usually 1or 2 hour after going to bed prompting sit up ,stand up ,going to
window for air
Berhanu s. 4
5. Epidemiology
• Shortness of breath is the primary reason 3.5% of people present to
the emergency department in the United States.
• Of these approximately 51% are admitted to hospital and 13% are
dead within a year.
• Some studies have suggested that up to 27% of people suffer from
dyspnea, while in dying patients 75% will experience it.
Berhanu s. 5
6. Mechanisms of Dyspnea
• Respiratory sensations are the consequence of interactions between
the efferent, or outgoing, motor output from the brain to the
ventilatory muscles (feed-forward) and the afferent, or incoming,
sensory input from receptors throughout the body (feedback), as well
as the integrative processing of this information that we infer must
be occurring in the brain.
Berhanu s. 6
7. Sensory afferents
• Afferent neurons significant in dyspnea arise from a large number of
sources including the carotid bodies, medulla, lungs, and chest wall.
• Chemoreceptors_ supplyinformation regarding the blood gas levels of
O2, CO2 and H+.
• Mechanoreceptors in the lungs, when stimulated by bronchospasm,
lead to a sensation of chest tightness
• juxtacapillary (J) receptors -pulmonary interstitial edema.
Berhanu s. 7
8. • pulmonary vascular receptors, activated by acute changes in
pulmonary artery pressure, appear to contribute to air hunger
• Muscle spindles in the chest wall signal the stretch and tension of the
respiratory muscles.
Berhanu s. 8
9. Motor Efferents
• Disorders of the ventilatory pump, most commonly increase airway
resistance or stiffness (decreased compliance) of the respiratory
system, are associated with increased work of breathing or a sense of
an increased effort to breathe.
• When the muscles are weak or fatigued, greater effort is required,
even though the mechanics of the system are normal.
• The increased neural output from the motor cortex is sensed via a
corollary discharge, a neural signal that is sent to the sensory cortex
at the same time that motor output is directed to the ventilatory
muscles
Berhanu s. 9
10. Integration: Efferent-Reafferent Mismatch
• A discrepancy or mismatch between the feed-forward message to the
ventilatory muscles and the feedback from receptors that monitor the
response of the ventilatory pump increases the intensity of dyspnea.
Berhanu s. 10
12. Assessing Dyspnea
Quality of Sensation
• As with pain, dyspnea assessment begins with a determination of the
quality of the discomfort .
• Dyspnea questionnaires, or lists of phrases commonly used by
patients, assist those who have difficulty describing their breathing
sensations.
Berhanu s. 12
14. Sensory Intensity
• A modified Borg scale or visual analogue scale can be utilized to
measure dyspnea at rest, immediately following exercise, or on recall
of a reproducible physical task, e.g., climbing the stairs at home.
• An alternative approach is to inquire about the activities a patient
can do, i.e., to gain a sense of the patient's disability.
Berhanu s. 14
15. MRC Breathlessness ScaleGrade Degree of
dyspnea
• 0 no dyspnea except with strenuous exercise
• 1 dyspnea when walking up an incline or hurrying on the level
• 2 walks slower than most on the level, or stops after 15 minutes of
walking on the level
• 3 stops after a few minutes of walking on the level
• 4 with minimal activity such as getting dressed, too dyspneic to
leave the house.
Berhanu s. 15
16. Differential Diagnosis
• Dyspnea is the consequence of deviations from normal function in
the cardiopulmonary systems.
• Classified in to:
1 Respiratory System Dyspnea
2 Cardiovascular System Dyspnea
3 others
Berhanu s. 16
17. 1 respiratory system dyspnea
Diseases of the Airways
• Asthma and COPD, the most common obstructive lung diseases, are
characterized by expiratory airflow obstruction, which typically leads
to dynamic hyperinflation of the lungs and chest wall.
• stimulation of pulmonary receptors.
• hypoxemia and hypercapnia from ventilation-perfusion ( /Q)
mismatch .
Berhanu s. 17
18. Diseases of the Chest Wall
• Conditions that stiffen the chest wall, such as kyphoscoliosis,
• or that weaken ventilatory muscles, such as myasthenia gravis or the
Guillain-Barré syndrome, are also associated with an increased effort
to breathe.
Berhanu s. 18
19. Diseases of the Lung Parenchyma
.Interstitial lung diseases _increased stiffness (decreased
compliance) of the lungs and increased work of breathing.
.In addition, v /Q mismatch, and destruction and/or thickening
of the alveolar-capillary interface may lead to hypoxemia and an
increased drive to breathe.
.Stimulation of pulmonary receptors may further enhance the
hyperventilation characteristic of mild to moderate interstitial
disease.
Berhanu s. 19
20. 2 Cardiovascular System Dyspnea
Diseases of the Left Heart
• Diseases of the myocardium_ greater left-ventricular end-diastolic
volume and an elevation of the left-ventricular end-diastolic, as well
as pulmonary capillary pressures.
• interstitial edema and stimulation of pulmonary receptors;
hypoxemia
Berhanu s. 20
21. Diseases of the Pulmonary Vasculature
• Pulmonary thromboemoblic disease and primary diseases of the
pulmonary circulation (primary pulmonary hypertension, pulmonary
vasculitis) cause dyspnea via
• increased pulmonary-artery pressure and stimulation of pulmonary
receptors.
• hypoxemia may be present.
Berhanu s. 21
22. Diseases of the Pericardium
• Constrictive pericarditis and cardiac tamponade are both associated
with increased intracardiac and pulmonary vascular pressures, which
are the likely cause of dyspnea in these conditions.
• To the extent that cardiac output is limited, at rest or with exercise,
stimulation of metaboreceptors and chemoreceptors (if lactic acidosis
develops) contribute as well.
Berhanu s. 22
23. 3 others
• Anemia :Increase Co, which may necessitate elevated left ventricular
volume and pulmonary vascular pressures
• Obesity _impaired ventilatory pump function (decreased compliance
of the chest wall).
• Neurological conditions .
Berhanu s. 23
25. HISTORY
the patient should be asked to describe in his/her own words
what the discomfort feels like, as well as the effect of position,
infections, and environmental stimuli on the dyspnea
Chest tightness or constriction
Increased work or effort of breathing
Air hunger, need to breathe, urge to breathe
Heavy breathing, rapid breathing, breathing more
Berhanu s. 25
26. Rate of onset of shotness of breath(sudden or gradual
Intermitent or persistent
Agravating or relieving factor
Berhanu s. 26
27. Berhanu s.
Number pillow of they use,is that awake from sleep during night
time, chestpain,palpitation,leg swelling, nocturnal cough
hx of hypertension ,diabetes mellitus ,alcoholism,CHD ,smoking
,family history of heart disease
27
28. Berhanu s.
wheezing , coughing which are variable bot spontaneously or with
therapy,
Cough worse at night and typically awoke amorning hour and
increased mucus secretion typically tenacious mucus
28
29. • Any hx of allergy ,drug (beta blocker, aspirin ),stress,
irritant(house hold spray ,fumes), family history
asthma
• Occuational exposur{coal miners and contact with},
ciggarate smoking ,low socio economic status,
• Weight loss, hemoptysis, bone pain,weakness,fever
Berhanu s. 29
30. • Ask self or family of heart disease ,asthma, hypertention,
Berhanu s. 30
31. Fracture,hip or knee replacement,
major surgery , major trauma
,chemotherapy,
pevious VTE,immobility ,
old age, bed rest
Berhanu s. 31
34. Respiratory system
Focus on:
Inspection
clubing
Look for cyanosis
Use of accessory muscle,subcostsl or
intercostal retraction
Symmetrry of movement of chest
Audible hearing sound (wheezing,stridor)
Shape of chest :barrel for COPD
Berhanu s. 34
36. Berhanu s.
Auscultation
wheezes, rhonchi, prolonged expiratory phase, diminished breath
sounds, which are clues to disorders of the airways, and interstitial
edema or fibrosis
36
37. Cardiac examination focus on
signs of elevated right heart pressures
jugular venous distention
Edema
accentuated pulmonic component to the second
heart sound
left ventricular dysfunction
S3 and S4 gallops
valvular disease (murmurs)
Berhanu s. 37
38. examining the abdomen
Berhanu s.
Look for
paradoxical movement of the abdomen
(inward motion during inspiration)
a sign of diaphragmatic weakness
rounding of the abdomen during exhalation is suggestive of
pulmonary edema
Look for hepatomegaly
Abdominojugular reflux(pressing on abdomen increases jugular vein
distension)
38
39. Musculo skeletal :
look for edema ,calf tenderness ( for
DVT)
Patients with exertional dyspnea should be asked to
walk under observation in order to reproduce the
symptoms.
Berhanu s. 39
40. INVESTIGATION
chest radiograph should be obtained
The lung volumes should be assessed
hyperinflation indicates obstructive lung disease
low lung volumes suggest interstitial edema or fibrosis
diaphragmatic dysfunction, or impaired chest wall motion.
Berhanu s. 40
41. The pulmonary parenchyma should be examined for
evidence of interstitial disease and emphysema
Prominent pulmonary vasculature in the upper zones
indicates pulmonary venous hypertension
enlarged central pulmonary arteries suggest
pulmonary artery hypertension
enlarged cardiac silhouette suggests a dilated
cardiomyopathy or valvular disease
Berhanu s. 41
42. Bilateral pleural effusions are typical of CHF and
some forms of collagen vascular disease
Unilateral effusions raise the specter of carcinoma
and pulmonary embolism but may also occur in heart
failure
Computed tomography (CT) of the chest
for further evaluation of the lung parenchyma
(interstitial lung disease) and possible pulmonary
embolism.
Berhanu s. 42
43. electrocardiogram
look for evidence of ventricular hypertrophy and prior
myocardial infarction
Echocardiography: is indicated
whom systolic dysfunction
pulmonary hypertension
valvular heart disease is suspected
Berhanu s. 43
44. Bronchoprovocation testing is useful in patients
with intermittent symptoms suggestive of asthma
but normal physical examination and lung function; up
to one-third of patients with the clinical diagnosis of
asthma do not have reactive airways disease when
formally tested
Berhanu s. 44
45. Distinguishing Cardiovascular from
Respiratory System Dyspnea
Respiratory system
If, at peak exercise, the patient achieves predicted maximal
ventilation, demonstrates an increase in dead space or hypoxemia, or
develops bronchospasm,
if the heart rate is >85% of the predicted maximum, if anaerobic
threshold occurs early, if the blood pressure becomes excessively high
or decreases during exercise, if the O2 pulse (O2 consumption/heart
rate, an indicator of stroke volume) falls, or if there are ischemic
changes on the electrocardiogram
Berhanu s. 45
47. Treatment
• The first goal is to correct the underlying problem responsible for the
symptom
• If this is not possible, one attempts to lessen the intensity of the
symptom and its effect on patient quality of life
Berhanu s. 47
48. • . Supplemental O2 should be administered if the resting O2 saturation
is 89% or if the patient's saturation drops to these levels with activity
• For patients with COPD, pulmonary rehabilitation programs have
demonstrated positive effects on dyspnea, exercise capacity, and
rates of hospitalization
Berhanu s. 48
Left atrial myxoma or hepatopulmonary syndrome should be considered when the patient complains of platypnea, defined as dyspnea in the upright position with relief in the supine position.
Alternatively a scale such as the MRC Breathlessness Scale might be used - it suggests five different grades of dyspnea based on the circumstances in which it arises
Large pleural effusions may contribute to dyspnea, both by increasing the work of breathing and by stimulating pulmonary receptors if there is associated atelectasis.
which may arise from infections, occupational exposures, or autoimmune disorders, are associated with
resulting from coronary artery disease and nonischemic cardiomyopathies result in
These elevated pressures lead to interstitial edema and stimulation of pulmonary receptors, thereby causing dyspnea
hypoxemia due to /Q mismatch may also contribute to breathlessness.
This is thought to be related to stimulation of metaboreceptors.
spinal cord injury, phrenic nerve injuries, Guillain-Barre syndrome, amyotrophic lateral sclerosis, multiple sclerosis can all cause an individual to experience shortness of breath