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PRESENTER:- BERHANU SHETIE
MESFIN KETEMA
MODERATOR:- Dr. ELSAH
DR.BIMEREW 1
june 24/06/2015.
Berhanu s.
outline
• Definition of dyspnea
• Mechanism of dyspnea
• Assesing dyspnea
• DDx
• approach
Berhanu s. 2
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
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
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
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
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
• 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
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
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
Berhanu s. 11
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
Berhanu s. 13
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
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
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
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
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
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
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
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
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
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
Approach to the Patient: Dyspnea
Berhanu s. 24
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
Rate of onset of shotness of breath(sudden or gradual
Intermitent or persistent
Agravating or relieving factor
Berhanu s. 26
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
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
• 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
• Ask self or family of heart disease ,asthma, hypertention,
Berhanu s. 30
Fracture,hip or knee replacement,
major surgery , major trauma
,chemotherapy,
pevious VTE,immobility ,
old age, bed rest
Berhanu s. 31
Physical Examination
GENERAL APPERANCE:
Acute sick looking or well looking
Wether in CRD or not
Nutritional status
Position of bed
Berhanu s. 32
VITAL SIGN
Blood pressure,pulse rate, respiratory
rate,To
HEENT
Sign of anemia(pale conjuctivae)
Berhanu s. 33
 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
Cont…
Berhanu s.
Percusion
Dullnes : pleurar effusion
Bilateral Hyper resonant :emphysema,bronchial asthma
Unilateral hyper resonant :pneumothorax
35
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
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
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
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
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
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
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
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
 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
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
summary
Berhanu s. 46
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
• . 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
referrence:
Internet
Berhanu s. 49

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dyspnea.pptx

  • 1. PRESENTER:- BERHANU SHETIE MESFIN KETEMA MODERATOR:- Dr. ELSAH DR.BIMEREW 1 june 24/06/2015. Berhanu s.
  • 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
  • 24. Approach to the Patient: Dyspnea Berhanu s. 24
  • 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
  • 32. Physical Examination GENERAL APPERANCE: Acute sick looking or well looking Wether in CRD or not Nutritional status Position of bed Berhanu s. 32
  • 33. VITAL SIGN Blood pressure,pulse rate, respiratory rate,To HEENT Sign of anemia(pale conjuctivae) Berhanu s. 33
  • 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
  • 35. Cont… Berhanu s. Percusion Dullnes : pleurar effusion Bilateral Hyper resonant :emphysema,bronchial asthma Unilateral hyper resonant :pneumothorax 35
  • 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

Editor's Notes

  1. 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.
  2. 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
  3. Large pleural effusions may contribute to dyspnea, both by increasing the work of breathing and by stimulating pulmonary receptors if there is associated atelectasis.
  4. which may arise from infections, occupational exposures, or autoimmune disorders, are associated with
  5. 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.
  6. 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