MEDICINE
DYSPNEA AND EDEMA
DRA. LABRADOR
JANUARY 6, 2020
-Objectives:
 Definition
 Mechanisms of dyspnea
 Differentiate cardiogenic vs. noncardiogenic dyspnea
 Differential diagnosis
 Approach to the patient with dyspnea
DYSPNEA: DEFINITION
AMERICAN THORACIC SOCIETY:
 “subjective experience of breathing discomfort that
consists of qualitatively distinct sensations that vary
in intensity experience”
 multiple physiological, psychological, social and
environmental factors.
 a symptom, can be perceived only by the person
experiencing it and, therefore, must be self-reported.
 In contrast, signs of increased work of breathing,
such as tachypnea, accessory muscle use, and
intercostal retraction, can be measured and reported
by clinicians.
MECHANISMS UNDERLYING DYSPNEA
Afferent i nformation fro m the receptors throughout the
respi ratory system projects directly to the sensory cortex
to contri bute to primary qualitative sensory experiences
and to provide feed back on the action of the ventilatory
pump. Affrents also project to the areas of the brain
responsible for control of ventilation. The motor cortex,
respo n d i n g to i n put fro m the control centers, sends
neural messages to the ventil atory muscles and a
corollary discharge to the sensory cortex (feed-forward
with respect to the instructlons sent to the muscles). If the
feed-forward and feedback messages do not match, and
error signal is generated and the intensity of dyspnea
increases. An increasin g body of data supports the
contribution of affective inp uts to the ultimate perception
of unpleasant respiratory sensation.
 Afferent sensory are your chemoreceptors,
mechanoreceptors and metaboreceptors will
somehow trigger the respiratory center. The
chemoreceptors will trigger the sensory cortex, the
mechanoreceptors will somehow help in the
feedback. Your efferent will stimulate the motor
cortex and the ventilator muscles.
 Dyspnea can arise from a variety of pathways,
including generation of afferent signals from the
respiratory system to the central nervous system
(CNS), efferent signals from the CNS to the
respiratory muscles, and particularly when there is a
mismatch in the integrative signaling between these
two pathways, termed “efferent-reafferent mismatch”
AFFERENT SIGNALS
 Afferent signals trigger the CNS (brainstem and/or
cortex) and include primarily:
A. Peripheral chemoreceptors in the carotid
body and aortic arch and central
chemoreceptors in the medulla that are
activated by hypoxemia, hypercapnia, or
B. academia, and might produce a sense of “air
hunger”
C. Mechanoreceptors in the upper airways,
lungs (including stretch receptors, irritant
receptors, and J receptors), and chest wall
(including muscle spindles as stretch receptors
and tendon organs that monitor force
generation) that are activated in the setting of
an increased work load from a disease state
producing an increase in airway resistance that
may be associated with symptoms of chest
tightness
D. Mechanoreceptors in the lungs:
Bronchospasm: chest tightness (asthma)
E. J-receptors: interstitial edema
F. Pulmonary vascular receptors: due to acute
changes in pulmonary artery pressure; will
trigger air hunger
G. Hyperinflation: Associated with the sensation
of an inability to get a deep breath/ unsatisfying
breath
H. Metaboreceptors:located in the skeletal
muscle
-Local biochemical changes during exercise
-Can cause Breathing discomfort
MOTOR EFFERENTS
 Efferent signals are sent from the CNS (motor
cortex and brainstem) to the respiratory muscles.
 Disorders of the ventilator pump will cause
dyspnea including:
 Disorder of ventilator pump
 Increased airway resistance/ stiffness (COPD)
 Associated with increased work of breathing or a
sense of an increased effort to breathe
ANXIETY
 Changes in the interpretation of sensory data
 Heightens physiologic abnormalities in the
respiratory system
Hyperinflation, increased work and effort of breathing
ASSESSING DYSPNEA
 Quality of Sensation
 Determination of the quality of the disorder
 Mild, moderate or severe. We say severe when
patient is almost in respiratory failure and can
hardly talk.
Like pain assessment, dyspnea assessment begins
with a determination of the quality of the patient' s
discomfort (Table47e-1)
 Sensory Intensity
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.
BORG SCALE FOR PERCEIVED DYSPNEA
 Measure dyspnea at rest, then immediately after
exercise
 The higher the number, the poorer the performance
 Just ask the patient and look where the patient fits
0 NOTHING 6
0.5 Very, very 7 Very
weak strong
1 Very weak 8
2 Weak (light) 9
3 Moderate 10 maximal
4 Somewhat
strong
5 Strong (heavy)
 Alternative approach
 For a sensation to inquire about the activities a
patient can do.
 The Baseline Dyspnea Index and the Chronic
Respiratory Disease Questionnaire are
commonly used tools for this purpose
 GOLD 2017 criteria advocate use of a dyspnea
assessment tool such as the Modified Medical
Research Council Dyspnea Scale to assess
symptom/impact burden in COPD. Higher the
score, worse the dyspnea
 Affective Dimension
 For a sensation to be reported as a symptom, it
must be perceived and interpreted as abnormal.
It’s supposed to be an unpleasant sensation
DIFFERENTIAL DIAGNOSIS
 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
 Patients with acute bronchoconstriction also
report a sense of tightness ， which can exist
even when lung function is still within the
normal range. These patients are commonly
tachypneic; this condition leads to hyperinflation
and reduced respiratory system compliance
and also limits tidal volume.
 DISEASES OF THE CHEST WALL Conditions that
stiffen the chest wall, such as kyphosιoliosis, or that
weaken ventilatory muscles, such as myasthenia
gravis or the Guillain-Barré syndrome
 DISEASES OF THE LUNG PARENCHYMA
Interstitial lung diseases, which may arise from
infections occupational exposures or autoimmune
disorders, are associated with increased stiffness
(decreased compliance) of the lungs and increased
work of breathing.
 CARDIOVASCULAR SYSTEM DYSPNEA
1. DISEASES OF THE LEFT HEART
-Diseases of the myocardium resulting from coronary
artery disease and nonischemic cardiomyopathies cause
a greater left-ventricular end-diastolic volume and an
elevation of the left-ventricular end-diastolic as well as
pulmonary capillary pressures. These elevated pressures
lead to interstitial edema and stimulation of pulmonary
receptors, thereby causing dyspnea; hypoxemia due to
V/Q mismatch may also contribute to breathlessness.
2. DISEASESOF THE PULMONARY VASCULATURE
Pulmonary thromboembolic disease and primary
diseases of the pulmonary circulation (primary pulmonary
hypertension, pulmonary vasculitis) cause dyspnea via
increased pulmonarγ artery pressure and stimulation of
pulmonarγ receptors. Hyperventilation is common, and
hypoxemia may be present.
-Use of supplemental oxygen has only a
minimal impact on the severity of dyspnea and
hyperventilation.
3. DISEASES OF THE PERICARDIUM
Constrictive pericarditis and cardiac
tamponade are both associated with increased
intracardiac and pulmonary vascular pressures, which
are the like cause of dyspnea in
these conditions.
DYSPNEA WITH NORMAL RESPIRATORY AND
CARDIOVASCULAR SYSTEMS
Mild to moderate anemia is associated with breathing
discomfort during exercise. This symptom is thought to
be related to stimulation of metaboreιeptors; oxygen
saturation is normal in patients with anemia.
The breathlessness associated with obesity is probably
due to multiple mechanisms, including high cardiac
output and impaired ventilatory pump function
(decreased compliance of the chest wall)
Cardiovascular deconditioning (poor fitness) is
characterized by the early development of anaerobic
metabolism and the stimulation of chemoreceptors and
metaboreceptors. Dyspnea that is medically unexplained
has been associated with increased sensitivity to the
unpleasantness of acute hypercapnia.
CARDIOVASCULAR SYSTEM DYSPNEA
1. HIGH CARDIAC OUTPUT
 Mild to moderate anemia: breathing discomfort
during exercise but at rest they are comfortable, but
when they climb stairs or walk faster, they start
complaining of breathing discomfort
 Left to right intracardiac shunts: may be complicated
by the development of pulmonary hypertension
 Breathlessness associated with obesity: due to
multiple mechanisms, including high cardiac output
and impaired ventilatory pump function.
2. NORMAL CARDIAC OUTPUT
• Cardiovascular deconditioning: early development of
anaerobic metabolism and simulation of chemo- and
metaboreceptors
• Diastolic dysfunction: common in the community due
to HPN, Aortic Stenosis, or hypertrophic
cardiomyopathy, common also in diabetic patients
• Pericardial disease: constrictive pericarditis
3. LOW CARDIAC OUTPUT
• Coronary artery disease and nonischemic
cardiomyopathies: pulmonary receptors are stimulated
APPROACH TO THE PATIENT
1. CLINICAL INDICATORS IN THE HISTORY
• Before we can classify dypnea as psychological we
have to rule out the other possibilities.
• Orthopnea: (difficulty of breathing in the supine
position) more commonly seen in patients with CHF,
mechanical impairment of the diaphragm in obesity, or
asthma triggered by esophageal reflux, so when the
patient lies down, the symptoms recur or occur
• Nocturnal dyspnea: CHF or asthma
• Acute, intermittent episodes: MI, bronchospasm, PE
(Pulmonary Embolism)
• Chronic persistent: COPD and interstitial lung disease
(interstitial lung disease includes idiopathic pulmonary
fibrosis, collagen vascular disease, drug or
occupation-induced pneumonitis, lymphangitic spread
of malignancy)
• Platypnea: ( dyspnea in the upright position with relief
in the supine position.) left atrial myxoma or
hepatopulmonary syndrome
2. PHYSICAL EXAMINATION
• History of the patient: 80%
physical examination:15%
lab tests: 5% ( we do the lab to confirm our diagnosis
not to indicate us the problem).
• We look for Inability of the patient to speak in full
sentences: the clue here is a problem with the
controller ventilatory pump. Ex. Asthma.
• Increased work of breathing (supraclavicular
retractions, use of accessory muscles, and the tripod
position, they cannot tolerate lying down and dyspneic
while sleeping): ventilatory pump problem, increased
airway resistance or stiff lungs and chest wall
• Evaluate vital signs. Look for:
-Respiratory rate normal RR: 12
 -examination for a pulsus paradoxus >10 mmHg:
ex. COPD
- -signs of anaemia (pale conjunctivae), cyanosis, and
cirrhosis (spider angiomata, gynecomastia)
• Anemia should be corrected especially with patients
with history of CHF, we don’t want tachycardia to
happen, because heart failure may be induced.
• Paradoxical movement of the abdomen (inward
motion during inspiration). Keep the patient in supine
position. normally, the abdomen is supposed to
expand during inhalation: diaphragmatic weakness.
• Clubbing of the digits: interstitial pulmonary fibrosis
• Joint swelling or deformation, change consistent with
Raynaud’s disease: collagen-vascular process
associated with pulmonary disease
• Physical examination of the Chest
o Symmetry of movement (lung expansion)
o Percussion (dullness indicative of pleural effusion,
hyper-resonance a sign of emphysema)
o Auscultation (wheezes, rales, rhonchi, prolonged
expiratory phase, diminished breath sounds)
o for percussion and auscultation, go back to that
table in Bate’s (last page) regarding those different
lung sounds, percussion notes and palpation
abnormalities
• Physical examination of the Heart
o signs of elevated right heart pressures (jugular
venous distention, edema, accentuated pulmonic
component to the second heart sound)
o left ventricular dysfunction (S3 and S4 gallops)
o valvular heart disease (murmurs)
DIAGNOSTIC EXAMS
• CXR
o Lung volumes
 hyperinflation: (film appears darker, lungs are
expanded, mediastinum is narrow, interspaces
are increased, ribs are further apart than usual)
seen in obstructive lung diseases
 low lung volumes: ex. interstitial edema or
fibrosis, diaphragmatic dysfunction, or impaired
chest wall motion
o Pulmonary parenchyma – look for interstitial
disease(fibrotic changes) and emphysema.
o Prominent pulmonary vasculature (look at the
hilum area)
 in the upper zones: pulmonary venous
hypertension
 enlarged central pulmonary arteries: pulmonary
artery hypertension
 enlarged cardiac silhouette: dilated
cardiomyopathy or valvular disease
o Bilateral pleural effusion: CHF and collagen
vascular disease
o Unilateral effusions: Carcinoma and Pulmonary
Embolism
• CT SCAN OF THE CHEST
Being expensive we do not do it right away.
o reserved for further evaluation of the lung
parenchyma (interstitial lung disease) and possible
Pulmonary embolism(spherical or helical CT scan
is recommended for PE)
• ECG
o Look for evidence of ventricular hypertrophy and
prior myocardial infarction.
In prior myocardial infarction there will be elevation on
Q-wave.
Algorithm will include this presented with the history of
dyspnea, go back to the history, look into the quality of
sensation, timing, etc, do your physical exam, and look
for clues and you may find something, example wheezes
and somehow you may have differentials in mind, from
there you may do your diagnostics. When you do your
X-ray, don’t forget to assess the cardiac signs, look for
signs of hyperinflation, pneumonia, effusions, for
evidence of CHF and then follow down the guide. Now if  INCREASED hyrdrostatic pressure (fluid exits
you have done everything, and then there’s still no actual the capillary at an increased rate =
diagnosis and you still can’t say whether it’s cardiac or interstitial/alveolar edema)
pulmonary in nature, that’s the time when you obtain  INCREASE pulmonary venous pressure
cardiopulmonary exercise test.  Exertional dyspnea and orthopnea
DISTINGUISHING CARDIOVASCULAR FROM  Physical Examination:
RESPIRATORY SYSTEM DYSPNEA o Increased intracardiac pressures (S3
CARDIOPULMONARY EXERCISE TEST gallop, elevated jugular venous pulse,
peripheral edema)
1. Determine which system is responsible for the o Rales and/or wheezes (asthma,
exercise limitation congestive heart failure) on auscultation
2. Cardiac if at peak exercise: of the chest
 Heart rate is >85% of the predicted maximum
 If anaerobic threshold occurs early  CXR:
 If the BP becomes excessively high or drops
 If the O2 pulse (O2 consumption/heart rate, an
indicator of stroke volume) falls
 If there are ischemic changes on the ECG
3. Pulmonary if at peak exercise:
 Achieves predicted maximal ventilation
 Demonstrates an increase in dead space or
hypoxemia (oxygen saturation below 90%)
 Develops bronchospasm

TREATMENT
 First goal: correct the underlying problem
responsible for the symptom
 Administration of supplemental O2 if the resting
O2 is saturation is less than or equal to 89% or if
the patients saturation drops to these levels with
activity.
 COPD patients: pulmonary rehabilitation
programs have demonstrated positive effects on
dyspnea, exercise capacity and rates of
hospitalization.
In order to treat dyspnea, you have to know the cause. If
you don’t know the cause it will be hard to treat dyspnea.
Generally, we give oxygen at the ER. For COPD patients,
pulmonary rehabilitation programs are not yet available
here in Pampanga. A patient who is referred to a rehab
will have better exercise tolerance compared to those
without.

PULMONARY EDEMA o Peribronchial thickening, Kerley B lines,

CARDIOGENIC VS NONCARDIOGENIC cardiomegaly
o Enlarged cardiac silhouette
1. CARDIOGENIC o Vascular redistribution
 o Interstitial thickening
o Perihilar alveolar infiltrates
o Pleural effusions
2. NONCARDIOGENIC
 NORMAL hydrostatic pressures
 Mild to severe dyspnea as manifested by
respiratory failure
 Categories:
o Direct
o Indirect
o Pulmonary Vascularity
 Physical Examination:
o Findings may be relatively normal in the
early stages
 CXR:
o Heart size is normal
o Uniform alveolar infiltrates
o Pleural effusions are uncommon
 Favors movement of fluid from capillary
into the interstitium
 Oncotic pressure
o Favors movement of fluid into the vessel
o Protein concentration, disruption of
endothelial barrier (movement of fluid
into the tissue of the lung)
STARLING FORCES
Starling forces have 4 components: Oncotic and
hydrostatic pressure of the vessels; oncotic and
hydrostatic pressure of the interstitial.
 TBW – 1/3 ECF
o 75% interstitial fluid
o Plasma
 Hydrostatic forces within capillaries, colloid
oncotic pressure (interstitial fluid) = fluid
movement from the vascular space to the
extravascular space
 Colloid oncotic pressure (plasma proteins) and
hydrostatic pressure (interstitial fluid) = fluid
movement into the vascular compartment
If you have problems with plasma proteins, you may have
problems with the liver and patient may manifest
pulmonary edema, etc.
 Imbalance: net movement of fluid from
intravascular to the interstitial spaces
DEFINITION
 EDEMA: clinically apparent increase in the
interstitial fluid volume
o Increase capillary pressure secondary to
increase venous load (localized or
generalized)
o Increase flow from vascular space to the
interstitium

EDEMA  Anasarca refers to gross, generalized edema.

(after auscultating the patient posteriorly, we see
OBJECTIVES: pitting on removal of the steth: there is already
 Definition of edema anasarca)
 Pathogenesis
 Factors involved  Ascites refer to accumulation of excess fluid in
 Clinical causes of edema the peritoneal cavity (common in cirrhotic
 Differential diagnosis patients)
 Approach to edema

 Hydrothorax is the accumulation of fluid in the

MECHANISMS OF FLUID ACCUMULATION pleural cavitiescaused by:
 Balance hydrostatic and oncotic forces within the  Capillary Damage
pulmonary capillaries  Drugs
 HYDROSTATIC PRESSURE:  Infections
  Thermal trauma  AGN (acute glomerulo nephritis): hematuria,
 Mechanical trauma proteinuria, hypertension
 Hypersensitivity  Primary retention of sodium and water by the
 Auto-immune diseses. kidneys
 Nephrotic syndrome- diminished colloid oncotic
pressure due to losses of large quantities of protein
Will cause a reduction of effective arterial volume and will into the urine.
lead to decrease renal circulation and will be interpreted  Severe hypoalbuminemia
by the JG cells to increase renin release; RAAS  severe nutritional deficiency states
activation.  severe, chronic liver disease
Arginine Vasopressin  protein-losing enteropathy
 Increase reabsorption of free water in the distal  Cirrhosis
tubules & collecting ducts of kidneys o Blockade of hepatic venous outflow
 Associated with decreased effective arterial Intrahepatic hypertension (renal sodium
volume retention with reduced effective arterial
 Commonly seen in patient with CHF blood volume)
Endothelin-1 Prevent dehydration to these patients because of
 Vasoconstrictor reduced arterial blood volume. You should be cautious in
giving diuretics. Monitor for the Intake and output of the
 Released by endothelin cells
patient
 Contributes to renal vasoconstriction, Na
retention, and edema in heart failure
 Drug induced edema
Natriuretic peptide
o Renal vasoconstriction (NSAIDS and
 Distention of the atrium cyclosporine)
 Elevated ANP and BNP (due o Arteriolar dilation (vasodilators)
to inc. ventricular diastolic pressure) o Augmented renal Na reabsorption
Sometimes we cannot identify if its acute coronoary (patients using steroid hormones)
syndrome or congestive heart failure. So we look for BNP. o Capillary damage (interleukin)
If there is elevation of BNP then we can say that the  Edema of Nutritional Origin
patient has heart failure. A diet grossly deficient in protein over a prolonged period
 Sometimes these are Not enough to prevent may produce hypoproteinemia and edema. The latter
edema formation may be intensified by the development of beriberi heart
disease, which also is of nutritional origin, in which
CLINICAL MANIFESTATION multiple peripheral arteriovenous fistulae result in
 Weight gain reduced effective systemic perfusion and
 Pitting edema effective arterial blood volume, thereby enhancing edema
 Puffiness of the face, periorbital areas formation.
 "pitting" edema
 Difficulty putting on shoes, particularly in the
evening

CLINICAL CAUSES

GENERALIZED EDEMA
DIFFERENTIAL DIAGNOSIS
 Congestive Heart Failure
 Elevated diastolic Pressure
 Accumulation Of blood in the Venous
Circulation
 Impaired Ventricular relaxation
 Increase Sympathetic Nervous system
stimulation will stimulate renal Vasoconstriction
which would further aggravate the condition.
 Renal disease
 LOCALIZED EDEMA
Causes of localized edema
 Obstruction of venous/lymphatic drainage of a
limb (localized edema)
 Transfer of fluid from the vascular to the
interstitial space (trapping)
 Thrombophlebitis, chronic lymphangitis,
resection of regional lymph nodes, filariasis.
Other causes
 Hypothyroidism (Myxedema)
 Hyperthyroidism (Pretibial myexedema
secondary to Graves disease)
o Nonpitting
 Estrogen
 Dyhydropyridines (amlodipine, nifedipine)
o Patient usually complain that their shoes
do not fit anymore. Consider changing
the medication.
DISTRI BUTION OF EDEMA
The distribution of edema is an important guide to its
cause.
 Edema associated with heart failure tends to be
more extensive in the legs and to be accentuated in
the evening, a feature also determined largely
byposture. When patients with heart failure are
confined to bed, edema may be most prominent in
the presacral region.
 Severe heart failure may cause ascites that may be
distinguished from the ascites caused by hepatic
cirrhosis by the jugular venous pressure which is
usually elevated in heart failure and normal in
cirrhosis.
 Edema resulting from hypoproteinemia, as occurs in
HISTORY LAB. FINDINGS the nephrotic syndrome, characteristically is
generalized, but it is especially evident in the very
Cardiac Dyspnea with Elevated BUN:crea soft tissues of the eyelids and face and tends to be
exertion ratio, Liver most pronounced in the morning owing to the
enzymes; BUA
recumbent posture assumed during the night.
Hepatic Alcohol abuse Hypo K,
 Less common causes of facial edema include
Respiratory trichinosis, allergic reactions and myxedema.
alkalosis (check  Edema limited to one leg or to one or both arms is
ABG) usually the result of venous and/or lymphatic
obstruction.
CRF(chronic Uremic s/sx Albuminuria, hyper
renal failure) K  Unilateral paralysis reduces lymphatic and venous
drain age on the affected side and may also be
Nephrotic Childhood DM, Proteinuria(3.5g/d) responsible for unilateral edema.
syndrome plasma cell ;  In patients with obstruction of the superior vena
dyscrasias hypoalbuminemia; cava, edema is
hypercholesterole confined to the face, neck, and upper extremities in
mia; microscopic which the venouspressure is elevated compared
hematuria
with that in the lower extremities.

APPROACH: Determine first if it is localized or generalized

REF:
HARRISONS. PPT. RECORDINGS. 2021TRANS