Dyspnea and Pulmonary Edema

Dyspnea
DYSPNEA
 American Thoracic Society
 dyspnea as a “subjective experience of breathing
discomfort that consists of qualitatively distinct
sensations that vary in intensity experience derives
from interactions among multiple physiological,
psychological, social, and environmental factors, and
may induce secondary physiological and behavioral
responses.”
MECHANISMS OF DYSPNEA
Motor Efferents
 Disorders of the ventilatory pump
 associated with increased work of breathing or a
sense of an increased effort to breathe

 The increased neural output from the motor cortex is

thought to be sensed due to a corollary discharge that is
sent to the sensory cortex at the same time that signals
are sent to the ventilatory muscles.
Sensory Efferents
 Chemoreceptors in the carotid bodies and medulla
 activated by hypoxemia, acute hypercapnia, and
acidemia; leads to an increase in ventilation, produce
a sensation of air hunger
 Mechanoreceptors in the lungs
 stimulated by bronchospasm; lead to a sensation of
chest tightness
 J-receptors, sensitive to interstitial edema, and
pulmonary vascular receptors
 activated by acute changes in pulmonary artery
pressure, appear to contribute to air hunger
Sensory Efferents
 Hyperinflation
 associated with the sensation of an inability to get a
deep breath or of an unsatisfying breath
 Metaboreceptors, located in skeletal muscle
 activated by changes in the local biochemical milieu of
the tissue active during exercise
 when stimulated, contribute to the breathing
discomfort
Anxiety
 Acute anxiety may increase the severity of dyspnea
 alteringthe interpretation of sensory data
 leading to patterns of breathing that heighten
physiologic abnormalities in the respiratory system
ASSESSING DYSPNEA
 Quality of Sensation
 determination of the quality of the discomfort
 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.
 alternative approach is 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.
 Affective Dimension
 for a sensation to be reported as a symptom, it must be perceived as
unpleasant and interpreted as abnormal.
DIFFERENTIAL DIAGNOSIS
Respiratory System Dyspnea
 Controller
 Stimulated by acute hypoxemia and hypercapnia
 Stimulation of pulmonary receptors: acute
bronchospasm, interstitial edema, and PE
 High altitude, high progesterone states (pregnancy),
aspirin
Respiratory System Dyspnea
 Ventilatory Pump
 Disorders of the airways (asthma, emphysema, chronic
bronchitis, bronchiectasis) lead to increased airway
resistance and work of breathing
 Hyperinflation  inability to get a deep breath

 Conditions that stiffen the chest wall (kyphoscoliosis)

and that weaken ventilatory muscles (MG and GBS)
associated with increased effort to breath
 Large pleural effusions increases the work of breathing
and stimulates pulmonary receptors if there is
associated atelectasis.
Respiratory System Dyspnea
 Gas Exchanger
 interfere with gas exchange: pneumonia, pulmonary
edema, and aspiration
 direct stimulation of pulmonary receptors: pulmonary
vascular and interstitial lung disease and pulmonary
vascular congestion

 relief of hypoxemia - small impact on dyspnea

Cardiovascular System Dyspnea
 High Cardiac Output
 Mild to moderate anemia: breathing discomfort
during exercise
 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
Cardiovascular System Dyspnea
 Normal Cardiac Output
 Cardiovascular deconditioning: early development of
anaerobic metabolism and stimulation of chemo- and
metaboreceptors
 Diastolic dysfunction: due to HPN, AS, or hypertrophic
cardiomyopathy
 Pericardial disease: constrictive pericarditis
Cardiovascular System Dyspnea
 Low Cardiac Output
 Coronaryartery disease and nonischemic
cardiomyopathies: pulmonary receptors are
stimulated
Approach to the Patient
 Clinical Indicators in the history
 Orthopnea: CHF, mechanical impairment of the
diaphragm in obesity, or asthma triggered by
esophageal reflux
 Nocturnal dyspnea: CHF or asthma

 Acute, intermittent episodes: MI, bronchospasm, PE

 Chronic persistent: COPD and interstitial lung disease

 Platypnea: left atrial myxoma or hepatopulmonary

syndrome
Approach to the Patient
 Physical Examination
 Inabilityof the patient to speak in full sentences:
problem with the controller ventilatory pump
 Increased work of breathing (supraclavicular
retractions, use of accessory muscles, and the tripod
position): ventilatory pump problem increased airway
resistance or stiff lungs and chest wall
Approach to the Patient
 Physical Examination
 vitalsigns, respiratory rate
 examination for a pulsus paradoxus >10 mmHg: COPD

 signs of anemia (pale conjunctivae), cyanosis, and

cirrhosis (spider angiomata, gynecomastia)
Approach to the Patient
 Physical Examination
 Paradoxical movement of the abdomen (inward
motion during inspiration): 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
Approach to the Patient
 Physical Examination of the Chest
 Symmetry of movement
 Percussion (dullness indicative of pleural effusion,
hyper-resonance a sign of emphysema)
 Auscultation(wheezes, rales, rhonchi, prolonged
expiratory phase, diminished breath sounds)
Approach to the Patient
 Physical Examination of the Heart
 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)

Approach to the Patient
 Diagnostic Exams
 CXR
 Lung volumes
 hyperinflation: obstructive lung disease
 low lung volumes: interstitial edema or fibrosis,
diaphragmatic dysfunction, or impaired chest
wall motion
 Pulmonary parenchyma - interstitial disease and
emphysema
Approach to the Patient
 Diagnostic Exams
 CXR
 Prominent pulmonary vasculature
 in the upper zones: pulmonary venous
hypertension
 enlarged central pulmonary arteries: pulmonary
artery hypertension
 enlarged cardiac silhouette: dilated
cardiomyopathy or valvular disease
Approach to the Patient
 Diagnostic Exams
 CXR
 Bilateral pleural effusions: CHF and collagen vascular
disease
 Unilateral effusions: CA and PE
Approach to the Patient
 Diagnostic Exams
 CT scan of the chest
 reservedfor further evaluation of the lung
parenchyma (interstitial lung disease) and possible PE

 ECG
 Lookfor evidence of ventricular hypertrophy and prior
myocardial infarction
Approach to the Patient
 Distinguishing Cardiovascular from Respiratory
System Dyspnea
 CARDIOPULMONARY EXERCISE TEST
 determine which system is responsible for the
exercise limitation
Approach to the Patient
 Distinguishing Cardiovascular from Respiratory
System Dyspnea
 CARDIOPULMONARY EXERCISE TEST
 PULMONARY IF AT PEAK EXERCISE:
 achieves predicted maximal ventilation
 demonstrates an increase in dead space or
hypoxemia (oxygen saturation below 90%)
 develops bronchospasm
Approach to the Patient
 Distinguishing Cardiovascular from Respiratory
System Dyspnea
 CARDIOPULMONARY EXERCISE TEST
 CARDIAC IF AT PEAK EXERCISE:
 heart rate is >85% of the predicted maximum
 if anaerobic threshold occurs early
 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
Treatment
 First goal: correct the underlying problem
responsible for the symptom
 Administration of supplemental O2

 COPD patients: pulmonary rehabilitation programs

have demonstrated positive effects on dyspnea,
exercise capacity, and rates of hospitalization
Pulmonary Edema
Pulmonary Edema
 fluid accumulation in the lungs caused by
extravasation of fluid from pulmonary vasculature
in to the interstitium and alveoli of the lungs

 is fluid accumulation in the air spaces and

parenchyma of the lungs.
 as a result of an alteration in one or more of
Starling's forces.
 The extent to which fluid accumulates in the
interstitium of the lung depends on the balance of
hydrostatic and oncotic forces within the pulmonary
capillaries and in the surrounding tissue.
 Hydrostatic pressure
 -favors movement of fluid from the capillary into the interstitium
 Oncotic pressure
 -favors movement of fluid into the vessel
 Maintenance
 -lymphatic in the tissue carry away the small amounts of protein
that may leak out
 -tight junction of endothelium are impermeable to protein
Pathophysiology
 imbalance of starling force
 increase pulmonary capillary pressure
 decrease plasma oncotic pressure
 increase negative interstitial pressure
 damage to alveolar- capillary barrier
 lymphatic obstruction
 Disruption of endothelial barrier allow protein to
escape capillary bed and enhance movement of
fluid in to the tissue of the lung
 idiopathic or unknown
Classification
 Based on underlining cause
 Cardiogenicpulmonary edema
 Non-cardiogenic pulmonary edema
Cardiogenic pulmonary edema
 Is Pulmonary edema due to increased pressure in
the pulmonary capillaries because of cardiac
abnormalities that lead to an increase in pulmonary
venous pressure.
 Hydrostatic pressure is increased and fluid exit
capillary at increased rate
Basic pathophysiology
 A rise in pulmonary venous and pulmonary
capillary pressures pushes fluid into the pulmonary
alveoli and interstitium.
Pathogenesis of CPE
 Left sided heart failure
 Decrease pumping ability to the systemic circulation
 Congestion & accumulation of blood in the pulmonary
area
 Fluid leaks out of the intravascular space to the
interstitium
 Accumulation of fluid

 Pulmonary edema
Causes of Cardiogenic PE
 LV failure is the most common cause.
 Dysrhythmia
 LV hypertrophy and cardiomyopathy
 LV volume over load
 Myocardia infarction
 left ventricular outflow obstruction
Non cardiogenic pulmonary edema
 It is defined as the evidence of alveolar fluid
accumulation with out hemodynamic evidence that
suggest a cardiogenic etiology.
 Hydrostatic pressure is normal
 Leakage of protein and other molecule in to the
tissue
Non cardiogenic PE
 Associated with dysfunction of surfactant lining the
alveoli, increased surface force and a propensity
for the alveoli to collapse at low volume.
 Characterized by intra pulmonary shunt with
hypoxemia and decrease lung compliance
Non cardiogenic PE
 Mechanism include:
 Increased alveolar–capillary membrane permeability
 Decreased plasma oncotic pressure

 Increased negativity of pulmonary interstitial pressure

 Lymphatic insufficiency or obstruction

Non cardiogenic PE
 Cause
 Directinjury to the lung
 Hematogenous injury to the lung

 possible lung injury plus elevated hydrostatic pressure

Unusual type pulmonary edema
 Neurogenic pulmonary edema
 Patientswith central nervous system disorders and
without apparent preexisting LV dysfunction
 head injury, intracranial surgery, grand mal seizures,
 subarachnoid or intracerebral hemorrhage, and
electroconvulsive therapy
 Re-expansion pulmonary edema
 Develops after removal of air or fluid that has been in
pleural space for some time, post- thoracentesis
 Patients may develop hypotension or oliguria resulting
from rapid fluid shifts into lung.
Cont
 High altitude pulmonary edema
 occurs in young people who have quickly ascended to
altitudes above2700m and who then engage in
strenuous physical exercise at that altitude, before they
have become acclimatized.
 Reversible (in less than48 hours)
Pathophysiology
 on ascending to high altitude, falling level of Po2
trigger hypoxic pulmonary vasoconstriction
 This directs blood flow away from hypoxic areas of
lung towards area that are well oxygenated
 This results in a rise in mean pulmonary artery
pressure & a heterogeneous blood flow to different
parts of the lung
 In areas that receive high blood flow the capillary
trans-mural pressure rises & walls of the capillary
&alveolus are exposed to stress failure
Cont
 Extensive damage to alveolar capillary membrane
 Edema which is rich in high molecular weight
proteins & RBCs to pass freely in to the alveoli &
impair oxygenation.
 patient present with
 Headache, Insomnia, Fluid retention, Cough,Shortness
of breath
Clinical Feature
 ACUTE
 Shortness of breath
 A Feeling of suffocating

 Anxiety ,restlessness

 Cough-frothy sputum that may be tinged with blood

 excessive sweating

 pale skin

 chest pain if PE is cause by cardiac abnormality

 palpitation
Cont
 Long term(chronic)
 Paraxosomal nocturnal dyspnea
 orthopnea
 Rapid weight gain

 Loss of appetite

 fatigue

 ankle and leg swelling

Distinguishing Cardiogenic from
Non-cardiogenic Pulmonary Edema
 Finding suggesting cardiogenic edema
 S3 gallop
 elevated JVP
 Peripheral edema
 Findings suggesting non-cardiogenic edema
 Pulmonary findings may be relatively normal in the
early stages
 Chest radiography
A cardiogenic cause is favored with
 Cardiomegaly
 Kerley B lines and loss of distinct vascular margins
 Cephalization: engorgement of vasculature to the apices
 Perihilar alveolar infiltrate
 Pleural effusion

 Non cardiogenic cause

 -Heart size is normal
 -Uniform alveolar infiltrate
 -pleural effusion is uncommon
 -lack of cephalization
cont
 Hypoxemia
 Cardiogenic
 due to ventilation perfusion miss match
 respond to administration of oxygen

 Non cardiogenic
 due to intrapulmonary shunting
 persist despite oxygen supplimentation
Patien Approach
 History Taking
 Exertional Dyspnea
 quality of sensation, timing, positional disposition,Persistent
vs. intermittent
 Orthopnea

 Aspiration of food or foreign body

 Direct Chest injuries

 Walking High altitude

 Chest Pain(right or left)

 Leg pain or swelling(Pulmonary Embolism)

 A cough that produces frothy sputum that may be

tinged with blood(cardiogenic)
cont
 Palpitations

 Excessive sweating
 Skin color change-Pale skin

 Chest pain(if it is Cardiogenic)

 Rapid weight gain(cardiogenic)

 Fatigue

 Loss of appetite

 Smoking History
 Past Medical History
 COPD,
 heart failure,
 HIV risk factors
 (pulmonary Kaposi’s sarcoma).
 Prior chest X-rays,
 CT scans,
 tuberculin testing (PPD).
 Medications
 Anticoagulants
 Aspirin
 NSAIDs
 Narcotic
 Heroin
 Morphine
 Methadone and
 Dextropropoxyphene
Cont
 Physical examination
 GA
 Speak in full sentences
 Agitation
 Anxious
 Diaphoric

 Vital sign
 Hypertension
 Tachycardia
 Tachypnea
Cont
 Respiratory system
 Rales
 Wheezing

 CVS
 S3 ,
 accentuation of pulmonic component of S2,
 jugular venous distention

 Cool extremities
Investigation
 Routine CBC
 Chest x-ray:
 Cardiogenic
 cardiomegaly
 vascular redistribution,
 interstitial thickening
 perihilar alveolar infiltrates(producing a characteristic
butterfly pattern)
 pleural effusions are common.
 Septal lines: Kerley A, B, C(fluid accumulation between the
lung lobules)
  Non-cardiogenic
 heart size is normal
 alveolar infiltrates are distributed more uniformly throughout
the lungs
 pleural effusions are uncommon

 ECG
 Used to identify cardiogenic causes
 Ischemia or MI
 Left ventricular or atrial hypertrophy
 Echocardiography
 dilated poorly contracting left heart
 reduced ejection fraction

 evidence of underlying valvular heart disease, septal

defect
 pulmonary capillary wedge pressure
 Swan-Ganz catheter measures PCWP that
 approximates the pulmonary venous pressure
 differentiate cardiogenic from non-cardiogenic causes

 Indications
 Uncertain causes
 Refractory to therapy
 Accompanied by hypotension

 Usually above
 20mmhg in cardiogenic &
 below18mmhg in noncardiogenic causes.
Management Principle
 Main aim:
 To support the circulation, gas exchange, and lung
mechanics.
 To correct conditions that frequently complicate
pulmonary edema.
 To identify the underlying cause.
Management Principle
 cardiogenic pulmonary edema
 -Sitting
position with the legs dangling beside the bed
and bed rest to decrease cardiac workload.
 Principles
 Assist oxygenation and ventilation
 Oxygen supplementation
 Positive pressure ventilation-nasal or face mask
 Mechanical ventilation&intubation
 decrease both preload and afterload
 redistribute lung water from intra alveolar to extra alveolar
space
 increase lung volume to prevent atelectasis
 Reduction of preload
 Diuretics
 loop diuretics-furosemide(initial dose<=0.5mg/kg higher
dose=1mg/kg), bumetanide, torsemide
 Nitrates
 nitroprusside, nitroglycerine,isosorbide dinitrate
 Pulmonary edema +hypertension=nitroprusside IV
 Pulmonary edema +hypotension=nitroglycerine IV

 3. Morphine(2-4mg IV)
 Transient venodilator
 4.ACE inhibitors
 Decrease both preload and afterload
 Inotropic and inodilator drugs
 Sympathomimetic amines=dopamine, dobutamine
 Stimulation of alvelar fluid clearance
 β adrenergic agonist
 Treat etiologic and precipitating factors:
 underling causes &precipitating factors of cardiac
failure must be treated accordingly.
 Management of Non-cardiogenic pulmonary edema
 Principles
 recognitionand treatment of the underlying medical
and surgical disorders (e.g., sepsis, aspiration, trauma)
 Oxygenation and Ventilation

 Diuretics
 Special conditions
 Re expansion pulmonary edema –
 Rx is mainly Ventilation+ fluid repletion and preload
reduction is contraindicated
 High-altitude pulmonary edema-
 RXis descent from altitude, bed rest, dexamethasone,
Oxygen and Nifedipine and inhaled NO are effective