1. Pulmonary edema occurs when fluid builds up in the tiny air sacs (alveoli) in the lungs, causing shortness of breath. 2. It can be caused by conditions that increase hydrostatic pressure in the pulmonary capillaries like heart failure (cardiogenic pulmonary edema) or disrupt the alveolar-capillary membrane like pneumonia or inhaled toxins (non-cardiogenic pulmonary edema). 3. The document provides definitions, classifications, signs and symptoms, differential diagnosis, and management approaches for dyspnea and pulmonary edema.

1. Approach to Dyspnea and Pulmonary Edema
Prepared By: Samuel Mesfin
Mikias Abera
Efrem Tamene
MODULATORS:- Dr. Kebede(Internist)

2. DEFINITION
The American Thoracic society(ATS) defned dyspnoea AS
 subjective experience of breathing discomfort that consists of
qualitatively distinct sensations that vary in intensity.
 The ATS also stated dyspnoea can only be perceived by the
person
experiencing it.

3. Dyspnoea
is a usual symptom related to disturbances in cardiovascular
and respiratory systems;
other potential causes that can cause dyspnoea include
metabolic,
infectious,
traumatic,
neuromuscular,
haematological and other conditions

4. Mechanism of Dyspnea
Respiratory sensations are the consequence of interactions
between
› Efferent or outgoing,
› Afferent or incoming, and
› Integrative center.
dyspnea sensations are more commonly viewed as holistic,
more akin to hunger or thirst.

5. Classification and Cause
Pulmonary parenchyma
– Acute pulmonary edema
– Acute infectious process (
pneumonia )
Pleural space
– Pneumothorax
Pulmonary vasculature
– Pulmonary embolis
Acute Dyspnea :
 Period of hours-
days
 Acute diseases :
Airways
Acute attack of asthma

6. Subacute Dyspnea :
Neuromuscular Diseases
• Guillian-Barre syndrome
• Myasthenia gravis
Pleural disease ( pleural effussion )
Chronic Cardiac Disease ( CHF )
Period of days-weeks
Airway Disease Exacerbation
Asthma/chronic bronchitis
Parenchymal infection or noninfectious
inflammatory process that proceed at
slow pace
 PCP in AIDS patients
 Mycobacterial/fungal pneumonia
 Eosinophilic pneumonea

7. Chronic dyspnea
Period of Months-Years
Chronic Obstructive Lung Disease ( COLD/COPD )
Chronic bronchitis/emphysema
Chronic interstitial lung disease
Chronic cardiac disease:heart failure,restrictive pericarditis

8. Differential Diagnosis

9. Degree of dyspnea
Freqently used scale to asses the degree of dyspnea due to lung
desease is that of the British medical researech council
Grade 0: dyspnea only during sterneus exercise
Grade 1: dyspnea only caused by brisk walking
Grade 2: brisk waking not possible due to shortness of
breath
Grade 3: stopping due to dyspnea after 100 m walking
Grade 4: doesn’t leave the due to shortness of breath

10. APPROACH TO PATIENTS
Exacerbating factor
activity?(quantify the level of
activity e.g.one flight of stairs, one block)
Is the shortness of breath related to
cold,exercise,or allergens
Alliating factor
rest
change in position
over the counter
prescription medicine?
HISTORY
Timing
Onset
Pattern
duration
Circumstance
toxic or environmental
exposure?
history of upper respiratory
infection?

11. Con’t…
Cardiovascular:
swelling?
 chest discomfort? if yes is it
pleuritic?
Pulmonary:
cough? if yes,specifically ask sputum
production and hemoptysis.
Gastrointestinal:
 heartburn?
 dysphagia?
Severity
 Does it stop the patient
from doing what they
want to do?
 Associated symptoms
Systemic: fever?
chills?
sweating?
weakness?

12. Con’t…
Relevant past history
Cardiac or pulmonary disease
 HTN,
 asthma,
 COPD,
 interstial lung disease or history of aspiration
DM
Recent trauma, or surgery , prolonged inactivity , stroke.
history of bleeding(including heavy menses)
Renal disease
Neuromuscular weakness

13. PHYSICAL EXAMINATION
 use of accessory muscles of
ventilation and
the tripod position.
Vital signs
 assess the respiratory rate
 measure the pulsus paradoxus if
it is >10 mmHg,
consider the presence of COPD
or acute asthma
General appearance
 In distress or not?
 pale or sweating?
 Inability of the patient to speak in
full sentences
 Evidence for Increased airway
resistance (stiff lung and chest
wall) includes:-
 increased work of breathing

14. Con’t…
PERCUSSION
 dullness indicative of pleural
effusion,
hyperresonance is a sign of
emphysema
AUSCULTATION
wheezes, rales, rhonchi,
prolonged expiratory phase,
diminished breath sounds, which
are clues to disorders of the airways,
HEENT
 Pale conjunctivae
 cyanosis
 icteric sclera
RESPIRATORY EXAMINATION
 INSPECTION
symmetry of movement
 PALPATION
deviated trachea

15. Cont…
 S3 and S4 gallops
 valvular disease
 murmurs
ABDOMEN
spider angiomata should be sought
paradoxical movement of the abdomen
Rounding of the abdomen during
exhalation
Clubbing of the digits
CARDIOVASCULAR
EXAMINATION
Focus on:-
signs of elevated right
heart pressures
jugular venous
distention
edema
left ventricular
dysfunction

16. Cont…
INVESTIGATIONS
ROUTINE: -
CBC: RBC,WBC & platlet count
RBC indicies :- MCV, MCH,MCHC
Hematocrit & hemoglobin
ESR
IMAGING:-
Chest X-Ray
CT scan
Electrocardiogram
Echocardiography
Bronchoprovocation testing
Cardiopulmonary Exercise Testing:
EXTREMITIES
joint swelling or deformation
Clubbing of the digits
Edema
Pulses
NEUROLOGIC EXAMINATION
 Cranial nerve palsies
 ptosis

17. Distinguishing Cardiovascular from Respiratory System
Dyspnea
Cardiovascular limitation Respiratory limitation
 Heart rate ≥85% of predicted
maximum
 Low anaerobic threshold
Reduced maximal oxygen consumption
Drop in blood pressure with exercise
Arrhythmias or ischemic changes on ECG
Does not achieve maximal predicted
ventilation
Does not have significant desaturation
Achieves or exceeds maximal predicted
ventilation
Significant desaturation (<90%)
Stable or increase dead space–to–tidal
volume ratio
 Development or bronchospasm with falling
FEV1
Does not achieve 85% of predicted maximal
heart rate
 No ischemic ECG changes

18. Management
ensuring and maintaining an open airway and providing
assistive ventilation
correct the underlying problem responsible for the symptom
Morphine may be given to reduce anxiety and extreme
discomfort of dyspnea that may occur with MI,PE,or terminal
illness, but contraindicated in asthma and COPD.

19. Pulmonary Edema

20. Definition
Pulmonary edema is a condition
characterized by fluid
accumulation in the lungs caused
by extravasation of fluid from
pulmonary vasculature into the
interstitium and alveoli of the lungs

21. 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

22. Epidemiology
Pulmonary edema occurs in about 1% to 2% of the general
population.
Between the ages of 40 and 75 years, males are affected more
than females.
After the age of 75 years, males and females are affected equally.
The incidence of pulmonary edema increases with age and may
affect about 10% of the population over the age of 75 years.

23. 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

24. Classification based on inciting mechanism
1. Imbalance of Starling force
A. Increased pulmonary capillary pressure
-left ventricular failure
-Volume overload
B. Decreased plasma oncotic pressure
- Hypoalbuminemia due to different
cause
C. Increased negativity of interstitial pressure
-Rapid removal of pneumothorax with large
applied negative pressures (unilateral)

25. Classification based on inciting agent…..
2. Altered alveolar-capillary membrane permeability
o Infectious pneumonia
o Inhaled toxins
o Circulating foreign substances
o Aspiration
o Endogenous vasoactive substances
o Disseminated intravascular coagulation
o Immunologic—hypersensitivity pneumonitis, drugs
o Shock lung in association with non-thoracic trauma
o Acute hemorrhagic pancreatitis

26. CON…
3. Lymphatic insufficiency
-After lung transplant
- Lymphangitic carcinomatosis
-Fibrosing lymphangitis
4. Unknown or incompletely understood
- High-altitude pulmonary edema
- Neurogenic pulmonary edema
- Narcotic overdose
- Pulmonary embolism
- Eclampsia

27. Based on Underlying cause
o Cardiogenic pulmonary edema: hose initiated by an
imbalance of Starling forces (Hydrostatic Pulmonary edema)
o Non-cardiogenic pulmonary edema :- those initiated by
disruption of alveolar-capillary membrane

29. Cardiogenic PE
Is Pulmonary edema due to increased pressure in the pulmonary capillaries
because of cardiac abnormalities that lead to an increase in pulmonary
venous pressure.
Increased hydrostatic pressure in the pulmonary capillaries is usually due to
elevated pulmonary venous pressure from increased left ventricular end-
diastolic pressure and left atrial pressure.
Mild elevations of left atrial pressure (18 to 25 mm Hg) cause edema in the
perimicrovascular and peribronchovascular interstitial spaces.
As left atrial pressure rises further (>25 mm Hg), edema fluid breaks through
the lung epithelium, flooding the alveoli with protein-poor fluid

30. Cont…
Due to cardiac abnormalities, pulmonary capillary pressure is increased that
increases the pulmonary venous pressure.
CAUSES :
o LV failure is the most common
o Dysrhythmia
o LV hypertrophy and cardiomyopathy
o LV volume overload
o Myocardial infarction
o LV outflow obstruction

31. Cont…
Flash pulmonary edema is a term that is used to describe a
particularly dramatic form of cardiogenic alveolar pulmonary edema.
Often, flash pulmonary edema is related to a sudden rise in left-sided
intracardiac filling pressures in the setting hypertensive urgency,
acute ischemia, new onset tachyarrhythmia, or obstructive valvular
disease.
Flash pulmonary edema rarely occurs among patients with chronic
dilated cardiomyopathies.

32. 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
`

33. Non-Cardiogenic PE
 Noncardiogenic pulmonary edema is a distinct clinical syndrome associated with
diffuse filling of the alveolar spaces caused by various disorders in which factors
other than elevated pulmonary capillary pressure are responsible for protein and
fluid accumulation in the alveoli
 By contrast, NCPE is caused by an increase in the vascular permeability of the lung
 pulmonary artery wedge pressure ≤18 mmHg
 The accumulation of fluid and protein in the alveolar space leads to decreased
diffusing capacity, hypoxemia, and shortness of breath.

34. Mechanism
include:
 Increased alveolar–capillary
membrane permeability
 Decreased plasma oncotic
pressure
 Increased negativity of
pulmonary interstitial pressure
 Lymphatic insufficiency or
obstruction

35. Cause NCPE

36. Staging of PE
Based on the degree of fluid accumulation
Stage- 1:all excess fluid can still be cleared by
lymphatic drainage
Stage- 2 presence of interstitial edema
Stage- 3 alveolar edema

37. Mild: Only engorgement of pulmonary vasculature.
Moderate: Extravasation of fluid into the interstitial space
due to changes in oncotic pressure
Severe: Alveolar filling occurs

38. Patients with noncardiogenic (or cardiogenic) pulmonary edema
rarely have unilateral edema.
Unilateral noncardiogenic pulmonary edema may be caused by
conditions ipsilateral to the edema such as aspiration, contusion,
re-expansion, and pulmonary vein occlusion (eg, veno-occlusive
disease or extrinsic compression) and by conditions contralateral
to the edema such as pulmonary embolism and lobectomy.
These lesions should be distinguished from unilateral cardiogenic
pulmonary edema, which is chiefly caused by eccentric mitral

40. Unusual type pulmonary edema
Neurogenic pulmonary edema
Patients with central nervous system disorders and
without apparent preexisting LV dysfunction
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

41. Re-expansion pulmonary edema —
Re-expansion pulmonary edema (RPE) usually occurs unilaterally
after rapid re-expansion of a collapsed lung (typically for greater
than three days) in patients with a pneumothorax, with rates
ranging from 16 to 33 percent.
Risk factors include diabetes, size of pneumothorax, and presence
of pleural effusion
It may rarely follow evacuation of large volumes of pleural fluid (>1
to 1.5 liters) (<1 percent) or removal of an obstructing

42. Reperfusion pulmonary edema
Reperfusion pulmonary edema appears to represent a form of
high-permeability lung injury that is limited to those areas of lung
from which proximal thromboembolic obstructions have been
removed.
It may appear up to 72 hours after surgery and is highly variable in
severity, ranging from a mild form of edema resulting in
postoperative hypoxemia to an acute, hemorrhagic and fatal
complication.

43. Viral infections
Rapidly progressive noncardiogenic pulmonary edema associated
with profound hypotension and a high case fatality rate has been
described with hantavirus infection and with dengue
hemorrhagic fever/dengue shock syndrome.
Enteroviral 71 infection in young children and coronavirus infection
in adults are other causes of viral-induced noncardiogenic
pulmonary edema and hemorrhage.

44. Con…
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 than

45. o on ascending to high altitude, falling level of Po2 trigger hypoxic
pulmonary vasoconstriction
o This directs blood flow away from hypoxic areas of lung towards area
that are well oxygenated
o This results in a rise in mean pulmonary artery pressure & a
heterogeneous blood flow to different parts of the lung

46. Cont…
In areas that receive high blood flow the capillary trans-mural pressure
rises & walls of the capillary &alveolus are exposed to stress failure
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

47. Clinical Presentation
Symptoms:
ACUTE
Severe shortness of breath
Cough- with pink frothy sputum
Profuse sweating
Cyanosis
Anxiety, restlessness
Palpitation
Chest pain

48. LONG TERM (CHRONIC)
Paroxysmal nocturnal dyspnea
Orthopnea
Rapid weight gain
Loss of appetite
Fatigue
Ankle and leg swelling

49. Sign
Crepitant rales, ronchi or wheeze
CVS findings:
S3,
accentuation of pulmonic
component of S2,
jugular venous distension
Tachycardia
Tachypnea
Confusion
Agitation, anxious
Diaphoriesis
Hypertension
Cool extremities

50. Complication
leg edema
Ascites
Pleural effusion
Congestion and swelling of liver
Myocardial infarction
Cardiogenic shock } Arrythmias
Electrolyte disturbances
Mesenteric insufficiency
Protein enteropathy
Respiratory arrest and death

51. Exertional Dyspnea
Orthopnea
Aspiration of food or foreign body
Direct Chest injuries
Walking High altitude
Chest Pain(right or left)
Leg pain or swelling(Pulmonary Embolism)
History Taking
Approach a Patient with Pulm.Edema

52. 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

53. Past Medical History
COPD,
 heart failure,
 HIV risk factors
(pulmonary Kaposi’s sarcoma).
 Prior chest X-rays,
CT scans,
tuberculin testing (PPD).

54. Medications
Anticoagulants
Aspirin
NSAIDs
Narcotic
Heroin
Morphine
Methadone and
Dextropropoxyphene

55. Physical Examination
respiratory distress
anxiety
diaphoresis
 pallor (note whether the patient appears ill or well).
General Appearance

56. Cont…
Temperature
respiratory rate (tachypnea),
 pulse rate(tachycardia),
BP (hypotension);
 assess hemodynamic status.
Vital Signs

57. HEENT
Nasal or oropharyngeal lesion
tongue lacerations;
Telangectasias on buccal mucosa (Rendu-Osler-Weber disease);
ulcerations of nasal septum (Wegener's granulomatosus),
jugulovenous distention,
 gingival disease (aspiration).
Cont…

58. Lymph Nodes
 Cervical, supraclavicular adenopathy(Virchow's nodes,
intrathoracic malignancy).
Cont…

59. Respiratory System
 using respiratory accessory muscles
 acral cyanosis and central cyanosis of the tongue and buccal
membranes
 Stridor,
 tenderness of chest wall;
 apical crackles(tuberculosis);
 localized wheezing (foreign body, malignancy),
 basilar crackles (pulmonary edema),
 Pleural friction rub, breastmasses (metastasis).
Cont..

60. Cardiovascular System
Jugular venous distention
Mitral stenosis murmur (diastolic rumble), right ventricular
S3 gallop;
accentuated second heart sound (pulmonary embolism).
Cont….

61. Musculoskeletal System
Calf tenderness,
calf swelling (pulmonary embolism);
clubbing (pulmonary disease),
 edema,
bone pain (metastasis).
Cont…

62. Laboratory Investigations
Routine(CBC,
Liver function tests
Electrolites
Renal Function Tests
CXR
SPIROMETRY
ECG,Echo

63. MANEGMENT
Immediate, aggressive therapy is mandatory for survival.
• Seat pt upright to reduce venous return.
• Administer 100% O2 by mask to achieve PaO2 > 60 mmHg; in
pts who can tolerate it, continuous positive airway pressure (10
cmH2O pressure) by mask improves outcome. Assisted
ventilation by mask or endotracheal tube is frequently
necessary.

64. Cont…
• Intravenous loop diuretic (furosemide, 40–100 mg, or bumetanide,
1 mg); use lower dose if pt does not take diuretics chronically.
• Morphine 2–4 mg IV (repetitively); assess frequently for
hypotension or respiratory depression; naloxone should be
available to reverse effects ofmorphine if necessary.

65. Cont…
Additional therapy may be required if rapid improvement does not
ensue:
• The precipitating cause of cardiogenic pulmonary edema should
be sought and treated, particularly acute arrhythmias or infection.
• Several noncardiogenic conditions may result in pulmonary edema
in the absenceof left heart dysfunction; therapy is directed toward
the primary condition.
• Inotropic agents, e.g., dobutaminein cardiogenic pulmonary edema
with shock.

66. Con…
 Reduce intravascular volume by phlebotomy (removal of ~250 mL through
antecubital vein) if rapid diuresis does not follow diuretic administration.
 Nitroglycerin (sublingual 0.4 mg × 3 q5min) followed by 5–10 μg/min IV.
Alternatively, nesiritide [2-μg/kg bolus IV followed by 0.01 (μg/kg)/min] may be
used.
 For refractory pulmonary edema associated with persistent cardiac ischemia,
early coronary revascularization may be life-saving.
 For noncardiac pulmonary edema, identify and treat/remove cause