Definition abnormal accumulation of extravascular fluid in the lung parenchyma. diminished gas exchange at alveolar level, potentially causing respiratory failure. Etiology cardiogenic noncardiogenic

1. Pulmonary Edema
Muneer M
Second year MSc Nursing

2. Definition
•abnormal accumulation of extravascular
fluid in the lung parenchyma.
•diminished gas exchange at alveolar level,
•potentially causing respiratory failure.

3. Etiology
1. cardiogenic
2. noncardiogenic

4. Cardiogenic or volume-overload pulmonary edema
• Due to rapid elevation in hydrostatic pressure of pulmonary
capillaries.
1. LV systolic & diastolic dysfunction
• acute myocarditis, other etiologies of non-ischemic cardiomyopathy
• acute myocardial infarction,
2. valvular dysfunction
• AS, AR,MS, MR
3. Arrhythmias
• AF with rapid ventricular response
• VT
• high degree, & third-degree heart block

5. Noncardiogenic pulmonary edema
• Due to lung injury causing increase in pulmonary vascular
permeability
• movement of proteins rich fluid to alveolar & interstitial
compartments.
• Acute lung injury with severe hypoxemia = acute respiratory distress
syndrome (ARDS)
directly affecting lungs Indirectly,
Pneumonia
Inhalational injury
sepsis
acute pancreatitis
severe trauma with shock
multiple blood transfusions

6. Pathophysiology
• increased extravascular fluid content in lung is
common to all forms of pulmonary edema

7. • Starling equation
• The rate of fluid filtration is determined by differences in
hydrostatic & oncotic pressures between pulmonary
capillaries & interstitial space

8. In non cardiogenic PE
1.Imbalance of starling force
 Increase in intravascular hydrostatic pressure
 Increase in interstitial hydrostatic pressure
 Decrease plasma oncotic pressure

9. 2. Endothelial injury & disruption of epithelial barriers
3. Lymphatic insufficiency
4. Disruption of endothelial barrier allow protein in to escape
capillary bed and enhance movement of fluid in to the tissue of
the lung.

10. Clinical features
• common to both cardiogenic & noncardiogenic
pulmonary edema:
• Progressively worsening dyspnea
• Tachypnea
• rales (or crackles)
• hypoxia

11. Cardiac aetiology:
• Cough with pink frothy sputum dt hypoxemia from alveolar
flooding
• auscultation of an S3 gallop
• murmurs, elevated JVP, peripheral edema
Non-cardiogenic aetiology,
• symptoms of infections -fever, cough with expectoration, dyspnea
pointing to likely pneumonia,
• recent trauma,
• blood transfusions

12. •In all patients with respiratory symptoms:
Auscultation remains the mainstay of bedside
assessment.
Fine crackles are heard in cardiogenic pulmonary
edema.
exclusively heard in inspiratory phase when small
airways, which were shut during expiration, open
abruptly

13. Investigations
• ECG to rule out the cardiogenic cause.

14. Lab investigations
Brain-type natriuretic peptide (BNP) –
• secreted by cardiac myocytes of LV in response to stretching due
to
• increased ventricular blood volume or increased intracardiac
pressures.
• Elevated BNP levels correlate with LV end-diastolic pressure &
pulmonary occlusion pressure
a)BNP levels <100 pg/ml heart failure is less likely,
b)> 500 pg/ml  high likelihood of heart failure
c)between 100 and 500 pg/ml do not help in diagnosis of heart
failure often seen in critically ill patients

15. • Troponin elevation
1. If damage to myocytes, (acute coronary syndrome).
2. also elevated in severe sepsis

16. • Hypoalbuminemia (≤3.4 g/dL)
• independent marker of increased mortality for pts with a/c
decompensated heart failure.
• Low albumin in isolation does not lead to pulmonary edema as there is a
concurrent drop in pulmonary interstitial and plasma albumin levels
preventing the creation of a transpulmonary oncotic pressure gradient.
• serum electrolyte levels, inc renal function, serum osmolarity,
toxicology screening, help in patients with pulmonary edema due
to toxic ingestion.
• lipase & amylase levels -acute pancreatitis.

17. Chest X Ray
• Pleural effusions are more commonly seen in the cardiogenic type
Cardiogenic
pulmonary edema
Noncardiogenic pulmonary edema
1.central edema,
2.pleural effusions,
3.Kerley B septal lines,
4.peribronchial cuffing,
5. enlarged heart size.
1.typically patchy
2. peripheral ground-glass opacities
3. consolidations with air
bronchograms.

22. •Echocardiography
Assists in the diagnosis of LVF & valvular dysfunction.
•Lung Ultrasound
It helps detect the accumulation of extravascular lung water
(EVLW)

23. Pulmonary Artery Catheterization
• gold standard in determination of etiology of pulmonary
edema,
• invasive test
• helps monitor systemic vascular resistance, cardiac output,
and filling pressures.
• An elevated pulmonary artery occlusion pressure > 18 mm
Hg is helpful in the determination of cardiogenic pulmonary
edema.

24. Treatment / Management
•Therapeutic goals in pulmonary edema :
1. alleviation of symptoms
2. treatment of underlying pathologic condition.

25. Ventilatory support
NONINVASIVE & INVASIVE
1.improve oxygenation,
2.direct alveolar and interstitial fluids back into
capillaries,
3.improve hypercarbia & hence reverse respiratory
acidosis,
4. improve tissue oxygenation.
5.It also aims at reducing the work of breathing.

26. •In patients on invasive mechanical ventilation,
continuous monitoring of hemodynamics is
essential as
a reduction in preload reduced CO & thus a fall in SBP.is
Aw
lower occurrences of respiratory muscle fatigue
&
 reduction in invasive ventilation

27. Diuretics
• remain the mainstay of treatment, furosemide –most common
used medication.

28. Vasodilators
• adjuvant therapy to the diuretics in pulmonary edema
IV Nitroglycerin (NTG) 0.6 ml/hrs
• lowers preload & pulmonary congestion.
• NTG should only be used when SBP is > 110 mm Hg.

29. Nesiritide is a recombinant brain natriuretic peptide
• has vasodilatory properties.f ischemia or MI
• reduce pulmonary capillary wedge pressure & filling pressures,
but no subsequent improvement in dyspnea has been noted.
Serelaxin, a recombinant human form of relaxin,
• induces Nitric Oxide activation, which causes vasodilation.
Clevidipine is an ultra-short-acting calcium channel blocker,
initiated very early in presentation
• reduced length of stay, improved dyspnea, and less frequent ICU
admission.

30. Nifedipine
• prophylaxis and treatment of high altitude pulmonary edema (HAPE).
• Counter acts the hypoxia-mediated vasoconstriction of pulmonary
vasculature.
• lowering of pulmonary arterial pressure &
• improvements in gas exchange, exercise capability, and chest radiography
• Nifedipine is only used as a prophylactic strategy when altitude
acclimatization cannot be achieved in
high-risk individuals &
 situations, increases extreme physical exertion, recent respiratory tract
infection, and low altitude of native place of residence

31. Inotropes
Dobutamine & dopamine, are used in pulmonary congestion
when:
low SBP and signs of tissue hypoperfusion.
Side effects tachyarrhythmias, ischemia, and hypotension.
Milrinone is an IV inotrope with vasodilatory properties ne)
but it increase the post-discharge mortality

32. Morphine
• venodilator
• reduces systemic vascular resistance
• acts as an analgesic & anxiolytic.
• used in of pulmonary edema secondary to ACS
• But, it may cause respiratory depression needing
intubation.
• generally not recommended

33. Management of ACS
• Early primary PCI is the method of choice;
• alternatively, a fibrinolytic agent should be
administered.
• Early coronary angiography & revascularization
by PCI or CABG also are indicated for non-ST
elevation ACS.

34. Extracorporeal Membrane Oxygenation (ECMO)
• For patients with acute, severe non-cardiogenic edema with a
potential rapidly reversible cause
• in highly selected patients as a temporizing supportive
measure to achieve adequate gas exchange

35. Prevention
• High-altitude pulmonary edema
prevented by Treatment
• dexamethasone,
• Calcium channel–blockers,
• long-acting inhaled β2-
agonists
• descent from altitude,
• bed rest,
• oxygen,
• if feasible, inhaled nitric
oxide
• nifedipine

36. • For pulmonary edema dt upper airway obstruction,
• recognition of the obstructing cause is key,
• since treatment then is to relieve or bypass the obstruction.