1) Cardiogenic pulmonary edema (CPE) occurs when increased hydrostatic pressure in the pulmonary capillaries causes fluid to leak into the lungs due to left ventricular dysfunction or elevated left atrial pressure. 2) Diagnosis is based on history, physical exam findings of tachypnea, tachycardia, crackles on auscultation, and tests like chest x-ray, EKG, BNP, echocardiogram and pulmonary artery catheter. 3) Treatment focuses on reducing preload and afterload through medications like nitrates, ACE inhibitors, diuretics and vasodilators, as well as providing supportive care through oxygen, ventilation if needed, and inotro

1. IN THE NAME OF GOD
CARDIOGENIC PULMONARY
EDEMA
1

2. Cardiogenic pulmonary
edema
2

3. CPE
CPE due to:
• increased capillary hydrostatic pressure
secondary to elevated pulmonary venous
pressure
3

4. following major pathophysiologic
mechanisms:
• Imbalance of Starling forces - Ie, increased
pulmonary capillary pressure, decreased plasma
oncotic pressure, increased negative interstitial
pressure
• Damage to the alveolar-capillary barrier
• Lymphatic obstruction
• Idiopathic (unknown) mechanism
4

5. Mechanism of CPE
• alveolar-capillary membrane
• Increase of net flux of fluid from the
vasculature into the interstitial space
• Net flow of fluid across a membrane is
determined by applying the following
equation:
Q = K(Pcap - Pis) - l(Pcap - Pis)
• 5

6. 6

7. Lymphatics
• 10-20 mL/h
• acute rise in pulmonary arterial capillary
pressure (ie, to >18 mm Hg)
• chronically elevated LA pressure, the rate
of lymphatic removal can be as high as
200 mL/h
7

8. Stages
Stage 1
• elevated LA pressure→ distention and
opening of small pulmonary vessels
• blood gas exchange does not deteriorate
8

9. Stage 2
• fluid and colloid shift into the lung
interstitium from the pulmonary
capillaries→but an initial increase in
lymphatic outflow efficiently removes the
fluid
• may overpower the drainage capacity of
the lymphatics
9

10. Stage 2
• mild hypoxemia
• Tachypnea→stimulation of
juxtapulmonary capillary (J-type)
10

11. Stage 3
• alveolar flooding
• abnormalities in gas exchange
• vital capacity and other respiratory
volumes are substantially reduced
• hypoxemia becomes more severe
11

12. Cardiac disorders manifesting
as CPE
• Atrial outflow obstruction
• LV systolic dysfunction
• LV diastolic dysfunction
• Dysrhythmias
• LV hypertrophy and cardiomyopathies
• LV volume overload
• Myocardial infarction
• LV outflow obstruction 12

13. Presentation
• History
• Physical Examination
13

14. History
Symptoms
• Sudden (acute)
• Long-term (chronic)
14

15. Sudden (acute)
• Extreme shortness of breath or difficulty
breathing (dyspnea) that worsens when lying
down
• A feeling of suffocating or drowning
• Wheezing or gasping for breath
• Anxiety, restlessness or a sense of apprehension
• A cough that produces frothy sputum that may
be tinged with blood
15

16. Sudden (acute)
• Excessive sweating
• Pale skin
• Chest pain, if pulmonary edema is caused
by heart disease
• A rapid, irregular heartbeat (palpitations)
16

17. Long-term (chronic)
• Having more shortness of breath than normal
when you're physically active
• Difficulty breathing with exertion, often when
you're lying flat as opposed to sitting up
• Wheezing
• Awakening at night with a breathless feeling
that may be relieved by sitting up
• Rapid weight gain
17

18. Long-term (chronic)
• Swelling in your legs and ankles
• Loss of appetite
• Fatigue
• Ortner sign?
18

19. Physical Examination
• Tachypnea
• Tachycardia
• sitting upright→air hunger
• Confuse
• agitate
• anxious
• diaphoretic 19

20. • Hypertension
• Hypotension indicates severe LV systolic
dysfunction and the possibility of
cardiogenic shock
• Cool extremities may indicate low
cardiac output and poor perfusion.
20

21. 21

22. Auscultation
• fine, crepitant rales
• rhonchi or wheezes may also be present
• Cardiovascular findings→S3,accentuation
of the pulmonic component of S2, jugular
venous distention
• Auscultation of murmurs→acute valvular
disorders
22

23. Auscultation
• Aortic stenosis→ harsh crescendo-
decrescendo systolic murmur, which is heard
best at the upper sternal border and radiating to
the carotid arteries
• acute aortic regurgitation→short, soft diastolic
murmur
• Acute mitral regurgitation produces a loud
systolic murmur heard best at the apex or lower
sternal border 23

24. • Mitral stenosis typically produces a loud
S1, opening snap, and diastolic rumble at
the cardiac apex
• skin pallor or mottling→peripheral
vasoconstriction, low cardiac output
24

25. Severe CPE→mental status→hypoxia or
hypercapnia
hypercapnia with respiratory acidosis may be seen
in patients with severe CPE or underlying
chronic obstructive pulmonary disease (COPD).
25

26. Diagnostic Considerations
Cardiogenic pulmonary edema (CPE) should be
differentiated from pulmonary edema associated
with injury to the alveolar-capillary membrane,
caused by diverse etiologies.
26

27. DDx
• Acute Respiratory Distress Syndrome
• Asthma
• Cardiogenic Shock
• Chronic Obstructive Pulmonary Disease
• Emphysema
• Goodpasture Syndrome
• Myocardial Infarction 27

28. DDx
• Pneumothorax
• High-altitude pulmonary edema
• Neurogenic pulmonary edema
• Pulmonary embolism
• Respiratory failure
28

29. DDx
• Pneumocystis (carinii) jiroveci
Pneumonia
• Pneumonia, Bacterial
• Pneumonia, Viral
29

30. differentiate CPE from NCPE
• In CPE, a history of an acute cardiac
event is usually present
• low-flow state
• S3 gallop
• jugular venous distention
• crackles on auscultation
30

31. differentiate CPE from NCPE
Patients with NCPE have a warm periphery, a
bounding pulse, and no S3 gallop or jugular
venous distention
Definite differentiation is based on pulmonary
capillary wedge pressure (PCWP) measurements.
The PCWP is generally >18 mm Hg in CPE and <
18 mm Hg in NCPE, but superimposition of chronic
pulmonary vascular disease can make this
distinction difficult to assess.
31

32. Workup
Lab studies
• Complete blood count
• Serum electrolyte measurements
• Blood urea nitrogen (BUN) and creatinine
• Pulse oximetry
• Arterial blood gas analysis
32

33. Electrocardiography
• LA enlargement
• LV hypertrophy
• acute tachydysrhythmia
• bradydysrhythmia
• acute myocardial ischemia or infarction
33

34. BNP
EFFECTS
1.Vasodilation
2. Diuresis
3. Natriuresis
4. Suppression of Renin Angiotensin Sys
34

35. BNP testing
• high negative predictive value; that is, in
patients with BNP value of under 100 pg/mL,
heart failure is unlikely
Values of 100-400 pg/mL may be related to
various pulmonary conditions, such as cor
pulmonale, COPD, and pulmonary embolism.
35

36. Radiography
Chest radiography is helpful in distinguishing CPE from other
pulmonary causes of severe dyspnea.
Features that suggest CPE rather than NCPE and other lung
pathologies include the following:
• Enlarged heart
• Inverted blood flow
• Kerley lines
• Basilar edema (vs diffuse edema)
• Absence of air bronchograms
• Presence of pleural effusion (particularly bilateral and
36
symmetrical pleural effusions)

37. 37

38. 38

39. 39

40. 40

41. 41

42. Echocardiography
important diagnostic tool in determining the etiology of
pulmonary edema
helpful in identifying a mechanical etiology for pulmonary
edema, such as the following:
• Acute papillary muscle rupture
• Acute ventricular septal defect
• Cardiac tamponade
• Contained LV rupture
• Valvular vegetation with resulting acute severe
42
mitral, aortic regurgitation

43. Pulmonary Arterial Catheter
PCWP can be measured with a pulmonary arterial catheter
(Swan-Ganz catheter)
This method helps in differentiating CPE from NCPE
A PCWP exceeding 18 mm Hg in a patient not known to
have chronically elevated LA pressure indicates CPE.
43

44. Treatment
Following initial management, medical treatment of CPE
focuses on 3 main goals
(1) reduction of pulmonary venous return (preload
reduction)
(2) reduction of systemic vascular resistance (afterload
reduction)
(3) inotropic support
44

45. Treatment
Patients with severe LV dysfunction or acute valvular
disorders may present with hypotension. These patients
may not tolerate medications to reduce their preload and
afterload. Therefore, inotropic support is necessary in
this subset of patients to maintain adequate blood
pressure.
45

46. Ventilatory Support
• Noninvasive pressure-support ventilation
• Mechanical ventilation
46

47. Preload Reduction
• Nitroglycerin
• Diuretics
• Morphine sulfate
• Nesiritide
47

48. Afterload Reduction
• ACE inhibitors
• Angiotensin II receptor blockers
• Nitroprusside
• Phosphodiesterase inhibitors
48

49. Inotropic support
• Dobutamine
• Dopamine
• Norepinephrine
• Phosphodiesterase inhibitors
• Calcium sensitizers
49

50. SUMMARY
ABC
REDISTRIBUTE FLUID OUT OF LUNGS!
1ST Line: Nitrates
2 ND Line: ACE Inhibitors
3RD Line: Diuretics
NIPPV – use early !
Milrinone – preferred inotrope
50

51. 51