8/10/2019 a-120226153104-phpapp01

1/51

IN THE NAME OF GOD

CARDIOGENIC PULMONARY

EDEMA

1

8/10/2019 a-120226153104-phpapp01

2/51

Cardiogenic pulmonary

edema

2

8/10/2019 a-120226153104-phpapp01

3/51

CPECPE due to:

increased capillary hydrostatic pressuresecondary to elevated pulmonary venous

pressure

3

8/10/2019 a-120226153104-phpapp01

4/51

8/10/2019 a-120226153104-phpapp01

5/51

Mechanism of CPE

alveolar-capillary membrane

Increase of net flux of fluid from thevasculature into the interstitial space

Net flow of fluid across a membrane is

determined by applying the followingequation:

Q = K(Pcap - Pis) - l(Pcap - Pis)

5

8/10/2019 a-120226153104-phpapp01

6/51

6

8/10/2019 a-120226153104-phpapp01

7/51

Lymphatics

10-20 mL/h

acute rise in pulmonary arterial capillarypressure (ie, to >18 mm Hg)

chronically elevated LA pressure, the rate

of lymphatic removal can be as high as200 mL/h

7

8/10/2019 a-120226153104-phpapp01

8/51

Stages

Stage 1

elevated LA pressure distention andopening of small pulmonary vessels

blood gas exchange does not deteriorate

8

8/10/2019 a-120226153104-phpapp01

9/51

Stage 2

fluid and colloid shift into the lung

interstitium from the pulmonarycapillariesbutan initial increase in

lymphatic outflow efficiently removes the

fluid may overpower the drainage capacity of

the lymphatics

9

8/10/2019 a-120226153104-phpapp01

10/51

Stage 2

mild hypoxemia

Tachypneastimulationofjuxtapulmonary capillary (J-type)

10

8/10/2019 a-120226153104-phpapp01

11/51

Stage 3

alveolar flooding

abnormalities in gas exchange

vital capacity and other respiratory

volumes are substantially reduced

hypoxemia becomes more severe

11

8/10/2019 a-120226153104-phpapp01

12/51

Cardiac disorders manifestingas CPE

Atrial outflow obstruction

LV systolic dysfunction LV diastolic dysfunction

Dysrhythmias

LV hypertrophy and cardiomyopathies

LV volume overload

Myocardial infarction

LV outflow obstruction 12

8/10/2019 a-120226153104-phpapp01

13/51

Presentation

History

Physical Examination

13

8/10/2019 a-120226153104-phpapp01

14/51

History

Symptoms

Sudden (acute)

Long-term (chronic)

14

8/10/2019 a-120226153104-phpapp01

15/51

Sudden (acute)

Extreme shortness of breath or difficulty

breathing (dyspnea) that worsens when lyingdown

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

8/10/2019 a-120226153104-phpapp01

16/51

Sudden (acute)

Excessive sweating

Pale skin

Chest pain, if pulmonary edema is caused

by heart disease

A rapid, irregular heartbeat (palpitations)

16

8/10/2019 a-120226153104-phpapp01

17/51

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

8/10/2019 a-120226153104-phpapp01

18/51

Long-term (chronic)

Swelling in your legs and ankles

Loss of appetite

Fatigue

Ortner sign?

18

8/10/2019 a-120226153104-phpapp01

19/51

Physical Examination

Tachypnea

Tachycardia

sitting uprightairhunger

Confuse

agitate

anxious

diaphoretic 19

8/10/2019 a-120226153104-phpapp01

20/51

Hypertension

Hypotension indicates severe LV systolicdysfunction and the possibility of

cardiogenic shock

Cool extremities may indicate lowcardiac output and poor perfusion.

20

8/10/2019 a-120226153104-phpapp01

21/51

21

8/10/2019 a-120226153104-phpapp01

22/51

Auscultation

fine, crepitant rales

rhonchi or wheezes may also be present

Cardiovascular findingsS3,accentuation

of the pulmonic component of S2, jugular

venous distention

Auscultation of murmursacutevalvular

disorders

22

8/10/2019 a-120226153104-phpapp01

23/51

Auscultation

Aortic stenosis harsh crescendo-

decrescendo systolic murmur, which is heardbest at the upper sternal border and radiating to

the carotid arteries

acute aortic regurgitationshort, soft diastolic

murmur

Acute mitral regurgitation produces a loud

systolic murmur heard best at the apex or lower

sternal border 23

8/10/2019 a-120226153104-phpapp01

24/51

Mitral stenosis typically produces a loud

S1, opening snap, and diastolic rumble atthe cardiac apex

skin pallor or mottlingperipheral

vasoconstriction, low cardiac output

24

8/10/2019 a-120226153104-phpapp01

25/51

Severe CPEmentalstatushypoxiaor

hypercapniahypercapnia with respiratory acidosis may be seen

in patients with severe CPE or underlying

chronic obstructive pulmonary disease (COPD).

25

8/10/2019 a-120226153104-phpapp01

26/51

Diagnostic Considerations

Cardiogenic pulmonary edema (CPE) should be

differentiated from pulmonary edema associatedwith injury to the alveolar-capillary membrane,

caused by diverse etiologies.

26

8/10/2019 a-120226153104-phpapp01

27/51

DDx

Acute Respiratory Distress Syndrome

Asthma

Cardiogenic Shock

Chronic Obstructive Pulmonary Disease

Emphysema

Goodpasture Syndrome

Myocardial Infarction 27

8/10/2019 a-120226153104-phpapp01

28/51

DDx

Pneumothorax

High-altitude pulmonary edema

Neurogenic pulmonary edema

Pulmonary embolism

Respiratory failure

28

8/10/2019 a-120226153104-phpapp01

29/51

DDx

Pneumocystis (carinii) jiroveci

Pneumonia Pneumonia, Bacterial

Pneumonia, Viral

29

8/10/2019 a-120226153104-phpapp01

30/51

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

8/10/2019 a-120226153104-phpapp01

31/51

differentiate CPE from NCPE

Patients with NCPE have a warm periphery, a

bounding pulse, andno S3 gallop or jugularvenous distention

Definite differentiation is based on pulmonary

capillary wedge pressure (PCWP) measurements.

The PCWP is generally >18 mm Hg in CPE and