1) Acute pulmonary edema is caused by fluid accumulation in the lungs due to increased pulmonary capillary pressure from conditions like heart failure. 2) It can be diagnosed based on symptoms of shortness of breath, chest imaging showing fluid in the lungs, and high BNP levels. 3) Initial treatment focuses on oxygen, diuretics to reduce fluid overload, vasodilators to reduce afterload, and in some cases non-invasive ventilation to help with breathing.

1. Acute pulmonary edema
By
Dr.kashif manzoor
Dr.anum
Dr.pakiza
Dr.ammara

2. Definition:
• Pulmonary Edema is a
condition characterized by fluid
accumulation in the lungs caused
by extravasation of fluid from
pulmonary vasculature in to the
interstitium and alveoli of the
lungs.

3. Pathopysiology:
• Pulmonary edema can be caused by the following
major pathophysiologic mechanisms:
• Imbalance of Starling forces i-e
• increased pulmonary capillary pressure,
• • decreased plasma oncotic pressure,
• • increased negative interstitial pressure
• Damage to the alveolar-capillary barrier
• Lymphatic obstruction
• Idiopathic (unknown) mechanism

4. Classification of pulmonary
edema:
•Cadiogenic
•noncadiogenic

5. Cardiogenic pulmonary edema
• Defined as pulmonary edema due to
increased Pulmonary capillary
hydrostatic pressure secondary to
elevated pulmonary venous pressure.

7. Causes of cpe:
• Atrial outflow obstruction(mitral stenosis, atrial
myxoma, thrombosis of a prosthetic valve, or a
congenital membrane in the left atrium)
• • LV systolic dysfunction
• • LV diastolic dysfunction
• • Dysrhythmias
• • LV hypertrophy and cardiomyopathies
• • LV volume overload
• • Myocardial infarction
• • LV outflow obstruction(acute stenosis of the aortic
valve, hypertrophic cardiomyopathy & elevated
systemic BP)

8. Stages of cpe:
• stage 1: fluid transfer is increased into the interstitial
tissue of the lung; because lymphatic flow also
increases, no net increase in interstitial volume occurs
• stage 2 maximum lymphatic drainage is reached and
fluid accumulates in the intestitial spaces surrounding
the bronchioles and lung vasculature
• stage 3, increasing pressure causes fluid to move into
the interstial space around the alveoli, disrupting the
alveolar membranes and finally flooding the alveoli. At
this stage, abnormalities in gas exchange are
noticeable, vital capacity and other respiratory volumes
are substantially reduced, and hypoxemia becomes
more severe.

9. Diagnosis:
• History. A careful history of previous cardiac or pulmonary
disease should be elicited. Pulmonary edema can result
from an exacerbation of previously known cardiac disease.
It can also be the presenting symptom in previously
undiagnosed cardiac disease. Because pulmonary edema
frequently arises from left ventricular failure, questions
concerning underlying causes for heart failure of left
ventricular origin should be asked: Has the patient had
chest pain? Is there any history of congenital or valvular
disease? Has the patient ever been treated for
hypertension?
• The possibility of recent infection should also be explored,
and any history of pulmonary disease should be obtained.
Specific questions should be addressed concerning
exposure to toxic inhalants, smoke, or possible aspiration.

10. Signs and symptoms:
• shortness of breath (dyspnea,
• orthopnea,
• wheezing
• anxiety
• restlesness
• cough with a frothy or pink sputum
• Chest pain
• excessive sweating
• sitting upright→air hunger • Confuse • agitate

11. Physical Examination
• Tachypnea
• Tachycardia
• Hypertension
• Hypotension indicates severe LV systolic
dysfunction and the possibility of cardiogenic shock
• Cool extremities may indicate low cardiac output
and poor perfusion.
• jugular venous distension, hepatojugularreflux,
• peripheral edema

12. Auscultation:
• fine, crepitant rales
• rhonchi or wheezes may also be present
• Cardiovascular findings→S3,gallop rhythum
• Auscultation of murmurs→Aortic stenosis,
acute aortic regurgitation, Acute mitral
regurgitation, Mitral stenosis

13. LABS:
• Complete blood count
• • Serum electrolyte measurements
• • Blood urea nitrogen (BUN) and creatinine
• • Pulse oximetry
• • Arterial blood gas analysis
• BNP

14. Role of bnp in cpe:
• Measurement of BNP levels in patients presenting to the
ED with acute dyspnea can be helpful in distinguishing
acute heart failure and CPE from other acute or chronic
lung diseases
• In the setting of acute heart failure and CPE, plasma
BNP levels increases
• a BNP level greater than 500 pg/mL makes acute heart
failure likely and is associated with a positive predictive
value of 90%.
• A BNP level less than 100 pg/mL makes acute heart
failure unlikely and is associated with a negative
predictive value of 90%.

15. Radiography in cpe:
• Enlarged heart
• Kerley B lines
• Absence of air bronchograms
• Presence of pleural effusion (particularly
bilateral and
• ymmetrical pleural effusions)
• bilateral infiltrates in a ‘‘bat wing’’ pattern

17. ECG:
• The ECG in pulmonary edema should be examined to aid
in defining the underlying etiology.
• Evidence of myocardial infarction (MI)
• LA enlargement
• LV hypertrophy
• arhythmias

18. ECG:

19. Echocardiography:
• Echocardiography can assist the physician in recognizing
valvular disease, which may lead to pulmonary edema.
• Abnormalities of left ventricular wall motion after MI
• poor left ventricular function in patients with
cardiomyopathy can easily be documented by
echocardiography.
1. Video: https://www.youtube.com/watch?v=SV2LLOhAs50
2. Video: https://www.youtube.com/watch?v=ICZmnCw0E5E
3. Video:
https://www.youtube.com/watch?v=jSbWs6A8qII&list=PLQR1tB
MKJLXwjcVCZRnsUNutfrTUX7uGB

20. Catheterization and angiography:
• 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.

21. Mitral regurtitaion

22. Dilated cardiomyopathy

23. Emergency management:
• Initial management of patients who experience CPE
should focus on the‘‘ABCs’’ of resuscitation.
• Large bore intravenous (IV) lines should be in place to
administer needed medications.
• Patients should be placed in an upright sitting position
attached to a cardiac monitor and pulse oximetry.
• Supplemental oxygen should be provided by way of a
facemask.
• If the patient remains persistently hypoxic despite the
supplemental oxygen, or if the patient develops
respiratory fatigue or a depressed level of
consciousness, mechanical ventilation should be
instituted

24. Emergency management:
• Treat the underlying etiology such as
• If a dysrhythmia has occurred, standard Advanced
Cardiac Life Support measures should be performed
• AMI, in which case appropriate anti-ischemia and
reperfusion therapies should be used
• Treatment should be aimed at redistributing the
excessive pulmonary interstitial fluid into the systemic
circulation, which improves gas exchange and hypoxia;
this can be done in three ways
• preload reduction
• afterload reduction
• In some cases, inotropic support is required also.

25. Preload reduction:
Nitrates
The mechanism of nitrate action is smooth muscle relaxation, causing venodilatation and
consequent preload reduction at low doses.13 Higher doses cause arteriolar dilatation,
resulting in reduced afterload and blood pressure. Specifically in the coronary arteries,
this dilatation results in increased coronary blood flow.9 These actions collectively
improve oxygenation and reduce the workload of the heart
Presentation and
administration
Dose Frequency Maximum dose
Glyceryl trinitrate
spray
400 microgram (2
puffs)
repeat every 5 min 1200 microgram
Glyceryl trinitrate
sublingual tablet
300–600 microgram repeat every 5 min 1800 microgram
Glyceryl trinitrate
intravenous
infusion*
5–10 microgram per
min
double every 5 min 200 microgram per
min

26. Diuretics:Loop diuretics such as
furosemide reduce preload
Presentation and
administration
Dose Frequency
Slow intravenous bolus repeat after 20 min if
necessary
– normal renal function 40–80 mg –
– renal insufficiency or
severe heart failure
up to 160–200 mg –
– chronic loop diuretic
users
initial intravenous dose
equal to maintenance oral
dose,* titrate to response
–
Intravenous infusion 5–10 mg per hour continuous

27. Afterload reduction:
• Angiotensin converting enzyme inhibitors
(ACEIs) are effective afterload-reducing agent
• The administration of sublingual (captopril) to
patients who develop CPE is associated with
reductions in systemic vascular resistance
(afterload) and improvements in PCWP
(preload), stroke volume, cardiac output, and
mitral regurgitation without causing adverse
changes in heart rate or mean arterial
pressure

28. Inotropic support
• Dobutamine provides the advantage of inducing mild
reductions in preload and afterload in addition to
inotropic support; however, dobutamine occasionally
causes a reduction in blood pressure due to peripheral
vasodilation.
• • Dopamine (Moderate dosages of 5-10 mcg/kg/min
stimulate beta-receptors in the myocardium, increasing
cardiac contractility and heart rate. High dosages of 15-
20 mcg/kg/min stimulate alpha-receptors, resulting in
peripheral vasoconstriction (increased afterload),
increased blood pressure, and no further improvement
in cardiac outpu
• • Norepinephrine

29. Phosphodiesterase inhibitors
• PDEIs(Milrinone) work by increasing
intracellular cyclic adenosine monophosphate
levels, which produces a positive inotropic
effect on the heart, induces peripheral
vasodilation, and reduces pulmonary vascular
resistance
• PDIs do not depend on adrenoreceptor activity.
Therefore, patients are less likely to develop
tolerance to PDIs than they are to other
medications

30. Calcium sensitizers
Levosimendan is a calcium sensitizer that is used to
manage moderate to severe heart failure. It has
inotropic, metabolic, and vasodilatory effects.
Levosimendan increases contractility by binding to
troponin C. It does not increase myocardial oxygen
demand, and it is not a proarrhythmogenic agent
Levosimendan opens potassium channels sensitive to
adenosine triphosphate (ATP), causing peripheral
arterial and venous dilatation. It also increases
coronary flow reserve.

31. Intra-Aortic Balloon Pumping
• IABP may be a life-saving intervention in
patients with acute mitral regurgitation
secondary to papillary muscle rupture or in
patients with ventricular septal defect as a
complication of MI. IABP reduces afterload and
thereby reduces the severity of mitral
regurgitation. It enhances forward cardiac
output, reduces LA pressure, and improves
pulmonary edema. Furthermore, IABP
decreases LV afterload and improves cardiac
output.

32. Oxygen Therapy
• If required, oxygen should be administered to
achieve a target oxygen saturation of 92–96%.
Depending on the clinical scenario, oxygen
titration can occur using a number of oxygen
delivery devices. These include up to 4 L/minute
via nasal cannulae, 5–10 L/minute via mask, . For
patients with chronic obstructive pulmonary
disease, the target oxygen saturation is 88–92% and
the use of a Venturi mask with inspired oxygen set
at 28% is recommended
• If the patient has respiratory distress, acidosis or
hypoxia, despite supplemental oxygen, non-
invasive ventilation is indicated.

33. Types of NIPPV
• There are two types of NIPPV,
• continuous positive airway pressure (CPAP):In
CPAP, the patient breaths against a continuous
flow of positive airway pressure. CPAP
maintains the same positive-pressure support
throughout the respiratory cycle.
• bilevel positive airway pressure (BiPAP):In
BiPAP, the patient receives additional positive
pressure during inspiration.it increases airway
pressure more during inspiration than during
expiration

35. Mechanical ventilation
• mechanical ventilation provides definitive
airway support and allows for maximal
oxygenation and ventilation.
• Once ETI is accomplished, positive end
expiratory pressure (PEEP) should be added to
the ventilator settings. The addition of PEEP
produces the same hemodynamic benefits as
NPPV, including improvements in preload,
afterload, and cardiac output, and decreases
the duration of mechanical ventilation.