Pulmonary edema
Introduction
• It is an abnormal accumulation of fluid in
the alveoli and interstitial spaces of the
lungs.
• Pulmonary edema can be defined as an
abnormal accumulation of extravascular
fluid in the lung parenchyma.
• This process leads to diminished gas
exchange at the alveolar level,
progressing to potentially causing
respiratory failure.
• It is a complication of various heart,
kidney and lung diseases.
• It is considered a medical emergency
and maybe life threatening.
• If fluid continues to leak from the pulmonary
capillaries, it will enter the alveoli. This stage is
referred to as alveolar edema.
• Pulmonary edema interferes with gas exchange by
causing an alteration in the diffusing pathway
between the alveoli and the pulmonary capillaries.
• Normally, there is balance between the
hydrostatic and oncotic pressures in the
pulmonary capillaries.
• If the hydrostatic pressure increases or the
colloid oncotic pressure decreases, the net
effect will be fluid leaving the pulmonary
capillaries and entering the interstitial space.
• This stage is referred to as interstitial edema.
• At this stage, the lymphatics cannot usually
drain away the excess fluid.
•Its etiology is either due to a
cardiogenic process with the inability to
remove sufficient blood away from the
pulmonary circulation or non-
cardiogenic precipitated by injury to the
lung parenchyma.
Etiology
• Cardiogenic or volume-overload pulmonary edema
arises due to a rapid elevation in the hydrostatic
pressure of the pulmonary capillaries. This is typically
seen in disorders involving left ventricular systolic
and diastolic function (acute myocarditis including
other etiologies of non-ischemic cardiomyopathy,
acute myocardial infarction), valvular function
(aortic/mitral regurgitation and stenosis in the
moderate to the severe range), rhythm (atrial
fibrillation with a rapid ventricular response,
ventricular tachycardia, high degree, and third-
degree heart block)
• Noncardiogenic pulmonary edema is caused by lung
injury with a resultant increase in pulmonary vascular
permeability leading to the movement of fluid, rich in
proteins, to the alveolar and interstitial
compartments. Acute lung injury with severe
hypoxemia is referred to as acute respiratory distress
syndrome (ARDS) and is seen in various conditions
directly affecting the lungs, such as pneumonia,
inhalational injury, or indirectly, such as sepsis, acute
pancreatitis, severe trauma with shock, multiple
blood transfusions.
Epidemiology
• More than 1 million patients are admitted each
year with a diagnosis of pulmonary edema
secondary to cardiac causes (heart failure)
• An estimated 190,000 patients are diagnosed with
acute lung injury each year
• About 1.5 to 3.5 cases/100,000 population are
diagnosed with ARDS.
Pathology
• The resultant pathology of increased extravascular
fluid content in the lung remains common to all
forms of pulmonary edema. However, the underlying
mechanism leading to the edema arises from the
disruption of various complex physiologic processes,
maintaining a delicate balance of filtration of fluid
and solute across the pulmonary capillary
membrane.
This imbalance can be from one or more of the
following factors:
• Increase in intravascular hydrostatic pressure
• Endothelial injury and disruption of epithelial barriers
• Decrease in oncotic pressure due to underlying
hepatic, renal, malnutrition, and other protein-losing
states.
• Lymphatic insufficiency
• Increased negative interstitial pressure
Pathophysiology
• Pulmonary edema most commonly occurs as a
result of increased microvascular pressure from
abnormal cardiac function.
• The backup of blood into the pulmonary
vasculature resulting from inadequate left
ventricular function causes an increased
microvascular pressure, and fluid begins to leak
into the interstitial space and the alveoli.
• Other causes of pulmonary edema are hypervolemia
or a sudden increase in the intravascular pressure in
the lung.
• One example of this is in the patient who has
undergone pneumonectomy. When one lung has
been removed, all the cardiac output then goes to
the remaining lung.
• If the patient’s fluid status is not monitored closely,
pulmonary edema can quickly develop in the
postoperative period as the patient’s pulmonary
vasculature attempts to adapt.
Clinical manifestations
• The patient has increasing respiratory distress,
characterized by dyspnea, air hunger and central
cyanosis.
• The patient is usually very anxious and often agitated.
• As the fluid leaks into the alveoli and mixes with air, a
foam or froth is formed. The patient have foamy, frothy,
and often blood-tinged secretions.
• The patient has acute respiratory distress and may
become confused or stuporous.
Cardiogenic
cause
• Cough with pink frothy
sputum noted due to
hypoxemia from alveolar
flooding and auscultation
of an S3 gallop.
• The presence of
murmurs, elevated
jugular venous pressure,
peripheral edema
Non-Cardiogenic
cause
 fever, cough with
expectoration, dyspnea
pointing to likely
pneumonia, recent
trauma
 Blood transfusions should
be carefully assessed as
these patients may
progress to acute
respiratory distress
syndrome.
Diagnosis
• Progressively worsening dyspnea, tachypnea, and
rales (or crackles) on examination with associated
hypoxia are present both in cardiogenic and
noncardiogenic pulmonary edema.
Diagnosis
• Auscultation reveals crackles in the lung bases
(especially in the posterior bases) that rapidly progress
toward the apices of the lungs.
• These crackles are due to the movement of air through
the alveolar fluid.
• The chest x-ray reveals increased interstitial markings.
• The patient may be tachycardic, the pulse oximetry
values begin to fall and arterial blood gas analysis
demonstrates increasing hypoxemia.
Lab findings
• Elevated BNP levels
• Troponin elevation is commonly noted in patients
with damage to myocytes
• Hypoalbuminemia (≤3.4 g/dL)
Management
• Management focuses on correcting the underlying
disorder.
• If the pulmonary edema is cardiac in origin, then
improvement in left ventricular function is the goal.
Vasodilators, inotropic medications,afterload or preload
agents, or contractility medications may be given.
Additional cardiac measures (eg, intra-aortic balloon
pump) may be indicated if the patient does not
respond.
• If the problem is fluid overload, diuretics are given and
the patient is placed on fluid restrictions.
• Oxygen is administered to correct the hypoxemia; in
some circumstances, intubation and mechanical
ventilation are necessary.
• The patient is extremely anxious and morphine is
administered to reduce anxiety and control pain.
Nursing management
• Nursing management of the patient with
pulmonary edema includes assisting with
administration of oxygen and intubation and
mechanical ventilation if respiratory failure occurs.
• The nurse also administers medications (ie,
morphine, vasodilators, inotropic medications,
preload and afterload agents) as prescribed and
monitors the patient’s response.
• Keen observation is a must :inform any untoward
incidence.
• Assist in MONA” – Morphine, Oxygen, Nitroglycerin
and Aspirin.
• Provide frequent mouth care to reduce dryness of
mucus membrane.
• Keep environment calm & quiet.
• Be alert for signs of increasing respiratory distress.
• Assess for edema especially in dependent areas
such as the ankles and sacrum.
Complication
• Multiorgan system involvement,
• Cardiogenic pulmonary edema can progress to
respiratory failure requiring the utilization of a
mechanical ventilator
• Thank You for watching and
sharing

Pulmonary edema.pptx

  • 1.
  • 2.
    Introduction • It isan abnormal accumulation of fluid in the alveoli and interstitial spaces of the lungs. • Pulmonary edema can be defined as an abnormal accumulation of extravascular fluid in the lung parenchyma. • This process leads to diminished gas exchange at the alveolar level, progressing to potentially causing respiratory failure. • It is a complication of various heart, kidney and lung diseases. • It is considered a medical emergency and maybe life threatening.
  • 3.
    • If fluidcontinues to leak from the pulmonary capillaries, it will enter the alveoli. This stage is referred to as alveolar edema. • Pulmonary edema interferes with gas exchange by causing an alteration in the diffusing pathway between the alveoli and the pulmonary capillaries.
  • 4.
    • Normally, thereis balance between the hydrostatic and oncotic pressures in the pulmonary capillaries. • If the hydrostatic pressure increases or the colloid oncotic pressure decreases, the net effect will be fluid leaving the pulmonary capillaries and entering the interstitial space. • This stage is referred to as interstitial edema. • At this stage, the lymphatics cannot usually drain away the excess fluid.
  • 5.
    •Its etiology iseither due to a cardiogenic process with the inability to remove sufficient blood away from the pulmonary circulation or non- cardiogenic precipitated by injury to the lung parenchyma.
  • 6.
    Etiology • Cardiogenic orvolume-overload pulmonary edema arises due to a rapid elevation in the hydrostatic pressure of the pulmonary capillaries. This is typically seen in disorders involving left ventricular systolic and diastolic function (acute myocarditis including other etiologies of non-ischemic cardiomyopathy, acute myocardial infarction), valvular function (aortic/mitral regurgitation and stenosis in the moderate to the severe range), rhythm (atrial fibrillation with a rapid ventricular response, ventricular tachycardia, high degree, and third- degree heart block)
  • 7.
    • Noncardiogenic pulmonaryedema is caused by lung injury with a resultant increase in pulmonary vascular permeability leading to the movement of fluid, rich in proteins, to the alveolar and interstitial compartments. Acute lung injury with severe hypoxemia is referred to as acute respiratory distress syndrome (ARDS) and is seen in various conditions directly affecting the lungs, such as pneumonia, inhalational injury, or indirectly, such as sepsis, acute pancreatitis, severe trauma with shock, multiple blood transfusions.
  • 8.
    Epidemiology • More than1 million patients are admitted each year with a diagnosis of pulmonary edema secondary to cardiac causes (heart failure) • An estimated 190,000 patients are diagnosed with acute lung injury each year • About 1.5 to 3.5 cases/100,000 population are diagnosed with ARDS.
  • 9.
    Pathology • The resultantpathology of increased extravascular fluid content in the lung remains common to all forms of pulmonary edema. However, the underlying mechanism leading to the edema arises from the disruption of various complex physiologic processes, maintaining a delicate balance of filtration of fluid and solute across the pulmonary capillary membrane.
  • 10.
    This imbalance canbe from one or more of the following factors: • Increase in intravascular hydrostatic pressure • Endothelial injury and disruption of epithelial barriers • Decrease in oncotic pressure due to underlying hepatic, renal, malnutrition, and other protein-losing states. • Lymphatic insufficiency • Increased negative interstitial pressure
  • 11.
    Pathophysiology • Pulmonary edemamost commonly occurs as a result of increased microvascular pressure from abnormal cardiac function. • The backup of blood into the pulmonary vasculature resulting from inadequate left ventricular function causes an increased microvascular pressure, and fluid begins to leak into the interstitial space and the alveoli.
  • 12.
    • Other causesof pulmonary edema are hypervolemia or a sudden increase in the intravascular pressure in the lung. • One example of this is in the patient who has undergone pneumonectomy. When one lung has been removed, all the cardiac output then goes to the remaining lung. • If the patient’s fluid status is not monitored closely, pulmonary edema can quickly develop in the postoperative period as the patient’s pulmonary vasculature attempts to adapt.
  • 13.
    Clinical manifestations • Thepatient has increasing respiratory distress, characterized by dyspnea, air hunger and central cyanosis. • The patient is usually very anxious and often agitated. • As the fluid leaks into the alveoli and mixes with air, a foam or froth is formed. The patient have foamy, frothy, and often blood-tinged secretions. • The patient has acute respiratory distress and may become confused or stuporous.
  • 14.
    Cardiogenic cause • Cough withpink frothy sputum noted due to hypoxemia from alveolar flooding and auscultation of an S3 gallop. • The presence of murmurs, elevated jugular venous pressure, peripheral edema Non-Cardiogenic cause  fever, cough with expectoration, dyspnea pointing to likely pneumonia, recent trauma  Blood transfusions should be carefully assessed as these patients may progress to acute respiratory distress syndrome.
  • 15.
    Diagnosis • Progressively worseningdyspnea, tachypnea, and rales (or crackles) on examination with associated hypoxia are present both in cardiogenic and noncardiogenic pulmonary edema.
  • 16.
    Diagnosis • Auscultation revealscrackles in the lung bases (especially in the posterior bases) that rapidly progress toward the apices of the lungs. • These crackles are due to the movement of air through the alveolar fluid. • The chest x-ray reveals increased interstitial markings. • The patient may be tachycardic, the pulse oximetry values begin to fall and arterial blood gas analysis demonstrates increasing hypoxemia.
  • 17.
    Lab findings • ElevatedBNP levels • Troponin elevation is commonly noted in patients with damage to myocytes • Hypoalbuminemia (≤3.4 g/dL)
  • 18.
    Management • Management focuseson correcting the underlying disorder. • If the pulmonary edema is cardiac in origin, then improvement in left ventricular function is the goal. Vasodilators, inotropic medications,afterload or preload agents, or contractility medications may be given. Additional cardiac measures (eg, intra-aortic balloon pump) may be indicated if the patient does not respond. • If the problem is fluid overload, diuretics are given and the patient is placed on fluid restrictions.
  • 19.
    • Oxygen isadministered to correct the hypoxemia; in some circumstances, intubation and mechanical ventilation are necessary. • The patient is extremely anxious and morphine is administered to reduce anxiety and control pain.
  • 20.
    Nursing management • Nursingmanagement of the patient with pulmonary edema includes assisting with administration of oxygen and intubation and mechanical ventilation if respiratory failure occurs. • The nurse also administers medications (ie, morphine, vasodilators, inotropic medications, preload and afterload agents) as prescribed and monitors the patient’s response. • Keen observation is a must :inform any untoward incidence.
  • 21.
    • Assist inMONA” – Morphine, Oxygen, Nitroglycerin and Aspirin. • Provide frequent mouth care to reduce dryness of mucus membrane. • Keep environment calm & quiet. • Be alert for signs of increasing respiratory distress. • Assess for edema especially in dependent areas such as the ankles and sacrum.
  • 22.
    Complication • Multiorgan systeminvolvement, • Cardiogenic pulmonary edema can progress to respiratory failure requiring the utilization of a mechanical ventilator
  • 23.
    • Thank Youfor watching and sharing