MS 1

-Obstruction of the pulmonary arterial bed when a mass (such as a dislodged thrombus) lodges in the main pulmonary artery or branch, partially or completely obstructing it,resulting in ventilation-perfusion mismatch and hypoxemia

PULMONARY EMBOLISM

PULMONARY EMBOLISM

-originate(s) somewhere in the

venous system or in the right side of the heart.

typically originate from the deep veins of the legs, right

ventricle (RV) of the heart, or pelvis.

Venous thromboemboli (VTE)

Venous thromboemboli (VTE) typically originate from the deep veins of the

legs, right ventricle (RV) of the heart, or pelvis.

mainly originate from far release after skeletal injuries,

amniotic fluid, air, and foreign bo

Nonthrombotic emboli

Nonthrombotic emboli mainly originate from far release after

skeletal injuries, amniotic fluid, air, and foreign bodies.

Patients may be asymptomatic, but sometimes

causes rapid death from pulmonary infarction

Nonthrombotic emboli m

PULMONARY EMBOLISM PATHOPHYSIOLOGY

When thrombi are formed, break loose, and lodge in the pulmonary

vasculature, both respiratory and cardiovascular changes occur. Alveoli distal to

the occlusion become ventilated but not perfused. Gas exchange cannot occur,

and the level of CO2 decreases in this area. This decrease causes broncho-

constriction, which shunts blood to ventilated areas of lungs, increases

pulmonary resistance, and causes a ventilation-perfusion mismatch. This

mismatch causes hypoxia and increases the work of breathing for the patient.

When a PE obstructs more than 50% of the pulmonary vasculature,

pulmonary hypertension results. Pulmonary vasoconstriction occurs from the

release of mediators at the injury site and from hypoxia. As resistance increases,

the workload of the RV of the heart also increases. Failure of the RV eventually

occurs, which leads to failure of the left ventricle, decreased cardiac output,

decreased blood pressure, and eventually shock

PULMONARY EMBOLISM ETIOLOGY

A decrease in blood flow (venous stasis), a problem with blood clotting, and

some form of injury to the vessel wall are three factors that can lead to the

development of venous thrombi. These three factors together are called

Virchows triad.

• Atrial fibrillation

• Deep vein thrombosis (DVT)

• Pelvic , renal, and hepatic vein thrombosis

• Rarely, other types of emboli, such as bone, air, fat, amniotic fluid, tumor cells,

or a foreign body

• Right heart thrombus

• Upper extremity thrombosis

• Valvular heart disease

Complications of pulmonary embolism

pulmonary infarction

• pulmonary hypertension

• embolic extension

• hepatic congestion and necrosis

• pulmonary abscess

• shock

• acute respiratory distress syndrome

• massive atelectasis

• right-sided heart failure

• ventilation-perfusion mismatch

• death.

ASSESSMENT pulmonary embolism

Shortness of breath for no apparent reason

• Pleuritic pain or angina

• Tachycardia, weak and rapid pulse, hypotension

• Low-grade fever

• Productive cough, possibly with blood-tinged sputum

• Warmth, tenderness, and edema of the lower leg

• Restlessness

• Transient pleural friction rub, crackles

• Third and fourth heart sounds with increased intensity of the

pulmonic component of the second heart sound

• With a large embolus: cyanosis, syncope, distended jugular

DIAGNOSTICS PE

Arterial blood gas analysis shows hypoxemia.

• D-dimer level is elevated.

• Lung ventilation-perfusion (V/Q) scan shows a V/Q mismatch.

• Pulmonary angiography shows a pulmonary vessel filling defect or

an abrupt vessel ending and reveals the location and extent of

pulmonary embolism.

• Chest X-rays may show a small infiltrate or effusion.

• Spiral chest computed tomography scan may show central

pulmonary emboli.

• Electrocardiography may reveal right axis deviation and right

bundle-branch block; it may also show atrial fibrillati

shows a pulmonary vessel filling defect or

an abrupt vessel ending and reveals the location and extent of

pulmonary embolism.

Pulmonary angiography

may show a small infiltrate or effusion.

Chest X-ray

may show central

pulmonary emboli.

Spiral chest computed tomography

may reveal right axis deviation and right

bundle-branch block; it may also show atrial fibrillatio

Electrocardiography

• Electrocardiography may reveal

right axis deviation and right

bundle-branch block; it may also show atrial fibrillation

TREATMENT PE

Mechanical ventilation, if indicated; oxygen therapy

❑ Possible fluid restriction

❑ Medications: thrombolytics, anticoagulation ,

corticosteroids (controversial), diuretics, antiarrhythmics,

vasopressors (for hypotension), antibiotics (for septic

embolus)

❑ Surgery: vena caval interruption, vena caval filter placement,

pulmonary embolectomy

Medical and nursing health care provider in PE

focus on maximizing

oxygenation, maintaining cardiopulmonary function and

hemodynamic status, and reducing oxygen demand with rest and

limitation of activity

may be necessary to help with

activity limitations and energy conservati in pe

Physical and occupational therapy

KEY PATIENT OUTCOMES in PE

The patient will:

•Maintain patent airway and adequate ventilation

•Maintain adequate cardiac output

•Verbalize feelings of increased com

NURSING INTERVENTIONSin PE

1. 2. Give prescribed drugs; avoid I.M. injections.

Avoid massage of the lower legs; encourage early postoperative

ambulation.

3. Apply antiembolism stockings.

4. 5. 6. 7. Encourage use of incentive spirometry

Monitor vital signs, intake and output, respiratory status,

Pulse oximetry, signs of DVT, complications, coagulation

Study results, abnormal bleeding, and stools for occult blood

a severe form of acute lung injury

(ALI), consists of a systemic inflammatory process that causes increased

permeability of the alveolocapillary membrane and vasoconstriction of the

pulmonary vasculatur

ACUTE RESPIRATORY DISTRESS SYNDRO

alveolocapillary membrane and vasoconstriction of the

pulmonary vasculature. This inflammation causes noncardiogenic pulmonary

edema with severely impaired gas exchange. The mortality rate greater than

40%, mostly from multisystem organ failure. Of those who survive, many have

long term impairment of lung functi

ACUTE RESPIRATORY DISTRESS SYNDRO

ACUTE RESPIRATORY DISTRESS When an injury occurs to the lungs, an

inflammatory response is initiated by

the immune system. This response

stimulates the activation

stimulates the activation of

neutrophils, macrophages, and

endotoxins into the lungs and the

release of protein mediators.

Permeability of the alveolocapillary

membrane is increased, allowing large

molecules, such as protein-rich fluid,

to enter into the lung tissue, which

causes the alveoli to collapse and the

lungs to become very stiff (decreased

compliance). Severe hypoxia develops,

leading to

respiratory acidosis,

narrowing of small airways, and pulmonary vasoconstricti

As hypoxia increases, the patient

begins t

hyperventilate

As hypoxia increases, the patient

begins to hyperventilate, which

creates

fatigue and eventually

respiratory failure.

As hypoxia increases, the patient

begins to hyperventilate, which

creates fatigue and eventually

respiratory failure. Pulmonary

vasoconstriction can lead to

pulmonary hypertension with RV

dysfunction and decreased cardiac

output.

ACUTE RESPIRATORY DISTRESS SYNDROME

ETIOLOGY

1. Pulmonary and/or nonpulmonary insult to the alveolar–capillary membrane

causing protein-rich fluid leakage into interstitial and alveolar spaces, resulting

in edema.

a. Inflammation in the interstitium and alveolar space promotes atelectasis

and lung damage.

b. This is associated with severe hypoxemia and reduced pulmonary

compliance.

c. Fibroproliferative state is often accompanied by capillary thrombosis, lung

fibrosis, and neovascularization follows.

2. Diffuse alveolar damage with ventilation–perfusion (V/Q) mismatch caused

by shunting of blood

3. Mechanisms are unclear. Acute lung injury includes both pulmonary

capillary endothelium and alveolar epithelium. Etiologies are numerous and

can be pulmonary or non pulmonary.

Predisposing factors include (but are not limited to):

•Infections, including sepsis, pneumonia (usually bacterial or aspiration).

•Shock (any cause), trauma, pulmonary contusion, near drowning, direct or

indirect lung injury, burns, pancreatitis.

•Inhaled agents—smoke, high concentration of oxygen, corrosive substances.

•Major surgery including coronary artery bypass graft, fat emboli, lung or

bone marrow transplantation, transfusion of blood products, reperfusion

pulmonary edema.

Predisposing factors include (but are not limited to): ARDS

Predisposing factors include (but are not limited to):

•Infections, including sepsis, pneumonia (usually bacterial or aspiration).

•Shock (any cause), trauma, pulmonary contusion, near drowning, direct or

indirect lung injury, burns, pancreatitis.

•Inhaled agents—smoke, high concentration of oxygen, corrosive substances.

•Major surgery including coronary artery bypass graft, fat emboli, lung or

bone marrow transplantation, transfusion of blood products, reperfusion

pulmonary ede

ETIOLOGY (SPECIFIC CONDITION) ARDS

Acute miliary tuberculosis

❑ Anaphylaxis

❑ Aspiration of gastric contents

❑ Coronary artery bypass grafting

❑ Diffuse pneumonia (especially viral)

❑ Drug overdose

❑ Hemodialysis

❑ Idiosyncratic drug reaction

❑ Indirect or direct lung trauma (most common)

❑ Inhalation of noxious gases and vapors

❑ Leukemia

❑ Near drowning

❑ Oxygen toxicity

❑ Pancreatitis

❑ Thrombotic thrombocytopenic purpura

❑ Uremia

❑ Venous air em

ASSESSMENT FINDINGS ARDS

Clinical Manifestations

-Acute onset of severe dyspnea, tachypnea, tachycardia, use of accessory

muscles, cyanosis.

-Increasing requirements of oxygen therapy. Hypoxemia refractory to

supplemental oxygen therapy.

-Scattered crackles and rhonchi heard on auscultation.

-Decreased pulmonary compliance, evidenced by increasing pressure required

to ventilate patient on mechanical ventilat

DIAGNOSTIC EVALUATIONbARDS

a.Diagnosis is based on clinical, hemodynamic, and oxygen criteria. The

hallmark signs for ARDS include acute-onset, severe hypoxemia, despite

increasing oxygen therapy, and chest x-ray exhibiting bilateralinfiltrates.

b.Pulmonary artery catheter readings show pulmonary artery wedge pressure

greater than 18 mm Hg, absence of left atrial hypertension, and no clinical

signs of heart failur

MANAGEMENT ARDS

1.Current ARDS treatment is primarily supportive. The underlying cause for

ARDS should be determined so appropriate treatment can be initiated.

2. Mechanical ventilation is nearly always required to decrease work of

breathing and improve oxygenation.

a.Low VT by mechanical ventilation (6 mL/kg of predicted body weight)

reduces mortality compared to high-volume ventilation.

b.Protective ventilation (ie, maximum inspiratory pressure of less than 35 cm)

should be instituted.

c.PEEP should be used to improve PaO2 (keeps the alveoli open, thereby

improving gas exchange). Therefore, a lower oxygen concentration (FiO2) may

be used to maintain satisfactory oxygenation.

3. Fluid management must be maintained. The patient may be hypovolemic

because of the movement of fluid into the interstitium of the lung. Pulmonary

artery catheter monitoring and inotropic medication can be helpful.

4. Medications are aimed at treating the underlying cause. Corticosteroids are

used infrequently because of controversial benefits.

5. Adequate nutrition should be initiated early and maintain

COMPLICATIONS ARDS

1. Infections, such as pneumonia, sepsis.

2. Respiratory complications, such as pulmonary emboli, barotrauma, oxygen

toxicity, subcutaneous emphysema, or pulmonary fibrosis.

3. GI complications, such as stress ulcer, ileus, pancreatitis.

4. Cardiac complications, such as decreased cardiac output and dysrhythmias.

5. Renal failure, disseminated intravascular coagulation.

6. Multiorgan failure and sepsis, which may result in death.

7. Cognitive impairment

NURSING INTERVENTIONS ARDS

Care is similar to patient with respiratory failure )

1.Give prescribed drugs and monitor for adverse effects.

2.Maintain a patent airway, tracheal suctioning, and endotracheal tube care

according to facility policy.

*** PEEP may lower cardiac output, so monitor for hypotension, tachycardia,

and decreased urine output. To maintain PEEP, suction only as needed.

3. Reposition the patient often; consider prone positioning for alveolar

recruitment.

4. Provide alternative communication means, such as cards or a notepad.

5. Monitor pulse oximetry, hemodynamics, intake and output, respiratory

status (breath sounds, ABG results), mechanical ventilator settings, sputum

characteristics, level of consciousness, daily weight, and laboratory studi

Monitor the patient for complication in ARDS

including cardiac arrhythmias,

disseminated intravascular coagulation, GI bleeding, infection, sepsis,

malnutrition, and pneumothorax