Respiratory Emergencies Study Guide for the CEN

Pleural Effusion

A pleural effusion is a collection of fluid just outside the lungs that accumulates between the parietal and visceral pleura in the pleural space. It compresses the lungs and interferes with the ability to breathe. Causes of pleural effusion include:

congestive heart failure
lung infection
cancer
irritation

Assessment

The primary symptom of a pleural effusion is dyspnea due to the compression of the lungs. Auscultation of the lungs will reveal a distinctive pleural friction rub, best described as a grating sound. Other symptoms include:

tachypnea
chest tightness
coughing
hypoxia
heart palpitations
inability to take a deep breath

The diagnostic tests may include a chest CT, chest X-ray, or chest ultrasound. The fluid from the pleural effusion can be analyzed when removed to determine the cause of the pleural effusion and help determine the treatment method.

Treatment

The patient will require continuous pulse oximetry to monitor their oxygen saturation. The first line of treatment for pleural effusion is a thoracentesis to drain the fluid from around the lungs. If the pleural effusion recurs frequently, then surgical solutions may become necessary. A pleurodesis is a procedure in which a drug or chemical irritant is used to fuse parietal and visceral pleural together to prevent the reaccumulation of fluid.

A PleurX™ catheter is a device placed into the pleural space that remains in place so that fluid can be drained repeatedly without needing to make a new puncture every time. Patients can even use the PleurX catheter at home after receiving proper education. Treating the underlying cause of the pleural effusion is also key: a patient with cancer may receive chemotherapy, while a patient with pneumonia would receive antibiotics.

Pneumothorax

A pneumothorax is the leakage of air into the pleural space. The lungs normally stay inflated thanks to the negative pressure exerted by the pleural space. When enough air leaks and disrupts this negative pressure, the lung can collapse, which significantly impairs the patient’s ability to breathe. It generally occurs as a result of trauma, but can also occur spontaneously. Young patients who are tall and thin are particularly prone to spontaneous pneumothorax due to increased shearing forces on their lungs.

Assessment

Symptoms of a pneumothorax include:

dyspnea
a harsh dry cough
stabbing chest pain that worsens with inhalation
fatigue
cyanosis
low blood pressure
tachypnea
hypoxia
tachycardia

Auscultation of the lungs will reveal diminished or absent breath sounds on the affected side. Tachycardia and low blood pressure occur if the pneumothorax is significant enough to decrease the blood return to the heart as the body attempts to compensate for the decreased blood flow.

Severe pneumothoraces can lead to a buildup of air under the skin that produces a crackling sensation upon palpation called crepitus. The pneumothorax can be diagnosed using a chest X-ray or chest CT. The provider can also percuss the sternum while auscultating the affected side. The percussion will have a resonant, booming sound if there is a pneumothorax.

Treatment

When the patient has a small pneumothorax, the first line of treatment is monitoring. The patient will receive serial chest X-rays at least every 24 hours for several days to make sure that the pneumothorax doesn’t grow. Pulse oximetry should be checked at least several times daily with vital signs. If the pneumothorax does grow,, further intervention is needed.

The patient may require the use of supplemental oxygen for more significant pneumothoraces. In an emergency setting, a needle decompression can be used to rapidly drain the excess air from around the lung and allow it to reinflate. A chest tube with a negative one-way valve can be placed to drain the air as well and generally remains in place for several days. For recurring or persistent pneumothoraces, surgery may be needed to seal the leak, perform a pleurodesis to seal the parietal and visceral pleura, or even remove part of the lung as a last resort.

Noncardiac Pulmonary Edema

Noncardiac pulmonary edema is the accumulation of fluid in the lungs due to a cause other than cardiac dysfunction. It can be divided into acute, chronic, and high-altitude pulmonary edema (HAPE) subsets. Some of the causes include:

acute respiratory distress syndrome (ARDS)
pulmonary embolism
fluid overload
acute kidney disease
drowning
drug use
neurogenic pulmonary edema
viral illnesses
inhalation injuries
aspiration
allergic reaction

Assessment

Symptoms of noncardiac pulmonary edema vary depending on whether it is acute, chronic, or HAPE, although all types can result in hypoxia, and auscultation of the lungs will reveal crackles/rales. Acute symptoms include:

shortness of breath during activity or while lying down that improves with sitting up
productive cough with frothy, possibly bloody sputum
tachycardia
sensation of impending doom
wheezing or gasping for breath

Chronic symptoms include:

fatigue
new or worsening cough that does not produce frothy sputum
increased shortness of breath during activity or while lying down
wheezing
rapid weight gain
peripheral edema

HAPE symptoms include:

headache
initial shortness of breath during activity, then shortness of breath while sedentary
a cough that is initially dry but can become productive with bloody, frothy sputum
tachycardia and chest pain
generalized weakness
fever

Diagnostic tests for noncardiac pulmonary edema include a chest X-ray, chest CT, ABG test, and lung ultrasound. An electrocardiogram (EKG), echocardiogram, and B-type natriuretic peptide test (BNP) will rule out a cardiac cause for the pulmonary edema and determine whether the pulmonary edema affects cardiac function.

Treatment

The patient will be on continuous pulse oximetry and telemetry monitoring. Supplemental oxygen may be needed depending on the severity of the pulmonary edema. The primary treatment method is diuretics such as furosemide (Lasix®) or bumetanide (Bumex®) that can be provided orally or intravenously. Depending on whether the pulmonary edema has started to affect the heart, vasodilatory medications like nitroglycerin or nitroprusside may be used. Morphine can be given intravenously or orally to relieve the shortness of breath that the patient is experiencing.

If the patient experiences HAPE, they should immediately relocate to a lower altitude and receive supplemental oxygen. Their caretakers should make sure they remain warm and minimize their physical activity.

Pulmonary Embolus

A pulmonary embolus is a blood clot, fatty plaque, or air bubble that travels through the circulatory system until it reaches the pulmonary artery and blocks blood flow to the lungs. It most commonly originates from a deep vein thrombosis (DVT) in the legs or, less commonly, in the arms. Causes of a pulmonary embolus include:

genetic clotting disorders (e.g., factor V Leiden clotting disorder)
inactivity
major surgery such as a joint replacement
fat embolism from the fracture of a large bone (e.g., femur or tibia)
tumor
heart disease
smoking
cancer
air embolism

Assessment

Symptoms of a pulmonary embolus include:

dyspnea
bloody sputum
tachypnea
tachycardia
dyspnea
chest pain
cyanosis
hypoxia

It is common for multiple emboli to occur simultaneously. Lung sounds will reveal crackles/rales or wheezing. A pulmonary embolus can be diagnosed using a chest CT, pulmonary angiogram, V/Q scan, and MRI. A duplex ultrasound can be used to check for DVTs in the upper and lower extremities. A blood test called a D-dimer measures a protein formed when a blood clot dissolves (indicating that a fragment of a blood clot from the legs has broken off, for instance). An ABG test can provide valuable information about the patient’s oxygenation status. Pulmonary emboli will not show up on a chest X-ray.

Treatment

Supplemental oxygen and continuous pulse oximetry should be initiated immediately if a pulmonary embolus is suspected. If the patient is not already hospitalized, they should be transported rapidly to the nearest medical facility. Untreated pulmonary emboli carry a fatality rate of up to 30 percent, while treated emboli carry a fatality rate of only eight percent. A continuous heparin infusion will be initiated immediately, and an anti-Xa assay or an activated partial thromboplastin time (aPTT) test will be drawn on a regular basis, according to the healthcare facility’s policy, to make sure the heparin infusion is within the targeted range.

If it is not within range, the heparin infusion will be titrated accordingly. If the patient has a heparin allergy or a history of heparin-induced thrombocytopenia (HIT), an infusion of a medication like argatroban will be initiated instead. The patient will likely remain hospitalized for several days at the minimum before being transitioned to an oral anticoagulant such as warfarin. An inferior vena cava (IVC) filter can be placed to prevent pulmonary emboli in patients who can’t take anticoagulants.