Page 1 Pulmonary Study Guide for the CCRN®
Knowledge of the anatomy of the pulmonary system is not enough to sustain you as a critical care nurse. You’ll need to go further into the realm and know what to do and how to do it in emergency/life-threatening situations. Take a look at this study guide to review the concepts that will be tested by this type of question, which will always begin with a scenario, and which will occupy about 17% of the CCRN® exam.
Acute Events and Conditions
Acutely ill patients have increased risk of numerous conditions. The respiratory system provides ventilation and oxygenation of blood. When this process is interrupted, severe, sometimes fatal, events will occur.
Acute Pulmonary Embolism
Acute pulmonary embolism results in blockage of the pulmonary arteries. The embolus prevents flow of blood past the blockage, thus prohibiting oxygenation of the blood. Most emboli formations are from blood, particularly from clot formations in the pelvic veins, or as a result of a deep vein thrombosis or atrial fibrillation. Air, fat, and septic embolisms may also occur. Patients with this condition will often have ventilation/perfusion mismatching and intrapulmonary shunting as the body attempts to compensate for the decreased oxygen exchange. The patient will become hypoxic and hypercapnic (increased \(CO_2\)) and may also experience bronchoconstriction. If greater than 50% of the pulmonary vasculature is unable to be perfused, pulmonary hypertension may occur, increasing the morbidity and mortality of this condition.
For more information on arterial blood gases, see our related blog.
Patients at increased risk for an acute pulmonary embolism include those with limited mobility, long hospital stay, history of coagulation disorders, atrial fibrillation, pregnancy, and recent surgical procedure. Monitor for symptoms such as acute dyspnea, tachypnea, cyanosis, anxiety, chest pain, fever, new-onset rales, cough, and hemoptysis. Patients often state they experience an intense “feeling of doom” with this condition. Other findings may include mottling or color changes (grey/blue) from the nipple line up to the head and hemodynamic instability.
Nurses must anticipate performing a series of tests to help diagnose this condition. Arterial blood gases will show respiratory alkalosis with a decreased \(PaCO_2\) (hypoxemia), decreased \(HCO_3\) (hypocarbia), and increased pH. D-dimer testing will be elevated in the event of an acute pulmonary embolism. ECG may show sinus tachycardia while an echocardiogram may actually visualize the emboli and can assess the function of the right side of the heart. A spiral CT, V/Q scintigraphy, and pulmonary angiogram may all be used to positively confirm the presence of a pulmonary embolism.
Management of an acute pulmonary embolism begins with prevention strategies to avoid the event altogether. Patients with limited mobility should have their mobility maximized with progressive movement and stretching exercises. Use of TED hose and sequential devices, especially for patients in the intensive care unit, help to decrease risk of DVT formation. Ambulate patients after surgery as quickly as allowed.
If the nurse suspects a patient has a pulmonary embolism, immediately begin oxygen therapy to relieve hypoxemia. Work with the healthcare team to relieve any hypotension. Cardiac monitoring, if not already initiated, should be started. Patients will also need to be monitored for right-sided heart failure due to fluid overload due to the blockage(s) present. In some patient cases, placement of an IVC filter (percutaneous venous filter or Greenfield™) can help prevent a previously established thromboembolism from breaking off and travelling to the pulmonary system.
Medication management of an acute pulmonary embolism may include a variety of substances to provide both pulmonary and cardiac support while treating the embolism itself. IV dobutamine (Dobutrex®) or dopamine (Intropin®) assist with blood pressure regulation. Digitalis glycoside can help with congestive heart failure and atrial arrhythmias. Diuretics help reduce any concern for fluid overload. Analgesics help to reduce anxiety in this high-anxiety event. Anticoagulants such as heparin or warfarin (Coumadin®) can prevent further clot formation; however, they do not dissolve the clot themselves. Recombinant tissue-type plasminogen activator (rt-PA), instead, may be used to help break down and dissolve the clot.
Asphyxia occurs when the body is deprived of oxygen for an extended period of time, resulting in unconsciousness or even death. It can occur from different conditions, including near-drowning and traumatic injury.
In near-drowning asphyxia, also known as submersion asphyxiation, the central nervous system, pulmonary structures, and other organs may become significantly and irreversibly damaged both due to the lack of oxygen and presence of aspirated fluids. Many times the body will respond to a drowning event by becoming hypothermic. This bodily reaction can help protect the vital organs by shunting blood toward the brain and heart and away from the other tissues of the body.
Treatment for near-drowning asphyxia includes establishing an airway to ensure breathing and circulation are appropriate for the patient. Pulmonary care should involve at least 72 hours of respiratory monitoring to evaluate for pulmonary deterioration. Oxygen support should be provided as needed to keep \(SPO_2\) greater than 94%. If the patient must be intubated, minimizing excessive use of positive-end expiratory pressure (PEEP) is recommended to avoid barotrauma and changes to cardiac output.
Patients must also have frequent neurologic assessments to identify changes in consciousness or other signs of increased intracranial pressure (e.g., headache, nausea, vomiting, asymmetric or dilated pupils). A nasogastric (NG) tube may be placed to provide gastric decompression and reduce the risk of aspiration. Patients, if they are hypothermic due to the near-drowning event, should be rewarmed slowly. Warming should not occur faster than 0.5-1 degrees centigrade per hour.
Traumatic asphyxia may occur due to a variety of injuries. Thoracic crush injuries are the most common injury that causes this condition. In crush injuries, the lungs are generally not the only organ damaged in the event. The patient may also have injury to the heart, liver, spleen, abdomen, and other organs depending on the location and duration of the crushing event.
Traumatic asphyxia may also occur from strangulation or choking. Nurses should understand common findings of each type of strangulation injury: manual, ligature, and hanging. In manual strangulation, the patient may present with crush injuries of the throat with or without bruising, discoloration (cyanosis) of the face not matched on the rest of the body, and facial petechiae. Ligature strangulation is similar to manual strangulation, though the throat markings differ. Instead of crushing, there is an indented area surrounding the neck in ligature strangulation. Neck markings in hanging appear as a v-shaped marking on the throat that does not completely surround the neck.
Priority nursing interventions for traumatic asphyxia include establishing the ABCs of airway, breathing, and circulation. Some patients may need to be prepped for surgery, especially if their asphyxia is caused by persistent airway obstruction. While bronchoscopy may be helpful in the event of choking, some patients may need placement of a temporary (or permanent) airway via tracheostomy to restore airflow to the pulmonary system.
Acute Respiratory Distress Syndrome (ARDS)
Acute respiratory distress syndrome (ARDS) is a sudden and potentially devastating condition. It is classified as damage to the pulmonary vasculature with an increased permeability of the alveolar-capillary membranes. In other words, ARDS is precedented by an acute lung injury (ALI). This is generally caused by substances such as gastric fluids, bacteria, chemicals, and other toxins. It may also be secondary to an inflammatory-mediated response due to underlying pathology or injury. Surfactant, the primary lubricator for the alveoli, becomes significantly reduced, causing the alveoli to fill with blood and protein-rich fluids. This leads to pulmonary edema and potentially infection. The alveoli will continue to enlarge with air (hyperinflation) to compensate for the decreased perfusion ability until they rupture and collapse.
Symptoms of ARDS include rales, wheezing, decreased pulmonary compliance, expiratory grunting, cyanosis, mottling, hypotension, and tachycardia. If fluid overload is also present, patients may have decreased heart sounds with a missing third heart sound and/or jugular venous distention (JVD). Patients may become hypoxic and tachypneic to compensate for a normal \(PaCO_2\). Nurses should anticipate early identification of these symptoms, particularly in patients less than 72 hours post surgical or other serious events. Respiratory failure and multi-organ dysfunction syndrome (MODS) will develop if ARDS is left untreated.
In addition to the symptoms of ARDS, nurses should be aware of the chemical changes that may occur in the body based on the severity of the disease process. Arterial blood gas (ABG) readings are critical in diagnosing and understanding the extent of pulmonary involvement in ARDS. Initial ABG results, in the event of early ARDS, will show respiratory alkalosis. This would be represented by \(PaCO_2\) less than 35, \(HCO_3\) between 22-26 (or less than 22 if compensated, although unlikely), and a pH greater than 7.45 (or between 7.35-7.45 if compensated). As ARDS progresses, the patient will experience hypercarbia and respiratory acidosis. This would be represented by a \(PaCO_2\) greater than 45, \(HCO_3\) between 22-26 (or greater than 26 if compensated), and a pH less than 7.35 (or between 7.35-7.45 if compensated).
Patients should be monitored for signs of respiratory distress. In mild ARDS, oxygen administration via nasal cannula or face mask may be sufficient to keep \(O_2\) saturation greater than 90%. Regardless of the patient’s saturation reading, always administer 100% \(O_2\) to help compensate for ventilation (V) and perfusion (Q) mismatch. The patient’s \(PaO_2\), as indicated on the ABG, should read between 55-80 mmHg and the \(SpO_2\) between 88-95%.
In the event that the patient’s \(SpO_2\) decreases or the \(CO_2\) rises, endotracheal intubation will occur to provide supportive pulmonary ventilation. Know it is important to avoid hyperinflation of the lungs to prevent pulmonary structure collapse. It is recommended to maintain low tidal volumes (6 mL/kg) with an increased PEEP (12+ \(cmH_2O\)) to provide gentle, yet effective respiratory support.
In severe cases of ARDS, prone positioning may be implemented for 18-24 hours a day to provide a decreased workload on the pulmonary system. Nurses will prepare the prone patient for optimal respiratory function by supporting the patient’s chest and pelvis with cushions or positioning devices while allowing the patient’s abdomen to hang freely. This allows the diaphragm to expand posteriorly and increases the patient’s functional residual capacity (FRC). Many hospitals today have special beds that help with rotated and prone positioning to maximize these efforts.
Patients with ARDS will likely be on several medications to improve pulmonary compliance, reduce pulmonary damage, and manage other existing conditions. Corticosteroids, despite the potential to increase the patient’s mortality, are often prescribed to reduce inflammation in the lungs. Corticosteroids are often used in conjunction with other anti-inflammatory medications to ensure the body’s inflammatory response system is managed to help avoid further tissue damage. Inhaled nitrous oxide has been shown to improve oxygenation. Some patients may be prescribed and administered inhaled surfactant to reduce alveolar collapse and pulmonary resistance. Antibiotics may be used if infection or sepsis is present. It is also important to treat any underlying conditions the patient may have that will complicate ARDS.
As with any disease, prevention of the disease process is preferred to treating the actual disease. Patients’ risks for acquiring ARDS should be evaluated early on in their hospital stays. Patients in the ICU are at particular risk for developing ARDS. Conservative fluid management and early-onset enteral nutrition within 24 hours of ICU admission or intubation should be considered. Medications may also be used to prevent ARDS. Enoxaparin 40 mg subcutaneously daily helps to prevent the formation of blood clots which may turn into pulmonary embolisms. Sucralfate, an antacid, 1 g either orally or via a nasogastric tube four times a day and omeprazole, a proton pump inhibitor, 40 mg intravenous daily may be used to prevent GI upset leading to gastric reflux or vomiting and aspiration. Other interventions include early mobilization of patients to prevent fluid stasis and initiation of pulmonary therapies (e.g., incentive spirometer, percussion, and intrapulmonary percussive ventilator (IPV).
Acute Respiratory Failure
Acute respiratory failure is caused by inadequate pulmonary gas exchange. The five most common symptoms of this condition include tachypnea, tachycardia, anxiety, restlessness, and diaphoresis. It can be caused by obstruction, organ injury, heart failure, and infection. Early assessment of acute respiratory failure will show changes in the depth and pattern of respirations, nasal flaring, retractions, expiratory grunting, wheezing, and extended expiration. Late symptoms include cyanosis, changes in level of consciousness, cardiac arrhythmias, bradycardia, hypotension or hypertension, and dyspnea. If left untreated, acute respiratory failure will progress to stupor, coma, and death due to decreased oxygenation of the blood and decreased perfusion of the critical organs.
Acute respiratory failure may be hypoxic or hypercapnic in nature. In hypoxemic respiratory failure, symptoms appear suddenly as the exchange of oxygen and carbon dioxide cannot meet the body’s demand. This can occur in patients due to low-inhaled oxygen events, in high elevations, or due to smoke inhalation. In a hypoxic event, the arterial blood gas would read: \(PaO_2\) <60 mmHg, \(PaCO_2\) >40 mmHg, and arterial pH <7.35. This would be classified as respiratory acidosis. The patient may also experience alveolar hypotension, ventilation-perfusion mismatch, intrapulmonary shunts, and diffusion impairment.
Hypercapnic respiratory failure also results in respiratory acidosis; however, the patient’s \(PaCO_2\) will reach between 45-50 mmHg. This type of respiratory failure may occur due to neurologic damage, muscle damage, chest wall disorders, airway obstruction, burns, infection, hypermetabolism, scoliosis, and drug overdose. Patients who have a condition or conditions that decrease their minute ventilation, increase the lung dead space, or increase production of \(CO_2\) are all at increased risk for hypercapnic respiratory failure.
Nursing interventions can be used to both prevent and treat acute respiratory failure. Patients must first have any underlying causes addressed. This includes the possibility of surgical repair of a defect, diuresis to reduce fluid overload, and antibiotics for infection. Appropriate nursing interventions include turning or repositioning the patient every two hours, elevating the head of bed, encouraging early ambulation, implementing cough and deep breathing exercises, using pulmonary vibration or percussion techniques, and making sure the patient is adequately hydrated. Patients should also have consistent intravenous access, likely via a central line, for medications, laboratory draws, and fluid administration. Oxygen therapy should be implemented to reverse hypoxemia, though careful titration is indicated. Intubation may be indicated if the patient has refractory hypoxemia and collapsed alveoli.
Acute Respiratory Infection
Acute respiratory infection is caused by an infiltration of a foreign substance, such as bacteria, viruses, parasites, or fungi, in the lungs. Another term for acute respiratory infection is pneumonia. Pneumonia may be community-acquired (CAP), chemical, or hospital-acquired (HAP).
Community-acquired pneumonia has a variety of causes; however, Streptococcus pneumoniae, Legionella species, Haemophilus influenzae, Mycoplasma pneumoniae, Staphylococcus aureus, and viruses are the most common offenders. Chemical pneumonia results from aspiration or inhalation of irritating substances (smoke, vape, etc.). Hospital-acquired pneumonia can be subdivided into numerous sections, including healthcare-associated pneumonia (HCAP) and ventilator-acquired pneumonia (VAP). Hospital-acquired pneumonia occurs only after at least 48 hours of hospital admission. Healthcare-associated pneumonia (HCAP) must occur within 90 days of a hospitalization of at least two days in an acute care unit. Ventilator-associated pneumonia (VAP) is defined as pneumonia that develops at least 48 hours after ETT intubation.
Characterization of pneumonia is based on the location of the patient’s infiltrates. Pneumonia may be either lobar, bronchial/lobular, or interstitial. Lobar pneumonia may be considered single/unilateral or double/bilateral pneumonia based on how many lobes of the lungs are affected. Bronchial/lobular pneumonia involves the bronchioles and sometimes the lobules. This may appear as scattered patches of consolidation throughout the lung. Interstitial pneumonia involves the interstitium and alveoli, causing inflammation, remodeling and stiffening as the healthy pulmonary tissues are destroyed.
Treatment for pneumonia includes antibiotic therapy to treat any bacteria that may be present in the exudate, isolation precautions to avoid transmission of infection to other patients, and maintaining patient ventilation. Nurses should frequently monitor a patient’s respiratory status and work of breathing. Patients, when possible, should be in a semi-Fowler’s position with their head of bed elevated at least 30 degrees. For patients who are intubated, frequent oral care and following ventilator cleaning/changing tubing part protocol should be implemented to help prevent VAP.
Medications may be used to treat the pneumonia. Considerations to what bacteria are treated can help identify appropriate antibiotic therapy. Common antibiotics that are used in these discussed pneumonias include ceftazidime, cefepime, imipenem, piperacillin/tazobactam, ciprofloxacin, and Levaquin®. Nurses should review common adult doses, side effects, and administration of these medications.