Respiratory Study Guide for the CCRN

General Information

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 12% 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 and sometimes fatal events will occur.

Acid-Base Imbalances

Acid-base balance is the body’s ability to keep the blood’s pH within a specific range (7.35 to 7.45). This balance is regulated by two main organ systems: the lungs and kidneys. Any imbalance can result in impaired organ function. Imbalances can lead to acidosis (pH <7.35) or alkalosis (pH >7.45). Furthermore, they can be classified as respiratory (lung related) or metabolic (kidney/GI related). Carbon dioxide, or CO2 , is the main acid the lungs control and has an inverse relationship with pH. The higher the CO2, the lower the pH, and the lower the CO2, the higher the pH. The normal value for CO2 is 35 to 45 mmHg. Bicarbonate (can be abbreviated bicarb), or HCO3-, is the main base the kidneys control and has a direct relationship with pH. The higher the bicarb, the higher the pH, and the lower the bicarb, the lower the pH. The normal value for HCO3- is 22 to 26 mEq/L.

Compensation

When the body recognizes an acid-base imbalance it may try to compensate to try to restore balance.

• The lungs compensate for metabolic problems by changing CO2 levels: They breathe faster to remove acid in metabolic acidosis or slower to retain acid in metabolic alkalosis.

• The lungs can begin compensating almost immediately and have obvious signs (changes in respiration).

• The kidneys compensate for respiratory problems by adjusting bicarbonate: They retain the base to counteract respiratory acidosis and excrete it in respiratory alkalosis. The kidneys take longer to begin compensating (hours to days) and do not show obvious signs, as most of this work is internal.

Compensation is further classified as either partially compensated or fully compensated. Partial compensation is when the body is trying to correct the acid-base imbalance, but the pH remains out of range still. Full compensation is when the body has successfully corrected the pH back into normal range. Compensation is simply the body’s survival mechanism and does not fix the underlying problem.

Causes and Diagnosis

Respiratory imbalances occur with changes in ventilation. Respiratory acidosis can be caused by things that cause hypoventilation, such as opioid overdose and neurological injury, or poor gas exchange, such as airway obstruction and COPD exacerbation. Respiratory alkalosis can be caused by things that cause hyperventilation, such as anxiety, pain, fever, and pulmonary embolism.

Metabolic imbalances occur with changes in the bicarbonate levels or the body’s acid. Metabolic acidosis can be caused by things that lead to the loss of bicarbonate, such as frequent diarrhea, or to the gain of acid, such as diabetic ketoacidosis (DKA), lactic acidosis from shock, and renal failure. Metabolic alkalosis can be caused by things that lead to a loss of acid, such as frequent vomiting and nasogastric suction, or to a gain of bicarbonate, such as excessive antacid use.

Acid-base balance is typically assessed using an arterial blood gas (ABG) test. This is a blood test using arterial blood and shows the values we have discussed before—pH, carbon dioxide, and bicarbonate—as well as values that show how well the blood is oxygenated, such as partial pressure of oxygen (PaO2). Although a very accurate clinical tool, it is invasive and, if a patient does not already have an arterial line, will require a poke through the artery. Sometimes the clinician will use a venous blood gas (VBG) as a less invasive alternative, though it is slightly less accurate as it uses venous blood.

Signs and Symptoms

The signs and symptoms of acid-base imbalances depend on the underlying cause, so be sure to study the most common causes further. Abnormal pH itself produces general symptoms: acidosis can cause confusion, lethargy, hypotension, and dysrhythmias, while alkalosis can cause lightheadedness, tingling, muscle cramps or tetany, and irritability. In addition to these general effects, there are causative and compensatory respiratory signs. You may see hyperventilation in respiratory alkalosis (causative) and in metabolic acidosis (compensatory response also referred to as Kussmaul respirations). Similarly, hypoventilation may occur in both respiratory acidosis (causative) and in metabolic alkalosis (compensatory response).

Treatment and Nursing Considerations

Nurses focus on monitoring, providing supportive care, and identifying the underlying cause. ABGs should be obtained as ordered and the results communicated with the physician. The frequency of these depends on the patient’s status, but in the critically ill patient, they are usually taken every couple of hours or daily. These patients may be unable to maintain a patent airway so therefore are intubated and on mechanical ventilation. ABG values can help guide the physician and treatment team to adjust ventilator settings to help correct the imbalance.

Additionally, it is important to note that electrolyte imbalances usually occur simultaneously as these play a role in pH regulation, so electrolytes should be monitored closely and supplemented as needed. Nurses should assess these patients frequently including neurological status, vital signs, respiratory patterns, and cardiac rhythm. Treatment also varies greatly on the cause such as antiemetics for vomiting, bronchodilators for COPD exacerbations, fluids and insulin for DKA, etc.

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 (DVT) or atrial fibrillation. Air, fat, and septic embolisms may also occur.

Symptoms

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 \(\text{CO}_2\)) 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.

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, newly onset rales or wheezing, cough, and hemoptysis. Patients often state they experience an intense “feeling of impending 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.

Diagnosis

Nurses must anticipate performing a series of tests to help diagnose this condition. Arterial blood gases will show respiratory alkalosis. D-dimer testing will be elevated in the event of an acute pulmonary embolism. ECG may show sinus tachycardia. The gold standard for diagnosing a pulmonary embolism is a computed tomography pulmonary angiography or CTPA. This test includes injecting contrast through an IV to highlight the pulmonary arteries, revealing any clots. When IV contrast or radiation is contraindicated, a ventilation-perfusion or V/Q scan is typically performed.This test uses a radioactive substance referred to as a tracer, and it tracks blood flow and compares it with the airflow in the lungs. Several other tests can aid in diagnosis or help rule out other conditions including echocardiogram, MRI, and chest X-ray.

Treatment

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. Patients may also be put on prophylactic blood thinning medications such as heparin or low-molecular weight heparin, such as enoxaparin or Lovenox®, given via subcutaneous injection.

If the nurse suspects a patient has a pulmonary embolism, immediately begin oxygen therapy and sit the patient upright 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 related 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 traveling 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. Intravenous 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. For larger clots, surgical removal of the clot, called a thrombectomy, may be needed.

Acute Pulmonary Edema

Acute pulmonary edema occurs when there is excess fluid in the lungs, causing a buildup of fluid in the alveoli, decreasing the oxygen movement through the lungs and subsequently increasing respiratory effort. It most often occurs in light of congestive heart failure but can also occur in patients with pneumonia, toxin exposure, adverse drug reactions (cocaine, heroin, aspirin), chest trauma, and high elevation.

Symptoms

Onset of this condition is usually sudden, with symptoms such as extreme shortness of breath, feeling of suffocating or drowning that is worse when lying down, wheezing or crackles, cold/clammy skin, anxiety, tachycardia, cyanosis, and frothy pink sputum.

Diagnosis and Treatment

The patient’s exam may identify abnormal heart sounds, lung rales, tachycardia, and tachypnea. Diagnostic testing for this condition includes an ECG, echocardiogram, and ultimately a chest X-ray to confirm diagnosis. Pulse oximetry testing should be implemented to monitor for hypoxia. Treatment includes placing patients in high Fowler’s position with 100% oxygen administered via face mask or nasal cannula to achieve a PaO2 of greater than 60%.

In some cases, positive end-expiratory pressure (PEEP) by the way of BiPaP or mechanical ventilation may be indicated to help open the airways, recruit the alveoli, and help with redistribution of the liquid within the lung. Diuretic medications help to alleviate extra fluid from the body. Pain should be controlled with analgesic medications such as 2 mg to 8 mg of IV morphine sulfate every two to four hours to decrease preload and anxiety. If not treated efficiently, pulmonary edema may result in death.

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. It is categorized on a mild, moderate, and severe scale based on oxygenation ratios and PEEP. This is generally caused by substances such as gastric fluids, bacteria, chemicals, and other toxins that damage the lungs. 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, which is also known as atelectasis.

Symptoms

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 \(\text{PaCO}_2\) or partial pressure of carbon dioxide. Nurses should anticipate early identification of these symptoms, particularly in patients less than \(72\) hours post surgical or other serious events. Respiratory failure and multiple 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. 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. As ARDS progresses, the patient will experience hypercarbia and respiratory acidosis.

Treatment

Patients should be monitored for signs of respiratory distress. In mild ARDS, oxygen administration via nasal cannula or face mask may be sufficient. The patient’s \(\text{PaO}_2\), as indicated on the ABG, should read between 55 and 80 mmHg and the \(\text{SpO}_2\) (peripheral oxygen saturation) between 88% and 95%.

In the event that the patient’s \(\text{SpO}_2\) decreases or the \(\text{CO}_2\) rises, endotracheal intubation will occur to provide supportive pulmonary ventilation. Know that it is important to avoid hyperinflation of the lungs to prevent pulmonary structure collapse. It is recommended to maintain tidal volumes of 6 mL/kg. PEEP should be at a minimum of \(5 \text{ cmH}_2\text{O}\) to provide gentle, yet effective respiratory support.

In severe cases of ARDS, prone positioning may be implemented for 18 to 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. Sepsis is the most common cause of 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 (Lovenox®) 40 mg subcutaneously daily helps to prevent the formation of blood clots, which may turn into pulmonary embolisms. Sucralfate (Carafate®), an antacid, 1 g either orally or via a nasogastric tube four times a day and omeprazole (Prilosec®), 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 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. 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.

Treatment

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) 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.

• Hospital-acquired pneumonia can be subdivided into numerous sections, including healthcare-associated pneumonia (HCAP) and ventilator-associated pneumonia (VAP). Hospital-acquired pneumonia occurs only after at least 48 hours of hospital admission. HCAP must occur within 90 days of a hospitalization with 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.

Diagnosis

Characterization of pneumonia is based on the location of the patient’s affected area. Pneumonia may be 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.

Chest X-rays are the standard imaging used when pneumonia is suspected. The film will often show white opaque areas called consolidation or infiltrates. Interstitial pneumonia involves the interstitium and alveoli, causing inflammation, remodeling, and stiffening as the healthy pulmonary tissues are destroyed.Sputum samples can be sent for culture to identify the organism responsible. Labs such as white blood cell count and SpO2 monitoring are useful in these patients as well.

Treatment

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. Encourage coughing and deep breathing. Use of incentive spirometer can help keep the alveoli inflated and prevent further fluid buildup. Patients, when possible, should be in a semi-Fowler’s position with their head of bed elevated at least 30 degrees and fluids should be encouraged to thin mucus unless otherwise contraindicated. 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 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. Viral and fungal pneumonia cannot be treated with antibiotics and instead should be treated with either antivirals or antifungals. Some mild cases of these types of pneumonia may clear up with supportive care.