CLASS 2-Gas Exchange I-January 25th

Acute Respiratory Failure

(ARF) occurs when oxygenation, ventilation, or both are inadequate. ARF is not a disease. It is a symptom that reflects lung function. For example, not enough O2 is transferred to the blood or inadequate CO2 is removed from the lungs. Conditions that interfere with adequate O2 transfer result in hypoxemia. This causes a decrease in arterial O2 (PaO2) and saturation (SaO2) to less than the normal values. Insufficient CO2 removal results in hypercapnia. It causes an increase in arterial CO2 (PaCO2). Arterial blood gases (ABGs) are used to assess changes in pH, PaO2, PaCO2, bicarbonate, and SaO2. We use pulse oximetry to assess arterial O2 saturation (SpO2). We classify ARF as hypoxemic or hypercapnic

Central Nervous System Problems in Hypercapnic respiratory failure

A number of CNS problems can suppress the drive to breathe. A common example is an overdose of a respiratory depressant drug (e.g., opioids). In a dose-related manner, CNS depressants decrease CO2 reactivity in the brainstem. This allows arterial CO2 levels to rise. A brainstem infarction or TBI may interfere with normal function of the respiratory center in the medulla. Patients are then at risk for acute hypercapnic respiratory failure because the medulla does not change the respiratory rate in response to a change in PaCO2. High-level spinal cord injuries can affect nerve supply to the respiratory muscles of the chest wall and diaphragm. Brain injury with a decreased level of consciousness can hinder the patient's ability to protect the airway, breathe, or manage secretions.

Shunt

A shunt occurs when blood exits the heart without having taken part in gas exchange. A shunt is an extreme V/Q mismatch. There are 2 types of shunt: An anatomic shunt occurs when blood passes through an anatomic channel in the heart (e.g., a ventricular septal defect) and bypasses the lungs. An intrapulmonary shunt occurs when blood flows through the pulmonary capillaries without taking part in gas exchange. It is seen in conditions in which the alveoli fill with fluid (e.g., pneumonia) and gas exchange is severely impaired at the alveolar-capillary membrane. O2 therapy alone is not effective at increasing the PaO2 if hypoxemia is due to shunt. Patients with a shunt are usually more hypoxemic than patients with V/Q mismatch. They often need mechanical ventilation with a high fraction of inspired O2 (FIO2) to improve gas exchange.

Clinical Manifestations of respiratory failure

A sudden decrease in PaO2 and/or a rapid rise in PaCO2 implies a serious respiratory condition, which can rapidly become a life-threatening emergency. An example is the patient with asthma who develops severe bronchospasm and a marked decrease in airflow, resulting in respiratory muscle fatigue, acidemia, and ARF. Signs of respiratory failure are related to the extent of change in PaO2 or PaCO2, the speed of change (acute versus chronic), and the patient's ability to compensate for this change. When the patient's compensatory mechanisms fail, respiratory failure occurs. Because clinical signs vary, frequent patient assessment is a priority. A lack of O2 affects all body systems For example, a decreased level of consciousness may occur without enough blood, O2, and glucose supplied to the brain. Permanent brain damage can result if hypoxia is severe and prolonged. Gastrointestinal (GI) system changes include tissue ischemia and increased intestinal wall permeability. Bacteria can migrate from the GI tract into systemic circulation. Renal function may be impaired. Sodium retention, peripheral edema, and acute kidney injury may occur. One of the first signs of acute hypoxemic respiratory failure is a change in mental status. Mental status changes occur early because the brain is extremely sensitive to changes in O2 (and to a lesser degree CO2) levels and acid-base balance. Restlessness, confusion, and agitation suggest inadequate O2 delivery to the brain. On the other hand, a morning headache and slow respiratory rate with decreased level of consciousness may indicate problems with CO2 removal. Tachycardia, tachypnea, slight diaphoresis, and mild hypertension are early signs of ARF. These changes indicate attempts by the heart and lungs to compensate for decreased O2 delivery and rising CO2 levels. It is important to understand that cyanosis is an unreliable indicator of hypoxemia. It is a late sign in ARF. It often does not occur until hypoxemia is severe (PaO2 45 mm Hg or less). The priority for the patient with ARF is immediate assessment of the patient's ability to breathe and providing any assistive measures needed. Depending on the severity of the respiratory failure and hemodynamic status, this may involve intubation and starting mechanical ventilation. Observing the patient's position helps assess the effort associated with the work of breathing (WOB). WOB is the effort needed by the respiratory muscles to inhale air into the lungs. Patients with mild distress may be able to lie down. In moderate distress, patients may be able to lie down but prefer to sit. With severe distress they may be unable to breathe unless sitting upright. The tripod position helps decrease the WOB in patients with moderate to severe COPD and ARF. The patients sit with the arms propped on the overbed table or on the knees. Propping the arms increases the anteroposterior diameter of the chest and changes pressure in the thorax. The patient in ARF may have a rapid, shallow breathing pattern (hypoxemia) or a slower respiratory rate (hypercapnia). Both changes predispose the patient to insufficient O2 delivery and CO2 removal. Increased respiratory rates require a substantial amount of work and can lead to respiratory muscle fatigue. A change from a rapid rate to a slower rate in a patient in respiratory distress, such as that seen with acute asthma, suggests severe respiratory muscle fatigue. There is an increased chance for respiratory arrest. The patient's ability to speak is related to the severity of dyspnea. The dyspneic patient may be able to speak only a few words at a time between breaths. For example, the patient may have "2-word" or "3-word" dyspnea. This means the patient can say only 2 or 3 words before pausing to breathe. You may see dyspneic patients using pursed-lip breathing. This technique increases SaO2 by slowing respirations, increasing time for expiration, and preventing small bronchioles from collapsing. You may see retraction (inward movement) of the intercostal spaces or supraclavicular area and use of the accessory muscles (e.g., sternocleidomastoid) during inspiration or expiration. Use of the accessory muscles often signifies a moderate degree of respiratory distress. Paradoxical breathing occurs with severe respiratory distress. Normally, the thorax and abdomen move outward on inspiration and inward on exhalation. With paradoxical breathing, the abdomen and chest move in the opposite manner—outward during exhalation and inward during inspiration. Paradoxical breathing results from maximal use of the accessory muscles of respiration. The patient may be extremely diaphoretic from the increased WOB. Auscultate breath sounds. Note the presence and location of any abnormal breath sounds. Fine crackles may occur with pulmonary edema. Coarse crackles heard on expiration indicate fluid in the airways. This may be a sign of pneumonia or a degree of HF. Absent or decreased breath sounds occur with atelectasis, pleural effusion, or hypoventilation. Bronchial breath sounds over the lung periphery occur with lung consolidation from pneumonia. You may hear a pleural friction rub if pneumonia involves the pleura.

Complications

Abnormal Lung Function Most patients will recover from ARDS within 6 months. Many will have normal to near normal lung function. However, not all patients regain normal lung function. Sometimes, abnormal lung function can persist for years. Ventilator-Associated Pneumonia Risk factors for ventilator-associated pneumonia (VAP) include impaired host defenses, invasive monitoring devices, aspiration of GI contents (especially in patients receiving enteral nutrition), and prolonged mechanical ventilation. prevention of VAP: elevating the head of bed 30 to 45 degrees strict infection control measures frequent oral care Barotrauma occurs when fragile alveoli are overdistended with excess pressure during mechanical ventilation. The high peak airway pressures needed to ventilate the lungs predispose patients with ARDS to this complication. Barotrauma results in alveolar air escaping from ruptured alveoli. This can lead to pulmonary interstitial emphysema, pneumothorax, subcutaneous emphysema, pneumopericardium, and tension pneumothorax. Providing ventilation with a smaller VT (e.g., 4 to 8 mL/kg) and varying amounts of PEEP minimizes the risk for barotrauma. Stress Ulcers Patients with ARF and ARDS are at high risk for stress ulcers because of blood being diverted from the GI to respiratory system to help meet the body's demand for O2. Management strategies include correcting predisposing conditions, such as hypotension, shock, and acidosis. Prophylactic management includes antiulcer drugs, such as proton pump inhibitors (e.g., pantoprazole [Protonix]) and mucosal-protecting drugs (e.g., sucralfate [Carafate]). Early initiation of enteral nutrition helps prevent mucosal damage. Venous Thromboembolism (VTE) ARDS patients are susceptible to the effects of immobility and venous stasis. They are at risk for deep vein thrombosis (DVT) and pulmonary emboli. Prophylactic management may include intermittent pneumatic compression stockings, anticoagulation (e.g. low-molecular-weight heparin), and, when possible, early ambulation. Acute Kidney Injury Acute kidney injury (AKI) can occur from decreased renal perfusion and subsequent decreased delivery of O2 to the kidneys. This most often occurs in ARDS because of hypotension in septic shock. It may also result from hypoxemia or nephrotoxic drugs (e.g., vancomycin) used to treat ARDS-related infections. Management strategies for AKI include careful monitoring of intake and output, obtaining daily creatinine and urea levels, and, when needed, dialysis therapy. Continuous renal replacement therapy (CRRT) is often used. Patients with ARDS are often hemodynamically unstable and need vasopressors and/or inotropes to maintain heart rate and BP. They cannot tolerate the large volumes of fluid that would be removed during traditional hemodialysis. CRRT is slow, gentle, and continuous. The patient can receive CRRT 24 hours a day. The overall mortality rate for ARDS patients is higher in those who need CRRT. Psychological Issues Recovery is far from complete for the patient who survives ARDS. Survivors may have anxiety, issues with memory and attention, inability to focus, nightmares, depression, and in some instances, various degrees of posttraumatic stress disorder (PTSD). PTSD can occur in ARDS survivors up to 5 years later.

Acute Respiratory Distress Syndrome

Acute respiratory distress syndrome (ARDS) is a sudden and progressive form of ARF in which the alveolar-capillary membrane becomes damaged and more permeable to intravascular fluid ARDS accounts for about 10% of all adult ICU admissions. The incidence of ARDS in the United States is estimated at more than 200,000 cases each year. Despite supportive therapy, the mortality rate from ARDS is around 50%.

Alveolar hypoventilation

Alveolar hypoventilation is a decrease in ventilation that results in an increase in the PaCO2. It may be caused by central nervous system (CNS) conditions, chest wall dysfunction, acute asthma, or restrictive lung diseases. Although alveolar hypoventilation is mainly a mechanism of hypercapnic respiratory failure, it contributes to hypoxemia.

Analgesia and Sedation

Analgesia and sedation, either by direct IV or continuous IV infusion, are important. Analgesia and sedation decrease the discomfort associated with the presence of an ET tube, help reduce WOB, and prevent ventilator dyssynchrony. Patients who breathe asynchronously with mechanical ventilation may benefit from an adjustment of ventilator inspiratory flow rates or other settings. Patients who stay asynchronous with mechanical ventilation despite aggressive analgesia and sedation may need a neuromuscular blocking agent (NMBA). These drugs, such as vecuronium, pancuronium (Pavulon) or cisatracurium (Nimbex), relax skeletal muscles and promote synchrony with mechanical ventilation. Remember that a patient receiving neuromuscular blockade can appear to be asleep, but still be awake and in pain. For this reason, simultaneous administration of analgesia and sedation with NMBAs is essential. Monitoring levels of sedation in patients receiving NMBA is challenging. Levels of drug paralysis are monitored primarily by clinical assessment, including heart rate and BP, but more importantly, respiratory rate and whether the patient is taking breaths above the set rate on the ventilator.

Reduce Anxiety, Pain, and Restlessness

Anxiety, pain, and restlessness may result from hypoxia. They increase O2 consumption and CO2 production (from an increased metabolic rate) and increase WOB. For the nonintubated patient, this may cause tachypnea and ineffective ventilation. For the intubated patient, this may cause ventilator dyssynchrony and increase the risk for unplanned extubation. We promote patient comfort in several ways. Benzodiazepines (e.g., lorazepam, midazolam), and opioids (e.g., morphine, fentanyl) may decrease anxiety, restlessness, and pain. They are often given IV.

Etiology of ARDS

Causes: sepsis multiple organ dysfunction syndrome (MODS) Either a direct or indirect lung injury In direct lung injury, the pathogen comes into contact with the tissue of the lung. For example, aspiration of gastric contents into the lung will immediately initiate the inflammatory response. In an indirect injury, ARDS develops due to a problem somewhere else in the body. For example, necrotizing pancreatitis or bowel obstruction with perforation cause widespread inflammation and infection. As a result, septic mediators gain entrance to the bloodstream and often move toward the lungs, which provide a favorable, dark, moist environment for their proliferation. This is the beginning of acute lung injury.

Chest Physiotherapy

Chest physiotherapy is indicated for all patients who are producing sputum or have evidence of severe atelectasis or pulmonary infiltrates on chest x-ray. Postural drainage percussion vibration to the affected lung segments help move secretions to the larger airways. Then, they can be removed by coughing or suctioning. Contraindications TBI increased intracranial pressure (ICP) unstable orthopedic injuries (e.g., spinal fractures, fractured ribs, fractured sternum) recent hemoptysis

Reduce Airway Inflammation and Bronchospasm

Corticosteroids (e.g., IV methylprednisolone [Solu-Medrol]) are often used in combination with other drugs, such as bronchodilators, for relief of inflammation and bronchospasm. It may take several hours to see their effects. Inhaled corticosteroids require 4 to 5 days for optimum therapeutic effects, so they will not relieve ARF. IV Corticosteroids • Monitor potassium levels. Corticosteroids worsen hypokalemia caused by diuretics. • Prolonged use causes adrenal insufficiency. Relief of bronchospasm increases alveolar ventilation. In acute bronchospasm, short-acting bronchodilators (e.g., albuterol), may be given at 15- to 30-minute intervals until a response occurs. Give these drugs using a hand-held nebulizer or a metered-dose inhaler with a spacer. Side effects tachycardia and hypertension Prolonged use can increase the risk for dysrhythmias and cardiac ischemia

Humidification

Humidification is an adjunct in secretion management. We can thin secretions with aerosols of sterile normal saline or mucolytic drugs (e.g., acetylcysteine mixed with a bronchodilator) given by nebulizer. O2 given by aerosol mask can thin secretions and promote their removal. Aerosol therapy may cause bronchospasm and severe coughing, causing a decrease in PaO2. Frequent assessment of the patient's tolerance to therapy is critical. Closely monitor the patient's respiratory status.

Consequences of Hypoxemia

Hypoxemia can lead to hypoxia if not corrected. occurs when the PaO2 falls enough to cause signs and symptoms of inadequate oxygenation. If hypoxia or hypoxemia is severe, the cells shift from aerobic to anaerobic metabolism. Anaerobic metabolism uses more fuel, produces less energy, and is less efficient than aerobic metabolism. The waste product of anaerobic metabolism is lactic acid. Lactic acid is harder to remove from the body than CO2, because it must be buffered with sodium bicarbonate. When the body does not have enough sodium bicarbonate to buffer the lactic acid, metabolic acidosis occurs. Left uncorrected, tissue and cell dysfunction, and ultimately cell death, occurs.

Hypoxemic vs Hypercapnic Respiratory Failure

Hypoxemic respiratory failure is a PaO2 less than 60 mm Hg when the patient is receiving an inspired O2 concentration of 60% or more. In hypoxemic respiratory failure (also called oxygenation failure), the main problem is inadequate exchange of O2 between the alveoli and pulmonary capillaries. The PaO2 level shows inadequate O2 saturation. A less than optimal PaO2 level exists despite supplemental O2. Hypercapnic respiratory failure (or ventilatory failure) is a PaCO2 greater than 50 mm Hg with acidemia (arterial pH less than 7.35). The main problem is insufficient CO2 removal. This causes the PaCO2 to be higher than normal. For whatever reason, the body is unable to compensate for the increase. This allows acidemia to occur. Patients may have both types of respiratory failure at the same time. For example, a patient with chronic obstructive pulmonary disease (COPD) who has pneumonia could have "acute-on-chronic" respiratory failure. In other words, the patient has an underlying chronic respiratory problem. The new infection, in addition to the chronic problem, results in the "acute-on-chronic" clinical picture. Significant changes in PaO2 and PaCO2 occur with ARF. These may develop over several minutes to a few hours to 1 or 2 days. The patient may have hemodynamic instability (e.g. tachycardia, hypotension), increased respiratory effort, and decreased level of consciousness. Urgent intervention is required. Chronic respiratory failure develops more slowly, over days to weeks. The patient is usually more stable as the body had time to compensate for the small, but subtle, changes that have occurred.

Positive Pressure Ventilation

If initial measures do not improve oxygenation and ventilation, enhanced ventilatory assistance may be needed. During Noninvasive positive pressure ventilation (NIPPV), a mask is placed tightly over the patient's nose or nose and mouth. When the patient breathes spontaneously, a mechanical ventilator or table-top unit delivers PPV to the patient. With NIPPV, it is possible to provide O2 and decrease WOB, avoiding the need for endotracheal intubation. NIPPV is not appropriate for patients who have a decreased level of consciousness, high O2 requirements, facial trauma, hemodynamic instability, or excessive secretions. NIPPV used after extubation can help avoid reintubation. There are 2 forms of NIPPV used for patients with ARF. Continuous positive airway pressure (CPAP) delivers 1 level of pressure—a constant pressure—to the patient's airway during inspiration and expiration. Bilevel positive airway pressure (BiPAP) uses 2 different levels of positive pressure (one on inspiration, another on expiration). With both CPAP and BiPAP, the patient must be awake and alert, have stable vital signs, and be able to support spontaneous ventilation. The most often used NIPPV for ARF is BiPAP. BiPAP provides O2 therapy and humidification, decreases WOB, and reduces respiratory muscle fatigue. It helps open collapsed airways and decrease shunt. If respiratory status worsens with NIPPV, PPV via mechanical ventilation and higher O2 concentrations is needed.

Hypercapnic Respiratory Failure

In acute hypercapnic respiratory failure, sometimes referred to as ventilatory failure, the lungs are often normal. In this situation, the respiratory system cannot keep CO2 levels maintained within normal limits. This often occurs from an increase in CO2 production or a decrease in alveolar ventilation. Causes: (1) CNS problems (2) neuromuscular conditions (3) chest wall abnormalities, (4) problems affecting the airways and/or alveoli.

Ventilation-Perfusion Mismatch

In normal lungs, the volume of blood perfusing the lungs and the amount of gas reaching the alveoli are almost identical. So, when you compare normal alveolar ventilation (4 to 6 L/min) to pulmonary blood flow (4 to 6 L/min), you have a V/Q ratio of 0.8 to 1.2 In a perfect match, ventilation and perfusion would yield a V/Q ratio of 1:1, expressed as V/Q = 1. When the match is not 1:1, a V/Q mismatch occurs. This example implies that ventilation and perfusion are perfectly matched in all areas of the lung. This situation does not normally exist. In reality, some regional mismatch occurs. For example, at the apex of the lung, V/Q ratios are greater than 1 (more ventilation than perfusion). At the base of the lung, V/Q ratios are less than 1 (less ventilation than perfusion). Because changes at the lung apex balance changes at the base, the net effect is a close overall match. O2 therapy is an appropriate first step to reverse hypoxemia caused by V/Q mismatch. O2 therapy increases the PaO2 in the blood leaving normal gas exchange units, causing a higher-than-normal PaO2. This blood mixes with the poorly oxygenated blood from damaged areas, raising the overall PaO2 level in the blood leaving the lungs. The best way to treat hypoxemia caused by a V/Q mismatch is to treat the cause. The most common are those in which increased secretions are present in the airways (e.g., COPD) or alveoli (e.g., pneumonia) or bronchospasm is present (e.g., asthma). V/Q mismatch may result from pain, alveolar collapse (atelectasis), or pulmonary emboli. Pain interferes with chest and abdominal wall movement and increases muscle tension. This often compromises ventilation. The patient is often unwilling to take big, deep breaths. As a result, short, shallow respirations contribute to the development of atelectasis. This worsens V/Q mismatch. Pain activates the stress response, increasing baseline metabolic state. This increases O2 consumption and CO2 production (as a by-product of cellular and tissue metabolism). The increased O2 demand, increased CO2, and decreased O2 supply increase ventilation demands. Since there is no effect on blood flow to the lungs, the result is V/Q mismatch. Pulmonary emboli affect the perfusion part of the V/Q relationship. When a pulmonary embolus occurs, it limits blood flow distal to the occlusion. Areas of normal lung ventilation remain, but there is decreased perfusion due to the vessel occlusion. This results in a V/Q mismatch. If the embolus is large, it can cause hemodynamic instability due to blockage of a large pulmonary artery. O2 therapy is an appropriate first step to reverse hypoxemia caused by V/Q mismatch. O2 therapy increases the PaO2 in the blood leaving normal gas exchange units, causing a higher-than-normal PaO2. This blood mixes with the poorly oxygenated blood from damaged areas, raising the overall PaO2 level in the blood leaving the lungs. The best way to treat hypoxemia caused by a V/Q mismatch is to treat the cause.

Relieve Pulmonary Congestion

Interstitial fluid can accumulate in the lungs because of direct or indirect injury to the alveolar capillary membrane from HF or fluid overload. Use of IV diuretics (e.g., furosemide [Lasix]), morphine, or nitroglycerin can decrease pulmonary congestion caused by HF. Use extreme caution when giving these drugs. Changes in heart rate and rhythm and significant decreases in BP are common.

Treat Infection

Lung infections (e.g., pneumonia, acute bronchitis) can result in excessive mucus production, fever, increased O2 consumption, and inflamed, fluid-filled, and/or collapsed alveoli. Alveoli that are fluid filled or collapsed cannot take part in gas exchange. Consequently, pulmonary infections can either cause or worsen ARF. IV antibiotics are often given to treat infection. Chest x-rays can show the location and extent of an infection. Sputum cultures help identify the organisms causing the infection and their sensitivity to antimicrobial drugs.

Maintaining Fluid Balance and Nutrition

Maintaining fluid balance and nutrition is challenging. Increasing pulmonary capillary permeability results in fluid in the lungs and causes pulmonary edema. At the same time, the patient may be intravascularly volume depleted and at risk for hypotension and decreased CO from mechanical ventilation and PEEP. Monitor hemodynamic parameters (e.g., CVP, stroke volume variation) and daily weights to assess the patient's fluid volume status. Monitor intake and output hourly. Keep the ARDS patient on the "dry" side. In other words, avoid aggressive resuscitation with IV fluids. ARDS patients typically have increased WOB because the alveoli, lungs, and spaces between the alveoli are partially or completely fluid filled. Since ARDS is an inflammatory process, diuretics play a minimal role. Maintaining protein and energy stores is important. Nutritional depletion causes a loss of muscle mass, including the respiratory muscles, which may prolong mechanical ventilation and delay recovery. Ideally, enteral or parenteral nutrition should be started within 24 to 48 hours.

Respiratory Therapy

Mechanical Ventilation Pressure-control ventilation helps to keep the inspiratory and plateau pressures from becoming too high. This prevents alveolar overdistention and rupture. By reducing the amount of pressure going into the stiff, noncompliant lungs, we can help prevent further lung injury. However, no mode of mechanical ventilation is superior to the others. Low Tidal Volume (VT) Ventilation Patients with ARDS are ventilated with a low VT of 4 to 8 mL/kg. The delivery of a large VT into stiff lungs is associated with volutrauma and barotrauma. Volutrauma causes alveolar fractures (damage or tears in the alveoli) and movement of fluids and protein into the alveolar spaces. Permissive Hypercapnia As a result of delivering a lower than normal VT to the patient with ARDS, the PaCO2 level will slowly rise above normal limits. This is known as permissive hypercapnia. A PaCO2 of up to 60 mm Hg is acceptable in the early phase of ARDS. The patient usually tolerates this rise in PaCO2 if it is gradual, allowing the brain and systemic circulation to compensate. Permissive hypercapnia is not used for the patient with TBI or increased ICP. Frequent ABG samples are needed, with careful monitoring of the pH, PaO2, and PaCO2 values. As per the ARDSNet protocol, the pH is kept between 7.30 and 7.45. CO2 is a powerful stimulant to breathe. When permissive hypercapnia is used, the patient is usually given continuous IV analgesia and sedation. Positive End-Expiratory Pressure (PEEP) During PPV, it is common to apply PEEP at 5 cm H2O to compensate for loss of glottic function caused by the ET. PEEP increases functional residual capacity, or the volume of air left in the lungs at the end of a normal expiration. PEEP also helps open up ("recruit") collapsed alveoli. We typically apply PEEP in increments of 3 to 5 cm H2O until oxygenation is adequate, with an FIO2 of 60% or less (if possible). PEEP may improve ventilation in respiratory units that collapse at low airway pressures, thus allowing the FIO2 to be lowered. Patients with ARDS may need higher levels of PEEP (e.g., 10 to 20 cm H2O). There is no identified optimal level of PEEP for patients with ARDS. PEEP is not without complications. The added intrathoracic and intrapulmonic pressures generated by positive pressure remaining in the lungs and transmitted to surrounding structures (e.g., inferior vena cava, heart) at end expiration can compromise venous return. This in turn has the potential to decrease the amount of blood returning to both the right and left sides of the heart. Dramatic reductions in preload, CO, and BP can occur. High levels of PEEP or excess inspiratory pressures can cause barotrauma and volutrauma. Prone Positioning In the early phases of ARDS, fluid moves freely throughout the lung. Because of gravity, fluid pools in dependent regions of the lung. As a result, some alveoli are fluid filled (dependent areas) while others are air filled (nondependent areas). When the patient is supine, the heart and mediastinal contents place added pressure on the lungs. Consequently, the supine position predisposes all patients, including those with ARDS, to atelectasis. Prone positioning is an option for patients with refractory hypoxemia who do not respond to other strategies to increase PaO2. By turning the patient prone, perfusion may be better matched to ventilation. Air-filled alveoli in the anterior part of the lung become dependent. Alveoli in the posterior part of the lungs are "recruited" (given the opportunity to reexpand), improving oxygenation. Some patients will have a big improvement in PaO2 when prone with no change in FIO2. The improvement in ventilation may be enough to allow a reduction in FIO2 or PEEP. You may see hemodynamic instability (dysrhythmias, a decrease in BP) from fluid shifts when the patient is prone. There may be more need for airway suctioning as secretions are mobilized. Best practice suggests that patients be positioned prone early in the course of ARDS. They can stay in the prone position for up to 16 hours per day. Placing a patient prone requires the presence of an ICU intensivist, respiratory therapist, and at least 3 to 4 nurses. Special attention must be given to securing the airway. Once prone, the patient should be positioned in a side-lying position. Extracorporeal Membrane Oxygenation (ECMO) is used most often in specialized ICUs in major cities. Like hemodialysis, a large blood vessel is cannulated (most often the internal jugular, femoral artery, or femoral vein) and a catheter is inserted. The catheter is then connected to a device that allows the blood to exit the patient and pass across a gas-exchanging membrane outside the body. Within the ECMO unit, O2 is delivered into the blood and CO2 removed. Oxygenated blood is returned back to the patient. ECCO2R is like ECMO. It does not require as high of blood flow rates. It is only used to enhance oxygenation. Both ECMO and ECCO2R are expensive and require specially trained nurses and other personnel.

Problems of the Airway and Alveoli

Patients with asthma, COPD, and cystic fibrosis have a high risk for hypercapnic respiratory failure because the underlying pathophysiology results in airflow obstruction and air trapping. Respiratory muscle fatigue and ventilatory failure occur from the added work of breathing needed to inspire air against increased airway resistance and air trapped within the alveoli.

Patient Positioning

Position the patient upright, either by elevating the head of the bed at least 30 degrees or by using a reclining chair or chair bed. This helps maximize respiratory expansion, decrease dyspnea, and mobilize secretions. A sitting position improves pulmonary function by promoting downward movement of the lungs. When lungs are upright, ventilation and perfusion are best in the lung bases. If there is a chance for aspiration, position the patient side-lying. Patients with one-sided lung disorders may be placed in a lateral or side-lying position. This position, called good lung down, allows for improved V/Q matching in the affected lung. Pulmonary blood flow and ventilation are better in dependent lung areas. This position allows secretions to drain out of the affected lung so they can be removed with suctioning. For example, place a patient with right-sided pneumonia on the left side. This will maximize ventilation and perfusion in the "good" lung and aid in secretion removal from the affected lung (postural drainage). Patients with ARF often have problems with both lungs. They may need repositioning at regular intervals on both sides to optimize air movement and drainage of secretions.

Chest Wall Abnormalities

Several conditions can prevent normal movement of the chest wall or diaphragm and limit lung expansion. In patients with flail chest, fractures prevent the rib cage from expanding normally. With kyphoscoliosis, the change in spinal configuration compresses the lungs and prevents normal expansion of the chest wall. In those with severe obesity, the weight of the chest and abdominal contents limit lung expansion.

Suctioning

Suctioning may be needed if the patient is unable to expectorate secretions. Suctioning through an artificial airway (e.g., endotracheal tube [ET], tracheostomy) is done only as needed. Complications hypoxia increased ICP dysrhythmias hypotension (from sudden elevation in intrathoracic pressure) hypertension tachycardia (from noxious stimulation) bradycardia (possible vasovagal response).

Consequences of Hypercapnia

The body can tolerate increased CO2 levels far better than low O2 levels. This is because with slow changes in PaCO2, the body may have time for compensation to occur. For example, consider the patient with COPD who has a slow increase in PaCO2 after an upper respiratory tract infection. Because the change occurred over several days, there is time for the kidneys to compensate (e.g., by retaining bicarbonate). This will initially minimize the change in arterial pH. Unless the primary cause is identified and corrected, the patient's condition will likely get worse.

Medical Supportive Therapy

The entire interprofessional team have important roles in the care of the patient with ARDS. All mechanically ventilated patients with ARDS in the ICU will have continuous heart rate, respiratory rate, BP, MAP, and SpO2 monitoring. EtCO2 monitoring is standard in the care of ARDS patients. Other positioning strategies for patients with ARDS include continuous lateral rotation therapy (CLRT) and kinetic therapy. CLRT provides continuous, slow, side-to-side turning of the patient by rotating the actual bed frame less than 40 degrees. The bed's lateral movement is maintained for 18 of every 24 hours to simulate postural drainage and help mobilize pulmonary secretions. The bed may contain a vibrator pack that provides chest physiotherapy. This feature assists with secretion mobilization and removal. Kinetic therapy is like CLRT in that patients are rotated side-to-side 40 degrees or more. It is important to obtain baseline assessments of the patient's pulmonary status (e.g., respiratory rate and rhythm, breath sounds, ABGs, SpO2) and continue to monitor the patient throughout the therapy.

Fibrotic or Fibroproliferative Phase

The fibrotic phase (chronic or late phase) of ARDS occurs 2 to 3 weeks after the initial lung injury. Not all patients who develop ARDS enter the fibrotic stage. For those who never fully recover from ARDS, the lung is completely remodeled by collagenous and fibrous tissues. Diffuse scarring of the lungs, interstitial fibrosis, and alveolar duct fibrosis result in decreased lung compliance. This reduces the surface area for gas exchange because the interstitium is fibrotic, and hypoxemia continues. Varying degrees of pulmonary hypertension may result from pulmonary vascular destruction and fibrosis.

Clinical Manifestations and Diagnostic Studies

The initial presentation of ARDS is often subtle. At the time of the initial injury, and for 24 to 72 hours, the patient may not have respiratory symptoms or may have only mild dyspnea, tachypnea, cough, and restlessness. Lung auscultation may be normal or reveal fine, scattered crackles. ABGs may show mild hypoxemia and respiratory alkalosis caused by hyperventilation. The chest x-ray may be normal or reveal diffusely scattered, but minimal, interstitial infiltrates. As ARDS progresses, symptoms worsen because of fluid in the lung parenchyma and alveoli and increased secretion accumulation in the airways. Respiratory distress becomes evident as WOB increases. Tachypnea and intercostal and suprasternal retractions may be present. Tachycardia, diaphoresis, changes in mental status, cyanosis, and pallor may occur. Lung auscultation usually reveals scattered to diffuse crackles and coarse crackles on expiration. After 72 hours, the chest x-ray often shows diffuse and extensive bilateral interstitial and alveolar infiltrates As ARDS progresses, ABGs reflect changes in oxygenation and ventilation. Refractory hypoxemia is the hallmark characteristic of ARDS. Hypercapnia often signifies that respiratory muscle fatigue and hypoventilation have severely affected gas exchange, and respiratory failure is imminent. To help evaluate the severity of hypoxemia in ARDS, we can calculate the PaO2/FIO2 (P/F) ratio . This measure reflects the ratio of the patient's PaO2 to the FIO2 that the patient is receiving. Under normal circumstances (e.g., PaO2 80 to 100 mm Hg; FIO2 0.21 [room air]), the P/F ratio is greater than 400 (e.g., 95/0.21 = 452). With the onset and progression of lung injury and impairment in O2 delivery through the alveolar-capillary membrane, the PaO2 may remain lower than expected despite increased FIO2. The P/F ratio distinguishes among mild (<300), moderate (<200), and severe (<100) ARDS As ARDS progresses, it is associated with profound dyspnea, hypoxemia, increased WOB, and respiratory distress, which require endotracheal intubation and PPV. The chest x-ray is often called "whiteout" (or white lung) because consolidation and infiltrates are widespread throughout the lungs, leaving few recognizable air spaces. Pleural effusions may be present. Severe hypoxemia, hypercapnia, metabolic acidosis, and organ dysfunction often accompany ARDS and provide additional challenges.

Diagnostic Studies for respiratory failure

The most common diagnostic studies used to evaluate ARF are chest x-ray and ABG analysis. A chest x-ray helps identify possible causes of respiratory failure (e.g., atelectasis, pneumonia). ABGs evaluate oxygenation (PaO2) and ventilation (PaCO2) status and acid-base (pH, bicarbonate) balance. Pulse oximetry monitors oxygenation status indirectly. Other diagnostic studies: complete blood cell count serum electrolytes urinalysis 12-lead ECG

Pathophysiology of ARDS

The pathophysiologic changes in ARDS are divided into 3 phases: (1) injury or exudative phase (2) reparative or proliferative phase (3) fibrotic or fibroproliferative phase.

Oxygen Therapy

The primary goal of O2 therapy is to correct hypoxemia. Closely monitor patients for changes in mental status, respiratory rate, and ABGs, until their PaO2 level has reached their baseline normal value. Ideally, the selected O2 delivery device must maintain PaO2 at 60 mm Hg or higher and SaO2 at 90% or higher. Breathing high O2 concentrations for prolonged periods is not without potential adverse effects. Exposure to higher FIO2 (greater than 60%) for longer than 48 hours poses a risk for O2 toxicity. In this situation, oxygen free radicals from the high O2 levels cause inflammation and cell death, by disrupting the alveolar-capillary membrane. Absorption atelectasis is another risk. O2 has the ability to replace nitrogen and other gases normally present in the alveoli. Without nitrogen to help maintain size and shape of the alveolus, structural support is lost and the alveolus collapses. Other effects of prolonged exposure to high levels of O2 include increased pulmonary capillary permeability, decreased surfactant production, surfactant inactivation, and fibrotic changes in the alveoli. Another risk of O2 therapy is specific to patients with chronic hypercapnia (e.g., patient with COPD). Chronic hypercapnia blunts the response of chemoreceptors to high CO2 levels as a respiratory stimulant. Initial O2 therapy may be provided to patients with chronic hypercapnia through a low-flow device, such as a nasal cannula at 1 to 2 L/min or a Venturi mask at 24% to 28%. The patient with COPD who does not respond to O2 therapy or other interventions may need mechanical ventilation with higher FIO2.

Reparative or Proliferative Phase

The reparative or proliferative phase of ARDS begins 1 to 2 weeks after the initial lung injury. During this phase, there continues to be an influx of neutrophils, monocytes, lymphocytes, and fibroblasts as part of the inflammatory response. Increased pulmonary vascular resistance and pulmonary hypertension may occur because fibroblasts and inflammatory cells destroy the pulmonary vasculature. Lung compliance continues to decrease due to interstitial fibrosis. Hypoxemia worsens because of the thickened alveolar membrane. This causes V/Q mismatch, diffusion limitation, and shunting. Airway resistance is severely increased from fluid in the lungs and secretions in the airways. The proliferative phase is complete when the diseased lung is replaced by dense, fibrous tissue. If the reparative phase persists, widespread fibrosis results. If the reparative phase stops, the lesions will often resolve.

Hydration

Thick, viscous secretions are hard to expel. Unless contraindicated, adequate fluid intake (2 to 3 L/day) keeps secretions thin and easier to remove. The patient who is unable to take enough fluids orally needs IV hydration. Assess cardiac and renal status to determine whether the patient can tolerate the IV fluid volume and avoid HF and pulmonary edema.

Promoting Tissue Perfusion

Those on PPV and PEEP often have decreased CO. One cause is decreased venous return from the PEEP-induced increase in intrathoracic pressure. Impaired contractility and decreased preload can decrease CO. Changes in intrathoracic or intrapulmonary pressures from PPV can also decrease CO. Patients with an exacerbation of COPD or asthma and those receiving PPV are at risk for alveolar hyperinflation, increased right ventricular afterload, and excess intrathoracic pressures. These changes can limit blood flow from the right side of the heart, through the pulmonary vasculature, to the left side of the heart, and cause hemodynamic compromise (e.g., decreased CO). Blood return from the systemic circulation to the right side of the heart may be impaired, decreasing preload and CO. Hemodynamic monitoring (e.g., CVP, CO, ScvO2, SvO2) is essential. This allows you to see trends, detect changes, and adjust therapy as needed. BP and mean arterial pressure (MAP) are important indicators of the adequacy of CO. Closely monitor BP and indicators of CO and tissue perfusion (SaO2, mixed venous O2 saturation) with the start of or changes in mechanical ventilation. A decrease in CO is treated by giving IV fluids, drugs, or both. (Chapter 66 discusses drugs used to treat decreased CO and shock.)

Neuromuscular Conditions

Various neuromuscular problems place patients at risk for respiratory failure. For example, patients with Guillain-Barré syndrome and multiple sclerosis have respiratory muscle weakness or paralysis. As a result, they cannot eliminate CO2 and maintain normal PaCO2 levels. Exposure to toxins (e.g., carbamate/organophosphate pesticides, chemical nerve agents) can interfere with the nerve supply to muscles and lung ventilation. Respiratory muscle weakness can occur from muscle wasting during a critical illness or peripheral nerve damage.

Effective Coughing

When secretions are present, encourage the patient to cough. Augmented coughing (quad coughing) may benefit some patients. To aid with augmented coughing, place 1 or both hands at the anterolateral base of the patient's lungs. As you observe deep inspiration end and expiration begin, move your hands forcefully upward. This increases abdominal pressure and helps the patient cough. It increases expiratory flow and promotes secretion clearance. Huff coughing is a series of coughs performed while saying the word "huff". This technique prevents the glottis from closing during the cough. The patient takes a deep breath, holds the breath for 2 or 3 seconds, and then exhales. The huff cough is effective in clearing central airways. It may help move secretions upward. COPD patients generate higher flow rates with a huff cough than with a normal cough, and it is less tiring. The staged cough also helps clear secretions. To perform a staged cough, the patient assumes a sitting position, breathes in and out 3 or 4 times through the mouth, then coughs while bending forward and pressing a pillow inward against the diaphragm.

hypoxemia

decreased level of oxygen in the blood r/t (5) high altitudes diffusion hypoventilation shunting V/Q mismatch

Diffusion Limitation

occurs when gas exchange across the alveolar-capillary membrane is compromised by a process that damages or destroys the alveolar membrane or affects blood flow through the pulmonary capillaries Causes: pulmonary fibrosis interstitial lung disease ARDS The accumulation of fluid, white blood cells, or protein in the alveoli can decrease gas exchange between the alveolus and the capillary bed. A common example is pulmonary edema. The classic sign of diffusion limitation is hypoxemia that is present during exercise but not at rest. During exercise, blood moves more quickly through the lungs. This decreases the time for diffusion of O2 across the alveolar-capillary membrane. Diffusion limitation can occur in conditions in which CO is markedly increased (e.g., high-output heart failure [HF], severe traumatic brain injury [TBI]). As blood circulates rapidly through the pulmonary capillary bed, there is less time for gas exchange to occur.

Nursing Implementation Prevention

teaching patients about deep breathing and coughing use of incentive spirometry early ambulation. Preventing atelectasis pneumonia complications of immobility optimizing hydration and nutrition

Injury or Exudative Phase

usually occurs 24 to 72 hours after the initial insult (direct or indirect). It generally lasts up to 7 days. Engorgement of the peribronchial and perivascular interstitial space causes interstitial edema. Fluid in the parenchyma of the lung surrounding the alveoli crosses the alveolar membrane and enters the alveolar space. V/Q mismatch and intrapulmonary shunt develop because the alveoli fill with fluid. Blood in the capillary network cannot be oxygenated. Hypoxemia and the stimulation of juxtacapillary receptors in the stiff lung parenchyma (J reflex) initially cause an increase in respiratory rate and a decrease in tidal volume (VT). This breathing pattern increases CO2 removal, producing respiratory alkalosis. CO increases in response to hypoxemia, a compensatory effort to increase pulmonary blood flow. However, as atelectasis, pulmonary edema, and pulmonary shunt increase, compensation fails and hypoventilation, decreased CO, and decreased tissue O2 perfusion occur. Severe V/Q mismatch and shunting of pulmonary capillary blood result in hypoxemia unresponsive to increasing concentrations of O2. This is the classic signs of ARDS, called refractory hypoxemia. In other words, despite receiving higher concentrations of O2, the patient's condition does not improve but continues to get worse. Diffusion limitation, caused by hyaline membrane formation, contributes to and worsens hypoxemia. As the lungs become less compliant because of decreased surfactant, pulmonary edema, and atelectasis, the patient must generate higher airway pressures to inflate "stiff" lungs. Reduced lung compliance increases the patient's WOB. At this point, the patient needs mechanical ventilation.