Pulmonary Embolism Explained PDF

PULMONARY EMBOLISM A pulmonary embolism (PE) is defined as the obstruction of one or more of the branches of the pulmonary artery (PA) by particulate matter that has an origin elsewhere in the body. A pulmonary embolus is most commonly caused by a thrombus. A pulmonary embolus can also be caused by...

PULMONARY EMBOLISM A pulmonary embolism (PE) is defined as the obstruction of one or more of the branches of the pulmonary artery (PA) by particulate matter that has an origin elsewhere in the body. A pulmonary embolus is most commonly caused by a thrombus. A pulmonary embolus can also be caused by a piece of tumor, amniotic fluid, air, or fat, referred to as a nonthrombotic pulmonary embolus (NTPE; Table 27.1). NTPE are incredibly dangerous, with amniotic fluid embolus (AFE) holding a 17% rate of failure to rescue being fatal to the mother in two-thirds of the cases. This figure rises to more than 30% when the AFE occurred concurrently with another complication. The nurse must possess astute surveillance skills and knowledge of complications to intervene early in these emergencies. Epidemiology There are many risk factors for PE, but by far, the greatest risk factor is the presence of a deep vein thrombosis (DVT). Virchow's triad of venous stasis, vessel wall damage, and hypercoagulability is the major predisposing factor for the development of a DVT. The most common cause of DVT is prolonged immobility (Table 27.2). Table 27.1 Sources of Pulmonary Emboli Type Source Deep vein thrombus Clot breaks loose from site of origin, most often from the deep veins of the leg or pelvis, then travels to the pulmonary vasculature. Fat Long-bone fracture Osteomyelitis Liposuction Air Central venous catheter (CVC) insertion---negative intrathoracic pressure can allow air to enter a CVC on insertion or if disconnected from a fluid source. Cardiopulmonary bypass Hemodialysis Amniotic fluid Amniotic fluid can move into the vascular space during delivery through placental vessels. Tumor Tumor sloughs off, and tumor particles travel to the pulmonary vasculature. Table 27.2 Virchow's Triad Predisposing Factor Causes Hypercoagulability Cancer Oral contraceptives Dehydration/hemoconcentration Sickle cell anemia Polycythemia vera Abrupt discontinuation of anticoagulants Venous stasis Prolonged bedrest/immobility Obesity Burns Pregnancy Vasculitis/thrombophlebitis Bacterial endocarditis Any postoperative patient Intimal damage of vessels Trauma IV drug use Atherosclerosis Other risk factors for DVT include: Obesity Smoking Chronic heart or vascular disease Fracture (hip or leg) Hip or knee replacement Major surgery Major trauma Spinal cord injury History of previous venous thromboembolism Malignancy Age \>50 years Estrogen use (i.e., oral contraceptives) Pregnancy Prior to 2020, the incidence of PE was approximately 1 to 2 per 1,000 persons in the United States, with 50,000 to 100,000 patients dying from PE. PE was a common complication of SARS-CoV-2 virus with more than 15% of patients developing a PE. More than 40% of patients diagnosed with PE also have diagnosed DVT. Venous thromboembolism (VTE) occurrence 30 days after COVID-19 infection is 50.99 per 1,000 persons, compared to 2.37 per 1,000 persons in noninfected patients. PE is the third most common cause of death in patients who are hospitalized for other reasons. Older adult patients are the most likely recipients of knee or hip replacement surgery. Due to the fact that many of these patients experience limited mobility due to the pain from their disease and have a higher risk for DVT due to aging changes, these patients are at high risk for PE. The nursing assessment must be aimed at early identification of PE as a possible postoperative complication. Pathophysiology When a blood clot or other particulate matter travels to the lungs, it lodges in the PA and blocks blood flow (Fig. 27.1). This obstruction results in an impaired ventilation-to-perfusion ratio (V/Q ratio) described as decreased or blocked blood flow or perfusion to functioning alveoli. This is called a ventilation--perfusion mismatch (V/Q mismatch), a decreased blood flow to functioning alveoli or areas of the lung where gas exchange can take place if perfusion is adequate. A PE results in a high-ventilation/low-perfusion scenario---a high V/Q mismatch. This prevents gas exchange at the alveolar level, leading to hypoxemia (low blood oxygen levels) and local vasoconstriction in the affected pulmonary vascular bed. The PE also results in an increase in pulmonary vascular resistance (PVR) because blood flow cannot move past the venous obstruction. If the right ventricle cannot overcome this increased PVR, then left ventricular preload (blood flow to the left ventricle) is reduced. This leads to decreased oxygenation, decreased cardiac output, and hypotension. The combination of decreased oxygenation and reduced cardiac output results in inadequate tissue perfusion and hypoxia (inadequate oxygenation at the cellular level). The increased PVR also leads to pulmonary hypertension (high pressures in the pulmonary vasculature), causing a backflow of blood into the right ventricle and right heart failure. This can exacerbate if the vascular obstruction continues to grow. FIGURE 27.1 Pulmonary embolism. Acute pulmonary emboli are classified as massive (high risk), submassive (intermediate risk), or low risk (Table 27.3). Massive pulmonary emboli occur abruptly, with a sudden onset of symptoms following obstruction. An acute massive PE can rapidly cause right ventricular heart failure and death. A massive PE is present if more than 50% of the blood flow through the PA is obstructed. A submassive PE is present when there is right heart dysfunction seen on echocardiogram but no hemodynamic instability. A low-risk PE presents with no indications of heart dysfunction, elevated biomarkers, or hypotension. Pulmonary emboli are further categorized by the placement of the embolus. A saddle PE is one that straddles the bifurcation of the PA, either fully or partially obstructing both branches of the PA. This type of PE very often results in sudden death. A central PE is an embolus or emboli found in the main branch of the PA or in either the right or left branch of the PA. A peripheral PE is an embolism or emboli found in the peripheral or smaller branches of the pulmonary arteries. Clinical Manifestations The sudden onset of intense dyspnea, pleuritic chest pain, and tachypnea is usually the first indication that the patient has an acute PE (Box 27.1). PE should be suspected in any postoperative patient, especially those following long-bone surgeries with a new onset of shortness of breath. The pain is attributed to the inflammatory mediators that have been released. In the cases of massive PE, acute right ventricular failure may present with jugular venous distention (JVD). Because of the decreased cardiac output, the patient may become hypotensive and tachycardic. The patient may also become tachycardic because of the hypoxemia caused by the increase in dead-space ventilation (nonperfused functioning alveoli). Cerebral perfusion may become compromised, making the patient anxious, restless, and/or confused. If pulmonary infarction has occurred because of hypoxia of pulmonary tissue, the patient may have hemoptysis (bloody sputum). Table 27.3 Pulmonary Embolism Classification Type Manifestations Massive or high risk Acute pulmonary embolism with: Prolonged hypotension requiring pharmacological support Right and left ventricular dysfunction Shock and/or cardiac arrest Submassive or intermediate risk Acute pulmonary embolism with: Normal blood pressure Right ventricular dysfunction---evidenced by echocardiogram Myocardial necrosis, indicated by elevated troponin I and elevated brain natriuretic peptide (BNP) Low risk Acute pulmonary embolism with: Normal blood pressure No right ventricular dysfunction No elevated biomarkers (troponin or BNP) Box 27.1 Common Signs and Symptoms of Pulmonary Embolism Dyspnea Accessory muscle use Pleuritic chest pain Tachycardia Tachypnea Crackles upon auscultation Cough Hemoptysis Unilateral lower extremity edema due to the presence of a deep vein thrombus (DVT); pain in extremity, with redness and warmth Interprofessional Management Medical Management Diagnosis Imaging Studies The diagnosis of PE is done through imaging studies and laboratory studies. If a patient is presenting with chest pain, an electrocardiogram (ECG) should be performed immediately to rule out a myocardial infarction (MI). There may be ECG changes in the case of massive PE, but they are nonspecific and not sensitive. Ischemic changes may be seen as inverted T waves and ST changes. Damage to the myocardium is represented by new Q waves and right bundle branch blocks. The predominant value of the ECG is to rule out myocardial infarction (MI). An initial chest x-ray may be done preliminarily to rule out other causes of the respiratory distress. While it may show atelectatic changes similar to those of pneumonia and infiltrates at the area of the embolism, a chest x-ray alone is not sufficient to diagnose a PE. Spiral computed tomography (CT) scan with intravenous contrast is the most commonly ordered test to diagnose a PE. The scan can effectively identify central as well as peripheral emboli. The nuclear medicine ventilation--perfusion scan (V/Q scan) can be utilized if a CT scan is not available. A V/Q scan can identify areas of the lungs that are ventilated but not perfusing effectively. This is an indication of obstruction of the pulmonary vasculature or PE. The phrase "high probability" indicates that there is a V/Q mismatch. A CT scan is preferred over a V/Q scan because the VQ scan has lower specificity and sensitivity to a CT scan, and a V/Q scan can take up to 60 minutes, which is significantly more time. The most definitive study for the diagnosis of PE is pulmonary angiography. This test allows for visualization of the pulmonary vasculature and therefore the detection of any obstruction. The invasive nature of this examination, coupled with the time it takes to perform the examination, limits its use when the patient is unstable. It also exposes the patient to more radiation than CT. This test is completed only if other studies are not conclusive and only in a stable patient. Once the patient with an acute PE has been stabilized, a lower extremity venous ultrasound is usually conducted to determine the presence and extent of any DVT. Recurrent PE is a major cause of mortality for patients who have endured an acute PE. Discovery of a DVT helps guide inpatient and post-discharge therapy and education. Laboratory Testing A plasma D-dimer level is a very specific indicator of the possibility of the presence of a thrombus in the body. This level increases as the body removes clots through lysis as part of the normal clot-removal process. The D-dimer is the fibrin left behind from that lysis. A negative D-dimer rules out the possibility of a clot. A positive D-dimer indicates the presence of a clot but requires further testing. This is the first blood test done when a PE is suspected. If a patient is experiencing respiratory distress, an arterial blood gas (ABG) will be performed. Evaluation of ABGs in the presence of a PE will most likely reveal hypoxemia (PaO2 less than 80 mm Hg) and respiratory alkalosis (PaCO2 less than 35) due to the patient's increased respiratory rate. The hypoxemia is more profound in direct relation to the amount of pulmonary vessel obstruction the patient is experiencing. The ABGs may later reveal metabolic acidosis due to the hypoxemia because the body switches to anaerobic metabolism in the face of hypoxemia in the later stages of a PE. As discussed previously, an acute PE may have cardiac manifestations. Because of the strain on the ventricles brought on by the PE, B-type natriuretic peptide (BNP) may be elevated. This peptide is released by overstretched ventricles under physiological stress. Levels above 100 pg/mL indicate heart failure. BNP is an insensitive test because not all patients with an acute PE have heart failure. Troponin I and troponin T may also rise, but this elevation is transient when compared with MI. Treatment Treatment for symptomatic PE includes supportive care to ensure oxygenation, as well as curative care to remove or reduce the clot and prevent further clot growth and formation. Providers will choose treatment for a PE based on the patient presentation, risk factors, and comorbidities. Medication therapy when treating a patient with acute PE is primarily anticoagulation. Anticoagulation does not reduce the clot size; it keeps the clot from getting larger and also helps to reduce the formation of other clots. In asymptomatic patients with a low-risk clot, anticoagulation usually consists of initiation of an oral factor Xa inhibitor that inhibits the conversion of prothrombin to thrombin. These patients do not require hospitalization. If a patient is symptomatic with a PE, the patient is hospitalized and intravenous heparin therapy is initiated. Heparin is initiated for any type of symptomatic pulmonary embolus: blood clot, air, fat, or other particulate matter---because platelets will aggregate and blood clots will adhere to any of those substances, making the obstruction larger. Typically, patients are started on IV heparin with a bolus followed by a continuous drip. The dosages are based on the patient's weight. Heparin therapy is monitored through the activated partial thromboplastin time (aPTT). Prior to the initiation of therapy, an aPTT is drawn and then repeated every 4 to 6 hours to monitor therapy. The therapeutic goal is 1.5 to 2.5 times the normal value, or 40 to 90 seconds. If the initial aPTT is below the designated therapeutic level, an additional heparin bolus may be given along with an increase in the rate of the infusion. If the aPTT is above therapeutic, the rate of the infusion will be reduced. In the cases of very high aPTT levels, the infusion may be held for a specified period of time before restarting the infusion at a lower rate. Once the aPTT is in the therapeutic range for two consecutive iterations, it is evaluated once every 12 or 24 hours. Each facility has established protocols for the assessment of aPTT for a patient receiving heparin. Reaching a therapeutic aPTT level within 24 hours has been shown to have better outcomes. Protamine sulfate is the reversal agent to heparin and must be readily available if active bleeding occurs. Subcutaneous low-molecular-weight heparin, fondaparinux, or unfractionated heparin may be prescribed in lieu of instituting a weight-based heparin protocol. Patients need to be on anticoagulation at least 3 months post-discharge. Agents used may be subcutaneous low-molecular-weight heparin, factor Xa inhibitors, or warfarin. Warfarin (Coumadin) therapy is monitored using the lab value international normalized ratio (INR). The therapeutic anticoagulation goal is an INR of 2.0 to 3.0. It takes approximately 3 to 5 days to reach a therapeutic level, so initially, the two medications, heparin and warfarin, are prescribed concurrently. See Table 27.4 for information on anticoagulants and reversal agents. If a patient is hemodynamically compromised, thrombolytic therapy (alteplase) should be considered. Contrary to anticoagulation, systemic thrombolysis is responsible for lysis or removal of the clot from the PA. The adverse effects of systemic thrombolytic agents may preclude their use. The risk of bleeding is of paramount concern. The main concern in the older adult patient is cerebral hemorrhage. Patients typically have IV heparin administration discontinued during the alteplase infusion. It is restarted after the infusion is complete. Absolute and relative contraindications must be considered before initiating this therapy (Table 27.5). Patients who are hemodynamically unstable may be candidates for catheter-directed thrombolysis (CDT) using a low-dose hourly infusion of tissue plasminogen activator (tPa) or urokinase. This therapy will administer the medication directly to the clot at the site, resulting in lysis of the clot and reducing the risk of bleeding complications. This therapy is considered safe and beneficial for patients with massive PE and those with submassive PE. Intravenous isotonic fluid is used to decrease the viscosity of the blood. Caution must be exercised to maintain a safe fluid balance. In cases of recognized right ventricular compromise, IV fluid may be held, and an inotropic pharmacological agent that increases cardiac contractility, such as dobutamine, may be administered to overcome PVR and afterload and allow the left ventricle to maximize cardiac output. Hypotension can be managed with vasopressors like norepinephrine and vasopressin if it is not resolved with single-medication therapy. Surgical Management Surgical management is considered for acute massive PE resulting in hemodynamic instability where thrombolytic agents are contraindicated. The procedure is an embolectomy, or physical removal of the clot. There are two types of embolectomy, catheter or surgical. In addition to the CDT previously discussed, rheolytic or rotational catheter embolectomy may be an option. In a rheolytic catheter embolectomy, pressurized saline is used to erode the clot. It requires a large venous catheter or sheath, so bleeding is a major risk. Another type of catheter embolectomy is the rotational embolectomy. A rotating tool is used to break down the clot. A standard cardiac catheter is used, so there is less risk to the patient. In general, catheter embolectomy is used for clots in the main and segmented or lobar PA branches. The efficacy of catheter embolectomy is still being studied, but each method has a mortality rate of approximately 20%. Table 27.4 Medications Used in the Treatment of Pulmonary Embolism Medication Classification Mechanism of Action Exemplars Nursing Implications Unfractionated heparin   Binds to antithrombin and stimulates it to inactivate factor Xa, stopping the clotting cascade Heparin SQ- Used for VTE prevention, treatment for uncomplicated or asymptomatic VTE. No laboratory monitoring required. IV- Used for treatment of symptomatic or unsymptomatic VTE and PE. Adjustments required to maintain a therapeutic range for aPTT. Blood draws every 4-6 hours to measure aPTT. May be used as a "bridge" to maintain anticoagulation while patient is initiating warfarin. Supratherapeutic aPTT increases the risk for bleeding complications. Maintain adequate IV access if giving IV Initiate bleeding precautions Educate patient/family about bleeding risk, precautions, and s/s of bleeding Reversal agent: Protamine sulfate Monitor aPTT Monitor platelets to monitor for heparin-induced thrombocytopenia Monitor BUN/creatinine as heparin is excreted via the kidneys Low-molecular weight heparin (LMWH) Binds to antithrombin and stimulates it to inactivate factor Xa, stopping the clotting cascade; more specific than unfractionated heparin because it does not bond to thrombin and has less activity against factor IIa; more bioavailable than unfractionated heparin Enoxaparin, Dalteparin Used for treatment of PE No laboratory monitoring required. Initiate bleeding precautions Educate patient/family about bleeding risk, precautions, and s/s of bleeding Reversal agent: Protamine sulfate Monitor platelets to monitor for heparin-induced thrombocytopenia Monitor BUN/creatinine as LMWH is excreted via the kidneys Patient/family education with teach-back if patient will be self-administering LMWH at home   Vitamin K antagonist Interferes with the vitamin K synthesis needed in the clotting cascade, inhibiting factors II, VII, IX, and X Warfarin Given PO Takes a few days of daily administration to reach therapeutic level Monitored using the international normalized ratio (INR); therapeutic level for anticoagulation is 2-3 Routine blood testing is required Reversal agent: Vitamin K Educate patient/family about bleeding risk, precautions, and s/s of bleeding Xa inhibitors   Selectively binds to factor Xa, inhibiting its role in the clotting cascade, inhibiting the generation of thrombin Rivaroxaban (PO) Apixaban (PO) Fondaparinux (SQ) Can be seen on a lab draw (assay), but not routinely necessary Reversal agent: andexanet alfa Educate patient/family about bleeding risk, precautions, and s/s of bleeding Thrombolytics Enzymes which break down fibrin and dissolve clots Streptokinase Urokinase Alteplase (rt-PA) Used for emergent situations, like a PE causing profound hemodynamic instability that will lead to death Diagnosis must be confirmed prior to initiating therapy Higher risk of bleeding complications, including intracerebral bleeding Breaks down any clot, including the clot being targeted Strict inclusion and exclusion criteria Astute (q 15 minute -- 1 hour monitoring during and after administration) to assess for bleeding complications -- complications may lead to death if not noticed/intervened upon Table 27.5 Contraindications to Thrombolytic Therapy Absolute Relative History of hemorrhagic stroke Active intracranial neoplasm Recent surgery Recent trauma (less than or equal to 2 months) Active or recent internal bleeding (6 months) Severe hypertension (SBP greater than 200 mm Hg or DBP greater than 110 mm Hg) Nonhemorrhagic stroke (within 2 months) Surgery in past 10 days Thrombocytopenia (platelets less than 100,000) History of bleeding tendencies DBP, Diastolic blood pressure; SBP, systolic blood pressure. The more common type of embolectomy is the surgical embolectomy. This is a complex thoracic surgical procedure that requires cardiopulmonary bypass. Again, this procedure is usually performed when the patient has systemic hypotension and the use of thrombolytics is contraindicated. New studies indicate that the use of CDT could be an appropriate choice in lieu of a surgical approach, especially in the face of severe hemodynamic instability. The major determinant of the success of these procedures is when they can be performed prior to the onset of cardiogenic shock or cardiac arrest. Inferior vena cava (IVC) filters are placed to prevent recurrent PEs (Fig. 27.2). The indications for IVC filter placement are active bleeding that disqualifies anticoagulation therapy, recurrent PE despite adequate anticoagulation therapy, or evidence that hemodynamic or respiratory dysfunction is severe enough that another PE could be fatal. The filter allows for blood passage but is designed to trap any further emboli originating in the lower extremities. Complications of IVC filter placement are rare but include filter migration, erosion of the vena cava wall, obstruction due to filter thrombosis, and procedural complications. Retrievable IVC filters are now available with the goal being the removal of the IVC when anticoagulation is again advisable. FIGURE 27.2 Inferior vena cava (IVC) filter placement. The filter allows for blood passage but traps emboli originating in the lower extremities, preventing travel to the heart and lungs. Nursing Management Assessment and Analysis Assessment of a patient at risk for an acute PE requires astute monitoring. The clinical manifestations are nonspecific. Sudden onset of pleuritic chest pain, dyspnea, and tachypnea are the most common initial assessment findings. The presence of a PE has two distinct cardiac manifestations. If PVR is elevated, the early signs of right ventricular failure, such as JVD, may be seen. With a massive PE, preload to the left side of the heart may be dramatically reduced, causing a decrease in cardiac output and hypotension. A sudden change in mental status may occur if cerebral perfusion pressure is compromised. The patient may become anxious or express feelings of impending doom. A sudden PE may be a cause of pulseless electrical activity cardiac arrest, in which cardiopulmonary resuscitation should be initiated, and the cause treated. Nursing Diagnoses/Problem List Impaired gas exchange related to interruption of pulmonary blood flow Ineffective breathing pattern: tachypnea related to pain and hypoxemia Decreased cardiac output related to increased PVR Risk for bleeding related to anticoagulant/thrombolytic therapy Nursing Interventions Assessments Airway Is breathing effective to maintain oxygenation? Is the patient breathing comfortably or in respiratory distress? Mechanical ventilation may be required. Oxygenation The pulse oximetry reading decreases from baseline as a result of increased dead-space ventilation; blood is not properly oxygenated in the lungs. Frequent vital signs The pulse increases because of hypoxemia; blood pressure may decrease from baseline in cases of massive PE because of decreased left heart preload; tachypnea may occur due to decreased oxygenation and pain; fever may develop because of the inflammatory response. Chest pain Sudden-onset chest (pleuritic) pain with dyspnea and tachypnea is usually the first sign of acute PE, resulting from the release of inflammatory mediators. Laboratory values ABGs (onset) Tachypnea causes respiratory alkalosis; PaO2 is reduced because of increased dead-space ventilation. ABGs (as disease progresses) Metabolic acidosis results from hypoxia and the subsequent transition to anaerobic metabolism. Lactic acid levels An increase confirms anaerobic metabolism. Coagulation studies APTT levels are monitored if the patient is on heparin; the prothrombin time (PT)/INR is followed if the patient is on warfarin. Monitor urine output. Urine output less than 0.5 mL/kg/hr is an early sign of shock. Actions Elevate the head of the bed. This allows the diaphragm to drop, facilitating less work of breathing and better oxygenation. Administer IV fluids. This decreases viscosity of blood; caution must be used in cases of right ventricular overload. Administer anticoagulation medications as ordered. Heparin infusion, warfarin, and factor Xa inhibitors limit the growth of PE and DVT and decrease the formation of new clots. Administer thrombolytic medications if ordered. Thrombolytics degrade the clot; if not contraindicated, they are used when patients are hemodynamically compromised. Administer inotropic agents if ordered. Inotropic agents increase cardiac contractility in an effort to augment cardiac output if the patient is hemodynamically unstable. Administer norepinephrine or vasopressin as ordered. These vasoconstrictive medications are given, if necessary, to maintain a systolic BP of at least 80 mm Hg. Institute bleeding precautions. The use of anticoagulants and/or thrombolytics can result in bleeding; minimize venipunctures; watch for blood in urine, stool, and sputum; watch for unusual bruising. Be prepared for intubation and resuscitation. Massive PE may result in cardiogenic shock and sudden death. Teaching Disease process/lifestyle modifications The patient should understand the risks of PE and how to avoid future occurrences via lifestyle modifications. Exercise regimen that includes aerobic exercise Exercise strengthens the patient's heart and cardiovascular system, improves venous return to the heart, and assists in the loss of weight. Cardiac-prudent diet that minimizes saturated fats A heart-healthy diet reduces damage to vasculature. Adequate fluid intake; at least eight 8-ounce glasses of water spread across each day This maintains hydration and decreases blood viscosity. Smoking cessation Smoking cessation reduces intimal damage to vasculature; decreases vasoconstriction caused by smoking, which decreases risk of clot formation in vasoconstricted vessels; and improves overall health. Medications Explain the mechanism of action of anticoagulants and thrombolytics; the patient will be required to have follow-up laboratory samples drawn if on warfarin to determine effective dosing of outpatient anticoagulants. Regular laboratory testing not necessary for patients on factor Xa inhibitors. Bleeding precautions Encourage the use of electric razors; use soft toothbrushes, no flossing. Avoid activities with a risk of bleeding, such as football. The patient should be educated on the signs of abnormal bleeding, like bleeding around the gums and excessive bruising. Diet Limit foods high in vitamin K; these foods interfere with the efficacy of warfarin. Signs and symptoms of a recurrent PE/DVT Be aware of the occurrence of unilateral lower extremity edema and pain in the extremity, with redness and warmth, which may be due to the presence of a DVT. Pleuritic chest pain and dyspnea may indicate recurrent PE. Evaluating Care Outcomes Patients who have experienced a PE have an increased incidence of recurrent PE. By adhering to a medication regimen, improving diet, beginning an exercise program, staying adequately hydrated, and quitting smoking, the patient should remain free of a recurrence of a PE as well as reducing the most common cause, DVT of the lower extremities. Quick recognition and identification of an acute PE is crucial in reducing failure to rescue and ensuring survival to hospital discharge. A massive PE can happen suddenly and is a cause of pulseless electrical activity cardiac arrest. Once a patient exhibits signs and symptoms of a PE, the nurse must quickly notify a provider or rapid response team, coordinate supportive and resuscitative care, and continuously reassess for complications. Massive and submassive PE hold a mortality rate of 16% at 30 days, with 14% of patients experiencing major bleeding as a complication of treatment. Connection Check 27.1 After oxygen has been administered, the next priority intervention the nurse would initiate for a patient with a pulmonary embolus is the administration of which of these therapies? A.  Normal saline IV fluid B.  IV heparin C.  Platelet administration D.  Antibiotics for inflammatory fever ACUTE RESPIRATORY FAILURE Epidemiology Acute respiratory failure is when one or both of the gas-exchange functions of the lungs are compromised. The gas-exchange functions of the lungs are oxygenation and ventilation or carbon dioxide (CO2) removal. Compromise of these functions leads to hypoxemia and/or hypercapnia, also referred to as hypercarbia (increased PaCO2). There are two types of respiratory failure: type I, or hypoxemic respiratory failure, and type II, or hypercapnic respiratory failure. Hypoxemic respiratory failure (type I) is characterized by a PaO2 of less than 60 mm Hg despite increased inspired oxygen with a normal or low PaCO2. Hypercapnic respiratory failure (type II) is characterized by a respiratory acidosis, a PaCO2 greater than 50 mm Hg and pH less than 7.35. Hypoxemia may or may not be present. The prevalence of acute respiratory failure varies depending on the definition, but it is a life-threatening disorder with a high mortality rate. Risk factors for hypoxemic respiratory failure include disease processes that produce a V/Q mismatch or impair oxygen diffusion at the alveolar level, such as pulmonary edema, pneumonia, or pulmonary embolus. Risk factors for hypercapnic respiratory failure include diseases that impair ventilation or cause hypoventilation. This type of respiratory failure is seen in patients with impaired chest-wall movement and thus impaired ventilation, such as acute asthma and narcotic overdose, or in patients with peripheral nervous system disorders that impair chest-wall movement, such as myasthenia gravis. This may also be seen in patients with chest-wall injury due to trauma that results in ventilatory impairment. Typically, these patients also present with hypoxemia if the cause is not quickly reversed. Risk factors are noted in Table 27.6. Table 27.6 Risk Factors for Acute Respiratory Failure Impaired Ventilation (Hypoventilation) Ventilation--Perfusion Mismatch Impaired Diffusion (Alveolar) Airway obstruction Respiratory muscle weakness/paralysis that can occur with neuromuscular disease such as myasthenia gravis Chest-wall injury Anesthesia Opioid administration COPD Restrictive lung diseases (sarcoidosis, pulmonary fibrosis) Atelectasis Pulmonary embolus Pneumothorax ARDS Pulmonary edema ARDS ARDS, Acute respiratory distress syndrome; COPD, chronic obstructive pulmonary disease. Pathophysiology Hypoxemic respiratory failure is characterized by impaired gas exchange and oxygenation because of a V/Q mismatch, a shunt, or impaired diffusion. In the case of V/Q mismatch, one scenario is that the lungs are adequately ventilated but not perfused (dead-space ventilation), as in the case of a patient with a PE (high V/Q); air is entering the lung, but the blood is blocked from reaching the alveoli due to the embolism, and thus no gas exchange occurs. The second scenario is when the lungs are perfused but inadequately ventilated (shunt), as in the case of the patient with atelectasis or pneumonia (low V/Q; Fig. 27.3). Blood is perfusing the lungs, but air cannot get to the alveoli due to fluid or exudate in the air spaces. An extreme V/Q mismatch is an intrapulmonary shunt, where there is no gas exchange at all because of a shunting of blood past collapsed alveoli, as in the case of atelectasis. Impaired diffusion occurs at the alveolar level. Either the distance for diffusion (gas exchange) is increased or the permeability of the alveolar-capillary membrane (ACM) is reduced. This is due to either collapsed alveoli; fluid in the alveoli or small airways, such as in pulmonary edema; or exudate in the small airways and/or alveoli, such as in pneumonia. The primary result is hypoxemia. In hypercapnic respiratory failure, impaired ventilation occurs when there is a reduced ability of the lungs and respiratory apparatus to adequately expand (hypoventilation). The amount of air moved by the lungs is suboptimal. This means that the elimination of CO2 does not take place adequately. Hypercarbia is the initial result, but hypoxemia eventually occurs without adequate treatment. Clinical Manifestations Acute respiratory failure results in hypercapnia and hypoxemia. Hypercapnia can produce headache, confusion, and a decreased level of consciousness or increased somnolence. The patient may be tachycardic, tachypneic, and may also appear dizzy and flushed, with a pink coloring to the skin. In hypoxemia, clinical manifestations include increases in heart rate, respiratory rate, and blood pressure in an effort to increase oxygenation and perfusion. As the patient becomes more hypoxemic, there is less cerebral perfusion. This may manifest as restlessness, confusion, and/or anxiety. Eventually, without adequate treatment, the patient will present cyanotic with a greatly decreased level of consciousness or coma. It is important to remember that the patient will present not only with the clinical manifestations of respiratory failure but also with the clinical manifestations of the underlying cause or disease process (Table 27.7). FIGURE 27.3 Ventilation--perfusion mismatch. Connection Check 27.2 A patient with a diagnosis of pneumonia complains of a new onset of slight shortness of breath. For which of the following assessment findings would the nurse call the primary care provider immediately? (Select all that apply.) A.  The patient is voiding, but the amounts are decreasing. B.  The patient is sleeping more than usual. C.  There is a pink coloration to the skin. D.  The patient's secretions are thin and milky colored. E.  The patient thought it was the third instead of the fifth of the month. Interprofessional Management Medical Management Diagnosis Laboratory and diagnostic tests include ABGs, venous oxygen saturation, hemoglobin and hematocrit, chest x-ray, and sputum cultures. ABGs are an excellent tool to assess the adequacy of both oxygenation and ventilation in the lungs. Hypoxemic respiratory failure has an initial period of respiratory alkalosis due to hyperventilation along with hypoxemia. Once the initial blood gases have been analyzed and treatment has been initiated, pulse oximetry can be used to monitor oxygenation. The goal is to have an SpO2 greater than 94% (which correlates to a PaO2 of approximately 80 mm Hg). Special care is taken for the patient with chronic obstructive pulmonary disease (COPD) because of the hypoxic drive to breathe (see Safety Alert). Table 27.7 Clinical Manifestations of Respiratory Failure Early Intermediate Late Dyspnea Restlessness Anxiety Fatigue Increased blood pressure (from baseline) Tachycardia Confusion Lethargy (due to increased CO2) Pink skin coloration (due to increased CO2) Cyanosis Coma Normal ventilation is stimulated by the buildup of CO2 in the blood. Chemoreceptors detect a hypercapnic (elevated CO2) state, and the respiratory cycle is stimulated to breathe faster and more deeply. This is called the "hypercapnic drive." In some patients with COPD, the body's chemoreceptors become less sensitive to CO2 because it is retained at higher levels as a result of the disease process. Over time, the patient with COPD develops a "hypoxic drive" to breathe. It is the lack of oxygen in the blood that causes these patients to breathe. It is because of this hypoxic drive that patients with known COPD may not tolerate high oxygen concentrations when being given supplemental oxygen therapy. The increased amount of oxygen may cause the patient to stop breathing. Careful, continuous monitoring must be used when providing increased oxygen levels to these patients. Hypercarbic respiratory failure results in ABGs with a pH of less than 7.35 and a PaCO2 of greater than 45 mm Hg. The PaO2 may or may not be decreased initially but will eventually decrease without adequate treatment. Venous oxygen saturation measures the amount of oxygenated blood returning to the heart to determine the adequacy of perfusion at the tissue level. It is correlated with perfusion failure or increased tissue oxygen demands. A normal venous oxygen saturation is 60% to 80%. A decreased venous oxygen saturation indicates inadequate cardiac output; the tissues are extracting more oxygen than normal because of the decreased oxygen delivery. A more detailed description of venous oxygen saturation and hemodynamic monitoring is given in Chapter 32. The patient's hemoglobin and hematocrit should be analyzed to make certain that there are enough binding sites for oxygen to ensure adequate oxygen-carrying capacity. Red blood cells carry oxygen to the cells for cellular oxygenation. If there are not sufficient red blood cells, the oxygen-carrying capacity of the blood is diminished. A chest x-ray may show an underlying pathology, such as heart failure, pulmonary congestion, pneumonia, or pneumothorax that can explain the respiratory failure. As discussed earlier, PE as a cause of respiratory failure is diagnosed through laboratory testing and a CT scan. A sputum culture should be obtained to rule out a pathogenic (i.e., bacterial or viral) cause of the failure. Treatment Respiratory failure is not a disease---it is a condition caused by another disease or disorder. It is vital to treat not only the respiratory failure but also the underlying cause. If the cause is pulmonary edema, that issue must be addressed as well as the oxygenation issues associated with the resulting respiratory failure. Careful attention to nutrition is also imperative to provide calories and energy for the increased work of breathing, as well as adequate hydration to keep secretions thin. The treatment of respiratory failure begins with oxygen. In many cases of respiratory distress, minimal supplemental oxygen may help the patient's hypoxemic status. The use of a nasal cannula or Venturi mask may provide adequate support. This is not the case when a patient is suffering from respiratory failure. The patient in acute respiratory failure who has not responded to traditional methods of oxygen administration may be placed on a nonrebreather mask with 100% FIO2. The mask is placed over the patient's nose and mouth and then secured to the patient using the elastic band. The oxygen flow meter is then turned on to its maximum setting. The reservoir bag of the mask should be inflated to ensure that the patient is receiving 100% oxygen. An oxygen delivery method, high-flow nasal cannula (HFNC), has been increasingly studied. HFNC is a nasal cannula that has thicker tubing and prongs and is able to generate higher flows of oxygen (up to 60L/minute) at higher and more precise fraction of inspired oxygen (FiO2), up to 100%. The oxygen delivery is also warm and humidified. This advance in oxygen delivery enhances patient comfort by potentially avoiding noninvasive positive pressure ventilation or mechanical ventilation. HFNC works by delivering a higher flow and percentage of oxygen, which reduces anatomic deadspace and provides a nominal end expiratory pressure. This reduces respiratory effort and work of breathing. While still being studied, HFNC has been low-to-moderately shown to reduce mortality, reduce hospital-acquired pneumonia, reduce intubations, and enhance patient comfort. In cases of severe V/Q mismatches where shunting of blood is occurring past nonfunctioning alveoli, supplemental oxygenation may not be sufficient to improve the patient's oxygenation status. In these cases, noninvasive or invasive positive-pressure ventilation may be necessary to open the alveoli to allow gas exchange. Noninvasive positive-pressure ventilation (NPPV), such as bilevel positive airway pressure (BiPAP) or continuous positive airway pressure (CPAP), administered via a tight-fitting face mask, can be used to help increase oxygenation. In BiPAP, the patient receives two different pressures. A higher-pressure during inhalation assists with the opening of the alveoli, and a lower pressure during exhalation keeps the alveoli from collapsing during/at the end of exhalation but also allows ease of exhalation. In contrast, CPAP maintains one continuous pressure throughout the respiratory cycle to help keep the alveoli open through inspiration and expiration. Invasive positive-pressure ventilation requires an advanced airway, such as an endotracheal tube (ETT) or a tracheostomy tube, and mechanical ventilation. As with CPAP, during mechanical ventilation, positive pressure is maintained throughout the ventilatory cycle in the form of positive end-expiratory pressure (PEEP). The pressure is measured at the end of expiration, thus the name, but as stated, the positive pressure is maintained throughout the cycle. Mechanical ventilation is discussed in detail in Chapter 7. Connection Check 27.3 The nurse understands that oxygen therapy for a patient with COPD requires close monitoring because of which of the following? A.  Hypoxic respiratory drive B.  Hypercapnic respiratory drive C.  Acidotic respiratory drive D.  Alkalotic respiratory drive Medications Medications such as inhaled bronchodilators, inhaled steroids, diuretics, sedation, and antibiotics are used in cases of acute respiratory failure. Bronchodilators open the airways by stimulating beta-2 receptors within the lungs. This helps to improve airflow because of an increase in the diameter of the airways. Inhaled steroids help decrease the inflammatory response, decreasing bronchoconstriction and increasing the airway diameter. The combination of bronchodilators and steroids provides a more therapeutic response than either medication alone. This is known as a synergistic response. Diuretics are used to decrease pulmonary congestion, especially in cases where pulmonary edema is the underlying cause of failure. Sedation is used to control agitation and anxiety that increase the work of breathing and oxygen consumption, and it is especially needed if the patient requires mechanical ventilation. Antibiotics may be initially broad spectrum to treat a suspected pneumonia and are adjusted if the sputum culture is positive for a bacterial infection. Complications If supplemental oxygen, mechanical ventilation, and medications do not halt the progression of respiratory failure, the patient is at high risk for cardiac failure, multiple organ dysfunction, and death. Nursing Management Assessment and Analysis The clinical manifestations are due to the hypoxemia and hypercapnia of acute respiratory failure. ABG analysis reveals a decreasing oxygenation status and/or increased CO2 levels due to impaired oxygenation or ventilation. Changes in mental status may indicate a decrease in cerebral perfusion. Agitation indicates hypoxia; somnolence indicates hypercarbia. New-onset dyspnea, increased work of breathing, and tachypnea are early indicators of impending respiratory compromise. Tachycardia and hypertension are present initially as a compensatory response. Nursing Diagnoses/Problem List Impaired gas exchange related to alveolar hypoventilation, V/Q mismatching, and/or intrapulmonary shunting Ineffective breathing pattern related to muscular fatigue and/or neurological impairment Nursing Interventions Assessments Airway Assess for airway patency, increased work of breathing, noisy ventilation (normal ventilation should be silent), excess secretions/need for assistance with excess secretions. Vital signs and oxygen saturation Blood pressure, pulse, and respiratory rate increase as a compensatory mechanism in an attempt to increase oxygenation in the presence of hypoxemia. To ease the work of breathing, the patient may breathe in a tripod position. Once respiratory failure progresses the patient will breathe slower or cease breathing. Fever may develop because of inflammation and/or infection. The pulse oximetry reading decreases from baseline because of the V/Q mismatch, impaired diffusion, and/or alveolar hypoventilation. ABGs Hypoventilation of type II failure results in CO2 retention, acidosis, and ultimately, decreased PaO2; V/Q mismatch or diffusion defects of type 1 failure result in a decreased PaO2. Cardiac monitoring Hypoxia and increased oxygen demand due to tachycardia may lead to dysrhythmias. Neurological assessment A change in mental status may be an early indication of impending respiratory failure. Anxiety A patient experiencing respiratory compromise may feel anxious or have a feeling of impending doom. Once respiratory failure progresses, the patient will have a decreased level of consciousness. Agitation Agitation is caused by hypoxemia. Somnolence Somnolence is caused by hypercapnia. Breath sounds The underlying cause of respiratory failure may result in crackles (pulmonary edema) or rhonchi (pneumonia, COPD) or diminished or absent breath sounds (hypoventilation, obstruction, pneumothorax). Skin coloration Careful monitoring of skin coloration can be helpful in identifying changes in the patient. Cyanosis may be visible in the nail beds and around the mouth in the initial stages of hypoxemia; as central cyanosis sets in, the body may take on a blue or gray tinge. A deep pink coloration to the skin is highly indicative of increased CO2 levels. Actions Administer oxygen (with humidity) as ordered. Supplemental oxygen is necessary to treat hypoxemia. Humidity helps to prevent mucosal drying and helps keep secretions thin so that they can be more easily coughed or suctioned up. Medication administration Administer bronchodilating medications as ordered. Bronchial smooth muscle relaxants help open the airways. Administer steroids as ordered. Steriods reduce inflammation due to a synergistic effect with bronchodilating agents (administer bronchodilator medications first, then inhaled steroids to allow the steroids to be inhaled more easily into the bronchial tree). Administer diuretics as ordered. Diuretics help decrease the pulmonary congestion that impairs ventilation. Administer sedation as ordered (typically only in mechanically ventilated patients). Sedation helps decrease anxiety and agitation, helping to decrease the work of breathing and oxygen consumption. Elevate the head of the bed; sit the patient up in a chair. Positioning with the head elevated optimizes gas exchange, aids in the work of breathing, and decreases the risk of aspiration. Position patient with the "good lung down." If the underlying disease is unilateral, positioning with the good lung down improves gas exchange by optimizing the V/Q ratio; gravity ensures the healthy lung maintains adequate blood flow to optimize ventilation to perfusion. Chest physical therapy and suctioning; ambulate as able. If excessive sputum is part of the underlying cause, positioning, postural therapy, percussion, vibration, and ambulation combined with assisted coughing or suctioning help mobilize and clear secretions. Administer IV fluids/hydration. This decreases viscosity of secretions and helps maintain intravascular volume. Administer nutritional support. The patient's metabolic needs must be met to promote healing. Be prepared for noninvasive or invasive positive-pressure ventilatory support. A severe V/Q mismatch may require the addition of positive pressure to adequately promote gas exchange. Teaching Disease process The patient should understand the risk factors and causes of acute respiratory failure and how to avoid future occurrences. Medications Explain the mechanism of action and the rationale for each medication. Dosing instructions, missed dosing, and the treatment regimen must be addressed. Pulmonary rehabilitation Breathing techniques Techniques such as pursed-lip breathing and diaphragmatic breathing allow for better alveolar ventilation and improve gas exchange. Energy conservation Work with the patient to determine priorities in daily living. Exercise Aerobic exercise helps improve respiratory status. Infection prevention Hand washing and pneumococcal and influenza vaccinations help decrease the likelihood of infection. Diet and adequate hydration Adequate caloric intake is necessary for healing; adequate hydration helps ensure thin secretions. Small, frequent, nutrient-dense meals and supplements may be necessary as often patients lack energy or desire to eat. Smoking cessation Smoking cessation improves overall health and respiratory functioning and reduces incidences of pulmonary disease and cancer. Evaluating Care Outcomes The initial goal of treatment for the patient with acute respiratory failure is to improve gas exchange. Pulmonary rehabilitation in the form of exercise training, nutritional counseling, and breathing strategies should be implemented to assist in the recovery from respiratory failure. The patient successfully treated is able to return to baseline respiratory function. Except in cases where the use of supplemental oxygen is the patient's underlying norm, a well-managed patient should not require supplemental oxygenation upon discharge. The patient should be able to return to baseline activities of daily living, work, and social commitments. CASE STUDY: EPISODE 2 After stabilization of his injuries, J.T. is admitted to the intensive care unit (ICU). The bleeding into the thoracic cavity has stopped, but the lung has not fully expanded. On the second day in the unit, it is noted that his pulse oximetry readings continue to decline in spite of increased FIO2 via 100% nonrebreather. He is tachypneic and tachycardic. A chest x-ray shows diffuse infiltrates bilaterally. An ABG shows the following: pH 7.50, PaCO2 of 32, PaO2 of 50, and HCO3 of 28 while on 70% FIO2. It is determined that J.T. has developed acute respiratory distress syndrome (ARDS). J.T. is intubated, and mechanical ventilation is initiated... ACUTE RESPIRATORY DISTRESS SYNDROME Epidemiology Prior to the COVID-19 pandemic, there were approximately 190,000 new cases of acute respiratory distress syndrome (ARDS) annually. It is estimated that COVID-19 more than doubled the annual number of ARDS cases in the United States. Research shows that the prevalence of ARDS is between 15% and 18% of all mechanically ventilated patients. Despite the most modern technology and after numerous studies, mortality rates for ARDS remain high. Death is not usually due to respiratory failure but due to multiple organ dysfunction caused by the massive inflammatory response brought on by hypoxia and/or infection. There are more than 50 causes for the development of ARDS. The most common cause is sepsis. Other causes include pneumonia, severe trauma, aspiration, massive transfusions, cigarette smoking, cardiopulmonary bypass, pneumonectomy, PE, and drug/alcohol overdose. A way of classifying ARDS is to determine if the cause is due to direct or indirect injury. Direct injury refers to damage or disruption of the respiratory system. Indirect causes are those processes or disorders that occur outside the respiratory system but have a deleterious effect on the lungs. Table 27.8 outlines a partial list of causes of ARDS; it is not meant to be a complete list. Pathophysiology and Clinical Manifestations ARDS is defined by the following characteristics: acute onset of less than 7 days, refractory hypoxemia, and bilateral infiltrates ruling out cardiac pulmonary edema as the cause. It is further classified in terms of severity through evaluation of the PaO2/FIO2 ratio, the ratio of the partial pressure of oxygen over the fraction of inspired oxygen. To determine this ratio, divide PaO2 by FIO2. In a healthy individual, the PaO2 averages 90 mm Hg (normal is 80 to 100). Breathing room air, the FIO2 is 21% (or 0.21), so the equation is 90/0.21 or a PaO2/FIO2 ratio of approximately 428. If a patient has a PaO2 of 70 mm Hg while receiving 70% (0.7) FIO2, the ratio is 100, which is diagnostic for severe ARDS (Table 27.9). Table 27.8 Direct and Indirect Causes of ARDS Direct Injury Indirect Injury Aspiration Chest trauma Pneumonia (infectious or aspiration) Pulmonary contusion Inhalation injury (smoke; toxins) Pulmonary embolus Sepsis, shock Pancreatitis Burns Multiple blood transfusions; transfusion-related acute lung injury (TRALI) Cardiopulmonary bypass Drug/alcohol overdose ARDS, Acute respiratory distress syndrome. Table 27.9 ARDS Severity Level of ARDS PaO2/FIO2 Ratio Mortality Rate Mild ARDS 200--300 on ventilator settings that include positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥5 cm H2O 27% Moderate ARDS 100--200 on ventilator settings that include PEEP ≥5 cm H2O 32% Severe ARDS Less than 100 on ventilator settings that include PEEP ≥5 cm H2O 45% ARDS, Acute respiratory distress syndrome. There are three phases of ARDS: exudative, proliferative, and fibrotic. The exudative phase typically occurs within 24 to 48 hours after injury. In this phase, as a result of the activation and release of inflammatory mediators, there is a disruption of the ACM. The ACM becomes dilated due to the inflammatory mediators, and this disturbance allows fluid to move from the capillaries into the interstitial space and into the alveoli. The disruption of the ACM also allows protein to move from the vascular space. The presence of protein in the vascular space helps to maintain the colloid oncotic pressure. Loss of protein from the vascular space lessens the oncotic forces, worsening the movement of fluid into the alveoli. The alveolar and interstitial edema results in a severe V/Q mismatch, inadequate ventilation occurring in the face of adequate perfusion or blood flow, which results in hypoxemia; blood is shunted past the fluid-filled alveoli without being oxygenated. In addition to the alveolar and interstitial edema, there is damage to the alveolar cells that produce surfactant. Surfactant is responsible for maintaining alveolar surface tension. Alveolar surface tension keeps the alveoli from fully collapsing at the end of expiration. If alveolar surface tension is lost, then the alveoli collapse. This is referred to as atelectasis. Clinical manifestations in this phase include hyperventilation and tachycardia as a compensatory response to hypoxemia. ABGs reveal a respiratory alkalosis due to the hyperventilation. Cardiac output increases in an attempt to increase blood flow through the lungs. The chest x-ray reveals the increased alveolar fluid as bilateral infiltrates and is referred to as pulmonary edema. Unlike the pulmonary edema associated with a heart failure exacerbation (see Chapter 30), there is no evidence of increased left atrial or ventricular pressure, which would indicate left heart failure. This is referred to as noncardiogenic pulmonary edema. In the proliferative phase, neutrophils and other inflammatory mediators cross the damaged ACM and release toxic mediators that further damage both the alveolar and capillary epithelium. Diffusion defects result. The V/Q mismatch worsens, and pulmonary hypertension occurs because of locally occurring vasoconstriction in the lung caused by the hypoxemia. This results in right-sided heart failure due to the increase in PVR or high vascular pressures in the lung. Widespread fibrotic changes occur throughout the diseased lung tissue. The lungs become stiff and noncompliant, increasing the work of breathing. Clinical manifestations in this phase include hypercarbia and worsening hypoxemia. As the process continues, PaCO2 begins to rise despite hyperventilation. Increases in delivered oxygen do not alleviate the dropping PaO2 caused by the increasingly impaired oxygen exchange across the fluid-filled and damaged ACM. This is refractory hypoxemia, meaning that in spite of increasing oxygen delivery to the patient, the hypoxemia does not improve and will eventually worsen. Lung compliance continues to deteriorate, continuing to increase the work of breathing. If the patient is on a ventilator, peak inspiratory pressures rise because of decreased compliance within the lung, requiring more pressure to deliver ventilatory volume. In the fibrotic phase, there is diffuse fibrosis and scarring, resulting in greatly impaired gas exchange and compliance. Pulmonary hypertension worsens, as does the accompanying right-sided heart failure. Clinical manifestations in this phase include a decreased left-heart preload due to the right heart failure and reduced capacity of the right ventricle to deliver blood to the lungs and on to the left side of the heart. This results in decreased blood pressure and cardiac output. The severe V/Q mismatch, diffusion defects, and intrapulmonary shunting result in refractory hypoxemia. The overall result is severe tissue hypoxia and lactic acidosis. Connection Check 27.4 The pulmonary edema associated with ARDS is caused by A.  increased permeability of the ACM. B.  right ventricular failure with pulmonary hypertension. C.  left ventricular failure due to poor oxygenation. D.  fluid overload related to resuscitation in the first phase. Interprofessional Management Medical Management Diagnosis Imaging Studies The key imaging procedure to help identify and guide treatment for ARDS is the chest x-ray. During the early phases of ARDS, serial chest x-rays can be used to identify the bilateral infiltrates that are the hallmark sign of this disease process. This is sometimes described as a "ground-glass appearance" and is also characterized as a "snow-screen effect" or whiteout effect on the chest x-ray. Laboratory Testing Laboratory testing includes ABGs; complete blood count (CBC) with differential; sputum, blood, and urine cultures; coagulation studies; electrolyte panels; and liver function tests. ABGs initially show hypoxemia and hypocapnia as alveolar compromise develops. A CBC with differential is done to determine if the cause is infection. An abnormally high white blood cell count (above 10,000) is indicative of an infectious process. Sputum, blood, and urine cultures are used to determine the source of any infection. Comprehensive metabolic panels, coagulation studies, and liver and renal function tests may be used to determine the cause of ARDS but are also used to determine if the hypoxia from the disease process is affecting other body systems. In some cases of ARDS, there is a disruption of the normal clotting cascade, resulting in impaired fibrinolysis. This can result in disseminated intravascular coagulopathy, discussed in Chapter 14. Treatment Mechanical Ventilation Mechanical ventilation is the primary treatment for the refractory hypoxemia of ARDS. It is initiated as lung compliance decreases, work of breathing increases, and oxygenation continues to be refractory regardless of interventions such as NPPV and other oxygen therapies. There are several modes of ventilation used in ARDS. The most common is lung-protective ventilation using reduced tidal volumes and higher PEEP. Because of the loss of lung compliance, research has demonstrated that using lower tidal volumes---the volume of air moved with one breath, one inhalation and exhalation---with mechanical ventilation can help improve oxygenation while also reducing the occurrence of ventilator-induced lung injury (VILI), lung damage due to mechanical ventilation such as inflammatory-cell infiltrates, increased vascular permeability, pulmonary edema, and barotrauma such as alveolar rupture. The reduced tidal volumes result in hypercapnia, which is accepted as a side effect. Permissive hypercapnia, although not fully understood, has been demonstrated to have some protective effects for the lungs. Hypercapnia should be carefully monitored or avoided in a patient with increased intracranial pressure because it results in vasodilation, which increases cerebral blood flow and increases intracranial pressure. The use of a low tidal volume is combined with higher PEEP. This allows the alveoli to open and remain open while at the same time keeping peak airway pressures low. As discussed earlier, PEEP keeps the alveoli from collapsing, allowing maximum gas exchange to continue throughout the respiratory cycle. Other ventilatory modes sometimes used in the treatment of ARDS are high-frequency oscillating ventilation and airway pressure-release ventilation (APRV). High-frequency oscillating ventilation delivers very small tidal volumes at high frequencies. It avoids lung overdistention and VILI while facilitating alveoli recruitment. APRV utilizes an inverse inspiratory/expiratory ratio (longer inspiration than expiration) to facilitate oxygenation and gas exchange. It is a form of elevated or higher-than-baseline CPAP that has timed, regular, brief reductions in the set airway pressure or CPAP level. Oxygenation is supported during the timed, higher pressure. Removal of CO2 is facilitated during the timed reduction in pressure. This mode of ventilation allows for spontaneous breathing, reduces the need for sedation or neuromuscular blockade, and reduces VILI. A mode of oxygenation in ARDS that was studied heavily during the COVID-19 pandemic is HFNCs. There is much research testing this treatment in the early phase of ARDS and in mild ARDS as a form of noninvasive ventilation (NIV). In this form of oxygenation, high-flow oxygen is humified, warmed, and delivered through soft, wide-bore nasal prongs. The high flow rate results in a "washout" of nasopharyngeal dead space, optimizing alveolar ventilation, and also increases nasopharyngeal airway pressure, producing a CPAP effect. The use of HFNC can improve oxygenation, decrease the work of breathing, and decrease the risk of nosocomial infection associated with invasive ventilation modes. As with other forms of NIV, some studies have shown a failure rate as high as 40%, requiring intubation and mechanical ventilation, indicating more research is required. Another treatment to support gas exchange in severe ARDS is extracorporeal membrane oxygenation (ECMO). This technique uses a pump to circulate blood through an artificial lung outside of the body (extracorporeal), where oxygenation and CO2 removal takes place. Blood is then returned into the bloodstream. This is a very invasive form of therapy with many inherent risks and complications, but recent technological improvements have made it safer, increasing its use. More research is needed to determine more clearly what subset of patients will benefit from this therapy. Positioning Patient positioning can be utilized as an adjunctive therapy in ARDS---specifically, placing the patient in a prone position. The proning of a patient while on mechanical ventilation may improve oxygenation through increased recruitment of collapsed posterior alveolar units and reduction in the V/Q mismatch. Via gravity, blood flow is directed to the better-aerated anterior portion of the lungs. It is best used in patients with severe ARDS if other ventilator strategies have not been successful. Careful, well-planned teamwork is required to put a critically ill patient with many IV lines and tubes in a prone position successfully and safely (see Box 27.2 for a description of the care of a patient using prone positioning; also see Evidence-Based Practice: Awake Self-Proning). Box 27.2 The Use of Prone Positioning in the Patient With ARDS Benefits: Dorsal lung reexpansion with improved oxygenation Aiding in secretion and extravascular water distribution, which decreases stress on the soft tissues of the lung Improved lung recruitment---opens more alveoli, improving oxygenation Reducing the need for higher PEEP and FIO2, decreasing ventilator-induced lung injury (VILI) Overall effects reduce mortality in the ARDS patient Implementation: Should be implemented within 72 hours of diagnosis Up to 20 hours per day in the prone position is recommended for the best results Can be accomplished by manually turning the patient in bed or by using a mechanical device that can turn the patient as needed and place the patient in the Trendelenburg or reverse Trendelenburg position as needed Contraindications: Spine instability Conditions that increase intracranial pressure Pregnancy---possible adverse effects Abdominal wounds---possible adverse effects Unstable peripheral fractures or rib fractures---possible adverse effects Need for frequent airway access---possible adverse effects Nursing Considerations: Any change in baseline oxygenation parameters after proning should be cause for a new ABG determination. Eye and facial skin care must be an integral part of the patient's ongoing care, including eye lubricant and padding of areas of the face as required. Pressure injury and eye hemorrhage and edema with permanent vision loss are preventable complications of prone positioning. Sedation may be required due to patient anxiety during the process. Care should be taken when enteral feeds are administered while the patient is in the prone position to prevent aspiration. A post-pyloric feeding tube may be considered. Ensure all tubes are free of compromise during the proning procedure and evaluated frequently during the process. Have a plan in place for a rapid return to the supine position in the case of hemodynamic compromise or cardiac arrest. CPR may be started in the prone position understanding that a return to the supine position quickly is ideal for quality compressions Educate the family members on this process---including the pros and the cons---and answer all questions related to this treatment modality. ABG, Arterial blood gas; ARDS, acute respiratory distress syndrome; PEEP, positive end-expiratory pressure. Evidence-Based Practice Awake Self-Proning Prone positioning has been used for decades in patients with ARDS. The COVID-19 pandemic necessitated a spotlight on the care of respiratory failure in an attempt to prevent its transition to ARDS. Prone positioning is proven to enhance lung perfusion, support alveolar inflation, and improve clearance of secretions. Awake self-proning was utilized and studied during the COVID-19 pandemic showing improved oxygenation and patient comfort, which may have prevented ARDS and intubation and mechanical ventilation. Additional studies are needed to confirm this correlation. Seckel, M. A. (2021). Awake self-prone positioning and the evidence. Critical Care Nurse, 41(4), 76-79. Medications If the cause of ARDS is infection, antibiotics are administered, broad spectrum initially, then narrow spectrum after the causative pathogen is identified (Table 27.10). Corticosteroids are also used to decrease the inflammatory response, but their use for the treatment of a patient with ARDS is controversial. There is no evidence that the use of steroids improves mortality and morbidity, but the anti-inflammatory properties are thought to reduce the migration of white blood cells to the affected areas of the lung. There is also some research that shows that there are less fibrotic changes in the lung during the fibrotic phase of the process. On the negative side, the use of corticosteroids can blunt the body's inflammatory response, making the patient more susceptible to secondary infections. Research regarding steroid use in ARDS is ongoing. Neuromuscular blocking agents or paralytics are sometimes used when patients are mechanically ventilated. Neuromuscular blocking agents reduce the risk of barotrauma because they control patient--ventilator synchrony; the patient cannot take a breath out of sync with the ventilator. They also reduce oxygen demand by limiting muscle movement. If neuromuscular blocking agents are used, the patient must also receive pain and sedative medication to ensure optimum comfort during treatment (Table 27.11). As stated earlier, the patient can be managed with the judicious use of sedatives without the use of paralyzing medications if on APRV mechanical ventilation. Paralytic agents are most often used for patients with severe ARDS, and their use must be reevaluated daily for each patient. Fluid Management Fluid management is an important component in the care of a patient with ARDS. Adequate hydration is necessary to maintain circulatory volume and also avoid issues with thick, dry secretions that may be difficult to clear and potentially cause plugged airways. Conversely, ARDS in sepsis is caused by massive vasodilation and capillary leaking, which causes intravascular fluid to enter the lungs. Fluid resuscitation may exacerbate this phenomenon. Many cases of ARDS necessitate the use of diuretics to help shift fluid out of the lungs. Complicating the management of fluid balance is a decrease in venous return to the right side of the heart because of the increased intrathoracic pressure associated with the use of PEEP. This results in a decrease in cardiac output and systemic blood pressure, potentially requiring fluid resuscitation. If too much fluid is given, ARDS can worsen because of the increased permeability of the ACM. If an insufficient amount of fluid is administered, preload and blood pressure may decrease, resulting in decreased perfusion to the brain and other vital organs. The patient's urine output and hemodynamic volume status should be carefully monitored via a central venous or PA catheter. Hemodynamic monitoring is discussed in detail in Chapter 32. Table 27.10 Medications Used in the Treatment of ARDS Medication Classification Mechanism of Action Exemplars Nursing Implications Antibiotics Antibiotics may be broad spectrum (utilized for a diverse population of microbes) or targeted (for a specific microbe). If pneumonia is suspected, broad spectrum antibiotics will be initiated. Antibiotics will be targeted once culture results return, which takes a few days. Antibiotics in the intensive care setting are given IV piggyback. Vancomycin Piperacillin/Tazobactam (Zosyn) Doxycycline Maintain patent IV access Monitor fluid status Give antibiotics on time every time If possible, obtain cultures prior to administering antibiotics Be mindful of IV compatibility if using Y site for other agents Monitor for signs and symptoms of allergic reaction Monitor for signs and symptoms of skin reactions, like vancomycin flushing syndrome If using peripheral IV access, assess frequently for infiltration and extravasation DVT prophylaxis with unfractionated heparin or low-molecular-weight heparin (LMWH) The risk of venothromboembolism is high in patients in ARDS due to immobility and the body's increased inflammatory response to critical illness. Unfractionated or low-molecular-weight heparin is used prophylactically to interrupt the clotting cascade and lower the threshold for clot formation. Heparin Enoxaparin Initiate bleeding precautions Monitor for s/s bleeding Educate patient/family about bleeding risk, precautions, and s/s of bleeding Reversal agent: Protamine sulfate Rotate subcutaneous injection sites Glucocorticoids Glucocorticoids are used in patients with refractory ARDS (not responsive to aggressive therapies and lung-protective ventilation). Critical illness often results in adrenal fatigue as a result of the massive inflammatory response. Glucocorticoids suppress cell-mediated immunity, meaning they suppress the body's massive inflammatory response to critical illness. Methylprednisolone IV push Dexamethasone IV push Give each dose on time and as ordered Do not stop glucocorticoids abruptly Once therapy is no longer needed, the dose will be tapered, not stopped abruptly Maintain patent IV access Monitor blood pressure and hemodynamic status on initiation and throughout therapy Insulin May be given subcutaneously or in a continuous infusion. Insulin brings glucose into the cells to aid in metabolism. Patients experiencing critical illness often develop insulin resistance even if they do not have a medical history of diabetes. Insulin Monitor blood glucose as ordered Monitor for signs and symptoms of hypoglycemia Maintain patent IV access Rotate subcutaneous injection sites Table 27.11 Medications Used When Sedation and/or Paralysis Are Utilized in the Treatment of a Mechanically Ventilated Patient Medication Classification Mechanism of Action Exemplars Nursing Implications Opioids   Opioids inhibit neurotransmitter release. The most common opioid used in the intensive care setting for sedation is fentanyl, which is a µ-opioid receptor agonist. Fentanyl is 100 times more potent than morphine and has a short half-life, which allows a large effect with a smaller volume while also being able to lose its effect quickly when pausing the drug, for example, if the team needs to perform a neurologic exam. Fentanyl is preferred in ARDS because it decreases the response to carbon dioxide, which promotes ventilator synchrony. Fentanyl continuous IV or IV push Maintain assessment of sedation status using the RASS scale Only sedate the patient as ordered Only deeply sedate a patient who is on a ventilator Reversal agent: naloxone (Narcan) Fentanyl may lower blood pressure High doses may cause chest wall rigidity Benzodiazepines The most common benzodiazepine used in the critical care setting is midazolam. Midazolam is a γ-aminobutyric acid A (GABA-A) receptor agonist which results in sedation, anxiolysis, and amnesia. Midazolam (versed) Lorazepam (ativan) Can be given continuous or IV push, per order Maintain patent IV access Maintain assessment of sedation status using the RASS scale Only sedate the patient as ordered Only deeply sedate a patient who is on a ventilator May lower blood pressure Reversal agent: Flumazenil General systemic anesthetics Propofol induces deep sleep and sedation by enhancing inhibitory function of GABA-A receptors. Propofol Given continuous IV infusion Give only as ordered and be aware most states do not allow RNs to give propofol IV push -- know the nurse practice act in your state Maintain patent IV access Maintain assessment of sedation status using the RASS scale Propofol should not be initiated or maintained unless a patient is on a ventilator -- this drug can cause apnea Can cause profound hypotension Very short half life -- patients begin waking up within minutes of pausing the drug Monitor cholesterol and lipid levels Monitor kidney function Sedatives Activates 2-adrenoceptors, decreasing sympathetic tone. Precedex induces sedation and anxiolysis while maintaining arouseability decreasing the incidence of delirium. Dexmedetomidine (precedex) Given continuous IV infusion Maintain patent IV access Maintain assessment of sedation status using the RASS scale Monitor heart rate -- can cause profound bradycardia Titrated every 30 minutes and can take a few hours to reach a therapeutic effect Neuromuscular blocking agents   NMBAs paralyze skeletal muscles by blocking the transmission of nerve impulses at the myoneural junction. Succinylcholine Vecuronium Rocuronium Can be given IV push or continuous IV infusion Maintain patent IV access Ensure the patient is appropriately sedated prior to initiation Ensure the patient is on a ventilator with a ventilator-controlled respiratory rate prior to administration Monitor SpO2 and ETCO2 Nutrition Adequate nutrition is a very important component of care for a critically ill patient with ARDS. ARDS is associated with a proinflammatory, hypermetabolic state. Without adequate nutrition, malnutrition, loss of body mass, and reduced respiratory muscle strength can result. Enteral (nasogastric tube feedings through the gastrointestinal \[GI\] tract) or parenteral (IV nutrition via a peripheral or central venous catheter) nutrition should be initiated within 48 to 72 hours of the initiation of mechanical ventilation. Enteral nutrition is the preferred method unless contraindicated because of GI issues. Both have risks associated with them. Tube feedings are associated with aspiration, so care must be given to ensure that the feeding tube is properly placed, the head of the bed is elevated, and the tube feeding is turned off during those times when the patient is completely supine. Parenteral nutrition may be associated with increased infections via the venous catheter. Complications Ventilator-Associated Events (VAE) A complication that occurs as a result of being on the ventilator is called a ventilator-associated event. These complications are identified through the need for sustained ventilatory support after periods of stable or decreasing support. They may be infectious, an infection-related ventilator-associated complication (IVAC), or a noninfectious ventilator-associated complication (VAC). Pneumonia, sometimes referred to as ventilator-associated pneumonia (VAP), is an infectious complication. Atelectasis and the risk of high volume and pressure problems associated with mandatory modes of ventilation combined with poor lung compliance are examples of noninfectious complications (see Evidence-Based Practice: Preventing Ventilator-Associated Events). Infection-Related Ventilator-Associated Complication --- Pneumonia When a patient has an artificial airway in place, normal mechanisms to protect the patient from pneumonia are compromised. The primary risks for pneumonia include the inability of the epiglottis to close and the potential drying out of the trachea and upper airways. Pneumonia is difficult to detect when a patient is already ventilated because of ARDS, but there are some assessment findings that indicate its occurrence. Development of fever, leukocytosis, increased respiratory effort, and purulent secretions are hallmark signs of pneumonia. Sputum cultures will indicate infection. The earlier pneumonia is diagnosed, the earlier it can be treated. Pneumonia can be prevented by instituting some basic preventive techniques, such as regular mouth care. Suctioning of the ETT must be performed routinely as needed, as well as oropharyngeal suctioning to remove secretions from the mouth and throat. The ventilator circuit should be changed per hospital protocol, and care must be taken to avoid water buildup in the circuit. Sterile water should be used for the humidification of the air being delivered to the patient. Noninfectious Ventilator-Associated Complication --- Barotrauma Another common VAC is barotrauma. ARDS results in a stiffening of the lungs and a loss of compliance (elasticity), requiring careful application of tidal volume and PEEP to maximize oxygenation without causing volume and pressure problems or barotrauma. Barotrauma is when the alveoli rupture due to increased intrathoracic pressure. Alveolar or lung rupture, may result in pneumomediastinum (air in the mediastinal space) or pneumothorax (air in the pleural space), causing further hypoxemia. The nurse's assessment and interventions are crucial in preventing barotrauma. Peak pressures on the ventilator should be continuously monitored. Suctioning in ARDS should be done judiciously (only as needed) as any disruption in pressure can lead to barotrauma. Low-tidal volume protective lung ventilation is managed and monitored astutely with serial ABGs and measurement of plateau pressure to provide ventilation while protecting the fragile lung parenchyma. Sedation and paralysis should be maintained per order to promote ventilator synchrony. Evidence-Based Practice Preventing Ventilator-Associated Events The recommendations to prevent VAE are categorized as essential or additional in the updated 2022 guidelines Essential: Avoid intubation if possible; consider HFNC Daily toothbrushing Perform daily spontaneous awakening trials in an effort to evaluate the patient and minimize sedation Additional: Utilize ETT with subglottis secretion drainage: (reclassified from essential) ETTs with an extra port above the inflated cuff that is connected to low continuous suctioning. This prevents secretions that sit above the cuff from becoming infected with bacteria and then oozing down around the cuff into the airway, infecting the airway. Consider postpyloric rather than gastric feeding Consider early tracheostomy Klompas, M., Branson, R., Cawcutt, K., Crist, M., Eichenwald, E. C., Greene, L. R.,... & Berenholtz, S. M. (2022). Strategies to prevent ventilator-associated pneumonia, ventilator-associated events, and nonventilator hospital-acquired pneumonia in acute-care hospitals: 2022 Update. Infection control and hospital epidemiology, 43(6), 687-713. Renal Failure/Multisystem Organ-Dysfunction Syndrome Renal failure is a frequent complication of ARDS due to hypotension and the use of nephrotoxic medications to treat infection. It also may indicate the progression of ARDS to multisystem organ-dysfunction syndrome (MODS). MODS results from prolonged refractory hypoxemia, hemodynamic instability, and the inflammation associated with sepsis. MODS is discussed in detail in Chapter 14. Nursing Management Assessment and Analysis The clinical manifestations of ARDS are due to the refractory hypoxemia, pulmonary edema, and lung parenchymal damage. The patient's increased work of breathing, evidenced by dyspnea, tachypnea, and accessory muscle use, may be the first indication present. Auscultation of breath sounds reveals crackles associated with pulmonary edema. Later, breath sounds may be diminished or absent because of the fibrotic lung changes and atelectasis. Anxiety and agitation may result from hypoxemia. The SpO2 continues to decrease despite increasing FIO2 levels. Initially, the ABGs demonstrate respiratory alkalosis due to hyperventilation. Later, respiratory acidosis develops. Nursing Diagnoses/Problem List Impaired gas exchange related to disrupted pulmonary function as evidenced by increased work of breathing, refractory hypoxemia, and increased oxygen demand Anxiety related to hypoxemia, lack of cerebral perfusion, and loss of personal control Imbalanced nutrition, less than body requirements, related to increased metabolic demand Nursing Interventions Assessments Hemodynamic monitoring Vital signs The pulse increases because of hypoxemia; this is a compensatory mechanism of the sympathetic nervous system in an attempt to increase oxygenation. The respiratory rate increases also in an attempt to increase oxygenation. Blood pressure may be decreased because of right-side heart failure and the increased intrathoracic pressure, thus the decreased venous return associated with PEEP. SpO2/pulse oximetry The pulse oximetry reading may be low because of the V/Q mismatch and intrapulmonary shunting. Central venous pressure (CVP) or pulmonary artery (PA) pressure monitoring The CVP or PA pressure may be variable. They may be decreased because of the decreased venous return related to increased intrathoracic pressure. They may also be increased due to increased vasoconstriction in the lung. Neurologic assessment: level of consciousness (LOC) and pupillary assessment The patient with ARDS is at risk for neurological compromise due to the refractory hypoxemia and potential increase in PaCO2 that can result in cerebral vasodilation. Frequent checks are necessary, especially if the patient is heavily sedated and chemically paralyzed or has a decreased ability to communicate due to intubation and mechanical ventilation. Sedation Regularly assess sedation using a standardized tool, like the Richmond Agitation-Sedation Scale (RASS) to promote ventilator synchrony and patient comfort and to help manage sedative medication. Lung sounds Crackles may be auscultated because of fluid buildup in the alveoli due to increased capillary permeability. Later, they may be diminished because of atelectasis and fibrotic changes in the lungs. Quantity and quality of airway secretions Airway secretions may be thick or thin, possibly indicating infection or fluid overload, respectively. A change in amount or quality of secretions may indicate a change in condition and should be reported to the provider. Monitor urine output. A decreased urine output is an early sign of poor oxygen delivery to the tissues and shock. Monitor mechanical ventilation. Frequent monitoring of airway pressure on the ventilator is vital. Increases in airway pressure may indicate the presence of secretions or worsening lung compliance. Decreases in airway pressure may indicate a leak in the system. Consistent high airway pressure may lead to barotrauma. Coordinate with the respiratory therapist to frequently monitor plateau pressure, which is used to guide treatment. Continuous cardiac monitoring and ECG. Hypoxemia can lead to cardiac dysrhythmias. Laboratory tests ABGs Initially, hypoxemia and respiratory alkalosis secondary to poor gas exchange and hyperventilation are present. Later, respiratory acidosis may occur because of increased PaCO2 levels and the permissive hypercapnia of low-tidal-volume ventilation. Later, metabolic acidosis may be present because of worsening hypoxemia and decreased oxygen delivery to the tissues, signaling the transition to anaerobic metabolism. Frequent, timely ABGs are collected to determine the P/F ratio and guide treatment. Serum lactate level Increased serum lactate confirms anaerobic metabolism. Liver/renal function blood tests Abnormal renal and liver values indicate the progression of ARDS to MODS. Blood/sputum cultures/CBC Positive cultures may indicate the cause of ARDS. Later, positive cultures may be present because of complications associated with critical illness, such as indwelling lines and catheters or VAP. A CBC indicating an increased white blood cell count is another indicator of infection. Basic metabolic panel and electrolytes Critical illness results in many fluid and electrolyte shifts that require frequent, timely management. This is especially true for intracellular ions like potassium and magnesium. These electrolytes are often replaced using a nurse-driven protocol. Skin assessment Patients are at increased risk for skin breakdown due to immobility, hypoxemia/hypoxia, hypermetabolic state, and hemodynamic changes. Chest x-ray Daily chest x-rays are done to monitor the progression or improvement of ARDS. Actions Airway suctioning when indicated by the presence of secretions to ensure that the ETT is clear The ETT must remain clear of secretions to facilitate the delivery of ventilatory volume; increased secretions require increased pressure to deliver the preset volume or may actually block the ETT. Secretions are also a source of infection. Care should be made to coordinate ETT assessment and suctioning with the respiratory therapist. Suctioning should occur as needed, as unnecessary suctioning can lead to barotrauma and harm the patient. Medication administration Administer paralytic agents, analgesics, and sedative medications as ordered. Allows for maximum patient comfort during mechanical ventilation. Respiratory effort and patient--ventilator synchrony must be optimized to avoid barotrauma. Administer inotropic/vasoactive agents as ordered. Inotropic medications are used to augment cardiac output; vasoactive medications may be necessary to support blood pressure. Administer antibiotics as ordered. Antibiotics are necessary to treat infection if that is the cause or a complication of the critical illness. Patient positioning/activity Placing the patient in the prone position---proning Proning allows for better oxygenation and alveolar recruitment. Proning increases the recruitment of collapsed posterior alveolar units and reduces the V/Q mismatch via gravity as blood flow is directed to the better-aerated anterior portion of the lungs. Elevate the head of the bed. Elevating the head of the bed allows for better lung expansion and reduces the risk of aspiration. Frequent position changes Frequent changes of position help prevent skin breakdown. Range-of-motion (ROM) exercises Range-of-motion exercises are necessary in the sedated or medically paralyzed bed-bound patient to preserve limb functioning and decrease the incidence of contracture (severe joint stiffness). Infection protection/prevention Hand washing Hand washing is the number one intervention in the effort to prevent infection. Monitoring and care of central IV lines Central lines are a significant source of infection. Maintenance of strict sterile technique on insertion is key to infection prevention. Routine monitoring for redness or drainage at the insertion site, dressing changes per hospital protocol, IV tubing changes per hospital protocol, and evaluation of the continued need for many invasive lines are also key to preventing central line infection. Foley catheter care Increased risk for iatrogenic infections such as urinary tract infection (due to Foley catheter) requires routine Foley catheter care and evaluation of necessity of continued use. Diligent mouth care Increased risk for VAP due to intubation requires mouth care every 2 hours, which includes brushing teeth at least daily. The use of chlorhexidine (previously encouraged) is no longer recommended. Teaching Disease process The patient and the patient's support system should understand the pathophysiology of ARDS, the severity of the disease, and the treatment required. Understanding the medications, invasive lines, and mechanical ventilation may help decrease anxiety and provide some sense of control. Providing time for visiting as possible may help the family stay engaged and involved in the family member's care. Visiting also provides tremendous support for the patient. Evaluating Care Outcomes Successful treatment of a patient with ARDS should be considered a victory because of the high mortality rate. The optimal outcome for a patient with ARDS is to return to baseline respiratory function and a return to a lifestyle similar to that prior to the illness. Ideally, there are no long-term respiratory issues, but in reality, ARDS can do significant damage to the lungs and thereby impacts the patient's life post-discharge. Some patients do continue to live with chronic pulmonary fibrosis after surviving ARDS. The incidence of this is currently unknown following the COVID-19 pandemic. The physical weakness, early fatigue, and change in lifestyle can take a tremendous toll on the patient. Helping the patient mentally adjust to any residual physical limitations is something that should be stressed for both family members and the healthcare team. Depression and post-traumatic stress disorder after critical illness for the patient and the family is common but not well studied or documented. Mental healthcare may be required. Consistent medical follow-up and a realistic rehabilitation regimen maximize the patient's recovery. CHEST TRAUMA Epidemiology Thoracic (chest) trauma accounts for approximately 16,000 deaths annually. Thoracic trauma is the direct cause in 20% to 25% of all trauma-related deaths and is a contributory cause for an additional 20% to 25% of deaths. MVCs are the most prevalent cause of thoracic injuries seen in emergency departments and trauma centers. In 2016, there were 34,439 MVCs resulting in fatality, with an overall number of 37,461 fatalities. These numbers have been decreasing over the past few years, most likely because of the increase in air bags in new cars and the improvement in car manufacturing to decrease crash fatalities. Older drivers (greater than 60 years of age) are more susceptible to injury. Other risk factors for injury include rate of speed, size of the vehicle, and seat belt use or lack thereof. At speeds greater than 25 miles per hour, the vehicle's occupants are more likely to be injured. At greater speeds, driver reaction time is increased, meaning it takes longer to process and react to danger; there is a greater collision impact and a higher chance that objects may enter the passenger compartment on impact. This is called intrusion and can cause injury secondary to the collision. In a vehicle-to-vehicle collision, a smaller car provides limited protection, especially if struck by a larger vehicle. Finally, not wearing a seat belt puts drivers and passengers at risk of injury because of the collision with hard surfaces in the car, such as the dash, steering wheel, or windshield. Pathophysiology Chest trauma is divided into two types: blunt-force and penetrating trauma. Blunt chest trauma is the result of a blunt object hitting the chest or the chest striking a blunt surface such as a steering wheel, seat belt, or air bag. Blunt-force injuries can be further characterized as acceleration or deceleration injuries. Deceleration is when the movement of the body is suddenly stopped, but the internal organs remain in motion and collide with the chest wall. Acceleration injury occurs when the body is abruptly set in motion (rear-end collisions) or when the body is hit by a rapidly moving object. When either occurs, chest organs and tissues are subject to impact and shearing forces. Blunt-force trauma is more diffuse than penetrating trauma and may cause injuries that may not be obvious at the time of initial assessment. Penetrating trauma is the result of sharp objects such as knives or bullets entering the chest and causing damage to internal structures or organs. Other causes of penetrating injury are objects that enter a motor vehicle during a collision (intrusion) or shrapnel from explosions. The depth, angle, and location of the penetration can differentiate whether the penetrating trauma is a superficial wound or is potentially life-threatening. A gunshot wound into the lateral right chest, missing all major vessels, may be superficial. A gunshot wound to the middle of the left chest is life-threatening. Common injuries as a result of chest trauma occur within the thoracic cavity and may include the heart, lungs, or vessels. This includes fractured ribs, pneumothorax, hemothorax, cardiac contusion, and cardiac tamponade. Fractured ribs are the most common injury associated with chest trauma. Normal chest wall movement---the diaphragm moving downward and the external intercostal muscles moving the rib cage up and outward---assists in generating the negative pressure required for inspiration and effective ventilation. When ribs are fractured, the integrity of the entire thorax and chest-wall movement are compromised. The patient cannot take deep, effective breaths, largely because of pain, effectively limiting the ability to maintain normal tidal volumes with each breath. Also, depending on the location of the rib fractures, there may be collateral penetrating damage to organs and vessels located near the site of injury, such as the liver. A flail chest is defined as three or more adjacent ribs that have been fractured in two or more places as a result of blunt or crush chest trauma, resulting in a "free" segment of the ribs. "Paradoxical" chest-wall movement is the hallmark sign associated with a flail chest. With each inhalation, the damaged area moves inward; on exhalation, this section of the chest wall moves outward (Fig. 27.4). As with rib fractures, chest-wall movement is compromised largely because of pain and may result in respiratory insufficiency. The severity of the injury and the treatment are determined by the extent of the underlying lung injury or contusion more so than by the fractures themselves. FIGURE 27.4 Flail chest. Paradoxical chest wall movement; on inhalation, the damaged area moves inward; on exhalation, the damaged area moves outward. A pneumothorax may result from severe blunt or penetrating chest trauma. Typically penetrating chest trauma results in an open pneumothorax. Blunt chest trauma may result in a closed or open pneumothorax. Both cause a disruption of the integrity of the lung parenchyma (Fig. 27.5). Pneumothorax is defined as the collection of air in the pleural space. A normal lung inflates during inspiration because of negative thoracic pressure in relationship to atmospheric pressure. As the diaphragm descends, the lung expands; air enters the airways and eventually fills the alveoli via the terminal bronchioles. When a pneumothorax occurs, there is a reduction in the negative thoracic pressure because of the presence of air in the pleural space. This makes inspiration more difficult, and the lung cannot adequately expand. This results in a reduction of gas exchange at the alveolar level, resulting in hypoxemia. FIGURE 27.5 Pneumothorax. There is a reduction in the negative thoracic pressure because of air in the pleural space, resulting in an inability of the lung to fully expand. This is due to either a closed (blunt chest trauma) or open (penetrating or blunt chest trauma) injury. A, Closed pneumothorax. B, Open pneumothorax. Different from a pneumothorax, a hemothorax is the presence of blood in the pleural space. It occurs if there has been a laceration of a pulmonary vessel with blunt or penetrating trauma. A hemothorax may result in two problems for the patient. As with pneumothorax, as blood fills the pleural space, the negative pressure is lost, limiting the lung's ability to expand. Second, the loss of blood from the vascular space may result in hemodynamic compromise. Drainage greater than 1,500 mL is considered massive, and the patient may become hemodynamically unstable. Clinical Manifestations With all chest trauma, clinical manifestations may include decreased oxygenation and ventilation. The patient will become tachypneic in an attempt to improve oxygenation. Because of the inability to fully inflate the lungs, gas exchange is compromised, resulting in decreased oxygenation. Initially, hyperventilation occurs in an effort to increase oxygen availabilit