Learning Material on Responses to Altered Ventilatory Function PDF

1 MMSU-CHS-Department of Nursing RESPONSES TO ALTERED VENTILATORY FUNCTIONS This chapter covers nursing management to a critically ill patient that affects the body’s ventilatory function. It contains relevant assessment techniques and findings...

1 MMSU-CHS-Department of Nursing RESPONSES TO ALTERED VENTILATORY FUNCTIONS This chapter covers nursing management to a critically ill patient that affects the body’s ventilatory function. It contains relevant assessment techniques and findings that will be useful in identifying nursing interventions that focuses on the emergency relief and prevention of potential complications. ASSESSMENT FOR THE HIGH-RISK RESPIRATORY PATIENT I. HISTORY AND INTERVIEW The clinical history of the respiratory system is divided into six Keep in Mind. components: (1) chief complaint, (2) history of present illness, Build your patient’s health history (3) past health history, (4) family history, (5) personal and social by asking short, open-ended history, and (6) review of systems. questions. Conduct the interview in several short sessions if you Begin by asking why your patient is seeking care. Because many have to, depending on the severity of your patient’s respiratory disorders are chronic, ask how the patient’s latest condition. Ask his family to acute episode compares with previous episodes and what relief provide information, if your measures are helpful and unhelpful. patient can’t. The patient’s history starts with the chief complaint and information about the present illness. Often, if the patient is very ill, a relative or friend provides more information. Data about the present illness and any symptoms are thoroughly investigated using the mnemonic NOPQRST (image on the left) Focused Health History Subjective information about the respiratory history can be taken from the patient if they are awake, or from other sources (e.g. family, caregivers, or patient notes). Principal symptoms that should be investigated in more detail commonly include dyspnea, chest pain, sputum production, and cough, shortness of breath, wheezing, chest pain and sleep disturbance. An overview of the patient’s past medical history and family’s respiratory history, as well as personal and social history, may uncover elements that are contributing to the patient’s current health problem. II. PHYSICAL ASSESSMENT In most cases, you should begin the physical examination after you take the patient’s history. However, you may not be able to take a complete history if the patient develops an ominous sign such as acute respiratory distress. If your patient is in respiratory distress, establish the priorities of your nursing assessment, progressing from the most critical factors (airway, breathing, and circulation [the ABCs]) to less critical factors. 2 MMSU-CHS-Department of Nursing Physical assessment of the respiratory system is a reliable means of gathering essential data and is guided by the information obtained through the history. A thorough physical assessment includes inspection, palpation, percussion, and auscultation. Recall your previous subjects. III. RESPIRATORY MONITORING Specific respiratory monitoring may be indicated during the care of a critically ill patient. An understanding of the indications and practices associated with these monitoring devices will ensure accuracy of the results. In addition to the respiratory monitoring described in this section, the following systems will provide further support for the respiratory assessment and care of the patient: chest X-ray, mechanical ventilation waveform analysis and blood gas analysis a. PULSE OXIMETRY: This provides continuous, non-invasive measurement of oxygen saturation in arterial blood (SpO2 ). Pulse oximetry is used to assess for hypoxemia, to detect variations from the patient’s oxygenation baseline (e.g. due to procedures or activity level), and to support the use of oxygen therapy. Nursing Alert Pulse oximetry measures the oxygen content bound to haemoglobin, not the oxygen content dissolved in the blood. It also does not identify whether the patient is making any respiratory effort, oxygen consumption, or carbon dioxide retention. b. ARTERIAL BLOOD GAS (ABG) ANALYSIS Arterial blood gas (ABG) monitoring is frequently performed in critically ill patients to assess acid- base balance, ventilation, and oxygenation. Here’s a summary of commonly assessed ABG values and what the findings indicate: ✓ pH measurement of the hydrogen ion (H+) concentration is an indication of the blood’s acidity or alkalinity. ✓ Partial pressure of arterial carbon dioxide (Paco2) reflects the adequacy of ventilation of the lungs. ✓ Pao2 reflects the body’s ability to pick up oxygen from the lungs. ✓ Bicarbonate (HCO3 – ) level reflects the activity of the kidneys in retaining or excreting bicarbonate. ✓ Oxygen saturation (Sao2) is the percentage of hemoglobin saturated with oxygen at the time of measurement. c. CAPNOGRAPHY / END TIDAL CARBON DIOXIDE (ETCO2) MONITORING End-tidal carbon dioxide (ETCO2) monitoring measures the level of carbon dioxide at the end of Because ETCO2 exhalation. ETCO2 values are obtained by monitoring samples of provides continuous expired gas from an endotracheal tube, an oral airway, or a estimates of alveolar nasopharyngeal airway. ventilation, its measurement is useful The exhaled carbon dioxide waveform is displayed on the monitor as a for monitoring the patient plot of ETCO2 versus time called a capnogram, which provides the nurse during weaning from a with a continuous graphic reading of the patient’s ETCO2 level with each ventilator, in exhaled breath. cardiopulmonary resuscitation, and in endotracheal intubation 3 MMSU-CHS-Department of Nursing Changes in the waveform indicate clinical abnormalities, mechanical abnormalities, or both and require immediate assessment by the nurse or other trained professional. On a capnogram, the waveform is composed of four phases, each one representing a specific part of the respiratory cycle. 1. The first phase is the baseline phase, which represents both the inspiratory phase and the very beginning of the expiratory phase, when carbon dioxide–free air in the anatomical dead space is exhaled. This value should be zero or negligible in a healthy adult. pling device dead space. However, if the CO2 level is significant this indicates re-breathing of exhaled gas. The commonest causes are failure of the expiratory valve to open during mechanical ventilation, or an inadequate amount of fresh gas in the reservoir of a non-rebreathing face mask. 2. The second phase is the expiratory upstroke, which represents the exhalation of carbon dioxide from the lungs. Any process that delays the delivery of carbon dioxide from the patient’s lungs to the detector prolongs the expiratory upstroke. Conditions such as COPD and bronchospasm are known physiological causes of prolonged expiratory upstroke. Mechanical obstructions, such as kinked ventilator tubing, may also cause prolonged expiratory upstroke. 3. The third phase begins as carbon dioxide elimination rapidly continues; a plateau on the capnogram indicates the exhalation of alveolar gases (AKA alveolar plateau). The ETCO2 is the value generated at the very end of exhalation, indicating the amount of carbon dioxide exhaled from the least ventilated alveoli. 4. The fourth phase is known as the inspiratory downstroke. The downward deflection of the waveform is caused by the washout of carbon dioxide that occurs in the presence of the oxygen influx during inspiration. IV. RESPIRATORY DIAGNOSTIC STUDIES ✓ Chest radiography This is an essential noninvasive diagnostic tool for evaluating respiratory disorders, infiltration, and abnormal lung shadows, as well as identifying foreign bodies. Chest x-rays in critical care settings are also used to check and monitor the effectiveness and placement of tubes and lines such as an endotracheal tubes, chest tubes, and pulmonary artery lines. Normal lung fields appear black because they are air-filled spaces. Thin, wispy white streaks are seen as vascular markings. Blood vessels can also appear gray. However, grayness in the lung fields usually suggests pleural effusion. Light white areas indicate fluid, blood, or exudate. VENTILATION–PERFUSION SCANNING Ventilation–perfusion scanning is a nuclear imaging test used to evaluate a suspected alteration in the ventilation– perfusion relationship. A ventilation– perfusion scan is helpful in detecting the percentage of each lung that is functioning normally, diagnosing and locating pulmonary emboli, and assessing the pulmonary vascular supply. 4 MMSU-CHS-Department of Nursing V scans aren’t The ventilation–perfusion scan consists of two parts: a ventilation scan commonly used for and a perfusion scan. In the ventilation scan, the patient inhales patients on mechanical radioactive gas, which follows the same pathway as air in normal ventilators because the breathing. In pathological conditions, the diminished areas of ventilation ventilation portion of the are visible on the scan. In the perfusion scan, a radioisotope is injected test is difficult to perform. (Pulmonary intravenously, enabling visualization of the blood supply to the lungs. angiography is the When a pulmonary embolus is present, the blood supply beyond the preferred test for a embolus is restricted, revealing poor or no visualization of the affected critically ill patient with a area suspected pulmonary embolus.) You may recall your previous subjects in studying these other tests. ✓ Pulmonary angiogram ✓ Sputum culture ✓ Bronchoscopy ✓ Pulmonary function test (PFTs) ✓ Thoracentesis PNEUMOTHORAX ▪ Pneumothorax occurs when the parietal or visceral pleura is breached and the pleural space is exposed to positive atmospheric pressure. ▪ Hemothorax is the collection of blood in the chest cavity because of torn intercostal vessels or laceration of the lungs injured through trauma. ▪ Hemopneumothorax occurs when both blood and air are found in the chest cavity. Types of Pneumothorax 1. Simple Pneumothorax ▪ It occurs when air enters the pleural space through a breach of either the parietal or visceral pleura. o Most commonly this occurs as air enters the pleural space through the rupture of a bleb or a bronchopleural fistula. 2. Traumatic Pneumothorax ▪ It occurs when air escapes from a laceration in the lung itself and enters the pleural space or from a wound in the chest wall. o It may result from blunt trauma (eg, rib fractures), penetrating chest or abdominal trauma (eg, stab wounds or gunshot wounds), or diaphragmatic tears. o It may also occur during invasive thoracic procedures (ie, thoracentesis, transbronchial lung biopsy, insertion of a subclavian line) in which the pleura is inadvertently punctured, or with barotrauma from mechanical ventilation. 5 MMSU-CHS-Department of Nursing ▪ Open pneumothorax is one form of traumatic pneumothorax. It occurs when a wound in the chest wall is large enough to allow air to pass freely in and out of the thoracic cavity with each attempted respiration. ▪ Traumatic open pneumothorax calls for emergency interventions. Stopping the flow of air through the opening in the chest wall is a life-saving measure. 3. Tension Pneumothorax ▪ It occurs when air is drawn into the pleural space from a lacerated lung or through a small hole in the chest wall; and is trapped with each breath. ▪ It may be a complication of other types of pneumothorax. o Tension builds up in the pleural space, causing lung collapse. o Mediastinal shift (shift of the heart and great vessels and trachea toward the unaffected side of the chest) is a life-threatening medical emergency. o Both respiratory and circulatory functions are compromised. Clinical Manifestations ▪ Sudden pleuritic pain ▪ Minimal respiratory distress with small pneumothorax; acute respiratory distress if large. ▪ The patient may have only minimal respiratory distress with slight chest discomfort and tachypnea with a small simple or uncomplicated pneumothorax. If the pneumothorax is large and the lung collapses totally, acute respiratory distress occurs. ▪ Anxiety, dyspnea, air hunger, use of accessory muscles, and central cyanosis (with severe hypoxemia). ▪ In a simple pneumothorax, the trachea is midline, expansion of the chest is decreased, breath sounds may be diminished, and percussion of the chest may reveal normal sounds or hyperresonance depending on the size of the pneumothorax. ▪ In a tension pneumothorax, the trachea is shifted away from the affected side, chest expansion may be decreased or fixed in a hyperexpansion state, breath sounds are diminished or absent, and percussion to the affected side is hyperresonant. Diagnostic Tests ▪ Chest x-ray (color will be blacker than black), computed tomography (CT), or ultrasound will indicate presence of fluid buildup causing a pneumothorax. ▪ ABGs will indicate a respiratory alkalosis if the patient is in the early stages and a respiratory acidosis if the patient develops hypercarbia (later). 6 MMSU-CHS-Department of Nursing Medical Management o The goal is evacuation of air or blood from the pleural space. ▪ A small chest tube is inserted near the second intercostal space for a pneumothorax. o This space is used because it is the thinnest part of the chest wall, minimizes the danger of contacting the thoracic nerve, and leaves a less visible scar. ▪ A large-diameter chest tube is inserted, usually in the fourth or fifth intercostal space, for hemothorax. ▪ Autotransfusion is begun if excessive bleeding from chest tube occurs. ▪ For traumatic open pneumothorax: o Anything may be used that is large enough to fill the chest wound—a towel, a handkerchief, or the heel of the hand. o In the hospital, the opening is plugged by sealing it with gauze impregnated with petrolatum. o If conscious, patient is asked to inhale and strain against a closed glottis to eject air from the thorax. o The pleural cavity can be decompressed by needle aspiration (thoracentesis) o Chest tube drainage of the blood or air. o Antibiotics to combat infection from contamination. o Thoracotomy if more than 1,500 mL of blood is aspirated initially by thoracentesis (or is the initial chest tube output) or if chest tube output continues at greater than 200 mL/h. ▪ For tension pneumothorax: o High concentration of supplemental oxygen to treat the hypoxemia o Pulse oximetry should be used to monitor oxygen saturation. o In an emergency situation, a tension pneumothorax can be decompressed or quickly converted to a simple pneumothorax by inserting a large-bore needle (14-gauge) at the second intercostal space, midclavicular line on the affected side. o A chest tube is then inserted and connected to suction to remove the remaining air and fluid, reestablish the negative pressure, and re-expand the lung. Nursing Management ▪ Promote early detection through assessment and identification of high-risk population; report symptoms. ▪ Assist in chest tube insertion; maintain chest drainage or water-seal. ▪ Monitor respiratory status and re-expansion of lung, with interventions (pulmonary support) performed in collaboration with other health care professionals (eg, physician, respiratory therapist, physical therapist). ▪ Provide information and emotional support to patient and family. 7 MMSU-CHS-Department of Nursing PULMONARY EMBOLISM ▪ It refers to the obstruction of the pulmonary artery or one of its branches by a thrombus (or thrombi) that originates somewhere in the venous system or in the right side of the heart. ▪ Gas exchange is impaired in the lung mass supplied by the obstructed vessel. ▪ Massive PE is a life-threatening emergency; death commonly occurs within 1 hour after the onset of symptoms. ▪ Most thrombi originate in the deep veins of the legs. Risk Factors ▪ Venous Stasis (slowing of blood flow in veins) o Prolonged immobilization (especially postoperative) o Prolonged periods of sitting/traveling o Varicose veins o Spinal cord injury ▪ Hypercoagulability (due to release of tissue thromboplastin after injury/surgery) o Injury o Tumor (pancreatic, GI, GU, breast, lung) o Increased platelet count (polycythemia, splenectomy) ▪ Venous Endothelial Disease o Thrombophlebitis o Vascular disease o Foreign bodies (IV/central venous catheters) ▪ Certain Disease States (combination of stasis, coagulation alterations, and venous injury) o Heart disease (especially heart failure) o Trauma (especially fracture of hip, pelvis, vertebra, lower extremities) o Postoperative state/postpartum period o Diabetes mellitus o Chronic obstructive pulmonary disease ▪ Other Predisposing Conditions o Advanced age o Obesity o Pregnancy o Oral contraceptive use o History of previous thrombophlebitis, pulmonary embolism o Constrictive clothing Clinical Manifestations Symptoms depend on the size of the thrombus and the area of the pulmonary artery occlusion. ▪ Dyspnea ▪ Tachypnea 8 MMSU-CHS-Department of Nursing ▪ Chest pain, usually sudden in onset and pleuritic in nature; it can be substernal and may mimic angina pectoris or a myocardial infarction. ▪ Anxiety, fever, tachycardia, apprehension, cough, diaphoresis, hemoptysis, syncope, shock, and sudden death may occur. ▪ Clinical picture may mimic that of bronchopneumonia or HF. ▪ In atypical instances, PE causes few signs and symptoms, whereas in other instances it mimics various other cardiopulmonary disorders. Assessment and Diagnostic Methods ▪ Because the symptoms of PE can vary from few to severe, a diagnostic workup is performed to rule out other diseases. ▪ The initial diagnostic workup may include: o Chest x-ray o ECG o ABG analysis o Ventilation–perfusion scan ▪ Pulmonary angiography is considered the best method to diagnose PE Prevention ▪ Ambulation or leg exercises in patients on bed rest ▪ Application of sequential compression devices ▪ Anticoagulant therapy for patients whose hemostasis is adequate and who are undergoing major elective abdominal or thoracic surgery Medical Management Immediate objective is to stabilize the cardiopulmonary system. General Measures to Improve Respiratory and Vascular Status ▪ Nasal oxygen is administered immediately to relieve hypoxemia, respiratory distress, and central cyanosis. ▪ IV infusion lines are inserted to establish routes for medications or fluids that will be needed. ▪ A perfusion scan, hemodynamic measurements, and ABG determinations are performed. Spiral (helical) CT or pulmonary angiography may be performed. ▪ Hypotension is treated by a slow infusion of dobutamine (Dobutrex), which has a dilating effect on the pulmonary vessels and bronchi, or dopamine (Intropin). ▪ The ECG is monitored continuously for dysrhythmias and right ventricular failure, which may occur suddenly. ▪ Digitalis glycosides, IV diuretics, and antiarrhythmic agents are administered when appropriate. ▪ Blood is drawn for serum electrolytes, complete blood cell count, and hematocrit. ▪ If clinical assessment and ABG analysis indicate the need, the patient is intubated and placed on a mechanical ventilator. ▪ If the patient has suffered massive embolism and is hypotensive, an indwelling urinary catheter is inserted to monitor urinary output. ▪ Small doses of IV morphine or sedatives are administered to relieve patient anxiety, to alleviate chest discomfort, to improve tolerance of the endotracheal tube, and to ease adaptation to the mechanical ventilator. 9 MMSU-CHS-Department of Nursing Pharmacologic Therapy ▪ Anticoagulation Therapy o Anticoagulant therapy (heparin, warfarin sodium [Coumadin]) o Patients must continue to take some form of anticoagulation for at least 3 to 6 months after the embolic event. o Major side effects are bleeding anywhere in the body and anaphylactic reaction resulting in shock or death. Other side effects include fever, abnormal liver function, and allergic skin reaction. ▪ Thrombolytic Therapy o Thrombolytic therapy may include urokinase, streptokinase, and alteplase. It is reserved for PE affecting a significant area and causing hemodynamic instability. o Bleeding is a significant side effect; nonessential invasive procedures are avoided. Surgical Management ▪ A surgical embolectomy is rarely performed but may be indicated if the patient has a massive PE or hemodynamic instability or if there are contraindications to thrombolytic therapy. ▪ Transvenous catheter embolectomy with or without insertion of an inferior vena caval filter (eg, Greenfield). Nursing Management ▪ Minimizing the Risk of PE o The nurse must have a high degree of suspicion for PE in all patients, but particularly in those with conditions predisposing to a slowing of venous return. ▪ Preventing Thrombus Formation o Encourage early ambulation and active and passive leg exercises. o Instruct patient to move legs in a “pumping” exercise. o Advise patient to avoid prolonged sitting, immobility, and constrictive clothing. o Do not permit dangling of legs and feet in a dependent position. o Instruct patient to place feet on floor or chair and to avoid crossing legs. o Do not leave IV catheters in veins for prolonged periods. ▪ Monitoring Anticoagulant and Thrombolytic Therapy o Advise bed rest, monitor vital signs every 2 hours, and limit invasive procedures. o Measure international normalized ratio (INR) or activated partial thromboplastin time (PTT) every 3 to 4 hours after thrombolytic infusion is started to cofirm activation of fibrinolytic systems. o Perform only essential ABG studies on upper extremities, with manual compression of puncture site for at least 30 minutes. ▪ Minimizing Chest Pain, Pleuritic o Place patient in semi-Fowler’s position; turn and reposition frequently. o Administer analgesics as prescribed for severe pain. ▪ Managing Oxygen Therapy o Assess the patient frequently for signs of hypoxemia and monitors the pulse oximetry values. o Assist patient with deep breathing and incentive spirometry. o Nebulizer therapy or percussion and postural drainage may be necessary for management of secretions. 10 MMSU-CHS-Department of Nursing ▪ Alleviating Anxiety o Encourage patient to express feelings and concerns. o Answer questions concisely and accurately. o Explain therapy, and describe how to recognize untoward effects early. ▪ Monitoring for Complications o Be alert for the potential complication of cardiogenic shock or right ventricular failure subsequent to the effect of PE on the cardiovascular system. ▪ Providing Postoperative Nursing Care o Measure pulmonary arterial pressure and urinary output. o Assess insertion site of arterial catheter for hematoma formation and infection. o Maintain blood pressure to ensure perfusion of vital organs. o Encourage isometric exercises, antiembolism stockings, and walking when permitted out of bed; elevate foot of bed when patient is resting. o Discourage sitting; hip flexion compresses large veins in the legs. ▪ Promoting Home- and Community-Based Care o Teaching Patients Self-Care Before discharge and at follow-up clinic or home visits, teach patient how to prevent recurrence and which signs and symptoms should alert patient to seek medical attention. Teach patient to look for bruising and bleeding when taking anticoagulants and to avoid bumping into objects. Advise patient to use a toothbrush with soft bristles to prevent gingival bleeding. Instruct patient not to take aspirin (an anticoagulant) or antihistamine drugs while taking warfarin sodium (Coumadin). Advise patient to check with physician before taking any medication, including OTC drugs. Advise patient to continue wearing antiembolism stockings as long as directed. Instruct patient to avoid laxatives, which affect vitamin K absorption (vitamin K promotes coagulation). Teach patient to avoid sitting with legs crossed or for prolonged periods. Recommend that patient change position regularly when traveling, walk occasionally, and do active exercises of legs and ankles. Advise patient to drink plenty of liquids. Teach patient to report dark, tarry stools immediately. Recommend that patient wear identification stating that he or she is taking anticoagulants. PULMONARY HYPERTENSION ▪ ▪ Pulmonary Arterial hypertension (PAH) is a progressive, life-threatening disorder of the pulmonary circulation characterized by high pulmonary artery pressures exceeding 30 mm Hg or mean pulmonary artery pressure exceeding 25 mm Hg. ▪ This persistent high pulmonary artery pressure ultimately leads to right ventricular failure. 11 MMSU-CHS-Department of Nursing Two Forms 1. Primary or idiopathic pulmonary hypertension ▪ Occurs most often in women aged 20 to 40 years, either sporadically or in patients with a family history, and is usually fatal within 5 years of diagnosis. ▪ There are several possible causes, but the exact cause is unknown. ▪ The clinical presentation may occur with no evidence of pulmonary or cardiac disease. 2. Secondary pulmonary hypertension ▪ More common and results from existing cardiac or pulmonary disease. ▪ The prognosis depends on the severity of the underlying disorder and the changes in the pulmonary vascular bed. ▪ A common cause of pulmonary arterial hypertension is pulmonary artery constriction due to hypoxemia from COPD (cor pulmonale). Classifications According to its Causes and Associated Underlying Condition (WHO) ▪ Group 1: Pulmonary arterial hypertension (PAH) refers to increased pressure in the vessels caused by obstruction in the small arteries in the lung, for a variety of reasons. ▪ Group 2: Pulmonary hypertension due to left-side heart disease. ▪ Group 3: Pulmonary hypertension caused by underlying lung diseases or hypoxemia. ▪ Group 4: CTEPH (chronic thromboembolic pulmonary hypertension ▪ Group 5: Pulmonary hypertension from numerous other disorders. This group includes any other cause that doesn’t fit under another heading. Pathophysiology ▪ The underlying process of pulmonary hypertension varies, and multiple factors are often responsible. ▪ Normally, the pulmonary vascular bed can handle the blood volume delivered by the right ventricle. It has a low resistance to blood flow and compensates for increased blood volume by dilation of the vessels in the pulmonary circulation. ▪ However, if the pulmonary vascular bed is destroyed or obstructed, as in pulmonary hypertension, the ability to handle whatever flow or volume of blood it receives is impaired, and the increased blood flow then increases the pulmonary artery pressure. ▪ As the pulmonary arterial pressure increases, the pulmonary vascular resistance also increases. Both pulmonary artery constriction (as in hypoxemia or hypercapnia) and a reduction of the pulmonary vascular bed (which occurs with pulmonary emboli) result in an increase in pulmonary vascular resistance and pressure. ▪ This increased workload affects right ventricular function. The myocardium ultimately cannot meet the increasing demands imposed on it, leading to right ventricular hypertrophy (enlargement and dilation) and failure. 12 MMSU-CHS-Department of Nursing Clinical Manifestations ▪ Dyspnea, the main symptom, is noticed first with exertion and then at rest. ▪ Substernal chest pain is common. ▪ Weakness, fatigability, syncope, and occasional hemoptysis may occur. ▪ Signs of right-sided HF (peripheral edema, ascites, distended neck veins, liver engorgement, crackles, heart murmur) are noted. ▪ Anorexia and abdominal pain in the right upper quadrant may also occur. ▪ PaO2 is decreased (hypoxemia). ▪ ECG changes (right ventricular hypertrophy) are seen, with right axis deviation and tall, peaked P waves in inferior leads and tall anterior R waves and ST-segment depression or T-wave inversion anteriorly. Assessment and Diagnostic Findings ▪ In some cases, a lung biopsy, performed by thoracotomy or thoracoscopy, may be needed to make a definite diagnosis. ▪ Cardiac catheterization of the right side of the heart reveals elevated pulmonary arterial pressure. ▪ An echocardiogram can assess the progression of the disease and rule out other conditions with similar signs and symptoms. ▪ The ECG reveals right ventricular hypertrophy, right axis deviation, and tall peaked P waves in inferior leads, tall anterior R waves, and ST-segment depression and/or T-wave inversion anteriorly. ▪ The PaO2 also is decreased (hypoxemia). ▪ A ventilation–perfusion scan or pulmonary angiography detects defects in pulmonary vasculature, such as pulmonary emboli. ▪ Pulmonary function studies may be normal or show a slight decrease in vital capacity (VC) and lung compliance, with a mild decrease in the diffusing capacity. Medical Management ▪ Administration of oxygen ▪ Avoidance of contributing factors o Air travel o Decongestant medications o Pregnancy o Tobacco use ▪ For cor pulmonale o fluid restriction and diuretics to decrease fluid accumulation o Cardiac glycosides (eg, digitalis) to improve cardiac function o Calcium channel blockers for vasodilation o Rest 13 MMSU-CHS-Department of Nursing ▪ Anticoagulants such as warfarin (Coumadin) for chronic pulmonary emboli. ▪ Heart – lung transplantation in select patients with primary hypertension who have not been responsive to other therapies. ▪ Newer Medical Treatment Options A. Prostacyclin therapy is a potent vasodilator of both the systemic and pulmonary arterial vascular beds and is an inhibitor of platelet aggregation. a. Remodulin (treprostinil sodium) is given continuous subcutaneous or intravenous infusion. It causes reduction in pulmonary artery pressure through direct vasodilation of the pulmonary and systemic arterial vascular beds, thereby improving systemic oxygen transport and increasing cardiac output with minimal alteration of the heart rate b. Veletri (epoprostenol sodium room temperature stable): Epoprostenol has 2 major pharmacological actions: (1) direct vasodilation of pulmonary and systemic arterial vascular beds, and (2) inhibition of platelet aggregation. It is a continuous intravenous infusion. c. Ventavis (iloprost sodium) and Tyvaso (treprostinil sodium) are intermittent inhalation treatments using medication specific nebulizers but cannot be administered during invasive mechanical ventilation. Both drugs, dilate systemic and pulmonary arterial vascular beds. B. Endothelin receptor antagonists block the neurohormone endothelin from binding in the endothelium and vascular smooth muscle. a. Tracleer (bosentan) and Letairis (ambrisentan) are oral agents. C. Phosphodiesterase inhibitors blocks phosphodiesterase type 5 which is responsible for the degradation of cyclic guanosine monophosphate (cGMP). Increased cGMP concentration results in pulmonary vasculature relaxation; vasodilation in the pulmonary bed and the systemic circulation (to a lesser degree) may occur. a. Revatio (sildenafil) and Adcirca (tadalafil) are oral agents specific for use in patients with pulmonary hypertension. NOTE: The most effective treatment for pulmonary hypertension associated with lung respiratory disease or hypoxia, or both, is treatment of the primary disorder. Nursing Management ▪ The major nursing goal is to identify patients at high risk for pulmonary hypertension, such as those with COPD, pulmonary emboli, congenital heart disease, and mitral valve disease. ▪ The nurse also must be alert for signs and symptoms, administer oxygen therapy appropriately, and instruct patients and their families about the use of home oxygen supplementation. 14 MMSU-CHS-Department of Nursing ACUTE RESPIRATORY DISTRESS SYNDROME ▪ Acute respiratory distress syndrome (ARDS; previously called adult respiratory distress syndrome) is a severe form of acute lung injury; it is a clinical syndrome characterized by a sudden and progressive pulmonary edema, increasing bilateral infiltrates on chest x-ray, hypoxemia refractory to oxygen supplementation, and reduced lung compliance. These signs occur in the absence of left-sided heart failure. ▪ Acute respiratory distress syndrome (ARDS) represents a complex clinical syndrome (rather than a single disease process) and carries a high risk for mortality. ARDS is defined as a type of acute, diffuse, inflammatory lung injury that leads to increased pulmonary vascular permeability and loss of aerated lung tissue. ▪ ARDS occurs when inflammatory triggers initiate the release of cellular and chemical mediators, causing injury to the alveolar capillary membrane in addition to other structural damage to the lungs. Factors associated with the development of ARDS include direct injury to the lungs (eg, smoke inhalation) or indirect insult to the lungs (eg, shock). Risk Factors ▪ Genetic Predisposition ▪ Direct Lung Injury o Aspiration (gastric fluids, near drowning) o Infectious pneumonia o Lung contusions with trauma o Toxic inhalation o Upper airway obstruction o Severe Acute Respiratpry Syndrome (SARS) coronavirus o Neurogenic pulmonary edema o Acute eosinophilic pneumonia ▪ Indirect Lung Injury o Sepsis o Burns o Trauma o Blood transfusion o Lung or bone marrow transplantation o Drug or alcohol overdose o Drug reaction o Cardiopulmonary bypass o Acute pancreatitis o Multiple fractures o Venous air embolism o Amniotic fluid embolism Pathophysiology: ▪ The clinical presentation consists of hypoxemia, bilateral lung opacities, increased physiological dead space, and decreased lung compliance. The acute phase is characterized by diffuse alveolar damage (i.e. oedema, inflammation, or hemorrhage). 15 MMSU-CHS-Department of Nursing ▪ Inflammatory triggers initiate the release of cellular and chemical mediators, causing injury to the alveolar capillary membrane in addition to other structural damage to the lungs. Severe V./Q. mismatching occurs. Alveoli collapse because of the inflammatory infiltrate, blood, fluid, and surfactant dysfunction. Small airways are narrowed because of interstitial fluid and bronchial obstruction. ▪ Lung compliance may markedly decrease, resulting in decreased functional residual capacity and severe hypoxemia. The blood returning to the lung for gas exchange is pumped through the nonventilated, nonfunctioning areas of the lung, causing shunting. This means that blood is interfacing with nonfunctioning alveoli and gas exchange is markedly impaired, resulting in evere, refractory hypoxemia. In stage 1, diagnosis is difficult because the signs of impending ARDS are subtle. Clinically, the patient exhibits increased dyspnea and tachypnea, but there are few radiographic changes. At this point, neutrophils are sequestering; however, there is no evidence of cellular damage. In Stage 2 (within 24 hours, a critical time for early treatment), the symptoms of respiratory distress increase in severity, with cyanosis, coarse bilateral crackles on auscultation, and radiographic changes consistent with patchy infiltrates. A dry cough or chest pain may be present. It is at this point that the mediator-induced disruption of the vascular bed results in increased interstitial and alveolar edema. The endothelial and epithelial beds are increasingly permeable to proteins. This is referred to as the “exudative” stage. The hypoxemia is resistant to supplemental oxygen administration, and mechanical ventilation will most likely be commenced in response to a worsening ratio of arterial oxygen to fraction of inspired oxygen (PaO2:FiO2 ratio). In Stage 3, the “proliferative” stage, develops from the 2nd to the 10th day after injury. Evidence of SIRS is now present, with hemodynamic instability, generalized edema, possible onset of nosocomial infections, increased hypoxemia, and lung involvement. Air bronchograms may be evident on chest radiography as well as decreased lung volumes and diffuse interstitial markings. Stage 4, the “fibrotic” stage, develops after 10 days and is typified by few additional radiographic changes. There is increasing multiorgan involvement, SIRS, and increases in the arterial carbon dioxide tension (PaCO2) as progressive lung fibrosis and emphysematous changes result in increased dead space. Fibrotic lung changes result in ventilation management diffi culties, with increased airway pressure and development of pneumothoraces. Clinical Manifestations The 2012 Berlin definition of ARDS changed the terminology and diagnostic criteria that had previously been used. The phrase ‘acute lung injury’ is no longer to be used, and ARDS is now categorized as mild, moderate, or severe. Initially, ARDS closely resembles severe pulmonary edema. Recognizing the dynamic nature of the morphological changes involved with ARDS enables the nurse to understand the changes in physical assessment, mechanical ventilation strategies, treatment, and management that occur throughout the patient’s critical care stay. 16 MMSU-CHS-Department of Nursing Diagnostic Tests ▪ Refractory hypoxemia (hypoxemia that does not improve with oxygen administration) is the hallmark of ARDS. Arterial blood gases initially show hypoxemia with a PO2 of less than 60 mmHg and respiratory alkalosis due to tachypnea. Chest x-ray changes may not be evident for as long as 24 hours after the onset of ARDS. Diffuse, bilateral pulmonary infiltrates without increased cardiac size are seen initially, progressing to a “white out” pattern. Chest CT scan provides a better illustration of the pattern of alveolar consolidation and atelectasis in ARDS (Fishman et al., 2008). Pulmonary function testing shows decreased lung compliance with reduced vital capacity, minute volume, and functional vital capacity Pulmonary artery pressure monitoring shows normal pressures in ARDS, helping distinguish ARDS from cardiogenic pulmonary edema. 17 MMSU-CHS-Department of Nursing Medical Management ▪ The primary focus in the management of ARDS includes identification and treatment of the underlying condition. Treatment is supportive; that is, contributing factors are corrected or reversed, and while the lungs heal, care is taken so that treatment does no further damage. In addition, extensive work has gone into creating “bundles,” which are elements of care considered core to the management and treatment of specific critical illnesses in intensive care units (ICUs). The image lists essential critical care bundles that apply to managing ARDS. 1. Improving Oxygenation: Administer high Fio2 levels with high-flow system or rebreathing mask. A constant positive airway pressure (CPAP) mask may be tolerated in alert, cooperative patients. Continuous, vigilant monitoring for contraindications of noninvasive CPAP (decreased loss of consciousness, nausea/vomiting, increased dyspnea or panic) is imperative. 2. Improving Ventilation: a. Intubation and mechanical ventilation if cardiovascular instability is present, severe hypoxemia persists, or if fatigue develops. The best treatment is to initiate PEEP after mechanical ventilation. b. Humidified oxygen delivery through a tightfitting mask and using CPAP may be adequate. ET intubation and mechanical ventilation are commonly required. PEEP may prevent alveolar collapse. High frequency jet ventilation is sometimes used. Suctioning as necessary removes accumulated secretions from the tracheobronchial tree c. Ventilation is usually started with Lung-protective ventilation strategies such as low tidal volumes (