ARF

Stages of Edema Formation in ARDS

8 Stages of edema formation in ARDS. A, Normal alveolus and pulmonary capillary. B, Interstitial edema occurs with increased flow of fluid into the interstitial space. C, Alveolar edema occurs when the fluid crosses the alveolar-capillary membrane.

Range of ventilation to perfusion (V/Q) relationships

A, Absolute shunt, no ventilation because of fluid filling the alveoli. B, V/Q mismatch, ventilation partially compromised by secretions in the airway. C, Normal lung unit. D, V/Q mismatch, perfusion partially compromised by emboli obstructing blood flow. E, Dead space, no perfusion because of obstruction of the pulmonary capillary (vent without perfusion)

Interprofessional Care Acute Respiratory Failure

Diagnostic Assessment • Vital signs • History and physical examination • Arterial blood gases (ABGs) • Pulse oximetry • Chest x-ray • CBC and differential( know CBC( hemoglobin is there) inclusion and differential is WBC) • Serum electrolytes • 12-Lead ECG • Blood, sputum, and/or urine cultures (if indicated) • Hemodynamic monitoring: CVP, SVV, PAWP (if indicated) Management Respiratory Therapy • O2 therapy • Mobilization of secretions • Positioning • Effective coughing • Chest physiotherapy • Suctioning of the airway • Oral and/or IV hydration • Humidification (of O2) • Ambulation (early mobility) • Positioning: head of bed elevated • Positive pressure ventilation (PPV) • Noninvasive positive pressure ventilation (e.g. CPAP, BiPAP) • Intubation with positive pressure ventilation Drug Therapy Reduce airway inflammation (e.g., corticosteroids) Relief of bronchospasm (e.g., albuterol) Reduce pulmonary congestion (e.g., furosemide [Lasix], morphine) Treat pulmonary infections (e.g., antibiotics) Reduce anxiety, pain, and restlessness (e.g., lorazepam, fentanyl, morphine) Supportive Therapy • Management of the underlying cause of respiratory failure • Monitor hemodynamic status • Optimize balance between activity and rest • Monitor for deterioration in patient condition CVP, Central venous pressure; SVV, stroke volume variation; PAWP, pulmonary artery wedge pressure.

Diffusion limitation

Exchange of CO2 and O2 cannot occur because of the thickened alveolar-capillary membrane.

Nursing Implementation Prevention

For the patient at risk for ARF, prevention and early recognition of respiratory distress are important. This is especially important for patients with neuromuscular diseases, cardiac problems, or respiratory problems (e.g., COPD). Do a thorough history and physical assessment to identify risk factors, then start appropriate interventions. Early strategies may include teaching patients about deep breathing and coughing, use of incentive spirometry, and early ambulation. Preventing atelectasis, pneumonia, and complications of immobility, and optimizing hydration and nutrition, can decrease the risk for ARF. Those patients at high risk should be assessed more often with attention given to preventive measures.

Drug Alert

IV Corticosteroids Monitor potassium levels. Corticosteroids worsen hypokalemia caused by diuretics. Prolonged use causes adrenal insufficiency. · Relief of bronchospasm increases alveolar ventilation. · In acute bronchospasm, short-acting bronchodilators (e.g., albuterol), may be given at 15- to 30-minute intervals until a response occurs. · Give these drugs using a hand-held nebulizer or a metered-dose inhaler with a spacer. · Side effects include tachycardia and hypertension. · Prolonged use can increase the risk for dysrhythmias and cardiac ischemia. It is important to monitor the patient's vital signs and ECG for any changes.

Nursing Diagnoses

Impaired gas exchange Impaired respiratory system function

common s/s of hypoxemia

Respiratory Dyspnea Tachypnea Prolonged expiration Nasal flaring Intercostal muscle retraction Use of accessory muscles in respiration ↓ SpO2 (<90%) Paradoxical chest or abdominal wall movement with respiratory cycle (late) Cyanosis (late) Nonspecific Central Nervous Agitation Confusion Disorientation Restless, combative behavior Delirium ↓ Level of consciousness Coma (late) Cardiovascular Tachycardia Hypertension Skin cool, clammy, and diaphoretic Dysrhythmias (late) Hypotension (late) Other Fatigue Inability to speak in complete sentences without pausing to breathe

Common s/s of hypercapnia

Respiratory Dyspnea Use of tripod position Pursed-lip breathing Limited chest wall movement ↓ Respiratory rate or rapid rate with shallow respirations ↓ Tidal volume ↓ Minute ventilation Nonspecific s/s Central Nervous Morning headache Disorientation, confusion Agitation Progressive somnolence ↑ ICP Coma (late) Cardiovascular Dysrhythmias Hypertension Tachycardia Bounding pulse Neuromuscular Muscle weakness ↓ Deep tendon reflexes Tremors, seizures (late)

hypoxemic respiratory failure

Respiratory System • ARDS • Hepatopulmonary syndrome (e.g., low-resistance flow state, V/Q mismatch) • Massive pulmonary embolism (e.g., thrombus emboli, fat emboli) • Pneumonia • Pulmonary artery laceration and hemorrhage • Toxic inhalation (e.g., smoke inhalation) Cardiac System • Anatomic shunt (e.g., ventricular septal defect) • Cardiogenic pulmonary edema • Cardiogenic shock (decreasing blood flow through pulmonary vasculature) • High cardiac output states: diffusion limitation

hypercapnic respiratory failure

Respiratory System • Asthma • COPD • Cystic fibrosis Central Nervous System • Brainstem injury or infarction • Sedative and opioid overdose • Spinal cord injury • Severe head injury Chest Wall • Kyphoscoliosis • Pain • Severe obesity • Thoracic trauma (e.g., flail chest) Neuromuscular System • Amyotrophic lateral sclerosis • Critical illness polyneuropathy • Guillain-Barré syndrome • Muscular dystrophy • Multiple sclerosis • Myasthenia gravis • Phrenic nerve injury • Poliomyelitis • Toxin exposure or ingestion (e.g., tree tobacco, acetylcholinesterase inhibitors, carbamate or organophosphate poisoning)

Nursing Assessment Acute Respiratory Failure

Subjective Data Important Health Information • Past health history: Age, weight, altered level of consciousness, tobacco use (pack-years), alcohol or drug use, hospitalizations related to either acute or chronic lung disease, thoracic or spinal cord trauma, occupational exposures to lung toxins • Medications: Use of home O2, inhalers (bronchodilators), home nebulization, over-the-counter drugs; immunosuppressant (e.g., corticosteroid) therapy, CNS depressants, illicit substances • Surgery or other treatments: Intubation and mechanical ventilation, recent thoracic or abdominal surgery Functional Health Patterns • Health perception-health management: Exercise, self-care activities, immunizations (flu, pneumonia, hepatitis) • Nutritional-metabolic: Eating habits, bloating, indigestion; recent weight gain or loss, change in appetite. Use of vitamins or herbal supplements • Activity-exercise: Fatigue, dizziness, dyspnea at rest or with activity, wheezing, cough (productive or nonproductive), sputum (volume, color, viscosity), palpitations, swollen feet, change in exercise tolerance • Sleep-rest: Changes in sleep pattern, use of CPAP • Cognitive-perceptual: Headache, chest pain or tightness, chronic pain • Coping-stress tolerance: Anxiety, depression, feelings of hopelessness. Risk for drug and/or alcohol use, nicotine withdrawal Objective Data General • Restlessness, agitation Integumentary • Pale, cool, clammy skin or warm, flushed skin. Peripheral and central cyanosis. Peripheral dependent edema Respiratory • Shallow, increased respiratory rate progressing to decreased rate. Use of accessory muscles with evidence of retractions, increased diaphragmatic excursion or asymmetric chest expansion, paradoxical chest and abdominal wall movement. Tactile fremitus, crepitus, or deviated trachea on palpation. Absent, decreased, or adventitious breath sounds. Pleural friction rub. Bronchial or bronchovesicular sounds heard in other than normal location, inspiratory stridor Cardiovascular • Tachycardia progressing to bradycardia, dysrhythmias, extra heart sounds (S3, S4). Bounding pulse. Hypertension progressing to hypotension. Pulsus paradoxus, jugular venous distention, pedal edema Gastrointestinal • Abdominal distention, ascites, epigastric tenderness, hepatojugular reflex Neurologic • Somnolence, confusion, slurred speech, restlessness, delirium, agitation, tremors, seizures, coma, asterixis, ↓ deep tendon reflexes, papilledema Possible Diagnostic Findings • ↓/↑ pH, ↑/↓ PaCO2, ↑/↓ bicarbonate, ↓ PaO2, ↓ SaO2, abnormal hemoglobin, ↑ WBC count, changes in serum electrolytes. Abnormal findings on chest x-ray. Abnormal central venous or pulmonary artery pressures. Initially cardiac output may be ↑ due to the stress response. As hypoxemia, hypercapnia, and acidosis become more severe, cardiac output will ↓.

Respiratory Therapy

The goals of respiratory care include maintaining adequate oxygenation and ventilation and correcting acid-base imbalance. Interventions include O2 therapy, mobilization of secretions, and positive pressure ventilation (PPV)

Planning

The overall goals for the patient with ARF include (1) independently maintain a patent airway, (2) absence of dyspnea or recovery to baseline breathing patterns, (3) effectively cough and able to clear secretions, (4) normal ABG values or values within the patient's baseline, and (5) breath sounds within the patient's baseline.

Regional V/Q differences in the normal lung

This difference causes the PaO2 to be higher at the apex of the lung and lower at the base. Values for PaCO2 are the opposite (i.e., lower at the apex and higher at the base). Blood that exits the lung is a mixture of these values

Common cause of resp. failure

hypoxemic resp. failure hypercapnic res. failure

Central Nervous System Problems

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

Shunt- perfusion no vent

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

Nursing Assessment

· A thorough assessment may result in early detection of respiratory insufficiency · This allows us to intervene sooner and can prevent worsening respiratory failure. · Monitor patients with preexisting cardiac and/or respiratory disease closely. · A slight change in their overall condition can cause significant decompensation. · It is important to observe trends in ABGs, pulse oximetry, and assessment findings. · You must identify the changes that are occurring from hypoxemia or hypercarbia. · Your ability to detect problems, notify the HCP, implement appropriate treatment, and evaluate response to therapy is essential.

Acute Respiratory Distress Syndrome

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

Alveolar Hypoventilation

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

Nursing and Interprofessional Management: Acute Respiratory Failure

· Because many different problems cause ARF, initial management and specific care varies. · Factors taken into consideration include patient age, severity of onset of respiratory failure, underlying co-morbidities, and suspected or most likely cause of the respiratory failure. · We then tailor management strategies to what best meets the patient's unique needs. · This section discusses general assessment and interventions most commonly used for patients with ARF. · In acute care settings, collaboration between nursing and the interprofessional team (e.g., ICU physicians, respiratory therapists, pharmacists) is essential. · In severe ARF, the patient will be cared for in an intensive care unit (ICU). · ICU care will include central venous pressure (CVP) and arterial BP monitoring. · Arterial BP will be monitored at least hourly. · Central or mixed venous O2 saturation [ScvO2 or SvO2] data help determine the adequacy of tissue perfusion and the patient's response to treatment. · The patient may need advanced hemodynamic monitoring to evaluate parameters such as CO and pulmonary capillary wedge pressure (PCWP).

Chest Physiotherapy

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

Reduce Airway Inflammation and Bronchospasm

· Corticosteroids (e.g., IV methylprednisolone [Solu-Medrol]) are often used in combination with other drugs, such as bronchodilators, for relief of inflammation and bronchospasm. · It may take several hours to see their effects. Inhaled corticosteroids require 4 to 5 days for optimum therapeutic effects, so they will not relieve ARF.

Drug Therapy

· Drug therapy depends on several factors. · These include the cause of ARF, the patient's preexisting medical condition, and whether infection is present. · Goals of drug therapy include to (1) reduce airway inflammation and bronchospasm, (2) relieve pulmonary congestion; (3) treat infection; and (4) reduce anxiety, pain, and restlessness.

Consequences of Hypoxemia

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

Positive Pressure Ventilation

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

Ventilation-Perfusion Mismatch

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

Relieve Pulmonary Congestion

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

Treat Infection

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

Nutritional Therapy

· Maintaining protein and energy stores is especially important in patients with ARF. · The hypermetabolic state in critical illness increases the caloric requirements needed to maintain a stable body weight and muscle mass. · Nutritional depletion causes a loss of muscle mass, including the respiratory muscles, which may delay recovery · . The dietitian often determines the best method of feeding and optimal caloric and fluid requirements. · Ideally, enteral or parenteral nutrition should be started within 24 to 48 hours

Gerontologic Considerations: Acute Respiratory Failure

· Many factors contribute to an increased risk for respiratory failure in older adults. · The reduced ventilatory capacity that accompanies aging places the older adult at risk for ARF. · Physiologic changes in the lungs include alveolar dilation, larger air spaces, and loss of surface area for gas exchange. · Decreased elastic recoil within the airways, decreased chest wall compliance, and decreased respiratory muscle strength occur · In older adults, the PaO2 falls further and the PaCO2 rises to a higher level before the respiratory system is stimulated to change the rate and depth of breathing. · This delayed response contributes to the development of respiratory insufficiency. · A history of tobacco use is a major risk factor that can accelerate age-related respiratory changes. · Poor nutritional status and less physiologic reserve in the cardiopulmonary system increases the risk for further compromising respiratory function and leading to ARF.

Conceptual Focus

· Nursing and interprofessional management of patients with ARF and ARDS focus on interventions to promote adequate oxygenation, ensure effective ventilation, identify and treat the underlying causes, and prevent complications. · When respiratory function is insufficient, all body systems are affected · PA is the only artery carrying deoxygenated blood

Problems of the Airway and Alveoli

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

Patient Positioning

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

s/s

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

Mobilization of secretions

· Retained pulmonary secretions may cause or worsen ARF · This occurs because the movement of O2 into the alveoli and removal of CO2 is severely limited or blocked. · Secretions can be mobilized by proper positioning, effective coughing, chest physiotherapy, suctioning, humidification, hydration, and, when possible, early ambulation.

Chest Wall Abnormalities

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

Suctioning

· Suctioning may be needed if the patient is unable to expectorate secretions. · Suctioning through an artificial airway (e.g., endotracheal tube [ET], tracheostomy) is done only as needed · Perform suctioning beyond the posterior oropharynx with caution, while monitoring the patient for complications. · These include hypoxia, increased ICP, dysrhythmias, hypotension (from sudden elevation in intrathoracic pressure), hypertension and tachycardia (from noxious stimulation), and bradycardia (possible vasovagal response).

Consequences of Hypercapnia

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

Acute Respiratory Failure

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

Diagnostic Studies

· The most common diagnostic studies used to evaluate ARF are chest x-ray and ABG analysis. · include history and physical exam · A chest x-ray helps identify possible causes of respiratory failure (e.g., atelectasis, pneumonia). · ABGs evaluate oxygenation (PaO2) and ventilation (PaCO2) status and acid-base (pH, bicarbonate) balance. · Pulse oximetry monitors oxygenation status indirectly. · Other diagnostic studies that may be done include a complete blood cell count, serum electrolytes, urinalysis, and 12-lead ECG · . Blood and sputum cultures (Gram stain, culture and sensitivity) may reveal infection. · A CT scan or V/Q lung scan may be done if a pulmonary embolus is suspected · . For the patient in severe ARF who needs intubation, end-tidal CO2 (EtCO2) may be used during ventilator management to assess trends in lung ventilation. · CBC

Neuromuscular Conditions

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

Effective Coughing

· When secretions are present, encourage the patient to cough. · Unfortunately, not all patients will have enough strength or force to produce a cough that will clear the airway of secretions. · Augmented coughing (quad coughing) may benefit some patients. · To aid with augmented coughing, place 1 or both hands at the anterolateral base of the patient's lungs · As you observe deep inspiration end and expiration begin, move your hands forcefully upward. · This increases abdominal pressure and helps the patient cough. · It increases expiratory flow and promotes secretion clearance. · Huff coughing is a series of coughs performed while saying the word "huff" (This technique prevents the glottis from closing during the cough. The patient takes a deep breath, holds the breath for 2 or 3 seconds, and then exhales. The huff cough is effective in clearing central airways. It may help move secretions upward. COPD patients generate higher flow rates with a huff cough than with a normal cough, and it is less tiring.The staged cough also helps clear secretions. To perform a staged cough, the patient assumes a sitting position, breathes in and out 3 or 4 times through the mouth, then coughs while bending forward and pressing a pillow inward against the diaphragm.

Chronic respiratory failure

· failure develops more slowly, over days to weeks. · The patient is usually more stable as the body had time to compensate for the small, but subtle, changes that have occurred.

Hypoxemic respiratory failure

· is a PaO2 less than 60 mm Hg when the patient is receiving an inspired O2 concentration of 60% or more · In hypoxemic respiratory failure (also called oxygenation failure), the main problem is inadequate exchange of O2 between the alveoli and pulmonary capillaries The PaO2 level shows inadequate O2 saturation A less than optimal PaO2 level exists despite supplemental O2.

Hypercapnic respiratory failure

· or ventilatory failure) is a PaCO2 greater than 50 mm Hg with acidemia (arterial pH less than 7.35). The main problem is insufficient CO2 removal. This causes the PaCO2 to be higher than normal. · For whatever reason, the body is unable to compensate for the increase. · This allows acidemia to occur · Patients may have both types of respiratory failure at the same time. · For example, a patient with chronic obstructive pulmonary disease (COPD) who has pneumonia could have "acute-on-chronic" respiratory failure. · In other words, the patient has an underlying chronic respiratory problem. · The new infection, in addition to the chronic problem, results in the "acute-on-chronic" clinical picture. · Significant changes in PaO2 and PaCO2 occur with ARF. · These may develop over several minutes to a few hours to 1 or 2 days. · The patient may have hemodynamic instability (e.g. tachycardia, hypotension), increased respiratory effort, and decreased level of consciousness. · Urgent intervention is required.

Reduce Anxiety, Pain, and Restlessness

• Anxiety, pain, and restlessness may result from hypoxia. • They increase O2 consumption and CO2 production (from an increased metabolic rate) and increase WOB. • For the nonintubated patient, this may cause tachypnea and ineffective ventilation. • For the intubated patient, this may cause ventilator dyssynchrony and increase the risk for unplanned extubation. • We promote patient comfort in several ways. • Benzodiazepines (e.g., lorazepam, midazolam), and opioids (e.g., morphine, fentanyl) may decrease anxiety, restlessness, and pain. • They are often given IV. • For the nonintubated patient, they should be started at the lowest dose possible. • Address treatable causes of restlessness (e.g., hypoxemia, pain, delirium). • Often, restlessness and mental status changes are the first signs of hypoxemia or ventilator dyssynchrony. • You should address the causes and not depend solely on the use of analgesics and sedatives.

Hypoxemic Respiratory Failure Etiology and Pathophysiology

• Four physiologic mechanisms may cause hypoxemia and hypoxemic respiratory failure: (1) mismatch between ventilation (V) and perfusion (Q), often referred to as V/Q mismatch air is not going through supposed to be 1:1; when one is more than the other too much 02 less blood coming through then there is a mismatch • (2) shunt • (3) diffusion limitation-ex COPD pt • (4) alveolar hypoventilation. • The most common causes are V/Q mismatch and shunt.

Medical Supportive Therapy

• Goals and interventions targeted to improving the patient's oxygenation and ventilation status are essential to improve O2 delivery. • The primary goal is to treat the underlying cause of the ARF. • Patients with V/Q mismatch, shunting, or diffusion limitation are managed differently, depending on the underlying cause. • Patients are continuously monitored for their response to therapy, including changes in respiratory status, trends in ABGs, and signs of clinical improvement.

Humidification

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

Hypercapnic Respiratory Failure

• In acute hypercapnic respiratory failure, ventilatory failure, the lungs are often normal • In this situation, the respiratory system cannot keep CO2 levels maintained within normal limits • This often occurs from an increase in CO2 production or a decrease in alveolar ventilation. • Hypercapnic respiratory failure can be acute or chronic. It often reflects significant problems with the respiratory system. • Many conditions can cause impaired ventilation. • We group into 4 categories: (1) CNS problems, (2) neuromuscular conditions, (3) chest wall abnormalities, and (4) problems affecting the airways and/or alveoli. • Acute hypercapnic respiratory failure can occur with CNS problems, neuromuscular conditions, and chest wall abnormalities in the presence of normal lungs.

Safety Alert Managing Restlessness and Sedation

• Pain, hypoxemia, electrolyte imbalance, TBI, and drug reactions can cause restlessness. • Assess and aggressively treat all reversible causes of restlessness. • Monitor patients closely for CNS, cardiac, and respiratory depression when giving sedative and analgesic drugs, especially in the nonintubated patient. • Sedative and analgesic drugs may have a prolonged effect in critically ill patients. This can delay weaning from mechanical ventilation and increase length of stay.

Interrelationship of Mechanisms

• Rarely is acute hypoxemic respiratory failure caused by a single factor. • More often, it is a combination of 2 or more factors. • For example, the patient with ARF from pneumonia may have a V/Q mismatch and shunt. • Inflammation, edema, and exudate obstruct the airways (V/Q mismatch) and fill the alveoli with exudate (shunt). • Other contributing factors include increases in O2 demand with anxiety and unrelieved pain.

Oxygen therapy

• The primary goal of O2 therapy is to correct hypoxemia. • This requires O2 administration. • Always administer O2 at the lowest possible FIO2 (O2 concentration) needed to keep SpO2 and PaO2 within patient-specific goals. • Never withhold O2 from a patient. It is essential to observe the patient's response to O2 therapy. • Closely monitor patients for changes in mental status, respiratory rate, and ABGs, until their PaO2 level has reached their baseline normal value. • Several methods are available to provide O2 to patients in ARF • The device selected depends upon the patient's overall condition, degree of respiratory failure, ability to maintain a patent airway, the amount of FIO2 that the device can deliver, and, most importantly, the patient's ability to breathe spontaneously. Ideally, the selected O2 delivery device must maintain PaO2 at 60 mm Hg or higher and SaO2 at 90% or higher. • The patient is often agitated, disoriented, and restless. • A face mask, though appropriate, may cause anxiety from feelings of claustrophobia. • Anxiety can cause dyspnea and increase O2 consumption and CO2 production. • The patient may try to remove the mask. • In this case, you need to explore other O2 therapy options. • Breathing high O2 concentrations for prolonged periods is not without potential adverse effects. Exposure to higher FIO2 (greater than 60%) for longer than 48 hours poses a risk for O2 toxicity • . In this situation, oxygen free radicals from the high O2 levels cause inflammation and cell death, by disrupting the alveolar-capillary membrane. • Absorption atelectasis is another risk. O2 has the ability to replace nitrogen and other gases normally present in the alveoli • . Without nitrogen to help maintain size and shape of the alveolus, structural support is lost and the alveolus collapses. • Other effects of prolonged exposure to high levels of O2 include increased pulmonary capillary permeability, decreased surfactant production, surfactant inactivation, and fibrotic changes in the alveoli. • Another risk of O2 therapy is specific to patients with chronic hypercapnia (e.g., patient with COPD). • Chronic hypercapnia blunts the response of chemoreceptors to high CO2 levels as a respiratory stimulant. • Initial O2 therapy may be provided to patients with chronic hypercapnia through a low-flow device, such as a nasal cannula at 1 to 2 L/min or a Venturi mask at 24% to 28%. • The patient with COPD who does not respond to O2 therapy or other interventions may need mechanical ventilation with higher FIO2.

Hydration

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

Diffusion limitation occurs when gas exchange across the alveolar-capillary membrane is

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