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Respiratory failure update Dr Ahmed Elmasry MD, chest diseases, Ain Shams University PhD, respiratory medicine, Uppsala University Acute Respiratory Failure • Failure in one or both gas exchange functions: oxygenation and carbon dioxide elimination • In practice: PaO2<60mmHg or PaCO2>46mmHg • Derangements in ABGs and acid-base status HYPERCAPNIC RESPIRATORY FAILURE At a constant rate of carbon dioxide production, PaCO2 is determined by the level of alveolar ventilation (Va), where VCO2 is ventilation of carbon dioxide and K is a constant value (0.863). Va = (K x VCO2)/PaCO2 ALVEOLAR-ARTERIAL OXYGEN DIFFERENCE The efficiency of lungs at carrying out of respiration can be further evaluated by measuring alveolar-to-arterial PaO2 difference. This difference is calculated by the following equation: ALVEOLAR –ARTERIAL OXYGEN DIFFERENCE PaO2 = FIO2 x (PB – PH2 O) – PaCO2/R For the above equation, PaO2 = alveolar PO2, FIO2 = fractional concentration of oxygen in inspired gas, PB = barometric pressure, PH2 O = water vapor pressure at 37°C, PaCO2 = alveolar PCO2, assumed to be equal to arterial PCO2, and R = respiratory exchange ratio. R depends on oxygen consumption and carbon dioxide production. At rest, VCO2/VO2 is approximately 0.8. SHUNT EFFECT Shunt is defined as the persistence of hypoxemia despite 100% oxygen inhalation. The deoxygenated blood (mixed venous blood) bypasses the ventilated alveoli and mixes with oxygenated blood that has flowed through the ventilated alveoli, consequently leading to a reduction in arterial blood content. SHUNT EFFECT The shunt is calculated by the following equation: QS/QT = (CCO2 – CaO2)/CCO2 – CVO2) QS/QT is the shunt fraction, CCO2 (capillary oxygen content) is calculated from ideal alveolar PO2, CaO2 (arterial oxygen content) is derived from PaO2 using the oxygen dissociation curve, and CVO2 (mixed venous oxygen content) can be assumed or measured by drawing mixed venous blood from pulmonary arterial catheter. SHUNT EFFECT Even normal lungs have some degree of V/Q mismatching and a small quantity of right-toleft shunt, alveolar PO2 is slightly higher than arterial PO2. However, an increase in alveolarto-arterial PO2 above 15-20 mm Hg indicates pulmonary disease as the cause of hypoxemia. Mortality/Morbidity The mortality rate associated with respiratory failure varies according to the etiology. For acute respiratory distress syndrome, the mortality rate is approximately 50% in most studies. Acute exacerbation of COPD carries a mortality rate of approximately 30%. The mortality rates for other causative disease processes have not been well described. Criteria for the diagnosis of ARDS • Clinical presentation - Tachypnea and dyspnea; crackles upon auscultation • Clinical setting - Direct insult (aspiration) or systemic process causing lung injury (sepsis) • Radiologic appearance - Three-quadrant or 4quadrant alveolar flooding • Lung mechanics - Diminished compliance ( <40 mL/cm water) • Gas exchange - Severe hypoxia refractory to oxygen therapy (PaO2/FIO2 <200) • Normal pulmonary vascular properties - Pulmonary capillary wedge pressure <18 mm Hg CAUSES Central nervous system disorders • A variety of pharmacological, structural, and metabolic disorders of the CNS are characterized by depression of the neural drive to breathe. • This may lead to acute or chronic hypoventilation and hypercapnia. • Examples include tumors or vascular abnormalities involving the brain stem, an overdose of a narcotic or sedative, and metabolic disorders such as myxedema or chronic metabolic alkalosis. CAUSES Disorders of the peripheral nervous system, respiratory muscles, and chest wall • These disorders lead to an inability to maintain a level of minute ventilation appropriate for the rate of carbon dioxide production. • Concomitant hypoxemia and hypercapnia occur. • Examples include Guillain-Barré syndrome, muscular dystrophy, myasthenia gravis, severe kyphoscoliosis, and morbid obesity. CAUSES Abnormalities of the airways • Severe airway obstruction is a common cause of acute and chronic hypercapnia. • Examples of upper airway disorders are acute epiglottitis and tumors involving the trachea; lower airway disorders include COPD, asthma, and cystic fibrosis. CAUSES Abnormalities of the alveoli • The diseases are characterized by diffuse alveolar filling, frequently resulting in hypoxemic respiratory failure, although hypercapnia may complicate the clinical picture. • Common examples are cardiogenic and noncardiogenic pulmonary edema, aspiration pneumonia, or extensive pulmonary hemorrhage. These disorders are associated with intrapulmonary shunt and an increased work of breathing. Common causes of type I (hypoxemic) respiratory failure Chronic bronchitis and emphysema (COPD) Pneumonia Pulmonary edema Pulmonary fibrosis Asthma Pneumothorax Pulmonary embolism Pulmonary arterial hypertension Pneumoconiosis Granulomatous lung diseases Cyanotic congenital heart disease Bronchiectasis Adult respiratory distress syndrome Fat embolism syndrome Kyphoscoliosis Obesity Common causes of type II (hypercapnic) respiratory failure Chronic bronchitis and emphysema (COPD) Severe asthma Drug overdose Poisonings Myasthenia gravis Polyneuropathy Poliomyelitis Primary muscle disorders Porphyria Cervical cordotomy Head and cervical cord injury Primary alveolar hypoventilation Obesity hypoventilation syndrome Pulmonary edema Adult respiratory distress syndrome Myxedema Tetanus Laboratory Studies • Arterial blood gases in all patients who are seriously ill or in whom respiratory failure is suspected. • A complete blood count; anemia can contribute to tissue hypoxia, whereas polycythemia may indicate chronic hypoxemic respiratory failure. • Abnormalities in renal and hepatic function may either provide clues to the etiology of respiratory failure or alert the clinician to complications associated with respiratory failure. • Abnormalities in electrolytes such as potassium, magnesium, and phosphate may aggravate respiratory failure. Laboratory studies • Measuring serum creatine kinase with fractionation and troponin I helps exclude recent myocardial infarction in a patient with respiratory failure. • An elevated creatine kinase with a normal troponin I may indicate myositis, which occasionally can cause respiratory failure. • In chronic hypercapnic respiratory failure, serum thyroid-stimulating hormone should be measured to evaluate the possibility of hypothyroidism, a potentially reversible cause of respiratory failure. Imaging Studies Chest radiograph • Chest radiography is essential because it frequently reveals the cause of respiratory failure. However, distinguishing between cardiogenic and noncardiogenic pulmonary edema often is difficult. • Increased heart size, vascular redistribution, peribronchial cuffing, pleural effusions, septal lines, and perihilar bat-wing distribution of infiltrates suggest hydrostatic edema; the lack of these findings suggests ARDS. Imaging studies Echocardiography • Echocardiography need not be performed routinely in all patients with respiratory failure. However, it is a useful test when a cardiac cause of acute respiratory failure is suspected. • The findings of left ventricular dilatation, regional or global wall motion abnormalities, or severe mitral regurgitation support the diagnosis of cardiogenic pulmonary edema. • A normal heart size and normal systolic and diastolic function in a patient with pulmonary edema would suggest ARDS. • Echocardiography provides an estimate of right ventricular function and pulmonary artery pressure in patients with chronic hypercapnic respiratory failure. Pulmonary function tests Patients with acute respiratory failure generally are unable to perform pulmonary function tests (PFTs). However, PFTs are useful in the evaluation of chronic respiratory failure. • Normal values of forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) suggest a disturbance in respiratory control. • A decrease in FEV1 -to-FVC ratio indicates airflow obstruction, whereas a reduction in both the FEV1 and FVC and maintenance of the FEV1 -to-FVC ratio suggest restrictive lung disease. • Respiratory failure is uncommon in obstructive diseases when the FEV1 is greater than 1 L and in restrictive diseases when the FVC is more than 1 L. ECG An ECG should be performed to evaluate the possibility of a cardiovascular cause of respiratory failure; it also may detect dysrhythmias resulting from severe hypoxemia and/or acidosis. Right heart catheterization • This remains a controversial issue in the management of critically ill patients. • Invasive monitoring probably is not routinely needed in patients with acute hypoxemic respiratory failure, but when significant uncertainty about cardiac function, adequacy of volume resuscitation, and systemic oxygen delivery remain, right heart catheterization should be considered. • Measurement of pulmonary capillary wedge pressure may be helpful in distinguishing cardiogenic from noncardiogenic edema. • The pulmonary capillary wedge pressure should be interpreted in the context of serum oncotic pressure and cardiac function. MEDICAL CARE • A patient with acute respiratory failure generally should be admitted to a respiratory care or intensive care unit. • Most patients with chronic respiratory failure can be treated at home with oxygen supplementation and/or ventilatory assist devices along with therapy for their underlying disease. MEDICAL CARE Airway management • Assurance of an adequate airway is vital in a patient with acute respiratory distress. • The most common indication for endotracheal intubation (ETT) is respiratory failure. • ETT serves as an interface between the patient and the ventilator. • Another indication for ETT is airway protection in patients with altered mental status. MEDICAL CARE Correction of hypoxemia • After securing an airway, attention must turn to correcting the underlying hypoxemia, the most lifethreatening facet of acute respiratory failure. • The goal is to assure adequate oxygen delivery to tissues, generally achieved with a PaO2 of 60 mm Hg or an arterial oxygen saturation (SaO2) of greater than 90%. • Supplemental oxygen is administered via nasal prongs or face mask; however, in patients with severe hypoxemia, intubation and mechanical ventilation often are required. MEDICAL CARE Coexistent hypercapnia and respiratory acidosis may need to be addressed. This is done by correcting the underlying cause or providing ventilatory assistance. • Mechanical ventilation is used for 2 essential reasons: (1) to increase PaO2 and (2) to lower PaCO2. • Mechanical ventilation also rests the respiratory muscles and is an appropriate therapy for respiratory muscle fatigue. MEDICAL CARE Overview of mechanical ventilation • Positive-pressure versus negative-pressure ventilation • Controlled versus patient-initiated (ie, assisted) • Pressure-targeted versus volume-targeted: MEDICAL CARE Interface between patient and ventilator (mask vs endotracheal intubation) • Mechanical ventilation requires an interface between the patient and the ventilator. In the past, this invariably occurred through an endotracheal or tracheostomy tube, but in recent years, an increasing trend has occurred towards noninvasive ventilation, which can be accomplished by the use of either a full face mask or a nasal mask. • Following intubation, the position of the tube in the airway should be confirmed by auscultation of the chest and, ideally, by a carbon dioxide detector. As a general rule, the endotracheal tube should be inserted to an average depth of 23 cm in men and 21 cm in women (measured at the incisor). Confirm proper placement with a chest radiograph. • The tube should be secured. The pressure in the cuff generally should not exceed 25 mm Hg. • Endotracheal suctioning can be accomplished by either open-circuit or closedcircuit suction catheters. MEDICAL CARE Specific modes of ventilatory support • Pressure support ventilation (PSV) • Intermittent mandatory ventilation (IMV) (SIMV) • Assist-control ventilation • Volume-control ventilation. • Pressure-control ventilation • Pressure-control inverse-ratio ventilation (PCIRV) MEDICAL CARE Triggering mechanism: pressure versus flow triggering • In patient- assisted ventilation, the ventilator must sense the patient's inspiratory effort in order to deliver assistance. • With pressure-triggering, in a patient on no positive endexpiratory pressure (PEEP) with a trigger sensitivity set at 1 cm water, a breath is triggered whenever airway pressure falls below -1 cm water. In a patient on 5-cm water PEEP with the same trigger sensitivity, a breath is triggered whenever airway pressure falls below +4 cm water. • In flow-triggering, a flow sensitivity is selected. When the patient makes an inspiratory effort, the ventilator senses the decrease in flow returning through the circuit, and a breath is triggered. One problem with flow-triggering is that autotriggering sometimes results from leaks in the ventilator circuit. MEDICAL CARE Positive end-expiratory pressure • PEEP may recruit atelectatic alveoli and prevent their collapse • PEEP shifts lung water from the alveoli into the perivascular interstitial space and helps with recruitment of alveoli. • However, it does not decrease the total amount of extravascular lung water. • In patients with ARDS or ALI, PEEP is applied to recruit atelectatic alveoli, improving oxygenation and allowing a reduction in FiO2 to nontoxic levels (FiO2 <0.6). MEDICAL CARE Positive end-expiratory pressure •PEEP of 3-5 cm water to prevent a decrease in functional residual capacity in patients with normal lungs is a common practice. • Higher PEEP produces better oxygenation and lung compliance but no benefit to survival, time on ventilator, or nonpulmonary organ dysfunction. • Ideal PEEP helps to achieve adequate oxygenation and decrease the requirement for high FiO2 without causing harmful effects of PEEP. • Current evidence does not support routine application of high PEEP strategy in people with ALI or ARDS. • PEEP causes an increase in intrathoracic pressure, which may decrease venous return and cardiac output, particularly in patients with hypovolemia. MEDICAL CARE Inspiratory flow • In volume-targeted ventilation, inspiratory flow is a variable that is set by the physician or respiratory therapist. The inspiratory flow rate is selected on the basis of a number of factors, including the patient's inspiratory drive and the underlying disease. Two flow patterns are used commonly: (1) a constant-flow (ie, square-wave) pattern and (2) a decelerating-flow pattern. With a constant-flow pattern, inspiratory flow is held constant throughout the breath, whereas with a decelerating-flow pattern, flow rises quickly to a maximal value and then decreases progressively throughout the breath. MEDICAL CARE Inspiratory flow •In pressure-targeted ventilation, the inspiratory flow rate is a dependent variable that varies as a function of the preset pressure and the patient's own inspiratory effort. Because airway pressure is held constant while alveolar pressure rises during inspiration, the pressure difference between airway and alveoli decreases, leading to a decelerating pattern of inspiratory flow. MEDICAL CARE Determinants of ventilator-associated lung injury •Mechanical ventilation is associated with a variety of insults to the lung. •In the past, physicians focused on barotrauma, including pneumothorax, pneumomediastinum, and subcutaneous and pulmonary interstitial emphysema. The manifestations of barotrauma likely occur because of excessive alveolar wall stress. Excessive airway pressure by itself does not appear to cause barotrauma. In critically ill patients, the manifestations of barotrauma can be subtle, the earliest sign of pneumothorax in supine patients may be the deepsulcus sign or a collection of air anteriorly along cardiophrenic angle. MEDICAL CARE Determinants of ventilator-associated lung injury •More recently, lung damage indistinguishable from ARDS has been recognized to possibly be caused by certain patterns of ventilatory support. The mechanism was thought to be due to direct parenchymal injury and altered microvascular permeability secondary to high peak alveolar pressures. Recently, other investigators have shown that excessive tidal volumes resulting in alveolar overdistension are the most important factor in ventilatorassociated lung injury. •A strategy of using low tidal volumes in patients with ARDS who are on mechanical ventilation has led to a reduced incidence of barotrauma and improved survival rates in recently published clinical trials. MEDICAL CARE Mechanical ventilation in specific diseases General guidelines • The mode of ventilation should be suited to the needs of the patient. Following the initiation of mechanical ventilation, the ventilator settings should be adjusted based on the patient's lung mechanics, underlying disease process, gas exchange, and response to mechanical ventilation. • SIMV and assist-control ventilation often are used for the initiation of mechanical ventilation. • In patients with intact respiratory drive and mild-to-moderate respiratory failure, PSV may be a good initial choice. Supplemental oxygen • The lowest FiO2 that produces an SaO2 greater than 90% and a PaO2 greater than 60 mm Hg generally is recommended. • The prolonged use of FiO2 less than 0.6 is unlikely to cause pulmonary oxygen toxicity. MEDICAL CARE Acute respiratory distress syndrome •The primary objective is to accomplish adequate gas exchange while avoiding excessive inspired oxygen concentrations and alveolar overdistension. •Repeated cycles of opening and collapsing of inflamed and atelectatic alveoli are detrimental to the lung. Failure to maintain a minimum alveolar volume may further accentuate the lung damage. Transalveolar pressure (reflected by plateau pressure) exceeding 25-30 cm water is a risk factor for stretch injury to the lungs. •Patients with ARDS should receive a tidal volume of 6 mL/kg. The set tidal volume should be based on ideal rather than actual body weight. If the plateau pressure remains excessive (>30 cm water), further reductions in tidal volume may be necessary. This strategy may lead to respiratory acidosis, which requires either high respiratory rates and or sodium bicarbonate infusion. MEDICAL CARE Acute respiratory distress syndrome •Application of PEEP sufficient to raise the tidal volume above the lower inflection point (Pflex) on the pressure-volume curve may minimize alveolar wall stress and improve oxygenation. A pressure-volume curve can be constructed for an individual patient by measuring plateau pressures at different lung volumes. Pflex is the point at which the slope of the curve changes, indicating that the lung is operating at the most compliant part of the curve. •A lung-protective strategy where the PaCO2 is allowed to rise (permissive hypercapnia) may reduce barotrauma and enhance survival. •In some patients with ARDS, the prone position may lead to significant improvements in oxygenation; whether this translates to improved outcome is unknown. MEDICAL CARE Obstructive airway diseases •In patients with COPD or asthma, institution of mechanical ventilation may worsen dynamic hyperinflation (auto-PEEP or intrinsic PEEP [PEEPi]). The dangers of auto-PEEP include a reduction in cardiac output and hypotension and barotrauma. •The goals of mechanical ventilation in obstructive airway diseases are to unload the respiratory muscles, achieve adequate oxygenation, and minimize the development of dynamic hyperinflation. •Patients with status asthmaticus frequently develop severe dynamic hyperinflation. This can be minimized by delivering the lowest possible minute ventilation in the least possible time. Therefore, the initial ventilatory strategy should involve the delivery of relatively low tidal volumes (eg, 8-10 mL/kg) and lower respiratory rates (eg, 8-12 breaths per min) with a high inspiratory flow rate. MEDICAL CARE Obstructive airway diseases •In the absence of hypoxia, even marked levels of hypercapnia are preferable to normalize the PCO2, which could lead to dangerous levels of hyperinflation. •Patients often require large amounts of sedation and occasionally paralysis until the bronchoconstriction and airway inflammation have improved. •To measure trapped-gas volume (VEI), as recommended by some investigators, an attempt should be made to keep it below 20 mL/kg. The measurement of plateau pressure and auto-PEEP provide similar information and are much easier to perform. •A goal of mechanical ventilation is to unload the respiratory muscles while minimizing the degree of hyperinflation. The use of extrinsic PEEP may be considered in spontaneously breathing patients in order to reduce the work of breathing and to facilitate triggering of the ventilator. Avoid causing further hyperinflation, level of PEEP should be less than the level of auto-PEEP. MEDICAL CARE Facilitating patient-ventilator synchrony •Many patients experience asynchrony between their own spontaneous respiratory efforts and the pattern of ventilation imposed by the ventilator. This can occur with both controlled and patient-initiated modes of ventilation. •To achieve synchrony, the ventilator must not only sense and respond quickly to the onset of the patient's inspiratory efforts, it also must terminate the inspiratory phase when the patient's "respiratory clock" switches to expiration. Asynchronous interactions, commonly referred to as "fighting the ventilator," may occur when ventilator breaths and patient efforts are out of phase. This may lead to excessive work of breathing, increased respiratory muscle oxygen consumption, and decreased patient comfort. •Patient-ventilator asynchrony should be minimized. Modern ventilators are equipped with significantly better valve characteristics. Flow-triggering (with a continuous flow rate) appears to be more sensitive and more responsive to patient's spontaneous inspiratory efforts. •Patient-ventilator asynchrony often occurs in the presence of auto-PEEP. AutoPEEP creates an inspiratory threshold load and thereby decreases the effective trigger sensitivity. This may be partially offset by the application of external PEEP. •Sometimes, additional sedation may be necessary to achieve adequate patientventilator synchrony. Noninvasive ventilatory support •Noninvasive ventilation should be considered in patients with mildto-moderate acute respiratory failure. The patient should have an intact airway, airway-protective reflexes, and be alert enough to follow commands. •NPPV has proven beneficial in acute exacerbations of COPD and asthma, decompensated CHF with mild-to-moderate pulmonary edema, and pulmonary edema from hypervolemia. •In acute exacerbations of obstructive lung disease, NPPV decreases PaCO2 by unloading the respiratory muscles and supplementing alveolar ventilation. The results of several clinical trials support the use of NPPV in this setting. •The use of NPPV was shown to reduce complications, duration of ICU stay, and mortality. In patients in whom NPPV failed, mortality rates were similar to the intubated group (25% vs 30%). NPPV was administered on the ward. Long-term outcome of patients treated with NPPV is better. Noninvasive ventilatory support •NPPV also helps maintain an adequate PaO2 until the patient improves. •In cardiogenic pulmonary edema, NPPV improves oxygenation, reduces work of breathing, and may increase cardiac output. •When applied continuously to patients with chronic ventilatory failure, NPPV provides sufficient oxygenation and/or carbon dioxide elimination to sustain life by reversing or preventing atelectasis and/or resting the respiratory muscles. •Patients with obesity-hypoventilation syndrome benefit from NPPV by reversal of the alveolar hypoventilation and upper airway obstruction. •Most trials have used inspiratory pressures of 12-20 cm water; expiratory pressures of 0-6 cm water; and excluded patients with hemodynamic instability, uncontrolled arrhythmia, or a high risk of aspiration. Weaning from mechanical ventilation •Weaning or liberation from mechanical ventilation is initiated when the underlying process that necessitated ventilatory support has improved. In some patients, such as those recovering from uncomplicated major surgery or a toxic ingestion, withdrawal of ventilator support may be done without weaning. •A patient who has stable underlying respiratory status, adequate oxygenation (eg, PaO2/FiO2 >200 on PEEP <10 cm water), intact respiratory drive, and stable cardiovascular status should be considered for discontinuation of mechanical ventilation. •Over the years, many criteria have been used to predict success in weaning, including a minute ventilation of less than 10 L/min, maximal inspiratory pressure more than -25 cm water, vital capacity more than 10 mL/kg, absence of dyspnea, absence of paradoxical respiratory muscle activity, and agitation or tachycardia during the weaning trial. However, recent studies suggest that the rapid-shallow breathing index, ie, the patient's tidal volume (in liters) divided by the respiratory rate (breaths per min) during a period of spontaneous breathing, may be a better predictor of successful extubation. In a recent study, a daily trial of spontaneous breathing in patients with a rapid-shallow breathing index of less than 105 resulted in a shorter duration of mechanical ventilation. A spontaneous breathing trial of only 30 minutes appears adequate to identify patients in whom successful extubation is likely. Weaning from mechanical ventilation •In patients who are not yet ready to be liberated from the ventilator, one should focus on the cause of ventilator dependency, such as excessive secretions, inadequate respiratory drive, impaired cardiac function, and ventilatory muscle weakness, rather than the type of ventilator or the mode of assistance. •The weaning protocol could be designed with assist-control ventilation, with gradually increasing time spent in trials of spontaneous breathing or by gradually reducing the level of PSV. •SIMV appears to result in less rapid weaning than PSV or trials of spontaneous breathing. •Patient-ventilator desynchrony is an important component in a carefully designed weaning protocol. •Attention must be directed towards patient comfort, avoidance of fatigue, adequate nutrition, and prevention and treatment of medical complications during the weaning period. •Ventilator monitoring: Peak inspiratory and plateau pressures should be assessed frequently. Attempts should be made to limit the plateau pressure to less than 25 cm water. Expiratory volume is checked initially and periodically (continuously if ventilator-capable) to assure that the set tidal volume is delivered. In patients with severe airflow obstruction, auto-PEEP (PEEPi) should be monitored on a regular basis. MEDICAL CARE Monitoring of patients with acute respiratory failure •A patient with respiratory failure requires repeated assessments, which may range from bedside observations to the use of invasive monitoring. •These patients should be admitted to a facility where close observation can be provided. Most patients who require mechanical ventilation are critically ill; therefore, constant monitoring in a critical care setting is a must. •Cardiac monitoring, blood pressure, pulse oximetry, SaO2, and capnometry are recommended. An arterial blood gas determination should be obtained 15-20 minutes after the institution of mechanical ventilation. The pulse oximetry readings direct efforts to reduce FiO2 to a value less than 0.6, and the PaCO2 guides adjustments of minute ventilation. MEDICAL CARE Treatment of underlying cause •After the patient's hypoxemia is corrected and the ventilatory and hemodynamic status have stabilized, every attempt should be made to identify and correct the underlying pathophysiologic process that led to respiratory failure in the first place. •The specific treatment depends on the etiology of respiratory failure. THANK YOU