الفهرس 
Respiratory Failure
Invasive Mechanical VentilationOnly 14 pages are availabe for public view
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Abstract
Summary
Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, it may be classified as either hypoxemic or hypercapnic.
Hypoxemic respiratory failure (type I) is characterized by an arterial oxygen tension (Pa O2) lower than 60 mm Hg with a normal or low arterial carbon dioxide tension (Pa CO2). This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.
Hypercapnic respiratory failure (type II) is characterized by a PaCO2 higher than 50 mm Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (eg, asthma and chronic obstructive pulmonary disease [COPD]) .
Respiratory failure may be further classified as either acute or chronic. Although acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent .
Acute hypercapnic respiratory failure develops over minutes to hours; therefore, pH is less than 7.3. chronic respiratory failure develops over several days or longer, allowing time for renal compensation and an increase in bicarbonate concentration. Therefore, the pH usually is only slightly decreased .
The distinction between acute and chronic hypoxemic respiratory failure cannot readily be made on the basis of arterial blood gases. The clinical markers of chronic hypoxemia, such as polycythemia or corpulmonale, suggest a long-standing disorder.
Arterial blood gases should be evaluated in all patients who are seriously ill or in whom respiratory failure is suspected.
Hypoxemia is the major immediate threat to organ function. 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.
Respiratory failure may be associated with a variety of clinical manifestations. However, these are nonspecific, and very significant respiratory failure may be present without dramatic signs or symptoms. This emphasizes the importance of measuring arterial blood gases in all patients who are seriously ill or in whom respiratory failure is suspected. Chest radiography is essential. Echocardiography is not routinely done but is sometimes useful. Pulmonary functions tests (PFTs), if feasible, may be helpful. Electrocardiography (ECG) should be performed to evaluate the possibility of a cardiovascular cause of respiratory failure; it also may detect dysrhythmias resulting from severe hypoxemia or acidosis. Right-sided heart catheterization is controversial. Once respiratory failure is suspected on clinical grounds, arterial blood gas analysis should be performed to confirm the diagnosis and to assist in the distinction between acute and chronic forms. This helps assess the severity of respiratory failure and helps guide management .
A complete blood count (CBC) may indicate anemia, which can contribute to tissue hypoxia, whereas polycythemia may indicate chronic hypoxemic respiratory failure .
A chemistry panel may be helpful in the evaluation and management of a patient in 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 and other organ f unction .
Measuring serum creatine kinase with fractionation and troponin I helps exclude recent myocardial infarction in a patient with respiratory failure. An elevated creatine kinase level with a normal troponin I level may indicate myositis, which occasionally can cause respiratory failure .
In chronic hypercapnic respiratory failure, serum levels of thyroid-stimulating hormone (TSH) should be measured to evaluate the possibility of hypothyroidism, a potentially reversible cause of respiratory failure .
Chest radiography is essential in the evaluation of respiratory failure because it frequently reveals the cause (see the images below). However, distinguishing between cardiogenic and noncardiogenic pulmonary edema is often 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 acute respiratory distress syndrome (ARDS) .
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.
Patients with acute respiratory failure generally are unable to perform PFTs; however, these tests are useful in the evaluation of chronic respiratory failure.
Normal values for forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) suggest a disturbance in respiratory control. A decrease in the FEV1 -to-FVC ratio (FEV1/FVC) indicates airflow obstruction, whereas a reduction in both FEV1 and FVC and maintenance of FEV1/FVC suggest restrictive lung disease .
Respiratory failure is uncommon in obstructive diseases when FEV1 is greater than 1 L and in restrictive diseases when FVC is greater than 1 L .
The risks of oxygen therapy are oxygen toxicity and carbon dioxide narcosis. Pulmonary oxygen toxicity rarely occurs when a fractional concentration of oxygen in inspired gas (FI O2) lower than 0.6 is used; therefore, an attempt to lower the inspired oxygen concentration to this level should be made in critically ill patients .
Carbon dioxide narcosis occasionally occurs when some patients with hypercapnia are given oxygen to breathe. Arterial carbon dioxide tension (Pa CO2) increases sharply and progressively with severe respiratory acidosis, somnolence, and coma. The mechanism is primarily the reversal of pulmonary vasoconstriction and the increase in dead space ventilation .
Hypoxemia is the major immediate threat to organ function. 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 .
Patients generally are prescribed bed rest during early phases of respiratory failure management. However, ambulation as soon as possible helps ventilate atelectatic areas of the lung.
Mechanical ventilation is used for 2 essential reasons: (1) to increase Pa O2 and (2) to lower Pa CO2. Mechanical ventilation also rests the respiratory muscles and is an appropriate therapy for respiratory muscle fatigue .
The use of mechanical ventilation during the polio epidemics of the 1950s was the impetus that led to the development of the discipline of critical care medicine. Before the mid-1950s, negative-pressure ventilation with the use of iron lungs was the predominant method of ventilatory support. Currently, virtually all mechanical ventilatory support for acute respiratory failure is provided by positive-pressure ventilation. Nevertheless, negative-pressure ventilation still is used occasionally in patients with chronic respiratory failure.
Over the years, mechanical ventilators have evolved from simple pressure-cycled machines to sophisticated microprocessor-controlled systems. The following is a brief overview of the basic principles of their use .
For air to enter the lungs, a pressure gradient must exist between the airway and the alveoli. This can be accomplished either by raising pressure at the airway (positive-pressure ventilation) or by lowering pressure at the level of the alveolus (negative-pressure ventilation).
The iron lung or tank ventilator is the most common type of negative-pressure ventilator used in the past. These ventilators work by creating subatmospheric pressure around the chest, thereby lowering pleural and alveolar pressure and facilitating flow of air into the patient’s lungs. These ventilators are bulky and poorly tolerated and are not suitable for use in modern critical care units. Positive-pressure ventilation can be achieved via an endotracheal or tracheostomy tube or noninvasively through a nasal mask or face mask .
Ventilatory assistance can be controlled or patient-initiated. In controlled ventilation, the ventilator delivers assistance independent of the patient’s own spontaneous inspiratory efforts. In contrast, during patient-initiated ventilation, the ventilator delivers assistance in response to the patient’s own inspiratory efforts. The patient’s inspiratory efforts can be sensed either by pressure or flow-triggering mechanisms .
During positive-pressure ventilation, either pressure or volume may be set as the independent variable.
In volume-targeted (or volume preset) ventilation, tidal volume is the independent variable set by the physician or respiratory therapist, and airway pressure is the dependent variable. In this type of ventilation, airway pressure is a function of the set tidal volume and inspiratory flow rate, the patient’s respiratory mechanics (compliance and resistance), and the patient’s respiratory muscle activity .
In pressure-targeted (or pressure preset) ventilation, airway pressure is the independent variable, and tidal volume is the dependent variable. The tidal volume during pressure-targeted ventilation is a complex function of inspiratory time, the patient’s respiratory mechanics, and the patient’s own respiratory muscle activity .
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, Sa O2, 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 FI O2 to a value less than 0.6, and the Pa CO2 guides adjustments of minute ventilation.