<p> THE KURSK STATE MEDICAL UNIVERSITY DEPARTMENT OF SURGICAL DISEASES № 1</p><p>RESPIRATORY FAILURE</p><p>Information for self-training of English-speaking students The chair of surgical diseases N 1 (Chair-head - prof. S.V.Ivanov)</p><p>BY ASS. PROFESSOR I.S. IVANOV </p><p>KURSK-2010 Respiratory failure</p><p>Respiratory failure: </p><p>Impairment of gas exchange between ambient air and circulating blood, occurring in intrapulmonary gas exchange or in the movement of gases in and out of the lungs.</p><p>In intrapulmonary gas exchange, O2 is transferred to arterial blood (oxygenation) and CO2 eliminated from it. Impaired intrapulmonary gas exchange usually results primarily in hypoxemia, because the diffusing capacity of CO2 is so much greater than that of O2 and because regional zones of hypoventilation (inadequate alveolar ventilation) with poor CO2 removal can be compensated for by increased ventilation of normal lung units. The process of moving gases in and out of the lungs may be inadequate (global or generalized hypoventilation), producing primarily hypercapnia, although hypoxemia occurs as well. Many pathologic processes cause simultaneous failure of both of these functions, but selective or disproportionate impairment of one or the other is more common.</p><p>Hypoxemia </p><p>The following mechanisms may act alone or together to cause arterial hypoxemia:</p><p>A decrease in the partial pressure of inspired O2 (PIO2) occurs at high altitude (in response to reduced barometric pressure), during toxic gas inhalation, and near fires, which consume O2.</p><p>Hypoventilation causes levels of alveolar O2 (PAO2) and arterial O2 (PaO2) to fall. During the initial phase of hypoventilation or apnea, PaO2 may fall more precipitously than arterial CO2 levels (PaCO2) rise because body stores of O2 are modest while those of CO2 are much greater. However, as the PaCO2 and PACO2 increase (the PaCO2 increases by 3 to 6 mm Hg/min in a totally apneic patient), the PAO2 must fall because the steady state concentration of PAO2 has a fixed relationship to PaCO2, as predicted by the alveolar gas equation PAO2 = PIO2 - PaCO2/R. R is the respiratory exchange ratio (the ratio of CO2 production to O2 consumption at steady state). When intrapulmonary gas exchange is normal, the</p><p>PAO2/PaO2 gradient remains unchanged, and the fall in PaO2 approximates the fall in PAO2.</p><p>Impaired diffusion is produced by physical separation of gas and blood (as in diffuse interstitial lung disease) or by shortened transit time of RBCs through the capillaries (as in pulmonary emphysema with loss of capillary bed).</p><p>Regional ventilation/perfusion ( / ) mismatching almost always contributes to clinically important hypoxemia. Lung units ventilated poorly in relation to perfusion result in desaturation; the effect depends partly on the O2 content of mixed venous blood. A reduced venous O2 content worsens the hypoxemia further. The most common causes are disorders that result in poorly ventilated lung units (eg, airway obstruction, atelectasis, consolidation, or edema of cardiogenic or noncardiogenic origin). The degree of hypoxic pulmonary vasoconstriction, which diverts blood from poorly ventilated lung zones, determines how much a reduction in ventilation contributes to hypoxemia. Because the capillary blood that exits from well-ventilated lung units is already saturated with O2, hyperventilation with an increase in the PAO2 does not fully compensate for / mismatching. However, O2 supplementation impressively reverses hypoxemia when / mismatching, hypoventilation, or impaired diffusion is the cause, because the PAO2 of even poorly ventilated units increases enough to allow full saturation of Hb. When patients breathe 100% O2, only perfused alveoli that are totally unventilated (shunt units) contribute to hypoxemia.</p><p>Shunt (the direct bypass of systemic venous blood to the arterial circulation) can be intracardiac, as in cyanotic right-to-left congenital heart disease, or can result from blood passing through abnormal vascular channels within the lung (eg, pulmonary arteriovenous fistulae). The most common causes are pulmonary diseases that produce regional / mismatching, with regional ventilation being nearly or totally absent.</p><p>The admixture of abnormally desaturated venous with arterial blood lowers</p><p>PAO2 in patients with pulmonary disease and impaired intrapulmonary gas exchange. Mixed venous O2 saturation (S O2) is directly influenced by any imbalance between O2 consumption and O2 delivery. Thus, anemia uncompensated for by increased cardiac output or a cardiac output insufficient for metabolic needs can cause S O2 and PaO2 to decrease, even when lung pathology remains unchanged.</p><p>Hypercapnia </p><p>Major mechanisms that can cause or contribute to hypercapnia are insufficient respiratory drive, a defective ventilatory pump, a workload so great that respiratory muscle fatigue develops, and intrinsic lung disease with severe / mismatching. The last two mechanisms often coexist.</p><p>Although an increase in the partial pressure of inspired CO2 (eg, in proximity to an indoor fire or with deliberate inhalation of CO2) may occasionally cause hypercapnia, hypercapnia almost always indicates ventilatory insufficiency or failure.</p><p>The PaCO2 is proportional to CO2 production ( CO2) and is inversely proportional to alveolar ventilation ( A) according to the standard equation (where k = a constant) An increase in CO2 due to fever, seizures, agitation, or other factors is usually compensated for by an immediate increase in A. Hypercapnia develops only if the increase in A is inappropriately low.</p><p>Hypoventilation is the most common cause of hypercapnia. In addition to an elevated PaCO2, respiratory acidosis is present in proportion to the extent of tissue and renal buffering.</p><p>A reduced A can be due to a decrease in total minute ventilation ( E)--often called global hypoventilation--or to an increase in dead space ventilation per minute ( D). ( E equals exhaled volume per breath [tidal volume] times respiratory rate per minute.)</p><p>A drug overdose with suppression of the brain stem respiratory centers is one cause of global hypoventilation.</p><p>Dead space (VD), or wasted ventilation, occurs when lung regions are well ventilated but underperfused or, conversely, when well-perfused alveoli are ventilated with gas that contains a high fraction of CO2. Such regions eliminate less than their normal share of CO2. The fraction of each tidal breath not involved in CO2 exchange (VD/VT), called the physiologic dead space fraction, can be estimated as follows:</p><p>(PECO2 = mixed expired concentration of CO2.) An alternative equation shows how an elevation in dead space contributes to hypercapnia; CO2, E, and VT are assumed to be constant.</p><p>Etiology </p><p>Respiratory failure (resulting in hypoxemia and/or hypercapnia) may be caused by airway obstruction; dysfunction of lung parenchyma but not of the airways; and ventilatory pump failure.</p><p>For effective ventilation, negative pleural pressure must be generated by the respiratory muscles acting in a coordinated fashion on an intact rib cage. Ventilatory pump failure may be caused by primary dysfunction of the CNS respiratory centers, dysfunction of the ventilatory neuromuscular apparatus, or structural abnormalities of the chest wall that prevent effective transmission of respiratory muscle forces. The airways and lung parenchyma may be anatomically normal. For example, disorders (eg, flail chest, kyphoscoliosis) that alter the structure of the chest wall can cause inefficient coupling of muscle contraction and pleural pressure generation. Hypoventilation can also occur when the inspiratory muscles of the diaphragm and rib cage contract asynchronously (eg, during diaphragmatic paralysis, quadriplegia, or acute stroke).</p><p>Often, the primary reason for pump dysfunction is reduced muscular power. The endurance of muscle fibers is determined by the balance of nutritional supply and demand. Therefore, respiratory muscles deprived of nutrients because of hypotension or hypoxemia perform inefficiently and become fatigued.</p><p>Acute hyperinflation severely reduces the efficiency of the ventilatory pump even when the strength of individual muscle fibers remains normal. Not only are the inspiratory muscle fibers foreshortened so that they produce less force, but also the work that the muscles must do is increased because of residual end-expiratory alveolar recoil tension and reduced compliance of the lung's connective tissue at high lung volumes. Furthermore, altered geometry (eg, flattened diaphragm, expanded rib cage) limits the pleural pressure change that can be generated during forceful contraction. During positive pressure ventilation, acute hyperinflation is associated with a positive end-expiratory difference between alveolar and central airway pressures (auto-PEEP).</p><p>Symptoms and Signs </p><p>The clinical symptoms and signs of respiratory failure are nonspecific and may be minimal even when hypoxemia, hypercarbia, and acidemia are severe. The primary physical signs of ventilatory fatigue are vigorous use of accessory ventilatory muscles, tachypnea, tachycardia, declining tidal volume, irregular or gasping breathing patterns, and paradoxical abdominal motion.</p><p>Acute hypoxemia may cause diverse problems, including cardiac arrhythmia and coma. Some alteration of consciousness is typical, and confusion is common.</p><p>Chronic reduction in PaO2 is generally well tolerated by patients with adequate cardiovascular reserve. However, alveolar hypoxia (PAO2 < 60 mm Hg) can induce pulmonary arteriolar vasoconstriction and increase pulmonary vascular resistance, leading, over weeks to months, to pulmonary hypertension, right ventricular hypertrophy (cor pulmonale), and eventual right ventricular failure.</p><p>Hypercapnia may produce acidemia. Sudden increases in PaCO2 occur much faster than compensatory increases in extracellular buffer base. Acute decreases in cerebral pH increase ventilatory drive; however, over time, buffering capacity in the CNS increases, eventually blunting the decrease in cerebral pH and reducing ventilatory drive.</p><p>The effects of acute hypercapnia are much less well tolerated than those of chronic hypercapnia. Acute hypercapnia may cause changes in sensorium ranging from subtle personality changes and headache to marked confusion and narcosis. Hypercapnia also causes cerebral vasodilation and increased CSF pressure, a major problem in patients with acute head injury. Acute CO2 retention causes acidemia, which when severe (pH < 7.3), contributes to pulmonary arteriolar vasoconstriction, systemic vascular dilation, reduced myocardial contractility, hyperkalemia, hypotension, and cardiac irritability, with the potential for life- threatening arrhythmias.</p><p>Diagnosis </p><p>Blood gas measurement (PaO2, PaCO2, and pH) is the main tool for diagnosing and judging the severity of respiratory failure. In many cases, it must be repeated frequently to assess deterioration or improvement.</p><p>Neuromuscular function is evaluated by observing the ventilatory pattern and measuring vital capacity, tidal volume, breathing frequency, and maximal inspiratory pressure. The ratio of breathing frequency to tidal volume is particularly helpful; > 100 breaths/min/L indicates severe weakness or fatigue. The intensity of ventilatory drive is most practically assessed by looking for signs of patient distress (respiratory rate > 30/min, vigorous use of accessory ventilatory muscles, paradoxical abdominal motion) and by examining PaCO2 in relation to the expired minute ventilation ( E) requirement. For example, if PaCO2 is high (> 45 mm Hg) and E and breathing frequency are modest or low, drive may be suppressed or mechanics impaired; the presence of agitation or distress argues for the latter.</p><p>If the cause of ventilatory failure is not obvious, certain bedside measurements help define the responsible mechanisms. The workload of breathing is reflected in the E, by the vigor of respiratory muscle activity, and in such indexes of breathing workload as the mean, plateau, and peak inspiratory pressures during passive machine inflation. Calculating the dead space fraction (VD/VT) and measuring</p><p>CO2 production may help define factors contributing to the ventilatory requirement. In acute ventilatory failure, impedance of chest inflation is difficult to assess precisely, except during mechanical ventilation, when it is best gauged by simple measures of chest mechanics (eg, airway resistance and respiratory system compliance).</p><p>Treatment </p><p>The primary aims are to maintain adequate O2 delivery, to alleviate an excessive breathing workload, and to establish electrolyte and pH balance while preventing further damage from O2 toxicity, barotrauma, infection, or other iatrogenic complications. Atelectasis, fluid overload, bronchospasm, increased respiratory secretions, and infection yield to specific measures, but treatment of other problems (eg, adult respiratory distress syndrome [ARDS], respiratory muscle fatigue, and structural abnormalities of the lung and chest wall) is largely supportive.</p><p>O2 therapy: Increasing the fraction of inspired O2 (FIO2) increases PaO2 whenever true shunt is not responsible for hypoxemia. Under usual circumstances, the goal is to increase Hb saturation to at least 85 to 90% without causing O2 toxicity. Many patients with chronic hypoxemia tolerate a PaO2 < 55 mm Hg; however, whatever the cause for ventilatory failure, a PaO2 between 60 and 80 mm Hg is usually desirable for adequate O2 delivery to tissues and for amelioration of pulmonary hypertension induced by hypoxemia. Because of the sigmoidal nature of the oxyhemoglobin dissociation curve, a PaO2 > 80 mm Hg does not significantly increase the O2 content of blood. The lowest FIO2 that provides an acceptable PaO2 should be selected. For patients with pulmonary insufficiency caused by / imbalances and diffusion limitation (eg, in obstructive pulmonary disease), an FIO2 < 40% usually suffices, with 25 to 35% being adequate for most patients. O2 toxicity is both concentration- and time-dependent. Sustained elevations in FIO2 > 60% result in inflammatory changes, alveolar infiltration, and, eventually, pulmonary fibrosis. An FIO2 > 60% should be avoided unless necessary for the patient's survival. An FIO2 < 60% is well tolerated for long periods without clinically evident toxicity.</p><p>An FIO2 < 40% can be given via nasal cannulas or a face mask. With a face mask, the flow of O2 required depends on the FIO2 desired and the mask design. With nasal cannulas, an O2 flow of 2 to 4 L/min ordinarily can raise PaO2 to therapeutic levels. However, the FIO2 delivered to the patient can only be estimated. Such estimates require knowing the total minute ventilation ( E) of the patient breathing room air and the duration of inspiration and expiration. If the time in both phases of ventilation is equal, only the flow of 100% O2 from the O2 reservoir is delivered to the patient. Thus, for a minute ventilation of 10 L/min with a 4-L/min flow of</p><p>100% O2 through a nasal cannula, the FIO2 delivered to the patient is estimated at (2 × 100%) + (8 × 21%)/10 L = 37% O2. If minute ventilation rises and O2 flow is unchanged, the FIO2 decreases. Because of the uncertainties in such estimates (eg, admixture of O2 with room air, mouth breathing, varying respiratory rate), the PaO2 or arterial O2 saturation (SaO2), measured by noninvasive oximetry, must be monitored regularly.</p><p>Excessive O2 administration is a common cause of respiratory depression in the management of CO2 retention. With chronic hypercapnia, the respiratory center may become insensitive to changes in PaCO2 and respond primarily to hypoxic stimuli. If PaO2 is raised excessively, the hypoxic ventilatory drive is obliterated, and further CO2 retention may ensue with worsening respiratory acidosis. Such a complication is prevented by judicious use of O2 and is detected at an early stage most effectively by arterial blood gas monitoring. If supplying O2 during spontaneous ventilation leads to a rising PaCO2 and acidemia, mechanical assistance is necessary. Use of positive pressure: Continuous positive airway pressure (CPAP), bilevel positive airway pressure (BiPAP), positive end-expiratory pressure (PEEP), and specialized techniques for increasing mean alveolar pressure (eg, inverse ratio ventilation) often reopen closed alveolar units, thereby reducing right-to-left shunt and the need for supplemental O2.</p><p>CPAP, a nonventilator technique that uses a face mask, recruits lung volume and often improves the PaO2/FIO2 ratio. It is most often used in patients with modest ventilatory requirements and acute atelectasis or pulmonary edema. BiPAP varies airway pressure about two levels, accomplishing both ventilatory assistance and higher end-expiratory lung volumes.</p><p>PEEP at low levels (3 to 5 cm H2O) can benefit virtually all intubated, mechanically ventilated patients with respiratory failure; it helps compensate for the volume loss that accompanies the supine posture and translaryngeal intubation. The optimal level of PEEP to be used is a function of tidal volume; higher levels of PEEP are usually required with small tidal volumes (< 7 mL/kg). PEEP may need to be > 15 cm H2O to effect acceptable arterial oxygenation at a well-tolerated FIO2. PEEP's volume-recruiting effects and ability to improve the PaO2 can be negated if vigorous expiratory muscle contraction forces lung volume lower than the relaxed end-expiratory (equilibrium) position. When this breathing pattern is evident, sedation or paralysis can help. When pulmonary infiltration is predominantly unilateral, delivering the same level of PEEP to both lungs may be ineffective, because it diverts blood from the healthy lung to the diseased one. With independent lung ventilation, the pattern of lung inflation, FIO2, and PEEP may be tailored to each lung.</p><p>Specific measures: Some measures can help compensate for impaired O2 exchange. Optimizing Hb concentration can improve O2-carrying capacity, although if the Hct becomes too high, O2 delivery can be impaired because of increased blood viscosity. Although controversial, the optimal Hb for most acutely ill patients with severe hypoxemia may be in the range of 10 to 12 g/dL. Correcting acute alkalemia improves Hb performance.</p><p>Reducing tissue O2 requirements can be as effective as improving O2 delivery. Fever, agitation, overfeeding, vigorous respiratory activity, shivering, sepsis, burns, tissue injury, seizures, and other common clinical conditions increase O2 consumption; aggressive steps should be taken to control them. Sedation and pharmacologic paralysis reduce O2 consumption in patients who remain agitated or who fight the ventilator. However, protracted paralysis must be avoided because it silences the cough mechanism, creates a monotonous breathing pattern that encourages secretion retention in dependent regions, and may accentuate muscle weakness and atrophy. Maintaining cardiac output by the appropriate use of fluids and inotropic drugs is crucial in the treatment of hypoxemia. Because extravascular water accumulates readily in many lung conditions, fluids should be used judiciously. A delicate balance must be maintained because severe fluid restriction, although often reducing lung water and improving O2 exchange, may compromise perfusion of the gut, kidneys, and other vital organs.</p><p>Assisting failing circulation, whether from cardiac or noncardiac causes, may help correct a low PaO2; measures include fluid manipulation, pressors, inotropic drugs, and reduction of O2 consumption. In patients with pulmonary edema, diuretics and other measures may help mobilize extravascular lung water, thereby increasing lung compliance, reducing cardiac asthma, and lessening the workload of the respiratory muscles. Relieving cardiac ischemia, lessening left ventricular afterload, or using a calcium channel blocker may decrease pulmonary vascular congestion and hypoxemia in patients with diastolic cardiac dysfunction.</p><p>Corticosteroids should not be used routinely for diffuse parenchymal pulmonary diseases, pulmonary edema, or ARDS the increased catabolism, protein wastage, and risk of infection far outweigh the potential therapeutic benefit in the first phase of respiratory failure. Nonetheless, certain patients (eg, those with proven vasculitis, fat embolism, acute eosinophilic pneumonia, or allergic reactions that contribute to the hypoxemia) may benefit. Corticosteroids may help more consistently in the later fibroproliferative stage of ARDS. Corticosteroids also benefit patients with acute asthma or an exacerbation of COPD.</p><p>Position changes may be beneficial. The change from the supine to upright position produces an increase in lung volume equivalent to about 5- to 12-cm H2O PEEP, depending on thoracic compliance. When possible, recumbent bedridden patients should be turned often (especially during coma or paralysis). Alternating lateral decubitus positions maximally stretches different regions of the lung and improves secretion drainage. When one lung is affected disproportionately, oxygenation may improve dramatically when the good lung is in the dependent position. However, care should be taken to ensure that secretions from the infiltrated lung are not aspirated into the airways of the other. Furthermore, certain patients with ARDS undergo marked O2 desaturation when repositioned (for reasons that are poorly understood). The prone position is often dramatically effective in the early stages of ARDS. Although the reason for this response is not completely understood, redistribution of resting lung volume with expansion of the dorsal areas is likely to be the primary benefit.</p><p>Clearing secretions from upper and lower airways is crucial. Parenteral hydration may help keep secretions adequately liquefied. Occasionally, mucolytic drugs (eg, potassium iodide preparations, acetylcysteine) are used if secretions remain tenacious despite adequate hydration and humidification of inspired air. Antibiotics and corticosteroids may help reduce the volume of secretions in selected patients. If the patient's own coughing efforts are ineffective, chest physiotherapy techniques (positioning, chest percussion) may be helpful. Secretions retained despite these measures must be removed by suctioning. Secretions in the lower airways can be sucked out through a catheter introduced past the vocal cords via the nose. If this method is unsuccessful or the lower airway secretions are too copious, an artificial airway is usually required. For short periods, an oral or nasal endotracheal tube can be used; if suctioning is required for prolonged periods, a tracheostomy may be necessary.</p><p>Moistening all inspired gas mixtures delivered to the trachea helps ensure the reduced viscosity of secretions. A heated humidifier moisturizes the inspiratory air stream most effectively; alternatively, hygroscopic disposable humidifiers (artificial noses) can be placed in the common channel of the ventilator circuit to recover exhaled moisture and return it to inhaled air.</p><p>Bronchodilators are indicated when bronchospasm and bronchial edema are factors. Airway resistance can be decreased and gas exchange improved by - adrenergic or anticholinergic drugs given as aerosols and by theophylline derivatives or corticosteroids given IV or orally. Nebulizers to deliver the aerosols may be attached to a mechanical ventilator or driven by a source of pressurized gas. Metered-dose inhalers can be used with or without a ventilator.</p><p>Antibiotics are given to control infection.</p><p>Precautions to minimize complications: In patients with acute lung injury, positive airway pressure, O2, and vasopressors and vasodilators are potentially dangerous. Thus, the need for PEEP, the level of ventilator support, and the FIO2 level should be frequently reassessed. Mean intrathoracic pressure can often be reduced by allowing the patient to provide as much ventilatory power as is compatible with comfort, eg, using intermittent mandatory ventilation.</p><p>Often, semiconscious, agitated, confused, or disoriented patients who receive mechanical ventilation must be restrained and sedated, because abrupt ventilator disconnection and accidental extubation can rapidly produce lethal bradyarrhythmias, hypoxemia, asphyxia, or aspiration of gastric contents. In patients with pulmonary edema, the interruption of PEEP for even brief periods (eg, during suctioning or tubing changes) may cause profound desaturation that is difficult to reverse as lung volume falls and the airways flood with edematous fluid. Paralyzed patients must be carefully monitored because ventilation is totally machine-dependent. Because air swallowing and ileus are common, the stomach should be decompressed in most recently intubated patients. The clinician must be ready to decompress a lung tension cyst or a pneumothorax immediately.</p><p>Mechanical Ventilation In current practice, positive pressure ventilation (PPV) is the only form of support for acute respiratory failure. Ventilators that apply negative pressure to the chest (tank, cuirass, poncho-wrap) require a rigid structural support for the vacuum compartment that greatly impedes intensive care nursing.</p><p>Criteria for intubation and mechanical ventilation include progressive acidemia, hypoxemia, and circulatory dysfunction. Before instituting mechanical ventilation, the clinician must select the mode of ventilation (the type and frequency of machine-supported cycles), the FIO2 to be delivered, the sensitivity of the machine to patient efforts, and the applied level of PEEP. Machine cycles can be either pressure- or flow-regulated and either volume-, flow-, time-, or pressure-cycled.</p><p>Pressure-cycled ventilators are simple in design and low in cost. However, because the tidal volume delivered during each respiratory cycle depends on the duration of the inspiratory phase and the impedance of the chest (resistance, compliance), these ventilators do not reliably provide a specified tidal volume or minute ventilation. Their use is confined to nonintubated patients requiring insufflation of bronchodilators or large tidal volumes to reverse atelectasis.</p><p>Volume-cycled ventilation has long been the standard type of ventilatory support for all forms of severe respiratory failure. All modern ventilators can provide it as well as several other modes that vary in ventilatory waveform, cycles, percentage of support provided, and method of terminating the machine-aided cycle. For many patients with moderate illnesses who can tolerate a pressurized nasal or orofacial mask, ventilation can be accomplished without tracheal intubation.</p><p>Full ventilatory support is designed to perform the complete work of breathing and attempts to provide an adequate tidal volume at a specified frequency. Flow- regulated volume-cycled breaths are the standard. The clinician selects the desired tidal volume, inspiratory flow waveform (eg, constant or decelerating), and peak flow rate. Once these are selected, peak airway cycling pressure varies depending on inflation impedance and end-expiratory alveolar pressure. When the pressure- regulated time-cycled variant (pressure-controlled ventilation) is used, pressure and inspiratory duration are selected and tidal volume is allowed to vary with inflation impedance. Either type of cycle can be set to occur at a fixed rate (controlled ventilation) or in response to patient effort (assist/control mode ventilation). A backup frequency rate is specified to trigger the machine if the patient does not do so.</p><p>Partial ventilatory support is indicated when the patient can comfortably perform a portion of the breathing workload, as during the process of machine withdrawal (weaning). Assistance can be provided for every spontaneous breath with pressure support, a flow-cycled technique that rapidly builds airway pressure to a fixed level with every breath. High or low levels of assistance can be provided, depending on the pressure selected. On newer equipment, the shape of the pressure waveform and the flow off-switch criterion can be adjusted. Pressure support helps to overcome endotracheal tube resistance, which can be surprisingly high during respiratory failure. When the appropriate level of pressure is given, pressure support tends to be comfortable in that the patient has some control over the flow profile and cycle duration. Synchronized intermittent mandatory ventilation uses either flow-regulated, volume-cycled or pressure-regulated, time-cycled breaths to provide the machine support at a frequency determined by the clinician. The level of support is varied not by adjusting the cycle characteristics but by adjusting the number of machine-aided cycles. This type of ventilation is often combined with pressure support to achieve optimum patient comfort during weaning.</p><p>Other forms of mechanical ventilation are less commonly used. High-frequency ventilators (jet or oscillators) cycle small pulses of gas rapidly, achieving gas exchange with very small excursions of tidal volume. Their usefulness has been limited in adult patients with respiratory failure, in part because establishing adequate gas exchange is largely an empiric process requiring considerable operator skill. Inverse ratio ventilation prolongs the inspiratory phase to occupy >= 50% of the inspiratory cycle, thereby raising mean alveolar pressure and slowing end-inspiratory flow. This type of ventilation is usually used with sedation and paralysis as supportive therapy for oxygenation failure. Some of the newest modes regulate the degree of partial ventilatory support to satisfy tidal volume and/or minute ventilation criteria with the least required pressure. PEEP (see above) can be added to systems that provide high-frequency or inverse ratio ventilation as well as to all conventional modes of ventilation.</p><p>Complications: Any mechanical ventilator may decrease venous return to the thorax, cardiac output, and systemic BP, especially if the driving pressure into the lung is high. These problems are likely to occur with high inspiratory pressure, hypovolemia, and inadequate vasomotor control due to drugs, peripheral neuropathy, or muscle weakness.</p><p>Barotrauma--damage to the lung induced by high cycling pressures--may take the form of tissue rupture (eg, pneumomediastinum, pneumothorax, subcutaneous emphysema, systemic gas embolism), parenchymal lung injury (bronchopulmonary dysplasia), or pulmonary edema. Such damage is likely to occur when pressures distending the alveoli are excessive (> 35 cm H2O) or when large tidal volumes (> 12 mL/kg) are used with PEEP insufficient to prevent the collapse of unstable lung units.</p>