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MD Consult: Books: Goldman: Cecil Medicine: SPECIFIC COMMON TREATMENT SCENARIOS

Goldman: Cecil Medicine, 23rd ed.

Copyright © 2007 Saunders, An Imprint of Elsevier


Initiation of Mechanical Ventilation

The initiation of mechanical ventilation involves several steps in clinical decision making ( Table 106-1 ). Despite the utility of such guidelines, each patient must be evaluated for specific factors that could modify the recommendation or mandate an alternative.

TABLE 106-1   — 

   1.    Ventilatory mode

   Unintubated patients:
       NIPPV for patients with COPD and acute hypercapnic respiratory failure if alert, cooperative, and hemodynamically stable
       NIPPV not routinely recommended for acute hypoxemic respiratory failure
   Intubated patients:
       Assist/control with volume-limited ventilation as initial mode
       Consider specific indications for PCV or HFOV (see text) in acute lung injury
       SIMV: consider if some respiratory effort, dyssynchrony
       PSV: consider if patient’s effort good, ventilatory needs moderate to low, and patient more comfortable during PSV trial
   2.    Oxygenation

       If infiltrates on chest radiograph, then

   FIO2: begin with 0.8–1.0, reduce according to SpO2
   PEEP: begin with 5 cm H2O, increase according to PaO2 or SpO2, FIO2 requirements, and hemodynamic effects; consider PEEP/FIO2 “ladder” (see Fig. 106-4 ); goal of SpO2 >90%, FIO2 ≤ 0.6
       No infiltrates on chest radiograph (COPD, asthma, PTE),

   FIO2: start at 0.4 and adjust according to SpO2 (consider starting higher if pulmonary embolism is strongly suspected)
   3.    Ventilation

       Tidal volume: begin with 8 mL/kg PBW (see Fig. 106-4 for formulas); decrease to 6 mL/kg PBW over a few hours if acute lung injury present (see Fig. 106-4 )
       Rate: begin with 10–20 breaths/min (10–15 if not acidotic; 15–20 if acidotic); adjust for pH; goal pH >7.3 with maximal rate of 35; may accept lower goal if minute ventilation high
   4.    Secondary modifications

       Triggering: in spontaneous modes, adjustment of sensitivity levels to minimize effort
       Inspiratory flow rate of 40–80 L/min; higher if tachypneic with respiratory distress or if auto-PEEP present, lower if high pressure in ventilator circuit leads to a high-pressure alarm
       Assessment of auto-PEEP, especially in patients with increased airways obstruction (e.g., asthma, COPD)
       I : E ratio: 1 : 2, either set or as function of flow rate; higher (1 : 3 or more) if auto-PEEP present
       Flow pattern: decelerating ramp reduces peak pressure
   5.    Monitoring

       Clinical: blood pressure, ECG, observation of ventilatory pattern including assessment of dyssynchrony, effort or work by the patient; assessment of airflow throughout expiratory cycle
       Ventilator: tidal volume, minute ventilation, airway pressures (including auto-PEEP), total compliance
       Arterial blood gases, pulse oximetry

COPD = chronic obstructive pulmonary disease; ECG = electrocardiogram; FIO2 = fraction of inspired oxygen; HFOV = high-frequency oscillatory ventilation; I:E ratio = inspiratory-to-expiratory ratio; NIPPV = noninvasive positive pressure ventilation; PaO2 = partial pressure of oxygen in arterial blood; PBW = predicted body weight; PCV = pressure control ventilation; PEEP = positive end-expiratory pressure; PSV = pressure support ventilation; PTE = pulmonary thromboembolism; SIMV = synchronized intermittent mandatory ventilation; SpO2 = arterial oxygen saturation by pulse oximetry.

* Decisions within this algorithm will be influenced by the specific conditions of the individual patient.

Acute Respiratory Distress Syndrome

Patients with ARDS ( Chapter 105 ) have noncardiogenic pulmonary edema, with a reduced functional residual capacity and a mortality rate of 30 to 60%. Although therapy may be available for the underlying disease process that led to the development of ARDS (e.g., antibiotics for a predisposing pneumonia), no effective therapy is directly aimed at the diffuse alveolar damage. These patients require mechanical ventilation as supportive therapy to improve oxygenation and to decrease the oxygen cost of breathing until their lungs recover from the primary insult that led to the alveolar damage.

The lungs in a patient with ARDS are stiff and are characterized on computed tomographic scans by patchy, heterogeneous infiltrates that consist of airless atelectatic or consolidated regions. Many patients have a dependent region that is consolidated, atelectatic, or fluid filled, a nondependent region that looks relatively normal, and a middle region that has some areas that look like the dependent regions but can be recruited to resemble the nondependent regions if high enough tidal volumes and/or increased levels of airway pressure are used transiently; these latter approaches are called recruitment maneuvers.

The challenge in ventilating patients with ARDS is to provide adequate gas excharge while at the same time not causing further lung injury (see earlier). Arterial oxygen saturation can often be increased by high tidal volumes but at the expense of regional overdistention of those lung units that were not affected by the disease process itself, thereby improving oxygen saturation initially but, over time, worsening lung injury and clinical outcome.

The injury caused by mechanical ventilation can be reduced by using ventilatory strategies that avoid or minimize regional lung overdistention: limiting inspiratory pressure to some “safe” level and/or using smaller tidal volumes to limit end-inspiratory stretch. However, in some patients, this lower “dose” of ventilation results in higher levels of Paco2 (so-called permissive hypercapnia) and a lower pH. Higher tidal volumes (12 mL/kg predicted body weight) yield more normal blood gases, but lower tidal volumes (6 mL/kg predicted body weight) that permit hypercapnia decreased mortality by 22% (from an absolute value of 40 to 31%) in a large clinical trial ( Fig. 106-4 ).

FIGURE 106-4  Ventilatory strategy for patients with the acute respiratory distress syndrome (ARDS). Several caveats should be considered when using the low tidal volume strategy: (1) tidal volume (Vt) is based on predicted body weight (PBW),1 not actual body weight; PBW tends to be about 20% lower than actual body weight; (2) the protocol mandates decreases in the Vt lower than 6 mL/kg of PBW if the plateau pressure (Pplat) is greater than 30 cm H2O and allows for small increases in Vt if the patient is severely distressed and/or if there is breath stacking, as long as Pplat remains at 30 cm H2O or lower; (3) because arterial carbon dioxide (CO2) levels will rise, pH will fall; acidosis is treated with increasingly aggressive strategies dependent on the arterial pH; (4) the protocol has no specific provisions for the patient with a stiff chest wall, which in this context refers to the rib cage and abdomen; in such patients, it seems reasonable to allow Pplat to increase to more than 30 cm H2O, even though it is not mandated by the protocol; in such cases, the limit on Pplat may be modified based on analysis of abdominal pressure, which can be estimated by measuring bladder pressure. RR = respiratory rate; Spo, = oxygen saturation based on pulse oximeter.

Positive End-Expiratory Pressure

PEEP has been used traditionally to improve oxygenation while at the same time allowing reduction in Fio2 to relatively nontoxic levels. Within the context of the current paradigm of trying to minimize iatrogenic complications of mechanical ventilation, PEEP is viewed as a therapy that potentially can abrogate or minimize the injury caused by ventilation at low lung volumes, by recruiting lung units and keeping them open. No definitive answer exists regarding how PEEP levels should be set in patients with ARDS; outcomes appear to be similar with the routine use of higher (∼13 cm H2O) and lower (∼8 cm H2O) levels of PEEP.[2] The critical issues are how to assess the level of PEEP in an individual patient and how to determine whether the procedures to recruit the lung units and keep them open are less harmful than allowing the lung units to remain de-recruited. One experimental option is chest computed tomography to assess whether areas of the lung are recruited, but this technique is not practical for routine assessment. A second approach is to measure the mechanical properties of the respiratory system by generating a pressure-volume curve (see Fig. 106-2 ). Investigators have suggested that the optimal strategy is to set PEEP just higher than the lower inflection point, which is thought to represent the opening pressure of the lung, and to adjust tidal volume so Pplat is just lower than the upper inflection point, where compliance decreases. Although lung continues to be recruited well above the lower inflection point, and the upper inflection point may not indicate overdistention, two clinical studies that based their lung protection strategies on the pressure-volume curve demonstrated reductions in mortality; however, both studies also included other features to reduce lung injury, so use of the pressure-volume curve to set PEEP levels and tidal volume (or pressure limits) cannot be recommended at this time. In the trial that demonstrated the benefit of lower tidal volumes, PEEP levels were individualized based on a PEEP/Fio2 table (see Fig. 106-4 ); a subsequent trial using PEEP about 5 cm H2O higher found no additional benefit.[2]

Obstructive Airways Diseases

The major pathophysiologic abnormality in patients with obstructive airways diseases is an increase in airway resistance leading to expiratory airflow limitation; patients may also have a concomitant increase in minute ventilation. These factors may lead to dynamic hyperinflation, which is associated with numerous complications, including respiratory muscle compromise, an increased oxygen cost of breathing, and hemodynamic compromise. Thus, the main goals in the ventilatory support of patients with obstructive airway diseases (COPD, asthma) are to rest the respiratory muscles, to maintain adequate gas exchange, and to decrease the oxygen cost of breathing while simultaneously minimizing the iatrogenic complications of mechanical ventilation and allowing time for the successful diagnosis and treatment of the primary cause of the exacerbation and the resulting increase in airway obstruction ( Chapters 87 and 88 ).

Noninvasive Ventilation

For patients with acute respiratory failure resulting from an exacerbation of COPD, the preferred approach is NIV using a mask if the patient is hemodynamically stable, alert, and cooperative and does not need to be intubated to protect the airway.[3] It is important to choose a comfortable mask and to reassure the patient because some people find the mask difficult to tolerate. This strategy may be applied using several ventilation modes, including pressure support or bilevel positive airway pressure. The ventilation settings are adjusted to improve gas exchange and to ensure the patient’s comfort. Despite this approach, some patients with COPD require intubation and ventilation because of cardiac or respiratory arrest, agitation, increased sputum, or other concomitant severe disorders.

Intubation and Ventilation

The key goal after intubation is to minimize the detrimental effects of dynamic hyperinflation. The most effective way to minimize dynamic hyperinflation is to decrease the minute ventilation, even if this means an increase in Paco2, a strategy known as permissive hypercapnia or controlled hypoventilation. Judicious use of sedation may decrease carbon dioxide production and improve patient-ventilator dyssynchrony. Care must be taken in the use of paralytic agents, especially when patients with asthma are also receiving corticosteroids, because such patients may have an increased risk of myopathy. The duration of use of paralytic agents should be minimized to reduce the risk of myopathy.

Increasing expiratory time by using a higher peak inspiratory flow may be somewhat helpful, but it is not nearly as effective as decreasing minute ventilation. What level of Paco2 (and pH) should be tolerated is not known with certainty, but maintaining pH higher than approximately 7.15 is a reasonable target, although much lower values have been reported in clinical studies.

In patients with COPD who are spontaneously breathing, the addition of external (set) PEEP at a level that is just less than what is necessary to overcome the auto-PEEP fully will decrease the inspiratory effort that the patient needs to generate to initiate inspiratory airflow and will not increase Pplat. This strategy does not appear to be as effective in patients with status asthmaticus, in whom it may cause an increase in Pplat. Measurements of auto-PEEP by airway occlusion may be inaccurate in some patients with status asthmaticus, likely because of gas trapping at the end of expiration with closed off lung regions that do not communicate with the central airways.

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