1. assist-control
a) background:
(1) ventilator provides full tidal volume at a minimum preset rate
(2) additional full tidal volumes given if the patient initiates extra breaths
b) advantages:
(1) provides near complete resting of ventilatory muscles
(2) can be effectively used in awake, sedated, or paralyzed patients
c) disadvantages:
(1) patients can hyperventilate and become alkalotic
(2) patients can "stack" breaths (air trapping) and develop barotrauma
(3) patients can develop "autoPEEP" with barotrauma or hypotension
d) initial settings:
(1) tidal volume = 8-10 ml/kg (6 ml/kg in ARDS)
(2) rate = 12
(3) FiO2 = 1.0
(4) peak inspiratory flow = 60 liters/minute
2. synchronized intermittent mandatory ventilation (SIMV)
a) background:
(1) ventilator provides set tidal volume at a preset rate
(2) when a ventilator breath is programmed to occur, the ventilator waits a predetermined trigger period; any patient-initiated breath during this trigger period results in a programmed ventilator delivered breath
(3) the patient can take additional breaths but tidal volume of these extra breaths is dependent on the patient's inspiratory effort
b) advantages:
(1) in theory, results in improved blood return to the right ventricle owing to intermittent negative pressure (spontaneous) breaths
(2) patients often more comfortable since they have more control over their ventilatory pattern and minute ventilation
c) disadvantages:
(1) can result in chronic respiratory fatigue if set rate is too low; in this situation, the following may be seen:
(a) high respiratory rate
(b) rising pCO2
(2) air trapping can occur
d) initial settings:
(1) tidal volume = 8-10 ml/kg (6 ml/kg in ARDS)
(2) rate = 12
(3) FiO2 = 1.0
(4) peak inspiratory flow = 60 liters/minute
3. pressure support (Dekel, 1996)
a) background:
(1) not a volume-cycled mode
(2) when the patient triggers the ventilator, a set pressure (1-100 cm) during the patient's inspiration; this air pressure is stopped when the patient ceases to inspire
(3) tidal volume and minute ventilation are dependent on the patient
b) advantages:
(1) avoids patient-ventilator aschrony
(2) patients often more comfortable since they have full control over their ventilatory pattern and minute ventilation
(3) often avoids breath stacking and autoPEEP (especially in patients with COPD)
(4) ability to permit self-determination of respiratory rate and to permit forced exhalation offers substantial advantages in status asthmaticus (Meduri, 1996)
c) disadvantages:
(1) cannot be used in heavily sedated, paralyzed, or comatose patients
(2) respiratory muscle fatigue can develop if the pressure support is set too low
d) initial settings:
(1) set pressure support at the pressure required to generate a tidal volume of 8-10 ml/kg
(a) this will usually be about the same as the plateau pressure
(b) 30-35 cm will usually give full ventilatory support
(2) FiO2 = 1.0
4. pressure control (Marik, 1997)
a) background:
(1) the breath is pressure limited rather than volume limited
(2) best reserved for patients with ARDS
b) advantages:
(1) in ARDS, pO2 may increase 10-15%
c) disadvantages:
(1) there is no guaranteed tidal volume and thus there is no guaranteed minute ventilation
(2) you must be very attentive to changes in the patients respiratory mechanics since unstable reactive airways disease can dramatically affect minute ventilation
(3) air trapping can be a problem
(4) CO2 retention frequently occurs (although this may be acceptable in "permissive hypercapnia" strategies for ventilation of some patients with acute respiratory failure)
(5) in general, patients must be heavily sedated since this is an uncomfortable mode for most patients
d) initial settings:
(1) set PEEP (generally 7 - 12)
(2) set maximum inspiratory pressure (generally < 35 cm)
(3) set rate (this will vary in order to achieve a desired minute ventilation)
(a) real time flow-time curves can facilitate optimization of pressure control settings
(4) FiO2 = 1.0
5. positive end-expiratory pressure (PEEP)
a) background:
(1) ventilator provides a fixed positive airway pressure at the end of expiration
(2) when used with assist-control ventilation, the term PEEP is used
(3) when used with spontaneous breathing, the term CPAP (continuous positive airway pressure) is used
b) advantages:
(1) opens closed alveolar units thus improving lung compliance and oxygenation
(2) to a point, peak and plateau airway pressures actually decrease since there are more alveoli open at the beginning of inspiration
(3) may improve secretion drainage from otherwise closed alveoli
(4) can reduce right ventricular venous return and also lower left ventricular afterload
(5) can be given on the ventilator or via a CPAP mask in the non-intubated patient
c) disadvantages:
(1) barotrauma
(2) can be risky and counterproductive in patients with obstructive airways disease
(3) may worsen hypoxemia in patients with localized (as opposed to diffuse) lung disease (eg, pneumonia)
(4) hypotension and reduced cardiac output
(5) increased cardiac shunt (especially PFOs)
(6) increased intracranial pressure
(7) decreased renal perfusion
(8) hepatic congestion
d) initial settings:
(1) 5 cm is fairly standard and in many hospitals is used on most patients initially placed on the ventilator
(2) changes in PEEP may not be reflected by changes in arterial blood gases for 20-30 minutes so changes in the PEEP setting should usually not be made faster than this
(3) the ventilator circuit should not be broken unless absolutely neccessary; disconnecting the patient (for example, to transport him/her) can result in an immediate loss of the benefit of PEEP which can require 20-30 minutes or more to restore
(4) PEEP is added in increments of 2-5 cm until the "best PEEP" is obtained
(a) there is no optimal way to assess "best PEEP"
(b) some PEEP authorities choose the level which provides the highest static compliance (in other words, the lowest airway plateau pressure)
(c) in general, use the lowest amount which gives the desired effect on pO2 without lowering blood pressure, reducing cardiac output, or increasing the plateau pressure on the ventilator
(5) PEEP over 20 cm is rarely beneficial and usually results in additional pressure-induced lung injury
6. airway pressure release ventilation (APRV) (Downs, 1987)
a) background:
(1) ventilator supplies a low level of CPAP alternating with a relatively high level of CPAP
(2) it can be coupled with pressure support
(3) at intermittant times the higher CPAP level is reduced for 1 or more breaths, permitting rapid exhausting of the gas in the expiratory reserve volume and resulting in a higher tidal volume
(4) when used in a patient who is not spontaneously breathing, this mode is no different than pressure control ventilation
b) advantage:
(1) potential for barotrauma and overdistension is reduced
(2) venous return is preserved
(3) permits spontaneous breaths
c) disadvantages:
(1) requires the use of relatively high CPAP levels
(2) CPAP reductions can result in hypoxemia
(3) better for post-op and mildly diseased lungs and role in severe respiratory failure is unclear
1. patients with high plateau airway pressures (> 35 cm)
a) causes:
(1) excessively high tidal volume
(2) pneumothorax or massive pleural effusion
(3) microatelectasis (due to ARDS, etc.)
(4) cardiogenic pulmonary edema
(5) secretions or foreign body in the airway
(6) kinking or obstruction of the endotracheal tube or ventilator tubing
(7) ascites or abdominal distension
(8) bronchospasm
(9) severe intrinsic lung disease (pulmonary fibrosis, etc.)
(10) patient "fighting" the ventilator
b) treatment:
(1) insure that the patient is optimally suctioned and that all bronchospasm is being treated
(a) when giving bronchodilators by MDI to ventilated patients, more puffs should be given - generally 4 puffs of albuterol; attention should be given to the manner that MDIs are introduced into the ventilator circuit since directing the MDI spray toward the wall of the ventilator tubing drastically reduces the delivered dose (Fink, 1996)
(2) check a chest x-ray to insure that there is no pneumothorax
(3) treat the underlying cause of stiff lungs (diuresis for pulmonary edema, antibiotics for diffuse pneumonia, etc.)
(4) insure that total body oxygen requirements are maximally reduced:
(a) treat fever
(b) sedate patients who are moving a great deal
(c) treat infection
(5) optimize oxygen delivery
(a) transfuse patients with severe anemia (the optimal hemoglobin in acute respiratory failure has not been determined and probably depends on the individual patient but pending definitive studies, a useful rule is to keep the hemoglobin > 9 gm)
(6) add PEEP to the "best PEEP" level to optimally open otherwise closed alveoli during expiration and therefore reduce the pressure required to open these alveoli during inspiration
(7) reduce peak inspiratory flow rate
(a) this will effectively increase inspiratory time and decrease expiratory time
(b) in its extreme, it results in "inverse ratio ventilation" with an I:E ratio < 1:1 (a normal ventilated patient has an I:E ratio of about 1:2 or 1:3)
(8) reduce tidal volume
(a) if the respiratory rate is unchanged, this can result in so called "controlled hypoventilation" when the minute ventilation is allowed to decrease below the patient's natural minute ventilation (by either a decrease in the tidal volume or a decrease in the respiratory rate); this can result in an increase in pCO2 ("permissive hypercapnia") and usually requires the patient to be heavily sedated since hypercapnia can be quite uncomfortable
(b) the lowest tolerable pH during controlled hypoventilation is unclear but pending definitive studies, it is probably desirable to keep the pH > 7.20 during hypoventilation
(9) sedation and/or paralysis (see below)
(10) change to pressure control ventilation mode
2. patients with persistent hypoxemia despite FiO2 > 50%
a) causes:
(1) underlying intrinsic lung disease (pneumonia, pulmonary edema, etc.)
(2) central airway obstruction (bronchospasm, secretions, foreign body, neoplasm, etc.)
(3) intra cardiac shunt (especially patent foramen ovale)
(4) pulmonary embolus
(5) other pulmonary vascular disease (pulmonary hypertension, etc.)
(6) autoPEEP
b) treatment:
(1) suction the airways to remove secretions, etc.
(2) administer bronchodilators if indicated
(3) therapeutic bronchoscopy if there is evidence of atelectasis or lobar collapse
(4) add PEEP to the optimal level
(5) diagnose and treat underlying causes (above), especially pulmonary embolus
(6) transfuse to keep hemoglobin > 9 gm to insure sufficient oxygen delivery despite low pO2
(7) in patients with severe ARDS or alveolar hemorrhage, consider placing the patient in the prone position as this can improve oxygenation by up to 15% in these situations (Chatte, 1997)
3. patients with autoPEEP
a) causes:
(1) fundamentally, this is the pressure associated with an end-expiratory volume which is higher than the normal functional residual capacity (FRC)
(a) this is most commonly seen in patients with obstructive airways disease in whom there is insufficient time for full exhalation resulting in "air trapping" and associated progressive hyperinflation
(b) it can also occur in persons without obstructive airways disease who have insufficient time for normal exhalation (eg, hyperventilation or too high of a tidal volume)
(2) autoPEEP should be suspected when:
(a) any patient with obstructive airways disease is receiving mechanical ventilation
(b) any patient with unexplained hypotension after initiating mechanical ventilation
(c) any patient with unexplained tachycardia after initiating mechanical ventilation
(3) autoPEEP can be inferred by any of three findings:
(a) an expired air volume that is less than the inspired volume (trapped air)
(b) a flow-time graphic (available on many newer ventilators) showing that flow never reaches 0 before the next breath (in other words, the patient is still expiring when the next breath is delivered)
(c) chest auscultation demonstrating that expiratory noises (wheezing, etc.) are audible all the way up until the next breath is delivered
(4) cannot be measured directly from the ventilator dials
(a) autoPEEP represents the pressure in the alveoli and not the pressure in the ventilator circuit; therefore, there can be life-threatening autoPEEP despite an end-expiratory pressure of 0 on the ventilator pressure meter (Leatherman, 1996)
(b) the expiratory port of the ventilator circuit must be occluded in order to allow the pressure within the airway to equilibrate and register on the pressure dial
b) treatment:
(1) reduce tidal volume
(2) increase peak inspiratory flow (allowing more expiratory time)
(3) reduce respiratory rate
(4) sedate the hyperventilating patient
(5) permit controlled hypoventilation (see below)
(6) treat any bronchospasm
(7) consider switching to pressure support mode
4. patients with ARDS
a) a low tidal volume strategy of 6 ml/kg was associated with a 22% improvement in mortality (31% vs. 39%) and a greater number of ventilator-free days in the first 4 weeks of hospitalization (12 vs. 10) compared to a traditional/high tidal volume ventilation strategy of 12 ml/kg. There was also less multiple organ system failure and lower blood interleukin-6 levels in the low tidal volume group (ARDS network, N Engl J Med 2000)
b) pressure control ventilation can be useful on occasion
c) PEEP needs to be judiciously adjusted and can result in substantially improved oxygenation
d) prone ventilation can result in improved oxygenation
1. early:
a) hypoxemia due to prolonged attempts
b) right mainstem intubation
c) intubation of esophagus
d) upper airway trauma
e) aspiration
f) hypotension immediately following intubation
(1) this is usually multifactorial and etiologies include:
(a) effect of sedatives and/or paralytics used for intubation
(b) diminished blood return to the thorax due to positive pressure ventilation
(c) auto-PEEP with breath stacking (especially in patients with COPD)
(d) diminished LV output due to compression of the LV by the interventricular septum
(2) treatment:
(a) reduce tidal volume (often gives the most immediate improvement)
(b) fluid bolus (usually all that is required unless breath stacking occurs)
(c) reverse Trendlenberg position (until fluid bolus is given)
(d) reduce PEEP
(e) vasopressors with predominately alpha adrenergic properties (eg, levarterenol)
2. late:
a) cuff leak
b) sinusitis
c) upper airway injury/stenosis
d) unplanned (self) extubation
1. disconnection
2. malfunction
1. hypoxemia
a) patients should always be pre-oxygenated with 100% oxygen prior to suctioning
b) suction time should be limited
2. arrhythmias
1. nosocomial infections (Kollef, 1999)
a) usually gram negative rods and staph
b) factors decreasing pneumonia probability:
1) early removal of NG tubes
2) hand washing
3) semirecumbant positioning of patient
4) adequate nutrition
5) avoid gastric overdistension
6) avoid nasal intubation (as opposed to oral intubation)
7) continuous subglottic suctioning
8) stress ulcer prophylaxis
(a) sucralfate is associated with less pneumonia than H2 blockers
c) early diagnosis of the specific organism(s) is critical for optimal survival
1) in a multicenter study of 413 patients with ventilator-associated pneumonia, compared to use of tracheal aspirates to guide antibiotic selection, early use of quantitative bronchoalveolar lavage or quantitative protected brush cultures to guide antibiotic selection was associated with (Ann Intern Med 2000; 132:621-30):
(a) decreased mortality (16% vs. 26%)
(b) lowered Sepsis Organ Failure Assessment scores (4.9 vs. 5.8)
(c) more antibiotic free days in the first month (11 vs. 7)
2. hemodynamic effects:
a) decreased cardiac output due to impaired venous return to the right heart and increased pulmonary venous resistance due to positive pressure alveolar distension
b) autoPEEP
3. barotrauma:
a) rare if plateau pressure is < 35
(1) for this reason, we generally use a plateau pressure < 35 as a major goal of mechanical ventilation and check plateau pressures frequently
b) often heralded by interstitial air on the chest x-ray
c) pneumomediastinum & subcutaneous emphysema
(1) does not need to be treated
(2) indicates high risk for pneumothorax
d) pneumothorax
(1) always treat with a chest tube in patients receiving positive pressure ventilation because of the risk of tension pneumothorax
(2) bronchopleural fistula can be difficult to resolve until the patient is off mechanical ventilation - the best treatment for a bronchopleural fistula is treatment of the underlying lung disease
4. oxygen toxicity
a) can occur as early as 24 hours after high oxygen exposure
b) more frequent if the FiO2 is > 0.5
c) clinically resembles adult respiratory distress syndrome
d) very important to avoid since this often results in an inescapable vicious cycle of high oxygen requirements ultimately resulting in fatal respiratory failure
5. respiratory alkalosis
6. increased intracranial pressure
7. atelectasis (especially the left lower lobe)
1. non-ventilator derived parameters
a) awake and off sedatives (as much as possible)
(1) be aware of depression as a psychological limitation to weaning
b) proper position (upright, ideally sitting)
c) adequate nutrition
d) optimal fluid status
e) no infection
f) hemodynamically stable
(1) preferably off vasopressors
(2) angina optimally controlled
(3) no active bleeding
g) no metabolic alkalosis
h) normal electrolyte status
(1) calcium
(2) phosphorus
(3) potassium
(4) magnesium
i) afebrile
j) bronchospasm controlled
k) mechanical airway obstruction treated
(1) for lung tumors, placement of a bronchial stent can permit extubation
l) normal thyroid function
m) re-establishment of normal sleep-wake cycling
2. weaning parameters (Yang, 1991)
a) f/Vt < 100 breaths/min./liter
(1) calculation:
(a) disconnect the patient from the ventilator for 1 minute
(b) measure the spontaneous minute ventilation and the respiratory rate
(c) calculate the average tidal volume (in liters) as the minute ventilation ÷ the respiratory rate
(d) f/Vt = respiratory rate ÷ average tidal volume
(2) in one study (Yang, 1991), this was the single best predictor of success in weaning patients from mechanical ventilation
(a) sensitivity 97%, specificity 64%
b) maximal inspiratory pressure (also mistakenly referred to as "NIF") more negative than -20
(1) sensitivity 100%, specificity 14%
c) minute ventilation (VE) < 10 liters/min.
(1) sensitivity 31%, specificity 61%
d) tidal volume (Vt) > 4 ml/kg
(1) sensitivity 94%, specificity 39%
e) vital capacity > 10 ml/kg
f) FiO2 < 40% with pO2 > 60 mm Hg
3. intrinsic PEEP
a) common in patients with obstructive lung disease (eg, COPD)
b) untreated, it can lead to increased work of breathing
c) it can be overcome by adding ventilator-delivered PEEP at pressures less than 85% of the intrinsicic PEEP
1. T-piece
a) theoretic advantages:
(1) simple
(2) provides strenuous exercise to the ventilatory muscles followed by periods of full ventilatory muscle rest; this is theoretically the best way to condition the inspiratory muscles
b) technique:
(1) match pCO2 and tidal volume to the patient's baseline prior to initiating weaning attempt
(2) increase FiO2 by 10% at initiation of weaning
(3) stop trial if :
(a) resp. rate increases > 10
(b) pCO2 rises > 5
(c) pulse rises > 20
(d) blood pressure rises > 20 mm systolic
(4) attempt trials at least twice per day with a minimum of 1 hour between trials
(5) extubation can be considered if the patient breathes on their own for at least 2 hours without distress
c) disadvantages:
(1) removes the internal resistance of the ventilator but does not alter the resistance due to the endotracheal tube
(a) resistance is proportional to length and inversely proportional to the 4th power of the radius
(b) some examples of endotracheal tube resistances:
i) 6.0 tube = 3.2 cm/liter/sec
ii) 7.0 tube = 2.5 cm/liter/sec
iii) 8.0 tube = 1.4 cm/liter/sec
iv) 9.0 tube = 0.5 cm/liter/sec
(c) this added resistance can pose a great deal of extra work for the patient over and above that of breathing spontaneously without an endotracheal tube
2. SIMV
a) technique:
(1) decrease rate of support by 2-4 breaths per trial as tolerated
(2) return to full support between trials
(3) extubate when rate close to or equal to zero
b) theoretic advantages:
(1) allows gradual switch from fully supported to fully independent breaths
(2) prevents patients from "fighting" the ventilator
(3) reduces respiratory muscle fatigue
(4) allows some normal venous return to the right heart due to some negative pressure (spontaneous) breaths
c) problems:
(1) work of breathing and oxygen consumption can increase as much as 2-fold due to work necessary to activate the demand valve (Sasoon, 1989)
(2) flow triggering results in 30-40% less inspiratory effort than presssure triggering
3. pressure support
a) theoretic advantages:
(1) augments a spontaneous breath with positive pressure
(2) counteracts extra work of breathing due to resistance of the tubing
(3) in patients with volume overload or left ventricular failure, rapid changing to spontaneous breathing (eg, T-piece trials) can result in lung flooding and rapid failure of weaning; pressure support avoids this by gradually reducing positive pressure and thus permitting gradual correction of fluid status by diuresis, etc.
b) technique:
(1) start at a pressure support sufficient to provide a tidal volume of 8-10 ml/kg (this will usually be about equal to the plateau pressure while the patient is on assist-control)
(2) reduce support by 2-5 cm as tolerated
(3) extubate when pressure support is equal to the calculated resistance of the ventilator circuit (eg. endotracheal tube, tubing, expiratory valves, etc.); this is usually about 5 cm
c) problems:
(1) requires physician to make frequent ventilator setting decisions
4. recent comparative studies:
a) Brochard, 1994
(1) randomized multicenter study of 456 patients
(2) all patients initially underwent a 2 hour trial of spontaneous breathing; if they had respiratory distress (109 patients) then they were assigned to 1 of 3 weaning modes:
(a) T-piece
(b) SIMV
(c) pressure-support
(3) outcome was measured as the percentage of patients extubated by 21 days:
(a) T-piece = 64%
(b) SIMV = 60%
(c) pressure-support = 90%
(4) conclusion: pressure-support resulted in the most patients extubated by 21 days
b) Esteban, 1995
(1) randomized multicenter study of 546 patients
(2) all patients initially underwent a 2 hour trial of spontaneous breathing; if they had respiratory distress (130 patients) then they were assigned to 1 of 4 weaning modes:
(a) IMV
(b) pressure support
(c) T-piece (2 or more trials per day)
(d) T-piece (once daily trial)
(3) outcome was measured by time until extubation:
(a) IMV = 5 days
(b) pressure support = 4 days
(c) T-piece (2 or more/day) = 3 days
(d) T-piece (1/day) = 3 days
(4) conclusion: T-piece trials result in the most rapid successful extubation
c) Ely, 1996
(1) randomized single hospital study of 300 patients
(2) control patients underwent daily respiratory function screening
(3) study patients underwent daily respiratory function screening and underwent a T-piece trial for up to 2 hours if the screening criteria were met; if the patient satisfactorily completed the trial, the attending physician was notified
(4) for the screening criteria to be met:
(a) pO2:FiO2 ratio > 200
(b) PEEP ² 5
(c) cough reflex intact
(d) f/Vt ² 105
(e) no continuous infusion of vasopressors or sedatives
(5) time to extubation:
(a) study group = 4.5 days
(b) control group = 6 days
(6) complication rate:
(a) study group = 20%
(b) control group = 41%
(7) ICU costs:
(a) study group = $15,740
(b) control group = $20,890
(8) conclusion: daily screening for "weanability" results in shorter days on the ventilator, fewer complications, and lower ICU costs
d) Girqult, 1999
(1) randomized single hospital study of 33 patients who failed a 2 hour T-piece trial
(2) patients were assigned to early extubation with immediate institution of non-invasive ventilation using pressure support or to continued mechanical ventilation via an endotracheal tube until a T-piece trial was successfully performed
(3) There was no difference in complication rates or survival but patients in the study group had a significantly decreased duration of mechanical ventilation
e) Henneman, 2001
(1) 124 patients had weaning facilitated by a collaborative weaning flowsheet and were compared to 77 patients weaned per the previous usual practice of the ICU
(2) Patients weaned using the "weaning board" and "weaning flowsheet" came off of the ventilator an average of 3.6 days faster than patients weaned per the previous usual practice of the ICU.
e) Krishnan, 2004
(1) 145 patients in an academic medical center ICU staffed 24 hours per day
(2) No differences in weaning rate by physician-directed weaning versus protocol-directed weaning.
(3) Findings may relate to the presence of 24-hour per day physician availability therefore, protocol-driven weaning may still be appropriate for ICUs that are not staffed 24 hours per day.
5. my personal philosophy:
a) all patients should have a weaning assessment to include f/Vt daily
b) SIMV is probably never the best mode of weaning medical patients; it is acceptable for uncomplicated post-operative patients because of its simplicity and because almost any weaning mode works well in these patients
c) T-piece weaning is better (more rapid) for medical patients who are rapidly improving
d) pressure-support is better for some medical patients who are improving slowing
e) the combination of pressure-support + SIMV as a weaning mode is unnecessarily confusing and adds little to pressure-support alone
6. rapid weaning in patients who fail an initial T-piece trial may be warrented in COPD patients if extubated to full face mask non-invasive ventilation (Nava, 1998).
1. hypoxemia
a) diffuse pulmonary disease
b) focal pulmonary disease (pneumonia, etc.)
c) pulmonary edema
(1) removal of positive pressure can increase preload and lead to worsened heart failure, especially in patients with diastolic dysfunction which should be suspected in patients who become unexpectedly tachycardic and/or hypertensive during weaning; these patients often require a calcium channel blocker (verapamil or diltiazem) or a beta blocker for control of diastolic dysfunction before weaning will be successful
2. insufficient ventilatory drive
a) response to pathologic metabolic alkalosis
b) inadequately functioning CNS respiratory drive center
(1) sedatives
(2) malnutrition
(3) myxedema
(4) primary CNS disease
3. excessive ventilatory demands
a) excessive CO2 production
(1) sepsis
(2) agitation
(3) fever
(4) high carbohydrate intake
4. respiratory muscle weakness
a) neuromuscular disease
b) malnutrition
c) drugs
(1) neuromuscular blocking agents
(2) corticosteroids
(3) aminoglycosides
d) low magnesium, potassium, phosphorus
5. excessive work of breathing
a) airway obstruction
(1) bronchospasm
(2) secretions
(3) bronchitis
(4) kinked endotracheal tube
(5) mechanical airway obstruction (tumor, bronchostenosis, tracheo-bronchial malacia)
b) endotracheal tube too small
c) chest motion restriction (bandages, positioning, etc.)
6. acid-base disorders
7. phrenic nerve injury
a) esp. following open heart surgery
b) unilateral diaphragm paralysis rarely symptomatic unless there is substantial contralateral pulmonary disease
8. psychological factors
a) sleep deprivation
b) anxiety
c) depression
d) confusion
e) pain
Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342.
Antonelli M, Conti G, Rocco M, Bufi M, De Blasi RA, Vivino G, Gasparetto A, Meduri GU. A coparison of noninvasive positive-pressure ventilation and conventional mechanical ventilation in patients with acute respiratory failure. N Engl J Med 1998; 339:429-35.
Baratz DM, Westbrook PR, Shah PK, Mohsenifar Z. Effect of nasal continuous positive airway pressure on cardiac output and oxygen delivery in patients with congestive heart failure. Chest 1992; 102:1397-401.
Bennett SN. McNeil MM. Bland LA. Arduino MJ. Villarino ME. Perrotta DM. Burwen DR. Welbel SF. Pegues DA. Stroud L. et al. Postoperative infections traced to contamination of an intravenous anesthetic, propofol. NEJM 1995; 333:147-54.
Bott J, Carroll MP, Conway JH, Keilty SE, Ward EM, Brown AM, et al. Randomized controlled trial of nasal ventilation in acute ventilatory failure due to chronic obstructive airways disease. Lancet 1993; 341:1555-7.
Bradley TD, Holloway RM, McLaughlin PR, Ross BL, Walters J, Liu PP. Cardiac output response to continuous positive airway pressure in congestive heart failure. Am Rev Resp Dis 1992; 145:377-82.
Bradley TD, Takasaki Y, Orr D, Popkin J, Liu P, Rutherford R. Sleep apnea in patients with left ventricular dysfunction: beneficial effects of nasal CPAP. Prog Clin Biol Res 1990; 345:363-8.
Brochard L, Isabey D, Piquet J, Amaro P, Mancebo J, Messadi AA, et. al. Reversal of acute exacerbations of chronic obstructive lung disease by inspiratory assistance with a face mask. N Engl J Med 1990; 323:1523-30.
Brochard L, Rauss A, Benito S, Conti G, Mancebo J, et al. Comparison of three methods of gradual withdrawal from ventilatory support during weaning from mehcanical ventilation. Am J Respir Crit Care Med 1994; 150:896-903.
Chatte G, Sab JM, Dubois JM, Sirodot M, Gaussorgues P, Robert D. Prone position in mechanically ventilated patients with severe acute respiratory failure. Am J Respir Crit Care Med 1997; 155:473-8.
Confalonieri M, Parigi P, Scartabellati A, Aiolfi S, Scorsetti S, Nava S, Gandola L. Noninvasive mechanical ventilation improves the immediate and long-term outcome of COPD patients with acute respiratory failure. Eur Resp J 1996; 9:422:30.
Cujec B, Polasek P, Mayers I, Johnson D. Positive end-expiratory pressure increases the right-to-left shunt in mechanically ventilated patients with patent foramen ovale. Ann Intern Med 1993; 119:887-94.
Dekel B, Segal E, Perel A. Pressure support ventilation. Arch Intern Med 1996; 156:369-73.
Deppe SA. Sipperly ME. Sargent AI. Kuwik RJ. Thompson DR. Intravenous lorazepam as an amnestic and anxiolytic agent in the intensive care unit: a prospective study. Crit Care Med 1994; 22:1248-52
Downs JB, Klein EF Jr, Desautels D, Modell JH, Kirby RR. Intermittent mandatory ventilation: a new approach to weaning patients from mechanical ventilators. Chest 1973; 64:331-5.
Downs JB, Stock MC. Airway pressure release ventilation: a new concept in ventilatory support. Crit Care Med 1987; 15:459-461.
Ely EW, Baker AM, Dunagan DP, Burke HL, Smith AC, Kelly PT, Johnson MM, Browder RW, Bowton DL, Haponik EF. Effect on the duration of mechanical ventilation of identifying patients capable of breathing spontaneously. N Engl J Med 1996; 335:1864-9.
Esteban A, Frutos F, Tobin MJ, Alía I, Solsona JF, et al. A comparison of four methods of weaning patients from mechanical ventilation. N Engl J Med 1995; 332:354-50.
Henneman E, Dracup K, Ganz T, Molayeme O, Cooper C. Effect of a collaborative weaning plan on patient outcome in the critical care setting. Crit Care Med. 2001 Feb;29(2):297-303.
Hess D. Ventilator modes used in weaning. Chest 2001; 120: 474-6S.
Hillberg RE, Johnson DC. Non-Invasive Ventilation. N Engl J Med 1997; 337:1746-52
Fink JB, Dhand R, Duarte AG, Jenne JW, Tobin MJ. Aerosol delivery from a metered-dose inhaler during mechanical ventilation. An in vitro model. Am J Resp Crit Care Med 1996; 154:382-7.
Hall JB, Wood LDH. Liberation of the patient from mechanical ventilation. JAMA 1987; 257:1621-8.
Hunter JM. New neuromuscular blocking drugs. N Engl J Med 1995; 332:1691-9.
Isenstein DA, Venner DS, Duggan J. Neuromuscular blockade in the intensive care unit. Chest 1992; 102:1258-66.
Krishnan JA, Moore D, Robeson C, Rand CS, Fessler HE. A prospective, controlled trial of a protocol-based strategy to discontinue mechanical ventilation. Am J Respir Crit Care Med 2004; 169: 673-8.
Javaheri S, Parker TJ, Wexler L, Michaels SE, Stanberry E, Nishyama H, Roselle GA. Occult sleep-disordered breathing in stable congestive heart failure. Ann Intern Med 1995; 122:487-92.
Kollef MH. The prevention of ventilator-associated pneumonia. N Engl J Med 1999; 340:627-34.
Leatherman JW, Ravenscraft SA. Low measured auto-positive end-expiratory pressure during mechanical ventilation of patients with severe asthma: hidden auto-positive end-expiratory pressure. Crit Care Med 1996; 24:541-6.
Marik PE, Krikorian J. Pressure-controlled ventilation in ARDS: A practical approach. Chest 1997; 112:1102-6.
Meduri GU, Abou-Shala N, Fox RC, Jones CB, Leeper KV, Wunderink RG. Noninvasive face mask mechanical ventilation in patients with acute hypercapnic respiratory failure. Chest 1991; 100:445-54.
Meduri GU, Cook TR, Turner RE, Cohen M, Leeper KV. Noninvasive positive pressure ventilation in status asthmaticus. Chest 1996; 110:767-74.
Meyer TJ, Hill NS. Noninvasive positive pressure ventilation to treat respiratory failure. Ann Intern Med 1994; 120:760-70.
Mirenda J, Broyles G. Propofol as used for sedation in the ICU. Chest 1995; 108:539-48.
Naughton MT, Rahman MA, Hara K, Floras JS, Bradley TD. Effect of continuous positive airway pressure on intrathoracic and left ventricular transmural pressures in patients with congestive heart failure. Circulation 1995; 91:1725-31.
Nava S, Ambrosino N, Clini E, Prato M, Orlando G, Vitacca M, Brigada P, Fracchia C, Rubini F. Noninvasive mechanical ventilation in the weaning of patients with respiratory failure due to chronic obstructive pulmonary disease. A randomized, controlled trial. Ann Intern Med 1998; 128:721-8.
Rasanen J, Nikki P, Heikkila H. Acute myocardial infarction complicated by respiratory failure: the effects of mechanical ventilation. Chest 1984; 85:21-8.
Rasanen J, Heikkila J, Downs J, Nikki P, Vaisanen IT, Viitanen A. Continuous positive airway pressure by mask in acute cardiogenic pulmonary edema. Am J Cardiol 1985; 55:296-300.
Sasoon CSH, Giron AE, Ely E, Light RW. Inspiratory work of breathing on flow-by and demand-flow continuous positive airway pressure. Crit Care Med 1989; 17:1108-14.
Society of Critical Care Medicine: "Practice Parameters For Systemic Intravenous Analgesia And Sedation For Adult Patients In The Intensive Care Unit"; September, 1995
Tobin MJ. Principles and Practice of Mechanical Ventilation. New York, McGraw-Hill; 1st edition, 1994.
Watling SM, Dasta JF. Prolonged paralysis in intensive care unit patients after the use of neuromuscular blocking agents: a review of the literature. Crit Care Med 1994; 22:884-93.
Yang KL, Tobin MJ. A prospective study of indexes predicting the outcome of trials of weaning from mechanical ventilation. N Engl J Med 1991; 324:1445-50.
Updated 5/29/2006