Ventilator Management | Emergency Critical Care

Mech ventilated patients have a dead space to alveolar ratio of 1:1 as opposed to the 1:2 in a normal patient

If a 70kg man needs >8400 cc/minute either deadspace for production of CO2 is elevated.

0022
VENTILATION WITH LOWER TIDAL VOLUMES AS COMPARED WITH CON-
VENTIONAL TIDAL VOLUMES FOR PATIENTS WITHOUT ACUTE LUNG
INJURY – A PREVENTIVE RANDOMIZED CONTROLLED TRIAL
M. J. Schultz*, R. M. Determann, E. K. Wolthuis
Intensive Care, Academic Medical Center, Amsterdam, Netherlands
INTRODUCTION. Recent cohort studies have identiﬁed ventilator settings as a major risk
factor for development of lung injury in mechanically ventilated patients who do not have
acute lung injury at the onset of mechanical ventilation. However, randomized controlled
trials have not been performed.
METHODS. To compare pulmonary inﬂammation and development of lung injury during
mechanical ventilation with conventional or lower tidal volumes in patients without acute
lung injury we performed a randomized controlled non–blinded preventive trial on patients
without acute lung injury at the onset of mechanical ventilation. Patients were randomly
allocated to mechanical ventilation with a tidal volume of 10 ml per kilogram of predicted
body weight or a tidal volume of 6 ml per kilogram of predicted body weight.
RESULTS. The trial was stopped after 150 patients were enrolled because development of
lung injury was higher in the group treated with conventional tidal volumes as compared to
the lower tidal volume group (13.5% vs. 2.6%, P = 0.01). Analysis of the lavage ﬂuid
cytokine proﬁles revealed no differences over time between the two ventilation groups. The
relative risk of acute lung injury for patients ventilated with conventional tidal volumes was
5.1 (95% CI 1.2 – 22.6).
CONCLUSION. Mechanical ventilation with conventional tidal volumes contributes to
development of lung injury. (ESICM 2008 in Lisbon Abstract 22 in Inten Care Med)

High PEEP causes right ventricular problems mostly by increased right vent afterload, not decreased preload. But you can still overcome this by fluid as shown by the PLR abolishment of the effects (CCM 2010;38(3):802-807)

Higher PEEP associated with increased survival in ARDS patients in SR/MA (JAMA 2010;303(9):865)

If you place a patient on 100% for 5-15 minutes, P (A-a) is entirely from shunt, divide by 20 to get shunt fraction

The total work of breathing can be partitioned between an elastic and resistive work. By analogy, the pressure needed to inflate a balloon through a straw varies; one needs to overcome the resistance of the straw and the elasticity of the balloon.

When airflow is stopped in a passively ventilated patient by occlusion of the expiratory circuit valve at end inspiration (plateau pressure) and end expiration (total PEEP), the pressure needed to overcome the elastic recoil of the lungs and chest wall during delivery of the tidal volume is given as the difference in these values. Dividing the delivered tidal volume by this difference quantifies the respiratory system compliance.

Predicted body weight (PBW) can be calculated by the following formula:
in men, PBW (kg)=50+0.91 (centimeters of height–152.4);
in women, PBW (kg)=is 45.5+0.91 (centimeters of height–152.4)

Hyperoxia screws up left ventricular function and filling pressures (Chest 2001;120(2):467)

Doppler study of healthy volunteers shows that hyperoxia screws up heart function (Cardiovasc Ultrasound 2004;2(22):

positive intrathoracic pressure decreases venous return but also decreases afterload

In supine pts, spont breathing distributes air preferentially to dependant regions. In positive pressure, distribution is to non-dependant regions.

Invasive Mechanical Ventilation

Invasive Ventilator Settings/Modes

What you need to know for each mode is the trigger, the limit, and the cycle. The trigger begins inspiration, the limit determines rate of airflow, and the cycle ends respiration.

CMV-vents at preset Vt and Rate, no patient initiated breaths allowed. Patient breathing against closed system, so they must fully sedated with no respiratory effort.

A/C-vents at preset Vt and Rate, if pt initiates a breath, it is given at preset Vt. Machine tries to match the pt's breaths; if patient breathing above set rate then all breaths are patient initiated.

IMV- mandatory preset vent rate/Vt. Pt initiated breaths are through vent circuit without assistance. No synchronization between pt and mandatory breaths

SIMV-Same as IMV, but pt’s breaths will keep mandatory breaths from triggering preventing stacking of a mechanical breath at end of pt breath. Can add a small amount of PSV to overcome tube resistance

PRVC-pressure regulated, volume controlled. Combination of pressure and volume ventilation, computer makes breath by breath determination of ideal pressure to deliver set tidal volume

PSV-usually added to spontaneous breaths, but can be used as vent mode at levels of 20-25. Some vents add PSV settings on top of PEEP, i.e.. PSV settings of 10 and PEEP of 5 would give the equivalent of BiPAP at 15 and 5, others ignore PEEP value, i.e.. same 10/5 settings give equivalent BiPAP of 10 and 5. Wean down to PSV of 5. Active with SIMV and CPAP modes.

Inspiratory Flow Rate (IFR)-Typically 60 L/min, change to 80-100 L/min in Asthma/COPD

Alarm Settings

Inspiratory/Trigger Sensitivity

is the amount of negative pressure that the patient must establish for the machine to sense patient effort. Usually set to -1 to -2 cm H2O. Machine adjusts based on PEEP

High Pressure

Low Pressure with PPV

Low PEEP

Low Minute Volume

High Breath Rate

Apnea Interval

Back Up Breath Rate

Keep PIP<50 and Plateau Press<30-35. Plateau is what the alveoli actually experiences

Permissive Hypercapnia

decrease Vt to 5-6 cc/kg, 8-10 bpm. Increase inspiratory flow rate to 80-100, Keep PIP<50. 8-9.0 Tube cut to size.

Adding PEEP to RAD patients may help in two ways. It may splint open airways that would otherwise close at exhalation leading to occult auto-peep. It also allows pt to breathe spontaneously, otherwise the autopeep would have to overcome in order to take a breath in. Autopeep leads to constant exhalation pressure from stretching the chest wall. In order to breathe in, you must overcome. Adding PEEP counters this force as long as it is equal to or less than autopeep.

Testing Vent for Leaks

Power-up the ventilator. Occlude the outlet of the circuit with your hand. Have your partner press the Inspiratory Hold button during inspiration and continue pressing it to create a pause of approximately 2 seconds. As the ventilator cycles observe the manometer needle closely. Pressure should reach a high peak value, drop quickly and then plateau for 2 seconds without dropping further. If the manometer needle does NOT reach a pressure of > 40 cmH2O and/or does NOT maintain a constant plateau, check for leaks at all connections.

Hyperoxia

Inverse Ratio Ventilation (IRV)

Increases the inspiratory time to greater than the expiratory time leaving the lungs inflated more of the time. Leads to better oxygenation, but respiratory acidosis from ventilatory inadequacy. Very uncomfortable for patients; they need to be heavily sedated.

How do I set PEEP for my patient?

Remember that the objective of using PEEP is to 1) restore functional residual capacity, & 2) to increase mean airway pressure and improve oxygenation by reducing ventilation-perfusion mismatch. The required PEEP depends on:

1) The extent of lung injury: determined by the alveolar-arterial oxygen gradient (or the PaO2/FiO2 ratio).

2) The patient's chest wall compliance. As stated previously (click here), additional weight to the chest reduces FRC, by reducing the tendency of the chest wall to spring outwards; the chest wall compliance. This is examplified in obese patients, and explains their chronic respiratory failure. Low chest wall compliance can be acquired in critical illness due to circumferential chest dressings, extensive edema, and, in particular, raised abdominal pressure. Patients who have had large volume fluid resuscitation develop extensive tissue edema, bowel distension, ascites and abdominal hypertension. The diaphragmatic excursion is limited, and dependent atelectasis results. Moreover, the heart increases in size and weight and compresses the left lower lobe.
The result of this is that patients with low chest wall compliance, such as surgical critically ill patients, require higher trans-alveolar pressure to achieve the same tidal volumes, which means higher PEEP to restore FRC. Elderly patients, particularly those with COPD, may have very high chest wall compliance, and require relatively low levels of pressure to generate target tidal volumes.

What is the extent of the patient's lung injury?	What is the patient' chest wall (C_w) compliance?
Target PaO₂>60-80 What FiO₂ is required to achieve this?	NORMAL	LOW -obesity -edema -abdominal hypertension
FiO₂	Normal C_w Compliance PEEP in cmH₂O	Low C_w Compliance PEEP in cmH₂O
0.3	5	10
0.4	8	12
0.5	10	14
0.6*	12	16
0.7*	14	18
0.75*	16	20
0.8*	18	22
0.9*	20	22
1*	22	24

*Consider alternative methods of increasing mean airway pressure such as prolonging the duration of inspiration - by increasing inspiratory time in pressure control or adding an inspiratory pause in volume control.

The static respiratory system pressure-volume (P-V) curve is often measured in intubated, mechanically ventilated patients to make inferences about the mechanical properties of the lungs. Although the utility of P-V measurements in clinical decision-making remains to be established, the determinants of the P-V relationship should nevertheless be understood. The P-V curve is generated by inflating and deflating the relaxed respiratory system in a stepwise fashion between residual volume and total lung capacity. The airway occlusion pressure at each volume defines the corresponding elastic recoil pressures of the lungs and chest wall. Because the inflation and deflation relationships differ from each other, the resulting curve is often referred to as a P-V loop. The respiratory system P-V loop is the summation of individual lung and chest wall P-V loops, termed a Rahn diagram

increased baseline airway pressures using CPAP, and restoration of lung volumes.

Resistive: initial airway pressure which must be overcome to inflate lungs (airway and lung compliance), peak pressure

Pressure will have a square shaped pressure wave while volume will peak and the slope down

limit/control=the parameter that is limited and kept constant throughout inspiration

rise time-as it goes from rapid to slow, it takes longer to get to peak airway pressure, peak flow decreases, time to get to same Vt is increased

EARLY PEEP is better than late, b/c ards turns from fluid to gel, and pneumonias organize

Cycle is time, flow, or volume. what makes vent switch from inspiration to expiration

anesthesia vents in the or are just bags in a bottle allowing control of tidal volume, respiratory rate and fiO2

Pts tend to hyperventilate as they emerge from sedation in this mode and there is no weaning component

triggers used to be negative pressure, but modern vents have a small amount of constant flow, differences in this flow caused by the patient is a better trigger

Look at the shape, if flat on top then pressure control, if sloped up then volume breath

Is there autopeep? If there is the new flow will start before return to baseline

In SIMV, on the flow screen, a Pressure supported breath can be distinguished by a shark fin shape and on the rpessure it will be flat topped

In pressure control the flow will end at end inspiration while in pressure support, flow ends before end inspiration

SIMV adds a second circuit with an FiO2 filled bag so patient can take spontaneous breaths in between mandatory breaths

Constant flow rate will cause more shear injury to the lung b/c mean airway pressures will be higher

flow is decel b/c pressure continues to remain the same even after it has equilibrated with alveoli because the vent sets the time of inspiration

decel flow patterns allow the flow to equilibrate even to non-compliant areas of the lung

Inspiratory time is usually set at 1 sec, but in can be increased if needed to relieve hypoxia

Patient controls everything but the pressure limit, they take as much flow as they want and breath continues until flow reaches preset point, usually 25% of peak.

they can get the same tidal volume without having to generate as much negative pressure

If patients can not get flow, they suck against the closed valve of the vent, this is bad

Only occurs in volume, in pressure modes, patients can get as much flow as they like

the pressure in pressure modes is peak pressure b/c it is easier for the machine to measure

Traumatic patients have limited abdominal excursion. Abd must always be considered part of the resp system

Pulmonary hypoxic vasoconstriction is sacrificed when r ventricle is hyperdynamic

In volume mode, when compliance is decreased, more pressure is needed to deliver the same volume

pressure of the heart and the ventricles occurs when trying to ventilate non-compliant lungs

In volume mode, if high volumes are chosen, the healthy lung gets the brunt of the pressure

Descriptions of ventilatory modes usually refer to the inspiratory component b/c there is very little aside from CPAP to do to expiration.

halfway measure, better to wean with AC (pressure or volume) if patient not ready to control their depth of inspiration or if they are, use PSV without mandatory breaths

Can prolong Insp Time to 1.0-1.5 if patient still hypoxemic, but beware of autopeep

Endotracheal Tube Management

study of pts intubated >24 hours showed ~10% loss of diameter increased more c increased duration of intubation (crit care med 2004 32(1):120)

Make sure artificial nose is not clogged with water or it can destroy patency of ventilator circuit

Edema is evenly distributed throughout the lungs due to increased hydrostatic pressure. Heart and diaphragm squeezes gas out of dependent regions, leading to classic CT appearance. Spontaneous breathing can reverse these changes

First of all I would probably discourage the use of APRV (when used in the traditional fashion)in the face of large air leaks. I think that it is counterproductive. I'm sure some would argue but I disagree. VERY efficacious when there is recruitable lung process....but not so much when there is a large pulmonary leak. Difficult to generate "effective" mean airway pressure, and large pressure swings dont do the fistulae any favors. Note that I said "traditional". I have set up APRV on a test lung, using a time high of 0.1 seconds, and a time low, of 0.1 seconds and have achieved "oscillator like" results. Has anyone ever used this on a patient??

Using PEEP to overcome autopeep: if in a volume mode keep increasing the level until plateau increases then drop down to previous level

ARDSnet Protocol

N Engl J Med. 2000 May 4;342(18):1301-8. Links
Comment in:
ACP J Club. 2001 Jan-Feb;134(1):16.
N Engl J Med. 2000 May 4;342(18):1360-1.
N Engl J Med. 2000 Sep 14;343(11):812-3; author reply 813-4.
N Engl J Med. 2000 Sep 14;343(11):812; author reply 813-4.
N Engl J Med. 2000 Sep 14;343(11):813; author reply 813-4.
Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network.
[No authors listed]
BACKGROUND: Traditional approaches to mechanical ventilation use tidal volumes of 10 to 15 ml per kilogram of body weight and may cause stretch-induced lung injury in patients with acute lung injury and the acute respiratory distress syndrome. We therefore conducted a trial to determine whether ventilation with lower tidal volumes would improve the clinical outcomes in these patients. METHODS: Patients with acute lung injury and the acute respiratory distress syndrome were enrolled in a multicenter, randomized trial. The trial compared traditional ventilation treatment, which involved an initial tidal volume of 12 ml per kilogram of predicted body weight and an airway pressure measured after a 0.5-second pause at the end of inspiration (plateau pressure) of 50 cm of water or less, with ventilation with a lower tidal volume, which involved an initial tidal volume of 6 ml per kilogram of predicted body weight and a plateau pressure of 30 cm of water or less. The primary outcomes were death before a patient was discharged home and was breathing without assistance and the number of days without ventilator use from day 1 to day 28. RESULTS: The trial was stopped after the enrollment of 861 patients because mortality was lower in the group treated with lower tidal volumes than in the group treated with traditional tidal volumes (31.0 percent vs. 39.8 percent, P=0.007), and the number of days without ventilator use during the first 28 days after randomization was greater in this group (mean [+/-SD], 12+/-11 vs. 10+/-11; P=0.007). The mean tidal volumes on days 1 to 3 were 6.2+/-0.8 and 11.8+/-0.8 ml per kilogram of predicted body weight (P<0.001), respectively, and the mean plateau pressures were 25+/-6 and 33+/-8 cm of water (P<0.001), respectively. CONCLUSIONS: In patients with acute lung injury and the acute respiratory distress syndrome, mechanical ventilation with a lower tidal volume than is traditionally used results in decreased mortality and increases the number of days without ventilator use.

PEEP in airway obstruction, some patients have paradoxical improvement (Crit Care Med 2005;33(7):1519)

high outward recoil of chest wall generated by persistent activation of inspiratory muscles during expiration

this results in diversion of blood away from areas of normally ventilated lungs due to overdistension

need several seconds to measure a Pplat on insp hold, b/c of need for continued equilibration

Mech Vent with ARDSNET strategy decreases markers of inflammation in patients without preexisting injury (Anesth 2008;108:46)

Patients with ALI often require PEEP to maintain alveolar distention and arterial oxygenation. Positive-pressure ventilation decreases intrathoracic blood volume,¹⁰⁴ and PEEP decreases it even more^125,126 without altering LV contractile function.¹⁶⁴ However, increases in airway pressure may not reflect increases in ITP, because patients with ALI have varying degrees of increased lung stiffness and decreased chest wall compliance. Further, it is the increase in lung volume, not airway pressure, that determines the degree of increase in ITP during positive-pressure ventilation.⁵ Lessard and colleagues, in a study of nine patients with ARDS, found no significant hemodynamic differences among volume-controlled, pressure-controlled, and pressure-controlled inverse ratio ventilation adjusted to keep total PEEP and tidal volume consistent among treatment arms. (Crit Care Text Online)

Systolic RV pressure approximates transmural systolic pulmonary artery pressure when no pulmonary stenosis is present. Transmural pulmonary artery pressure can increase by one of two mechanisms: (1) an increase in pulmonary artery pressure without an increase in pulmonary vasomotor tone, as occurs with increases in blood flow (exercise) or passive increases in outflow pressure (LV failure), or (2) an increase in pulmonary vascular resistance. Usually any increase in transmural pulmonary artery pressure during positive-pressure ventilation is due to an increase in pulmonary vascular resistance, because neither instantaneous cardiac output⁶¹ nor LV filling¹¹ increases. Increases in transmural pulmonary artery pressure impede RV ejection,⁶² decreasing RV stroke volume⁶³ and causing RV dilatation and passive obstruction to venous return,^64,65 which can rapidly progress to acute cor pulmonale.⁶⁶ If RV dilatation and pressure overload persist, RV free wall ischemia and infarction may develop.⁶⁷ Importantly, rapid fluid challenges in the setting of acute cor pulmonale can precipitate profound cardiovascular collapse due to excessive RV dilatation, RV ischemia, and compromised LV filling through the process of ventricular interdependence (discussed later). During normal end-inspiration, mild hypoxemia (arterial O₂ partial pressure >65 mm Hg) and low levels of PEEP (<7.5 cm H₂O) should minimally increase transmural pulmonary artery pressure. If slight increases in transmural pulmonary artery pressure are sustained, however, fluid retention occurs, either by intrinsic humeral mechanisms (increased atrial natriuretic peptide secretion) or by therapeutic intravascular volume infusion,⁶⁸ resulting in an increase in RV end-diastolic volume and maintenance of cardiac output.^60,69

The decrease in venous return during positive-pressure ventilation is often lower than one might expect based on the increase in right atrial pressure. Because a large proportion of venous blood is in the abdomen, the net effect of PEEP is to increase mean systemic pressure and right atrial pressure. Accordingly, the pressure gradient for venous return may not be reduced by PEEP, especially in patients with hypervolemia. In fact, abdominal pressurization by diaphragmatic descent may be the major mechanism by which the decrease in venous return is minimized during positive-pressure ventilation.^71,112-115 When cardiac output is restored to pre-PEEP levels by fluid resuscitation^71,116 and PEEP is maintained, liver clearance mechanisms increase above pre-PEEP levels.^116-119 These data are consistent with a PEEP-induced alteration in intrahepatic blood flow distribution. Thus, ventilation may have less of an effect on venous return than was originally postulated. Van den Berg and colleagues examined the effects of varying levels of CPAP on right atrial pressure, intra-abdominal pressure, and cardiac output in 42 postoperative cardiac surgery patients.¹²⁰ Up to 20 cm H₂O, CPAP did not significantly decrease cardiac output, as measured 30 seconds into an inspiratory hold maneuver. The reason for this apparent paradoxical effect became obvious when the investigators compared the associated changes in right atrial pressure, abdominal pressure, and RV end-diastolic volume (Fig. 64-9). They found that only 30% of the increased airway pressure was transmitted to the right atrium; however, and perhaps more important, most of the increase in right atrial pressure was realized by an increase in intra-abdominal pressure. Thus, it was not surprising that RV end-diastolic volume fell by less than 8% from pre-CPAP values. These data demonstrate that in fluid-resuscitated patients, institution of positive-pressure ventilation may not result in a decrease in blood flow. However, if intra-abdominal pressure is allowed to decrease, as would occur with an open laparotomy and decompression of tense ascites, a marked preload-responsive effect of positive-pressure ventilation should occur.

Hyperinflation can create significant pulmonary hypertension and may precipitate acute RV failure (acute cor pulmonale)⁸⁸ and RV ischemia.⁶⁷ Thus, PEEP may increase pulmonary vascular resistance if it induces overdistention of the lung above its normal functional residual capacity. Recently, the effect of inflation on RV input impedance was validated in humans using echocardiographic techniques.⁸⁹ Similarly, if lung volumes are reduced, increasing lung volume back to baseline levels by the use of PEEP decreases pulmonary vascular resistance by reversing hypoxic pulmonary vasoconstriction.⁹⁰

In the normal lung, expiratory driving pressure is determined by the difference between alveolar pressure and airway opening pressure. In the relaxed or paralyzed state, this driving pressure is the respiratory system recoil pressure at that particular end-inspiratory lung volume. In normal lungs, the net driving pressure may be reduced by the application of extrinsic PEEP, which serves as a load that must be overcome before volume can be expired. Consequently, in a volume-preset ventilatory mode, this would result in reduced expiratory flow, hyperinflation, and elevated peak airway pressures over subsequent breaths. As explained in Figure 64-7, if extrinsic PEEP does not affect expiratory flow, flow limitation is present. In other words, in patients with severe airway obstruction who are breathing in the tidal volume range, end-inspiratory recoil pressure far exceeds that required for maximal expiratory flow. These patients would not exhibit reductions in expiratory flow in response to the application of small levels of extrinsic PEEP.³⁵ Accordingly, as shown in Figure 63-11, the application of up to 5 cm H₂O of extrinsic PEEP in an obstructed patient fails to raise volume or peak pressure.

In PS mode, the transition from inspiration to expiration, known as cycling, occurs when instantaneous inspiratory flow (V'insp) decreases to a predetermined fraction of peak inspiratory flow (V'insp/V'peak), often referred to as an 'expiratory trigger' (ET) [15]. In an ideal situation, cycling coincides with the end of the patient's inspiratory effort. Prolonged pressurization by the machine into the patient's expiratory phase is known as delayed cycling. Delayed cycling can lead to expiratory asynchrony and increased WOB [14,33]. Delayed cycling has been shown to occur mostly in patients with obstructive airways disease [34-36]. On many ventilators, the cutoff value of ET is pre-determined, usually at a default setting of 0.25; that is, the ventilator cycles when V'insp has decreased to 25% of V'peak. However, when airway resistance increases, the profile of the inspiratory flow curve changes, the curve spreading out and becoming flatter (Figure 3). Hence, the 0.25 point will be reached later, which in turn increases the likelihood of delayed cycling. The adverse consequences of delayed cycling are summarized in Figure 4. Consequently, setting a higher value of ET should theoretically decrease the magnitude of delayed cycling [35], and thereby alleviate some of the adverse consequences outlined above (Figure 5). This hypothesis was tested in a recent study in which intubated COPD patients on PS were studied at various ET settings, ranging from 0.10 to 0.70 [37]. The study showed that at the higher ET values, the magnitude of delayed cycling was reduced, entailing as predicted a reduction in PEEPi, ineffective inspiratory attempts and inspiratory muscle workload [37].
During NIV, additional factors can contribute to delayed cycling. Calderini and colleagues [8] showed that leaks around the mask led to a prolonged pressurization by the ventilator, in turn leading to an insufficient decrease in V'insp to the cycling threshold. Consequently, cycling was considerably delayed, the patients were attempting to cycle the ventilator by active expiration [33] and WOB was increased [8]. The authors convincingly showed that relying on time rather than on flow cycling, that is, by limiting the maximum inspiratory time, delayed cycling, the magnitude of inspiratory efforts and WOB were all markedly reduced [8]. Naturally, reducing leaks can also contribute to alleviate this problem, but tight-fitting masks are a source of discomfort for patients, which can lead to overall intolerance to NIV and reduce its chances of success. Finally, delayed cycling can also occur as a result of increased leaks caused not by an insufficient mask seal but by a high pressurization rate [9].
Go to source: Critical Care | Full text | Clinical review: Patient-ventilator interaction in chronic obstructive pulmonary disease

During PS, the slope of pressurization, that is, the incremental increase in per time unit, can be adjusted on most Paw ventilators [19]. The steeper the slope, the faster Paw will rise to its target value. Studies performed in patients with obstructive mechanics have demonstrated that, compared to a slow pressurization rise time, a steep slope is associated with less WOB, and the steeper the slope the lower the WOB [25]. The same observation was made by Chiumello and colleagues [26], their results also showing that comfort was at its lowest at both the lowest and highest pressurization rates. During NIV, a study performed in COPD patients showed that the diaphragmatic pressure-time product was lower at the fastest pressurization rate, which was associated with a significant increase in air leaks and proved to be the most uncomfortable for the patients [9]. Therefore, it is probably wise not to decrease the PS rise time to <100 ms, and, if a patient exhibits discomfort, to increase the time up to 200 ms.
Go to source: Critical Care | Full text | Clinical review: Patient-ventilator interaction in chronic obstructive pulmonary disease

Lancet. 1999 Nov 27;354(9193):1851-8. Related Articles, Links
Supine body position as a risk factor for nosocomial pneumonia in mechanically ventilated patients: a randomised trial.

HMEs not worse than heated humidifiers; both help to prevent VAP (Crit Care Med 2007;35:2843)

PEEP

they are summarized in an editiorial (JAMA 2008;299(6):691), the articles prove that the higher PEEP levels are safe and that in the sickest patients, the high PEEP strategy is the way to go

To the Editor: Limiting plateau pressures in the respiratory system of patients with acute lung injury and acute respiratory distress syndrome (ALI/ARDS) to 28 to 30 cm H₂O may help guarantee lung protection.¹ In the large multicenter Express trial, Dr Mercat and colleagues² set positive end-expiratory pressure (PEEP) as high as possible to avoid plateau pressure above 28 to 30 cm H₂O (mean, 27.5 cm H₂O). In the lower PEEP (minimal distention) group in the Express trial, plateau pressure was kept as low as possible to maintain oxygenation targets (mean, 21 cm H₂O). There was no difference in mortality between the 2 groups, but the higher PEEP/plateau pressure (increased recruitment) group showed a greater number of ventilator-free and organ failure–free days. Plateau pressure in the increased recruitment group dropped to 24 cm H₂O within the first week.

Two smaller trials (n = 53³ and n = 103⁴) showed that higher PEEP levels, comparable with the Express trial (14-16 cm H₂O), can reduce mortality in ARDS, despite using plateau pressures that have been considered unsafe. Both studies started out with a plateau pressure of 32 and 31 cm H₂O, respectively, but within 1 week they only needed a plateau pressure of 24 to 26 cm H₂O.

There are 2 main differences between these studies and the Express trial. In the smaller trials, plateau pressure before lung protective ventilation was 30 to 32 cm H₂O compared with 23 cm H₂O in the Express study, at comparable PEEP levels (8 cm H₂O) and tidal volumes. Also, both smaller studies used standardized ventilator settings with the patients to see whether ARDS criteria (ratio of partial pressure of arterial oxygen over fraction of inspired oxygen [PaO ₂:FIO ₂]<200 mm Hg) were maintained over a set time period.

Alterations in chest wall mechanics may also result in marked differences in the real transpulmonary pressure, leading to progressive lung derecruitment and ventilator-induced lung injury (VILI).⁵ Recruitment maneuvers may improve lung function by allowing ventilation on the deflation limb of the pressure-volume curve, resulting in higher end-expiratory lung volumes at similar airway pressures and potentially minimizing VILI.⁵

Arbitrarily limiting plateau pressure without individualized settings, with potential resultant progressive lung derecruitment, may prevent advances in lung protective ventilation. An individually titrated recruitment maneuver leading to an early short-term increase in plateau pressure, especially in more severely hypoxemic patients with altered chest wall mechanics, may result in better oxygenation, rapid lowering of plateau pressure in the first week, and possibly improved outcome.

Jack J. Haitsma, MD, PhD
jack.haitsma@utoronto.ca
Interdepartmental Division of Critical Care Medicine
St Michael's Hospital
Toronto, Ontario, Canada

Paolo Pelosi, MD
Department of Ambient Health and Safety
University of Insubria
Varese, Italy

1. Terragni PP, Rosboch G, Tealdi A; et al. Tidal hyperinflation during low tidal volume ventilation in acute respiratory distress syndrome. Am J Respir Crit Care Med. 2007;175(2):160-166. FREE FULL TEXT

PEEP's effect on Cardiac Output

Fig. 3 Various possible effects of PEEP on cardiac output, illustrated with Guyton’s graphical analysis: a with normal cardiac function, b with depressed cardiac function. In both panels a and b, right atrial pressure is measured relative to atmosphere, i.e., it represents the intracavitary pressure. This is the reason why PEEP shifts the cardiac function curve to the right (see left lower part of Fig. 4 in Part I). PEEP shifts the venous return curve as shown in Fig. 3 of Part I, i.e., the zero flow intercept (which is MSFP) and the critical pressure (Pcrit, at the intersection of the oblique and plateau parts) are increased by approximately equal amounts, while the maximal venous return (height of the plateau part) is depressed. Volume expansion shifts the venous return curve “rightwards” (see Footnote 2 in Part I), whereas hypovolemia has the opposite effect. Pcrit is not affected by changes in volemia. Further explanations in the text (“Effects of PEEP on cardiac output”)

Asthma

new form of trauma=biotrauma lungs are little factories to produce inflammatory mediators

	Trigger	Limit/Control/Target	Cycle
Volume AC	Time	Flow	Volume
Pressure AC	Time	Pressure	Time
PRVC AC	Time	Pressure (Volume)	Time
PSV	Patient	Pressure	Flow