Best Textbook (Tobin MJ Principles and Practice of Mech Vent) Handout for Studs Review Article for Residents My Vent Lecture Handout Mech ventilated patients have a dead space to alveolar ratio of 1:1 as opposed to the 1:2 in a normal patient Va for a normal CO2 is 60 cc/kg/min, so we need to double that (120 cc/kg/min) If a 70kg man needs >8400 cc/minute either deadspace for production of CO2 is elevated. Doubling the minute volume will send CO2 from 40 to 30 quadrupling the minute volume will send it from 40 to 20 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 nonblinded 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) (Final In-Press) 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 Normal shunt fraction is 3% Always consider atelectasis as shunt fraction > 40-50%, increasing FiO2 will not change SaO2 
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. Oxygen Physiology PAO2=PIO2((760-47)x0.21 or 150 on room air)-PaCO2/R(0.8) Amount of O2 dissolved in the blood 1.34xHbx(SaO2/100) + 0.003 x PO2=20.8 DO2=(1.39 x Hb x SaO2 + (0.003x PaO2)) x Q Q=cardiac Output Predicted body weight (PBW) can be calculated by the following formula: in men, PBW (kg)=50+0.91 (centimeters of height152.4); in women, PBW (kg)=is 45.5+0.91 (centimeters of height152.4) each time we disconnect the vent, we cause derecruitment 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 pts 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 Peep-during mechanical ventilation, keeps airways open during expiration If chest tube is present, consider HFOV
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
10 to 15 above PIP, set at 50
Low Pressure with PPV
5-10 below PIP, only active with vent initiated breath
Low PEEP
Set 2-3 less than PEEP setting
Low Minute Volume
1-3 L below minute volume
High Breath Rate
24-28
Apnea Interval
10 seconds
Back Up Breath Rate
give a reasonable rate ~10 Keep PIP<50 and Plateau Press<30-35. Plateau is what the alveoli actually experiences
Permissive Hypercapnia
Shoot for I:E 1 to 4 or 5 instead of 1:2 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
Testing for Leaks: Set the machine to the following settings: Mode: Assist/Control (A/C) Wave form: Square Normal Vt: 200 ml Normal pressure limit: Maximum setting Flow rate: 40 l/m Rate: 12 breaths/minute PEEP: OFF Sensitivity: – 2 cmH2O Sigh controls: Off O2 %: 21 Pressure Support: 0 Low pressure alarm: Off (0) 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.
Back to topHyperoxia
Inten Care Med 2006;32:1979 14 pt study high fiO2 without sig. PEEP led to derecruitment. Obviated by ~15 of PEEP 60% vs. 100% fiO2 was the comparision 100% fiO2 during anesthesia induction leads to atelectasis even if done for only a few minutes (Lancet 1995;345:1387)
Back to topInverse 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 (Cw) compliance? Target PaO2>60-80 What FiO2 is required to achieve this? NORMAL LOW -obesity -edema -abdominal hypertension FiO2 Normal Cw Compliance PEEP in cmH2O Low Cw 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 Failure to oxygenate is treated by recruitment methods, increased baseline airway pressures using CPAP, and restoration of lung volumes. Equation of movement describes gas physics in ventilation Two forces must be overcome for inspiration Resistive: initial airway pressure which must be overcome to inflate lungs (airway and lung compliance), peak pressure Elastic: to keep lungs open, (lung compliance), plateau pressure Trachea is the biggest resistor, and by extension, the ET tube. P is pressure V is volume v with dot over it is flow Volume mode can have constant flow of gas or be set with a decel pattern Pressure is always decel pattern Paw is airway pressure Pressure will have a square shaped pressure wave while volume will peak and the slope down Formats Trigger, Limit, Cycle flow cycled=25% of peak flow 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 trigger=what sets it off limit/control=the parameter that is limited and kept constant throughout inspiration cycle=what causes shift to expiration 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 MMV-spont breathing, but ensures minute volume EARLY PEEP is better than late, b/c ards turns from fluid to gel, and pneumonias organize set Fm near pt’s own rate ǿaw=mean airway pressure Paw=airway pressure Control is volume, pressure, or dual Cycle is time, flow, or volume. what makes vent switch from inspiration to expiration Triggering is time, pressure, or flow what makes vent start inspiration breaths are either mandatory, assisted, or spontaneous Flow pattern constant, sinusoidal or decelerating anesthesia vents in the or are just bags in a bottle allowing control of tidal volume, respiratory rate and fiO2 Volume Assist Control Set Vt, Peak Inspiratory Flow, and RR Pts tend to hyperventilate as they emerge from sedation in this mode and there is no weaning component Flow is given at peak flow until preset volume is reached 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 Waveform Analysis Look at the pressure screen, you can see the CPAP Look for negative deflections and note whether these are triggering the vent Look at the shape, if flat on top then pressure control, if sloped up then volume breath Look at flow screen If the flow is constant then it is volume controlled if it is decel then either pressure or volume with flow alteration 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 Peak flow is usually set at 4 times the minute volume 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 Setting the Peak Flow set higher if using a decel flow pattern if the patient is dysynchronous, give more flow Pressure Controlled conventionally, pressure control refers to CMV but SIMV is also possible 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 There is unlimited flow to the patient’s own inspiratory efforts Set the inspiratory pressure to achieve a Vt of 5-6 cc/kg Inspiratory time is usually set at 1 sec, but in can be increased if needed to relieve hypoxia The higher the insp time, the more potential for auto-peep Pressure Assist Ventilation Pressure Control without a preset rate Pressure Support Ventilation 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. CPAP restores the FRC Press support compensates for loss of lung compliance they can get the same tidal volume without having to generate as much negative pressure Patient Ventilator Dysynchrony 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 Inverse ratio instead of 1:2 I:E uses 4:1, very uncomfortable for the patient optimal peep will be at Pflex 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 pleural pressure manipulation prone positioning spontaneous breaths sit on chest strap bar on chest push on chest all recruitment methods they force the pressure into other parts of the lung 100% o2 results in absorption atelectasis 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 While venous return is obstructed, there is easier ventricular emptying as well In volume mode, if high volumes are chosen, the healthy lung gets the brunt of the pressure Airway resistance is ET tube, bronchoconstriction and mucus plugging PRVC uses flow rate and Ti to keep both pressure and guarantee volume Descriptions of ventilatory modes usually refer to the inspiratory component b/c there is very little aside from CPAP to do to expiration. SIMV with Pressure Support 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 Set rate at 12 Set Vt 6 cc/kg Set PF to 50 L/min Flow Trigger Decel flow pattern PS of 20 cmH20 Reset to Plat-PEEP if machine can measure Volume Assist Control Set Vt 6 cc/kg Set PF to 50 L/min Flow Trigger Decel flow pattern Pressure Assist Control Set PEEP Rate of 12 Adjust Insp Press to get Vt of 6cc/kg, Start high and work lower Insp time 0.5-0.8 seconds flow trigger Set Insp Flow to optimum level Can prolong Insp Time to 1.0-1.5 if patient still hypoxemic, but beware of autopeep Wean down to pressure Assist or PSV Pressure Support Ventilation Set Press Support to 20 Adjust to Vt of 5-6 cc/kg Increase support if compliance decreases
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 Spontaneous Breathing 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 Open Lung Concept early and sustained lung recruitment PaO2 should be >450 when breathing 100% (Mount Sinai Journal of Medicine 2002;Jan/Mar 69:73) 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
Back to topARDSnet 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. ARDSnet does not increase sedation needs (Crit Care 2007;11:R77) Wolthuis EK MA of lung protective (Ann intern med 2009;151:566) low Vt reduces mortality maintaining Plat <30 with higher Vt was not inferior to low Vt Higher PEEP as long as plat < 30 was safe Another opinion on ARDSNet ARMA trial Long-term outcome with ALI patients and ARDSnet (BMJ. 2012 Apr 5;344:e2124. doi: 10.1136/bmj.e2124) great review article on peep and cardiac output (Crit Care 2005;9:Luecke) PEEP in airway obstruction, some patients have paradoxical improvement (Crit Care Med 2005;33(7):1519) Best review on Auto-PEEP and why to give PEEP to these patients (Cleveland Clinic Journal of Med 2005;72(9):801 Auto-positive end-expiratory pressure: mechanisms and treatment) Review article on ventilation in severe asthma (Intensive Care Med 2006;32:501) high outward recoil of chest wall generated by persistent activation of inspiratory muscles during expiration diagrams indicate that asthmatic lungs are “baby lungs” just like ARDS 
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 Trial that high peep low tidal volume is better (Crit Care Med 2006;34(5):1311)
Low Volume Ventilatory Strategies in Patients without Lung Injury
Mech Vent with ARDSNET strategy decreases markers of inflammation in patients without preexisting injury (Anesth 2008;108:46) Determann Prospective RCT(Crit Care 2010;14:R1) Crit Care Med 2007;35:1660 Anesth 2006;105:689 Anesth 2008;108:46 Meta-Analysis (Critical Care 2014, 18:211 ) 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 more125,126 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 resuscitation71,116 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 VENTILATION AS EXERCISE page 486 
page 487 Spontaneous ventilatory efforts are induced by respiratory muscle contraction. Blood flow to these muscles is derived from several arterial circuits whose absolute flow is believed to exceed the highest metabolic demand of maximally exercising skeletal muscle.16 Thus, under normal cardiovascular conditions, blood flow is not the limiting factor determining maximal ventilatory effort. Although ventilation normally requires less than 5% of total O2 delivery to meet its demand,16 in lung disease states in which the work of breathing is increased, such as pulmonary edema or bronchospasm, the work of breathing can increase metabolic demand for O2 to 25% or 30% of total O2 delivery.16-19 Further, if cardiac output is limited, blood flow to other organs and to the respiratory muscles may be compromised, inducing both tissue hypoperfusion and lactic acidosis.20-23 Starting mechanical ventilation may reduce metabolic demand, increasing venous O2 saturation for a constant cardiac output and arterial oxygen content (CaO2). Intubation and mechanical ventilation, when adjusted to the metabolic demands of the patient, may dramatically decrease the work of breathing, resulting in increased O2 delivery to other vital organs and decreased serum lactic acid
levels. These cardiovascular benefits can also be realized with the effective use of noninvasive continuous positive airway pressure (CPAP) by ventilation mask.24 The obligatory increase in venous O2 saturation will result in an increase in arterial O2 partial pressure if fixed right-to-left shunts exist, even if mechanical ventilation does not alter the ratio of shunt blood flow to cardiac output. Finally, if cardiac output is severely limited, respiratory muscle failure will develop despite high central neuronal drive, such that many patients with heart failure die of respiratory failure before cardiovascular standstill.25 Go to source: Critical Care Online 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. during normal tidal volume breathing (30% to 70% vital capacity) High vs. Lower PEEP no difference in outcomes (NEJM 2004;351:327) 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
Two new articles published simul. in JAMA add to the PEEP question 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 JAMA 2008;299(6):646 and 637 Express trial and LOV trial Ventilation Strategies for Acute Lung Injury and Acute Respiratory Distress Syndrome 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 failurefree 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. Financial Disclosures: None reported. Jack J. Haitsma, MD, PhDjack.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 
2. Mercat A, Richard JC, Vielle B; et al, Expiratory Pressure (Express) Study Group. Positive end-expiratory pressure setting in adults with acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008;299(6):646-655. FREE FULL TEXT 3. Amato MB, Barbas CS, Medeiros DM; et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med. 1998;338(6):347-354. FREE FULL TEXT 4. Villar J, Kacmarek RM, Perez-Mendez L, Aguirre-Jaime A. A high positive end-expiratory pressure, low tidal volume ventilatory strategy improves outcome in persistent acute respiratory distress syndrome: a randomized, controlled trial. Crit Care Med. 2006;34(5):1311-1318. FULL TEXT | ISI | PUBMED 5. Quintel M, Pelosi P, Caironi P; et al. An increase of abdominal pressure increases pulmonary edema in oleic acid-induced lung injury. Am J Respir Crit Care Med. 2004;169(4):534-541. FREE FULL TEXT
Decremental PEEP Trial
Decremental PEEP trialResp Care 2006;51(10):1132CPAP of 40 cm H20 for 40 secthen set PEEP at 20then decrease fiO2 until Sat 90-94%then PEEP was dropped by 2 every few minutesPEEP just before the drop was considered optimal PEEPthe pt was then recruited again
Back to topPEEP’s effect on Cardiac Output
Fig. 3 Various possible effects of PEEP on cardiac output, illustrated with Guytons 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) best article
Asthma
new form of trauma=biotrauma lungs are little factories to produce inflammatory mediators oxytrauma=from high fiO2 In the OR, spont ventilations prevent ventral redistribution (Anesthesiology 2012;116(6):1227)
Equilibration Times
It is a common practice in intensive care, before assessing the effects of changes of the ventilator setting on relevant variables, to wait for an ‘‘equilibration time.’’ As an example, it was found that after changing FiO2, the oxygenation reaches its equilibrium in\100 [9, 10], while, when total ventilation is increased, the PaCO2 falls exponentially, reaching its equilibrium in 10–200. In contrast, when ventilation is decreased, the rate of change of PaCO2 is far lower, and the equilibration time requires up to 45–600 [11, 12]. The present study was designed to describe the equilibration time of oxygenation-, ventilation- and respiratory mechanics-related variables after incremental or decremental PEEP. We arbitrarily set the time 600 as the longest time allowed for equilibration, assuming that a longer period could imply, in some patients, a dramatic change of the underlying pathophysiological conditions of the lung, which may confound the effects of PEEP alone. Tugrul et al. [7], after setting PEEP values according to the inflection point of the pressure volume curve, found 200 sufficient to reach 90 % of the PaO2 recorded at time 600, which was assumed as a ‘‘full equilibration time.’’ In contrast, in our study, we found that each group of variables reached its equilibrium When PEEP was decreased, the PO2 and the other oxygenation- related variables significantly decreased within 50 and remained unmodified in the following 550, suggesting that the oxygenation equilibrium was reached almost immediately. The PaO2 decrease is likely due to the immediate collapse of the most dependent lung regions, as observed by CT scan [13], which remain perfused. The initial collapse is primarily due to the gravity-dependent closure of the small airways (‘‘loose’’ atelectasis). If the inspiratory pressure is sufficient to open them, an opening/closing phenomenon is generated [14]. With time the ‘‘loose’’ atelectasis may become ‘‘sticky’’ because of the gas reabsorption, and the opening pressure become greater [15]. This phenomenon may affect the lung mechanics but is probably irrelevant for oxygenation, which is impaired in the presence of either loose or sticky atelectasis, provided that atelectatic regions are perfused. It is also possible that, when atelectasis shifts from an opening/closing to always closed status, which should lead to a further deterioration of oxygenation, more blood flow is diverted to aerated regions, limiting the fall of PO2 (hypoxic vasoconstriction) [16, 17]. Independently from the causative mechanism, however, the PO2 values after 50 are highly representative of the values observed up to 600 (see Fig. 3). In contrast, when PEEP was increased, the PO2 continuously rose, suggesting that equilibrium was not reached even at time 600. In our setting, the PO2 increase was likely due to recruitment of previously collapsed and perfused pulmonary units, as FiO2, minute ventilation and hemodynamics were unchanged. The slow PaO2 increase confirms that, although most of the recruitment occurs rapidly, the remaining opening is a ‘‘slow’’ phenomenon [18]. In fact, recruitment depends on the interaction between the increase of opening pressure (the plateau pressure raised proportionally to the PEEP value) and the increased threshold for closing pressure (higher PEEP maintains open regions that would collapse at lower PEEP) [14, 19, 20]. Whatever the mechanism underlying the
recruitment, it is obvious that its early assessment by observing PO2 variations during incremental PEEP may be misleading because of the slow equilibration time of the oxygenation-related variables. However, the PO2 values obtained after 50, although not in equilibrium, may be sufficient to indicate the oxygenation trend (see Fig. 3). (Intensive Care Med (2013) 39:1377–1385)
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