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Objec ctives
To understand: How positive pressure ventila ation helps
Reduce the work of breathing Restore adequate gas exchange
The basics of
Invasive positive pressure ventilat tion (IPPV) Noninvasive positive pressure ven ntilation (NIPPV)
ComplianceR
Neuromuscular disorders
AW=Airrway; R=respiratroy system; VE = minute ventilation, VO O2 = Oxygen consumption, VCO2=carbon dioxide production
Others
Intubation to facilitate procedure (bron nchoscopy), bronchial suctioning
Lungs L
- Barotrauma - Ventilator-induced lung injury pp g - Air trapping
Gas exchange
- May increase dead space (compression of capillaries) e increase in vascular resistance in the normal lung - Shunt (e.g., unilateral lung disease - the associated with PPV tends to redirect blood flow in the abnormal lung)
Reduced afterload
Lung expansion increases extramural pressure (which helps pump blood out of the thorax) and thereby reduces LV afterload. When the cardiac performance is mainly de etermined by changes in afterload than in preload conditions (e.g., hypervolemic patient with systolic heart failure), PPV may be associated with an improved stroke volume. PPV is very he elpful in patients with cardiogenic pulmonary edema, as it helps to reduce preload (lung congestion) and afterload. As a result stroke volume tends to increase. increase
Oxygen transport
Note that as airway pressure increases s above a certain level (e.g., high PEEP [positive end-expiratory end expiratory pressur re]):
Oxygen transport start to decline despite th he rising PaO2 as cardiac output starts falling. Dead space also tends to increase due to compression of alveolar capillaries by high alveolar pressure, creating ventilated but poorly perfused alveolar units.
Lungs of dogs ventilated for a few hours with large tidal volume demonstrate extensive hemorrhagic injury.
P elastic
P resistive
P elastic
Where CR = compliance of the respiratory system, Ti = inspiratory time and VT/Ti = Flow, RR = resistance of the respiratory system and PEEP total = the alveolar pressure at the end of expiration = externa al PEEP + auto (or intrinsic) PEEP, if any. Auto PEEP = PEEP total P e one needs to generate a tidal breath. extrinsic (PEEP dialed in the ventilator) adds to the inspiratory pressure
Work of Breathing B
Work per breath is depicted as a pressure-volume area Work per breath (Wbreath) = P x tidal vo olume (VT) Wmin = wbreath x respiratory rate
WEL = elastic work Volume e Volume e Volume e WR = resistive i ti work k
VT
Pressure
Press sure
Pressure
The total work of breathing can be partitioned between an elastic and re esistive work. By analogy, the pressure needed to inflate a balloon through a straw varies; one needs to overcome the resistance of the str raw and the elasticity of the balloon.
Volume
VT
VT
Dynamic Hyperinflation
PEEPi = intrinsic or auto PEEP; green triangle = tidal elastic work; red d loop = flow resistive work; blue rectangle = work expended in offsetting intrinsic PEEP (an expiratory driver) during inflation
The Pressure and Work of f Breathing can be Entirely Provided by the Ventilator (Passive Patient)
Ventilator
+ + +
When the lung is inflated by constant flow flow, time e and volume are linearly related related. Therefore Therefore, the monitored airway pressure tracing (Paw) re eflects the pressure-volume work area during inspiration. A pressure-sensing esophageal balloon reflects the average pressure change in est wall expansion. the pleural space and therefore the work of che
PAW
patient i machine hi
PES
Paw = Airway pressure, Pes= eso ophageal pressure
time
Relationship Between th he Set Pressure Support Level and the Patien nts nt s Breathing Effort
The changes in Pes (esophageal pressure) and in the diaphragmatic activity (EMG) associated i t d with the increase in the level of mask pressure (Pmask = pressure support) indicate transfer of the work of breathing from the patient to the ventilator.
Partitioning of the Worklo oad Between the Ventilator and the e Patient
How the work of breathing partitions betw ween the patient and the ventilator depends on:
Mode of ventilation (e.g., in assist control mo ost of the work is usually done by the ventilator) Patient effort and synchrony with the mode of o ventilation Specific p settings g of a g given mode ( (e.g., g level of p pressure in PS and set rate in SIMV) )
Combination modes
SIMV with PS and either volume or pressure-targeted mandatory cycles
VT
AssistAssist -control
Set variables
Volume, TI or flow rate, frequency, flow w profile (constant or decel) PEEP and FIO2
Mandatory breaths
Ventilator delivers preset volume and preset flow rate at a set back-up rate
Spontaneous breaths
Additional cycles can be triggered by t the patient but otherwise are identical to the mandatory breath.
SIM MV
Key set variables
Targeted volume (or pressure target), flow rate (or inspiratory time, Ti), mandated frequency PEEP FIO2, pressure support PEEP,
Mandatory breaths
Ventilator delivers a fixed number of cycles with a preset volume at preset flow rate. Alternatively, a preset pressure is applied f for a specified f Ti
Spontaneous breaths
Unrestricted number, , aided by y the selected d level of p pressure support pp
+
_ _
meanPaw
+
_
Palveolar
_
Ppleural External PEEP
Intrinsic PEEP
The difference between the Ppeak and Pplat tracks the resistive pressure as dictated by the equatio pressure, on of motion. motion During an inspiratory pause, flow becomes zero, the resi istive pressure is eliminated and the airway pressure drops from its peak to the plateau pressure.
Mandatory breaths
Ventilator generates a predetermined press sure for a preset time
Spontaneous breaths
PCV-AC mode: same as mandatory breaths s PCV-SIMV mode: unsupported or PS
Important caveat
It is important to understand that in pressure e-controlled ventilation the relation between the set rate and minute ventilation is complex. p Abov ve a certain frequency q y( (e.g., g , when intrinsic PEEP is created due to a reduced expiratory time), the driving pressure starts to drop--and so does the delivered tidal volume. A pneumothorax or other adverse change in n the mechanics of the respiratory system will not trigger a high alarm pressure but a low tidal volume alarm instead instead.
Pressure e Support
Pressure = set variable. Mandatory breaths: none none. Spontaneous breaths
Ventilator p provides a p preset p pressure a assist, , which terminates when flow drops p to a specified fraction (typically 25%) of its maximum. Patient effort determines size of breath h and flow rate.
Change in mechanics
A AutoPEEP
Inspiratory time
Note that AutoPEEP is not equivalent to air trapping. Active expira atory muscle contraction is an often under appreciated contributor (left panel) to positive press sure at the end of expiration
Press sure
AutoPEEP is commonly measured by performing a pause at the end of expiration. In a passive patient, flow interruption is associated with pressure p tracks the mean alveolar pressure caused by dynamic equilibration through the entire system. In such conditions, proximal airway pressure hyperinflation.
Hypercapnic Acidosis
Determinants of PaCO2
PACO2 = 0.863 x VCO2/VA VA = VE (1-VD/VT)
C Causes of fh hypercapnia i
Inadequate minute ventilation (VE) Dead space ventilation (VD/VT) CO2 production (VCO2 )
VD = dead space VA = alveolar ventilation VE = minute ventilation VT = tidal volume VCO2 = CO2 production
Reduced FiO2 (e.g., (e g toxic fume es altitude) es, Hypoventilation Impaired diffusion Ventilation/perfusion (VA/Q) mis smatching
High VA/Q ( = Shunt) Low VA/Q (0 = Dead-Space) Dead Space)
Shunting
If significant shunting is present, the F FIO2 requirement is typically > 60%
The relationship between PaCO2 and minu ute ventilation is not linear. In patients with hypoventilation, small changes in min nute ventilation may have large effect on the PaCO2.
Note that as the % of shunt rises, increasing the FIO2 has h l less and dl less i impact t on P PaO O 2. Under such conditions, reducing the shunt fraction is key to the ability to improve gas exchange, and this typically requires PPV and PEEP. PEEP
0 mmHg 70%
SvO2
Shunt fraction
50%
In normal lungs, the inspiratory resistive pressure is similar to the ex xpiratory resistive pressure (light shaded area under the airway pressure-time curve) so that mean airway pressure (Paw) can be us sed to track mean alveolar pressure (Palv).
CPAP
Lung regions with shunt tend to distribute preferentially in the dependent regions. Tidal ventilation helps open collapsed regions, and PEEP helps to maintain those regions open throughout expiration an nd to reduce shunt. Note that level of PEEP required to achieve such varies along the gravitational axis.
Approac ch to MV
Is MV indicated ? Y YES NO Contraindica ation to NIPPV ? Conservative treatment and periodic reassessment NO
Y YES
Invas sive MV
Noninvasive e Ventilation
Disadvantages of NIPPV
Less airway pressure is tolerated Does not protect against aspiration No access to airway for suctioning
Initiating g NIPPV
Initial settings:
Spontaneous trigger mode with backu up rate Start with low pressures
- IPAP 8 - 12 cmH2O - PEEP 3 - 5 cmH H 2O
Adjust inspired O2 to keep O2 sat > 90 0% Increase IPAP gradually up to 20 cm H2O (as tolerated) to:
alleviate dyspnea decrease respiratory rate increase tidal volume establish p patient-ventilator synchrony y y
Conclu usions
A good understanding of respir ratory physiology is required for the judicious mechanical ventila ation. Unless contraindicated, NIPPV V is becoming the first modality to try in many settings. Monitoring key variables such a as Pplateau and auto-PEEP is mandatory d t t safe to f and d effective ff ti e practice. ti
Quest tion 1
Answ wer 1
If in a ventilated patient, FIO2 > 60% is needed, shunt is certainly the main cause for the hypoxem mia (correct response: 2). As a rule, increasing the FIO2 w will compensate for VA/Q mismatching i t hi b but t not tf for shunt. h t W Wh VA/Q mismatching When i t hi i is present, hypoxemia typically co orrects with an FIO2 < 60%. Altered diffusion is rarely a clinically relevant issue issue. Increasing the ventilation rate w will not exert a significant impact on oxygenation unless it contribute es to air trapping and auto-PEEP. auto PEEP.
Quest tion 2
Which of the following ventilatory s setting changes is the next best step to reduce shunt and incre ease the PaO2/FIO2 ratio (a bedside index of oxygen exchange)
1. 2. 3. 4. Increase PEEP to 10 cmH20 Increase the FIO2 to 100% Add an inspiratory pause of 1 second Increase respiratory rate to 30/min
Answ wer 2
Interventions that target mean airw way pressure are the most helpful. They help recruit flooded or collapsed alveoli and maintain the recruited alveoli open for gas exchange (red duced shunt). Increasing PEEP is the first interve ention to consider; extending the inspiratory time and I:E ratio is a secondary option to raise mean airway pressure. In the p presence of shunt, increasin ng g the FIO2 would reduce the ratio. Although increasing rate may affec ct mean Paw, its impact is overall minor. Rate adjustment is mainly u used to control minute ventilation and its consequences on:
air trapping PaCO2 and pH
Quest tion 3
PEEP is increased to 10 cmH H20 P O2 is PaO i now 85 mmHg, H P Pplat l t is i 45 45, and dP Ppeak k 50 cmH H2O The high pressure alarm is no ow triggered. Your next step is:
1. 2. 3. 4. 5. Reset the alarm pressure to 55 cmH H20. Disconnect the p patient from the ven ntilator and start manual ventilation (bagging). ( gg g) Order a stat chest x-ray to assess fo or a pneumothorax. Reduce the tidal volume slowly until the alarm turns off. None of the above
Answ wer 3
The correct answer is 5. Option 1 does not ad ddress the issue of the excessive tidal volume and airway pressure. The rise in airway pressure that triggered the a alarm was predictable following the increase in PEEP level. l l Th There i is th thus no need df for 2 and d 3. Tidal volume is never titrated to an arbitrary se et alarm pressure. Pplat, which tracks alveolar pressure and the risk of developing ventilator-induced lung injury (VILI) is an easy and accessible bedside para (VILI), ameter used to assess the risk of alveolar overdistension. In this patient, it is the high Pp plat associated with the choice of an excessive tidal volume that puts the patient at risk of VILI. Patients with ARDS have reduced aerated lun ng volume (baby lungs) and need to ventilated with small tidal volumes: e.g., 6 ml/kg predicted ide eal body weight. This patient is clearly ventilated with an excessive tidal volume for his size (ideal or r predicted body weight). The tidal volume must be reduced. A tidal volume and PEEP combinatio on associated with a Pplat of less than 25 cmH2O is generally considered safe. Concerns regarding the risk of overdistension and VILI is significant when Pplat is > 30 cmH2O. Remember, however, that the actual distendin ng alveolar pressure is the transpulmonary pressure (Pplat- Ppleural). Higher Pplat can be accepte ed in a patient with low chest wall compliance, as less alveolar distension will be present for the same Pplat Pplat, everything else being equal equal.
Cas se 2
67-year-old female (weight 50 kg) with h severe emphysema is admitted for COPD decompensation. She failed NIPPV and required sedation, paralysis, and intubation. Soon after intubation and initiation of m mechanical ventilation, she became hypotensive (BP dropped from 170/95 5 to 80/60). She has cold extremities, distended neck veins, midline trachea a, distant heart sounds, and symmetrical breath sounds with prolonged expirato ory phase. Ventilatory settings are: assist control, tidal volume 500ml 500ml, rate 15/min 15/min, PEEP 5 cmH2O, FIO2 1.0 (100%) ABG: pH 7.20, PaO2 250 mmHg, PaC CO2 77 mmHg Measured variables: rate 15/min, VE = 7.5 l/min, Ppeak 45 cmH2O, Pplat 30 cmH2O
Ques stion 1
The next step p in this p patients man nagement g should be:
1. 2 2. 3. Order a stat echocardiogram to ass sess for tamponade. Order a stat AngioCT to assess for pulmonary p lmonar embolism embolism. Measure AutoPEEP, disconnect the e patient briefly from the ventilator, then resume ventilation with a lower tidal volume and rate and administer intravenous fluid. Start the patient on intravenous dop pamine and adjust the ventilator to normalize the PaCO2.
4.
Answ wer 1
The correct answer is 3. Remember that t gas trapping is your key concern in the ventilated patient with obstructive physio ology. A quick i kl look k at t th the expiratory i t fl flow t tracin i g and d performing f i an expiratory i t pause maneuver demonstrated that the patient t has developed severe dynamic hyperinflation and intrinsic PEEP (15 cmH2O). Brief B i f disconnection di ti (1 - 2 minutes) i t )f from the th ventilator til t while hil continuously ti l monitoring it i oxygen saturation is safe in this conditio on and allows for the lung to empty, intrinsic PEEP to decrease--thus restoring venou us return, preload, stroke volume, and BP. The restoration of BP following g ventilator disc connection is not specific p for air trapping. pp g Therefore, intrinsic PEEP needs to be m measured to confirm the diagnosis. It is also important to consider the possibility of a tension pneumothorax in this patient. The symmetrical y chest and midline trach hea did not suggest gg this p possibility y here. Also notice that Pplat was elevated (due e to gas trapping), but in contrast to a patient with stiff lungs (ARDS), there is a large d difference between Ppeak and Pplat because airway y resistance is markedly y elevated in p patients with COPD.
Question 2
You change the ventilators tidal volume to 300 ml and the rate to 15/min. After 1 liter of physiologi p y gic saline is infused, , the BP is now 100/70 mmHg and heart rate is 120/min. ABG: pH 7.30, PaO2 250 mmHg, PaCO2 60 mmHg. Meas sured variables: rate 20/min, VE = 6.0 l/min, Ppeak 37 cmH2O, Pplat 25 5 cmH2O, Intrinsic PEEP is now 7cmH2O (total PEEP=12 cmH2O O). The best next step is to:
1. 2. 3. 4. Continue with bronchodilators and t tolerate the current mild respiratory acidosis. Increase the rate to normalize PaCO O2. Increase the tidal volume but only to o normalize the pH. Ask for another ABG since you do n not believe the drop in PaCO2--minute ventilation declined.
Answ wer 2
The best next step is continue e with bronchodilator and tolerate th current the t mild ild respiratory i t ac cidosis id i (RA) (RA).
The patient has no contraindications s to mild RA (history of an acute or chronic central nervous system problem, tha at may be worsened by the increase in intracranial pressure associated wit th RA, RA heart failure, failure cardiac ischemia ischemia, or arrhythmia. Although less than present initially, dynamic hyperinflation is still an issue (high Pplat and relatively low BP). Thus, i increasing the minute ventilation to normalize the pH or PaCO2 will make this wors se. The reduction in PaCO2 is due to le ess air trapping, with improved venous return and reduced dead space ventilation n. Hyperinflation tends to compress capillaries and thus promote ventilation of unperfused alveolar units (dead space).