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Basics of Mechanical l Ventilation

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)

The principles of bedside mo onitoring


Pressure and volume alarms Flow and pressure time curves

Physiopathology of Respiratory R Failure30


ResistanceAW VA/ /Q Work of Breathing Fatig gue Hypoxemia Hyperca apnia VE
VO2 VCO2 pH

ComplianceR

Neuromuscular disorders

AW=Airrway; R=respiratroy system; VE = minute ventilation, VO O2 = Oxygen consumption, VCO2=carbon dioxide production

Indications and Ration nale for Initiating IPPV


Unprotected and unstable airways s (e.g,, coma)
Intubation and IPPV allows to
- Secure the airways y - Reduce the risk of aspiration - Maintain adequate alveolar ventilation

Hypercapnic respiratory acidosis


IPPV and NIPPV
- Reduce the work of breathing and thus s prevents respiratory muscle fatigue or speeds recovery when fatigue is already prese ent - Maintain adequate alveolar ventilation (prevent or limit respiratory acidosis as needed)

Hypoxic respiratory failure


IPPV and NIPPV help correct hypoxem mia as it allows to
- Deliver a high g FiO2 ( (100% if needed d during g IPPV) ) - Reduce shunt by maintaining flooded o or collapsed alveoli open

Others
Intubation to facilitate procedure (bron nchoscopy), bronchial suctioning

Important Pitfalls and Problems Associated with PPV


Potential detrimental effects ass sociated with PPV
Heart and circulation
- Reduced venous return and afterload - Hypotension and reduced cardiac outpu ut

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)

Important Effects of PPV on Hemodynamics


Decreased preload
Positive alveolar pressure lung volume e compression of the heart by the inflated lungs the intramural p pressure of the heart cavi ities rises ( (e.g., g , RAP) ) venous return decreases preload is reduced stroke volume dec creases cardiac output and blood pressure may drop. This can be minimized with i.v. fluid, w which helps restore adequate venous return and preload. Patients P ti t who h are very sensitive iti t to change h i in preload l d conditions diti ( (e.g., presence of f hypovolemia, tamponade, PE, severe air t trapping) are particularly prone to hypotension when PPV is initiated.

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

Effects of PPV on n Hemodynamics


Generally speaking, the effects of f PPV on the cardiac chamber transmural pressures vary in para allel with:
Airway pressure Lung compliance Chest wall stiffness (e.g., air rway pressure venous return) (e.g., co ompliance venous return) (e.g., in th he obese patients, a given change in airway pressure a and lung volume will have more impact on the hemodyna amics, given that the pressure rise around the heart is go oing to be higher than in patients with compliant t chest wall, everything else being equal)

Marini, Wheeler. Crit Care Med. The Essentials. E 1997.

Alveolar Pressure and Gas Exchange


Intens sity of the ef ffects Dead space PaO2

Oxygen transport

Alveolar Pre essure

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.

Adapted from: Marini, et al. Crit Care C Med. 1992.

Other Potentially Advers se Effects of Mechanical Ventilation


Excessive airway pressure and tid dal volume can lead to lung injury (ventilatorinduced lung injury) an nd contribute to increased mortality mortality.

Lungs of dogs ventilated for a few hours with large tidal volume demonstrate extensive hemorrhagic injury.

The Acute Respiratory Distress Syndrome Network. N Engl J Med. 2000;342:1301-1308.

Other Potentially Advers se Effects of Mechanical Ventilation


In the setting of obstructive physio ology (e.g., asthma and COPD), adjustment of the tidal volume and d rate minute ventilation to restore a normal pH and PaCO2 can lead to o air trapping, pneumothoraces, and severe hy ypotension.
Up pper Panel: When airway resistances are high, there is for a few breath more air going in than coming out of the lungs (dynamic hyperinflation). Subsequently, a new equilibrium is reached. The amount of air trapped can be estimated in a passive patient by discontinuing ventilation and collecting the expired volume (lower panel). l) Th he volume of trapped gas is largely determined by: 1. 2. 3. The severity of airway obstruction The ventilator settings (see advance course for details) details). Of all the settings, the imposed minutes ventilation (set rate x VT) and the most important one. The time left between tidal breath for exhalation is less important if a low VT and VE are targeted.

Tuxen et al. Am Rev Resp Dis 198 87;136:872.

Positive Pressu ure Ventilation: on of Motion The Equatio


In a passive subject, airway pressure r represents the entire pressure (P) applied across the respiratory p y system. y The work required to deliver a tidal bre eath (Wb) = tidal volume (VT) x airway pressure The p pressure ( (P) ) associated with the d delivery y of a tidal breath is defined by y the simplified equation of motion of the res spiratory system (lungs & chest wall):

P = VT/CR+ VT/Ti x RR + PEEP total

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.

Intrinsic PEEP and d Work of Breathing


When present, intrinsic PEEP contrib butes to the work of breaking and can be offset by applyi ing external PEEP.

Volume

VT

VT

FRC Pressur re PEEPi

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

+ + +

Work of Breathing Und der Passive Conditions

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

The Work of Breathing ca an be Shared Between the Ventilator an nd the Patient


The ventilator generates positive press sure within the airway and the patients inspiratory muscles generate nega ative pressure in the pleural space space.
AC mode

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.

Carrey et al. Chest. 1990;97 7:150.

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) )

Common Mode es of Ventilation

Volume targeted ventilation (flow w controlled controlled, volume cycled)


AC

Pressure targeted ventilation


PCV (pressure controlled, time cycled) PS

Combination modes
SIMV with PS and either volume or pressure-targeted mandatory cycles

Pressure and Volume e Targeted Ventilation


In pressure-targeted ventilation: an n airway pressure target and inspiratory p y time are set, , while flow a and tidal volume become the dependent variables. In volume I l targeted t t d ventilation til ti (flow (fl w-controlled, t ll d volume l cycled), l d) a t target t volume and flow (or inspiratory time e in certain ventilator) are preset and pressure and inspiratory time (or flo ow in the ventilator where inspiratory time is preset) ) become the dependent variables. The tidal volume is the integral of th he flow during inspiration = area under the curve of the flow time curve during inspiration (see next slide).

Pressure and Volume e Targeted Ventilation

VT

Marini, Wheeler. Crit Care Med. The e Essentials. 1997.

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

Peak Alveolar and Tran nspulmonary Pressures


P(t) = VT/CR+ Flow w x RR + PEEP tot

+
_ _

Peak Airway Pressure Alveolar Pressure Plateau pressure

meanPaw

+
_

Palveolar

_
Ppleural External PEEP

Intrinsic PEEP

Ptranspulmonary = Palveolar - Ppleural

Pplat = Maximum Palveolar

Transpulmonary pressure is a key d determinant of alveolar distension distension.

Monitoring Pressure e in Volume Targeted Ventilation


Plateau pressure tracks the highes st tidal alveolar pressure, a key determinant of alveolar distension distension. Plateau pressure (Pplat) is, howeve er, only a surrogate of peak alveolar distending gp pressure ( (transpulmona p ary y pressure p = Pplat p p pleural pressure).
e.g., in a patient with a low chest wall c compliance, a given Pplat is typically associated with a higher g p pleural p pressu ure but less alveolar distension (smaller ( transpulmonary pressure) than in a pat tient with a compliant chest wall.

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.

Airway Resistance an nd Respiratory System Comp pliance


Under conditions of consta ant flow, the difference between peak and plateau airway pressures drives end-inspiratory flow. When airflow is stopped in a passively ventilated patient by occlusion of the e expiratory circuit valve at end inspiration (plateau pre essure) and end expiration (t t l PEEP) (total PEEP), the th pressure needed d dt to overcome th the elastic recoil of the lungs and chest wall during delivery of the tidal volume is given as the difference in these values. l Di Dividing idi th the d deliver li red d tid tidal l volume l b by thi this difference quantifies the respiratory system compliance. p

Mean Airwa ay Pressure


Although measured in the connecting circuit, mean airway pressure is a valid measure of t p the p pressure applied pp across the lung and chest wall, averaged a across both phases of the ventilatory cycle - but only unde er passive conditions. Changes in mean airway pressu ure are produced by changes in minute ventilation, PEEP, and I:E ratio. Mean airway yp pressures affect p pleural p pressure and lung g distention. Therefore, changes in mean air rway pressure during passive inflation may influence:
Arterial oxygenation Cardiac output

Pressure Contro olled Ventilation


Key set variables:
Pressure, TI, and frequency PEEP and FIO2

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.

PCV: Key Paramet ter to Monitor is VT


What Causes a Decreased VT During g PCV?
airway resistance: . e.g., bronchospasm b h respiratory system compliance . .e.g, pulmonary edema, pneumothorax

Change in mechanics

A AutoPEEP

expiratory resistance expiratory time e.g., g , rate

Inspiratory time

e.g., rate if I:E ratio constant

AutoAuto -PEEP (Intrin nsic PEEP, PEEPi)

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

Marini, Wheeler. Crit Care Med. Th he Essentials. 1997.

Suspecting and Me easuring AutoPEEP


Suspect AutoPEEP if flow at the end of expiration does not return to the zero baseline.

End expirat tory pause

Press sure

Total PEEP PEEPe PEEPi Time Ti

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.

Interim Summary y and Key Points


Mechanical ventilation helps to improve respiratory gas exchange and can provide com mplete or partial work of breathing assistance. Safe and effective implementati p ion of mechanical ventilation requires understanding the equation of motion for the respiratory system. Monitoring dynamic and static a airway pressures and flows yields vital information for interpreting the mechanics of the respiratory system and for adjusting machine settings for optimal performance. performance

Mechanical Ven ntilation and Gas Exch hange


Respiratory y acidosis Hypox xemia

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

Corrective measures for respira atory acidosis


When appropriate, increase the minute ventilation (e.g., the rate or the tidal ou e) volume

Mechanism for Arterial A Hypoxemia

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%

Minute Ventilation and Gas Exchange

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.

Shunting: Effects s of FiO2 on PaO2

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

Key Factors Determining g the Effects of Shunting on Arterial O2 Saturation


Note that inpatients with shunt physiology a reduction in arterial O2 saturation may be due to a change in: the intraparenchymal shunt fraction (e.g., atelectasis) or the SvO2 (e.g., drop in cardiac output). A sudden drop in O2 saturation in patients with ARDS warrants a thorough assessment of the respiratory and cardiovascular system.

450 mmHg 100% 85%


50%

0 mmHg 70%

SvO2
Shunt fraction
50%

Mean Airway and Alveolar A Pressures

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).

Adapted from: Ravenscraft et al. Crit Ca are Med. 1992.

PEEP, Regional Lung Volume, V and Shunting


ZEEP

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.

Effect of PEEPPEEP-in nduced Alveolar Recruitmen nt on PaO2

Malbuisson et al. AJRCCM. 2001:163:1444-1450.

Approac ch to MV
Is MV indicated ? Y YES NO Contraindica ation to NIPPV ? Conservative treatment and periodic reassessment NO

NIPPV YES Success ? NO

Y YES

Invas sive MV

Noninvasive e Ventilation

Ventilatory support provided with hout invasive airway control


No tracheostomy No ETT

Key Differences Betw ween NIPPV and IPPV


Advantages of NIPPV
Allows the patients to maintain normal functions
Speech Eating

Disadvantages of NIPPV
Less airway pressure is tolerated Does not protect against aspiration No access to airway for suctioning

Helps avoid the risks and complications p related to:


Intubation Sedation Less ventilator-associated pneumonia

Clinical Use of NIPP PV in Intensive Care


Decompensated p COPD ( (Hyperc yp capnic p Respiratory p y Failure) ) Cardiogenic pulmonary edema Hypoxic respiratory failure Other possible indications
Weaning g (p (post-extubation) ) Obesity hypoventilation syndrome Patients deemed not to be intubated Post-surgery g y Asthma

Adapted from: Am J Respir Crit Care Med. 20 001;163:283-291.

Contraindicati ions to NIPPV


Cardiac or respiratory arrest Nonrespiratory organ failure Severe encephalopathy (e.g., G GCS < 10) Severe upper gastrointestinal b bleeding Hemodynamic instability or uns stable cardiac arrhythmia Facial surgery, g y trauma, or defo ormity y Upper airway obstruction Inability to cooperate/protect th he airway Inability to clear respiratory sec cretions High risk for aspiration
Adapted from: Am J Respir Crit Care Med. 2001;163:283-291.

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

Success and Failure Criteria for NPPV


Improvements in pH and PCO2 o occurring within 2 hours predict the eventual success of NPPV. NPPV If stabilization or improvement has not been achieved during thi ti this time period, i d th the patient ti t shou h uld ld b be considered id d an NPPV failure and intubation must be st trongly considered. Other criteria for a failed NPPV t trial include: worsened encephalopathy or agitation, ina ability to clear secretions, inability to tolerate any available e mask mask, hemodynamic instability, worsened oxygenatio on.

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

Post Module Testing: T Case 1


29-year-old patient (weight 120 kg, height 170 cm) ARDS secondary to bilateral pneumonia Ventilator settings: AC with VT 8 800 ml and back-up rate 10/min, PEEP 5 cmH2O, FIO2 80 % Measured variables: rate 25, VE = 20 l/min, Ppeak 40 cm H2O, P l t 35 cm H2O Pplat ABG: pH 7.40, PaO2 55 mmHg, PaCO2 38 mmHg, O2 saturation 85%

Quest tion 1

Wh t mechanism What h i b best t explains l i the patients ti t hypoxemia? h i ?


1. 2. 3. 4 4. V/Q mismatch Shunt Abnormal diffusion Inadequate oxygen delivery and high h tissue extraction

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).

References and Su uggested Readings


Hubmayr RD, Abel MD, Rehder K. . Physiologic approach to mechanical ventilation Crit Care Med. 1990;18 ventilation. 8:103-13. 8:103-13 Tobin MJ. Mechanical ventilation. N Engl J Med. 1994;330;1056-61. Marini JJ. Monitoring during mecha anical ventilation. Clin Chest Med. 1988;9:73-100. Brochard L. Noninvasive ventilatio on for acute respiratory failure. JAMA. 2002;288:932-935. 2002;288:932-935 Calfee CS, Matthay MA. Recent ad dvances in mechanical ventilation. Am J Med. 2005;118:584-91.