Chapter 43 Physiology of Ventilatory Support

Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc.

Chapter 43

Physiology of Ventilatory Support


Learning Objectives

Discuss the pressures and pressure gradients that affect gas delivery during spontaneous breathing and negative and positive pressure ventilation

Discuss are the effects of mechanical ventilation on ventilation, oxygenation, and lung mechanics.

Discuss the currently available modes of mechanical ventilation

Discuss the indications and physiologic effect of PEEP

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Learning Objectives (cont.)

Describe the cardiovascular effects of positive and negative pressure ventilation

Describe the effects of positive pressure ventilation on other body systems.

Describe and list the complications and hazards of providing mechanical ventilatory support.

Discuss how to minimize the adverse effects of mechanical ventilation.

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Pressure & Pressure Gradients

Gas flows only when pressure gradient exists To understand pulmonary gas flow, must

understand: Pressure at airway opening (Pawo)

Alveolar pressure (Palv)

Intrapleural pressure (Ppl)

Atmospheric or pressure at body surface (Pbs)

See Figure 33-1 Review Chapter 10 on normal ventilation

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Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc. 5

Pressure, Volumes, & Flows During Negative-Pressure MV

Mimics spontaneous ventilation: creates negative pressure at chest wall at beginning of inspiration Pbs transmitted to pleura ( P⇓ pl) and alveoli ( P⇓ alv)

As Pawo is atmospheric, a pressure gradient between Pawo and Palv causes gas flow into lungs

Expiration is passive during spontaneous, negative pressure, & positive pressure ventilation

• Lung recoil creates positive Palv compared to Pawo, creating gradient for gas flow out of lungs

See Figure 43-4



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Pressure, Volumes, & Flows During Positive-Pressure MV

Inspiration occurs due to positive Pawo creating gradient compared to Palv, causing gas to enter lung Entering gas increases airway pressure and volume,

expanding lungs Ppl often becomes positive as compressed between

expanding lung and chest wall Positive pressures exist in thorax from beginning of

inspiration until near end of exhalation • Quite different than normal ventilation

See Figure 43-4



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Ventilation

Minute ventilation (VE): VE = VT f Indication for MV is acute hypercapnic

respiratory failure, aka ventilatory failure Increased PaCO2 with decreased pH

Assumption that MV will improve VE and thus VA by which PaCO2 will be normalized

• Accomplished by increasing VT, f, or both

. . . .

. . . .


After obtaining an arterial blood gas from a patient who is on MV, the respiratory therapist determines the patient is hypercapnic. What ventilator settings changes can the therapist recommend to normalize the PaCO2?

A.Decrease VT, respiratory rate or both

B.Increase VT, respiratory rate or both

C.Increase Positive End Expiratory Pressure

D.Increase the FIO2


Effects of Mechanical Ventilation

Alveolar ventilation (VA): (VA = VCO2 0.863)/PaCO2

As PaCO2 is inversely related to VA, improved VA will decrease PaCO2 & vice versa

• ⇓VA or ⇑VCO2 may cause an ⇑PaCO2 and acute ventilatory failure

Increased V/Q mismatch PPV increases ventilation to nondependent regions Blood flow greatest to dependent regions Therefore, PPV tends to worsen V/Q and contribute to &

increased P(A – a)O2

See Figure 43-5

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Effects on Alveolar & arterial carbon dioxide Normally PACO2 & PaCO2 equal 40 mm Hg as

equilibration occurs across A/C membrane ⇑VCO2 or V⇓ A may cause PaCO⇑ 2

⇑VD/VT can also PaCO⇑ 2

• Occurs due to excessive PEEP, pulmonary embolus, or emphysema

• Results in high V/Q ratio as all ventilation in excess of perfusion is wasted

. . ..

. . . .



Changes in acid-base balance Respiratory acidemia (PaCO2 > 45, pH < 7.35) indicates

inadequate VA: increase VE to correct

• Patient anxiety may cause ventilator asynchrony

• Can occur with a small VT and V⇑ D/VT

Respiratory alkalemia (PaCO2 < 35, pH > 7.45)

• Indicates VA is too high, decrease VE to correct

• Caused by anxiety, pain, or inappropriate set VE

Changes in acid-base status impact electrolyte balance and O2Hb dissociation curve, which affect loading and unloading of O2

. . . .

. . . .

. .


A patient in the ED has experienced an increase in ventilatory dead space. Which of the following can occur with this patient?

A.Increased PaO2

B.Increased PaCO2

C.Decreased PaCO2

D.Increased FIO2


Effects of Mechanical Ventilation on Oxygenation

Increased Inspired Oxygen Mechanical ventilators deliver increased inspired

oxygen concentration (FIO2)

Increase FIO2 may restore PAO2 and PaO2 to normal with appropriate management


Effects of Mechanical Ventilation on Oxygenation (cont.)

FIO2 available: 0.21–1.0 May restore PAO2 and PaO2 to normal, particularly

if hypoxemia is caused by V/Q mismatch Hypoxemia caused by diffusion defect or shunt

responds best to PEEP and increased FIO2

Hypoventilation induced hypoxemia improves with MV as it increases VA

. . . .

. .



Alveolar oxygen & alveolar air equation Increasing FIO2 increases PAO2 predictably:

PAO2 = FIO2 (PB – 47) – PaCO2 (FIO2 + (1 – FIO2/R) Even with changes in PaCO2 and R, PAO2

changes proportionally to FIO2

How PaO2 responds to changes in FIO2 depends on pathology that has caused it to fall



Arterial oxygenation & oxygen content (CaO2) Fick’s law of diffusion: Diffusion =

[A D (P1 – P2)]/Twhere A = surface area, D = diffusion coefficient, P1 = PAO2, P2 = PcO2 or capillary PO2, T = tissue

thickness. If PAO2 is low (P1), decreased gradient and low PaO2

• ⇑VA and FIO⇑ 2 reestablishes PaO2

Need PEEP and FIO⇑ 2 reestablishes PaO2

• Diffusion defects: Increased tissue thickness (T)• ALI increases T & decreases A



Arterial oxygenation & oxygen content (CaO2) CaO2 determined by arterial oxygenation & [Hb]

as:

CaO2 = (1.34 Hb SaO2) + (PaO2 0.003)

where 1.34 = maximum oxygen a mg of Hb can carry, SaO2 = O2 saturation of Hb, 0.003 = ml of O2 dissolved in plasma for each mm Hg of PaO2

Normal ~19.8 ml O2/dl CaO2 alters with changes in Hb, SaO2, or PaO2



PEEP/CPAP is required to decrease shunt Helps maintain, open, and stabilize alveoli, increasing

surface area for gas exchange• Improves arterial oxygenation

Use carefully- may overdistend alveoli, sending blood to poorly ventilated alveoli worsening shunt

Tissue oxygen delivery (DO2) DO2 = CaO2 CO (normal 1000 ml/min)

Mechanical ventilation may impede venous return, so increased CaO2 can be offset by decreased CO


The physician has informed you that a ventilated patient has a severe shunt due to widespread atelectasis. In an effort to better oxygenate this patient, what should the respiratory therapist recommend?

A.Decrease PEEP

B.Increase PEEP

C.Decrease FIO2

D.Increase FIO2


Effects of Positive-Pressure Mechanical Ventilation on Lung Mechanics

Increased pressure Peak inspiratory pressure (PIP) is pressure

necessary to overcome airway resistance & lung & chest wall compliance

Pplat is static Palv at peak inspiration With square flow waveform, difference between

Pplat & PIP is due to Raw• Raw = (PIP – Pplat)/flow

Cstatic = VT/(Pplat – PEEP) common measurement of pulmonary compliance

• Tracks changing lung conditions Pplat should be kept <30 cm H2O


Effects of Positive-Pressure Mechanical Ventilation on Lung Mechanics (cont.) Mean airway pressure (see Box 43-1)

Average pressure across respiratory cycle Any changes in settings, PIP, VT, etc. alter MAP Most closely tied to oxygenation, direct

relationship Effect of peak airway pressure on lung

recruitment ⇑PIP recruits previously closed alveoli

• PEEP then maintains or keeps alveoli open Extrinsic PEEP controlled by PEEP control Intrinsic (auto) PEEP results from gas trapping

– Breath starts during ongoing expiratory flow.


Effects of Positive-Pressure Mechanical Ventilation on Lung Mechanics (cont.)

Tidal volume PCV, VT varies inversely with changes in Cstatic & often

Raw• If inspiratory time is sufficient, changes in Raw will not alter

VT but will shorten period of no flow

Functional residual capacity (FRC) Varies directly with PEEP level In restrictive disease as PEEP and FRC increases

lung compliance increases (⇑Cstatic) until lung overdistention occurs



P/V curve and lung recruitment in ARDS Set PEEP 2 cm H2O above lower Pflex

Avoid hitting upper Pflex as indicates overdistention

Note that Pflex points are often difficult to identify



P/V curve and lung recruitment in ARDS Lung recruitment (RM) has proved very useful

• Commonly 40–50 cm H2O applied over <3 minutes Recent approach to setting PEEP

• Decremental PEEP trial following RM• Best PEEP where highest compliance is noted• Recruit lung again, then set PEEP at best level

Decreased work of breathing (WOB) (see Figure 43-8) Properly set MV should alleviate or lessen WOB Continuum from full support (A/C) to little (CPAP)



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After increasing the PEEP for a mechanically ventilated patient who appears to have a severe shunt, which of the following has been directly affected by this increase?

A.VT

B.IRV

C.IC

D.FRC


Minimizing Adverse Pulmonary Effects of PPMV

Decreasing pressure Attempt to keep pressures as low as possible

PIP < 40 cm H2O, Pplat < 30 cm H2O

Use of diuretics, bronchodilators, inotropes may help to lower ventilating pressures

May need to decrease VT to keep pressures low

High MAP can impede venous return, reducing CO.

• Reduce by decreasing TI, VT, f, PEEP, or PIP


Minimizing Adverse Pulmonary Effects of PPMV (cont.)

PEEP/CPAP Used to improve oxygenation, particularly with

refractory hypoxemia (PaO2 < 50–60, FIO2 > 0.5)

Maintains open alveoli, increasing FRC, reducing shunt, often improving Cstatic & PaO2/FIO2 ratio

• Allows FIO2 to be reduced while maintaining PaO2



Effects of ventilatory pattern (flow waveform) Square waveform typical of VCV Decelerating waveform typical of PCV

• Compared to square waveform ⇓PIP, P⇓ plat, WOB, V⇓ ⇓ D/VT, PaCO⇓ 2, ⇑PaO2, and MAP⇑

PPV low flows can cause gas trapping and patientventilator asynchrony (especially in COPD, asthma).

• Minimize risk with higher flows and shorter TI, to allow more time for exhalation


Physiologic Effects of Ventilatory Modes

Volume-Control vs. Pressure Control Primary variable we wish to control is patient’s

minute ventilation Continuous Mandatory Ventilation-CMV

provides all breaths, even patient triggered, as mandatory breaths Mandatory breaths may be Volume Control-VC or

Pressure Control-PC


Physiologic Effects of Ventilatory Modes

Volume-controlled modes VC-CMV provides all breaths, even patient

triggered, as mandatory breaths.• Breaths at set VT but pressures will vary

• High MAP results

• For true control patients must be sedated Problem is muscle atrophy

• Must set trigger and flows to meet patients needs otherwise patient-ventilator asynchrony occurs

Graphics reflect needed adjustments


Physiologic Effects of Ventilatory Modes (cont.)

Volume-controlled modes VC-SIMV used for patients capable of providing

some ventilation, the mandatory breaths will be at set VT all other breaths are spontaneous

• Advantages Inspiratory muscle usage avoids atrophy ⇓MAP Reduced risk of cardiovascular compromise



Volume-controlled modes VT delivered to patient is less than set because

• Pressure compresses gas, occupy less volume • Ventilator circuits are compliant so under pressure they

expand, which takes volume Not critical unless ventilating with small VT

Minimized by using Low compliance tubing, low-volume humidifier Compensating for lost volume

– Adjust manually or use modern ventilator, which compensates for tubing compliance



Leaks in volume ventilation Noted two methods

• Inspired VT significantly greater than expired VT

• An abrupt, above baseline end to expired volume as seen on volume-time scalar


Physiologic Effects of Ventilatory Modes (cont. )


The respiratory therapist has intubated and placed a patient in the ICU on MV. Which of the following is the primary variable the therapist wants to initially control?

A.ICP

B.Minute ventilation

C.Arterial pressure

D.Mean airway pressure



Pressure-controlled modes PC-CMV, PC-SIMV, PSV, APRV, BiPAP, etc. All PC modes feature

Patient or time triggered to inspiration Pressure limited inspiration Decelerating flow waveform Time or flow cycled to expiration

Benefits include limitation of Palv and improved patient ventilator synchrony, possibly improves distribution of ventilation, oxygenation, and gas mixing



PC-CMV May reduce PIPs and Palv

Each breath has preset pressure, so constant PIP Volume & flow will vary with Cstatic and Raw

Commonly used to treat ALI/ARDS patients• May include lung protective strategy with permissive

hypercapnia CO2 allowed to rise gradually with pH >7.2 Thought to reduce risk of further lung injury



PC-IRV PC-CMV may be used by setting I:E >1:1 MAP increases proportional with I:E Suggested to treat severe hypoxemia when high

FIO2 and high PEEP fail as in ALI/ARDS Short time constants associated with ALI/ARDS so

less expiratory time required Depending on degree of IRV may cause auto-

PEEP If applied PEEP in conventional ventilation is equal

to total PEEP in IRV, oxygenation will be equivalent


A patient in the ED has been placed on PC-CMV. Which of the following variable is dependent on the patient’s lung compliance and airway resistance?

A.Pressure

B.Inspiratory Time

C.Tidal Volume

D.FIO2



APRV Variation on PC-IRV Patient breaths spontaneously at high and low levels

of CPAP, spontaneous effort may be PSV supported Most time is spent at high CPAP level with brief

periods of release (<1.5 seconds) to low CPAP During release patient exhales passively When pressure is restored to high CPAP, it causes a

mechanical inspiration Often fewer hemodynamic side effects than PC-IRV Less sedation may be required



PSV-Pressure Support Ventilation Patient triggered, pressure limited, flow cycled

• Flow cycle may be factory preset or adjustable

Minimal levels set to overcome Raw caused by ETT, secretions, bronchospasm, imposed WOB

Patient has control over f, TI, and flow

VT is determined by PSV level, patient effort, Cst, Raw

May decrease f, WOB, VO2, and increase VT

Patients generally prefer to other modes.

. .



VA-PSV (Volume Assured-PSV) Dual control mode Patient initiates all breaths, which most resembles

VC with constant flow If patient demand is greater then set flow, breath

becomes a pressure breath Breath ends when (1) volume is reached or (2) if

volume is exceeded, when patient’s flow falls back to set flow



CPAP Spontaneous breathing at elevated baseline pressure Positive pressure maintains higher alveolar inflation,

used to reestablish FRC in low FRC states• May reduce need of high FIO2, reduce shunt, V/Q⇑

Adaptive Support Ventilation (ASV) Automated dual-control mode, where support varies

based on patient effort Input: IBW, high pressure alarm, PEEP, FIO2, rise

time, flow cycle %, and % predicted VE desired Ventilator makes adjustments based on Otis “ideal”

ventilatory pattern

. . . .


A post operative patient has developed ARDS. Which of the following ventilator mode should the respiratory therapist recommend?

A.PC-IMV

B.PC-CSV

C.PC-CMV

D.VC-CSV



Proportional assist ventilation (PAV) RT sets proportional assist up to 80% of total effort Ventilator determines: Paw, flow, VT, IT based on

• Patient effort, elastance, and resistance

Patient affects everything, as only set parameter is that ventilator will perform a fixed proportion of work

Problems:• Little data to support use• Potential for runaway ventilation caused by

Leaks Overestimation of elastance and resistance



Automatic tube compensation (ATC) Calculates Raw associated with the artificial airway

Attempts to adjust Paw to keep tracheal pressure

constant at baseline pressure Goal to eliminate imposed WOB

• ATC % adjustable to compensate from as low as 10% to 100% of imposed work

If applied to expiration may cause early airway closure As ATC accounts for WOB imposed by ETT, some

consider equivalent to “electronic extubation”



Dual control modes with volume target Pressure-controlled breaths but target a volume

Volume support ventilation (VSV) Set: target VT, FIO2, PEEP, high pressure alarm

PSV with volume target IF PSV delivers an inaccurate VT

• Following breaths PSV adjusted a maximum of 3 cm H2O until volume target reestablished



PRVC (pressure-regulated volume control) PCV with a volume target – Dual control mode If volume target is not reached:

• Next breaths pressure will adjust in maximum of 3 cm H2O increments per breath until targeted volume attained

Use care in any dual-control mode as patient with strong drive may receive diminishing support with increased WOB (study by Jaber et al.)



Patient positioning to optimize oxygenation and ventilation Frequent turns are required to avoid atelectasis,

hypoxemia, secretion retention, pressure sores• Kinetic beds may help (controversial)

Unilateral lung disease, place good lung down as much as possible, improves V/Q and oxygenation

ARDS patients most often improve oxygenation in prone position, recruits alveoli, improves V/Q,

• Problems: Labor intensive, extubation, line displacements, corneal abrasion

. . . .

. . . .

. . . .

. . . .


Cardiovascular (CV) Effects of PPV Early studies show marked reduction in cardiac

output Amount of reduction proportional to pressure applied

PPV causes Ppl to become positive Intrathoracic veins are compressed, increased CVP

• Impedes venous return and venous pooling• Cardiac output (CO) decreases within few beats• Increases ICP with a reduction in cerebral perfusion, may

lead to cerebral ischemia/hypoxia Healthy persons minimized by autoregulation

• Compensatory mechanisms minimize CV affects Increase HR, SVR, blood to core organs


Cardiovascular Effects of PPV (cont.)

Pulmonary vascular pressure, blood flow, and pulmonary vascular resistance (PVR)

Normally PPV has minimal impact on all the above

If alveolar distention occurs, due to high VT or excessive PEEP, blood flow is impeded as the capillaries are compressed between over-distended alveoli Increases RV afterload and decreases CO The stiffer the lungs, the more this affect is minimized



Right and left ventricular function Normal CV systems: no significant effect Conditions that cause impairment

• Hypovolemia, excessive VT or PEEP

Effect with left ventricular dysfunction May improve CV function due to decreased afterload Endocardial blood flow may be impeded

• Determined by ΔP between Pdiastolic and wedge

• Decreased by excessive PEEP, MAP, high VT, long TI



CO, CI, and systemic blood pressure No alteration if CV system is normal and PPV is

normal High MAP may decrease all of these values Ways to minimize or avoid these affects are:

• Adequate fluid balance• Proper management of PPV

Lowest MAP and PEEP possible

• Use of vasopressors Most common cause of hypotension in PPV is

sepsis

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Positive pressure ventilation, especially when accompanied by PEEP, may cause which of the following negative effects on the cardiovascular system?

A.Increase CO

B.Decrease CO

C.Increase CI

D.Increase systemic arterial pressure


Minimizing the CV Effects of PPV

Mean pleural pressures (MPPs) Clinically monitored by following MAP

• Linear relationship Higher the MPP, greater the CV effects Effects are minimized in noncompliant lungs, i.e.,

stiff lungs seen in ARDS patients. Moderate increases in MPP have minimal effect in

most patients.• If patient is hypovolemic, a small change in MPP could

cause a serious decrease in CO.

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Minimizing the CV Effects of PPV (cont.)

Decreasing mean airway pressure (MAP) Determined by f, VT, TI, Ipause, ET, I:E, PIP, PEEP, &

inspiratory flow pattern Changes of above to decrease MAP

• If PaO2 is high, reduce PEEP: very effective Follow carefully to avoid desaturation

• Increased compliance PEEP and diuretics

• Decreased VT or PC level

• Decreased TI & I:E ratio

• Changing from A/C to SIMV or PSV


Minimizing the CV Effects of PPV (cont.)

Fluid management & cardiac output (CO) In face of sepsis, high PEEP & MAP, preload & CO

may decrease thus worsening DO2

• Fluid or blood administration to maintain CO Pharmacologic maintenance of CO and blood

pressure First line is fluid administration except CHF Shock

• Fluid to achieve CVP 8–10 or wedge of 18 mm Hg• Persistent shock, use dobutamine• If BP is low, dopamine


A patient in the ICU has been placed on positive pressure ventilation. Which of the following when increased may reduce cardiac output?

A.FIO2

B.PaO2

C.PaCO2

D.PEEP


Minimizing Effects of PPV on Other Body Systems

Increased ICP in traumatic brain injury (TBI) Hyperventilation ( PaCO⇓ 2) must be used with

caution as decreases ICP but also CBF resulting in ischemia

• Effects may be as short as 1 hour

Treatment of patient with closed head injury (severe TBI) Avoid hyperventilation in first 24 hours to avoid

ischemia• Exceptions

Use briefly while other therapies are initiated Use to treat transient spikes in ICP

If instituted, VT 8–10 ml/kg, higher f


Minimizing Effects of PPV on Other Body Systems (cont.)

Effect on renal function Directly reduces urine output by 30–50% by

reduction in mean arterial pressure or vascular redistribution

Indirectly PPV ⇑ADH, natriuretic hormone, ⇓which together cause fluid retention

Decreased liver and splanchnic perfusion Dysfunction caused by CO⇓

Decreased gastrointestinal function Stress ulcers (ischemia), gastric distention


Minimizing Effects of PPV on Other Body Systems (cont.)

Effects on the CNS: anxiety, fear, agitation due to Lose of control and autonomy in ICU Inability to communicate because of ETT

Sedatives, hypnotics, and neuromuscular blockers Targeted to relieve CNS side affects Sedation level based on Modified Ramsay Scale

• Level 3 responds to verbal commands (Box 43-3) Neuromuscular blockers should never be used with

out sedatives Daily sedation vacations to assess overall functions


Complications of Mechanical Ventilation

Negative-pressure ventilation Pulmonary complications

• Hypoventilation due to inadequate negative pressure or leaks, or hyperventilation, too negative pressures

Cardiovascular complications• Abdominal blood pooling, reducing venous return, CO,

and blood pressure, called tank shock

• With iron lung, patient isolation occurs, as all but head is inside the tank

Difficult to access lines, do patient care, etc.


Complications of Mechanical Ventilation (cont.)

Positive-pressure ventilation Artificial airway complications (see Chapter 33)

• Intubation trauma to eyes, teeth, soft tissues• Nasal ETT: epistaxis, sinusitis, necrosis of nares• Oral ETT: necrosis of lips, patient may bite the tube• Placement of ETT in esophagus or bronchus• Cuff leak: hypoventilation, aspiration, pneumonia• Excessive cuff pressure: tracheal necrosis, cuff rupture

(requires reintubation)• Tracheostomy tube: innominate artery erosion,

hemorrhage, tracheal stenosis, and cuff issues



Complications related to pressure Ventilator-associated lung injury (VALI)

High pressures are associated with barotrauma• Pneumothorax, pneumomediastinum,

pneumopericardium, subcutaneous emphysema

Pneumothorax has decreased chest movement, hyperresonance to percussion, on affected side

• If tension pneumothorax: medical emergency Relieved by needle insertion, then chest tube Use 100% oxygen to speed reabsorption



Volume related as a result of alveolar overdistention

Ventilator-induced lung injury (VILI) Increased A/C permeability, pulmonary edema, cell

damage & necrosis, diffuse alveolar damage Overdistention causes volutrauma and biotrauma. Recruitment-derecruitment of alveoli (atelectrauma)

• Led to lung protective (Pplat < 30 cm H2O) & open lung (recruit then set adequate PEEP) strategies

Biotrauma releases inflammatory mediators, results in inflammation, impaired DO2, and bacteremia

• Contribute to multisystem organ failure (MSOF)



Auto-PEEP (a.k.a.: occult or intrinsic PEEP) Airtrapping occurs if ET is too short for patient’s

condition• Expiratory flow is interrupted by next breath

• Greatest risk with R⇑ aw (obstructive disorder), C⇑ st

Not included in measured & displayed PEEP value so easy to overlook

Increases WOB by decreasing diaphragms effectiveness and making it difficult for patient to trigger (asynchrony)

• Minimize by ⇑ET, I⇓ T, & PEEP set until patient can trigger; ⇑watch auto-PEEP does not increase with PEEP


A patient in the ICU has been placed on positive pressure ventilation. It has been determined that the patient is trapping air in their lungs. Which of the following should the respiratory therapist recommend?

A.Increase FIO2

B.Decrease the inspiratory flow

C.Increase the inspiratory time

D.Decrease the inspiratory time



Oxygen toxicity Mimics ARDS: tissue damage with ⇑A/C

permeability Risks factors: length of exposure, FIO2,

susceptibility• Associated with FIO2 >0.5 for >24–48 hours

• Risk increases the higher the FIO2

Oxygen free radicals (OH, HO2, O2) increase with

⇑FIO2

• Impair type II cell production of enzyme superoxide dismutase, which detoxifies free radicals

• Increase A/C permeability• Decrease surfactant production

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Ventilator-associated pneumonia (VAP) Intubation increases risk, bypasses protection of URT

• Microaspiration of upper GI or pharyngeal bacteria

• Occurs around cuff or from ETT lumen

Prevention of VAP• Gentle suctioning

• Use of MDI rather than SVN

• Keep head elevated 30 to 45 degrees

• Ventilator circuit changed as seldom as possible

• Avoid or drain inspiratory tube condensation

• Daily sedation vacation to assess readiness to wean



Ventilator malfunction Patient circuit failure

• ETT problems: cuff rupture, mainstem intubation, soft tissue damage, and disconnection

• Circuit problems: leaks, humidifier overheating or not filled, expiratory valve failure

• Noted on ventilator by changes in f, VT, Paw

Ventilator failure• Failure of electrical system, microprocessor, gas supply,

or development of an internal leak



Ventilator malfunction Patientventilator asynchrony

• Airway, circuit, and ventilator functioning fine

• Patient is in distress as demonstrated by Dyspnea, tachypnea, tachycardia, hypotension,

diaphoresis, accessory muscle use, retractions, and paradoxical breathing pattern

• Patient is fighting the ventilation. See Table 43-3 for troubleshooting this condition

Chapter 43 Physiology of Ventilatory Support

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Transcript of Chapter 43 Physiology of Ventilatory Support