Principles of Mechanical Ventilation

NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning, LLC NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC 9781284202175_CH01_001_012.indd 1

© s_maria/Shutterstock Bibliography Case Study Summary Conditions LeadingtoMechanicalVentilation Oxygenation Failure Ventilatory Failure Dead SpaceVentilation Compliance Airway Resistance Introduction OUTLINE Failure ofVentilatory Pump Excessive Ventilatory Workload Depressed RespiratoryDrive Gas ExchangeAbnormalities Clinical SignsofHypoxia Hypoxemia andHypoxia Defects Diffusion Intrapulmonary Shunting Ventilation-Perfusion Mismatch Hypoventilation Physiologic DeadSpace Alveolar DeadSpace Anatomic DeadSpace onVentilationEffects andOxygenation Pressure-Volume Slope Plateau Pressure andPeakInspiratoryPressure Abnormal LungCompliance Measurement ofCompliance Waveform Displays onVentilationEffects andOxygenation Airway ResistanceandWork ofBreathing AirwayResistance Factors Affecting NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC Principles of Mechanical © Jones & Bartlett Learning LLC, an Ascend Learning Company. NOTFORSALEORDISTRIBUTION. LLC, anAscendLearning © Jones&Bartlett Learning NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC David W.Chang,EdD,RRT Ventilation C 1 NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning, LLC NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC hap t er OBJECTIVES peak inspiratorypressure oxygenation failure intrapulmonary shunting hypoxia hypoxemia dynamic compliance dead spaceventilation resistanceairflow KEY TERMS 2. 9. 8. 7. 6. 4. 3. 1. 5.

resistance. Define andexplaintheclinicalsignificanceofairflow mechanical ventilation. List thepulmonaryandnonpulmonaryconditionsleadingto failures. Define anddescribethecausesleadingtooxygenation failures. Define anddescribethecausesleadingtoventilatory rapid shallowbreathing pattern. Describe therelationship betweendeadspaceventilationand Describe theclinicalapplicationofPIP-Pplatpressure gradient. (compliance) slope. Describe theclinicalapplicationofpressure-volume peak inspiratorypressure. Describe theclinicalapplicationofplateaupressure and compliance anddynamiccompliance. Define andexplaintheclinicalsignificanceofstatic NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC NOT FORSALEORDISTRIBUTION © Jones&BartlettLearning,LLC ventilatory failure ventilation-perfusion static compliance pressure-volume slope plateau pressure mismatch 05/12/19 10:43 AM 1 2 CHAPTER 1 Principles of Mechanical Ventilation

© Jones &Introduction Bartlett Learning, LLC © JonesThere & Bartlett are many Learning,conditions that LLC can increase the airway resistance. Two common diseases with increased Mechanical ventilation is an invasive procedure to pro- NOT FOR SALE OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION airway resistance are asthma and COPD (e.g., emphy- vide partial or full support of a patient’s ventilation and sema, chronic bronchitis, and bronchiectasis). Me- oxygenation needs. Indications for mechanical ventila- chanical factors that increase airway resistance include tion include numerous clinical conditions that fail to foreign body aspiration, main stem intubation, and meet these gas exchange requirements. Examples include artificial airways for mechanical ventilation. Infectious abnormal functioning© of Jones the respiratory & Bartlett drive (e.g., Learning, drug LLC © Jones & Bartlett Learning, LLC processes include laryngotracheobronchitis (croup), overdose, postanesthesiaNOT recovery, FOR traumaticSALE OR brain DISTRIBUTION injury), NOT FOR SALE OR DISTRIBUTION epiglottitis, and bronchiolitis. ventilatory pump (e.g., flail chest, diaphragm), airway (e.g., The normal airway resistance (of the natural airways) epiglottitis, status asthmaticus), and lung parenchyma in adults is between 0.5 and 2.5 cm H O/L/sec. The total (e.g., acute respiratory distress syndrome [ARDS], chronic 2 resistance of all airways in the tracheobronchial tree is obstructive pulmonary disease [COPD]). referred to as airways resistance. It is higher in intu- Durations© Jones of & mechanical Bartlett ventilation Learning, range LLC from less © Jones & Bartlett Learning, LLC bated patients due to the small diameter of the ET tube. thanNOT an hour FOR (e.g., SALE postanesthesia OR DISTRIBUTION recovery) to years (e.g., NOT FOR SALE OR DISTRIBUTION Airway resistance varies directly with the length and high spinal cord injury). Locations for use of mechanical inversely with the diameter of the airway or ET tube. ventilation include acute care units, mass casualty situa- A shortened ET tube or tracheostomy tube facilitates tions, long-term care facilities, and at home. This chapter airway management and removal of secretions. It also covers the essential principles of normal and abnormal reduces mechanical dead space and airway resistance. © Jones & respiratoryBartlett physiologyLearning, for LLCspontaneous breathing and © Jones & Bartlett Learning, LLC However, the main determinant of increased airway NOT FOR SALEhow they OR relate DISTRIBUTION to the use of mechanical ventilation. NOT FOR SALE OR DISTRIBUTION resistance is the internal diameter of the ET tube. For this reason, the largest but appropriately sized ET tube Airway Resistance should be used for mechanical ventilation. Once the pa- Airway resistance (Raw) is a mechanical factor affecting tient is intubated, patency of the ET tube must be main- the airflow in the airways.© Jones Airflow & resistance Bartlett has Learning, a simi- LLCtained as secretions inside the© ET Jones tube greatly & Bartlett increase Learning, LLC lar definition, exceptNOT it can FOR be used SALE to describe OR DISTRIBUTIONthe con- the airway resistance. NOT FOR SALE OR DISTRIBUTION dition in the airways or in the lungs. Airway resistance Besides the ET tube, the ventilator circuit and con- is considered the nonelastic airflow resistance, because densation collected in it also contribute to the airflow the airway diameter changes minimally during respira- resistance. Pressure support ventilation (PSV) is often tion. The elastic recoil of the lungs contributes to the used to compensate for airflow resistance and to aug- elastic© Jones resistance & toBartlett gas flow. Learning, The total airflow LLC resistance ment spontaneous© Jones breathing & Bartlett efforts. Learning, LLC is theNOT sum FOR of nonelastic SALE and OR elastic DISTRIBUTION resistance. The de- NOT FOR SALE OR DISTRIBUTION gree of airway resistance is primarily determined by the Airway Resistance and Work of Breathing length, internal diameter, and patency of the airway. The Airway resistance (Raw) is calculated by pressure gradi- patency of the airway may be reduced in conditions of ent (ΔP)/flow: retained secretions, bronchospasm (nonelastic airflow Pressure gradient (P∆ ) © Jones & resistance),Bartlett Learning,or compression LLC of the lung parenchyma (i.e.,© Jones & BartlettRaw = Learning, LLC NOT FOR SALEelastic airflow OR DISTRIBUTION resistance). For mechanically ventilated NOT FOR SALE OR DISTRIBUTIONFlow patients, the endotracheal (ET) tube and ventilator cir- The pressure gradient (ΔP) in the equation reflects the cuit impose additional airflow resistance to the airways. work of breathing. Since Raw is directly related to ΔP, an Factors Affecting Airway Resistance increase in airway resistance will increase the work of breathing. If the work of breathing remains unchanged Airflow obstruction ©causes Jones different & Bartlett degrees Learning,of resis- LLCin the presence of increased airway© Jones resistance, & Bartlett the flow Learning, LLC tance in the airways.NOT It is increased FOR SALE when the OR patency DISTRIBUTION (or volume) will decrease. In NOTessence, FOR an increase SALE in OR DISTRIBUTION or diameter of the airways is reduced. Airflow obstruc- airway resistance will lead to an increase in work of tion may be caused by changes inside the airway (e.g., breathing or a decrease in flow (or volume). In a clini- retained secretions), in the wall of the airway (e.g., neo- cal setting, relief of airflow obstruction is an effective plasm of the bronchial muscle structure), or outside the way to improve ventilation and to reduce the work of airway© Jones (e.g., tumors & Bartlett surrounding Learning, and compressing LLC the breathing. © Jones & Bartlett Learning, LLC airway).NOT These FOR conditionsSALE OR reduce DISTRIBUTION the internal diameter NOT FOR SALE OR DISTRIBUTION of the airway and increase the airway resistance. The Effects on Ventilation and Oxygenation simplified Poiseuille’s law shows that when the radius An increase in airway resistance hinders ventilation of a circle is reduced by 50%, the driving pressure (∆P) and oxygenation. If an abnormally high airway resis- must increase by a factor of 16-fold to maintain the tance is sustained over a long time, respiratory muscle © Jones & sameBartlett airflow Learning, (V ). LLC © Jones & Bartlett Learning, LLC fatigue may occur. This leads to eventual ventilatory NOT FOR SALE OR DISTRIBUTION 4 NOT FOR SALE OR DISTRIBUTION Simplified form of Poiseuille’s law: ∆P = V /r and oxygenation failure. Ventilatory failure occurs when

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© Jones &the Bartlett patient’s Learning, minute alveolar LLC ventilation cannot keep up© Jones & Bartlett Learning, LLC with the metabolic rate or CO2 production. Oxygen- NOT FOR SALE OR DISTRIBUTION NOT FOR SALEation failure OR usuallyDISTRIBUTION follows when the cardiopulmonary system cannot provide adequate oxygen needed for PIP

metabolism. O) 2 Pplat Waveform Displays© Jones & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC

The airflow resistanceNOT of aFOR patient-ventilator SALE OR system DISTRIBUTION may w (cm H NOT FOR SALE OR DISTRIBUTION Pa Transairway be monitored using the pressure-volume (compliance) resistanceTransthoracic loop on the ventilator waveform display. An increased pressure bowing of the pressure-volume loop (Figure 1-1) suggests an overall increase in airflow resistance. The increase© Jones in airflow & Bartlett resistance Learning, may be due toLLC excessive © Jones &Time Bartlett (sec) Learning, LLC inspiratoryNOT FOR flow SALEor increased OR expiratoryDISTRIBUTION flow resistance. NOT FOR SALE OR DISTRIBUTION Another method to evaluate the airflow resistance Figure 1-2 Pressure-time waveform. PIP-Pplat gradient reflects of a patient-ventilator system is to use the peak inspi- airflow resistance. PIP, peak inspiratory pressure; Pplat, plateau ratory pressure-plateau pressure (PIP-Pplat) gradient pressure. on the pressure-time waveform obtained by a brief © Jones & end-inspiratoryBartlett Learning, pause. Figure LLC 1-2 shows the PIP and © Jonessame proportion.& Bartlett Likewise, Learning, when theLLC lung compliance NOT FOR SALEPplat (duration OR DISTRIBUTION of Pplat = pause time). PIP is the total NOTis FOR increased, SALE the ORPplat DISTRIBUTION will decrease causing the PIP to pressure needed to overcome the airflow resistance decrease by the same proportion. (nonelastic resistance) in the airways and the elastic recoil forces (elastic resistance) of the lung parenchyma. Compliance Since Pplat is the pressure needed to overcome the re- Lung compliance (Cl) describes the distensibility of the coil forces of the lungs,© Jones the PIP-Pplat & Bartlett gradient Learning, reflects LLClung parenchyma. The opposite© Jones of compliance & Bartlett is elas- Learning, LLC the airflow resistanceNOT characteristic FOR SALE of each OR volume- DISTRIBUTIONtance. Compliance is calculatedNOT by dividingFOR SALE the change OR DISTRIBUTION controlled breath. in volume (∆V) by change in pressure (∆P), or ∆V/∆P. The PIP-Pplat gradient is a steady indicator of airflow In volume-controlled ventilation, ∆V is the mechanical resistance and is not influenced by changes of the lung tidal volume and ∆P is the pressure needed to deliver compliance. As the lung compliance is decreased, the the tidal volume. In pressure-controlled ventilation, Pplat© willJones increase & Bartlett causing the Learning, PIP to increase LLC by the ∆P is the set© peak Jones inspiratory & Bartlett pressure Learning, and ∆V is the LLC NOT FOR SALE OR DISTRIBUTION volume deliveredNOT byFOR the pressure.SALE ORIt should DISTRIBUTION be noted that the required pressure (during volume-controlled 800 ventilation) and delivered volume (during pressure- 700 controlled ventilation) are variable for each breath, and 600 they are influenced by the changing airflow resistance © Jones & Bartlett Learning, LLC © Jonesand lung & Bartlettcompliance. Learning, LLC 500 NOT FOR SALE OR DISTRIBUTION NOT FORThe SALEcompliance OR equation DISTRIBUTION is a very useful tool in 400 mechanical ventilation. During volume-controlled ven- (mL)

T 300 tilation, a rising plateau pressure indicates a decreasing V 200 compliance (and vice versa). (Note: A rising peak inspi- 100 ratory pressure may be due to a decreasing compliance © Jones & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC 0 or an increasing airflow resistance.) During pressure- NOT FOR SALE OR DISTRIBUTIONcontrolled ventilation, a decreasingNOT volumeFOR SALE indicates OR a DISTRIBUTION decreasing compliance (and vice versa). 0210 0 30 40 50 60 P (cm H2O) Measurement of Compliance

© Jones & Bartlett Learning,A1 B1 LLC In mechanical© Jones ventilation, & Bartlettthe compliance Learning, measure- LLC NOT FOR SALE ORA DISTRIBUTION2 B2 ment can beNOT separated FOR into SALE dynamic OR and DISTRIBUTION static compliance. Dynamic compliance (Cdyn) is measured during Figure 1-1 Pressure-volume (compliance) loop shows increased a mechanical breath with gas movement (thus the term bowing (from dotted to solid lines) suggesting an increase in airflow dynamic). The ∆P used to calculate dynamic compli- resistance due to presence of excessive inspiratory flow or increased ance is the peak inspiratory pressure (PIP). Static © Jones & expiratoryBartlett resistance. Learning, Bowing from LLC A1 to A2 could be due to © Jonescompliance & Bartlett (Cst) is measuredLearning, during LLC an end-inspiratory excessive flow during inspiration, and since expiration is passive the NOT FOR SALE OR DISTRIBUTION NOTpause FOR where SALE gas ORmovement DISTRIBUTION is absent (thus the term bowing from B1 to B2 is likely due to expiratory flow obstruction. static). The ∆P in static compliance measurement is the

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© Jones & BartlettTable 1-1 Learning, LLC © Jonesthe alveolar & Bartlett opening Learning, pressure and LLCmakes lung inflation Steps to Measure Dynamic and Static Compliance NOTand FOR expansion SALE difficult. OR DISTRIBUTION The work of breathing is in- NOT FOR SALE OR DISTRIBUTION creased, and the patient typically adopts a rapid shallow 1. Calculate corrected tidal volume. breathing pattern. High compliance means diminished elastic recoil. This abnormal condition becomes evident 2. Obtain peak inspiratory pressure (PIP) during volume-controlled ventilation. during the expiratory phase, and it may lead to incom- © Jones & Bartlett Learning, LLCplete exhalation, incomplete ©CO Jones2 elimination, & Bartlett CO2 Learning, LLC 3. Obtain plateau pressure (Pplat) by applying a brief end- NOT FOR SALE OR DISTRIBUTIONretention, air trapping, and autoNOT positive FOR end-expiratory SALE OR DISTRIBUTION inspiratory pause or manually occluding the exhalation port at pressure (PEEP). Extreme low or high compliance ab- end inspiration. normalities are two contributing factors to increased 4. Obtain positive end-expiratory pressure (PEEP), if any. work of breathing and ventilatory failure.

5. Dynamic compliance (Cdyn) = Corrected tidal volume/ Low Lung Compliance ©(PIP Jones – PEEP) & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC NOTStatic compliance FOR SALE (Cst) = CorrectedOR DISTRIBUTION tidal volume/ In low lung NOTcompliance FOR (high SALE elastance) OR DISTRIBUTION conditions, a (Pplat – PEEP) higher than normal inspiratory pressure is required to inflate the lungs and deliver a set volume. The lungs are stiff or noncompliant. The work of breathing is in- plateau pressure (Pplat), also known as static pressure. creased proportionally to the decrease in compliance. © Jones & MostBartlett ventilators Learning, can measure LLC and display the dynamic © JonesAtelectasis & Bartlett and ARDS Learning, are two examples LLC that produce NOT FOR SALEand static OR compliance DISTRIBUTION values. A manual method to NOTlow FOR lung SALE compliance. OR DISTRIBUTIONThey are associated with refrac- measure and calculate static and dynamic compliance is tory hypoxemia, the type of hypoxemia that responds outlined in Table 1-1. poorly to oxygen therapy alone. Low lung compliance is usually related to conditions that reduce the patient’s Dynamic and Static Compliance functional residual capacity. Patients with noncompli- © Jones & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC Since Cdyn is measured during a mechanical breath, the ant lungs often have a restrictive lung defect, low lung rise and fall of PIP is NOTdetermined FOR by SALE two main OR factors: DISTRIBUTION volumes/capacities, and low minuteNOT FOR ventilation. SALE OR DISTRIBUTION airflow resistance (ventilator circuit, ET tube, airways) and total compliance (chest wall and lung parenchyma). High Lung Compliance In clinical practice, monitoring the PIP or Cdyn does High lung compliance means low elastance (less elastic not© offer Jones enough & Bartlettdetails for Learning,optimal patient LLC care. This is recoil during© exhalation). Jones & TheBartlett lungs areLearning, easily opened LLC because an increase in PIP (or a decrease in Cdyn) could NOT FOR SALE OR DISTRIBUTION and inflatedNOT at a givenFOR inspiratory SALE OR pressure. DISTRIBUTION Unlike low be caused by an increase in airflow resistance or a de- lung compliance, the problem with high lung compli- crease in lung compliance, or both. In most cases, care- ance occurs during the expiratory phase. The exhalation ful patient assessment can isolate the cause for the PIP is often incomplete due to the low elastic recoil property and Cdyn changes. For objective evaluation of a patient’s of the lung parenchyma. Emphysema is an example of status during mechanical ventilation, the Pplat and Cst high lung compliance with impaired gas exchange. This © Jones & shouldBartlett be measured Learning, along LLC with the PIP and Cdyn. © Jones & Bartlett Learning, LLC NOT FOR SALE OR DISTRIBUTION NOTcondition FOR SALE typically OR leads DISTRIBUTION to CO2 retention, chronic air Pplat is measured during a brief end-inspiratory trapping, destruction of lung tissues, and enlargement of pause. When flow is stopped momentarily, there is terminal and respiratory bronchioles. The lung functions no airflow resistance. For this reason, the Pplat is the will show increased residual volume, functional residual pressure needed to overcome the lung compliance (or capacity, and total lung capacity. Patients with extremely elastic force of the lungs) during a mechanical breath. © Jones & Bartlett Learning, LLCcompliant lungs often develop© ventilatory Jones & failure Bartlett and re Learning,- LLC Since Pplat is used in the Cst equation (see Table 1-1), quire noninvasive or invasive mechanical ventilation. Cst reflects the lungNOT compliance FOR characteristics.SALE OR DISTRIBUTION In this NOT FOR SALE OR DISTRIBUTION chapter, discussion on compliance refers to the total Plateau Pressure and Peak Inspiratory compliance (chest wall and lungs) unless it is specified as dynamic compliance (airway and lungs) or static Pressure compliance© Jones (lungs). & Bartlett Learning, LLC Pplat and PIP© Jonesare common & Bartlett measurements Learning, on the LLC AbnormalNOT FOR Lung SALE Compliance OR DISTRIBUTION pressure-timeNOT waveform. FOR SALE During ORvolume-controlled DISTRIBUTION ventilation, these pressure readings increase or de- Abnormally low or high lung compliance affects the crease in response to the breath-by-breath changes in work of breathing and hinders the normal process of airflow resistance or compliance. Conditions leading ventilation and oxygenation. Low compliance means to changes in plateau pressure and static compliance © Jones & highBartlett elastance Learning, (tendency toLLC recoil to size at rest), and it© Jonesinvoke & similar Bartlett changes Learning, in peak inspiratory LLC pressure and NOT FOR SALEis a problem OR affectingDISTRIBUTION the respiratory mechanics duringNOT dynamic FOR SALE compliance. OR DISTRIBUTIONFor example, atelectasis causes the inspiratory phase. This condition greatly increases an increase in plateau pressure and a decrease in static

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© Jones &compliance. Bartlett Learning, These changes LLC will lead to an increase in © JonesTable & 1-2Bartlett Learning, LLC peak inspiratory pressure and a decrease in dynamic NOT FOR SALE OR DISTRIBUTION NOT FORConditions SALE Leading OR toDISTRIBUTION Changes in Plateau Pressure compliance (Figure 1-3 [A to B]). With resolution of (Pplat) and Peak Inspiratory Pressure (PIP) atelectasis, the plateau and peak inspiratory pressures return to normal (see Figure 1-3 [B to A]). When the Pplat PIP Conditions plateau pressure and peak inspiratory pressure change ↑ ↑ ↓ lung compliance (proportional by the same proportion© Jones (increase & or Bartlett decrease), Learning, the LLC changes© Jones in PIP and & Pplat) Bartlett Learning, LLC lungs are responsibleNOT for the FOR changes. SALE In some OR cases,DISTRIBUTION NOT FOR SALE OR DISTRIBUTION the chest wall compliance may invoke similar changes ↑ ↑↑ ↓ lung compliance + ↑ airway resistance as in lung compliance. In conditions where the airway resistance is in- ↓ ↓ ↑ lung compliance (proportional creased (e.g., bronchospasm), the peak inspiratory changes in PIP and Pplat) pressure© Jones is increased & Bartlett and the Learning,dynamic compliance LLC is de- © Jones & Bartlett Learning, LLC creased. It is important to note that the plateau pressure ↓ ↓↓ ↑ lung compliance + ↓ airway NOT FOR SALE OR DISTRIBUTION NOT FOR SALEresistance OR DISTRIBUTION and static compliance remain unchanged (Figure 1-4 [A to B]). The plateau pressure and static compliance No change ↑ ↑ airway resistance stay unchanged because the lung parenchyma is not in- volved in the increase of airway resistance. When bron- No change ↓ ↓ airway resistance © Jones & chospasmBartlett is Learning, resolved, the LLC peak inspiratory pressure and© Jones↑ & BartlettNo change Learning,↓ lung compliance LLC and ↓ airway NOT FOR SALEdynamic OR compliance DISTRIBUTION measurements return to normal NOT FOR SALE OR DISTRIBUTIONresistance (see Figure 1-4 [B to A]). Table 1-2 shows examples of clinical conditions leading to changes in plateau pres- ↓ No change ↑ lung compliance and ↑ airway resistance sure and peak inspiratory pressure.

80 © Jones & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC AB NOT FOR SALE ORPIP DISTRIBUTION NOT FOR SALE OR DISTRIBUTION

O) PTA 2 PIP B PTA 30 cm H2O 20 cm H2O P (cm H Pplat Pplat © Jones & Bartlett Learning, LLC © Jones & Bartlett Learning,A LLC

NOT02 FOR1 SALE OR3 DISTRIBUTION45 76 NOTVolume FOR SALE OR DISTRIBUTION Time (sec)

Figure 1-3 Changes in plateau pressure (Pplat) and peak inspiratory pressure (PIP). In atelectasis, both Pplat and PIP increase © Jones & byBartlett the same proportion Learning, (from A LLCto B). Upon resolution of atelectasis,© Jones & Bartlett Learning, LLC NOT FOR SALEboth Pplat OR and PIP DISTRIBUTION return to normal (from B to A). NOT FOR SALE OR DISTRIBUTIONPressure Chang, DW. Respiratory Care Calculations. revised 4th ed. Jones and Bartlett Learning; 2021. Figure 1-5 Pressure-volume (P-V) display. Shifting of the P-V slope toward the pressure axis (from solid line to dotted line A) indicates a decrease in compliance. Shifting of the P-V slope toward the 80 AB volume axis (from solid line to dotted line B) indicates an increase in © Jones & BartlettPIP Learning, LLCcompliance. © Jones & Bartlett Learning, LLC O) 2 NOT FOR SALEP TAOR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION PIP Pressure-Volume Slope PTA 20 cm H2O

P (cm H 20 cm On the ventilator graphic, the pressure-volume (P-V) Pplat H O 2 Pplat display represents the compliance because C = ∆V/∆P. © Jones & Bartlett Learning, LLC The P-V slope© Jones shows the & Bartlettpatient’s compliance Learning, charac- LLC 021 3 45 76 Figure 1-5 NOT FOR SALE OR DISTRIBUTION teristics duringNOT mandatory FOR SALE breaths. OR DISTRIBUTION shows a Time (sec) P-V slope. A shift of the slope toward the pressure axis (from solid line to dotted line A) indicates a decrease in Figure 1-4 Changes in peak inspiratory pressure (PIP). Increase in compliance. A shift of the slope toward the volume axis airway resistance will increase the PIP, but not the plateau pressure (from solid line to dotted line B) indicates an increase in (Pplat) (from A to B). When the airway resistance is corrected, the PIP © Jones & returnsBartlett to normal Learning, (from B to A). LLC © Jonescompliance. & Bartlett Learning, LLC Interpretation of compliance should be made over NOT FOR SALEChang, DW. RespiratoryOR DISTRIBUTION Care Calculations. revised 4th ed. Jones and Bartlett Learning; NOT FOR SALE OR DISTRIBUTION 2021. time using a trend of serial measurements. In general,

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© Jones &gradual Bartlett changes Learning, in compliance LLC are usually related © JonesTable & 1-3Bartlett Learning, LLC to progressive conditions such as consolidation, NOT FOR SALE OR DISTRIBUTION NOT FORClinical SALE Conditions OR That DISTRIBUTION Increase Physiologic Dead atelectasis, and retained secretions. Sudden changes Space Ventilation in compliance are often due to urgent conditions such as tension pneumothorax, main stem intubation, and Cause of Increased Physiologic Dead Space Example mucus plugs. © Jones & Bartlett Learning, LLC↓ spontaneous tidal ©Neuromuscular Jones & diseases Bartlett Learning, LLC Effects on Ventilation and Oxygenation volume (Vt) Respiratory suppressing drug NOT FOR SALE OR DISTRIBUTION NOToverdose FOR SALE OR DISTRIBUTION Abnormal compliance impairs gas exchange. When an Respiratory muscle fatigue abnormally low or high compliance is uncorrected and Postanesthesia recovery prolonged, muscle fatigue may occur and lead to the development of ventilatory and oxygenation failure. ↑ alveolar dead space (due to Decreased cardiac output lack of matching pulmonary (e.g., congestive heart Ventilatory© Jones failure & Bartlett develops when Learning, the patient’s LLC minute perfusion) © Jones & Bartlettfailure, Learning,blood loss) LLC ventilationNOT FOR cannot SALE keep up OR with DISTRIBUTION the CO2 production. NOT FOR SALEObstruction OR DISTRIBUTIONor constriction Oxygenation failure usually follows when the cardiopul- of pulmonary vessels monary system cannot provide the oxygen demand for (e.g., pulmonary embolism, metabolism and increased work of breathing. hypoxic vasoconstriction)

© Jones & DeadBartlett Space Learning, Ventilation LLC © Jones & Bartlett Learning, LLC NOT FOR SALE OR DISTRIBUTION NOTperfusion FOR SALE in conditions OR DISTRIBUTION such as pulmonary embolism, Dead space ventilation is defined as the portion of tidal (2) decreased of global pulmonary perfusion in condi- volume that does not take part in gas exchange. It is also tions such as congestive heart failure and hypovolemia, called wasted ventilation or ventilation in excess of per- and (3) constriction of pulmonary blood vessels as in fusion. Dead space ventilation has three distinct types: hypoxic vasoconstriction. anatomic, alveolar, and© Jonesphysiologic. & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC Physiologic Dead Space NOT FOR SALE OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION Anatomic Dead Space Physiologic dead space is the total dead space volume Normally, the conducting airways make up about 30% that includes anatomic and alveolar dead space vol- of dead space ventilation. A tidal volume (Vt) of 500 mL umes. Under normal conditions, the physiologic dead normally has about 150 mL of anatomic dead space vol- space approximates the anatomic dead space. In clinical ume© (V Jonesd). This & anatomic Bartlett dV (i.e.,Learning, volume in LLC nasal cavity, conditions where© Jones alveolar & deadBartlett space Learning,is increased, phys-LLC trachea,NOT and FOR main SALE stem bronchi) OR DISTRIBUTION does not contribute to iologic deadNOT space FORbecomes SALE higher OR than DISTRIBUTION anatomic dead gas exchange because it is not in contact with the pul- space. Table 1-3 shows clinical conditions that increase monary capillaries where gas exchange takes place. The physiologic dead space ventilation. Vd/Vt can be measured or estimated (1 mL/lb predicted Physiologic dead space to tidal volume ratio (Vd/Vt) body weight). Decrease in tidal volume (shallow breath- can be calculated as follows: © Jones & ing)Bartlett results Learning,in a relatively higherLLC Vd/Vt %. For example,© Jones & Bartlett Learning, LLC Vd/Vt = (Paco2 – Pe-co2)/Paco2 NOT FOR SALEif the tidal OR volume DISTRIBUTION was decreased from 500 mL to NOT FOR SALE OR DISTRIBUTION 300 mL, the Vd/Vt% would increase from 30% Paco2 is arterial carbon dioxide tension and Pe-co2 is (150 mL/500 mL) to 50% (150 mL/300 mL). In con- Pco2 of a mixed expired gas sample. These two samples ditions leading to a shallow breathing pattern, the are collected simultaneously. In patients on mechanical spontaneous breathing frequency is often increased ventilation, Vd/Vt of less than 60% is considered ac- to maintain the minute© Jonesventilation. & ThisBartlett rapid Learning,shal- LLCceptable, and this value suggests© Jones adequate & ventilatory Bartlett Learning, LLC low breathing patternNOT is inefficient FOR SALE for gas OR exchange. DISTRIBUTION It function upon weaning from NOTmechanical FOR ventilation SALE OR DISTRIBUTION causes increased work of breathing, respiratory muscle and extubation. Severe and prolonged dead space venti- fatigue, and eventual ventilatory failure. In mechanical lation causes inefficient ventilation, muscle fatigue, and ventilation, the rapid shallow breathing index is used as ventilatory and oxygenation failure. an indication for mechanical ventilation and for making weaning© Jones and extubation & Bartlett decisions. Learning, LLC Ventilatory© Jones Failure & Bartlett Learning, LLC NOT FOR SALE OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION Alveolar Dead Space Ventilatory failure is a condition in which CO2 production exceeds CO2 removal. This imbalance leads to CO2 Alveolar dead space also contributes to wasted venti- retention, increase in Paco2, and respiratory acidosis. In lation. This occurs when alveoli receive normal venti- mild cases, the Paco2 exceeds its upper normal limit lation but it is not adequately perfused by pulmonary (45 mm Hg). In severe ventilatory failure, the Paco2 © Jones & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC NOT FOR SALEcirculation. OR This DISTRIBUTION high ventilation-perfusion (V/Q) mis-NOTmay FOR exceed SALE 80 mm OR Hg. DISTRIBUTION It is important to note that match may be due to (1) absence of regional pulmonary evaluation of ventilatory failure or respiratory acidosis

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© Jones &requires Bartlett an arterialLearning, blood LLCgas sample. The Paco2 is © Jonesventilation & Bartlett is in excess Learning, of perfusion, LLC this high V/Q the measurement used to evaluate how well a patient mismatch leads to dead space ventilation. Pulmonary NOT FOR SALE OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION is ventilating (i.e., ↑ Paco2 = hypoventilation and ↓ embolism is an example of conditions leading to dead Paco2 = hyperventilation). A patient’s spontaneous space ventilation. On the other extreme, low V/Q mis- frequency or tidal volume cannot be used to evaluate match causes intrapulmonary (right-to-left) shunting. hypoventilation or hyperventilation. Atelectasis is an example of conditions leading to intra- Hypercapnia (increase© Jones in Paco &2 )Bartlett is the key featureLearning, of LLCpulmonary shunting. Severe ©V/ QJones mismatch & Bartlett is respon- Learning, LLC hypoventilation or ventilatoryNOT FOR failure. SALE Since OR ventilation DISTRIBUTION sible for the development of hypoxemia.NOT FOR With SALE sufficient OR DISTRIBUTION is a key factor in gas exchange, hypoventilation almost pulmonary reserve, a patient can usually compensate always leads to hypoxemia. In general, hypoxemia due for the hypoxemic condition by increasing the heart rate to hypoventilation responds well to ventilation and low or spontaneous respiratory frequency. These cardiopul- concentration of supplemental oxygen. Without supple- monary compensations require work expenditure. If the mental© Jones oxygen, & the Bartlett degree of Learning,hypoxemia correlates LLC with patient cannot© Jones sustain this & Bartlettadditional Learning,workload over LLC a the severity of ventilatory failure. long period of time, ventilatory failure may result. The NOT FOR SALE OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION The primary conditions leading to ventilatory failure key management strategy for V/ Q mismatch is to iden- include (1) hypoventilation, (2) V/ Q mismatch, (3) in- tify its cause and to implement appropriate treatment trapulmonary shunting, and (4) diffusion defects. If un- plan before decompensation occurs. In uncomplicated corrected, these conditions inevitably lead to increased V/ Q mismatch, oxygen therapy can be very effective. If > © Jones & workBartlett of breathing, Learning, hypercapnia, LLC respiratory acidosis, © Jonesrefractory & Bartlett hypoxemia Learning, develops on LLC Fio2 0.5, presence NOT FOR SALEventilatory OR failure, DISTRIBUTION and mechanical ventilation. NOTof FOR intrapulmonary SALE OR shunting DISTRIBUTION should be investigated. Hypoventilation Intrapulmonary Shunting Hypoventilation is defined as a condition that results in Unlike dead space ventilation (high V/Q mismatch), intrapulmonary shunting is a condition in which perfu- an increased Paco2. It may be caused by a variety of clin- © Jones & Bartlett Learning, LLCsion is present but ventilation© is Jones diminished & Bartlettor absent Learning, LLC ical conditions, including high spinal cord injury, neuromuscular disorders, overdoseNOT FOR of analgesics SALE ORor sedatives, DISTRIBUTION (low V/Q mismatch). IntrapulmonaryNOT FOR shunting SALE is more OR DISTRIBUTION severe airway obstruction, and central sleep apnea. In difficult to manage because oxygen therapy alone can- a clinical setting, hypoventilation is characterized by a not correct refractory hypoxemia. Delivery of oxygen reduction of minute alveolar ventilation (V a) and an to the lungs requires ventilation—a component lacking in intrapulmonary shunting. Shunted pulmonary blood increase of Paco2. The following equation shows inverse flow is ineffective in gas exchange because the collapsed relationship© Jones between & Bartlett Va and Learning, Paco2: LLC © Jones & Bartlett Learning, LLC alveoli at the alveolocapillary interface are not venti- NOT FOR SALE = OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION Va Vco2 / Paco2 lated or do not carry oxygen. Minute alveolar ventilation is the product of respira- In healthy individuals, the physiologic shunt is about < tory frequency and the difference between tidal volume the same as the anatomic shunt ( 5%). For noncritically and dead space volume V a = f × (Vt – Vd). A decrease ill patients, the normal (acceptable) physiologic shunt © Jones & inBartlett frequency Learning, or tidal volume, LLC or an increase in dead © Jonesis less &than Bartlett 10%. In otherLearning, disease states,LLC the physiologic Table 1-4 NOT FOR SALEspace volume OR DISTRIBUTION will reduce the minute alveolar ventilationNOT shunt FOR may SALE be greater OR thanDISTRIBUTION 30%. provides interpretation of shunt percent in critically ill patients. and raise the Paco2. In essence, CO2 production, respiratory frequency, tidal volume, and dead space volume are The shunt percent can be calculated (classic shunt the main determinants of the adequacy of ventilation. equation) or estimated (estimated shunt equation). The During mechanical ventilation, hypoventilation classic shunt equation is more accurate, but it requires can be corrected by increasing© Jones the & frequencyBartlett or Learning, tidal LLCarterial and mixed venous blood© Jones gas samples. & Bartlett The Learning, LLC volume (in volume-controlledNOT FOR ventilation) SALE orOR the DISTRIBUTION peak NOT FOR SALE OR DISTRIBUTION inspiratory pressure (in pressure-controlled ventilation). Unlike tidal volume, dead space volume is difficult Table 1-4 to manage because anatomic dead space stays rather Interpretation of Physiologic Shunt Percent in constant and physiologic dead space is due to high V/ Q Critically Ill Patients mismatch© Jones (inadequate & Bartlett pulmonary Learning, perfusion). LLC © Jones & Bartlett Learning, LLC Physiologic Shunt Interpretation NOT FOR SALE OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION Ventilation-Perfusion Mismatch <10% Normal The V/Q ratio is the percent proportion of ventila- 10% to 19% Mild shunt tion in L/min to pulmonary perfusion in L/min. Since 20% to 29% Moderate shunt © Jones & bloodBartlett flow Learning,is gravity dependent, LLC the V/Q ratio ranges © Jones & Bartlett Learning, LLC NOT FOR SALEfrom about OR 0.4 DISTRIBUTION in the lower lung zone (more perfusion)NOT FOR≥30% SALE OR DISTRIBUTIONCritical and severe shunt to 3.0 in the upper lung zone (less perfusion). When

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© Jones &estimated Bartlett shunt Learning, equation LLCis easier to use as it requires © JonesTable & 1-5Bartlett Learning, LLC only an arterial blood gas sample. See Appendix B for NOT FORClinical SALE Conditions OR That DISTRIBUTION Reduce Gas Diffusion Rate NOT FOR SALEthese two OR shunt DISTRIBUTION equations. In significant or severe physiologic shunts, the Type of Diffusion Defect Clinical Condition cardiopulmonary system typically cannot sustain the ↓ P(a – a)o2 gradient (due to High altitude (↓Pb) workload to compensate for the refractory hypoxemia. ↓Pao2) Fire combustion (↓Fio2) Over time, respiratory© muscleJones fatigue & Bartlett and ventilatory Learning, LLC © Jones & Bartlett Learning, LLC ↓ Surface area of alveolo- Emphysema failure are the end results.NOT ThisFOR is SALEusually followedOR DISTRIBUTION by NOT FOR SALE OR DISTRIBUTION oxygenation failure if ventilatory interventions are capillary membrane Pulmonary fibrosis unsuccessful. In intrapulmonary shunting, lack of ad- ↑ Thickness of alveolar-capil- Pulmonary edema equate ventilation is due to collapsed or fluid-filled lung lary membrane Retained secretions units. PEEP and continuous positive airway pressure (CPAP) are two methods to reopen and ventilate these Insufficient time for gas Tachycardia © Jones & Bartlett Learning, LLC diffusion © Jones & Bartlett Learning, LLC lungNOT units. FOR Other SALE chapters OR describe DISTRIBUTION the use of PEEP or NOT FOR SALE OR DISTRIBUTION CPAP and other strategies to manage intrapulmonary shunting. Diffusion Defects cellular and tissue hypoxia. Regardless of the cause, mechanical ventilation may be indicated to reduce the © Jones & DiffusionBartlett ofLearning, oxygen and LLCcarbon dioxide across the © Joneswork of& breathing, Bartlett prevent Learning, depletion LLC of oxygen reserve, NOT FOR SALEalveoloca ORpillary DISTRIBUTION (A-c) membrane is mainly dependent NOTand FOR provide SALE oxygenation OR DISTRIBUTION to vital organs. on the gas pressure gradients. Oxygen diffuses from the = alveoli (Pao2 109 mm Hg) to the pulmonary capil- Hypoxemia and Hypoxia - = laries (Pvo2 40 mm Hg) with a pressure gradient of Hypoxemia 69 mm Hg. Carbon dioxide diffuses from the pulmo- is defined as lower than normal levels of - oxygen in blood, and this can be evaluated directly nary capillaries (Pvco©2 Jones= 46 mm & Hg) Bartlett to the alveoli Learning, LLC © Jones & Bartlett Learning, LLC by performing arterial blood gases or transcutaneous (Paco2 = 40 mm Hg)NOT with FORa net pressure SALE gradient OR DISTRIBUTION of NOT FOR SALE OR DISTRIBUTION blood gases (neonates) or indirectly by using pulse only 6 mm Hg. This low-pressure gradient for CO2 dif- oximetry (an estimation). Hypoxia is lack of sufficient fusion is possible because the CO2 diffusion coefficient is about 20 times higher than the diffusion coefficient oxygen in the tissues or organs. Presence of hypoxia for oxygen. may not be apparent but it should be implied whenever ©Diffusion Jones of & oxygen Bartlett is greatly Learning, impaired LLCin environ- hypoxemia ©is present.Jones It & should Bartlett be noted Learning, that hypoxia LLC mentsNOT with FOR low barometricSALE OR pressure DISTRIBUTION (Pb) and low in- can occur withoutNOT FOR hypoxemia. SALE For OR example, DISTRIBUTION anemic hypoxia can occur with a reduced hemoglobin level (e.g., spired oxygen tension (Pio2). Two examples show the anemia, sepsis) or an increased level of dysfunctional importance of adequate Pb and Pio2 for proper gas ↑ diffusion: At high altitude, the barometric pressure and hemoglobins (e.g., carboxyhemoglobin due to carbon inspired oxygen tension are lower than that at sea level. monoxide poisoning). Histotoxic hypoxia and circula- © Jones & ThisBartlett leads toLearning, hypoxic hypoxia. LLC Fire in an enclosure re- © Jonestory hypoxia & Bartlett can occur Learning, with cyanide LLC poisoning and decreased cardiac output, respectively. Hypoxia due NOT FOR SALEduces the OR Pio DISTRIBUTION2 because combustion consumes oxygen inNOT FOR SALE OR DISTRIBUTION the air. Patients with smoke inhalation are at risk of de- to dysfunctional hemoglobins typically shows normal or near normal Pao2 because this value is measured veloping hypoxic hypoxia (low Pio2) as well as anemic hypoxia (carbon monoxide inhalation). from the dissolved oxygen in the plasma. It is a grave In addition to the pressure gradient and diffusion oversight if the patient’s oxygenation status is based on coefficient, the gas ©diffusion Jones rate & isBartlett also affected Learning, by the LLCthe Pao2 (dissolved oxygen) alone© Jones because & over Bartlett 98% of Learning, LLC available oxygen is bounded to functional hemoglobin. thickness of the A-c NOTmembrane, FOR surface SALE area OR of theDISTRIBUTION A-c NOT FOR SALE OR DISTRIBUTION membrane, and time available for diffusion.Table 1-5 If the Pao2 is normal and the patient shows signs of outlines the clinical conditions that reduce gas diffusion hypoxia (e.g., complaint of dyspnea, deterioration of rate. Similar to other chronic cardiopulmonary diseases, vital signs, diminished mental status, cyanosis), arte- persistent reduction of gas diffusion rate may lead to rial oxygen content (Cao2) measured by CO-oximetry hypoxemia,© Jones hypoxia, & Bartlett hypoxic Learning, vasoconstriction, LLC pulmo- should be evaluated© Jones because & Bartlett it includes Learning, the oxygen LLC naryNOT hypertension, FOR SALE right ventricularOR DISTRIBUTION hypertrophy, and combined withNOT hemoglobin FOR SALE and theOR oxygen DISTRIBUTION dissolved in cor pulmonale. the plasma. With some exceptions noted, hypoxemia and hypoxia are closely related. Since Pao2 is often used to evaluate Oxygenation Failure a patient’s oxygenation status, Table 1-6 provides a © Jones & OxygenationBartlett Learning, failure is defined LLC as severe hypoxemia © Jonesquick reference& Bartlett for interpretationLearning, LLCof oxygenation status NOT FOR SALEdue to any OR condition DISTRIBUTION (e.g., high altitude, smoke inhala- NOTbased FOR on SALE Pao2 at OR sea levelDISTRIBUTION and 6000 ft above sea level tion, cardiopulmonary diseases) that lead to persistent (Denver, CO).

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© Jones & BartlettTable 1-6 Learning, LLC © JonesTable & 1-7Bartlett Learning, LLC NOT FOR SALEInterpretation OR DISTRIBUTION of Oxygenation Status Based on Pao2 atNOT FOREarly and SALE Late SignsOR DISTRIBUTION and Symptoms of Hypoxia Sea Level and 6000 ft Above Sea Level Category Early Phase Late Phase

Pao2 (Pb = Pao2 (Pb = Status 760 mm Hg) 609 mm Hg) Assessment Pallor Cyanosis findings Nasal flaring Respiratory arrest Normal ©80 toJones 100 mm &Hg Bartlett 60 to 79 Learning, mm Hg LLC Mouth breathing© JonesCardiac & Bartlettarrest Learning, LLC

Mild hypoxemiaNOT 60 to 79 FOR mm Hg SALE 50 toOR 59 mm DISTRIBUTION Hg Vital signs ↑ RespiratoryNOT FOR↓ Respiratory SALE OR DISTRIBUTION frequency frequency Moderate 40 to 59 mm Hg 40 to 49 mm Hg ↑ Heart rate ↓ Heart rate hypoxemia ↑ Blood pressure ↓ Blood pressure

Blood gases and Pao Pao Severe© Jones hypoxemia & Bartlett<40 mm HgLearning,<40 LLC mm Hg © Jones↓ &2 Bartlett ↓Learning,2 LLC oximetry ↓ Spo2 ↓ Spo2 NOT FOR SALE OR DISTRIBUTION NOT FOR↓ Cao2 SALE OR↓ DISTRIBUTIONCao2 Metabolic (lactic) acidosis Clinical Signs of Hypoxia Combined acidosis Results of arterial blood gases and pulse oximetry are with hypoventilation © Jones & commonlyBartlett usedLearning, to evaluate LLC how well a patient is venti-© JonesNeurologic & Bartlett signs AnxietyLearning, LLCConfusion NOT FOR SALElating and OR oxygenating. DISTRIBUTION Under certain hypoxic condi- NOT FOR SALE ORAgitation DISTRIBUTIONLoss of tions, Pao2 and Spo2 do not accurately reflect a patient’s Restlessness consciousness oxygenation status, especially at the tissue level. Normal Table data from Considine J. Emergency assessment of oxygenation. cellular metabolism under aerobic condition produces Acutecaretesting.org. https://acutecaretesting.org/en/articles up to 38 adenosine triphosphate (ATP) molecules (en- /emergency-assessment-of-oxygenation. Published January 2007; ergy units). Under hypoxic condition, only 2 ATPs are Rochester DF. Respiratory muscles and ventilatory failure. Am J Med Sci. © Jones & Bartlett Learning, LLC1993;205(6):394–402. © Jones & Bartlett Learning, LLC produced. This drasticNOT reduction FOR SALEof energy OR unit DISTRIBUTION shows NOT FOR SALE OR DISTRIBUTION the importance of adequate oxygenation at the cellular level. Recognition of the presence of hypoxia is there- ventilation usually have more ventilator-associated fore an important assessment tool, especially in the problems. Unless complications occur, nonpulmonary early stage of hypoxia. Early intervention of hypoxia is conditions usually have an uneventful course of mech- crucial for patient outcomes because untreated hypoxia © Jones & Bartlett Learning, LLC anical ventilation.© Jones The &next Bartlett sections Learning,describe the patho-LLC is one main reason for hospital and intensive care unit NOT FOR SALE OR DISTRIBUTION physiology ofNOT ventilatory FOR SALEfailure and OR the DISTRIBUTION rationales for (ICU) admissions. Table 1-7 outlines the early and late initiation of mechanical ventilation. signs and symptoms of hypoxia. Gas Exchange Abnormalities Conditions Leading © Jones & Bartlett Learning, LLC © JonesSevere & or Bartlett prolonged Learning, gas exchange LLC abnormalities (dead to Mechanical Ventilation space ventilation, diffusion defect, and shunting) often NOT FOR SALEMechanical OR ventilationDISTRIBUTION is frequently used to support a NOTlead FOR to ventilatorySALE OR and DISTRIBUTION oxygenation failure and the need patient’s ventilation and oxygenation needs. Hypoven- for mechanical ventilation. Dead space ventilation is a tilation will lead to immediate respiratory acidosis and perfusion problem. Lack of perfusion produces dead hypoxemia. Severe and prolonged hypoventilation space ventilation or “wasted ventilation.” A classic ex- often results in ventilatory© Jones failure, & oxygenationBartlett Learning, failure, LLCample of dead space ventilation© Jonesis pulmonary & Bartlett embolism Learning, LLC cellular and tissue hypoxia, anaerobic metabolism, lac- in which the amount of ventilation is not matched tic acidosis, hypoxic NOTbrain, andFOR cardiopulmonary SALE OR DISTRIBUTION arrest. proportionally by the amountNOT of pulmonary FOR SALE blood flow.OR DISTRIBUTION Severe hypoxia results in similar adverse outcomes. Diffusion defects occur at the alveolocapillary level Mechanical ventilation is often necessary to manage and they impede the normal gas diffusionfunctions— oxygenation failure. mainly oxygen diffusion from alveoli to pulmonary ©Inadequate Jones ventilation& Bartlett or Learning,oxygenation may LLC be caused capillaries. ©Emphysema Jones & is Bartlettan example Learning, of diffusion LLC by NOTpulmonary FOR or SALE nonpulmonary OR DISTRIBUTION conditions. ARDS is defect due toNOT loss FORof surface SALE area forOR gas DISTRIBUTION exchange. Pul- an example of a pulmonary condition commonly as- monary fibrosis is another example of diffusion defect sociated with mechanical ventilation. This condition in which the reduction in gas diffusion is due to the produces severe and progressive hypercapnia and re- increased thickening of A-c membrane. Absolute shunt fractory hypoxemia. Nonpulmonary conditions leading (true shunt, capillary shunt) occurs when the capillary © Jones & toBartlett hypoventilation Learning, and hypoxemia LLC include postanesthe-© Jonesblood &flow Bartlett is not matchedLearning, by alveolar LLC ventilation (i.e., NOT FOR SALEsia recovery, OR neuromuscularDISTRIBUTION diseases, and brain injury. NOTcomplete FOR SALE or near OR complete DISTRIBUTION absence of ventilation as In general, pulmonary conditions leading to mechanical in atelectasis). Relative shunt (shuntlike effect) refers

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© Jones &to Bartlett a condition Learning, in which capillary LLC perfusion is in excess © Jonesthe clinical & Bartlett outcomes Learning, as a result of LLC depressed respira- of ventilation (i.e., ventilation is present but at lesser NOTtory FOR drive. SALE OR DISTRIBUTION NOT FOR SALEdegrees). OR Therefore, DISTRIBUTION shunting is a ventilation problem. Classic examples of absolute shunt include atelectasis Excessive Ventilatory Workload and consolidation. Examples of relative shunt include Under normal conditions, the ventilatory workload ventilation-perfusion mismatch, and hypoventilation, is in balance with metabolic and oxygenation needs. diffusion defects. It should be noted that relative shunts © Jones & Bartlett Learning, LLCHowever, the workload is increased© Jones in conditions & Bartlett with Learning, LLC respond very well to supplemental ventilation and oxy- NOT FOR SALE OR DISTRIBUTIONhigh airflow resistance (e.g., NOTbronchospasm), FOR SALE low com-OR DISTRIBUTION genation. On the other hand, absolute shunts do not pliance (e.g., ARDS), and high metabolic rate or oxygen respond well to traditional methods of ventilation and consumption (e.g., fever). Other conditions may include oxygenation. increased dead space ventilation (e.g., rapid shallow Venous admixture is the end result of shunting breathing pattern), congenital heart disease, cardiovas- where the shunted, nonoxygenated blood is mixed with © Jones & Bartlett Learning, LLC cular decompensation,© Jones and& Bartlett shock. When Learning, the workload LLC reoxygenated blood distal to the alveoli with adequate NOT FOR SALE OR DISTRIBUTION exceeds the NOTpatient’s FOR physical SALE ability OR or DISTRIBUTIONendurance, ven- ventilation. Conditions resulting in venous admix- tilatory and oxygenation failures are the eventual out- ture usually respond well to traditional methods of comes. The patient will show cyanosis, tachycardia, and oxygenation. a rapid shallow breathing pattern. Arterial blood gases will show progression from respiratory alkalosis with © Jones & DepressedBartlett Learning, Respiratory LLC Drive © Joneshypoxemia, & Bartlett respiratory Learning, acidosis, impending LLC ventila- NOT FOR SALEDepressed OR or DISTRIBUTION absent respiratory drive often leads to NOTtory FOR failure, SALE ventilatory OR DISTRIBUTION failure, and oxygenation failure. Table 1-9 outlines common clinical conditions leading hypoventilation and hypoxemia. In spontaneously to excessive ventilatory workload. breathing patients, the tidal volume and frequency are decreased. Patients with reversible neurologic impair- Failure of Ventilatory Pump ment typically have normal© Jones lung & functions Bartlett in theLearning, early LLC © Jones & Bartlett Learning, LLC stage. The lung functions may quickly worsen with The ventilatory pump includes the diaphragm, thoracic complications from NOTintubation FOR and SALE mechanical OR DISTRIBUTIONven- skeletal structure, respiratoryNOT muscles, FOR and SALElung paren OR- DISTRIBUTION tilation. For reversible causes, mechanical ventilation chyma. Failure of one or more mechanical components is needed to support the ventilation and oxygenation will lead to increased work of breathing due to V/ Q mis- needs until the cause of insufficient respiratory drive match. If uncorrected, failure of the ventilatory pump Table 1-8 has© been Jones identified & Bartlett and resolved. Learning, LLC summarizes can result in© ventilatory Jones & and Bartlett oxygenation Learning, failure. Clinical LLC NOT FOR SALE OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION Table 1-8 Outcomes and Examples of Depressed Respiratory Drive

Type Outcome/Example

© Jones & BartlettAnesthesia orLearning, drug overdose LLC Central hypoventilation (narcotics,© sedatives) Jones & Bartlett Learning, LLC NOT FOR SALE OR DISTRIBUTIONAcute respiratory insufficiency (cocaine,NOT FORheroin, methadone,SALE ORpropoxyphene, DISTRIBUTION phenothiazine, alcohol, barbiturates) Severe pulmonary complications (poisons and toxins such as paraquat, petroleum distillates, organophos- phates, mushrooms of Amanita genus, hemlock, botulism)

High spinal cord injury Apnea (tetraplegic with injury at C1–C3 level) © Jones & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC Traumatic head injury Abnormal respiratory patterns (apnea, tachypnea, Cheyne-Stokes respiration, apneustic breathing, ataxic NOT FORbreathing) SALE OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION Neurogenic pulmonary edema (increase in intracranial pressure) Delayed pulmonary dysfunction (intrapulmonary shunt, increased pulmonary vascular resistance, VQ/ mismatch) Neurologic© Jones dysfunction & Bartlett ComaLearning, (anoxic brain) LLC © Jones & Bartlett Learning, LLC Reduced sensorium (hypoxic brain) NOT FOR SALE ORCerebrovascular DISTRIBUTION accident (stroke) NOT FOR SALE OR DISTRIBUTION

Sleep disorders Sleep apnea (central, obstructive, mixed)

Table data from Bach JR. Alternative methods of ventilatory support for the patient with ventilatory failure due to spinal cord injury. J Am Paraplegia Soc. 1991;14(4):159–174; Greene KE, Peters JI. Pathophysiology of acute respiratory failure. Clin Chest Med. 1994;15(1):1–12; Kelly BJ, Matthay MA. Prevalence and © Jones & Bartlettseverity of neurologic Learning, dysfunction LLCin critically ill patients—influence on need ©for continuedJones mechanical & Bartlett ventilation. Learning, Chest J. 1993;104:1818–1824; LLC Parsons PE. Respiratory failure as a result of drugs, overdoses, and poisonings. Clin Chest Med. 1994;15(1):93–102; Pierson DJ. Indications for mechanical ventilation in adults NOT FOR SALEwith acute OR respiratory DISTRIBUTION failure. Respir Care. 2002;47(2):249. NOT FOR SALE OR DISTRIBUTION

9781284202175_CH01_001_012.indd 10 05/12/19 10:43 AM Summary 11

© Jones & BartlettTable 1-9 Learning, LLC © JonesVentilatory & Bartlett and oxygenation Learning, failures LLC are two main rea- sons for mechanical ventilation. In turn, these failures NOT FOR SALEClinical OR Conditions DISTRIBUTION Leading to Excessive Ventilatory NOT FOR SALE OR DISTRIBUTION Workload can be caused by pulmonary and nonpulmonary conditions. Identification of the causes of ventilatory and oxy- Type Clinical Condition genation failure is important because the strategies for Increased air- Bronchospasm implementing mechanical ventilation are often patient flow resistance Asthma© Jones & Bartlett Learning, LLCspecific. The chapter covers© the Jones fundamental & Bartlett concepts Learning, LLC Chronic obstructive pulmonary disease (COPD) NOT FOR SALE OR DISTRIBUTIONin mechanical ventilation, includingNOT FOR airflow SALE resistance, OR DISTRIBUTION Acute epiglottitis compliance, dead space ventilation, and shunting. Clini- Endotracheal tube intubation cians should apply these concepts during mechanical Decreased lung Acute respiratory distress syndrome (ARDS) ventilation for better patient outcomes. and chest wall Atelectasis compliance Tension pneumothorax © Jones &Chest Bartlett trauma Learning, LLC © Jones & Bartlett Learning, LLC NOT FOR SALEObesity OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION Postthoracic surgery Case Study Increased Rapid shallow breathing pattern dead space Pulmonary embolism You are evaluating patients in the intensive care ventilation Decreased cardiac output unit (ICU). The first patient, 55-year-old Bill, is © Jones & Bartlett Learning,Congestive LLC heart failure © Jones & Bartlett Learning, LLC Emphysema on volume-controlled ventilation. Over the past NOT FOR SALE OR DISTRIBUTION NOT FOR6 hours, SALE the peak OR inspiratory DISTRIBUTION pressure (PIP) has Increased oxy- Fever increased from 40 cm H O to 44 cm H O. gen demand Increased work of breathing 2 2 Sepsis 1. What is the meaning of this increase in PIP? Patient-ventilator dyssynchrony The second patient, Pam, a 50-year-old with a re- Congenital Hypoplastic© Jones left heart & syndromeBartlett Learning, LLCcent onset of ARDS, has the© following Jones ventilator& Bartlett Learning, LLC heart disease TetralogyNOT of FORFallot SALE OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION Persistent pulmonary hypertension parameters during volume-controlled ventilation Left-to-right intra-atrial or intraventricular shunt (Vt 500 mL, f = 18/min): At 6:00 a.m., PIP 50 cm H O, plateau pressure (Pplat) 36 cm H O. At 8:00 Hypovolemic Blood loss 2 2 shock Sepsis a.m., PIP 46 cm H2O, Pplat 32 cm H2O. Congestive heart failure © Jones & Bartlett Learning, LLC 2. What ©is theJones main &reason Bartlett for the Learning, changes in LLC DrugNOT FOR SALEAcute pulmonary OR DISTRIBUTION edema (e.g., narcotics, PIP andNOT Pplat? FOR SALE OR DISTRIBUTION salicylates, nonsteroidal anti-inflammatory agent, naloxone, thiazide diuretic, insulin, The third patient, Hero, a 33-year-old, was recently contrast media) admitted to the ICU for overdose. The toxicology Bronchospasm (e.g., salicylates, nonsteroidal panel is pending. He is breathing spontaneously anti-inflammatory agent, hydrocortisone, on a high-flow nasal cannula (HFNC). The flow © Jones & Bartlett Learning,β-blocker, LLC neuromuscular blocking agents, © Jones & Bartlett Learning, LLC is set at 30 L/min with an Fio of 40%. Over the NOT FOR SALE OR DISTRIBUTIONcontrast media) NOT FOR SALE OR DISTRIBUTION2 past 30 minutes, his spontaneous frequency has Table data from Bach JR. Alternative methods of ventilatory support for the patient with ventilatory failure due to spinal cord injury. J Am Paraplegia changed from 18/min to 30/min. Soc. 1991;14(4):159–174; Greene KE, Peters JI. Pathophysiology of acute respiratory failure. Clin Chest Med. 1994;15(1):1–12; DiCarlo JV, Steven JM. 3. This change in breathing pattern (not Respiratory failure in congenital heart disease. Pediatr Clin North Am. considering the effects of Fio2 and HFNC) 1994;41:525–542; Hinson ©JR, MariniJones JJ. Principles & Bartlett of mechanical Learning,ventilator use LLC © Jones & Bartlett Learning, LLC in respiratory failure. Ann Rev Med. 1992;43:341–361. doi:10.1146/annurev will most likely result in which outcome? .me.43.020192.002013; KrausNOT P, Lipman FOR J, Lee SALE CC, et al. AcuteOR lung DISTRIBUTION injury at (A) increase in compliance,NOT (B) FOR decrease SALE in OR DISTRIBUTION Baragwanath ICU, an eight-month audit and call for consensus for other organ failure in the adult respiratory distress syndrome. Chest. 1993;103:1832–1836. compliance, (C) increase in dead space ventilation, (D) decrease in dead space ventilation. conditions that may lead to ventilatory pump failure 4. If Hero’s spontaneous breathing pattern include© Jones chest trauma & Bartlett (e.g., flail Learning, chest, pneumothorax), LLC persists,© Joneswhat is the& Bartlett likely outcome? Learning, (A) LLC prematurityNOT FOR (respiratory SALE distressOR DISTRIBUTION syndrome), electrolyte ventilatoryNOT failureFOR dueSALE to respiratory OR DISTRIBUTION muscle imbalance (e.g., hyperkalemia), and geriatric patients fatigue, (B) respiratory arrest due to decrease (e.g., fatigue or dysfunction of respiratory muscles). in compliance, (C) ventilatory failure due to Summary overdose of an unknown drug, (D) oxygen- © Jones & Bartlett Learning, LLC © Jonesation & Bartlett failure due Learning, to inadequate LLC flow by nasal NOT FOR SALEMechanical OR ventilation DISTRIBUTION is an invasive tool commonly NOT FORcannula. SALE OR DISTRIBUTION used to support a patient’s failing breathing efforts.

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Bibliography West JB. Pulmonary Pathophysiology—The Essentials. 6th ed. Balti- © Jones & Bartlett Learning, LLC © Jonesmore, & MD:Bartlett Lippincott Learning, Williams & Wilkins; LLC 2007. NOT FOR SALEAirway ORResistance DISTRIBUTION NOTWilkins FOR RL, SALE Dexter JR. OR Respiratory DISTRIBUTION Disease—Principles of Patient Care. 2nd ed. Philadephia, PA: FA Davis; 1998. Blanch L. Bernabe F, Lucangelo U. Measurement of air trapping, intrin- sic positive end-expiratory pressure, and dynamic hyperinflation in Oxygenation Failure mechanically ventilated patients. Respir Care. 2005;50(1):110–123. Chang DW. Clinical Application of Mechanical Ventilations. 4th ed. Considine J. Emergency assessment of oxygenation. Acutecaretesting.org. Clifton Park, NY: Delmar-Cengage© Jones Learning; & Bartlett 2014. Learning, LLCAvailable at https://acutecaretesting.org/en/articles/emergency-assess© Jones & Bartlett Learning,- LLC Myers TR. Use of heliox in children. Respir Care. 2006;51(6):619–631. ment-of-oxygenation Accessed May 14, 2019. Published January 2007. Rochester DF. RespiratoryNOT muscles FOR and ventilatory SALE failure. OR DISTRIBUTIONAm J Med Rochester DF. Respiratory muscles NOTand ventilatory FOR failure.SALE Am ORJ Med DISTRIBUTION Sci. 1993;205(6):394–402. Sci. 1993;205(6):394–402. Waugh JB, Deshpande VM, Brown MK, et al. Rapid Interpretation of Shapiro BA, Kacmarek RM, Cane RD, et al. Clinical Application of Re- Ventilator Waveforms. 2nd ed. Upper Saddle River, NJ: Pearson spiratory Care. 4th ed. St. Louis, MO: Mosby; 1991. Education; 2007. Conditions Leading to Mechanical Ventilation West© JB. Jones Pulmonary & Pathophysiology—TheBartlett Learning, Essentials LLC. 6th ed. Balti- © Jones & Bartlett Learning, LLC more, MD: Lippincott Williams & Wilkins; 2007. Bach JR. Alternative methods of ventilatory support for the patient NOT FOR SALE OR DISTRIBUTION with ventilatoryNOT failure FOR due SALEto spinal cordOR injury. DISTRIBUTION J Am Paraplegia Compliance Soc. 1991;14(4):159–174. Blanch L, Bernabe F, Lucangelo U. Measurement of air trapping, intrin- Chang DW. Clinical Application of Mechanical Ventilations. 4th ed. sic positive end-expiratory pressure, and dynamic hyperinflation Clifton Park, NY: Delmar Cengage Learning; 2014. in mechanically ventilated patients. Respir Care. 2005;50:110–123. Rochester DF. Respiratory muscles and ventilatory failure. Am J Med DiCarlo JV, Steven JM. Respiratory failure in congenital heart disease. © Jones & BartlettSci. 1993;205(6):394–402. Learning, LLC © JonesPediatr & Bartlett Clin North Am Learning,. 1994;41(3):525–42. LLC NOT FOR SALEWaugh JB, OR Deshpande DISTRIBUTION VM, Brown MK, et al. Rapid Interpretation ofNOT Freeman FOR SJ,SALE Fale AD. OR Muscular DISTRIBUTION paralysis and ventilatory failure caused Ventilator Waveforms. 2nd ed. Upper Saddle River, NJ: Pearson by hyperkalemia. Br J Anaesth. 1993;70:226–227. Education; 2007. Greene KE, Peters JI. Pathophysiology of acute respiratory failure. Clin Chest Med. 1994;15(1):1–12. Dead Space Ventilation Hinson JR, Marini JJ. Principles of mechanical ventilator use in respira- Chang DW. Clinical Application© Jones of Mechanical & Bartlett Ventilations Learning,. 4th ed. LLCtory failure. Ann Rev Med. 1992;43:341–361.© Jones doi:10.1146/annurev. & Bartlett Learning, LLC Clifton Park, NY: Delmar-Cengage Learning; 2014. me.43.020192.002013 Shapiro BA, Kacmarek RM,NOT Cane FORRD, et al. SALE Clinical ApplicationOR DISTRIBUTION of Re- Kelly BJ, Matthay MA. Prevalence andNOT severity FOR of neurologic SALE dysfunc OR -DISTRIBUTION spiratory Care. 4th ed. St. Louis, MO: Mosby; 1991. tion in critically ill patients—influence on need for continued mechanical ventilation. Chest J. 1993;104:1818–1824. Ventilatory Failure Kraus P, Lipman J, Lee CC, et al. Acute lung injury at Baragwanath ICU, an eight-month audit and call for consensus for other or- Greene KE, Peters JI. Pathophysiology of acute respiratory failure. Clin gan failure in the adult respiratory distress syndrome. Chest. ©Chest Jones Med. 1994;15(1):1–12. & Bartlett Learning, LLC 1993;103(6):1832–1836.© Jones & Bartlett Learning, LLC RochesterNOT DF. FOR Respiratory SALE muscles OR and DISTRIBUTION ventilatory failure. Am J Med Krieger BP. RespiratoryNOT FOR failure SALE in the ORelderly. DISTRIBUTION Clin Geriatr Med. Sci. 1993;205(6):394–402. 1994;10(1):103–119. Shapiro BA, Kacmarek RM, Cane RD, et al. Clinical Application of Re- Parsons PE. Respiratory failure as a result of drugs, overdoses, and poi- spiratory Care. 4th ed. St. Louis, MO: Mosby; 1991. sonings. Clin Chest Med. 1994;15(1):93–102. Shapiro BA, Peruzzi WT, Kozlowski-Templin R. Clinical Application of Pierson DJ. Indications for mechanical ventilation in adults with acute Blood Gases. 5th ed. St. Louis, MO: Mosby; 1994. respiratory failure. Respir Care. 2002;47(2):249. © Jones & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC NOT FOR SALE OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION

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