care of the intubated emergency department patient

A

The Journal of Emergency Medicine, Vol. 40, No. 4, pp. 419–427, 2011Copyright © 2011 Elsevier Inc.

Printed in the USA. All rights reserved0736-4679/$–see front matter

doi:10.1016/j.jemermed.2010.02.021

Best ClinicalPractice

CARE OF THE INTUBATED EMERGENCY DEPARTMENT PATIENT

Samantha Wood, MD and Michael E. Winters, MD, FAAEM, FACEP

Combined Emergency Medicine/Internal Medicine/Critical Care, University of Maryland Medical Center, Baltimore, MarylandReprint Address: Michael E. Winters, MD, FAAEM, FACEP, Combined Emergency Medicine/Internal Medicine/Critical Care, University of

Maryland School of Medicine, 110 S. Paca Street, 6th Floor, Suite 200, Baltimore, MD 21201

e Abstract—Background: Emergency physicians performtracheal intubation and initiate mechanical ventilation forcritically ill patients on a daily basis. With the currentnational challenges of intensive care unit bed availability,intubated patients now often remain in the emergency de-partment (ED) for exceedingly long periods of time. As aresult, care of the intubated patient falls to the emergencyphysician (EP). Given the potential for significant morbid-ity and mortality, it is crucial for the EP to possess the mostcurrent, up-to-date information pertaining to the care ofintubated patients. Discussion: This article discusses criti-cal aspects in the ED management of intubated and me-chanically ventilated patients. Specifically, emphasis isplaced on providing adequate sedation and analgesia, lim-iting the use of neuromuscular blocking agents, correctlysetting and adjusting the mechanical ventilator, utilizingappropriate monitoring modalities, and providing key sup-portive measures. Despite these measures, inevitably, somepatients deteriorate while receiving mechanical ventilation.The article concludes with a discussion outlining a step-wiseapproach to evaluating the intubated patient who developsrespiratory distress or circulatory compromise. With thisinformation, the EP can more effectively care for ventilatedpatients while minimizing morbidity, and ultimately, im-proving outcome. Conclusion: Essential components of thecare of intubated ED patients includes administering ade-quate sedative and analgesic medications, using lung-protective ventilator settings with attention to minimizingventilator-induced lung injury, elevating the head of the bed inthe absence of contraindications, early placement of an oro-gastric tube, and providing prophylaxis for stress-relatedmucosal injury and deep venous thrombosis whenindicated. © 2011 Elsevier Inc.

RECEIVED: 5 June 2009; FINAL SUBMISSION RECEIVED: 2 De
CCEPTED: 18 February 2010
419

e Keywords—endotracheal intubation; mechanical ventila-tion; ventilator-induced lung injury; neuromuscular block-ade; ventilator-associated pneumonia; stress-related mucosalinjury; capnography

INTRODUCTION

Emergency physicians perform tracheal intubation andinitiate mechanical ventilation for critically ill patientson a daily basis. With the current national challenges ofintensive care unit (ICU) bed availability, intubated pa-tients now remain in the emergency department (ED) forexceedingly long periods of time. As a result, care of theintubated patient falls to the emergency physician (EP).In fact, the EP is arguably the first “intensivist” thatprovides critical care to the intubated patient. The fol-lowing discussion will focus on critical aspects in the EDmanagement of intubated and mechanically ventilatedpatients. With this information, the EP can more effec-tively care for ventilated patients while minimizing mor-bidity and, ultimately, improving outcome.

DISCUSSION

Aside from treating the condition that resulted in intuba-tion and mechanical ventilation, essential components inthe care of the intubated ED patient include administer-ing adequate sedation and analgesia, accurately setting

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420 S. Wood and M. E. Winters

and adjusting the ventilator, appropriate physiologicmonitoring, and providing key supportive therapies.

SEDATION, ANALGESIA, ANDNEUROMUSCULAR BLOCKADE

Mechanically ventilated patients routinely experience painand anxiety (1–3). These symptoms often result from thepresence of an endotracheal tube, various ventilator modesor settings, placement of invasive catheters, surgical pro-cedures, or simply routine nursing care such as endotra-cheal suctioning or patient repositioning. Adverse effectsof unrelieved pain can include increased catecholaminerelease, hypercoagulability, immunosuppression, andmyocardial ischemia (3–5). Unfortunately, intubated pa-tients are often unable to communicate the presence ofpain or anxiety. As a result, physicians consistently un-derrate, and thereby inadequately treat, pain and anxietyin these non-communicative patients (6,7). In a recentretrospective study of intubated ED patients, Bonomo etal. demonstrated that 74% of patients received eitherinadequate or no anxiolysis, whereas 75% of patientsreceived either inadequate or no analgesia (8).

A number of instruments have been developed toassess pain (Numeric Rating Scale, Visual Analog Scale,Behavior Pain Scale, Critical Care Pain ObservationTool) and anxiety (Richmond Agitation-Sedation Scale,Sedation Agitation Scale) in critically ill patients (5,7,9–14). Protocols that incorporate these instruments in themanagement of intubated patients have demonstratedmore precise dosing, reduced medication side effects, ashorter duration of mechanical ventilation, and reducedICU and hospital length of stay (15–17). Although use-ful, no single instrument is universally accepted as thegold standard for assessing pain and anxiety in intubated,non-communicative patients. As such, current guidelinesrecommend monitoring a combination of physiologicand behavioral responses of intubated patients (5). Phys-iologic indicators of pain include increases in heart rate,blood pressure, and respiratory rate. Important behav-ioral responses that indicate pain or anxiety include fa-cial expression, body movements, muscle tension, andnon-compliance with mechanical ventilation.

When treating pain and anxiety in intubated ED pa-tients, it is important to focus first on providing analgesiabefore anxiolysis. Patients who receive analgesics beforeanxiolysis consistently achieve comfort goals with lesssupplemental anxiolytic medications (15,18,19). In addi-tion, these patients may have a shorter duration of me-chanical ventilation (19). Opiates remain the drugs ofchoice for analgesia in intubated patients (5,20). Com-monly used opiate medications include morphine, fenta-
nyl, hydromorphone, and remifentanil. Of these, the au- c
thors prefer fentanyl given its rapid onset of action, lackof histamine release, and lack of active metabolites.Fentanyl can be given in an initial intravenous dose of50–100 �g, followed by an infusion ranging from 50–350 �g/h.

After appropriate analgesia, sedative medications shouldbe given for anxiolysis and amnesia. Midazolam, loraz-epam, and propofol are common sedative medications usedin the intubated ED patient (3,21). When given by contin-uous infusions for prolonged periods, benzodiazepines pref-erentially accumulate in peripheral tissues, thereby pro-longing the sedative effect (3). This is most commonlyseen with prolonged infusions of midazolam (22–24).Patients with renal insufficiency also have prolongedsedation from midazolam, due to accumulation of itsactive metabolite, 1-hydroxylmethylmidazolam (25,26).In contrast, lorazepam is metabolized via hepatic glucu-ronidation to inactive metabolites that are then excretedby the kidney (21). Long-term infusions of lorazepam,however, have been associated with an increased risk ofdelirium and propylene glycol toxicity (15,27).

Propofol is increasingly used for sedation in intubatedpatients. Although the exact mechanism is unknown,propofol seems to act on the gamma-aminobutyric acidreceptor at a site different from that of benzodiazepines.Given its high lipophilicity, propofol rapidly crosses theblood-brain barrier, producing sedation in � 1 min.

ropofol can be given as an initial bolus of 0.25–1.0g/kg, followed by an infusion ranging between 25 and

5 �g/kg/min. Carson et al. demonstrated a decreaseduration of mechanical ventilation in patients receiving aontinuous infusion of propofol, compared to intermit-ent dosing of lorazepam (28). Important adverse effectsf propofol include hypotension, hyperlipidemia, andropofol-related infusion syndrome. Propofol-related in-usion syndrome is characterized by the onset of meta-olic acidosis, dysrhythmias, hyperkalemia, rhabdomy-lysis, and congestive heart failure (21).

In addition to analgesic and sedative medications, neu-omuscular blocking agents (NMBAs) are often given toacilitate mechanical ventilation. Common NMBAs used inhe ED include vecuronium, rocuronium, and pancuronium.mportantly, these medications do not have analgesic ormnestic properties. Furthermore, indiscriminate usean prolong recovery and may result in the developmentf “critical illness polyneuromyopathy” (29). Althoughhe exact pathophysiologic mechanisms remain incom-letely understood, critical illness polyneuromyopathyrolongs mechanical ventilation, increases ICU and hos-ital length of stay, and has been associated with in-reased mortality (29). Thus, NMBA use should be dis-
ontinued as soon as clinically possible (30).

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Care of the Intubated ED Patient 421

SETTING AND ADJUSTINGTHE VENTILATOR

Mechanical ventilation, like any medical therapy, can beharmful if not properly managed. Large tidal volumes,high pressures, and high inspired oxygen concentrationscan initiate and propagate lung injury, termed ventilator-induced lung injury (VILI). Although the exact patho-physiology remains incompletely understood, VILI isbelieved to occur as a result of the combination ofvolutrauma, atelectrauma, barotrauma, and biotrauma(31). Of these, volutrauma is likely the most significantcontributor to VILI and refers to the over-distension ofalveoli from large tidal volumes, resulting in rupture, dis-ruption of the capillary interface, and infiltration of theairspace with edema and inflammatory cells. Atelectraumais the shear stress and injury that is caused by repeatedopening and closing of alveolar units during ventilation.Barotrauma is characterized by extra-alveolar air that dis-sects along fascial planes, whereas biotrauma describes thesystemic release of inflammatory mediators resulting inextra-pulmonary organ dysfunction.

“Lung-protective” ventilatory strategies aim to reducethe risk of VILI by limiting volutrauma through the useof low tidal volumes, preventing atelectrauma by usingpositive end-expiratory pressure (PEEP) and recruitmentmaneuvers, reducing oxygen toxicity by decreasing in-spired oxygen concentrations, and decreasing biotrauma.Using these strategies, lower arterial partial pressures ofoxygen, higher arterial partial pressures of carbon diox-ide, and lower pH values are tolerated. In a landmarktrial, the ARDSnet group demonstrated improved mor-tality in patients with acute lung injury (ALI) and acuterespiratory distress syndrome (ARDS) who were venti-lated with lower tidal volumes while maintaining plateauairway pressures � 30 cm H2O (32).

Fortunately, the majority of patients intubated andventilated in the ED do not have evidence of ALI/ARDSat the time of intubation, thereby raising the question ofwhether low tidal volume ventilation is applicable. De-spite the paucity of randomized trials in patients with-out ALI/ARDS, any intubated patient is at risk ofdeveloping ALI. In fact, up to 25% of intubated patientsdevelop ALI/ARDS within 5 days of intubation (33).Furthermore, patients ventilated with higher tidal vol-umes and higher pressures are more likely to developALI (34). Until definitive evidence indicates otherwise,the EP should use lung protective ventilator settingswhen initiating and adjusting the mechanical ventilator.

As initial ventilator settings, we recommend a tidalvolume of 6 mL/kg of predicted body weight, a respira-tory rate of 18–22 breaths/min, PEEP of 5–7 cm H2O,nd a fractional inspired oxygen concentration (FiO2) of

100%. When making adjustments to ventilator settings, it r

is important to monitor plateau pressure, pH, andoxygenation. Plateau pressure provides information onlung compliance and is measured by performing anend-expiratory hold. If the plateau pressure is � 30 cmH2O, the tidal volume should be decreased in 1-mL/kgncrements until the plateau pressure is � 30 cm H2O or

the tidal volume reaches 4 mL/kg (32,35). Elevated par-tial pressures of carbon dioxide and lower pH values aretolerated in lieu of lower and safer distending pressures.If pH, however, falls below 7.15, the respiratory rateshould be increased until a maximum of 30–35 breaths/min is reached (31,32). If pH remains below 7.15 despitean increase in respiratory rate, the tidal volume should beincreased by 1 mL/kg (31,32).

High oxygen concentrations are known to cause lunginjury (31,36). Although the literature is not clear onwhat is a safe duration and concentration of oxygen, it isrecommended to maintain FiO2 � 60% when clinicallypossible (36). Provided the arterial partial pressure ofoxygen is � 55 mm Hg or the pulse oximetry is � 88%,

e recommend that the FiO2 be decreased in 10–20%increments until the FiO2 is � 60%. If the pulse oximetryeading falls below 88% with a FiO2 � 60%, we recom-end that the PEEP be increased in 2–3 mm Hg incre-ents until pulse oximetry readings are � 88%. In theRDSnet protocol, PEEP was titrated to a maximum of4 mm Hg to maintain oxygenation goals (32). Impor-antly, the titration of PEEP requires a balance betweenchieving oxygenation goals and avoiding the complica-ions of higher levels of PEEP. High levels of PEEP canver-distend normal alveoli and compress adjacent, lessompliant airspaces (31). In addition, high levels ofEEP can also compromise venous return, especially inolume-depleted patients (31). The decrease in cardiacutput and oxygen delivery caused by impaired venouseturn can easily offset the beneficial effects of PEEP.

MONITORING THE INTUBATED ED PATIENT

ulse Oximetry

ulse oximetry (SpO2) is widely regarded as one of theost important advances in critical care monitoring.

pO2 provides a continuous, non-invasive method toeasure arterial oxygen saturation and should be used on

very intubated ED patient. Displayed readings are de-ermined by the absorption spectra of both oxyhemoglo-in and deoxyhemoglobin and the characteristics of pul-atile blood. SpO2 is accurate to within � 2% for

saturations � 70% (37–39).Despite its utility for monitoring arterial oxygen sat-

uration, there are several limitations of SpO2 that must be
ecognized. Intubated patients who are hypotensive, hy-

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pothermic, or receiving vasoactive medications are likelyto have inaccurate readings (38,40). Any process thatalters the pulsatile component of arterial flow can affectsignal strength and quality. Additional inaccuracies arecaused by methylene blue, indocyanine green, sicklingred cells, and the presence of dyshemoglobinemias (40).Anemia and hyperbilirubinemia do not affect the accu-racy of SpO2 (40,41).

Importantly, SpO2 is a measure of arterial oxygenationaturation, not arterial oxygen tension (PaO2). Given the

characteristics of the oxygen dissociation curve, largefluctuations in PaO2 can occur despite minimal changesn SpO2. In addition to its inability to measure PaO2, SpO2

provides no measure of ventilation or acid-base status.Therefore, it cannot be used to determine arterial carbondioxide tension or pH. Significant increases in arterialcarbon dioxide can occur with normal readings in SpO2.Although useful for arterial oxygen saturation, SpO2

should not be assumed to provide information aboutventilation.

Capnography

End-tidal carbon dioxide monitoring (PetCO2) can pro-ide the EP with useful information regarding alveolarentilation in intubated patients. PetCO2 is the concen-ration of carbon dioxide at end-expiration and is deter-ined by tissue carbon dioxide production, pulmonary

erfusion, and alveolar ventilation. PetCO2 can be dis-layed either as a number (capnometry) or a waveformlotted against time (capnography). In hemodynamicallytable patients with minimal to no pulmonary pathology,

etCO2 generally underestimates arterial carbon dioxideby 2–5 mm Hg (38).

Capnography has several useful applications in theintubated ED patient (Table 1). Perhaps the most usefulapplication is in the detection of acute ventilator dys-function or endotracheal tube obstruction or dislodge-ment. The sudden loss of the entire capnogram waveformindicates endotracheal tube obstruction, accidental extu-bation, ventilator dysfunction, or the onset of cardiacarrest. A drop in the waveform to a low, but non-zero,

Table 1. Applications of Capnography in the IntubatedED Patient

Confirmation of endotracheal tube placementDetecting airway catastrophesDetection of hypercapniaDiagnosing pulmonary embolismDetermining the optimal level of PEEPEvaluation of weaning from mechanical ventilation

PEEP � positive end-expiratory pressure.

number signifies partial endotracheal tube obstruction, anairway leak, or the onset of hypotension. Finally, cap-nography can be useful for monitoring intubated patientsat risk for hypercarbia. Because PetCO2 routinely under-estimates arterial carbon dioxide, the gradient betweenarterial and end-tidal carbon dioxide is nearly alwayspositive (38). PetCO2 values � 40 mm Hg nearly alwaysequate to an equal, or higher, value for arterial carbondioxide (42). Elevated PetCO2 values for patients inwhich hypercarbia can be detrimental (elevated intracra-nial pressure) indicate the need for alterations in EDmanagement.

Intravascular Volume

Fundamental to the management of many critically illpatients is the accurate determination of volume status.To date, clinicians have relied upon static measurementssuch as central venous pressure (CVP) to determinevolume assessment and guide resuscitation. In fact, CVPis incorporated into existing guidelines for the resuscita-tion of patients with severe sepsis and septic shock (43).Unfortunately, CVP has many limitations that affect itsusefulness as a marker of volume status. CVP can beaffected by tricuspid valve disease, pericardial disease,abnormal right ventricular function, dysrhythmias, andmyocardial disease (44). In addition, CVP is affected bychanges in intrathoracic pressure produced by mechani-cal ventilation (44). Furthermore, a static CVP measure-ment does not provide the EP with any information aboutwhere a particular patient resides on their individualStarling curve. Some patients will have an elevated CVP,yet still increase cardiac output with additional bolusesof intravenous fluid. For these reasons, CVP is oftenunreliable in accurately assessing volume in intubatedpatients.

Recent literature has shifted focus to dynamic mea-surements of volume, such as systolic pressure variation,pulse pressure variation (PPV), and stroke volume vari-ation. Each measurement has demonstrated utility inassessing intravascular volume in mechanically venti-lated patients (45). Of these, PPV (the difference be-tween maximum pulse pressure during inspiration andminimum pulse pressure during expiration) seems to bethe most useful (46,47). PPV can be calculated by print-ing out a tracing from an arterial line and measuring themaximum pulse pressure during inspiration and the min-imum pulse pressure during expiration. A difference ofmore than 13% has been shown to be highly sensitive inidentifying hypovolemic patients and those that wouldbenefit from additional fluid therapy (48,49). PPV hasbeen primarily studied thus far in mechanically venti-
lated patients. Importantly, spontaneous breathing and

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dysrhythmias have been shown to adversely affect PPVreadings (47). Furthermore, PPV will not provide the EPwith information on actual cardiac function (47).

Intra-abdominal Pressure

Over the past decade, there has been increasing aware-ness of the importance of elevated intra-abdominal pres-sure (IAP) and its impact upon patient outcomes. Oncethought to occur strictly in blunt trauma patients, ele-vated IAP, resulting in intra-abdominal hypertension(IAH) or abdominal compartment syndrome (ACS), hasbeen shown to occur in both medical and surgical ICUpatients (50). IAH is defined as an IAP � 12 mm Hg,

hereas ACS is defined as a sustained IAP � 20 mm Hgssociated with new organ dysfunction (51,52). ElevatedAP can decrease preload, increase afterload, and in-rease organ dysfunction (51). For the intubated patient,AH and ACS can cause elevated peak pressures, hyp-xia, and impair ventilation (51).

Conditions that predispose patients to IAH includearge-volume fluid resuscitation (� 5 L), massive trans-usion, sepsis, hypothermia, coagulopathy, and mechan-cal ventilation with the use of PEEP (51). As such, it isecommended to measure an IAP in mechanically ven-ilated patients with organ dysfunction. IAP measure-ent via the bladder is currently the recommended mon-

toring method (53). Using a Foley catheter, IAP shoulde measured in the supine position at the end of expira-ion (51,54). In addition, the transducer should be zeroedt the mid-axillary line (51). Because definitive treatmentemains a decompressive laparotomy, obtain surgicalonsultation for any IAP over 12 mm Hg.

SUPPORTIVE CARE

entilator-associated Pneumonia

entilator-associated pneumonia (VAP) is defined asneumonia that develops � 48 h after endotracheal in-ubation and initiation of mechanical ventilation (55).AP is the most common infectious complication occur-

ing in ICU patients, resulting in prolonged mechanicalentilation, increased ICU and hospital length of stay,nd increasing the cost of care by approximately $40,000er patient (55–57). Attributable mortality rates for VAPange between 20% and 30% (55,58).

The principal pathogenic mechanisms that result inAP are bacterial colonization of the aerodigestive tract

nd aspiration of secretions into the lower airway (59).lthough the diagnosis of VAP is made in the ICU, it is

mperative to understand that the processes that initiate h

nfection begin while the patient remains in the ED. TheP should, therefore, implement several no-cost, non-harmacologic interventions that have been shown toecrease the incidence of VAP. These interventions aimo reduce bacterial colonization and decrease the inci-ence of aspiration. Proper patient positioning is, per-aps, the easiest intervention shown to positively affecthe incidence of VAP. The supine position has beenemonstrated to increase the risk of aspiration and inci-ence of VAP (55,60). Current evidence indicates that aeduction in VAP occurs when patients are placed in aemi-recumbent position (61,62). The Centers for Dis-ase Control recommends that intubated patients at highisk for aspiration be placed in the semi-recumbent po-ition (63). Provided there are no absolute contraindica-ions in intubated ED patients, the head of the bed shoulde elevated to 30–45 degrees.

Preventing aspiration of gastric contents or secretionsrom the oropharynx is critical to reducing the risk ofAP. Micro- or macro-aspiration of secretions from both

ocations is believed to be an essential step in developingAP. Some low-cost strategies that can be implemented

n the ED and are demonstrated to reduce VAP includeastric decompression with early placement of an oro-astric tube, maintaining endotracheal cuff pressures be-ween 25 and 30 cm H2O, and oral rinses with chlorhexi-ine solution (55,64,65).

Additional non-pharmacologic strategies to decreaseAP include adequate hand washing between ED patient

ncounters, limiting stress ulcer prophylaxis to onlyigh-risk patients (discussed below), and lung protectiveentilatory settings. The injured lung is more likely toevelop infection (55). Lung-protective ventilatory set-ings, as discussed above, reduce VILI through limitingolutrauma, barotrauma, and atelectrauma.

tress-related Mucosal Injury

n critically ill patients, stress-related gastric mucosalamage is nearly universal. In fact, gastric mucosal ero-ions are seen in 75–100% of patients within 24 h ofdmission to the ICU. These erosions are believed toccur as a result of decreased blood flow and increasedastric acidity (66). Fortunately, clinically significantastric hemorrhage is seen in only 3–4% (67).

Treatment with a proton pump inhibitor, histamineeceptor antagonist, or sucralfate has been shown toeduce the incidence of clinically significant gastric hem-rrhage. In a randomized trial of 1200 ventilated pa-ients, Cook et al. found ranitidine to be superior toucralfate for the protection from stress-related mucosalesions (68). Unfortunately, there was a trend toward
igher rates of VAP in the ranitidine group. Because the

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incidence of VAP, along with its increased mortality, ishigher than clinically significant gastric hemorrhage,routine prophylaxis for stress-related lesions is not indi-cated for all intubated patients. Current recommenda-tions state that patients at high risk of gastric hemorrhageshould receive a proton pump inhibitor, histamine recep-tor antagonist, or sucralfate (69). High-risk patients arethose who are coagulopathic, have a history of gastroin-testinal bleeding, gastritis, or peptic ulcer within the prioryear, or are ventilated for over 48 h (69). In addition,patients with two or more of the following should receiveprophylaxis: sepsis, renal failure, hepatic failure, hypo-tension, severe head injury, or concurrent glucocorticoidtherapy (69).

Deep Venous Thrombosis

Venous thromboembolism (VTE) develops in 13–30%of ICU patients during their entire hospital stay (70). Inntubated ED patients, VTE prophylaxis with unfraction-ted or low-molecular-weight heparin should be consideredor patients without contraindications. Contraindications toTE prophylaxis with heparin include intracranial bleed-

ng, spinal cord injury with hematoma, uncontrolled activeleeding, and uncorrected coagulopathy (70). In patients

Figure 1. The crashing ventilated patient.

with contraindications to heparin, mechanical methods ofVTE prophylaxis, such as pneumatic compression de-vices, are recommended (70). Because heparin dosingand protocols vary in the literature, the EP is advised tofollow institutional protocols for VTE prophylaxis.

THE “CRASHING” VENTILATED PATIENT

Despite receiving optimal care, inevitably, some intu-bated ED patients will deteriorate and develop respira-tory distress. The differential diagnosis of intubated pa-tients who deteriorate is broad and includes endotrachealtube malfunction, improper ventilator settings, pulmo-nary or extra-pulmonary processes, endotracheal tubecuff leak, pain, or anxiety. Given the potential for rapidprogression to cardiopulmonary arrest, these patients re-quire immediate attention and a step-wise approach toevaluation and management (Figure 1).

Hemodynamically unstable intubated patients with re-spiratory distress should immediately be disconnectedfrom the machine and manually ventilated with a FiO2 of00%. Once disconnected from the ventilator, among therst priorities should be to exclude a tension pneumo-

horax. The diagnosis of tension pneumothorax is clini-al; treatment with needle or tube thoracostomy should


not be delayed while awaiting a confirmatory chest X-raystudy. Once tension pneumothorax is excluded, auto-PEEP should be considered. Auto-PEEP, also calledintrinsic PEEP, primarily occurs as a result of incompleteexhalation. The dynamic hyperinflation that is createdwith incomplete exhalation increases intrathoracic pres-sure, decreases venous return, reduces preload, increasesright ventricular afterload, and decreases left ventricularcompliance (71). Although more common in patientswith asthma and chronic obstructive pulmonary disease(COPD), auto-PEEP can also occur in those withoutintrinsic expiratory flow limitations. In these patients,auto-PEEP occurs as a result of the combination of largeinspiratory volumes and short expiratory times. Auto-PEEP can be detected by examining end expiratory flowon the ventilator. If the end expiratory flow is not zero (orabove the set extrinsic PEEP), then dynamic hyperinfla-tion is occurring (71). An end-expiratory hold may alsobe performed to detect auto-PEEP. The treatment forpatients with auto-PEEP is to allow for adequate lungdeflation. Once the lungs have adequately exhaled, he-modynamic stability should return. When re-initiatingmechanical ventilation in patients who have developedauto-PEEP, it is important to allow for longer expiratoryphases by decreasing the respiratory rate, decreasing thetidal volume, or altering the inspiratory-to-expiratoryratio (72). Additional strategies to prevent recurrence ofauto-PEEP include adequate analgesia and sedation toreduce ventilatory demand and bronchodilators and cor-ticosteroids for patients with asthma or COPD (72).

Once tension pneumothorax and auto-PEEP havebeen excluded, the patient should be evaluated for anobstructed endotracheal tube or an endotracheal tube cuffleak. Causes of endotracheal tube obstruction are manyand include tube kinking, foreign bodies, copious secre-tions, stylet shearing, mucosal flaps, and blood clots (73).The primary clinical clue to endotracheal tube obstruc-tion is difficulty with or resistance to manual ventilation.When tube obstruction is suspected, an endotrachealsuction catheter should be passed. In some cases, a newendotracheal tube may need to be placed. Endotrachealtube cuff leaks render ventilation less effective and pre-dispose patients to aspiration. Sufficient cuff pressuremust be maintained to effectively ventilate patients. Todetect a cuff leak, the EP should listen for air escapingfrom the mouth or nose when manually ventilating (74).An additional clue before disconnection from the venti-lator is that the measured expiratory volume is consis-tently lower than the set tidal volume (74). If a leak issuspected, the cuff should be inflated until air is nolonger detected from the mouth or nose. Although itrequires assistance with respiratory therapy, cuff ma-nometry can be performed to determine an optimal cuff
pressure. Current evidence indicates that the goal cuff
pressure for effective ventilation while minimizing over-distension is 20–30 mm Hg (75).

Similar to unstable patients, hemodynamically stablepatients with respiratory distress require a systematicapproach to evaluation and management. In these pa-tients, the ventilator and ventilator circuit (tubing) shouldbe checked immediately (74). Patients in whom ventila-tor malfunction is suspected should be disconnectedfrom the ventilator and manually ventilated. The FiO2

should be increased to 100% until the etiology of distressis determined. A chest X-ray study should be performedto exclude pneumothorax. Bedside ultrasound evaluationof the pleural space to exclude pneumothorax is a skillmany EPs are developing and can be rapidly performedwhile awaiting chest X-ray study. Normally, the inter-face between the chest wall and lung produces a hyper-echoic line that moves easily with respiration, aptlytermed the sliding lung sign (76). In the presence of apneumothorax, the sliding lung sign disappears (77).

Measurement of both peak and plateau pressures in avolume-cycled ventilator mode can be useful in the he-modynamically stable patient with respiratory distress(74). Peak pressure, obtained during inspiration, reflectsresistance to airflow, whereas plateau pressure, obtainedduring an inspiratory pause, reflects pulmonary compli-ance. Increases in peak pressure without changes inplateau pressure indicate a problem with airflow. Com-mon causes of resistance to airflow include a kinked ortwisted endotracheal tube, tube obstruction, bronchos-pasm, or, less commonly, ventilator tubing obstructioncaused by the heat-moisture exchanger (74). Increase inboth peak and plateau pressure points to problems withlung compliance. Etiologies to consider include worseningpulmonary edema, pneumonia, ARDS, abdominal disten-sion, atelectasis, and mainstem intubation (74). Whether thecause is an increase in resistance or compliance, the treat-ment is aimed at correcting the underlying cause. Althougha diagnosis of exclusion, inadequate analgesia and sedationshould always be considered in the hemodynamically stablepatient with respiratory distress.

CONCLUSION

EPs intubate and initiate mechanical ventilation in criti-cally ill patients daily. Given the current environment ofdecreased ICU bed availability, many of these patientsremain in the ED for prolonged periods of time. Thus,initial care of these critically ill patients falls to the EP.Providing appropriate and adequate analgesia and seda-tion, utilizing lung-protective ventilator settings, recog-nizing the limitations of current monitoring methods, andinitiating simple low-cost interventions to decrease the
incidence of VAP and stress-related mucosal injury are


key components of the initial care of intubated ED pa-tients. Utilizing the recommendations discussed, the EPcan provide effective post-intubation care and, ulti-mately, decrease patient morbidity and mortality.

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