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coronary blood ow and/ or inotropes to enhance myocardial contractility.8 In contrast, while vasopressors may
be necessary to maintain systemic blood pressure in many
types of obstructive shock, inotropy is contraindicated in
cardiac tamponade45 and HOCM13 due to the associated
tachycardia that could worsen ventricular lling.
Echocardiography should also be used to evaluate for
resolution of obstruction or recurrence aer surgical treatment for HOCM38 and intracardiac myxoma.12 Aer a
pneumothorax has been treated with needle thoracostomy,
chest radiography or lung ultrasonography can monitor for
persistence of pneumothorax and chest tube placement.
5,41
erapeutic anticoagulation will need to be monitored and
SUBSEQUENTSTEPS
Aer initiating preliminary measures of cardiopulmonary
support, the next step is diagnosis- specic intervention
to correct the underlying pathophysiology of obstructive
shock. With cardiac tamponade, denitive treatment is
drainage of the eusion. is can be done by percutaneous
pericardiocentesis or as an open procedure in the operating
room with a pericardiotomy.45 Specic therapy for PE consists of anticoagulation, thrombolytics, and/ or embolectomy, while an acute worsening of pulmonary hypertension
maintained in patients with PE. Patients with pulmonary
hypertension should be followed by a specialist who can
modify the medication regimen and observe for worsening or improvement.
8,37
For abdominal compartment syndrome, periodic bladder pressure measurements may be
continued, as some patients remain at risk for recurrence.7
Patients who experience amniotic uid embolism have an
increased likelihood of developing disseminated intravascular coagulation21 and will require monitoring of coagulation.44 In cases of fat embolism, monitoring of respiratory
and neurologic status is necessary aer initial support.
20
could be treated with diuretics and pulmonary vasodilators
such as inhaled nitric oxide.8 Specic interventions for nonthrombotic causes of pulmonary emboli include prevention
CONCLUSION
of fat embolism by early long bone xation and avoidance of
increased intramedullary pressures during reaming; immediate delivery of the baby and correction of coagulopathy in
AFE; and halting further air entry, aspirating air from the
right heart, and placing the patient in the le lateral decubitus position inVAE.
18
In obstructive shock from increased intrathoracic or
intra- abdominal pressure, decompression of the compartment with elevated pressure reverses the shock state:needle
decompression with tension pneumothorax;5 complete
exhalation or circuit disconnection with auto- PEEP;6 and
medical or surgical abdominal decompression with abdominal compartment syndrome.45 Timely surgical intervention to remove intracardiac myxomas prevents embolism
e ow of blood through the circulatory system can be
obstructed in a variety of ways to cause obstructive shock.
Rapid diagnosis and supportive treatment with judicious
intravenous uid administration and vasopressors must be
initiated while the cause is elucidated via clinical features
and diagnostic tools. erapeutic interventions should target the specic cause of obstructive shock and can range
from disconnecting the endotracheal tube from the ventilator to relieve auto- PEEP to surgical interventions such as
laparotomy for abdominal compartment syndrome or pulmonary thrombectomy for massive PE. Aer obstructive
shock has resolved, monitoring for resolution of the under-
lying pathophysiology can prevent possible recurrence.
or sudden death.12 e goals of medical management in
HOCM are negative inotropy with beta blockade or other
agents and avoidance of sympathetic stimulation. Further
interventions include alcohol septal ablation or, preferably,
surgical septal myectomy.
13
CASE- BASED LEARNING DISCUSSION
1. What is the dierential diagnosis of obstructive shock
and what are the initial managementsteps?
FOLLOW- UP
2. e surgeons are in the process of reaming the femur
and report that blood loss is minimal. e patient
Interventions that remove the obstruction should rapidly
resolve the shock state and improve organ dysfunction.
Follow- up monitoring will need to be specically chosen
according to the cause of obstruction. In the case of tamponade, serial echocardiography ensures complete resolution and identies reaccumulation of pericardial uid.25
develops hemodynamic instability. e patient receives
a uid bolus, is given phenylephrine 200 micrograms
IV, and the FiO2 is increased to 100% on the ventilator,
but hemodynamic instability persists. Does this alter
the dierential diagnosis? What would be the next
diagnosticstep?
116 PART III.SHOCK
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117
3. e peak inspiratory pressures have increased. Upon
auscultation, diminished breath sounds and wheezing
are now noted. Aer administration of albuterol,
symptoms do not resolve. e ultrasound machine used
for the femoral block is in the operating room— what
information could this provide?
4. With a phased array probe, the apical four- chamber
view of the heart shows an underlled right heart, no
pericardial eusion, and a hyperdynamic le ventricle.
Lung sliding and A- lines are seen on the right chest, but
no lung sliding is noticeable on the anterior or lateral
aspects of the le chest. What is the next step in the
management of this patient?
5. Aer appropriate treatment, saturation and
hemodynamics improve. e intramedullary nail is
placed. e patient remains hemodynamically stable
throughout the rest of the case and is now ready
for emergence. Can this patient be extubated in the
operating room? What studies should be ordered for
this patient in the recovery room? Is this patient at risk
of having another similar event in the future?
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North America. 2014;32(4):747– 58.
2. Schairer JR, Biswas S, Keteyian SJ, Ananthasubramaniam K. A sys-
tematic approach to evaluation of pericardial eusion and cardiac
tamponade. Cardiology Review. 2011;19(5):233– 8.
3. Funk DJ, Jacobsohn E, Kumar A. Role of the venous return in
critical illness and shock:part II- shock and mechanical ventilation.
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4. Pepi M, Muratori M, Barbier P, etal. Pericardial eusion aer car-
diac surgery:incidence, site, size, and haemodynamic consequences.
British Heart Journal. 1994;72:327– 31.
5. Yarmus L, Feller- Kopman D. Pneumothorax in the critically ill
patient. Chest. 2012;141(4):1098– 1105.
6. Berlin D. Hemodynamic consequences of auto- PEEP. Journal of
Intensive Care Medicine. 2014;29(2):81– 6.
7. Cheatham ML. Abdominal compartment syndrome:pathophysiol-
ogy and denitions. Scandinavian Journal of Trauma, Resuscitation
and Emergency Medicine. 2009;17:10.
8. Matthews JC, McLaughlin V. Acute right ventricular failure in the
setting of acute pulmonary embolism or chronic pulmonary hypertension: a detailed review of the pathophysiology, diagnosis, and
management. Current Cardiology Reviews. 2008;4(1):49– 59.
9. Palmon SC, Moore LE, Lundberg J, Toung T. Venous air embo-
lism:a review. Journal of Clinical Anesthesia. 1997;9:251– 7.
10. Kotyra M, Houltz E, Ricksten SE. Pulmonary haemodynamics
and right ventricular function during cemented hemiarthroplasty
for femoral neck fracture. Acta Anaesthesiologica Scandinavica.
2010;54(10):1210– 6.
11. Davies S. Amniotic uid embolus: a review of the literature.
Canadian Journal of Anesthesia. 2001;48(1):88– 98.
12. Reynen K. Cardiac myxomas. New England Journal of Medicine.
1995;333(24):1610– 7.
13. Hensley N, Dietrich J, Nyhan D, Mitter N, Yee MS, Brady M.
Hypertrophic cardiomyopathy: a review. Anesthesia & Analgesia.
2015;120(3):554– 69.
14. Kirkpatrick AW, Ball CG, D’Amours SK, Zygun D. Acute resuscitation of the unstable adult trauma patient:bedside diagnosis and
therapy. Canadian Journal of Surgery. 2008;51(1):57– 69.
15. Rei DA, Haricharan RN, Bullington NM, Grin RL, McGwin G
Jr, Rue LW 3rd. Traumatic brain injury is associated with the development of deep vein thrombosis independent of pharmacological
prophylaxis. Journal of Trauma. 2009;66(5):1436– 40.
16. Shackford SR, Moser KM. Deep venous thrombosis and pulmonary
embolism in trauma patients. Journal of Intensive Care Medicine.
1988;3:87– 98.
17. Lipe B, Ornstein DL. Deciencies of natural anticoagulants, protein C, protein S, and antithrombin. Circulation.
2011;124(14):e365– 8.
18. Jorens PG, Van Marck E, Snoeckx A, Parizel PM. Nonthrombotic
pulmonary embolism. European Respiratory Journal.
2009;34(2):452– 74.
19. Motzer RJ, Bander NH, Nanus DM. Renal- cell carcinoma. New
England Journal of Medicine. 1996;335(12):865– 75.
20. Akhtar S. Fat embolism. Anesthesiol Clinics. 2009;27(3):533– 50.
21. Kanayama N, Tamura N. Amniotic uid embolism:Pathophysiolog y
and new strategies for management. Journal of Obstetrics and
Gynaecology Research. 2014;40(6):1507– 1517.
22. Sood J. Advancing frontiers in anaesthesiology with laparoscopy.
World Journal of Gastroenterology. 2014;20(39):14308– 14.
23. Hsu CW, Sun SF. Iatrogenic pneumothorax related to mechanical ventilation. World Journal of Critical Care Medicine.
2014;3(1):8– 14.
24. Manseld PF, Hohn DC, Fornage BD, Gregurich MA, Ota DM.
Complications and failures of subclavian- vein catheterization. New
England Journal of Medicine. 1994;331(26):1735– 8.
25. Imazio M, Brucato A, Rovere ME, et al. Contemporary features,
risk factors, and prognosis of the post- pericardiotomy syndrome.
American Journal of Cardiology. 2011;108(8):1183– 7.
26. Stathopoulos I, Kossidas K, Panagopoulos G, Garratt K. Cardiac
tamponade complicating coronary perforation during angioplasty: short- term outcomes and long- term survival. Journal of
Invasive Cardiology. 2013;25(10):486– 91.
27. Daugherty EL, Liang H, Taichman D, Hansen- Flaschen J, Fuchs
BD. Abdominal compartment syndrome is common in medical
intensive care unit patients receiving large- volume resuscitation.
Journal of Intensive Care Medicine. 2007;22:294– 9.
28. Balogh Z, McKinley BA, Cocanour CS, etal. Supranormal trauma
resuscitation causes more cases of abdominal compartment syndrome. Archives of Surgery. 2003;138(6):637– 42.
29. Vincent JL, De Backer D. Circulatory shock. New England Journal
of Medicine. 2013;369(18):1726– 34.
30. Argulian E, Messerli F. Misconceptions and facts about pericardial eusion and tamponade. American Journal of Medicine.
2013;126(10):858– 61.
31. Roberts DJ, Leigh- Smith S, Faris PD, etal. Clinical presentation of
patients with tension pneumothorax:a systematic review. Annals of
Surgery. 2015 Jan 5. [Epub ahead ofprint]
32. Kucher N, Goldhaber SZ. Management of massive pulmonary
embolism. Circulation. 2005;112(2):e28– 32.
33. Bakker J, Nijsten MW, Jansen TC. Clinical use of lactate monitoring
in critically ill patients. Annals of Intensive Care. 2013;3(1):12.
34. Eisenberg MJ, Munoz de Romeral L, Heidenreich PA, Schiller NB,
Evans GT. e diagnosis of pericardial eusion and cardiac tamponade by 12- lead ECG. Chest. 1996;110:318– 24.
35. Levis JT. ECG diagnosis: pulmonary embolism. Permanente
Journal. 2011;15(4):75.
OBSTRUCTIVESHOCK 117
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36. Perera P, Lobo V, Williams SR, Gharahbaghian L. Cardiac echocardiography. Critical Care Clinics. 2014;30(1):47– 92.
37. Simon MA. Perioperative management of pulmonary hypertensive
crisis. Advances in Pulmonary Hypertension. 2013;12(1):38– 9.
38. Patil PV, Wiegers SE. Echocardiography for hypertrophic cardiomyopathy. Progress in Cardiovascular Diseases. 2014;57(1):91– 9.
39. Gribaa R, Slim M, Kortas C. Right ventricular myxoma obstructing
the right ventricular outow tract:a case report. Journal of Medical
Case Reports. 2014;8:435.
40. Lacey BW, Lin A. Radiologic evaluation of right ventricular outow
tract myxomas. Texas Heart Institue Journal. 2013;40(1):68– 70.
41. Galbois A, Ait- Oufella H, Baudel JL, etal. Pleural ultrasound compared with chest radiographic detection of pneumothorax resolution aer drainage. Chest. 2010;138(3):648– 55.
42. Ding W, Shen Y, Yang J, He X, Zhang M. Diagnosis of pneumothorax by radiography and ultrasonography:a meta- analysis. Chest.
2011;140(4):859– 66.
43. Oren- Grinberg A, Gulati G, Fuchs L, Pinto DS. Hand- held echocardiography in the management of cardiac arrest. Anesthesia &
Analgesia. 2012;115(5):1038– 41.
44. Balogh ZJ, Malbrain M. Resuscitation in intra- abdominal hypertension and abdominal compartment syndrome. American Journal of
Surgery. 2011;77(Suppl 1):S31– 3.
45. Bodson L, Bouferrache K, Vieullard- Baron A. Cardiac tamponade.
Current Opinion in Critical Care. 2011;17:416– 424.
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PARTIV.
PULMONARYCRISES
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121
14.
INTRODUCTION TOPULMONARY URGENCIES AND EMERGENCIES
John D. Mitchell and Marek Brzezinski
CASE PRESENTATION
A 54- year- old woman with severe chronic obstructive pulmonary disease (FEV1/ FVC ratio 45%), hypertension, and
a new central le lung nodule presents for exible and rigid
bronchoscopy as well as endobronchial ultrasound with
biopsy for tissue diagnosis. Her medications include albuterol, atrovent, uticasone, motelukast, and hydrochlorothiazide. She is a current pack- a- day smoker and has a 2- liter
per minute home oxygen requirement. e patient is obese,
with a BMI of 35. Her airway is Malampatti classIII, but
the patient is edentulous with good neck motion and adequate thyromental distance. Your plan is for a total intravenous anesthetic with propofol and remifentanyl. Following
demonstration of easy mask ventilation, succinylcholine is
given and the rigid bronchoscope is introduced. Mechanical
jet ventilation is initiated uneventfully and the procedure
begins. 15 minutes into the procedure, the patient begins
to cough. You deepen the anesthetic, but notice the oxygen
saturation, previously 98%, has begun to rapidly decline
and is now88%.
PATHOPHYSIOLOGY OFRESPIRATORY FAILURE
From the mouth and nose to the level of the alveoli and pulmonary vasculature, issues can arise that interrupt the normal transfer of gasses. Respiratory failure can be grouped
into Types IthroughIV.
3,4
Type Irepresents hypoxemic respiratory failure, dened
as a PaO2 lower than 60mm Hg with a normal or low
PaCO2. It is characterized by ventilation perfusion mismatch or shunt due to malfunction of the pulmonary vasculature or alveoli. Examples include pneumonia, pulmonary
edema, pulmonary embolus, and alveolar hemorrhage.
In contrast, type II is hypercapnic respiratory failure,
characterized by a PaCO2 higher than 50mmHg due to
decreased minute ventilation or increased dead space ventilation. Lesions or medications interrupting normal function in the nervous system, musculature, neuromuscular
transmission, or airway structures can result in this type of
respiratory failure. Conditions such as COPD, neuromuscular diseases, or administration of narcotic or paralytic
medications are common examples.
Type III respiratory failure is combined failure of oxygenation and ventilation. It is common in the perioperative
REVIEW OFMAJOR PULMONARY FUNCTIONS
setting and thus important for the anesthesiologist to consider. It is sometimes considered a subset of type Ifailure,
e lungs are responsible for delivery of oxygen to and
removal of carbon dioxide from the bloodstream. ey are
delicate, hollow organs weighing less than a pound together,
yet are constructed to provide an incredibly ecient transfer of gases. e trachea and airways serve to transport gases
to and from the lungs, humidify the air, and lter impurities. e pulmonary arteries carry deoxygenated blood to
the lungs and may be impacted by levels of acid, carbon
dioxide, or disease processes that can alter the ow of blood
to the alveoli. e lungs also serve metabolic functions
including degradation of vasoactive mediators, conversion
of angiotensin Ito angiotensin II, and production of proteins. Figure 14.1 demonstrates the basic anatomy of the
respiratory system.
1,2
with atelectasis chief among its causes. Other contributors
include decreased functional residual capacity2, direct or
indirect eects of anesthetic agents, airway secretions, positioning of patients with obesity or ascites in the supine position, and upper abdominal incisions.
Type IV respiratory failure is due to shock states with
hypoperfusion. ese can be cardiogenic, hypovolemic, or
septic in nature. ese will be addressed more thoroughly
in other sections.
e chapters that follow in Part IV discuss in detail the
management of issues related to securing the airway, disruptions of airow, impaired diusion of gases, injuries to the
lung (pneumothorax), issues related to gas exchange involving the anesthesia machine, and airway res. We therefore
121
122
T
Diaphragm
Human Respiratory System
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Pulmonary
venule
Bronchus
Pulmonary
arteriole
rachea (windpipe)
Upper lobe
Heart
Lower lobe
conne the remainder of this introduction to the discus-
DIFFERENTIAL DIAGNOSIS
Alveoli
Figu re14.1 Respirator y system anatomy.
SOURCE:Purchased from iStockphoto.com,
Copyright:blueringmedia.
sion of an overarching approach to the management of the
patient under anesthesia with a deteriorating respiratory
status characterized by worsening oxygenation.
e unstable patient deserves rapid, systematic appraisal
and action both to temporize the episode and resolve the
underlying etiology. Respiratory emergencies can unfold
quickly, and desaturation is oen the rst detected sign
in the operating theater. Identication of risk factors for
e dierential diagnosis of desaturation can be divided
into decreased delivery of oxygen, decreased delivery of
blood, impaired oxygen exchange, or artifact. A thorough list is presented in Box 14.1. e most likely causes
are displacement of the saturation probe, apnea, hypoventilation, improper position of the endotracheal tube, or
laryngospasm.
7
desaturation and application of an appropriate algorithm
can facilitate diagnosis and management.
RISK FACTORS
INITIAL TREATMENTSTEPS
Cognitive aids, such as checklists, have been shown to
improve outcomes in crisis situations. COVER ABCDIn a large database review, general anesthesia was associated with over 90% of desaturation episodes. Nearly 75%
of cases were felt to be due entirely (57%) or in part due
to the administration of anesthesia. Events happened at all
points in the anesthetic. Most (88%) of events were respiratory, but 8% were circulatory in nature, and 3% machine
or equipment related. While most patients recovered completely, death occurred in 5.8% of hypoxic events. Complex
patients, incorrect diagnoses, inadequate knowledge, and
lack of supervision were contributing factors in deaths.
5
Review and regression analysis of intraoperative desaturation events in over 152,000 anesthetics revealed that risk
factors for desaturation included age under 5, American
Society of Anesthesiologists (ASA) class 3- 5, history of
upper respiratory tract infection or asthma, use of general
anesthesia, and durations of anesthesia over 30 minutes.
A SWIFT CHECK, developed by the Australian Patient
Safety Foundation, is based on expert consensus aer
reviewing cases from the Australian Incident Monitoring
System. e expert- developed consensus checklist
was applied to 2,000 events in the Australian Incident
Monitoring System to assess its degree of utility and to
develop subalgorithms, making it a robust, data- driven
tool. Importantly, it includes a desaturation subalgorithm.
Application of the primary algorithm achieved a working
diagnosis in greater than 99% of cases, and could facilitate
rapid correction of 62% of issues in less than a minute.
Of remaining problems, 37% were addressed by the subalgorithm for desaturation. As less than 1% of reported
problems would require additional algorithms to deal
with, this represents a very comprehensive approach to
6
the issue.
6,8,9
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123
e full pneumonic device and explanation can be
BOX 14.1 DIFFERENTIAL DIAGNOSIS OFDESATURATION
(TOP CAUSES INITALICS)
viewed in Box 14.2. In brief, the following should be evaluated sequentially:
Decreased Oxygen toLungs
Oxygen supply- lowFiO
Apnea/ hypoventilation
Low or inappropriateFGF
ETT advanced too far (right mainstem)
Airway position/ obstruction
Laryngospasm
Ventilator broken/ settings inadequate
Circuit kink, obstruction, or disconnect
2
Decreased Blood toLungs
Cardiacarrest
Cardiac pump dysfunction
Anaphylaxis
Pulmonary embolism(PE)
Diminished Oxygen Exchange or Increased Shunting(AV)
One lung ventilation
Pulmonaryedema
Aspiration
Lung contusion
Atelectasis
C Circulation,Color
O Oxygen, Oxygen Analyzer
V Ventilation, Vaporizer
E Endotracheal Tube, Eliminate anesthesia machine
R Review monitors, equipment
AAirway
B Breathing
C Circulation
DDrugs
A Aware of Air (embolism or intrapleural), Allergy,
Anaphylaxis
SWIFT CHECK— of patient, surgeon, medications,
history, and other relevant factors.
BOX 14.2 COVER ABCD- A SWIFTCHECK
C C1 Circulation— Check pulse and adequacy of
circulation— consider CPR. Consider also the rate,
rhythm, and quality of thepulse.
C2 Color— Evaluate for central cyanosis, check
saturation by pulse oximetry.
Consider testing oximeter on own nger while continuing
protocol.
Pneumothorax
Pneumoperitoneum
Pneumonia
Sepsis/ ARDS
Artifacts
Probe malposition
Hypothermia
Poor peripheral circulation
SOURCE:Adapted from The Anaesthetic Crisis Manual by David Borshoff.
Cambridge University Press, NewYork,2011.
INTRODUCTION TO PULMONARY URGENCIES AND EMERGENCIES 123
O O1 Oxygen— Ensure oxygen ow, rule out hypoxic
mixture or delivery failure.
O2 O2 Analyzer— Convert to 100% oxygen and establish
owmeter function.
V V1 Ventilation— Verify no overination of reservoir
bag. Check spill valve and scavenger line for blockage
or closure. Ventilate by hand to evaluate circuit and
airway patency and lung/ chest compliance and air
movement by “feel,” auscultation, and visualization of
chest movement. Provide a single recruiting breath at
40cm water to recruit possible atelectasis. Evaluate
capnography waveform.
(continued)
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Once the initial assessment is completed, application
BOX 14.2 CONTINUED
V2 Va+porizer— Evaluate levels and settings of inhaled
agents. Check for vaporizer leaks at ll sites, vent
seating rings, and gas ow for liquid or gas leaks.
Explore whether correct gas is in vaporizer.
of the desaturation subalgorithm is recommended. It was
deemed helpful in the potential management of 9% of
problems that remained aer ABCD- A SWIFT CHECK
was applied. e primary principles hereare:
1. Manual Ventilation at an FiO2 of100%
E E1 Endotracheal Tube— Check tube patency and
position with suction, auscultation, capnography, and
direct laryngoscopy. Assess for mainstem intubation
by deating cuff and withdrawing the tube during
laryngoscopy until the cuff is seen just below the
cords. Consider adjusting, removing, or replacing
endotrachealtube.
E2 Elimination— Remove the anesthetic machine from
the system by ventilating with a self- inating bag on an
alternate oxygen source such as a canister. Continue to
monitor line gases, staying alert to issues with sampling
from an open system.
R R1 Review Monitors— Assess all monitors applied. If not
present, consider adding oxygen analyzer, capnograph,
pulse oximeter, blood pressure monitor (direct or
indirect), electrocardiogram, temperature monitor,
and monitor of neuromuscular function. Ensure that
all monitors are positioned properly, calibrated, and
checked for function.
R2 Review Equipment— Check all other equipment being
used to provide care to verify appropriate function.
A Be Aware of Air (emboli or pneumothorax), Anaphylaxis,
or Allergic reaction.
SWIFT CHECK— Quickly evaluate issues related to patient
history, position, procedure, personnel (nursing and
surgeons), and current elements of the event. Engage
the team in a dialogue about situation. Review all
medications.
SOURCE:Adapted from Runciman WB, Sellen A, Webb RK, etal. Errors,
incidents and accidents in anesthetic practice. Anaesthesia and Intensive Care.
1993;21(5):506– 19.
2. Re- check of adequacy ofFiO
2
3. Conrmation that end- tidal CO2 levels are what they
should be.If they are abnormally low, the dierential
must include Air embolism, Pneumothorax,
Anaphylaxis, or low cardiac output,
4. Repeat auscultation to rule out endobronchial
intubation (the cause of over half of desaturation events
in the initial case series analysis)
10
If none of these represents the issue, other etiologies
must be considered and managed. Chief among these are
underlying cardiopulmonary problems (Table14.1).
Pulse oximeters may also malfunction and require
replacement of the probe (most common), cable, or module. Readings provided may also be unreliable in some
cases (1%) including polycythemia, Raynaud’s phenomenon, vasoconstriction, hypothermia, dark nail polish,
or the presence of an AV stula upstream of the probe.
Of note, acute tricuspid regurgitation has been reported
to cause the pulse oximeter to read the venous pulse and
display a corresponding saturation in the 70s, even in the
setting of adequate arterial oxygenation. Similarly, severe
methemoglobinemia can result in a displayed oxygen saturation of85%.
9
SUBSEQUENT TREATMENTSTEPS
In cases where desaturation continues despite troubleshooting, the procedure should be completed or terminated
TABLE14.1 OTHER ETIOLOGIES FORACUTE DESATURATION
The approach COVER ABCD- A SWIFT CHECK
can be used whether a patient is mechanically ventilated or spontaneously breathing. Of note, if a patient
is under sedation with an unprotected airway, maintenance of protective reflexes must be ensured in the setting of respiratory insufficiency. In such cases, the airway
and breathing portion (AB) of the approach should be
appliedfirst.
124 PART IV. PULMONARY CRISES
Bronchial Secretions Acute Shunt Pneumoperitoneum
Suction tube or
airways
Provide recruitment
breath
Consider CPAP/ PEEP
If oxygenation does not improve following COVER ABCD- A SWIFT CHECK and the
desaturation algorithm application, these factors must also be considered and treated.
Position patient
supine
Level patient Evaluate for gas
Release pressure
embolism
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125
as quickly as possible. Chest x- rays, blood gases, and TEE (if
REFERENCES
readily available), should be obtained to provide additional
information.
FOLLOW- UP
Follow- up will be determined by the etiology of the event,
resulting complications, and reversibility of the condition.
Specic disease states will be dealt with in more detail in
chapters to follow.
CASE- BASED LEARNING DISCUSSION
1. What is the dierential diagnosis for the rapid
desaturation in this patient?
2. What initial steps will you take to address the oxygen
saturation?
3. If the initial steps do not resolve the issue, what would
your next approachesbe?
4. Oxygenation stabilizes at 87%, but will not improve.
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3. Neema PK. Respiratory failure. Indian Journal of Anaesthesia.
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4. Melanson P, ed. Acute respiratory failure. http:// www.mcgill/ ca/
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desaturation. Journal of the Medical Association of ailand.
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6. Charuluxananan S, Suraseranivongse S, Punjasawadwong Y, et al.
Risk factors of intraoperative oxygen desaturation: a case- control
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Barker L. e Australian Incident Monitoring Study. Crisis management: validation of an algorithm by analysis of 2000 incident
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Should the procedural team abort the procedure?
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