Peri-opera)eve monitoring: De Swan-Ganz katheter in perspec)ef

16
Volume – Does it make a difference? Hemodynamische monitoring op Intensieve Zorgen: Het 6jdperk na de Swan-Ganz Katheter Prof. Dr. Steffen Rex Department of Anesthesiology University Hospitals Leuven Department of Cardiovascular Sciences KU Leuven [email protected] Peri-opera)eve monitoring: De Swan-Ganz katheter in perspec)ef PA-catheter: perioperatively Conflicts of interest – financial disclosures Company Nature of Affiliation Unlabeled Product Usage Edwards Speaker’s fees None

Transcript of Peri-opera)eve monitoring: De Swan-Ganz katheter in perspec)ef

Page 1: Peri-opera)eve monitoring: De Swan-Ganz katheter in perspec)ef

Volume – Does it make a difference?

HemodynamischemonitoringopIntensieveZorgen:Het6jdperknadeSwan-GanzKatheter

Prof. Dr. Steffen Rex Department of AnesthesiologyUniversity Hospitals Leuven

Department of Cardiovascular SciencesKU Leuven

[email protected]

Peri-opera)evemonitoring:DeSwan-Ganzkatheterinperspec)ef

PA-catheter: perioperatively

Conflicts of interest – financial disclosures

Company Nature of Affiliation

Unlabeled Product Usage

Edwards Speaker’s fees None

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PA - catheter: perioperatively

PA-catheter:Is it really time for the swan song?

ofMedicine and Physiology, Stanford University MedicalCenter, Stanford.

Reprint requests: Dr Robin, Physiology, Anatomy Building, Stan-ford University School ofMedicine, Stanford 94305

CHEST I 92 I 4 I OCTOBER, 1987 727

ACKNOWLEDGMENT: The authors wish to express their appreci-ation to the administration, medical record departments, andcardiology departments ofthe hospitals in the Worcester SMSA whoprovided access to their medical records; to Sandra Knowlton andGerrie Nespoli for data abstraction; to Donald Love and Marc Zivefor statistical analysis; and to Mary Larson for secretarial assistance.

REFERENCES

1 AlpertJS. Invasive hemodynamic monitoring. J Cardiovasc Med1980; 5:83-7

2 Swan HJC, Ganz W. Hemodynamic measurements in clinicalpractice: a decade in review. J Am Coil Cardiol 1983; 1:103-13

3 Gore JM, Alpert JS, Benotti JR, Kotilainen PW, Haffajee CI.Handbook of hemodynamic monitoring. Boston: Little Brown,1984:5-9

4 Dillon JC, Vasu CM, Berman DS, Goldstein S, Warren J. ThskForce III, Diagnostic procedures. 13th Bethesda Conference,Emergency cardiac care. Am J Cardiol 1982; 50:382-92

5 Goldenheim PD, Kazemi H. Cardiopulmonary monitoring ofcritically ill patients (part II). N Engl J Med 1984; 311:776-83

6 Swan HJC, Ganz W, Forrester J, Marcus H, Diamond G,Chonette D. Catheterization of the heart in man with use of aflow-directed balloon-tipped catheter. N EngI J Med 1970; 283:447-51

7 Murray IF Complications of invasive monitoring. Med Instrum1981; 15:85

8 Boyd KD, Thomas SJ, Gold J, Boyd AD. A prospective study ofcomplications ofpulmonary artery catheterization in 500 consec-utive patients. Chest 1983; 84:245-49

9 Rowley KM, Clubb KS, Smith GJW, Cabin HS. Right-sidedinfective endocarditis as a consequence of flow-directed pulmo-nary artery catheterization. N Engl J Med 1984; 311:1152-56

10 Keefer JR, Barash PG. Pulmonary artery catheterization, adecade ofclinical progress. Chest 1983; 84:241-42

11 Dalen JE. Bedside hemodynamic monitoring. N Engl J Med1979; 301:1176-78

12 Reeves TJ. Advances in cardiology and escalating costs to thephysician. Circulation 1985; 71:637-41

13 Goldberg RJ, Gore JM, Alpert JS, Dalen JE. Recent changes inthe attack rates and survival rates of acute myocardial infarction(1975-1981). The Worcester Heart Attack Study. JAMA 1986;255:2774-779

14 Goldberg R, Szklo M, TonasciaJ, Kennedy H. ‘lime trends in theprognosis of patients with myocardial infarction: A population-based study. Johns Hopkins Med J 1979; 144:73-80

15 Szklo M, Goldberg R, Kennedy H, Tonascia J. Survival ofpatients with nontransmural myocardial infarction: A population-based study. Am J Cardiol 1978; 42:648-52

16 Goldberg RJ, Gore JM, Alpert JS, Dalen JE. Non-Q wave myo-cardial infarction: Recent changes in occurrence and prognosis: Acommunity-wide perspective. Am Heart J 1987; 113:273-79

17 Merrell M, Shuiman LE. Determination ofprognosis in chronicdisease illustrated by systemic lupus erythematosis. J Chron Dis1955; 1:12-37

18 Peto R, Pike MC, Armitage P, Breslow NE, Cox DR, Howard SV,et al. Design and analysis ofrandomized clinical trials requiringprolonged observation of each patient. II. Analaysis and exam-pIes. Br J Cancer 1977; 35:1-39

19 Dalen JE, Goldberg RJ, Gore JM, Nespoli G, Struckus J, AlpertJS. lIme trends in the use ofselected procedures in patients withacute myocardial infarction-The Worcester Heart Attack Study(abstract). Circulation 1984; 70:642

20 Eisenberg PR, Jaffee AS, Schuster DR Clinical evaluationcompared to pulmonary artery catheterization in the hemo-dynamic assessment ofcritically illpatients. Crit Care Med 1984;12:549-53

21 Bayliss J, Norell M, Ryan A, Thurston M, Sutton CC. Bedsidehemodynamic monitoring: Experience in a general hospital. BrMed J 1983; 287:187-90

22 Parmley WW. The post MI role of hemodynamic monitoring.Hosp Prac 1982; 17:169-75

23 Gorlin R. Practical cardiac hemodynamics. N EngI J Med 1977;296:203-05

24 Robin ED. The cult of the Swan-Ganz catheter. Overuse andabuse of pulmonary flow catheters. Ann Intern Med 1985; 103:445-49

25 Weber KT, Janicki JS, Russell RO, Racldey CE. Identification ofhigh risk subsets ofacute myocardial infarction: derived from theMyocardial Infarction Research Unit cooperative study databank. Am J Cardiol 1978; 41:197-203

26 ForresterJS, Diamond GA, Swan HJC. Correlative classificationof clinical and hemodynamic function after acute myocardialinfarction. Am J Cardiol 1977; 39:137-45

27 Packer M, Medina N, Yushak M. Hemodynamic changes mim-icking a vasodilater drug response in the absence ofdrug therapyafter right heart catheterization in patients with chronic heartfailure. Circulation 1985; 71:761-66

28 Spodick DH. Physiologic and prognostic implications of invasivemonitoring: Undetermined risk/benefit ratios in patients withheart disease. Am J Cardiol 1980; 46:173-75

Death by Pulmonary Artery FlowDirectedCatheter (editorial)Time for a Moratorium?Eugene D. Robin, M.D.*

study by Gore et al in this issue ofChest (see page721) raises some critically important issues involv-

ing the safety of large numbers of patients.The impact ofthe use ofthe pulmonary artery flow-

directed catheter on patient outcome following acute(usually complicated) myocardial infarction wasanalyzed retrospectively in 3,263 patients. No benefit

in terms of mortality, length of hospital stay (longer inthose with the catheter), or long-term prognosis couldbe demonstrated. These findings, although not antici-pated by the overwhelming majority ofcatheter users,are scarcely surprising. The probable lack of benefitwas anticipated in 1980k and has been emphasizedsince 1982.2 A lack ofbenefit in the use of pulmonaryflow catheters in the ICU is also implicit in the data ofKnaus et al.5

The present study by Gore et al, however, surpris-ingly shows a very large excess mortality in patients in

Downloaded From: http://journal.publications.chestnet.org/ on 04/28/2014

CHEST I 92 I 4 I OCTOBER, 1987 727

PA - catheter: perioperatively

PA-catheter:Swan gone catheter ?

Crit Care Med 2011; 39:1613–1618

JAMA. 2007;298(4):423-429

PACman

ARDSnetwork

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PA - catheter: perioperatively

PA-catheter:Is it really time for the swan song?

PRO’s CON’s▪ The PAC is useless for most of the

indications it is used for: • assessment of cardiac preload • prediction of fluid responsiveness • detection of myocardial ischemia

▪ The PAC is dangerous: Complications ▪ Availability of less invasive

alternatives ▪ No improvement in outcome ▪ Practitioners are unable to

appropriately interpret PAC-derived variables

▪ Practitioners are insufficiently trained in the use of the PAC

▪ The PAC measures hemodynamic parameters that are difficult to assess with other techniques

▪ Other monitoring tools are also dangerous

▪ Alternatives are not equivalent ▪ Outcome studies are methodologically

flawed

Volume – Does it make a difference?PA-catheter: periopeatively

The PA-catheter:Measurement of filling pressures

N Engl J Med 1970; 283:447-451

Chatterjee K. The Swan-Ganz Catheters: Past, Present, and Future. A Viewpoint. Circulation. 2009;119:147-152

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Volume – Does it make a difference?PA-catheter: periopeatively

The PA-catheter is useless: Assessment of cardiac preload

Crit Care Med 2004; 32:691–699

Δ PCWP [mmHg]

[ml m-2]

-10 -5 0 5 10

-20

-10

0

10

20

Δ SVI

▪ Filling pressures ≉ filling status ▪ Filling pressures do not reflect cardiac preload!

Volume – Does it make a difference?PA-catheter: periopeatively

The PA-catheter is useless: Assessment of cardiac preload

RA

CVP PADP PAOP LAP LVEDP LVEDV

Pulmonary Vascular Resistance Heart Rate

Mitral Valve Pathology Heart Rate

Tricuspid Valve Pathology RV Diastolic Compliance

Alveolar pressure Pulmonary Venous Pressure

LV Diastolic Compliance

RV LV

LA PA

Ao PV CVP PAP

PAOP

LAP

LVP

! Myocardial edema (ischemia, sepsis, trauma) ! Hypertrophy (HOCM, hypertension) ! Increase of juxtacardial pressure (IPPV, PEEP, pericardial effusion) ! Impaired diastolic function (ischemia, CPB) ! Catecholamines ▪ Filling pressures ≉ filling status

▪ Filling pressures do not reflect cardiac preload!

S. Rex, W.F. Buhre: Pulmonary Artery Catheters. In: A. Klein, A. Vuylsteke, S.A.M. Nashef (ed): Core Topics in Cardiothoracic Critical Care. Cambridge University Press 2008

C = ΔV/ΔP ΔP = ΔV/C

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PA-catheter: perioperatively

The PA-catheter is useless: Prediction of fluid responsiveness

Crit Care Med 2007; 35:64–68

Pre

-Infu

sion

∆ CI > 15% ∆ CI < 15%

PA-catheter: perioperatively

The PA-catheter is useful: Complete and unique hemodynamic profile

Calculated variables

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PA-catheter: perioperatively

The PA-catheter is useless: Detection of myocardial ischemia

PA-catheter: perioperatively

The PA-catheter is useful: Lack of alternatives in OPCAB-surgery

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PA-catheter: perioperatively

The PA-catheter is dangerous

Malposition

Perforation

PA-catheter: perioperatively

The PA-catheter is dangerous

suture perforating/transfixing the catheter. Knotting can be seenon chest x-ray, but differentiating between an encircled or atransfixed catheter can be impossible. If the catheter is still fullyfunctional, this may favor an encircling suture, but this may notalways hold true. The authors therefore strongly caution againstthe application of increased force in an attempt to withdraw thePAC. Although 1 PAC in this series was dislodged (“moderateresistance” was reported by the surgeon) without any adverseevent, pulling the catheter with “moderate” force applied by thesurgeon in another case led to a tear at the right atrial inferiorvena cava junction, resulting in death. In 1 patient who had thePAC pulled with “moderate force” in the operating room (pa-tient no. 3), there were no immediate consequences, but she didgradually deteriorate over the next 7 days, with increasingright-heart failure. She was later diagnosed with a traumatictear of the septal leaflet of the tricuspid valve, which is mostlikely the result of “leveraging” of the PAC at the tricuspidvalve because of the entrapment point being in the main pul-monary artery.

Fluoroscopy19 or echocardiography21 are 2 types of imag-ing techniques that may be used to confirm the catheter’simmobility and the location of the entrapping suture. Inject-

ing contrast agent through the catheter may occasionallyshow a leak, suggesting a perforating suture.

The ideal method of removing the entrapped catheter is notclear and will depend on the location and type of entrapment,as well as the endovascular expertise available at the particularinstitution. There are many case reports of the nonsurgicalremoval of entrapped catheters17,20,25-32; most of these involvethe removal of catheters that have been knotted in the heart orhave been encircled by a suture in the right atrium.25 Nonsur-gical removal has also been reported in the case of a ventricularentrapment.17 In the case of knotted and encircled catheters,using an array of endovascular tools, the catheter can be un-knotted or cut and removed. The risk of bleeding in thissituation is usually minimal. However, these approaches re-quire considerable expertise by the interventional radiologyteam.

Surgical removal of catheters has been advocated in othersituations.10,20 Catheters that have been perforated or are firmlyattached to cardiac structures should be considered riskier clin-ical scenarios. In these situations, manipulation of the cathetercould either tear the perforating stitch (with the potential forcardiac suture line dehiscence) or could lead to a tear in the

Fig 1. Sites of pulmonary artery catheterentrapment. IVC, inferior vena cava; LPA, leftpulmonary artery; RPA, right pulmonary ar-tery; SVC, superior vena cava. Numbers 1 to8 correspond to the patients’ number withinTable 1. Site #4 reflects a left atrial septalsite.

373PULMONARY ARTERY CATHETERS

Jacobson E. et al. Morbidity and Mortality Associated With Accidentally Entrapped Pulmonary Artery Catheters During Cardiac Surgery: A Case Series. Journal of Cardiothoracic and Vascular Anesthesia, Vol 20, No 3 (June), 2006: pp 371-375

Catheter entrapment

Washington University School of Medicine, St Louis, USA 8 cases from 2000-2005

▪ All patients needed redo-surgery ▪ One patient died from exsanguination

subsequent to withdrawal attempt

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PA-catheter: perioperatively

The PA-catheter is dangerous

Zink W, Graf BM. Der Pulmonalarterienkatheter. Anaesthesist 2001 Aug;50(8):623-42

Complication Incidence (%)

Complications related to venopuncture

Arterial Puncture Pneumothorax

Neural Injury Air Embolism

1,2 0,3-4,5 0,3-1,3

0,5

Cardiac Arrhythmias Supraventricular Ventricular

Haemodynamic Relevance Right bundle branch block

15 13-78

2-3 3-6

Knotting/Entrapment Intravasal/Intracardial Unknown

Valvular Lesions Petechial Bleedings, Perforation

0,5-2

Pulmonary Infarction 0,8-1

Pulmonary Artery Rupture

0,064-0,2 (Mortality 25-83)

Infections Asymptomatic Colonisation Symptomatic Infection

Catheter related sepsis Endocarditis

22 11

0,5-1 <1,5

Thrombus Formation 66 PA-catheter: perioperatively

Not only the PA-catheter is dangerous

Zink W, Graf BM. Der Pulmonalarterienkatheter. Anaesthesist 2001 Aug;50(8):623-42

Complication Incidence (%)

Complications related to venopuncture

Arterial Puncture Pneumothorax

Neural Injury Air Embolism

1,2 0,3-4,5 0,3-1,3

0,5

Cardiac Arrhythmias Supraventricular Ventricular

Haemodynamic Relevance Right bundle branch block

15 13-78

2-3 3-6

Knotting/Entrapment Intravasal/Intracardial Unknown

Valvular Lesions Petechial Bleedings, Perforation

0,5-2

Pulmonary Infarction 0,8-1

Pulmonary Artery Rupture

0,064-0,2 (Mortality 25-83)

Infections Asymptomatic Colonisation Symptomatic Infection

Catheter related sepsis Endocarditis

22 11

0,5-1 <1,5

Thrombus Formation 66

CVC

CVC

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PA-catheter: perioperatively

Not only the PA-catheter is dangerous

for the rational use of imagingservices.18 In general, it is as-sumed that TEE is appropriatelyused as an adjunct or subsequenttest to transthoracic echocardiog-raphy (TTE) when suboptimalimages on TTE preclude obtain-ing a diagnostic study. The indi-cations for which TEE mayreasonably be the test of firstchoice include, but are not lim-ited to, aortic pathology, cardiacvalve dysfunction, percutaneous

noncoronary cardiac interventions, infective endocarditis, atrial fibril-lation or flutter, and embolic events.18,19

Although TEE is considered a safe and relatively noninvasive diag-nostic technique, severe, even life-threatening complications havebeen reported (Table 1, Figure 1). The infrequency of serious compli-cations and difficulties in evaluating rare events limit the identificationof TEE-associated predictors of increased morbidity or mortality.Several retrospective studies involving larger patient populationshave identified inherent risk factors associated with TEE. A literaturesearch was conducted via Medline and PubMed (1966 to June 1,2010), and the bibliographies of retrieved articles were also reviewed.

For practicing echocardiographers, it is important to be familiarwith potential complications of TEE to allow a thorough risk-benefitanalysis on an individual basis. This holds especially true for patientswith preexisting gastroesophageal disease, for whom the decisionabout the benefit versus potential harm of TEE can be difficult.

In this review, we summarize the available literature pertaining tothe risks, complication rates, and overall safety of TEE, with the goalof facilitating the identification of patients in whom alternative echo-cardiographic modalities or other invasive or noninvasive diagnosticstrategies should be considered.

GENERAL CLINICAL EXPERIENCE OF TRANSESOPHAGEALECHOCARDIOGRAPHIC SAFETY

Reported rates ofmajor TEE-related complications in ambulatory, non-operative settings range from 0.2% to 0.5%. TEE-associated mortalityhas been estimated to be <0.01% (Tables 2 and 3).20-23 These ratesof adverse outcomes are comparable with those associated withgastroscopy or esophagogastroduodenoscopy (EGD), for which theoverall risk for nonfatal complications is between 0.08% and 0.13%,and the reported mortality rate is approximately 0.004%.24,25 Incomparison with the use of TEE in a nonoperative setting,intraoperative TEE poses a slightly different risk profile, because itinvolves probe placement and manipulation in intubated patientsunder general anesthesia who have frequently receivedneuromuscular blocking drugs. These patients are unable to swallowto facilitate probe insertion and cannot respond to possibly injuriousprobe manipulations. Furthermore, several consecutivetransesophageal echocardiographic examinations or continuousintraoperative monitoring might be required for a subset of surgicalpatients. Overall rates of TEE-related morbidity with intraoperativeTEE, however, have been estimated to be similar to nonoperative pa-tients and range from 0.2% to 1.2%.26-29 In the largest study ofintraoperative TEE–related complications to date, a single-center caseseries of 7,200 patients, Kallmeyer et al.28 reported TEE-associated

morbidity and mortality of 0.2% and 0%, respectively. In contrast,Lennon et al.30 surveyed patients for later complications and suggestedthat rates of major gastrointestinal (GI) injuries (e.g., gastric laceration,hemorrhage, or perforation) could be as high as 1.2%. More than halfof the complications presented >24 hours postoperatively, with onepatient not presenting until day 11. The authors therefore suggestedthat the accurate assessment of overall risk for TEEmay have previouslybeen underestimated given a possible delay in the clinicalmanifestationof TEE-related GI injury.30

Table 1 TEE-related injuries

Site Injury

Oropharyngeal Lip bruising/laceration, loose/chipped tooth,displaced dentures, pharyngeal laceration,perforation of the hypopharynx, accidentaltracheal intubation

Esophageal Odynophagia, dysphagia, laceration/perforation,Mallory-Weiss tear

Gastric Laceration/perforation, hemorrhageMiscellaneous Splenic laceration, compression of mediastinal

structures, airway compromise, thermal injury/burn, tongue necrosis

Figure 1 Sites of potential injury related to TEE include oralinjury (e.g., lip or dental trauma), oropharyngeal injury (e.g., lac-eration, perforation), laryngeal injury (e.g., vocal cord trauma,compression of airway structures, inadvertent tracheal intuba-tion), esophageal injury (e.g., laceration, perforation, falsepassage into diverticulum), gastric injury (e.g., lacerations orperforation particularly of fundus or gastroesophageal junction),and gastric bleeding.

Abbreviations

EGD = Esophagogastro-duodenoscopy

GI = Gastrointestinal

ICU = Intensive care unit

TEE = Transesophagealechocardiography

TTE = Transthoracicechocardiography

1116 Hilberath et al Journal of the American Society of EchocardiographyNovember 2010

of 869 patients undergoing cardiac surgery (with and without TEE)and found that 4% subsequently had evaluation by barium swallowfor swallowing dysfunction. Older age was the strongest independentpredictor of swallowing dysfunction (P < .001), followed by theduration of postoperative intubation (P = .001), but the use of intra-operative TEE itself also appeared to be an independent risk factorfor dysphagia (odds ratio, 4.68; 95% confidence interval, 1.76–12.43;P = .003).

Although an association between intraoperative TEE and postoper-ative dysphagia or odynophagia has been suggested,28,32,33 anindependent correlation has not been consistentlydemonstrated.27,34,35 A prospective study byOwall et al.35 randomized57 patients undergoing cardiac surgery to either have or not have trans-esophageal echocardiographic monitoring and reported no significantdifferences in the rates of sore throat or odynophagia. Anothernonrandomized study prospectively examined 41 patients undergoingcardiac surgery with and 40 patients without TEE, as well as retrospec-tive analysis of another 200 cases, and found no difference in anorexia,dysphagia, and sore throat.27 These studies are limited by size and/orlack of randomization. Given the morbidity that may be associatedwith severe dysphagia, further study of this area is warranted.

The incidence of dental injury ranges from 0.03% to 0.1%28,31

and correlates with a patient’s overall dental health. Dentures canalso be dislodged by a TEE probe, highlighting a thoroughpreprocedural assessment of the oral cavity.36 Sriram et al.37 re-ported a case of tongue necrosis and formation of a permanent cleftassociated with TEE probe position in a prolonged cardiac opera-tion. Intraoperative tongue swelling in the setting of TEE has been

described in the past,38 but the majority of tongue pathology inthe perioperative period is attributed to endotracheal tube position,the duration of endotracheal intubation,39 or the surgical procedureitself (i.e., head and neck surgery, prone positioning, and risk forvenous congestion).40

TEE and Orogastric Tract Perforation

Upper GI perforations after TEE have been reported in both pediatricand adult surgical patients,29,30,41-49 with an estimated incidencebetween 0.01% and 0.04%.28,30 This incidence is consistent withthe approximate rate of one to three per 10,000 TEE-related perfora-tions in ambulatory, conscious, or semiconscious patients.21,23 GIperforation is associated with severe morbidity, and depending onmode of management (surgical vs medical) and time to diagnosis,mortality can range from 10% to 56%.25,50 Delayed recognition ofserious orogastric canal injury or perforation can be a problem inheavily sedated patients and in the setting of intraoperative TEE inanesthetized patients. Although evidence of rupture may bedramatic with the sudden appearance of the probe in the surgicalfield,41 excessive orogastric hemorrhage, or subcutaneous emphy-sema, the signs of perforation are frequently subtle and likely to bemasked by sedation or general anesthesia and postoperative intuba-tion and sedation. Patients may present much later with nonspecificsigns such as dyspnea, agitation, fever, or bloody nasogastric aspirates.Symptoms relating to spontaneous esophageal perforation such asMeckler’s triad of vomiting, pain, and subcutaneous emphysemaare rarely present, and according to one study of esophageal

Table 3 Complications of TEE in adult patients

Study Population Complications

Chan et al.69 1,700 ambulatory patients Complication rate 0.47% (accidental tracheal intubation,bronchospasm, atrial fibrillation); placement failure0.73%

Colreavy et al.89 255 critically ill patients Complication rate 1.6%; transient hypotension,oropharyngeal bleeding, pulmonary aspiration

Daniel et al.23 10,419 conscious/sedated patients Complication rate 0.18%; one mortality; placementfailure 1.9%

Hogue et al.33 869 cardiac surgical patients Risk for dysphagia independently correlated withintraoperative TEE, age, prolonged postoperativeintubation

Hulyalkar and Ayd27 Cardiac surgical patients No increase in incidence of 41 prospectively studiedpostoperative frank or occult patients, 40 controls;200 bleeding or gastroesophageal retrospectivelystudied complaints from controls

Kallmeyer et al.28 7,200 cardiac surgical patients Morbidity 0.2%, no deaths

Khandheria et al.20 7,134 conscious/sedated patients Complication rate 2.8%; major complications(laryngospasm, sustained ventricular tachycardia,congestive heart failure, death) 0.26%; one death

Lennon et al.30 516 cardiac surgical patients Major gastroesophageal complications 1.2%, fourgastroesophageal tears/ulcers, two gastricperforations, time of presentation < 11 days

Min et al.21 10,000 conscious/sedated patients Mortality 0%; orogastric perforation 0.03% (onehypopharyngeal, two cervical esophageal, no gastric)

Owall et al.35 57 cardiac surgical patients No increased rate of odynophagia, sore throat

Poelaert et al.93 108 critically ill patients One transient ventricular tachycardiaRousou et al.32 838 cardiac surgical patients Odds ratio 7.8 dysphagia

1118 Hilberath et al Journal of the American Society of EchocardiographyNovember 2010

Hilberath JN. et al. Safety of Transesophageal Echocardiography. J Am Soc Echocardiogr 2010;23:1115-27

PA-catheter: perioperatively

The PA-catheter Alternatives

PAC Alternative

Cardiac output COMinimally / less

invasive CO monitors

Echocardiography

Oxygen delivery / consumption SvO2 ScvO2

„Filling pressure“ PAOP E/E’ Echocardiography

RV - afterload SPAPMPAP

RVSPPAT Echocardiography

Continuous monitoring Intermittent monitoring

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PA-catheter: perioperatively

The PA-catheter Are the alternatives equivalent?

Cowie B, Kluger R, Rex S, Missant C Noninvasive estimation of left atrial pressure with

transesophageal echocardiography . Annals of Cardiac Anaesthesia | Jul-Sep-2015 | Vol 18 | Issue 3

Cowie, et al.: Noninvasive estimation of left atrial pressure with TOE

Annals of Cardiac Anaesthesia | Jul-Sep-2015 | Vol 18 | Issue 3 315

had 71% sensitivity and 60% specificity to predict a

PCWP ≥18 mmHg.

Figure 4 is a dot plot of the E/e’ values in patients

with PCWP <18 mmHg (median 8.2) and those with

PCWP ≥18 mmHg (median 11.4). This was significantly different (P = 0.004, Mann–Whitney U-test).

DISCUSSION

There is a modest correlation of E/e’ >10 and elevated

PCWP >18 mmHg. However, the clinical utility of this

is limited with many patients with elevated filling

pressures having normal E/e’ and many patients with

elevated E/e’ ratios having normal filling pressures.

In cardiology literature and TTE studies, E/e’ is routinely

measured to estimate left ventricular diastolic function

and to estimate LAPs.[13] However, recent data suggest

that there are significant limitations in this technique,

particularly in patients with normal left ventricular

structure and function, segmental wall motion

abnormalities, and mitral valve disease.[13] This greatly

limits the utility of this technique, in general, cardiac

surgical patients and would exclude many, if not all

patients.

Two recent publications post completion of our

study also suggested a poor correlation of E/e’ with

PCWP in cardiac surgical patients undergoing general

anesthesia.[16,17] In fact, correlations were poor in

patients with normal and impaired left ventricular

function under anesthesia.

Given the declining use of the PAC in cardiac anesthesia,

noninvasive estimation of intracardiac pressures is

required. However, we have shown that TOE is unable

to reliably estimate PCWP in cardiac surgical patients.

Nor is it able to reliably provide a cut-off value that rules

in or out elevated PCWP. As yet, there is no noninvasive

tool capable of reliably measuring this parameter and

a PAC or direct catheter in the LA remains the clinical

gold standard.

While TOE does not reliably estimate LAP with Doppler

indices, it does accurately measure left ventricular

volumes and ejection fraction with two-dimensional

biplane and newer three dimensional techniques.[18]

However, these are noncontinuous measurements at a

specific time point, requiring repeating with changes

in patient physiology.

LIMITATIONS

Our study includes using the lateral mitral annulus

for e’ measurements, which are different to septal e’.

In general, lateral e’ values are higher than septal,

and these values seem to correlate better with LAP

in patients with normal left ventricular function.

Averaging septal and lateral e’ values is recommended

in some guidelines, but this adds additional time and

complexity during a TOE study in the cardiac operating

room, without clear benefit.[13]

We did not specifically evaluate the E/e’ technique in

patients with different cardiac pathologies and it may be

Figure 3: Receiver operating characteristic curve for the use of

E/e’topredictpulmonarycapillarywedgepressure≥18mmHg.Youden index (maximumsumof sensitivity and specificity)represented by point where E/e’ = 10

Figure 4: Dot plot of E/e’ values in patients with pulmonary

capillary wedge pressure (PCWP) <18 mmHg and those with

PCWP≥18mmHg.Thetwosmallhorizontal linesrepresentthe medians of each group. The long dashed line represents

the optimum threshold value of E/e’

Cowie, et al.: Noninvasive estimation of left atrial pressure with TOE

314 Annals of Cardiac Anaesthesia | Jul-Sep-2015 | Vol 18 | Issue 3

ROC furthest from the line of equality (y = x). Mann–Whitney U-tests were used to compare nonnormally distributed data.

All statistical analyses were performed using Stata 12.1 (StataCorp, College Station, Texas, USA).

RESULTS

Measurement of E/e’ and PCWP was possible in all 91 patients.

A total of 38 patients underwent coronary artery bypass graft surgery, 24 valvular surgery, 17 combined coronary and valve surgery, 8 aortic surgery, and 4 others (septal defect repair and aneursymectomy).

No patients had known pulmonary arterial hypertension or pulmonary thromboembolic disease.

The patient characteristics are shown in Table 1.

The correlation between E/e’ and PCWP was modest with a Spearman rank correlation co-efficient of 0.29 (P = 0.005) [Figure 1].

The area under the ROC curve for using E/e’ to predict elevated PCWP (>12 mmHg) was 0.60 (95% confidence interval [CI]: 0.47–0.72), which is not significantly different from 0.5 which represents no predictive utility.

Figure 2 is a dot plot of the E/e' values in patients with normal PCWP (median 8.7) and those with an elevated PCWP (median 10.0). This was not significantly different (P = 0.15, Mann–Whitney U-test).

Guidelines suggest that an E/e’ <8 is associated with normal PCWPs. In our series, an E/e’ ratio of <8 had a sensitivity of 46% and specificity of 67% to detect normal PCWP.

Guidelines suggest that an E/e’ >15 is associated with elevated PCWPs. In our series, an E/e’ ratio of >15 had a sensitivity of 23% and specificity of 92% to detect an elevated PCWP (>12 mmHg).

The area under the ROC curve [Figure 3] for using E/e’ to predict elevated PCWP (≥18 mmHg) was 0.6825 (95% CI: 0.57–0.80), which is significantly different from 0.5 indicating some predictive utility. The optimum threshold value of E/e’ was 10 which

Table 1: Patient demographics with the age (years), weight (kg), height (cm), BMI (kg/m2), mitral inflow velocity (E cm/s), mitral annular velocity (e’ cm/s), ratio of mitral inflow velocity to mitral annular tissue velocity (E/e’) and PCWP (mmHg)

Age Weight Height BMI E e’ E/e’ PCWPMean 69 78.6 170.9 27 76.5 7.8 11.8 16.8SD 10.6 14 8.6 4.1 22.9 2.7 8 6.3Minimum 30 48 148 18 34 2 3.6 8Maximum 89 112 197 37.46 1.34 15 50 40

BMI: Body mass index, PCWP: Pulmonary capillary wedge pressure, SD: Standard deviation

Figure 1: Scatterplot of pulmonary capillary wedge pressure (PCWP) versus E/e’. The horizontal reference lines at 12 mmHg and 18 mmHg represent two clinically relevant cut-off values for PCWP. The two vertical dashed reference lines at 8 and 15 represent two commonly cited E/e’ cut-offs to predict PCWP over 12 mmHg

Figure 2: Dot plot of E/e’ values in patients with normal pulmonary capillary wedge pressure (PCWP) and those with an elevated PCWP (over 12 mmHg). The two horizontal dashed reference lines at 8 and 15 represent two commonly cited E/e’ cut-offs to predict PCWP over 12 mmHg

E/E’ vs. PCWP

Copyright © European Society of Anaesthesiology. Unauthorized reproduction of this article is prohibited.

CE: Swati; EJA-D-15-00267; Total nos of Pages: 6;

EJA-D-15-00267

interpercentile range, as the differences were not nor-mally distributed. All statistical analyses were performedusing Stata 12.1 (StataCorp, College Station, Texas,USA).

ResultsSimultaneous measurements of PAT and MPAP werepossible in all 98 patients. The patients’ characteristicsare summarised in Table 1. Forty patients (40.8%) hadpulmonary hypertension on the basis of a MPAP at least25 mmHg. Upper oesophageal views and appropriatealignment of the right ventricular outflow tract withpulsed wave Doppler were obtainable in 75% of patients,with a deep transgastric view required in 25% of patients.The severity of tricuspid regurgitation was graded, with93% of patients having trivial/mild tricuspid regurgitationand 7% of patients having moderate/severe tricuspidregurgitation. No patient had more than trivial/mildpulmonary regurgitation (Fig. 1).

The ROC curve for using PAT to predict pulmonaryhypertension is shown in Fig. 2. A PAT of less than

107 ms detected pulmonary hypertension with a sensi-tivity of 75% and specificity of 94.8%. The area under theROC curve was 0.87 [95% confidence interval (95% CI)0.80 to 0.95].

The relationship between PAT and MPAP was curvi-linear in nature (Fig. 3). Below a PAT of 107 ms, therelationship was relatively linear and could be describedby the equation MPAP (mmHg)¼ 77 – (0.49 x PAT).The standard error of this estimate was 6.9 mmHg. Inother words, there is a 95% chance that the true MPAPwill lie within 13.8 mmHg of the pressure predicted bythis equation. With a PAT at least 107 ms, the relation-ship was linear with approximately zero slope and couldbe described by the equation MPAP (mmHg)¼ 20.5 –(0.003 x PAT). The standard error of this estimate was5.1 mmHg. Therefore, there is a 95% chance the trueMPAP will lie within 10.2 mmHg of the pressure pre-dicted by this equation.

The PAT appeared to be a valid indicator of pulmonaryhypertension in patients with varying degrees of tricuspidregurgitation. For example, in the seven patients with

Estimating MPAP with pulmonary acceleration time 3

Table 1 Patient characteristics

Median Minimum Maximum 10th centile 90th centile

Age (years) 72 30 89 55 81Weight (kg) 77.5 48 112 62 97BMI (kg m"2) 26 18 37.5 22.3 33.1Mean PAP (mmHg) 23 11 61 15 38Systolic PAP (mmHg) 33 18 88 24 53PAT (ms) 118 50 200 85 150Cardiac output (l min"1) 4.8 2.7 8 3.1 5.8

Data are median, minimum, maximum along with the 10th and 90th centile values. PAP, pulmonary artery pressure; PAT, pulmonary artery acceleration time.

Fig. 2

1.000.750.500.250.00

0.00

0.25

0.50

Sen

siti

vity

0.75PAT = 107

1.00

1 - SpecificityArea under ROC curve = 0.8739

Receiver operating characteristic curve for the use of pulmonaryacceleration time to predict pulmonary hypertension. Youden index(maximum sum of sensitivity and specificity) represented by point wherePAT¼107 ms.

Fig. 1

Measurement of pulmonary acceleration time from an upperoesophageal view in a patient with pulmonary hypertension.PV, Pulmonary Valve Acceleration Time.

Eur J Anaesthesiol 2015; 32:1–6

Cowie B, Kluger R, Rex S, Missant C The relationship between pulmonary artery acceleration time and mean pulmonary artery pressure in patients undergoing cardiac surgery. An observational study. Eur J Anaesthesiol 2015; 32:1–6

PAT vs. MPAP

PA-catheter: perioperatively

The PA-catheter Are the alternatives equivalent?

number of subjects ranged from 79 to 61,7 and thenumber of comparative pairs of measurements rangedfrom 276 to 580.9 In most studies, an unequal number ofblood samples per subject was drawn,8–14,16,21,25 poten-tially resulting in an imbalanced statistical weight ofsubjects with exceedingly good or bad correspondencesof ScvO2 and SvO2. In addition, in some studies, bloodsamples were not drawn simultaneously, but sequen-tially during the advancement of the PA catheter,6–8,16,21

possibly causing arrhythmia31 and thus significantly al-tering hemodynamic variables, which may result in dif-ferent oxygen saturations at different sites of measure-ment.

Neither a power analysis nor an analysis of methodrepeatability was presented in previous investigations. Apower analysis has to be calculated on the basis of adifference between SvO2 and ScvO2 that is defined asclinically relevant before the study. Furthermore, this !(SvO2 " ScvO2) value serves as an a priori standard,

which is necessary to discuss the variability found in theactual study data. Evaluation of the repeatability of singlemeasurements is a very important issue because therepeatability of methods limits the amount of agreementthat is possible.27 Therefore, repeatability represents abaseline (within-method variability) to which the be-tween-method variability can be compared.

Most studies present the bias6–8,10,11,13,15–20 as well ascorrelation coefficients between the measurements.7–20,25

However, calculating bias and correlation coefficients forindividual values is not enough for evaluating the agree-ment of two different methods.26,27 Despite large differ-ences between individual values, the bias (i.e., mean of thedifferences between individual values) might be zero, andthe correlation coefficient measures proportionality, notagreement. In 1986, Bland and Altman26 recommended thecalculation of 95% limits of agreement of individual valuesfor method comparison studies. However, only 5 of 10investigations studying the equivalence of SvO2 and ScvO2 havepresented these limits of agreement since then.9–11,14,18 Fur-thermore, only 8 of 17 studies analyzed the agreement of thetrend of oxygen saturations measured at different sites inaddition to the agreement of absolute values.8–13,15,17

Fig. 2. Bland and Altman plots of the dif-ferences between mixed venous oxygensaturation (SvO2) and central venous ox-ygen saturation (ScvO2) at different timepoints. (T1) Supine position after induc-tion of anesthesia and insertion of cath-eters. (T2 and T3) During the neurosurgi-cal procedure in the sitting position, withan interval of at least 1 h between. (T4)Supine position after the neurosurgicalprocedure was completed. The brokenline indicates the mean difference (bias),and unbroken lines indicate 95% limits ofagreement (mean ! SD). Note the large95% limits of agreement.

Fig. 3. Changes in mixed venous ("SvO2) and central venousoxygen saturation ("ScvO2) between two measurements. n #182; r # 0.755; equation of the regression line: "ScvO2 # 1.084$ "SvO2 % 0.412.

Table 2. Correlation of Changes in Oxygen Saturation ofBlood Samples Taken from Different Sites

Changes in Oxygen Saturation between Different Time Points

Site n R P

PA vs. SVC!Diff!# 0% 182 0.755 $ 0.0001!Diff!# 5% 71 0.849 $ 0.0001!Diff!# 10% 23 0.930 $ 0.0001

PA vs. RA!Diff!# 0% 176 0.821 $ 0.0001!Diff!# 5% 70 0.916 $ 0.0001!Diff!# 10% 24 0.928 $ 0.0001

!Diff!% absolute value of the change in oxygen saturation between sequentialtime points; n % number of analyzed differences in oxygen saturation betweendifferent time points; P % P value; PA % pulmonary artery; R % Pearsoncorrelation coefficient; RA % right atrium; SVC % superior vena cava.

252 DUECK ET AL.

Anesthesiology, V 103, No 2, Aug 2005

number of subjects ranged from 79 to 61,7 and thenumber of comparative pairs of measurements rangedfrom 276 to 580.9 In most studies, an unequal number ofblood samples per subject was drawn,8–14,16,21,25 poten-tially resulting in an imbalanced statistical weight ofsubjects with exceedingly good or bad correspondencesof ScvO2 and SvO2. In addition, in some studies, bloodsamples were not drawn simultaneously, but sequen-tially during the advancement of the PA catheter,6–8,16,21

possibly causing arrhythmia31 and thus significantly al-tering hemodynamic variables, which may result in dif-ferent oxygen saturations at different sites of measure-ment.

Neither a power analysis nor an analysis of methodrepeatability was presented in previous investigations. Apower analysis has to be calculated on the basis of adifference between SvO2 and ScvO2 that is defined asclinically relevant before the study. Furthermore, this !(SvO2 " ScvO2) value serves as an a priori standard,

which is necessary to discuss the variability found in theactual study data. Evaluation of the repeatability of singlemeasurements is a very important issue because therepeatability of methods limits the amount of agreementthat is possible.27 Therefore, repeatability represents abaseline (within-method variability) to which the be-tween-method variability can be compared.

Most studies present the bias6–8,10,11,13,15–20 as well ascorrelation coefficients between the measurements.7–20,25

However, calculating bias and correlation coefficients forindividual values is not enough for evaluating the agree-ment of two different methods.26,27 Despite large differ-ences between individual values, the bias (i.e., mean of thedifferences between individual values) might be zero, andthe correlation coefficient measures proportionality, notagreement. In 1986, Bland and Altman26 recommended thecalculation of 95% limits of agreement of individual valuesfor method comparison studies. However, only 5 of 10investigations studying the equivalence of SvO2 and ScvO2 havepresented these limits of agreement since then.9–11,14,18 Fur-thermore, only 8 of 17 studies analyzed the agreement of thetrend of oxygen saturations measured at different sites inaddition to the agreement of absolute values.8–13,15,17

Fig. 2. Bland and Altman plots of the dif-ferences between mixed venous oxygensaturation (SvO2) and central venous ox-ygen saturation (ScvO2) at different timepoints. (T1) Supine position after induc-tion of anesthesia and insertion of cath-eters. (T2 and T3) During the neurosurgi-cal procedure in the sitting position, withan interval of at least 1 h between. (T4)Supine position after the neurosurgicalprocedure was completed. The brokenline indicates the mean difference (bias),and unbroken lines indicate 95% limits ofagreement (mean ! SD). Note the large95% limits of agreement.

Fig. 3. Changes in mixed venous ("SvO2) and central venousoxygen saturation ("ScvO2) between two measurements. n #182; r # 0.755; equation of the regression line: "ScvO2 # 1.084$ "SvO2 % 0.412.

Table 2. Correlation of Changes in Oxygen Saturation ofBlood Samples Taken from Different Sites

Changes in Oxygen Saturation between Different Time Points

Site n R P

PA vs. SVC!Diff!# 0% 182 0.755 $ 0.0001!Diff!# 5% 71 0.849 $ 0.0001!Diff!# 10% 23 0.930 $ 0.0001

PA vs. RA!Diff!# 0% 176 0.821 $ 0.0001!Diff!# 5% 70 0.916 $ 0.0001!Diff!# 10% 24 0.928 $ 0.0001

!Diff!% absolute value of the change in oxygen saturation between sequentialtime points; n % number of analyzed differences in oxygen saturation betweendifferent time points; P % P value; PA % pulmonary artery; R % Pearsoncorrelation coefficient; RA % right atrium; SVC % superior vena cava.

252 DUECK ET AL.

Anesthesiology, V 103, No 2, Aug 2005

ScvO2 vs. SvO2

Dueck MH et al. Trends but Not Individual Values of Central Venous Oxygen Saturation Agree with Mixed Venous Oxygen Saturation during Varying Hemodynamic Conditions. Anesthesiology 2005; 103:249 –57

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PA-catheter: perioperatively

PA-catheter and outcome

What/who does improve the outcome?

A diagnostic/monitoring tool cannot be expected to independently alter outcomes!

PA-catheter: perioperatively

The PA-catheter fails to improve outcome

JAMA. 2005;294:1664-1670

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Volume – Does it make a difference?PA-catheter: periopeatively

PAC outcome studies are methodologically flawed

The PA-catheter fails to improve outcome: WHY?

▪ Selection bias▪ Retrospective design▪ Inadequate blinding/randomization▪ Crossover▪ Lack of power▪ Therapeutic trespass of protocols▪ Caregiver non-compliance▪ Hawthorne effect▪ Questionable goals/endpoints Vender JS

Pulmonary Artery Catheter Utilization: The Use, Misuse, or Abuse.

JCTVA, Vol 20, 2006: pp 295-299

Volume – Does it make a difference?PA-catheter: periopeatively

The PAC fails to improve outcome: WHY? Inadequate knowledge/competency in the use of PACs

Crit Care Med 2002; 30:1197–1203

Figure 1. Pulmonary artery catheter (PAC) and pulmonary artery occlusion pressure (PAOP) items from survey.

1198 Crit Care Med 2002 Vol. 30, No. 6

The pulmonary artery occlusion pressurewaveform was interpreted accurately by only 61% of the respondents

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PA-catheter: perioperatively

The PAC fails to improve outcome: WHY? Inadequate training in the use of PACs

Journal of Critical Care (2013) 28, 857–861

PA-catheter: perioperatively

The PAC fails to improve outcome: WHY? Wrong/harmful therapeutic decisions

Anesth Analg 2011;113:994–1002

▪ prospective observational study

▪ 5065 CABG patients from 70 centers

▪ propensity score matched-pair analysis

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PA-catheter: perioperatively

The PAC fails to improve outcome: WHY? Wrong/harmful therapeutic decisions

▪ Historic cohort study using prospective data from the Western Denmark Heart Registry

▪ 6,005 cardiac surgery cases from three university hospitals

▪ Propensity matching on pre- and intraoperative variables for outcome analysis

▪ Subgroup of patients receiving inotropic therapy (n = 1,170) versus comparable nonreceivers (n = 1,170)

PA-catheter: perioperatively

The PAC fails to improve outcome: Really? Perioperative optimization

Anesth Analg 2011;112:1392–402

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PA-catheter: perioperatively

The PAC fails to improve outcome: Really? Time is organ

Volume – Does it make a difference?PA-catheter: periopeatively

▪ Not to be used routinely in low-risk patients (➪ less invasive alternatives)

▪ (Probably) not useful in patients with unimpaired cardiac function

▪ Gold-standard • in patients with (pending) acute LV/RV failure • in patients with cardiogenic shock • in patients with circulatory shock of unknown

origin (if echocardiography is not available) • for the continuous monitoring of RV-afterload

(SSLTX, ARDS with iNO-therapy, etc.) • during OPCAB-surgery and other high-risk

cardiac surgery

Conclusion:Indications

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Volume – Does it make a difference?PA-catheter: periopeatively

▪ Numbers do not cure patients! ▪ Diagnostic data have to be correctly

interpreted and converted to appropriate and timely delivery of care

▪ Failure to improve outcome is most probably due to: • inaccurate measurements and data

interpretation • inappropiate, scientifically unjustified

therapeutic interventions • delays in the timeliness of interventions • absence of a treatment to alter the outcome

of the underlying pathophysiological condition

▪ Training is indispensable!!!

Conclusion:Preventing misuse of the PAC

Vender JS Pulmonary Artery Catheter Utilization:

The Use, Misuse, or Abuse. JCTVA, Vol 20, 2006: pp 295-299