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Perioperative pulse contour cardiac output analysis in a patient with severe cardiac dysfunction.

SUMMARY

We describe a patient with severe left ventricular dysfunction simultaneously monitored with pulse contour cardiac output (PiCCO) analysis, a continuous cardiac output pulmonary artery catheter (continuous COPAC) and intraoperative transoesophageal echocardiography (TOE).

There was good agreement between cardiac output (CO) measurements obtained by the three techniques prior to cardiopulmonary bypass (CPB). Agreement of CO measurements following CPB was initially poor, but improved following recalibration of PiCCO.

PiCCO-derived global end-diastolic volume index (GEDVI) and cardiac function index (CFI), were assessed as markers of left ventricular preload and myocardial contractility, respectively. GEDVI correlated well with CO in the postoperative period.

CFI increased more than two-fold following coronary revascularization and milrinone administration, and there was also a temporal relationship between the CFI and the dose of milrinone in the first 24 hours of treatment. Global end-diastolic volume and cardiac function index may be useful additional measures of left ventricular preload and myocardial contractility in patients with severe left ventricular dysfunction.

Key Words: pulse contour cardiac output, PiCCO, cardiac function index, milrinone, global end-diastolic volume, cardiac surgery, haemodynamic monitoring

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Haemodynamic monitoring to guide inotropic and fluid therapy is an integral aspect of cardiac anaesthesia and intensive care management. This is particularly true of patients with poor left ventricular (LV) function who are undergoing cardiac surgery.

Standard pulmonary artery catheters (PAC) pro vide only intermittent analysis of CO. Continuous COPAC can provide continuous analysis of both CO and mixed venous oxygen saturations, but give pressure measures as surrogates of preload. Pulmonary artery occlusion pressure (PAOP) is affected by LV compliance (1) and is not a reliable measure of preload in patients following cardiac surgery (2).

Echocardiography gives images of global and regional LV performance and can provide CO estimation by assessment of trans-valvular Doppler flow. However, echocardiography requires specialized training and is not a continuous technique.

Pulse contour cardiac output (PiCCO) analysis provides continuous measures of CO, and has been used to monitor cardiac function during cardiac surgery, especially in cases conducted without cardiopulmonary bypass (2-8). Further, PiCCO estimates global end-diastolic volume index (GEDVI) and intra-thoracic blood volume index (ITBVI) from the transpulmonary thermodilutional cardiac output curve and these have been shown to be a better marker of LV preload than PAOP in the perioperative period of cardiac surgery (2,9). PiCCO-derived cardiac function index (CFI) provides a preload-independent measure of myocardial systolic function, and correlates well with LV fractional area of change measured by echocardiography (10).

There has been limited research examining the application of PiCCO in patients with severe LV dysfunction. We present a case report of a patient with severe left ventricular dysfunction undergoing cardiac surgery, simultaneously monitored with PiCCO, a COPAC, as well as TOE cardiography. Intraoperative data regarding cardiac output measures from the three techniques are presented, as are postoperative measure of LV preload and myocardial performance.

MATERIALS AND METHODS

The patient was enrolled in a study investigating the correlation between systolic pressure variation and PiCCO-derived stroke volume variation. Approval for this study was obtained from the Medical Centre Ethics Committee, and written informed consent was obtained from the patient.

A 5F femoral arterial catheter (PV2015L20A Pulsion Medical Systems, Munich, Germany) was inserted using the Seldinger technique, and transpulmonary thermodilution determination of CO was carried out using 15 ml of cooled normal saline. Readings were carried out in triplicate, and averaged by the device. Other readings derived from Pulse contour cardiac output were GEDVI, pulse contour cardiac output, systemic vascular resistance index (SVRI), and cardiac function index.

It is standard practice at the institution for patients with severe left ventricular dysfunction undergoing cardiac surgery to be monitored with continuous COPAC and TOE. A Swan-Ganz CCOmboV pulmonary artery catheter (Edwards Lifesciences, Irvine CA, U.S.A.) was introduced via a 9F introducer in the right internal jugular vein, and floated into the pulmonary artery under continuous pressure monitoring.

Transoesophageal echocardiography was performed by an anaesthetist experienced in the use of the technique. Two dimensional mid-oesophageal long axis four chamber views and trans-gastric short axis views were used to monitor global and regional LV performance. Using pulse wave Doppler ultrasound, the CO was calculated from the product of heart rate, cross sectional aortic valve area (obtained by triangulation), and the aortic valve velocity time integral(VTI).

Although the echocardiographer was aware of the trends in CO, he was blinded to the absolute value. Doppler CO was measured by obtaining the angle of insonnation required to achieve the greatest transvalvular peak velocity.

Intraoperative measurements of CO from PiCCO and the CCOPAC were recorded digitally every 10 minutes unless this had the potential to disrupt therapy.

Postoperative measurements of GEDVI and transpulmonary CO were obtained 4 to 6 hourly by the principal investigator, and recorded digitally for subsequent analysis. Measurements of CO and PAOP from the continuous COPAC were recorded by the attending nurse. All intraoperative and intensive care management was dictated by the attending anaesthetist and intensivist.

Statistical analyses

Correlations between GEDVI versus CO, and PAOP versus CO were analyzed using the Spearman-Rank linear regression analysis on MS Windows Statview (Abacus Concepts, Berkeley, CA, USA).

CASE STUDY

The patient was a 61-year-old male with a past medical history including oesophageal reflux and mild renal impairment (serum creatinine 0.12 mmol/l). He suffered a myocardial infarct 15 years prior to presentation, and had coronary risk factors including hypertension, dyslipidemia, a positive family history and a 100-pack-year history of smoking.

He presented to the emergency department of a nearby hospital with an anteroseptal ST-elevation myocardial infarct, and had a creatine kinase peak of 5800 IU despite thrombolysis. A coronary angiogram was performed because of post-infarction exertional angina and dyspnoea, and this demonstrated triple-vessel disease, a left ventricular end-diastolic pres sure of 23 mmHg, and severe segmental systolic dysfunction. A transthoracic echocardiogram showed a mildly dilated LV, moderate to severe segmental systolic dysfunction, with inferior wall akinesis and hypokinesis of the septum, apex and distal anterior wall. There was also mild to moderate mitral regurgitation. The estimated PAP was 42 mmHg+right atrial pressure and the LV fractional shortening was 20%.

A rest-redistribution thallium demonstrated nonviable myocardium in most of the left anterior descending (LAD) artery territory, with a moderate sized area of viable/ischemic myocardium at rest in the basal inferior and infero-lateral walls. The patient was booked for elective coronary arterial bypass graft surgery (CABGS).

After premedication with oral promethazine 25 mg, paracetamol 1g and diazepam 10 mg, invasive monitoring was performed as outlined above. Anaesthesia was induced with midazolam (3 mg) and fentanyl (total 750 ig), and endotracheal intubation was facilitated with rocuronium (50 mg). Prophylactic flucloxacillin and gentamicin were administered, and anesthesia was maintained with a fentanyl infusion and inhaled sevoflurane.

Following induction, the patient became brady-cardic (HR 42 bpm), and hypotensive (BP 97/ 59 mmHg). The mean PAP and central venous pressure (CVP) at this time were 42 mmHg, and 22 mmHg, respectively. The CO from the PAC was initially 3.6 l/min, and abruptly fell to 2.1 l/min. Two-dimensional TOE images revealed a severely dilated and hypokinetic left ventricule, with an akinetic septum and anterior wall, and mild to moderate lateral and posterior hypokinesis.

Treatment with atropine (total 1.2 mg), ephedrine (total 30 mg), and frusemide (total 240 mg, and infusion of 20 mg/h), resulted in reduced filling pressures (Figure 1) and increased cardiac output (Figure 2), before cardiopulmonary bypass (CPB).

[FIGURE 1 OMITTED]

[FIGURE 2 OMITTED]

Prior to CPB, there was good correlation between CO measures using PiCCO, continuous COPAC, and Doppler ultra sound (Figure 2). The patient underwent CABGS with left internal mammary artery grafted to the LAD, and saphenous venous grafts to the obtuse marginal and the posterior descending artery. Epicardial pacing wires were placed on the atrium and ventricle, and the patient was paced in DDD mode at 88 beats/min. Aortic cross clamp time and CPB time were 92 and 116 minutes, respectively. Concurrent with weaning from CPB, a loading dose of 50 [mu]g/kg milrinone was administered, followed by an infusion of 0.5 [mu]g/ kg/minute. Noradrenaline was commenced to maintain a mean arterial blood pressure >70 mmHg, and dose did not exceed 8 [mu]g/min. Revascularization and milrinone therapy lead to a substantial increase in CO (Figure 2). Agreement between CO from PiCCO and continuous COPAC was poor immediately after CPB, but improved after re-calibration of the PiCCO by transpulmonary thermodilution. TOE derived estimations of CO agreed better with PiCCO than continuous COPAC measures of CO (Figure2).

A TOE conducted prior to transfer to the intensive care unit (ICU) demonstrated improvement of anterior and septal contractility, although these regions remained moderately hypo kinetic. There was also recruitment of the lateral and posterior walls.

The patient was extubated 6 1/2 hours after returning to the ICU, and urinary output was enhanced with a frusemide infusion. The milrinone infusion was weaned over the next 72 hours, concurrent with the commencement of oral perindopril. The initial post operative course was complicated by bleeding requiring treatment with protamine (50 mg), 2 units of packed red blood cells, as well as 5 units each of cryoprecipitate, platelets and fresh-frozen plasma. The patient received 5,100 ml of fluid in the first 24 hours of the postoperative course, although the overall fluid balance was negative 90 ml for this period.

In the first 24 hours following surgery, there was a statistically significant correlation between the GEDVI provided by PiCCO and the PiCCO-derived transpulmonary thermodilution CO. A similar correlation was seen with the POAC and CO from the continuous COPAC (Figure 3).

The PiCCO-derived CFI was markedly depressed prior to CPB. Revascularization and intravenous milrinone resulted in a 2.2 fold increase in CFI (from 1.56 to 3.41 [min.sup.-1]). Concurrently, systemic vascular resistance fell by 40% (from 2823 to 1698 dyn.s.[cm.sup.-5].[m.sup.-2]), heart rate increased by 76% (from 50 to 88 beats/min), and GEDVI fell by 13% (from 1024 to 885 ml/[m.sup.2]).

In addition, the trend of the CFI followed the time course of milrinone weaning during the first 24 hours following surgery (Figure 4). The patient was discharged from the ICU after four days, and remained in hospital for a further four days before being discharged home.

[FIGURE 3 OMITTED]

DISCUSSION

We have described the use of PiCCO to assess perioperative haemodynamics in a patient with severe LV dysfunction undergoing coronary artery surgery, and documented for the first time the dynamic effects of milrinone on the PiCCO-derived CFI. Pulse contour cardiac output has been previously used to monitor cardiac surgical patients in the postoperative period, but the majority of patients had cardiac outputs greater than 3 l/min (3,4).

Two studies (6,8) have demonstrated a good correlation between the continuous cardiac output measurements derived from PiCCO and pulmonary artery catheter in a limited number of patients with pre-existing LV dysfunction (ejection fraction less than 45%, and CO down to 1.8 l/min). However, neither of these studies documented dynamic changes in cardiac output during the course of surgery or commented on changes in the cardiac function index and markers of left ventricular preload in the patients with severe LV dysfunction.

[FIGURE 4 OMITTED]

We found a good correlation between cardiac output estimates derived from PiCCO, continuous cardiac output catheters, and Doppler ultrasound before cardiopulmonary bypass. After cardiopulmonary bypass, PiCCO tended to underestimate cardiac output compared to continuous cardiac output catheters. This phenomenon has been attributed to changes in pulsatility of flow, and uneven rewarming following cardiopulmonary bypass (8). However, thermodilution cardiac output estimates have been found to be unreliable with very low cardiac output and may also be inaccurate following cardiopulmonary bypass (11). We found that the Doppler-derived measure of cardiac output in the immediate post bypass period agreed better with the PiCCO estimate of cardiac output than the continuous cardiac output catheter. Agreement between PiCCO and the continuous cardiac output catheter improved following calibration of the PiCCO with transpulmonary thermodilution. This is consistent with previous fi ndings that PiCCO requires recalibration after marked changes in the systemic vascular resistance (8). We feel that PiCCO may provide an additional technique for the assessment of cardiac output in low cardiac output states, but that recalibration is required after cardiopulmonary bypass.

Although the preload measures of global end-diastolic volume index and pulmonary artery occlusion pressure correlated with cardiac output (Figure 3) in the postoperative period, readings for both were substantially above the reference range. It would be desirable to apply these markers of preload in conjunction with a preload-independent measure of myocardial contractility (such as the PiCCO derived cardiac function index) to guide inotrope therapy.

We found the cardiac function index was markedly depressed before cardiopulmonary bypass, consistent with the severe LV dysfunction documented by intraoperative echocardiography. Revascularization and intravenous milrinone were associated with a 220% increase in cardiac function index and improved LV performance assessed by echocardiography, despite a 13.5% reduction in the preload measure global end-diastolic volume index. The improvement in the cardiac function index was proportionally greater than changes in systemic vascular resistance (35% decrease) and heart rate (76% increase).

These observations support the proposition that cardiac function index is a marker of LV contractility, and agree with a recent study involving 33 mechanically ventilated patients, that demonstrated a good correlation between cardiac function index and echocardiography measures of left ventricular fractional area of change (10). We found a lag between changes in milrinone dose and the effect on cardiac function index, which may be due to milrinone being slow to reach new equilibria (15). The effects of other vasoactive agents on dynamic changes in the cardiac function index need further investigation.

ACKNOWLEDGEMENTS

We would like to acknowledge Dr Moritoki Egi for his assistance in statistical analysis.

Accepted for publication on August 8, 2005.

REFERENCES

(1.) Rocca GD, Costa MG. Preload indexes in thoracic anesthesia. Curr Opin Anaesthesiol 2003; 16:69-73.

(2.) Sakka SG, Meier-Hellmann A. Evaluation of cardiac output and cardiac preload. In: Yearbook of intensive care and emergency medicine 2000, Ed J.L. Vincent. Springer Verlag: 671-679.

(3.) Godje O, Hoke K, Goetz A et al. Reliability of a new algorithm for continuous cardiac output determination by pulse-contour analysis during hemodynamic instability. Crit Care Med 2002; 30:52-58.

(4.) Zollner C, Haller M, Weis M, Morstedt K et al. Beat-to-beat measurement of cardiac output by intravascular pulse contour analysis: a prospective criterion standard study in patients after cardiac surgery. J Cardiothorac Vasc Anesth 2000; 14:125-129.

(5.) Godje O, Thiel C, Lamm P et al. Less invasive, continuous hemodynamic monitoring during minimally invasive coronary surgery. Ann Thorac Surg 1990; 68:1532-1536.

(6.) Rauch H, Muller M, Bauer H et al. Pulse contour analysis versus thermodilution in cardiac surgery patients. Acta Anaesthesiol Scand 2002; 46:424-429.

(7.) Buhre W, Weyland A, Kazmaier S et al. Comparison of cardiac output assessed by pulse-contour analysis and thermodilution in patients undergoing minimally invasive direct coronary artery bypass grafting. J Cardiothorac Vasc Anesth 1999; 13:437-440.

(8.) Rodig G, Prasser C, Keyl C et al. Continuous cardiac output measurement: pulse contour analysis vs thermodilution technique in cardiac surgical patients. Br J Anaesth 1999; 82:525-530.

(9.) Godje O, Peyerl M, Seebauer T et al. Central venous pressure, pulmonary capillary wedge pressure and intrathoracic blood volumes as preload indicators in cardiac surgery patients. Eur J Cardiothorac Surg 1998; 13:533-540.

(10.) Combes A, Berneau J-B, Luyt C-E, Trouillet J-L. Estimation of left ventricular systolic function by single transpulmonary thermodilution. Intensive Care Med 2004; 30:1377-1383.

(11.) van Grondelle A, Ditchey RV, Groves BM et al. Thermodilution method overestimates low cardiac output in humans. Am J Physiol 1983; 245:H690-H692.

(12.) Sakka SG, Ruhl CC, Pfeiffer et al. Assessment of cardiac preload and extravascular lung water by single transpulmonary thermodilution. Intensive Care Med 2000; 26:180-187.

(13.) Thomas B. Monitoring of cardiac output by pulse contour method. Acta Anaesth Belg 1978; 29:259-270.

(14.) Prielipp RC, MacGregor DA, Butterworth JF et al. Pharmocodynamics and pharmacokinetic of milrinone administration to increase oxygen delivery in critically ill patients. Chest 1996; 109:1291-1201.

D. JONES *, D. STORY ([dagger]), P. PEYTON ([double dagger]), R. BELLOMO ([section])

Department of Intensive Care, The Alfred Hospital, Departments of Anaesthesia and Surgery, Austin Hospital, Departments of Intensive Care and Medicine, Austin Hospital, Melbourne, Victoria

* B.Sc., (Hons) M.B., B.S., Intensive Care Registar.

([dagger]) M.B., B.S. (Hons) B. Med. Sci. (Hons) F.A.N.Z.C.A. M.D., Associate Professor.

([double dagger]) M.B., B.S., F.A.N.Z.C.A. M.D., Staff Anaesthetist.

([section]) M.B., B.S. F.R.A.C.P., F.J.F.I.C.M., Professor

Address for reprints: A/Prof. David A. Story, Department of Anaesthesia, Austin Health, Studley Rd, Heidelberg, Victoria 3084, Australia.
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Author:Jones, D.; Story, D.; Peyton, P.; Bellomo, R.
Publication:Anaesthesia and Intensive Care
Date:Feb 1, 2006
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