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Revista Brasileira de Anestesiologia

Print version ISSN 0034-7094

Rev. Bras. Anestesiol. vol.54 no.5 Campinas Sept./Oct. 2004

http://dx.doi.org/10.1590/S0034-70942004000500002 

SCIENTIFIC ARTICLE

 

Correlation between end-tidal carbon dioxide levels and cardiac output during cardiac surgery with cardiopulmonary bypass*

 

Evaluación de la correlación entre el dióxido de carbono expirado y el débito cardíaco en pacientes sometidos a la cirugía cardíaca con circulación extracorpórea

 

 

Karina Takesaki Miyaji, M.D.I; Roberto Iara Buscati, M.D.II; Antônio José Arraiz Rodriguez, M.D.II; Luciano Brandão Machado, TSA, M.D.III; Luiz Marcelo Sá Malbouisson, TSA, M.D.IV; Maria José Carvalho Carmona, TSA, M.D.V

IGraduanda do 6º ano da FMUSP. Bolsista de Iniciação Científica da FAPESP (Processo 99/06338-4)
IIAnestesiologista do Curso de Especialização em Anestesiologia e Pós-Operatório de Cirurgia Cardiovascular e Torácica do Instituto do Coração do HC-FMUSP
IIIPós-Graduando da Disciplina de Anestesiologia da FMUSP
IVDoutor pela Disciplina de Anestesiologia da FMUSP. Médico Assistente do Serviço de Anestesiologia do InCor-HCFMUSP
VProfessora Doutora da Disciplina de Anestesiologia da FMUSP. Médica Supervisora do Serviço de Anestesiologia e Terapia Intensiva Cirúrgica do InCor, HC-FMUSP

Correspondence

 

 


SUMMARY

BACKGROUND AND OBJECTIVES: End-tidal carbon dioxide (PETCO2) not only reflects pulmonary ventilation but also carbon dioxide production (metabolism) and pulmonary blood supply (circulation). During constant metabolism and ventilation, PETCO2 reflects pulmonary blood perfusion, thus cardiac output (CO). This study aimed at evaluating the correlation between PETCO2 levels and CO during cardiac surgery with cardiopulmonary bypass (CPB).
METHODS: Participated in this study 25 patients submitted to coronary artery bypass grafting (CABG) with CPB. End-tidal CO2 monitoring started after tracheal intubation. Cardiac output was determined by thermodilution with pulmonary artery catheter (Swan-Ganz). Carbon dioxide partial blood pressure (PaCO2) was obtained with arterial blood gases analysis. Studied parameters were evaluated in the following moments: immediately after general anesthesia induction, before cardiopulmonary bypass, at cardiopulmonary bypass completion and at surgery completion.
RESULTS: Statistical analysis has not shown correlation between PETCO2 and CO2, or between PETCO2-PaCO2 gradient (Ga-eCO2) and CO. There has been correlation between PETCO2, Ga-eCO2 and CO values variation as compared to baseline values before CPB, with loss of correlation after CPB until surgery completion.
CONCLUSIONS: In this study, where patients submitted to cardiac surgery with CPB were evaluated, ventilation/perfusion changes throughout the procedure might have been the factors determining decreased correlation between cardiac output and end tidal CO2.

Key Words: MONITORIZATION: end-tidal carbon dioxide, cardiac output; SURGERY, Cardiac


RESUMEN

JUSTIFICATIVA Y OBJETIVOS: El CO2 expirado (PETCO2) refleja, además de la ventilación pulmonar (eliminación), la producción de dióxido de carbono (metabolismo) y el flujo sanguíneo pulmonar (circulación). Cuando el metabolismo y la ventilación son constantes, el CO2 expirado refleja el flujo sanguíneo pulmonar y, de esta forma, el débito cardíaco (DC). Este estudio tiene como objetivo la evaluación de la correlación entre el dióxido de carbono expirado (PETCO2) y el débito cardíaco en pacientes sometidos a la cirugía cardíaca con circulación extracorpórea (CEC).
MÉTODO: Fueron estudiados 25 pacientes sometidos a la cirugía de revascularización miocárdica con CEC. Después de la intubación traqueal tuvo inicio la monitorización de la PETCO2. La determinación del débito cardíaco (DC) fue hecha por método de termodiluición con el uso de catéter de Swan-Ganz y la PaCO2 fue evaluada a través de gasometría arterial. Los parámetros del estudio fueron evaluados en cuatro momentos: luego después de la inducción de la anestesia general; antes de la circulación extracorpórea, al término de la circulación extracorpórea y al final de la cirugía.
RESULTADOS: El teste estadístico no demostró una correlación entre el CO2 expirado y el DC, así como el gradiente de dióxido de carbono arterial y expirado (Ga-eCO2) y el DC. Fue encontrada correlación entre la variación de los valores de la PETCO2, Ga-eCO2 y DC en relación al basal antes de la CEC con pérdida de la correlación después de la CEC hasta el final de la cirugía.
CONCLUSIONES: En este estudio, donde se evalúan pacientes sometidos a cirugía cardíaca con CEC, las alteraciones de relación ventilación/perfusión ocurridas a lo largo del procedimiento son, probablemente, los factores determinantes de la diminución de la correlación entre el débito cardíaco y el valor de dióxido de carbono expirado.


 

 

INTRODUCTION

End-tidal carbon dioxide (PETCO2) not only reflects pulmonary ventilation but also carbon dioxide production (metabolism) and pulmonary blood supply (circulation). During constant metabolism and ventilation, PETCO2 reflects pulmonary blood perfusion, thus cardiac output (CO).

When Fick’s equation is applied to carbon dioxide, the difference between mixed venous blood CO2 content and the arterial blood CO2 content is equal to the ratio between CO2 production and cardiac output 1, and this equation may be applied to CO2 to estimate cardiac output 2. There are already some commercially available monitoring equipment to indirectly and noninvasively analyze cardiac output as from end tidal CO2 evaluation 3-5.

This study aimed at evaluating the correlation between PETCO2 levels and CO during cardiac surgery with cardiopulmonary bypass (CPB).

 

METHODS

After the Scientific Committee, Instituto do Coração (INCOR) and Medical Ethics Committee, Hospital das Clinicas, Faculdade de Medicina, USP approval, participated in this study 25 patients submitted to coronary artery bypass grafting with cardiopulmonary bypass and monitoring through pulmonary artery catheter. Surgical risk was evaluated according to Higgin’s criteria 6.

Patients were premedicated with oral 0.1 to 0.2 mg.kg-1 midazolam 30 minutes before anesthetic induction until the maximum dose of 15 mg. At operating room admission, patients were monitored with continuous ECG with 5 electrodes evaluating DII and V5 leads and pulse oximetry, and were submitted to peripheral venoclysis with 16G catheter. Invasive blood pressure was monitored through radial artery puncture with 20G catheter. After oxygenation, general anesthesia was induced with fentanyl (20 a 30 µg.kg-1) and midazolam (0.1 a 0.3 mg.kg-1), followed by muscle relaxation with pancuronium (0.1 a 0.2 mg.kg-1).

Manual ventilation under mask was installed and tracheal intubation was achieved with a tube of adequate size, being then installed mechanically controlled ventilation with tidal volume of 8 mL.kg-1, respiratory rate of 12 incursions per minute, I:E ratio = 1:2 and FiO2 = 0.6 (oxygen and air). PETCO2 monitoring has started after tracheal intubation by the sidestream method, in addition to nasopharyngeal temperature and diuresis monitoring. Anesthesia was maintained with fractional fentanyl, midazolam and pancuronium doses associated to variable inhalational isoflurane concentrations.

Hemodynamic parameters were further monitored by 7F Swan-Ganz catheter introduction through right internal jugular vein puncture to monitor pulmonary artery pressure (PAP), systolic, diastolic and mean blood pressure, right atrium pressure (RAP), pulmonary capillary wedge pressure (PCWP), and cardiac output (CO) measured by thermodilution.

Three consecutive measures were taken and their mean value has been used. Cardiac index was obtained by the ratio between CO and patient’s body surface. PaCO2 was evaluated through arterial blood gases analysis. Oxygen alveolar-arterial gradient (GA-aO2) and pulmonary shunt were calculated from arterial and mixed venous blood gases analysis data.

All patients were submitted to cardiopulmonary bypass with membrane oxygenator (Braile, Brazil) with non-pulsatile flow and under moderate hypothermia (minimum temperature 32 oC). Vasodilators and/or inotropic drugs were introduced at cardiopulmonary bypass weaning in variable doses, according to clinical indication.

End tidal CO2 (PETCO2), partial arterial CO2 pressure (PaCO2), CO2 arterial-expired gradient (GA-eCO2), cardiac index, pulmonary shunt and oxygen alveolar-arterial gradient (GA-aO2) were evaluated in the following moments:

• Immediately after general anesthetic induction;
• Immediately before cardiopulmonary bypass;
• At cardiopulmonary bypass weaning;
• At surgery completion.

Analysis of Variance for repeated measures was used to evaluate end tidal CO2 (PETCO2) partial arterial CO2 pressure (PaCO2), CO2 arterial-expired gradient, cardiac index, pulmonary shunt and oxygen alveolar-arterial gradient, considering significant p < 0.05. Spearman correlation test was used to correlate CO2 arterial-expired gradient and cardiac index, and PETCO2 and cardiac index, considering significant p < 0.05. The same statistical test has also evaluated the correlation between PETCO2 variation (as compared to baseline values after anesthetic induction) and arterial-expired CO2 gradient and cardiac index.

 

RESULTS

From 25 studied patients, 20 were male and 5 females. Demographics data and CPB length are shown in table I.

Surgical risk classification 6 has shown 6 patients at minimum risk, 6 patients at low risk, 6 patients at moderate risk, 3 patients at high risk and 4 patients at extreme risk.

There have been significant changes in cardiac output (p < 0.001), pulmonary shunt (p < 0.001) and oxygen alveolar-arterial gradient (p = 0.038) throughout surgery. Results (Mean ± SD) of cardiac output, cardiac index, PETCO2, PaCO2, CO2 arterial-expired gradient, pulmonary shunt and oxygen alveolar-arterial gradient in different studied moments are shown in table II.

Figure 1 shows end tidal carbon dioxide (PETCO2) and cardiac index variations throughout the study.

Correlation between cardiac index and arterial - end tidal carbon dioxide arterial-expired gradient, PETCO2 and PaCO2 evaluated by Spearman correlation test are shown in table III. Correlation of variation (as compared to baseline) of cardiac index and carbon dioxide arterial-expired gradient, PETCO2 and PaCO2 are shown in table IV.

 

DISCUSSION

Carbon dioxide (CO2) is a product of organic cells metabolism, which is uptaken and transported by venous circulation to the lungs where it is excreted by alveolocapillary membrane 7. CO2 content is then exhaled and in normal ventilation/perfusion conditions (respiratory coefficient - RC = 0.8) end tidal CO2 (PETCO2) is an approximate reflex of partial arterial CO2 pressure (PaCO2). In these conditions, venous blood entering pulmonary circulation has PvO2 of approximately 46 mmHg and, for being an extremely diffusible gas, it is rapidly transferred to the alveoli. When this blood leaves exchange respiratory unit, there is a balance between CO2 concentrations in pulmonary capillary edge and alveoli.

In normal patients, the difference between PaCO2 and PETCO2 is 3 to 6 mmHg 8,9, which tends to increase with ventilation/perfusion ratio changes 3,10, the major example of which is the so-called dead space ventilation when there are's ventilated and not perfused alveoli, leading to increased PaCO2 and PETCO2 gradient.

The increasing importance of PETCO2 evaluation during cardiopulmonary resuscitation has been stressed 7,11. A rapid (in 1-2 minutes) and progressive decrease in capnography values and height is observed during acute pulmonary circulation or ventilation changes, such as cardiac arrest, pulmonary thromboembolism an sudden hypotension, conditions impairing pulmonary blood supply. Capnography may be a guide to optimize therapy during cardiopulmonary resuscitation 12,13 and to evaluate the quality of cardiac massage 13 or of post-resuscitation prognosis 14,15.

A previous study has shown direct correlation between end tidal CO2 (PETCO2) changes and cardiac output measured by thermodilution 16. This study has observed direct correlation between PETCO2 and cardiac output at CPB weaning. This same study has invariably correlated PETCO2 above 30 mmHg to cardiac output above 4 L.min-1 16. However, for higher cardiac output values, PETCO2 is constant or suffers minor changes, while pulmonary artery blood supply continues to increase. It has also been observed that PETCO2 may be poorly accurate when associated to chronic low cardiac output situations 17.

Initially, blood flow decrease corresponds to PETCO2 decrease until baseline values, beyond which it does not significantly change in spite of progressive pulmonary artery blood supply decrease. The explanation proposed is that persistent blood flow decrease would result in higher carbon dioxide release by tissues, resulting in gradual PETCO2 increase 18.

In our study, although the highest correlation between variation (as compared to baseline) of cardiac index and arterial-end tidal CO2 gradient, PETCO2 and PaCO2 has been observed before cardiopulmonary bypass, this result might have been influenced by the fact that cardiac patients often present chronically decreased cardiac output.

The evaluation of patients at different surgical risks and with different preoperative ventricular function may have contributed for the non-observation of correlations between PETCO2, PaCO2, CO2 and arterial-end tidal gradient with cardiac output at initial evaluation after anesthetic induction. Still, differences found in cardiac index and respiratory variables ratio in both moments (pre-CPB and after anesthetic induction) may have been at least partially due to increased myocardial contractility (inotropics used before CPB) or systemic vasodilation in general following loss of consciousness before CPB.

Pulmonary function changes observed during cardiac surgery with cardiopulmonary bypass depend on several factors, such as preoperative pulmonary function, surgery type and length, CPB length 8,10, surgical manipulation intensity and number of pleural drains. General anesthesia favors atelectasis which directly influences pulmonary function, changing pulmonary ventilation/perfusion ratio, increasing pulmonary shunt and potentially interfering with CO2 elimination 3.

Generalized systemic inflammatory response activation during CPB may cause edema, decreased ventricular contractility, increased patency and vascular resistance changes in different organs. There is increase in extravascular pulmonary water 19 with alveolar filling by inflammatory cells which leads to pulmonary surfactant inactivation and collapsing of some areas, with changes in pulmonary ventilation/perfusion ratio, decreased patency and increased respiratory work.

CO2 production depends on body metabolism which may be changed by anesthesia and body temperature, this latter also interfering with blood gas solubility 16,20. In addition, microvasculature barocompression may be observed in patients submitted to cardiac surgery 18, as well as potential embolism by microparticles which increases physiological dead space 8. Since CO2 elimination depends on alveolar ventilation, these dead space area decrease ventilation efficiency further changing ventilation/perfusion ratio. Such dead space changes may explain PETCO2 values above PaCO2 values observed in some cases.

Arterial-end tidal CO2 gradient (Ga-PETCO2) is influenced by ventilation and perfusion unbalance and gas composition of alveoli with low ventilation/perfusion ratio, which present CO2 pressure similar to venous value, interfering with Ga-PETCO2 even without influence of cardiac output. Alveolar factor is also very important for the intervention in respiratory mechanics and physiology to which cardiac surgery with CPB patients are submitted, with moments of pulmonary expansion interruption followed by positive pressure inflation, which contributes to increase ventilation/perfusion ratio disorder.

Added to this, there is blood volume manipulation by drugs and volume replacement, contributing to already mentioned disorders and decreased gases exchange by decreased blood components, among them hemoglobin. As a consequence, there will be Ga-PETCO2 increase at surgery completion, in spite of cardiac output values improvement with coronary artery bypass grafting.

So, patients submitted to cardiac surgery with cardiopulmonary bypass develop ventilation/perfusion ratio changes, with areas of atelectasis and pulmonary shunt 9,19. Such pulmonary conditions may change carbon dioxide elimination and, as a consequence, arterial- end tidal CO2 gradient 21.

In our study the changes in pulmonary function after CPB could had contributed with the loss of correlation between end tidal CO2 and cardiac output.

Based on noninvasive cardiac output evaluation through pulmonary blood supply evaluation with capnography, there are currently available devices made up of the union of a major flow capnographer, a variable hole pneumotacographer, a signal processor and an analysis software which allow the evaluation of alveolar dead space, of real minute ventilation and CO2 production through the study of this gas spirography 5,7. This tool may enhance the application of capnography through the use of two end tidal CO2 curve variables and the inference of cardiac output values in a noninvasive and continuous way 4. Still under evaluation, this method may have potential to be incorporated to modern monitoring armamentarium for critically ill patients 7,22.

In our study, where patients submitted to cardiac surgery with cardiopulmonary bypass were evaluated, the ventilation/perfusion ratio changes throughout the procedure, as confirmed by significant pulmonary shunt and oxygen alveolar-arterial gradient changes seen during surgery, are possibly the factors determining decreased correlation between cardiac output and arterial-end tidal CO2 gradient.

 

ACKNOWLEDGEMENTS

We acknowledge Fundação de Apoio à Pesquisa do Estado de São Paulo (Research Support Foundation of the State of São Paulo) and Prof. Dr. José Otávio Costa Auler Jr, Head Professor of Anesthesiology, Faculdade de Medicina, USP, and Director of the Anesthesiology Department, INCOR-HCFMUSP for the incentive during this research.

 

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Correspondence to
Dra. Maria José Carvalho Carmona
Rua Rodésia, 161/82 Vila Madalena
05435-020 São Paulo, Brazil
E-mail: maria.carmona@incor.usp.br

Submitted for publication August 4, 2003
Accepted for publication January 5, 2004

 

 

* Received from Faculdade de Medicina da Universidade de São Paulo, SP