**3.1 Monitoring and anesthesia**

Any operative procedure involving large vessels entail the risk of developing hemodynamic instability, mainly due to massive bleeding. Moreover, a number of specific conditions have to be taken into consideration, including coexisting multisystemic diseases, nonphysiological conditions associated with CPB and deep HCCA. In light of these concerns, patients undergoing cavo-atrial thrombectomy require extensive monitoring to provide early warning of conditions that may lead to potentially life-threatening states.

#### **3.1.1 Monitoring**

An intraoperative electrocardiogram, using the five-leads technique, is the standard monitoring procedure always recommended during surgery and anesthesia. In this setting, it is useful for the diagnosis of both myocardial ischemia (DII – V5 identify 90% of ischemic episodes) and dysrhythmias.

Intravascular pressure measurements represent the standard technique during this type of surgery. Arterial pressure is usually measured by placing a catheter in a peripheral (radial, ulnar, brachial) or central (femoral) artery. Direct arterial pressure measurement allows monitoring during the pre-CPB stage and nonpulsatile ECC. Moreover, during the post-CPB/HCCA period, patients are usually hemodynamically unstable, and close surveillance of arterial blood pressure, other than with blood-gas analysis, is of primary importance.

A central venous line (internal jugular, subclavian) for pressure monitoring (central venous pressure [CVP]) is influenced by circulating blood volume, venous tone and capacitance, and right ventricular function; therefore, a number of pieces of information can be obtained from the CVP. A central venous catheter (3 lumens, 7-8.5 Fr) can be used for both pressure measurement and inotropic-vasoactive drug administration. Central venous lines can also be used for pulmonary artery catheter (PAC) positioning if the patient's comorbidities suggest the monitoring of pulmonary artery pressures, the measurement of cardiac output and mixed venous oxygen saturation. Central venous cannulation should be performed under ultrasound guidance because up to 30% of patients have some abnormalities of the jugular vein anatomy (Carid et al., 1988; Bevilacqua et al., 2005).

Hemodynamic monitoring is completed with transesophageal echocardiography, which has gained widespread use in cardiac operating rooms (where this intervention for cavo-atrial invasion is usually performed) because it provides a great deal of information about the heart's global performance during systole and diastole, the valve function and cardiac volume loads, as well as morphologic details on thrombotic cardiac invasion from the inferior vena cava.

Hypothermic Cardiac Arrest to Remove Right Atrial Thrombi Due to Abdominal Malignancies 157

Renal function. Acute kidney injury (AKI) is one of the well-known complications occurring during CPB that has significant implications for both short- and long-term outcomes. The incidence of acute renal failure rages from 20 to 30% of patients (Kumar & Suneja, 2004). Pre-operative renal function is one of the most important factors related to post-CPB AKI. The major risk factors for AKI after CPB include advanced age, preexisting kidney disease, diabetes mellitus, chronic obstructive pulmonary disease, CPB duration, emergency surgery, female sex, left ventricle ejection fraction <40%, and hemodilution on CPB. Hemolysis always occurs during CPB, and serum hemoglobin levels rise; therefore, urine output should be maintained to avoid tubular damage. Diuretic therapies (mannitol is used routinely in CPB priming) are also useful for eliminating the hemodilution induced with the onset of CPB. As a consequence, urinary catheter positioning and urine output are the best

These patients usually require a smooth induction because wide modifications in vascular tone, myocardial contractility, and reductions in venous returns due to increased intrathoracic pressures under mechanical ventilation may worsen the organ and tissue perfusion. Midazolam or etomidate, in association with an opioid (remifentanil, fentanyl), are useful drugs for anesthesia induction; propofol and/or sevoflurane or desflurane can be used for anesthesia maintenance, and a nondepolarizing muscle relaxant should be administered for

**Hypnotics** Propofol 1-1.5 mg/Kg

**Opioids** Fentanyl 3-10 mcg/Kg

**Muscle relaxants** Cisatracurium 0.07- 0.1 mg/Kg

Cardiopulmonary bypass permits blood to bypass the heart and lungs (Fig. 6).

The choice of drug for anesthesia induction and maintenance depends on the patient's general conditions and, in particular, his/her heart, renal, and liver function. In addition, antibiotic prophylaxis should be administered at least 30 minutes before skin incision.

**3.2 Cardiopulmonary bypass, deep hypothermic circulatory arrest and neuroprotection** 

Venous blood is drained by gravity into an oxygenator (artificial lung), and a pump injects it, after oxygenation and removal of CO2, into a great artery (aorta, subclavian, femoral artery). Adequate anticoagulation is necessary during the CPB period, and an activated clotting time longer than 420-480 seconds is usually considered safe (the optimal target of

Table 1. Hypnotics, opioids, and muscle relaxants (induction doses)

**Drug Induction dose** 

Thiopental 3-4 mg/Kg Etomidate 0.2-0.3 mg/Kg Midazolam 0.1-0.2 mg/Kg

Sufentanyl 0.5-1 mcg/Kg

Vecuronium 0.07- 0.1 mg/Kg Rocuronium 0.6 mg/Kg

Remifentanil 0.1-0.75 mcg/Kg/min

monitoring systems for renal function evaluation.

the duration of the intervention (Table 1).

**3.2.1 Cardiopulmonary bypass** 

**3.1.2 Anesthesia** 

Temperature monitoring. Assessment of accurate central temperature is of primary importance in this setting. The core temperature (vital organ temperature) can be measured by means of a PAC thermistor, nasopharyngeal probe (provides accurate measurement of brain temperature during CPB and HCCA), bladder probe (it may be inaccurate when renal blood flow and urine output are decreased), CPB arterial line (temperature of the heat exchanger), CPB venous line (reflects core temperature well during CPB, when no active cooling or warming is ongoing), or rectal probe (when the tip of the probe rests in stool, the measurement may be imprecise) (FIG. 4 & 5).

Fig. 4. Monitoring. (NIRS, near infrared spectroscopy; CVC, central venous catheter).

Fig. 5. Near infrared spectroscopy. (DHCA Deep Hypothermic Circulatory Arrest; CPB, cardiopulmonary bypass).

Renal function. Acute kidney injury (AKI) is one of the well-known complications occurring during CPB that has significant implications for both short- and long-term outcomes. The incidence of acute renal failure rages from 20 to 30% of patients (Kumar & Suneja, 2004). Pre-operative renal function is one of the most important factors related to post-CPB AKI. The major risk factors for AKI after CPB include advanced age, preexisting kidney disease, diabetes mellitus, chronic obstructive pulmonary disease, CPB duration, emergency surgery, female sex, left ventricle ejection fraction <40%, and hemodilution on CPB. Hemolysis always occurs during CPB, and serum hemoglobin levels rise; therefore, urine output should be maintained to avoid tubular damage. Diuretic therapies (mannitol is used routinely in CPB priming) are also useful for eliminating the hemodilution induced with the onset of CPB. As a consequence, urinary catheter positioning and urine output are the best monitoring systems for renal function evaluation.

## **3.1.2 Anesthesia**

156 Front Lines of Thoracic Surgery

Temperature monitoring. Assessment of accurate central temperature is of primary importance in this setting. The core temperature (vital organ temperature) can be measured by means of a PAC thermistor, nasopharyngeal probe (provides accurate measurement of brain temperature during CPB and HCCA), bladder probe (it may be inaccurate when renal blood flow and urine output are decreased), CPB arterial line (temperature of the heat exchanger), CPB venous line (reflects core temperature well during CPB, when no active cooling or warming is ongoing), or rectal probe (when the tip of the probe rests in stool, the

Fig. 4. Monitoring. (NIRS, near infrared spectroscopy; CVC, central venous catheter).

Fig. 5. Near infrared spectroscopy. (DHCA Deep Hypothermic Circulatory Arrest; CPB,

cardiopulmonary bypass).

measurement may be imprecise) (FIG. 4 & 5).

These patients usually require a smooth induction because wide modifications in vascular tone, myocardial contractility, and reductions in venous returns due to increased intrathoracic pressures under mechanical ventilation may worsen the organ and tissue perfusion. Midazolam or etomidate, in association with an opioid (remifentanil, fentanyl), are useful drugs for anesthesia induction; propofol and/or sevoflurane or desflurane can be used for anesthesia maintenance, and a nondepolarizing muscle relaxant should be administered for the duration of the intervention (Table 1).


Table 1. Hypnotics, opioids, and muscle relaxants (induction doses)

The choice of drug for anesthesia induction and maintenance depends on the patient's general conditions and, in particular, his/her heart, renal, and liver function. In addition, antibiotic prophylaxis should be administered at least 30 minutes before skin incision.

#### **3.2 Cardiopulmonary bypass, deep hypothermic circulatory arrest and neuroprotection 3.2.1 Cardiopulmonary bypass**

Cardiopulmonary bypass permits blood to bypass the heart and lungs (Fig. 6).

Venous blood is drained by gravity into an oxygenator (artificial lung), and a pump injects it, after oxygenation and removal of CO2, into a great artery (aorta, subclavian, femoral artery). Adequate anticoagulation is necessary during the CPB period, and an activated clotting time longer than 420-480 seconds is usually considered safe (the optimal target of

Hypothermic Cardiac Arrest to Remove Right Atrial Thrombi Due to Abdominal Malignancies 159

approximately 70 mm Hg. During CPB and HCCA, the loss of flow auto regulation (<20°C and for several hours after HCCA) is still debated, but pressure levels as low as 30-40 mm Hg are considered safe values (Croughwell et al., 1992). Despite several techniques for cerebral protection have been developed, central nervous system dysfunction associated with cardiac surgery is very frequent, with an incidence that depends on the type of intervention (up to 65%) (Arrowsmith et al., 2000). Apart from ischemic events, cognitive dysfunction has been observed within the first postoperative week in more than 80% of patients undergoing coronary artery bypass grafting under CPB, and at five years after surgery, some degree of neuropsychological dysfunction can be observed in up to 35% of patients (Arrowsmith et al., 2000). A number of risk factors have been identified, and they can be divided into patient-related and technology-related factors. The patient-related factors are age>70 year old, cerebrovascular disease, aortic atherosclerosis, and diabetes mellitus; the technology-related factors are open chamber procedures, CPB duration >90 minutes, use of bubble rather than membrane oxygenators, and circulatory arrest. Apart from open chamber procedures, all the other risk factors have to be taken into consideration

After CPB has been started, the temporary interruption of cerebral blood flow is a necessary condition to remove the thrombus from the vena cava and, in such cases, from the right atrium. Interruption of cerebral blood flow has been associated with a high incidence of neurologic injury because the brain is susceptible to ischemic injury within minutes of the onset of circulatory arrest as a result of its high metabolic rate and limited reserves (Harrington et al., 2003). The physiologic basis for hypothermia as a neuroprotective strategy is its ability to reduce the cerebral oxygen metabolic rate and the accumulation of toxic metabolites. In adults, a decrease in core temperature leads to a reduction in the cerebral metabolic rate that increases in ischemic tolerance from 2-3 minutes (normothermia) to 20-34 minutes (17°C) (Reich et al., 1999). However, the optimal level of hypothermia is still debated. Studies based on electroencephalographic monitoring have shown that a median nasopharyngeal temperature of 18°C allows electrocortical silence (Stecker et al., 2001). Today, based on the results of several studies, HCCA at 18°C is considered safe for durations of up to 40 minutes (Griepp, 2001). It has been also suggested that hypothermia provides neurological protection through mechanisms other than the cerebral metabolic rate. In the face of an incomplete understanding of the involved mechanisms, hypothermia remains the most efficacious intervention for preventing ischemic brain injuries. In addition to systemic hypothermia, topical cooling, obtained by packing the head with ice, can be used to prevent passive warming of the brain during circulatory arrest, but consensus on this adjunctive strategy is still lacking because rewarming during circulatory arrest could be negligible (Reich et al., 1999). After the targeted core temperature has been reached, the pump is turned off, allowing brain protection during surgery performed in a bloodless field. HCCA has several potential adverse consequences. Achieving the target temperature prolongs the duration of the CPB period, thus amplifying problems related to CPB (loss of pulsatile flow, injury to blood elements, risk of embolization, coagulation system derangements, etc.). Re-warming increases the cerebral metabolic rate and has the potential to make the brain vulnerable to ischemic injury. With the aim of limiting brain injuries, a short period (10 minutes) of hypothermic

when cavo-atrial thrombectomy with CPB and HCCA is performed.

**3.2.2 Deep hypothermic circulatory arrest** 

Fig. 6. Cardiopulmonary bypass.

ACT is still debated). Anticoagulation is obtained with heparin 300-400 U/kg, and supplemental doses of 5000 U can be administered if necessary. Use of heparin-coated circuits does not eliminate the need for heparin. The pump flow has to be set at values that guarantee an adequate oxygen delivery. "Normal" pump flow is considered to be 2.4 l/min/m2, although recent studies have demonstrated that a redistribution of flow toward organs occurs during CPB in both normothermia and hypothermia (Slater et al., 2001). Muscle flow is significantly reduced during CPB, and if flow is reduced, splacnic, renal and cerebral flow decrease as well, in that order. During CPB, blood pressure depends on pump flow, total arterial impedance and haematocrit. During CPB, blood pressure is less important in determining global perfusion if pump flow is adequate, but minimal values of blood pressure may be significant in providing specific regional flows; therefore, during mild to moderate hypothermia (30-34°C), the blood pressure is generally maintained at approximately 70 mm Hg. During CPB and HCCA, the loss of flow auto regulation (<20°C and for several hours after HCCA) is still debated, but pressure levels as low as 30-40 mm Hg are considered safe values (Croughwell et al., 1992). Despite several techniques for cerebral protection have been developed, central nervous system dysfunction associated with cardiac surgery is very frequent, with an incidence that depends on the type of intervention (up to 65%) (Arrowsmith et al., 2000). Apart from ischemic events, cognitive dysfunction has been observed within the first postoperative week in more than 80% of patients undergoing coronary artery bypass grafting under CPB, and at five years after surgery, some degree of neuropsychological dysfunction can be observed in up to 35% of patients (Arrowsmith et al., 2000). A number of risk factors have been identified, and they can be divided into patient-related and technology-related factors. The patient-related factors are age>70 year old, cerebrovascular disease, aortic atherosclerosis, and diabetes mellitus; the technology-related factors are open chamber procedures, CPB duration >90 minutes, use of bubble rather than membrane oxygenators, and circulatory arrest. Apart from open chamber procedures, all the other risk factors have to be taken into consideration when cavo-atrial thrombectomy with CPB and HCCA is performed.

#### **3.2.2 Deep hypothermic circulatory arrest**

158 Front Lines of Thoracic Surgery

ACT is still debated). Anticoagulation is obtained with heparin 300-400 U/kg, and supplemental doses of 5000 U can be administered if necessary. Use of heparin-coated circuits does not eliminate the need for heparin. The pump flow has to be set at values that guarantee an adequate oxygen delivery. "Normal" pump flow is considered to be 2.4 l/min/m2, although recent studies have demonstrated that a redistribution of flow toward organs occurs during CPB in both normothermia and hypothermia (Slater et al., 2001). Muscle flow is significantly reduced during CPB, and if flow is reduced, splacnic, renal and cerebral flow decrease as well, in that order. During CPB, blood pressure depends on pump flow, total arterial impedance and haematocrit. During CPB, blood pressure is less important in determining global perfusion if pump flow is adequate, but minimal values of blood pressure may be significant in providing specific regional flows; therefore, during mild to moderate hypothermia (30-34°C), the blood pressure is generally maintained at

Fig. 6. Cardiopulmonary bypass.

After CPB has been started, the temporary interruption of cerebral blood flow is a necessary condition to remove the thrombus from the vena cava and, in such cases, from the right atrium. Interruption of cerebral blood flow has been associated with a high incidence of neurologic injury because the brain is susceptible to ischemic injury within minutes of the onset of circulatory arrest as a result of its high metabolic rate and limited reserves (Harrington et al., 2003). The physiologic basis for hypothermia as a neuroprotective strategy is its ability to reduce the cerebral oxygen metabolic rate and the accumulation of toxic metabolites. In adults, a decrease in core temperature leads to a reduction in the cerebral metabolic rate that increases in ischemic tolerance from 2-3 minutes (normothermia) to 20-34 minutes (17°C) (Reich et al., 1999). However, the optimal level of hypothermia is still debated. Studies based on electroencephalographic monitoring have shown that a median nasopharyngeal temperature of 18°C allows electrocortical silence (Stecker et al., 2001). Today, based on the results of several studies, HCCA at 18°C is considered safe for durations of up to 40 minutes (Griepp, 2001). It has been also suggested that hypothermia provides neurological protection through mechanisms other than the cerebral metabolic rate. In the face of an incomplete understanding of the involved mechanisms, hypothermia remains the most efficacious intervention for preventing ischemic brain injuries. In addition to systemic hypothermia, topical cooling, obtained by packing the head with ice, can be used to prevent passive warming of the brain during circulatory arrest, but consensus on this adjunctive strategy is still lacking because rewarming during circulatory arrest could be negligible (Reich et al., 1999). After the targeted core temperature has been reached, the pump is turned off, allowing brain protection during surgery performed in a bloodless field. HCCA has several potential adverse consequences. Achieving the target temperature prolongs the duration of the CPB period, thus amplifying problems related to CPB (loss of pulsatile flow, injury to blood elements, risk of embolization, coagulation system derangements, etc.). Re-warming increases the cerebral metabolic rate and has the potential to make the brain vulnerable to ischemic injury. With the aim of limiting brain injuries, a short period (10 minutes) of hypothermic

Hypothermic Cardiac Arrest to Remove Right Atrial Thrombi Due to Abdominal Malignancies 161

should be administered. During CPB, antifibrinolytic agents (ξ-aminocaproic acid or tranexamic acid) have beneficial effects in restoring coagulation equilibrium. Antifibrinolytics act as lysine analogues that bind to the lysine-binding sites of plasmin and plasminogen. ξ -aminocaproic acid can be administered at a dose of 100-150 mg/kg in bolus form, followed by 10-15 mg/kg/h or a 50 mg/kg bolus followed by 20-25 mg/kg/h. Tranexamic acid can be administered at a dose of 10-20 mg/kg followed by 1-2 mg/kg/h, although some centres prefer a 5 g bolus and repeat bolus to a total of 15 g. Post-bypass bleeding is common after CPB/HCCA. Evaluation of haemostasis and correct intervention are key factors for preventing indiscriminate use of transfusion medicine. After surgical haemostasis has been achieved, the first approach is the confirmation of adequate heparin neutralization (heparinase ACT, protamine titration test, thromboelastography-TEG). In addition, a test of platelet function should be available (TEG maximal amplitude, Platelet-Function-Analyzer-100). Finally, the fibrinolysis pathway must be explored (TEG lysis index). Packed red blood cells must be available at every moment of the intervention, and fresh frozen plasma and platelets should be prepared in case of established coagulation abnormalities (very frequent in this population of patients) to replace coagulation factors

In conclusion we think that CPB with HCCA should be considered for atrial thrombi removal in patient affected by several abdominal malignancies such as renal, adrenal carcinomas, primary liver tumours also in presence of a well compensated liver cirrhosis, uterine endometrial stromal tumours and intravascular leiomyomatosis, vena cava leiomysarcoma and others, because it is simpler and safer compared to CPB alone. It permits the careful cleaning of the vena cava, right atrium, ventricle and even of the pulmonary artery in a bloodless field which entails in a lower recurrence rate. Mortality and morbidity seem to be the same when compared to CPB alone but further studies are necessary due to

Akashi Y, Koreeda C, Enomoto S, et al. Prognosis of unresectable hepatocellular carcinoma:

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and platelets.

**4. Conclusions** 

**5. References** 

the small number of patients.

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reperfusion is achieved before re-warming, and maintaining a temperature gradient of less than 10°C in the heat exchanger and avoiding complete re-warming are usually performed.

Currently, there is no class of drug representing the standard of practice, but some drugs can be used as adjunctive strategies for cerebral protection. A number of drugs cause EEG burst suppression, resulting in a reduction in the cerebral metabolic rate by approximately 50%, but the most used of these drugs is thiopental at a dose of 5-8 mg/kg. The administration of thiopental results in EEG burst suppression for few minutes at normothermia. Thiopental and/or steroids are administered before circulatory arrest in some centres, without a clear demonstration of beneficial effects.

#### **3.2.3 pH management during hypothermia**

There is an inverse relationship between gas solubility and blood temperature. When blood temperature decreases, an apparent respiratory alkalosis occurs due to a decrease in PaCO2 and an increase in pH. To compensate for this PaCO2 reduction, CO2 can be added to the oxygenator (pH-stat management) or the CPB gas sweep rate can be reduced. The technique of pH-stat management was commonly used until the mid-1980s, but there is more recent evidence that pH-stat management can increase the incidence of postoperative cognitive dysfunction when CPB lasts longer than 90 minutes (Murkin et al., 1995). It has been suspected that the increase in CO2 should increase the cerebral blood flow during perfusion phases, uncoupling flow and metabolism. The most used α-stat (not temperature-correcting) requires that neutrality be maintained at only 37°C, and it permits hypothermic alkaline drift. Thus, additional CO2 is not needed. Cellular trans-membrane pH gradients, protein functioning, and enzyme activity are more normal when the pH is allowed to drift into the alkaline range, in parallel with the temperature-dependent pKa of protein and the neutral pH of water. Moreover, a relatively alkaline pH is beneficial before the ischemic insult of circulatory arrest. Despite considerable laboratory and animal research into these mechanisms, substantial controversy remains over which strategy produces the best clinical outcomes (Duebener et al., 2002).

#### **3.2.4 Coagulation management**

Coagulation system management during and after CPB is based on the administration of heparin, followed by neutralization with protamine, and this approach has been unchanged for almost 50 years. Heparin binds to antithrombin-III (AT-III), potentiating the action of AT-III (more than 1000-fold) to inhibit thrombin and factor Xa most importantly (but also factors IXa, XIa, and XIIa). After central venous administration, heparin's effect peaks within 1 minute. The onset of CPB increases the circulating blood volume by approximately 1500 ml, reducing the heparin blood concentration; therefore, 5000 U of heparin are added to the CPB prime. Before CPB, heparin is administered at a dose of 300-400 U/kg to obtain ACT for 420-480 seconds, and successive supplemental doses are guided by monitoring the ACT. Some centres monitor blood heparin concentrations. ACT is prolonged by hypothermia and hemodilution. After CPB weaning is successfully achieved and a satisfactory spontaneous circulation is restored, heparin anticoagulation must be reversed with protamine administration. The most used protamine-heparin ratio is 0.6-1 mg/100 U. Protamine must always be administered slowly to prevent adverse hemodynamic effects. After protamine administration, ACT should return to a value no more than 10% above the basic value. If more prolonged, heparin residual activity is likely, and additional doses of protamine should be administered. During CPB, antifibrinolytic agents (ξ-aminocaproic acid or tranexamic acid) have beneficial effects in restoring coagulation equilibrium. Antifibrinolytics act as lysine analogues that bind to the lysine-binding sites of plasmin and plasminogen. ξ -aminocaproic acid can be administered at a dose of 100-150 mg/kg in bolus form, followed by 10-15 mg/kg/h or a 50 mg/kg bolus followed by 20-25 mg/kg/h. Tranexamic acid can be administered at a dose of 10-20 mg/kg followed by 1-2 mg/kg/h, although some centres prefer a 5 g bolus and repeat bolus to a total of 15 g. Post-bypass bleeding is common after CPB/HCCA. Evaluation of haemostasis and correct intervention are key factors for preventing indiscriminate use of transfusion medicine. After surgical haemostasis has been achieved, the first approach is the confirmation of adequate heparin neutralization (heparinase ACT, protamine titration test, thromboelastography-TEG). In addition, a test of platelet function should be available (TEG maximal amplitude, Platelet-Function-Analyzer-100). Finally, the fibrinolysis pathway must be explored (TEG lysis index). Packed red blood cells must be available at every moment of the intervention, and fresh frozen plasma and platelets should be prepared in case of established coagulation abnormalities (very frequent in this population of patients) to replace coagulation factors and platelets.
