Physiological changes during Laparoscopy
The introduction of gas into the peritoneal cavity under pressure may cause pain, respiratory distress, and possibly cardiac embarrassment. Further, Trendelenburg’s position is necessary for access but extreme Trendelenburg’s position enhances respiratory and cardiac embarrassment.
Pneumoperitoneum at the time of laparoscopic surgery causes upward displacement of the diaphragm, resulting in the reduction in lung volumes including functional residual capacity. Pulmonary compliance is reduced and airway resistance is increased due to high intra-abdominal pressure. The anesthetist often uses high airway pressure to overcome the intra-abdominal pressure for a given tidal volume, which increases the risk of hemodynamic changes and barotraumas.
The impaired diaphragmatic mobility gives rise to uneven distribution of ventilation to the nondependent part of the lung, resulting in ventilation-perfusion mismatch with hypercarbia and hypoxemia. The ventilatory impairment is even more severe if there are associated with airway and alveolar collapse. Increased intra-abdominal pressure also predisposes to regurgitation of gastric contents and pulmonary aspiration.
The insufflation of CO2 is usually accompanied by hypercapnia. The reason initially proposed to explain this hypercapnia was that CO2 was reabsorbed from the peritoneal cavity. This explanation was all the more plausible in that it was based on the capacity of CO2 to diffuse, and the exchange capacities of the peritoneal serosa. Recent studies reveal a two-phase phenomenon, with absorption proportional to intraperitoneal pressure for low insufflation pressures, then a drop in the rate of this reabsorption probably due to the peritoneal circulation being crushed under the effect of the pressure. The variations in PaCO2 observed during the second phase with high intra-abdominal pressures which act against reabsorption essentially depend on a change in the ventilation/perfusion ratio with an increase in the dead space.
The hypercapnia mechanism is different from extraperitoneal insufflation. In this case, the pressure effect limiting reabsorption from the peritoneum no longer applies. The increase in pressure increases the diffusion space by dilacerations of the tissues, and thus the CO2 reabsorption surface. Reabsorption is thus directly proportional to the pressure and volume of CO2 insufflated in extraperitoneal insufflation. Severe hypercapnia is thus possible, if not to say frequent, in these situations. On the other hand, provided the hypercapnia is controlled, the circulatory effect of extraperitoneal insufflation is lower than those of intraperitoneal insufflation.
The increase in intrathoracic pressures induced by the increase in intra-abdominal pressure can be limiting factors for laparoscopic surgery in certain patients. Insufflation of the pneumoperitoneum in laparoscopic surgery is accompanied by a decrease of some 30 percent in pulmonary compliance. The resistance of the air passages increases in the same proportions. The resulting increase in pressure in the air passages can have adverse consequences for patients with bubbles of emphysema. These patients and all those who suffer from dystrophy of the pulmonary parenchyma will find it difficult to cope with the often considerable hyperventilation required by hypercapnia, with volumes per minute sometimes reaching 2 or 3 times than normal.
Venous gas embolism is a fatal complication of pneumoperitoneum. Veress needle or the trocar may directly puncture the arteries or blood flow across an opening in an injured vessel, may sometimes draw gas into the vessel, and lead to gas embolism. A slow infusion of air less than one liter/minute is absorbed across the pulmonary capillary-alveolar membranes without causing any damage. At higher infusion rates, the gas bubbles lodging in the peripheral pulmonary arterioles provokes neutrophil clumping, activation of the coagulation cascade and platelet aggregation.
This may lead to pulmonary vasoconstriction, bronchospasm, pulmonary edema, and pulmonary hemorrhage. Gas bubbles attached to fibrin deposits and platelet aggregates mechanically obstruct the pulmonary vasculature and increases the pulmonary vascular resistance. The increased right heart afterload leads to acute right heart failure with arrhythmia, ischemia, hypotension, and elevated central venous pressure. Sometimes, paradoxical embolism is seen through a patent foramen ovale.
Elevated intra-abdominal pressure produces physiological changes in the hemodynamic by its effects on systemic vascular resistance, venous return, and myocardial performance. Systemic venous return increases when Intraabdominal pressure is elevated. The effects on venous return and cardiac output depend on the magnitude of the intraabdominal pressure. Venous return initially increases with intra-abdominal pressure below 10 mm Hg. This paradox is due to a reduction in the blood volume sequestrated in the splanchnic vasculature which increases cardiac output and arterial pressure. When intra-abdominal pressure exceeds 20 mm Hg, the inferior vena cava is compressed. Venous return from the lower half of the body is impeded resulting in a fall in cardiac output.
A number of animal studies have been devoted to variations in cardiac output induced by the increase in intraperitoneal pressure. The results are consistent with a fall in cardiac output proportional to the intraperitoneal pressure. In low abdominal pressure (5 mm Hg), cardiac output remains unchanged. The drop in right transmural auricular pressure indicates a reduction in the venous return which is demonstrated by a reduction in flow, through the vena cava, the degree of which is proportional to the intraabdominal pressure.
The cardiac output is governed by the myocardial function, the post-loading, and by the venous return, the latter in turn depending on venous resistance and mean systemic pressure. With an intra-abdominal pressure of 5 mm Hg, the venous return improves. Under these conditions, the intraperitoneal pressure remains lower than the pressure in the vena cava which results in a flushing effect, with no obstructive phenomena in the lower vena cava. When the intraperitoneal pressure rises above the intravascular pressure, a sub-diaphragmatic narrowing of the lower vena cava slows the flow of blood. The abdominal blood volume is reduced due to the pressure and reflux into the venous system of the lower limb occurs.
The increase in vascular resistance can be explained by the splanchnic vascular compression, but the persistence of high resistance after exsufflation means a humoral factor could be suggested. During the increase in intraperitoneal pressure, a considerable rise in antidiuretic hormone is found, and its vasopressive effects are well-known. This secretion would seem to be dependent on the drop in cardiac flow rate. A simultaneous rise in the level of plasma norepinephrine, whose vasoconstrictor effects are equivalent to those of vasopressin, has also been reported. The increase in vascular resistance is correlated with a rise in arterial pressure insofar as inotropism is sufficient.
The circulation of the kidney becomes much compromised with increased intra-abdominal pressure. Renal blood flow and glomerular filtration rate decrease because of an increase in renal vascular resistance, reduction in glomerular filtration gradient, and a decrease in cardiac output. The increase in systemic vascular resistance impairs left ventricular function and cardiac output. Arterial pressure, however, remains relatively unchanged, which conceals the fall in cardiac output. High intrathoracic pressure during intermittent positive pressure ventilation adds in impairment of venous return and cardiac output, particularly if positive end-expiratory pressure (PEEP) is also applied. The elevation in intra-abdominal pressure produces lactic acidosis, probably by severely lowering cardiac output and by impairing hepatic clearance of blood lactate.
Stretching of the peritoneum sometimes leads to stimulation of vagus nerve and can provoke arrhythmias such as AV dissociation, nodal rhythm, sinus bradycardia, and asystole. This shock is more commonly seen with the rapid stretching of the peritoneum at the beginning of peritoneal insufflation.
Faulty pneumoperitoneum may give rise to subcutaneous emphysema, pneumomediastinum, pneumopericardium, and pneumothorax. However, gas can also dissect through existing defects in the diaphragm or along surgically traumatized tissue planes in the retroperitoneum, the diaphragm, or the falciform ligament. Gas can leak into the subcutaneous tissues connected with poor positioning of a trocar sleeve (2.7% of cases of severe hypercapnia in a series of cholecystectomies published by Wieden), CO2 is seen to spread outside the abdominal cavity during a laparoscopic-assisted hysterectomy, with or without lymphadenectomy, and during bladder neck suspensions.
In laparoscopic gynecological surgery, because this effusion originates in the pelvis, it mostly affects the sides and loins and generally remains hidden by the drapes until the end of the operation. Only the very abundant, rare forms can be diagnosed by the anesthetist during the operation, when they shift towards the upper part of the thorax. In this case, the capnographic signs (slow and regular increase in CO2 expired) will provide an alert during the anesthesia.
Evaluation and Preparation of Patient for Laparoscopic Surgery
There are laparoscopic operations that are emergencies. Therefore, all patients should receive the same evaluation and preparation that they would receive for an open, elective abdominal operation. There are several unique concerns with laparoscopy and the type of patients who undergo these procedures.
Many of the patients scheduled to undergo laparoscopic surgery are young women undergoing gynecological laparoscopy. Young women are at high-risk for postoperative nausea and vomiting following general anesthesia, and gynecological procedures may provoke nausea and vomiting as well. Laparoscopy itself is also associated with postoperative nausea and vomiting, probably due to the stretching of the abdominal cavity or residual irritant effects of retained carbon dioxide. Anesthesiologists should plan their anesthetic to prevent and treat postoperative nausea and vomiting in these patients.
The second group of patients that cause concern is those with significant cardiac disease. Most of these patients tolerate abdominal insufflation at low pressures currently used (< 18 mm Hg) surprisingly well. If the operation is to be of short duration, few patients with cardiac disease, other than those with severe congestive heart failure, require invasive monitoring. However, insufflation can be associated with a moderately reduced cardiac index, increased cardiac filling pressures, systemic blood pressure, and systemic vascular resistance. In addition, hypercarbia from insufflated carbon dioxide may be detrimental to patients with cardiac disease by stimulating the sympathetic nervous system and vasopressin release. Therefore, for extensive laparoscopic procedures direct arterial and pulmonary artery catheterization and/or transesophageal echocardiography may be necessary for monitoring.
The third group of patients of concern is those with severe emphysema, asthma, cystic fibrosis, or another pulmonary disease. Often these are patients who would benefit from a laparoscopic operation as opposed to an open procedure because of improved postoperative pulmonary function following procedures performed laparoscopically. However, some of these patients may not be able to be adequately ventilated to eliminate the carbon dioxide absorbed during laparoscopy. It is important for patients with severe lung disease to be in optimum medical condition prior to having surgery.
The anesthesiologist must be certain that the patient does not have an upper respiratory tract infection or other conditions that may impair pulmonary function at the time of surgery. Prior preparation with a course of bronchodilators, steroids and/or antibiotics may be necessary. In these patients, an intra-arterial catheter for arterial blood sampling for gas analysis as well as direct arterial pressure monitoring is essential, since the end-tidal carbon dioxide tension often does not accurately reflect the arterial carbon dioxide tension and may be significantly lower.
A laparoscopic surgeon should develop communication and understanding with his anesthetist. Adequate preoperative assessment of the patient and the disease minimizes the risk of general anesthesia. Necessary measures should be undertaken to correct any metabolic or hematological abnormalities. These include hypokalemia, hyponatremia, hyperglycemia, azotemia, anemia, and coagulation defects. All the required pre-anesthetic laboratory data should be available, including blood grouping and testing for the hepatitis B antigen and HIV. Patients should have an electrocardiogram and chest X-ray.
The introduction of gas into the peritoneal cavity under pressure may cause pain, respiratory distress, and possibly cardiac embarrassment. Further, Trendelenburg’s position is necessary for access but extreme Trendelenburg’s position enhances respiratory and cardiac embarrassment.
Pneumoperitoneum at the time of laparoscopic surgery causes upward displacement of the diaphragm, resulting in the reduction in lung volumes including functional residual capacity. Pulmonary compliance is reduced and airway resistance is increased due to high intra-abdominal pressure. The anesthetist often uses high airway pressure to overcome the intra-abdominal pressure for a given tidal volume, which increases the risk of hemodynamic changes and barotraumas.
The impaired diaphragmatic mobility gives rise to uneven distribution of ventilation to the nondependent part of the lung, resulting in ventilation-perfusion mismatch with hypercarbia and hypoxemia. The ventilatory impairment is even more severe if there are associated with airway and alveolar collapse. Increased intra-abdominal pressure also predisposes to regurgitation of gastric contents and pulmonary aspiration.
The insufflation of CO2 is usually accompanied by hypercapnia. The reason initially proposed to explain this hypercapnia was that CO2 was reabsorbed from the peritoneal cavity. This explanation was all the more plausible in that it was based on the capacity of CO2 to diffuse, and the exchange capacities of the peritoneal serosa. Recent studies reveal a two-phase phenomenon, with absorption proportional to intraperitoneal pressure for low insufflation pressures, then a drop in the rate of this reabsorption probably due to the peritoneal circulation being crushed under the effect of the pressure. The variations in PaCO2 observed during the second phase with high intra-abdominal pressures which act against reabsorption essentially depend on a change in the ventilation/perfusion ratio with an increase in the dead space.
The hypercapnia mechanism is different from extraperitoneal insufflation. In this case, the pressure effect limiting reabsorption from the peritoneum no longer applies. The increase in pressure increases the diffusion space by dilacerations of the tissues, and thus the CO2 reabsorption surface. Reabsorption is thus directly proportional to the pressure and volume of CO2 insufflated in extraperitoneal insufflation. Severe hypercapnia is thus possible, if not to say frequent, in these situations. On the other hand, provided the hypercapnia is controlled, the circulatory effect of extraperitoneal insufflation is lower than those of intraperitoneal insufflation.
The increase in intrathoracic pressures induced by the increase in intra-abdominal pressure can be limiting factors for laparoscopic surgery in certain patients. Insufflation of the pneumoperitoneum in laparoscopic surgery is accompanied by a decrease of some 30 percent in pulmonary compliance. The resistance of the air passages increases in the same proportions. The resulting increase in pressure in the air passages can have adverse consequences for patients with bubbles of emphysema. These patients and all those who suffer from dystrophy of the pulmonary parenchyma will find it difficult to cope with the often considerable hyperventilation required by hypercapnia, with volumes per minute sometimes reaching 2 or 3 times than normal.
Venous gas embolism is a fatal complication of pneumoperitoneum. Veress needle or the trocar may directly puncture the arteries or blood flow across an opening in an injured vessel, may sometimes draw gas into the vessel, and lead to gas embolism. A slow infusion of air less than one liter/minute is absorbed across the pulmonary capillary-alveolar membranes without causing any damage. At higher infusion rates, the gas bubbles lodging in the peripheral pulmonary arterioles provokes neutrophil clumping, activation of the coagulation cascade and platelet aggregation.
This may lead to pulmonary vasoconstriction, bronchospasm, pulmonary edema, and pulmonary hemorrhage. Gas bubbles attached to fibrin deposits and platelet aggregates mechanically obstruct the pulmonary vasculature and increases the pulmonary vascular resistance. The increased right heart afterload leads to acute right heart failure with arrhythmia, ischemia, hypotension, and elevated central venous pressure. Sometimes, paradoxical embolism is seen through a patent foramen ovale.
Elevated intra-abdominal pressure produces physiological changes in the hemodynamic by its effects on systemic vascular resistance, venous return, and myocardial performance. Systemic venous return increases when Intraabdominal pressure is elevated. The effects on venous return and cardiac output depend on the magnitude of the intraabdominal pressure. Venous return initially increases with intra-abdominal pressure below 10 mm Hg. This paradox is due to a reduction in the blood volume sequestrated in the splanchnic vasculature which increases cardiac output and arterial pressure. When intra-abdominal pressure exceeds 20 mm Hg, the inferior vena cava is compressed. Venous return from the lower half of the body is impeded resulting in a fall in cardiac output.
A number of animal studies have been devoted to variations in cardiac output induced by the increase in intraperitoneal pressure. The results are consistent with a fall in cardiac output proportional to the intraperitoneal pressure. In low abdominal pressure (5 mm Hg), cardiac output remains unchanged. The drop in right transmural auricular pressure indicates a reduction in the venous return which is demonstrated by a reduction in flow, through the vena cava, the degree of which is proportional to the intraabdominal pressure.
The cardiac output is governed by the myocardial function, the post-loading, and by the venous return, the latter in turn depending on venous resistance and mean systemic pressure. With an intra-abdominal pressure of 5 mm Hg, the venous return improves. Under these conditions, the intraperitoneal pressure remains lower than the pressure in the vena cava which results in a flushing effect, with no obstructive phenomena in the lower vena cava. When the intraperitoneal pressure rises above the intravascular pressure, a sub-diaphragmatic narrowing of the lower vena cava slows the flow of blood. The abdominal blood volume is reduced due to the pressure and reflux into the venous system of the lower limb occurs.
The increase in vascular resistance can be explained by the splanchnic vascular compression, but the persistence of high resistance after exsufflation means a humoral factor could be suggested. During the increase in intraperitoneal pressure, a considerable rise in antidiuretic hormone is found, and its vasopressive effects are well-known. This secretion would seem to be dependent on the drop in cardiac flow rate. A simultaneous rise in the level of plasma norepinephrine, whose vasoconstrictor effects are equivalent to those of vasopressin, has also been reported. The increase in vascular resistance is correlated with a rise in arterial pressure insofar as inotropism is sufficient.
The circulation of the kidney becomes much compromised with increased intra-abdominal pressure. Renal blood flow and glomerular filtration rate decrease because of an increase in renal vascular resistance, reduction in glomerular filtration gradient, and a decrease in cardiac output. The increase in systemic vascular resistance impairs left ventricular function and cardiac output. Arterial pressure, however, remains relatively unchanged, which conceals the fall in cardiac output. High intrathoracic pressure during intermittent positive pressure ventilation adds in impairment of venous return and cardiac output, particularly if positive end-expiratory pressure (PEEP) is also applied. The elevation in intra-abdominal pressure produces lactic acidosis, probably by severely lowering cardiac output and by impairing hepatic clearance of blood lactate.
Stretching of the peritoneum sometimes leads to stimulation of vagus nerve and can provoke arrhythmias such as AV dissociation, nodal rhythm, sinus bradycardia, and asystole. This shock is more commonly seen with the rapid stretching of the peritoneum at the beginning of peritoneal insufflation.
Faulty pneumoperitoneum may give rise to subcutaneous emphysema, pneumomediastinum, pneumopericardium, and pneumothorax. However, gas can also dissect through existing defects in the diaphragm or along surgically traumatized tissue planes in the retroperitoneum, the diaphragm, or the falciform ligament. Gas can leak into the subcutaneous tissues connected with poor positioning of a trocar sleeve (2.7% of cases of severe hypercapnia in a series of cholecystectomies published by Wieden), CO2 is seen to spread outside the abdominal cavity during a laparoscopic-assisted hysterectomy, with or without lymphadenectomy, and during bladder neck suspensions.
In laparoscopic gynecological surgery, because this effusion originates in the pelvis, it mostly affects the sides and loins and generally remains hidden by the drapes until the end of the operation. Only the very abundant, rare forms can be diagnosed by the anesthetist during the operation, when they shift towards the upper part of the thorax. In this case, the capnographic signs (slow and regular increase in CO2 expired) will provide an alert during the anesthesia.
Evaluation and Preparation of Patient for Laparoscopic Surgery
There are laparoscopic operations that are emergencies. Therefore, all patients should receive the same evaluation and preparation that they would receive for an open, elective abdominal operation. There are several unique concerns with laparoscopy and the type of patients who undergo these procedures.
Many of the patients scheduled to undergo laparoscopic surgery are young women undergoing gynecological laparoscopy. Young women are at high-risk for postoperative nausea and vomiting following general anesthesia, and gynecological procedures may provoke nausea and vomiting as well. Laparoscopy itself is also associated with postoperative nausea and vomiting, probably due to the stretching of the abdominal cavity or residual irritant effects of retained carbon dioxide. Anesthesiologists should plan their anesthetic to prevent and treat postoperative nausea and vomiting in these patients.
The second group of patients that cause concern is those with significant cardiac disease. Most of these patients tolerate abdominal insufflation at low pressures currently used (< 18 mm Hg) surprisingly well. If the operation is to be of short duration, few patients with cardiac disease, other than those with severe congestive heart failure, require invasive monitoring. However, insufflation can be associated with a moderately reduced cardiac index, increased cardiac filling pressures, systemic blood pressure, and systemic vascular resistance. In addition, hypercarbia from insufflated carbon dioxide may be detrimental to patients with cardiac disease by stimulating the sympathetic nervous system and vasopressin release. Therefore, for extensive laparoscopic procedures direct arterial and pulmonary artery catheterization and/or transesophageal echocardiography may be necessary for monitoring.
The third group of patients of concern is those with severe emphysema, asthma, cystic fibrosis, or another pulmonary disease. Often these are patients who would benefit from a laparoscopic operation as opposed to an open procedure because of improved postoperative pulmonary function following procedures performed laparoscopically. However, some of these patients may not be able to be adequately ventilated to eliminate the carbon dioxide absorbed during laparoscopy. It is important for patients with severe lung disease to be in optimum medical condition prior to having surgery.
The anesthesiologist must be certain that the patient does not have an upper respiratory tract infection or other conditions that may impair pulmonary function at the time of surgery. Prior preparation with a course of bronchodilators, steroids and/or antibiotics may be necessary. In these patients, an intra-arterial catheter for arterial blood sampling for gas analysis as well as direct arterial pressure monitoring is essential, since the end-tidal carbon dioxide tension often does not accurately reflect the arterial carbon dioxide tension and may be significantly lower.
A laparoscopic surgeon should develop communication and understanding with his anesthetist. Adequate preoperative assessment of the patient and the disease minimizes the risk of general anesthesia. Necessary measures should be undertaken to correct any metabolic or hematological abnormalities. These include hypokalemia, hyponatremia, hyperglycemia, azotemia, anemia, and coagulation defects. All the required pre-anesthetic laboratory data should be available, including blood grouping and testing for the hepatitis B antigen and HIV. Patients should have an electrocardiogram and chest X-ray.
