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In recent years laparoscopy has become the gold standard approach in many surgical procedures. It allows for better cosmesis, faster post-operative recovery and reduced pain. The formation of pneumoperitoneum however, does alter physiological processes which, unless appropriately safeguarded against by the surgeon and anaesthetistââ‚¬â„¢s monitoring and management, can become of clinical significance. One will aim to outline the main cardiovascular, pulmonary and renal physiological effects after induction of pneumoperitoneum. Importance will be given to their clinical significance and subsequent management, so as to prevent any pathophysiological complications, thus maintaining the safety of performing a surgical procedure laparoscopically.
Insufflation of the peritoneal cavity with carbon dioxide creates both metabolic and mechanical effects which both have an impact on the cardiovascular system. High levels of carbon dioxide (pCO2 above 55mmHg) may cause hypercarbia, inducing haemodynamic effects. Vasodilatation and myocardial depression may ensue which is commonly resolved by an autonomic sympathetic nervous system response, giving rise to a compensatory central vasoconstriction and tachycardia. This in turn causes a rise in central venous pressure and pulmonary capillary wedge pressure (PCWP) leading to increased cardiac output, thus counteracting the metabolic effects of hypercarbia.  The metabolic effects however, are outweighed by the mechanical changes that occur during pneumoperitoneum, causing an increased intra-abdominal pressure which wields physiological change. The exact physiological response depends on the amount of intra-abdominal pressure (IAP) exerted. Various clinical studies have been performed in order to gauge the optimum pressure during pneumoperitoneum, so as to reduce cardiovascular effects. Joris et al discovered that at an IAP level of 15mmHg with a 100 head-up tilt, the inferior vena cava (IVC) becomes partially occluded, thus decreasing venous return (VR) by increasing the central venous pressure (CVP) and PCWP and reducing cardiac preload.  This in turn increases systemic vascular resistance (SVR), reduces cardiac output and leads to an attempted compensatory increase in blood pressure and tachycardia so as to achieve an increased cardiac workload. De Waal and Kalkman however, demonstrated that when IAP is lower, e.g. as low as 5mmHg in during laparoscopic fundoplication procedures, the IVC is not compressed and therefore the increased IAP serves to enhance venous return thus increasing cardiac pre-load and an increased cardiac output of 22%.  These studies are therefore evident of the effects of changes in IAP on the cardiovascular system. Clinical complications relating to the cardiovascular system can be identified and adequately managed with this knowledge of the physiological changes during creation of pneumoperitoneum. Hypertension is a potentially dangerous consequence of increased IAP at the commencement of insufflation, when the IAP is still low enough to not compress the IVC and indeed increases venous return and pre-load as described above. Severe hypertension may cause cardiac overload leading to pulmonary oedema in patients who already have an element of congestive cardiac failure (CCF).  The opposite is true at higher IAPs during laparoscopic procedures; i.e. hypotension due to partial occlusion of the IVC, thus decreasing venous return and cardiac output, as described above. Arrhythmias have an incidence of 14-27% during laparoscopic surgery.  Many of these are directly related to the vagal nerve stimulation during fast peritoneal stretch at the establishment of pneumoperitoneum.  This causes bradyarrhythmias, which if left untreated may lead to cardiac arrest and become life-threatening. The European Association for Endoscopic Surgery (E.A.E.S) produced clinical guidelines about pneumoperitoneum within the context of laparoscopic surgery so as to provide a framework for surgical departments to follow in order to avoid complications relating to physiological change as described previously. With regard to the cardiovascular complications outlined above they advised that in ASA III-IV patients, invasive circulating volume measurements, e.g. a pulmonary artery catheter, should be used whilst also ensuring that these patients receive beta-blocker medication if hypertension is a risk or appropriate intravenous fluid therapy pre-operatively if hypotension is a risk.  Pneumatic compression stockings for the lower limbs and the head-up position are also advised due to venous blood pooling in the extremities as a consequence of reduced venous return at higher IAP levels. Patients with CCF or prone to arrhythmias are advised to have their pneumoperitoneums insufflated at very low pressures.7 All of these interventions help to prevent the cardiovascular complications, described above, that may occur during laparoscopy.
Pulmonary physiological changes also occur during laparoscopy. The increased IAP during the creation of pneumoperitoneum causes cephalad movement of the diaphragm, with a resultant reduction in movement and an increase in intra-thoracic pressure (ITP). A head-tilt position (Trendelenburg) may also contribute to an increased ITP. Both alveolar collapse and a reduced tidal volume occur, leading to a lower pulmonary compliance and decreased functional residual capacity (FRC). This causes increased ventilation and work of breathing. A ventilation-perfusion mismatch thus occurs which may promote hypoxaemia. A study by Hasukic et al demonstrated a reduction in forced vital capacity (FVC), forced expiratory volume in one second (FEV1) and peak expiratory flow rate (PEFR) in patients after laparoscopy.  Healthy patients with no respiratory morbidities pre-operatively are rarely affected by these physiological changes as they generate a faster ventilatory pattern thus preventing atelectasis, so as to increase oxygen consumption and elimination of CO2. Patients that are subjected to general anaesthesia during laparoscopy cannot breathe spontaneously and thus the prevention of atelectasis and hypoxaemia is achieved by large tidal volume controlled ventilation with the addition of positive end-expiratory pressure (PEEP) if required.1 PEEP must be used with caution however, as it has a detrimental effect on cardiac output by further increasing ITP and impeding venous return. A compromising measure is the alveolar recruitment strategy, which combines the use of manual ventilation with low levels of PEEP, so as to achieve effective ventilation and reduce hypoxaemia whilst also maintaining cardiovascular function.  Having established the pulmonary physiology one must be aware of the pulmonary complications that have the potential to arise from such physiological changes in relation to laparoscopy. Gas embolism and pneumomediastinum are respiratory complications of surgery but not necessarily specific to laparoscopy and will thus not be discussed at length. Patients with obstructive respiratory diseases such as COPD (chronic obstructive pulmonary disease) and severe asthma are prone to developing atelectasis and hypoxaemia due to the physiological changes described above. The EAES therefore recommends the carrying out of regular intra-operative and post-operative arterial blood gas monitoring, in addition to lowering the IAP and close controlled ventilation, in patients with pre-operative respiratory compromise, e.g. COPD.7 Barotrauma to the lungs is also a potential complication due to increased ventilator pressure and this is therefore another reason why low IAP levels are recommended by EAES in those with poor respiratory function.4,7
The creation of pneumoperitoneum also exerts renal physiological changes. Human studies have been conducted which show IAPs of 20mmHg or above to reduce urine output and glomerular filtration rate (GFR).1 The principle reason for this is due to direct compression of the renal vascular system by the pneumoperitoneum. The resulting effect is a reduced effective renal blood flow causing decreased perfusion to the kidneys. The renin-angiotensin-aldosterone system becomes activated, thus causing renal vasoconstriction and an increase in vasopressin (anti-diuretic hormone) resulting in fluid retention and consequential decreased urine production, oliguria. This physiological effect is however, not clinically significant in the majority of patients as the changes revert back to their pre-operative renal function approximately two hours post-operatively, i.e. acute renal failure.  Patients assessed pre-operatively to have impaired renal function proceed to undergo this physiological process during laparoscopy and are at an increased likelihood of developing renal tubular acidosis due to prolonged renal hypoperfusion.4 The EAES therefore recommends that intravenous volume loading pre-operatively and peri-operatively, in addition to a low IAP being applied, is of paramount importance is these patients.7 Prophylactic measures such as the avoidance of non-steroidal anti-inflammatory drugs (NSAIDs) are also advised in patients with impaired renal function.  This is due to their effect of vasoconstriction to an already vasoconstricted renal system, from the increased IAP levels during establishment of pneumoperitoneum, which may also lead to acute tubular necrosis.
Due to the less invasive approach of laparoscopic surgery in comparison to open surgery, the immunological stress response to injury is reduced due to a decrease in the level of trauma experienced by the patient. Studies however have shown that carbon dioxide gas may potentiate an inflammatory response.1 Sietses et al researched these effects on patients undergoing laparoscopic cholecystectomy.  They compared CRP levels in patients having pneumoperitoneum created by insufflations of CO2, helium and abdominal wall lifting. Results showed that the CRP level was significantly raised in patients who underwent CO2 insufflation compared to the other two techniques. Whilst the EAES does not recommend any specific alterations in management to reduce the stress response to injury during laparoscopy, this study could prompt anaesthetists and surgeons to be aware of the possible increased immunological effect of CO2 and therefore, use the lowest IAP possible to achieve the desired effect.
It is evident that the creation of pneumoperitoneum, which is required to perform effective laparoscopy, causes physiological changes to all the major systems of the human body. Knowledge of these changes is of the utmost importance so that one has increased awareness of when these changes can become pathophysiological, i.e. in patients with pre-operative co-morbidities. It is only from identification of patients at risk of pathophysiological effects from laparoscopy that one can implement appropriate monitoring and management techniques to avoid such complications. This therefore maintains the safety and often advantageous method of laparoscopic surgery over open surgical techniques.