The Greek e-journal of Perioperative Medicine

15-36

Authors: Petrou A, Christoforidis S

The tremendous impact of hypoxia on any critical organ, namely the brain and the heart, are well known, at least because of their obvious result. The question asked by many: “For how long can the patient tolerate apnoea?” cannot be answered with certainty for any given patient. The long list of possible problems that may arise during the transport of O2 from the anesthetic circuit to the very last cell of the human organism precludes any possibility of precise calculation. Hypoxia of critical tissues (the brain and the heart) has deleterious pathophysiologic effects on them. The abrupt and intense rise in systemic and pulmonary blood pressure combined with tachycardia, adds an excessive work load (and so an extra ATP deficit) to the myocardium. Thus it can increase morbidity from myocardial ischemia, rupture of aneurysms in the systemic and cerebral circulation, acute heart failure, pulmonary hypertension and failure of the right heart. The severity of these consequences may be augmented by the cellular effects of hypoxia like disruption of cell structure and sensitization to arrhythmias. The Central Nervous System accepts an excessive work load too. It has to fulfill auto regulation requirements: regulation of the perfusion pressure to the brain while systemic blood pressure presents with at least biphasic fluctuation during hypoxia and apnoea, manage the responses of reflex mechanisms, conservation of electrical activity in order to continue its central role as command center and sympathetic and parasympathetic outflow to the heart and other organs in gravely hypoxic conditions, over viewing hormonal and catecholamine discharge etc. All these responsibilities should have to be concluded in a milieu of strenuous efforts to conserve or replace ATP and get rid of the products of anaerobic metabolism. This is obviously a titanic work. It could be more devastating, if all these procedures should be completed in subjects who may already suffer from serious derangements of their physiology like systemic hypertension, coronary artery disease, carotid artery disease, chronic pulmonary disease, diabetes mellitus, intracranial hypertension and cerebral oedema. And it becomes worse, when hypoxia and apnoea ensues in patients, who are trying to conserve homeostasis while suffering from multiple trauma, sepsis or acute respiratory insufficiency. Finally, possibly under the systemic effects of anesthetic agents, cells of critical organs respond to protracted hypoxia with programmed cell death after stressful combat to retain structural and operational integrity. Some anesthetic agents are considered to have protective effects to the brain and the heart against ischemic – reperfusion injury. Unfortunately, we are lacking almost any data on their possible positive or negative effect on hypoxemic hypoxia during apnoea. A few agents have been discovered that could offer in time protection against hypoxia. Even less would be applicable in every day clinical practice, as the cases of difficult airway come up unexpectantly. So what should be done? Apparently we should be able to understand and learn any critical information that has been discovered about the systemic effects of hypoxia and apnoea. And most important, we should make any effort to continuously apply structured and well organized procedures of administering anesthesia in order to minimize the rate of hypoxic accidents and their effect on human tissues that are obviously completely dependant on oxygen.

54-65

Authors: Papagiannopoulou P, Didilis V, Ferdi E, Stam atiou G, Dragoum a nis Ch, Iatrou Ch, Vretzak is G

Cardiac stabilization during “off-pump” coronary revascularization (OPCAB) has been implicated in causing intraoperative hemodynamic disturbances. Stroke volume and cardiac output reductions may alter the ventilation/perfusion ratio in the lungs and compromise the gas exchange. This study was conducted to determine the impact of heart’s stabilization on arterial blood-gas profile in patients undergoing OPCAB surgery. After institutional approval and informed consent, 57 patients undergoing OPCAB procedures were studied. LIMA was anastomosed to LAD in all patients. In 20 patients a second coronary vessel received a graft, while in 5 patients a third vessel was also anastomosed under propofol-remifentanil (TIVA) anesthetic technique. FiO2 was equal to 1. Compression fork-type stabilizer was used. Full hemodynamic profile, mixed venous oxygen saturation, acid base status, end-tidal partial pressure of carbon dioxide and ST-segment changes were monitored before heart’s stabilization (T1 values-baseline), 5 minutes after stabilization (T2 values), before stabilizer’s removal (T3 values) and 10 minutes after stabilizer’s removal (T4 values). Oxygen delivery and consumption, VD/VT and Qs/Qt were calculated. Ventilation was kept unchanged during data collection. Statistical analysis for pairwise comparisons with baseline values (T1) was performed with Dunnett’s two-sided multiple-comparison procedure. Statistical analysis was performed using the t-paired test. A value of p<0.05 was considered statistically significant. During LIMA→LAD grafting (n=57) cardiac stabilization and anastomotic maneuvering caused significant hemodynamic changes. Cardiac output, stroke volume and mixed venous oxygen saturation decreased significantly (4.44 ± 1.0 → 3.43 ± 0.8 L/min, 70.6 ± 15.5 → 52.6 ± 14.2 ml, 83.5 ± 4.7 → 76.5 ± 8.0 % respectively; p<0.001 for all) while systolic, diastolic and mean pulmonary pressure, central venous pressure and capillary wedge pressure increased significantly during stabilizer’s application (T2, T3 values). Calculated O2 delivery and consumption were decreased. PH, bicarbonate and base excess decreased significantly at all times compared to baseline (7.45 ± 0.03 → 7.43 ± 0.03, 23.9 ± 1.44 → 22.9 ± 1.98 mEq/L, 0.06 ± 1.6 → -0.98 ± 1.9 respectively; p<0.001 for all) while arterial partial pressure and end-tidal partial pressure of carbon dioxide decreased at T2, T3 interval and increased at T4. Arterial partial pressure of oxygen increased significantly after stabilizer’s placement (T2, T3 interval) and decreased in stage T4. Qs/Qt was decreased during anastomotic maneuvering. IN OPCAB SURGERY, THE HEMODYNAMIC CHANGES DUE TO the heart’s stabilization caused significant changes in the arterial blood gas profile. The reduction of systemic flow and tissue perfusion led to increased plasma hydrogen ion concentration. Restoration of flow was followed by “wash-out” phenomena. Arterial tension and exhalation of CO2 were primarily influenced by the decreased O2 consumption, the increased VD/VT and the buffering of protons after the stabilizer’s removal. In this study population, the deterioration in gas exchange was minor. Although these changes are not persistent, they may have implications in the intraoperative management of patients with compromised alveolar gas-exchange.

73-79

Authors: Theodosiadis P, Grosomanidis V, Touroutoglou N

Neurolytic celiac plexus block (NCPB) is a useful technique for pain control in patients with intra-abdominal tumors or pain secondary to chronic pancreatitis that does not respond to other therapeutic modalities (not interventional). The anterior approach for NCPB has been considered a relatively safe approach, with a low rate of complications and little risk of neurologic injury secondary to the spread of a neurolytic agent. This is the first national case report of successful NCPB using the anterior approach under CT guidance.