Anaesthesia, Pain, Intensive Care and Emergency - Part 3 ppt

References 1. Sugerman HJ (1987) Pulmonary function in morbid obesity. Gastroenterol Clin North Am 16:225–237 2. Sugerman HJ (1995) Ventilation and obesity. Int J Obes Relat Metab Disord 19:686 3. Juvin P, Lavaut E, Dupont H et al (2003) Difficult tracheal intubation is more common in obese than in lean patients. Anesth Analg 97:595–600 4. Brodsky JB, Lemmens HJ, Brock-Utne JG et al (2002) Morbid obesity and tracheal intubation. Anesth Analg 94:732–736 5. Resta O, Foschino-Barbaro MP, Legari G et al (2001) Sleep-related breathing disorders, loud snoring and excessive daytime sleepiness in obese subjects. Int J Obes Relat Metab Disord 25:669–675 6. Strum EM, Szenohradszki J, Kaufman WA et al (2004) Emergence and recovery characteristics of desflurane versus sevoflurane in morbidly obese adult surgical pa- tients: a prospective, randomized study. Anesth Analg 99:1848–1853 7. Hofer RE, Sprung J, Sarr MG et al (2005) Anesthesia for a patient with morbid obesity using dexmedetomidine without narcotics. Can J Anaesth 52:176–180 8. Pelosi P, Ravagnan I, Giurati G et al (1999) Positive end-expiratory pressure improves respiratory function in obese but not in normal subjects during anesthesia and paraly- sis. Anesthesiology 91:1221–1231 9. Sprung J, Whalley DG, Falcone T et al (2003) Theeffectsoftidal volume and respiratory rate on oxygenation and respiratory mechanics during laparoscopy in morbidly obese patients. Anesth Analg 97:268–274 10. Visick WD, Fairley HB, Hickey RF (1973) The effects of tidal volume and end-expiratory pressure on pulmonary gas exchange during anesthesia. Anesthesiology 39:285–290 11. Bardoczky GI, Yernault JC, Houben JJ et al (1995) Large tidal volume ventilation does not improve oxygenation in morbidly obese patients during anesthesia. Anesth Analg 81:385–388 12. 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Rothen HU,SporreB,EngbergG et al(1996) Atelectasisandpulmonaryshuntingduring induction of general anaesthesia: can they be avoided? Acta Anaesthesiol Scand 40:524–529 19. Tusman G, Bohm SH, Vazquez de Anda GF et al (1999) ‘Alveolar recruitment strategy’ improves arterial oxygenation during general anaesthesia. Br J Anaesth 82:8–13 20. Whalen FX, Gajic O, Thompson GB et al (2006) The effects of the alveolar recruitment maneuver and positive end-expiratory pressure on arterial oxygenation during laparo- scopic bariatric surgery. Anesth Analg 102:298–305 82 J. Sprung 21. Sprung J, Whalley DG, Falcone T et al (2002) The impact of morbid obesity, pneumo- peritoneum, and posture on respiratory system mechanics and oxygenation during laparoscopy. Anesth Analg 94:1345–1350 22. Dreyfuss D, Soler P, Basset G et al (1988) High inflation pressure pulmonary edema: respective effects of high airway pressure, high tidal volume, and positive end-expira- tory pressure. Am Rev Respir Dis 137:1159–1164 23. Dreyfuss D, Saumon G (1992) Barotrauma is volutrauma, but which volume is the one responsible? Intensive Care Med 18:139–141 24. Pelosi P, Croci M, Ravagnan I et al (1998) The effects of body mass on lung volumes, respiratory mechanics, and gas exchange during general anesthesia. Anesth Analg 87:654–660 25. Squadrone V, Coha M, Cerutti E et al (2005) Continuous positive airway pressure for treatment of postoperative hypoxemia: a randomized controlled trial. JAMA 293:589–595 26. Duggan M, McCaul CL, McNamara PJ et al (2003) Atelectasis causes vascular leak and lethal right ventricular failure in uninjured rat lungs. Am J Respir Crit Care Med 167:1633–1640 Respiratory issues and ventilatory strategies for morbidly obese patients 83 FLUID AND ELECTROLYTE EMERGENCY Fluid and electrolyte emergency J. BOLDT Fluid deficits andelectrolyte imbalances are common among surgical,traumatised and intensive care unit (ICU) patients. Fluid deficits can occur in the absence of obvious fluid loss secondary to vasodilation or generalised alterations of the endothelial barrier resultingin diffuse capillary leak. Thus, especially inthe inflam- matory patient, large fluid deficits become obvious. This situation is characterised by panendothelial injury with subsequent development of increased endothelial permeability, leading to a loss of proteins and a fluid shift from the intravascular to the interstitial compartment and resulting in interstitial oedema. Fluid deficits (or overload) are often associated with compromised acid–base status and elec- trolyte imbalance (Fig. 1). Chapter 9 · Metabolic Acidosi s – Diabetic Ketoacidosis, lactic acidosis – Salicylate poisoning (children) – Methanol, ethylene glycol poisoning – Renal failure – Diarrhoea · Metaboli c Alkalosis – Prolonged votiming – Diuretic the rapy – Hyperadrenocortical disease – Exogeno us base (antacids, bicarbonate IV, citrate toxicity after massive blood transfu sions Causes of Acid-Base Imbalances Fig. 1. Some causes of derangement in acid–base balance Principles of fluid/volume replacement and maintenance of electrolyte balance Managing patients with fluid deficits and/or disturbed electrolyte balance demands some basic consideration of the mechanisms, reasons and regulation (Figs. 2–4): fluid administered may stay in the intravascular compartment or equilibrate with the interstitial/intracellular fluid compartments. The antinatriuretic system (ANH), the renin–aldosterone–angiotensin system (RAAS) and the sympathetic nervous system (SNS) and other hormone systems are involved in the control of volume and the composition of each body compartment. The principal action of these neurohumoural systems is to retain water in order to restore water or intra- vascular volume deficits, to retainsodium in order to restore theintravascularvolume, and to increase the hydrostatic perfusion pressure through vasoconstriction. En- hanced activity of ANH, RAA S and SNS is known to occur in stress situations, e.g., during surgery. Although the norm al response to surgery and starvation results in increased metabolic activity,a pre-existing deficit of water or intravascularvolume can be expected to increase this activity further. If water or intravascular volume deficits and the stress-related stimulus of ANH, RAA and SNS are additive, fluid management could inhibit this process through counterregulatory mechanisms. There have been several attempts to inhibit or attenuate the activity of ANH and RAAS by administering different volumes of isotonic crystalloid solutions. It is known that ANH production is dependent on the maintenance of the extracellular volume and, in particular, the intravascular compartment (“preload”). Admini- stration of a restricted amount of crystalloid could possibly replace a previous Fig. 2. Composition and fluid shifts of the different compartments 88 J. Boldt Fluid balance – Adequate water is pre- sent and is distributed among the various compartments accord- ing to the body’s needs – Many things are freely exchanged between fluid compartments (e.g. water) – Fluid movements by: · bulk flow (blood and lymph circulation) · diffusion and osmosis Fig. 3. Organs that are involved in guaranteeing adequate fluid balance Electrolyte Balance · Aldosterone  [Na + ] [Cl - ][H 2 O] ¯ [K + ] · At rial Natriuretic Peptide (opposite effect) · Ant idiuretic Hormone  [H 2 O] (¯ [solutes]) · Parathyroid Hormone  [Ca++] ¯ [HPO 4 - ] (opposite effect) · Calcitonin · Female sex hormones [H 2 O] Fig. 4. Some mechanisms that are involved in guaranteeing electrolyte balance Fluid and electrolyte emergency 89 deficit of water, but the replacement of an intravascular volume deficit would require a much greater volume to inhibit the secretory stimulus of all the hormone systems committed to maintainingit. Thus, it can beexpected thatthe replacement of water alone will not inhibit the normal response of ANH and RAAS, whereas administration of a combination of crystalloid and colloid solutions (replacement of water deficit simultaneously with improvement in the effective intravascular volume) may achieve this goal. The primary goal of volume administration is to guarantee stable haemodyna- mics by rapid restoration of circulating plasma volume. Excessive fluid accumula- tion, particularly in the interstitial tissue, should be avoided. Starling’s hypothesis describes and analyses the exchange of fluid across biological membranes. Colloid oncotic pressure (COP) is an important factor in the determination of fluid flux across the capillary membrane between the intravascular and interstitial spaces. Thus, manipulation of COP appears to be useful for guaranteeing adequate circu- lating intravascular volume. The magnitude and duration of this volume effect will depend on the specific water-binding capacity of the plasma substitute and on how much of the infused solution stays in the intravascular space. Because of varying physicochemical properties,the solutions commonly usedfor volume replacement differ widely in COP, initial volume effects, and duration of intravascular persis- tence. Special conditions: fluids, electrolytes and the renal system in the elderly Renal function declines with age, and diseases affecting the kidney become more prevalent. Body composition changes with age: there is a relative decrease in total body water and a relative increase in body fat. In 80-year-olds, there is a 10–15% loss of total body water, mostly limited to the intracellular compartment; plasma volume and extracellular volumes are maintained. This results in altered propor- tions of extracellular and intracellular fluids: there is decreased intracellular fluid in proportion to total body water but a relative increase in extracellular fluid [1]. Approximately 0.5–1% of nephrons are lost with each year of life, mostly from the cortex [2]. Serum creatinine, however, remains generally unchanged, since skeletal muscle mass decreases at a similar rate to glomerular filtration rate (GFR). The elderly mainly losecortical nephrons; the rem aining medullary nephrons have less concentrating ability and thus excrete more free water, after which the homeo- static mechanisms of sodium and water balance are impaired: renal tubular res- ponse to aldosterone is reduced, and thus the ability to conserve sodium. There is a slow response to a sodium load owing to reduced GFR and impaired tubular function, and the ability to excrete a free water load and mobilise third-space fluid is decreased. The elderly have increased osmoreceptor sensitivity—they release more antidiuretic hormone (ADH) in response to hypertonicity. End-organ res- ponse to ADH, however, is altered so that less water is retained than in the young [1, 3]. Thirst perception is altered, and associated disease states may reduce the amount of fluid ingested. 90 J. Boldt In the setting of abnormal cardiovascular compensatory mechanisms, conser- vation and delayed excretion of sodium and free water could potentially result in hypervolaemia or hypovolaemia [4]. The elderly are vulnerable to electrolyte disturbances owing to abnormal physiology, pathology and iatrogenic causes. Most serum electrolytes do not alter in the healthy elderly, but serum potassium may increase with age, even though total body potassium is reduced. There is a signifi- cant risk of hyponatraemia after surgery, owing to ADH secretion provoked by surgical stress, chronic disease and such medications as thiazide diuretics. This may be compounded by the use of hypotonic maintenance fluids after surgery. Finally, the elderly are at risk of hyper- and hypokalaemia, which can be due to concurrent medication, disease or inadequate potassium supplementation in in- travenous maintenance fluids. Possible strategies of fluid/volume replacement Crystalloids Hypotonic (e.g., dextrose in water), isotonic (e.g., normal saline solution; Ringer’s solution [RL]) and hypertonic crystalloids (e.g., 7.5% saline solution) have to be distinguished when using crystalloids for volume replacement. Crystalloids are freely permeable to the vascular membrane and are therefore distributed mainly in the interstitial and/or intercellular compartment. Only 25% of the infused crystalloid solution remains in the intravascular space, whereas 75% extravasates into the interstitium [5]. Dilution of plasma protein concentration may also be accompanied by a reduction in plasma colloid oncotic pressure (COP) sub- sequently leading to tissue oedema. It has been shown in animal experiments that even massive crystalloid resuscitation is less likely to achieve adequate restoration of microcirculatory blood flow than is a colloidal-based volume replacement strategy [6]. In a study in patients who underwent major abdominal surgery and in whom crystalloids (RL) or colloids were used for volume replacement, Prien et al. [7] demonstrated significantly more voluminous intestinal oedema with the use of RL than with colloids. In an experimental trauma–haemorrhage model either colloids (dextran) or crystalloids (Ringer’s acetate) were used to replace blood loss after surgical trauma [8]. The crystalloid group showed significantly larger amounts of tissue water in muscle and jejunum than the colloid-treated group of animals. Crystalloids are frequently preferred because they are inexpensive and appear to be almost free of significant negative side-effects, and especially of any linked with coagulation. Interest has recently beenfocused on theinfluence of crystalloids on haemostasis. There is convincing evidence that useof crystalloids has a substan- tial influence on coagulation. Ruttmann et al. [9, 10] and Ng et al. [11] showed that in vivo dilution with crystalloids resulted in significant enhancement of coagula- tion. The reason for the hypercoagulable state appears to be an imbalance between naturally occurring anticoagulants and activated procoagulants, a reduction in Fluid and electrolyte emergency 91 antithrombin III probably being the most important [9]. Other authors have also documented hypercoagulability with the use of crystalloids [12]. This increase in coagulation seems to be independent of the type of crystalloid that has been used [12]. An early study reported that the increase in coagulation in patient in whom crystalloids were given during surgery was associated with an increased incidence of deep vein thrombosis [13]. Thus, taking new data into account, crystalloids can no longer begenerallyconsidered as the “goodguys” with regard to the coagulation process. What’s new in fluid/volume replacement strategies and treatment of electrolyte imbalances? It is now generally accepted that significant alterations in acid–base balance de- velop in patients to whom considerable amounts of 0.9% saline solution are infused. This has been described as “hyperchloraemic acidosis” [14, 15]. Thus use of large amounts the “physiological”, normal (0.9%) saline (NS) solution should be urgently avoided, because of the risk of producing (hyperchloraemic) acidosis (Fig. 4). One study in patients undergoing major spine surgery showed that this phenomenon occurred only when considerable amounts of normal saline solution were infused; use of RL was not associated with hyperchloraemic acidosis [16]. Unfortunately, most of the available colloids are not “balanced”, but include unphysiologically high concentrations of sodium and chloride, so that they do not fit into the concept of a balanced fluid/volume replacement strategy. Use of large amounts of such colloids may also be associated with metabolic acidosis: acute normovolaemic haemodilution (ANH) using either5% albumin or6% HES 200/0.5 (aim: haematocrit 22%) in patients undergoing gynaecological surgery resulted in metabolic acidosis in both groups [17]. Dilution of extracellular bicarbonate or changes in strong iron differences and albumin concentration may be explanations of this type of acidosis. Others found decreases in base excess (BE) only after the use of standard HMW-HES and not after albumin [18]. Little information is available on the clinical value of this type of acidosis. Negative consequences of hyperchloraemic acidosis on organ function have been elucidated by some studies: in patients undergoing abdominal aortic aneurysm repair, either RL (total dose: 6,800 ml) or NS (total dose: 7,000 ml) was used for volume replacement in a double-blind fashion [19]. Only the NS-treated patients developed hyperchloraemic acidosis. They needed significantly more blood pro- ducts than the RL-treated patients. There is also some evidence that hyperchlorae- mic acidosis may impair end-organ perfusion and organ function (e.g. splanchnic perfusion [19]) or interfere with the cellular exchange mechanism [20]. In animal experiments, hyperchloraemic acidosis was associated with a reduction in renal blood flow (which was most probably due to vasoconstriction) and a negativeeffect on glomerular filtration rate [20]. In noncardiac surgical patients, Bennett-Guer- rero et al. [21] demonstrated that administration of unbalanced salt solutions resulted in reduced urine output and increased serum creatinine levels postopera- 92 J. Boldt tively. In elderly patients undergoing elective surgical procedures, either conven- tional HMW-HES (hetastarch) or a hetastarch in a balanced electrolyte andglucose formulation (Hextend â ) was used [19]. Only patients treated with the conventional hetastarch developed hyperchloraemic acidosis (postoperative BE: –0.2 versus –3.8 mmol/l). Gastric tonometry indicatedbetter gastric mucosal perfusion in thegroup treated with the balanced hetastarch solution (Hextend â ) than in the group treated with a hetastarch dissolved in saline. The search for more physiologically balanced i.v. fluids that fulfil the principle of a balanced volume and fluid replacement strategy is fundamentally important. In a prospective, randomised, controlled, and double-blind study conducted in patients undergoing major abdominal surgery, a total balanced volume replace- ment strategy including a new balanced hydroxyethyl starch solution (HES) and a balanced crystalloid solution was compared with a conventional, nonbalanced fluid regimen [22]. The new balanced 6% HES 130/0.42 contained Na + 140 mmol/l, Cl – 118 mmol/l, K + 4 mmol/l, Ca 2+ 2.5 mmol/l, Mg 2+ 1 mmol, acetate 24 mmol/l, malate 5 mmol/l (B Braun, Melsungen, Germany). The complete balanced volume replacement strategy, including a new balanced HES preparation, resulted in significantly fewer derangements in acid–base status than did a nonbalanced volume replacement regimen. How to avoid under-/overloading the patient? Although the principles of fluid/volume therapy are widely accepted (Fig. 5), esti- mating the necessary fluid/volume still remains a challenge. The question of how volume/fluid therapy should be guided has not yet been decided. In spite of some negative data, pulmonary artery (PA) catheters are still used in several centres, and data obtained by means of this monitoring instrument can be helpful in guiding volume therapy. It has to be emphasised that cardiac filling pressures (central venous pressure [CVP], pulmonary capillary wedge pressure [PCWP]) are often misleading as an index for assessing optimal LV loading. Cardiac filling pressure may be influenced by several factors other than blood volume, including those influencing cardiac performance, vascular compliance and intrathoracic pressure. Particularly in patients with altered ventricular compliance, commonly monitored parameters such CVP, right atrial pressure (RAP) or right ventricular pressure (RVP) have not always proved sufficiently valid to be used in judgement of loading conditions. Measurement of right ventricular end-systolic and end-diastolic vol- umes (RVESV, RVEDV) by the thermodilution (TD) technique is another easily performed bedside monitoring technique with noaccumulation of toxicindicators, and loading can probably be achieved more accurately by this means. It is unaf- fected by arbitrary and poorly reproducible zero points for pressure transducers and can be carried out at the bedside. Echocardiography appears to be the most reliable monitoring instrument; owing to its cost, however, it is not available for every cardiac surgery patient in the perioperative period. Measurement of intratho- racic blood volume (ITBV) by the PICCO system is another technique by which Fluid and electrolyte emergency 93 [...]... 121:2000–2008 13 Jardin F, Vieillard-Baron A (2006) Ultrasonographic examination of the venae cavae Intensive Care Med 32 :2 03 206 14 Reynolds RM, Padfield PL, Seckl JR (2006) Disorders of sodium balance BMJ 33 2:702–705 15 Saeed BO, Beaumont D, Handley GH et al (2002) Severe hyponatremia J Clin Pathol 55:8 93 896 16 Kumar S, Berl T (1998) Sodium Lancet 35 2:220–222 17 Yancey PH, Clark ME, Hand SC et al... syndrome? 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Schött U, Lindbom LO, Sjöstrand U (1988) Hemodynamic effects of colloid concentration in experimental hemorrhage: a comparison of Ringer’s acetate, 3% dextran-60 and 6% dextran-70 Crit Care Med 16 :34 6 35 2 9 Ruttmann TG, James MFM, Finlayson J (2002) Effects on coagulation of intravenous crystalloid or colloid in patients undergoing peripheral vascular surgery Br J Anaesth 89:226– 230 10 Ruttmann TG, James... and tubular creatinine secretion, thereby limiting rises in plasma creatinine [3, 4] Table 1 Estimated expected baseline creatinine (mmol/l) calculated (modified from [9]) for patients with glomerular filtration rate (GFR) assumed to be at the lower end of the normal 2 range (75 ml/min per 1. 73 m ) Age (years) Black men White men Black women White women 20–24 133 115 106 88 25–29 133 106 97 88 30 39 . Crit Care Med 167:1 633 –1640 Respiratory issues and ventilatory strategies for morbidly obese patients 83 FLUID AND ELECTROLYTE EMERGENCY Fluid and electrolyte emergency J. BOLDT Fluid deficits andelectrolyte. Hemodynamic effects of colloid concentra- tion in experimental hemorrhage: a comparison of Ringer’s acetate, 3% dextran-60 and 6% dextran-70. Crit Care Med 16 :34 6 35 2 9. Ruttmann TG, James MFM, Finlayson. Brock-Utne JG et al (2002) Morbid obesity and tracheal intubation. Anesth Analg 94: 732 – 736 5. Resta O, Foschino-Barbaro MP, Legari G et al (2001) Sleep-related breathing disorders, loud snoring and