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بسم الله الرحمن بسم الله الرحمن الرحيمالرحيم
Stress Response And Severely Obese For OP_CAB
Amr Abdelmonem , M.D.
By Amr Abdelmonem,MD.Assistant professor of anesthesia ,surgical intensive care and clinical nutrition in faculty of medicine, Cairo university
Member of North American Association For The Study Of Obesity
Member of the American society of regional anesthesia and pain medicine
Obesity is a well-recognized risk factor for mortality from cardiovascular diseasesMcGee DL.body mass index and mortality.Ann Epidemiol 2005;15:87-97
Obesity is associated with a 3-or-more-fold increase in the risk of fatal and nonfatal myocardial infarction
Dagenais GR, Yi Q, Mann JF et al. Prognostic impact of body weight and abdominal obesity in women and men with cardiovascular disease. Am Heart J 2005; 149:54–60.
The American Heart Association has reclassified obesity as a major, modifiable risk factor for coronary heart disease
Poirier P, Giles TD, Bray GA et al. Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss: an update of the 1997 American Heart Association Scientific Statement on Obesity and Heart Disease from the Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism. Circulation 2006; 113:898–918
Waist circumference maintains the strongest association with cardiovascular disease risk factors than other measures of obesity(BMI,TBF,%BF, skin fold thickness)
Andy M,et al .Measures of adiposity and cardiovascular disease risk factors .Obes Res.2007;15:785
Definition
Neurohormonal changes that are reproducible from patient to patient With a host of biologic alterations following tissue injuryNCHS.Advance report of final mortality statistics ,1992.Hyattsville,Maryland: US Department
of Health and Human services, Public Health Service ,CDC,1994
Biologic Adaptation
Cardiovascular alterationsCardiovascular alterations
Neurohormonal changesDesborough JP, Hall GM. Endocrine response to surgery. In: Kaufman L. Anaesthesia Review, Vol. 10. Edinburgh:
Churchill Livingstone,1993; 131–48 Autonomic nervous systemAutonomic nervous system Sympathetic nervous system activationSympathetic nervous system activationExcess release of Excess release of catecholamines (from nerves , ganglia catecholamines (from nerves , ganglia
and and the heartthe heart) )
Adrenal medullaAdrenal medulla Excess release of Excess release of catecholamines catecholamines (epinephrine and nor-epinephrine)(epinephrine and nor-epinephrine)
Adrenal cortex Adrenal cortex Excess release of Excess release of aldosteronealdosterone (mineralocoticoid) (mineralocoticoid)
Posterior pituitary glandPosterior pituitary glandExcess release of Excess release of vasopressinvasopressin (ADH) (ADH)
Patients with American Society of Anesthesiology physical status 1
SA node stimulationSA node stimulation ➞ ➞ tachycardiatachycardia ➞ ➞ ↑myocardial ↑myocardial oxygen demandoxygen demand
Re –entry excitationRe –entry excitation ➞ ➞ tachyarrhythmia'stachyarrhythmia's➞ ➞ ↑myocardial ↑myocardial oxygen demandoxygen demand
Stimulation of beta-adrenergic receptors on the cardiac Stimulation of beta-adrenergic receptors on the cardiac cell membranecell membrane ➞ ➞ ↑intracellular cAMP↑intracellular cAMP ➞ ➞ activating Caactivating Ca2+ 2+
channelschannels ➞ ➞ ↑contractility↑contractility ➞ ➞ ↑myocardial oxygen ↑myocardial oxygen demanddemand
Salt and water retentionSalt and water retention ➞ ➞ ↑preload↑preload➞ ➞ ↑myocardial ↑myocardial oxygen demandoxygen demand
Hypokalemia Hypokalemia ➞➞ tachycardiatachycardia ➞ ➞ ↑myocardial oxygen ↑myocardial oxygen demanddemand
The Myocardial Oxygen SupplyThe Myocardial Oxygen SupplyAlexander RW,Schlant RC,Fuster V,et al:Hurst's The Heart ,9th ed.New York,McGraw-Alexander RW,Schlant RC,Fuster V,et al:Hurst's The Heart ,9th ed.New York,McGraw-
Hill,1998Hill,1998
Normally CBF is coupled to ONormally CBF is coupled to O2 demand demand
CBF = 80 ml/min/100gCBF = 80 ml/min/100g
Normal ONormal O22 delivery= 16 ml/min/100g delivery= 16 ml/min/100g
Normal ONormal O22 consumption= 8-12 ml/min/100g consumption= 8-12 ml/min/100g
OO22 extraction ratio is 60-75% extraction ratio is 60-75%
Therefore the myocardium Therefore the myocardium
is supply dependentis supply dependent
SNS StimulationSNS Stimulation
αα adrenoceptors stimulation adrenoceptors stimulation ➞➞VCVC ➞ ➞ followed by VDfollowed by VD (sympatholysis)(sympatholysis)
The mechanismThe mechanism
↑↑myocardial Omyocardial O22 demand demand ➞ ➞ accumulation of VD metabolitesaccumulation of VD metabolites
Active hyperemiaActive hyperemia ➞ ➞ prolonged coronary VD (increased supply)prolonged coronary VD (increased supply) ➞ ➞ balancing the demandbalancing the demand ➞ ➞ no ischemiano ischemia
For OP-CAB patientsFor OP-CAB patients
InsulinReaven GM. Role of insulin resistance in human disease .Diabetes.1988;37:1595
Increased sodium retention
Increased sympathetic nervous system activity
Alteration in the mechanics of blood vessels
LeptinIoanna S,et al. Baroreflex sensitivity in obesity.Obes Res 2007;15:1685
Reduction of baroreflex sensitivity
Ventricular dilatation and eccentric hypertrophyPiercarlo B,et al . Impact of obesity on left ventricular mass . Obes Res 2007;15:2019
Diastolic dysfunction+ systolic dysfunctionKenchaiah S,et al .obesity and the risk of heart failure.N Engl J Med.2002;347:305
Obesity cardiomyopathy
↑myocardial O2 demandGalinier M,et al. obesity and cardiac failure .Arch Mal Coeur Vaiss.2005;98:39
↓
↓
↓
Kidney functions and electrolyte Kidney functions and electrolyte imbalanceDesborough JP. Physiological responses to surgery and trauma. In: Hemmings HC Jr, Hopkins PM, eds. Foundations of Anaesthesia.
London: Mosby, 1999: 713–20
ADH Catecholamines Aldosterone
SIADH Hypokalemia and hypomagnesemia
Hyponatremia + Hypokalemia + Hypomagnesemia
Patients with American Society of Anesthesiology physical status 1Patients with American Society of Anesthesiology physical status 1
Severe obese for OP-CAP
Fluid overload Hypokalemia+ ↓BRS Ioanna S,et al. Baroreflex sensitivity in obesity.Obes Res 2007;15:1685
Hypomagnesemia
CHFGalinier M,et al. obesity and cardiac failure .Arch Mal Coeur Vaiss.2005;98:39 Tachyarrhythmia
Ioanna S,et al. Baroreflex sensitivity in obesity.Obes Res 2007;15:1685
Cellular edemaSheeran P, Hall GM. Cytokines in anaesthesia. Br J Anaesth 1997; 78: 201–19
Intensify the stress responseTepaske R. Immunonutrition. Curr Opin Anaesthesiol 1997; 10: 86–91
Diffuse metabolic alterationsDiffuse metabolic alterations
1.Aantaa R, Scheinin M. Alpha2-adrenergic agents in anaesthesia. Acta Anaesthesiol Scand 1993; 37: 1–162. Cuthbertson DP. Observations on the disturbance of metabolism produced by injury to the limbs. Q J Med 1932; 1: 233–46 3. UKPDS group. Effect of intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risks of complications in patients with type 2 diabetes. Lancet 1998; 352: 837–53
Neurohormonal changesNeurohormonal changes
Autonomic nervous systemAutonomic nervous system Sympathetic nervous system activationSympathetic nervous system activationExcess release of catecholaminesExcess release of catecholamines Adrenal medullaAdrenal medulla Excess release of catecholamines Excess release of catecholamines (epinephrine and nor-epinephrine)(epinephrine and nor-epinephrine) Adrenal cortex Adrenal cortex Excess release of cortisol (glucocoticoid)Excess release of cortisol (glucocoticoid) Anterior pituitary glandAnterior pituitary gland Increased secretion of ACTH and Growth hormone.Increased secretion of ACTH and Growth hormone. Pancreas Pancreas
Increased glucagon secretion and Increased glucagon secretion and decreased insulin secretiondecreased insulin secretion Thyroid glandThyroid glandDecreased free TDecreased free T44 and free T and free T33 Increased conversion of Free TIncreased conversion of Free T44 to inactive T to inactive T33(rT(rT33)) White adipose tissueWhite adipose tissueDecreased leptin hormone secretionDecreased leptin hormone secretionZeev N,etal.Zeev N,etal.EndocrinologyEndocrinology.1999;84:2438.1999;84:2438
Glycogen
Glucose -6-phosphate
Liver Glucagon + epinephrine+ GH
Blood
Cells
Insulin Hypoinsulinemia +Insulin resistance
Cortisol +catecho +GH +FFA
Hyperglycemia
Adipocytes catecholamines FFA
25%oxidised
75%Re-esterified
hydrolysis
glycerol
Skeletal MuscleVisceral ptns
Cortisol +catecho aa
Diabetes of stress
Severely obese for OP-CAB
Insulin resistance
Cortisol FFA Cytokines
Type –II diabetes
+
Diabetes of stress
Diabetic ketoacidosis
Resistin
Neurohormonal changes Autonomic nervous systemAutonomic nervous systemSympathetic nervous system activationSympathetic nervous system activationExcess release of catecholaminesExcess release of catecholaminesAantaa R, Scheinin MAantaa R, Scheinin M. . Alpha2-adrenergic agents in anaesthesia. Alpha2-adrenergic agents in anaesthesia. Acta Anaesthesiol Acta Anaesthesiol
ScandScand 1993; 37: 1–16 1993; 37: 1–16
Adrenal medulla Adrenal medulla Excess release of catecholamines Excess release of catecholamines (epinephrine and nor-epinephrine)(epinephrine and nor-epinephrine)DesboroughDesborough J,et al . The J,et al . The stressstress responseresponse toto trauma and trauma and surgersurgery . y . Br J AnaesthBr J Anaesth 2000; 2000; 8585: :
109–17 109–17
Increased release of cytokinesIncreased release of cytokinesSheeran P, Hall GM. Cytokines in anaesthesia. Sheeran P, Hall GM. Cytokines in anaesthesia. Br J AnaesthBr J Anaesth 1997; 78: 201–19 1997; 78: 201–19
Patients with American Society of AnesthesiologyPatients with American Society of Anesthesiology physical status 1 physical status 1
Increased tendency toward hypercoagulabilityIncreased tendency toward hypercoagulability1.1. Increased conc. of plasma fibrinogenIncreased conc. of plasma fibrinogen
2.2. Increased platelets aggregation(PAF)Increased platelets aggregation(PAF)
3.3. Increased conc. of plasminogen activator inhibitor Increased conc. of plasminogen activator inhibitor (impaired fibrinolysis)(impaired fibrinolysis)
White blood cell and immune functionWhite blood cell and immune functionAbnormalities in cell mediated immunity Abnormalities in cell mediated immunity
Severely obese for OP-CAB
Tendency toward hypercoagulabilityTendency toward hypercoagulabilityRimm EB,et al. Body size and fat istribution as predictors of coronary heart disease ,Am J Rimm EB,et al. Body size and fat istribution as predictors of coronary heart disease ,Am J
Epidemiol.1995;141:1117 Epidemiol.1995;141:1117
1.1. Acute phase proteins (increased)Acute phase proteins (increased)2.2. Plasminogen activator inhibitor (increased)Plasminogen activator inhibitor (increased)
ConsequencesConsequencesClotting of grafts, acute coronary thrombosis and MIClotting of grafts, acute coronary thrombosis and MI
White blood cell and cell mediated immunityWhite blood cell and cell mediated immunityLow grade inflammationLow grade inflammationAllison D, et al . Obesity as a disease .Obes Res 2008;16:1161Allison D, et al . Obesity as a disease .Obes Res 2008;16:1161
Mechanisms responsible for surgical trauma-induced hormonal and autonomic changes
Neural stimuli arising at the site of injured tissues
↑CatecholaminesEgdahl RH. Pituitary–adrenal response following
trauma to the isolated leg. Surgery 1959; 6: 9–21
↑cortisolEnquist A, Brandt MR, Fernandes A, Kehlet H.
The blocking effect of epidural analgesia on the
adrenocortcial and hyperglycaemic response
s to surgery. Acta Anaesthesiol Scand 1977; 21: 330–35
Release of cytokinesHelmy SAK, Wahby MAM, El-Nawaway M. The effect of anaesthesia
and surgery on plasma cytokine production. Anaesthesia 1999; 54: 733–8
Hypothermia Frank SM,etal.Anesthesiology.1995;82:83
Transient hypotension ,hypoxemia and hypercarbia Michael J.Critical Care.1997
Hypoleptinemia (↓TSH)Zeev N.Clinical Endocrinology,1999
Hypomagnesemia Anastasios K.Endocrinology.2003
↑Acute phase proteins↓albumin &transferrin↓zinc&iron Kehlet H. Multimodal approach to control postoperative pathophysiolog
y and rehabilitation. Br J Anaesth 1997; 78
Sheeran P, Hall GM. Cytokines in anaesthesia. Br J Anaesth 1997
Anne-Sopie M,et al.Circulating IL-6 concentrations and abdominal adiposity.Obey Res2008;16:1487
The effect of anaesthesia on the stress
response to cardiac surgery
Large doses of morphine Large doses of morphine ((4 mg kg–1) block the 4 mg kg–1) block the secretion of growth hormone and inhibit cortisol release secretion of growth hormone and inhibit cortisol release until the onset of cardiopulmonary bypass (CPB). until the onset of cardiopulmonary bypass (CPB).
Desborough JPDesborough JP. . Physiological responses to surgery and trauma. In: Hemmings HC Jr, Hopkins PM, eds. Physiological responses to surgery and trauma. In: Hemmings HC Jr, Hopkins PM, eds. Foundations of Foundations of
AnaesthesiaAnaesthesia. London: Mosby, 1999: 713–20. London: Mosby, 1999: 713–20
Fentanyl Fentanyl ((50–100 µg kg–1), sufentanil (20 µg kg–1) and 50–100 µg kg–1), sufentanil (20 µg kg–1) and alfentanil (1.4 mg kg–1) suppress pituitary hormone alfentanil (1.4 mg kg–1) suppress pituitary hormone secretion for OP_CABsecretion for OP_CAB Desborough JP, Hall GM. Modification of the hormonal and metabolic Desborough JP, Hall GM. Modification of the hormonal and metabolic
response to surgery by narcotics and general anaesthesia. response to surgery by narcotics and general anaesthesia. Clin AnaesthesiolClin Anaesthesiol 1989; 3: 317–34 1989; 3: 317–34 . .
A A highhigh--dose opioid technique leads inevitably to dose opioid technique leads inevitably to prolonged ventilatory support prolonged ventilatory support
Kehlet H. Multimodal approach to control postoperative pathophysiology and rehabilitation. Br J Anaesth 1997; 78: 606–17
Perioperative thoracic epidural anaesthesia has been Perioperative thoracic epidural anaesthesia has been used successfully in the management of patients used successfully in the management of patients undergoing coronary artery bypass undergoing coronary artery bypass surgerysurgeryLiem TH, Hasenbos MAWM, Booij Liem TH, Hasenbos MAWM, Booij
LHDJ, Gielen MJM. Coronary artery bypass grafting using two different anaesthetic effects: Part 2: Postoperative outcome. LHDJ, Gielen MJM. Coronary artery bypass grafting using two different anaesthetic effects: Part 2: Postoperative outcome.
J Cardithorac Vasc AnesthJ Cardithorac Vasc Anesth 1992; 6: 156–61 1992; 6: 156–61
A study showed that thoracic epidural A study showed that thoracic epidural anaesthesia and general anaesthesia in anaesthesia and general anaesthesia in cardiac surgery attenuated the myocardial cardiac surgery attenuated the myocardial sympathetic response and was associated with sympathetic response and was associated with decreased myocardial damage as determined decreased myocardial damage as determined by less release of troponin Tby less release of troponin T
Loick HM, Schmidt C, van Aken H Loick HM, Schmidt C, van Aken H et al. et al. High thoracic epidural anesthesia, but not clonidine, attenuates the perioperative High thoracic epidural anesthesia, but not clonidine, attenuates the perioperative
stress response via sympatholysis and reduces the release of troponin T in patients undergoing coronary artery bypass stress response via sympatholysis and reduces the release of troponin T in patients undergoing coronary artery bypass
grafting. grafting. Anesth AnalgAnesth Analg 1999; 88: 701–9 1999; 88: 701–9
In medical patients, The sympatholytic effects of the blockade of cardiac sympathetic efferents and afferents may improve the balance of oxygen delivery and consumption
Meissner A, Rolf N, Van Aken H. Thoracic epidural anesthesia and the patient with heart disease: Meissner A, Rolf N, Van Aken H. Thoracic epidural anesthesia and the patient with heart disease:
benefits, risks and controversies. benefits, risks and controversies. Anesth AnalgAnesth Analg 1997; 1997; 8585: 598–612 : 598–612
Anesthetic Management of the Patient Receiving Unfractionated Heparin during cardiac surgery
Regional Anesthesia and pain medicine ,Vol 29,No 2 Suppl1(March-April),2004:pp1-11
Currently, insufficient data and experience are available to Currently, insufficient data and experience are available to determine if the risk of neuraxial hematoma is increased determine if the risk of neuraxial hematoma is increased when combining neuraxial techniques with the full when combining neuraxial techniques with the full anticoagulation of cardiac surgery. anticoagulation of cardiac surgery.
Combining neuraxial techniques with intraoperative anticoagulation with heparin during cardiac surgeries seems acceptable with the following cautions:
● Avoid the technique in patients with other coagulopathies.● Heparin administration should be delayed for 1 hour after needle
placement.● Indwelling neuraxial catheters should be removed 2 to 4 hours after the last heparin dose and the patient’s coagulation status is evaluated; ●Reheparinization should occur 1 hour after catheter removal.
● ● Monitor the patient postoperatively to provide early detection of motor blockade and consider use of minimal concentration of local anesthetics to enhance the early detection of a spinal hematoma.
● Although the occurrence of a bloody or difficult neuraxial needle placement may increase risk, there are no data to support mandatory cancellation of a case.
● Direct communication with the surgeon and a specific risk-benefit decision about proceeding in each case is warranted.
● Antiplatelet medications, low molecular weight heparin (LMWH) and oral anticoagulants may increase the risk of bleeding complications for patients receiving standard heparin.
Recommendations: Limiting, Diagnosing, and Treating Neuraxial Injury
ASRA practice Advisory on neurologic complications in regional anesthesia and pain medicine,Regional Anesthesia and pain medicine,Vol 33,No 5(september-
october)2008:pp4040-415
•• Epidural anesthetic procedures using the thoracic approach are neither safer nor riskier than using the lumbar approach. (Class I)
Surgical positioning and specific space-occupying extradural lesions (e.g., severe spinal stenosis, epidural lipomatosis, ligamentum flavum hypertrophy, or ependymoma) have been associated with temporary or permanent spinal cord injury in conjunction with neuraxial regional anesthetic techniques.
Awareness of these conditions should prompt consideration of risk vs. benefit when contemplating neuraxial regional anesthetic techniques. (Class II)
Diagnosis and treatment
• Magnetic resonance imaging (MRI) is the diagnostic modality of choice for suspected neuraxial lesions. Computed tomography (CT) should be used for rapid diagnosis if MRI is not immediately unavailable, especially when neuraxial compression injury is suspected.
(Class I)
•Diagnosis of a compressive lesion within or near the neuraxis demands immediate neurosurgical consultation for consideration of decompression. (Class I)
Home messageHome message
The stress response to surgery comprises a number of hormonal changes initiated by neuronal activation of the hypothalamic–pituitary–adrenal axis
The overall metabolic effect is one of catabolism of stored body fuels
In general, the magnitude and duration of the response are proportional to the surgical injury therefore exaggerated in cardiac surgeries
Understanding the neurobiological and pathophysiological natures of the of the severely obese patients will enable physicians and scientists to approach the proper management of their stress response especially for CAB surgeries
Regional anesthesia with low concentrations local anesthetic agents inhibits the stress response to surgery and can also influence postoperative outcome by beneficial effects on organ function.