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Stress response and OP_CAB for obese

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Title: Stress response and OP_CAB for obese Author: Amr Last modified by: Amr Created Date: 2/9/2005 11:14:53 AM Document presentation format: On-screen Show – PowerPoint PPT presentation

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Title: Stress response and OP_CAB for obese


1
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2
Stress Response
And
Severely Obese For OP_CAB

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
Amr Abdelmonem , M.D.

3
Obesity is a well-recognized risk factor for
mortality from cardiovascular diseases McGee
DL.body mass index and mortality.Ann Epidemiol
20051587-97
4
  • 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 1495460.
  •  
  • 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 113898918

5
  • 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.200715785

6
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8
Definition
Neurohormonal changes that are reproducible from
patient to patient With a host of biologic
alterations following tissue injury
NCHS.Advance report of final mortality statistics
,1992.Hyattsville,Maryland US Department of
Health and Human services, Public Health Service
,CDC,1994
9
Biologic Adaptation
10
Cardiovascular alterations
11
Neurohormonal changes Desborough JP, Hall GM.
Endocrine response to surgery. In Kaufman L.
Anaesthesia Review, Vol. 10. Edinburgh
Churchill Livingstone,1993 13148
  • Autonomic nervous system
  • Sympathetic nervous system activation
  • Excess release of catecholamines (from nerves ,
    ganglia and the heart)
  • Adrenal medulla
  • Excess release of catecholamines
  • (epinephrine and nor-epinephrine)
  • Adrenal cortex
  • Excess release of aldosterone (mineralocoticoid)
  • Posterior pituitary gland
  • Excess release of vasopressin (ADH)

12
Patients with American Society of Anesthesiology
physical status 1
  • SA node stimulation ? tachycardia ? ?myocardial
    oxygen demand
  • Re entry excitation ? tachyarrhythmia's?
    ?myocardial oxygen demand
  • Stimulation of beta-adrenergic receptors on the
    cardiac cell membrane ? ?intracellular cAMP ?
    activating Ca2 channels ? ?contractility ?
    ?myocardial oxygen demand
  • Salt and water retention ? ?preload? ?myocardial
    oxygen demand
  • Hypokalemia ? tachycardia ? ?myocardial oxygen
    demand

13
The Myocardial Oxygen Supply Alexander RW,Schlant
RC,Fuster V,et alHurst's The Heart ,9th ed.New
York,McGraw-Hill,1998
  • Normally CBF is coupled to O2 demand
  • CBF 80 ml/min/100g
  • Normal O2 delivery 16 ml/min/100g
  • Normal O2 consumption 8-12 ml/min/100g
  • O2 extraction ratio is 60-75
  • Therefore the myocardium
  • is supply dependent

14
SNS Stimulation
  • a adrenoceptors stimulation ?VC ? followed by VD
    (sympatholysis)
  • The mechanism
  • ?myocardial O2 demand ? accumulation of VD
    metabolites
  • Active hyperemia ? prolonged coronary VD
    (increased supply) ? balancing the demand ? no
    ischemia

15
For OP-CAB patients

16
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17
Insulin Reaven GM. Role of insulin resistance in
human disease .Diabetes.1988371595
Increased sodium retention Increased
sympathetic nervous system activity Alteration
in the mechanics of blood vessels
Leptin Ioanna S,et al. Baroreflex sensitivity in
obesity.Obes Res 2007151685
Reduction of baroreflex sensitivity
18
Ventricular dilatation and eccentric
hypertrophy Piercarlo B,et al . Impact of obesity
on left ventricular mass . Obes Res 2007152019
?
Diastolic dysfunction systolic
dysfunction Kenchaiah S,et al .obesity and the
risk of heart failure.N Engl J Med.2002347305
?
Obesity cardiomyopathy
?
?myocardial O2 demand Galinier M,et al. obesity
and cardiac failure .Arch Mal Coeur
Vaiss.20059839
19
Kidney functions and electrolyte
imbalance Desborough JP. Physiological responses
to surgery and trauma. In Hemmings HC Jr,
Hopkins PM, eds. Foundations of Anaesthesia.
London Mosby, 1999 71320
20
Patients with American Society of
Anesthesiology physical status 1
ADH
Catecholamines
Aldosterone
SIADH
Hypokalemia and hypomagnesemia
Hyponatremia Hypokalemia Hypomagnesemia
21
Severe obese for OP-CAP
Hypokalemia ?BRS Ioanna S,et al.
Baroreflex sensitivity in obesity.Obes Res
2007151685
Hypomagnesemia
Fluid overload
CHF Galinier M,et al. obesity and cardiac failure
.Arch Mal Coeur Vaiss.20059839
Tachyarrhythmia Ioanna S,et al. Baroreflex
sensitivity in obesity.Obes Res 2007151685
Cellular edema Sheeran P, Hall GM. Cytokines in
anaesthesia. Br J Anaesth 1997 78 20119
Intensify the stress response Tepaske R.
Immunonutrition. Curr Opin Anaesthesiol 1997 10
8691
22
Diffuse metabolic alterations
1.Aantaa R, Scheinin M. Alpha2-adrenergic agents
in anaesthesia. Acta Anaesthesiol Scand 1993
37 116 2. Cuthbertson DP. Observations on the
disturbance of metabolism produced by injury to
the limbs. Q J Med 1932 1 23346 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 83753
23
Neurohormonal changes
  • Autonomic nervous system
  • Sympathetic nervous system activation
  • Excess release of catecholamines
  • Adrenal medulla
  • Excess release of catecholamines
  • (epinephrine and nor-epinephrine)
  • Adrenal cortex
  • Excess release of cortisol (glucocoticoid)
  • Anterior pituitary gland
  • Increased secretion of ACTH and Growth hormone.
  • Pancreas
  • Increased glucagon secretion and decreased
    insulin secretion
  • Thyroid gland
  • Decreased free T4 and free T3
  • Increased conversion of Free T4 to inactive
    T3(rT3)
  • White adipose tissue
  • Decreased leptin hormone secretion
  • Zeev N,etal.Endocrinology.1999842438

24
Glycogen
Liver
Glucagon epinephrine GH
Glucose -6-phosphate
Hyperglycemia
Blood
Hypoinsulinemia Insulin resistance
Diabetes of stress
Insulin
Cells
25oxidised
Cortisol catecho GH FFA
hydrolysis
Adipocytes
catecholamines
FFA
75 Re-esterified
glycerol
Skeletal Muscle Visceral ptns
Cortisol catecho
aa
25
Severely obese for OP-CAB
Insulin resistance
FFA
Cytokines
Cortisol
Type II diabetes
Resistin

Diabetes of stress
Diabetic ketoacidosis
26
Hematologic Alterations
27
Neurohormonal changes
  • Autonomic nervous system
  • Sympathetic nervous system activation
  • Excess release of catecholamines
  • Aantaa R, Scheinin M. Alpha2-adrenergic agents in
    anaesthesia. Acta Anaesthesiol Scand 1993 37
    116
  • Adrenal medulla
  • Excess release of catecholamines
  • (epinephrine and nor-epinephrine)
  • Desborough J,et al . The stress response to
    trauma and surgery . Br J Anaesth 2000 85
    10917
  • Increased release of cytokines
  • Sheeran P, Hall GM. Cytokines in anaesthesia. Br
    J Anaesth 1997 78 20119

28
Patients with American Society of Anesthesiology
physical status 1
  • Increased tendency toward hypercoagulability
  • Increased conc. of plasma fibrinogen
  • Increased platelets aggregation(PAF)
  • Increased conc. of plasminogen activator
    inhibitor (impaired fibrinolysis)
  • White blood cell and immune function
  • Abnormalities in cell mediated immunity

29
Severely obese for OP-CAB
  • Tendency toward hypercoagulability
  • Rimm EB,et al. Body size and fat istribution as
    predictors of coronary heart disease ,Am J
    Epidemiol.19951411117
  • Acute phase proteins (increased)
  • Plasminogen activator inhibitor (increased)
  • Consequences
  • Clotting of grafts, acute coronary thrombosis and
    MI
  • White blood cell and cell mediated immunity
  • Low grade inflammation
  • Allison D, et al . Obesity as a disease .Obes Res
    2008161161

30
Mechanisms responsible for
surgical trauma-induced
hormonal and autonomic changes
31
Neural stimuli arising at the site of injured
tissues
Release of cytokines Helmy SAK, Wahby MAM,
El-Nawaway M. The effect of anaesthesia and
surgery on plasma cytokine production.
Anaesthesia 1999 54 7338
?Catecholamines Egdahl RH. Pituitaryadrenal
response following trauma to the isolated leg.
Surgery 1959 6 921
?cortisol Enquist 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 33035
?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
Hypothermia Frank SM,etal.Anesthesiology.1995828
3
Transient hypotension ,hypoxemia and
hypercarbia Michael J.Critical Care.1997
Hypoleptinemia (?TSH)Zeev N.Clinical
Endocrinology,1999
Hypomagnesemia Anastasios K.Endocrinology.2003
32
Anne-Sopie M,et al.Circulating IL-6
concentrations and abdominal adiposity .Obey
Res2008161487
33
The effect of anaesthesia on the stress response
to cardiac surgery
  • Large doses of morphine (4 mg kg1) block the
    secretion of growth hormone and inhibit cortisol
    release until the onset of cardiopulmonary bypass
    (CPB).
  • Desborough JP. Physiological responses to
    surgery and trauma. In Hemmings HC Jr, Hopkins
    PM, eds. Foundations of Anaesthesia. London
    Mosby, 1999 71320
  • Fentanyl (50100 µg kg1), sufentanil (20 µg
    kg1) and alfentanil (1.4 mg kg1) suppress
    pituitary hormone secretion for OP_CAB Desborough
    JP, Hall GM. Modification of the hormonal and
    metabolic response to surgery by narcotics and
    general anaesthesia. Clin Anaesthesiol 1989 3
    31734 .
  • A high-dose opioid technique leads inevitably to
    prolonged ventilatory support
  • Kehlet H. Multimodal approach to control
    postoperative pathophysiology and rehabilitation.
    Br J Anaesth 1997 78 60617

34
  • Perioperative thoracic epidural anaesthesia has
    been used successfully in the management of
    patients undergoing coronary artery bypass
    surgeryLiem TH, Hasenbos MAWM, Booij LHDJ, Gielen
    MJM. Coronary artery bypass grafting using two
    different anaesthetic effects Part 2
    Postoperative outcome. J Cardithorac Vasc Anesth
    1992 6 15661
  • A study showed that thoracic epidural anaesthesia
    and general anaesthesia in cardiac surgery
    attenuated the myocardial sympathetic response
    and was associated with decreased myocardial
    damage as determined by less release of troponin
    T
  • Loick HM, Schmidt C, van Aken H et al.
    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 grafting. Anesth Analg
    1999 88 7019

35
  • 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
    benefits, risks and controversies. Anesth Analg
    1997 85 598612

36
Anesthetic Management of the Patient Receiving
Unfractionated Heparin during cardiac
surgery Regional Anesthesia and pain medicine
,Vol 29,No 2 Suppl1 (March-April),2004pp1-11
  • Currently, insufficient data and experience are
    available to determine if the risk of neuraxial
    hematoma is increased when combining neuraxial
    techniques with the full 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 patients
    coagulation status is evaluated
  • ?Reheparinization should occur 1 hour after
    catheter removal.

37
  • ? 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.

38
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)20
08pp4040-415
  • 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)

39
  • 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)

40
Home message
41
  • The stress response to surgery comprises a number
    of hormonal changes initiated by neuronal
    activation of the hypothalamicpituitaryadrenal
    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.

42
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