ANESTHESIA CASE STUDY Objective Objectives 9/25/2012
9/25/2012 ANESTHESIA CASE STUDY Vasospastic Myocardial Infarction Objective Objectives Overview of coronary vasospasm mechanisms and risk factors Review of the perianesthesia events surrounding this actual case study Pharmacology gy review off medications associated w/ risk of coronary vasospasm Rx of patients suspected of having coronary vasospasm while under anesthesia, and while recovering from anesthesia 1 9/25/2012 “Just a TVH…” Relatively innocent sounding case (?) “really fast surgeon” “no significant PMH” “… yada yada…” Your check is in the mail… Many times you don’t suspect anything at all… And then the demons come out to play! 2 9/25/2012 Just the Facts, Ma’am… Heart Facts… The heart consumes the highest fraction of oxygen per tissue mass of any organ in our bodies At rest, O2 consumption is 250 ml/min, or 5 % of normal CO Blood flow to the myocardium occurs mainly during diastole Arterial O2 extraction in the myocardium is around 60- 80%, vs. ~ 20% in the rest of the body Increased O2 demand must be met by an increase in coronary flow vs. increase in O2 extraction Flow depends on… Jean Louis Marie Poiseuille 3 9/25/2012 Oh God, not Physics! … the volume of a homogeneous fluid passing per unit time through a capillary tube i directly is di l proportional i l to the pressure difference between its ends and to the fourth power of its internal radius, and inversely proportional to its length and to the viscosity of the fluid …* Coronary Vessel Diameter Intraluminal deposits Vasomotor tone (alpha) receptors (beta) receptors Muscarinic receptors AT (angiotensin) receptors ET (endothelin) receptors Physiology Review Coronary arterial tone exists along a physiological spectrum Pathophysiology alters the normal spectrum of vasomotor homeostasis Multiple p ffactors come into play… p y Neurological (autonomic) control Presence of pathophysiology of coronaries Metabolic demands Endothelial factors 4 9/25/2012 Let’s talk about those last bullet points, shall we? Autonomic Control Regular diurnal alterations in tone do exist, but are generally regarded as weak Epicardial coronaries generally have receptors (vasoconstriction) Intramuscular I l andd subendocardial b d di l coronaries i generally have receptors (vasodilation) Parasympathetic stimulation results in vasodilation via acetylcholine Metabolic Demands Local (cardiac) metabolic balance is the main regulatory player in arterial vasomotor tone Tissue hypoxia, increased tissue CO2 and tissue acidosis drive coronary vasodilation Adenosine is released and ATP-K+ channels are activated Pre-capillary sphincters are relaxed and more capillaries are recruited 5 9/25/2012 Endothelial Factors Vascular endothelium acts as a barrier b/w flowing blood and vascular wall Regulates vascular growth, platelet fxn, coagulation, vascular tone Responds to neural, humoral and mechanical (myogenic) stimuli Injury/Repair cycle Synthesizes/secretes vasoactive substances Responses d/o intact vascular endothelium Vascular Endothelium Single-cell lining of all blood vessels found in higher organisms Proteins, lipids, and vasoactive substances secreted by the endothelium Protects the vessels from environmental stress, oxidative damage and thrombosis Ensures delivery of O2 and nutrients to tissues As such, it is the largest endocrine organ of the body (surface area ~ 6 tennis courts!) Vasodilatory Influences Nitric oxide Acetylcholine, via release of nitric oxide Endothelium-derived Endothelium derived relaxing factor (EDRF) Prostacyclin Bradykinin 6 9/25/2012 Vasoconstrictor Influences Angiotensin II Enhances Ca2+ influx Causes release off endothelin ACE inactivates bradykinin Thromboxane A2 Balance The net effect on vasomotor tone is dependent upon the balance between the two opposing systems Mechanisms are unreliable in the presence of diseased vascular endothelium E.G. acetylcholine acts as a vasoconstrictor in atherosclerotic arteries,, opposite pp off its normal action Genetic polymorphisms that diminish endothelial nitric oxide production have been correlated with coronary vasospasm Vasospastic Imbalance… Heightened vasoconstrictor response to acetylcholine Enhanced vasodilator response to nitrates Endogenous nitric oxide deficiency Autonomic imbalance Sensitization towards vasoconstriction 7 9/25/2012 Predisposing Factors Genetic factors compromising endothelial NO production Markers of chronic low-level oxidative stress (monocyte counts, C-reactive protein levels, thioredoxin levels, etc.) Type A personality Panic disorder Severe S anxiety i t Incidence among Japanese elevated Gender preponderance unclear Presence of acknowledged ‘triggers’ in susceptible patients Vasospastic Triggers Hyperventilation Illicit drugs, especially cocaine Emotional stress Exposure to cold Tobacco use, especially smokingg Alcohol use Intracoronary provocative agents…Acetylcholine, ergonovine, histamine, serotonin OTC drugs, especially cold meds Thyroxin preparations (rare) Chemotherapy agents Hypersensitivity rxns to NSAIDs Abx and allopurinol NSAIDs, Induction of anesthesia Prescription drugs Non-selective -blockers, migraine medications Let’s take a moment to have a serious chat… 8 9/25/2012 A Word about Smoking… 20 X the risk of coronary vasospasm (CV) vs. non-smokers Causes vasoconstriction through adrenergic increase in vascular tone, and via increases in platelet and plasma levels of vasopressin and oxytocin Imposes endothelial damage Diminishes endogenous antioxidant activities (glutathione, etc.) P i smokers Passive k have h a 25% iincrease iin the h risk i k off all ll coronary M&M Passive smoking is the 3rd leading preventable cause of death after active smoking and alcohol abuse Case report relating that 1 cigarette during angiography provoked an incident of CV So, curious about the case?! CASE REVIEW 42 yo white female For TVH d/t fibroids, extreme menorrhagia, anemia Allergy: PCN Anesthesia complications: PONV PIV #18g x 1 9 9/25/2012 PMH Bilateral hip osteoarthritis (1999) Low grade astrocytoma of brainstem, inoperable, treated w/ XRT (transmastoid rad port), no major recent sequelae… S Sz diso disorder, de , none since early ea ly in astrocytoma ast ocytoma XRT Migraines, none ‘recent’ per patient report PMH (cont’d) She has chronic occipital pain as a consequence of the astrocytoma and/or Rx thereof, with exacerbations of this pain deemed to be migraines;on a tiered pain regimen Maxalt used for breakthrough migraines She Sh also l has h intermittent vertigo andd diplopia, d l speech hesitancy, and diminished hearing Hx bilateral TMJ syndrome Patient Profile PSH PSH: T & A, D & C, brainstem tumor bx 1999, sinus sx 2001. No history of anesthetic complications, except PONV MEDS MEDS: Arthrotec, Arthrotec FeSO4, FeSO4 Ca2+, Ca2+ MVI, MVI Singulair, Singulair Prozac, Zonegran. PRNs are Maxalt, Alleve, Toradol. By pt. report, no maxalt since 6-7 days prior to DOS LAB LAB: Hemoglobin approximately 3 weeks prior to surgery = 12.4 ** 10 9/25/2012 Patient Profile (cont’d) Pleasant lady with noticeable speech hesitancy Pupils dilated wider than usual for light conditions Mild nystagmus when looking to the right. Heart S1S2 RRR, Lungs CTA bilaterally Normal A/W exam, except TMD just slightly > 3 FBs Baseline HR in PAPA approx. 55-60 bpm, and SBP 90-100s. Preop EKG Operative Course Uneventful induction, using propofol, fentanyl, lidocaine, and divided dose of mivacron (total 12 mg)… easy intubation Maintenance with sevoflurane in Air and O2 (FiO2 ~ 56=58%) Post-induction, prolonged prep and drape* BP and HR b began ddrifting f down d Inhalational agent turned down as low as 1.5% inspired, IVF bolus Upon sustained hypotension, ephedrine 5 mg x 2 doses, approx. 3 minutes apart given. 11 9/25/2012 Operative Course Hypotension (SBP 69) worsens plus significant brady (HR 30s) with ventricular escape beats develops Robinul 0.2mg given, MDA paged by circulator BP recheck not improved, brady continues Ephedrine 10mg given, FiO2 changed to 100% Surgeon g requested q to not begin g pprocedure Sustained ventricular ectopy begins,and MDA arrives Total elapsed time from beginning of initial Rx for BP approx. 10 minutes. Intraoperative EKG Rhythms Intraop/Postop Rhythms 12 9/25/2012 There’s going to be, trouble… Interventions Sustained pulsatile monomorphic VT x approx 1-2 minutes, then nodal rhythm with salvos of polymorphic ventricular ectopy. Still hypotensive Extra lidocaine given, total of 100 mg Now,, ST 120s with hypertension, yp , initiallyy opposite pp electrical axis from baseline. Rx’d with esmolol 2 inches NTG paste to chest wall Postop Interventions Baseline axis in sinus resumed, with overt ST depression. Patient allowed to wake up and extubated without need for reversal agents. BP baseline briefly (100s/50s) To PACU. Placed on hi flow O2, 12 lead EKG obtained, showing 4-5mm ST depression in inferior,lateral, and v3-6 precordial leads BP now consistently hypotensive; IVF running at moderate pace, labs sent and dopamine gtt ordered Magnesium 2 gm infusion run started Cardiology consult placed; dopa gtt okayed with Cards 13 9/25/2012 Initial EKG in PACU Teamwork… Postop Course Serial EKGs show progressive improvement in ST depression Pt remains hypotensive, refractory to Rx including eventually a dopamine gtt up to 5 mcg/kg/min Cards in to see pt. pt and transferred to CCU Pt. denies discomfort of any kind, except for occipital h/a, throughout PACU stay 14 9/25/2012 Initial EKG CCU Course in CCU Ruled in for MI, peak CK 393, MB 47.9 Cardiac cath shows clean coronaries, Ao 90/60, Lvedp approx. 20 Echo shows mildly decreased EF (50%), with posterior- lateral dyskinesia/ hypokinesia, and inferior septal akinesia Pt. P remainedd markedly k dl hypotensive h on dopa d gtt, as muchh as 2 days postop She was eventually fluid challenged, and then transfused, with hemodynamic improvement Interesting Facts… Initial Hgb drawn in PACU was 8.9 Pt. recalled she did indeed have a dose of Maxalt 2 days y prior p to surgery Pt. admitted to having CP and unusual fatigue the day prior to surgery Told Cards that she does occasionally smoke, sometimes a great deal… 15 9/25/2012 Migraine Meds Cafergot, DHE 45, Midrin Triptans Axert, Almogran Relpax Frova, Migard, Frovamig Amerge, Naramig Maxalt Imitrex Zomig Triptans First introduced in the 1990s Used in the Rx of migraine/cluster headaches Acts by binding to serotonin subtype 5-HT1B and 5-HT1D receptors and constricting cranial blood vessels Also binds on receptors in the peripheral terminals of the trigeminal nerve that innervate the cranial blood vessels This leads to a subsequent decrease in release of nociceptive mediators (CGRP, substance P) Mean plasma half-life after oral dosing is 2 hours Triptans Contraindicated in IHD, variant angina, poorly controlled HTN Contraindicated in those taking ergot preparations within previous 24 hours Contraindicated in those taking MAOIs within prior 2 weeks Poses the risk of coronary vasospasm Poses the risk of serotonin syndrome if used in conjunction with SSRIs, SNRIs Should be used with caution in those with epilepsy 16 9/25/2012 Better Living thro Chemistry? So what the heck happened? Research re: CV continue to indicate many directions of thought… Autonomic tone influences, specifically vagal withdrawal: although -adrenergic input is not excluded as a factor Adrenergic agonist post-induction Local vasomotor hyperreactivity d/t receptor abnormality, endothelial d h li l dysfxn d f or platelet l l fxn f alteration l i (smoking) ( ki ) Vitamin E deficiency, allowing oxidative modification of LDL, which increases vasomotor reactivity (smoking) Central serotonin excess with prn 5HT agonist addition Case Reports CV reported with GA, GA +Epidural, SAB CV reported with triptans alone, or with SSRIs CV reported with ephedrine in pt. reporting ‘rare’ cocaine use CV reported with ephedrine use for hypotension in SAB cases in young smokers CV reported with induction free of hypotension, other agents 17 9/25/2012 CV Clinical Presentation (Preoperative Clues) Patients without usual risk factors for IHD Young, normotensive, no lipid abnormalities No prior hx IHD Transient/sustained ST segment elevation or depression, especially in a global pattern Global or focal transient/sustained T wave inversion Severe ventricular tachyarrhythmias and bradyarrhythmias up to & including AV block If awake, typical symptoms of angina and associated signs Important Principles of Perioperative CV Rx Rx of life-threatening arrhythmias Immediate application of nitrates IV/topical/SL Avoidance of non-selective blockers as blockade may exacerbate CV Intravenous calcium channel blockers are potentially of benefit Cards workup to rule out and/or treat atherosclerotic heart disease Avoid hyperventilation Avoidance of histamine releasing meds Ultimate Outcome LV fxn normalized after 2 weeks by echo Prozac dose reduced to 1/3 original dose Toradol T d l discontinued d d Maxalt discontinued Midrin used for migraines Surgery successfully completed 6 weeks later 18 9/25/2012 So, in Hindsight… Pt. was a smoker On generous dose of an SSRI (total 60mg/day prozac) On prn triptan that she regularly takes ? Up-regulated serotonergic receptors ? Altered autonomic responses d/t CNS lesion On anti-sz med that acts as a carbonic anhydrase inhibitor More volume-depleted and anemic than it appeared What we don’t say enough.. Questions, Comments, etc.? 19 9/25/2012 Thanks! 20
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