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Cardiovascular Anesthesia neurosurgery requires Ali Mohammadian Erdi, MD Assistant Professor of Anesthesiology & Fellow of Pain Medicine Ardabile-Iran 91/07/10 Management of anesthesia (I) Understanding of the pathophysiology of the disease process (2) Appropriate preoperative testing (3) Application of perioperative risk reduction strategies (4) Careful selection of anesthetic, analgesic, and neuromuscular and autonomic blocking drugs (5) Monitors to match the needs created by this disease. MI, presence of CHF & AS are the highest risk factors. Patient History History from patients with CAD before noncardiac surgery : (1) Evaluation of cardiac reserve : exercise tolerance : Inability to lie flat, awakening from sleep with angina or shortness of breath, or angina at rest or with minimal exertion) Patient History (2) Characteristics of their angina pectoris: - Stable and unstable - Prinzmetals, - Silent myocardial ischemia - 70% of ischemic episodes are not associated with angina pectoris and as many as 15% of acute MI are silent. - Females and individuals with DM are more likely to have painless myocardial ischemia and infarctions. - An increased HR is more likely than systemic hypertension to produce signs of myocardial ischemia . 5 A.Mohammadian Patient History (3) Previous occurrence MI: - delay elective surgery, especially thoracic,upper abdominal, or other major procedures, for a period (2 to 6 months) after a MI. - but the exact period of suggested delay is not clear. After 6 months: incidence of MI is about 50 times greater than in patients undergoing similar operations but in the absence of a previous MI. Most myocardial reinfarctions occur in the first 48 to 72 hours postoperatively. 6 A.Mohammadian FACTORS THAT INCREASE THE RISK FOR PERIOPERATIVE MI The site of the previous MI A history of prior (CAB G) surgery Intrathoracic or intra-abdominal operation > 3 hours Techniques used to produce anesthesia. Perioperative betablockade and clonidine reduces the risk for mortality . Perioperative betablocker started 7 to 30 days before surgery and continued for 30 days postoperatively has been shown to reduce the risk for cardiac morbidity by 90%. if started before surgery and continued for 7 days reduces the risk for by 50%. Close hemodynamic monitoring and prompt pharmacologic intervention with fluid infusion decrease the risk for peri operative cardiac morbidity in high-risk patients. Patient History (4) Medical, interventional cardiology, and cardiac surgical therapy for these conditions. Interactions of medications of CAD with anesthesia drugs. Coexisting noncardiac diseases: Hypertension peripheral vascular disease COPD Renal dysfunction associated with chronic hypertension DM 8 A.Mohammadian CURRENT MEDICATIONS Drugs encountered in patients with CAD are beta antagonists, nitrates, CA blockers,ACE inhibitors, lipid-lowering agents, diuretics, and platelet inhibitors. Pharmacology and adverse interactions with anesthetics. All patients with known CAD, peripheral vascular disease, or 2 risk factors for CAD (age > 60 years, HTN, DM, smoking history, cholesterol>240 mg/dL) should receive perioperative betablockers unless there is a specific contraindication. Reactive asthma, but not COPD is a contraindication to perioperative betablock. Despite the potential for adverse drug interactions, cardiac medications should be continued . Discontinuation increases peri operative morbidity and mortality. Risk Stratification versus Risk Reduction One of the standard approaches to the peri operative care of patients with cardiac disease is risk stratification. Consists of a preoperative history and physical examination, followed by a series of tests thought to predict perioperative cardiac morbidity and mortality. The results of these tests ( thalliumscintigraphy, echocardiography, Holter monitoring, dobutamine stress echocardiography, angiography) can justify subsequent angioplasty with or without an intracoronary stent or CABG . There is no evidence suggesting that preoperative risk stratification with invasive testing is superior to a careful history and physical examination, followed by prophylactic medical therapy. PERIOPERATIVE CARDIAC RISK REDUCTION THERAPY Recommendations have been established for the administration of prophylactic medical therapy to stable patients with known CAD or at risk for such disease . All patients who either have CAD, peripheral vascular disease, or 2 risk factors for coronary artery disease should receive perioperative beta blockers unless they have a specific intolerance to these drugs . If a patient has an absolute contraindication to perioperative betablockers, clonidine may be used as an alternative. Protocol for perioperative cardiac risk reduction : Evaluation of Left Ventricular Function Determinants of Myocardial Oxygen Requirements and Delivery Management of Anesthesia Intraoperative anesthetic management, as well as postoperative pain management in patients with CAD, should permit modulation of sympathetic nervous system responses and provide for rigorous control of hemodynamic variables. Anesthesia based on preoperative evaluation of LV function and maintenance of a favorable balance between myocardial oxygen requirements and delivery so that myocardial ischemia is prevented. Any event associated with persistent tachycardia, systolic hypertension, arterial hypoxemia, or diastolic hypotension can adversely influence this delicate balance. A common recommendation: maintain HR and systemic BP within 20% of awake values. . Management of Anesthesia A single I-minute episode of myocardial ischemia detected by I- mm segment elevation or depression on the ECG increases the risk for cardiac events 10-fold and for death 2-fold. - Tachycardia (> 105 beats/min) for 5 minutes in the postoperative period can increase the risk for death 10-fold. - The only clinically proven method to reduce the risk for perioperative myocardial ischemia and associated death is perioperative betablocker (atenolol or metoprolol) or alfa 2 agonist (clonidine) therapy. - Vasoconstrictors, betaagonists, betablockers, anticholinergics, and vasodilators should be immediately available PREOPERATIVE MEDICATION Preoperative anxiety can lead to preoperative myocardial ischemia. Preoperative beta-blocker therapy or clonidine reduces the incidence of myocardial ischemia. Patients should receive their routine medications except for oral hypoglycemic agents. Oral administration of benzodiazepines . Supplemental oxygen may be useful, especially if opioids are combined with benzodiazepines for sedation. INDUCTION OF ANESTHESIA Etomidate is a popular induction drug( limited inhibition of the sympathetic nervous system and minimal hemodynamic effects). Propofol is popular( antiemetic effects and rapid recovery, but the dose should be reduced to avoid undesirable degrees of hypotension). Fentanyl plus midazolam in combination with an infusion of phenylephrine and a NDNMB produces minimal changes in systemic BP and HR. - Ketamine is not popular. - If desflurane is chosen, care should be taken to not increase the dose rapidly to avoid sympathetic nervous system stimulation TRACHEAL INTUBATION TI is facilitated by SCH or a NDNMB. Myocardial ischemia result from the stimulation of laryngoscopy before tracheal intubation. A brief duration of direct laryngoscopy (preferably 15 seconds) is important for minimizing the circulatory changes. If duration of direct laryngoscopy is not likely to be brief or when systemic hypertension coexists, the addition of other drugs to minimize the pressor response produced by direct laryngoscopy may be a consideration( lidocaine 1- 2 mg/kg ) Opioids and BetaBlockers before laryngoscopy reduce the circulatory responses as. MAINTENANCE OF ANESTHESIA Choice of anesthesia is often based on the patient's LV function . patients with CAD but normal LV function, tachycardia and systemic hypertension are likely to develop in response to intense stimulation. Controlled myocardial depression produced by a volatile anesthetic, with or without N2O may be appropriate if the primary goal is to prevent increased myocardial oxygen requirements. Equally acceptable for maintenance of anesthesia: N2O - opioid technique with the addition of a volatile anesthetic as necessary. MAINTENANCE OF ANESTHESIA Avoiding tachycardia with the use of long acting betablockers is more important than the choice of anesthetic. - Impaired LV function:( previous MI), may not tolerate the direct myocardial depression produced by volatile anesthetics. Then short-acting opioids with N2O may be a more acceptable selection. - N2O + opioids may produce undesirable decreases in systemic BP and cardiac output. - High-dose fentanyl with benzodiazepines added to ensure amnesia, has been advocated for patients who cannot tolerate even minimal anesthetic-induced myocardial depression. There is no evidence to support the superiority of this technique over moderate-dose opioids with an inhaled agent or IV anesthetics. MAINTENANCE OF ANESTHESIA RA may be an appropriate technique in selected patients with CAD. It is important that flow through critically narrowed coronary arteries is pressure dependent. Therefore, decreases in systemic BP associated with a RA that are greater than 20% of the pre block value should probably be treated by the IV infusion or vasoconstrictor or both. Perioperative betablockers or clonidine should be administered to patients with known cardiac risk factors who are undergoing surgery with RA. NEUROMUSCULAR BLOCKING DRUGS The choice of NDNMB may be influenced by the circulatory effects & myocardial oxygen requirements and delivery. Vecuronium, rocuronium, and cisatracurium do not evoke histamine even with the rapid IV administration of large doses. Systemic BP –lowering effects of atracurium and mivacurium are usually modest, especially if these drugs are injected over a period of 30 to 45 seconds. It is unlikely that any of these drugs will adversely alter myocardial oxygen requirements. NEUROMUSCULAR BLOCKING DRUGS Pancuronium increases the HR and BP, but these changes are usually less than 15% above predrug values . the circulatory changes can be offset the negative inotropic and chronotropic effects of anesthetic drugs. One of the common causes of postoperative myocardial ischemia and MI is tachycardia after emergence, which may be the result of the combination of emergence, surgical pain, and reversal of drugs. - Long- acting IV betablockers may be added to decrease the incidence of tachycardia, which may lead to myocardial ischemia in this period. MONITORING The intensity of monitoring is influenced by the complexity of the operative procedure and the severity of the CAD. The five-lead ECG serves as a noninvasive monitor of the balance between myocardial oxygen requirements and delivery. V5 lead is for detecting ST-segment changes ( ischemia of the LV). Intra-arterial pressure monitoring can speed the identification and treatment of hemodynamic changes. Ventricular wall motion abnormalities observed by transesophageal echocardiography. MONITORING Tachycardia: is treated by atenolol, metoprolol, propranolol, or esmolol. Excessive BP:may respond to opioids, betablockers, vasodilators (nitroglycerin, nitroprusside), or increased delivered volatile anesthetics. Decreases in body temperature may predispose to shivering on awakening and increases in myocardial oxygen requirements. Postoperative Care Is based on provision of peri operative anti- ischemic drugs, analgesia, and if needed, sedation to blunt excessive sympathetic nervous system activity and facilitate rigorous control of hemodynamic variables. Intensive and continuous postoperative monitoring is useful for detecting myocardial ischemia, which is often asymptomatic. - It is more effective to prevent the occurrence of myocardial ischemia than to detect it. VALVULAR HEART DISEASE The most frequently forms of VHD produce: pressure overload (MS, AS) or volume overload (MR, AR) of the LV. Selection of anesthetic drugs and NMBD based on the probable effects of drug-induced changes in cardiac rhythm, HR, systemic BP, systemic vascular resistance and pulmonary vascular resistance relative to maintenance of CO in these patients. VALVULAR HEART DISEASE Although no specific type of GA has been shown to be superior, when cardiac reserve is minimal, an anesthetic combination that includes a high dose of a short-acting opioid, an amnestic benzodiazepine, and a low dose of a volatile anesthetic is common. Prophylactic infusion of a vasoconstrictor (phenylephrine) may reduce hemodynamic changes. Prophylactic AB for endocarditis. 29 A.Mohammadian Mitral Stenosis MS : mechanical obstruction to LV diastolic filling secondary to progressive decrease in the orifice of the mitral valve. The obstruction produces an increase in left atrial and pulmonary venous pressure. Distention of the left atrium predisposes to AF, which can result in stasis of blood, the formation of thrombi, and systemic emboli. Chronic anticoagulation or antiplatelet therapy (or both) can reduce the risk for systemic embolic events . Mitral Stenosis Patients with MS may be more susceptible to the ventilatory depressant effects of the sedative drugs used for preoperative medication. If patients are given sedative drugs, supplemental oxygen may increase the margin of safety. Most medications except anticoagulants, anti platelet drugs, and oral hypoglycemicdrugs, should be continued throughout the preoperative period. 31 A.Mohammadian Mitral Stenosis Digitalis should continue until surgery. Adequate digitalis effect for heart rate control is generally reflected by a ventricular rate less than 80 beats/min. Because diuretic therapy is common in these patients, the serum potassium is often measured preoperatively. Management of anticoagulant or antiplatelet therapy should be discussed with the surgeon and cardiologist. Patients should be switched from warfarin (Coumadin) to heparin therapy preoperatively, depending on the type of surgery. Anesthetic Considerations in Mitral Stenosis MANAGEMENT OF ANESTHESIA(MS) Intra-arterial pressure monitoring . Induction : with IV drugs ( possible exception of ketamine, which increase the HR). Tracheal intubation : is facilitated by neuromuscular blocking drugs with minimal effects on heart rate are commonly chosen. Drugs used for maintenance of anesthesia should cause minimal changes in heart rate and systemic and pulmonary vascular resistance. these drugs should not greatly decrease myocardial contractility. No one anesthetic has been proved to be superior. MANAGEMENT OF ANESTHESIA(MS) Combinations of an opioid and low concentrations of volatile anesthetics or IV anesthetics, with or without N2O. Although N2O can increase pulmonary vascular resistance, this increase is not sufficiently great to justify avoiding this drug . NDNMBD with minimal circulatory effects are useful. Pancuronium is less appropriate. Although there is no reason to avoid drug assisted antagonism of NDNMBD, it is desirable to avoid the adverse effects of druginduced tachycardia . An option :Allow the neuromuscular blockade to wane spontaneously with metabolism of the drug. MANAGEMENT OF ANESTHESIA(MS) Intraoperative fluid : titrated ,susceptible to intravascular volume overload and LV failure and pulmonary edema. The head-down position may not be well tolerated. Monitoring intraarterial pressure and possibly right atrial pressure is a helpful guide to the adequacy of IV fluid replacement. An increase in right atrial pressure could also reflect pulmonary vasoconstriction and thus suggests the need to check for causes, which may include nitrous oxide, desflurane, acidosis, arterial hypoxemia, increased MR, or light anesthesia. MANAGEMENT OF ANESTHESIA(MS) Postoperative: high risk for pulmonary edema and right heart failure. Mechanical support of ventilation of the lungs may be necessary, particularly after major thoracic or abdominal surgery. The shift from controlled to spontaneous ventilation with weaning and extubation of the patient's trachea may lead to increased venous return and increased central venous pressure with worsening of CHF. 37 A.Mohammadian Mitral Regurgitation Mitral regurgitation : left atrial volume overload and decreased left ventricular forward stroke volume as a result of the backflow of part of each stroke volume through the incompetent mitral valve back into the left atrium. MR secondary to rheumatic fever usually has a component of mitral stenosis. Dilated cardiomyopathy resulting from chronic myocardial ischemia, repeated MI, or viral infections may cause MR. MANAGEMENTOF ANESTHESIA(MR) should be designed to reduce the likelihood of decreases in forward left ventricular stroke volume. Conversely, cardiac output can be improved by mild increases in heart rate and mild decreases in systemic vascular resistance. MANAGEMENTOF ANESTHESIA(MR) GA is the usual choice for patients with MR. Although decreases in systemic vascular resistance are theoretically beneficial, the uncontrolled nature of this response with a RA may detract from the use of this technique. Maintenance of GA with volatile anesthetics, with or without N2O, or a continuous IV infusion of drugs. NDNMB that lack significant circulatory effects are useful. Pancuronium is acceptable because the increase in HR and forward left ventricular strok volume. IV fluid volume must be maintained by prompt replacement of blood loss to ensure adequate venous return and ejection of an optimal forward LV stroke volume. Aortic Stenosis Aortic stenosis is characterized by increased left ventricular systolic pressure to maintain the forward stroke volume. The combination of clinical symptoms (angina, congestive failure, fainting), signs (left ventricular dysfunction, progressive cardiomegaly), and reduced valve area suggests the presence of critical aortic stenosis requiring surgical replacemen. MANAGEMENTOF ANESTHESIA(AS) Goals : maintenance of normal sinus rhythm and avoidance of extreme and prolonged alterations in heart rate, systemic vascular resistance, and intravascular fluid volume. Preservation of normal sinus rhythm is critical because the left ventricle is dependent on properly timed atrial contractions to ensure optimal left ventricular filling and stroke volume. Increases in HR (>100 beats/min) can decrease the time for LV filling and ejection, whereas bradycardia (<60 beats/min) can lead to acute overdistention of the LV. Tachycardia may lead to myocardial ischemia and ventricular dysfunction. MANAGEMENTOF ANESTHESIA(AS) The most important technique: intra-arterial pressure monitoring with careful avoidance of hypotension. GA may be preferred over a RA because sympathetic nervous system blockade can lead to undesirable decreases in systemic vascular resistance. However, if the surgical site is on an extremity, a RA with intra-arterial pressure monitoring can be equally successful. Maintenance of GA can be achieved with volatile anesthetics, with or without N2O, or with intravenous drugs. A potential disadvantage of volatile anesthetics is depression of sinus node automaticity. IV fluid volume must be maintained by prompt replacement of blood loss and liberal IV administration of fluids. Defibrillator should be available because external cardiac compressions are unlikely to generate an adequate stroke volume across a stenosed aortic valve. Aortic Regurgitation Decreased forward LV stroke volume as a result of regurgitation of part of the ejected stroke volume from the aorta back into the LV through an incompetent aortic valve. Increased myocardial oxygen requirements secondary to left ventricular hypertrophy, plus a characteristic decrease in aortic diastolic pressure that decreases coronary blood flow, can manifested as angina pectoris in the absence of coronary artery disease. Management of anesthesia: is the same as described for patients with MR. Anesthetic Considerations in Patients with Mitral or Aortic Regurgitation Ventricular Premature Beats(PVC) Recognized on the ECG by (1) premature occurrence, (2) the absence of a P wave preceding the QRS complex, (3) a wide and often bizarre QRS complex, (4) an inverted T wave, and (5) a compensatory pause that follows the premature beat. Treatment:ed : lidocaine (1 to 2 mg/kg IV followed by 1 to 2 mg/min infusion) when : (1) are frequent (more than six premature beats/min) (2) multifocal (3) occur in salvos of three or more, or (4) take place during the ascending limb of the T wave (R on T phenomenon). The primary goal should be to identify the underlying cause (myocardial ischemia, arterial hypoxemia, hypercapnia, hypertension, hypokalemia, mechanical irritation of the ventricles) if possible and correct it. NEUROANESTHETIC MAINTENANCE ADEQUATE BRAIN RELAXATION Adequate oxygenation and ventilation (PaCO2 3335mmHg),, venous return, muscle relaxation, anesthetic depth Furosmide 10-20mg iv, Mannitol 0.5-1.5g/kg iv, iv thiopental, CSF drainage NEUROANESTHETIC MAINTENANCE STABLE ANESTHETIC STATE AND RAPID SMOOTH EMERGENCE Low after the craniotomy (brain is devoid of sensation) Isoflurane, Sevoflurane or Desflurane 0.5MAC & Propofol 50-150 ug/kg/min and Remifentanil 0.10.5ug/kg/min Muscle relaxant maintaining 2twitches (phenytoin may increase requirment of muscle relaxants) NEUROANESTHETIC EMERGENCE AVOID COUGHING STRAINING OR BP INCREASE Normalize gradually PaCO2 Full reversal of muscle relaxant IV Lidocaine IV labetolol, Nicardpine, NTP, NTG Brief neurological Assessment before leaving OR Pre emergence 1-2 hr before end Gradual decrease anesth aiming for bis 80 at end Treat post op htn before hand, I aim for SBP 110 Maintain solid reversible NMB!! IMMEDIATE POSTOPERATIVE CARE IN NEUROANESTHESIA ADEQUATE VENTILATION AND OXYGENATION HEAD OF BED (10-25C0 NEUROLOGIC FUNCTION CEREBRAL DYNAMICS MONITORING AND CONTROL SERUM ELECTROLYTE: SIADH (↓Na, ↓serum osm, ↑urine osmo) Treatment restrict water intake ‡meds DI (polyuria, ↑Na, ↑serum osmo, ↓urine osmo) Treatment Aqueous vasopressin 510USP units sq or 3units iv OR desmporessin 1-2 ug iv sq q6-12hr. Plus adequate fluid replacement SEIZURE (adequate oxygenation, ventilation and airway protection: midazolam (2- 4mg), thiopental (100-150mg), fosphenytoin 15-20mg/kg, 100 mg/min) POSTOPERATIVE IMAGING (CTScan, MRI, Angiography) TRANSPORT FROM OPERATING ROOM TRANSPORT FROM OPERATING ROOM TO NEURO-ICU OR PACU: PRIOR COMPLETE REPORT TO ACCEPTING UNIT WITH SET-UP NEEDED TRANSPORT ONLY WHEN PATIENT IS STABLE OR AS STABLE AS CAN BE DIRECT SUPERVISION OF ANESTHETIST HEMODYNAMIC AND RESPIRATORY SYSTEMS MONITORED AND CONTROLLED O2 SUPPLEMENT WORKING IV AND RUNNING INFUSION PUMPS BLANKETS AND HEAT LOSS PREVENTION EMERGENCY MEDS AND INTUBATION KIT ENDORSEMENT IS NOT COMPLETE UNTIL PATIENT IS STABLE AND COMPREHENSIVE REPORT HAS BEEN DELIVERED CAUSES OF POST-ANESTHETIC HYPOTENSION HYPOVOLEMIA ↑HR, RR, SKIN TURGOR, DRY MUCOUS MEMBRANE, OLIGURIA AND THIRST. INADEQUATE FLUID REPLACEMENT, ONGOING LOSS, OSMOTIC POLURIA, FLUID SEQUESTRATION (ASCITIS, INTESTINAL OBSTRUCTION A MEANINGFUL VOLUME CHALLENGE AND FURTHER ASSESSMENT (CAUTIOUS IN IMPAIRED BBB) IMPAIRED VENOUR RETURN JUGLAR VEIN DISTENTION, ↑CVP, ↓BREATH SOUNDS AND ↓HEART TONES. POSITIVE PRESSURE VENTILATION, PEEP, PNEUMOTHORAX, PERICARDIAL TAMPONADE. TREATED BY VOLUME AND THE CAUSE CAUSES OF POST-ANESTHETIC HYPOTENSION VASODILATION REWARMING, RESIDUAL INHALATION AGENTS, NEUROAXIAL ANESTHESIA, TRANSFUSION REACTION, ANAPHYLAXIS, INFLAMMATION, SEPSIS, ADRENAL INSUFFICIENCY, LIVER FAILURE DECREASED CARDIAC OUTPUT MYOCARDIAL ISCHEMIA, INFARCTION, CHF, NEGATIVE INOTROPIC DRUGS, SEPSIS, HYPOTHYRODISM, MALIGNANT HYPERTHERMIA DYSPNEA, DIAPHORESIS, CYANOSIS, JUGLAR VEIN DISTENTION, OLIGURIA, RHYTHM DISTURBANCES, WHEEZING, DEPENDENT CRACKLES, AND S3 GALLOP INOTROPIC AGENTS (e.g. DOPAMINE) AFTERLOAD REDUCTION (e.g.Nitrate) DIURESIS for fluid overload ANTIDYSRHYTHMICS OR ELECTRICAL CARDIOVERSION CAUSES OF POST-ANESTHETIC DYSRHYTHMIAS INCREASED SYMPATHETIC OUTFLOW (PAIN) HYPOXEMIA, PE HYPERCARBIA HYPO-HYPERTHERMIA HYPOVOLEMIA ELECTROLYTE AND ACID-BASE IMBALANCE DRUG TOXICITY THYROTOXICOSIS MALIGNANT HYPERTHERMIA MYOCARDIAL ISCHEMIA, CHF ELEVATED ICP COMMON TYPES OF POSTANESTHETIC DYSRHYTHMIAS SUPRAVENTRICULAR DYSRHYTHMIAS SINUS TACHYCARDIA SINUS BRADYCARDIA PAROXYSMAL SUPRAVENTRICULAR TACHYDYSRHYTHMIAS VENTRICULAR DYSRHYTHMIAS; STABLE PVCS VENTRICULAR TACHYCARDIA (NON-SUSTAINED) UNSTABLE VENTRICULAR TACHYCARDIA AND VENTRICULAR FIBRILLATION GENERAL TREATMENT OF POST-ANESTHETIC DYSRHYTHMIAS O2 SUPPLEMENT INCREASE PERFUSION TREAT THE CAUSE (S) Pain: Opiods Bradycardia: Atropine 0.2-0.4mg or glycopyrrolate 0.2mg Synchronized cardioversion if unstable arrthymia Adenosine 6mg then 12mg rapid to convert PACS B-adrenergic blockers (labetalol 5-20mg -2mg/min, esmolol 10-100mg or 25-300ug/kg/min, propranolol 0.5-1mg iv) Calcium-channel blockers (Verapamil 2.5-5mg increment, diltiazem 5-20mg iv or 0.25-0.35mg/kg iv then 5-15mg/hr Amiodarone 150mg over 10min then 1mg/min for 6hrs then 0.5mg/min Digoxin 0.25mg increment 1.5mg Ibutilide, Procainamide 20-30mg/min iv up 17mg/kg 1-2mg/min, Lidocaine 1.5mg/kg then 14mg/min PERIOPERATIVE FLUID MANAGEMENT IN NEUROANESTHESIA Avoid infusion of water or dextrose in water (Water freely passes through BBB) BBB is impermeable to most ions. Total osmolarity rather than oncotic pressure determine osmotic gradient. Maintenance of high serum osmolality decrease brain water content Large, polar substances cross poorly BBB e.g albumin If BBB is disrupted, permeability to mannitol, albumin, and saline increases and edema formation PERIOPERATIVE FLUID MANAGEMENT IN NEUROANESTHESIA Physiologic mainenance fluid given hourly without replacement of overnight deficit Third spacing is minimal during craniotomy surgery 2/3 of total intraoperative urine output is replaced with crystalloid Iso-osmolar crystalloid sol (0.9NS, 309 mOsm. Large quantity may cause metabolic acidosis) Hypokalemia secondary to steriod, porassium-wasting diuretics, hyperventilation. Hyponatremia caused by SIADH and diuretic used Brain Death Determination Apnea test Disconnect the ventilator Deliver 100% FIO2 via t-piece/trach collar Monitor for ventilatory effort until ABG confirms a PaCO2 greater than 60 mm Hg Reconnect ventilator If patient becomes unstable, terminate apnea test Patient is considered apneic if PaCO2 is > 60 and there is no respiratory effort Have A Nice Day