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Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
Ischaemic heart disease & its anaesthetic implications
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Ischaemic heart disease & its anaesthetic implications

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  • Myocardial oxygen consumption (MVO2) is required to regenerate ATP which is needed for contraction & relaxation of the heart muscles
  • n Fick's original method, the "organ" was the entire human body and the marker substance was oxygen. the total uptake of (or release of) a substance by the peripheral tissues is equal to the product of the blood flow to the peripheral tissues and the arterial-venous concentration difference (gradient) of the substance
  • The constant 0.0031 represents the amount of oxygen dissolved in plasma. The constant, 1.36, is the amount of oxygen (ml at 1 atmosphere) bound per gram of haemoglobin
  • Isolated hypoxemia (i.e., diminished transport of oxygen by the blood) induced by cyanotic congenital heart disease, severe anemia, or advanced lung disease is less deleterious than ischemia
  • Increased hr = less diastolic filling time hence less coronary blood flow.
  • Angina pectoris reflects intracardiac release of adenosine and bradykinin during ischemia. These substances stimulate cardiac chemical and mechanosensitive receptors whose afferent neurons converge with upper thoracic sympathetic fibers and other somatic nerve fibers in the spinal cord and ultimately produce thalamic and cortical stimulation that results in the typical chest pain of angina pectoris.
  • Nearly all improve supply by coronary vasodilation……… Nitrates relax all vascular smooth muscle but have a much greater effect on venous than on arterial vessels. Decreasing venous tone and reducing venous return to the heart (cardiac preload) reduce wall tension and afterload……….B.blockers decrease myocardial oxygen demand by reducing heart rate and contractility Calcium channel blockers reduce myocardial oxygen demand by decreasing cardiac afterload. Verapamil and diltiazem also reduce demand by slowing the heart rate.
  • The normal ST segment does not deviate by more than 1 mm above or below the isoelectric line.
  • Several schemes for estimated perioperative risk have been used over the years. Although perhaps the most subjective, the American Surgical Association/Dripps classification is still commonly used by anesthesiologists. The Goldman Index was the first risk stratification method to use modern statistical methods and identified 9 clinical factors which correlated with cardiovascular risk and death. A weight was assigned to each risk factor based on the strength of the statistical risk and it was possible, using this method, to assign a number of points and use this point score, generally to place a patient in one of four risk categories. Although popular at the time, this was based primarily on the data from a single hospital (Mass General) and was subsequently shown to underestimate risk in certain populations, including the elderly, obese and those with vascular disease. The Detsky Index was a take-off of the Goldman Index which empirically added a number of additional clinical characteristics known to be associated with perioperative risk. Recommended today, and the focus of the remainder of this presentation are the joint recommendations of the AHA and ACC.
  • The Detsky Index was a take-off of the Goldman Index which empirically added a number of additional clinical characteristics known to be associated with perioperative risk
  • Major predictors mandate intensive management, intermediate predictors are markers of enhanced risk and require careful preoperative assessment, and minor predictors are recognized markers of cardiovascular disease that have not clearly been shown to independently increase perioperative risk. Patients with major predictors should undergo noninvasive cardiac evaluation and, when appropriate.
  • In 1996, a 12-member task force of the American College of Cardiology and the American Heart Association (ACC/AHA) published The principal theme of the guidelines is that preoperative intervention is rarely necessary just to lower the risk of surgery. An intervention is indicated or not indicated irrespective of the need for surgery. Preoperative testing should be performed only if it is likely to influence perioperative management Provide a risk profile based on pt’s medical status and make recommendations concerning the management cardiac problems over the entire perioperative period
  • Multiples of the baseline MET value can be used to express aerobic demands for specific activities. Perioperative cardiac and long-term risks are increased in patients unable to meet a 4-MET demand during most normal daily activities capacity can be expressed in metabolic equivalent (MET) levels
  • The urgency with which surgery is required has been shown to be an important predictor of risk. In fact, studies have shown that surgery performed on an emergent basis is associated with a 3-5 times increased risk compared with the same surgery conducted on an elective basis. Beyond the issue of urgency is the degree of risk arising from the type/complexity of surgery
  • The overriding theme is No test should be performed unless it is likely to influence patient treatment. who cannot exercise are to increase myocardial oxygen demand (by pacing or intravenous dobutamine) and to induce hyperemic responses by pharmacological vasodilators such as intravenous dipyridamole or adenosine. Are necessary for definitive diagnosis of ischaemia & quantify the damage.
  • Poor LV function preop correlates well with postop CHF & death/ The ventricular wall motion abnormalities CORRESPOND to the site of myocardial ischemia, thereby localizing the obstructive coronary lesion. reliably predict the location of the obstructive coronary lesion.
  • These drugs dilate normal coronary arteries but evoke minimal or no change in the diameter of atherosclerotic coronary arteries. A significant coronary obstructive lesion causes less blood flow and thus less tracer activity
  • when a diseased coronary artery is of reasonable size, has a high-grade proximal stenosis, and is free of significant distal plaques. The most suitable atherosclerotic lesion for coronary angioplasty is discrete, concentric, proximal, noncalcified, and less than 5 mm in length.
  • Troponin is more specific than CK-MB ; increases within 4 hours after AMI & remains elevated up to 1 wk . CPK-MB elevates within 4-6 hours after an acute MI; peaks in 18-24 hours; it then returns to normal within 3-4 days LDH elevates in 24-48 hours and peaks in 48-72 hours after the episode.
  • At risk patients need to be managed with pharmaco­logic and other perioperative interventions that can ame­liorate perioperative cardiac events. Three therapeutic options are available before elective noncardiac surgery.­
  • patient-specific strategy for perioperative aspirin management that weighs the risks of stopping aspirin with those associated with its continuation. Most patients, especially those taking aspirin for secondary cardiovascular prevention, should have their aspirin continued throughout the perioperative period. When aspirin is held preoperatively, the aspirin withdrawal syndrome may significantly increase the risk of a major thromboembolic complication. For many operative procedures, the risk of perioperative bleeding while continuing aspirin is minimal, as compared with the concomitant thromboembolic risks associated with aspirin withdrawal. ■ Continue beta blockers ; they were found to increase long-term survival in patients with IHD. ■ Calcium channel blockers do not increase the negative inotropic & vasodilatory effects of inhalational agents but may potentiate the effects of depolarizing & nondepolarizing muscle relaxants. ■ Stop ACE inhibitors the night before surgery to avoid severe hypotension intraoperatively. ■ Stop aspirin 1 wk before surgery if possible; anticoagulation must be held to decrease risk of bleeding.
  • Acute postopera­tive stent thrombosis has been reported when anti-plate­let agents were temporarily held preoperatively to reduce chance of bleeding. Continuing the therapy can lead to significant postoperative bleeding.
  • In general all agents can be used safely if given slowly in small increments
  • Decrease bp . Pancuronium bp & hr increase.
  • Opoid alone does not cause total amnesia …. volatile anesthetic agents are coronary vasodilators the mechanism is not clear, it may involve activation of ATP-sensitive K + channels and stimulation of adenosine (A 1 ) receptors. …
  • Blood pressure-invasive & noninvasive
  • the requirement of fluid volume or inotropes can be judiciously calculated and response monitored closely TEE =high cost & complex technique
  • Kinotropes like digoxin ,dopamine dobutamine
  • Transcript

    • 1. Ischaemic Heart disease &its Anaesthetic Management.Dr. Swadheen kumar Rout1styear P.GDept. of AnaesthesiologyM.K.C.G College & hospital
    • 2. Overview:-• Leading cause of death & health care expenditure.• 5% of patients over 35 years of age have asymptomaticischaemic heart disease.• May be present in up to 30% of older pts ( >65 yrs)undergoing surgery.• ↑ incidence of peri- & post-operative MI in patients withknown coronary disease.
    • 3. Blood supply of heart:-
    • 4. Blood supply of heart:-
    • 5. Physiology:- supply & demand• Oxygen demand is a concept that is closely relatedto the oxygen consumption of an organ.• The two terms are often used interchangeablyalthough they are not equivalent.• Demand is related to need ,whereas consumption isthe actual amount of oxygen consumed per minute.• Under some conditions, demand may exceedconsumption because the latter may be limited by thesupply of oxygen to the organ.
    • 6. Organ VO2 (ml O2/min/100g)Brain 3Kidney 5Skin 0.2Resting muscle 1•Highly oxidative organs such as the heart have a high demand foroxygen and therefore have a relatively high oxygen consumption.Physiology:- supply & demandCARDIAC STATE MVO2 (ml O2/min/100g)Arrested heart 2Resting heart 8Heavy exercise 70VO2 = O2 consumption/demandMVO2 = Myocardial O2consumption/demand
    • 7. Physiology:- demand•In order to support MVO2, particularly during times of increasedoxygen demand (e.g., during exercise), the heart must extract oxygenfrom the arterial blood supplying the myocardium.Myocardial Oxygen DemandMyocardial LV wall tensionHeart rateCardiac contractility(preload & afterload)
    • 8. Physiology:-Cont..Fick’s Principle- (CO)•States that blood flow to an organ can be calculated using amarker substance if the following is known:-Amount of marker substance(Consumption) taken up by the organ per unit time (VO2)-Concentration of marker substance in arterial blood supplying the organ (Ca)-Concentration of marker substance in venous blood leaving the organ (Cv)•Applying Fick’s principle to coronary circulation, myocardial O2 consumption(MVO2) can be calculatedMV02 = CBF× (CaO2 – CvO2)• CBF = Coronary blood flow (ml/min)• CaO2 – CvO2 = Arterio-venous O2 content difference(ml O2/ml blood)
    • 9. Physiology:-SupplyMVO2 = (CBF ×CaO2) – (CBF × CvO2)• In another wayCBF × CaO2 is the oxygen supply (or delivery)to the myocardium.CBF × CvO2 is the unextracted oxygen leaving theheart via the venous circulation.•The delivery of oxygen(MDO2) to the myocardium (oxygensupply) is determined by two factors:• CBF (Coronary blood flow)• CaO2 (Oxygen content of the arterial blood)(O2 Delivery) MDO2 = CBF × CaO2
    • 10. OXYGEN content of blood:-CaO2 (O2 content) = ( Hgb x 1.36 x SaO2) + (0.0031 x PaO2)• CaO2: Directly reflects the total number of oxygen molecules inarterial blood (both bound and unbound to haemoglobin).• Hgb = haemoglobinNormal range(Adults): Male: 13-18 g/dl Female: 12-16 g/dl• SaO2 = % of haemoglobin saturated with oxygen(Normal range: 93-100%)• PaO2= Arterial oxygen partial pressure(Normal range: 80-100 torr)
    • 11. Myocardial Ischemia :- AetiologyDemand > SupplyMyocardial hypoxia↓ Availability of nutrient substrates•Results due to Imbalance between Myocardial oxygen supplyand demand.↓ removal of metabolites
    • 12. Increase in O2 demand may be due to:• Tachycardia• Hypertension• Stress.• Drugs• Severe painMyocardial Ischemia :- AetiologyHowever, 50% or more of the ischemic episodes may beunrelated to increased demand suggesting that decreasedoxygen supply is the primary cause.
    • 13. Potential aetiologies for ↓myocardial O2 supply include:External factors:• Hypotension ,Tachycardia, Increased filling pressure,Anaemia, Hypoxemia, and ↓ Cardiac output.Internal factors:• Acute coronary artery thrombosis & spasm.• Myocardial O2 supply/demand mismatch is the maintrigger of myocardial injury.Myocardial Ischemia :- Aetiology
    • 14. Risk factors:-Risk factorsNon-modifiable/irreversible Modifiable/reversible•Male sex•Age•Genes
    • 15. Risk factors:-Risk factorsNon-modifiable/irreversible Modifiable/reversible•Male sex•Age•Genes
    • 16. Modifiable factors:-
    • 17. Myocardial Ischemia:-•More than 90% of cases, the cause of myocardial ischemia isreduction in coronary blood flow due to atherosclerotic coronaryarterial obstruction.•Hence often termed coronary artery disease (CAD).•Limits normal rise in coronary blood flow in response to↑myocardial oxygen demand
    • 18. Clinical manifestation:-– Myocardial necrosis (infarction)– Ischaemia (usually angina)– Arrhythmias (resulting in sudden death)– Ventricular dysfunction (CHF) – ischemic cardiomyopathy
    • 19. Clinical manifestation:-• Patients with IHD can present with chronic stable angina orwith Acute coronary syndrome.Which includes ST elevation myocardial infarction(STEMI)/non–ST elevation myocardial infarction (NSTEMI) onpresentation and unstable angina• Chronic stable angina: Chronic pattern of transientangina pectoris precipitated by physical activity oremotional upset, relieved by rest with in few minutes.• Unstable angina: Increased frequency and duration ofAngina episodes, produced by minimal exertion or at rest(high frequency of MI if not treated)
    • 20. Treatment of IHD:-• The general approach– Prevent progression of disease by correcting risk factors-lifestyle modification to prevent stress & improve exercisetolerance.– Correction of complicating medical condition like,HTN, Anemia, Hypoxemia, Thyrotoxicosis, Infection.– Pharmacological therapy aimed in restoring balance betweenmyocardial oxygen supply and demand.– Surgical correction of Coronary lesion• Percutaneous coronary intervention (PCI).• Coronary artery bypass surgery (CABG).• Pharmacological agents– Calcium channel blockers– β-blockers– Nitrates
    • 21. Anti-ischemic Rx. effect on myocardial O2Demand Heart Rate Contractility Preload AfterloadNitrates No ,  No ,   β-blockers   No ,  NoDHP*  No No V / D**  No ,  No Supply Regional CBF Diastolic filling timeNitrates  +/-β-blockers  DHP*  V / D**  Demand:Supply:
    • 22. Anaesthesia :- Pre-operative AssesmentGOALS:A. Evaluate patient’s current medical status.B. To estimate peri-operative CV risk.(Risk Stratification)C. Know when to perform stress testing or specialinvestigations pre-operatively.D. Pre-operative management to reduce risk peri-operatively in those at higher risk
    • 23. Evaluation of current medical status:-History:Symptoms such as angina and dyspnoea may be absent at rest. Emphasizing the importance of evaluating the patientsresponse to various physical activities such as walking orclimbing stairs. Limited exercise tolerance in the absence of significant lungdisease is very good evidence of decreased cardiacreserve. If a patient can climb two to three flights of stairs withoutsymptoms, it is likely that cardiac reserve is adequate.• Previous Myocardial Infarction.• Co-Existing Noncardiac Diseases• Current Medications
    • 24. Physical examination:-
    • 25. Routine investigations:-• Blood chemistry tests-• Chest X-RAY - excluding cardiomegaly or pulm. Congestionsecondary to ventricular disfunction.• Standard ECG - changes of a previous MI – abmormal Q waves.- loss of R waves.• Suggest myocardial ischaemia - ST segment depression- ST elevation (variant angina)- Flattening of T waves- Inverted T waves- Abnormally tall T waves• Resting ECG may be normal in 50% of patients with IHD• Also detect conduction defects, ventricular hypertrophy,& arrhythmias
    • 26. Anaesthesia :- Pre-operative AssesmentGOALS:A. Evaluate patient’s current medical status.B. To estimate peri-operative CV risk.(Risk Stratification)C. Know when to perform stress testing or specialinvestigations pre-operatively.D. Pre-operative management protocol to reduce risk peri-operatively in those at higher risk
    • 27. Risk Stratification:-Estimate peri-operative CV risk• Numerous risk indices and predictors have been used over theyears for estimating peri-operative risk .•The Goldman Index was the first risk stratification method to usemodern statistical methods and identified 9 clinical factors whichcorrelated with cardiovascular risk and death.•A weight was assigned to each risk factor based on the strengthof the statistical risk and it was possible, using this method, toassign a number of points and use this point score, generally toplace a patient in one of four risk categories.Demerit - underestimate risk in certain populations (elderly,obese)
    • 28. Goldman Risk Index:- (1977)
    • 29. Goldman Risk Index:- (1977)
    • 30. Goldman Risk Index:- (1977)
    • 31. Detsky modified Index:- 1986
    • 32. Detsky modified Index:-Class Points Cardiac riskI 0 to 15 LowII 20 to 30 ModerateIII 31 + high High
    • 33. Clinical Predictors of IncreasedPerioperative Cardiovascular Risk
    • 34. J Am Coll. Cardiol, 2007; 50:1707-1732ACC/AHA Guidelines:- (2007)• Based on - Active cardiac conditions.- Surgery-Specific Risk- Functional Capacity- Cardiac risk factors
    • 35. Active Cardiac Conditions:- for Which the Patient Should UndergoEvaluation and Treatment Before Surgery
    • 36. Cardac risk factors:-
    • 37. Functional Capacity :Metabolic Equivalents (METs)• One MET is the basal oxygen consumption (VO2) of a 70Kg ,40 yr old man in resting state (3.5 ml/kg/min).• Multiples of the baseline MET value can be used toexpress aerobic demands for specific activities .• Perioperative cardiac and long-term risks are increasedin patients unable to meet a 4-MET demand during mostnormal daily activities.
    • 38. Functional Capacity : Duke Activity Status Index
    • 39. Surgery-Specific Risk:-• Urgency.• Type/complexity of surgery.
    • 40. ACC/AHAStepwise approach to perioperative cardiac assessmentCardiologyconsultationCardiologyconsultation
    • 41. ACC/AHAStepwise approach to perioperative cardiac assessmentCardiologyconsultationCardiologyconsultation
    • 42. Anaesthesia :- Pre-operative AssesmentGOALS:A. Evaluate patient’s current medical status.B. To estimate peri-operative CV risk.(Risk Stratification)C. Know when to perform stress testing orspecial investigations pre-operatively.D. Pre-operative management protocol to reduce risk peri-operatively in those at higher risk
    • 43. Special Cardiac Investigation :-• 1) Non-invasive tests.• 2) Invasive testsAssesment of LV functionNoninvasive Stress Testing- Active cardiac conditions.- 3 or more clinical risk factors & poorfunctional capacity (less than 4 METs)requiring high risk surgery.
    • 44. Special Cardiac Investigation:-Noninvasive tests• Holter Monitoring- Continuous ambulatory ECGmonitoring.• Evaluating the severity and frequency of ischemic episodes &arrhythmias• Excellent negative predictive valuefor perioperative cardiac complications.
    • 45. Special Cardiac Investigation:-Noninvasive testsExercise electrocardiography-•Contraindications include severe aortic stenosis, severe HTN,limited exercise tolerance, uncontrolled heart failure and IE.•Normal test does not necessarily exclude CAD but suggests thatsevere disease is not likely.
    • 46. Echocardiography-• Can be used to assess globalcardiac function.• Assess regional wall motionabnormalities & detect thepresence of previous myocardialinjury.• LV function assessment is amajor determinant of long-termprognosis.• Ejection fraction < 50% (pooroutcome)Special Cardiac Investigation:-Noninvasive tests
    • 47. Myocardial perfusion scans-• Nuclear tracers (thallium-201 or technetium-99m) are used tomeasure coronary blood flow to myocardium.• IV dipyridamole or adenosine (coronary dilator) produces ahyperemic response similar to exercise.• A significant coronary obstructive lesion causes less bloodflow and thus less tracer activity.Size of the perfusion abnormalityis the most important indicatorof the significance of CAD.Special Cardiac Investigation:-Noninvasive tests
    • 48. • Coronary angiography- indicated in patients who continueto have angina pectoris despite maximal medical therapy/ fordefinitive diagnosis.• Gold standard to evaluate CAD.• Provides information about thecoronary anatomy & locationthe extent & of the lesions.Determine need of coronaryrevascularization & the feasibilityof PCI/CABG depending on thecharacteristics & location of the lesions.Special Cardiac Investigation:- Invasive tests
    • 49. Supplemental Preoperative Evaluation:When and Which Test
    • 50. Other investigations:-Cardiac enzymes- Cardiac-specific Troponins (T or I). Creatinine kinase (MB isoenzyme). Lactate dehydrogenase (type 1 isoenzyme). Myoglobins.
    • 51. Anaesthesia :- Pre-operative AssesmentGOALS:A. Evaluate patient’s current medical status.B. To estimate peri-operative CV risk.(Risk Stratification)C. Know when to perform stress testing or specialinvestigations pre-operatively.D. Pre-operative management to reduce riskperi-operatively in those at higher risk.
    • 52. Preoperative management:-• At risk patients need to be managed with pharmacologic andother pre-operative interventions that can ameliorateperioperative cardiac events.Optimisation of medicalmanagement.Coronary revascularization(PCI / CABG)
    • 53. Optimisation of medical management:-• Continue cardiac medications (beta blockers, CCBs, Nitrates)till morning of surgery.Sudden withdrawal of antianginal medication canprecipitate a sudden increase in ischemic episodes (rebound).Prophylactic -adrenergic blockade has been shown to reducethe incidence of intra-op & post-op ischemic episodes.■ ACE inhibitors – Severe hypotension.• Anti platelet therapy-Aspirin- patient-specific strategy. (Risk/Benefit)(Risk of perioperative bleeding while continuing aspirin is, as compared withconcomitant thromboembolic risks associated with aspirin withdrawal)• Stop ticlodipine & clopidrogel
    • 54. Coronary ArteryDiseasePatient Scheduled for Surgery WithTwo Risk Factors:Age > 65HypertensionDiabetesCholesterol > 240 mg/dlSmokingBeta Blockers:Atenolol 25 mg po qd to start, if heart rate greaterthan 60 and systolic blood pressure greater than120 mmHg. Titrate dose to effect.Atenolol or Metoprolol IV on day of surgery.Atenolol or Metoprolol IV post op until taking POthen.Atenolol 100 mg PO qd for at least a week post op(hold for heart rate less than 55 or systolic bloodpressure less than 100 mmHg)If known CAD continue beta blocker indefinitely.If patient has a specific contraindication(asthma not COPD) to beta blockers:Clonidine 0.2 mg PO tablet night beforesurgeryClonidine TTS#2 Patch (0.2 mg/24 hours)night before surgeryClonidine 0.2 mg PO table morning of surgery.Hold for systolic blood pressure less than 120.If Unable to take beta blockersProceed with SurgeryPerioperative Cardiac Risk ReductionTherapy (PCRRT)α2 agonists by virtue of itssympatholytic effects is usefulin patients where beta blockers arecontraindicated.
    • 55. Coronary Revascularization:- PCI/CABG• Guided by patients cardiaccondition & potential consequenceof delaying surgery for recoveryafter coronary revascularization.• Patients who underwent coronaryvascularization had better outcomeafter noncardiac surgery.Stent / baloon(per-cutaneous Angioplasty)Coronary artery bypass graft
    • 56. Delaying surgery after PCI:-
    • 57. Anaesthesia:- PremedicationGoal- Allaying anxiety minimizes the sympathetic systemeffects on the myocardium decreasing possibility of ischemicevents perioperatively.• Benzodiazepine, alone or with opioid are m/c used.• Excellent results can be obtained by a combination ofmorphine (0.1–0.15 mg/kg) and scopolamine (0.2–0.4 mg)IM.• Concomitant administration of oxygen helps avoid hypoxemiafollowing premedication.
    • 58. Choice of Anesthesia:-• Regional anesthesia may be preferred togeneral anesthesia if possible, as it tendsto better block the stress response tosurgery.• Hypotension associated can be correctedby fluids & sympathomimetic agents.• Potential benefits include excellent paincontrol, decreased incidence of deep veinthrombosis in some patients, and theopportunity to continue the block into thepostoperative period.• However, the incidence of postoperativecardiac morbidity and mortality does notappear to be significantly different betweengeneral and regional anesthesia.Anaesthetic management skillsmore important than technique
    • 59. General anesthesia:-■ Induction :➣ The main goal duringinduction is to avoid haemodynamic alteration (minimizeextreme variation in HR & BP), thereby decreasing drasticcardiac events.➣.Produce reliable loss of consciousness, & provide sufficientdepth of anaesthesia
    • 60. • In general all agents can be used safely if given slowly insmall increments. However Ketamine due to its indirectsympathomimetic effects can adversely affect the myocardialoxygen demand–supply balance.Intravenous anaesthetics-1) Thiopentone - Reduces myocardial contractility, preload andBP & slight increase in HR. It should be administered slowlyand with caution.2) Propofol - Reduces arterial BP & HR significantly. There isdose dependent reduction in myocardial contractility. It can beused in with good ventricular function but is not good inductionagent for patients with CAD.General anesthesia:-Choice of agent
    • 61. 3) Midazolam - It produces decrease in mean arterial pressureand increase in heart rate. It provides excellent amnesia and iswidely used for patient with CAD.4) Etomidate - It causes minimum haemodynamic changes. It isexcellent for induction in patients with poor cardiac reserve.General anesthesia:-Choice of agent
    • 62. Intubation : choice of muscle relaxant• Rocuronium, vecuronium, pipecuronium, and doxacuriumproduce minimum haemodynamic alterations & safe in IHD.• Histamine releasing drugs better avoided.General anesthesia:-• Control cardiovascular response to tracheal intubation bykeeping low duration of laryngoscopy(<15sec) or bypharmacologic means.• Pharmacologic interventions include lidocaine IV (1.5–2mg/kg), 1.5 to 2 min before intubation intratracheal lidocaine (2mg/kg) at the time of laryngoscopy, IV fentanyl ,IV esmolol orIV nitroprusside.
    • 63. • Volatile anaesthetics (isoflurane, desflurane & sevoflurane) aresafe in IHD. Volatile agents generally have a favorable effect onmyocardial oxygen balance, reducing demand & increasing suppl(administered alone or in combination with nitrous oxide.)• Alternately nitrous oxide – opioid combination with the additionof a low dose of volatile anesthetic to treat any undesirableincreases in blood pressure can also be used.Opoids:-Morphine is the preferred drug for its relative cardiac stability &very good analgesic effect. It produces arterial and venousdilatation resulting in reduction of afterload and preload. Neweragents like fentanyl, alfentanyl and sufentanil also provideadequate cardiac stability and pain relief.General anesthesia:- Maintenance
    • 64. GOALS• Stable haemodynamics. (A common recommendation is to keepthe heart rate and blood pressure within 20% of the normal awake value)• Prevent MI by optimizing myocardial oxygen supply andreducing oxygen demand.• Monitor for ischaemia.• Treat ischemia or infarction if it develops.• Normothermia.• Avoidance of significant anaemiaIntraoperative management:-
    • 65. Intraoperative management:-• Maintenance of balance between myocardial O2 supply &demand is more important than the specific anaesthetictechnique or drugs selected to produce anaesthesia andmuscle relaxation.Intraoperative Events That Influence the Balance BetweenMyocardial O2 supply & demand
    • 66. Triggers •Surgical Trauma•Anesthesia/analgesia•Intubation/extubation•Pain•Hypothermia•Bleeding/anemia•Fasting
    • 67. • BP-invasive & noninvasive• Pulse oximetry,Temp.• In addition an important goalwhen selecting monitors forpatients with IHD is to selectthose allowing early detectionof myocardial ischemia.• Most myocardial ischemiaoccurs in the absence ofhemodynamic alterations.• One should be cautious whenendorsing routine use ofexpensive or complexmonitors to detect myocardialischemia.
    • 68. Monitors used depend on disease severity & operativeprocedure complexity➣ ECG: Simplest & Cost effective. ST-segment changes areprincipally used to diagnose myocardial ischaemia.➣ Pulmonary artery catheter: Ischaemia manifests as a suddenincrease in PCWP (not specific). more useful as a guide in thetreatment of myocardial dysfunction.➣ Central venous pressure may correlate with PCWP if EF >0.5 & there is no evidence of LV dysfunction.➣ Transesophageal echocardiography: Most sensitive todetect intraoperative myocardial ischemia by detecting newonset of regional wall motion abnormality.
    • 69. Intraoperative Management of MyocardialIschemia• If patient is haemodynamically stable-IV Beta blockers like metoprolol / Esmolol (associated with tachycardia).IV Nitroglycerine (associated with HTN).Heparin after consultation with surgeon.• If patient is haemodynamically unstable-Support with inotropes.Use of intraoperative ballon pump may be necessary.Urgent consultation with cardiologist to plan for earliest possible cardiaccatheterization.
    • 70. Reversal and recovery:• Muscle relaxants can be reversed with neostigmine incombination with glycopyrrolate, as the latter produces lesstachycardia. Nevertheless, atropine can be used with noadverse effects as long as the pt is adequately beta blocked.• Early extubation is desirable in many patients as long as they fulfillthe criteria for extubation.• However, patients with IHD can become ischemic duringemergence from anesthesia or weaning with an increased heartrate and blood pressure.• These hemodynamic alterations must be managed diligently.Pharmacologic therapy with a β-blocker or combined α- and β-blockers such as labetalol can be very helpful.
    • 71. Postoperative Management:-• The goals are to prevent ischemia, monitor for myocardialinjury, and treat myocardial ischemia/infarction.• Supplemental oxygen is crucial.• Adequate Pain control to avoid excessive sympathetic nervoussystem stimulation.• 12-lead ECG as a baseline for detecting ischaemia.• Prevention of shivering & maintenance of normothermia iscrucial to avoid oxygen desaturation & sympathetic overactivity.• Maintaining adequate oxygenation & tight pain control for48 to 72 hr post-op is very important, since this is the periodwhen the likelihood of developing AMI is highest.

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