Ischaemic heart disease & its anaesthetic implications

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Ischaemic heart disease & its anaesthetic implications

  1. 1. Ischaemic Heart disease &its Anaesthetic Management.Dr. Swadheen kumar Rout1styear P.GDept. of AnaesthesiologyM.K.C.G College & hospital
  2. 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. 3. Blood supply of heart:-
  4. 4. Blood supply of heart:-
  5. 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. 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. 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. 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. 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. 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. 11. Myocardial Ischemia :- AetiologyDemand > SupplyMyocardial hypoxia↓ Availability of nutrient substrates•Results due to Imbalance between Myocardial oxygen supplyand demand.↓ removal of metabolites
  12. 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. 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. 14. Risk factors:-Risk factorsNon-modifiable/irreversible Modifiable/reversible•Male sex•Age•Genes
  15. 15. Risk factors:-Risk factorsNon-modifiable/irreversible Modifiable/reversible•Male sex•Age•Genes
  16. 16. Modifiable factors:-
  17. 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. 18. Clinical manifestation:-– Myocardial necrosis (infarction)– Ischaemia (usually angina)– Arrhythmias (resulting in sudden death)– Ventricular dysfunction (CHF) – ischemic cardiomyopathy
  19. 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. 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. 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. 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. 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. 24. Physical examination:-
  25. 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. 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. 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. 28. Goldman Risk Index:- (1977)
  29. 29. Goldman Risk Index:- (1977)
  30. 30. Goldman Risk Index:- (1977)
  31. 31. Detsky modified Index:- 1986
  32. 32. Detsky modified Index:-Class Points Cardiac riskI 0 to 15 LowII 20 to 30 ModerateIII 31 + high High
  33. 33. Clinical Predictors of IncreasedPerioperative Cardiovascular Risk
  34. 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. 35. Active Cardiac Conditions:- for Which the Patient Should UndergoEvaluation and Treatment Before Surgery
  36. 36. Cardac risk factors:-
  37. 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. 38. Functional Capacity : Duke Activity Status Index
  39. 39. Surgery-Specific Risk:-• Urgency.• Type/complexity of surgery.
  40. 40. ACC/AHAStepwise approach to perioperative cardiac assessmentCardiologyconsultationCardiologyconsultation
  41. 41. ACC/AHAStepwise approach to perioperative cardiac assessmentCardiologyconsultationCardiologyconsultation
  42. 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. 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. 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. 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. 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. 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. 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. 49. Supplemental Preoperative Evaluation:When and Which Test
  50. 50. Other investigations:-Cardiac enzymes- Cardiac-specific Troponins (T or I). Creatinine kinase (MB isoenzyme). Lactate dehydrogenase (type 1 isoenzyme). Myoglobins.
  51. 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. 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. 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. 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. 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. 56. Delaying surgery after PCI:-
  57. 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. 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. 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. 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. 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. 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. 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. 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. 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. 66. Triggers •Surgical Trauma•Anesthesia/analgesia•Intubation/extubation•Pain•Hypothermia•Bleeding/anemia•Fasting
  67. 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. 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. 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. 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. 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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