Ischemic Heart Disease Student PDF

ISCHEMIC HEART DISEASE NRAN 80413 SPRING 2024 RON ANDERSON, M.D. 1 OUTLINE Anatomy of the Coronary Circulation Coronary Blood Flow Pathophysiology of Ischemic Heart Disease Known or Suspected Coronary Artery Disease Coronary Artery Disease 2 ANATOMY OF THE CORONARY CIRCULATION Coronary Arterial Syst...

ISCHEMIC HEART DISEASE NRAN 80413 SPRING 2024 RON ANDERSON, M.D. 1 OUTLINE Anatomy of the Coronary Circulation Coronary Blood Flow Pathophysiology of Ischemic Heart Disease Known or Suspected Coronary Artery Disease Coronary Artery Disease 2 ANATOMY OF THE CORONARY CIRCULATION Coronary Arterial System Origin Distribution Dominance Collateral Circulation Coronary Venous System 3 CORONARY ARTERIAL SYSTEM Resting coronary blood flow ~ 225-250 ml/min, or ~ 5% of the cardiac output Left main and RCA originate from proximal aorta behind left and right aortic valve leaflets 4 GUYTON LEFT MAIN DISTRIBUTION Left Anterior Descending (LAD) – Further divides into several branches Supplies – Anterior wall of LV – Anterior 2/3 of interventricular septum – Apex of RV Left Circumflex Supplies – Lateral wall of LV – Part of posterior wall of LV – Occasionally SA node 5 RIGHT CORONARY DISTRIBUTION Supplies – Anterior and Posterior walls of RV – Right atrium (typically including SA node) – Upper half of atrial septum – Posterior third of interventricular septum – Inferior wall and posterior base of LV – AV node 6 ARTERIAL DISTRIBUTION ANTERIOR POSTERIOR 7 BARASH DOMINANCE Right or left dominance determined by which artery, the RCA or Left Circumflex supplies the Posterior Descending coronary artery 8 COLLATERAL CIRCULATION Extensive superficial (epicardial) and deep (subendocardial) plexuses Anastamotic connections may form, producing collateral circulation between branches of a coronary artery or between two coronary arteries. 9 BARASH CORONARY MICROCIRCULATION Ratio of myocardial capillary blood vessels to myofibrils ~ 1:1. Decreased capillary density in interventricular septum and AV node which may explain vulnerability of these tissues to ischemia. 10 CORONARY VENOUS SYSTEM Great cardiac vein (runs with LAD) Anterior cardiac vein (runs with RCA) Middle cardiac vein (runs with posterior descending branch) Terminate in coronary sinus which empties into right atrium – ~75% of coronary venous blood 11 CORONARY VENOUS RETURN Left Ventricle – ~85% returns via coronary sinus – Remainder empties directly into the atria and ventricles via thebesian veins Right Ventricle – Primarily via the anterior cardiac veins which empty directly into the right atrium 12 CORONARY BLOOD FLOW Mechanical Effects Regulation of Coronary Blood Flow Metabolic Control Neural Control 13 FACTORS AFFECTING LV BLOOD FLOW Coronary Perfusion Pressure – (Aortic pressure – LVEDP) Vascular resistance – Related to radius of vessel to 4th power Vessel length Blood viscosity 14 EFFECTS OF EXTRAVASCULAR COMPRESSION ON CORONARY BLOOD FLOW 15 BARASH GUYTON EFFECTS OF EXTRAVASCULAR COMPRESSION ON CORONARY BLOOD FLOW Intense LV muscular contraction limits systolic capillary blood flow, particularly to subendocardial region Large epicardial coronary vessels act as capacitors Driving pressure for perfusion essentially becomes the average aortic root pressure during diastole 16 FACTORS WHICH FURTHER COMPROMISE SUBENDOCARDIAL BLOOD FLOW Coronary artery disease Left ventricular hypertrophy Tachycardia Decreased aortic-intraventricular pressure gradient Decreased aortic diastolic pressure Increased LVEDP 17 MAJOR DETERMINANTS OF MYOCARDIAL OXYGEN CONSUMPTION Heart Rate Myocardial Contractility Wall Stress 18 KAPLAN DPTI / SPTI RATIO More accurate (but not perfect) picture in normal animal model. 19 KAPLAN REGULATION OF CORONARY BLOOD FLOW Myocardial blood flow is primarily under metabolic control Coronary blood flow is tightly linked to myocardial oxygen consumption Exact mechanism, or mediator, has not been identified 20 METABOLIC CONTROL Myocardial O2 extraction is near maximal in resting myocardium Increases in oxygen supply are therefore dependent on increased blood flow Local mechanisms likely dependent on depletion of oxygen or accumulation of products of metabolism result in release of one or more unspecified mediators of vasodilation – – – – – Adenosine Bradykinin Nitric oxide CO2, H+ ions etc 21 NEURAL CONTROL Direct Effects – Action of Ach, NE, and Epi on the coronary vessels Minimal parasympathetic innervation, however effect of released Ach is coronary vasodilation Much greater sympathetic innervation and effect dependent on preponderance of receptor type – α – receptors more prevalent in epicardial vessels – β – receptors more prevalent in the intramuscular arteries Indirect Effects – Much more significant than the direct effects – Changes in heart rate and contractility (produced by Ach, NE, and Epi) alter myocardial metabolism and affect coronary blood flow via local metabolic mechanisms 22 FAILURE OF AUTOREGULATION Increasing occlusion results in dilation of capillary beds to maintain flow Coronary Flow Reserve decreases, and when exhausted, autoregulation begins to fail CBF reverts to dependence on pressure gradients rather than metabolic control Tachycardia markedly increases the MAP at which autoregulation fails due to: – Increased myocardial O2 consumption – Decreased diastolic perfusion time 23 PATHOPHYSIOLOGY OF ISCHEMIC HEART DISEASE Atherosclerosis Acute Coronary Syndromes Coronary Steal Silent Ischemia 24 ATHEROSCLEROSIS An inflammatory process Intimal lipid plaque producing chronic stenosis and episodic thrombosis Most often occurring in an epicardial artery Characteristics of a vulnerable plaque – – – – High lipid content Thin, fibrous cap Decreased number of smooth muscle cells Increased macrophage activity 25 ACUTE CORONARY SYNDROMES Resulting from sudden decreases in CBF Nearly always caused by thrombosis of a coronary artery Damage varies by extent of thrombosis and duration of occlusion The degree of stenosis is much less important than the extent of plaque rupture 26 OTHER CAUSES OF MI Excessive metabolic demands – Severe left ventricular hypertrophy – Vasoactive drug ingestion – Thyrotoxicosis, sepsis Coronary artery vasospasm Subendocardial infarction can occur with decreased coronary perfusion pressure due to: – Decreased diastolic aortic pressure – Increased LVEDP 27 ST ELEVATION MI (STEMI) Management Goals – – – – Hemodynamic stability Increase O2 supply Decrease myocardial O2 demand Reperfusion Thrombolytic therapy PCI CABG – Emergent CABG has a high mortality and is typically reserved for patients with: » Anatomy non-conducive to PCI » Failed PCI » Associated injury requiring surgery 28 UNSTABLE ANGINA/ NON-ST ELEVATION MI (UA/NSTEMI) Management Goals – Low risk patients typically managed medically Decrease myocardial O2 demand Increase myocardial O2 supply Prevent ongoing thrombus formation – ASA, heparin, LMWH, etc – Higher risk patients considered for early invasive evaluation and intervention 29 PREDICTORS OF LONG-TERM PROGNOSIS Degree of left ventricular dysfunction Degree of residual ischemia Potential for malignant ventricular dysrhythmias 30 ARRYTHMIAS 20 ISCHEMIA Ventricular arrythmias most likely to occur in first 10 minutes following acute occlusion 3 Primary Mechanisms – Failure of repolarization of ischemic myocytes leading to repolarization dyssynchrony – Activation of the sympathetic nervous system – LV dilatation or aneurysm formation leading to abberant impulse conduction and dyssynchrony 31 CORONARY STEAL Ischemic area distal to a high grade stenosis has maximally dilated microvasculature Increased oxygen demand produces vasodilation in vessels supplying adjacent normal myocardium Blood flow may be redistributed away from the ischemic area via collateral vessels 32 SILENT ISCHEMIA Most often associated with elevations in heart rate or blood pressure Closely related to circadian sleep-wake cycles Study of patients presenting for CABG – 42% had perioperative ischemic episodes – 87% of these episodes were silent – Few precipitated by adverse hemodynamics 33 KNOWN OR SUSPECTED CORONARY ARTERY DISEASE Preoperative Assessment History Physical Exam Preoperative Testing Risk Stratification Algorithms Preoperative intervention 34 CARDIAC HISTORY Chest Pain (Character, severity, frequency, progression, last episode) Non-Cardiac Stable (No change in severity, frequency, no recent MI or intervention) Cardiac Unstable “Do you have any trouble with your heart, any chest pain, or shortness of breath?” No. Is this consistent with H&P, ECG? (Silent ischemia?) Active “Can you climb a flight of stairs without getting SOB?” Progressive At Rest Shortness of Breath “When active, or at rest?” “Do you wake up at night short of breath? Do you sleep flat on your back?” Stable (Consistent with CXR, physical exam?) 35 PATIENT HISTORY Cardiac – Previous myocardial infarction – Stent placement Bare-metal Drug-eluting Associated Non-Cardiac – – – – Syncope Cough, shortness of breath Diabetes mellitis Renal insufficiency 36 PREOPERATIVE MEDICATIONS Most drugs are continued throughout the perioperative period with the exception of hypoglycemic agents and drugs affecting coagulation Beta-blockers – Avoid abrupt discontinuation in the perioperative period Angiotensin converting enzyme inhibitors – Controversial (Some d/c 24 hours preop) Antiplatelet drugs – Typically, but not always discontinued preoperatively – Consider effect on central neuraxis anesthesia 37 PHYSICAL EXAM BASIC – Airway – Heart Rhythm Murmurs 3rd Heart sound – Lungs Air movement Wheezes Rales TARGETED – Additional auscultation – Neck -JVD – Orthostasis – Extremities Cyanosis Edema 38 PREOPERATIVE TESTING Only indicated if management of the patient will change based on results. Limited value in patients whose cardiac function is: – Stable – Able to be assessed clinically 39 LEE REVISED CARDIAC RISK INDEX High-risk surgery Ischemic heart disease Congestive heart failure Cerebrovascular disease Insulin-dependent diabetes Preop serum creatinine > 2.0 mg/dl 40 STOELTING ACC/AHA TESTING GUIDELINES 41 STOELTING ACC/AHA TESTING GUIDELINES $ Non-invasive Testing – Able to exercise Stress ECG – Unable to exercise Stress Echo Thallium Stress – Dipyridamole-thallium scintigraphy $$$ Positron emission tomography 42 VALUE OF CARDIAC PET SCAN 43 44 PREOP CARDIAC INTERVENTION Options – Revascularization (CABG) Risk of planned surgery must exceed risk of cardiac cath + CABG + planned surgery(in revascularized pt.) – Percutaneous Coronary Intervention (PCI) Angioplasty + stenting – Consider timing and anticoagulation issues – Optimizing medical management 45 MEDICAL THERAPY INTERVENTION COMMENTS RECOMMENDATION Perioperative beta-blockade Oral therapy initiated at least 30 days preop and IV therapy intraop and postop α2 - agonists Oral clonidine at least 90 min preop and oral/transdermal/IV for 72 hours postop Class IIa Statin therapy Initiated at least 45 days preop and extended-release form day of surgery. Reumed postop Class IIa ACE inhibitors Class I Class IIb Ca++ channel blockers Decreased SVT following non-cardiac surgery. Limited evidence for use in vascular surgery Class IIb Nitroglycerin Not indicated for prophylaxis or initial treatment of myocardial ischemia Class III CORONARY ARTERY DISEASE Intraoperative Management General Principles Induction and Laryngoscopy Maintenance Muscle Relaxants Monitoring Management of Ischemia Postoperative Management 47 GENERAL PRINCIPLES Optimize the myocardial oxygen supply/demand ratio Monitor for ischemia and treat aggressively General Goal: – Maintain heart rate and blood pressure within 20% of baseline 48 HINES IMPORTANCE OF HEART RATE STOELTING 49 INDUCTION AND LARYNGOSCOPY Induction – Most any induction technique is acceptable if done properly Likely would avoid ketamine as primary induction agent Laryngoscopy – Minimize the sympathetic pressor response Short duration Lidocaine Narcotic Esmolol 50 MAINTENANCE Volatile anesthetics – Widely used – Decrease myocardial oxygen requirements – Excessive decrease in blood pressure may compromise coronary perfusion Narcotic technique + – – – – Nitrous Benzodiazipines Low-dose volatile Low-dose propofol infusion General vs. Regional – Avoidance of hypotension with Central Neuraxis Anesthesia – ? Morbidity and Mortality? 51 MUSCLE RELAXANTS Minimal effect on hear rate and blood pressure – Rocuronium – Vecuronium – Cisatracurium Histamine release – Atracurium Increased heart rate and blood pressure – Pancuronium As needed – Succinylcholine – look at Reversal – Glycopyrrolate may produce less tachycardia than atropine – Dosage adjustment 52 MONITORING ECG – ST segment depression or elevation Degree parallels severity of ischemia Occurrence and duration correlate with incidence of perioperative MI – T-wave inversion – R-wave changes HINES 53 MONITORING Pulmonary artery occlusion pressure – Disadvantages Intermittent Relatively insensitive in absence of global ischemia or with papillary muscle dysfunction Not likely to improve outcomes except in carefully selected populations Transesophageal echocardiography – Gold standard for intraoperative diagnosis of ischemia – Disadvantages Expensive Extensive training required ( limits availability) Unavailable during anesthetic induction 54 INTRAOPERATIVE MANAGEMENT OF ISCHEMIA Prompt management of any hemodynamic derangements – Tachycardia (considerations) Beta blockade Deepen anesthetic – Hypotension (considerations) Sympathomimetics Fluids Lighten anesthetic Inotropes IABP In the absence of hemodynamic derangement consider coronary vasodilation with nitroglycerin 55 MANAGEMENT OF ISCHEMIA 56 STOELTING POSTOPERATIVE MANAGEMENT Increased potential for myocardial ischemia combined with a reduction in the acuity of patient care Particular concerns: – Hypothermia and shivering – Pain – Inadequate ventilation Hypoxia Hypercarbia – – – – Infection Unreplaced or ongoing blood loss Continuation of beta-blockade Metabolic regulation 57 THE TRANSPLANTED HEART First 6-12 months No parasympathetic, sympathetic or sensory innervation After 6-12 months Partial reinnervation Results: Higher than normal resting heart rate No sympathetic response to laryngoscopy Light anesthesia/ pain produces less of a heart rate increase May see two P waves on the ECG Unable to detect anginal pain Dependent on preload and the Frank-Starling mechanism to maintain cardiac output – Slow to compensate for hypovolemia with increased heart rate 58 THE TRANSPLANTED HEART Autonomic nervous system is disrupted but alpha and beta receptors are present on the transplanted heart Direct-acting drugs = normal effect Indirect-acting drugs = blunted effect Consider: – Atropine – Neuromuscular blockade reversal 59 SOURCES Anesthesia and Coexisting Disease –Hines. 2022. 8th Edition Textbook of Medical Physiology –Guyton and Hall. 2021. 14th Edition Kaplan’s Cardiac Anesthesia –Kaplan. 2016. 7th Edition Clinical Anesthesia –Barash. 2017. 8th Edition 60