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Cardiovascular Pathophysiology (2/4) Ricardo L. Garcia MD TODAY’S LECTURE } Ischemic Heart Disease } Valvular Heart Disease } Congenital Heart Disease Ischemic Heart Disease examen One of your patients complains of chest pain while you were re-evaluating him at recovery area. You notice a...

Cardiovascular Pathophysiology (2/4) Ricardo L. Garcia MD TODAY’S LECTURE } Ischemic Heart Disease } Valvular Heart Disease } Congenital Heart Disease Ischemic Heart Disease examen One of your patients complains of chest pain while you were re-evaluating him at recovery area. You notice a ST depression on the electrocardiogram (ECG). As part of the next management no arrhythmia steps for this scenario you may administer all of the following agents, EXCEPT: A. Procainamide -> used O to manage arrhytmias B. Oxygen C. Opioids for analgesia D. Beta blockers E. Aspirin Item Weight: 1.0 of the patient is determined by the following: The cardiac output a. Heart rate Question #: 20 volume ESK-EDV= SV b. Stroke c. Heart rate and stroke volume CO HR XSV 0 blood pressure Youd.are Stroke caring Volume for a 32and y/o female with mitral stenosis who is undergoing a large abdominal e. Heart Rate and contractility surgery. What special consideration you must have? -> = A 35-year-old male was involved in a motor vehicle accident. He suffered severe traumatic brain injury A. with an epidural hematoma. He is being taken to OR for decompresive craniotomy. Upon Promote tachycardia evaluation patient HR:anesthetics 50 BP: 180/99 RR: 14 (on MV) and Saturation 100%. These B. Use potent has volatile vital signs are compatible with: C. Avoid hypervolemia usually seen in brain injury NBP HHR irregular breathing a. Cushing reflex 0 D. Use potent intravenous sedatives b. Vaso vagal reflex faint/suncope inpH and 02 Will see resp A's E. No special consideration this scenario carotid/aorta respond to c. Chemoreceptor reflex inlocated in response to Matrial pressure HR d. Bainbridge reflex Baroreceptor reflex circulatory homeostasis Iteme.Weight: 1.0 . - - - - - . . Ischemic Heart Disease } Important Prevalence: up to 30% of patients who undergo surgery } First manifestation could be: } } } Myocardial infarction (MI) Angina Pectoris Sudden Death } } Cardiac Dysrhytmias Most important risk factors } } male gender increasing age Ischemic Heart Disease } Risk Factors } } } } } } } } } Male gender Increasing age Hypercholesterolemia Hypertension Cigarette smoking Diabetes mellitus Obesity Sedentary lifestyle Genetic factors / family history menopause it risk ↳ female in Arterial Supply Determinants Of Coronary Perfusion } Coronary perfusion is intermittent compared to continuous in other organs } CPP = Aortic diastolic pressure – LVEDP } LV is perfused entirely during diastole } RV is perfused during both systole & diastole Myocardial Ischemia desbalance duplido d demande } Results when there is an imbalance between myocardial oxygen supply and demand } Most occurs because of atherosclerotic plaque with in one or more coronary arteries } Limits normal rise in coronary blood flow in response to increase in myocardial oxygen demand Ischemic Heart Disease (IHD) } Patients with IHD may have: } Chronic Stable Angina } Acute Coronary Syndrome (ACS) } ST elevation Myocardial Infarction (STEMI) } Unstable angina/non-ST elevation Myocardial Infarction (UA/NSTEMI) Stable Myocardial Ischemia } Also know as: Angina Pectoris } An imbalance between coronary blood flow (supply) and myocardial oxygen consumption (demand) can precipitate ischemia. } Stable angina seen with partial occlusion or significant (>70%) chronic narrowing. } There is an intracardiac release of adenosine, bradykinin, and other substances during ischemia. } } } i que hasen These mediators promote the development of pain. Slow atrioventricular nodal conduction and decrease cardiac contractility. (Improving balance between demand and supply). Atherosclerosis is the most common cause of impaired coronary blood flow resulting in angina pectoris. Angina Pectoris } Diagnosis } History and Physical Exam } } } } -> Retrosternal Chest discomfort Pain Pressure or heaviness Shortness of breath elephant in chest -> pesado no in essharp el . pecto } Usually last several minutes and is crescendo / decrescendo. } Sharp pain for few seconds or dull ache rarely is myocardial in nature } Rest or nitroglycerin alleviate it. f Angina Pectoris } Stable versus unstable } Chronic stable angina refers to chest pain or discomfort that does not change appreciably in frequency or severity over 2 months or longer. - - } Unstable angina is defined as angina at rest, angina of new onset, or an increase in the severity or frequency of previously stable angina without an increase in levels of mas risk de infarto cardiac biomarkers. - Angina Pectoris } ECG Findings } } Standard 12-lead electrocardiogram (ECG) demonstrates ST-segment depression (characteristic of subendocardial ischemia) that coincides in time with anginal chest pain. May have transient symmetrical T-wave inversion. } Patients with chronically inverted T waves resulting from previous MI may manifest a return of the T waves to the normal upright position (pseudonormalization of the T wave) during myocardial ischemia. cambios este ↳O en es order - Angina Pectoris cambios en ST while stress stress Stop test ! . Angina Pectoris Ø Electrocardiography Ø Nuclear Cardiology Techniques Ø Echocardiography Ø Coronary Angiography no exament Modality Exercise electrocardiography Exercise SPECT Adenosine SPECT Exercise echocardiography Dobutamine echocardiography Sensitivity 0.68 0.88 0.90 0.85 0.81 Specificity[†] 0.77 0.72 0.82 0.81 0.79 Saber I Angina Pectoris } Important prognostic determinants : } } } } Right Marginal Artery Greater than 50% stenosis of the left main coronary artery is associated with a mortality rate of 15% per year. Vulnerable plaques, that is, those most likely to rupture and form an occlusive thrombus, have a thin fibrous cap and a large lipid core containing a large number of macrophages. } } Artery Left main coronary artery disease is the most dangerous anatomic lesion and is associated with an unfavorable prognosis when managed with medical therapy alone. } } the anatomic extent of the atherosclerotic disease, the state of left ventricular function (ejection fraction), the stability of the coronary plaque. Right coronary presence of vulnerable plaque predicts a greater risk of MI regardless of the degree of coronary artery stenosis. Most common cause of inferret Acute MI most often results from rupture of a plaque that had produced less than 50% stenosis of a coronary artery. } Currently, there is no satisfactory test to measure the stability of plaques 18 Gen mon 19 Angina Pectoris } Treatment involves } } } } } } Identification and treatment of diseases that can precipitate or worsen ischemia; Reduction of risk factors for coronary artery disease; Lifestyle modification; Pharmacologic management of angina; and Revascularization by coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI) with or without placement of intracoronary stents. The goal of treatment of patients with chronic stable angina is to achieve complete or almost complete elimination of anginal chest pain and a return to normal activities with minimal side effects. Angina Pectoris } Reduction of risk factors for coronary artery disease and Lifestyle modification: } Imbalance in oxygen supply and demand } } } } } } } } Sepsis Fever Hypoxia Cessation of smoking maintenance of an ideal body weight by consumption of a low-fat, lowcholesterol diet Regular aerobic exercise Blood pressure control HDL bueno" it"malo" Lowering the low-density lipoprotein (LDL) cholesterol level by diet and/or drugs such as statins is associated with a substantial decrease in the risk of death due to cardiac events. Angina Pectoris } Medical management of Myocardial Ischemia } Antiplatelet Drugs } Nitrates } B blockers } Calcium Channel blockers } ACE inhibitors - dilation ↓ Oz consumption ↓after load 11 to consumpt Angina Pectoris } } Medical management: Antiplatelet Drugs plaquetas no I } irreversible aspirinay Three classes: dias days quitar } aspirin surgery } thienopyridines (clopidogrel and prasugrel) } platelet glycoprotein IIb/IIIa inhibitors (eptifibatide, tirofiban, and abciximab) - antes de se juntan se ran 10-14 PLT life espera esto ya que se crean PLT nuer as = A fourth class of antiplatelet drug, which affects platelet cyclic adenosine monophosphate (dipyridamole), is not widely used. no examen Medial management: Antiplatelet drugs Angina Pectoris } Medical Management: Organic Nitrates } } } - vasodilator Decrease the frequency, duration, and severity of angina pectoris Increase exercise tolerance The antianginal effects of nitrates are greater when used in combination with β-blockers or calcium channel blockers. I Goal ! } Mechanism of action: } } } disminuir Elmen consumo myocardium de 02 : en el Dilate coronary arteries and collateral blood vessels Decrease peripheral vascular resistance, which reduces left ventricular afterload and myocardial oxygen consumption. The venodilating effect of nitrates decreases venous return and hence left ventricular preload and myocardial oxygen consumption. Angina Pectoris } Medical Management: Organic Nitrates } Nitrates are contraindicated in the presence of hypertrophic cardiomyopathy or severe aortic stenosis and should not be used within 24 hours of sildenafil, tadalafil, or vardenafil because this combination may produce severe hypotension. } Administration of sublingual nitroglycerin by tablet or spray produces prompt relief of angina pectoris. } The most common side effect of nitrate treatment is headache. } The therapeutic value of organic nitrates is compromised by the development of tolerance. To avoid nitrate tolerance, a daily 8to 12-hour interval free of nitrate exposure is recommended. Angina Pectoris } Medical Management: β-Blockers } } } } } } } antiischemic, antihypertensive, and antidysrhythmic properties. Decreases the risk of death and myocardial reinfarction in patients who have had an MI. Drug-induced blockade of β1-adrenergic receptors (atenolol, metoprolol, acebutolol, bisoprolol) results in heart rate slowing and decreased myocardial contractility that are greater during activity than at rest. The decrease in heart rate also increases the length of diastole and thereby coronary perfusion time. β2-Adrenergic blockers (propranolol, nadolol) can increase the risk of bronchospasm in patients with reactive airway disease. β1 and β2 effects, all β-blockers seem to be equally effective in the treatment of angina pectoris. The most common side effects of β-blocker therapy are fatigue and insomnia. How they work Medical Management: β-Blockers know this Angina Pectoris } Medical Management: Long acting calcium channel blockers } } Ninfedipine Similar effects to B blockers Mechanism: decrease vascular smooth muscle tone, dilate coronary arteries, decrease myocardial contractility and oxygen consumption, and decrease systemic blood pressure. Many calcium channel blockers are potent vasodilators and are useful in treating both hypertension and angina. Common side effects: hypotension, peripheral edema, and headache. Calcium channel blockers are contraindicated in patients with severe congestive heart failure or severe aortic stenosis. - } } } Angina Pectoris } Medical Management: ACE inhibitors } ACE inhibitors are recommended for patients with coronary artery disease, especially those with hypertension, left ventricular dysfunction, or diabetes. } Angiotensin receptor blockers offer similar benefits. } Contraindications to ACE inhibitor use include documented intolerance or allergy, hyperkalemia, bilateral renal artery stenosis, and renal failure. Angina Pectoris } Medical Management: Revascularization } Revascularization by CABG or PCI with or without placement of intracoronary stents is indicated when optimal medical therapy fails to control angina pectoris. } Revascularization is also indicated for: } } } left main coronary artery stenosis of more than 50% or the presence of a 70% or greater stenosis in an epicardial coronary artery. In patients with significant coronary artery disease with evidence of impaired left ventricular contractility (ejection fraction of <40%). Angina Pectoris } Medical Management: Revascularization specially if } CABG is preferred over PCI ①LAD } Significant left main artery disease } Three-vessel coronary artery obstruction } Diabetic patients who have two- or three-vessel coronary artery disease. } Operative mortality rates for CABG surgery currently range from 1.5% to 2%. Acute Coronary Syndrome (ACS) } ACS represents a hypercoagulable state. } } } se compe la place Focal disruption of an atheromatous plaque triggers the coagulation cascade with subsequent generation of thrombin and partial or complete occlusion of the coronary artery by a thrombus. Imbalance of myocardial oxygen supply and demand leads to ischemic chest pain. Ischemic chest pain can be categorized based on 12-lead ECG. } } STEMI I UA/NSTEMI know difference 34 ACS STEMI - · st segment elevation know Troponin/CKMB positive · NSTEMI · NO ST eler . Tro pun in positive CMB positive -are re Trop/CKMB & df ⑧ ⑧ : Acute Coronary Syndrome (ACS) } ST Elevation Myocardial Infarction (STEMI) } Mortality decreased because of early interventions } Early intervention 6.5% vs 20% late intervention } Advance age the worst prognostic factor } Almost all STEMI are caused by thrombotic occlusion of a coronary artery } Ifunction Long term prognosis depends on the residual function: specially measured 3-4 months afterwards Acute Coronary Syndrome (ACS) } STEMI: Pathophysiology } } } ↑ Atherosclerosis an inflammatory disease STEMI occurs when coronary blood flow decreases abruptly } Acute thrombus formation } Atherosclerotic plaque fissures, ruptures or ulcerates Various chemical mediators such as collagen, ADP, epinephrine, and serotonin stimulate platelet aggregation. is vasoconstrict } Potent vasoconstrictor thromboxane A2 released } Glycoprotein IIb/IIIa receptors on the platelets are activated, which causes growth and stabilization of the thrombus. 38 ACS } Diagnosis } } } } Diagnosis of acute MI requires the typical rise and subsequent fall in plasma levels of biochemical markers of myocardial necrosis in combination with at least one of the following: (1) ischemic symptoms, (2) development of pathologic Q waves on the ECG, (3) ECG changes indicative of ischemia (ST-segment elevation or depression), and ECHO card (4) imaging evidence of a new loss of viable myocardium or new regional wall motion abnormality. : } ACS } } } seriht } Almost two thirds of patients describe new-onset angina pectoris or a change in their anginal pattern during the 30 days preceding an acute MI. The pain is often more severe than the previous angina pectoris and does not resolve with rest. About a quarter of patients, especially the elderly and those with diabetes, have no or only mild pain at the time of MI. At PE patients typically appear anxious, pale, and diaphoretic. } } } } Sinus tachycardia is usually present. most on arhy nmia during Hypotension caused by left or right ventricular dysfunction or cardiac dysrhythmias may be present. Rales signal congestive heart failure due to left ventricular dysfunction. A cardiac murmur may indicate ischemic mitral regurgitation. ACS } Laboratory Evaluation; Troponin I } Cardiac-specific protein and biochemical marker acute MI. } Levels of cardiac troponins (troponin T or I) increase within 3 hours after myocardial injury and remain elevated for 7 to 10 days. } Elevated troponin levels and the ECG are powerful predictors of adverse cardiac events in patients with anginal pain. } Troponin is more specific than CK-MB. } The currently accepted definition of MI recommends assessing the magnitude of the infarction by measuring how much the cardiac biomarker level is elevated above the normal reference range ACS } Treatment: } } } } Evaluate hemodynamic stability 12 lead ECG Administrer Oxygen Pain relief } } } } Nytroglycerin Aspirin (clopidrogel) B blokers } } Morphine IV Contarindicated in cardiogenic shock, or hemodynamically unstable PRIMARY GOAL: Reestablish blood flow in the obstructed coronary ¨ Time to reperfusion influences outcome ACS: STEMI ACS: STEMI } Reperfusion Therapy } Thrombolytic therapy with streptokinase, tissue plasminogen activator, reteplase, or tenecteplase should be initiated within 30 to 60 minutes of hospital arrival, and within 12 hours of symptom onset. } Thrombolytic therapy restores normal antegrade blood flow in the occluded coronary artery. Dissolution of the clot by thrombolytic therapy becomes much more difficult if therapy is delayed. } The most feared complication: intracranial hemorrhage. } } most likely in elderly patients (>75 years of age) uncontrolled hypertension. ACS: STEMI } Percutaneus Coronary Intervention (PCI) } PCI may be preferable to thrombolytic therapy if appropriate resources are available. } } Treatment choice in patients with a contraindication to thrombolytic therapy and those with severe heart failure and/or pulmonary edema. } } Angioplasty should be performed within 90 minutes of arrival at the health care facility and within 12 hours of symptom onset. About 5% may require emergency cardiac surgery because of failed PCI with intracoronary stents and antiplatelet drugs (aspirin, clopidogrel or prasugrel, and a platelet glycoprotein IIb/IIIa inhibitor) during emergency PCI provides the maximum chance of achieving normal antegrade coronary blood flow. ACS: STEMI } Coronary Bypass Surgery (CABG) } CABG can restore blood flow in an occluded coronary artery, but reperfusion can be achieved faster with thrombolytic therapy or coronary angioplasty. } Emergency CABG is usually reserved for patients in whom angiography reveals coronary anatomy that precludes PCI, patients with a failed angioplasty, and those with evidence of infarction-related ventricular septal rupture or mitral regurgitation. } Patients with ST-segment elevation who develop cardiogenic shock, left bundle branch block, or a posterior wall MI within 36 hours of an acute STEMI are also candidates for early revascularization. } Mortality from CABG is significant during the first 3 to 7 days after an acute MI. ACS: STEMI } Adjuvant Therapies } } Intravenous Heparin ACE inhibitors } } } } } } } } Heart failure of EF<40% Diabetes Receive β-blockers as early as possible Prophylactic administration of lidocaine or other antidysrhythmic drugs is not recommended. Calcium channel blockers should not be administered. Glycemic control is part of the standard care of diabetic patient. Routine administration of magnesium is not recommended. Statins have strong immune-modulating effects and should be started as soon as possible after MI, especially in patients receiving long-term statin therapy. ACS: Unstable Angina / Non-STEMI UA/NSTEMI results from a reduction in myocardial oxygen supply. Pathophysiologic processes: } } } } } } } (1) rupture or erosion of a coronary plaque that leads to nonocclusive thrombosis; examen (2) dynamic obstruction due to vasoconstriction (Prinzmetal's variant angina, cold, cocaine use); (3) worsening coronary luminal narrowing due to progressive atherosclerosis, in-stent restenosis, or narrowing of coronary artery bypass grafts; (4) inflammation (vasculitis); (5) myocardial ischemia due to increased oxygen demand (sepsis, fever, tachycardia, anemia). Troponin M1(biomarkers) it biomarkers/Troponin @ IS anging ACS: Unstable Angina / Non-STEMI last Usual Presentations: } longer } Angina at rest (usually lasting more than 20 minutes unless interrupted by antianginal medication), } Chronic angina pectoris that becomes more frequent and more easily provoked,;and } New-onset angina that is severe, prolonged, or disabling. UA/NSTEMI can also present with hemodynamic instability or congestive heart failure. } O } 50% have significant ECG abnormalities, including transient ST-segment elevation, ST depression, and T-wave inversion. } Significant ST-segment depression in two or more contiguous leads and/or deep symmetrical T-wave inversion, especially in the setting of chest pain, is highly consistent with a diagnosis of myocardial ischemia and UA/NSTEMI. Elevated levels of cardiac biomarkers establish the diagnosis of acute MI. } ACS: Unstable Angina / Non-STEMI } Treatment / Goals } Decreasing myocardial oxygen demand: Bed rest, supplemental oxygen, analgesia β-blocker therapy are indicated. } } ¨ } Calcium channel blockers can also be used. Sublingual or intravenous nitroglycerin may improve myocardial oxygen supply. Limiting thrombus formation by inhibiting platelet activation and Alparinized aggregation. } -> } } } Aspirin, clopidogrel, or prasugrel and 48 hours of heparin therapy are strongly recommended to decrease further thrombus formation. Thrombolytic therapy is not indicated in UA/NSTEMI and has been shown to increase mortality. Older age (>65 years), positive finding for cardiac biomarkers, rales, hypotension, tachycardia, and decreased left ventricular function (ejection fraction of <40%) are associated with increased mortality. ACS: Unstable Angina / Non-STEMI Patients at high risk: } } } } } } } } } } Elderly ischemic symptoms in the preceding 48 hours prolonged chest pain (>20 minutes) those with heart failure or hemodynamic instability Presence of ventricular dysrhythmias, PCI within the past 6 months or had prior CABG surgery elevated troponin levels angina at low-level activity Older age (>65 years), positive finding for cardiac biomarkers, rales, hypotension, tachycardia, and decreased left ventricular function (ejection fraction of <40%) are associated with increased mortality. Complications of Acute Myocardial Infarction Cardiac Dysrhytmias – common cause death } Ventricular fibrilation (3-5%) Ventricular Tachycardia Atrial Fibrilation / atrial Flutter (20%) Sinus Bradycardia } } } } } Heart Block 20% patients with inferior wall MI Pericarditis } } } } 10-15% in 1-4 days after MI Pleuritic pain Dressler’s Syndrome: 4 weeks later Complications of Acute Myocardial Infarction Mitral Regurgitation } } } } } ischemic injury to the papillary muscles and/or the ventricular muscle to which the papillary muscles attach. Severe mitral regurgitation is 10 times more likely to occur after an inferior wall MI than after an anterior wall MI Total papillary muscle rupture usually leads to death within 24 hours. Prompt surgical repair is required. Ventricular Septal Rupture } } } } Anterior wall MI High mortality Emergency surgical repair Complications of Acute Myocardial Infarction } CHF / Cardiogenic Shock } Restricted to an advanced form of acute heart failure } Hypotension and oliguria persist } Systolic blood pressure is low, and there may be associated pulmonary edema and arterial hypoxemia. } Cardiogenic shock is usually a manifestation of infarction of more than 40% of the left ventricular myocardium. } In the setting of an acute MI, the mortality of cardiogenic shock exceeds 50%. Complications of Acute Myocardial Infarction CHF / Cardiogenic Shock } Management is directed at the prompt treatment of: } } } } (1) rupture of the left ventricular free wall, septum, or papillary muscles; (2) cardiac tamponade; and (3) acute, severe mitral regurgitation. Circulatory assist devices can help sustain viable myocardium and support cardiac output until revascularization can be performed. } } } Left ventricular assist intraaortic balloon pumps (much more widely available) Complications of Acute Myocardial Infarction Myocardial Rupture } } Acute cardiac tamponade Right Ventricular Infarction } } } } Associated with acute inferior wall MI Heart block 50% TRIAD: ¨ ¨ ¨ Hypotension JVD (kussmaul sign) Clear lung fields Stroke } } } Infarct of the apex and anterior wall Hemorrhagic stroke (0.3-1%) Anesthesia Considerations Perioperative: PCI Mechanically opening a blood vessel by angiography causes vessel injury, especially destruction of the endothelium. } } } } } Prone to thrombosis. It takes about 2 to 3 weeks for the vessel to reendothelialize after balloon angioplasty. After bare metal stent placement, reendothelialization can take up to 12 weeks, and a drug-eluting stent may not be completely endothelialized even after 1 year. Thus, thrombosis after angioplasty and stent placement is a major concern. Perioperative: PCI Percutaneous coronary angioplasty (PTCA) was introduced as an alternative to CABG to mechanically open stenosed coronary arteries. } } Effective, but restenosis occurred in 15% to 60% of patients } Stents coated with drugs (drug-eluting stents) were then introduced to reduce neointimal hyperplasia and subsequent stenosis. } The two principal issues related to PCI with stent placement are thrombosis and an increased risk of bleeding due to dual antiplatelet therapy. Perioperative: PCI Surgery and Risk of Stent Thrombosis } } } Bare Metal Stents: The risk of death, MI, stent thrombosis, and urgent revascularization is increased by 5% to 30% if surgery is performed within 6 weeks of bare metal stent placement. } Drug Eluting Stents: In the nonsurgical population, the chance of late stent thrombosis is higher. } Incidence of major adverse cardiac events is quite significant if dual antiplatelet therapy is discontinued and noncardiac surgery is performed within 1 year of drug-eluting stent placement. Emergency Surgery: In patients with bare metal stents the adverse event rate is threefold higher over elective surgery. For patients with drug-eluting stents, data indicate a 3.5-fold increase in adverse events. Perioperative: PCI } Risk of Bleeding with Antiplatelet Agents } Continuing aspirin therapy increases the risk of bleeding by a factor of 1.5, but the severity of adverse events is not increased. } The risk of bleeding in patients undergoing noncardiac surgery who are taking clopidogrel has not been extensively studied. The addition of clopidogrel to aspirin increases the relative risk of bleeding by 50%. } So far no increase in mortality has been noted except for intracranial surgery. Perioperative: PCI } Management of Patients with Stents } Factors to consider: 1. 2. 3. 4. 5. timing of the operation after PCI, also called the PCI-tosurgery interval; continuation of dual antiplatelet therapy; perioperative monitoring strategies; anesthetic technique; and immediate availability of an interventional cardiologist. Perioperative: PCI } PCI to Surgery Interval Procedure Angioplasty without stenting Bare metal stent placement Coronary artery bypass grafting Drug-eluting stent placement Drug Clopidogrel Ticlopidine Prasugrel Ticagrelor Time to wait for elective surgery 2-4 wk At least 6 wk; 12 wk preferable At least 6 wk; 12 wk preferable At least 12 mo Time before puncture/catheter manipulation or removal 7 days 10 days 7-10 days 5 days Time after puncture/catheter manipulation or removal After catheter removal After catheter removal 6 hr after catheter removal 6 hr after catheter removal Perioperative: PCI Monitoring } High index of suspicion } } } Intraoperative monitoring for ST changes on ECG carde Any angina should prompt MI evaluation - eval Anesthetic technique } Neuroaxial anesthetic: Controversial Neuroaxial blockade not encouraged } } } } 2 leads High risk for spinal hematoma Availability of Interventional cardiologist at institution Perioperative MI } The incidence of perioperative cardiac injury is a cumulative result. } Risk of perioperative death due to cardiac causes is less than 1% in patients without IHD.-schemic heart disease } Incidence of perioperative MI in elective high-risk vascular surgery 5% - 15% } The risk is even higher for emergency surgery. } Patients who undergo urgent hip surgery have an incidence of perioperative MI of 5% to 7%, whereas fewer than 3% of patients who undergo elective total hip or knee arthroplasty have a ↳ 45 year perioperative MI. } Perioperative MIs are associated with a 20% mortality. Perioperative MI: Pathophysiology } } } } } Ischemia occurs early in the postoperative period and is associated with development of a perioperative MI. eval E , Contemporary studies indicate that most perioperative MIs occur in the first 24 to 48 hours after surgery. Many postoperative MIs are NSTEMIs and can be diagnosed by release of cardiac biomarkers and/or ECG changes. These MIs are usually preceded by tachycardia with ST depression, and are often silent. Hypothesis: perioperative myocardial injury develops as a consequence of increased myocardial oxygen demand (increased blood pressure and heart rate) in the context of underlying compromised myocardial oxygen supply. OR Response to strass to surgery Perioperative MI: Pathophysiology