Perioperative MI: Diagnosis PDF

Perioperative MI: Diagnosis } } An acute increase introponin levels should be considered Risk to indicate MI. troponin There is also a significant association between increased troponin levels and short- and long-term morbidity and mortality in surgical patients. } This association exists for card...

Perioperative MI: Diagnosis } } An acute increase introponin levels should be considered Risk to indicate MI. troponin There is also a significant association between increased troponin levels and short- and long-term morbidity and mortality in surgical patients. } This association exists for cardiac death, MI, myocardial ischemia, congestive heart failure, cardiac dysrhythmias, and stroke } An increase in troponin level postoperatively, even in the 0 absence of clear cardiovascular signs and symptoms, is an important finding that requires careful attention and referral to a cardiologist for further evaluation and management Perioperative Assessment in IHD } History } } } } } } evaluation Evaluate Severity, Progression and functional limitations Clinical Risk Factors History of prior MI more risk for infarct Presence of Aortic Stenosis Look for co-existing non-cardiac diseases Medication therapy which one - - } Adequate BP control DBPS } ?? no canclas Physical Examination } } } } } Maybe normal Carotid bruit: cerebrovascular disease Orthostatic hypotension Gallops, rales Peripheral edema surgery Perioperative Assessment in IHD } Specialized Preoperative Testing } } } Exercise ECG Echocardiography Thallium Scintigraphy scan diff Nuclear studies CT Scan / MRI PET Scan . } } } to see how parts of blood is heart reaching Clinical predictors of increased perioperative cardiovascular risk MAJOR •Unstable coronary syndromes •Acute or recent MI with evidence of important ischemic risk based on clinical symptoms or noninvasive study •Unstable or severe angina * combensado •Decompensated heart failure actionality •Significant dysrhythmias •High-grade atrioventricular block •Symptomatic ventricular dysrhythmias in the presence of underlying heart disease •Supraventricular dysrhythmias with uncontrolled ventricular rate •Severe valvular heart disease ↑ * Clinical predictors of increased perioperative cardiovascular risk INTERMEDIATE Mild angina pectoris Previous MI based on history or Q waves on ECG Compensated or previous heart failure Diabetes mellitus (particularly insulin dependent) uncontrolled/long standing diabetes affect perfusion infarct risk Renal insufficiency - of MINOR Advanced age (>70 years) Abnormal ECG (left ventricular hypertrophy, left bundle branch block, ST-T abnormalities) Rhythm other than sinus arrhythmias Low functional capacity History of stroke Uncontrolled systemic hypertension - Management of Anesthesia: IHD } } The preoperative management of patients with ischemic heart disease or risk factors for ischemic heart disease has the following goals: (1) determining the extent of ischemic heart disease and any previous interventions (CABG, PCI), } (2) assessing the severity and stability of the disease, } (3) reviewing medical therapy and noting any drugs that can increase the risk of surgical bleeding or contraindicate use of a particular anesthetic technique. } The first two goals are important in risk stratification. Management of Anesthesia: IHD Cardiac Risk Factors 1. High-risk surgery 1. Abdominal aortic aneurysm 2. Peripheral vascular operation 3. Thoracotomy 4. Major abdominal operation 2. Ischemic heart disease 1. History of myocardial infarction 2. History of a positive finding on exercise testing 3. Current complaints of angina pectoris 4. Use of nitrate therapy 5. Presence of Q waves on electrocardiogram } Management of Anesthesia: IHD 1. Congestive heart failure 1. History of congestive heart failure 2. History of pulmonary edema 3. History of paroxysmal nocturnal dyspnea 4. Physical examination showing rales or S3 gallop 5. Chest radiograph showing pulmonary vascular redistribution 2. Cerebrovascular disease 1. History of stroke 2. History of transient ischemic attack Wen for 3. Insulin-dependent diabetes mellitus 4. Preoperative serum creatinine concentration >2 mg/dL HD Management of Anesthesia: IHD Management of Anesthesia: IHD } Clinical risk factors identified from the history, physical examination, and review of the ECG are grouped into three categories: } Major clinical risk factors may require delay of elective surgery and cardiologic evaluation. Intensive preoperative management is necessary if surgery is urgent or emergent. } Moderate clinical risk factors are well-validated markers of an enhanced risk of perioperative cardiac complications. } Minor clinical risk factors are recognized markers of coronary artery disease that have not been proven to independently increase perioperative cardiac risk. Management Anesthesia: IHD Management After Risk Stratification } The fundamental reason for risk stratification is to identify patients at increased risk so as to manage them with pharmacologic and other perioperative interventions that can lessen the risk and severity of perioperative cardiac events. } Therapeutic options are available before elective noncardiac surgery: } } } (1) revascularization by surgery (CABG) (2) revascularization by PCI (with and without stent) (3) optimal medical management. Management After Risk Stratification } Pharmacologic Management } use of β-blockers } } } } } } } Acute High dose no benefit Continue it’s use prior to surgery Start at least one week before Promote use of statins at least 4 weeks before Alfa blockers may be considered on patients that do not tolerate beta blockers Glycemic control Because several pathophysiologic mechanisms can trigger a perioperative MI, it seems reasonable to think that multimodal therapy with β-blockers or α2-agonists, statins, and insulin may be more beneficial than treatment with any single drug Management After Risk Stratification Paranagement Management After Risk Stratification } Intraoperative management } } } Prevent Myocardial Ischemia Monitor for Ischemia Treat ischemia aggressively if it develops see } Events that Influence Myocardial Oxygen delivery vs Consumption: } Decreased Delivery Decreased CBF ¨ Tachycardia ↓ time in diast ¨ Hypotension ¨ Hypocapnia ¨ Coronary artery spasm ¨ Anemia not enough blood ¨ Hypoxia not enough oxygen ¨ Alkalosis ¨ . Management After Risk Stratification } Events that Influence Myocardial Oxygen delivery vs Consumption: } Increased Consumption Sympathetic stimulation ¨ Tachycardia ¨ Hypertension ¨ Increased contractility ¨ Increased Afterload ¨ Increased preload strech ¨ of ↑ consumption Intraoperative management } Induction } Intravenous induction drugs } } } } Avoid ketamine use T BD Use muscle relaxant Avoid prolonged laryngoscopy Maintenance } } } } } Controlled blood pressure through volatile agents consider ? May consider opioids in impaired left ventricular function opiod platelets and May use regional anesthesia: Remember the history of STENTS defar el el baseline Control tachycardia: goal around 80 bpm Reversal of neuromuscular blockade: Glycopyrrolate (less tachycardia) - - - en - Robinol ↳ anticholinergic usually given Neostigmine - with Inhibit ach Intraoperative management } most effective Monitoring: } } } } 2leads : lead E is (precordial ECG: most effective early detection Changes in the ST segment, characterized as elevation or depression of at least 1 mm and T-wave inversions. The degree of ST-segment depression parallels the severity of myocardial ischemia. Because visual detection of ST-segment changes is unreliable, computerized ST-segment analysis has been incorporated into ECG monitors. Traditionally, monitoring of two leads (leads II and V5) has been the standard, but it appears that monitoring three leads (leads II,V4, and V5, or else V3,V4, and V5) improves the ability to detect ischemia. There is a correlation between the lead of the ECG that detects myocardial ischemia and the anatomic distribution of the diseased coronary artery Intraoperative management sabet - no Intraoperative management of Ischemia } Treatment of myocardial ischemia should be instituted when there are 1-mm ST-segment changes on the ECG. ↳ ischema ? pain , enture 02 , maintain BP } Prompt pharmacologic treatment of changes in heart rate and/or blood pressure is indicated. } Nitroglycerin is an appropriate choice when myocardial ischemia is associated with a normal or modestly elevated blood pressure. } A persistent increase in heart rate in the setting of normal or high blood pressure can also be treated by administration of a β-blocker such as esmolol. Intraoperative management of Ischemia } Hypotension is treated with sympathomimetic drugs to restore coronary perfusion pressure. vaso , neo } In addition to administration of vasoconstrictor drugs, fluid infusion can be useful to help restore blood pressure. } In an unstable hemodynamic situation, circulatory support with inotropes or an intra-aortic balloon pump may be necessary. It may also be necessary to plan for early postoperative cardiac catheterization. Postoperative Management } The goals of postoperative management: } } } prevent ischemia monitor for myocardial injury Risk treat myocardial ischemia or infarction. -> of death up to Mohrs } Any situation that leads to prolonged and significant hemodynamic perturbations can stress the heart. } Although most adverse cardiac events occur within the first 48 hours postoperatively, delayed cardiac events can occur within the first 30 days and can be the result of secondary stresses. It is imperative that patients taking β-blockers continue to receive these drugs throughout the perioperative period. Until next time! Cardiac Transplantation } Preoperative EF usually less than 20% } Patients may come for cardiac transplantation with inotropic, vasodilator, or mechanical circulatory support. } They should be in hemodynamically stable condition before induction of anesthesia. } Etomidate is preferred as an induction agent because it has little effect on hemodynamics. } An opioid technique is often chosen for maintenance of anesthesia. risk to hypotension Volatile anesthetics may produce undesirable degrees of myocardial depression and peripheral vasodilation. more } Nitrous oxide is rarely used because significant pulmonary hypertension & is often present. - hypoxia Cardiac Transplantation lack · } Operative technique } } } CPB Anastomosis Aorta, PA, LA, RA transplant vagal Innervation : - If depend wont respond to atropine On catecholamines . The denervated transplanted heart initially assumes an intrinsic heart rate of about 110 beats per minute, which reflects the absence of normal vagal tone. due to lack of vagal innervation } Stroke volume responds to an increase in preload by the Frank-Starling mechanism. These patients tolerate hypovolemia poorly. } The transplanted heart does respond to direct-acting catecholamines, but drugs that act by indirect mechanisms, such as ephedrine, have a less intense effect. Cardiac Transplantation } Post Operative Complications B adrenergic stimulation for 3-4 days motropic } Early complicat CHE ↓regulation } - } } } Sepsis Rejection of receptors Late } } } } Infection Rejection Cancer Diffuse Obliterative Coronary artheriopathy artheroscleros Risk Infarct is Cardiac Transplantation } Anesthesia Considerations } hemodynamic function of the transplanted denervated heart, the side effects of immunosuppressive therapy, the risk of infection, the potential for drug interactions given the complex drug regimens, and the potential for allograft rejection. If NHR } } Isoprotene 10/ Watch for present infections For transplanted ot w . beta immunosuppressive +x If hepatic and renal function are normal, there is no contraindication to the use of any anesthetic drug. prograft - vasoconst ↓ · afferent GFR Prerenal azotemia agonist Cardiac Transplantation already transplanted } intubation alt i : I in preload intrathoracic pressure . Anesthesia Considerations } The transplanted heart has no sympathetic, parasympathetic, or sensory innervation, and the loss of vagal tone results in a higher than normal resting heart rate. } Carotid sinus massage and Valsalva's maneuver have no effect on heart rate. wont work o innervation } There is no sympathetic response to direct laryngoscopy and tracheal intubation, and the denervated heart has a blunted heart rate response } The transplanted heart is unable to increase its heart rate immediately in response to hypovolemia or hypotension but responds instead with an increase in stroke volume via the Frank-Starling mechanism. first } choice -> volume Cardiac output is dependent on venous return until the heart rate increases after several minutes in response to the effect of circulating catecholamines. Because α- and β-adrenergic receptors are intact on the transplanted heart, it will eventually respond to circulating catecholamines. Summary of lecture stress test } The exercise ECG is most likely to indicate myocardial ischemia when there is at least 1 mm of horizontal or down-sloping STsegment depression during or within 4 minutes after exercise. The greater the degree of ST-segment depression, the greater the likelihood of significant coronary disease. } Noninvasive imaging tests for the detection of ischemic heart disease are used when exercise ECG is not possible or interpretation of ST-segment changes would be difficult. Administration of atropine, infusion of dobutamine, institution of cardiac pacing, or administration of a coronary vasodilator such as adenosine or dipyridamole creates cardiac stress. After stress is induced, either echocardiography to assess myocardial function or radionuclide imaging to assess myocardial perfusion is performed. Summary of lecture } β-Blockers are the principal drug treatment for patients with angina pectoris. } Long-term administration of β-blockers decreases the risk of death and myocardial reinfarction in patients who have had an MI, presumably by decreasing myocardial oxygen demand. } This benefit is present even in patients in whom β-blockers were traditionally thought to be contraindicated, such as those with congestive heart failure, pulmonary disease, or advanced age. S ↑ + Summary of lecture Pathophy Siology and biorn. of NSTEMI STEMI Patients with acute coronary syndrome can be categorized based WSTEMI on a 12-lead ECG. Patients with ST elevation at presentation are d considered to have STEMI. Patients who have ST-segment +bromdepression or nonspecific ECG changes can be classified based on the level of cardiac-specific troponins or CK-MB. Elevation of paincardiac-specific biomarkers indicates NSTEMI. If levels of cardiacchest specific biomarkers are normal, then unstable angina is present. } table biorSTEMI occurs when coronary blood flow decreases abruptly. } } Typically, vulnerable plaques—that is, those with rich lipid cores and thin fibrous caps—are most prone to rupture. Plaques that rupture are rarely of a size that causes significant coronary obstruction. By contrast, flow-restrictive plaques that produce angina pectoris and stimulate development of collateral circulation are less likely to rupture. Summary of lecture } The primary goal in the management of STEMI is reestablishment of blood flow in the obstructed coronary artery as soon as possible. This can be achieved by reperfusion therapy or coronary angioplasty with or without placement of an intracoronary stent. } Thrombolytic therapy is associated with hemorrhagic stroke in 0.3% to 1% of patients. } NSTEMI and unstable angina result from a reduction in myocardial oxygen supply. Rupture or erosion of an atherosclerotic coronary plaque leads to thrombosis, inflammation, and vasoconstriction. Embolization of platelets and clot fragments into the coronary microvasculature leads to microcirculatory ischemia and infarction and results in elevation of cardiac biomarker levels. Summary of lecture } } Acute MI (1 to 7 days previously), recent MI (8 to 30 days previously), and unstable angina are associated with the highest risk of perioperative myocardial ischemia, MI, and cardiac death. need antiplatelet Coronary artery stent placement (drug-eluting or bare metal stent) is routinely followed by dual antiplatelet therapy to prevent acute coronary thrombosis and maintain long-term patency of the vessel. Elective noncardiac surgery should be delayed for 6 weeks after a PCI with bare metal stent placement and for at least 12 months after a PCI with drug-eluting stent placement to allow endothelialization of the stent and completion of dual antiplatelet therapy. Summary of lecture } The transplanted heart has no sympathetic, parasympathetic, or sensory innervation, and the loss of vagal tone results in a higher avold Nitric than normal resting heart rate. 3 1 100 } Carotid sinus massage and Valsalva's maneuver have no effect on heart rate. } There is no sympathetic response to direct laryngoscopy and tracheal intubation, and the denervated heart has a blunted heart rate response to light anesthesia or intense pain. Valvular heart Disease CHAMBERS OF THE HEART Heart Sounds S1 · produced by ·best heard Loud closure of tricuspid and mitral : Cardiac apex : mitral stenosis Se ·soft/absent si -> 5th intercostal space , values at ; the end of a filling phase mid clavicular line (early) immoble mitral or regurgitation ; late mitral stenosis that lead to mitral S2 produced by Best heard Physiologic Narrowing · widening : S2 the closure of the P2-> splitting Expiration : : 2nd Inspiration L (Pz) pulmonic parasternall and ICS aortic value (A2) Az-> 2ndR ; onset of diastole parasternal ICS regurgitation -> onset of systole ATRIOVENTRICULAR & SEMILUNAR VALVES Perioperative Evaluation } Assessment of } } } } Severity of cardiac Disease Degree of Impaired Myocardial Contractility Prescence of associated major organ system disease History and PE } NY Heart Classification } Evidence of CHF Suplo } Heart Murmur (systolic vs dyastolic) } Atrial fibrillation } Age (increased incidence of IHD) Murmur diastolic -- Regurgitation aortic & Pulmon value lic ⑭ Mitral o Tricuspid Regurgitation Classification not fortest New York Heart Association functional classification of patients with heart disease: Class Description I Asymptomatic II Symptoms with ordinary activity but comfortable at rest III Symptoms with minimal activity but comfortable at rest IV Symptoms at rest (worst artere slooke Tol Perioperative Evaluation } Assessment of } Drug Therapy } β-blockers, calcium channel blockers, and digitalis for heart rate control; } angiotensin-converting enzyme inhibitors and vasodilators to control blood pressure and afterload; } diuretics, inotropes, and vasodilators as needed to control heart failure. } Antidysrhythmic therapy may also be necessary. } Certain cardiac lesions such as aortic and mitral stenosis require ⑧ a slow heart rate to prolong the duration of diastole and improve left ventricular filling and coronary blood flow. } The regurgitant valvular lesions such as aortic and mitral regurgitation require afterload reduction and a somewhat fasternormal preload heart rate to shorten the time for regurgitation.. after load Perioperative Evaluation } Assessment of } Laboratory Data } ECG } Chest Xray } Echocardiography Determine significance of cardiac murmurs ¨ Identify hemodynamic abnormalities associated with physical findings ¨ Determine transvalvular pressure gradient ¨ Determine valve area ¨ Determine ventricular ejection fraction ¨ Diagnose valvular regurgitation ¨ Evaluate prosthetic valve function ¨ Perioperative Evaluation } Assessment of } Presecnce of Prothetic Valves G - mitral aortic } Asses function: transthoracic Echocardiography } Complications ¨ ¨ ¨ ¨ ¨ ¨ Valve thrombosis Systemic embolization Structural failure Hemolysis Paravalvular leak Endocarditis - Click most common " COMO reloj un aortic } Anticoagulation therapy have mas ruido Perioperative Evaluation } Management: Anticoagulation therapy } The risk of thromboembolism is estimated to be about 5% to 8%. thromboembolk event } Anticoagulation may be continued in patients with prosthetic heart valves who are scheduled for minor surgery in which blood loss is expected to be minimal. } In major surgery warfarin is typically discontinued 3 - 5 days preop. Intravenous unfractionated heparin or subcutaneous low-molecularweight heparin is administered after discontinuation of warfarin and continued until the day before or the day of surgery. } } The heparin can be restarted postoperatively when the risk of bleeding has lessened and can be continued until effective anticoagulation is again achieved with oral therapy. When possible, elective surgery should be avoided in the first month after an acute episode of arterial or venous thromboembolism. Prophylaxis antibiotic ex : Perioperative Evaluation } Prevention of Bacterial Endocarditis } } } problem convalvula malq . pt valuula prost I parcho" device . Cre Prosthetic cardiac valve or prosthetic material used for cardiac valve repair Previous infective endocarditis Congenital heart disease } Unrepaired cyanotic congenital heart disease, including palliative shunts and conduits Completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure[*] } Repaired congenital heart disease with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization) Cardiac transplantation recipients who develop cardiac valvulopathy } } dentist Mitral Stenosis Mitral Stenosis Overview } Definition: Obstruction of LV inflow that prevents proper filling during diastole } Normal MV Area: 4-6 cm2 } Transmitral gradients and symptoms begin at areas less than 2 cm2 } Rheumatic carditis is the predominant cause } Most common in females } Prevalence and incidence: decreasing due to a reduction of rheumatic heart disease. not as common Etiology of Mitral Stenosis } Rheumatic heart disease: 77-99% of all cases } Infective endocarditis: 3.3% } Mitral annular calcification: 2.7% atrium enlarged At T workload · pulmonary HTN MS Pathophysiology T in pressure amdilation Progressive Dyspnea (70%): LA dilation à pulmonary congestion (reduced emptying) } } worse with exercise, fever, tachycardia, and pregnancy } Increased Transmitral Pressures: Leads to left atrial enlargement and atrial fibrillation. } Right heart failure symptoms: due to Pulmonary venous HTN } Hemoptysis: due to rupture of bronchial vessels due to elevated pulmonary pressure Natural History of MS } Disease of plateaus: } } } Mild MS: 10 years after initial RHD insult Moderate: 10 years later Severe: 10 years later dt saS Mortality: Due to progressive pulmonary congestion, infection, and thromboembolism. - } Physical Exam Findings of MS A i dIt } in workload t atrium is hypertrophy Prominent "a" wave in jugular venous pulsations } Due to pulmonary hypertension and right ventricular hypertrophy } Signs of right-sided heart failure: in advanced disease } Diastolic Murmur; opening snap } Worse symptoms when gradient across the valve higher than 10 (normal < 5mmHg) ??? de mayor presion a menor presion Evaluation of MS } ECG: may show atrial fibrillation and LA enlargement } CXR: LA enlargement and pulmonary congestion. Occasionally calcified MV } ECHO: The GOLD STANDARD for diagnosis. Asses mitral valve mobility, gradient and mitral valve area Treatment of MS } Control Heart Rate } } } issue / artenal : aggregation plaquetaria Digoxin Beta Blockers Calcium Channels blockers - warfarn : venous stases } Anticoagulation } Surgical correction indicated if worsening symptoms and pulmonary hypertension develops. } } stenotic value Percutaneous Open repair or replacement - can leak or this Management of Anesthesia } } Management of anesthesia for noncardiac surgery in patients with mitral stenosis includes prevention and treatment of events that can decrease cardiac output or produce pulmonary edema. Events that impact MS } } } } Sinus tachycardia or a rapid ventricular response during atrial fibrillation Marked increase in central blood volume, as associated with overtransfusion or head-down positioning Drug-induced decrease in systemic vascular resistance Hypoxemia and hypercarbia that may exacerbate pulmonary hypertension and evoke right ventricular failure avoid nitrous oxide Management of Anesthesia } Preoperative medications } } } } donopin Decrease anxiety Continue HR control meds Neuroaxial anesthesia is an acceptable technique - Induction Anesthesia } Intravenous induction } } } Avoid ketamine - va TIVA a causar prob . con afterload , MBD Avoid Hypertension and tachycardia during intubation Maintenance Combination volatile agents: do not alter pulmonary resistance, decrease on contractility or changes on HR } Control volume status (euvolemia) O } - Management of Anesthesia } Monitoring } } ECG, CVP, and Depending on the surgery: A line, PA catheter Post Operative } Risk of pulmonary edema and right heart failure it dt too much analges/9 } Pain and hypoventilation with subsequent respiratory acidosis and hypoxemia may be responsible for increasing heart rate and pulmonary vascular resistance. } Decreased pulmonary compliance and increased work of breathing may necessitate a period of mechanical ventilation, particularly after major thoracic or abdominal surgery. } Relief of postoperative pain with neuroaxial opioids can be very useful in selected patients. } Anticoagulation therapy should be restarted as soon as the risk of perioperative bleeding has diminished. Mitral Regurgitation Mitral Regurgitation (MR) } Definition: Backflow of blood from the LV to the LA during systole Strivial } MR-gotio algo atrio normal) Mild (physiological) MR is seen in 80% of normal individuals. Causes of MR } Endocarditis / rheumatic fever } Acute MI: } } Rupture of Papillary Muscle Malfunction or disruption of prosthetic valve congenital 17 Disease } CHD } Cardiomyopathy syst Inflammatory . } SLE, etc , Lupus MR: pathophysiology hemodynamic derangement in mitral regurgitation is a decrease in forward left ventricular stroke volume and cardiac output. } Patients with a regurgitant fraction of more than 0.6 are 0 considered to have severe mitral regurgitation. } - affect } 11 performance The fraction of left ventricular stroke volume that regurgitates into the left atrium depends on: } } } size of the mitral valve orifice; heart rate, which determines the duration of ventricular ejection; pressure gradients across the mitral valve. afterload in } more regurgitation Pharmacologic interventions that increase or decrease systemic vascular resistance have a major impact on the regurgitant fraction in patients with mitral regurgitation. ⑪ after load MR: pathophysiology } Myocardial ischemia secondary to MR is uncommon } In Chronic MR the volume overload produced by MR transforms the left ventricle into a larger, more compliant chamber that is able to deliver a larger stroke volume. } Development of ventricular hypertrophy and increased compliance of the left atrium permit the accommodation of the regurgitant volume without a major increase in left atrial pressure. } Patient maybe asymptomatic for many years. > } Diagnosis of MR } Holosystolic Murmur ↳ dura todo mid el systolic systole a mitad } Echocardiography } Presence of V wave in a PA Catheter occlusion Treatment of MR } Early surgery may be warranted to prevent left ventricular muscle dysfunction from becoming severe or irreversible. } Symptomatic patients should undergo mitral valve surgery even if ⑧ ④ the ejection fraction is normal. Mitral valve repair, if possible, is ② preferred to mitral valve replacement. } - Although vasodilators are useful in the medical management of acute mitral regurgitation, there is no apparent benefit to longterm use of these drugs in asymptomatic patients with chronic mitral regurgitation. Observation afterload reducer yet - } no . For symptomatic patients, angiotensin-converting enzymefor inhibitors alrial Kick or β-blockers (particularly carvedilol) and & biventricular pacing have all been shown to decrease functional mitral regurgitation and improve symptoms and exercise tolerance. MR: Anesthesia Considerations } Prevent bradycardia } Prevent increases in systemic vascular resistance keep contractility } Minimize drug-induced myocardial depression } Monitor the magnitude of regurgitant flow with a pulmonary artery catheter (size of the V wave) and/or echocardiography MR: Anesthesia Management } Induction } } Avoid Hypertension or bradycardia Maintenance } Volatile anesthesisc desirable } Avoid hypotension to avoid Pulm HIN Ventilator with low volume pressures (Pulm hypertension) . } } Monitoring } } Usual if asymptomatic If not consider CVP, PA catheter, A line Mitral Valve Prolapse } Mitral valve prolapse (MVP) is defined as the prolapse of one or both mitral ↳ leaflets into the left atrium during systole with or without mitral regurgitation. } Associated with the auscultatory findings of a midsystolic click and a late systolic murmur. } ⑧ MVP is the most common form of valvular heart disease, affecting 1% to 2.5% of the U.S. population. } It is more common in young women. } MVP can be associated with Marfan's syndrome, rheumatic ⑧ carditis, myocarditis, thyrotoxicosis, and systemic lupus erythematosus. MVP: Management Management of anesthesia for noncardiac surgery in patients with MVP follows the same principles outlined earlier for patients with mitral regurgitation. } } Management is influenced primarily by the degree of depend regurgitation mitral regurgitation. on and usual of pr management Degree of MVP can be affected by left ventricular dimensions and is more dynamic than mitral valvular disease. dt strech } - } A larger ventricle will often have less prolapse (and regurgitation) than a smaller ventricle. So events that affect how much the left ventricle fills or empties with each cardiac cycle will affect the amount of mitral regurgitation. MVP } Perioperative events that enhance left ventricular emptying include; } } } increased sympathetic activity that increases myocardial contractility, decreased systemic vascular resistance, assumption of the upright posture. } Hypovolemia reduces left ventricular filling. } Events that decrease left ventricular emptying and increase left ventricular volume may decrease the degree of MVP. These include hypertension or vasoconstriction, druginduced myocardial depression, and volume resuscitation. MVP: Preoperative Evaluation } Systolic Click and murmur ⑧} Female above 45 } Medication usage: Beta blockers } Aspirin use } Signs of CHF MVP: Anesthesia } If normal LV function general and or regional well tolerated. } Avoid hypovolemia discase MU · · Stenosis. so } Induction with Etomidate considered · it Regurg -keep } Avoid Ketamine Slow can - - fill rapid contractility Preload depend avoid - hypovolem forward } Maintenance with low dose volatile anesthetics } Routine monitoring used in OR flow . Aortic Stenosis Aortic Stenosis Overview: } Normal Aortic Valve Area: 2.5- 3.5cm2 } Symptoms: Occur when valve area is 1/4th of normal area. ( 25 % } Gradient across valve above 50 mmHg } Types: } Supravalvular I above value Subvalvular I below value } Valvular } Etiology of Aortic Stenosis } Common Valvular lesion } Associated factors: } } } } } degeneration and calcification of the aortic leaflets and subsequent stenosis; bicuspid rather that a tricuspid aortic valve. Aortic stenosis develops earlier in life (30 to 50 years of age) in individuals with a bicuspid aortic valve than in those with a tricuspid aortic valve (60 to 80 years of age). Other causes include rheumatic heart disease and infective endocarditis. Aortic stenosis is associated with risk factors similar to those of ischemic heart disease, such as systemic hypertension and hypercholesterolemia. Pathophysiology of Aortic Stenosis } } } A pressure gradient develops between the left ventricle and the aorta. (increased afterload) LV function initially maintained by compensatory pressure hypertrophy When compensatory mechanisms exhausted, LV function declines. Presentation of Aortic Stenosis } Syncope: (exertional) } Angina: (increased myocardial oxygen demand; demand/supply mismatch) } Dyspnea: on exertion due to heart failure (systolic and diastolic) } Sudden death Diagnosis you can tell this a } Slow rising carotid pulse (pulsus tardus) & decreased pulse amplitude (pulsus parvus) } Heart sounds- soft and split second heart sound, S4 gallop due to LVH. se escuchathrombo atrio } de ventriculo Systolic ejection murmur- cresendo-decrescendo character. This peaks later as the severity of the stenosis increases. } } a Loudness does NOT tell you anything about severity About 75% symptomatic patients will die within 3 years of diagnosis if not replaced. Evaluation of AS } } Echocardiography is the most valuable test for diagnosis, quantification and follow-up of patients with AS. Two measurements obtained are: a) Left ventricular size and function: LVH, Dilation, and EF b) Doppler derived gradient and valve area (AVA) Management of AS } General- IE prophylaxis in dental procedures with a prosthetic AV or history of endocarditis. } Medical - limited role since AS is a mechanical problem. Vasodilators are relatively contraindicated in severe AS ↓ BP in valvular problem infarct } lead to syncope Aortic Balloon Valvotomy- shows little benefit. It dilation } can in value is insufficient Surgical Replacement: Definitive treatment Management Anesthesia } Maintain normal sinus rhythm } Avoid bradycardia or tachycardia } Avoid hypotension At } lack of blood in coronary . Avoid hypowlemia Optimize intravascular fluid volume to maintain venous return and left ventricular filling Induction of Anesthesia } General anesthesia preferred } } } Intravenous Volatile (carefull) Avoiod Ketamine ↳ ↑ afterload ! I demands Maintenance Anesthesia } Goals: } Maintain Blood Pressure } Keep stable SVR } Adequate CO } Treat hypotension agressively; } } Phenylephrine · Alpha Avoid tachycardia Monitoring Anesthesia } ECG } CVP } A line } Watch for signs of ischemia Pathologic Aortic Regurgitation Sangre unelve atras T diastolic en Aortic Regurgitation or Insuficiency } Definition: Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps } Etiologies: } Related to damage of the leaflets } Related to the aortic root Pathophysiology Recordina ventricle ejection time Treatment of Aortic Regurgitation } Surgical Replacement * Afterload Reducers Ok } Operative mortality 4% } Mortality Rate in asymptomatic patients less than 0.2% vs 10% in symptomatic ones. } Alternative to replacement * } } } * Pulmonic ROSS procedure ↳ most Aortic Valve Reconstruction common value in Peds eval . E change Medical management } Decrease SVR } } Nifedipine hydralazine - ↓ regurgitation Pulmonic value to artic w . a homo value . Management of Anesthesia } Avoid bradycardia becauseregur happens me todia Avoid increases in systemic vascular resistance Minimize myocardial depression } INDUCTION } - } } } } Inhaled anesthetic or an intravenous induction drug. Ideally the induction drug should not decrease the heart rate or avoid increase systemic vascular resistance. Ketamine MAINTENANCE } } } e Inhaled anesthetic's Avoid hypertension Avoid Bradycardia Management of Anesthesia } MONITORING } } } ECG Watch for signs of ischemia CVP pt need to be envolemic - Right sided valves } Tricuspid Regurgitation } causes } } Tricuspid Stenosis causel} } RV Failure Pulmonary Hypertension Rare I most seen in Peds Pulmonic Valve Regurgitation cause } Pulmonar Hypertension } Pulmonic Stenosis causes} CHD Congenital Heart Disease Congenital Heart Disease Acyanotic Heart Disease ↳ blood } } } } } } } mix : blood without of mix w . 02 Atrial Septal Defect Ventricular Septal Defect Patent Ductus Arteriosus Aorticopulmonary Fenestration Aortic Stenosis Pulmonic Stenosis Coarctation of the Aorta no Cyanotic Heart Disease 0 } Tetralogy of Fallot } } } } } } } } } Eisenmenger's Syndrome Ebstein's Anomaly Tricuspid Atresia Transposition of the Great Arteries Mixing of Blood between the Pulmonary and Systemic Circulations Truncus Arteriosus Partial Anomalous Pulmonary Venous Return Total Anomalous Pulmonary Venous Return Hypoplastic Left Heart Syndrome examen Congenital Heart Disease } Congenital heart disease is the most common form of congenital disease and accounts for approximately 30% of all congenital diseases that occur. } Ventricular septal defects (VSDs) remain the most commonly encountered congenital cardiac abnormality in infants and children. } Transthoracic and transesophageal echocardiography facilitates early and accurate diagnosis of congenital heart disease. Recording 23 : look up 00 Congenital Heart Disease balance } between blood w . Oe : mixed venous saturation and wo 02 Understanding of the relationship between systemic and pulmonary vascular resistance is essential to determine appropriate anesthetic management. } } } For example, in patients with cyanotic heart disease, ventilation with high airway pressures can increase pulmonary vascular resistance, compromise venous return, and exacerbate right-toleft shunt physiology. Placement in Trendelenburg's position can increase central venous (superior vena cava) pressure and cause cerebral hypoperfusion in a patient who has a Glenn shunt or has undergone Fontan's procedure. In those patients with large ASDs, inadequate anesthesia and sympathetic nervous system stimulation might increase systemic vascular resistance, exacerbate left-to-right shunting, and reduce cardiac output. e 33 01 : avoid hypoxia For de elamen ! Congenital Heart Disease } Modalities to decrease pulmonary vascular resistance are important in the management of CHD. } Management of pulmonary vascular resistance and hence prevention of pulmonary hypertension is essential for better hemodynamic stability in the intraoperative and postoperative environment as well as for improved long-term outcomes. } Prevention and treatment of pulmonary hypertensive crisis in congenital heart disease patients includes hyperventilation (with 1.0 fractional inspired oxygen concentration), correction of acidosis, avoidance of sympathetic nervous system stimulation, maintenance of normothermia, minimization of intrathoracic pressure, and use of inotropic support. } Inhaled nitric oxide may be useful for sudden increases in pulmonary vascular resistance in patients at high risk. TO Be continued } Abnormalities on cardiac Conduction } Independent Reading: Chapter 7-8 } Pericardial Disease / Cardiac Trauma } Vascular Disease