Cardiology [MYOCARDIAL ISCHEMIA] Introduction Myocardial ischemia is produced where there is an occlusion to blood flow. It’s caused by chronically progressive atherosclerosis limiting perfusion to the myocardium. This produces ischemia when cardiac demand increases; there’s an imbalance in the demand to supply ratio. When an acute thrombus forms from endothelial injury the lumen can quickly become occluded (an MI). Over time, the patient will undergo infarction with permanent loss of myocardial tissue. Risk Factors HTN Smoking Dyslipidemia DM Cocaine Risk Factors Since this is a result of progressive atherosclerosis those things which perpetuate atherosclerosis will lead to ischemic heart disease. Risk factors provide something to fix and help steer the diagnosis. What makes this interesting is HOW you fix these risk factors. They’re HTN, smoking, dyslipidemia, diabetes, and drug use (i.e. cocaine). Patient Presentation Myocardial ischemia on its own is painful. It causes a crushing, retrosternal chest pain that will radiate down the arm and up the jaw. It may also present with dyspnea. Ischemia on its own will not cause mechanical failure. Other signs and symptoms will be a result of myocardial infarction and necrosis. If the Left Heart fails it’s pulmonary edema. If the Right Heart fails it’s hypotension and peripheral edema. Any infarct can produce arrhythmias: atrial, ventricular - whatever. Separating severity of ischemia is typically based on whether or not the pain is relieved with rest and/or nitrates. Beyond that, laboratories are needed to differentiate between the “bad ones” (STEMI, NSTEMI). Diagnosis The first test is the ECG. It’s noninvasive, cheap, and able to detect the highest acuity disease (STEMI). It also establishes an admission baseline for comparison. A 12-Lead ECG is best. ST segment elevation = transmural infarct = STEMI. To rule out active myocardial infarct you need cardiac biomarkers (Troponins, CKMB, etc). These are released from dying or dead myocytes. They separate unstable angina from NSTEMI. Pain Relief Biomarkers ST ∆s Pathology Stable Angina Exercise Rest + Nitrates Ø Ø 70% Unstable Angina @ rest Ø NSTEMI STEMI @ rest Ø @ rest Ø Ø Ø 90% ↑ Ø 90% ↑ ↑ 100% Typical Levine Sign Crushing Chest Pain Pale, Cool, Diaphoretic Sense of Impending Doom Diagnosis In Acute disease (guy in the ER with active chest pain) get EKG, Troponins, and Cath. In Chronic disease (guy in office with an h/o chest pain) get an EKG and Echo/Stress Test. Chest Pain ST ∆s EKG Multiple options exist for confirming the diagnosis of myocardial ischemia based on severity and acuity. There is the stress test (for someone who has neither NSTEMI nor STEMI) and the best test which is coronary catheterization. The higher the acuity, the more likely the cath. Let’s talk about the low-acuity setting first. Able to Exercise STEMI Emergently ST∆s Routine tests such as CXR / CBC / TSH / CMP are obtained but do not influence the diagnosis or management. Atypical Fatigue Malaise SOB CATH NSTEMI Biomarkers Troponin, CKMB Unstable Angina Stress Test Unable To Exercise Treadmill Dobutamine or Adenosine Normal EKG Abnormal EKG EKG test Echo or Thallium Treat with medications then… Manage Medically © OnlineMedEd. http://www.onlinemeded.org Cardiology 1. 2. 1. 2. 3. 4. [MYOCARDIAL ISCHEMIA] Diagnostic Modalities The stress test a) Treadmill stress test - Requires the patient to be able to exercise (80% of max heart rate) and requires a normal ECG. Send him/her on an exercise and stop the test when there are EKG changes (ST depression or T wave inversion) or Chest Pain. If positive, go immediately to cath. b) Dobutamine Stress Test – Uses a pharmacological challenge and an Echo. Under the challenge (85% max HR), the echo will pick up hypokinesis or akinesis (decreased wall motion). Areas that are infarcted will persist with akinesis even at rest. Areas that become ischemic under stress (become akinetic) will move again after dobutamine is removed (revealing salvageable tissue). c) Nuclear Stress Test – Thallium looks like sodium to the heart. It will be picked up by myocytes and light up healthy tissue. Infarcted tissue will not under both rest and exercise. Ischemic tissue will not under stress, but will at rest (revealing salvageable tissue). Catheterization This is the best test for the diagnosis of coronary artery disease. It assesses the severity of stenosis AND helps rule out Prinzmetal’s angina (clean coronary arteries producing ischemia as a product of vasospasm - treat with CCB). Therapy Adjust risk factors a. LDL – the goal is to ↓ LDL < 100 or <70 for active disease and get ↑HDL > 40. Do this with statins. Other drugs exist, but start with statins. Use Fibrates if there is a contraindication to statins. b. DM – tight glucose control to near normal values (80-120 or HgbA1C < 7%) with oral medications or insulin. c. HTN – regular control of blood pressure to <140 / <90 with Beta-Blockers (reduce arrhythmias) and ACE-inhibitors. Titrate heart rate to between 50-65bpm and 75% of the heart rate that produced symptoms on stress test. Reduce Risk of Thrombosis Manage this with either Aspirin (Cox-Inhibitor) or Clopidogrel (ADP-inhibitor) long term. Those spiffy Glycoprotein IIb/IIIa inhibitors like Abciximab are useful in the patient going for cath with stenting for additional antiplatelet effect, but they are not for long term. Surgical Management Surgical management choices are angioplasty or CABG. The decision is made based on the severity of occlusive disease. If it’s really bad (i.e. requires multiple stents) do a CABG. If the atherosclerosis is global and no ground can be found for the stent, do CABG. Stents are now drug-eluding (require Clopidogrel) or bare-metal (do not require Clopidogrel) Thrombolytics Either the administration of tPA (within 12 hours of onset) or heparin is done only when catheterization is not available AND they are in an acute disease (NSTEMI or STEMI). Can’t Exercise: Peripheral Vascular Disease, Claudication, vasculitis, diabetic ulcers, SOB at rest, etc. Can’t Read ECG: Any BBB or old infarct “Dead Things Don’t Move” Stress Normal Wall Motion Akinesis Akinesis No Dz Ischemia Infarct Normal Wall Motion Normal Wall Motion Akinesis At Rest Acute Presentation: MONA-BASH Morphine Beta-Blocker Oxygen ACE-inhibitor Nitrates Statin Aspirin Heparin Treatment Statins β-Blockers ACE-i ASA Clopidogrel Angioplasty CABG tPA Heparin When to use it Goals Any ACS LDL < 70 HDL > 40 Any ACS SBP < 140 DBP < 90 Any ACS SBP < 140 DBP < 90 Any ACS No goal ASA allergy or No goal drug-eluding stents ST↑ or + Stress; 1 or 2 vessel disease ST↑ or + Stress; Left-Mainstem or 3 vessel disease ST↑ or + Stress; no PCI available, no transport ST↑ or + Stress; contraindication to tPA, CATH Angioplasty (PCI) Left Mainstem 1,2 Vessel CATH CABG 3 Vessel Disease Surgery = Left Mainstem OR 3-vessel disease; surgery = CABG Angioplasty = 1,2 Vessel Disease © OnlineMedEd. http://www.onlinemeded.org