Transcript Slide 1
Acute Coronary Syndrome APS Fleming College What is an ACS? A sudden event during which the myocardium suffers from a relative or a complete lack of perfusion Covers the continuum between angina and MI This is reflected in: Signs and symptoms Electrocardiographic changes Biochemical changes Symptoms of ACS Pain – Pressure – Burning (hot) – Chest/arms/jaw/back Sympathetic response – Sweats – Tachycardia – Cool, clammy skin Parasympathetic response – Nausea – Vomiting – Weak Inflammatory response Other – Mild fever – Dyspnea – Asymptomatic Physical Findings Inspection BP - often increase anterior MI - often decrease inferior MI HR - often increase anterior MI - often decrease inferior MI RA po - increase in RV MI Stable CAD Acute Coronary Syndromes Unstable angina Non-ST Elevation MI (Non-Q-wave MI) ST-Elevation MI (Q-wave MI) The continuum of acute coronary syndromes ranges from unstable angina, through non-ST-elevation myocardial infarction (also referred to as “non-Q-wave” myocardial infarction [MI]), to ST-elevation MI (also referred to as “Q-wave” MI). Platelets & ACS Platelets become activated by various stimuli Binds to fibrinogen and serves to crosslink and aggregate platelets Platelet plug becomes the centre of a larger thrombus Triggers to Plaque Rupture Inflammatory cytokines Vulnerable Plaque Plaque Rupture Physical Stress Emotional Stress Extent of Myocardial Injury Determined by: muscle mass perfused by vessel Magnitude/Duration of flow Oxygen demand of affected tissue Adequacy of collaterals Tissue response to ischemia Preventing ACS / Reducing Infarct Size Primary prevention -lifestyle Stabilizing plaque Preventing platelet aggregation Decreasing preload and afterload Decreasing cardiac workload Reperfusion Treating arrhythmia Which ones do you as medics do?? Pathophysiology of ACS Myocardial ischemia >>> infarction 1. Plaque formation with narrowing of coronary artery lumen 2. Plaque rupture 3. Thrombus formation with platelet activation and aggregation 4. Ischemia in downstream territory with reversible cell injury 5. Myocardial cell death Cardiovascular Pathology Angina Unstable angina Myocardial Infarction Congestive heart failure Valvular dysfunction Cardiogenic shock Aneurysms Deep vein thrombosis/arterial occlusion Ischemic Chest Pain Good history and physical exam 3 & 12/15lead ECG OPQRST to guide history investigation Differential diagnosis Chapter 27 27.24-27.36 OPQRST Onset - when did it start? Provoked - at rest, exertion, better or worse? Quality - sharp, dull, ache, heaviness? Radiating - to shoulder, back, jaw? Severity - on a scale of 1-10? Time - does it come and go? Myocardial Ischemia Blood supply and demand Causes of ischemia – too slow or too fast vasospasm (Prinzmetals) coronary artery occlusion narrowing of coronary arteries low blood pressure hypoxemia HR Coronary Artery Disease Poor dietary habits Imbalance between good cholesterol (HDL) and bad cholesterol (LDL) Atherosclerosis That’s why there are angiograms! Angina or MI?? myocardial ischemia Decreased perfusion angina Supply and demand unstable angina myocardial infarction CP pattern changes or complicated Total occlusion and necrosis Consequences of Coronary Thrombosis Lilly. Pathophysiology of Heart Disease, 4th Ed. Lippincott Williams, 2007. Page 173 The Importance of History Someone with angina knows their typical pattern In addition to OPQRST, take an AMPLE history “are you SOB?” Similar pain? MI in past? Is this pain similar? Other cardiac Hx? e.g. CABG, angioplasty ,stress testing, hospitalizations etc. Angina Lasts less than 30 minutes Heaviness, dull, tight or even sharp pain Can radiate but less common Usually on exertion and dissipates with rest Temporary drop in coronary artery blood flow Rule out rate related problems Angina Management Rest/relaxation (Be calm!) O2 therapy IV access ? ASA 160mg chewed & swallowed Vitals Nitroglycerin 0.4mg SL q 5 min. if SBP >100 and HR > 60 but less than 160 bpm HR and blood pressure parameters…why? Hemodynamic Parameters SBP < 100 preload reduction - vasodilation decreased coronary perfusion HR < 60 bpm or > 160 bpm rate related ischemia? Ischemic Chest Pain Nitroglycerin 0.4mg SL, q 5 min. PRN Assess VS after each dose d/c if SBP <100 or SBP drops by 1/3 d/c if HR <60 or >160 bpm ASA 160mg chewable tablets Morphine Sulphate 2mg IV, q 5 min. x 3 PRN Unstable Angina Indicates a progression towards serious myocardial disease 5 Indicators of Unstable Angina new angina pain change in the duration change in Rx (e.g increased NTG use) onset at rest change in quality (e.g now radiates) Acute Myocardial Infarction Definition: Necrosis of heart muscle due to absolute or relative lack of blood supply to the myocardium. The site of infarction is determined by the location of the arterial occlusion. Myocardial Infarction Killing of myocardial tissue Conventional treatment will only save ischemic zone Thrombolytics Necrotic zone Ischemic zone Presentation of Myocardial Infarction Varies widely from patient to patient Typical vs. Atypical (e.g.. weakness or SOB) The elderly, alcoholics, and women CP unresolved with rest or NTG 12 Lead shows acute ST elevation, Flipped T waves or Q waves (old) Electrocardiographic Changes Change in rate and rhythm Most often sinus with: No discernible change Hyper-acute T-waves T wave flattening or inversion ST segments up or down Q waves Biochemical Markers of ACS Enzymes which are unique to cardiac myocytes Released into the circulation by dead cells Thus a rise in these indicates that myocardium has suffered damage Biochemical Markers Troponin (remember its role in actin/myosin binding??) CPK (Creatine Phosphokinase) Specifically one isoenzyme -MB band LDH (Lactose dehydrogenase) AST Hospital staff will draw blood for these tests early but do NOT generally help in the decision making Cardiac Markers Myoglobin is found in cardiac and skeletal muscle Very sensitive if measured early Not specific Not often used Use of Nitrates in ACS Nitrates, typically nitroglycerin Nitrous Oxide acts as a smooth muscle relaxant leading to vasodilatation Transdermally, sublingually and/or parenterally Benefits of Nitrates Reduce preload and afterload Dilate coronary arteries Assists coronary perfusion Disadvantages of Nitrates Not useful in patients who are reperfused May cause hypotension Severe hypotension in patients with RV dysfunction May cause hypotension in inferior MI 30% have RV involvement-check!!! b-blockers Multi-purpose in the setting of ACS Anti-arrhythmic Anti-ischemic Anti-hypertensive b-blockers Decrease myocardial oxygen demand heart rate – increases diastole Decreased myocardial contractility Decreased MAP Decreased Advantages of b-blockers Reduction in pain Decreased morbidity and mortality Decreased risk of arrhythmia Decreased infarct size Decreased risk of re-infarction Treatment with a b-blocker is a standard of care ASA Anti-inflammatory prevents the formation of arachidonic acid A pathway that can be blocked to prevent platelet aggregation Does not block all platelet activators Other Treatment Modalities in ACS Heparins (LMWH) Reperfusion PCI Mechanical (the digger!) Thrombolytic agents Antiarrhythmic agents Focus of ACS Common reason for transport Much can be done during transfer Reduce risk of morbidity and mortality The first step = recognizing the ACS Signs and symptoms ECG changes Biochemical changes Summary Strategies for reducing morbidity and mortality Reduce cardiac workload Improve perfusion to cardiac tissue Reduce risk of fatal arrhythmias Reduce extension of clot formation Reperfuse the ischemic myocardium Myocardial Infarction ASA (2 x 80 mg) P.O. O2 therapy IV access NTG via SL, transdermal, and/or IV Morphine (ACP) Heparin and/or Beta blockers (Hosp) 12/15 Lead ECG as soon as possible Angioplasty (hosp) Thrombolytics if PCI not available or contraindicated PCI Pre-hospital Thrombolysis Oshawa Land ALS Northern Ornge Bases Frequent Southern Ornge Bases Carry use it Positive empirical trends Pre-hospital Thrombolysis prolonged transport time no thrombolysis at the sending facility Long delays Indications - Thrombolysis Ischemic Less C.P. than 6 hours duration Ischemic Chest Pain? O - at rest or with exertion P – better or worse Q - heaviness, tightening, sharp, weakness etc R - neck, jaw and/or left arm S - varies T - consistent, does NOT come & go 12 Lead ECG Criteria ST segment elevation New onset Left Bundle Branch Block with S&S? Some acute coronary syndromes (A.C.S.) do not benefit from thrombolysis Next We will be looking at 12 leads specifically Look at the hand powerpoint (12lead) Read the sample handouts Read your text 12 lead ECG (big book)