Objectives. Identify early signs and symptoms of Acute Coronary Syndrome Initiate proper protocol for ACS patient 10/2013 2

Transcription

1 10/2013 1

2 Objectives Identify early signs and symptoms of Acute Coronary Syndrome Initiate proper protocol for ACS patient 10/2013 2

3 Purpose of this Education Module: Chest Pain Center Accreditation involves the management of chest pain anywhere in the hospital. Intensive Care and Step down Units along with Emergency Department staff care for many patients who have or are at a high risk for heart disease. Knowledge of ACS pathophysiology and early recognition is key to impacting patient outcomes. Early recognition reduces the time it takes for patients experiencing symptoms of possible ACS to see a physician thus decreasing the time to treatment which is critical in the early stages when treatment is most effective. September

4 Background Coronary Artery Disease (CAD) = #1 killer of men and women in U.S. Affects about 12 million Americans In the US, CAD claims more lives each year than the next 7 leading causes of death combined! Myocardial Infarction (MI) or Heart attack 1.1 million people affected each year About half present at ED triage not using EMS 460,000 deaths annually from MI Half of these deaths occur before reaching hospital Estimated average number of years of life lost due to a heart attack is 14.2 Average delay in presentation about 3 hours from onset on symptoms! 10/2013 4

5 Acute Coronary Syndrome refers to a state of symptomatic ischemia or infarction resulting from a completely or partially clot-obstructed coronary artery. ST elevated MI (Complete occlusion) Non ST elevation MI (Partial occlusion) 10/2013 5

6 Cardiac Risk Factors Non-Modifiable Risk Factors Previous history Family history 1 st degree relative (parents, siblings) Men < 55; Women < 65 Age Gender Socioeconomic Factors and Ethnicity 9 easily measured and potentially modifiable risk factors account for over 90% of the risk of an initial acute MI Smoking Hypertension Dyslipidemia Diabetes Obesity Metabolic Syndrome Inactivity Alcohol 10/2013 6

7 Assessment of Pain Linking Patient History and Risk factors Cardiac Biomarkers ECG Findings 10/2013 7

8 Assessment of cardiac pain N = Normal (What is the patient s baseline?) O = Onset (sudden/gradual?) P = Precipitation / provoking / palliative factors Q = Quality or quantity (have patient describe in own words) R = Radiation and region S = Severity (pain scale) T = Time (continuous/intermittent?) 10/9/2013 8

9 ACS Symptoms Classic Symptoms Symptom Variations Stable angina Unstable angina MI Women Elderly Diabetics 10/9/2013 9

10 Angina Stable Occurs with physical exertion or emotional stress Relieved by rest or sublingual nitroglycerin Predictable pattern Predictable = triggered by the same amount of physical or emotional stress and should be easily relieved by rest or sublingual nitroglycerin. Unstable Occurs with minimal exertion OR increased dose of nitroglycerin is required to achieve relief. Prolonged rest angina is also considered unstable angina. Angina that increases in severity or is very severe on first presentation Caused by unstable or ruptured plaque that causes abrupt closure of a coronary artery which may spontaneously reperfuse. 10/

11 Characteristics of Angina Sensation of pressure, tightness, heaviness, burning, or squeezing. Rarely described as a sharp or stabbing pain. Should not worsen with changes in position or respiration. Location behind the sternum and in the upper back, shoulder, arm, jaw, or epigastric area. Not usually located in the middle to lower abdomen and usually does not radiate to the lower extremities. Associated symptoms (or stand alone symptoms) of dyspnea, nausea, palpitations, or diaphoresis. Duration typically defined in minutes. Not typically defined in seconds or hours. CAUTION WHEN ASKING THE PATIENT ABOUT PAIN! May deny pain but may state pressure, fullness or heaviness. 10/

12 Symptoms in Special Populations ACS in Women Delay presenting with symptoms Attribute symptoms to other non-cardiac causes Presentation epigastric discomfort less specific complaints: dyspnea or fatigue symptoms of discomfort from nose to navel should be evaluated for presence of heart disease Older women have higher incidence of complications ACS in the Elderly Generalized symptoms Dyspnea, diaphoresis, N&V, and syncope Confusion Symptoms often attributed to the aging process such as activity intolerance ACS in the Diabetic Patient Autonomic dysfunction can affect symptoms experienced with angina Less likely to experience pain. 25% of all patients presenting with ACS are diabetic Have severe multi-vessel disease Have higher rates of complications Have a greater proportion of ulcerated plaques resulting in intracoronary thrombi 10/

13 Cardiac Biomarkers Released into the blood when necrosis occurs as a result of membrane rupture of the myocytes Used in the evaluation of ACS Myoglobin Rises the earliest Within 2 hours after damage Very sensitive, not specific CK (creatine kinase) Enzyme present in the heart, brain, and skeletal muscle Elevations are not specific to myocardial damage. CK-MB More specific to the heart Helpful in identifying more than minor amounts of myocardial damage Rapidly rises in the presence of myocardial damage. 10/

14 Cardiac Biomarkers Troponin I and T Found only in cardiac muscle Most sensitive indicator of myocardial damage Capable of diagnosing small amounts of myocardial necrosis not measured by rises in CK-MB levels Approximately 30% of patients with NSTEMI and normal CKMB levels will test positive Of equal sensitivity and specificity Troponin remains elevated for a long period (late presentation) Positive troponin + ECG changes of injury / ischemia = infarct Non CAD causes of troponin elevation (sepsis, pulmonary emboli and chronic kidney disease) Troponin I more specific in renal dysfunction 10/

15 Cardiac Biomarker Summary Cardiac Biomarker Specificity / Sensitivity Rise Peak Duration Myoglobin Sensitive but not specific Within 2 hours 4 to 10 hours < 24 hours CK-MB (more specific to the heart than CK levels) Highly specific 4 to 6 hours 18 to 24 hours 2 to 3 days Troponin I or T Highly specific and sensitive 4 to 6 hours 18 to 24 hours 10 or more days 10/

16 ECG Findings A discussion of injury/ischemia ECG findings is beyond the scope of this module. Key tips Mark chart copy as pain free or with pain on top of ECG ECG Critical Values at Aultman include the following and require physician notification Acute MI Bradycardia <45 beats Ventricular Tachycardia 10/

17 STAT ECG Indications Chest pain or severe epigastric pain, non traumatic in origin, with components typical of myocardial ischemia or MI: Central/substernal compression or crushing chest pain Pressure, tightness, heaviness, cramping, burning, aching sensation Unexplained indigestion, belching, epigastric pain Radiating pain in neck, jaw, shoulders, back, or 1 or both arms If non diagnostic: Associated dyspnea Associated nausea/vomiting Repeat every 15 to 30 minutes Associated diaphoresis Use ST segment monitoring Consider right-sided/posterior ECG 10/

18 SCREEN for ACS if > 30 years old with any of the following: Chest discomfort of any kind Heartburn, indigestion, or epigastric pain Complaints of heart racing (HR >150 or irregular and >120) Complaints of heart too slow (HR < 50 and symptomatic) Syncopal episode or severe weakness in patients > 45 years old Difficulty breathing (no obvious non cardiac cause) </= 30 with any of the above PLUS: Prior Cardiac disease Family history of early heart disease Diabetes mellitus Severe Obesity Recent cocaine use Remember: Women and diabetic patients are more likely to present with atypical symptoms When in doubt, do the ECG! Elderly patients may have symptoms such as generalized weakness, altered mental status, shortness of breath, or syncope, as their only sign of acute heart attack. 10/

19 < 25% of ACS patients Complete occlusion of a vessel by a thrombus Fibrin stable clot (red clot) Classified more specifically by the portion of the left ventricle suffering injury. Mortality is greatest within the first 24 to 48 hours of symptom onset TREATMENT FOCUS = REPERFUSION 10/

20 Acute MI Symptoms Symptoms occur spontaneously and are not relieved by rest or nitroglycerin Chest pressure or discomfort may be accompanied by nausea, vomiting, or diaphoresis Patient may have hemodynamic instability or cardiac arrest from ventricular fibrillation Acute MI patients have positive biomarkers and are classified as STEMI or NSTEMI based on ECG presentation 10/

21 STEMI Management Reperfusion is number one treatment strategy Primary Coronary Intervention (PCI) preferred treatment strategy if within 90 minutes Goal: 90 minutes from 1 st medical contact Fibrinolytics within 30 minutes of hospital presentation (or 30 minutes from EMS to fibrinolytics) Facilitated PCI with full dose fibrinolytics is not recommended. Rescue PCI may be done after failed fibrinolytics 10/

22 Reperfusion Therapy Fibrinolytic Therapy Primary PCI The Winner! Primary PCI has clear outcome advantage in those > 65 years: Mortality Stroke Intracranial Hemorrhage Reperfusion has proven benefit up to age /

23 Medical Management of STEMI ASA Clopidogrel (with or without reperfusion) Oxygen NTG MS D/C NSAIDS Beta-blockers (within 24 hours) Reperfusion is primary management strategy. ACE Inhibitors (within 24 hours with impaired EF, HTN, diabetes or chronic kidney disease) Anticoagulants (related to reperfusion strategy) Intravenous insulin may be indicated in first 24 to 48 hours after STEMI to tightly control blood sugars. 10/

24 Treatment of NSTEMI / UA: New Guidelines ASA Oxygen (1 st 6 hours) NTG Medical Supportive Therapy: Similar to STEMI IV in first 48 hours for persistent ischemia, HTN, HF Should not interfere with mortality reducing beta blockers or ace inhibitors MS (if NTG unsuccessful and other anti ischemic drugs on board ) Beta Blockers (within 24 hours) Start PO when hemodynamically stable May use IV if hypertensive ACE Inhibitors (within 24 hours) In select patients pulmonary congestion or LVEF < 40%) may also be used in other patients DC NSAIDS 10/

25 Complications of MI Hemodynamic Alterations Ventricular Arrhythmias Atrial Arrhythmias Pericarditis Ventricular Aneurysms Mechanical Complications Myocardial Rupture (free wall or VSD) Papillary Muscle Rupture Long Term: Ventricular Remodeling 10/

26 New addition to all admission power plans In order to improve our patient care for an In house STEMI patient a communication order will be added to each admission power plan. This order is prechecked and states Stat ECG will be obtained in the setting of a Rapid Response for suspected heart attack signs or symptoms This will allow the rapid response team to immediately obtain an ECG allowing quicker diagnosis and STEMI alert will be called if ECG is diagnostic for STEMI. 10/

27 Information that needs charted with In House STEMI patient Onset of symptoms EKG time Notification of physician Time STEMI called Departed from floor ( to either Heart Cath lab or CCU) It is important to accurately chart the times the above occurs. Use IP phone or computer for atomic time. Atomic time is a synchronized time and is very important when tracking quality data. This patient may be in three different locations during this quality data collection and each area using this atomic time will allow accurate data collection. This data will be tracked and used as quality data to improve our care for the In house STEMI patient. 10/

28 Summary Remember, time is muscle! Save hearts and lives by knowing the signs/symptoms of ACS Activate the rapid response team and notify the physician Obtain an EKG 10/