Acute Coronary Syndrome

Slides:



Advertisements
Similar presentations
Acute Coronary Syndrome
Advertisements

Acute coronary syndrome : Risk stratification – markers of myocardial necrosis Paul Calle Emergency Department Ghent University Hospital Belgium.
“ If physicians would read two articles per day out of the six million medical articles published annually, in one year, they would fall 82 centuries behind.
British Cardiac Intervention Society Risk Assessment In Acute Coronary Syndromes Dr David Newby BHF Senior Lecturer in Cardiology Associate Director of.
A few basics of cardiac surgery…. Brett Sheridan, MD Assistant Professor Department of Surgery.
Myocardial Infarction
Ischemic Heart Diseases IHD
Chest Pain Dr. Shamim Nassrally BSc (Hons) MB ChB MRCP(UK)
 Decide on the correct management of patients with acute coronary syndrome based on the findings of a clinical history, examination and relevant test.
ACUTE CORONARY SYNDORME EARLY RISK STRATIFICATION Sarah Jamison March 2003.
Acute Coronary Syndrome. Acute Coronary Syndrome (ACS) Definition of ACS Signs and symptoms of ACS Gender and age related difference in ACS Pathophysiology.
1 Dr. Zahoor Ali Shaikh. 2 CORONARY ARTERY DISEASE (CAD)  CAD is most common form of heart disease and causes premature death.  In UK, 1 in 3 men and.
Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. Chapter 53 Management of ST-Elevation Myocardial Infarction.
1 What is… ? Disparities Among Women in Acute Cardiac Care Frances Canet, MD Cath Conference Thursday, May 26, 2011.
Indication and contra-indications for cardiac catheterization
Chest Pain & Unstable Angina Eugene Yevstratov MD Based on UCLA protocol of the management of Chest Pain & Unstable Angina.
ACUTE CORONARY SYNDROME (ACS). ACS Pathophysiology is that of a ruptured or eroded atheromatous plaque. Pathophysiology is that of a ruptured or eroded.
Management of Stable Angina SIGN 96
VBWG OASIS-5 The Fifth Organization to Assess Strategies in Acute Ischemic Syndromes trial.
Management of Chronic Stable Angina AIMGP Seminar Series Mirek Otremba 2007.
ACUTE CORONARY SYNDROME
1 DIAGNOSTICS OF Acute Coronary Syndromes At the end of this self study the participant will: Verbalize meanings of specific ECG changes: –ST Elevation.
Amy Gutman MD EMS Medication Director
CARDIOVASCULAR CARE of the OUTPATIENT Diane M. Enzweiler, MSN, ANP-BC St. Elizabeth Physicians: Heart and Vascular.
DR. ZAHOOR 1.  A 50 year old man presents to clinic with a complaint of central chest discomfort of 2 weeks’ duration, occurring after walking for more.
Ischemic Heart Disease CVS3 Hisham Alkhalidi. Ischemic Heart Disease A group of related syndromes resulting from myocardial ischemia.
Myocardial infarction My objectives are: Define MI or heart attack Identify people at risk Know pathophysiology of MI Know the sign & symptom Learn the.
Elsevier items and derived items © 2006 by Elsevier Inc. Coronary Artery Disease Includes stable angina pectoris and acute coronary syndromes Ischemia:
Myocardial Ischemia: Concepts in Management Topics in Clinical Medicine February 14, 2007.
1 Pathophysiology & Clinical Presentations Acute Coronary Syndromes.
Acute Coronary Syndrome Sofiya Lypovetska, MD PhD Ternopil State Medical University Ukraine.
Jump to first page Chapter 10 Cardiac Emergencies.
6/04 CRUSADE: A National Quality Improvement Initiative C an R apid Risk Stratification of U nstable Angina Patients S uppress AD verse Outcomes with E.
ACUTE CORONARY SYNDROMES Part I. Definition Acute coronary syndrome (ACS) describes a spectrum of clinical conditions ranging from ST segment elevation.
Acute Coronary Syndrome
Diagnosis, Management, & Follow-up Care Of CAD/AMI BARRY BERTOLET, MD CARDIOLOGY ASSOCIATES OF NORTH MS.
Acute Coronary Syndromes
The INT egrelin and E noxaparin R andomized assessment of A cute C oronary syndrome Treatment T rial Sponsored by the Canadian Heart Research Centre, Key.
Acute Coronary Syndromes. Learning outcomes To understand the clinical spectrum of coronary disease To recognise different presentations of the disease.
Acute Coronary Syndrome David Aymond, MD. ACS Definition: Myocardial ischemia typically due to atherosclerotic plaque rupture  Coronary thrombosis ACS.
Dr. Sohail Bashir Sulehria
Coronary Heart Disease (CHD) László Tornóci Inst. Pathophysiology Semmelweis University.
MYOCARDIAL INFARCTION. CASE 1 Mr. A: 38 years old He smokes 1 pack of cigarettes per day He has no other past medical history 8 hours ago, he gets sharp.
Acute Coronary Syndromes Risk-Stratification Pathophysiology Diagnosis Initial Therapy Risk-Stratification Risk-Stratification Invasive vs Conservative.
ADMIRALADMIRAL Abciximab before Direct Angioplasty and Stenting in Myocardial Infarction Regarding Acute and Long term follow-up ADMIRAL Study ADMIRAL.
Ischemic Heart Disease CVS3 Hisham Alkhalidi. Ischemic Heart Disease A group of related syndromes resulting from myocardial ischemia.
Myocardial Infarction (MI) Prepared by Miss Fatima Hirzallah RNS, MSN,CNS.
Acute Coronary Syndromes Chapter 12 Cardiovascular Disorders Medical Surgical Nursing II.
Chest Pain in the Emergency Department Junior Teaching C. Brown August 2015.
Acute Coronary Syndrome
CPR in ACUTE CORONARY SYNDROM
Cardiac causes of cardiac arrest
Chest Pain & Unstable Angina Eugene Yevstratov MD
Coronary artery disease
Acute coronary syndrome
By Saranya Temprasertrudee M.D.
CORONARY ARTERY DISEASE
CHEST PAIN.
Management of ST-Elevation Myocardial Infarction
Ischaemic Heart Disease Acute Coronary Syndrome
Coronary artery disease
Unstable Angina and Non–ST Elevation Myocardial Infarction
Nursing Management: Patients With Coronary Vascular Disorders
Chapter 28 Management of Patients With Coronary Vascular Disorders
European Heart Association Journal 2007 April
© 2004 American Heart Association
Acute Coronary Syndrome (1)
Myocardial Infarction
Management of AMI in patients presenting with STEMI
Presentation transcript:

Acute Coronary Syndrome

Objectives Define & delineate acute coronary syndrome Review Management Guidelines Unstable Angina / NSTEMI STEMI Review secondary prevention initiatives

Scope of Problem (2004 stats) CHD single leading cause of death in United States 452,327 deaths in the U.S. in 2004 1,200,000 new & recurrent coronary attacks per year 38% of those who with coronary attack die within a year of having it Annual cost > $300 billion

Expanding Risk Factors Smoking Hypertension Diabetes Mellitus Dyslipidemia Low HDL < 40 Elevated LDL / TG Family History—event in first degree relative >55 male/65 female Age-- > 45 for male/55 for female Chronic Kidney Disease Lack of regular physical activity Obesity Lack of Etoh intake Lack of diet rich in fruit, veggies, fiber

Acute Coronary Syndromes Unstable Angina Non-ST-Segment Elevation MI (NSTEMI) ST-Segment Elevation MI (STEMI) Similar pathophysiology Similar presentation and early management rules STEMI requires evaluation for acute reperfusion intervention

Diagnosis of Acute MI STEMI / NSTEMI At least 2 of the following Ischemic symptoms Diagnostic ECG changes Serum cardiac marker elevations

Diagnosis of Angina Typical angina—All three of the following Substernal chest discomfort Onset with exertion or emotional stress Relief with rest or nitroglycerin Atypical angina 2 of the above criteria Noncardiac chest pain 1 of the above

Diagnosis of Unstable Angina Patients with typical angina - An episode of angina Increased in severity or duration Has onset at rest or at a low level of exertion Unrelieved by the amount of nitroglycerin or rest that had previously relieved the pain Patients not known to have typical angina First episode with usual activity or at rest within the previous two weeks Prolonged pain at rest

STEMI Unstable Angina NSTEMI Occluding thrombus Complete thrombus Non occlusive thrombus Non specific ECG Normal cardiac enzymes Occluding thrombus sufficient to cause tissue damage & mild myocardial necrosis ST depression +/- T wave inversion on ECG Elevated cardiac enzymes Complete thrombus occlusion ST elevations on ECG or new LBBB Elevated cardiac enzymes More severe symptoms

Acute Management Initial evaluation & stabilization Efficient risk stratification Focused cardiac care

Occurs simultaneously Evaluation Occurs simultaneously Efficient & direct history Initiate stabilization interventions Plan for moving rapidly to indicated cardiac care Directed Therapies are Time Sensitive!

Chest pain suggestive of ischemia Immediate assessment within 10 Minutes Initial labs and tests Emergent care History & Physical IV access Cardiac monitoring Oxygen Aspirin Nitrates Establish diagnosis Read ECG Identify complications Assess for reperfusion 12 lead ECG Obtain initial cardiac enzymes electrolytes, cbc lipids, bun/cr, glucose, coags CXR

Focused History Aid in diagnosis and rule out other causes Palliative/Provocative factors Quality of discomfort Radiation Symptoms associated with discomfort Cardiac risk factors Past medical history -especially cardiac Reperfusion questions Timing of presentation ECG c/w STEMI Contraindication to fibrinolysis Degree of STEMI risk

Targeted Physical Examination Recognize factors that increase risk Vitals Cardiovascular system Respiratory system Abdomen Neurological status Recognize factors that increase risk Hypotension Tachycardia Pulmonary rales, JVD, pulmonary edema, New murmurs/heart sounds Diminished peripheral pulses Signs of stroke

ECG assessment ST Elevation or new LBBB STEMI NSTEMI Unstable Angina ST Depression or dynamic T wave inversions NSTEMI Non-specific ECG Unstable Angina

Normal or non-diagnostic EKG

ST Depression or Dynamic T wave Inversions

ST-Segment Elevation MI

New LBBB QRS > 0.12 sec L Axis deviation Prominent R wave V1-V3 Prominent S wave 1, aVL, V5-V6 with t-wave inversion

Cardiac markers Troponin ( T, I) CK-MB isoenzyme Very specific and more sensitive than CK Rises 4-8 hours after injury May remain elevated for up to two weeks Can provide prognostic information Troponin T may be elevated with renal dz, poly/dermatomyositis CK-MB isoenzyme Rises 4-6 hours after injury and peaks at 24 hours Remains elevated 36-48 hours Positive if CK/MB > 5% of total CK and 2 times normal Elevation can be predictive of mortality False positives with exercise, trauma, muscle dz, DM, PE

Prognosis with Troponin Mortality at 42 Days 831 174 148 134 50 67  %

Risk Stratification STEMI Patient? - Assess for reperfusion Based on initial Evaluation, ECG, and Cardiac markers STEMI Patient? YES NO - Assess for reperfusion - Select & implement reperfusion therapy - Directed medical therapy UA or NSTEMI - Evaluate for Invasive vs. conservative treatment - Directed medical therapy

Cardiac Care Goals Decrease amount of myocardial necrosis Preserve LV function Prevent major adverse cardiac events Treat life threatening complications

STEMI cardiac care STEP 1: Assessment Time since onset of symptoms 90 min for PCI / 12 hours for fibrinolysis Is this high risk STEMI? KILLIP classification If higher risk may manage with more invasive rx Determine if fibrinolysis candidate Meets criteria with no contraindications Determine if PCI candidate Based on availability and time to balloon rx

Fibrinolysis indications ST segment elevation >1mm in two contiguous leads New LBBB Symptoms consistent with ischemia Symptom onset less than 12 hrs prior to presentation

Absolute contraindications for fibrinolysis therapy in patients with acute STEMI Any prior ICH Known structural cerebral vascular lesion (e.g., AVM) Known malignant intracranial neoplasm (primary or metastatic) Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours Suspected aortic dissection Active bleeding or bleeding diathesis (excluding menses) Significant closed-head or facial trauma within 3 months

Relative contraindications for fibrinolysis therapy in patients with acute STEMI History of chronic, severe, poorly controlled hypertension Severe uncontrolled hypertension on presentation (SBP greater than 180 mm Hg or DBP greater than 110 mmHg) History of prior ischemic stroke greater than 3 months, dementia, or known intracranial pathology not covered in contraindications Traumatic or prolonged (greater than 10 minutes) CPR or major surgery (less than 3 weeks) Recent (within 2-4 weeks) internal bleeding Noncompressible vascular punctures For streptokinase/anistreplase: prior exposure (more than 5 days ago) or prior allergic reaction to these agents Pregnancy Active peptic ulcer Current use of anticoagulants: the higher the INR, the higher the risk of bleeding

STEMI cardiac care STEP 2: Determine preferred reperfusion strategy Fibrinolysis preferred if: <3 hours from onset PCI not available/delayed door to balloon > 90min door to balloon minus door to needle > 1hr Door to needle goal <30min No contraindications PCI preferred if: PCI available Door to balloon < 90min Door to balloon minus door to needle < 1hr Fibrinolysis contraindications Late Presentation > 3 hr High risk STEMI Killup 3 or higher STEMI dx in doubt

Comparing outcomes

Comparing outcomes

Medical Therapy MONA + BAH Morphine (class I, level C) Analgesia Reduce pain/anxiety—decrease sympathetic tone, systemic vascular resistance and oxygen demand Careful with hypotension, hypovolemia, respiratory depression Oxygen (2-4 liters/minute) (class I, level C) Up to 70% of ACS patient demonstrate hypoxemia May limit ischemic myocardial damage by increasing oxygen delivery/reduce ST elevation

Nitroglycerin (class I, level B) Analgesia—titrate infusion to keep patient pain free Dilates coronary vessels—increase blood flow Reduces systemic vascular resistance and preload Careful with recent ED meds, hypotension, bradycardia, tachycardia, RV infarction Aspirin (160-325mg chewed & swallowed) (class I, level A) Irreversible inhibition of platelet aggregation Stabilize plaque and arrest thrombus Reduce mortality in patients with STEMI Careful with active PUD, hypersensitivity, bleeding disorders

Beta-Blockers (class I, level A) 14% reduction in mortality risk at 7 days at 23% long term mortality reduction in STEMI Approximate 13% reduction in risk of progression to MI in patients with threatening or evolving MI symptoms Be aware of contraindications (CHF, Heart block, Hypotension) Reassess for therapy as contraindications resolve ACE-Inhibitors / ARB (class I, level A) Start in patients with anterior MI, pulmonary congestion, LVEF < 40% in absence of contraindication/hypotension Start in first 24 hours ARB as substitute for patients unable to use ACE-I

Heparin (class I, level C to class IIa, level C) LMWH or UFH (max 4000u bolus, 1000u/hr) Indirect inhibitor of thrombin less supporting evidence of benefit in era of reperfusion Adjunct to surgical revascularization and thrombolytic / PCI reperfusion 24-48 hours of treatment Coordinate with PCI team (UFH preferred) Used in combo with aspirin and/or other platelet inhibitors Changing from one to the other not recommended

Additional medication therapy Clopidodrel (class I, level B) Irreversible inhibition of platelet aggregation Used in support of cath / PCI intervention or if unable to take aspirin 3 to 12 month duration depending on scenario Glycoprotein IIb/IIIa inhibitors (class IIa, level B) Inhibition of platelet aggregation at final common pathway In support of PCI intervention as early as possible prior to PCI

Additional medication therapy Aldosterone blockers (class I, level A) Post-STEMI patients no significant renal failure (cr < 2.5 men or 2.0 for women) No hyperkalemis > 5.0 LVEF < 40% Symptomatic CHF or DM

STEMI care CCU Monitor for complications: recurrent ischemia, cardiogenic shock, ICH, arrhythmias Review guidelines for specific management of complications & other specific clinical scenarios PCI after fibrinolysis, emergent CABG, etc… Decision making for risk stratification at hospital discharge and/or need for CABG

Unstable angina/NSTEMI cardiac care Evaluate for conservative vs. invasive therapy based upon: Risk of actual ACS TIMI risk score ACS risk categories per AHA guidelines Low High Intermediate

Risk Stratification to Determine the Likelihood of Acute Coronary Syndrome Assessment Findings indicating HIGH likelihood of ACS Findings indicating INTERMEDIATE likelihood of ACS in absence of high-likelihood findings Findings indicating LOW likelihood of ACS in absence of high- or intermediate-likelihood findings History Chest or left arm pain or discomfort as chief symptom Reproduction of previous documented angina Known history of coronary artery disease, including myocardial infarction Age > 50 years Probable ischemic symptoms Recent cocaine use Physical examination New transient mitral regurgitation, hypotension, diaphoresis, pulmonary edema or rales Extracardiac vascular disease Chest discomfort reproduced by palpation ECG New or presumably new transient ST-segment deviation (> 0.05 mV) or T-wave inversion (> 0.2 mV) with symptoms Fixed Q waves Abnormal ST segments or T waves not documented to be new T-wave flattening or inversion of T waves in leads with dominant R waves Normal ECG Serum cardiac markers Elevated cardiac troponin T or I, or elevated CK-MB Normal

TIMI Risk Score Predicts risk of death, new/recurrent MI, need for urgent revascularization within 14 days

ACS risk criteria Low Risk ACS Intermediate Risk ACS No intermediate or high risk factors <10 minutes rest pain Non-diagnositic ECG Non-elevated cardiac markers Age < 70 years Intermediate Risk ACS Moderate to high likelihood of CAD >10 minutes rest pain, now resolved T-wave inversion > 2mm Slightly elevated cardiac markers

High Risk ACS Elevated cardiac markers New or presumed new ST depression Recurrent ischemia despite therapy Recurrent ischemia with heart failure High risk findings on non-invasive stress test Depressed systolic left ventricular function Hemodynamic instability Sustained Ventricular tachycardia PCI with 6 months Prior Bypass surgery

Low High risk risk risk Conservative therapy Invasive therapy Intermediate risk High risk Chest Pain center Conservative therapy Invasive therapy

Invasive therapy option UA/NSTEMI Coronary angiography and revascularization within 12 to 48 hours after presentation to ED For high risk ACS (class I, level A) MONA + BAH (UFH) Clopidogrel 20% reduction death/MI/Stroke – CURE trial 1 month minimum duration and possibly up to 9 months Glycoprotein IIb/IIIa inhibitors

Conservative Therapy for UA/NSTEMI Early revascularization or PCI not planned MONA + BAH (LMW or UFH) Clopidogrel Glycoprotein IIb/IIIa inhibitors Only in certain circumstances (planning PCI, elevated TnI/T) Surveillence in hospital Serial ECGs Serial Markers

Secondary Prevention Disease Behavioral Cognitive HTN, DM, HLP smoking, diet, physical activity, weight Cognitive Education, cardiac rehab program

Secondary Prevention disease management Blood Pressure Goals < 140/90 or <130/80 in DM /CKD Maximize use of beta-blockers & ACE-I Lipids LDL < 100 (70) ; TG < 200 Maximize use of statins; consider fibrates/niacin first line for TG>500; consider omega-3 fatty acids Diabetes A1c < 7%

Secondary prevention behavioral intervention Smoking cessation Cessation-class, meds, counseling Physical Activity Goal 30 - 60 minutes daily Risk assessment prior to initiation Diet DASH diet, fiber, omega-3 fatty acids <7% total calories from saturated fats

Thinking outside the box…

Or maybe just move….

Secondary prevention cognitive Patient education In-hospital – discharge –outpatient clinic/rehab Monitor psychosocial impact Depression/anxiety assessment & treatment Social support system

Medication Checklist after ACS Antiplatelet agent Aspirin* and/or Clopidorgrel Lipid lowering agent Statin* Fibrate / Niacin / Omega-3 Antihypertensive agent Beta blocker* ACE-I*/ARB Aldactone (as appropriate)

Prevention news… From 1994 to 2004 the death rate from coronary heart disease declined 33%... But the actual number of deaths declined only 18%  Getting better with treatment… But more patients developing disease –need for primary prevention focus

Summary ACS includes UA, NSTEMI, and STEMI Management guideline focus Immediate assessment/intervention (MONA+BAH) Risk stratification (UA/NSTEMI vs. STEMI) RAPID reperfusion for STEMI (PCI vs. Thrombolytics) Conservative vs Invasive therapy for UA/NSTEMI Aggressive attention to secondary prevention initiatives for ACS patients Beta blocker, ASA, ACE-I, Statin