![(1) plaque rupture or erosion with a
superimposed nonocclusive thrombus
NSTEMI may occur with downstream
embolization of platelet aggregates and/or
atherosclerotic debris;
(2) dynamic obstruction [e.g., coronary spasm,
as in Prinzmetal's variant angina (PVA)
(3) progressive mechanical obstruction [e.g.,
rapidly advancing coronary atherosclerosis
or restenosis following percutaneous
coronary intervention (PCI)]
(4) UA secondary to increased myocardial
oxygen demand and/or decreased supply
(e.g., tachycardia, anemia).](https://image.slidesharecdn.com/acs-140710120722-phpapp01/75/Acute-coronary-syndrome-29-2048.jpg)
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Acute coronary syndrome
Coronary artery disease (CAD) is a major cause of death in India. Atherosclerosis underlies most CAD cases. Unstable angina and NSTEMI are types of acute coronary syndrome (ACS) caused by a reduction in oxygen supply to the heart. The clinical presentation of ACS can include chest pain and other symptoms. Diagnosis involves ECG, cardiac biomarkers, and risk stratification. Treatment focuses on anticoagulation, antiplatelet therapy, and revascularization. Myocardial infarction (MI or heart attack) occurs when an atherosclerotic plaque ruptures completely blocking a coronary artery. This leads to necrosis of heart muscle cells. Diagnosis of MI requires specific ECG changes and elevated cardiac
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Acute coronary syndrome
- 2. EPIDEMIOLGY • Main causeof death • The highest rate is in south India. • It has been estimated that India had the highest number of deaths in the world due to CAD in 2002, nearly 1.5 million and which is expected to double by 2015. • Atherosclerosis remains the major cause of death and premature disability
- 3. MEANING • Atherosclerosis : athere=fatty mush,skleros = hard. • Atherosclerosis = “hardening of the arteries”
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- 9. Non modifiable RiskFactors • Heredity • Age • Personality factors • Gender
- 10. Modifiable Risk Factors •Smoking • Hypertension • Elevated serum cholesterol level • Diabetes • Obesity • Physical Inactivity
- 11. Contributing Risk Factors •Response to stress • Homocysteine Level • Inflammatory Level • Menopause • Type A Behavioural Patterns, TABP • Hemostatic factors
- 12. Novel risk factors •Homocysteine • CRP • Plasma fibrinogen • Fibrin D dimer • Lipoprotein
- 13. CAUSES OF ACS •Decrease in the oxygen available to the myocardium – Nonobstructive clot on an atherosclerotic plaque. – Coronary vasospasm. – Atherosclerotic obstruction without clot or vasospasm. – Inflammation or infection. – Unstable angina due to a non cardiac cause. – Thrombus formation with subsequent coronary artery occlusion
- 14. CAUSES OF ACS •Increase in the oxygen demand
- 15. PATHOPHYSIOLOGY • Initiation ofAtherosclerosis • Leukocyte Recruitment • Foam-Cell Formation • Atheroma Evolution and Complications • Microvessels • Calcification • Plaque Evolution
- 19. Deterioration of astable atherosclerotic plaque Exposing the intima to blood Stimulating platelet aggregation Local vasoconstriction Thrombus formation Partially occluded by the thrombus (manifesting UA/NSTEMI) or totally occluded by a thrombus (STEMI) A C S A C S
- 22. Criteria for diagnosisof ACS Major criteria Minor criteria A diagnosis of ACS can be made if one or more of the following major criteria are present: ST elevation or LBBB in the setting of recent (<24hrs) or ongoing angina New or presumably new, ST segment depression (≥0.05mV) or T wave inversion (≥ 0.2mV) with rest symptoms Elevated serum markers of myocardial damage (ie, Troponin I, T and CK-MB) In the absence of a major criterion, a diagnosis of ACS requires the presence of at least one item from both column 1 and 2 1 2 Prolonged (ie, >20mts) chest, arm/shoulder, neck or epigastric discomfort New onset chest, arm/ shoulder, neck, or epigastric discomfort at rest , minimal exertion or ordinary activity Previously documented chest, arm/ shoulder, neck, or epigastric discomfort which has become distinctly more frequent or longer in duration Typical/ atypical angina Male> 40yrs or female>60yrs Known CAD HF, hypotension or transient mitral valve regurgitation by examination DM Extracardiac disease Pathologic Q wave on ECG Abnormal ST segment or T wave abnormalities not known to be new
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- 24. Definition Stable angina pectorisis characterized by chest or arm discomfort that may not be described as pain but is reproducibly associated with physical exertion or stress and is relieved within 5–10 minutes by rest and/or sublingual nitroglycerin.
- 25. Unstable Angina isdefined as angina pectoris or equivalent ischemic discomfort with at least one of three features: (1) it occurs at rest (or with minimal exertion), usually lasting >10 minutes; (2) it is severe and of new onset (i.e., within the prior 4–6 weeks); and/or (3) it occurs with a crescendo pattern
- 26. The diagnosis ofNSTEMI is established if a patient with the clinical features of UA develops evidence of myocardial necrosis, as reflected in elevated cardiac biomarkers.
- 27. Canadian Cardiovascular Society -Classification of Angina CLASS ACTIVITY EVOKING ANGINA LIMITS TO ACTIVITY I II III IV Prolonged exertion Walking>2 blocks Walking<2 blocks Minimal or rest None Slight Marked Severe
- 28. Pathophysiology A reduction inoxygen supply and/or by an increase in myocardial oxygen demand superimposed on a lesion that causes coronary arterial obstruction, usually an atherothrombotic coronary plaque
- 29. (1) plaque ruptureor erosion with a superimposed nonocclusive thrombus NSTEMI may occur with downstream embolization of platelet aggregates and/or atherosclerotic debris; (2) dynamic obstruction [e.g., coronary spasm, as in Prinzmetal's variant angina (PVA) (3) progressive mechanical obstruction [e.g., rapidly advancing coronary atherosclerosis or restenosis following percutaneous coronary intervention (PCI)] (4) UA secondary to increased myocardial oxygen demand and/or decreased supply (e.g., tachycardia, anemia).
- 30. Clinical Presentation • Typicalchest and associated symptoms (not related to trauma):
- 31. Atypical symptoms • Neck,throat, jaw or tooth discomfort • Shoulder or arm pain • Numbness or tingling in the chest or related area • Fullness or burning in the chest • Epigastric discomfort which is described as indigestion • Discomfort between scapula or in the midback region • Dizziness/ light headedness with or without syncope • Fatigue or weakness not related to neurologic problems • Palpitation of new onset with no history of dysrhythmia • Mid back pain (not related to degenerative joint diseases)
- 32. Diagnostic Pathways • Clinicalhistory • ECG • Cardiac markers • Stress testing (coronary imaging is an emerging option).
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- 36. Biochemical cardiac markers •Creatine kinase (CK-MB) • Troponin I and T and/ or • Myoglobulin
- 37. Medical Treatment • Bedrest • Continuous ECG monitoring for ST- segment deviation and cardiac arrhythmias. • Ambulation is permitted if the patient shows no recurrence of ischemia and does not develop a biomarker of necrosis for 12–24 h.
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- 44. Anti-ischemic treatment • Toprovide relief and prevention of recurrence of chest pain • Initial treatment should include – bed rest – nitrates, and – beta blockers
- 45. Antithrombotic Therapy: • Othermain component of treatment for UA/NSTEMI • Initial treatment should begin with the platelet cyclooxygenase inhibitor aspirin. • The typical initial dose is 325 mg/d, with lower doses (75–162 mg/d) recommended for long-term therapy.
- 46. Anticoagulant therapy • Unfractionatedheparin (UFH • The low-molecular-weight heparin (LMWH), enoxaparin • The indirect Factor Xa inhibitor, fondaparinux • Bivalirudin
- 47. Unstable Angina Risk Stratification oLow risk – New-onset exertional angina – Minor chest pain during exercise – Pain relieved promptly by nitroglycerine o Management – Can be managed safety as an outpatient (assuming close follow-up and rapid investigation)
- 48. Unstable Angina Risk Stratification oIntermediate risk – Prolonged chest pain – Diagnosis of rule-out MI o Management – Observe in the ER or Chest Pain Unit – Monitor clinical status and ECG – Obtain cardiac enzyme (troponin T or I) every 8 to 12 hours
- 49. Unstable Angina Risk Stratification oHigh risk – Recurrent chest pain – ST-segment change – Hemodynamic compromise – Elevation in cardiac enzyme o Management – Monitor in the coronary Care Unit
- 50. Risk Stratification byECG The risk of death or MI at 30 days is stongly related to the ECG at the time of chest pain • ST depression 10 % • T-wave inversion 5 % • No ECG changes 1~2 %
- 51. PRINZMETAL'S VARIANT ANGINA (PVA) •A syndrome of severe ischemic pain that occurs at rest but not usually with exertion and is associated with transient ST- segment elevation. • This syndrome is due to focal spasm of an epicardial coronary artery, leading to severe myocardial ischemia
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- 53. Treatment of PVA •Nitrates and calcium channel blockers • Aspirin may actually increase the severity of ischemic episodes, possibly as a result of the exquisite sensitivity of coronary tone to modest changes in the synthesis of prostacyclin. • The response to beta blockers is variable. • Coronary revascularization
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- 55. DEFINITION • A dynamicprocess by which one or more regions of the heart experience a severe and prolonged decrease in oxygen supply because of insufficient coronary blood flow; subsequently, necrosis or death•to the myocardial tissue occurs.
- 56. Pathophysiology slowly developing high gradestenosis of epicardial coronary arteries complete occlusion , but do not precipitate MI Development of collateral circulation atherosclerotic plaque rupture exposure of substances that promote platelet activation and aggregation thrombin generation thrombus formation interrupt blood supply and leads imbalance between O2 demand and supply myocardial necrosis contractile function of the heart stops at necrotic area
- 57. • The coronaryplaques prone to disruption are those with a rich lipid core and a thin fibrous cap. disrupted plaque Formation of an initial platelet monolayer activation of various agonists promote platelet activation release of thromboxane A2 further platelet activation potential resistance to fibrinolysis develops.
- 58. Platelet activation change inthe glycoprotein IIb/IIIa receptor develops a high affinity for soluble adhesive proteins (i.e., integrins) such as fibrinogen platelet cross-linking and aggregation
- 59. Disrupted plaque exposure oftissue factor in damaged endothelial cells at the site coagulation cascade is activated Factors VII and X are activated the conversion of prothrombin to thrombin converts fibrinogen to fibrin autoamplification reaction further activation of the coagulation cascade Artery is occluded by a thrombus containing platelet aggregates and fibrin strands.
- 60. The amount ofmyocardial damage caused by coronary occlusion depends on (1) the territory supplied by the affected vessel (2) whether or not the vessel becomes totally occluded (3) the duration of coronary occlusion (4) the quantity of blood supplied by collateral vessels to the affected tissue (5) the demand for oxygen of the myocardium whose blood supply has been suddenly limited (6) endogenous factors that can produce early spontaneous lysis of the occlusive thrombus, and (7) the adequacy of myocardial perfusion in the infarct zone when flow is restored in the occluded epicardial coronary artery.
- 61. Location of Infarction Locationof MI Primary siteof occlusion Inferior MI RCA (80-90%), LCX (10- 20%) Inferolateral MI LCX Posterior MI RCA/ LCX Anterior MI LAD Anterior septal MI LAD Lateral MI LAD/LCX Right ventricular RCA
- 62. KILLIPS CLASSIFICATION Killip class I Individualswith no clinical signs of heart failure Killip class II Individuals withrales or crackles in the lungs , an S3, and elevated JVP Killip class III Individuals with frank acute pulmonary edema Killip class IV Individuals with cardiogenic shock/ hypotension and evidence of peripheral vasoconstriction (oliguria, cyanosis or sweating)
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- 64. Involved layers ofheart muscle – Transmural (Q wave) infarction - area of necrosis occurs throughout the entire thickness of the heart muscle. – Subendocardial (nontransmural/non Q-wave) infarction area of necrosis is confined to the innermost layer of the heart lining the chambers.
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- 66. Clinical features • Diaphoresis,cool clammy skin, facial pallor. • Hypertension or hypotension and Bradycardia or tachycardia • Premature ventricular and/or atrial beats • Palpitations, severe anxiety, dyspnea • Disorientation, confusion, restlessness • Fainting, marked weakness • Nausea, vomiting, hiccups
- 68. Atypical symptoms • Epigastricor abdominal distress • dull aching or tingling sensations • shortness of breath • extreme fatigue
- 70. Physical Signs • Fourthand third heart sounds • Decreased intensity of the first heart sound • Paradoxical splitting of the second heart sound • A pericardial friction rub (transmural STEMI) • Temperature elevations up to 38°C.
- 71. Diagnostic Evaluation (1) ECG (2)serum cardiac biomarkers (3) cardiac imaging (4) nonspecific indices of tissue necrosis and inflammation
- 72. Physical Examination • mufflingof sounds • presence of gallop • arrhythmia, and • accentuation of pulmonary second sound
- 73. WHO criteria fordiagnosis of MI: It requires atleast two of the following three elements • A history of ischemic type chest discomfort • Evolutionary changes on serially obtained ECG tracing • Typical rise and fall in serum cardiac markers
- 74. ECG Changes – STsegment depression and T wave inversion indicate a pattern of ischemia. – ST elevation indicates an injury pattern. – Q waves indicate tissue necrosis and are permanent
- 75. Location of MIPrimary siteof occlusion Primary ECG changes Complications Inferior MI RCA (80-90%) LCX (10-20%) L II,III, aVF First and second degree AV block, right ventricular infarct Inferolateral MI LCX L II, III, aVF, V5,V6 Third degree heart block, left HF, CMP, left ventricular rupture Posterior MI RCA/ LCX No lead truly looks at posterior surface. Look for reciprocal changes in V1 and V2- tall, broad R waves; ST depression and tall T waves. Posterior leads V7,V8 and V9 may be recorded and evaluated First, second, and third degree heart block, HF, bradydysrhythmias Anterior MI LAD V2- V4 Third degree heart block, HF, bundke branch block Anterior septal MI LAD V1-V3 Second and third degree heart block Lateral MI LAD/LCX V5, V6, I, aVL HF Right ventricular RCA V4R Right precordial leads V1R – V6R may be recorded and evaluated Increased RAP, decreased CO, bradydysthymias, heart blocks, hyptension, cardiogenic shock
- 76. ECG leads showingchanges Location of infarct V1-V3 Anteroseptal V4- V6, L1 and aVL Anterolateral aVF,L2 and L3, ST depression in V1 and V2 Inferior wall Presence of tall R wave and upright T waves in V1 and V2 True posterior infarct ST elevation in Rt sided chest leads and Q waves (V3R, V4R) Right ventricular infarct
- 77. Cardiac Markers • Nonspecificmarkers – lactate dehydrogenase – aspartate aminotransferase – myoglobin • Specific cardiac markers – Troponin (troponin C, troponin I and troponin T). – Creatine kinase (CK)
- 78. Marker Rise in serum levelfrom onset Peak level Time to return to normal Time for blood collection SGOT (5- 40u/l) 8-12 hrs 18-36hrs 3-4 days Once n 12hrs LDH (20- 220IU/L) 10hrs 24-48hrs 10- 14 days 24hrs CK-MB 3-12hrs 24hrs 48-72 hrs Every 12hrs for 3 days C TnT 3-12hrs 12hrs-2 days 5-14 days Once atleast every 12 hrs C TnI 3-12hrs 24hrs 5-10days Once atleast every 12 hrs
- 80. • Chest xray:Prominent pulmonary vascular markings on x ray indicate left ventricular failure. Chest film helps to exclude other causes of chest pain such as pneumothorax, pulmonary infarction with effusion, aortic dissection and skeletal fractures. • Echocardiogram: – used to evaluate ventricular function. – used to assist in diagnosing an MI, especially when the ECG is nondiagnostic.
- 82. • CT Scan:to reveal cavity dimensions, wall thickness, aneurysms and intracardiac thrombi. • Nuclear imaging : to study nature of myocardial lesion, its viability and prognosis • MRI scan: to assess the perfusion of infracted and noninfarcted tissue as well as the state of reperfused myocardium
- 83. Other Findings • ElevatedCRP and lipoprotein • Abnormal coagulation studies • Elevated white blood cell (WBC) count and sedimentation rate • Radionuclide imaging allows recognition of areas of decreased perfusion. • PET determines the presence of reversible heart muscle injury and irreversible or necrotic tissue; extent to which the injured heart muscle has responded to treatment can also be determined.
- 84. Management • Prehospital care: 1)recognition of symptoms by the patient and prompt seeking of medical attention; (2) rapid deployment of an emergency medical team capable of performing resuscitative maneuvers, including defibrillation; (3) expeditious transportation of the patient to a hospital facility that is continuously staffed by physicians and nurses skilled in managing arrhythmias and providing advanced cardiac life support; and (4) expeditious implementation of reperfusion therapy
- 87. Emergency department • Goals: –control of cardiac discomfort, – rapid identification of patients who are candidates for urgent reperfusion therapy, – triage of lower-risk patients to the appropriate location in the hospital, and – avoidance of inappropriate discharge of patients with STEMI.
- 88. • Aspirin :Rapid inhibition of cyclooxygenase-1 in platelets followed by a reduction of thromboxane A2 • Supplemental O2: when hypoxemia is present, O2 should be administered by nasal prongs or face mask (2–4 L/min) for the first 6–12 h after infarction
- 89. Control of Discomfort •Sublingual nitroglycerin • Morphine • Intravenous beta blockers
- 90. Management Strategies: Initial 12-leadECG ST-segment elevation of at least 2 mm in 2 contiguous precordial leads and 1 mm in 2 adjacent limb leads is present a patient should be considered a candidate for reperfusion therapy • Gold hour = first 60 mts. Total ischemic time : 120 mts
- 91. Primary Percutaneous Coronary Intervention •PCI, usually angioplasty and/or stenting without preceding fibrinolysis, referred to as primary PCI • It is effective in restoring perfusion in STEMI when carried out on an emergency basis in the first few hours of MI.
- 92. • Advantage: – patientswho have contraindications to fibrinolytic therapy – More effective than fibrinolysis in opening occluded coronary arteries
- 93. PCI • Indication: – Whenthe diagnosis is in doubt – Cardiogenic shock is present – Bleeding risk is increased, or – Symptoms have been present for at least 2–3 h when the clot is more mature and less easily lysed by fibrinolytic drugs.
- 95. Fibrinolysis • Ideally initiatedwithin 30 min of presentation (door-to-needle time 30 min). • Goal of fibrinolysis is prompt restoration of full coronary arterial patency.
- 96. Fibrinolytic agents • Tissueplasminogen activator (tPA), streptokinase, tenecteplase (TNK), and reteplase (rPA) – First generation drugs- streptokinase, urokinase – Second generation- TPA, anioylated plasminogen streptokinase – Third generation- reteplase, TNK • These drugs are promoting the conversion of plasminogen to plasmin, which subsequently lyses fibrinthrombi.
- 97. Thrombolysis in myocardial infarction(TIMI) grading system • Grade 0 - Complete occlusion of the infarct-related artery • Grade 1 - Some penetration of the contrast material beyond the point of obstruction but without perfusion of the distal coronary bed; • Grade 2 - Perfusion of the entire infarct vessel into the distal bed, but with flow that is delayed compared with that of a normal artery • Grade 3 - Full perfusion of the infarct vessel with normal flow
- 98. CONTRAINDICATIONS OF FIBRINOLYSIS • Historyof cerebrovascular hemorrhage, a nonhemorrhagic stroke or other cerebrovascular event within the past year • Suspicion of aortic dissection • Active internal bleeding (excluding menses). • Advanced age associated with an increase in hemorrhagic disorders
- 99. Relative contraindications: • Currentuse of anticoagulants (INR- 2) • A recent (<2 weeks) invasive or surgical procedure or prolonged (>10 min) cardiopulmonary resuscitation • Known bleeding disorders • Pregnancy • A hemorrhagic ophthalmic condition (e.g., hemorrhagic diabetic retinopathy) • Active peptic ulcer disease • A history of severe hypertension that is currently adequately controlled. • Because of the risk of an allergic reaction, patients should not receive streptokinase if that agent had been received within the preceding five days to two years.
- 100. Hospital Management • CoronaryCare Units • Diet • Bowel Management • Sedation
- 101. Interventional Cardiology: • Percutaneoustransluminal coronary angioplasty • Intracoronary stent
- 102. Surgical Revascularization • CoronaryArtery Bypass Graft • Minimal Invasive Coronary Artery Surgery • Transmyocardial revascularization
- 103. Cardiac Rehabilitation • Medicallysupervised program consisting of exercise training, education on heart healthy living, and counseling to reduce stress and help patients return to an active lifestyle and recover more quickly
- 104. Components • Physician-prescribed exercise • Cardiacrisk factor modification (education, counseling and behavioral intervention) • Psychosocial assessment • Outcomes assessment • Individualized treatment plan
- 105. Complications • Ventricular Dysfunctionand Congestive Heart Failure STEMI left ventricle begins to dilate results from expansion of the infarct resulting in disproportionate thinning and elongation of the infarct zone lengthening of the noninfarcted segments occurs overall chamber enlargement HEART FAILURE
- 106. EARLY COMPLICATIONS • Hypovolemia •Cardiogenic Shock • Right Ventricular Infarction • Arrhythmias • Ventricular Premature Beats • Ventricular Tachycardia and Fibrillation • Sinus Bradycardia
- 107. LATE COMPLICATIONS • LeftVentricular Aneurysm • Dressler’s syndrome • Shoulder hand syndrome
- 108.
- 109. Nursing Assessment • Gatherinformation regarding the patient's chest pain: • Evaluate cognitive, behavioral, and emotional status. • Prior health status with emphasis on current medications, allergies • Analyze information for contraindications for thrombolytic therapy and PCI. • Gather information about presence or absence of cardiac risk factors. • Identify patient's social support system and potential caregivers. • Identify significant other's reaction to the crisis situation.
- 110. • Acute painrelated to decreased blood supply to the myocardium
- 111. • Ineffective tissueperfusion : cardiopulmonary related to reduced coronary blood flow from coronary thrombus and atherosclerotic plaque
- 112. • Anxiety relatedto pain and fear of death
- 113. • Risk fordecreased cardiac output related to decrease in LV function
- 114. • Activity intolerancerelated to imbalance between oxygen demand and supply
- 115. • Ineffective copingrelated to life threatening diagnosis
- 116. • Risk forbleeding
- 117.
- 118. BIBLIOGRAPHY • Braunwald, Fauci,Kasper,Hauser, Longo,Jameson.Harrison’s Principles of Internal Medicine. 15th ed. Vol 1. New York:McGraw-Hill;2001 • K.V Krishnadas. Textbook of Medicine. 5th ed. Delhi: Jaypee brothers;2008 • Bonow. Mann. Zipes, Libby. Braunwald’s Heart disease. 9th ed. India; Elsevier publication; 2011. • Joyce M Black, Jane Hokanson Hawks. Medical Surgical Nursing. 8th ed. Vol-2. India: Saunders Elsevier publishers; 2010