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SGD 1: AMI. CL, 55y/o M, CEO, severe substernal chest heaviness. SALIENT FEATURES. 55 y/o M, CEO severe substernal chest heaviness accompanied by nausea and vomiting History of having episodes of mild substernal chest tightness for the last 5 yrs - PowerPoint PPT Presentation

Text of SGD 1: AMI

  • CL, 55y/o M, CEO, severe substernal chest heavinessSGD 1: AMI

  • SALIENT FEATURES 55 y/o M, CEO severe substernal chest heaviness accompanied by nausea and vomiting History of having episodes of mild substernal chest tightness for the last 5 yrs a known hypertensive for 6 yrs (Usual BP: 130/80, Highest BP: 170/100) Irregular intake of Nifedipine 30mg

  • SALIENT FEATURES 40 pack years of cigarette smoking heavy alcohol beverage drinker Family History (+ ) premature CAD sister, 38 and brother, 45 (+ ) HTN father (+ ) DM mother

  • SALIENT FEATURES Soft S1 murmur on PE Laboratory tests 12 lead ECG: NSR, ST segment elevation I, aVL, V1-V6; ST segment depression II, III, aVF Troponin I 1.5ng/mL CPK-MB 256u/L CXR: cardiomegaly

  • SALIENT FEATURESContd Echo Doppler: Eccentric LVH w/ segmental wall motion abnormalityEjection fraction at 48%Doppler evidence off impaired LV relaxationDilated LA Dilated Aortic RootAortic Sclerosis

  • Ischemic Cardiac Disease with an Eccentric Left Ventricular Hypertrophy with segmental wall motion abnormality, a Dilated Left Atrium and Aortic Root, and Aortic Sclerosis with evident ST Elevation Myocardial Infarction (STEMI) and Normal Sinus Rhythm, of Class IV-D Functional DisabilityDiagnosis

  • 2. Differentiate between ATHEROGENESIS and ATHEROTHROMBOSIS

  • Atherogenesis The process of forming atheromas, plaques in the inner lining (the intima) of arteries. It involves elements of inflammation , a process that provides a unifying theme in the pathogenesis of atherosclerosis

  • Atherogenesis

  • AtherothrombosisCharacterized by an unpredictable, sudden disruption (rupture or erosion/fissure) of an atherosclerotic plaque, which leads to platelet activation and thrombus formation. It is the underlying condition that results in events leading to myocardial infarction, ischemic stroke, and vascular death.

  • Atherothrombosis

  • 3. What are the risk factors for CAD?


  • RISK FACTORS PRESENT IN THE PATIENT(+) Family history of premature CAD (sister at age 38 and brother at age 45)

    Sex (Male)

    Age (55 years old)

    Known hypertensive for 6 yearsHighest BP = 170/100 mmHgIrregular intake of Nifedipine 30 mg

    Forty (40) pack years of cigarette smoking

    Stress Occupation: CEOHad an argument during regular board meeting

    Heavy alcoholic beverage drinker

  • 4. What are the WHO criteria for acute myocardial infarction? Are they present in this patient?

  • WHO CRITERIA FOR AMI (1979):1. Clinical history of ischemic type of chest pain lasting for more than 20 minutes.

    A patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:

  • WHO CRITERIA FOR AMI (1979):2. Changes in serial ECG tracings.

    A patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:

  • WHO CRITERIA FOR AMI (1979):3. Rise and fall of serum cardiac biomarkers such as creatinine kinase-MB fraction and troponin.

    A patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:

  • REDEFINED WHO CRITERIA FOR AMI (2000):Cardiac troponin rise accompanied by either: Typical symptoms Pathological Q waves ST elevation or depression Coronary intervention

    The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers.

  • IN THE PATIENT: Severe substernal heaviness (experienced about 1 hour)

    ST segment elevation I, aVL, V1-V6

    Troponin I: 1.5ng/mL (NV: 0 0.4 ng/mL) CPK-MB: 256 u/L (NV: 20 mins

    Changes in serial ECG tracings

    Rise and fall of cardiac biomarkers

    Cardiac troponin rise accompanied by ST depression CRITERIA:

  • 5.What are the clinical features(Sx and PE) of AMI? Are they present in this patient?

  • Symptoms and PE of AMIChest pain described as a pressure sensation, fullness, or squeezing in the midportion of the thorax may radiate to the arms, jaw or teeth, shoulder, and/or backAssociated diaphoresis or sweating palpitations, weakness

    Substernal chest pain for >30 mins and diaphoresis strongly suggests STEMI

    Presence of a precipitating factor:Vigorous physical activityEmotional stressIllness: medical or surgical

  • Symptoms and PE of AMIAssociated with dyspnea or shortness of breathAssociated epigastric discomfort with or without nausea and vomitingSyncope or near-syncope without other causeImpairment of cognitive function without other cause lightheadedness or loss of consciousness a look of anxiety, or a sense of impending doom or death It may occur at any time of the day, but most appear to be clustered around the early hours of the morning, are associated with demanding physical activity, or both

  • PESigns of ventricular dysfunction:(+) S3 and S4Decreased intensity of S1Paradoxical splitting of S2Transient midsystolic or late systolic apical systolic murmur (mitral valve apparatus dysfunction)Anterior infraction (1/4 of pxs): sympathetic hyperactivityTachycardia, hypertensionPosterior infarction (1/2 of pxs): parasympathetic hyperactivityBradycardia, hypotensionCarotid pulse decreased in volume (reduced stroked volume)1st week after STEMI: temp. up to 38 Cin transmural STEMI: (+) pericardial friction rubSymptoms and PE of AMI

  • Symptoms and PE seen in AMI which is present in our patient(+) precipitating factorEmotional stress: started after argument during board meeting(+) Chest pain (severe substernal chest heaviness) not relieved by rest(+) weakness, sweating ( due to sympathetic activity), nausea, vomiting anxietySoft S1

  • 6. What is the ECG pattern of STEMI and NSTEMI?

  • Normal ECG PAttern

  • STEMI ECG FINDINGSST-segment elevation of at least 1 mm in two or more limb leads

  • STEMI ECG FINDINGSAt least 2 mm ST segment elevation in two or more precordial leads

  • STEMIST segment elevationQ wave inversion

  • Non-ST Elevation Myocardial InfarctionExample of an acute coronary syndrome closely related to unstable anginaDifference primarily in whether the ischemia is severe enough to cause sufficient myocardial damage to release detectable quantities of a marker of myocardial injuryDiagnosis of NSTEMI is established if a patient with the clinical features of UA develops evidence of myocardial necrosis, as reflected in elevated cardiac biomarkers

  • PathophysiologyMost commonly caused by a reduction in oxygen supply and/or by an increase in myocardial oxygen demand superimposed on an atherosclerotic coronary plaque, with varying degrees of obstruction

  • History and Physical ExamClinical Hallmark: chest paintypically located in the substernal region or sometimes in the epigastrium, that radiates to the neck, left shoulder, and left armLarge area of myocardial ischemia or a large NSTEMIDiaphoresispale cool skinsinus tachycardiaa third and/or fourth heart soundbasilar ralessometimes hypotension

  • ECG NSTEMIIn UA,ST-segment depressiontransient ST-segment elevationT-wave inversion

  • Non-ST Elevation InfarctionST depression & T-wave inversionThe ECG changes seen with a non-ST elevation infarction are:Before injuryNormal ECGST depression & T-wave inversion ST returns to baseline, but T-wave inversion persists

  • Classify AMI as to location based on ECG.

  • LocationLeadsVesselAnteriorV3-V4LCASeptalV1-V2LADInferiorII, III, AVFRCALateralV5-V6L circumflexPosteriorII, III, AVF, rV4 or marked depression V1-V4RCA




  • What is the location of the AMI in this patient based on his ECG?

  • Location of AMI based on ECG ANTERIOR

  • ECG of the PatientST segment depression on II, III and aVFMarked ST elevation on I, aVL, V1-V6

  • Early Management of AMIKey pointsRecognition of symptoms by the patient and prompt seeking of medical attentionRapid deployment of emergency medical team capable of performing resuscitative measuresExpeditious transport of patient to hospitalEarly treatment without more delay

  • Early Management of AMI

    Goals of ManagementControl of cardiac discomfortRapid identification of patients in need of urgent reperfusion therapy

  • Early Management of AMITreatment:1. Aspirin- rapidly inhibits COX-1 in platelets and reduces thromboxane A2.- chewed 160- 325 mg tablet 2. Presence of hypoxemia- Oxygen supplementation (2-4 L/ min)3. Nitroglycerin(sublingual) 3 doses of 0.4 mg at 5 min intervals to relieve chest pain and decrease preload and dilate infarcted coronary or collateral vessels.

  • Early Management of AMI4. Nitroglycerin (intravenous)- given when there is return of chest pain accompanied with ST-segment of T-wave shifts.5. Beta-blockers- diminish myocardial O2 demand and ischemia, reduces the risk of ventricular fibrillation.6. Reperfusion therapy- by fibrinolysis or primary Percutaneous Coronary Intervention.- done if ST- segment elevation is at least 2mm in 2 contiguous precordial leads and 1 mm in 2 adjacent limb leads present

  • 8. What are the possible complications of AMI?

  • ComplicationsVentricular remodelingleft ventricle undergoes a series of changes in shape, size, and thickness in both the infarcted and noninfarcted segmentsPrecedes clinically evident CHF in months to years after infarctionProgressive dilation and its clinical conse