Emergency Cardiovacular Care (ECC)

Emergency Cardiovacular Care (ECC)Dr. Erwin Sukandi, SpPD, K-KV, FINASIMCardiology DivisionInternal Medicine Department

ECCAcute Coronary SyndromeUnstable Angina PectorisNon ST Elevation Myocardial InfarctionST Elevation Myocardial InfarctionAcute Heart FailureMalignant ArrhythmiaACUTE CORONARY SYNDROMES LEARNING OBJECTIVES

Define acute coronary syndromes (ACS)Understand the pathophysiologyBe capable of risk stratificationAware of medications and strategies employed to manage ACSUse basic principles of ECG interpretation and infarct localizationApply knowledge to case studies

Acute Coronary SyndromeUnstable Angina PectorisNon-ST segment elevation myocardial infarction (NSTEMI, usually non Q wave MI)ST segment elevation myocardial infarction (STEMI, usually Q wave MI)

Goal of ACS Management:

REDUCE PATIENT SYMPTOMSREDUCE MORTALITYLIMIT MYOCARDIAL DAMAGEPRESERVE LV FUNCTION

TIME IS MUSCLE ACUTE CORONARY SYNDROMESStable Angina

Does not predict acute eventsMarker of established coronary artery disease (CAD)Fixed lesion / partially occluded vesselMismatch in oxygen supply and demandPrecipitants:ExerciseColdStressDuration: 30 minutes Pain relieved byRestNitroglycerin15Symptoms -Angina PectorisGreat anxiety/FearFixation of the body Pale, ashen, or livid faceDyspnea (SOB) may be associated16Symptoms -Angina PectorisNauseaDiaphoresisBP usually up during attackDysrhythmia may be presentTHE ELECTROCARDIOGRAM12 lead EKG Cornerstone of initial evaluationWithin 10 minutes of presentationPrevious EKG tracingsCompareSerial EKGs Essential

THE ELECTROCARDIOGRAM1. ST segment elevation 2mm (2 contiguous leads), new LBBB, true posterior ischemiaSTEMIEMERGENT REPERFUSION

2. ST depression >1mm, marked symmetrical T wave inversions >2 mm or Wellens pattern, dynamic ST-T changes with painUA/NSTEMI LIKELYMEDICAL MANAGEMENT +/- URGENT IMAGING

3. Non-diagnostic or normal ECGACS LESS LIKELYRISK STRATIFY

THE ELECTROCARDIOGRAMINFARCT LOCATIONII, III, AVF : InferiorV1 - V4 : AnteroseptalI, aVL: High lateralI, aVL, V5-V6 : LateralI,aVL, V1-V6: Extensive anteriorV1-V2 tall R, ST depression: True posterior

ELECTROCARDIOGRAM

Anterior Myocardial Infarction

Occlusion of the left coronary arteryleft anterior descending branch ECG changes: ST segment elevation with tall T waves and taller-than-normal R waves in leads V3 and V4Inferior Myocardial Infarction

Occlusion of the right coronary arteryposterior descending branch ECG changes: ST segment elevation in leads II, III, and aVFLateral Myocardial Infarction

Occlusion of the left coronary arterycircumflex branch ECG changes: ST segment elevation in leads I, aVL, V5, and V6Septal Myocardial Infarction

Occlusion of the left coronary arteryleft anterior descending branch ECG changes: pathological Q waves; absence of normal R waves in leads V1 and V2Posterior Myocardial Infarction

Occlusion of the right coronary artery (posterior descending branch) or the left circumflex artery Tall R waves and ST segment depression possible in leads V1, V2, V3, and V4 ST segment elevation in true posterior leads, V8 and V9Cardiac enzyme Marker

Cardiac enzyme Marker Initial elevation after AMIMean time to peak elevations Time to return to baseline Myoglobin 1-4hr 6-7hr 18-24hr CTnI3-12hr 10-24hr 3-10 dayCTnT3-12hr

12-48hr 5-14 dayCKMB4-12 hr10-24hr 2-3day TCK 2-6 hr 4.7hr(3-5)72hr(50-96) KILLIP SCORE

Management of Cardiac Chest Pain

MANAGEMENT STEMI ACS

Urgent reperfusion:

FIBRINOLYSIS

PERCUTANEOUS CORONARY INTERVENTION

ACUTE PULMONARY EDEMAMost commonly due to left ventricular dysfunctionUsually occurs in the setting of chronic congestive heart failureAlso commonly occurs with myocardial infaction (usually anterior infarction)Less frequently due to acute valvular dysfunction (mitral or aortic)SVT or AF can cause APEAcute myocarditis can also cause APEAlways associated with elevated pulmonary venous pressurePrecipitating FactorsChronic LV dysfunction, most commonlyNa and or fluid overloadViral and or bacterial infectionMyocardial ischemiaNew arrhythmia: atrial fibrillationAcute valvular dysfunctionAcute ischemia precipitating or worsening mitral regurgitationDiagnosis Broad differential for acute dyspneaDyspnea due to CHFBNP level > 100 pg/mL in patient with acute dyspnea carry 12X risk of CHF etiologyBNP level > 500 pg/mL, CHF is nearly certain and therapy ca be institutedChest X-rayCardiomegalyCephalization of vesselsInterstitial edemaBNP level and ches x-ray finding are independent predictor for CFF etiology

Treatment Treat precipitating factorsPreload reductionIntravenous nitratesDiureticsAfterload reduction (if blood pressure telerates)Inotropic agentsTreatmentLMNOPFurosemide (Lasix)Morphine, intravenous, caution with nauseaNitrates, most important agentsOxygen Posture (uprightMalignant ArrhythmiaSupraventriclar ArrhythmiaAtrial FibrillationAtrial FlutterSupraventricular TachycardiaVentricular (Lethal) ArrhythmiaVentricular TachycardiaVentricular FibrillationPEA (Pulseless Electrical Activity)AsystoleSUPRAVENTRICULAR ARRHYTHMIA

VENTRICULAR ARRHYTHMIA

SEVERITY CLASSLV FUNCTION IN AMI

INo crackles, no S3

IIaCrackles < 50 % lung fields,

no S3

IIbCrackles < 50 % lung fields,

S3 present

IIICrackles > 50 % lung fields, pulmonary edema

IVCardiogenic Shock