blok 19 emergency cardiovacular care

7/31/2019 Blok 19 Emergency Cardiovacular Care

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Emergency CardiovacularCare (ECC)

Dr. Erwin Sukandi, SpPD, K-KV, FINASIM

Cardiology Division

Internal Medicine Department


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ECC

Acute Coronary Syndrome Unstable Angina Pectoris

Non ST Elevation Myocardial Infarction

ST Elevation Myocardial Infarction Acute Heart Failure

Malignant Arrhythmia

Aortic Dissection Cardiac Tamponade

Infective Endocarditis


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ACUTE CORONARY SYNDROMESLEARNING OBJECTIVES

Define acute coronary syndromes (ACS)

Understand the pathophysiology

Be capable of risk stratification

Aware of medications and strategiesemployed to manage ACS

Use basic principles of ECG interpretation

and infarct localization Apply knowledge to case studies


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Acute Coronary Syndrome

Unstable Angina Pectoris

Non-ST segment elevation myocardialinfarction (NSTEMI, usually non Q wave

MI)

ST segment elevation myocardialinfarction (STEMI, usually Q wave MI)


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REDUCE PATIENT SYMPTOMS

REDUCE MORTALITY

LIMIT MYOCARDIAL DAMAGE PRESERVELVFUNCTION

TIME IS MUSCLE

Goal of ACS Management:


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ACUTE CORONARY SYNDROMES

Unstable Angina

Clinical Presentation:

I. New Onset Angina Within past 1-2 months

CCS III or IV

II. Crescendo Angina Previous stable angina which has become more

frequent, severe, prolonged, easily induced or lessresponsive to nitroglycerine

III.Rest Angina Angina occurring at rest and lasting more than 15-20

minutes


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ACUTE CORONARY SYNDROMESUnstable Angina/NSTEMI

UA/NSTEMI Patent culprit artery, ulcerated plaque and associated thrombus

Significant risk of of thrombotic reocclusion

Unstable Angina = ACS withoutabnormal levelsof serum biomarkers for myocardial necrosis(Ti,Tt,CK-MB)

NSTEMI =ACSwithpositive markers


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ACUTE CORONARY SYNDROMESSTEMI

STEMI Complete thrombotic occlusion of a major epicardial artery

Presentation: Characteristic symptoms of cardiac ischemia

More prolonged and severe symptoms

Little response to nitroglycerine

Specific EKG changes on serial EKGs

Elevation of serum markers for cardiac injury

WHO definition of AMI


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Diagnosis

Cardiac Chest pain

ECG chages Cardiac enzymes


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Symptoms -Angina

PectorisPainSubsternal

Squeezing/Crushing/HeavinessMay radiate to arms, shoulders,jaw, upper back, upper abdomenback

May be associated with shortnessof breath, nausea, sweating

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Symptoms -Angina

Pectoris

Pain usually associated with 3Es

Exercise

Eating

Emotion

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Symptoms -Angina

PectorisPain seldom lasts > 30 minutes

Pain relieved by

Rest

Nitroglycerin

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Symptoms -Angina

PectorisGreat anxiety/Fear

Fixation of the bodyPale, ashen, or livid face

Dyspnea (SOB) may be

associated

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Symptoms -Angina

PectorisNausea

Diaphoresis

BP usually up during attack

Dysrhythmia may be present


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THE ELECTROCARDIOGRAM

12 lead EKG

Cornerstone of initial evaluation

Within 10 minutes of presentation

Previous EKG tracings Compare

Serial EKGs

Essential


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THE ELECTROCARDIOGRAM

1. ST segment elevation 2mm (2 contiguous leads), new LBBB, trueposterior ischemia

STEMI

EMERGENT REPERFUSION

2. ST depression >1mm, marked symmetrical T wave inversions>2 mm or Wellens pattern, dynamic ST-T changes with pain

UA/NSTEMI LIKELY

MEDICAL MANAGEMENT +/- URGENT IMAGING

3. Non-diagnostic or normal ECGACS LESS LIKELY

RISK STRATIFY


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THE ELECTROCARDIOGRAMINFARCT LOCATION

II, III, AVF : Inferior

V1 - V4 : Anteroseptal I, aVL : High lateral

I, aVL, V5-V6 : Lateral

I,aVL, V1-V6 : Extensive anterior

V1-V2 tall R, ST depression : True posterior


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ELECTROCARDIOGRAM


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Anterior MyocardialInfarction

Occlusion of the leftcoronary arteryleftanterior descendingbranch

ECG changes: STsegment elevationwith tall T waves and

taller-than-normal Rwaves in leads V3and V4


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Inferior MyocardialInfarction

Occlusion of the rightcoronary arteryposteriordescending branch

ECG changes: STsegment elevation inleads II, III, and aVF


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Lateral Myocardial Infarction

Occlusion of the leftcoronary arterycircumflex branch

ECG changes: STsegment elevation inleads I, aVL, V5,and V6


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Septal Myocardial Infarction

Occlusion of the leftcoronary arteryleftanterior descendingbranch

ECG changes:pathological Qwaves; absence of

normal R waves inleads V1 and V2


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Posterior Myocardial Infarction

Occlusion of the rightcoronary artery(posterior descendingbranch) or the left

circumflex artery Tall R waves and STsegment depressionpossible in leads V1,V2, V3, and V4

ST segment elevationin true posterior leads,V8 and V9


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Cardiac enzyme Marker

CardiacenzymeMarker

Initialelevationafter AMI

Mean timeto peakelevations

Time toreturn tobaseline

Myoglobin 1-4hr 6-7hr 18-24hr

CTnI 3-12hr 10-24hr 3-10 day

CTnT 3-12hr 12-48hr 5-14 day

CKMB 4-12 hr 10-24hr 2-3day

TCK 2-6 hr 4.7hr(3-5) 72hr(50-96)


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KILLIP SCORE

SEVERITY CLASS LV FUNCTION IN AMI

I No crackles, no S3

IIa Crackles < 50 % lung fields,no S3

IIb Crackles < 50 % lung fields,S3 present

III Crackles > 50 % lung fields,

pulmonary edemaIV Cardiogenic Shock


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Management of Cardiac

Chest Pain


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MANAGEMENT STEMI ACS

Urgent reperfusion:

FIBRINOLYSIS

PERCUTANEOUS CORONARYINTERVENTION


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ACUTE PULMONARYEDEMA Most commonly due to left ventricular

dysfunction Usually occurs in the setting of chronic

congestive heart failure

Also commonly occurs with myocardialinfaction (usually anterior infarction) Less frequently due to acute valvular

dysfunction (mitral or aortic) SVT or AF can cause APE Acute myocarditis can also cause APE Always associated with elevated pulmonary

venous pressure


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Precipitating Factors

Chronic LV dysfunction, most commonly

Na and or fluid overload

Viral and or bacterial infection

Myocardial ischemia

New arrhythmia: atrial fibrillation

Acute valvular dysfunction

Acute ischemia precipitating orworsening mitral regurgitation


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Diagnosis Broad differential for acute dyspnea

Dyspnea due to CHF

BNP level > 100 pg/mL in patient with acutedyspnea carry 12X risk of CHF etiology

BNP level > 500 pg/mL, CHF is nearly certainand therapy ca be instituted

Chest X-ray

Cardiomegaly

Cephalization of vessels

Interstitial edema

BNP level and ches x-ray finding are

independent predictor for CFF etiology


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Treatment

Treat precipitating factors

Preload reduction

Intravenous nitrates

Diuretics

Afterload reduction (if blood pressuretelerates)

Inotropic agents


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Treatment

LMNOP

Furosemide (Lasix)

Morphine, intravenous, caution withnausea

Nitrates, most important agents

Oxygen

Posture (upright


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Malignant Arrhythmia

Supraventriclar Arrhythmia

Atrial Fibrillation

Atrial Flutter

Supraventricular Tachycardia

Ventricular Arrhythmia

Ventricular Tachycardia

Ventricular Fibrillation Torsades de Pointes

Asystole


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SUPRAVENTRICULARARRHYTHMIA


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VENTRICULARARRHYTHMIA


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THANK YOU !!!

blok 19 emergency cardiovacular care

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