ACUTE CORONARY SYNDROMES

Dr. Ravi KantAssistant Professor

Department of General Medicine

LECTURE OUTLINE

• INTRODUCTION – EPIDEMIOLOGY/PREVALENCE/DEFINITION

• PATHOPHYSIOLOGY OF ACUTE CORONARY SYNDROMES

• APPROACH TO SUSPECTED ACUTE CORONARY SYNDROME – GUIDELINE UPDATE

• TREATMENT/MANAGEMENT UPDATE

INTRODUCTION

• Coronary Artery Disease – leading cause of morbidity & mortality in industrialized nations.

• Although decrease in cardiovascular mortality still major cause of morbidity & burden of disease.

DEFINITIONS

• CAD is a continuum of disease….• Angina -> unstable angina -> AMI -> sudden cardiac

death• Acute coronary syndrome encompasses unstable

angina, NSTEMI, STEMI• Stable angina – transient episodic chest pain d/t

myocardial ischaemia, reproducible, frequency constant over time.usually relieved with rest/NTG.

• Classification of angina – Canadian Cardiovascular Society classification.

Canadian Cardiovascular Association Classification of Angina

CLASS 1 NO PAIN WITH ORDINARY PHYSICAL ACTIVITY

CLASS 2 SLIGHT LIMITATION OF PHYSICAL ACTIVITY –PAIN OCCURS WITH WALKING, CLIMBING STAIRS,STRESS

CLASS 3 SEVERE LIMITATION OF DAILY ACTIVITY – PAIN OCCURS ON MINIMAL EXERTION

CLASS 4 UNABLE TO CONDUCT ANY ACTIVITY WITHOUT PAIN, PAIN AT REST

UNSTABLE ANGINA

• Pain occurring at rest – duration > 20min, within one week of first visit

• New onset angina – ~ Class 2 severity, onset with last 2 months

• Worsening of chest pain – increase by at least 1 class, increases in frequency, duration

• Angina becoming resistance to drugs that previously gave good control.

• NB! ECG – normal, ST depression(>0.5mm), T wave changes

ACUTE MYOCARDIAL INFARCTION

• ECC/ACC DEFN –rise and fall in cardiac enzymes with one or more of the following:

• Ischaemic type chest pain/symptoms• ECG changes – ST changes, pathological Q waves• Coronary artery intervention data• Pathological findings of an acute MI• NSTEMI = UNSTABLE ANGINA SYMPTOMS/FINDINGS +

POSITIVE CARDIAC ENZYMES• STEMI = ST ELEVATION ON ECG + SYMPTOMS

APPROACH

• Identifying those with chest pain suggestive of IHD/ACS.• Thorough history required:• Character of pain• Onset and duration• Location and radiation• Aggravating and relieving factors• Autonomic symptoms• TYPICAL VS ATYPICAL HISTORY• Failure to recognise symptoms other than chest pain ->

approx 2 hr delay in seeking medical attention

CHARACTERISTICS OF TYPICAL ANGINAL CHEST PAIN (ADAPTED FROM ROSEN’S, EMERGENCY MEDICINE)

CHARACTERISTIC SUGGESTIVE OF ANGINA

LESS SUGGESTIVE OF ANGINA

TYPE OF PAIN DULL PRESSURE/CRUSHING PAIN

SHARP/STABBING

DURATION 2-5 MIN, <20 MIN SECONDSTO HOURS/CONTINUOUS

ONSET GRADUAL RAPID

LOCATION/CHEST WALL TENDERNESS

SUBSTERNAL, NOT TENDER TO PALP.

LATERAL CHEST WALL/TENDER TO PALP.

REPRODUCIBALITY WITH EXERTION/ACTIVITY

WITH BREATHING/MOVING

AUTONOMIC SYMPTOMS

PRESENT USUALLY ABSENT

TOOLS USED IN RISK STRATIFICATION

• HISTORY

• ECG

• BIOCHEMICAL MARKERS

ECG

• First point of entry into ACS algorithm• Abnormal or normal• Neither 100% sensitive or 100% specific for AMI• Single ECG for AMI – sensitivity of 60%, specificity

90% Normal ECG does not exclude ACS – 1-6% proven to

have AMI, 4% unstable angina

• GUIDELINES:• Initial 12 lead ECG – goal door to ECG time 10min, read

by experienced doctor.

• If ECG not diagnostic/high suspicion of ACS – serial ECGs initially 15 -30 min intervals.

• ECG adjuncts – leads V7 –V9, RV 4

• Continuous 12 lead ECG monitoring reasonable alternative to serial ECGs.

Thanking You

Electrocardiography

Dr. Ravi KantAssistant Professor

Department of General Medicine

Introduction

• An electrocardiogram (ECG or EKG) is a graphic recording of electric potentials generated by the heart.

• The signals are detected by means of metal electrodes attached to the extremities and chest wall and then are amplified and recorded by the electrocardiograph.

• ECG leads actually display the instantaneous differences in potential between the electrodes.

ECG Waveforms and Intervals• The ECG waveforms are

labelled alphabetically, beginning with the P wave, which represents atrial depolarization .

• The QRS complex represents ventricular depolarization, and the ST-T-U complex represents ventricular repolarization.

• The J point is the junction between the end of the QRS complex and the beginning of the ST segment.

• The QRS-T waveforms of the surface ECG correspond in a general way with the different phases of simultaneously obtained ventricular action potentials, the intracellular recordings from single myocardial fibber's.

• Conditions that prolong phase 2 (amiodarone, hypocalcemia) increase the QT interval.

• In contrast, shortening of ventricular repolarization (phase 2), such as by digitalis administration or hypercalcemia, abbreviates the ST segment

ECG Leads• The 12 conventional ECG leads record the

difference in potential between electrodes placed on the surface of the body.

• These leads are divided into two groups: six limb (extremity) leads and six chest (precordial) leads.

• The limb leads record potentials transmitted onto the frontal plane and the chest leads record potentials transmitted onto the horizontal plane

Genesis of the Normal ECG• P Wave• The normal atrial depolarization vector is oriented downward and

toward the subject's left, reflecting the spread of depolarization from the sinus node to the right and then the left atrial myocardium.

• Since this vector points toward the positive pole of lead II and toward the negative pole of lead aVR, the normal P wave will be positive in lead II and negative in lead aVR. By contrast, activation of the atria from an ectopic pacemaker in the lower part of either atrium or in the AV junction region may produce retrograde P waves (negative in lead II, positive in lead aVR).

• The normal P wave in lead V1 may be biphasic with a positive component reflecting right atrial depolarization, followed by a small (<1 mm2) negative component reflecting left atrial depolarization.

QRS Complex

• Normal ventricular depolarization proceeds as a rapid, continuous spread of activation wave fronts.

• This complex process can be divided into two major sequential phases, and each phase can be represented by a mean vector

• The first phase is depolarization of the interventricular septum from the left to the right and anteriorly (vector 1).

• The second results from the simultaneous depolarization of the right and left ventricles; it normally is dominated by the more massive left ventricle, so that vector 2 points leftward and posteriorly.

• Therefore, a right precordial lead (V1) will record this biphasic depolarization process with a small positive deflection (septal r wave) followed by a larger negative deflection (S wave).

T Wave and U Wave• Normally, the mean T-wave vector is oriented roughly concordant with the

mean QRS vector (within about 45° in the frontal plane). Since depolarization and repolarization are electrically opposite processes, this normal QRS–T-wave vector concordance indicates that repolarization normally must proceed in the reverse direction from depolarization (i.e., from ventricular epicardium to endocardium).

• The normal U wave is a small, rounded deflection (1 mm) that follows the T wave and usually has the same polarity as the T wave.

• An abnormal increase in U-wave amplitude is most commonly due to drugs (e.g., dofetilide, amiodarone, sotalol, quinidine, procainamide, disopyramide) or to hypokalemia.

• Very prominent U waves are a marker of increased susceptibility to the torsades de pointes type of ventricular tachycardia Inversion of the U wave in the precordial leads is abnormal and may be a subtle sign of ischemia.

Major ECG Abnormalities

Cardiac Enlargement and Hypertrophy

• Right ventricular hypertrophy due to a pressure load (as from pulmonic valve stenosis or pulmonary artery hypertension) is characterized by a relatively tall R wave in lead V1 (R S wave), usually with right axis deviation alternatively, there may be a qR pattern in V1 or V3R. ST depression and T-wave inversion in the right-to-midprecordial leads are also often present.

• This pattern, formerly called right ventricular "strain," is attributed to repolarization abnormalities in acutely or chronically overloaded muscle.

• Prominent S waves may occur in the left lateral precordial leads. Right ventricular hypertrophy due to ostium secundum–type atrial septal defects, with the accompanying right ventricular volume overload, is commonly associated with an incomplete or complete right bundle branch block pattern with a rightward QRS axis.

Bundle Branch Blocks

Clinical Interpretation of the ECG• Accurate analysis of ECGs requires thoroughness and care. • The following 14 points should be analyzed carefully in every ECG: • 1 standardization (calibration) and technical features (including lead placement and

artefact's)• 2 rhythm• 3 heart rate• 4 PR interval/AV conduction• 5 QRS interval• 6 QT/QTc interval• 7 mean QRS electrical axis • 8 P waves• 9 QRS voltages • 10 precordial R-wave progression • 11 abnormal Q waves • 12 ST segments • 13 T waves • 14 U waves

Myocardial Ischemia and Infarction• The ECG is a cornerstone in the diagnosis of acute and chronic ischemic heart disease.• Ischemia exerts complex time-dependent effects on the electrical properties of

myocardial cells. Severe, acute ischemia lowers the resting membrane potential and shortens the duration of the action potential.

• These currents of injury are represented on the surface When the acute ischemia is transmural, the ST vector usually is shifted in the direction of the outer (epicardial) layers, producing ST elevations and sometimes, in the earliest stages of ischemia, tall, positive so-called hyperacute T waves over the ischemic zone. With ischemia confined primarily to the subendocardium, the ST vector typically shifts toward the subendocardium and ventricular cavity, so that overlying (e.g., anterior precordial) leads show ST-segment depression (with ST elevation in lead aVR). Multiple factors affect the amplitude of acute ischemic ST deviations. Profound ST elevation or depression in multiple leads usually indicates very severe ischemia. From a clinical viewpoint, the division of acute myocardial infarction into ST-segment elevation and non-ST elevation types is useful since the efficacy of acute reperfusion therapy is limited to the former group

ECG sequence with anterior q wave infraction

ECG sequence with inferior q wave infraction

Computerized Electrocardiography

• Computerized ECG systems are widely used for immediate retrieval of thousands of ECG records.

• Computer interpretation of ECGs still has major limitations.

• Incomplete or inaccurate readings are most likely with arrhythmias and complex abnormalities. Therefore, computerized interpretation should not be accepted without careful clinician review.