ECG Interpretation for Ischemia

Cardiac Conduction System Revision

The heart has four chambers and is a metabolically active organ with its own wiring system. Cardiac myocytes are electrically active. The sinoatrial (SA) node, located at the top of the right atrium, is the pacemaker and is regulated by the autonomic nervous system and hormones like thyroid hormone and the sympathetic nervous system.

Conduction passes through the right atrium and Bachmann's bundle to the left atrium, pausing at the atrioventricular (AV) node near the intraventricular septum, where the bundle of His is located. It then moves down the intraventricular septum through the left and right bundle branches. The left bundle branch has anterior and posterior fascicles, terminating in the Purkinje fibers. This coordinated propagation of action potentials leads to mechanical contractility in a distinct order.

The surface ECG (electrocardiogram) measures this net process. The P wave correlates to atrial depolarization, the QRS complex to ventricular depolarization, and the T wave to ventricular repolarization.

Blood Supply and Territories

Understanding the blood supply to the heart is crucial as it helps correlate electrical changes in the heart, seen on the surface ECG, with ischemia and infarction. The anatomy is correlated to electrical changes on the surface ECG in ischemia and infarction. Advanced material may cover the mechanisms behind these ECG changes, correlating the surface ECG to areas of the heart supplied by major coronary arteries.

Surface ECG Revision

Think about the surface ECG and consider the following:

  • What are the chest leads?
  • What are the limb leads?
  • Where is the rhythm strip?
  • Where is the calibration pulse?

Also, think about the paper speed on a standard ECG and how to determine the rate and rhythm.

Standard ECG paper speed is 25 millimeters per second.

Rate and Rhythm Calculation

Heart rate can be roughly calculated by looking at the gaps between RR waves. For example, if there are a bit less than three big boxes between RR waves, the heart rate is a bit less than 100 beats per minute.

The rhythm is determined by the presence of P waves and regularity. Sinus rhythm implies the presence of P waves.

ECG Lead Presentation

The standard presentation of an ECG includes limb leads (I, II, III, AVR, AVL, AVF) on the left side and chest leads (V1 to V6) on the right. Lead II is often recapitulated at the bottom as a rhythm strip.

It's important to note that limb leads and chest leads are not all taken simultaneously. The leads above each other are simultaneous, but from left to right, it's sequential (each 2.5 seconds). The rhythm strip (lead II) shows the entire ten seconds, which is important for evaluating the rhythm.

Lead II is used as the rhythm strip because it provides a good view of the P waves due to the vector direction.

Signal Amplitude and Calibration Pulse

The calibration pulse on an ECG is a standardization that can be adjusted to accentuate certain features. A standard ECG is 10 millimeters per millivolt.

Paper Speed and Time Measurement

Paper speed on an ECG is 25 millimeters per second. One small box represents 40 milliseconds, and one large box represents 200 milliseconds. Five big boxes between RR waves indicate 60 beats per minute.

Components of a Normal ECG

The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. The segment is from the end of the P wave.

Segments like TP or TQ are not clinically relevant. The PQRST segments are named by mathematical Cartesian convention.

The PQRST complex represents a vector sum of action potentials moving in different directions in the heart. The P wave represents atrial depolarization initiated by the sinoatrial node. During atrial depolarization, when there is no net electrical activity, the ECG should be isoelectric (flat).

The impulse is delayed at the AV node, determining the length of the PR interval. The QRS complex represents depolarization through the ventricular septum, followed by a period when depolarization is complete (ST segment). The ST segment should be isoelectric.

Ventricular repolarization begins at the apex, causing the T wave, and when complete, the ECG should be isoelectric once again.

Heart Rate Calculation Examples

Calculate heart rates on ECGs. A heart rate more than 100 bpm is considered tachycardic, while less than 60 bpm is bradycardic. However, normal heart rates vary.

ECG Recording and Leads

An ECG measures the electrical potential difference between two points on the body. Electrodes are placed on the body, connected to an instrumentation amplifier. A wave of depolarization passing between two electrodes elicits a positive deflection if moving towards the electrode and a negative deflection if moving away.

There are 10 physical electrodes but a 12-lead ECG. Six electrodes are placed across the precordium, and three limb electrodes are used, plus a neutral one.

Why all these leads? They provide vectors to precisely localize changes in the electrical activity of the heart. Limb electrodes are in a vertical plane, while chest leads are in a horizontal plane. This allows determination of where in three-dimensional space abnormal electrical activity originates. It allows localization of myocardial infarcts or scars and other pathology like hypertrophy or chamber enlargement.

Limb Leads

Limb leads are placed on the left arm/shoulder, right arm/shoulder, and left leg/hip. Bipolar leads are generated using both ends of the poles. From right arm to left arm is lead I, from right arm to left leg is lead II, and from left arm to left leg is lead III.

Augmented leads are unipolar, derived from the Wilson Central Terminal, an imaginary point in the middle of the body with zero potential. By reorienting vectors from leads I, II, III, and the augmented leads through a central point, a Cartesian plane is created. Einthoven's triangle divides the heart into 12 segments.

Chest Leads

Chest leads are unipolar. V1 is at the right sternal edge, V2 at the left sternal edge, around to the apex or axilla for V6.

Myocardial Ischemia and Infarct

The clinical history of chest pain is vital. The absence of chest pain often negates the possibility of myocardial ischemia. Typical chest pain is central, crushing, and tight, radiating to the jaw or arm, described as vice-like or like an elephant sitting on the chest, with sweating and shortness of breath. However, variations exist. Biomarkers like troponin and creatine kinase rise and fall in myocardial infarcts.

ECG changes are vital and sometimes diagnostic. Imaging like CT coronary angiography or coronary angiography may support a diagnosis.

Coronary Artery Anatomy

The right coronary artery (RCA) supplies the right ventricle and the inferior portion of the heart. The left main coronary artery bifurcates into the circumflex artery (supplying the lateral wall) and the left anterior descending (LAD) artery, which supplies most of the anterior myocardium and the apex.

Pathophysiology of Myocardial Ischemia

Myocardial ischemia results from an imbalance between oxygen supply (blood flow delivery) and oxygen demand (metabolic requirements). It is potentially reversible if this mismatch is rebalanced.

Relative imbalance occurs when increased oxygen demand (e.g., exercise) and narrowed coronary artery due to stenosis don't cause a problem under normal conditions but cause ischemia when demand increases.

Absolute imbalance occurs when there's normal oxygen demand but severely reduced supply due to pinhole narrowing or complete occlusion.

Factors regulating myocardial oxygen supply include oxygen-carrying content of blood and coronary blood flow. Factors regulating oxygen demand include heart rate, contractility, and wall stress.

Wall stress = rac{Pressure imes Radius}{Wall thickness}

Left ventricular hypertrophy is a compensatory mechanism to reduce wall stress by increasing wall thickness.

Changes After Coronary Occlusion

After coronary occlusion, subcellular changes (ATP reduction, acidosis) occur first, then affect contractility and relaxation. Heart pressures fill up, affecting wall stress, and ECG changes are seen on the surface.

Consequences of Prolonged Ischemia

Ischemia can lead to:

  • Reversible ischemia: No persistent damage.
  • Injury: prolonged or repetitive ischemia causing subcellular changes without cell death, leading to stunning (reduced myocardial function) or preconditioning (adaptation to resist future injury).
  • Infarction: Cell death or necrosis, with the degree and size dependent on blood vessel size, collaterals, duration of ischemia, and metabolic demands.

Occluded Coronary Artery

Sustained ischemia can lead to a zone of necrosis. The endocardium is the first area at risk due to being farthest from the supplying coronary artery. This results in endocardial ischemia, then infarction, before becoming transmural. Time is muscle. Restore blood flow as quickly as possible.

Other blood flow disturbances include:

  • Plaque rupture with thrombus.
  • Vasospasm or endothelial dysfunction.
  • Gradual atherosclerosis leading to critical stenosis.

Diastolic vs Systolic Function in Ischemia

Diastolic function is affected before systolic function in ischemia due to the myofibrillar apparatus and cross-bridges, and relaxation properties being more sensitive to changes in ATP.

Ischemic Discomfort

Supply-demand imbalance without acute thrombosis can occur. Small thrombi can form due to plaque rupture, traveling to smaller vessels causing pain. Complete vessel occlusion due to plaque rupture and thrombosis can lead to ST elevation on an ECG.

ECG Patterns in Subendocardial Ischemia or Infarction

Unstable angina pectoris (UAP) and non-ST elevation MI (NSTEMI) are types of acute coronary syndromes (ACS) due to subendocardial or non-transmural ischemia or infarction.

Ischemia usually affects the subendocardial region first. An NSTEMI involves seeing an enzyme leak. ST depression or T wave inversion may be observed. Weeks later, findings tend to normalize, and pathological Q waves are not typically seen.

ST Depression

ST depression is a characteristic of acute subendocardial ischemia, seen in demand ischemia and used for stress testing. It is defined as a horizontal or downsloping depression in the ST segment of more than half a millimeter in two contiguous leads. Leads V1 and V2, V5 and V6, or leads II, III, and AVF are contiguous.

ECG Changes in Established Subendocardial Infarct

In an established subendocardial infarct: T wave inversion may persist. ST segments tend to normalize. No pathological Q wave is present. Persistent R waves may be reduced. After weeks or months, the necrotic area becomes fibrotic, and ST and T wave changes resolve, although not always.

Case 1: 72-year-old Male

72-year-old male with type 2 diabetes and hypertension presents with a three-hour history of on-and-off central chest tightness. ECG shows sinus rhythm with T wave inversion in leads I, AVL, V4, V5, and V6. The clinical history of chest pain is concerning. Until troponin levels are seen, it is not known if this is just angina or an infarct. The ST and T wave changes are generally non-localizing.

Case 2: 55-year-old Female

55-year-old female, active smoker, presents with central chest tightness lasting 50 minutes radiating to the left arm. ECG shows sinus rhythm with ST segment depression, particularly in lead II, V4, and V6, with some ST elevation in AVR and V1/V2. The ST depression is widespread, and it is not specified which region of the heart is affected. The clinical context is worrying, and the patient should be triaged and treated appropriately.

T wave inversion is non-specific to ischemia because it can be seen in almost any pathology of the heart affecting the myocardium. In this context, it's abnormal. So it is not diagnostic of a heart attack.

ST Elevation Myocardial Infarct (STEMI)

ECG changes occur with complete coronary occlusion, causing transmural ischemia or infarction.

Definition of ST Segment Elevation

The initial onset of a Q wave serves as a reference point. If there is no Q wave, the inflection point that initiates the R wave is used. The J point (the point after the Q-wave flexion) is compared to the isoelectric line.

During STEMI, pathology involves occluding a large coronary vessel supplying a large area of myocardium, causing necrosis from subendocardium to epicardium. This can affect a large area of heart muscle. Acute and evolving ECG changes can be observed, but they don't necessarily occur, and it depends on when the ECG is performed.

Early on (minutes), there is quickly upsloping ST elevation. Over time (hours), the ST elevation flattens, and the amplitude of the R waves decreases. A pathological Q wave may be seen, along with deep T-wave inversion. Days later, ST segments may normalize, and T waves may remain inverted. Later, everything may resolve with the exception of the pathological Q waves.

The evolution involves changes from ischemia to infarction. Within a couple of days, when there has been transmural necrosis, T wave inversion may begin, ST elevation will decrease, and a significant Q wave is present. Over time, fibrosis and remodeling can develop, with persistent ST elevation. If there is occlusion, there will be ST elevation or hyperacute T waves to start with. If there is no occlusion, there may be ST depression or T wave inversion, and potentially there may be nothing seen at all.

Localizing the Problem

The location of ST elevation on a surface ECG indicates the affected part of the heart and potentially the affected coronary artery. Note that the ECG alone is not diagnostic. Other pathologies can cause ST elevation. Patient history, risk factors, and biomarkers should all be considered.

How ECG Leads Help Localize Myocardial Injury

The limb leads (vertical plane) and augmented limb leads at the shoulders and inferiorly generate Einthoven's Triangle. The chest leads provide different information about the axis.

V5 and V6 give us the closest window to cellular necrosis (anterolateral). the key is that the ECG leads that are looking most directly at the region of interest in parallel, remember at the beginning I talked about the action potential and positive negative deflections, you'll get the most deflection if you're looking directly towards or directly away from where the depolarization is occurring.

ECG Leads and Cardiac Anatomic Regions

  • Anterior/Septal Regions: V1 to V4 (anteroseptal leads in blue)
  • Anteroapical Leads: V3/V4
  • Lateral: V5/V6 (anterolateral). Changes will be seen on the limb leads I and AVL
  • Inferior: Leads II, III, and AVF. V5 and V6 do not show ST elevation when the bottom of the heart is affected, so there won't necessarily be changes on the anterior leads. note, inferior/posterior aspects of the heart demonstrate ST elevation

Posterior Leads

Posterior leads (V7 and V8 - placed on the back) provide an inverted version of the anterior leads on the posterior aspect. Marked ST depression in V1 and V2 suggests ST elevation on V7 and V8, indicating a posterior infarct.

Coronary Artery Supply

  • Anterior: Left Anterior Descending Artery (LAD)
  • Lateral : Circumflex Artery
  • Posterior/Inferior : Right Coronary Artery (RCA) or PDA (Posterior Descending Artery)

STEMI 1

Leads II, III, and AVF demonstrate strong ST elevation with tombstoning. The RCA supplies the territory. Reciprocal depression in Leads I and AVL.

STEMI 2

Leads V2, V3, V4, and V5 have abnormalities. There are no R waves. The LAD artery is the likely culprit. There is also a very low voltage. The rhythm strip has an early beat with a broad complex.

STEMI 3

Lead II is positive. The amplitude has reduced. Ventricular ectopic beat. Effectively V1 to V5 demonstrate ST elevation. Demonstrate Q waves here in V2 to V6 and effective lack of R wave.

STEMI 4

Lead I is negative. Anteroapical instead of anteroseptile. Multi vessel disease but LAD is still blocked.

STEMI 5

There is more than 2 mL elevation, but the most notable is in AVL and Lead 1, demonstrating lateral. V6 and V5 are not demonstrating any majorly obvious ST elevation. Occluded circumflex vessel that supplies the lateral wall.

STEMI Criteria

Contiguous Leads - adjacent leads look at adjacent regions or the same region

  • Anterior - V2 or V3 - more than 2 mL in men younger than 40, 1.5 in women, and with other leads being more than 1mL
  • Reciprocal Change from the Leads should be checked on the anteriorly facing leads.
  • Left Bundle Branch Block - can fit in STEMI, especially if the patient has chest pain along with this block.
  • Prior ECG - always good to be looked over, as comparing it to previous scans can make or break the interpretation for patients that don't seek out help until much later.

Other Causes of ST Elevation

Reasons that may cause ST elevation include, but are not limited to:

  • History
  • Risk Factors
  • Biomarkers (STEMI still must be treated right away)
  • Benign Early Repolarization
  • Ventricular Hypertrophy
  • Aneurysm
  • Electrolyte Abnormalities
  • Cardiomyopathy
  • Brugada Syndrome

In cases, as well, as Pericarditis, there will be ST segments effectively going across all the leads. This being due to all types of inflammation of the lining of the heart rather than necessarily in a region.

Coronary Thrombosis/Fixed Stenosis Without Thrombosis

  • Coronary Thrombosis (STEMI) - large vessel is occluded and prolonged with ischemia - ST elevation and Q waves are seen + biomarkers
  • Coronary Thrombosis with (NSTEMI) - ST depression with T wave inversion = biomarker test is proven to be positive / if it is not proven to be STEMI then this is proven to be stable OR unstable angina . Unstable is a partial thrombus, and stable if symptoms do not worsen.
  • Fixed Non-Obstructive Stenosis / Symptoms - these would likely have no symptoms/ ECG changes, and could even sometimes heal.

Important diagnostic notes

The IMPORTANT ones are ST elevation in STEMI and often Q waves with this. - The site of Injury must be noted based on ECG leads - There are a lot of different things that may cause/ or appear to be similar in the ECG.

Membrane Potential + ST Segment Changes

Changes in membrane will create current on the surface depending on direction of the depolarization. Resting membrane potential will mean how the single myocyte at rest and has potentially different intracellular/extracellular space by ion channels - it is maintained negatively to the outside but a 90 mV of difference.

With Depolarisation - the changes will have membrane potential and will have the inside less negative - therefore current goes negative - positive.

To illustrate how to explain ST changes. Normal resting myocyte, the resting membrane potential is 90mv by extracellular vs fluid. The net change will see it positively.
What if the cell has injury? Will get leakages and pumps. The membrane will have less - negative insides vs outsides.
Normal change - Action potential of electrical systole. Will result in Ischemic cardiomyopathy + reduced resting membrane - action will be small -
This cell injured or harmed on normal

In this case: Cell has injury. The extra cellular space has the charged negative against normal . In electrical diastole this will produce current as well as a negative reflection. And rather than just being a normal ST segment. This compensation will result in the ST Elevation.

Systole vs Diastole

Systole will show strong current toward the injured / ST is already elevated. Diastole current must move to resting cell.
Injured is negative, Normal is Positive.

Cardiac Cell Status

Normal = more + outside than the insides; injured is less minus inside vs the outside RELATIVELY outside

Rather than DIA theory, but the electrical force systolic pushed everything up in the ST Theory.

Q Wave Meaning

An ECG shows normal wave + pathological - This could result from myocardial damage + or myocardial infarct. In the end - inert inactive and this one is not good. 1/3 more than R waves - there is significant damage and these become bad

Necrotic muscle. But no depolarisation and propagated through septal and is always directed toward the way to left to a point, so will produce what is normal with Q - but in a high infarct - the right still is moving but very little electrical with it. So still will see negative with this!

In addition - the necrotic areas. So in very large areas can start to create a window where it allows better view across that window - allowing stronger more dominant to produce positive as R Wave with electricals on the opposite.

Vector Activity

A vector is just directional from the point spread across hearts and is more directional for one to be high to the other side and to be diminished. Think frontal limbs can be used to know any of these is useful - chest will have almost anything + will require math and time in between to focus too much for the point.

A vector can easily change. If the conduction is not one side or parts or both or the muscle increased. Normal axis, positive = to QRS and the electrical will move. Remember P wave is not a vector, P wave demonstrates atrial depolarisation.

So for the Axis.

RATE then RHYTHM then focus in complexes and the rest.

Normal = anything from positive, 90* to -30 degrees
To be normal - look only at 2 or 3 leads for focus - 2 MUST be positive. It will lead negative direction in direction with heart!
Remember 6 lead limbs. If positive, + normal leads there needs to be a - on one that runs negatively towards the end to provide direction!
When 2 is done positive and both are at the + side vs one not - 2 will generally always show high amplitudes.

In left, lead 1 can be be positive and lead 2 positive then its extremely to the left/ shifted! Look at AVL - if lead is positive AVF will be negatively.
Right Axis: opposite of vector if not, and both have + values - the leads that will change are commonly the - ones.

Case : Rate around 100. And variable. Atrial activity but no normal p + no regular! That, with a slightly left deviation that lead 1 is positive vs AVF is negative.

Hypertrophy

Increased muscle (hypertrophy) = increase the amplitude for complexes to depolarise. 5 waves are higher there will also be + in V4-V6 as right values. Look SV1++5 is >35mm then diagnosis can be LVH. Another isolation/11mm example in AVL with this.
For more massive - Cardiac MRI. BUT more likely show something like HCM 11 11
For right more high from right chest that is 1 + V and like from -1 and lead should increase that amplitude + high