CVPR 03-31-14 10-11am Introduction to the ECG - Horwitz Flashcards Preview

CVPR Unit 1 > CVPR 03-31-14 10-11am Introduction to the ECG - Horwitz > Flashcards

Flashcards in CVPR 03-31-14 10-11am Introduction to the ECG - Horwitz Deck (46):

Cardiac Conduction System

Sinoatrial (SA) node is normally the heart’s pacemaker ---> Electrical impulses initiated there proceed through internodal tracts ---> activate wave of depolarization in the atrium that converges on the atrioventricular (AV) node ---> brief delay ---> impulses rapidly flow through the Bundle of His & activate the ventricles through the right & left bundles ---> impulses then diverge into Purkinje fibers ---> activate ventricular myocardial cell depolarization & contraction.


ECG – different waves & causes

[SA node firing unseen on ECG] 1. P wave = initial deflection, due to atrial depolarization….. 2. QRS = next deflection, due to ventricular depolarization; Q is negative, R is positive, & S is a late negative deflection; One, two, or all of these deflections may be present in a given lead; Normal duration of QRS is 0.06-0.10 seconds…… 3. T wave = due to ventricular repolarization….. 4. U waves = inconstant


ECG – paper, lines

Paper speed is 25 mm/second….. Thin vertical lines (small squares) are 0.04 seconds apart ….. Thick vertical lines (large squares) are 0.2 seconds apart


ECG – PR interval

PR interval = from onset of P wave to onset of QRS = a measure of AV node conduction time, since most of the interval reflects delay in traversing the node (the “pause”)…..Normal PR interval = 0.12-0.20 seconds


ECG – QT interval

QT interval = represents total duration of depolarization & repolarization


Heart Rate on ECG

Paper speed = 25mm/sec….. Light lines (1mm) = 0.04 s….. Heavy lines (5mm) = 0.2 s….. HR = 300 / # of heavy lines between QRS’s….. OR….. HR = 1500 / # mm between QRS’s


EKG leads

Electrodes which measure the difference in electrical potential between either: 1. Two different points on the body (bipolar leads)….. 2. One point on the body and a virtual reference point w/zero electrical potential, located in the center of the heart (unipolar leads)



Left ventricle is the dominant determinant of the depolarization direction of the ventricles….. Depolarization moving toward an electrode produces a positive deflection (electrode sitting next to the apex of the heart, for example)….. QRS will be upright (+) in left and lateral leads (near left ventricle) & downward (-) in right-sided leads (area in opposite to left ventricle)


Summary of leads

Bipolar limb leads = I, II, III (standard limb leads…both arms & left leg)…. Unipolar limb leads = aVR, aVL, aVF (augmented limb leads; both arms & left leg)….. Unipolar Precordial leads = V1-V6 (on chest wall)


Lead 1 - polarity

= positive in left arm, negative in rt arm


Lead II - polarity

+ lt food, - left arm


Lead III - polarity

- sort of perpendicular to direction of depolarization --- predominantly + in left foot, +in lt arm


AVF - polarity

positive (toward left food)


AVL - polarity

Everything’s away from AVR (typically all are negative


AVR - polarity

negative in all direction


Precordial leads - names & placements

V1 (rt of sternum, near SA node)…V2 (rt side of heart)…. V3/4/5/6 (left ventricle)


Limb leads reflecting lateral wall changes

“Lateral leads” = I and AVL (high lateral leads)


Limb leads reflecting inferior wall changes

“Inferior elads” = II, III, AVF


Right chest leads

V1 & V2 = moniter the RV as well as ventricular septum


Left chest leads

V5 & V6 = monitor the LV


Ventricular hypertrophy & ECG

More muscle (bigger size of cells) = more volts = great amplitude


Left ventricular hypertrophy on ECG

Big + R waves in Left-sided leads (I & aVL (lateral leads), V5 & V6 (left-sided precordial leads)


Right ventricular hypertrophy on ECG

Big + R waves in right-sided leads (V1, V2 (right-sided precordial leads)) – usually see no/diminutive R wave from right-sided leads


Ischemia – when it occurs

Occurs when body supply is insufficient to meet oxygen demand in the ventricles


Ischemic changes in EKG

Alter ventricular repolarization and affect the ST segment and the T wave…. Ischemia due to SUDDEN HIGH oxygen demand (exercise, etc.) in the presence of fixed coronary obstruction causes depression of the ST segment…. Ischemia due to acute coronary artery obstruction during LOW oxygen demand (when you’re just sitting around) causes T wave inversion (becomes negative when it should have been positive in that lead)


ST depression - cause

Ischemia due to sudden HIGH oxygen (exercise/stress test) demand in the presence of fixed coronary obstruction (plaques in coronary vessels, for example) = Increased oxygen consumption w/inability to increase coronary flow appropriately [ECG on slide 17]


T wave inversion - cause

Ischemia due to acute coronary artery obstruction during LOW oxygen demand = ischemia due to decrease coronary flow w/out increased oxygen consumptions [ECG on slide 18]


ST elevation - cause

ST segment and actual T wave are almost the same height = A sign of transmural injury in acute coronary syndrome, usually with a clot due to platelet aggregation obstructing the coronary artery (transmural ischemia)…. Most commonly, injury is associated w/acute MI….. If obstructed artery is quickly opened w/angioplasty or thrombotic agent, ST elevation may partially/entirely reverse w/much (rarely all) injury avoided


Necrosis after infarct – effect on ECG

Q waves appear or become more substantial in size


Q wave – meaning

Very small Q waves may not be pathological, but generally the development of a sizable Q wave is due to transmural NECROSIS


Q wave - location

Infarcts usually involve only the left ventricle; when Q waves develop in leads which would normally be positive, they give info on localization of the infart: 1. Q waves in INFERIOR leads (II, III, aVF) are due to INFERIOR infarcts….. 2. Q waves in leads V1-V4 are due to anterior wall infarcts….. Leads I, aVL and the anterolateral leads (V5, V6) are associated with lateral wall infarcts


Determining if a Q wave is “significant”

1. Greater than/equal to 1/4 the R wave amplitude…. 2. Greater than/equal to one small box wide (0.04 s)….. 3. Seen in at least 2 leads reflecting same region of the left ventricle (otherwise may be some sort of artifact or something)


Transmural Myocardial Infarct – Stages of its Evolution on ECG

Typically, a transmural acute MI evolves over time … First, would see Giant, upright “hyperacute” T waves, but rarely seen b/c often lasts only a few minutes…… Next stage: T wave inverts (“ischemia w/out injury”) and ST segments elevates (“current of injury”) --- ST elevation may occur simultaneously w/ OR after T inversion….. Final stage: All together, Q wave develops (typically last thing seen), ST elevates, and T wave inverts


Transmural infarcts vs. Subendocardial infarcts

Transmural = Involve full thickness of left ventricular wall & tend to be large ---> ST elevation w/Q waves…… Smaller infarcts may be localized to inner layer of left ventricular wall (subendocardium) ST depression w/out Q wave


Subendocardial infarcts – ECG findings

NO Q waves or ST elevation….Rather, persistent ST depression…..While ST depression may reflect transient ischemia w/out necrosis, ST depression lasting 2-3 days probably reflects a subendocardial infarct.


Anterior vs. Inferior infarct location from leads

V1-2 = anteroseptal wall infarct….. V3-4 = anterior wall infarct….. V5-6 = anterolateral wall infarct ….. II, III, Avf, = inferior wall infarct ….. I, aVL = high lateral wall infarct


QT interval & Arrhythmias

When QT interval is altered, susceptibilities to arrhythmias increase….. Especially likely w/QT prolongation…..Congenital QT prolongation syndromes are associated w/serious, sometimes fatal arrhythmias; More common are QT prolongations acquired due to electrolyte abnormalities or drugs….. A QT depends on heart rate, but the rule of thumb (compared to RR interval) here is easier to remember than specific time intervals


Prolonged QT interval – rule of thumb defn.

Prolonged if QT interval is more than 1/2 the RR interval


Prolonged QT interval – causes

Causes: HYPO-calcemia/kalemia/magnesia; Class 1A or 3 anti-arrhythmic drugs; Hypothermia; Congenital Long QT syndrome


Calcium levels & Arrhythmias

Both hypercalemia & hypocalcemia can predispose to arrhythmias…… HYPERcalcemia shortens the QT interval; The commonest cause is hyperparathyroidism…… HYPOcalcemia lengthens the QT interval, is more commonly encountered, has many causes, and may be associated with life threatening ventricular arrhythmias


Hypokalemia – causes

Extremely common; A common cause of arrhythmias <--- Overuse of diuretics, vomiting, and diarrhea are most common causes; Alkalosis, K+-losing nephropathies, and excess aldosterone are among other causes


Hypokalemia on ECG

T waves are flattened & possibly inverted…..also, QT interval is generally prolonged, prominent U waves are frequent ….. ECG changes are not specific and serum K+ levels should be checked to confirm the Dx.


Hyperkalemia & Arrhythmias

Distinctive changes are induced by EXCESS K+, depending on level of elevation of K+


Mild hyperkalemia on ECG

At slightly elevated K+ levels (normal is 3.5-5.0 mml/L…. this elevation would be between 5.5-7.5mmol/L)….. Increased T wave voltages with a distinctive peaked, symmetrical appearance


Moderate hyperkalemia

At higher K+ levels (7.5-9.0 mmol/L), P & R waves may flatten…. QRS & T waves widen…… A broad S wave often appears


Severe hyperkalemia

At very high levels, a sinusoidal pattern appears (P & R waves gone; S & T waves broaden)…… Renal failure is the commonest cause…… If unrecognized hyperkalemia often causes fatal arrhythmias.

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