Flashcards in Chapter 268 - Electrocardiography Deck (74):
"ECG leads actually display the instantaneous differences in potential between the electrodes."
True or False?
What is the clinical utility of electrocardiogram (ECG)? Name the main conditions that might be diagnosed using this test.
"The clinical utility of the ECG derives from its immediate availability as a noninvasive, inexpensive, and highly versatile test. In addition to its use in detecting arrhythmias, conduction disturbances, and myocardial ischemia, electrocardiography may reveal findings related to life-threatening metabolic disturbances (e.g., hyperkalemia) or increased susceptibility to sudden cardiac death (e.g., QT prolongation syndromes)."
The ECG only records the depolarization (stimulation) and repolarization (recovery) potentialts generated by the "working" atrial and ventricular myocardium.
True or False?
What is the characteristic feature of sinoatrial cells that explain why they are the main pacemaker cells of the heart?
In comparison to other cells with this feature, sinoatrial cells have the quickest automaticity and, therefore, they are responsible for heart rhythm in physiological conditions.
Explain the normal depolarization wavefront of the heart.
"The first phase of cardiac electrical activation is the spread of the depolarization wave through the right and left atria, followed by atrial contraction. Next, the impulse stimulates pacemaker and specialized conduction tissues in the atrioventricular (AV) nodal and His-bundle areas; together, these two regions constitute the AV junction. The bundle of His bifurcates into two main branches, the right and left bundles, which rapidly transmit depolarization wavefronts to the right and left ventricular myocardium by way of Purkinje fibers. The main left bundle bifurcates into two primary subdivions: a left anterior fascicle and a left posterior fascicle. The depolarization wavefronts then spread through the ventricular wall, from endocardium to epicardium, triggering ventricular contraction."
How does one explain the inherent limitations of ECG sensitivity and specificity?
"The ECG records the complex spatial and temporal summation of electrical potnetials from multiple myocardial fibers conducted to the surface of the body. This principle accounts for inherent limitations in both ECG sensitivity (activity from certain cardiac regions may be canceled out or may be too weak to be recorded) and specificity (the same vectorial sum can result from either a selective gain or a loss of forces in opposite directions)."
What is J point in ECG?
J point corresponds to the junction of QRS with the beginning of ST-segment.
How do you identifiy atrial repolarization in ECG?
"Atrial repolarization (STa and Ta) is usually too low in amplitude to be detected, but it may become apparent in conditions such as acute pericarditis and atrial infarction."
Explain the correlation between the action potential of a single myocardial fiber and the ECG wavefront.
"The QRS-T waveforms of the surface ECG correspond in a general way with the different pahses of simultaneously obtained ventricular action potentials, the intracellular recordings from single myocardial fibers. The rapid upstroke (phase 0) of the action potential corresponds to the onset of QRS. The plateau (phase 2) corresponds to the isoelectric ST segment, and active repolarization (phase 3) corresponds to the inscription of the T-wave."
Explain the different phases of myocardial cell depolarization as well as the different factors that might impair the normal duration of these phases. Also, explain the correlation between these factors and the alterations in the ECG.
"Factors that decrease the slope of phase 0 [rapid upstroke] by impairing the influx of Na+ (e.g., hyperkalemia and drugs such as flecainide) tend to increase QRS duration. Conditions that prolong phase 2 [plateau] (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."
How can one radiply ascertain the heart rhythm by looking at an ECG?
"The heart rate (beats per minute) can be computed readily from the interbeat (RR) interval by dividing the number of large (0,20s) time units between consecutive R waves into 300 or the number of small (0,04s) units into 1500."
What are the normal times for the following intervals: (i) PR segment; (ii) QRS complex; (iii) QTc interval.
(ii) Less than 100-110ms
(iii) Equal or less than 0,44s "(Some refences give QT upeer normal limits as 0,43s in men and 0,45s in women. Also, a number of different formulas have been proposed, without consensus, for calculating the QTc.)"
How do you calculate "corrected" QT? Therefore, what is the relation between QT interval and heart rate?
"The QT interval includes both ventricular depolarization and repolarization times and varies inversely with heart rate. A rate-related ("corrected") QT interval, QTc, can be calculated as QT/√RR"
The limb leads record potentials transmitted onto the frontal plane, and the chest leads record potentials transmitted onto the horizontal plane.
True or False?
Where should one place the precordial leads for body surface ECG?
"lead V1, fourth intercostal space, just to the right of the sternum; lead V2, fourth intercostal space, just to the left of the sternum; lead V3, midway between V2 and V4; lead V4, midclavicular line, fifth intercostal space; lead V5, anterior axillary line, same level as V4; and lead V6, midaxillary line, same level as V4 and V5. Additional posterior leads are sometimes placed on the same horizontal place as V4 to facilitate detection of acute posterolateral infarction (V7, midaxillary line; V8 posterior axillary line; and V9, posterior scapular line)."
V7-V9 leads and V3R/V4R have the same significance for ECG interpretation.
True or False?
V7-V9 are used to identify acute posterolateral myocardial infarction (of the left ventricle), while V3R/V4R are used to identify acute right ventricular ischemia.
What are the characteristic of the normal P-wave on ECG? Which signs would you look for if you suspect an ectopic pacemaker rhythm?
"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 O wave in lead V1 may be biphasic with a positive component reflecting right atrial depolarization, followed by a small (less than 1 mm2) negative component
reflecting left atrial depolarization."
How does one explain the normal QRS in leads V1 and V6 regarding the two phases of myocardial depolarization?
"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 large negative deflection (S wave). A left precordial lead, e.g., V6, will record the same sequence with a small negative deflection (septal q wave) followed by a relatively tall positive deflection (R wave)."
Define normal R-wave progression and transition zone concepts.
"Intermediate leads show a relative increase in R-wave amplitude (normal R-wave progression) and a decrease in S-wave amplitude progressing across the chest from right to left. The precordial lead where the R and S waves are of approximately equal amplitude is referred to as the transition zone (usually V3 or V4)."
What is the normal QRS axis range?
-30º to +100º
Name the causes for left axis deviation.
"[it] may occur as a normal variant but is more commonly associated with left ventricular hypertrophy, a block in the anterior fascicle of the left bundle system (left anterior fascicular block or hemiblock), or inferior myocardial infarction."
Name the causes of right axis deviation.
"Right axis deviation also may occur as normal variant (particularly in children and young adults), as a spurious finding due to reversal of the left and right arm electrodes, or in conditions such as right ventricular overload (acute or chronic), infarction of the lateral wall of the left ventricle, dextrocardia, left pneumothorax, and left posterior fascicular block."
What is the normal polarity of the T-wave and U-wave? Explain the electrophysiology of T-wave.
"Normally, the mean T-wave vector is oriented roughly concordant with the mean QRS vector (within about 45º 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 (equal or less than 1mm) that follows the T wave and usually has the same polarity as the T wave."
Which conditions might be associated with an abnormal U-wave? What are the risks associated with this abrnomality?
"An abnormal increase in U-wave amplitude is most commonly due to drugs (e.g., dofetilide, amiodarone, sotalol, quinidine) 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."
Explain the pathophysiology of pathological P-waves on ECG. Apply the terms "P-pulmonale" and "P-mitrale" to this explanation.
"Right atrial overload (acute or chronic) may lead to an increase in P-wave amplitude (≥2,5mm), sometimes referred to as "P-pulmonale". Left atrial overload typically produces a biphasic P wave in V1 with a broad negative component or a broad (≥120msw), often notched P wave in one or more limb leads. This pattern, previously referred to as P-mitrale", may also occur with left atrial conduction delays in the absence of actual atrial enlargement, leading to the more general designation of left atrial abnormality."
What are the indicators of right ventricular hypertrophy/overload?
"Right ventricular hypertrophy due to a sustained, severe pressure load (e.g., due to tight pulmonic valve stenosis or certain pulmonary artery hypertension sydnromes) 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-midprecodial 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, is commonly associated with an incomplete or complete right bundle branch block pattern with a rightward QRS axis."
What is the characteristic ECG of acute cor pulmonale due to pulmonary embolism?
None is characteristic, although many features might be indicative.
"Acute cor pulmonale due to pulmonary embolism, for example, may be associated with a normal ECG or a variety of abnormalities. Sinus tachycardia is the most common arrhythmia, although other tachyarrhythmias, such as atrial fibrillation or flutter, may occur. The QRS axis may shift to the right, sometimes in concert with the so-called S1Q3T3 pattern (prominence of the S-wave in lead I and the Q wave in lead III, with T-wave inversion in lead III). Acute right ventricular dilation also may be associated with slow R-wave progression and ST-T abnormalities in V1 to V4 simulating acute anterior infarction. A right ventricular conduction disturbance may appear."
Chronic cor pulmonale is associated with tall R-waves in the right precordial leads.
True or False?
"Chronic cor pulmonale due to obstructive lung disease usually does not produce the classic ECG patterns of right ventricular hypertrophy noted above. Instead of tal right precordial R waves, chronic lung disease more typically is associated with small R waves in right-to-midprecordial leads (slow R-wave progression) due in part to downward displacement of the diaphragm and the heart. Low-voltage complexes are commonly present, owing to hyperaeration of the lungs."
Name two groups of patients in which ECG has a lower sensitivity for detecting left ventricular hypertrophy.
Obese and smokers.
Left ventricular hypertrophy is a major noninvasive marker of increased risk of cardiovascular morbidity and mortality rates, including sudden cardiac death.
True or False?
How does one differentiate incomplete from complete bundle branch block?
"With complete bundle branch blocks, the QRS interval is ≥120ms in duration; with incomplete blocks, the QRS interval is between 100 and 120ms."
What are the typical ECG patterns of both left and right complete bundle branch blocks?
"with right bundle branch block, the terminal QRS vector is oriented to the right and anteriorly (rSR' in V1 and qRS in V6, typically). Left bundle branch block alters both early and late phases of ventricular depolarization. The major QRS vector is directed to the left and posteriorly. In addition, the normal early left-to-right pattern of septal activation is disrupted such that septal depolarization proceeds from right to left as well. As a result, left bundle branch block generates wide, predominantly negative (QS) complexes in lead V1 and entirely positive (R) complexes in lead V6. A pattern identical to that of left bundle branch block, preceded by a sharp spike, is seen in most cases of electronic right ventricular pacing because of the relative delay in left ventricular activation."
Which type of block is more frequent in the subset of patients with both a bundle branch block and no structural heart disease?
Right bundle branch block.
Name the most frequent conditions associated with left bundle branch block. Does its presence have prognostic significance?
"Left bundle branch block is often a marker of one of four underlying conditions associated with increased risk of cardiovascular morbidity and mortality rates: coronary heart disease (frequently with impaired left ventricular function), hypertensive heart diease, aortic valve disease, and cardiomyopathy."
Bundle branch blocks might be chronic or intermitent as wel as rate-related.
True or False?
What is the correlation between T-wave and QRS polarity in bundle branch block?
T-wave is usually inverse in polarity in comparison to the last wave of the QRS.
What is the pathophysiology of QRS-T discordance in primary and secondary repolarization abnormalities?
"With bundle branch blocks, the T wave is typically opposite in polarity to the last deflection of the QRS. This discordance of the QRS-T wave vectors is caused by the altered sequence of repolarization that occurs secondary to altered depolarization. In contrast, primary repolarization abnormalities are independent of QRS changes and are related instead to actual alterations in the electrical properties of the myocardial fibers themselves (e.g., in the resting membrane potential or actioan potential duration), not just to changes in the sequence of repolarization."
Which ST-T alterations might lead to suspicion of subjacent mycoardial ischemia if one has bundle branch block?
"Primary and secondary T-wave changes may coexist. For example, T-wave inversions in the right precordial leads with left bundle branch block or in the left precordial leads with right bundle branch block may be important markers of underlying ischemia or other abnormalities."
Which type of block does Brugada pattern simulate?
Right bundle branch block.
Fascicular blocks are usually associated with prolongation of the QRS duration as well as a shift in the frontal plane of the QRS axis.
True or False?
False: "Partial blocks (...) generally do not prolong the QRS duration substantially".
True: "[Partial blocks] are assocaited with shifts in the frontal plane QRS axis"
What is the most common cause of leftward shift of the QRS axis in adults?
"Left anterior fascicular block (QRS axis more negative than -45º) is probably the most common cause of marked left axis deviation in adults."
Left posterior fascicular block (QRS axis more rightward than +110-120º) is extremely rare as an isolated finding and requires exclusion of other factors causing right axis deviation.
True or False?
How does one define bifascicular and trifascicular block?=
"Examples of bifascicular block include right bundle branch block and left posterior fascicular block, right bundle branch block with left anterior fascicular block, and complete left bundle branch block."
"Alternation of right and left bundle branch block is a sign of trifascicular disease" which would be defined by left anterior and posterior bundle branch block plus right bundle branch block.
Chronic asymptomatic bifascicular block is associated with an increased risk of progression to high-degree AV heart block.
True or False?
It should be noted that the risk is relatively low.
Name one situation with a high risk of progression of bifascicular block to complete heart block.
New bifascicular block with acute anterior myocardial infarction.
PR prolongation with bifascicular block is always associated with trifascicular block.
True or False?
"the presence of a prolonged PR interval and bifascicular block does not necessarily indicated trifascicular involvement, since this combination may arise with AV node disease and bifascicular block."
Name four factors that slow intraventricular conduction.
Hyperkalemia and drugs (such as class 1 antiarrhythmic agents, tryclic antidepressants and phenotiazines).
Prolongation of the QRS is always indicative of an intraventricular conduction delay.
True or False?
"Prolongation of QRS duration does not necessarily indicate a conduction delay but may be due to preexcitation of the ventricles via a bypass tract, as in Wolff-Parkinson-White patterns and related variants."
What is the characteristic triad for Wolff-Parkinson-White (WPW) diagnosis?
"The diagnostic triad of WPW consists of a wide QRS complex associated with a relatively short PR interval and slurring of the initial part of the QRS (delta wave), with the latter effect being due to aberrant activation of ventricular myocardium."
Is there any consequence due to a bypass tract in Wolff-Parkinson-White (WPW) that is associated with increased morbidity and mortality?
"The presence of a bypass tract predisposes to reentrant supraventricular tachyarrhythmias."
How does one explain ECG alterations due to ischemia and myocardial infarction? Explain the pathophysiology.
"Ischemia exerts complex time-dependent effects on the electrical properties of myocardial cells. Severe, acute ischemia lowers the resting membrane potencial and shortens the duration of the action potential. Such changes cause a voltage gradient between normal and ischemic zones. As a consequence, current flows between those regions. These currents of injury are represented on the surface ECG by deviation of the ST segment. 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 erliest 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 precordal) leads show ST-segment depression (with ST elevation in lead aVR)."
Profound ST elevation or depression in multiple leads usually indicates very severe ischemia.
True or False?
What are the leads indicative of the following: (i) acute anterior transmural ischemia; (ii) "posterior" wall ischemia; (iii) inferior wall ischemia; (iv) right ventricular wall ischemia.
(i) V1-V6 and D-I, aVL
(ii) V1-V3 ("reciprocal" ST depressions which should be interpreted as an ST elevation "equivalent" acute coronary syndrome)
(iii) D-II, D-III and aVF
(iv) Right precordial leads (V3R/V4R)
Name three situations associated with reversible transmural ischemia.
Prinzmetal's variant angina, possibly Takotsubo cardiomyopathy syndrome and very early reperfusion in acute coronary syndrome.
How does one define pseudonormalization?
"patients whose baseline ECG already shows abnormal T-wave inversions may develop T-wave normalization (pseudonormalization) during episodes of acute transmural ischemia."
Patients with ischemic hcest pain who present with deep T-wave inversions in multiple precordial leads (e.g., V1-V4, I and aVL) with or without cardiac enzyme elevations typically have severe obstruction in the left anterior descending coronary artery system.
True or False?
A subendocardial infarction is always a "non-Q-wave" infarct, while transmural infarction is usually a "Q-wave" infarction.
True or False?
"Previously, abnormal Q waves were considered markers of transmural myocardial infarction, whereas subendocardial infarcts were thorugh not to produce Q waves. However, careful ECG-pathology correlative studies have indicated that transmural infarcts may occur without Q waves and that subendocardial (nontransmural) infarcts sometimes may be associated with Q waves."
Increased R-wave amplitude in V1 and V2 without diagnostic Q waves might be an indicator of previous myocardial infarct.
True or False?
"Loss of depolarization forces due to posterior or lateral infarction may cause reciprocal increases in R-wave amplitudes in leads V1 and V2 without diagnostic Q waves in any of the conventional leads."
What are the ECG abnormalities in atrial infarction?
"Atrial infarction may be associated with PR-segment deviations due to an atrial current of injury, changes in P-wave morphology, or atrial arrhythmias."
Persistent elevation of the ST-segment is indicative of frank ventricular aneurysm following myocardial infarction.
True or Fase?
"St-segment elevations that persist for several weeks or more after a Q-wave infart usually correlate with a severe underlying wall motion disorder (akinetic or dyskinetic zone), although not necessarily a frank ventricular aneurysm."
Normal ECG throughout the course of an acute infarct is distincly uncommon.
True or False?
Which conditions might mask evolving myocardial infarction?
Left bundle branch block, electronic ventricular pacemaker patterns and Wolff-Parkinson-White preexcitation.
Which conditions might lead to ST-segment elevations due to a noncoronary cause?
"ST-segment elevations simulating ischemia may occur with acute pericarditis or myocarditis, as a normal variant (including the typical "early repolarization pattern"), or in a variety of other conditions"
"ST-segment elevations and tall, positive T waves are common findings in leads V1 and V2 in left bundle branch block or left ventricular hypertrophy in the absence of ischemia."
Other ST-segment elevations include: acute pulmonary embolism, Brugada patterns, class 1C antiarrhythmic drugs, DC cardioversion, hypercalcemia, hyperkalemia, hypothermia (J Osborn waves), tumor invading left ventricle and trauma to ventricles.
Which conditions might produce tall T-waves due to a noncoronary event?
"tall, positive T waves do not invariably represent hyperacute ischemic changes but may also be caused by normal variants, hyperkalemia, cerebrovascular injury and left ventricular volume overload due to mitral or aortic regurgitation, among other causes."
What is the differential diagnosis of Q waves?
"The differential diagnosis of Q waves include physiologic or positional variants, ventricular hypertrophy, acute or chronic noncoronary myocardial injury, hypertrophic cardiomyopathy, and ventricular conduction disorders."
Which factors are associated with ST-segment depression other than subendocardial ischemia?
"Digoxin, ventricular hypertrophy, hypokalemia, and a variety of other factors may cause segment depression mimicking subendocardial ischemia."
Which conditions might be associated with T-wave inversions other than ischemia?
"Prominent T-wave inversions may occur with ventricular hypertrophy, cardiomyopathies, myocarditis, and cerebrovascular injury, particularly intracranial bleeds), among many other conditions."
In a patient with progressive hyperkalemia, what is the pathophysiologic sequence of the ECG?
"Hyperkalemia produces a sequence of changes, usually beginning with narrowing and peaking (tenting) of the T waves. Further elevation of extracellular K+ leads to AV conduction disturbances, diminution in P-wave amplitude, and widening of the QRS interval. Severe hyperkalemia eventually causes cardiac arrest with a slow sinusoidal type of mechanism ("sine-wave" pattern) followed by asystole."
A "scooping" of ST-T wave is characteristic of which drug?
Which conditions are assocaited with prominent U waves?
Which conditions are associated with either prolonged or shortened QT interval?
"Prolongation of the QT interval is also seen with increase the duration of the ventricular action potential: class 1A antiarrhythmic agents and related drugs (e.g., quinidine, disopyramide, procainamide, tricyclic antidepressants, phenothiazines) and class III agents (e.g., amiodarone, dofelitide, dronedarone, sotalol, ibutilide). Marked QT prolongation, sometimes with deep, wide T-wave inversions, may occur with intracranial bleeds, particularly subarachnoid hemorrhage ("CVA T-wave" pattern). Hypocalcemia typically prolongs the QT interval (ST portion), whereas hypercalcemia typically shortnes it."
Name the conditions associated with "nonspecific ST-T wave changes", either pathological or physiological.
"Many other are associated with ECG changes, particularly alterations in ventricular repolarization, T-wave flattening, minimal T-wave inversions, or slight ST-segment depression ("nonspecific ST-T wave changes") may occur with a variety of electrolyte and acid-base disturbances, a number of infectious processes, central nervous system disorders, endocrine abnormalities, many drugs, ischemia, hypoxia, and virtually any type of cardiopulmonary abnormality. Although subtle ST-T wave changes may be markers of ischemia, transient nonspecific repolarization changes may also occur after a meal or with postural (orthostatic) change, hyperventilation, or exercise in healthy individuals."
Name conditions associated with low QRS voltage.
Pericardial and pleural effusions, chronic obstructive pulmonary disease, infiltrative cardiomyopathies and anasarca.