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Principles 2 > ECG Arrhythmias > Flashcards

ECG Arrhythmias Flashcards

1
Q

What are some factors that can contribute to ECG changes in the OR?

A

-General Anesthetics: Halothane, Ketamine (remember: Halothane sensitizes myocardium to Epi, causing V Tach)
-Local Anesthetics: Cocaine. Sympathectomy leading to bradyarrhythmias.
-ABGs: Low PaCO2 = lower K+
-Intubation: Most common cause!
-Vagal response: bradycardia and asystole, paroxysmal tachyarrhythmias
-Reflexes: Vagal stimulation, carotid sinus stimulation during jugular venous cannulation
-CNS stimulation: Inc ICP = QT interval and ST segment changes, QT prolongation, ST-segment depression, negative T waves, sinus bradycardia, Osborn wave
-Pre-existing cardiac disease: espec if disease is close to SA/AV Node
-Central Venous Cannulation: arrhythmias can occur as cannula is passed through the RV.

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2
Q

What are Obsorn Waves (J Waves)?

A

Positive deflection at the end of QRS complex in J-point (Junction between QRS and ST segment).
-Prominent Jpoint waves have: amplitude > 2 mm, duration of > 20 ms.
-Also called “Camel-hump sign”
-Usually due to severe hypothermia, hypercalcemia, vasospastic angina (Printzmetal’s), ventricular fibrillation, or brain injuries

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3
Q

What does the presence of an Atrial Premature Contraction indicate?

A

Presence indicates a higher than normal risk in the elderly, in high risk surgeries, or medically /surgically unstable

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4
Q

What are the concerns with Ventricular Premature Contractions?

A

Concerning if lasts for >5 minutes, multifocal, or runs
-R on T phenomenon can occur (can lead to Torsades)
-“Non-sinus rhythm and greater than 5 PVCs on resting EKG were independent predictors of increased perioperative risk after noncardiac surgery”

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5
Q

What are atrial arrhythmias usually associated with?

A

Underlying heart disease.
-Seen in patients with pulm HTN, enlarged R atrium causing stress.

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6
Q

Describe Atrial Fibrillation

A

“irregularly irregular”
-Incidence of Afib in patients undergoing CAB is 20-30%.
-Sustained Afib present in 10% of population over the age of 60.

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7
Q

Describe Atrial Flutter.

A

Depending on rate of conduction from atrium to ventricle, can have a rate of 300 and then 2:1 or 3:1 block. Not all flutter waves are transmitted to the ventricle.
-Occurs with CAD, valvular disease, myocarditis, or longstanding pulmonary dz

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8
Q

Describe the pathway of electrical impulses through the heart.

A

1) SA node (pacemaker of the heart) sends an action potential
2) AP spreads to cardiac myocytes through the internodal atrial pathways
3) AP arrives at AV node. Delay occurs (allows for mechanical to catch up and ensure you have filling of ventricles before they are rapidly depolarized)
4) Then, rapid depolarization of the Bundles and Purkinje fibers occurs.

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9
Q

What is a Mobitz 1 (Wenkebach)?

A

-Pathology at the level of the AV node
-Progressive prolongation of the PRI until an atrial beat is dropped – rarely progresses to CHB

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10
Q

What causes a Mobitz 1 (Wenkebach)?

A

-Inferior MI
-drugs (CCBs, BBs, digitalis)
-increased vagal tone

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11
Q

What is a Mobitz II?

A

-Pathology is infranodal (below the level of the node), in the His-Purkinje system.
-Dropped beats without PRI prolongation
-Normal beat, all of a sudden random p wave, normal beat
-Can progress to CHB

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12
Q

What causes a Mobitz II?

A

-ALWAYS associated with significant CAD
-Calcification of conducting system; anteroseptal MI

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13
Q

What is third degree AV heart block?

A

-No atrial impulses reach the ventricles
-Slower escape rhythm & prolonged QRS (compared to 2nd degree)
-P waves will march out, but are not associated with the QRS.
-Wide QRS
-Cancel case if able
-Have external pacer applied and be ready to pace

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14
Q

What cause 3rd degree AVB?

A

-Inferior or anterior ischemia/infarct

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15
Q

What are the characteristics of a Right Bundle Branch Block (BBB) on ECG?

A

-Prolonged QRS (>0.12 sec)
-RSR’ configuration in leads V1 and V2
-R wave of not blocked; R’ of the blocked bundle
-QRS has double-peaked appearance.
-Then, look at I, V5, and V6. Will see a negative QRS in lead 1, and a widened QRS in V5 and V6.
-A good sign of RBBB is if the S wave has a “slurred” appearance or the end of the wave doesn’t return sharply back up to baseline.

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16
Q

What is a Right BBB?

A

-Delayed activation of the right ventricle
-Conduction defect in the Bundle of His
-Ability to diagnose infarct not affected (Delayed activation of the right ventricle but since initial forces of septal depolarization are not affected: ability to diagnose infarction not affected)
-Usually accompanied by ST depression and T-wave inversion in leads V1-V3

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17
Q

What causes a Right BBB?

A

-Lung disease
-ASDs

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18
Q

Describe normal conduction through the bundle of His?

A

In the absence of BBB, passage of the depolarizing impulse down the His bundle and bundle branches is rapid and activation of the right and left ventricles is simultaneous and synchronous. The individual QRS complexes of the right and the left ventricles superimpose on each other and produce a composite QRS complex that is narrow in width (< 120 ms). In BBB, irrespective of whether it is right or left, activation of the ventricles becomes asynchronous: Depolarization of the ventricle on the blocked side is delayed. This delay causes the individual QRS complex of the blocked ventricle to be wider than normal and appear after the individual QRS complex of the not-blocked ventricle. As a result, the composite QRS complex is > 120 ms wide and has RSR’ waves: the R wave belongs to the individual QRS of the not-blocked ventricle and the R’ wave to the individual QRS of the blocked ventricle.

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19
Q

What is a Left Bundle Branch Block (BBB)?

A

Prolonged QRS with generalized abnormal septal depolarization.
-lose ability to diagnose ischemia and impending infarction
-Usually due to LVH
-May progress to CHB
-Caution with PAC insertion

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20
Q

A pre-existing Left BBB can mask:

A

-ischemia and impending infarction
-Left ventricular hypertrophy

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21
Q

What does a new Left BBB mean?

A

-Consider recent MI
-Needs evaluation

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22
Q

What about if your patient gets a Left BBB under anesthesia?

A

Ominous sign of ischemia and infarction
-Look at hemodynamics, oxygenation. Are they hypotensive?

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23
Q

How do you assess a Left BBB on ECG?

A

-Look first at I, V5, and V6. If the QRS is wide, mostly upright, and the T waves are inverted, it’s LBBB
-Then, look at V1-V3. If QRS complexes are mostly negative, and T waves are upright, then definitely LBBB.

Will also see ST segment and T Wave Discordance (lose ability to see if there are ST segment changes)

24
Q

What is a Bifascicular Block?

A

-RBBB in combination with a block of one of the L branches
-Rare progression to CHB

25
Q

What is a Trifascicular Block?

A

-Bifascicular block (Right BBB and a block of 1 of the branches on the Left) and a prolonged PRI
-Considerable risk of progression to CHB
-Need backup pacing available

26
Q

What does LVH predict?

A

LVH is an independent predictor of perioperative risk after noncardiac surgery
-Strain pattern

27
Q

What will Hyperkalemia do to the ECG?

A

-Tall, peaked T waves
-U Waves

28
Q

What will Hypercalcemia and Hypermagnesemia do to the ECG?

A

Shortened QTc

29
Q

What will Hypocalcemia and Hypomagnesemia do to the ECG?

A

-Prolonged QTc
-Increased incidence of Torsades Des Pointes

30
Q

What can COPD do to the ECG?

A

-Low voltage QRS: distance between electrical activity on the heart and on the surface of the body
-Right Axis Deviation (RAD): if they have pulmonary HTN, RVH
-Poor R wave progression in the precordial leads
-Due to lung hyperinflation and RV enlargement

31
Q

What can a Pulmonary Embolism do to the ECG?

A

-Sudden, massive PE = RBBB, R ventricular strain, ST changes, or A fib.
-Causes prevention of forward flow from R side of the heart, resulting in RV strain and RBBB
-Not very specific or sensitive. Lots going on and may miss ECG changes with sudden, massive PE.

32
Q

What is a Prolonged QT Interval?

A

-QT interval is corrected for HR.
-If a rate corrected QT interval is > 0.44 = increased susceptibility to life-threatening dysrhythmias
-Caused by congenital syndromes (r/t sudden death due to cardiac dysrhythmias), electrolyte abnormalities, medications

33
Q

What is important to know regarding Automated ST segment Analysis?

A

-Low cost, non-invasive, widespread availability
-Sensitivity and specificity (mid 70%) for detecting ischemia
-Anesthetist should periodically examine the criteria of the machine to ensure that measurements are properly placed (can be affected by placement of electrodes/leads due to patient positioning or incision site)

34
Q

What ECG criteria is required to diagnose Ischemia?

A

->1 mm horizontal ST depression (from the J Point)
->1 mm upsloping or downsloping depression (downsloping is typically much worse - indicates increased # of diseased coronary arteries and increased mortality. More indicative of significant ischemia)
->1 mm ST elevation

35
Q

The combination of __________ and ___________ indicates a high incidence of Left Main disease and death.

A

The combination of ST depression and T Wave inversion indicates a high incidence of Left Main disease and death.

36
Q

What is the difference between Upsloping and Downsloping?

A

-Amount of ST depression corresponds to the degree of ischemia
-Downsloping ST depression is associated with an increased number of diseased coronary arteries and an increased mortality
-Upsloping more often benign especially if less than 2 mm

37
Q

What does ST elevation represent?

A

ST elevation may represent acute myocardial ischemia (preinfarction), coronary vasospasm, epicardial ischemia

38
Q

Describe a normal T wave

A

Indicates ventricular repolarization
-Should be rounded, should follow the ST segment, and is never taller than height of the QRS (otherwise, think of hyperK+)
-Normally upright in I, II, and V3-V6
-Inverted in aVR

39
Q

Inverted T waves in the Inferior (II, III, and aVF) and Anterolateral (I, aVL, V3-V6) leads indicates what?

A

-May be seen in Papillary muscle ischemia
-Occurs due to altered repolarization of ischemic myocardial cells

40
Q

What are causes of ST/T wave changes?

A

-Drugs: diuretics, digoxin, quinidine, insulin
-Electrolyte disturbances: hypokalemia
-Conduction disturbances: BBB
-LVH
-Pericarditis
-Subarachnoid Hemorrhage (SAH)
-Prone position
-Acute abdomen, hiatal hernia, gallbladder disease

41
Q

Which leads indicate the Inferior (diaphragmatic) area of the heart?

A

II, III, aVF

42
Q

What supplies blood flow to the inferior area of the heart?

A

RCA; PDA

43
Q

Which leads indicate the Lateral Wall area of the heart?

A

I, aVL, V5, V6
-I and aVL = high lateral
-V5 and V6 = low lateral

44
Q

What supplies blood flow to the Lateral Wall area of the heart?

A

Primarily Left Circumflex

45
Q

Which leads indicate the Septal area of the heart?

A

V1, V2

46
Q

What supplies blood flow to the Septal area of the heart?

A

Primarily LAD, some Left Circumflex

47
Q

Which leads indicate the Anterior Wall of the heart?

A

V3, V4

48
Q

What supplies blood flow to the Anterior Wall of the heart?

A

LAD, Diagonals

49
Q

Which leads indicate the Posterior Wall of the heart?

A

Reciprocal changes in V1 and V2.
-Visualizing electrical activity passing through the damaged part of the heart to the front part.
-See reciprocal changes in anteroseptal leads
-Look in V1 & V2 for tall R waves that will not be accompanied by right axis deviation. This is often confused with right ventricular hypertrophy. Careful with this one!!

50
Q

What supplies blood flow to the Posterior Wall of the heart?

A

PDA
-So, RCA in 80% of people or LAD in 20% of people
-If patient is R dominant, PDA perfuses post. part of the heart 80% of the time. 20% of the time, the PDA comes off of the LAD.

51
Q

What does the RCA supply?

A

-SA and AV nodes
-Proximal Bundle of HIS
-Posterior fascicle of the LBBB

Risk of profound bradycardia

52
Q

What is important to know about ST segment elevation in V1 and V2?

A

Careful, don’t overdiagnose the ST segments in V1 & V2. They are often normally elevated somewhat!

53
Q

What will you see in Lead II in the setting of an early, inferior wall MI?

A

-Flattening of the originally concave ST segment and it eventually becomes convex as infarction progresses
-Hyperacute T waves, upsloping of ST elevation, furthers ST elevation
-Get pathologic Q waves

ST elevation typically transmural injury; ST depression subendocardial ischemia

54
Q

What is a Q Wave?

A

-Normally produced in Lead I by initial depolarization of the interventricular septum (with electrical vector directed to the right and downward)
-Septum is relatively thin and depolarizing occurs quickly, generating only a small, short-lived action potential.
-Resultant q wave is small amplitude, and short duration.

55
Q

What changes occur to the Q wave in the setting of MI?

A

-In MI, dead muscle tissue produces no action potentials
-ECG “looks through” infarcted area to pick up electrical forces from the opposite side of the heart, which are directed away from Lead I
-Q wave in MI is of substantial amplitude and duration
-End up getting a rly big Q wave, more than 25% of the R wave, and of a longer duration.

56
Q

What kind of arrhythmias are due to an Inferior MI?

A

Occurs closer to SA Node area.
Narrow complex dysrhythmias
-Profound Sinus Bradycardia
-Junctional
-3rd degree AVB with junctional escape rhythm

57
Q

What kind of arrhythmias are due to an Anterior MI?

A

Wide complex dysrhythmias
-Mobitz II
-3rd degree with ventricular escape rhythm

Principles 2 (45 decks)

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