Cardiac Rhythm Study Guide

Question 1

0.04 seconds

Answer 1

1 little box

Question 2

0.20 seconds

Answer 2

1 big box

Question 3

1 second

Answer 3

5 big boxes

Question 4

3 seconds

Answer 4

15 big boxes

Question 5

6 seconds

Answer 5

30 big boxes

Question 6

Take a 6 second strip (30 big boxes) and count the number of beats
Multiply the number of beats x 10- that is the heart rate

Answer 6

Irregular rhythms

Question 7

1500 method – Count the number of small boxes between two p waves or QRS waves then divide into 1500. 1500 divided by 20 small boxes = 75 bpm

Answer 7

Regular rhythms

Question 8

Heart Rate Determination
Rhythm Determination
P Wave Evaluation
PR Interval Evaluation
QRS Complex Evaluation

Answer 8

Questions to ask to determine rhythm/arrhythmia

Question 9

The first thing to assess when evaluating a rhythm strip is the ventricular rate. Regardless of the dysrhythmia involved, the ventricular rate and blood pressure are key to whether a patient can tolerate the dysrhythmia (i.e., maintain CO and mentation). Once the patient can no longer tolerate the dysrhythmia, often a ventricular rate greater than 200 or less than 30, emergency measures must be started to correct the condition. A detailed analysis of the underlying rhythm disturbance can proceed later, once the patient’s clinical condition has stabilized.
The three methods for calculating rate are as follows:
Number of R-R intervals in 6 seconds times 10 (30 big boxes. ECG paper is usually marked at the top in 3-second increments, making a 6-second interval easy to identify).
Number of large boxes between QRS complexes divided into 300
Number of small boxes between QRS complexes divided into 1500

Answer 9

Heart Rate Determination

Question 10

The term rhythm refers to the regularity with which the P waves or R waves occur. Calipers assist in determining rhythm. One point of the calipers is placed on the beginning of one R wave, and the other point is placed on the next R wave. Leaving the calipers “set” at this interval, each succeeding R-R interval is checked to be sure it is the same width as the first one measured.
Regular: the R-R intervals are the same, within 10%.
Regularly irregular: the R-R intervals are not the same, but some sort of pattern is involved, which could be grouping, rhythmic speeding up and slowing down, or any other consistent pattern.
Irregularly irregular: the R-R intervals are not the same, and no pattern can be found.

Answer 10

Rhythm Determination

Question 11

The P wave is analyzed by considering whether the P wave is present or absent.
If present, is each P wave associated with a QRS complex?
It is expected that one P wave will be in front of every QRS.

Answer 11

P Wave Evaluation

Question 12

The duration of the PR interval, is 0.12 to 0.20 second
The PR is measured from the start of a visible P wave to the beginning of the next QRS complex. All PR intervals on the strip are verified to be sure they have the same duration as the original interval.

Answer 12

PR Interval Evaluation

Question 13

The entire ECG strip must be evaluated to ascertain that the QRS complexes are consistently the same shape and width.
The normal QRS complex duration is 0.06 to 0.10 second (60 to 110 ms).
The QRS complex is measured from where it leaves the baseline to where it returns to the baseline
Any QRS longer than 0.10 second is considered abnormal.
If more than one QRS shape is visible on the strip, each QRS complex must be measured.

Answer 13

QRS Complex Evaluation

Question 14

Regularity: Regular
Rate: Atrial: 60-100 bpm (beats per minute); Ventricular: 60-100 bpm
P Waves: One P wave precedes every QRS; P waves are consistent in shape. All upright in II, III, AVF and Biphasic in MCL1. All followed by a QRS complex.
PR Interval: 0.12-0.20 sec. (second) and is consistent.
QRS: 0.04 - 0.12 sec. Normal configuration and consistent. A QRS follows each P wave.
Interpretation: Sinus Rhythm represents normal functioning of the conduction system. Sinus Rhythm is the “gold standard” against which all other rhythms are compared.
Significance: Sinus rhythm represents normal functioning of the conduction system. Therefore, it is characterized by normal values of rate, regularity, and intervals.

Answer 14

Sinus Rhythm (SR)

Question 15

Regularity: Regular
Rate: Atrial: >100- <160 bpm, Ventricular:>100- <160 bpm
P Waves: One P wave precedes every QRS; P waves are consistent in shape.
PR Interval: 0.12-0.20 sec. and consistent.
QRS: 0.04-0.12 sec. QRS is normal configuration. A QRS follows each P wave.
Interpretation: In ST, the impulse is generated in the SA node at a rate that is faster than normal. The rote is through the conduction system is normal. ST meets all criteria for SR except for the rate.
Causes: Can be normal response to situations that create an increase in demand for cardiac output such as exercise, pain, stress, fever, hypovolemia, or strong emotions, such as fear and anxiety. Can also occur as a compensatory mechanism in conditions, such as heart failure, shock and pericarditis, anemia, respiratory distress, pulmonary embolism, sepsis, and hyperthyroidism. Drugs may cause ST: atropine, isoproterenol (Isuprel), aminophylline, dopamine, dobutamine, epinephrine, alcohol, caffeine, nicotine, cocaine, and amphetamines.)
Significance: ST increases myocardial oxygen demand. Tachycardia decreases the time for ventricular filling time which decreases cardiac output, cause hypotension, and hypoperfusion. Tachycardia increases heart work and myocardial oxygen demand, while decreasing oxygen supply by decreasing coronary artery filling time
Treatment: Treat the underlying cause. Nursing interventions to relieve pain, anxiety may be useful. In urgent cases of symptomatic ST, some drugs that slow the heart rate include beta-blockers, calcium-channel blockers, or digoxin.

Answer 15

Sinus Tachycardia (ST)

Question 16

Regularity: Regular
Rate: Atrial: <60 bpm Ventricular: <60 bpm
P Waves: One P wave precedes every QRS; P waves are consistent in shape.
PR Interval: 0.12-0.20 sec. and consistent.
QRS: 0.04-0.12 sec. QRS is normal configuration. A QRS follows each P wave.
Interpretation: In SB, the impulse is being generated in the SA node at a rate that is slower than normal. The route through the conduction system is normal. Therefore, SB meets all criteria for Sinus Rhythm except the rate.
Causes: SB may be normal physiological variant, especially in athletes or during sleep. Some pathologies associated with SB include myxedema coma, increased intracranial pressure, and glaucoma. Conditions that increase vagal tone or stimulation, for example vagal maneuvers such as Valsalva or carotid sinus massage, can slow the rate. Drugs that slow the heart rate include beta-blockers, calcium-channel blockers, and digoxin. SB often occurs inferior MI.
Significance: Bradycardia may result in low cardiac output with clinical sighs of hypotension and decreased organ perfusion.
Treatment: Treat only if symptomatic. For symptomatic patients (hypotension, chest pain, shortness of air, dizziness, lethargy, s/s CHF, syncope) treatment is necessary to rise the HR to establish optimal cardiac output. Urgent situations may require atropine, isupril, temporary pacemaker, or permanent pacemaker placement.

Answer 16

Sinus Bradycardia (SB)

Question 17

Regularity: Irregular
Rate: Atrial: 60-100 bpm Ventricular: 60-100 bpm
P Waves: One P wave precedes every QRS; P waves are consistent in shape.
PR Interval: May vary slightly but is within normal limits. 0.12-0.20 sec. and consistent.
QRS: 0.04-0.12 sec. QRS is normal configuration. A QRS follows each P wave.
Interpretation: The sinus node is firing in a slightly irregular pattern, usually caused by fluctuations of autonomic tone. Sinus arrhythmia meets all criteria for Sinus Rhythm except regularity.
Causes: Is commonly seen as a cyclic pattern that varies with respiration. The heart rate increases on inspiration and decreases on exhalation. Can be caused by the increase in intrathoracic pressures created by mechanical ventilation. It is also common in the young and athletic. A non-respiratory form can be present in diseased hearts. In this cases the irregularity is usually more pronounced.
Significance: Usually not clinically significant
Treatment: Treatment is not usually required unless symptomatic bradycardia is present.

Answer 17

Sinus Arrhythmia

Question 18

Regularity: Grossly irregular
Rate: Atrial: Indeterminate, >400 bpm. Ventricular: Varied depending on the AV node’s ability to conduct to the ventricles; if uncontrolled generally160-180 bpm, controlled generally at 60-70 bpm.
P waves: No discernable P waves, as the atria never depolarize as a whole. Atria are quivering and not contracting. The baseline is chaotic and may appear fine or coarse. T waves may also be difficult to distinguish within the chaotic baseline.
PR Interval: None, due to a lack of P wave
QRS: Typically normal, unless aberrant conduction occurs causing widening of the QRS complex which is common at faster rates.
Interpretation: Multiple ectopic sites within the atria firing rapidly. This arrhythmia may be acute (< 48 hours), paroxysmal (intermittent), or chronic (< 1 month)
Cause: CAD, MI, ischemia, rheumatic heart disease, valvular heart disease, pericarditis, cardiomyopathy, CHF, hypermetabolic states, pulmonary disease, stimulants/intoxicants, hypokalemia, cardiac surgery, chronic HTN, and hypoxia.
Significance: Loss of atrial kick with attributes to 10 – 20% of ventricular filling which decreases cardiac output. High ventricular response rates exacerbate decreased cardiac output due to decreased filling times. Commonly blood clots form in the atria that may manifest as emboli.
Treatment: Rhythm control: antidysrhythmic medication, synchronized cardioversion. Catheter procedure: radiofrequency catheter ablation. Rate control: slow conduction through the AV node: calcium channel blockers, beta blockers, and digoxin. Prevent thrombi & emboli: If pt in a. fib > 48 hours, they must be anticoagulated with Warfarin for at least 3 weeks with an INR of 2.0 – 3.0 before cardioverting.
When the ventricular rate is greater than 100 in the presence of atrial fibrillation, the person is said to have atrial fibrillation with a “rapid ventricular response” or “RVR”. Atrial fibrillation is sometimes abbreviated as “Afib”. Thus a “rapid afib” or atrial fibrillation with RVR is sometimes abbreviated as “afib with RVR”.
Very similar to SVT but is irregular rate, where SVT is regular rate

Answer 18

Atrial Fibrillation (A-Fib) - Atrial Arrhythmias

Question 19

SVT describes a varied group of dysrhythmias that originate above the AV node. SVT is not a specific term; it includes sinus tachycardia, atrial tachycardia, multifocal atrial tachycardia, atrial flutter, atrial fibrillation, and junctional tachycardia. SVT may also be described as a narrow complex tachycardia
Regularity: Regular
Rate: Atrial: 150-250 bpm, Ventricular: 150-250 b bpm (that’s less than 2 big boxes between QRSs)
P Waves: Very difficult to see, generally lost in the preceding QRS or T wave. One P wave precedes every QRS; P waves are consistent in shape. To determine which SVT the patient is presenting with, an ECG with a faster sweep speed is necessary to spread everything out.
PR Interval: Generally constant but often indeterminate since the P waves are not visible.
QRS: 0.04-0.12 sec. QRS is normal configuration. A QRS follows each P wave.
Interpretation: SVT describes all tachydysrhythmias that originate above the bundle of His. The term relates to a dysrhythmia with rapid ventricular rate and a narrow QRS complex. The specific origin is unknown unless more advanced testing is done.
Causes: Stress, valvular heart disease, stimulants, bronchodilators, CAD, hypokalemia, hypoxia.
Significance: Usually well tolerated and often paroxysmal in nature. If rate is rapid and sustained, cardiac output will be decreased, and hemodynamic instability will result.
Treatment: Treat the underlying cause of the fast heart rate. Valsalva (Vagal) maneuver to decrease rate emergently. 6 mg IV rapid push Adenosine may break the rhythm or allow slowing to better determine underlying rhythm. diltiazem, verapamil, amiodarone, or digoxin may be used to slow AV conduction. Synchronized cardioversion if symptomatic. If refractory/chronic ablation procedures may eliminate reentrant dysrhythmias.

Answer 19

Supraventricular Tachycardia (SVT) - Atrial Arrhythmias

Question 20

If the SVT starts and ends abruptly, it’s called Paroxysmal Supraventricular Tachycardia (PSVT)

Answer 20

Paroxysmal Supraventricular Tachycardia (PSVT) - Atrial Arrhythmias

Question 21

Regularity: Regular The premature beat (PVC) will interrupt the regularity of the underlying rhythm. The R-R will be regular
Rate: Atrial: depends on the underlying rhythm Ventricular: depends on the underlying rhythm
P Waves: P waves are not seen for the PVC. A PVC occurring late in diastole may occur after the normal P-wave, in such a case, the P-R interval will be shortened. The electrical impulse from the ventricle may conduct retrograde to the atria; in such a case the P-wave, if seen will be inverted in lead II and will follow the QRS.
PR Interval: A P-R interval is not measured for the PVC
QRS: The PVC will have a wide, bizarre QRS with a QRS duration of > 0.12 sec.
Interpretation: A PVC is an ectopic ventricular beat that occurs before a normal sinus beat, therefore there is an underlying rhythm. The name of the underlying rhythm is included in the description of the rhythm. For example: sinus rhythm with PVC or sinus bradycardia with a PVC or atrial fibrillation with a PVC.
PVC’s that are consistently the same shape (morphology) are described as unifocal. PVC’s that are different in morphology are described as multifocal.
PVC’s may occur as isolated beats, or consecutively as two beats (couplets). When three or more PVC’s occur consecutively, it’s called ventricular tachycardia. PVC’s may alternate with normal beats of the underlying rhythm (bigeminy) or after every 2 beats (trigeminy) or after every 3 beats (quadrigeminy)
Causes: PVC’s resulting from enhanced normal automaticity may be a normal occurrence, if infrequent.
Frequent PVCs (> 6 per minute) and couplets may be caused by electrolyte abnormalities (hypokalemia, hyperkalemia, hypomagnesemia, and hypocalcemia), ischemia, MI, hypoxemia, acidosis, and cardiomyopathies.
Other causes include increase sympathetic stimulation, sympathomimetics drugs (epinephrine, isoproterenol), caffeine, alcohol, tobacco, drug intoxication (cocaine, amphetamines, tricyclic antidepressants),
Mechanical irritation by a pacemaker wire or PA catheter
Antiarrhythmic medication may have a proarrhythmic effect, as do medications that prolong the QT interval.
Significance: Usually well tolerated and often paroxysmal in nature. If rate is rapid and sustained, cardiac output will be decreased, and hemodynamic instability will result.
Treatment: Treat the underlying cause (correct electrolyte imbalance, restrict caffeine. . .). Antiarrhythmic medications may suppress PVCs (Amiodarone, Lidocaine, Pronestyl, beta-blockers)

Answer 21

Pre-Ventricular Contraction (PVC) - Rhythms originating in the Ventricles

Question 22

Lethal Dysrhythmia
Any wide complex Tachycardia is V-Tach until proven otherwise
Regularity: Regular during tachycardia. May be slightly irregular at onset and cessation of tachycardia “run”
Rate: Atrial: depends on the underlying rhythm. It’s usually impossible to calculate the rate. Ventricular: > 100 bpm
P Waves: Usually not seen. If seen, p-waves are dissociated from the QRSs.
PR Interval: If p-waves are noted, the P-R will vary.
QRS: a wide, bizarre QRS with a QRS duration of > 0.12 sec.
Interpretation: A PAC or PVC may trigger V-Tach; repetitive beating occurs because of reentry.
V-Tach may be sustained (continuous) or non-sustained (short bursts < 30 seconds). Some will call a 3 – 8 beat run of V-tach a “salvo’.
Dissociated P-waves, when they can be found, are diagnostic for V-Tach, as they indicate the ventricular rhythm does not result from atrial activity.
V-Tach where the morphology (shape) of the QRS complexes change across the strip is called polymorphic V-Tach.
A polymorphic V-Tach that produces a gradual increase and decrease in the QRS amplitude, producing a characteristic spindle shape is called Torsades des Points, or twisting of the points.
Causes: Acute MI, electrolyte abnormalities, hypoxemia, acidosis, ischemia, MI, or variable refractory periods between tissue due to the effects of antiarrhythmic drugs. A persistent V-Tach may be the result of altered tissues bordering infarcted and scarred tissue, congenital dysplasia of the myocardium, or interstitial fibrosis in cardiomyopathy, a prolonged QT interval, R on T shock.
Significance: Immediately assess the patient with V-tach. Responses range from asymptomatic to loss of consciousness and pulse. The response depends on the rate and duration of the V-tach and the contractility of the ventricles.
Treatment: Treat the underlying cause.
Stable patient: IV antiarrhythmic medications: amiodarone, lidocaine
Unstable but conscious patient: synchronized cardioversion
Pulseless patient: CPR, defibrillation, and IV medications: epinephrine (given to all pulseless rhythms), amiodarone (antiarrhythmic), lidocaine (antiarrhythmic)
Management of recurrent V-tach may include, antiarrhythmic medication and/or ICD.

Answer 22

Ventricular Tachycardia (VT) - Rhythms originating in the Ventricles

Question 23

Lethal Dysrhythmia!
Vfib is a PULSELESS Rhythm. Verify and defibrillate immediately.
Regularity: irregular
Rate: Atrial: none Ventricular: none
P Waves: none
PR Interval none
QRS: none
Interpretation: Irregular, chaotic fibrillatory waves. They may be course or fine.
Causes: Severe hypoxemia, ischemia, MI, acidosis, profound electrolyte imbalance, severe hypothermia, electric shock, drug toxicity (digoxin, quinidine, procainamide), V-tach may deteriorate to V-fib.
Significance: The ventricles are not beating (just quivering) so there is no cardiac output.
Treatment: The only effective treatment is defibrillation. CPR is required until defibrillation is available. If initial defibrillation attempts and supplemental oxygen are ineffective, epinephrine may increase ventricular irritability and improve the likelihood of success with subsequent attempts.

Answer 23

Ventricular Fibrillation (V Fib) - Rhythms originating in the Ventricles

Question 24

Lethal Dysrhythmia
Regularity: irregular
Rate: Atrial: none Ventricular: none
P Waves: none
PR Interval none
QRS: none
Interpretation: No waveforms are seen. The ECG tracing is flat, or may have a slight, slow fluctuation in the baseline. Confirm rhythm in more than one lead.
Causes: Severe hypoxemia, hypovolemia, electrolyte imbalance or acidosis. Hypothermia, cardiac tamponade, tension pneumothorax, massive pulmonary embolus, drug overdose. Failure of the SA node, pacemaker generator battery malfunction.
Significance: The ventricles are not beating (just quivering) so there is no cardiac output.
Treatment: Initiate CPR. epinephrine, consider atropine

Answer 24

Asystole - Rhythms originating in the Ventricles

Question 25

Regularity: Atrial and ventricular rhythms are regular.
Rate: Atrial: Dependent on underlying rhythm, Ventricular: Dependent on underlying rhythm. Same as atrial rate
P Waves: The P waves will be normal size and configuration; each P wave followed by a QRS complex
PR Interval: The PR interval will be constant, but prolonged (> 0.20 sec)
QRS: Since depolarization will usually occur normally through the ventricles, the QRS has a normal configuration and duration of 0.04 – 0.12 sec
Interpretation: First degree AV block is a rhythm disturbance that co-exists with an underlying rhythm (i.e. sinus rhythm with a first-degree AV block, sinus brady with a first degree AV block). There is a constant delay in the conduction of electrical impulses through the AV node. It’s characterized by prolonged PR intervals that are greater than 0.20 seconds and constant.
Causes: May appear without any apparent cause. Commonly occurs with acute inferior MI. Chronic causes: fibrosis and sclerosis of the conduction system, lack of blood supply to the conduction system secondary to coronary artery disease (CAD), valvular heart disease, myocarditis, and various cardiomyopathies. Can also be attributed to degenerative changes in the heart associated with aging. Acute causes is of much greater concern. Causes include medication toxicity related to digoxin, beta blockers, or amiodarone administration; acute myocardial ischemia or MI; hyperkalemia; edema after valvular heart surgery; and increased vagal tone
Significance: Generally first-degree AV block produces no signs or symptoms.
Treatment: In general, no treatment except to identify and correct the underlying cause.

Answer 25

1st Degree Heart Block - AV Heart Blocks

Question 26

Regularity: Atrial rhythm is regular. Ventricular rhythm is irregular. The R-R interval is irregular in a pattern of group beating. The R-R interval gets progressively shorter as the PR interval gets progressively longer
Rate: Atrial: Exceeds the ventricular rate because of blocked Ps, Ventricular: Less than atrial rate
P Waves: The P waves will be normal size and configuration; some P waves not followed by QRS complexes
PR Interval: The PR interval gets progressively longer until one P wave is not followed by a QRS complex. After the blocked beat (dropped QRS), the cycle starts again (group beating). (The PR gets longer, longer, longer, then there’s a p wave without a QRS.)
QRS: Since depolarization will usually occur normally through the ventricles, the QRS has a normal configuration and duration of 0.04 - 0.12 sec.
Interpretation: Occurs when each successive impulse from the SA node is delayed slightly than the previous impulse. The pattern of progressively longer PR intervals continues until an impulse fails to reach the ventricles (dropped QRS). This type of AV block is usually distinguished by group beating, referred to as footprints of Wenckebach.
Causes: Include inferior wall MI, digoxin toxicity, ischemic heart disease, acute rheumatic fever, post-cardiac surgery, electrolyte imbalance; Drugs such as beta blockers, Quinidine and Procainamide.
Significance: Second-degree AV block, type 1 is commonly transient and reversible. May occur in otherwise healthy people. Although many cases are asymptomatic and resolved when the causative factor is corrected, the AV block may progress to a more serious form. If beats are frequently dropped, cardiac output can be compromised.
Treatment: Treatment is seldom necessary. The underlying cause should be identified and treated. If hypotension and bradycardia are present, administer atropine. The goal is to increase cardiac output via increasing the heart rate

Answer 26

2nd Degree Heart Block Type I (Wenckebach, Mobitz I) - AV Heart Blocks

Question 27

(Wide QRS complexes indicate origin of block is below the Bundle of His, leading to a higher incidence of lethal complications, If QRS narrow, block is above the Bundle of His, and is not associated with high mortality)
Regularity: Atrial rhythm is regular, Ventricular rhythm can be regular or irregular. Pauses correspond to dropped beats. When the block is intermittent or when the conduction ratio is variable, the ventricular rhythm is irregular. When there is a constant conduction ratio, the ventricular rhythm is regular.
Rate: Atrial: Exceeds the ventricular rate because of blocked Ps Ventricular: Less than atrial rate.
P Waves: The P waves will be normal size and configuration; some P waves not followed by QRS complexes.
PR Interval: PR interval is within normal limits or prolonged, but constant
QRS: If the block occurs at the bundle of His, the QRS will have a normal configuration and duration of 0.04 – 0.12 sec, If the block occurs at the bundle branches, the QRS will be wide >0.12 sec.
Interpretation: This rhythm looks like sinus rhythm with nonconducted p wave(s). The PR interval does not vary before a dropped beat, so there are no warning signs. More than one nonconductor beat can occur in succession.
Causes: Extensive damage to the bundle branches following an acute anterior or anteroseptal MI, degenerative changes in the conduction system, or severe coronary artery disease.
Significance: Second-degree AV block, type II can range benign to lethal. If beats are frequently dropped, cardiac output can be compromise causing syncope and angina.
Treatment: Asymptomatic patients: monitor closely.
Symptomatic patients: Transcutaneous pacing should be immediately available and applied. Second degree type II AV block may progress to a complete heart block, prepare for transcutaneous cardiac pacing.
** Giving atropine in the setting of Second degree type II AV block can worsen the block and increase the risk of complete heart block or asystole.

Answer 27

2nd Degree Heart Block Type II (Mobitz II) - AV Heart Blocks

Question 28

Above the Bundle of HIS
(Narrow QRS complexes indicate high block (above the Bundle of His) Usually benign. Usually associated with ischemia or toxic drug effects.)
Below the Bundle of HIS
Regularity: Atrial rhythm is regular, Ventricular rhythm is regular.
Rate: Atrial: Generally under the control of the SA node, 60 – 100 bpm, Ventricular: With a junctional escape rhythm the ventricular rate usually 40 – 60 bpm. With a ventricular escape rhythm the ventricular rate is usually below 40 bpm, Ventricular rate is less than the atrial rate.
P Waves: The P waves will be normal size and configuration. Some p-waves may be buried in the QRS complex or T-wave (the QRS complex or T wave will look distorted or different than the other QRS complexes.)
PR Interval: There is no PR interval. Any p-wave that occurs before a QRS complex is incidental.
QRS: Configuration depends on location of escape mechanism pacing the ventricles. If junctional escape rhythm, the QRS will appear normal (0.04 – 0.12 sec.). If ventricular escape rhythm the QRS will be widened (>0.12 sec)
Interpretation: The atria and ventricles are depolarized from different pacemakers and beat independently of each other (AV dissociation). Complete absence of impulse conduction between the atria and ventricles. There are two independent rhythms. Atrial rate > ventricular rate.
Causes: Can be caused by increased parasympathetic tone, inferior wall MI, anterior/anteroseptal MI, AV node damage or ischemia, acute myocarditis, electrolyte imbalance or toxic drug effects (beta blockers, digoxin)
Significance: This dysrhythmia can range benign to lethal. Because the ventricular rate in CHB is usually slow, the cardiac output is significantly low. There is no atrial kick because the atria and ventricles are beating independently.
Treatment: Asymptomatic patients: monitor closely.
Symptomatic patients: The goal is to increase cardiac output via increasing the heart rate. Positive chronotropic drugs such as isoproterenol, epinephrine or low-dose dopamine are used to increase heart rate. Transcutaneous pacing should be immediately available and applied. A transvenous or transcutaneous temporary pacemaker may be used until a permanent pacemaker can be inserted.

Answer 28

3rd Degree Heart Block (Complete Heart Block) - AV Heart Blocks

Question 29

Ventricular Pacemaker (Spikes followed by wide qrs complexes) be aware of potential for pacemaker failure, electrical capture without mechanical capture. (CHECK PULSE)
Pacing stimuli can be seen on the ECG tracing as “spikes”; the size of the spike and whether you can see them at all is determined by the type of pacemaker.
Pacing stimuli are delivered directly to the myocardium, and so do not take advantage of the specialized conduction system. The impulse must then travel from cell to cell to depolarize the rest of the heart. As a result, paced beats are wide waveforms on the ECG
There are four primary problems that can be identified on the surface ECG:

Answer 29

Pacemaker

Question 30

Undersensing occurs when the pacemaker is unable to detect the intrinsic electrical waveform. Put simply, the pacemaker doesn’t “see” the P-wave (atrial pacing lead) or the QRS (ventricular pacing lead).
This is identified on the ECG strip when a pacing spike is seen soon after the waveform (P-wave for an atrial pacing lead, QRS for a ventricular pacing lead).
Adjustment of the pacemaker’s settings may resolve this problem. In some cases, repositioning or replacing the electrode/lead is required.

Answer 30

Undersensing

Question 31

Oversensing occurs when the pacemaker senses waveforms other than those it is intended to sense. Most commonly, this is a ventricular lead sensing a T-wave.
This is identified on the ECG strip when pacing occurs at a slower rate that the programmed rate.
Adjustment of the pacemaker’s settings will resolve this problem.

Answer 31

Oversensing

Question 32

Failure to capture occurs when the pacemaker stimulus fails to capture (trigger depolarization) of the intended chamber.
This is identified on the ECG strip when a pacemaker spike, falling at a time that the heart should be able to respond, fails to produce a depolarization waveform (P-wave for an atrial spike; QRS for a ventricular spike).
Adjustment of the pacemaker’s settings may resolve this problem. In some cases, repositioning or replacing the electrode/lead is required.

Answer 32

Underpacing (failure to capture)

Question 33

No output occurs when no pacemaker stimuli reach the heart.
This is identified on the ECG strip when the patient’s heart rate is slower than the rate the pacemaker is programmed for, and no pacemaker spikes are seen.
This can be due to a loss of power from the generator, or due to a disruption along the electrode/lead. If this is a temporary pacemaker, check the power source and all connections.

Answer 33

No output