D. AV Blocks
Blocks can be transient, intermittent, or permanent and complete or incomplete. Blocks are caused by physiologic, pharmacologic, and pathologic processes. The site of a block is localized with a His bundle electrogram. The H represents impulse conduction over the His bundle and occurs between the A (atrial) and V (ventricle) deflections. The conduction time from the atria to the bundle is the A-H interval. The conduction time from the His bundle to the ventricle is the H-V interval. The bundle of His travels in posterior part of interventricular septum.
Traditional Classification of AV Blocks:
• 1st degree AV block
• 2nd degree AV block — Mobitz I (Wenckebach phenomenon) and Mobitz II
• High degree AV block — momentary absence of conduction for several seconds
• 3rd degree AV block — complete heart block
Newer, more useful classification of AV Blocks:
• Diagnosis cannot be made on basis of surface ECG; requires invasive cardiac electrophysiology study (EPS) — His bundle ECG.
• Type I AV block — block located in the AV node; supra-Hisian (above His bundle); better prognosis.
A-H prolongation during acute MI is often caused by ischemia, not necrosis. Thus, tend not to be permanent.
A-H interval prolonged.
A-H (atrial-His) interval makes up most of the PR interval on the surface ECG.
Hallmark of blocks in the supra-Hisian region = PR prolongation.
If A-H prolongation progresses to the point that the impulse fails to get through at all (3° block) a stable, dependable junctional escape rhythm generally tends to takeover and sustain life. If it is too slow, it can be pharmacologically by atropine but atropine only lasts about 20 min/dose.
If complete heart block develops it does so gradually and predictably and thus can be anticipated.
Transition usually takes place over several days in the setting of acute MI.
• Type II AV block — block located in the bundle branches or fascicles; infra-Hisian (below the AV node); worse prognosis.
H-V (His-ventricular) interval represents time from His bundle depolarization until the beginning ofventricular depolarization; the impulse travels very fast once it gets out of the AV node so this interval is normally short. The H-V interval could double without a noticeable 1st degree AV block on the surface ECG.
Hallmark of blocks in the supra-Hisian region = bundle branch and fascicular blocks.
H-V prolongation during acute MI is usually caused by necrosis or other irreversible causes; requires permanent pacemaker.
If H-V prolongation progresses to the point that 3° block develops, there may be no escape rhythm at all (ventricular standstill), or, at best, a slow and unpredictable idioventricular escape rhythm. Because the block is below pacer cells in the AV junction, junctional impulses will be blocked from conducting to the ventricles.
Idioventricular rhythms do not respond to atropine and thus Isuprel must be used which is extremely potent and difficult to titrate.
Isuprel may D idioventricular rhythm to ventricular tach. Lidocaine cannot be given for V.
tach. in this setting as it might completely suppress the rhythm Æ complete asystole.
Only thing you can do is increase the Isuprel drip.
Onset of complete heart block is often sudden and unanticipated.
1. First Degree Block — discussed under 12-lead ECG interpretation.
• Prolonged PR interval only (> 0.20 sec).
• All sinus impulses conduct to the ventricles.
• Causes — inferior MI, other cardiac disease, digitalis, ? b-blockers, degenerative changes with aging.
• Relatively benign; rarely advances to complete block.
• Treatment — none if chronic. Watch if new or progressive.
2. Second Degree Block
There are two types of 2° block; the differential dx. depends on the PR interval and the QRS complexes.
Mobitz I (Wenckebach):
• Mobitz I block is more common than Mobitz II.
• Mobitz I block is often a/w R CAD and is usually transient.
• It is a/w a prolonged A-H interval and irregular rhythm.
• QRS duration is normal and the P is upright and uniform.
• P-P interval is constant, but not all Ps are 1:1 with the QRSs.
• The R-R gets shorter as PR interval gets longer until an impulse is not conducted.
• Refers to a gradual prolongation of the PR interval, with occasional failure to conduct a P wave through the AV node to the ventricle.
• Characteristics ( some or all of these may be present):
_ Start with normal or prolonged PR interval (underlying 1° block is most common); then with each successive beat the PR interval gradually lengthens until a beat is dropped. Usually due to prolonged A-H time.
_ Following the dropped beat, the PR returns to what it was and the sequence is repeated.
_ The greatest increase in the PR interval develops between 1st and 2nd beats in the cycle.
_ R-R interval tend to shorten until the dropped beat. P-P interval should be normal and non-changing. P waves occur closer and closer to the preceding T wave.
_ The longest cycle (containing the dropped beat) is less than two of the shorter cycles because is contains the shortest PR interval. (Less than double the R-R.)
_ Tends to produce small groups of beats, esp. pairs because 3:2 Wenckebachs (3 P waves with 2 QRSs) are common.
Can occur as 2:1 Wenckebach. Most 2:1 blocks are Wenckebach.
• By itself, it is a benign condition.
• Etiology — Most common cause is an inferior wall MI (usually there is transient ischemia of the AV node so the block may be reversible). Mobitz I blocks may be seen with disease in the AV node, digitalis toxicity (particularly when it occurs in combination with atrial tachycardia), and parasympathetic (vagal) tone . Commonly seen in athletic young patients, particularly during sleep.
• Distinguished from 2° AV Nodal Block, Mobitz type II by the fact that the PR interval of the P wave that follows the non-conducted P wave is at least 10 msec shorter than the PR interval of the P wave that precedes the non-conducted P wave.
Typically, the QRS complex is unchanged from the patient's normal QRS morphology.
By contrast, the PR interval does not change in Mobitz type II block.
• Management — Therapy may not be necessary. If it is, atropine is the drug of choice, although a temporary pacemaker may be inserted. If the patient was receiving digitalis, it should be D.C.'d.
Mobitz II
• This block originates below the bundle of His in the BB system.
• Usually an intermittent trifascicular block. Usually one bundle branch or fascicle is already permanently damaged, then damage occurs to the other. Sometimes one bundle vacillates between conducting and not conducting so that every other impulse is conducted resulting in a 2:1 block.
• 70% of the wide QRS blocks are Mobitz II, the others are Mobitz I.
Rare and often misdiagnosed.
• There are 2 types of Mobitz II blocks — constant or periodic.
The constant type is regular; the periodic type is irregular.
• Mobitz II rates are slow (1/2-1/3 of the normal rate).
• The patient will have s/s, if the cardiac output decreases.
• Characteristics:
_ P wave is upright, uniform, and of SA origin.
_ There is more than one P/QRS (2:1, 3:1, 4:1).
_ PR interval is constant (but it can be prolonged).
• Refers to occasional failure to conduct a P wave through the AV node to the ventricle without a change in the PR interval after the nonconducted P wave compared with before the nonconducted P wave.
• A dangerous condition because it can progress to complete heart block and death without warning.
• Placement of an external pacemaker may be lifesaving if a temporary pacemaker cannot be placed immediately. This condition, while dangerous, is very unusual.
• QRS complex is usually wide, due to extensive disease of the His-Purkinje system, although a narrow QRS complex does not exclude the diagnosis.
• Clinician should measure the change in PR interval carefully, as described for 2° AV nodal block, Mobitz Type I.
• Etiology of Mobitz II — includes anterior MIs, extensive destruction of the septum, shock and ventricular ectopic beats. This one is not caused by digitalis toxicity. It may progress to third degree block or ventricular standstill. This rhythm is usually irreversible.
• Management — includes the administration of atropine, epinephrine, or Isuprel or the insertion of a temporary pacemaker followed by a permanent pacer. This rhythm is often not responsive to drug therapy. Usually not reversible.
3. 2° Atrioventricular Nodal Block (2:1 AV Block)
• Diagnosed when the entire rhythm strip shows only conduction of every other P wave to the ventricle.
• Because the record does not show two consecutive P waves that conduct to the ventricle, it is not possible to measure prolongation of the PR interval, so that it is not possible to distinguish between 2° AV nodal block, Mobitz type I and the dangerous 2° AV nodal block, Mobitz type II . By convention, recordings obtained at other recent times are used to make this distinction.
4. High Degree AV Block — block which results in many dropped QRS complexes (vent. standstill).
• Type I (supra-Hisian) — benign phenomenon.
May be seen with vasovagal reactions.
In vagally mediated blocks, the sinus rate slows down and/or the PR interval _ prior to the dropped QRSs. The vagal stimulation affects both the SA node and AV conduction.
Sinus Slowing and PR Lengthening Prior to High Grade AV Block.
• Type II (infra-Hisian) — seen in association with Mobitz II can be extremely dangerous.
If pt. with inferior MI and some degree of AV block (?1° or Wenckebach) vomits, the vagal stimulation may produce several seconds of complete block.
Reverses after the vagal influence is gone.
Treatment — same as for Mobitz II.
5. Complete Heart Block (Third Degree)
• There is no SA impulse conduction to the ventricles with this rhythm.
• The ventricular beat is idiojunctional if the AV junctional area is controlling the ventricular rhythm or idioventricular if the ventricle is controlling it.
• May be transient and cease after 2-4 days.
• There is a decrease in cardiac output, and angina, CHF, or syncope may develop.
• P waves are uniform.
• There is more than one P for each QRS, but the P is not related to the QRS.
• P-P and R-R intervals are regular.
• PR interval does not really exist since there is no relationship between the P and QRS.
• P waves sometimes fall on the QRS.
• QRS configuration is normal if the escape focus pacer is junctional and it is wide if the pacer is ventricular (focus is below BB bifurcation).
• Characterized by failure of conduction from the atria through the AV node to the ventricles.
• Atrial rhythm is independent of the ventricular rhythm, unless an accessory pathway that conducts antegrade is present.
• It is most easily distinguished from high-grade AV nodal block when the atrial and ventricular rhythms are regular but have different rates. Because of weak coupling between the chambers by the autonomic nervous system, these rates can be very close to each other and in fact can oscillate around each other.
• Complete heart block is one of three forms of AV dissociation. The other two forms are:
_ Sinus arrest or sinus bradycardia with junctional rhythm or Idioventricular rhythm.
_ Ventricular tachycardia.
Of these three forms, only complete heart block results from antegrade conduction block from the atria to the ventricles.
• Etiology — Complete block is seen after an inferior MI; sometimes after an anterior MI with RBBB and L axis deviation; rarely congenital; also seen with degeneration with age, myocarditis, cardiac surgery, and digitalis toxicity.
• Management — Isuprel may be used to treat the patient while preparing for pacemaker insertion.
Interventions for Blocks Associated With Inferior Infarction
• Determine if the patient is symptomatic from a slowed ventricular rate (check BP, urine, etc.).
• Monitor for development of Mobitz I or third degree block.
• Have atropine at bedside.
Interventions for Blocks Associated With Anterior Infarction
• Determine if patient is symptomatic from slowed ventricular rate (check BP, urine, etc.).
• Monitor for development of Mobitz II or third degree block .
• Have Isuprel and pacemaker at bedside .
Interventions for Blocks Associated With Drug Toxicity
• Check digitalis and potassium levels.
PART IV: DIAGNOSIS OF DYSRHYTHMIAS
Always state the impulse origin first and then add additional descriptions (e.g., sinus rhythm with right bundle branch block, first degree AV block, and frequent left ventricular PVCs). If there are two pacemakers driving the heart, mention the "higher" pacemaker first (e.g., sinus tachycardia with complete AV block and an idioventricular escape rhythm).
Remember, TREAT THE PATIENT, NOT THE RHYTHM!
Questions for Every Rhythm:
What is the rate of the QRS?
Rate > 100 is called tachycardia.
Rate < 60 is called bradycardia.
Is the QRS regular or irregular?
Irregular — atrial fibrillation, extra beats superimposed on sinus, sinus arrhythmia, others.
Is the QRS narrow or wide?
A wide QRS (> 3 small boxes) indicates a conduction delay or impulse arises in the ventricle.
Are there P waves?
Look at more than one lead if in doubt.
Does a P wave precede ever QRS?
Is the PR interval constant? (> 1 large box = prolonged PR [1° AV block].)
Definitions:
Cycle — one complete systole and diastole sequence; may be measured from P-P or R-R or T-T intervals.
Premature — occurs early or ends a cycle shorter than the dominant cycle (active).
Escape — occurs late or ends a cycle longer than the dominant cycle (passive).
Ectopic — arises from outside the normal pacemaker of the heart; can arise from the atria, AV junction, or ventricles; can be premature beats, escape beats, or a continuous rhythm.
Block — an abnormal delay or failure of conduction; must be differentiated from normal physiologic delays (e.g., atrial flutter with 2:1 conduction or sinus node suppression following atrial ectopy.)
A. Sinus rhythms
1. Normal Sinus Rhythm — discussed under section on 12-lead ECG interpretation.
2. Sinus Bradycardia — discussed under section on 12-lead ECG interpretation.
3. Sinus Tachycardia — discussed under section on 12-lead ECG interpretation.
4. "Relative" Sinus Bradycardia — heart rate slows down sufficiently to make the patient symptomatic, esp. if normal rate was previously rapid (from 110 to 70 bpm).
5. Sinus Arrhythmia:
• Irregular rhythm representing a cardiac adjustment to respiratory or neurologic Ds.
Rate varies — during inspiration due to the baroreceptor response to increasing negative pressure; during expiration, there is a increase rate.
• Rate is like a NSR, 60-100 bpm. Usually a benign finding.
• P-P regularly irregular.
• PR interval normal.
• QRS for each P.
• Treatment — none. Considered normal variant.
• Sinus arrhythmias are normal in kids. Non-respiratory (pathologic) sinus arrhythmias are seen in elderly patients who have SA node disease or digitalis toxicity.
6. Sinus Arrest
• Results from failure of the sinus node to activate the atria.
• Usually benign when duration short (less than one to two seconds).
• Can be life-threatening (because of the potential for longer periods of sinus arrest with asystole) when duration long (_ 3 seconds).
• Causes— medications, including as b-blockers, some Ca++ blockers such as diltiazem, Aldomet, and digitalis or quinidine toxicity, excess vagal stimulation, hyperkalemia, stress, or vasoconstriction.
• Can also be part of the sick sinus ("tachy-brady") syndrome, one of the leading indications for implantation of permanent pacemakers in this country.
• With sinus arrest or pause, the impulse is never formed.
7. Sino-Atrial Block — unclear whether the sinus node pacer cells generate impulses which fail to be conducted out of the sinus node (SA exit block) or whether the pacer cells fail to generate impulses (SA arrest). Can be manifested by any of the following:
• Extremely slow sinus rate (e.g., 25/min) which cannot be justified simply as sinus bradycardia (may be 2:1, 3:1 etc. exit block).
• Occasional dropped beats (i.e., the entire P-QRS-T sequence is missing); may be sinus Wenckebach.
• No P waves at all (complete SA block or standstill).
One of 3 things can happen when you have complete SA block:
_ Cardiac standstill and death (rare).
_ Lower pacemaker comes to the rescue and takes over (junctional escape or ventricular escape rhythm).
_ Chronic atrial fibrillation, typically with a slow ventricular rate.
• Causes of SA block:
Digitalis, b-blockers, quinidine, etc.
Hyperkalemia
SA node ischemia/infarction (RCA or Cx artery disease).
Vagal stimulation.
Other cardiac disease.
Degenerative Ds with aging.
• Treatment of SA block:
Hold drug until toxicity ruled out.
Atropine and/or temporary pacing if patient symptomatic.
Permanent pacing if block persists and is not due to some reversible situation.
• SA node and intra-atrial blocks are rare. Blocks can be transient, intermittent, or permanent and complete or incomplete.
8. Sick Sinus Syndrome — Brady-Tachy Syndrome
• ECG manifestations:
Marked sinus bradycardia or arrest often resistant to atropine or Isuprel.
Longer (~ 12 sec) asystolic pause than can be explained by simple SA node suppressions following:
A single PAC.
DC cardioversion.
Spontaneous conversion of atrial flutter or fibrillation.
Rapid atrial pacing.
Periods of atrial fibrillation (or less commonly atrial flutter) either with a slow or rapid ventricular response alternating with periods of asystole, junctional escape rhythm, or ventricular escape rhythm or extremely slow junctional rate (< 40/min).
• Causes — same as for SA block.
• Symptoms:
Palpitations (either during tachy or brady phase).
Syncope or near syncope (during asystolic or bradycardic periods).
CHF (inadequate CO because of slow heat rate, rapid heart rate, and loss of atrial kick).
Increased angina (inadequate CO) in patients with coronary artery disease (CAD).
• Treatment:
Permanent pacing. (Rapid rate cannot be treated with usual methods due to risk of bradycardia.)
After pacer inserted, drugs to convert atrial fibrillation or to slow ventricular rate in chronic atrial fib.
• Sick sinus syndrome may coexist with atrial flutter or fibrillation in elderly.
9. Hidden Atrial Activation
• Activation of the atrium by the sinus node can be inferred from surrounding sinus P waves. For example, if the P wave following a PVC (VPC) occurs at the time that would have been expected had the premature complex not occurred, then in can be inferred that the atrium was not activated retrogradely by the premature complex and that a hidden, or obscured, P wave did occur.
• Such an inference can be confirmed during invasive electrophysiologic study.
B. Ectopic Atrial Rhythms
1. Premature Atrial Contractions (PACs)
• Earlier than expected P waves — morphology of premature P wave usually differs from the sinus P.
• Atrial P wave often falls near the T wave and distorts it — P is flat, notched, or lost in the T in at least one lead.
• PR interval is usually normal.
• Rhythm is regular except for the premature contraction.
• PAC will have 1 of 3 fates: it will be non-conducted, conducted normally, or conducted aberrantly.
Non-conducted PACs arrive at the AV junction before it has repolarized. Because the junction is refractory, the QRS is missing and there is no contraction for that beat.
As Dr. Marriott observes, "the commonest causes of pauses are non-conducted atrial premature complexes."
Nonconducted PACs
Conduction can be normal with a PAC if the PAC arrives at AV junction after it has repolarized; can then be transmitted to ventricles, initiating a normal, narrow QRS.
Aberrant conduction — traverses the bundle branches of the His-Purkinje system while one or both is in its relatively refractory period; resulting QRS complexes are wider than normal and have the morphology of BBB pattern.
• Atrial premature complexes are a normal finding in adults of all ages; frequency can increase during stress, ingestion of caffeine, after a heavy meal, and sympathomimetic drugs such as some OTC cold remedies.
• PACs are also seen in rheumatic heart dz., ischemia, hyperthyroidism, digitalis toxicity, MI, CHF, CAD, and hypokalemia.
2. Aberrant Conduction
• Occurs when the AV node is partially refractory and usually results in a RBBB pattern; impulse arrives at the LBB after it has repolarized, but at the RBB before it has repolarized; QRS is distorted (aberrantly conducted) because the impulse will be conducted normally to the LV, but relayed by aberrant pathways to the RV.
• V1 and V6 are triphasic and predominantly positive with aberrant PACs.
• Aberrant PACs look a lot like PVCs.
• Differential diagnosis should focus on whether a premature P wave precedes the wide QRS and whether a RBBB pattern occurs in V1 or V6.
Best criteria to support the dx. of aberrant supraventricular contraction is the presence of a premature P wave. Unfortunately the P wave of PAC may be buried so you may not see it; if a P wave precedes a PVC, it is usually sinus and not premature.
Aberrantly Conducted PAC
(1) Normal supraventricular conduction.
(2) Normal conduction in the left bundle branch.
(3) Blocked conduction at the right bundle branch which is still refractory.
(4) Normal conduction in the left ventricle.
(5) Abnormal, delayed conduction in the right ventricle by aberrant pathways.
• Cycle is reset with PACs.
Look at the duration between the beat that precedes the one with the wide QRS and the normal beat which follows it.
A less than compensatory pause is often seen with PACs because of retrograde discharge of the SA node and resetting of cycle. The distance is less than you would expect from 2 normal beats.
(You have a compensatory pause with PVCs.)
3. Atrial Couplet
• Pair of atrial premature complexes in a row.
• Less common in normal subjects than are PACs, it can still be benign.
• Appearance of atrial couplets should also raise the index of suspicion for susceptibility to atrial fibrillation, atrial flutter, and supraventricular tachycardia (SVT).
4. Atrial Multiform Couplet
• Pair of PACs, with differing P wave morphologies, in a row.
• Unusual in normal subjects, but is itself benign.
• Appearance of multiform atrial couplets, esp. in patients with pulmonary dz., should raise the indexof suspicion for susceptibility to multifocal atrial tachycardia, atrial fibrillation, and atrial flutter.
5. Wandering Atrial Pacemaker
• Supraventricular rhythm resulting from multiple ectopic foci in the atria.
• Characterized by 3 or more P wave morphologies.
• Rate < 100 bpm.
• Sinus rhythm gives way to an ectopic or junctional rhythm. May see fusion beats at the transitions.
Two opposing electrical currents (sinus and atrial ectopic) within the same chamber at the same time Æ P wave often narrower and of lesser amplitude than the normal sinus P wave.
• Benign, but reflects electrical abnormalities in one or both atria that increase the likelihood of multifocal atrial tachycardia or other atrial arrhythmias.
6. Multifocal Atrial Tachycardia (MFAT)
• Supraventricular rhythm resulting from multiple ectopic foci in the atria.
• Characterized by 3 or more P wave morphologies.
• Rate _ 100 bpm.
• Seen most frequently in patients with severe pulmonary disease.
• Rapid ventricular rate can be symptomatic (hypotension, angina, CHF).
• Treatment — improvement of the concomitant pulmonary disease and consideration of administration of verapamil. Digoxin is not effective in treatment of this rhythm.
Multifocal Atrial Tachycardia
7. Atrial Escape Complex
• P wave that occurs later than would be expected from the sinus rate.
• Like all escape complexes, it can occur only when the normal cardiac pacemaker does not function, as in sinus arrest.
8. Atrial Tachycardia
• Abnormal supraventricular rhythm.
• Results from either an atrial automatic focus or a reentrant circuit that lies entirely within the atrium.
• Rate > 100 bpm.
• P wave morphology is usually different from that of the sinus P wave.
• Can be intermittent or incessant (present more than 50% of the time).
When incessant, it can cause symptomatic dilated cardiomyopathy that is reversible with control of the tachycardia.
• Can result from digitalis toxicity, particularly when it occurs in combination with 2° AV nodal block, Mobitz Type I (Wenckebach).
• Emergency treatment of this rhythm (when patient is symptomatic) — synchronized cardioversion with appropriate anesthesia.
• Short-term pharmacologic control — drugs that decrease AV nodal conduction (b-blockers, Ca++ blockers).
9. Atrial Flutter
• Atrial rate = 250-350 bpm; ventricular response usually ~ 75, 150, or 300 bpm.
• Atrial beats are regular.
• Ventricular beats are also usually regular but you may see a variable block, because the junctional area blocks some beats.
• Causes decreased filling of the ventricle if ventricular rate is too fast.
• P wave is called an F wave and has a sawtooth, picket fence shape in leads II, III, aVF, and V1.
• Even if flutter waves are not found, this rhythm should be suspected when the ventricular rate ranges from 140-160 bpm and there is no clear evidence of atrial activity.
• PR interval is unknown.
• QRS is normal (narrow) but not 1:1 with the F (P) waves.
• At least 2 different types (FYI) — one with regular morphology and a rate of 240-350 bpm and a rapid type with a rate greater than 350 bpm. The rapid type is difficult to treat and often Ds to V fib.
• Carotid massage may slow the ventricular rate so flutter waves become apparent but massage does not terminate the dysrhythmia.
• Treated if the ventricular rate is rapid or patient symptomatic — b- or Ca++ channel-blockers or digoxin; then either synchronized cardioversion or pacing.
• Rapid atrial pacing may be used to interrupt flutter. For example, if the flutter rate is 280 bpm, the heart could be paced at 320 bpm. Pacing may produce A fib, which is easier to treat than flutter.
• Supraventricular rhythm resulting from a reentrant circuit that lies within the R atrium or a single ectopic focus.
Usually begins with a premature beat and then is supported by reentry beats.
Can occur alone, but is usually associated with hypertensive cardiomyopathy, COPD, cor pulmonale, CAD, rheumatic heart dz., congestive cardiomyopathy, or hyperthyroidism.
• New onset is seen in about 5% of cases of acute MI. Clinician may also want to check for CHF, since worsening CHF can present with these rhythms.
10. Atrial Fibrillation
• P wave is called an f or fibrillatory wave and consists of a wavy line that is seen best in the inferior leads (I, II, aVF).
• PR interval — none.
• QRS is normal or aberrant.
• Atrial and ventricular rate and rhythm are irregular.
• R-R interval and baseline are variable.
• Atrial rate is > 350 bpm; the ventricular rate is 40-170 bpm. Ventricle response may be slow (< 60) or rapid (> 100).
• Characterized by an irregularly irregular ventricular rate that is usually rapid in young patients, but may be normal or even bradycardic in elderly patients or patients taking medications that cause AV nodal blockade.
• Most common supraventricular rhythm — found in 4/100 people age 55-64; 9/100 of those over 65.
• Seen more frequently in males than females.
• Ineffective quiver that occurs with A fib results in the loss of the atrial kick; also results in decreased CO, increased O2 demand, and an enlarged left atrium (? cause or effect).
• Usually due to re-entrant excitation with multiple reentry circuits within either atria, or both.
• May be chronic or paroxysmal.
• Can occur alone, but is usually a/w hypertensive cardiomyopathy, COPD, or congestive cardiomyopathy.
• New onset of either atrial flutter or A. fib. is seen in about 5% of cases of acute MI. Clinician may also want to check for CHF, since worsening CHF can present with these rhythms.
• Pulse deficit occurs — apical pulse is > than radial because some contractions are so feeble.
• Well tolerated by most patients. There are four different types (types I-IV) of A. fib.
• Peripheral arterial emboli due to thrombi in the atria are seen in 30% of the patients; a/w an increased incidence of CVA after age 59, because the risk of emboli is 4-5x normal.
Low dose anticoagulation with warfarin significantly Æ the stroke rate without significantly increasing the hemorrhage rate.
Goal = 1.3 to 1.6 x normal PT (or an INR of 2.0-3.0).
ASA does not decrease risk of emboli in people over 70 y.o. as well as it does in middle-aged people.
HTN predisposes to emboli risk in A. fib. patients.
• Seen with atrial muscle dz., atrial distention, SA node dz., CHF with hypoxemia, stress, pericarditis, drug toxicity, hyperthyroidism, mitral stenosis, HTN, cerebral or cardiac ischemia, PE, Rh heart disease, acute infection, MI, cardiomyopathy, COPD, and digitalis toxicity.
• Treatment
Cardioversion can be accomplished with antiarrhythmic drugs or electrically.
Antiarrhythmic drug therapy may be 6 doses of flecainide or quinidine and, if that does not work, synchronous cardioversion may be used.
Anticoagulation therapy is begun 3 weeks before and continued 4 weeks after synchronous cardioversion.
Digitalis decreases the AV block and allows increased ventricular filling, so it is used to treat rapid ventricular responses.
Quinidine, propranolol, verapamil, and Pronestyl (also used to control rate) are also used.
Catheter ablation of the His bundle to create a 3° AV block is used for the patient with a rapid ventricular rate that does not respond to medications. This requires a permanent pacemaker.
Clonidine also used to treat A. fib. with a rapid ventricular response.
Clonidine decreases sympathetic outflow from brain, and increases parasympathetic outflow, thus slowing conduction across the AV node, decreases the ventricular response rate, and sometimes converting A. fib. to NSR; can be used in place of b- and Ca++ blockers (with CHF), in place of b-blockers (asthma), and in place of digitalis (hypertrophic obstructive cardiomyopathy).
• Digitalis toxicity is suggested by a regular ventricular response (accelerated junctional rhythm) in combination with atrial fibrillation.
• In the presence of an accessory AV pathway, atrial fibrillation can manifest as a rapid, irregularly irregular wide complex tachycardia that can resemble ventricular tachycardia closely; should be suspected particularly in young patients with very rapid tachycardia that is well tolerated hemodynamically; close examination of the ECG will reveal irregularly irregular RR intervals.
• Important to obtain a 12-lead ECG before cardioversion because the location of the pathway, and therefore the risks of a subsequent curative catheter-mediated radiofrequency ablation procedure, can be estimated fairly accurately from the 12-lead ECG.
• Do NOT give digitalis or verapamil to try to slow ventricular response if an accessory pathway is suspected. These drugs can accelerate conduction over accessory pathways, resulting in even more rapid ventricular activation which can, in turn, induce ventricular fibrillation.
• Four issues related to care of patients with atrial fibrillation:
1. Control of the rate of the ventricular response,
2. Conversion of the atrial rhythm to sinus rhythm,
3. Maintenance of sinus rhythm following conversion, and
4. Prevention of embolic stroke from thrombi that form in the fibrillating left atrium.
11. Supraventricular Tachycardia
• A generic name for a variety of specific supraventricular rhythms, including Atrioventricular Reentrant Tachycardia, Atrioventricular Nodal Reentrant Tachycardia, and Atrial Tachycardia.
• Also used in reference to any narrow complex rhythm to distinguish it from wide-complex rhythms that could arise in the ventricle.
• Use of the term includes atrial fibrillation, atrial flutter, junctional tachycardia, accelerated junctional rhythm, and multifocal atrial tachycardia.
12. Paroxysmal Supraventricular Tachycardia (PSVT)
• Old name was paroxysmal atrial tachycardia (PAT); no longer called PAT unless P waves are clearly seen.
• PSVT rhythms start and stop suddenly in comparison to sinus tachycardia, which begins and ends gradually.
• PSVT is also differentiated from sinus tachycardia by altered configuration of the P waves.
• PSVT is supported by either an AV nodal reentry circuit (AV nodal reentry tachycardia — AVNRT) or an AV reentry circuit using the AV node and an accessory pathway (circus movement tachycardia — CMT). Rate 170-250 bpm.
13. Atrioventricular Nodal Reentrant Tachycardia (AVNRT)
• Rate — 150-250 bpm (rarely above 250).
• QRS that is usually normal in contour and duration.
• P waves may or may not be seen; follow closely after the QRS if they are seen; retrograde P is usually lost in the QRS.
• A reentrant supraventricular rhythm whose circuit is located in the region of the AV node.
Two functionally separate pathways down to the AV node — a slow (posterior) pathway and a fast (anterior) pathway). Slow pathway has the shortest refractory period.
When an early atrial beat arrives at the AV node, it may be conducted only down the slow pathway to the ventricles, turning around in the AV node to return to the atria via the fast pathway.
Atria and ventricles are activated simultaneously.
Following a PAC, the PR interval at the onset of the tachycardia is long as the impulse uses the slower pathway.
Subsequent P waves are buried in the QRS (retrograde activation.) QRS complexes are narrow.
• Only about 60% of narrow-complex tachycardias have this mechanism but 20% of all narrow-complex tachycardias are AVNRT, which use a concealed accessory pathway for retrograde conduction.
AV Nodal Reentry Tachycardia
(2 beats sinus, early beat, long PR Æ impulse "jumps over to slow pathway)
• Clinical significance of this rhythm depends on the rate.
• Most often paroxysmal and benign. Stops abruptly with effective treatment.
Usual initial treatments are the Valsalva maneuver, then IV adenosine (Adenocard).
Adenocard stimulates K+ conductance producing hyperpolarization, leading to AV block and coronary dilation.
If these are unsuccessful, one can try medication that reduces conduction through the AV node.
Rhythm can now be cured by catheter-mediated radiofrequency ablation.
In some cases it may be recurrent, symptomatic, and refractory to medical therapy.
• Presence is usually unrelated to preexisting heart disease.
• AVNRT is usually initiated by a PAC, and maintained by a reentry mechanism; impulse moves in an anterograde direction over a slow conducting pathway and retrograde over a more rapid pathway.
• Atria contract against closed AV valves, causing a reflux up the jugular vein.
• Other s/s are dyspnea, anginal pain, perspiration, fatigue, anxiety, dizziness, and polyuria; in the presence of heart dz., you may see CHF or shock.
• AV Nodal Pathways: 2 separate pathways leading to a common AV node exist in many normal individuals. Normally, impulses travel through the conduction fibers in an even and synchronous manner and collide with each other in the potential circuits. Ischemia can depress conduction or convert fast cells to slow cells setting up an environment for AV node reentry tachycardia (AVNRT).
14. AV Reciprocating Tachycardia (AVRT or "Circus Movement" Tachycardia)
• Orthodromic Tachycardia — most common form, proceeds antegrade (from atrium to ventricle) over the AV node, and retrograde over an accessory pathway.
Pt. has two AV pathways — the normal AV node and His bundle + an accessory pathway.
Usually initiated by a PAC but may be initiated by a PVC.
Impulse enters ventricles via the AV node and His bundle and returns to the atria via a rapidly conducting accessory pathway placing the P' wave close to the preceding QRS.
Impulse circulates around and around in this sequence.
Initial PR interval not prolonged.
Also a common arrhythmia in WPW syndrome.
• Antidromic Tachycardia — proceeds in the reverse direction; a wide QRS tachycardia except when the accessory pathway is located in the right anteroseptal location very close to the His bundle.
• When multiple pathways are present, it is also possible for the circuit to use 2 pathways as a circuit.
• P waves may or may not be seen, but they usually do not follow closely after the QRS if they are seen.
• Clinical significance — depends on the rate.
• Stops abruptly with effective treatment.
Usual initial treatments — Valsalva maneuver, then IV adenosine.
If these are unsuccessful, one can try medication that reduces conduction through the AV node, except that verapamil and digitalis SHOULD NOT BE GIVEN.
Can now be cured by catheter-mediated radiofrequency ablation.
C. Accessory AV Pathways
• "Preexcitation syndrome" is the term used to describe pathways that bypass the AV node and cause short PR intervals. Those pathways that insert into the ventricle wall produce delta waves that are seen in sinus rhythms.
Delta waves result from a fusion complex (2 beats trying to control ventricles at same time).
• There are three common bypass systems:
_ Wolff-Parkinson-White (WPW) Syndrome:
The abnormal pathway is called the Kent bundle or accessory AV connection. This pathway bypasses the normal AV conduction system and connects the atria directly to the ventricles.
There is a delta wave and the PR is short. WPW is the most common preexcitation system.
Term used to describe the presence of one or more accessory AV pathways that conduct in the antegrade direction, with or without retrograde conduction.
Patients with this syndrome are susceptible to AV reentrant tachycardia and atrial fibrillation.
_ Mahaim Fiber: The abnormal pathway for this system is a fasciculo-ventricular or a nodo-ventricular connection. The pathway originates below the AV node and bypasses part or all of the ventricular conduction system and inserts directly into the ventricle wall. The pathway
connects the lower AV node or bundle of His directly to the ventricle. The PR is normal, but a delta wave is produced.
_ Lown-Ganong-Levine Syndrome: The abnormal pathway for this system is the James bundle (atrio-Hisian tract). This pathway inserts into the conduction system just below the AV node, thus connecting the atria to the lower part of AV junction. A short PR is seen but there is no delta wave with this pathway.
Reciprocal Complex — A QRS complex that is caused by activation of a reentrant circuit rather than by the sinus node. This can be harbinger of AV nodal tachycardia or AV tachycardia.
Retrograde Atrial Activation — A P wave that occurs because of activation of a portion of the heart below the sinus node, including elsewhere in the atrium, the AV node (via the fast or a slow AV nodal pathway) or the ventricle (via an accessory pathway). Retrograde P waves typically are inverted in the inferior and right precordial ECG leads (II, III, aVF, and V1), in which the normal sinus P wave is upright.
E. Junctional Ectopic Beats and Rhythms
1. Junctional Dysrhythmias
• It is really the tissue around the AV node that is normally conductive.
• Junctional dysrhythmias are significant because they may be too fast or too slow to provide adequate cardiac output.
• Depending on the timing of retrograde conduction, the P occurs before (high junctional), after (low junctional), or during (mid junctional) the QRS.
• Junctional dysrhythmias often signal digitalis toxicity.
UNCOMPLICATED NODAL RHYTHMS
2. Junctional Escape Complexes
• Junctional escape rhythms originate low in the AV node, high in the common bundle. They may be recognized by following clues
• The first beat of a junctional escape occurs later in the cycle than the next expected beat; the escape beat occurs after a beat has been missed
• Rate of 40-60 (inherent rate of junctional cells)
• The rhythm is regular
• P — inverted in II, III, and aVF (atria depolarization is retrograde)
• P and QRS not 1:1
• There is no PR interval unless the P appears before the QRS, then it is less than normal.
• QRS has normal morphology for the patient that is not preceded by a P wave and occurs later than would be expected from the sinus rate.
• Like all escape complexes, it can occur only when the normal cardiac pacemaker does not function, as in sinus arrest.
3. Junctional Premature Complexes
• Treated like premature atrial beats.
• If the atria and ventricles contract together, blood is forced back to the vena cava causing distended neck veins.
• QRS complex that occurs earlier than would be expected from the sinus rate, and that usually has a normal morphology for the patient.
• It can fail to conduct retrograde through the AV node, in which case it results in a compensatory pause. (The next P wave occurs at the same time as would be expected had the JPC not occurred.)
• More usually, it does conduct through the AV node, so that the following P wave may occur either sooner or later than would be expected.
• Relatively uncommon.
• Can be seen with increased frequency during stress, with ingestion of caffeine, and with sympathomimetic drugs such as some over-the-counter (OTC) cold remedies.
• Can also be misdiagnosed when the P wave of a PAC is obscured by the preceding T wave.
4. Junctional Premature Couplets
• An unusual rhythm, and most likely represents two cycles of one of the supraventricular tachycardias.
5. Junctional Rhythms
• A slow rhythm, with rates ranging from 40 to 60 beats per minute.
• QRS complexes have the patient's normal morphology.
• Usually, no P waves are seen. When P waves are present, they follow closely after the QRS complexes.
• Results from the backup pacemaker capability of the AV node during sinus arrest.
6. Accelerated Junctional Rhythms
• A supraventricular rhythm resulting from a focus in or near the AV junction.
• Rate ranges from 60 to 100 bpm.
• An abnormal rhythm that can result from digitalis toxicity, particularly when it occurs in combination with atrial fibrillation.
• Can also result from physiologic stress and other causes of increased sympathetic nervous system tone.
7. Junctional Tachycardia
• A supraventricular rhythm resulting from a focus in or near the AV junction.
• Rate is around 100 bpm.
See also: accelerated junctional rhythm.
• Usually results from a primary arrhythmia rather than as a response to physiologic stimulation.
• ECG usually cannot distinguish this rhythm from the more common types of supraventricular tachycardia, for which different treatments may be appropriate.
• Junctional tachycardia can be of several types — AVNRT (150-250), enhanced automaticity tachycardia (100-150), or accelerated junctional rhythm (digitalis induced) (65-100).
8. Interventions for Junctional Rhythms:
• Assess the ventricular rate, BP, sensorium, urine output, and skin changes • Determine if the dysrhythmia is due to digitalis
• Assess other possible causes like ischemia, infarction, heart disease