β-Blockers are used for rate control, but are not appropriate in patients with acute HF. In ill patients with acute HF, some degree of tachycardia may be tolerated to prevent a shock state (heart rate of 100–110 bpm). Anti-congestive measures and afterload reduction improve the AF rate; if needed, digoxin and IV amiodarone may be added for rate control.
H. Accelerated junctional rhythm (also called non-paroxysmal junctional tachycardia)
The accelerated junctional rhythm is an automatic rhythm originating from the AV node at a rate of 70–130 bpm, often ~80 bpm. The junctional rhythm is faster than the sinus rhythm, which leads to AV dissociation. Sometimes, the junctional and sinus rhythms compete at close rates, leading to isorhythmic AV dissociation, i.e., some beats may be sinus beats preceded by sinus P waves, while the other beats may be junctional beats dissociated from P waves and showing up at any deceleration of the sinus P rate (see Chapter 13, Figure 13.9). The QRS is narrow, except in patients with a baseline bundle branch block. This rhythm may occur with inferior MI, is benign and transient, and does not generally require any specific therapy unless the patient is in shock. In shock, atrial pacing at a rate faster than the junctional rhythm may be performed to promote AV synchrony and a more appropriate rate for shock.
Persistent sinus tachycardia is a strong negative prognostic marker; it often signifies pump failure from a large MI. Do not necessarily attempt to slow it down, and avoid β-blockers in the first 24 hours if the heart rate exceeds 110 bpm. One may attempt to slow it down in young patients with hyperdynamic circulation and limited-size MI. Sinus tachycardia may improve with anticongestive measures and afterload reduction.
V. Bradyarrhythmias, bundle branch blocks, fascicular blocks
A. Inferior MI
The sinus nodal artery originates from the proximal RCA (60%) or the LCx (40%). The AV nodal artery originates from the AV groove con- tinuation of a dominant RCA (90%) or a dominant LCx (10%).
In inferior MI, sinus bradycardia and AV blocks may develop in the first 24 hours, at which time they are usually brief and result from the increased vagal tone that accompanies inferior MI. Beyond 24 hours, the AV block is due to ischemia and edema of the AV node and is more persistent, but eventually resolves within a few days (<1 week). The AV node is resistant to ischemia, and therefore it almost never infarcts. When AV block is seen along with a fast P-wave rate, the block is due to nodal ischemia or edema, rather than a high vagal tone.
The AV block being at the nodal level, it may manifest as first-degree AV block, second-degree type I AV block, or complete AV block with a junctional rhythm (rate 40–100). Those blocks are usually well tolerated, develop gradually (first-degree to second-degree then third-degree AV block), and resolve gradually. Complete AV block is seen in ~4-5% of inferior MIs, mostly on the first day.150,151
Complete AV block is associated with a larger MI, more RV MI, and a 2-fold higher in-hospital mortality.150,151 Patients who survive to hospital discharge, however, do not have an increase in long-term mortality in some,152 but not all studies.150
Treatment – AV block that occurs in the first 24 hours responds to atropine, which should be used in case of hemodynamic instability. Since it is not driven by a high vagal tone, later AV block (>24 hours) does not typically respond to atropine but may respond to aminophylline (adenosine-receptor blocker) (ACC); being usually well tolerated with a good escape, complete AV block does not require pacing. It only requires temporary transvenous ventricular pacing in case of shock, HF, or low-output signs.
Symptomatic sinus bradycardia or pauses are initially treated with up to 2 mg of atropine. Transcutaneous or transvenous pacing may be used if symptomatic bradycardia persists.
B. Anterior MI
The bundle branches and fascicles are, at least partially, supplied by the LAD. Anterior MI may lead to bundle branch blocks and AV block. The AV block is Hisian or infra-Hisian and is usually preceded by bundle branch blocks. A high-degree AV block is seen in ~1-2% of anterior MIs and portends a very high mortality related to pump failure (3–4 times increase in mortality; mortality was >50% in the pre-reperfusion era).152,153 The anterior MI’s AV block often resolves but may recur in a minority of patients.153
Transvenous pacing, while indicated for any high-grade second- or third-degree AV block occurring with anterior MI, even if asymp- tomatic, does not improve the grim overall prognosis that is dictated by the pump function. Permanent pacing is indicated for persistent, infranodal second- or third-degree AV block.
C. Bundle branch and fascicular blocks
Approximately 2–8% of STEMI patients develop some form of new intraventricular block, LAFB being the most common block. Note the following arterial supply:154
The right bundle mainly has a single arterial supply from the LAD (first septal branch).
The left anterior fascicle has a single arterial supply from the LAD (first septal branch).
The His bundle, the main left bundle, and the posterior fascicle have a dual supply from the LAD septal branches and the AV nodal artery. Thus, the composite of the anterior and posterior fascicles, the branching left bundle, usually has a dual supply. This explains why it is difficult to infarct the left bundle and why most new LBBBs are non-ischemic in nature.
RBBB or LAFB are most commonly seen in anterior MI,155 but may also be seen in inferior MI if the LAD has severe disease and is dependent on the RCA for collaterals. LBBB may result from either anterior or inferior MI, and is more likely seen when both RCA and LAD are com- promised, with one acutely occluded and the other chronically obstructed (in the GUSTO trial, LBBB was associated with an RCA culprit at least as much as an LAD culprit).10,156
The conduction system is more resistant to ischemia than the myocardium, as the myocardial cells require much more O2 for their continuous mechanical work than the electrical cells, which also frequently receive dual or collateral supply. This explains why conduction blocks are frequently due to edema or ischemia rather than necrosis and are frequently reversible (25-75% of the cases).155,156 If not reversible, and if secondary to MI rather than degenerative disease, the myocardial injury is usually quite extensive (e.g., persistent RBBB or LBBB).
While a chronic bundle branch block (BBB) has a very low risk of progression to complete AV block, 20% of acute BBBs progress to complete AV block, and 25–40% of acute bifascicular blocks progress to complete AV block.
Beside the risk of progressing to complete AV block, a new BBB is independently associated with a two- to threefold increase in in-hospital mortality, HF, and VF, particularly because it correlates with a more extensive infarction (mortality 18% vs. 11% in GUSTO-I trial; 35–50% in the pre-reperfusion era).156 Up to 75% of these blocks are transient, and transient blocks do not portend any increase in mortality.155,156 Old BBBs do not portend any increase in mortality either. Both RBBB and LBBB are associated with the same increase in mortality. 155,156
A standby temporary transcutaneous or transvenous pacemaker is indicated for a new BBB or bifascicular block occurring in anterior MI.
VI. LV aneurysm and LV pseudoaneurysm
A. LV aneurysm
Dyskinesis signifies that a non-contractile myocardial segment moves out during myocardial contraction and moves in during relaxation (paradoxical motion). LV aneurysm is an extreme form of dyskinesis and consists of a thin area of infarcted,