Download Arrhythmias Complicating AMI

Arrhythmias Complicating
Acute Myocardial
Infarction
Sinus Bradycardia





Most common arrhythmia occurring during the early
hours after MI and may occur in up to 40% of
inferior and posterior infarcts.
May be related to autonomic imbalance or to atrial
and sinus node ischemia or both.
Profound bradycardia may predispose the patient to
ventricular ectopy.
Usually resolves spontaneously, treatment is reserved
for hemodynamically symptomatic arrhythmias and
those with bradycardia dependent vent. Arrhythmias.
Atropine usually successful for symptomatic
bradycardia. Temporary pacing is rarely required.
Indications for Temporary Pacing
in the Peri-infarct Period








Sinus bradycardia with hypotension, bradydependent vent. arrhythmias, angina,
syncope/presysnope, or congestive heart failure
and refractory to atropine.
Accelerated idioventricular rhythm with
symptoms and rate less than 40 beats/min.
Prolonged (>3 s) sinus pauses.
Atrial fibrillation with inadequate vent. response.
Asystole.
Mobitz II second degree AVB.
Third degree block
New or progressive bifascicular block
Sinus Tachycardia






May occur in up to 1/3 of patients in the peri-infarct period,
esp. with ant. MI.
The ischemic left ventricle may have a relatively fixed
stroke volume; thus augmenting CO by increasing HR.
It may occur as a result of sympathetic stimulation from
locally released and circulating catecholamines, concurrent
anemia, hypo or hypervolemia, hypoxia, pericarditis,
inotropic drugs, pain, fever.
Treatment includes optimizing hemodynamics, oxygenation,
correction of anemia, electrolyte and acid base
abnormalities, pain control, and anxiolytic agents.
Beta blockers are indicated for patients without evidence of
significant LV dysfunction or hypovolemia.
Persistent sinus tachycardia as an early manifestation of
heart failure is an indicator of poor prognosis.
Premature atrial Contractions
Up to one half of patients with MI
 May be due to atrial or sinus node ischemia,
atrial fibrillation, pericarditis, anxiety or pain.
 The combination of atrial asystole and rapid
ventricular rate markedly decreases cardiac
output and increase oxygen demands.
 Attempts should be made to restore sinus rhythm;
if not, rate should be controlled aggressively to
minimize oxygen demand.
 May have no prognostic significance after MI.

First degree AVB




5 % to 10 % patients with MI at some times during
peri-infarct period.
Almost all have supra-Hisian conduction abnormalities.
Rare cases of infranodal block are seen with anterior
MI and associated fascicular block; these patients are
at risk for progressive block, including third degree
block with ventricular asystole.
May be associated with drugs that prolong AV
conduction.
nd
2
degree Mobitz Type I Block
May be seen with up to 10% cases of MI,
typically inferior infarcts, and is due to increased
vagal tone and ischemia.
 Conduction defect is usually in the AV node.
 When seen early after MI, usually responds to
atropine and resolves within 48-72 hours.
 Late occurring Wenckebach is less sensitive to
atropine and may be due to recurrent ischemia.
 Very rarely it may progress to higher grades of
block that require permanent pacing.
 It has no impact on long-term prognosis.

Second-degree Mobitz Type II Block






1% of cases of MI and more common with anterior
MI.
High risk of progression to higher degrees of block,
including sudden complete heart block with
ventricular asystole.
Should have temporary pacing wire placed
prophylactically.
Conduction defect is most likely infranodal.
Most patients need permanent pacing and if it is
uncertain, EP evaluation should be performed before
discharge to assess integrity of the infranodal
conduction system.
Long term prognosis is related to size of infarct rather
than conduction abnormality.
Complete Heart Block





With either anterior or inferior infarct.
With inferior infarcts , the defect is likely to be in the
AV node, with escape rhythms exceeding 40 beats/min
and exhibiting a narrow QRS complex.
With anterior infarct, the conduction defect is
infranodal and the escape rhythm (if present) is usually
less than 40 beats/min with a wide QRS complex.
Typically CHB seen with ant. MI is preceded by
progressive fascicular, bundle, or mobitz type II block.
Temporary pacing may be required with inferior MI if
the patient is hemodynamically unstable. It should
always be used with anterior MI if progressive or CHB
is present.
Complete Heart Block - Continued




Permanent pacing is almost always required for high
grade block in the setting of anterior MI.
The prognosis is poor for these patients because of
the large amount of myocardium involved.
EP evaluation should be considered for patients with
Anterior MI and transient CHB to assess the integrity
of the infranodal conduction system.
Transient CHB with inferior MI rarely requires
permanent pacing and usually resolves spontaneously.
BBB
New BBB has been reported in about 15% of
cases of MI and is associated with an increased
risk of CHB, CHF, cardiogenic shock, vent.
arrhythmias and sudden death.
 Most commonly seen is RBBB; LBBB or
alternating BBB being less common. This may
be related to discrete anatomical location of RB
compared to broad, fan shaped LB.
 The highest incidence of BBB occurs with LAD.

BBB



Progressive infra-Hisian block indicates a
significant risk of sudden CHB and asystole, and
patients demonstrating progression should have
temporary pacing wires placed.
Persistent BBB confers a significantly higher
mortality, because of the large amount of
myocardium that must be involved to include the
BB.
Thrombolytic therapy and catheter-based early
reperfusion appear to decrease the incidence of
BBB in the peri-infarct period.
Intraventricular Block
New isolated LAFB occurs in 3% to 5% of
patients with MI; New isolated LPFB
occurs in 1% to 2% of patients with acute
MI.
 Anatomically, LPFB is larger; hence a large
infarct is required to produce block.
Mortality is greater among those patients.
 LAFB with new RBBB is also indicative of
a larger infarct and higher subsequent
mortality.

Ventricular arrhythmias - Factors



Damaged myocardium: A substrate for development of
reentrant circuits. Large MI, Early LV dilatation and
remodeling, perhaps due to ventricular stretching and
electromechanical feedback.
Arrhythmia trigger: spontaneous ventricular
arrhythmias, variation in cycle length and HR.
Electrolyte Imbalance, autonomic nervous system
dysfunction/imbalance, increased catecholamines,
continued ischemia, impaired LV function.
Mechanism


Changes in the resting membrane potential and the
inward and outward ionic fluxes during action
potential lead to alterations in the conduction,
refractoriness, and automaticity of cardiac muscle
cells.
Increase in QT dispersion due to inhomogeneity in
myocardial cells may be a contributing factor. The
central ischemic zone has decreased impulse
velocity and increased refractoriness; the normal
zone has increased or normal impulse velocity
with decreased refractoriness; and the area in
between has intermediate properties.
Mechanism


Less negative resting membrane potential due to loss of
energy dependent ATP-ase pump and consequently
decrease K influx and increased K loss.
The ventricular arrhythmias after MI can be divided into
early ( upto 30 minutes after total occlusion of artery)
and delayed phase (3 to 6 hours and as long as 3 days).
Early phase is further divided into 1a (2-10 minutes after
total occlusion of artery) or 1b (10 to 30 minutes).
According to animal studies arrhythmias occurring in 1a
phase are mainly due to re-entry. Occasionally it may be
due to nonreentry initiated PVBs which may precipitate
eventually reentry arrhythmias.
Mechanism



1b phase has no clear mechanism established but it
is thought to be due to abnormal automaticity.
Arrhythmias occurring in late phase are thought to
be due to surviving purkinje tissue located within
the subendocardium which displays abnormal
automaticity. It also shows increase sensitivity to
catecholamines.
Arrhythmias occurring in chronic phase (after 3
days) - reentry.
Ventricular Fibrillation



Incidence of primary VF in MI is about 5% in patients
in whom a documented rhythm is obtained. It occurs
without antecedent warning arrhythmias in over half.
The true incidence of primary VF is probably higher
because it has been estimated that one-half of all
patients with coronary artery disease die of sudden
death presumably VF.
Factors associated with an increased incidence of VF
include current smoking, LBBB and hypokalemia.
Ventricular Fibrillation
Patients with Ant. MI and VF have worse longterm prognosis than those with inferior MI.
 VF may occur with reperfusion after
thrombolytics or catheter-based therapy.
 Treatment with prompt defibrillation. Beta
blockers appear to decrease the incidence of
lethal vent arrhythmias including VF, in the
peri-infarct period

Ventricular Tachycardia



VT occurs in 10% to 40% of cases of MI. Early VT
during the first 24 hours is usually transient and
benign.
Late occurring VT is associated with transmural
infarction, LV dysfunction, hemodynamic
deterioration, and a markedly higher mortality, both
in-hospital and long-term.
If the rate is slow and hemodynamically tolerated,
cardioversion with drugs may be attempted. Rapid VT
(>150 beats/min) or VT with hemodynamic
deterioration should be treated with prompt DC
cardioversion.
Accelerated Idioventricular rhythm







Rate faster than the normal ventricular escape rhythm
but slower than the VT.
Onset and offset is usually gradual, and isorhythmic
dissociation is often present.
Has been reported in 10% to 40% of cases of MI,
especially but not necessarily with early reperfusion.
The incidence is equal in anterior and inferior infarcts
and not related to infarct size.
Not related to increased mortality or VF.
May also be seen with dig toxicity, myocarditis, and
cocaine use..
Symptoms are usually related to loss of AV synchrony
or slow ventricular rates or both.
Premature ventricular Complexes





Occur frequently during MI.
Their significance preceding VT and VF is unclear.
Treatment of PVCs in the peri-infarct period has not
been shown conclusively to decrease incidence of
malignant vent. Arrhythmias or to improve mortality.
The pooled data of randomized trials in which PVCs
were treated prophylactically in the peri-infarct period
with lidocaine demonstrated an increased mortality.
Beta blockers may be the best option for treating PVCs
and preventing malignant arrhythmias
Reperfusion Arrhythmias


Typically accelerated idioventricular rhythm has
been credited with being a marker of reperfusion,
However, any arrhythmia or no arrhythmia may be
seen with reperfusion; conversely, AIVR may
occur without reperfusion. Other clinical factors
should be considered when deciding whether
reperfusion has occurred.
The appearance of reperfusion arrhythmias is
related to size of infarct, length and severity of
ischemia, rate of reperfusion, HR, extracellular K
concentration, and the presence of congestive
heart failure or LVH or both.
Asystole and EMD
Occur in a small fraction of patients with
MI and are usually associated with large
infarcts.
 The prognosis is extremely poor even with
aggressive therapy.
 Defibrillation should be attempted in
patients with apparent systole, because the
rhythm may be actually fine VF

Other Miscellaneous

T-Wave alternans: Transient finding
usually seen with ischemia and most
pronounced in leads overlying the affected
myocardium.
Other Miscellaneous


Regional pericarditis sometimes seen after Qwave MI may present with PR depression, but
more commonly with atypical ST-segment and Twave changes. These changes typically consist of
gradual premature reversal of initially inverted T
waves or persistent/recurrent ST-segment
elevation or both.
Persistent ST-segment elevation after infarct may
be due to continuing ischemia or aneurysm
formation or may herald free wall rupture
Other Miscellaneous





LV free wall rupture occurs in approximately 10%
cases of fatal transmural MI.
EKG finding include failure of the characteristic
evolution of the ST segment, T wave or both.
Persistent, progressive, or recurrent ST-segment
elevation in the absence of recurrent ischemia may be
seen.
Failure of T waves to invert or initial inversion
followed by reversion may be seen.
Abrupt bradycardia responsive to atropine may occur
and is believed to mark the time or rupture