(Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries), (Assessment of Pexelizumab in Acute Myocardial Infarction).
(See Chapters 36 and 37)
Vagotonia refers to a condition of excessive stimulation of the parasympathetic nerve fibers carried by the vagus. nerve increased activity in the vagus nerve tends to slow the heart, constrict bronchial passages in the airway, and increase digestive activity.
bundle branch block
(See Chapters 37 and 38)
See Chapter 38.
Electrical complications of mi
Electrical Complications of MI
Dr. Virbhan Balai
Department of cardiology
National heart institute, Delhi
Cardiac Arrhythmias and Their Management
During Acute Myocardial Infarction
• All forms of tachycardia and bradycardia can
• Myocardial oxygen consumption
• Optimal rate - 60 to 80 beats/min.
• Loss of the atrial contribution to ventricular
• Loss of atrial transport ↓ LV output by 15%-
• In patients with STEMI, atrial systole boosts
– End-diastolic volume by 15%
– End-diastolic pressure by 30%
– Stroke volume by 35%.
• “warning arrhythmias.” Presage VF.
1. Frequent VPCs = >5/min
2. VPCs with a multiform configuration
3. Early coupling (the “R-on-T” phenomenon)
4. Couplets or salvos
• Primary VF
– Occurs without antecedent warning arrhythmias
– May even develop despite suppression of warning
• Primary VF and VPCs (esp. R-on-T beats)
– Occur during the early phase of STEMI
• The incidence of VF in pt`s with STEMI declined.
• Prophylactic suppression of VPCs with
antiarrhythmic drugs is not indicated .
• Suppression may ↑the risk for fatal bradycardic
and asystolic events.
• Do not routinely prescribe antiarrhythmic drugs,
other than beta blockers.
• Determine recurrent ischemia or electrolyte or
metabolic disturbances .
• When VPCs are accompanied by sinus
tachycardia → sympatho adrenal stimulation.
• Use beta-adrenergic blockade.
• Early administration of an IV beta blocker
reduces the incidence of VF in cases of
Accelerated Idioventricular Rhythm
• Occurs during the first 2 days
• Equal frequency in anterior and inferior
• Most episodes are of short duration.
• Often observed shortly after successful
reperfusion established with fibrinolytic
• Frequent AIVR in pt`s without fibrinolysis &
following pri PCI have diff implications .
• AIVR does not affect prognosis.
• Routine Tt is not required.
Ventricular Tachycardia and
• Mechanism - re entry
• Caused by inhomogeneity of the electrical
characteristics of ischemic myocardium.
• Cellular mechanisms for reperfusion
– Washout of various various ions such as lactate, k+
and toxic metabolic substances that have
accumulated in the ischemic zone.
• Late VT / VF more common in pt`s with
transmural infarction and LV dysfunction
• More frequently associated with hemodynamic
• Hypokalemia increases the risk for VT
• Low K+ levels should be treated promptly.
• Pt`s with STEMI have reduced intracellular
– not adequately reflected by serum measurements.
• Magnesium should be repleted, achieve a
serum level of 2 mEq/liter.
• Early beta blocker use reduces VF and can be
instituted in pt`s without CI.
• Lidocaine prophylaxis to prevent primary VF
is no longer advised.
• Unstable VT or VF -Electrical cardioversion
• I/V Amiodarone- prevention of refractory
• Sod bicarbonate- X, bcz of high osmotic load
• Hyperventilation is a more suitable means of
clearing the acidosis.
• Revascularization- Urgent, if caused by
• Antiarrhythmic drug- extended therapy
• Failure of electrical cardioversion
1. Rapidly recurrent VT or VF
2. Electromechanical dissociation
3. Electrical asystole.
• GUSTO-I study, among pt`s who under went
fibrinolysis ~10% experienced VT/VF.
• APEX-AMI study,-pt`s treated with pri PCI,
sustained VT/VF developed in 5.7%.
• Worse clinical outcomes in pts with VT/VF
than in those without VT/VF.
• Early versus late VT/VF, at 90 days doubles.
• VT/VF after(> 48 hrs) without reversible
cause, ICD for sec preventions before
• VT/VF before reperfusion therapy-only beta
• Inf. & post. infarctions
• ↑ vagal tone produces sinus bradycardia
• May be beneficial
• Reduces myocardial O2 demand.
• Mortality rate similar
• No hypotension or VPCs- observed
• IV atropine –In the first 4 to 6 hrs after
• If the sinus rate <40/min and associated with
• Doses 0.3 -0.6 mg every 3 to 10 min.
• Total dose should not exceed 3 mg.
• Can produce conduction block at any level
• AV or intraventricular conduction system.
– AV node
– Bundle of His
• Produce various grades of AV block
• LBBB –
First-Degree Atrioventricular Block
• Does not generally require specific Tt.
• Beta blockers & CCB- D/c could ↑ischemia
• Do not ↓the dosage unless the PR> 0.24 sec
• Stopped if a higher-degree block or
• Atropine- If excessive vagotonia associated
with sinus bradycardia and hypotension
• Continued ECG monitoring
Second-Degree A-V Block
• First-degree and type I second-degree AV
blocks do not affect survival
• Commonly associated with occlusion of
• Caused by ischemia of the AV node
• Specific therapy is required in pt`s with
second-degree type I AV block when-
1. Vent rate >50 beats/min and PVCs
2. Heart failure
3. Bundle branch block are present.
• Atropine (0.3 to 0.6 mg)
• Temporary pacing systems-not required.
• Type II second-degree AV block
• Inferior/posterior STEMI
• Usually temporary
• Narrow-complex/ junctional escape rhythm.
• Managed conservatively.
• Anterior/lateral STEMI- :
• Type II second-degree AV block usually
originates from below the bundle of His.
• May progress to CHB,
• Temporary external or trans venous demand
• Inferior or anterior infarction
• More common in inferior than in anterior MI.
• Often progressing from a first-degree or type I
second-degree block –
– In pt`s with inf infarction
• The escape rhythm is typically stable without
asystole and often junctional.
• This form of complete AV block is often
• May respond to pharmacologic antagonism of
adenosine with methylxanthines
• Resolves in most patients within a few days
• Pt`s with inferior infarction often have
concomitant ischemia or infarction of the AV
node secondary to hypoperfusion of the AV node
artery, but the His-Purkinje system usually
escapes injury in such individuals.
• Pt`s with inf STEMI and AV block have larger
infarcts and more depressed RV and LV function
than do pts with an inf infarct and no AV block.
• junctional escape rhythms with narrow QRS
complexes occur commonly in this setting.
• Pacing is generally NOT necessary in pt`s with
inferior wall infarction
• Complete AV block is often transient in nature
• Pacing is indicated
1. if symptoms related to a ventricular rate emerge
2. if ventricular arrhythmias
3. hypotension is present
4. if pump failure develops
• Atropine only rarely useful
• Only when CHB develops in <6 hrs after the
onset of symptoms is atropine likely to abolish the
AV block or cause acceleration of the escape
• In such cases the AV block is more likely to be
transient and to be related to increases in vagal
• More persistent block seen later in the course of
STEMI, which generally requires cardiac pacing.
• In pt`s with ant infarction, third-degree AV block
can occur suddenly 12 to 24 hours after the onset
• It is usually preceded by an intraventricular block
and often a type II (not first-degree or type I) AV
• Such pt`s typically have unstable escape rhythms
with wide QRS complexes and rates <40
• ventricular asystole may occur quite suddenly.
• In pt`s with ant infarction, AV block generally
develops as a result of extensive septal
necrosis involving the bundle branches.
• The high rate of mortality in this group of pts
is the consequence of extensive myocardial
necrosis resulting in severe left ventricular
failure and frequently shock .
• Whether temporary transvenous pacing per se
improves survival in pt`s with anterior STEMI
• Pacing protects against asystole and may
protect against transient hypotension, with its
attendant risks of extending the infarction and
precipitating malignant ventricular
• The right bundle branch and the left posterior
division have a dual blood supply from the
LAD and RCA
• Left anterior division is supplied by septal
perforators originating from the LAD.
• Not all conduction blocks in patients with
STEMI are complications of infarcts.
• STEMI and bundle branch blocks have higher
peak biomarker levels, lower EF, and ↑ed in-
hospital and long-term mortality rates.
• In the prefibrinolytic era, IVCD of the His-
Purkinje system occurred in 5% -10% of pt`s
• In the reperfusion era intraventricular blocks
occur in ~2% - 5% of pt`s with MI.
Isolated Fascicular Blocks
• An isolated left anterior divisional block is
unlikely to progress to a complete AV block.
• Mortality is increased in these pt`s
• The post. fascicle is larger than the ant.
fascicle, and in general, a larger infarct is reqd
to block it.
• Complete AV block is not a frequent
complication of either form of isolated
Right Bundle Branch Block
• Can lead to AV block bcz it is often a new
lesion associated with antero septal infarction.
• Isolated RBBB is associated with an increased
risk for mortality in patients with anterior
– Even if complete AV block does not occur,
– But if accompanied by CHF
Bifascicular Block, Including Left
Bundle Branch Block
• The combination of RBBB with either Lt. ant. or
post. divisional block is known as bidivisional or
• If a new block occurs in two of the three divisions
of the conduction system, the risk for
development of a complete AV block is quite
• Mortality is also high because of the occurrence
of severe pump failure secondary to the extensive
myocardial necrosis required to produce such an
extensive intraventricular block.
• Preexisting BBB or divisional block is less
often associated with the development of
complete AV block in pt`s with STEMI.
• Bidivisional block in the presence of
prolongation of the PR interval may indicate
disease of the third subdivision rather than
disease of the AV node and is associated with a
greater risk for complete heart block than if
first-degree AV block is absent
• Complete BBB (either Lt or Rt), the combination
of RBBB and left anterior fascicular block, and any
of the various forms of trifascicular block are all
more often associated with anterior than with
• All these forms are more frequent with large
• Older patients and have a higher incidence of
other accompanying arrhythmias.
Use of Pacemakers in Patients with
Acute Myocardial Infarction
• Temporary Pacing
• Just as is the case for complete AV block,
transvenous ventricular pacing has not resulted
in a statistically demonstrable improvement in
prognosis in patients with STEMI in whom
intraventricular conduction defects develop.
• Temporary pacing is advisable in some of
these patients, however, because of the high
risk for development of a complete AV block.
• Temporary pacing
• Pt`s with new bifascicular bundle branch block
(i.e., RBBB with Lt. ant. or post. divisional
block and alternating Rt. and Lt. BBB)
• An isolated new block in only one of the three
fascicles, even with PR prolongation and pre
existing bifascicular block and a normal PR
interval, poses somewhat less risk;
• These pt`s should be monitored closely, with
insertion of a temporary pacemaker deferred
unless a higher-degree AV block occurs.
• The presence of apparent ventricular asystole on
monitor displays of continuously recorded ECGs
may be misleading in that the rhythm may
actually be fine VF.
• The predominance of VF as the cause of cardiac
arrest in this setting suggests electrical counter
shock as initial therapy, even if definitive
electrocardiographic documentation of this
arrhythmia is not available.
• Permanent Pacing
• The advisability of permanent pacemaker
insertion is complicated because not all sudden
deaths in pt`s with STEMI and conduction defects
are caused by high-grade AV block.
• A high incidence of late VF occurs in CCU
survivors with anterior STEMI complicated by
either right or left bundle branch block.
• VF rather than asystole caused by failure of AV
conduction and infranodal pacemakers could be
responsible for late sudden death.
• Permanent Pacing
1. when CHB persists throughout the hospital phase in a pt
2. when sinus node function is markedly impaired, or
3. when type II second-degree or third-degree block occurs
4. When high-grade AV block is associated with newly
acquired BBB or other criteria for conduction system
impairment, prophylactic long-term pacing may be
justified as well.
• Pt. who is candidate for an ICD or has severe heart
failure might improve with biventricular pacing.
• Sinus Tachycardia
• Augmented sympathetic activity
• Common causes -anxiety, persistent pain, LV
failure, fever, pericarditis, hypovolemia,
• Administration of drugs such as atropine,
epinephrine, or dopamine; rarely, it occurs in
pt`s with atrial infarction.
• Common in pt`s with anterior infarction, LV
• ↑ myocardial O2 consumption &↓time for
coronary perfusion→ intensifying the
myocardial ischemia & myocardial necrosis.
• Persistent sinus tachycardia
1. Persistent heart failure
2. Poor prognosis and excess mortality.
• Tt cause
• Analgesics for pain
• Diuretics for heart failure
• Oxygen, beta blockers, and nitroglycerin for
• Aspirin for fever or pericarditis.
• Beta blockers - sinus tachycardia caused by
pain, anxiety, or fever
• Beta blockers - CI in pt`s who are tachycardic
bcz of pump failure.
Atrial Flutter and Fibrillation
• Usually transient in pt`s with STEMI
• Augmented sympathetic stimulation of the
• Reduced cardiac output-
– ↑ed vent rate
– Loss of the atrial contribution to LV filling
• AF during STEMI is associated with ↑ed
mortality and stroke
– esp. in pt`s with AWMI
2. Ongoing ischemia
3. Heart failure
• Beta blocker- In stabilized pt`s and in the
absence of CI
• Digitalis - when AF with ventricular
• Oral anticoagulants -to reduce the risk for
• Even if sinus rhythm is present at the time of