Download Tachycardia during Myocardial Infarction

Tachycardia during
Myocardial Infarction
Alireza Heidari Bakavoli, M.D
Mashhad University of Medical Science
Introduction
• Ventricular tachyarrhythmia has been
one of the most frequent cause of sudden
cardiac death in AMI
• In one report(1985), 60 % of deaths
associated with acute MI occurred within
the first hour and were related to a
ventricular arrhythmia, particularly vf
Introduction
• Arrhythmic Mortality and Overall in hospital Mortality
have been decreased in recent years
• Ventricular arrhythmias, ranging from isolated
ventricular premature beats to VF, are common in
the immediate postinfarction period
• Observations in the prefibrinolytic era :
– VPBs 10 to 93 percent
– VT
3 to 39 percent
– VF
4 to 20 percent
Introduction
• Early series underestimated the incidence of
unstable VT and VF,
– they did not include out-of-hospital sudden cardiac
death (SCD)
• The incidence of ventricular arrhythmias appears to
be higher with STEMI than NSTEMI
• VT is less common than VF in the periinfarction
period.
Introduction
• Early (≤4 hours) primary VF (ie, VF in the absence
of heart failure or shock) occurred in 3.1 percent.
• VF recurred during the hospitalization in 11 percent
of these patients.
• Late VF (>4 to 48 hours) occurred in 0.6 percent
and was recurrent in 15 percent.
Introduction
• Most peri-infarct arrhythmias are benign and selflimited
• However, those that result in hypotension, increase
myocardial oxygen requirements, and/or predispose
the patient to develop additional malignant
ventricular arrhythmias should be aggressively
monitored and treated.
Pathophysiology of arrhythmic
complications
• Autonomic dysfunction:
– Electrolyte imbalances (eg, hypokalemia and
hypomagnesemia) and hypoxia further contribute to the
development of cardiac arrhythmia.
• The damaged myocardium acts as substrate for reentrant circuits, due to changes in tissue
refractoriness.
Classification of peri-infarction
arrhythmias
• Supraventricular tachyarrhythmias
– Sinus tach , PACs, PSVT, AFL, Afib
• Accelerated Junctional Rhythm
• Bradyarrhythmias
• Ventricular arrhythmias
– PVCs, accelerated idioventricular rhythm, ventricular
tachycardia, and ventricular fibrillation
– Reperfusion arrhythmias
persistent sinus tachycardia
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Pain
Anxiety
Heart failure
Hypovolemia
Hypoxia
Anemia
Pericarditis
Pulmonary embolism
Sinus tachycardia
• Treatment strategies:
– Pain medication
– Diuresis to manage heart failure
– Oxygenation
– Volume repletion for hypovolemia
– Administration of anti-inflammatory agents to treat
pericarditis
– Beta-blockers and/or NTG to relieve ischemia
Premature atrial contractions
• Often before the PSVT, AFL, or A fib.
• The usual cause:
– Atrial distention due to LV diastolic pressure or
inflammation associated with pericarditis
• No specific therapy is indicated
• Attention should be given to identifying the
underlying disease process, particularly occult heart
failure
Paroxysmal supraventricular
tachycardia
• The incidence: less than 10%.
• In the absence of definitive data in the patient with AMI,
the consensus is that adenosine can be used when
hypotension is not present.
• In patients without clinically significant LV failure,
intravenous diltiazem or a beta-blocker can be used
instead.
• In patients who develop severe heart failure or
hypotension, synchronized electrical cardioversion is
required.
Atrial flutter
• Occurs in less than 5% of patients with AMI.
• Is usually transient and results from sympathetic
overstimulation of the atria
• Treatment strategies(same as A fib )
– Rate control with drugs is less easy in AFL than with A fib
• Synchronized DC shock
(50 J, or the biphasic equivalent) may be needed
• If AFL is refractory to medical therapy
– overdrive atrial pacing may be considered.
Atrial fibrillation
• The rate:10-15%
• A fib in the first hours of AMI is usually caused by
– LV failure
– Ischemic injury to the atria
– RV infarction
– Pericarditis
– All conditions leading to elevated LA pressure
Atrial fibrillation
• The presence of A fib during an AMI is associated
with an increased risk of
– mortality
– stroke,
– particularly in patients who have anterior-wall MIs.
Atrial fibrillation
• Immediate DC cardioversion is indicated for the
patient in unstable condition
– New or worsening ischemic pain
– Hypotension.
– Synchronized DC cardioversion to treat A fib begins with
200 J (or the biphasic equivalent).
– Conscious sedation (preferred) or general anesthesia is
advisable prior to cardioversion.
Atrial fibrillation
• In stable condition
– rate control
• If the A fib does not respond to cardioversion, IV
amiodarone[2] or IV digoxin (in patients with LV dysfx
or HF) can be used to achieve rate control.
Atrial fibrillation
• For patients who do not develop hypotension, a betablocker can be used.
– metoprolol 5-mg IV boluses every 5-10 min, with a maximum
dose of 15 mg.
• IV diltiazem Is an alternative but it should be used with
caution in patients with moderate-to-severe heart
failure.
• In patients with new-onset sustained tachycardia
(absent before MI), conversion to sinus rhythm should
be considered as an option.
• A fib and AFL confer an increased risk of
thromboembolism
• Therefore, anticoagulation with either unfractionated
heparin or low molecular weight heparin (LMWH)
should be started if contraindications are absent.
• It is unclear whether anticoagulation is needed in
cases of transient atrial fibrillation and how long
after the onset of atrial fibrillation should the
anticoagulation be started.
Accelerated junctional rhythm
and junctional tachycardia
• A rhythm results from increased automaticity of the
junctional tissue that leads to a heart rate of 70-130
bpm.
• This type of dysrhythmia is most common in
patients who develop inferior myocardial infarctions.
• Treatment is directed at correcting the underlying
ischemia.
Ventricular Arrhythmias
Premature ventricular
contractions
• In the past, frequent PVCs were considered to
represent warning arrhythmias and indicators of
impending malignant ventricular arrhythmias.
• However, presumed warning arrhythmias are
frequently observed in patients who have an acute
AMI and who never develop VF.
• On the converse, primary VF often occurs without
antecedent premature ventricular ectopy
Premature ventricular
contractions
• For these reasons, prophylactic suppression
of PVCs with lidocaine, is no longer
recommended.
• Prophylaxis has been associated with an
increased risk of fatal bradycardia or asystole
because of the suppression of escape
pacemakers.
Management
• A conservative approach
• Do not routinely administer prophylactic
antiarrhythmics.
• Attention should be directed toward correcting any
electrolytic or metabolic abnormalities, plus
identifying and treating recurrent ischemia
Accelerated idioventricular
rhythm
• In as many as 20% of patients who have an AMI.
• A ventricular rhythm characterized by a wide QRS
with a regular escape rate faster than the atrial rate,
but less than 100 bpm.
• AV dissociation is frequent.
• Slow, nonconducted P waves are seen; these are
unrelated to the fast, wide QRS rhythm.
AIVR
• Most episodes are short and terminate
spontaneously.
• Equal frequency in anterior and inferior infarctions.
• The mechanism
– (1) the sinoatrial node or the AV node, which may
sustain structural damage and depress nodal
automaticity, and/or
– (2) an abnormal ectopic focus in the ventricle that takes
over as the dominant pacemaker
Management of AIVR
• The presence of accelerated idioventricular
rhythm does not affect the patient's prognosis
• This rhythm occurs somewhat more frequently
in patients who develop early reperfusion than
in others; however, it is neither sensitive nor
specific as a marker of reperfusion.
Management of AIVR
• Temporary pacing is not indicated unless the rhythm is
sustained and results in hypotension or ischemic
symptoms.
• An accelerated idioventricular rhythm represents an
appropriate escape rhythm.
• Suppression of this escape rhythm with an
antiarrhythmic drug can result in clinically significant
bradycardia or asystole.
• Therefore, an accelerated idioventricular rhythm should
be left untreated.
Nonsustained VT
• is defined as 3 or more consecutive ventricular
ectopic beats at a rate of greater than 100 bpm
• and lasting less than 30 seconds.
• In patients who experience multiple runs of
nonsustained ventricular tachycardia, the risk for
sudden hemodynamic collapse may be substantial.
Non sustained VT
• NSVT in the immediate peri-infarction period does not
appear to be associated with an increased mortality
risk,
• No evidence suggests that antiarrhythmic treatment
offers a morbidity or mortality benefit.
• However, NSVT occurring more than 48 hours after MI
in patients with LV systolic dysfx (LV EF< 0.40) poses
an increased risk for sudden cardiac death;
• If VT is inducible during EPS ICD is indicated (class I,
Level of evidence B).
NSVT
• Multiple episodes of NSVT require intensified
monitoring and attention to electrolyte imbalances.
• Serum potassium levels should be maintained
above 4.5 mEq/L, and serum magnesium levels
should be kept above 2.0 mEq/L.
• Ongoing ischemia should aggressively be sought
and corrected if found
Sustained VT
• Defined as 3 or more consecutive ventricular ectopic
beats at a rate greater than 100 bpm and lasting longer
than 30 seconds or causing hemodynamic compromise
that requires intervention.
• Monomorphic VT is most likely to be caused by a
myocardial scar,
• Polymorphic ventricular tachycardia may be most
responsive to measures directed against ischemia.
• Sustained polymorphic ventricular tachycardia after an
AMI is associated with a hospital mortality rate of 20%
Sustained VT
• Emergency treatment is mandatory because of its
hemodynamic effects and because it frequently
deteriorates into V fib .
• Rapid polymorphic VT (rate >150 bpm) associated with
hemodynamic instability should be treated with
immediate direct-current unsynchronized cardioversion
of 200 J (or biphasic energy equivalent).
• Monomorphic VT should be treated with a
synchronized discharge of 100 J (or biphasic energy
equivalent).
Sustained VT
• If VT is well tolerated
– Amiodarone (drug of choice)
– or procainamide may be attempted before DC cardioversion.
• Precipitating causes, such as electrolyte abnormalities,
acid-base disturbances, hypoxia, or medication, should
be sought and corrected.
• For persistent or recurrent VT , overdrive pacing may
be effective in electrically converting the patient's
rhythm to a sinus rhythm.
Ventricular fibrillation
• The incidence of primary ventricular fibrillation is
greatest in the first hour after the onset of infarct
(4.5%) and declines rapidly thereafter.
• Approximately 60% of episodes occur within 4
hours, and 80% occur within 12 hours.
Late VF
• Secondary( late VF) occurring more than 48 hours after
an MI is usually associated with pump failure and
cardiogenic shock.
• Risk factors :
– Large MI
– IVCD
– Anteroseptal AMI.
• Secondary VF in conjunction with cardiogenic shock is
associated with an in-hospital mortality rate of 40-60%.
VF treatment
• Treatment for VF is unsynchronized electrical
countershock with at least 200-300 J (or biphasic
energy equivalent) administered as rapidly as possible.
• Each minute after the onset of uncorrected VF is
associated a 10% decrease in the likelihood of survival
• Electromechanical dissociation, or pulseless electrical
activity is generally due to extensive myocardial
ischemia and/or necrosis or cardiac rupture.
VF treatment
• IV amiodarone and lidocaine, facilitate successful
electrical defibrillation and help prevent recurrent or
refractory episodes.
• After VF is successfully converted, antiarrhythmic
therapy is generally continued as a constant IV infusion
for 12-24 hours.
• Prophylactic lidocaine is not used because it seems to
be associated with an excessive mortality risk owing to
bradycardic and asystolic events[4] .
• Early use of beta-blockers reduces the VF/death