Tachyarrhythmia's
In Acute Myocardial Infarction ( AMI)
Dr.Fawzia Al-kandari Consultant Cardiologist Division of electrophysiology Chest Diseases Hospital-Kuwait Done By AMNA
In MI we have area of necrotic zone that develops early, and depending of the degree of infarction, u may see a bigger zone of necrosis in AMI
Huge Thrombus in LAD
This slide just to show a thrombus sitting on the coronary artery and occluding it
Coronary Thrombus after A/S STEMI
This is an angiogram showing clot that is sitting on the left anterior descending artery in the coronary artery
Last Pt – diseased LAD
Patient with anterior MI (ST elevation seen in leads V2, V3, V4)
Acute inferior MI, ST elevation seen on leads I, II, aVF
Complications of STEMI
Hemodynamic
Cardiogenic Shock Acute LVF
Complications
Mechanical Arrhythmias
Rupture of Muscle Rupture of Chords Rupture of Papillary Muscles
*Abnormal cardiac rhythm has been noted in 72
to 96 per cent of patients with AMI treated in CCU.
*The incidence is higher among those presented earlier after the onset of symptoms. *Many Arrhythmias occur before hospitalization.
Some of them occur at home and patient may not reach the hospital and
dieing bcoz of malignant ventricular arrhythmias or ventricular fibrillation
Mechanisms
Activation of receptors within atrial and ventricular myocardium by necrotic tissue may cause enhanced efferent sympathetic activity ,increased concentrations of circulating catecholamines ,and release of catecholamines from nerve endings within the heart.
Ischaemic myocardium may be hyperreactive to the ÷ arrhythmogenic effect of norepinephrine.
Sympathetic stimulation of the heart may also enhance automaticity of ischaemic Purkinje fibres. Transmural infarct can interrupt both the afferent and efferent limbs of sympathetic nervous system innervating "distal" myocardium.
Coronary occlusion produce produces a wide variety of changes in extracellular K,pH,Po2 ,and Pco2 .
The rate and magnitude of those changes are inhomogeneous ,both within and at the margins of ischaemic zone resulting in variable intraventricular conduction velocity.
The nonuniform conduction velocity produces the electrical substrate for reentry. Enhanced Automaticity is another important mechanism.
Re-entry
In the normal heart, we have normal homogenous conduction But if patient get scar or dead area on the conduction pathway, slow and abnormal conduction will trigger the development of certain arrhythmias
Increased/Abnormal Automaticity
Sinus tachycardia
Ectopic atrial tachycardia
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Junctional tachycardia
….Require vigorous treatment when :
Impair haemodynamics.(as hypotensive pulmonary edema)
Compromise myocardial viability by augmenting myocardial oxygen requirements. Malignant ventricular arrhythmias, i.e., V.Tachy., VF ,or a systole.
Cardiac TachyArrhythmias during Acute Myocardial Infarction
Sinus Tachycardia. Atrial Fibrillation. Atrial Flutter. Paroxysmal Supraventricular tachycardia. Accelerated AV junctional Rhythm and junctional tachycardia. Ventricular Arrhythmias : Ventricular Tachycardia ,Ventricular Fibrillation Accelerated idioventricular rhythm .
Sinus Tachycardia
*Defined as sinus rate exceeding 100 beats per minute. *Non-specific finding: pain ,anxiety , fever ,volume depletion ,pericarditis , pulmonary embolus , and cardio-accelerator drugs may produce S.tachy. *Persistent S.tachy may be an ominous sign reflecting heart failure. *Aim of treatment : Reduce heart rate to diminish myocardial oxygen demands. *Treatment : is that of the cause. * The role of Beta-adrenergic blockers. Is
given for persistent sinus tachy to reduce the myocardial oxygen demands
Sinus tachy is very common in patient with . AMI If we need to treat , usually we treat the causes of sinus tachy rather than treating it by itself For example: If patient is in pain we should relieve the pain If the volume is depleted, we give fluid If there are complications, we should deal with them
In sinus tachy, u will see normal P-wave before each QRS with heart rate more than 100 bpm
Supraventricular tachycardia *Infrequent arrhythmia following MI.
The problem here is the fast HR that may coz haemodynamic compromise in patient with preexisting MI
*Treatment objectives : Reduce ventricular rate ; restore Sinus rhythm. *Treatment : Cardioversion ,verapamil ,cardiac glycosides, BB ,and Vagal maneuvers.
Example of AVNRT
There is no P-wave and irregular narrow complex tachy suggesting supra ventricular tachycardia
Atrial tachycardia
Atrial tachycardia is usually a narrow complex tachyarrhythmia accounting for 10% of supraventricular tachycardias. The mechanism of atrial tachycardia is usually re-entrant but may be due to enhanced automaticity of the atrial myocardium. The atrial rate is between 120 and 240 bpm. At higher rates there may be variable AV block.
Multifocal atrial tachycrdia
3 or more P waves morphologies, irregular QRS. Most commonly occur in COPD. Correct hypoxia and hypercapnia. Consider verapamil if rate remains > 110bpm.
Atrial Flutter
Less commonly seen
*Organized rhythm with the atrial rate 280-320 beats per minute .It is usually associated with a 2:1 AV conduction ratio. * Seen in less than 5 % of patients with MI. *Treatment objectives : Reduce ventricular rate ; restore sinus rhythm. *Rather difficult to treat. * Treatment : Cardioversion, Rapid atrial pacing , Digitalis and anticongestive measures. .
Atrial Flutter
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Most cases of atrial flutter are caused by a large reentrant circuit in the wall of the right atrium Biphasic “sawtooth” flutter waves at a rate of ~ 300 bpm
EKG Characteristics:
Flutter waves have constant amplitude, duration, and morphology through the cardiac cycle
There is usually either a 2:1 or 4:1 block at the AV node, resulting in ventricular rates of either 150 or 75 bpm
Atrial Fibrillation
*The most common atrial tachyarrhythmia
complicating MI. *Often, intermittent. *In association with Inferior Infarct may be due to left atrial ischaemia. *Requires treatment as the loss of synchronized atrial contraction and the rapid irregular ventricular rate may produce hemodynamic impairment. *Treatment: Digitalis ,BB ,Verapamil , Amiodarone and Synchronized cardioversion.
.
AF
Atrial Fibrillation
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Atrial fibrillation is caused by numerous wavelets of depolarization spreading throughout the atria simultaneously, leading to an absence of coordinated atrial contraction.
Atrial fibrillation is important because it can lead to:
Hemodynamic compromise Systemic embolization Symptoms
Ventricular Tachycardia
*Definition : 3 or more consecutive ectopic beats occurring in a frequency exceeding 120 beats per minute. *Incidence In MI : 10-40 %.(common in MI) * Early after MI ( within 24 hours) , benign.(doesn’t affect the prognosis of the patient), Later : associated with high mortality (affect patient prognosis) * The role of hypokalemia and hypomagnesemia.(trigger this type of arrhythmias) *Frequently deteriorates into VF (if not treated) *Therapeutic options : Antiarrhythmic agents ; cardioversion / defibrillation.
What is this arrhythmia?
Ventricular tachycardia
(Wide complex tachy) Ventricular tachycardia is usually caused by reentry, and most commonly seen in patients following myocardial infarction.
SVT w/ aberrancy
Accelerated Idioventricular Rhythm (AIVR)
Ventricular Fibrillation Occurs in 4-18 % of patients with AMI Rare in patients with Non-Q MI. Nearly , 60 % of episodes occurs within 4 hours and 80 % occurs within 12 hours of the onset of symptoms., Primary VF Late VF is explained by heart failure , while patients with anteroseptal MI and associated RBBB or LBBB are particularly vulnerable.
Management : electrical countershock , as rapid as possible , Often recurs rapidly :continued CPR ,prompt implementation of pharmacological and ventilatory maneuvers and treatment with antiarrhythmic drugs and repeated countershocks. The role of epinephrine and Ca.gluconate in facilitating success of countershocks on interrupting VF rhythm as brain damage may occur as soon as 2 minutes.. ( fine VF ).
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