Dr. Mobeen discusses following topics in the context of multifocal atrial tachycardia.
- Terms and definition of abnormal rate
- Definition of MAT
- Causes of MAT
- EKG representation
- Diagnostic criteria
- Pathological mechanisms behind the causative factors
- Non-nodal cardiac tissue that incorrectly starts to generate new impulses without the need to be triggered by another impulse. These ectopic foci are called drivers instead of pacemakers.
- Entrapment of an impulse originated somewhere else in a reentrant circuit.
- As the impulse cycles in this reentrant circuit, it sends new impulses to the neighboring cells.
- An impulse giving rise to further impulses due to the abnormal state of myocardial cells.
- Note: these cells in the abnormal state cannot produce a new impulse on their own, they need an impulse acting as a trigger.
- Drugs that prolong action potential duration (APD), e.g. class III antiarrhythmic, can cause triggered activity.
- This triggered activity is called afterdepolarization (AD). It is of two types.
- Early Atrial Depolarization (AED). Caused by slow activation and prolonged action potential.
- Delayed afterdepolarization (DAD). Caused by the Ca++ overload.
(A type of Supraventricular Tachycardia)
- Irregular rhythm occurring at the rate of 100 to 200 bpm.
- The rate can be less than 100 bpm somtimes. In such cases, the arrhythmia is called wandering atrial pacemaker (WAP) or multifocal atrial rhythm.
- Wandering atrial pacemaker can be detected in healthy individuals too.
- If the rate is lesser than or equal to 60 then the term is multifocal atrial bradycardia.
- MAT occurrs due to the random firing of several different atrial foci.
- Common in patients with severe lung disease.
- Older people with the chronic obstructive pulmonary disease (COPD,) and hypoxia.
- Theophylline toxicity can also cause MAT. (Given in COPD.)
- MAT can occur with myocardial infarction.
- Low blood magnesium levels1 (<1.5 mg/dl) can lead to MAT.
- Diuretics can cause hypomagnesemia.
- Mg acts similar to Ca++ channel blockers.
- Mg depletion reduces Na+/K+ pump action, leading to intracellular K+ depletion.
- Hypokalemia can lead to MAT. (<3.5 mg/dl or severe hypokalemia <2.5 mg/dl.)
- Rarely, digitalis toxicity in patients with heart disease can cause MAT.
- Treatment is usually not needed other than fixing the underlying disease.
- Carotid massage has no effect as the rate is not originating from a pacemaker.
- Patients are often asymptomatic.
- Exacerbated underlying disease symptoms may be present.
- Shortness of breath, wheezing, productive cough, or the symptoms of acute metabolic derangement.
- Irregular heart rate/pulse.
- Heart rate > 100 bpm.
- Can worsen the systemic oxygenation in patients with advanced COPD.
- Can worsen the cardiovascular dynamics in patients with coronary artery disease or heart failure.
- Signs and symptoms of exacerbated heart disease may be observed e.g. angina, dyspnea, and orthopnea.
MAT’s Diagnostic Criteria
- As the P waves appear from many different sites in the atria. The shapes of the P waves vary.
- For diagnosing MAT:
- One must find three morphologies (shapes) of the P waves.
- Note: one shape of a P wave can appear for a few beats before another shape of the P wave appears.
- P waves must be separated by isoelectric lines.
- Varying PR intervals, R-R intervals duration, and R-R intervals are observed.
- QRS complexes are of narrow type (no problem in the ventricle.)
- Unless there are ventricular conduction pathologies present too.
- MAT is observed in about 3 patients out of every 1000 hospitalized adults.
(Credit: By Jer5150 - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=20243829)
Note the varying shapes of the p waves in the v6 rhythm lead at the bottom of this EKG image. You have to find at least three different shapes of p waves.
Difference of MAT and Atrial Fibrillation
- MAT usually has easily identifiable P waves before the QRS complex.
- There are clear isoelectric intervals between the P waves. Atrial fibrillation either does not have easily discernable P waves, or the P waves appear on the EKG with a higher frequency than the QRS complexes without isoelectric intervals between them.
- In atrial fibrillation, there is no discernible association between the P waves and the QRS complexes.
- In MAT PR intervals vary in size. Depends on the distance of the impulse origin from the AV node.
Chronic obstructive pulmonary disease (COPD) and MAT
- Hypoxia causes cell depolarization.
- Na+/K+ pump function decreases due to the lack of ATP.
- Reduced levels of hyperpolarizing currents.
- Reduced pump activity leads to increased extracellular K+ levels. Which initially cause hyperpolarization but then cause depolarization because of increase extracellular K+ concentration.
- Reduced ATP also slows down Na+ channels which causes action potential duration (APD) to become variable.
- Hypoxia affects the L-type Ca++ channel’s function.
- These channels are important for the plateau phase of the cardiac action potential.
- Disturbance in these L-type Ca++ channel function can result in life threatening arrhythmia. This happens as some cells end up with longer action potential duration and some with shorter durations. (An abnormal function of the L-type Ca++ channels.)
- In patients of severe COPD hypercapnia causes vasodilatation.
- This, in turn, causes low blood pressure and the release of norepinephrine. Elevated levels of norepinephrine can cause arrhythmia.
- Norepinephrine acts on beta receptors and triggers cAMP dependent PK-A. PK-A, in turn, acts on the L-type Ca++ channels in the cell membrane to increase Ca++ influx. PK-A also acts on the sarcoplasmic reticulum to release Ca++. Both of these effects increase the cardiac cell contractility. (In the heart the action is predominantly via beta 1 receptors.)
- Norepinephrine also increases heart rate by its action on the Ca++ channels in the nodal tissue.
Treatment of the multifocal atrial tachycardia (MAT)
- Treat the underlying cause.
- Electrical cardioversion has no effect.
- Carotid massage has no effect.
- The following therapy can be applied (if the tachycardia due to MAT is causing hemodynamic issues.)
- Ca++ channel blockers (verapamil.)
- Verapamil is negatively inotropic and a vasodilator. It can cause severe hypotension in patients with heart failure. Use with caution.
- Beta blockers (metoprolol.)
- Patients with severe lung disease often cannot tolerate beta blockers.
- Verapamil and beta blockers should not be given to patients with sinus node dysfunction or existing second or third-degree block without a pacemaker.
- In patients with pulmonary disease start with calcium channel blockers. Use beta blockers with lots of care.
- In patients who do not have pulmonary disease, you can start with beta blockers.
- Amiodarone is effective but dangerous.
- Long-term therapy with amiodarone is avoided due to its toxicity, especially pulmonary fibrosis.
- Simultaneously correct magnesium and potassium levels.
- Radiofrequency ablation of the AV node with a pacemaker installation is indicated in patients who are not responding to the drug therapy or who cannot tolerate drug therapy.
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