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
• Treatment

Abnormal Impulse Terms

• Automaticity

  • Change in the heart rate driven by the pacemaker cells.

  • Sinus Tachycardia
  • Sinus Bradycardia
  • Sick sinus syndrome (alternating sinus tachycardia and sinus bradycardia.)

• Drivers

  • 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.

• Reentry

  • 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.

• Triggered activity

  • 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.

MAT

(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.

Clinical Presentation

• 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.

EKG Presentation

(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.
    • APD shortening, resting membrane potential hyperpolarization, development of early afterdepolarizations cause arrhythmias.
    • https://books.google.com.pk/books?id=moq9BAAAQBAJ&pg=PA46&lpg=PA46&dq=mechanism+adrenaline+induced+arrhythmia&source=bl&ots=dQG2U-1x2L&sig=L4639d7lmGbSVsAVjq6MFDelo-w&hl=en&sa=X&ved=0ahUKEwiVyKad3rrVAhVKvI8KHfEcCb44ChDoAQgpMAI#v=onepage&q=mechanism%20adrenaline%20induced%20arrhythmia&f=false
  • 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.
  • Oxygen
  • 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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