Clinical Significance And Presentation Of Atrial Flutter And Atrial
Pictorial diagram of Atrial Flutter
This is an uncommon arrhythmia in which the atria contract at the rate of 300/min. The mechanism is one of re-entrant tachycardia affecting the atria. Since the A-V node cannot conduct impulses at this rate, a physiological block develops and only half, a third, or a fourth of the atrial impulses are transmitted to the ventricles. The ventricles contract at a lower rate, but regularly. Flutter waves are seen in the jugular vein. Carotid pressure increases the block and reduced the ventricular rate further.
Treatment: Digoxin either abolishes the arrhythmia or converts it into atrial fibrillation. On withdrawing digoxin, normal rhythm is restored. Quinidine is also effective in the treatment of atrial flutter. Generally, atrial flutter is resistant to drug treatment, but it responds to DC shock readily (50 joules may be sufficient).
This is the condition in which the coordinated contraction of the atrium is abolished and the atrial muscle fibrillates. Abnormality of atrial activation is caused by impulses arising from different foci at the rate of 400-600/min. Since coordinated contraction at this rate is not possible, fibrillation sets in.
Atrial fibrillation may be due to different causes. In the order of frequency, there are:
- Rheumatic mitral valvular disease- mixed mitral lesions, mitral stenosis and mitral regurgitation
- Ischemic heart disease
- Digoxin toxicity
- Chronic pericardial disease, and
Rare causes include aortic and pulmonary valve diseases ad congenital heart disease. At times, atrial fibrillation ma occur without any predisposing disease (lone atrial fibrillation). Infections and alcoholic bouts may precipitate the attacks in persons who are predisposed for recurrent episodes of atrial fibrillation.
Pathophysiology: Ectopic impulses arise in the atria at the rate of 400-600/min. They reach the A-V node at irregular intervals. Many of them find the A-V node totally or partially refractory and, therefore, conduction to the ventricle is totally irregular. Ventricular contraction occurs irregularly- both in rhythm as well as in force. The ‘a’-wave in the jugular vein disappears since the atrium fails to contract as a whole. Loss of atrial contraction abolishes the augmented transit of atrial blood into the ventricle during end diastole, thereby abolishing the stretch to the ventricular muscle preceding systole (atrial booster effect). In normal hearts, this may not be clinically significant, but in a diseased heart, AF precipitates cardiac failure because of the loss of atrial booster effect. Thrombi form in the atria as a result of stagnation. These embolise periodically resulting in systemic or pulmonary embolism.
© 2014 Funom Theophilus Makama