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Cardiac Arrhythmias, Animation

(USMLE topics, Cardiology) Cardiac Arrhythmias Overview: Sinus, Atrial and Ventricular Rhythms, Anatomy and ECG/EKG, Animation. Purchase a license to download a non-watermarked copy of this video on AlilaMedicalMedia(dot)com ©Alila Medical Media. All rights reserved. Voice by: Abbie Drum All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Cardiac arrhythmias classified by site of origin: Sinus rhythms, from the SA node; Atrial rhythms the atria; Ventricular rhythms from the ventricles. Sinus bradycardia and sinus tachycardia may be normal or clinical depending on the underlying cause. Cardiac arrhythmias that originate from other parts of the atria are always clinical. The most common include: atrial flutter, atrial fibrillation and AV nodal re-entrant tachycardia. These are forms of supraventricular tachycardia or SVT. Atrial flutter or A-flutter is caused by an electrical impulse that travels around in a localized self-perpetuating loop, most commonly located in the right atrium. This is called a re-entrant pathway. For each cycle around the loop, there is one contraction of the atria. The atrial rate is regular and rapid - between 250 and 400 beats per minute. Ventricular rate, or heart rate, however, is slower, thanks to the refractory properties of the AV node. The AV node blocks part of atrial impulses from reaching the ventricles. In this example, only one out of every three atrial impulses makes its way to the ventricles. The ventricular rate is therefore 3 times slower than the atrial rate. This is an example of a “3 to 1 heart block”. On an ECG atrial flutter is characterized by absence of normal P wave. Instead, flutter waves, or f-waves are present in saw-tooth patterns. Atrial fibrillation is caused by multiple electrical impulses that are initiated randomly from many ectopic sites in and around the atria, commonly near the roots of pulmonary veins. These un-synchronized, chaotic electrical signals cause the atria to quiver or fibrillate rather than contract. The atrial rate during atrial fibrillation can be extremely high, but most of the electrical impulses do not pass through the AV node to the ventricles, again, thanks to the refractory properties of the cells of the AV node. Those do come through are irregular. Ventricular rate or heart rate is therefore irregular and can range from slow to rapid. On an ECG, atrial fibrillation is characterized by absence of P-waves and irregular narrow QRS complexes. The baseline may appear undulating or totally flat depending on the number of ectopic sites in the atria. In general, larger number of ectopic sites results in flatter baseline. AV nodal re-entrant tachycardia or AVNRT is caused by a small re-entrant pathway that involves directly the AV node. Every time the impulse passes through the AV node, it is transmitted down to the ventricles. The atrial rate and ventricular rate are therefore identical. Heart rate is regular and fast, ranging from 150 to 250 beats per minute. Ventricular rhythms are the most dangerous (lethal rhythms). Ventricular tachycardia or V-tach is most commonly caused by a single strong firing site or circuit in one of the ventricles. It usually occurs in people with structural heart problems such as scarring from a previous heart attack or abnormalities in heart muscles. Impulses starting in the ventricles produce ventricular premature beats that are regular and fast, ranging from 100 to 250 beats per minute. On an ECG V-tach is characterized by wide and bizarre looking QRS complexes. P wave is absent. V-tach may occur in short episodes of less than 30 seconds and cause no or few symptoms. Sustained v-tach lasting for more than 30 seconds requires immediate treatment to prevent cardiac arrest. Ventricular tachycardia may also progress into ventricular fibrillation. Ventricular fibrillation or v-fib is caused by multiple weak ectopic sites in the ventricles. These un-synchronized, chaotic electrical signals cause the ventricles to quiver or fibrillate rather than contract. The heart pumps little or no blood. V-fib can quickly lead to cardiac arrest. V-fib ECG is characterized by irregular random waveforms of varying amplitude, with no identifiable P wave, QRS complex or T wave. Amplitude decreases with time, from initial coarse v-fib to fine v-fib and ultimately to flatline.