Dawn's picture

This rhythm strip is recorded in two simultaneous leads, which is always preferable to one single lead.  It is a good example of atrial fibrillation with a rapid ventricular response.  Atrial fib that has not been treated will usually have a rapid ventricular rate.  This reflects the ability of the AV node to conduct a tachycardia, within limits.  The natural slow conduction of the AV node allows it to act as a "filter", preventing the huge numbers of impulses generated by the atrial fibrillation from reaching the ventricles.  In this case, about 140 beats per minute are able to make it through the AV node into the ventricles.   In some patients, preexisting cardiac conditions such as valve insufficiency or CHF may make this rate dangerous for the patient.  The rate may lower cardiac output in some people, and this must be considered in light of the fact that the loss of P waves in atrial fib also lowers cardiac output significantly.

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ekgpress@mac.com's picture


To amplify what Dawn describes regarding the relationship between AFib and cardiac output — Consider the following:
  • The “atrial kick” (ie, contribution of atrial contraction at the end of diastole to cardiac filling) — generally contributes between 5-to-40% of cardiac output. This lower range (ie, ~5-10% of cardiac output) — is what is seen in younger healthy individuals with normal size and relaxation capacity ventricles (that fill nearly completely during the earlier passive phase of diastole). In contrast, in older individuals (especially older women with longstanding hypertension and resultant diastolic dysfunction) — there is LV thickening (LVH) and associated greatly reduced LV compliance (relaxation capacity) — such that passive filling of the LV is incomplete. These patients depend much more on the “atrial kick” for their contribution to cardiac output (which may attain 30-40% of their total cardiac output! ). It is precisely in these older individuals in whom cardiac output may be reduced already — that sudden loss of atrial contractile function (from new-onset AFib) is most likely to precipitate sudden severe acute heart failure
  • The cardiac mechanical cycle is divided into the period of ventricular systole and ventricular diastole. At a normal heart rate — diastole tends to last longer — however LV filling occurs during diastole. The KEY point — is that the period of systole cannot be shortened by very much — because regardless of heart rate, the ventricle still needs to go through all of the phases of cardiac contraction. In contrast — with ANY tachycardia (including sinus tachycardia) — the R-R interval shrinks primarily because of reduction in duration of diastole. This explains why cardiac output will decrease to at least some extent with ANY tachycardia (because the period of ventricular diastole during which LV filling occurs is disproportionately shortened compared to the reduction in duration of systole).
Given that new-onset AFib is generally associated with a rapid ventricular response — the combination of loss of “atrial kick”+ reduction in time for LV filling (caused by the rapid rate) explains why new-onset AFib in an older hypertensive adult (with diastolic dysfunction) is so prone to present to the emergency department in acute pulmonary edema ...

  • For a quick VIDEO REVIEW on the ECG Diagnosis of AFib (and the various rates of the ventricular response to AFib)CLICK HERE
  • For those wanting a Linked Contents of my 2-Hour Long, Basics of Rhythm Interpretation VideoCLICK HERE
 

Ken Grauer, MD  www.kg-ekgpress.com   [email protected] 

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