It is a well known cardiac auscultatory sign, S 1 becomes variable in intensity with the onset of atrial fibrillation.
In physiology , the intensity of S 1 is determined by many factors.
- The valve morphology(Thickness, Calcium , Rigidity )
- Valve mobility
- PR interval
- Force of LV contraction
- Preceding RR interval (4 and 5 are inter related)
- Insulation and auditory factors (Thick chest wall etc)
How does atrial fibrillation modify the intensity of S1 ?
It is to be noted , atrial fibrillation alters only one of the above factors, namely the RR interval which becomes irregular.
The mix of short and long RR intervals occurs at random . A short RR interval, results in a relatively softer S1 and vice versa . The mechanism is directly attributable to the degree of LV filling and subsequent change in force of contraction .
Many times , at fast ventricular rates (Say >150) the distinction between short- long cycles is negligible in terms of net cardiac cycle.
If the RR interval , is too prolonged there can be an inverse relationship with s 1 intensity .It gets muffled as the mitral valve floats back to it’s orifice and a partial or even complete closure occurs , making force of LV contraction irrelevant in the genesis of S1 .
The vanishing act of PR interval in atrial fibrillation.
It does not require great brains to understand , if P waves are absent , PR interval must also be absent !
If PR interval is absent , there can be no influence of it on the first heart sound. Logic demands absence of PR interval must have some sort of influence on the intensity of S1. As far as i know cardiology literature has not answered this query.
What are the two types of S 1 variation ?
Experince has shown us , the variation of S1 can be of two types*.
Sequence 1 : Varying between , Loud -Louder- Loudest -pounding
Sequence 2: Varying between , Loud -Normal – soft -Muffled
* Applicable only for those with shrewed ears !
S 1 intensity with reference to underlying pathology : Valvular vs Non valvular atrial fibrillation
It is obvious the impact of varying RR interval on the intensity of S1 will directly depend upon the underlying pathology. The intensity of S1 in non valvular AF (Like , lone AF, Thyrotoxic AF, Hypoxic AF ,Ischemic AF etc) are more vulnerable to changing RR interval .
In rheumatic heart disease , the influence of valve morphology , rigidness, calcification and presence of MR generally prevail over the impact of changing RR interval .So, in a case of tight mitral stenosis and AF it is expected the sequence 1 is more common .
In lone AF or AF due to CAD , sequence 2 is more likely * Associated LV dysfunction , and ischemic MR may further dampen the intensity of S1 .
Hearing few occasional loud S1 in AF , is an indirect indication that underlying LV function is good, as it reflects the force of LV contraction .
Some hearts are notoriously silent even in the midst of AF. If the silence is not due to obesity or other insulation defects, it suggests a sinister diagnosis , like severely dysfunctional ventricle like DCM etc.
As a corollary, it is often noticed , palpitations* are , often not felt by patients with dysfunctional ventricles in spite of atrial fibrillation. (As loud S 1 is rare with dysfunctional ventricle)
*Palpitation is a symptom that equates to Dp/Dt of ventricles.
What happens to mid diastolic murmur in AF ?
The murmur length varies linearly with reference to RR interval. The pre systolic accentuation disappears ,but pre-systolic component may persist .
Simple, bed side auscultation during atrial fibrillation can give us vital clues about the etiology, and the underlying LV function . Let us not be ashamed to talk about clinical cardiology . . .at least in the bed side !