Posts Tagged ‘loud s1’

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.

  1. The valve morphology(Thickness, Calcium , Rigidity )
  2. Valve mobility
  3. PR interval
  4. Force of LV contraction
  5. Preceding RR interval (4 and 5 are inter related)
  6. 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 .

Clinical implication

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 .

Silent AF

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 .

Final message

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 !

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Cannon Sound

A loud first heart sound (S 1)   which is  heard intermittently in patients with complete heart block (CHB)  is  often referred to as  cannon sound .

What is the mechanism of loud S1 in CHB ?

We know , the intensity of S 1 is  mainly determined by the  relative position of mitral leaflet (To be precise, the  anterior mitral leaflet(AML) )   at the onset of systole.  We also know the  PR interval  has an intricate relationship to  mitral leaflet  position .

The shorter it is ,  wider the leaflet separation  and a longer PR interval makes a mitral leaflet assume a almost closed position   by the time the ventricle contracts.this happens because  a long drawn PR interval fills the ventricle more completely and LVEDV  reaches the maximal levels and LV blood column lifts up the mitral leaflets , and hence the LV  contraction  which follows does not close it with a  bang. In a short PR interval the opposite happens and hence a loud S1 .

In CHB we have variety of PR intervals ranging between  very short to long   ( falling just before the qrs complex) It is not difficult to understand this , as P waves are totally dissociated with the QRS complex  in CHB.In fact p waves have a liberty to fall any where in the ECG tracing , some call this as marching through the qrs complex !.

Hence typically the S1 is variable in intensity , varying between loud to soft.  When  P wave falls just behind a QRS complex , it generates a very  loud S 1  that is called cannon sound .This happens intermittently.

Cannon wave

This is entirely different phenomenon except that it shares the word cannon . Cannon a wave is  a visual finding on the jugular venous pulse.(JVP) .It is a systolic event . It is also seen in CHB as like a cannon sound

This is a giant a wave  in  JVP  when the right atrium contracts against a closed tricuspid valve. In physiological situations atrium contracts with an open AV valves , so that ventricle gets  filled . So atrial contraction  does not does not cause any reflux of blood back into vena cava.

But, when the atrium  contracts and  finds , the AV valve closed  there is no other option   for the incoming blood  to reflux  back into  the neck veins. This is seen as giant a waves called as cannon ” a “waves

With reference to ECG  location ,  this cannon”  a” wave occurs   whenever p wave falls within the ventricular systole ie  the QT interval .The cannon waves also occur intermittently like the  cannon sounds.

What is the  peculiar relationship between cannon a wave and   sound ?

In fact , it is  a non- relationship.  Though  , both the sound and wave   can occur in a given  patient with CHB ,   they can not occur simultaneously .This is because ,  for cannon sounds   to occur  the  P  wave has to fall before  QRS  and for cannon waves to occur the  p   waves must fall after QRS  ie with QT interval .

Clinical significance  of  cannon wave

Complete heart block is the most common situation for cannon waves to occur.

Ironically ,the VVI pacemaker which is used  to treat CHB does not prevent the cannon waves , and atrial contractions continue to occur at random , causing various degrees of intermittent venous reflux into the veins .This may produce, worrisome venous palpitation in some (Usually settles down after few weeks !)

Some attribute , the so called pacemaker syndrome ie giddiness, dizziness to this abnormal venous waves triggering the carotid baroreceptors (Venous -artery spillover )

Will DDD pacemakers  eliminate venous cannon waves ?

We hoped so , it does in fact . But,  it really happens only if the A sense V pace mode . A pace V pace mode with programmed PR interval is not a realiable way to produce AV synchrony. It is  common ,  many of the DDD pacemakers fall back to VVI mode either intentionally or by mode switching  for various reasons.


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