That’s how one of the patient presented to our hospital . An echo documented severe aortic stenosis with a peak aortic gradient of 80mmhg and a bounding systolic blood pressure of 180 mmhg . Is that an exception ?
I recall the early days of medical school when we are fervently taught that systolic blood pressure is primarily determined by stroke volume and LV contractility .
The above example clearly proves this is explicitly wrong .
Now , we understand systolic blood pressure have many determinants . Stroke volume is just one of them .
The tone , distensibility of major blood vessels arising from aorta determine how a pressure wave is going to get amplified .
If you say stroke volume is not major determinate of systolic blood pressure . . . . does it imply , the antique bed side cardiac sign Pulsus parvus et- tardus a myth ?
No , it still holds good . But it is not a hard sign . We realise now , a patient with a well felt carotid can have a severe Aortic stenosis .
- Pre- existing systemic hypertension is a valid explanation.
- The other popular explanation for loss of systolic decapitation due to associated aortic regurgitation may be acceptable . (Not really proven though ! )
What will be the central aortic pressure in critical Aortic stenosis ?
It is definitely lower than brachial cuff pressure .This will explain the systolic blood pressure is actually an amplified signal .
Dr.S.Venkatesan MD 
Thank you for the post Dr.Venkatesan,
a related question of AS+HTN
so , in your practise, if you find a patient in your ER with
1.murmur of Aortic stenosis, radiating to carotids (later confirmed to be moderate AS on echo)
2.high BP
3.new ischemic changes in ECG and chest pain.
4. HR-120/min
what drug would you choose?
nitrates? hoping to achieve a double effect of reducing ischemia and at the same time reduce the preload and hence prevention of overloading the LV with AS
or
ACEI? hoping to reduce the BP. But at the risk of dereasing the gradient across stenosis and at the same time contraindications and cautions of ACEI and other vasodilators causing evere hypotension in an already supposedly low stroke volume patient prevail in AS.
or Betablocker? hoping to cotrol the HR,which would further have beneficial effects on ischemia, BP…but then again at the risk of further having a depressive effect of heart.
or
All of them in moderation?
looking forward to your answer,
Thank you
Hi Dr.Rajin Choudhury
Thank you for your interesting comments .
I believe more in beta blockers than the other two .
Heart rate optimisation is best modality in any heart that is under distress.
The myocardial depression is generally a not a major issue considering the fact it is useful even in advanced failure .
venkatesan
Hi SIr
This is DR R Ramesh from Madurai Medical college and your proud student too
sir does this systolic decapitation occurs in patients with AR / AS in the lower limb BP thus attenuating the Hill ” s sign and does this apply to LL BP
Thanks Ramesh for your comments.
There will always be difficulty in explaining BP changes with obstructive or regurgitant cardiac lesions as long as we ignore the peripheral amplifying and dampening factors.
If at all one wave in pulse , that is more related to stoke volume it is the percusion wave. Here too, it is the rate of raise that is determined by contractility, the peak gets modified by fusion of reflected tidal wave.
Though peripheral vascular resistance determine the diastolic pressure, the aortic recoil is an important determinant of maintaining diastolic pressure. The aortic recoil pressure is actually stored potential energy accrued during systolic expansion.So, technically (and really too )systolic BP do influnce diastolic BP if PVR is kept constant.
Under these condtions we have to analyse the BP response in various clinical entities.So , Imagine the complexities.
Systolic decapitation is indeed well observed clinical sign, as always exception are there.
One important caveat with intra arterial pressure measurement and cuff pressure is, catheters measure pressures as blood is flowing in the lumen.As expected pressure variations are reported in end and side hole.
Cuff pressure is actually the
vessel wall occluding pressure, that gets released when phase 1 kortocoff occur.
By definition cuff pressure will be close to physiological pressure as BP is the lateral pressure it exerts on vessel as it flows.We also know, lateral pressure drops as velocity increase.We dont know how important is this as we meaure within the lumen.
The recent obsevation that Hills sign is artifact was a revelation.Many may not accept that.
If we say hill sign is an artifact it may also mean the normal amplification of peripheral systolic pressure is also an artifact, which is well proven.
I agree with you decapitation in combined AS and AR may blunt Hill sign.
Ramesh, can you do one simple study , I have in mind, that can clarify few issues on this.Call me when free.
Wishes to you
Venkatesan