Why does blood flows with increased velocity across the stenosed valve in Aortic Stenosis
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aortic stenosis increased velocity across stenotic valve Bernoulli continuity equation
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Why does blood flows with increased velocity across the stenosed valve in Aortic Stenosis
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aortic stenosis increased transvalvular jet velocity continuity equation Bernoulli ASE
Blood velocity rises across a stenosed aortic valve because the same stroke volume must pass through a much smaller opening during systole.
By the continuity equation:
[
Q = A \times v
]
where (Q) is flow rate, (A) is valve area, and (v) is velocity. If flow (Q) is roughly maintained but the valve area (A) decreases, velocity (v) must increase.
Example: If the effective valve area becomes one-quarter of normal, blood needs to travel roughly four times faster through that narrowed orifice to deliver the same volume per second.
The left ventricle produces a higher pressure to force blood through the narrow valve. As blood enters the narrow opening, some of this pressure energy is converted into kinetic energy, producing a high-velocity jet just beyond the valve. This also creates a large pressure gradient:
[
\Delta P \approx 4V^2
]
So velocity and pressure gradient have a squared relationship. A jet velocity of 4 m/s corresponds to an estimated peak pressure gradient of about (4 \times 4^2 = 64) mmHg.
This is why Doppler echocardiography measures peak aortic jet velocity and uses the continuity equation to calculate valve area. ASE guidance identifies peak velocity, mean transvalvular gradient, and continuity-equation valve area as the main haemodynamic measures of aortic stenosis severity, as described in the ASE valve-stenosis guideline.
In pulmonary hypertension pulmonary artery constricts or dilates?
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pulmonary hypertension pulmonary artery vasoconstriction vascular remodeling overview
In pulmonary hypertension, the small pulmonary arteries and arterioles predominantly constrict and remodel, which increases pulmonary vascular resistance and raises pulmonary artery pressure.
- Early or reversible component: vasoconstriction, especially with hypoxia.
- Chronic component: thickening of the vessel wall from smooth-muscle hypertrophy, intimal fibrosis, and loss/narrowing of small vessels. This can become fixed.
However, the main pulmonary artery and its large branches may become dilated over time because they are exposed to persistently high pressure.
So the key distinction is:
| Vessel level | Typical change |
|---|---|
| Small pulmonary arteries/arterioles | Constriction and narrowing |
| Main pulmonary artery | Often dilates secondarily from chronic high pressure |
Pulmonary arterial hypertension is driven by sustained vasoconstriction plus vascular remodeling, as described in Fishman's Pulmonary Diseases and Disorders and summarized by this NCBI review.
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