Test: Measurement Of Blood Pressure, Regulation Of Blood Pressure - NEET PG MCQ

“Constriction of an artery increases the velocity of blood flow through the constriction, producing turbulence and sound beyond the constriction. Examples are bruits heard over arteries constricted by atherosclerotic plaques and the sounds of Korotkoff heard when measuring blood pressure.”

Right ventricular peak systolic pressure: 17–32 mm Hg, End diastolic pressure: 1–7 mm Hg
Left ventricular peak systolic pressure: 90–130 mm Hg, End diastolic pressure: 5–12 mm Hg.

Mean BP = DBP + 1/3 pulse pressure = DBP + 1/3 (SBP – DBP)
= (3DBP + SBP – DBP)/3
= 2/3 DBP + 1/3 SBP = (SBP + 2DBP)/3

“The arterial pressure is conventionally written as systolic pressure over diastolic pressure, for example, 120/70 mm Hg. One millimeter of mercury equals 0.133 kPa, so in SI units this value is 16.0/9.3 kPa.”

There is stretching of aorta and arteries during systole due to ejection of blood from ventricle. During ventricular diastole the previously stretched aorta and arteries recoil. The volume of blood that is displaced by the recoil furnishes continuous capillary flow throughout diastole. The lateral pressure exerted by this flowing blood is diastolic pressure.

Sphygmomanometer always underestimates systolic pressure and overestimate diastolic BP (not always). So, better answer: intra-arterial is higher than sphygmomanometer measurement.

Auscultatory gap gives falsely low BP measurement.

Diastolic BP indicated by fifth phase of Korotkoff sound.

Shape of the pressure pulsation is not linear because of elastic expansion of arterial wall (expansion causes dampening of pressure).
The shape progressively changes towards peripheral arteries. The cause of this shape change is resistance to blood movement in the vessels. So, resistance of vessel is the main factor determining shape of arterial pulse. Resistance indirectly depends on cross sectional area (diameter).

“Occluding the two common carotid arteries, reduces the carotid sinus pressure; as a result, the baroreceptors become inactive and lose their inhibitory effect on the vasomotor center. The vasomotor center then becomes much more active than usual, causing the aortic arterial pressure to rise and remain elevated.”

Low-pressure baroreceptor are located within the wall of both right (main), left atrium and pulmonary artery.

Baroreceptor directly activated by the increase BP. Active baroreceptor inhibits vasomotor center and activates vagal center. Vagal center stimulation decreases HR.
When BP falls, the baroreceptors become inactive and lose their inhibitory effect on the vasomotor center. The vasomotor center then becomes much more active than usual (Tonically active), and causes vasoconstriction via sympathetic system. So, it is not direct effect of baroreceptor but the effect of tonically active VMC.

“Volume receptors are low-pressure baroreceptor located within atrium.
The stretch receptors in the atria are of two types: those that discharge primarily during atrial systole (type A), and those that discharge primarily late in diastole, at the time of peak atrial filling (type B).”
Cardiac output will affect the high pressure baroreceptor (carotid sinus and aortic arch) not the volume receptor.

Baroreceptor stimulation inhibits vasomotor center and stimulates cardiovagal center. So, Sympathetic system will be inhibited and parasympathetic will be stimulated.

Pressure on carotid sinus activates baroreceptors. Active baroreceptor reflexly decreases HR by inhibiting vasomotor center and stimulating cardiac vagal center.

Active baroreceptor inhibits rostral ventrolateral medulla (vasomotor center). All other center in the options are activated.

VMC is a tonically active center. Disinhibition of VMC leads to spontaneous activation of sympathetic system. Although stimulation of vagal center may decrease BP, the effect is not significant.

Baroreceptor respond much more to a rapidly changing pressure than to a stationary pressure. “These receptors (baroreceptor) are most sensitive to changes in pulse pressure but also respond to changes in mean arterial pressure.”

Vineet: At 85 mm Hg: during this time Baroreceptors are still active (in a lesser degree). Active Baroreceptor inhibits VMC/Sympathetic system(means during this time, Baroreceptor still has some inhibitory effect on VMC). So, cutting the sinus nerve during this time, all inhibitory effect on VMC will be lost, BP will rise (although rise will not be very severe).
Kamlesh: At 60 mm Hg: during this time Baroreceptors are completely inactive, but chemoreceptors are active. Active chemoreceptor stimulates VMC/sympathetic system (means during this time, Chemoreceptor is trying to rise the BP by stimulatory effect on VMC).
So, cutting the sinus nerve during this time, excitatory effect on VMC due to chemoreceptor will be lost, BP will fall.
So, Vineet will record increase in BP, Kamlesh will record decrease in BP (option a).

Clamping above carotid sinus, increases sinus pressure and activate baroreceptor.