Short-term blood pressure regulation

Flow equals the pressure difference divided by resistance (F = ΔP / R). With resistance fixed, doubling the pressure difference doubles the flow.

• It halves to 2.5 L/min:
• It stays at 5 L/min:
• Correct: It doubles to 10 L/min:

Norepinephrine binds beta-1 receptors on SA node cells and speeds the pacemaker potential, so heart rate rises. Acetylcholine from the vagus nerve does the opposite. The SA node receives both sympathetic and parasympathetic fibers.

• Correct: It speeds the pacemaker potential, so heart rate rises:
• It slows the pacemaker potential, so heart rate falls:
• It has no effect; only the vagus nerve reaches the SA node:

Cardiac output = heart rate × stroke volume = 60 × 80 mL = 4,800 mL/min, which is 4.8 L/min.

• Correct: 4.8 L/min:
• 1.3 L/min:
• 140 mL/min:

Start with MAP = CO × TPR = 4.5 × 20 = 90 mm Hg. A 20 percent fall in TPR gives 20 × 0.8 = 16 mm Hg·min/L. New MAP = 4.5 × 16 = 72 mm Hg. With cardiac output fixed, MAP falls by the same 20 percent as TPR.

• 70 mm Hg: This subtracts 20 mm Hg from the starting MAP of 90. The drop was 20 percent of TPR, not 20 mm Hg of pressure, so the new MAP is 4.5 × 16 = 72 mm Hg.
• 86 mm Hg: This is too small a fall. MAP is proportional to TPR when cardiac output is fixed, so a 20 percent fall in TPR gives a 20 percent fall in MAP, from 90 to 72 mm Hg.
• Correct: 72 mm Hg: Correct. MAP = 4.5 × (20 × 0.8) = 4.5 × 16 = 72 mm Hg.
• 112 mm Hg: This divides the starting MAP by 0.8, as if pressure rose when resistance fell. Lower resistance with the same flow means a lower pressure, not a higher one.

Standing moves blood into the leg veins. Venous return, end-diastolic volume, stroke volume, cardiac output and MAP fall in a chain, and baroreceptor firing falls with MAP. That fall in firing is the signal that starts the reflex a moment later.

• Venous return: down. Gravity pools blood in the stretchy veins of the legs and abdomen, so less blood reaches the right atrium.
• Stroke volume: down. Less venous return means a smaller end-diastolic volume, so by the Frank–Starling mechanism each beat ejects less blood.
• Mean arterial pressure: down. Cardiac output falls with stroke volume, and MAP = CO × TPR, so MAP falls.
• Baroreceptor firing rate: down. Lower arterial pressure stretches the carotid sinus and aortic arch walls less, so the baroreceptors fire fewer action potentials.
• Plasma protein concentration: no change. Pooling moves whole blood into the leg veins within seconds. It does not change what the plasma contains.

Norepinephrine constricts arterioles by binding alpha-1 receptors on their smooth muscle. With those blocked, TPR cannot rise when he stands, so MAP = CO × TPR stays low. His heart rate still rises, which shows the sensors, afferent nerves, control center and sympathetic output to the heart all work.

• His baroreceptors no longer sense the fall in pressure: If the baroreceptors missed the fall, nothing would drive his heart rate up. The rise from 70 to 94 shows they did sense it.
• His cardiovascular center no longer raises sympathetic output: His heart rate rose, and much of that rise comes from increased sympathetic output. The control center is responding.
• His SA node no longer responds to sympathetic signals: The SA node responds through beta-1 receptors, which the drug does not block. His heart rate did rise.
• Correct: His arterioles cannot constrict in response to norepinephrine: Correct. The effector that fails is arteriole smooth muscle, because its alpha-1 receptors are blocked.

Baroreceptors adapt. If pressure stays at a new level for a day or two, their firing settles back toward its usual rate at that level, so they stop signaling a change. This makes the reflex a fast corrector, not a setter of long-term pressure.

• Correct: The baroreceptors reset and treat the higher pressure as normal: Correct. Resetting shifts the pressure the baroreceptors report as normal.
• Baroreceptors respond only to falls in pressure, never to rises: Baroreceptors fire steadily at normal pressure, so they report both rises and falls. A rise increases their firing.
• The vagus nerve cannot slow the heart for more than a few hours: Vagal output can stay raised for as long as the control center drives it. The reflex fades because its sensors reset, not because the vagus tires.
• Higher pressure damages the carotid sinuses within the first day: Resetting is a normal adaptation of the nerve endings over a day or two, not damage. The sinuses still work, around a new level.

While the cuff blocked flow, the forearm's cells kept working. Oxygen fell and carbon dioxide, hydrogen ions, potassium ions and adenosine built up in the interstitial fluid. These relax arteriole smooth muscle, so when the cuff came off, the arterioles were wide open and flow surged until the metabolites washed out. This is metabolic autoregulation.

• Sympathetic nerves to the forearm fire faster once the cuff is released: Faster sympathetic firing would constrict the arterioles and reduce flow, not raise it. The response is local, with no nerve involved.
• Baroreceptors in the arm sense the fall in pressure and dilate its arteries: The arm has no baroreceptors that control its arteries. Arterial baroreceptors sit in the carotid sinuses and aortic arch and act through the brainstem.
• Correct: Metabolites built up during the blockage and dilated the forearm's arterioles: Correct. Local metabolites dilated the arterioles, and flow stays high until the extra flow washes them away.
• The cuff stretched the arterioles, which now contract through the myogenic response: The myogenic response to stretch is contraction, which would narrow the arterioles and reduce flow. It cannot explain a rise in flow.

The immediate change is a fall in venous return, cardiac output and MAP, sensed as reduced baroreceptor firing. Within a minute the reflex raises heart rate, contractility, venous tone and TPR. MAP climbs back toward normal, at the cost of lower flow to the skin and gut, while the brain and heart keep their flow.

• Mean arterial pressure, first few seconds: down. Less blood volume means less venous return, a smaller stroke volume and lower cardiac output, so MAP = CO × TPR falls.
• Baroreceptor firing, first few seconds: down. Lower arterial pressure stretches the carotid sinus and aortic arch walls less.
• Heart rate, one minute later: up. The cardiovascular center raises sympathetic output and lowers vagal output to the SA node.
• Total peripheral resistance, one minute later: up. Norepinephrine on alpha-1 receptors constricts arterioles in the skin, gut, kidneys and resting muscle.
• Mean arterial pressure one minute later, compared with its lowest point: up. Higher heart rate, contractility, venous tone and TPR push MAP back up toward normal.
• Blood flow to the skin, one minute later: down. Skin arterioles constrict strongly under sympathetic stimulation, which is why a bleeding person looks pale and feels cool.