Control of heart rateAQA A-Level Biology: Revision notes
Section 1
The heartbeat is myogenic
Cardiac muscle is myogenic: it can contract and relax without receiving nerve impulses. The sinoatrial node (SAN), a small patch of tissue in the wall of the right atrium, initiates the heartbeat. It acts as the heart's pacemaker, generating regular waves of electrical excitation.
The nervous system does not start the heartbeat. It only changes the rate set by the SAN.
Do not say that the brain makes the heart beat. The brain only speeds it up or slows it down.
Section 2
Spread of excitation through the heart
- The SAN produces a wave of excitation that spreads over both atria, causing them to contract.
- A layer of non-conducting tissue between the atria and ventricles stops the wave passing directly to the ventricles.
- The wave reaches the atrioventricular node (AVN), which delays it by about 0.1 s. This gives the atria time to empty into the ventricles.
- The wave then passes down the bundle of His, which divides into Purkyne tissue, conducting it rapidly to the apex of the heart.
- The wave spreads upwards through the ventricle walls, so the ventricles contract from the apex upwards, pushing blood out into the arteries.
Section 3
Chemoreceptors and pressure receptors
Heart rate is adjusted by receptors that monitor the blood.
- Chemoreceptors in the walls of the carotid arteries and the aorta detect changes in blood pH, which is lowered by a rise in carbon dioxide concentration (they also respond to changes in oxygen concentration).
- Pressure receptors (baroreceptors) in the walls of the carotid arteries and the aorta detect changes in blood pressure.
Both send impulses to the cardiac centre in the medulla of the brain.
Section 4
The autonomic nervous system
The autonomic nervous system controls heart rate involuntarily. It acts on the SAN, which is the effector.
- Sympathetic neurones (the accelerator nerve) carry impulses to the SAN that increase the heart rate.
- Parasympathetic neurones (the vagus nerve) carry impulses to the SAN that decrease the heart rate.
Exercise: more carbon dioxide, so lower pH. Chemoreceptors send more impulses to the cardiac centre, which sends more impulses along sympathetic neurones to the SAN, so heart rate increases.
High blood pressure: pressure receptors send more impulses to the cardiac centre, which sends more impulses along parasympathetic neurones to the SAN, so heart rate decreases.
Low blood pressure has the opposite effect.
Name the full pathway: receptor, impulses to the cardiac centre in the medulla, then sympathetic or parasympathetic neurones to the SAN (effector), then the change in heart rate.
That's the notes covered.
Carry on to the next subtopic.
Exam questions on Control of heart rate
- A mammalian heart is removed from the body and placed in warm, oxygenated saline solution. All the nerves to it have been cut. The heart continues to beat rhythmically for several minutes.Explain why the wave of excitation is carried by Purkyne tissue down the septum to the apex of the heart before it spreads upwards through the ventricle walls.2 marks
- A volunteer holds her breath for 30 seconds. During this time the carbon dioxide concentration of her blood rises and her heart rate increases from 70 to 85 beats per minute.Explain how the rise in carbon dioxide concentration leads to the increase in her heart rate.2 marks
- Physiologists investigate how the autonomic nervous system controls the heart rate of an anaesthetised mammal at rest. With all nerves intact, the resting heart rate is 90 beats per minute. When the parasympathetic nerve to the sinoatrial node (SAN) was cut, the rate rose to 110 beats per minute. When the sympathetic nerve to the SAN was cut instead, the rate fell to 80 beats per minute. When both nerves were cut, the heart continued to beat at 100 beats per minute.The blood pressure of this mammal suddenly rises. Describe how pressure receptors lead to a return of the heart rate towards normal.3 marks
Written by the Exaim team, led by Shaun Daswani (Head of Upper Secondary, Improve ME Institute; MSc Financial Mathematics, Imperial College London; BSc, UCL) and Jason Daswani (operational lead, Improve ME Institute; LSE).