Heart rate is one of the two factors (the other being stroke volume) that determines cardiac output.
Heart rate (also called chronotropy) normally falls in the range of 60-100 beats per minute (bpm). However in special circumstances, such as during exercise, the heart needs to be able to change this rate to either increase or decrease cardiac output accordingly.
In this article, we will discuss how hormones and nerve impulses work to control the heart rate and the baroreceptor reflex, which can change the heart rate.
Sinoatrial Node (SAN) and Atrioventricular Node (AVN)
Heart rate (or chronotrophy) is established by the sinoatrial node (SAN) – this is a cluster of pacemaker cells which sits in the right atrium. In the absence of any external influences, the SAN pacing rate is about 100 beats per minute (bpm). However, heart rate and cardiac output must be able to vary in response to the needs of the body.
By influencing cells in the SAN, nerve impulses and hormones can affect the speed at which the SAN generates an electrical impulse. This affects the heart rate, which in turn affects cardiac output.
The atrioventricular node (AVN) sits above the ventricular septum at the junction between the atria and the ventricles. Its function is to pass on the impulse from the atria to the ventricles. However, as the conduction velocity of the AVN is much slower than the SAN, this creates a delay of about 0.15 seconds. This 0.15s delay is what allows the atria to finish contracting and the atrioventricular valves to close before the ventricles start to contract – this prevents blood from regurgitating back into the atria during ventricular contraction. This delay is also one of the reasons why despite the SAN having a pacing rate of 100bpm, the actual heart rate is usually lower, at around 70bpm.
The Autonomic Nervous System
The autonomic nervous system (ANS) is responsible for controlling many physiological functions. It induces the force of contraction of the heart and its heart rate. In addition, it controls the peripheral resistance of blood vessels. The ANS has both sympathetic and parasympathetic divisions that work together to maintain balance.
Parasympathetic input to the heart is via the vagus nerve (CN X). The vagus nerve synapses with postganglionic cells in the SAN and atrioventricular node (AVN). When stimulated, acetylcholine binds on to M2 receptors, which act to decrease the slope of the pacemaker potential. This leads to a decrease in heart rate (a negative chronotropic effect).
Sympathetic input to the heart is via the postganglionic fibres from the superficial and deep cardiac plexuses, which innervate the SAN and AVN. The postganglionic fibres release noradrenaline, which acts on B1 adrenoreceptors to increase the slope of the pacemaker potential. This increases the heart rate (a positive chronotropic effect), as well as the force of contraction (positive inotropic effect).
At rest, parasympathetic input to the SAN dominates, giving a normal resting heart rate of around 60bpm. A reduction in parasympathetic outflow results in an increase in heart rate, reaching over 100bpm. This is further brought about by an increase in sympathetic outflow.
Baroreceptors are mechanoreceptors located in both the carotid sinus and aortic arch. They are sensitive to changes in stretch and tension in the arterial wall. Additionally, they detect changes in arterial pressure and communicate this to the medulla oblongata in the brainstem via the glossopharyngeal nerve (CN IX) and vagus nerve (CN X). The medullary centres in the brain are responsible for the overall output of the autonomic nervous system, and use the information fed back from baroreceptors to coordinate a response:
- If an increase in arterial pressure is detected by the baroreceptors, the parasympathetic pathway is activated. This impulse is carried the glossopharyngeal (CN IX) and vagus (CN X) nerves to the medulla oblongata oblongata, where they activate cardiac decelerator centre. These cardioinhibitory centres carry impulses back to the heart via the vagus nerve (CN X) to reduce the heart rate. This, along with increasing vasodilation of vessels, acts to reduce the arterial pressure.
- If a decrease in arterial pressure is detected by the baroreceptors, there is no parasympathetic activation. Therefore the sympathetic pathway is activated. The cardiac accelerator centre in the medulla oblongata is activatedto increase the heart rate and the contractility of the heart. This, along with increasing vasoconstriction of vessels, acts to increase the arterial pressure.
Hormones also have the ability to affect heart rate. For example, adrenaline is released from the medulla of adrenal glands during times of stress. This results in a number of effects that occur during a stress response such as an increase in heart rate.
Clinical Relevance – Tachycardia
Tachycardia is defined as a heart rate that exceeds the normal resting rate (over 100bpm). This can be normal in the case of exercise, however, tachycardia at rest is generally due to causes such as:
- Problems with conductance in the heart
Tachycardias due to conductance within the heart can be classified as narrow or wide complex tachycardia depending on the length of the QRS complex on an ECG. Narrow complex tachycardias include sinus tachycardia, atrial fibrillation and atrial flutter. Wide complex tachycardias include ventricular tachycardia and Wolff-Parkinson-White Syndrome.
In narrow complex tachycardias, vagal manoeuvres (e.g. Valsalva manoeuvre or carotid sinus massage) or IV adenosine can be used to attempt to revert to a normal rhythm. If the patient is haemodynamically unstable then DC cardioversion may be necessary.
For broad complex tachycardias, amiodarone can be given if a patient is stable, however, if a patient is unstable DC cardioversion may be needed. It is important to note that in the case of Wolff-Parkinson-White syndrome with atrial fibrillation, AV node blocking drugs must not be used as they will increase conduction down the abnormal pathway.
Some disorders such as atrial fibrillation can be rate controlled using drugs such as beta-blockers, with accompanying anti-coagulants.