Part of the TeachMe Series

Control of Heart Rate

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Original Author(s): Aarushi Khanna
Last updated: 22nd April 2018
Revisions: 13

Original Author(s): Aarushi Khanna
Last updated: 22nd April 2018
Revisions: 13

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The heart rate is established by the Sinoatrial Node (SAN) – the pacemaker of the cardiac muscle. In the absence of any influences the SAN pacing rate would be 100 bpm, however heart rate and cardiac output must be able to vary in response to the needs of the body.

By influencing the cells in the SAN, nerve impulses and hormones can affect the speed at which the SAN generates electrical impulse. This affects the heart rate (or chronotrophy), which in turn affects the cardiac output. In this article we will discuss how hormones and nerve impulses work to control the rate of the heart.

The Autonomic Nervous System

The ANS is responsible for controlling many physiological functions: inducing the force of contraction of the heart, peripheral resistance of blood vessels and the heart rate. The ANS has both sympathetic and parasympathetic divisions that work together to maintain balance.


The parasympathetic input into the heart is via the vagus nerve (CN X). The vagus nerve forms synapses with postganglionic cells in SAN and AVN. When stimulated, acetylcholine which binds on to M₂ receptors, which acts to decrease the slope of the pacemaker potential, leading to a decrease in heart rate (a negative chronotropic effect).


The sympathetic input into the heart is via the postganglionic fibres from the sympathetic trunk which innervate the SAN and AVN. The post ganglionic fibres release noradrenaline, which acts on B₁ adrenoreceptors to increase the slope of the pace maker potential, thereby increasing the heart rate (a positive chronotropic effect), as well as increasing the force of contraction (positive inotropic effect).

The parasympathetic input on the SAN dominates at rest, to give a normal resting heart rate of around 60bpm. Any initial increases in heart rate are brought about by a reduction in parasympathetic outflow, and increasing the heart rate over 100bpm is via an increase in sympathetic outflow.

Fig 1 – Diagram giving an overview of autonomic innervation to the heart.

Baroreceptor Reflex

Baroreceptors are mechanoreceptors located in both the carotid sinus and the aortic arch, which are sensitive to stretch. Their function is to detect changes in arterial pressure and communicate this to the medulla oblongata in the brainstem. 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 increased arterial pressure is detected, the parasympathetic pathway is activated to reduce heart rate. This, along with increasing vasodilation of vessels, acts to reduce the arterial pressure.
  • If a decrease in arterial pressure is detected, the sympathetic pathway is activated to increase the heart rate and the force of contraction of the heart. This, along with increasing vasoconstriction of vessels, acts to increase the arterial pressure.

    Fig 2 – Diagram showing the action of the baroreceptor reflex.

Hormonal Control

Hormones also have the ability to affect the heart rate. One example would be adrenaline, which is released from the medulla of adrenal glands. This hormone can be released into the blood stream at a time when a person encounters a stressful situation. The release of this hormone can result in a number of effects one of which is increasing of the heart rate.

Clinical Relevance – Tachycardia

Tachycardia is defined as a heart rate that exceeds the normal resting rate, it is normally a rate of over 100 beats per minute. This can be normal in the case of exercise, but tachycardia at rest is generally due to another cause, such as:

  • Anxiety
  • Infection
  • Hypoglycaemia
  • Hypovolaemia
  • Hyperthyroidism
  • 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 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 the case of narrow complex tachycardias vagal manoeuvres 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 for 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-coagulative measures.

Fig 3 – ECG showing Sinus Tachycardia with a heart rate of 150bpm.