Part of the TeachMe Series

Control of Heart Rate

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Original Author(s): Aarushi Khanna
Last updated: 7th February 2021
Revisions: 18

Original Author(s): Aarushi Khanna
Last updated: 7th February 2021
Revisions: 18

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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 an 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 heart rate.

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.


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 (atrioventricular node). 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).


The sympathetic input into the heart is via the postganglionic fibres from the sympathetic trunk 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).

The parasympathetic input on the SAN dominates at rest, giving a normal resting heart rate of around 60bpm. A reduction in parasympathetic outflow results in an initial increase in heart rate, reaching over 100bmp. This is further brought about by an increase in sympathetic outflow.

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

Baroreceptor Reflex

Baroreceptors are mechanoreceptors located in both the carotid sinus and the 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. 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, the parasympathetic pathway is activated 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, the sympathetic pathway is activated to increase the heart rate and the contractility 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. 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 100 beats per minute). This can be normal in the case of exercise, however, tachycardia at rest is generally due to causes 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 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 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 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-coagulative measures.

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