Control Of Heart Rate

  • Created by: Rachelezy
  • Created on: 14-02-20 14:44

Myogenic Stimulation

1) SAN produces a wave of electrical excitation that spreads across atria and cause them to contract

2) Wave is prevented from spreading to the ventricles by the atrioventricular septum

3) Wave enters the AVN

4) There is a short delay. Then, the AVN sends a wave of excitation along a series of Purkyne fibres (form bundles of His)

5) The wave travels through the atrioventricular septum (to the base of ventricles) down the bundle of His and branch into the smaller Purkyne fibres.

6) Wave released from these fibres causes ventricles to contract in unison from bottom upwards

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Role of the Atrioventricular Node (AVN)


  • Second clump of specialised cells
  • LOCATION: inferior part of the right atria in the septum
  • Delays impulses from spreading to the ventricles - pause depolarises and transmits to the atrioventricular bundle 
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Role of the Sinoatrial Node (SAN)


  • Clump of specialised myocardial conducting cells
  • LOCATION: superior and posterior walls in the right atrium (close to vena cava)
  • Establishes normal cardiac rhythm 
  • Has highest rate of depolarisation - initiates synus rythm
  • Impulse spreads through atria through internodal pathways that lead directly from the SAN to the AVN
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Purkyne Tissue/Fibres

Purkyne Tissue/Fibres:

  • Forms bundle of His
  • Conducts electrical activity rapidly down the wall between ventricles to the bottom of the heart
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Role of Chemoreceptors


  • 'chemical' receptors
  • LOCATION: aorta, medulla oblongata, and carotid arteries
  • Monitor the pH levels in the blood (e.g. exercising )
  • 1) CO2 in the blood increase and lowers the pH of the blood
  •  2) Chemoreceptors detect this change and signal to the centre in the medulla oblongata (increases heart rate)
  •  3) Centre sends more frequent impulses along sympathetic nerves to the SAN
  •  4) Waves by SAN increases which leads to an increased heart rate as more CO2 is removed
  •  5) As the CO2 concentration in the blood decreases, receptors detect this change stop being stimulated (heart rate is back to normal)
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Role of Pressure Receptors

Pressure Receptors:

(Same process as chemoreceptors - only difference is it is in terms of blood pressure rather than pH)

  • The pressure of blood is maintained at a set level - pressure receptors measure changes in pressure
  • LOCATION: Aorta and carotid arteries

Both chemoreceptor and pressure receptor mechanisms are examples of negative feedback

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Role of the Autonomic Nervous System


  • Input into the heart via the vagus nerve
  • Nerves form synapses with postganglionic cells in the SAN and AVN
  • When stimulated, it decreases action potential, decreasing heart rate



  • Input into the heart via the postganglionic fibres
  • Fibres increase action potential, increasing the heart rate


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Effect of Blood Pressure on Heart Rate (+ Stroke V


  • Pressure receptors detect an increase in blood plasma content
  • Impulses from pressure receptors to the medulla
  • Impulses from the medulla to the SAN (along parasympathetic nerves)
  • Results in a decrease in heart rate back to its normal level


  • Pressure receptors detect low blood plasma content
  • Impulses from pressure receptors to the medulla
  • Impulses from the medulla to SAN (along sympathetic nerves)
  • Results in an increase in heart rate back to its normal level.


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Role of Medulla Oblongata + Heart Modification

Medulla Oblongata:

  • Controls rate at which sinoatrial node fibres are unconsciously controlled

Has two centres:

  • 1) Links to sinoatrial node via a parasympathetic nerve  (INCREASING HEART RATE)
  • 2) Links to sinoatrial node via a sympathetic nerve (DECREASING HEART RATE)

How can the heart be modified?

  • Changing the heart rate
  • Changing the contraction strength of the ventricles
  • Changing the volume of blood transported in each stroke
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