Neural and chemical control of cardiorespiratory function

• Respiratory control

  The process of regulating breathing to match metabolic demand
• At rest, body cells use around 200mls of oxygen each minute
• Rhythm of respiration

  Controlled by 2 separate interacting neural mechanisms:

  1. Voluntary System – cerebral cortex

  2. Automatic System – medulla and pons
• Basic rhythm of respiration

  Controlled by two specialised groups of neurons in the brain stem:

  Medulla Oblongata – controls the basic rhythm of respiration (Respiratory Rhythmicity Centre – RRC). Dorsal group – inspiration. Ventral group - expiration

  Pons – adjusts the activity of the RRC in response to input from other areas of the brain – rate and depth of inspiration
• Pons

  • Pneumotaxic area helps to turn off the inspiratory area "prematurely", shortens the duration of inhalation, increases breathing rate

  Apneustic area sends excitatory impulses to inspiratory area to "keep going", facilitates respiration, prolongs inhalation - Long deep inhalation

  Controlled mechanically to prevent over-inflation and Barotrauma (Hering-Breuer Reflex)
• Normal quiet breathing

  • Normal quiet inspiration = diaphragm and external intercostals contract
  • Normal quiet exhalation = diaphragm and external intercostals relax followed by elastic recoil of lungs
• Forceful breathing

  • Forceful inhalation = inspiratory area active -> diaphragm, sternocleidomastoid, scalene contract
  • Forceful exhalation = inspiratory area activates expiratory area -> internal intercostals and abdominals contract
• Basic rhythm of respiration

  Set and co-ordinated by respiratory area in Medulla Oblongata, but rate is modified by:

  Chemical Stimuli

  Non-chemical stimuli

  Other factors (medication, limbic system)
• Chemoreceptor regulation

  Certain chemical stimuli determine how quickly and deeply we breathe:

  O2, CO2, H+ ions

  Raised PCO2/H+ ions or lowered O2 levels increase respiratory centre activity

  Lowered PCO2/H+ions or raised O2 levels decrease respiratory centre activity
• Central chemoreceptors

  • Found on the ventral surface of the medulla near, but not part of the respiratory centre

  Superficial enough to be bathed in CSF, as well as being surrounded by the brain's extra cellular fluid

  Respond to a change in concentration of H+ ions and levels of CO2 in these fluids
• Location of the peripheral chemoreceptors

  • Two carotid bodies – near the bifurcation of the carotid artery at each side

  Two or more aortic bodies- near the aortic arch

  Mainly react to arterial hypoxemia , less so to H+ ions and CO2

  Carotid bodies more sensitive than aortic bodies (consider brain)
• CO2 hydration

  CO2 + H2O ⇌ H2CO3 ⇌ H+ + HCO3-

  Changes in CO2 causes local changes in H+ ion concentration

  Central chemoreceptors sensitive to this change

  Effects of CO2 on respiration depend on the hydration and subsequent dissociation of CO2 into H+ ions which then stimulate the central chemoreceptors
• Increased CO2 (PCO2 = 5.3 KPa (40 mmHg))

  Increase in PCO2 (hypercapnia) - increases H+ ions - stimulates central and to a lesser extent peripheral chemoreceptors

  Highly activated inspiratory area – rate and depth of breathing increases – hyperventilation

  Continues or increases as output of PCO2 and decreased pH is produced
• Decreased CO2 (below 5.3 KPa (40mmHg) – hypocapnia)


  Central and peripheral receptors not stimulated – lack of stimulus to inspiratory area

  Inspiratory area sets a slow pace (rate/depth) until CO2 accumulates and rises to 5.3 KPa (40mmHg)
• Severe deficiency of O2

  Depresses the central chemoreceptor activity and inspiratory area

  Stops responding effectively to any inputs and sends fewer impulses to respiratory muscles

  Decreases breathing rate – worsening situation

  Hypoxaemia can kill in minutes
• If PaO2 drops to 8KPa (60mmHg) the peripheral chemoreceptors in carotid bodies will stimulate the inspiratory centre
• Other factors affecting respiration

  Limbic system in brain – emotional anxiety /exercise anticipation/performance stress - excitatory

  Temperature increases (fever and vigorous muscular exercise ) – increases rate

  Temperature decreases (hypothermia ) – decreases rate

  Proprioceptors – exercise, your rate and depth of breathing increases even before changes in chemical – proprioceptors that monitor joint and muscle movement send signals to medulla
• Cardiovascular control

  Lungs and heart work together, one can help the other (to a certain extent), both fulfil same overall role in homeostasis

  The heart also has specific and specialist mechanisms for ensuring cardiovascular demand meets supply
• Regulation of the heart

  Adjustments to the heart rate are important in the short term control of Cardiac Output and Blood Pressure

  CO = SV x HR

  BP = CO x SVR

  CO = Cardiac Output, SV = Stroke Volume, HR = Heart Rate, BP = Blood Pressure, SVR = Systemic Vascular Resistance
• Regulation of Heart

  Left to self – SA node – sets rate at a constant e.g., 100 beats/min

  Different volumes of blood required by tissues under different conditions

  Exercise – cardiac output increases to supply working muscles with more O2 and nutrients
• Systems of Regulation

  Autonomic Nervous System

  Hormones released by Adrenal Glands
• Autonomic Nervous System

  Nervous system regulation of heart originates in CV centre of Medulla

  Receives input from a variety of sensory receptors and higher centres in brain – cerebral cortex and Limbic system

  CV Centre – directs appropriate output by increasing and decreasing frequency of nerve impulses sent out to ANS

  Both Sympathetic and Parasympathetic branches
• Sympathetic system

  CV centre excites Sympathetic neurons which up-regulate heart rate

  Via cardiac accelerator nerve which innervates conducting system - atria and ventricles of heart

  Cardiac accelerator nerve releases nor-epinephrine (nor-adrenaline) to increase heart rate
• Parasympathetic system

  CV centre excites Parasympathetic neurons which down-regulate heart rate

  Via Vagus nerve (cranial nerve X) which innervates conducting system – atria

  Neurotransmitter they release is – acetylcholine – slowing activity of SA node
• Normal Resting Heart Rate

  Balance between SNS and PNS

  To increase HR – ↑ SNS activity, ↓ PNS activity, or both

  To slow HR – ↓ SNS activity, ↑ PNS activity, or both
• Stroke Volume Control

  ↑ SNS activity enhances myocardial contractility, leads to better emptying of the ventricles

  ↑ Venous return, greater stretch of ventricular walls prior to contraction, further increases SV

  Known as Frank-Starling Law of the Heart, ensures demand and supply meet
• Sensory Receptors - Baroreceptors

  • Neurones sensitive to changes in BP

  Located in the Arch of the Aorta and Carotid Arteries

  Increased BP – baroreceptors send impulses along sensory neurons to CV centre in medulla

  CV centre responds - more impulses along parasympathetic (motor) nerve and decrease in accelerator output, ↓ Heart rate, ↓ CO, and thus ↓ BP
• Decrease in BP

  Baroreceptors do not stimulate CV centre, lack of stimulus, ↑ HR, ↑ CO and this leads to ↑ BP to normal levels
• Sensory Receptors - Chemoreceptors

  • Sensitive to O2, CO2, H+

  Located in Carotid Arteries and Arch of Aorta

  Hypoxia, Acidity (pH), Hypercapnia stimulate the chemoreceptors to send information to CV centre in medulla

  ↑ Sympathetic stimulation to peripheral arterioles and veins, producing ↑ vasoconstriction and ↑ BP

  Also ↑ HR and ↑ force of contraction, supply matched to demand
• Chemical Regulation

  Hormones:

  Epinephrine and norepinephrine – Adrenal medulla

  Enhance the hearts effectiveness as a pump, ↑ HR and force of contraction

  Excitement, Stress , Exercise - Adrenal Medulla – produce these hormones

  Longer-term changes (revising for exam!)