Control of heart rate and stroke volume

Question 1

What controls heart rate?

Answer 1

• Cardiac output = heart rate x SV (SV = EDC -ESV)
• Changes in any of these will alter cardiac output to ensure it meets the metabolic demand
• Specialised cells have the ability to produce electric activity (originates from SA node)
• Resting heart rate and changes in heart rate are primarily controlled by the autonomic nervous system
• Parasympathetic (craniosacral outflow) and sympathetic (thoracolumbar outflow, T1-T4) innervation work in an antagonistic manner where sympathetic nerves increase chronotropy, dromotropy, inotropy, and lusitropy, parasympathetic decrease effects
• Sympathetic innervation of T1-T4 origins synapse in sympathetic chain, give off cervical and thoracic nerves which supply the heart
• Parasympathetic innervation originates from dorsal vagal motor muscles, have long presynaptic fibres that supplies heart by synapse of cardiac plexus, supplies visceral of abdomen, and visceral of pelvis
• Parasympathetic nerve = vagus nerve: leaves brain stem, travels to SA node and alters heart rate (vagus can also innervate AV node to innervate ventricles)
• Sympathetic fibres travel from brain stem to spinal cord, short pre-ganglionic nerve synapse and run beside spinal cord but long post-ganglionic nerves innervate SA node, AV node and ventricles

Question 2

What is EDV determined by?

Answer 2

• EDV (also known as preload on cardiac muscle): volume of blood in ventricles at end of diastole (rest =120ml) and is determined by cardiac filling during end of diastole (determined by venous return related to stretching)
• Venous return is determined by central venous pressure (pressure in thoracic vena cava near right atrium) and by:
  1. Skeletal muscle pump: helps maintain venous return and cardiac output by compressing underlying veins to increase blood flow back to the heart
  2. Respiratory pump: diaphragm lowering causes an increase pressure in abdominal cavity, whilst chest wall expands which reduces pressure in thorax, right atrial pressure is also reduced during inspiration, these pressure changes help to move blood from abdominal vena cava to thoracic vena cava, aiding in EDV
  3. Blood volume: increased total blood volume leads to increases in venous return
  4. Venous tone: veins can stretch easily so can hold large volumes of blood within a small increase in internal pressure (venoconstriction increases venous return as less blood in veins so more blood in heart)
  5. Gravity: lying down, same gravitational forces are acting throughout body, but standing, gravity acts on vascular volume, causes blood to accumulate in venous system of legs so volume and pressure increases in legs and feet upon standing decreasing blood volume in thorax, decreasing central venous pressure

Question 3

Difference between Preload and Afterload

Answer 3

• Preload = stretching of cardiac myocyte prior to contraction (EDV = preload)
• Increasing preload means stretching sarcomere and stretching myocyte resulting in an increased force of contraction and so increased SV
• Afterload = load to overcome to eject SV (aortic pressure = afterload)
• Decreasing afterload, by working against less resistance, increases SV
• In congestive failure, can use ECG to know if preload has increased in the first stage
• Increase in preload let to increase in diameter of heart so greater distance between actin and myocyte (no longer contracting) and so greater EDV
• Increasing afterload means increase in internal dimension of ventricle at systole so not constricting as well, reducing SV
• Once heart is stretched, it cannot recoil and so will continue to stretch until it no longer meets metabolic demand
• Increasing both preload and afterload causes morphological remodelling (increase in EDV and ESV), functional loss (heart rate is maintained but reduced CO and reduced contractility)

Question 4

Contractility equation

Answer 4

• Left ventricular ejection fraction (around 55-65%) is the percentage of blood that is ejected from the ventricle during systole
• LVEF = ((LVEDD^2 - LVESD^2)/LVEDD^2)/100
• Increase sympathetic activity results in increased inotropic effect and increase contractility due to increase of intracellular calcium allowing for more actin-myosin cross bridges to be formed
• Excitation-contraction coupling is the process where an action potential triggers a myocyte to contract followed by subsequent relaxation
• Increasing the sarcomere length during diastole increases the calcium sensitivity of the contractile apparatus, increasing the rate of cross bridge attachment and detachment and so the amount of tension developed by the muscle fibre

Question 5

Sequence of events at the SA node

Answer 5

• Produces spontaneous action potentials, has a steady depolarisation which takes the membrane up to threshold
• Autonomic nervous system alters the slope of the depolarisation so alters time taken for the cell to reach threshold
• Noradrenaline is released from post-ganglionic fibres and acts on β-receptors on the SA node, circulating adrenaline released from the medulla will act on the same receptors and so have the same effect
• Stimulation of sympathetic nervous system of SA node increases permeability of cells to Na+ and Ca2+ , so cell reaches threshold sooner allowing more action potentials to be generated per minute, increasing heart rate (positive chronotropic effect)
• Stimulation of SA node through parasympathetic nervous system leads to a fall in heart rate
• Acetylcholine released from vagal nerve endings bind to muscarinic receptors, which hyperpolarises the cell making it harder to reach threshold, reduces Na+ current so takes longer to reach threshold (negative chronotropic effect)
• SA node produces action potentials at an intrinsic rate of 100 action potential per minute but resting heart rate is around 70 beats per minute, this is due to tonic activity where vagal influence is dominant over sympathetic influence so reduces heart rate

Question 6

Control of ESV

Answer 6

• Advantageous to have reserve blood in ventricle at end systole as it is possible to change SV by ejecting more blood so reducing ESV meaning it is possible to increase the SV without changing the filing of the heart
• Changing the SV without changing the ESV is due to contractility, if the contractility of the ventricular muscles increased, this would make the Starling’s curve steeper so there would be a larger SV for any given EDV
• increase in sympathetic nerve activity and/or circulating noradrenaline acting at β-receptors on ventricular cells increases contractility
• stimulation of the β-receptor increases the calcium influx into the ventricular cells and also increases the calcium released from the sarcoplasmic reticulum
• Overall increase of intracellular calcium leads to increased cross bridge formation in the myocyte which leads to greater force of contraction so increase in SV
• Afterload also affects SV and it is the load against which the heart must contract to eject the stroke volume
• For the left ventricle, the afterload is the aortic pressure which is high, whereas for the right ventricle, the afterload is the pulmonary pressure and the pulmonary circulation is a low resistance circulation and so afterload is lower