The Heart as a Pump

Question 1

Describe what is caused by an action potential in cardiac muscle.

Answer 1

• Action potential causes L-type dihydropyridine (DHP) channels to open.
  
  • Large influx of extracellular Ca²⁺ but only ~10% of this contributes to contraction.
  • Cardiac muscle T-tubules 5x greater in diameter than skeletal muscle (25x more volume).
  • Cardiac T-tubule mucopolysaccharides sequester Ca²⁺. This keeps calcium in high concentration in the extracellular environment.

Question 2

What is the effect of dihydropyridine receptor activation?

Answer 2

• DHP receptor activation causes release of Ca²⁺ from sarcoplasmic reticulum via ryanodine release channels.
• At resting heart rates, the rise in intracellular Ca²⁺ due to influx and sarcoplasmic release is insufficient to cause maximal contractile force.

Question 3

Describe the refractory period of the heart.

Answer 3

• Cardiac twitches involve all fibres of the myocardium.
• You can not significantly summate contractions of cardiac muscle.
• Refractory period due to inactivation of Na²⁺ channels.

Question 4

Compare and contrast the contraction and refractory period of skeletal and cardiac muscle.

Answer 4

• Skeletal muscle
  
  • Absolute refractory period of 1-2ms
  • Period of contraction of 20-100ms
• Cardiac muscle
  
  • ​Absolute refractory period (ARP) ~245ms
  • Relative refractory period (RRP) - a stronger-than-normal signal can cause a contraction to occur.
  • Period of supranormal excitability (SNP) - a lower-than-normal signal can cause the cell to depolarise again.
  • Period of contraction 250ms

Question 5

Describe the contraction of cardiac muscle.

Answer 5

• Spread of an action potential across the surface of the cardiac muscle cell which is stimulated upstream by the SA node, driving electrical activity from nodal tissue to muscle fibres.
• The wave of depolarisation spreads down the T-tubules, causing a conformational change in the DHP-related Ca²⁺ channels.
• High concentration of calcium stored in the T-tubule mucopolysaccharides allows calcium in.
  
  • No direct physical connection here, it is only the increase in calcium concentration causing a change in the ryanodine receptors which opens pores in the sarcoplasmic reticulum.
• This calcium release drives the contraction; cross-linking of actin and myosin.
• The more calcium released from the sarcoplasmic reticulum, the more actin-myosin cross bridges become involved in the process, and the stronger the muscle contracts.
• You can modify how strongly each individual muscle cell contracts by changing the regulation of calcium here.

Question 6

Describe how the contractile process in cardiac muscle is stopped.

Answer 6

• To stop the contractile process, we need to get rid of the calcium from the extracellular environment.
• We can do this either by repackaging it back into the sarcoplasmic reticulum, or by putting it back out into the extracellular environment.
  
  • These are energy-dependent processes (either directly, such as the ATPase pump which pushed calcium back into the sarcoplasmic reticulum, or in exchange for sodium which is driven by the sodium-potassium ATPase pump.
    
    • Some treatments such as digoxin has some action on these ATPase pumps and influences how calcium is stored and packaged.

Question 7

How can the action of ATPase pumps and sodium-potassium ATPase pumps in cardiac muscle be modified?

Answer 7

• The reaction of these pumps is modifiable. We can influence how effectively we repackage calcium either into the sarcoplasmic reticulum or back out into the extracellular environment.
• In doing so, this is a way to modify how much calcium you have stored inside the sarcoplasmic reticulum.
• If you favour pushing more calcium back into the sarcoplasmic reticulum, the whole time the process loops over and starts again, when you open the sarcoplasmic reticulum stores, a higher concentration of calcium comes out and the extracellular calcium concentration becomes higher which increases the force of contraction.

Question 8

Describe the relationship among pressure (aortic, atrial and ventricular), ventricular volume, ECG and phonocardiogram during the cycle of systole and diastole.

Answer 8

Question 9

What is systole? What happens during this period?

Answer 9

• Systole is the period of contraction.
• Contraction of the ventricles occurs between the first and second heart sounds of the cardiac cycle. It causes the ejection of blood into the aorta and pulmonary trunk.

Question 10

What is diastole? What happens during this period?

Answer 10

• Diastole is the period of relaxation.
• During diastole, the thick muscular walls of the ventricles relax. The pressure in the ventricles falls low enough for the mitral valve to open.

Question 11

Describe the role of the atria as primer pumps.

Answer 11

• ~80% of ventricular filling is passive due to normal blood flow.
• Atrial contraction ‘tops up’ the remaining 20% volume.

Question 12

Describe the role of the ventricles as pumps.

Answer 12

• Isovolumetric (isometric) period of contraction.
• Period of rapid ejection (1/3) when 70% of stroke volume is ejected.
• Period of slow ejection (2/3) when the remaining 30% of stroke volume is ejected.
• Isovolumetric (isometric) period of relaxation.

Question 13

What happens to blood pressure in the arteries?

Answer 13

Blood pressure in the arteries oscillates.

Question 14

Compare and contrast the pressure in the aorta and in the pulmonary circulation.

Answer 14

• Systolic blood pressure in the aorta
  
  • ​~120mmHg
• Diastolic blood pressure in the aorta
  
  • ​~80mmHg
• Pressure in the pulmonary circulation is much lower
  
  • ​Much less resistance to flow.
  • Right side of the heart needs to do less work.
  • Right ventricle walls contain less muscle mass.
• Pulmonary systolic pressure
  
  • ​~30mmHg
• Pulmonary diastolic pressure
  
  • ​~12mmHg

Question 15

Describe the intrinsic mechanisms used to control stroke volume.

Answer 15

• Self-regulation
• Frank-Starling mechanism
• Increased end diastolic volume (EDV) causes increased force of contraction.
• Intrinsic mechanism causes EDV to change. EDV is influenced by preload and changes via the Frank-Starling mechanism.

Question 16

Describe preload.

Answer 16

• Preload is the initial length to which the muscle is stretched prior to contraction.
• It is defined by the venous pressure and venous return to the heart (EDV/EDP).

Question 17

Describe afterload.

Answer 17

• All the forces against which cardiac muscle must contract to generate pressure and shorten.
• It is defined by the aortic and pulmonary artery pressure.

Question 18

What are the extrinsic mechanisms used to control stroke volume?

Answer 18

• Sympathetic nerves

Question 19

What is the main principle of Frank-Starling’s law of the heart?

Answer 19

• Allows for automatic adjustment for small imbalances between the left ventricle and the right ventricle.
• Essentially balancing cardiac output from the left side of the heart with volume returning to the right side.

Question 20

Describe the effect of ANS stimulation on the contractility of the heart.

Answer 20

• Sympathetic innervation
  
  • Throughout the entire heart
  • Has a positive ionotropic effect
• Noradrenaline on β₁ receptors
  
  • ​Enhances Ca²⁺ influx
  • Promotes storage and release of Ca²⁺ from sarcoplasmic stores
    
    • Therefore there is increased contractility
    • Therefore there is increased speed of relaxation
• Parasympathetic innervation
  
  • ​Mostly to the SA node
  • Main effect is decreased rate

Question 21

Describe the effect on the length-tension relationship of Frank-Starling’s law of the heart plus ionotropic stimulation.

Answer 21

• The ionotropic effect can be modified by the degree of sympathetic stimulation.

Question 22

What is the end systolic volume (ESV)?

Answer 22

The volume in the ventricle at the end of systole.

Question 23

What is the end diastolic volume (EDV)?

Answer 23

The volume in the ventricle at the end of diastole.

Question 24

What is the stroke volume?

Answer 24

• EDV - ESV.
• It is the quantity of blood expelled per beat (L).

Question 25

What is the cardiac output?

Answer 25

• SV x HR
• It is the volume of blood pumped by the heart (L/min).

Question 26

Describe the cycle of left ventricular volume.

Answer 26

Question 27

Describe the Fick principle for determining cardiac output.

Answer 27

Question 28

Describe the relationship between cardiac output, stroke volume and heart rate.

Answer 28

Question 29

What are the elements which affect venous return?

Answer 29

• Sympathetic innervation
• Muscle pumps
• Insipratory movements
• Blood volume

Question 30

Describe the effect of inspiratory movements on venous return.

Answer 30

• Diaphragm descends
  
  • ​Causes increased abdominal pressure
  • Blood is transmitted passively to intraabdominal veins
• Decreased pressure in the thorax
  
  • ​Causes decreased pressure in the intrathoracic veins and right atrium.
• Therefore, there is an increased pressure difference between peripheral veins and the heart.

Question 31

Describe the effect of sympathetic innervation on venous return.

Answer 31

• Sympathetic innervation of veins increases venous return to the heart, therefore increases cardiac output.
  
  • Important in exercise, blood loss etc.