Martini Chapter 20 Heart Physiology p695-715

Question 1

Which two muscle cells are involved in the normal heartbeat? What do they do?

Answer 1

Muscle cells of the Conducting System control and coordinate the heartbeat.

Contractile cells produce the powerful contractions that propel blood.

Question 2

What does each heartbeat begin with?

Then what happens to the action potential?

How can this be measured? What is produced?

Answer 2

Each heartbeat begins with an action potential generated at the pacemaker called the SA node, which is part of the conducting system.

This electrical impulse is then propagated by the conducting system and distributed so that the stimulated contractile cells will push blood in the right direction at the proper time.

This can be monitored from the surface of the body through electrocardiography, the printed record of which is an electrocardiogram (ECG or EKG)

Question 3

What does blood flow into and through in a heartbeat?

Answer 3

The atria contract first, driving blood into the ventricles through the AV valves, then the ventricles contract driving blood out of the heart via the semilunar valves.

Question 4

What is the name of the period between the start of one heartbeat and the start of the next?

Answer 4

The cardiac cycle

Question 5

How is the heartbeat different from any other muscle contraction in the body?

Answer 5

In contrast to skeletal muscle, cardiac muscle contracts on its own, in the absence of neural or hormonal stimulation. This is automaticity, or autorhythmicity.

Question 6

Why does the actual contraction of a heartbeat lag behind the beginning of an electrical impulse?

Answer 6

The delay represents the time it takes for calcium ions to enter the sarcoplasm and activate the contraction process.

Question 7

What are the elements of the conducting system of the heart? (5)

Answer 7

• The sinoatrial node (SA node) located in the wall of the right atrium
• The internodal pathways in the atria comprised of conducting cells which run between the SA and AV nodes. (The electrical impulse can also travel through contractile cells in the atria to reach the AV node in the same time)
• The atrioventricular (AV) node located at the junction between the atria and ventricles
• The AV bundle and bundle branches in the interventricular septum
• The Purkinje fibres which distribute the stimulus to the ventricular myocardium.

Question 8

How do conducting cells of the heart compare to contractile cells?

How are Purkinje cells different from other contractile cells?

What characeristic do cells of the SA and AV node share?

Answer 8

Most cells of the conducting system are smaller than contractile cells of the myocardium and contain very few myofibrils.

Purkinje cells, however, are much larger than contractile cells in diameter and as a result they conduct action potentials more quickly than other conducting cells.

Conducting cells of the SA and AV cannot maintain a stable resting potential. After each repolarisaion, their membranes gradually drift towards threshold. This is called prepotential or pacemaker potential.

Question 9

How does the rate of spontaneous depolarisation differ in different parts of the conducting system of the heart?

How does this help you to diagnose damage to the heart?

Answer 9

Depolarisation is fastest in the SA node, which normally generates action potentials at 80-100bpm.

Isolated cells of the AV node depolarise more slowly, at 40-60bpm. However, in a healthy heart the SA node sets the rate of depolarisation of the AV node cells.

Certain cells in the Perkinje fibres depolarise spontaneously at an even lower rate: 20-40bpm

If the SA node is damaged, the heart will continue to beat at the rate dictated by the AV node. If both SA and AV node are damaged, the Perkinje fibres can cause the heart to beat slower still.

Question 10

What can happen if cells in the AV node or Purkinje fibres begin to depolarise spontaneously when the SA node is functional, what can happen?

Answer 10

The heart may no longer pump blood effectively, and it may result in dealth if the problem persists.

Question 11

Where is the SA node located?

What are the alternative names for the SA nodes, and what specialised cells does it contain?

Answer 11

The SA node is in the posterior wall of the right atrium, near the entrance of the superior vena cava.

The SA node is also known as the cardiac pacemaker or natural pacemaker and contains pacemaker cells.

Question 12

What happens after the SA node fires, and the action potential travels towards the AV node?

Which part of the heart is not affected by this and why?

Answer 12

An cation potential travels along internodal pathways to the AV node, which takes about 50msec. Along the way, the conducting cells pass the stimulus to contractile cells of both atria. The action potential then spreads across the atrial surface by cell-to-cell contact.

The stimulus does not affect the ventricles becasue the cardiac skeleton insulates the atrial myocardium from the ventricular myocardium.

Question 13

Where is the AV node?

How does the rate of conduction change when the action potential reaches the AV node? Why?

How long does it take the impulse to pass through the AV node?

Answer 13

The AV node is in the floor of the right atrium near the opening of the coronary sinus.

The rate of propagation of the impulse slows as it leaves the internodal pathways and enters the AV node because the nodla cells are smaller in diameter than the conducting cells.

Nodal cells are also less efficient at relaying the impulse from one cell to another than the conducting cells are.

As a result it takes 100msec for the impulse to pass through the AV node.

Question 14

What is the purpose of the delay in electrical conduction at the AV node?

Answer 14

This delay ensures that the atria contract completely Otherwise the contraction from the powerful ventricles would close the AV valves and prevent blood flowing from the atria into the ventricles.

Question 15

What is the maximum normal heart rate, and what is this determined by?

Why is this limitation important?

When do rates above the normal maximum occur?

At what rates does pumping effectiveness become dangerously, if not fatally, reduced?

Answer 15

The maximum normal heart rate is 230bpm, and this is determined by the AV node, which can conduct electrical impulses at this rate and no faster. Even if the SA node produces electrical impulses at over 230bpm, the contraction of the heart will be at 230bpm.

This limitation is important becasue mechanical factors begin to decrease the pumping efficiency of the heart at ratres above approx 180bpm.

Rates above 230bpm only occur when the conduction system of the heart has been damamges, or it has been stimulated by drugs.

The theoretical maximum rate of ventricular contraction is 300-400bpm, at which sppeds pumping effectiveness becomes dangerously, if not fatally, reduced.

Question 16

Where does the electrical impulse travel once it is through the AV node? (6 structures)

What is the difference between the two main pathways?

Answer 16

Into (1) the AV bundle (bundle of His (pronounced hiss))

then to (2) the interventricular septum where it enters (3) the left and right bundle branches.

The left bundle branch supplies the massive left ventricle and is much larger than the right bundle branch. Both branches extend towards the apex of the heart, turn and fan out deep to the endocardial surface.

As the branches diverge, they conduct the impulse to (4) Purkinje fibres and, through (5) the moderator band, to the (6) papillary muscles of the right ventricle.

Question 17

How quickly do Purkinje fibres conduct action potentials?

Answer 17

Purkinje fibres conduct action potentials very quickly, as fast as small myelinated axons. Within about 75msec, the signal to begin a contraction has reached all the ventricular cardiac muscle cells.

Question 18

What are the moderator band and papillary muscles for?

Answer 18

Becasue the bundle branches deliver the impulse across the moderator band to the papillary muscles directly, rather than by way of Purkinje fibres, the papillary muscles begin contracting before the rest of the ventricular musculature does.

Contraction of the papillary muscles applies tension to the chordae tendinae, which braces the AV valves and prevents backflow of blood into the atria when the ventricles contract.

Question 19

What abnormalities in the conducting system of the heart can cause decrease in efficiency of the pumping of the heart? (2)

How are they diagnosed?

Answer 19

If the SA node or internodal pathways are damaged, the AV node will assume command and the heart will beat normally, but at a slower rate.

If an abnormal conducting cell or ventricular muscle cell begins generating action potentials at a higher rate, the impulses can override those of the SA or AV node. The origin of these abnormal signs is called an ectopic pacemaker, and it disrupts the timing of ventricular contraction.

These conditions are diagnosed with an electrocardiogram.

Question 20

What does an ECG do, and what aspects of the heart do clinicians use it to assess (3)?

Answer 20

An ECG intrgrates electrical information obtained by placing electrodes at different locations on the body surface. Clinicians use an ECG to assess performance of specific nodal, conducting and contractile components of the heart.

Question 21

In a normal situation with a healthy heart, what does the appearence of an ECG vary with?

Answer 21

The appearence of an ECG varies with the placement of monitoring electordes, or leads. There are certain standard configurations.

Question 22

Describe the classic electrocardiogram pattern. What does each deflection of the ECG line correspond to?

Answer 22

P wave: depolarisation of the atria. The atria begin contracting about 25msec after the start of the P wave.

QRS complex: depolarisation of the ventricles. The ventricles begin to contract shortly after the R peak.

T wave: ventricular repolarisation.

Atrial repolarisation is masked by the QRS complex.

Question 23

What are the 2 segments and 4 intervals of an ECG?

Answer 23

The PR segment is the flat part between the end of the P wave and the beginning of the QRS complex.

The ST segment is the flat part between the end of the QRS complex and the start of the T wave

The PR interval is between the start of the P wave and the start of the QRS complex

The QRS interval is the duration of the QRS complex

The QT interval is between the start of the QRS complex and the end of the T wave

The ST interval is between the end of the QRS complex and the end of the T wave.

Question 24

What do you measure when analysing an ECG?

What are the two elements of particular diagnostic importance?

Answer 24

You measure the size of voltage changes and determine durations and temporal relationships of components.

The amount of depolarisation occuring during the P wave and the QRS complex are of particular importance.

Question 25

What does an excessively large QRS complex indicate?

What does a small QRS complex indicate?

What might the size and shape of the T wave be affected by?

What length of PR interval is considered too long, and what can this be casued by?

What can the QT interval be lengthened by?

Answer 25

Large QRS complex: the heart has become enlarged

Small QRS complex: the mass of the heart muscle has decreased (although probelms using the ECG are more often repsonsible)

Size and shape of the T wave can be affected by starvation, low cardiac energy reserves, coronary ischaemia, abnormal ion concentrations.

PR interval of more than 200msec is too long, and can indicate damage to the conducting pathways or AV node.

The QT interval can be lenthened by electrolyte disturbances, some medications, conduction problems, coronary ischaemia or myocardial damage. A congenital heart defect which can cause sudden death without warning can be detected as a prolonged QT interval.

Question 26

There is a varielty of sophisticated techniques for visualising the heart, but the ECG is still the most useful diagnostically.

What is an ECG especially useful for diagnosing? Whwn might this become dangerous? What might this be casued by? (4)

Answer 26

ECG is especially useful for diagnosing cardiac arrythmias. Some arrythmias are not dangerous - 5% of healthy people have a few abnormal heartbeats each day.

Clinical problems appear when arrythmias reduce the pumping efficiency of the heart. Serious arrythmias may indicate damage to the myocardium, injuries to pacemakers or conduction pathways, exposure to drugs, abnormalities in the electrolyte composition of extracellular fluids.

Question 27

When an action potential reaches a cardiac contractile cell, what 2 stages occur (the same as in a skeletal muscle cell)

How does the process differ in a cardiac muscle cell when compared to a skeletal muscel cell? (3)

Answer 27

1) the action potential leads to the appearence of Ca2+ among the myofibrils
2) the Ca2+ binds to the troponin on the thin filaments, which initiates the contraction.

The duration of action potential is much longer in a cardiac muscle cell

The source of the Ca2+ is extracellular for cardiac muscle cells, but comes from stores in the sarcoplasmic reticulum for skeletal muscle cells.

The duration of the resulting contraction is 30 times longer in a cardiac muscle cell than a skeletal muscle cell.

Question 28

What is the resting potential of a ventricular contractile cell? An atrial contractile cell? Which side of the cell membrane is positively charged, and which side is negatively charged at rest?

What is the resting potential of a skeletal muscle cell?

What is the threshold potential which will lead to an action potential in a cardiac muscle cell?

Answer 28

Resting potential of a ventricular contractile cell: -90mV.

Resting potential of an atrial contractile cell: -80mV.

The internal side of the cell membrane is negatively charged.

Resting potential of a skeletal muscle cell: -85mV.

The threshold potential which will lead to an action potential in a cardiac muscle cell is -75mV.

Question 29

Describe the three main steps of the action potential

Answer 29

Step 1 - Rapid Depolarisation. At threshold, voltage gated sodium channels open (fast sodium channels), and the cell membrane becomes permeable to Na+ ions, which enter the cell resulting in the sudden depolarisation of the membrane.

Step 2 - The Plateau. As the transmembrane potential reaches +30mV, the voltage gated sodium channnels close and the cell begins actively pumping out Na+. However, a net loss of positive charge does not contiunue because as the sodium channels close, calcium channels are opening and Ca2+ enters the cell, roughly balancing the loss of Na+. These channels are called slow calcium channels becasue they open slowly and remain open for a long time, 175msec. The transmembrane potential remains at about 0mV for 100msec, this is the plateau and does not occur in skeletal muscle cells, only cardiac muscle cells.

Step 3 - Repolarisation. The slow calcium channels begin to close and slow potassium channels begin to open, causing K+ to rush out of the cell, resulting in rapid repolarisation that restores the resting potential.

Question 30

What is the stage after an action potential on a cell membrane? What is it divided into?

Why does this stage occur?

How long does each division last?

Answer 30

The Refractory Period - containing the absolute refactory period and the relative refractory period.

For some time after an action potential, the cell membrane will not respond normally to a second stimulus. Initially, in the absolute refractory period, the membrane cannot react at all because the sodium channels are either already open or are closed and inactivated.

In a ventricular muscle cell, the absolute refactory period lasts 200msec, spanning the duration of the plateau and rapid repolarisation.

The relative refractory period is shorter, 50msec, and during this period the voltage gated sodium channels are closed but can open. The membrane can respond to a stronger-than-normal stimulus by initiating another action potential.

Question 31

What is the shape of the graph of the action potential of a cardiac muscle cell - mV plotted against time? How does the contraction of the cell relate to the action potential?

Answer 31

Question 32

What are the two steps by which calcium ions are made available for a contraction in cardiac muscle cells?

What are cardiac muscle cells therefore very sensitive to?

Answer 32

1) Calcium ions cross the cell membrane and enter the cell during the palteu phase of the action potential. This provides about 20% of the calcium ions required for contraction.
2) The arrival of extracellular calcium is a trigger for the release of additional Ca2+ from reserves in the sarcoplasmic reticulum.

Extracellular calcium therefore have direct and indirect effects on cardiac muscle contraction, so cardiac cells are very sensitive to changes in the concentration of Ca2+ in extracellular fluid.

Question 33

Describe the difference in contraction between skeletal muscle and cardiac muscle in terms of the movement of Ca2+

Answer 33

In a skeletal muscle fibre, the action potential is relatively brief and ends as the related twitch contraction begins. The twitch contraction is short and ends as the sarcoplasmic reticulum reabsorbed the Ca2+ it released.

In a cardiac muscle cell, the action potential is longer amd calcium ions continue to enter the cell throughout plateau. As a result, the period of active muscle cell contraction continues until the plateu ends. As the slow calcium channels close, the intracellular calcium ions are absorbed by the sarcoplasmic reticulum or are pumped out of the cell, and the muscle cell relaxes.

Question 34

What is tetanus? Can it occur in skeletal muscle cells or cardiac muscle cells, and why?

Answer 34

Tetanus is a sustined contraction of a muscle cell, where no relaxation can take place between action potentials.

This can only happen in skeletal muscle cells, as the refractory period in a skeletal muscle cell ends before the peak of the contraction. Therefore another action potential can occur and cause another twitch contraction before the muscle cell has had time to relax. This is summation.

In cardiac muscle cells, the absolute refractory period continues until relaxation is under way. Therefore, summation and tetanus cannot occur, regardless of the frequency or intentisty of stimulaiton. This is vital, as a heart in tetany could not pump blood.

Question 35

Where does the heart obtain energy and oxygen for contraction?

Answer 35

The heart gains energy by the breakdown of fatty acids (stored as lipid droplets) and glucose (stored as glycogen). These aerobic reactions can occur only when oxygen is available.

In addition to obtianing oxygen from the coronary circulation cardiac muscle cells maintain their own sizeable reserves of oxygen, bound to the heme units of myoglobin molecules.

Normally, the combination of circulatory supply plus myoglobin reserves is enough to meet oxygen demands of the heart, even when it is working at its maximum capacity.

Question 36

What is each heartbeat followed by?

What is the period between the beginning of one heartbeat and the next?

For each chamber of the heart, what can this period be divided into?

Answer 36

Each heartbeat is followed by a resting phase, which allows time for the chambers to relax and prepare for the next heartbeat.

The period between the begniining of one heartbeat and the next is the cardiac cycle.

For each chanber of the heart, the cardiac cycle is divided into systole and diastole - systole is contraction of the chamber, and diastole is relaxation of the chamber.

Question 37

When will blood flow from one heart chamber into another, ot into an artery?

Answer 37

Only when the pressure in the first chamber exceeds that of the second.

Question 38

What state is the heart in at the beginning of the cardiac cycle?

Describe the blood flow during atrial systole.

How long does atrial systole last?

Answer 38

At the beginning of the cardiac cycle, all four chambers of the heart are relaxed, with the ventricles partly filled with blood.

During atrial systole, the atria contract and fill the ventricles completely with blood.

Blood cannot flow into the atria becasue atrial pressure exceeds venous pressure. Despite this, there is very little backflow into the veins, even though the connection with the venous system lacks valves, becasue the blood takes the path of least resistance.

Resistence to blood flow through the broad AV valves into the ventricles is less than the resistance provided by the smaller, angled openings of the large veins.

Atrial systole lasts 100msec

Question 39

Describe atrial distole and ventricular systole, and the flow of blood.

How long does ventricular systole last at a bpm of 75?

Answer 39

Atrial diastole and ventricular systole begin at the same time. During this period, blood is pushed through the systemic and pulmonary circuits towards the atria.

Ventricular systole lasts 270msec at 75bpm.

Question 40

Describe ventricular diastole.

How long does this last at a bpm of 75?

Answer 40

During ventricular diastole, which lasts for 530msec at 75bpm (the remaining 430msec of the cariac cycle and 100msec of the next cardiac cycle), filling occurs passively and both the atria and the ventricles are relaxed.

The next cardiac cycle begins with atrial systole and complete ventricular filling.

Question 41

When heart rate increases what happens to the phases of the cardiac cycle?

Answer 41

When heart rate increases all the phases of the cardiac cycle are shortened. The greatest reduction is in the time spent in diastole.

When the heart rate climbs from 75 to 200bpm, the time in systole drops by less than 40%, but the time in diastole drops by 75%.

Question 42

Describe the two stages of ventricular systole

Answer 42

Ventricular systole stage 1 - Ventricular contraction pushes the AV valves closed but does not create enough pressure to open semilunar valves. The ventricles contract isometrically, generate tension and ventricular pressure rises. This is Isovolumetric Contraction - all the hearts valves are closed, the volumes of the ventricles remain constant and the ventricular pressure rises.

Ventricular systole stage 2 - As ventricular pressure rises and exceeds the pressure in the arteries, the semilunar valves open and blood is ejected.This is ventricular ejection.

Question 43

Describe the two stages of ventricular diastole

Answer 43

Ventricular diastole early stage - As ventricles relax, pressure in the ventricles drops rapidly. This is a period of isovolumetric relaxation. In the main arteries, blood flows back against cusps of the semilunar valves and forces them closed. Blood flows into the relaxed atria, but not into the ventricles as ventricular pressure is still higher than atrial pressure.

Ventricular diastole stage 2 - When ventricular pressure falls below atrial pressure, the AV valves open. All chambers are relaxed and the ventricles fill passively. Ventricular pressure continues to drop, as the ventricular chambers expand.

The ventricles are almost three quarters full of blood before the cardiac cycle ends.

Question 44

Just before atrial systole, what capacity of the ventricles is already filled with blood?

What is the name for the amount of blood in the venticles after atrial systole? What is this volume in an adult?

Answer 44

70% of the ventricles is filled with blood before atrial systole due to passive blood flow during the end of hte previous cardiac cycle. The contraction of the atria essentially tops up the ventricles.

At the end of atrial systole, each ventricel contains the maximum amount of blood that it will hold in the cardiac cycle. This is called the End Diastolic Volume (EDV). In an adult this is about 130ml.

Question 45

What is an isotonic contraction of a muscle?

What two types of contraction can isotonic contraction be divided into?

Answer 45

Isotonic contraction: tension rises and the skeletal muscles length changes.

Isotonic contraction can be concentric or eccentric.

In concentric contraction, the muscle tension exceeds the load and the muscle shortens.

In eccentric contraction, the muscle tension does not exceed the load, and the muscle extends.

When you lift weights at the gym, you use both concentric and eccentric contractions - concentric to lift a weight, eccentric to lower it. This is easily visualised in the flexion and extension at the elbow.

Question 46

What is an isometric contraction of a muscle?

Answer 46

In an isometric contraction, the muscle as a whole does not change length and the tension produced never exceeds the load.

Many reflexive muscle contractions that keep the body upright upon standing or sitting involve isometric contractions of the muscles that oppose the forces of gravity.

Question 47

At what point do cardiac mucle cells contract isometrically, and at what point do they contract isotonically?

Answer 47

Cardiac muscle cells of the ventricles contract isometrically during the first stage of ventricular systole - the cells do not change shape. They generate tension and the ventricular pressure rises, but the ventricular pressure is not yet higher than the pressure in the great arteries.

These same cells contract isometrically during the second stage of venrticular systole, when the pressure in the ventricles exceeds the pressure in the great arteries and ventricular ejection occurs. The muscle cells shorten and tension production remains relatively constant.

Question 48

Describe the diagram of:

1) Aortic pressure
2) Ventricular pressure
3) Atrial pressure
4) Ventricular volume
5) the electrocardiogram
6) the phonocardiogram
7) the opening and closure of the heart valves:

during the stages of the cardiac cycle: atrial systole, isovolumetric contraction, ventricular ejection, isovolumetric relaxation, rapid inflow and diastasis.

Answer 48

Question 49

How does the pressure of the left and right atria and ventricles compare?

What is the name of the volume of blood ejected into the main arteries from the heart, and how does it compare on the left and right sides?

At rest, what percentage of the end diastolic volume (EDV) is expelled in the stroke volume (SV)? What is this known as?

Approximately how large is the SV in an adult?

Answer 49

The pressure in the right atrium and ventricle are much lower than the left atrium and ventricle.

The blood ejected from the left and right ventricles at ventricular systole is the stroke volume (SV) and it is the same on each side, even though the pressure on the two sides of the heart are different.

At rest 60% of the end diastolic volume (EDV) is expelled in the stroke volume (SV). This is known as the ejection fraction, and it can vary depending on the demands on the heart.

In an adult the stroke volume is approximately 70-80ml

Question 50

As the end of ventricular systole approaches, what happens to ventricular pressure?

How does this affect the pressure in the aorta?

Answer 50

As the end of ventricular systole approaches, the pressure in the ventricles decreases rapidly. This casues blood in the aorta and pulmonary trunk to flow back towards the ventricles, which closes the semilunar valves.

As the backflow begins, pressure decreases in the aorta. When the semilunar valves close, pressure rises again as the elastic arterial walls recoil. This small temporary rise produces a valley in the pressure tracing which is called a dicrotic.

Question 51

What is the name given to the volume of blood left in the ventricles when the semilunar valves close?

How big is this volume in an adult at rest?

How big is this volume compared to the EDV (end diastolic volume)?

Answer 51

The End Systolic Volume (ESV) is the blood remaining in the ventricles once the semilunar valves have closed.

At rest the ESV is about 50ml, 40% of the EDV.

Question 52

If the atria are severely damaged and function poorly, what effect might this have on a patient?

If the ventricles are severely damaged and function poorly, what effect might this have on a patient?

Answer 52

Atrial systole makes a relatively minor contribution to ventricular filling, so a patient can survive quite normally with damaged atria.

In contrast, damage to one or both ventricles can leave the heart unable to maintain adequate blood flow through peripheral tissues and organs. This causes a condition of heart failure.

Question 53

Describe the four heart sounds and the events of the cardiac cycle which cause them.

Answer 53

S1 (lubb) - produced by the closure of the AV valves. Marks the start of ventricular contraction.

S2 (dubb) - produced by the closure of the semilunar valves. Marks the start of ventricular filling.

S3 - faint sound - seldom audible in a helathy adult - caused by blood flowing into the ventricles.

S4 - faint sound - seldom audible in a helathy adult - caused by atrial contraction

Question 54

What is a heart murmur and what is it caused by?

Answer 54

Heart murmurs are caused by regurgitation at the AV valve - blood backflowing into the atria. The sound is a rushing, gurgling noise. It can be caused by malformation of the valve cusps, or problems with the papillary muscles or chordae tendinae which lead to an incomplete closure of the AV valves.

Question 55

What is the term given to the movements and forces generated during cardiac contractions?

What is:

End-Diastolic Volume

End-Systolic Volume

Stroke Volume

Ejection Fraction

Answer 55

Cardiodynamics

End-Diastolic Volume (EDV) The amount of blood in each ventricle at the end of ventricular diastole (the start of ventricular systole)

End-Systolic Volume (ESV) The amount of blood remaining in each ventricle at the end of ventricular systole (the start of ventricular diastole)

Stroke Volume (SV) The amount of bl;ood pumped out of each ventricle during a single beat; it can be expressed as SV=EDV-ESV

Ejection Fraction: The percentage of the EDV represented by the SV

Question 56

What relative size of EDV and ESV provides the largest SV?

What measure do physicians use to investigate cardiac function over time? How is it calculated?

Answer 56

The largest stroke volume is provided when the EDV is as large as it can be and the ESV is as small as it can be.

Cardiac output (CO) is used to measure cardiac function over time - this is the amount of blood pumped byt the left ventricle in one minute.

CO (ml/min) = HR (beats/min) X SV (ml/beat)

Question 57

How much can the heart rate and stroke volume increase to supply an increased demand from the body?

Answer 57

Heart rate can increase by 250%

Stroke volume in a normal heart can almost double

Changes in cardiac output generally reflect changes in both heart rate and stroke volume.

Question 58

What means of inernal communication can influence the heart rate?

How can the stroke volume be altered?

What factors can affect cardiac output in abnormal circumstances? (3)

Answer 58

The autonomic nervous system and circulating hormones can affect heart rate.

The stroke volume can be adjusted by changing the EDV or ESV or both.

Various drugs, changes in ion concentrations and changes in body temperature can alter the basic rhythm of contraction established by the SA node.

Question 59

How do caffeine and nicotine increase the heart rate?

How can ion concentrations affect the heart rate?

How can temperature changes affect the heart rate?

Answer 59

Caffeine acts directly on the conducting system and increases the rate of depolarisation of the SA node.

Nicotine acts directly by stimulating the activity of sympathetic neurones that innervate the heart.

Abnormal ion concentrations can change both the contractility of the heart by affecting the cardiac muscle cells, and the heart rate by affecting the SA nodal cells. The most obvios and clinically important are problems with concentrations of Ca2+ and K+.

Temperature changes affect metabolic operations throughout the body. For example, a reduction in temperature slows the rate of depolarisation at the SA node, lowers the heart rate and reduces the strength of cardiac contractions. Elevated body temperature accelerates the heart rate and contractile force.

Question 60

Which divisions of the nervous system inntervate the heart by means of the cardiac plexus?

What structures do both ANS divisions innervate? (3)

Answer 60

The sympathetic and parasympathetic divisions of the autonomic nervous system innervate the heart by means of the cardiac plexus.

Both ANS divisions innervate the SA and AV nodes and the atrial muscle cells. Although ventricular muscle cells are also innervated by both divisions, sympathetic fibres far outnumber parasympathetic fibres there.

Question 61

Where does the sypathetic innervation of the heart arise from?

Where does the parasympathetic innervation of the heart arise from?

Answer 61

The sympathetic innervation of the heart arises from the spinal cord, specifically the sympathetic paravertebral ganglia of the cervical region, and the superior part of the thoracic region (T1-T4). The fibres which directly innervate the heart are sympathetic postganglionic fibres originating from these ganglia.

The parasympathetic innervation of the heart arises from the right and left vagus nerves (cranial nerve 10). Parasympathetic fibres synapse either to the cardiac plexus, or directly to the walls of the atria.

Question 62

Describe the effect of sympathetic (2) and parasympathetic (3) stimulation upon the heart.

Answer 62

Stimulation of the sympathetic system:
increases heart rate; and
increases the force of contraction.

Stimulation of the parasympathetic system:
decreases heart rate;
reduces force of contraction; and
constricts the coronary arteries.