Cardiac Cycle Overview

Question 1

Cardiac PV diagram with valves

Answer 1

Question 2

Aortic systole and diastole represented on PV curve and Wigger’s diagram

Answer 2

Question 3

Three types of cell that are electrically active in cardiac conduction

Answer 3

1. Pacemakers
2. Purkinje fibres
3. Cardiac muscle

Question 4

Ion transporters that maintain cardiac conduction system’s poise

Question 5

The transmembrane potential of a myocyte at rest

Answer 5

About -90 mV

the inside of the cell is negative relative to the outside. This contributes to the rapidity of Na+ diffusion in action potential (since it is going down both a chemical and electrical gradient)

Question 6

fast sodium channels

Answer 6

Closed at the resting potential ( -90 mV ), opens during depolarization, but then spontaneously closes. Must be repolarized to resting potential to ‘reload’.

Question 7

How fast sodium channels respond to slow depolarization

Answer 7

If the transmembrane voltage of a cardiac cell is slowly depolarized and maintained chronically at levels less negative than the usual resting potential, inactivation of channels occurs without initial opening and current flow. As long as this partial depolarization exists, the closed, inactive channels cannot recover to the resting state.

This is the typical case in cardiac pacemaker cells, which rest above -70 mV for the entire cardiac cycle. As a result, the fast sodium channels in pacemaker cells are persistently inactivated and do not play a role in the generation of the action potential.

Question 8

inward rectifier potassium channels

Answer 8

Cardiac myocytes contain a set of potassium channels that are open in the resting state, when Na and Ca channels are closed. These generate the potassium equilibrium potential in ventricular myocytes at -91 mV.

Question 9

Constituent ion contributions to potential throughout depolarization in myocyte

Answer 9

Question 10

The resting state before depolarization is known as __ of the action potential.

Answer 10

his resting state before depolarization is known as phase 4 of the action potential.

Question 11

Threshold potential in cardiac myocytes

Answer 11

−70 mV

Potential at which enough fast Na+ channels have opened to generate a self-sustaining inward Na+ current. The entry of positively charged Na+ ions exceeds the charge imbalance that was caused by K+ ion movement at rest, such that the cell depolarizes, transiently, to a net positive potential.

Question 12

The prominent influx of sodium ions is responsible for ___ of the action potential.

Answer 12

The prominent influx of sodium ions is responsible for the rapid upstroke, or phase 0, of the action potential.

Question 13

Phase 1

Answer 13

Following rapid phase 0 depolarization into the positive voltage range, a brief current of repolarization returns the membrane potential to approximately 0 mV. The responsible current is carried by the outward flow of K+ ions through a type of transiently activated potassium channel.

Question 14

Phase 2

Answer 14

Balance of an outward K+ current in competition with an inward Ca++ current, which flows through specific L-type calcium channels. They begin to open during phase 0, when the membrane voltage reaches approximately −40 mV, allowing Ca++ ions to flow into the cell. Charge is balanced by outflow of potassium via delayed rectifier potassium channels, such that there is no net current. This is known as the plateau.

Question 15

Phase 3

Answer 15

Final phase of repolarization. Ca++ ions are removed by the sarcolemmal Na+-Ca++ exchanger and to a lesser extent by the sarcolemmal Ca++-ATPase. The corrective exchange of Na+ and K+ across the cell membrane is mediated byNa+K+-ATPase. Potential returns to -90 mV.

Question 16

Purkinje fibres behave similarly to cardiac muscle in conduction, except . . .

Answer 16

. . . they have a lower resting potential and phase 0, the upstroke, is significantly shorter.

Question 17

Action potential plot for a pacemaker cell

Answer 17

When the threshold potential is reached, at about −40 mV, the upstroke of the action potential follows. The upstroke of phase 0 is less rapid than in nonpacemaker cells because the current represents Ca++ influx through the relatively slow calcium channels.

Question 18

Three ways action potential from pacemakers differs from normal cardiomyocytes

Answer 18

1. The maximum negative voltage −60 mV
2. Phase 4 of the pacemaker cell action potential is not flat but has an upward slope, representing spontaneous gradual depolarization (the pacemaker current).
3. The phase 0 upstroke of the pacemaker cell action potential is less rapid and reaches a lower amplitude than that of a cardiac muscle cell (remember that fast sodium channels are inactive, so they rely on the slower calcium channels).

Question 19

Cardiac refractory period

Answer 19

Compared with electrical impulses in nerves and skeletal muscle, the cardiac action potential is much longer in duration. This results in a prolonged refractory period during which the muscle cannot be restimulated.

Such a long period is physiologically necessary because it allows the ventricles sufficient time to empty their contents and refill before the next contraction.

Question 20

Refractory period graph showing different levels of refractoriness

Answer 20

Question 21

Different levels of refractoriness represent. . .

Answer 21

. . . the number of fast Na+ channels that have recovered from their inactive state and are capable of reopening. As phase 3 of the action potential progresses, an increasing number of Na+ channels recover and can respond to the next depolarization.

Question 22

absolute refractory period

Answer 22

time during which the cell is completely unexcitable to a new stimulation

Question 23

effective refractory period

Answer 23

includes the absolute refractory period but extends beyond it to include a short interval of phase 3, during which stimulation produces a localized action potential that is not strong enough to propagate further.

Question 24

relative refractory period

Answer 24

Interval during which stimulation triggers an action potential that is conducted, but the rate of rise of the action potential is lower during this period because some of the Na+ channels are inactivated and some of the delayed rectifier K+ channels remain activated, thus reducing the available net inward current.

Question 25

“supranormal” period

Answer 25

Following the relative refractory period, a short “supranormal” period is present in which a less-than-normal stimulus can trigger an action potential.

Question 26

Dependence of speed of repolarization on resting potential

Answer 26

Question 27

____ participate in the propagation of the impulse from the SA to the AV node

Answer 27

Ordinary atrial muscle fibers participate in the propagation of the impulse from the SA to the AV node

Question 28

Fibrous tissue surrounds the tricuspid and mitral valves, such that . . .

Answer 28

Fibrous tissue surrounds the tricuspid and mitral valves, such that there is no direct electrical connection between the atrial and ventricular chambers other than through the AV node

Question 29

As the electrical impulse reaches the AV node, a delay in conduction (approximately 0.1 sec) is encountered. This delay occurs because . . .

Answer 29

. . . the small-diameter fibers in this region conduct slowly, and the action potential is of the “slow” pacemaker type (recall that the fast sodium channels are permanently inactivated in pacemaker tissues, such that the upstroke velocity relies on the slower calcium channels).

fter traversing the AV node, the cardiac action potential spreads into the rapidly conducting bundle of His and Purkinje fibers

Question 30

Cardiac actin-myosin diagram

Answer 30

Question 31

Titin

Answer 31

a protein that helps tether myosin to the Z line of the sarcomere and provides elasticity to the contractile process.

Question 32

The troponin subunits

Answer 32

The troponin T (TnT) subunit links the troponin complex to the actin and tropomyosin molecules. The troponin I (TnI) subunit inhibits the ATPase activity of the actin–myosin interaction. The troponin C (TnC) subunit is responsible for binding calcium ions that regulate the contractile process.

Question 33

Calcium regulation during contraction

Answer 33

Question 34

Contraction cycle

Answer 34

Question 35

Adrenergic and Cholinergic cardiac input (regulation of calcium)

Answer 35

Question 36

phospholamban

Answer 36

The return of Ca++ from the cytosol to the SR is regulated by phospholamban. In its dephosphorylated state, PL inhibits Ca++ uptake by SERCA.

However, β-adrenergic activation of protein kinases causes PL to become phosphorylated, an action that blunts PL’s inhibitory effect. The subsequently greater uptake of calcium ions by the SR hastens Ca++ removal from the cytosol, promoting myocyte relaxation.

Question 37

Systole and Diastole sounds on ventricular pressure plot

Answer 37

Question 38

Atrial pressure: a wave, c wave, and v wave

Answer 38

• a wave: generated by the force of atrial contraction
• c wave: generated by the closing of the atrioventricular valves and their bulging into their respective atria.
• v wave: result of passive filling of the atria from the systemic and pulmonary veins during systole

Question 39

Although the duration of systole remains constant from beat to beat, . . .

Answer 39

Although the duration of systole remains constant from beat to beat, the length of diastole varies with the heart rate:

the faster the heart rate, the shorter the diastolic phase​

Question 40

Time of systole is approximated as

Answer 40

S1 to S2

Question 41

Time of diastole is approximated as

Answer 41

S2 to S1

Question 42

The JVP is an accurate measure of . . .

Answer 42

. . . the pressure in the right atrium. Remember, there are no structures in between the internal jugular vein, superior vena cava, and right atrium.

Question 43

JVP wave graph

Answer 43

• a wave: transient venous pressure from RA contraction
• x descent: declining pressure from RA contraction
• c wave: short upward deflection in x descent from closing of tricuspid valve
• v wave: passive filling of RA from venous pressure during systole, when the tricuspid valve is closed
• y descent: the fall in pressure due to the opening of the tricuspid valve and filling of the RV

Question 44

Prominent a wave on JVP

Answer 44

Indicates possible right ventricular hypertrophy or tricuspid stenosis. Corresponds to an increased pressure in the right atrium while it is contracting.

Question 45

Prominent v wave on JVP

Answer 45

Indicates tricuspid regurgitation. Corresponds to an increased pressure in the right atrium during right ventricular contraction, which means fluid is being forced through the weakened tricuspid valve.

Question 46

Prominent y descent on JVP

Answer 46

Indicates constrictive pericarditis. Corresponds to a rapid fall in pressure from rapid emptying of the right atirum into the right ventricle.

Question 47

Heart failure is present when the heart is unable to . . .

Answer 47

. . . pump blood forward at a sufficient rate to meet the metabolic demands of the body (forward failure), or is able to do so only if the cardiac filling pressures are abnormally high (backward failure), or both.

Question 48

Four fundamental isotonic / isochoric contraction relationships

Answer 48

1. The tension generated by the fiber is equal to afterload
2. The greater the load opposing contraction, the less the muscle fiber can shorten
3. If the fiber is stretched to a longer length before stimulation but the afterload is kept constant, the muscle will shorten a greater distance to attain the same final length at the end of contraction
4. The maximum tension that can be produced during isotonic contraction is the same as the force produced by an isometric contraction at that initial fiber length

Question 49

Key mediators of cardiac output

Answer 49

Question 50

Effects of varying preload, afterload, and contractility on a left ventricular PV plot

Answer 50

Question 51

Ventricular end-systolic volume depends on . . .

Answer 51

Ventricular end-systolic volume depends on the afterload and contractility but not on the preload.