The Cardiac Pressure-Volume Cycle

Question 1

What is the role of potassium (K+) in the cell?

Answer 1

Potassium helps in repolarizing the cell by letting K+ out of the cell.

Question 2

What happens when the membrane potential (Vm) goes below -60 mV?

Answer 2

Inward rectifier K+ channels open.

Question 3

Which type of channels are more open when cells are at rest?

Answer 3

Inward rectifier K+ channels.

Question 4

What is the function of inward rectifier K+ channels?

Answer 4

Inward rectifier K+ channels help in clamping the membrane potential (Vm) at rest.

Question 5

When do delayed rectifier K+ channels open?

Answer 5

Delayed rectifier K+ channels open when the membrane depolarizes.

Question 6

What are the possible causes of intrinsic depolarization?

Answer 6

Intrinsic depolarization can be caused by a nearby cell depolarizing or synaptic transmission (neurotransmitter).

Question 7

What happens when a few Na+ channels open during depolarization?

Answer 7

Na+ permeability increases, leading to Na+ current flowing into the cell.

Question 8

What is the threshold voltage for the cell to be committed to an action potential (AP)?

Answer 8

When the voltage exceeds the threshold voltage (approximately -50 mV), the cell is committed to an AP.

Question 9

What occurs during repolarization of the basic action potential?

Answer 9

Na+ channel inactivation decreases the Na+ current going in, while delayed rectifier K+ channels open, increasing the K+ going out.

Question 10

What happens during after-hyperpolarization of the basic action potential?

Answer 10

Inward rectifier K+ channels open again, increasing K+ permeability and decreasing Na+ permeability. This moves the membrane potential (Vm) closer to the equilibrium potential for K+ (EK).

Question 11

What is the refractory period of the basic action potential?

Answer 11

The refractory period is the period during which the cell cannot reinitiate an action potential. It mostly occurs during the after-hyperpolarization phase.

Question 12

What happens during Phase 0 of the ventricular myocyte action potential?

Answer 12

Na+ channels open with positive feedback, allowing Na+ to enter the myocyte and causing depolarization.

Question 13

Which channels are responsible for the transient outward current in Phase 1 of the ventricular myocyte action potential?

Answer 13

Delayed rectifier K+ channels open during Phase 1, allowing K+ to leave the myocyte.

Question 14

What occurs during the plateau phase (Phase 2) of the ventricular myocyte action potential?

Answer 14

Ca2+ channels open in a time and voltage-dependent manner, allowing Ca2+ to enter the myocyte while K+ continues to leave.

Question 15

What happens during Phase 3 of the ventricular myocyte action potential?

Answer 15

Ca2+ channels close, and K+ continues to leave the myocyte, resulting in rapid repolarization.

Question 16

Which current is responsible for the resting potential (Phase 4) of the ventricular myocyte action potential?

Answer 16

Inward rectifier K+ current helps maintain the resting potential as K+ leaves the myocyte.

Question 17

How does the duration of a cardiac action potential compare to a nerve cell action potential?

Answer 17

Cardiac action potentials can vary in duration and can last up to 500 ms, whereas nerve cell action potentials are typically around 1 ms.

Question 18

What is the refractory period like in cardiac muscle action potentials?

Answer 18

Cardiac muscle action potentials have a long refractory period, which prevents tetany (sustained muscle contraction) from occurring.

Question 19

What is the characteristic of pacemaker tissues in cardiac APs?

Answer 19

Pacemaker tissues exhibit spontaneous depolarization, lack an inward K+ rectifier current, and are not stable at rest.

Question 20

What is responsible for the depolarization in Phase 4 of pacemaker tissues?

Answer 20

The depolarization in Phase 4 is due to the “funny” current (If), which is carried by inward flow of Ca2+ rather than Na+.

Question 21

Which phase(s) are absent in the nodal action potential?

Answer 21

Phases 1 and 2 do not exist in the nodal action potential.

Question 22

What is the role of the “funny” current (If) in auto-rhythmicity?

Answer 22

The “funny” current (If) is responsible for making the SA node cells spontaneously active, contributing to cardiac auto-rhythmicity. It leads to a net inward current and depolarizes the cell towards 0 mV.

Question 23

What does the “funny” current (If) involve in terms of ion flow?

Answer 23

The “funny” current (If) involves a large inward Na+ current and a small outward K+ current.

Question 24

What is the distinction between “sodium channels” and channels that conduct sodium?

Answer 24

All channels that conduct sodium are not necessarily classified as “sodium channels.” While they conduct sodium ions, the term “sodium channels” specifically refers to a specific type of ion channel.

Question 25

What are intercalated discs in cardiac muscle?

Answer 25

Intercalated discs are specialized junctions that join adjacent cardiac myocytes. They consist of desmosomes for structural support, adherens junctions for anchoring thin filaments, and gap junctions for ion movement.

Question 26

What is the significance of gap junctions in intercalated discs?

Answer 26

Gap junctions in intercalated discs provide low electrical resistance and high ion permeability. They allow action potentials to pass easily from one cardiac myocyte to another, facilitating coordinated contraction.

Question 27

What is a functional syncytium?

Answer 27

A functional syncytium refers to a multinucleated cell resulting from the fusion of multiple cells. In the case of cardiac muscle, intercalated discs allow the formation of functional syncytia in the atria and ventricles, ensuring coordinated contraction.

Question 28

What is the significance of AV node conduction in the heart?

Answer 28

AV node conduction is the slowest conduction pathway in the heart, with a delay of approximately 120-200 ms. This delay allows the atrial contraction to complete before the ventricular contraction, ensuring efficient pumping of blood.

Question 29

How is the conduction velocity in the AV node controlled?

Answer 29

The conduction velocity in the AV node is regulated by the autonomic nervous system. Sympathetic stimulation (noradrenaline, b1 receptors) increases cAMP and enhances conduction velocity, while vagal stimulation (ACh, muscarinic receptors) decreases cAMP and slows conduction velocity.

Question 30

Which drugs can affect AV node conduction?

Answer 30

Drugs such as bisoprolol (b1 receptor antagonist), verapamil (L-type Ca channel blocker), and digoxin (increases vagal tone) can slow AV node conduction.

Question 31

What does Starling’s law describe in cardiac muscle?

Answer 31

Starling’s law states that the force of cardiac muscle contraction increases with increasing myocardial stretch (preload). It is based on the relationship between ventricular filling and stroke volume.

Question 32

How does the sarcomere structure contribute to Starling’s law?

Answer 32

When the myocyte (cardiac muscle cell) is stretched, there is an increased overlap of thick and thin filaments within the sarcomere. This increased overlap leads to increased actin-myosin cross-bridging, resulting in increased force generation and a stronger contraction.

Question 33

How does myocyte stretch affect the force and duration of contraction?

Answer 33

Increased myocyte stretch leads to an increased overlap of thick and thin filaments, which results in more actin-myosin cross-bridging. This leads to an increase in the force of contraction and an extended duration of contraction.

Question 34

What is the intrinsic regulation of contractile force?

Answer 34

Intrinsic regulation, also known as the Starling mechanism, involves the increase in force and duration of contraction due to increased myocardial stretch. It is driven by the increased cross-bridge formation between actin and myosin.

Question 35

What is the extrinsic regulation of contractile force?

Answer 35

Extrinsic regulation involves sympathetic stimulation, where the force of contraction is increased but the duration remains similar. This is achieved by the activation of the sympathetic nervous system, which leads to a faster and stronger contraction without changing the number of cross-bridges.

Question 36

What happens to left ventricular (LV) volume during the cardiac cycle?

Answer 36

LV volume reduces progressively during systole (contraction) and increases progressively during diastole (relaxation).

Question 37

What does the Wiggers diagram illustrate?

Answer 37

The Wiggers diagram represents the different phases of the cardiac cycle and displays various parameters such as ventricular pressure, aortic pressure, and electrocardiogram (ECG) changes.

Question 38

How can the LV pressure: volume loop be interpreted?

Answer 38

The LV pressure: volume loop provides a graphical representation of the changes in left ventricular pressure and volume throughout the cardiac cycle. It includes isovolumic contraction (a), ejection (b), isovolumic relaxation (c), and diastolic filling (d).

Question 39

What are the key components of the troponin complex in thin filaments?

Answer 39

The troponin complex consists of troponin T (Tn-T), troponin C (Tn-C), and troponin I (Tn-I). Tn-T binds the complex to tropomyosin, Tn-C binds calcium ions (Ca2+) during excitation-contraction coupling, and Tn-I inhibits cross-bridging to myosin heavy chains.

Question 40

What is the role of creatine kinase (CK)?

Answer 40

Creatine kinase moves high-energy phosphate from ATP in the mitochondria to ADP in the cytoplasm, replenishing ATP stores. CK-MB is a subtype of creatine kinase that is more specific to cardiac muscle.

Question 41

Why are cardiac biomarkers important?

Answer 41

Cardiac biomarkers, such as troponin and CK-MB, are used to detect myocardial damage. Elevated levels of these biomarkers indicate injury or stress to the heart muscle and can aid in diagnosing conditions like myocardial infarction.