Lecture 1 – The Heart’s Conduction System

1) The plasma membrane of nodal cells has Ca⁺⁺, Na⁺ and K⁺ voltage gated channels. What does it mean the calcium channels are ‘fast’ and the sodium channels are ‘slow’?

In nodal cells, calcium channels are considered “fast” because they allow a large, rapid influx of Ca²⁺ when open, while sodium channels are “slow” because they permit only a gradual, steady leak of Na⁺ into the cell.

2) What is the resting membrane potential for a nodal cell within the SA node of the heart? What is the threshold membrane potential? What is the is peak membrane potential?

The resting membrane potential of a nodal cell within the SA node is –60 mV. The threshold membrane potential is –40 mV, and the peak membrane potential is just above 0 mV.

3) Which voltage gated ion channel opens at RMP creating the SA nodal cells pacemaker potential? What direction does the ion move?

At resting membrane potential, voltage-gated sodium (Na⁺) channels open, allowing sodium ions to slowly leak into the cell. This gradual inward movement of sodium creates the pacemaker potential.

4) Which voltage gated ion channel opens at threshold? What direction does the ion move?

When the cell reaches threshold, fast voltage-gated calcium (Ca²⁺) channels open, and calcium ions move into the cell, causing depolarization.

5) Which voltage gated ion channel is stimulated to open at threshold but doesn’t fully open until peak membrane potential? What direction does the ion move once the channel is fully open?

At threshold, voltage-gated potassium (K⁺) channels are stimulated to open, but they do not fully open until peak membrane potential is reached. Once fully open, potassium ions move out of the cell, leading to repolarization.

6) What is the definition of pacemaker potential? Are SA nodal cells the only cells in the body that have pacemaker potential?

Pacemaker potential is defined as the ability of a cell to generate an action potential and reach threshold without any external stimulation. SA nodal cells are not the only cells in the body with pacemaker potential, because AV nodal cells can also generate action potentials, although at a slower rate.

7) How do most excitable cells in the body (i.e. neurons, skeletal muscle fibers) reach threshold?

Most excitable cells in the body, such as neurons and skeletal muscle fibers, reach threshold when chemically gated ion channels open in response to neurotransmitters, allowing ions to flow and depolarize the membrane.

8) The nodal cells within the SA node naturally generate how many action potentials each minute? What about the nodal cells in the AV node?

The nodal cells within the SA node naturally generate about 100 action potentials per minute, while the nodal cells in the AV node generate action potentials at a slower rate of about 40–50 per minute.

9) Why must the action potential go through the AV node (i.e. What is electrically separating the atrial myocytes from the ventricular myocytes)? What type of tissue is this structure composed of?

The action potential must pass through the AV node because the fibrous skeleton electrically isolates the atrial myocytes from the ventricular myocytes. This structure is composed of dense irregular connective tissue.

10) What structural characteristics of the AV node cause the action potential to slow down?

The action potential slows down at the AV node because the nodal cells there have smaller fiber diameters and fewer gap junctions.

11) Why is the slowing of the action potential at the AV node so important to the function of the heart?

Slowing of the action potential at the AV node is important because it allows the ventricles to fill completely with blood before they contract.

12) What two structures within the ventricles keep the AV valves from prolapsing during ventricular contraction?

The two structures within the ventricles that prevent the AV valves from prolapsing during ventricular contraction are the papillary muscles and the chordae tendineae.

13) List the ways in which cardiac myocytes differ from skeletal muscle fibers.

Cardiac myocytes differ from skeletal muscle fibers in several ways. At rest, their filaments are not at optimal overlapping, but they reach this optimal overlap when the myocardium is stretched as blood fills the chamber. They are able to use a wide variety of energy sources, including glucose, fatty acids, lactate, amino acids, and ketone bodies. In addition, cardiac myocytes are electrically connected at intercalated discs, which is not the case in skeletal muscle fibers.

14) Intercalated discs contain two important membrane junctions. What are they and why are they important?

Intercalated discs contain two important types of membrane junctions: desmosomes and gap junctions. Desmosomes anchor the plasma membranes of cardiac cells together, preventing the cells from being pulled apart during chamber filling. Gap junctions allow ions to move directly from one myocyte to the next, enabling the action potential to spread and cause the chamber to contract as a functional syncytium.

15) What is the RMP for cardiac myocytes? Do they have a threshold, why or why not?

The RMP for cardiac myocytes is –90 mV. Cardiac myocytes do not have a threshold because they do not generate their own action potentials. Instead, they conduct action potentials that are passed to them from nodal cells through gap junctions.

16) What ion channel is stimulated to open as an action potential enters through a gap junction?

When an action potential enters a cardiac myocyte through a gap junction, fast voltage-gated sodium (Na⁺) channels are stimulated to open, and sodium floods into the cell, causing depolarization

17) What two ion channels open when the cardiac myocytes reach peak (+30mV) membrane potential? Which direction is each ion moving?

At the peak membrane potential of +30 mV, slow voltage-gated calcium (Ca²⁺) channels open and calcium flows into the cell, while voltage-gated potassium (K⁺) channels open and potassium flows out of the cell.

18) These ions flowing in opposite direction cause a plateau in the action potential making it last longer than most action potentials. How does this affect the myocytes absolute refractory period? Can another action potential be generated while a cardiac myocyte is within the absolute refractory period?

The plateau makes the absolute refractory period longer in cardiac myocytes. Because the cell is still in an action potential during this time, another action potential cannot occur. As a result, myocytes cannot generate tetany like skeletal muscle and must go through a full contraction/relaxation cycle before contracting again.

19) Where are the cardiac centers in the brain?

The cardiac centers are located in the medulla oblongata of the brain.

20) What is a chronotropic agent? What is an inotropic agent?

A chronotropic agent is a factor that changes heart rate, while an inotropic agent is a factor that changes the strength of contraction by altering calcium concentrations within the myocytes

21) The parasympathetic division slows the heart rate by decreasing the number of action potentials the nodal cells in the SA node can generate. How? (mention ion involved and how it affects the cells, i.e. depolarizes the cell, hyperpolarizes the cell)

The parasympathetic division slows the heart rate because Ach binds to muscarinic receptors on the nodal cells, opening K⁺ channels. It Hyperpolarizes the cells. Negative Chronotropic Agent

22) The sympathetic division speeds up the heart rate by increasing the number of action potentials the nodal cells in the SA node can generate. How?

The sympathetic division speeds up the heart rate because NE released from sympathetic stimulation, as well as EPI and NE from the adrenal medulla, bind to beta-1 receptors on the nodal cells. This causes the opening of Ca²⁺ channels, leading to faster depolarization and more frequent action potentials. Positive Chronotropic Agent

23) The sympathetic division also increases the strength of the contractions of the cardiac myocytes. How? (mention ion involved and how it affects the cell)

The sympathetic division increases the strength of cardiac contractions because EPI/NE increase Ca²⁺ concentrations within the cytoplasm of the myocytes. The higher calcium levels allow more cross-bridges to form, resulting in stronger contractions.