Cardiac Muscle Physiology

Flashcards covering cardiac cell types, pacemaker and myocyte action potentials, and excitation-contraction coupling based on BMS 1004 lecture notes.

How does the initiation of contraction in cardiac myocytes differ from that in skeletal muscle?

Cardiac muscle generates its own electrical stimulation spontaneously through action potentials without needing nervous system signals, whereas skeletal muscle requires direct stimulation from the nervous system.

What specialized role do pacemaker cells perform in the heart?

Pacemaker cells are modified myocytes in the cardiac conduction system that have lost the ability to contract and are specialized for initiating and conducting action potentials.

What is the primary function of the sinoatrial (SA) node?

The SA node acts as the primary pacemaker of the heart, initiating all heartbeats, controlling heart rate, and firing action potentials simultaneously that spread across atrial contractile myocytes.

Why do electrical impulses slow down when they reach the atrioventricular (AV) node?

The impulses slow down briefly at the AV node to allow the atria to contract fully before the electrical signal spreads through the ventricular myocytes.

What role do gap junctions in intercalated discs play in heart muscle function?

Gap junctions form channels between myocytes that allow ions to flow rapidly from cell to cell, electrically coupling neighboring cells into a functional syncytium so signals propagate rapidly.

How are ion concentration gradients arranged across a resting cardiac myocyte membrane?

Resting cardiac cells have higher extracellular concentrations of $\text{Na}^+$ and $\text{Ca}^{2+}$, and a higher intracellular concentration of $\text{K}^+$.

How does an SA node pacemaker cell reach threshold potential from its starting voltage?

Starting at about $-60\,\text{mV}$, funny channels open at membrane voltages lower than $-40\,\text{mV}$ to allow a slow influx of $\text{Na}^+$ (the pacemaker potential) until the cell reaches the threshold of $-40\,\text{mV}$.

What ion flows are responsible for the rising and falling phases of an SA node action potential?

The rising phase is caused by $\text{Ca}^{2+}$ influx through voltage-gated $\text{Ca}^{2+}$ channels; the falling phase is driven by $\text{K}^+$ efflux through opened $\text{K}^+$ channels after $\text{Ca}^{2+}$ channels inactivate.

How does depolarization spread from one contractile myocyte to trigger threshold in an adjacent myocyte?

When a myocyte depolarizes, stored $\text{Na}^+$ and $\text{Ca}^{2+}$ leak through gap junctions into the neighboring myocyte, raising its membrane voltage from a resting $-90\,\text{mV}$ to its threshold of $-70\,\text{mV}$.

What ion channel activity creates the sharp depolarization phase in contractile myocytes at $-70\,\text{mV}$?

Fast $\text{Na}^+$ channels open at threshold ($-70\,\text{mV}$), causing a rapid influx of $\text{Na}^+$ and a sharp voltage rise.

What creates the plateau phase during a contractile myocyte action potential, and how long does it last?

The plateau phase lasts about $200\,\text{msec}$ and is maintained by a balance between steady $\text{Ca}^{2+}$ influx through L-type (slow) $\text{Ca}^{2+}$ channels and $\text{K}^+$ efflux through voltage-gated $\text{K}^+$ channels.

Why is the long absolute refractory period ($250\,\text{msec}$) critical for cardiac muscle function?

It ensures the cardiac muscle completely relaxes before responding to a new stimulus, preventing summation and tetanus, which would stop the heart from pumping.

In this diagram of myocyte ultra-structure, what function do the T-tubules perform?

T-tubules are sarcolemmal extensions that increase cell surface area and carry electrical impulses deep into the cell near the sarcoplasmic reticulum.

What is meant by $\text{Ca}^{2+}$-induced $\text{Ca}^{2+}$ release in cardiac myocyte contraction?

It is the process where a small influx of extracellular $\text{Ca}^{2+}$ across the sarcolemma triggers a much larger release of stored $\text{Ca}^{2+}$ from the sarcoplasmic reticulum.

Based on this figure, what happens to tropomyosin and actin when $\text{Ca}^{2+}$ binds to troponin C?

Binding of $\text{Ca}^{2+}$ to troponin C causes tropomyosin to slide off the actin filament, exposing the myosin-binding sites so myosin heads can bind.

How do myosin heads interact with actin to cause physical myocyte contraction?

Myosin heads perform a power stroke that pulls actin and myosin filaments past each other to shorten the muscle, consuming ATP and repeating the cycle as long as $\text{Ca}^{2+}$ is present.

What role does SERCA play during cardiac myocyte relaxation?

SERCA (sarco-endoplasmic reticulum calcium-ATPase) is an ATP-dependent pump that actively sequesters cytosolic $\text{Ca}^{2+}$ back into the sarcoplasmic reticulum.

As shown in this relaxation pathway diagram, how is cytosolic $\text{Ca}^{2+}$ moved out across the sarcolemma?

Cytosolic $\text{Ca}^{2+}$ is transported out of the myocyte into the extracellular fluid by the $\text{Na}^+/\text{Ca}^{2+}$ exchange pump.