Cardiac Muscle

What is systole?

Contraction of the ventricles (ventricular systole = contraction phase).

What is diastole?

The relaxation phase of the cardiac cycle.

What is the source of Ca2+ in skeletal muscle?

Ca2+ comes from the sarcoplasmic reticulum (SR) only.

What is the source of Ca2+ in cardiac muscle?

Ca2+ comes from both the sarcoplasmic reticulum and the extracellular fluid.

How is skeletal muscle excited?

It requires nervous system stimulation for excitation.

How is cardiac muscle excited?

It has inherent (spontaneous) excitation.

What type of innervation does skeletal muscle receive?

Somatic motor innervation.

What type of innervation does cardiac muscle receive?

Autonomic nervous system innervation.

What is the refractory period of skeletal muscle?

About 3 milliseconds.

What is the refractory period of cardiac muscle?

Long, approximately 200+ milliseconds.

Relate electrical events (ECG) to mechanical events.

Depolarization initiates contraction; repolarization is slow, prolonging contraction. P wave → atrial depolarization/contraction; QRS → ventricular systole; T wave → ventricular diastole.

What ion is responsible for the plateau phase in cardiac muscle?

Calcium (Ca2+).

What is the role of the plateau phase?

Extends the absolute refractory period so the contractile response is more than half over before another can begin.

Why is the long refractory period necessary in cardiac muscle?

Prevents tetanus, which would stop the heart from pumping effectively.

Identify the absolute and relative refractory periods in the cardiac cycle.

Absolute refractory period: during systole. Relative refractory period: during diastole.

What are the two systems that control cardiac function?

Autoregulation via Starling's Law; autonomic control via autonomic nerves.

Describe Starling's Law.

The heart pumps all the blood that returns to it. ↑ Venous Return → ↑ EDV → muscle fibers stretch → ↑ force of contraction → ↑ Stroke Volume.

Which parts of the heart are innervated by both PANS and SANS?

SA node, AV node, and both atria.

Which parts of the heart are innervated only by SANS?

The ventricles (primarily sympathetic fibers).

What is the name of the PANS nerve that innervates the heart?

The vagus nerve (Cranial Nerve X).

What are the PANS (ACh) effects on the heart? (↓ HR)

↑ K⁺ permeability; membrane becomes hyperpolarized; decreases prepotential slope (takes longer to reach threshold).

What are the SANS (NE/Epi) effects on the heart? (↑ HR & contractility)

↑ Ca²⁺ permeability; increases prepotential slope (faster to threshold). In ventricles: ↑ intracellular Ca²⁺ → stronger contraction; ↑ Ca²⁺ reuptake → shortens repolarization/QT interval.

What is the effect of ↑ temperature on cardiac performance?

↑ HR → ↓ filling time → ↓ stroke volume → ↔ cardiac output (CO).

What is the effect of ↓ temperature on cardiac performance?

↓ HR → ↑ filling time → ↑ stroke volume → ↔ cardiac output (CO).

Why does cardiac output stay the same when only temperature changes?

Changing temperature alone does not alter metabolic needs, so CO does not need to change.

Why does altering temperature change heart rate?

Temperature changes alter the rate of diffusion of ions across the cell membrane, which alters the prepotential slope.

What is vagal tone?

Continuous parasympathetic stimulation of the SA node (via the right vagus nerve) that suppresses the intrinsic rate of discharge.

What happens when vagal tone is eliminated?

The heart rate increases to the intrinsic denervated rate of 100-110 beats per minute.

What is the initial effect of increased PANS stimulation?

Slowing of the ventricular contraction rate → temporary vagal arrest (the heart may stop beating).

What causes vagal arrest?

Intense PANS stimulation causes the prepotential slope to approach zero, stopping spontaneous depolarization of pacemaker cells.

What allows vagal escape to occur?

Another part of the conducting system (likely the AV node) takes over as pacemaker and begins discharging.

What is the effect of vagal stimulation after administering atropine?

No effect on heart rate; atropine blocks vagus nerve action by antagonizing acetylcholine receptors.

Why does epinephrine increase CO while increased temperature leaves CO unchanged?

Epinephrine acts like SANS, increasing contractility and ejection fraction → ↑ CO to meet metabolic needs. Increased temperature does not change metabolic needs, so CO remains unchanged.

What happens when the ventricle is stimulated during systole vs. diastole?

During systole: no effect (absolute refractory period). During diastole: causes an extra systole (premature beat).

Explain the extra systole and compensatory pause.

The extra systole occurs because the stimulus hits during the relative refractory period; the premature beat disrupts timing and leads to a prolonged compensatory pause before normal rhythm resumes.

How does Starling's Law explain the small extra systole and large post-pause beat?

Premature beat → ↓ filling time → ↓ EDV → ↓ force. After the pause → ↑ filling time → ↑ EDV → ↑ force.

What is the difference in what initiates vagal arrest vs. a compensatory pause?

Vagal arrest: caused by increased PANS stimulation. Compensatory pause: triggered by a large extrinsic stimulus delivered to the ventricle.

Explain Stannius's experiments.

Ligating the sinus venosus (SA node) stopped the heart, proving it as primary pacemaker. A second ligature lower down caused the ventricle to beat again at a slower rate, showing pacemaker cells exist throughout cardiac tissue (latent pacemakers).