Study Guide 9: Properties of Cardiac Muscle

Experiment #9

Systole

Contraction of the heart

Diastole

Relaxation of the heart

Source of Calcium in Skeletal Muscle

Sarcoplasmic Reticulum

Means of Excitation in Skeletal Muscle

Nervous System

Innervation in Skeletal Muscle

Somatic

Length of Refractory Period in Skeletal Muscle

3 msec

Source of Calcium in Cardiac Muscle

Sarcoplasmic reticulum and extracellular fluid

Means of Excitation in Cardiac Muscle

Inherent

Innervation in Cardiac Muscle

Autonomic

Length of Refractory Period in Cardiac Muscle

200+ msec

Ion responsible for the long plateau phase of the ventricular muscle action potential

Calcium

Role of the plateau phase in the long refractory period seen in cardiac muscle

Sustains depolarized state of cell membrane, allowing for a prolonged contraction period

Why is a long refractory period necessary for cardiac muscle?

Ensures that the heart pumps blood effectively

Absolute refractory period occurs during (systole/diastole)

During systole

Relative refractory period occurs during (systole/diastole)

During diastole

Two systems of control over cardiac function

Autoregulation via Starling’s Law

Autonomic control via autonomic nerves

Starling’s Law states that

The force of the heart's contraction increases in proportion to the stretch of its muscle fibers

What is the role of venous return, EDV, and cardiac muscle fiber length in relation to Starling’s Law?

Venous return ∝ EDV ∝ muscle fiber length

Parts of the heart innervated by both the parasympathetic and sympathetic nervous system

SA node

AV node

Atria

Parts of heart innervated by only sympathetic nervous system

Ventricles

Name of the parasympathetic nerves that innervate the SA node (sinus venosus)

Vagus nerves

PANS secretes ____________ (cholinergic agonists)

Acetylcholine

SANS secretes __________ (also epinephrine/adrenergic agonists)

Norepinephrine

PANS

Role of pacemaker cells

↓ heart rate

↑ K⁺ permeability

↓ membrane potential (hyperpolarized)

↓ prepotential slope

What does a decreased prepotential slope mean

Takes longer to reach threshold

SANS

Role of pacemaker cells

↑ heart rate

↑ Ca²⁺ permeability

↑ prepotential slope

SANS

Role of ventricular muscle cells

↑ contractility

Shortens relaxation time

↑ intracellular Ca2+

↑ rate of re-uptake of Ca²⁺ by SR

How does ↑ rate of re-uptake of Ca²⁺ by SR impact the ventricular action potential

Shortens plateau phase of ventricular fast response action potential or QT interval, making faster heart rate possible

↑ temperature of fluid bathing in sinus venosus causes a (increased/decreased) heart rate

Increased heart rate

↑ temperature of fluid bathing in sinus venosus causes a (increased/decreased) force of contraction (stroke volume)

Decreased force of contraction (stroke volume)

Explain why altering the temperature of the Ringer’s solution bathing the sinus venosus changes heart rate

↑ temperature = ↑ diffusion rate = steeper prepotential slope = ↑ HR

Define vagal tone

Measure of the activity level of the vagus nerve

Describe the effects of eliminating vagal tone

Removes parasympathetic braking on the heart, causing increased heart rate & cardiac output

In the turtle heart experiment, describe what happened initially to heart rate with increased parasympathetic stimulation via the right vagus nerve

Increased PANS stimulation → decreased force of contraction → decreased HR

What causes vagal arrest

Intense parasympathetic stimulation causes prepotential slope to approach zero. Spontaneous depolarization of pacemaker cells stop. Transmission of action potentials to the ventricle will cease. As a result, the heart may stop beating.

What permits vagal escape to occur?

When the AV node becomes the pacemaker and spontaneously stimulates ventricular contraction

Result of vagal stimulation follow addition of atropine

Vagal stimulation has no effect because acetylcholine cannot bind to its receptors.

With an injection of epinephrine, heart rate and ejection fraction both increase, leading to an increase cardiac output.

What happens to venous return and filling time?

Increased venous return

Decreased filling time

What happens to heart rate and force of contraction when the temperature of the pericardial fluid increases?

Increased heart rate

Decreased force of contraction

Effect of stimulating turtle heart ventricle with a large extrinsic stimulus during systole

No effect due to absolute refractory period

Effect of stimulating turtle heart ventricle with a large extrinsic stimulus during diastole

Premature contraction due to relative refractory period

What causes the extra systole and compensatory phase?

An artificial stimulus during diastole depolarizes the ventricle before the next normal pacemaker impulse, causing a premature contraction

How does Starling’s Law account for the small size of the extra systole?

A premature beat occurs before the ventricles have fully filled, giving a low EDV and therefore a weaker contraction

How does Starling’s Law account for the larger than normal beat following the compensatory pause?

Allows extra time for ventricular filling, increasing EDV and stretch, which produces a stronger contraction

Distinguish between vagal arrest and the compensatory pause

Vagal Arrest - temporary stoppage of heart due to increased parasympathetic stimulation

Compensatory Pause - prolonged interval after an extra systole during which heart resets its rhythm

How did the Stannius experiments work

A tight ligature was tied around a section of cardiac muscle, which prevented electrical excitation from passing throughout the heart

Where was Stannius Ligature I tied?

It is tied around the junction of the sinus venosus and right atrium. Conduction from the sinus to the rest of the heart is prevented

Where was Stannius Ligature II tied?

It is tied between the atria and ventricles. The ventricles stop, then resume beating at an even slower and more irregular rate than the atria