Week 2

Question 1

Name 4 types of anti-arrhythmic therapies.

Answer 1

1. Drugs (Na channel blockers, K channel blockers, Ca channel blockers, Beta blockers)
2. Radio-frequency ablation
3. DC cardioversion
4. Implantable Cardioverter-Defibrillator (ICD)

Question 2

Which part of the sarcomere are T-tubules positioned?

Answer 2

Z-line

Question 3

Which part of the SR releases Ca2+?

Which part of the SR does Ca reuptake?

Answer 3

• Released at terminal cisternae (near T-tubule/Z-line)

- Reuptake at longitudinal cisternae (over rest of sarcomere)

Question 4

In E-C coupling, what are the 3 methods by which cytosolic Ca2+ can be removed?
How much does each method contribute, about?

Answer 4

1. SERCA to SR (80%)
2. Ca efflux via NCX (18%)
3. Ca efflux via sarcolemma Ca pump (2%)

Question 5

What regulates contraction amplitude in cardiac vs skeletal m. cells?

Answer 5

Cardiac: contraction amplitude regulated by Ca influx via slow Ca current and SR Ca content

Skeletal: contraction amplitude regulated by AP frequency and central recruitment of m. fibers

Question 6

What is the force-frequency relationship?

Answer 6

The beating rate and rhythm of the heart (cycle length) influences cardiac contraction amplitude by altering contractility. Changes in cycle length alter the TIME available for intracellular Ca2+ handling, which alters contractility.

Question 7

What is positive staircase (treppe)?

Explain the mech.

Answer 7

As HR increases, the strength of contraction increases

1. Greater Ca++ influx per unit time, and less time for Ca efflux via NCX
2. Increase SR content/CICR = larger contraction strength

Question 8

What is negative staircase?

Explain the mech.

Answer 8

As HR decreases, the strength of contraction decreases

1. Less Ca2+ influx per unit time, and more time for Ca efflux via NCX
2. Decrease SR content/CICR = weaker contraction strength

Question 9

When would you see a premature beat resulting in a weaker strength of contraction?

Answer 9

• Going from slow to fast (first beat would be weaker)

- Or after a premature beat

Question 10

What is post-extrasystolic potentiation (PESP)?

When would you see it physiologically?

Answer 10

Stronger than normal contraction of the beat following a premature beat.
- Going from fast to slow (first beat would be stronger)

Question 11

Why would a PESP result in larger contraction strength?

Answer 11

• More time for recovery of L-type current
• More time for recovery of SR release channels
• More time for redistribution of Ca stores in terminal SR cisternae
• -> Greater CICR, greater strength of contraction

Question 12

Why, mechanistically, would a premature beat result in weaker than nl contraction strength?

Answer 12

• Less time for recovery of L-type Ca current
• Less time for recovery of SR release channels
• Less time for redistribution of Ca stores in terminal SR cisternae
• -> Smaller CICR, smaller strength of contraction

Question 13

What causes a systolic murmur?

Answer 13

Caused by turbulent blood flow through either a stenotic or

incompetent heart valve during systole.

Question 14

What causes a diastolic murmur?

Answer 14

Caused by turbulent blood flow through either a stenotic or

incompetent heart valve during diastole.

Question 15

What is physiological splitting?

What’s the cause of it?

Answer 15

When the closure of the aortic valve (A2) and the pulmonic valve (P2) are not synchronized in time (A2 followed by P2).
- Decrease in intrathoracic pressure increases right
ventricular end-diastolic volume (filling). This delays closure of the pulmonic valve at
the end of systole (delays P2). As a result, physiological splitting is exaggerated and paradoxical splitting is attenuated.

Question 16

When is physiological splitting considered to be normal?

Answer 16

It is physiologically normal to hear a “splitting” of the second heart sound in younger people, and during inspiration.

Question 17

What is pathological splitting?

Answer 17

Caused when A2 is delayed due to Left Bundle Branch Block (LBBB) (P2 followed by A2).

Question 18

What are the 3 major factors that affect SV?

Answer 18

1. Myocardial contractility
2. Preload
3. Afterload

Question 19

What is preload dependent on?

Answer 19

End-diastolic volume

Question 20

What is afterload?

Answer 20

Any force that resists muscle shortening (arterial pressure is main one)

Question 21

Define contractility.

How is it related to preload and afterload?

Answer 21

The inherent ability of actin and myosin to form cross-bridges and generate contractile force–primarily determined by intracellular [Ca2+]. *AKA inotropy.
- It’s independent of preload and afterload

Question 22

If a muscle is unable to generate enough force to meet the afterload, then the contraction is ___________.

Answer 22

Isometric

Question 23

During a normal cardiac cycle, cardiac muscle initially generates _________ tension and then __________ contractions.

Answer 23

Isometric

Isotonic

Question 24

A decrease in compliance _________ the slope of the resting tension curve.
Is heart tissue more or less compliant than skeletal m. tissue?

Answer 24

increases

- less

Question 25

An increase in contractility (positive inotropic effect) will shift the slope of the active tension curve _____ and _____.

Answer 25

up and left

Question 26

How does an increase in preload cause an increase in tension development?

Answer 26

a) Creates more optimal overlap between thin and thick filaments. b) Increases Ca2+ sensitivity of myofilaments.

Question 27

In terms of cardiac function, how does increasing contractility affect m. shortening amount? Velocity of shortening? Rate of relaxation?

Answer 27

*Increases them all (rate of relaxation increased due to symp stim.) Decreasing contractility has the opposite affect

Question 28

When would you see the theoretical maximal isometric force of contraction in the heart?

Answer 28

When the muscle is unable to meet the afterload because the afterload's force is greater than the muscle fibers' ability to shorten

Question 29

At any given afterload, how does preload affect a heart muscle's velocity of shortening? Does Vmax change?

Answer 29

* Increases velocity w/increasing preload, decreases velocity w/decreasing proload - No, Vmax doesn't change

Question 30

At any given afterload, how does contractility affect a heart muscle's velocity of shortening? Does Vmax change?

Answer 30

* Positive inotropy increases velocity, negative inotropy decreases velocity - Yes, Vmax increases or decreases w/inotropy change

Question 31

In terms of cardiac function, how would an increase in afterload affect velocity of m. shortening? Amount of m. shortening?

Answer 31

- Decrease | - Decrease

Question 32

At any given afterload, an increase in preload will _________ the velocity of shortening.

Answer 32

Increase

Question 33

In the P-V loop, the top segment is not flat (as in skeletal muscle). Why?

Answer 33

Because the afterload is not constant. Therefore, during the ejection phase the heart generates an isotonic contraction with a changing (rather than constant) afterload.