Cardiac Cell Regulation and ECGs

Question 1

Chronotropy, inotropy, dromotropy, lusitropy

Answer 1

Heart rate, contractions, cell-cell conduction, relaxation

Question 2

Parasympathetic effect on heart rate

Answer 2

Decreases heart rate

Question 3

Effects of parasympathetic inhibition vs effects of sympathetic inhibition

Answer 3

Administer atropine (muscarinic antagonist, block parasympathetic), heart rate rises rapidly. Administer propranolol, heart rate decreases a little. The effects of para inhibition are greater than symp inhibition.

Question 4

Sympathetic vs parasympathetic stimulation. Why does this occur?

Answer 4

Sympathetic effects are slower and more even, parasympathetic effects are quick. Parasympathetic effects don’t require an intermediate enzyme (just BG subunit), sympathetic effects require AC to convert ATP to cAMP.

Question 5

How does the parasympathetic system act on the heart?

Answer 5

Release of acetylcholine from the vagus binds to muscarinic receptor in SA and AV nodes only. Linked to Gi, so decrease in AC, cAMP, PKA. But more importantly, beta and gamma subunits of Gi will directly activate the acetylcholine-sensitive K current.

Question 6

I (k,ACh)

Answer 6

Acetylcholine-sensitive K current, activated by B and G subunits of GPC muscarinic receptor. This will allow for K release from cell, repolarizing the membrane, and slowing firing rate.

Question 7

How does activation of I (K, ACh) slow heart rate?

Answer 7

K will escape and repolarize membrane, lengthening the time required to depolarize membrane.

Question 8

Where do sympathetic effects on the heart occur?

Answer 8

SA node, AV node, and ventricle.

Question 9

How does sympathetic stimulation of the heart work in SA node?

Answer 9

NE or Epi binds to B receptor, which is coupled to Gs. Activates AC, cAMP, PKA. cAMP will directly activate funny current. Increased depolarizing Na+ will increase SA nodal firing rate.

Question 10

HCN

Answer 10

Hyperpolarization activated, cyclic nucleotide gated. cAMP turns on funny current.

Question 11

Sympathetic effects on ventricles. How?

Answer 11

Stronger contractions, faster relaxation. PKA from B adrenergic receptor activation will phosphorylate L-type Ca channels, phospholamban, Ryr, and troponin.

Question 12

Effect of PKA on L type Ca channel

Answer 12

Increased Ca flux, higher SR Ca load, stronger contractions.

Question 13

Effect of PKA on SERCA pump

Answer 13

Will phosphorylate phospholamban, which relieves inhibition on SERCA, pumping Ca in more efficiently.

Question 14

B adrenergic activation causes shift to new steady state. How?

Answer 14

Increased Ca through L-type channels and increased Ca uptake into SR by SERCA. More Ca entering than exiting, more Ca uptake then release. More Ca released next few beats.

Question 15

What is the structure in cardiac muscle that is key for AP propagation?

Answer 15

Gap Junctions

Question 16

Gap Junction structure

Answer 16

Connexins arrenged in a connexon channel.

Question 17

What determines how fast AP’s propagate?

Answer 17

Number of gap junctions. Also, inward current responsible for AP upstroke (Na) because the speed of the upstroke is proportional to the speed of conduction.

Question 18

Difference between measuring APs and ECG

Answer 18

AP measures V_inside - V_outside.

With an ECG, both leads are outside and = V₂ - V₁

And, because voltage outside is the inverse of voltage inside, V2 - V1= AP1-AP2

Question 19

Cellular basis for T wave

Answer 19

Epicardium depolarizes after and repolarizes before endocardium.

Epicardium has a shorter AP

Question 20

Fundamental principles of electocardiography

Answer 20

1) Voltages outside the heart are transmitted to body surface
2) Electrodes don’t measure absolute voltages, just differences between each other
3) We only see ECG deflections when voltages in the heart and changing with respect to location
4) A depolarization wave moving towards an electrode gives a positive deflection.
5) An orthogonal depolarization or repolarization produces no signal.
6) The strength of a given signal depends not only on propagation direction, but also on the mass of tissue contributing to the signal.
7) Signals in additional directions can be derived by combining signals in the known directions accordingly.

Question 21

Depolarization towards a positive electrode = ? deflection

Depolarization away from a positive electrode = ? deflection

Repolarization towards a positive electrode = ? deflection

Repolarization away from a positive electrode = ? deflection

Answer 21

Positive

Negative

Negative

Positive

Question 22

Why no signal from orthogonal AP?

Answer 22

No difference in voltage between leads.

Question 23

Einthoven’s Triangle

Answer 23

RA, LA, LL leads

Question 24

Vi = ?

Vii= ?

Viii=?

Answer 24

Vi = LA-RA

Vii= LL-RA

Viii= LL-LA

Question 25

Unipolar Leads

Answer 25

Question 26

Six ECG leads in the frontal plane

Answer 26

Question 27

What do the precordial leads do?

Answer 27

Placed in a transverse plane and provide info about activity along anterior-posterior directions

Question 28

P Wave

QRS Complex

T Wave

Correspond to?

Answer 28

Atrial Depolarization

Ventricular Depolarization

Ventricular Repolarization

Question 29

Why is there no atrial repolarization signal?

Answer 29

Not strong enough, small mass

Question 30

QT interval events

Answer 30

Ventricular depolarization to repolarization (AP duration)

Typically 300ms

Question 31

PR interval events

Answer 31

Atrial to ventricular polarization (propagation through AV node)

Typically 120-200 ms

Question 32

Why is AV nodal propagation slow?

Answer 32

Upstrokes caused by slower L-type Ca current

Question 33

Why does parasympathetic activation cause negative dromotropy?

Answer 33

Negative dromotropy = slower conduction through AV node.

Activation of mAChRs inhibit AC and reduce activation of PKA. L type Ca channel is not phosphorylated causing slower current and slower upstroke.

Question 34

Why does sympathetic activation cause positive dromotropy?

Answer 34

Activation of AC through B adrenergic receptors, P of L type ca channels.

Question 35

Boxes in EKGs

Answer 35

One small box = 40 ms

Large box = 200ms

5 large boxes = 1 s

Question 36

Estimating electrical axis

Answer 36

To determine the dominant location that the depolarization wave travels

1) Look for maximum positive R with no negative, this is closest
2) Look for cloest QRS to zero, this is perpendicular
3) If 2 R waves are equally tall, the axis is between these

Question 37

Why would electrical axis deviate?

Answer 37

Hypertrophy

Question 38

Why does lead II QRS have multiple phases?

Answer 38

Question 39

Narrow vs Wide QRS complexes

Answer 39

Narrow = depolarization through conduction system is fast

Wide= depolarization through ventricular propagation, which is slow

Wide is caused when spontaneous Ap fires in ventricles, and cannot use purkinje system to zip around ventricles.

Question 40

Answer 40

Sinus bradycardia. Long spaces between R waves. Normally indicates dysfunction SA node

Question 41

What is this?

Answer 41

First degree AV block. Delayed PR interval, which should be <200ms. All p waves are followed by QRS

Question 42

What is this?

Answer 42

Second degree AV block. Some impulses fail to propagate towards ventricles

Question 43

What is this?

Answer 43

Atrial Fibrillation

P waves are random and indistinct. R-R intervals are irregular.

Question 44

What is this?

Answer 44

Premature ventricular contractions. Wide QRS complexes, so ventricles are exciting themselves. Also, they have difference shapes, meaning there are multiple foci of self-excitation. Caused by spontaneous ca release.

Question 45

What is this?

Answer 45

Monomorphic Ventricular Tachycardia. Wide QRS, Complexes are similar.