Heart 2

Question 1

Intercalated disc

Answer 1

Specialized region of intercellular connections between cardiac cells

Question 2

Three types of adhering junctions within an intercalated disc

Answer 2

Fascia adherens, macula adherens, and gap junctions

Question 3

Fascia adherens

Answer 3

Anchoring sites for actin that connect to the closest sarcomere

Question 4

Macula adherens

Answer 4

Holds cells together during contraction by binding intermediate filaments, joining the cells together (desmosomes)

Question 5

Gap junctions

Answer 5

Low-resistance connections that allow current (AP’s) to conduct between cardiac cells

Question 6

How close are cell membranes in heart cells?

Answer 6

2-4 nanometers

Question 7

Connexon channels

Answer 7

Create intracellular connections

Question 8

Primary determinant of internal resistance in cardiac tissue

Answer 8

Gap junctions

Question 9

“Healing over”

Answer 9

Increase in internal resistance that results from a decrease in the number of open gap junctions

Question 10

What causes healing over?

Answer 10

Increase in intracellular (cytosolic) calcium and/or hydrogen ions

Question 11

Clinical application of healing over

Answer 11

Damaged tissue from a myocardial infarction will become electrically isolated

Question 12

Three factors that determine cardiac conduction

Answer 12

Length constant, and rate of rise AND amplitude of action potential

Question 13

Membrane resistance is inversely related to __ __.

Answer 13

potassium permeability

Question 14

Internal resistance is inversely related to . . .

Answer 14

the number of gap junction connections AND to cell diameter

Question 15

What is shown on a graph showing the relationship between the number of available fast Na+ channels and the membrane potential before stimulation of an action potential?

Answer 15

Shows that all the sodium channels have already been activated during depolarization and are no longer open to continue working. The number hits zero around -50mV, which is right about where the depolarization happens

Question 16

Conditions that influence the AP upstroke due to changes in the RMP

Answer 16

Hyperkalemia, premature excitation during relative refractory period, ischemia/myocardial injury

Question 17

What effect does hyperkalemia have on the upstroke of the AP waveform?

Answer 17

The fast upstroke will not be present, as the sodium channels have been deactivated already from the membrane potential being so close to threshold. Creates a slow waveform

Question 18

Other than elevated blood levels of potassium, how else can hyperkalemia be stimulated?

Answer 18

If there is an infarct in an area of the heart, the injured cells can leak out potassium and increase the concentration of potassium in the local ECF

Question 19

During infarction, how high can the local potassium concentration reach?

Answer 19

Up to 20 mEq/L

Question 20

P-R interval

Answer 20

Conduction time from atria to ventricular muscle

Question 21

QRS interval

Answer 21

Intraventricular conduction time (i.e., conduction through ventricles)

Question 22

Why does the AV node delay?

Answer 22

To allow time for optimal ventricular filling

Question 23

Why is AP slow at the AV node

Answer 23

Due to slow inward calcium current

Question 24

How is the long refractory period of the AV node beneficial?

Answer 24

Protects the ventricles from abnormally high atrial rates (i.e., atrial fibrillation or atrial flutter)

Question 25

Clinical determinant of AV nodal conduction time

Answer 25

P-R interval

Question 26

First degree heart block

Answer 26

Abnormal prolongation in P-R interval greater than 0.20 seconds

Question 27

Second degree heart block

Answer 27

Some atrial impulses fail to activate ventricles; not all P waves are followed by a QRS complex

Question 28

Third degree heart block

Answer 28

Complete AV nodal block; no consistent P-R interval

Question 29

Typical method of travel through the His-Purkinje system

Answer 29

Rapid conduction that brings the electrical impulse to the endocardial surface, resulting in endocardial and epicardial activation of the ventricles

Question 30

How long is the QRS complex normally?

Answer 30

Less than 100 msec in duration; narrow

Question 31

Clinical determinant of intraventricular conduction time

Answer 31

Duration of QRS complex

Question 32

Why does the QRS complex need to be so short?

Answer 32

Syncrhonized ventricular activation to give a concise and strong contraction

Question 33

Possible causes of slurred QRS complexes

Answer 33

Hyperkalemia, ischemia, ventricular tachycardia

Question 34

Notched QRS complex

Answer 34

Indicates asynchronous electrical activation of the left and right ventricles

Question 35

Possible causes of a notched QRS complex

Answer 35

Right and/or left bundle branch blocks

Question 36

Supraventricular tachycardia

Answer 36

Conduction through the ventricles is normal, just rapid; the impulse still comes from the atria and travels through the AV node into the His-Purkinje system.

Question 37

Ventricular wall motion and QRS during supraventricular tachycardia

Answer 37

QRS duration is normal because ventricles are firing normally, just more frequently. Ventricular wall motion is normal

Question 38

Ventricular tachycardia

Answer 38

Conduction through the ventricles is not normal, because the impulse originates within the ventricular muscle and not through the His-Purkinje system

Question 39

EKG findings and ventricular wall motion during ventricular tachycardia

Answer 39

QRS duration is prolonged (slurred) and the wall motion is abnormal. This causes a compromise in stroke volume

Question 40

What determines atrial conduction?

Answer 40

The shape of the P wave of an EKG

Question 41

Which is more fatal: a-fib or v-fib?

Answer 41

V-fib, since that is what is responsible for getting the blood oxygenated and perfused to the body. Atrial dysrhythmia will still get enough blood through to sustain life

Question 42

What is the life-threatening secondary effect of atrial fibrillation?

Answer 42

Clotting due to pooling of blood in the atrial appendages, increasing potential for stroke, MI, or PE

Question 43

How does acetylcholine act in the heart?

Answer 43

Via muscarinic receptors

Question 44

What is the effect of the ACh release in the heart?

Answer 44

Increases K permeability directly via G-proteins, hyperpolarizing the membrane and decreasing the chance for action potential

Question 45

What is the other secondary effect of ACh release on the heart?

Answer 45

Inhibition of adenylate cyclase activity and cAMP synthesis, decreasing slow inward calcium current indirectly

Question 46

ACh directly inhibits these structures in the heart

Answer 46

Atrial muscle, SA node, and AV node

Question 47

What are the effects of ACh on an EKG?

Answer 47

Lengthened P-R interval, lengthened R-R interval

Question 48

What does ACh not directly effect?

Answer 48

Basal ventricular muscle function

Question 49

Atropine

Answer 49

Pharmaceutical agent that blocks the muscarinic ACh receptors

Question 50

What areas of the heart does norepinephrine affect?

Answer 50

All areas

Question 51

What is the primary receptor acted on by norepinephrine in the heart?

Answer 51

Beta-1 adrenergic receptors

Question 52

When NE binds its receptors, what intracellular signal is released?

Answer 52

cAMP

Question 53

On what gradient does NE have an effect?

Answer 53

Positive effect on slow inward calcium current

Question 54

EKG changes seen after NE release

Answer 54

Decreased R-R interval, decreased P-R interval

Question 55

Inotropic effect

Answer 55

Hormonal reaction that changes contractility of the heart