Unit 4 - Wk 1 Physiology

Front 1

Myogenic

Back 1

Myocyte contraction that originates from the myocyte itself

Front 2

How are signals conducted in myocytes?

Back 2

Gap junctions

Front 3

If the electrical wave is passing towards the positive electrode in what direction does the tracing deflect?

Back 3

Upward

Front 4

If the electrical wave is passing towards the positive negative in what direction does the tracing deflect?

Back 4

Downward

Front 5

Sympathetic Effects on HR

Back 5

NE release at sympahtetic ending
Causes increased sinus node discharge
Increases rate of conduction of impulse
Increases force of contraction in atria and ventricles

Front 6

Parasympathetic Effects on HR

Back 6

Vagal nerves release ACh; innervate SA node and AV junctional fibers proximal to AV node
Cause hyperpolarization bc of increase K permeability in response to acetylcholine which causes a decreased transmission of impulses

Hyperpolarize the cell via increasing potassium conductance in SA nodal cells. Thus, it takes longer to reach threshold and the intrinsic firing rate decreases; there may also be a decrease in the slope of the prepotential

Front 7

Which cardiac action potential does this describe?

Back 7

AP at the SA node

Front 8

Which cardiac AP does this describe?

Back 8

Ventricular action potential

Front 9

Describe the cardiac conduction pathway

Back 9

SA node -> atrial muscle -> AV node (delay) -> Purkinje fibers -> ventricular muscle

Front 10

What is the fastest cardiac conducting fiber?

Back 10

Purkinje Cell

Front 11

What is the slowest conducting fiber?

Back 11

AV node

Front 12

Where are gap junctions located on caradiac cells?

Back 12

intercalated disks

Front 13

what is a unique contracticle feature of cardiac cells?

Back 13

require extracellular calcium to replace depleted intracellular from SR

Front 14

Is there summation in muscle contraction?

Back 14

NO; this allows for orderly blood flow

There is a long refractory period so a secondary contraction can't sum on top of the first; thus the heart won't tetanize

Front 15

T tubules in cardiac muscle compared to skeletal muscle

Back 15

T tubules are 25x larger in cardiac muscle

Front 16

What is the correlation between extracellular calcium concentration and strength of the contraction

Back 16

Direct relationship;

Front 17

What happens to calcium after a contraction?

Back 17

Cytosolic calcium is pumped out of the cardiac muscle into the t-tubule, a small amount is pumped back into the SR

Front 18

Describe actin based regulation of contraction

Back 18

Calcium binds troponin to move the troomyosin off of the actin filament to allow actin and myosin to bind/crossbridge cycle

Front 19

How is the length tension curve in cardiac muscle different from skeletal

Back 19

In skeletal, increasing sacromere length (stretching the muscle) too far ends up decreasing muscle tension past an optimal point
In cardiac muscle, a connective tissue skeleton prevents cardiac sarcomeres from overlengthening; if the heart overfills and reaches its limit of stretching, there will be an increase in blood pressure (but NOT a lack of blood flow)

Front 20

Effects of Sympathetics

Back 20

Slope of prepotential increases; threshold is reached sooner; the intrinsic firing rate increases (via increased calcium conductance of nodal fibers)

Front 21

P Wave?

Back 21

Represents atrial depolaization
Does not include atrial repolarization, which is 'buried' in the QRS complex

Front 22

PR interval?

Back 22

Is th einterval from the beginning of the P wave to the beginning of hte Q wave (initial depolarization of the ventricle)
varies w/ CONDUCTION VELOCITY THROUGH AV NODE (if AV nodal conduction decreases the PR interval increases)
Is decreased by sympathetic stimulation
Is increased by parasympathetic stimulation

Front 23

QRS complex?

Back 23

Represents depolarization of the ventricles

Front 24

Phase 0

Back 24

Upstroke of the AP
rapid Na influx depolarizes membrane
At the peak of the AP, the membrane potential approaches the Na equilibrium potential

Front 25

Phase 1

Back 25

Initial repolarization; part bc of K+ ions move outward and a decrease in Na+ conductance

Front 26

Phase 2

Back 26

Plataeu of the action potential
Caused by a transient increase in Ca2+ conductance = inward Ca+ current
During phase 2 outward and inward currents are approximately equal, so the membrane potential is stable at the plateau level

Front 27

Phase 3

Back 27

Repolarization
Ca2+ conductance decreases and K+ conductance increases and predominates
The high K+ conductance results in large OUTWARD K+ current (Ik) which hyperpolarizes the membrane back toward the K+ equilibrium potential

Front 28

Phase 4

Back 28

Resting membrane potential
Inward/outward currents (Ik1) are equal and the membrane potential approaches the K+ equilibrium potential

Front 29

Phase 0

Back 29

Upstroke
Inward Ca2+ current; drives membrane potential towards Ca+ equilibrium potential
Note: ionic basis for phase 0 in the SA node is diff from that in ventricles, atria and purkinje fibers (where it is due to Na current)

Front 30

Phase 3

Back 30

Repolarization
Outward K current

Front 31

Phsae 4

Back 31

Slow depolarization
Accounts for pacemaker activity of the SA node (automaticity)
Increase in Na conductance, which results in an inward Na current called If
If is turned on by repolarization of the membrane potential during the preceding action potential

Front 32

Phase 1 and 2?

Back 32

Not present in the SA node action potential

Front 33

Where is conduction velocity fastest?

Back 33

in the Purkinje system

Front 34

Where is conduction velocity slowest?

Back 34

In the AV node (seen as the PR interval on the ECG); allows time for ventricular filling before ventricular contraction

if conduction through AV node is increased, ventricle filling may be compromised

Front 35

Einthoven's Law

Back 35

I + III = II

If the electrical potential of any two leads is known the potential of the third can be determined

Front 36

Back 36

Cardiac Cycle; know it

Front 37

Systole

Back 37

Heart squeezing blood out; increases pressure in the arterial system

Front 38

Diastole

Back 38

Heart relaxes and refills; pressure decreases during this time bc the heart isn't pushing any blood into the system

Front 39

Wave perpendicular to ECG vector

Back 39

no deflection

Front 40

Wave moving away from ECG vector

Back 40

Needle moves down; moves down less if wave is moving away at an angle

Front 41

Wave moving in the same direction from ECG vector

Back 41

Needle moves up; moves less if wave is moving with it at an angle

Front 42

Right shoulder negative -> left shoulder positive

Back 42

Lead I; since vector is down and to the left you get a smaller positive PQRS complex

Front 43

Right shoulder negative -> left leg as positive

Back 43

Lead II; depolarization vector parallel so large positive PQRS complex

Front 44

Right shoudler negative -> right leg positive

Back 44

Lead III; wve of depolarization almost perpendicular but still aligned so decrease PQRS complex

Front 45

Which precordial leads are considered the septal leads (record heart activity from septum)

Back 45

V1 and V2

Front 46

Which precordial leads capture the anterior wall of the heart, and which is the apical lead?

Back 46

V2, V3, V4

V4 is considered the apical lead

Front 47

Which precordial leads are considered the lateral leads which give a view of the sidewall of the heart?

Back 47

V4, V5, V6

Front 48

What does the left main coronary give rise to?

Back 48

LLC
LAD

Front 49

What does the right coronary give rise to

Back 49

Posterior Descending Coronary Artery; supplies the inferior posterior portion of the heart

Front 50

Which leads view the bottom of the heart?

Back 50

Front 51

Which leads view the antero-septal wall, supplied by the LAD?

Back 51

Front 52

What does the LLC give rise to?

Back 52

Obtuse marginal branch; supplies lateral wall

Front 53

Which leads view the lateral wall?

Back 53

V5, V6 (low lateral)
I, aVL (high lateral)

Front 54

Myocardial infarction

Back 54

Type of IHD; ischemia causes the death of heart muscle

Front 55

Angina pectoris

Back 55

Type of IHD; ischemia is of insufficient severity to cause infarction but may be a harbinger of MI

Front 56

paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort (variously described as constricting, squeezing, choking, or knifelike) caused by transient (15 seconds to 15 minutes) myocardial ischemia that falls short of inducing myocyte necrosis.

Back 56

Angina pectoris (literally chest pain)

Front 57

Stable Angina and EKG changes

Back 57

Imbalance in coronary perfusion (due to chronic stenosis coronary atherosclerosis) relative to myocardial demand; relieved by rest and administering nitro

ST segent depression

Front 58

Retrosternal chest pain on exertion

Back 58

Stable angina

Front 59

ST segment depression

Back 59

Stable angina

Front 60

What causes prinzmetal/variant angina?

Back 60

Coronary artery spasm; episodic myocardial ischemia

the anginal attacks are unrelated to physical activity, heart rate, or bp