X_Cardiology_Hour3 Exam1 Dcom Oms2

Front 1

what are the basic features of cardiac cells that make them distinct from skeletal muscle: (x3)

Back 1

1. electrically connected through gap junctions
2. action potential in a single cell brings neighboring cells to threshold
3. nerves regulate but do not drive

Front 2

the highest rate of spontaneous depolarization in the heart is in cells of what:

Back 2

the sinoatrial (SA) node – the normal pacemaker.

Front 3

what is the secondary pacemaker of the heart:
tertiary:

Back 3

atrial foci
AV junction

Front 4

how is cardiac contraction similar to muscle contraction:

Back 4

actin/myosin regulated by troponin C as in skeletal muscle

Front 5

how does cardiac contraction differ from skeletal muscle:

Back 5

Cardiac cells depend on extracellular calcium for contraction through calcium influx during the action potential, while skeletal muscle lacks a calcium current during its action potential

Front 6

in the cardiac muscle, what is preload:

where is it measured in the cardiac cycle:

Back 6

degree of tension on the muscle just before contraction

end of diastolic volume (when the ventricles have become filled)

Front 7

in the cardiac muscle with is afterload:

when is it measured:

Back 7

the load against which the muscle exerts its contractile force

pressure in the artery leaving from the ventricle

Front 8

what is frequency in the biophysics of cardiac muscle contraction:

recruitment:

Back 8

how many contractions per unit of time

not possible in the heart; all cells fire in each beat

Front 9

what is contractility in the biophysics of cardiac muscle contraction: (think mechanism)

Back 9

making the heart more/less responsive to the preload mechanism

Front 10

how do you control contractility:

Back 10

extrinsic control → autonomics, hormones, drugs

Front 11

what is diastole:

Back 11

period of relaxation and chamber filling
continues until the next contraction begins

Front 12

what is systole:

Back 12

onset of contraction and continues until relaxation begins

Front 13

the best measure of preload is sarcomere length immediately before contraction begins - impractical

what is the measures of left ventricular preload in descending order of reliability: (x8)

Back 13

1. muscle fiber length
2. left ventricular volume
3. left ventricular diameter
4. left ventricular end diastolic pressure
5. left atrial pressure
6. pulmonary capillary wedge pressure
7. pulmonary artery pressure
8. central venous pressure

Front 14

what is the force-velocity relationship in muscle contraction:

Back 14

the velocity of muscle shortening is inversely proportional to the load it must move

put another way, the greater the afterload, the slower the velocity of shortening

Front 15

how can the force-velocity relationship in cardiac muscle and skeletal muscle be altered:

Back 15

force-velocity relationship can be altered by extrinsic regulatory mechanisms, such as sympathetic nerves

Front 16

the contractile mechanism of the heart is the same as in skeletal muscle; what is it:

Back 16

energized myosin heads bind to an active site on actin, which is regulated by binding of calcium to troponin

Front 17

what is the difference between skeletal and cardiac muscle in the control of intracellular free calcium concentration during the calcium pulse of the active state:

Back 17

Skeletal muscle: no calcium current influx during the action potential

Cardiac muscle: Ca++ influx through L-type, voltage-gated channels

Front 18

where does the Ca++ that binds to troponin during cardiac contraction come from: (% comes from where)

Back 18

70% of Ca++ released from the SR

30% of Ca++ influx through L-type, voltage-gated channels

Front 19

___ triggers release of Ca++ from the SR by binding to ___

Back 19

Ca++ influx through L-type voltage-gated channels

ryanodine receptors (RYRs)

Front 20

how is the efflux of Ca++ accomplished in the cardiac cell: (x3)

Back 20

1. 70% resequestered into SR by a Ca++-ATPase
2. Na+/Ca++ exchanger
3. 2% via Ca++-ATPase of the sarcolemma

Front 21

in the heart, there is a dangerous Ca++ uptake by mitochondria during ___

Back 21

ischemia

Front 22

why is there a long action potential in the heart:

(what is the mechanism and what controls the duration)

Back 22

L-type channels produces long calcium pulse - duration is controlled by rate of resequestration and efflux of calcium

Front 23

reduced extracellular calcium concentration in the heart, causes what:

but does not change what:

Back 23

decreased active force

the duration of force production

Front 24

what do drugs that block L-type calcium channels (calcium blockers) do:

Back 24

reduce active force

Front 25

why are refractory periods long in cardiac muscle:

Back 25

prevents summation and tetanic contractions

Front 26

what is tetanic contraction:

Back 26

when a motor unit has been maximally stimulated by its motor neuron

Front 27

decreased Ca++ influx also decreases ___, which does what:

Back 27

release of Ca++ from SR

reduces force

Front 28

active force of the cardiac muscle is directly related to what 2 things:

Back 28

1. intracellular Ca++
2. preload

Front 29

what are the proposed mechanisms of the interaction of preload and contractility:

Back 29

1. stretching brings actin and myosin filaments closer together because of elastic elements, this makes more crossbridge attachments possible.
2. stretching increases sensitivity to calcium, possibly due to same effect on distance.

Front 30

extrinsic mechanisms of regulation of force do what in the cardiac contraction: (think in general terms)

Back 30

change amount of response to preload and afterload

Front 31

what are examples of extrinsic mechanisms that effect contractility: (x4)

Back 31

autonomic nerves
hormones
drugs and toxins
damage

Front 32

what is chronotrophy:

Back 32

heart rate

Front 33

what is lusitropy:

Back 33

rate of relaxation also conduction velocity

Front 34

___ is the amount of active force at a single preload that can be changed

Back 34

contractility

Front 35

what is contractility:

Back 35

amount of active force at a single preload can be changed

Front 36

any influence that increases contractility is referred to as what:

Back 36

positive inotropic

Front 37

any influence that decreases contractility is referred to as what:

Back 37

negative inotropic

Front 38

what is the Frank-Starling law of the heart:

Back 38

Input = output
or
Cardiac output = venous return

Front 39

As venous return increases it stretches the cardiac muscle. This increase of ___ increases cardiac force by the ___ mechanism. The more forceful beat matches the output to the input

Back 39

preload
intrinsic

Front 40

the cardiac muscle gets 90% of its energy from what:

Back 40

oxidation of fatty acids

Front 41

the heart is highly dependent on oxygen and contraction fails within 30 seconds after what:

Back 41

complete occlusion of blood supply

Front 42

there is a direct relationship between
cardiac ___, cardiac ___
and coronary blood flow

Back 42

work
oxygen consumption

Front 43

the failing of heart contractions after complete occlusion of blood supply is not simply due depletion of ATP or creatine phosphate, it is due what 6 factors:

Back 43

1. slight (↓)ATP → (↓)(↓)ATP/ADP

2. loss of allosteric effects of ATP on L-type Ca++ channels → transient decrease influx

3. (↓)ATP inhibits SR release

4. (↓)ATP/ADP → (↓)energy of hydrolysis of ATP required for contraction force

5. inability to resequester or pump Ca++ out poisons mitochondrial energy production

6. (↑) myoplasmic Ca++ → (↑)risk of free radical damage

Front 44

what kind of neural receptors are primarily on cardiac cells:

Back 44

β1-adrenergic receptors

Front 45

what neurotransmitters stimulate the β1-adrenergic receptors on the cardiac cells: (x2)

Back 45

1. norepinephrine released from sympathetic efferents
2. circulating epinephrine and norepinephrine

Front 46

epinephrine and norepinephrine stimulate the ___ receptors on the cardiac cells

Back 46

β1-adrenergic

Front 47

norepinephrine is released from what: (think nervous system)

Back 47

sympathetic efferents

Front 48

what is the effect of sympathetic stimulation on the cardiac cells: (x4)

Back 48

1. Alter ion conductance mainly via cAMP
2. (↑)Ca++ influx and release of Ca++ by SR
3. (↑)rate of transport and resequestration
4. stronger, faster, shorter duration

Front 49

what are the receptors for acetylcholine:

Back 49

muscarinic M2 receptors

Front 50

what are the parasympathetic effects on cardiac tissue: (x3)

Back 50

1. (↓)cAMP
2. weaker, slower, longer duration
3. (↑)conductance of potassium

Front 51

what occurs as a consequence and a contributing factor to many cardiac pathologies:

Back 51

remodeling of the heart

Front 52

remodeling of the heart occurs why:

Back 52

consequence and a contributing factor to many cardiac pathologies

Front 53

in remodeling of the heart, what occurs due to hypertension: (3 steps)

Back 53

hypertension → chronic high afterload → concentric left ventricular hypertrophy

Front 54

physiologic hypertrophy with exercise conditioning and hypertension or failure of contractility causing dilated failure are both examples of ___

Back 54

remodeling

Front 55

what is ultimately responsible for remodeling of the heart:

Back 55

altered gene expression