Catos Cardiology Phys 1&2

Front 1

Types of cardiac muscle cells involved in fast response action potentials

Back 1

Atrial
Ventricular
Bundle of His
Purkinje

Front 2

Types of cardiac muscle cells involved in slow response action potentials

Back 2

SA node
AV node

Front 3

Fast response phase 0

Back 3

Rapid depolarization (-80 to +20mV) due to influx of sodium via voltage gate channels

Front 4

What two drugs can eliminate Phase 0 in fast response? How?

Back 4

Tetradotoxin and Saxitoxin by inhibiting sodium voltage gated channels

Front 5

Fast Response Phase 1

Back 5

Repolarization to 0mV via efflux of K

Front 6

Fast Response Phase 2

Back 6

Prolonged depolarization
Plateau is caused by efflux of K balancing influx of Ca (and Na)
L-type Ca (long lasting)
T-type Ca (inactivate quickly, less common in cardiac muscle)

Front 7

Fast Response Phase 3

Back 7

Rapid Repolarization (to -80)
L-type Ca closes and 3K channels open (Na pump, Ca/Na exchanger)

Front 8

Fast Response Phase 4

Back 8

Remains at resting potential (diastole)

Front 9

What three phases in fast response are involved in systole?

Back 9

Phases 0-3

Front 10

What are some key differences between slow and fast response action potentials?

Back 10

Fast
Phase 0 +Na
Resting mem pot = -80mV
Slow
Phase 0 +Ca
Resting mem pot = -40mV
No response in phase 1&2

Front 11

What phase in fast and slow are affected by Nitrendipine and Nitedipine and why?

Back 11

Fast Phase 2
Slow Phase 0
These drugs are Ca channel blockers, and these phases use L-type Ca

Front 12

What is resting membrane potential determined by?

Back 12

The equilibrium potential of the most permeable ion. In this case, Potassium

Front 13

Slow Response Phase 0

Back 13

Rapid rise in membrane potential (+20mV) due to the opening of L-type Ca channels

Front 14

Slow Response Phase 1

Back 14

No response

Front 15

Slow Response Phase 2

Back 15

No response

Front 16

Slow Response Phase 3

Back 16

Repolarization (to -40mV) via efflux of K.

Front 17

Slow Response Phase 4

Back 17

Slow Depolarization (-40 to -20mV) due to Na and Ca conductance

Front 18

What happens if the SA node (pacemaker) is nonfx?

Back 18

AV will drive heart rate (slower) and if that also fails, ectopic foci in atrial and ventricular muscle can set heart rate

Front 19

Can summation occur in cardiac muscle?

Back 19

There is limited temporal summation due to a long refractory period (need to relax)
No Spatial Summation bc they function as a syncytium

Front 20

How is the heart beat initiated? How does it spread? What determines the speed of its spread?

Back 20

Pacemaker cells in SA node initiate it. It spreads via electical conduction via gap Jx. It spreads at a rate determined by the magnitude of the action potential and rate of rise of the action potential.

Front 21

SA node excites...
AV node excites...

Back 21

Atria
Ventricles

Front 22

What will sympathetic stimulation do to the speed of slow response? Parasymp stim?

Back 22

Symp Increase (tachycardia)
Para Decrease (bradycardia)

Front 23

How is cardiac muscle innervated?

Back 23

Autonomically, symp and para

Front 24

Which type of a response is capeable of a plateau phase?

Back 24

Fast response due to delayed rectifying K and maintained Ca current

Front 25

In cardiac contraction the length tension curve is really a...

Back 25

Volume-Pressure Curve

Front 26

How is the cardiac length tension curve different?

Back 26

Its a volume-pressure curve.
It shows degree of shortening, not max tension.
Passive part is different bc cardiac muscle displays passive tension at all lengths(preload)

Front 27

Is cardiac muscle as elasticic as skeletal muscle?

Back 27

Not at all

Front 28

Which type of a response is capeable of a plateau phase?

Back 28

Fast response due to delayed rectifying K and maintained Ca current

Front 29

In cardiac contraction the length tension curve is really a...

Back 29

Volume-Pressure Curve

Front 30

How is the cardiac length tension curve different?

Back 30

Its a volume-pressure curve.
It shows degree of shortening, not max tension.
Passive part is different bc cardiac muscle displays passive tension at all lengths(preload)

Front 31

Is cardiac muscle as elasticic as skeletal muscle?

Back 31

Not at all

Front 32

Define contractility. What can affect it?

Back 32

Contractility is the active length tension relationship.
Ionotropic agents

Front 33

What potentially occurs if contractility increases?

Back 33

Potential maximal tension increases, ie muscle shortens more, work imparted to blood.

Front 34

What are the 5 positive ionotropic agents?

Back 34

Symp stim
Horomones
Increased Ca loading
Increased Heart Rate
Hypertrophy

Front 35

What are the 2 negative ionotropic agents?

Back 35

Parasympathetic Stim
Heart Damage

Front 36

What is residual volume?

Back 36

The volume of blood remaining after the rapid and reduced ejection phases.

Front 37

In regards to location and pressure, explain:
Initial Pressure
Rapid Ejection Phase
Reduced Ejection Phase
Residual Volume
Rapid Filling Phase
Reduced Filling Phase

Back 37

Decription
Then it all repeats
Note** Atrium fills passively and doesn't actively fill the ventricle.

Front 38

Describe the afterload.

Back 38

The the pressure of the ventricular blood equals the pressure of the blood in the aorta - aortic valve opens, and muscle shortens at constant pressure

Front 39

Cardia Output (mls/min) equals the product of:

Back 39

Stroke volume (mls/beat) and Heart Rate (beats/min)

Front 40

If you increase the force of contraction you will also increase

Back 40

the stroke volume

Front 41

Starlings Law of the Heart relationship btween

Back 41

preload and stroke volume

Front 42

In regards to systemic circulation, where does the largest blood pressure drop occur?

Back 42

In the arterioles

Front 43

Capillaries

Back 43

Have intima only.

Front 44

Arteries
Veins

Back 44

High Pressure, low volume
Low pressure, High volume

Front 45

A ventricular function curve plots

Back 45

Stroke volume and diastolic pressure. It reaches a plateau but NEVER reaches a point where tension begins to fall.

Front 46

What will positive ionotropic agents do to a ventricular function curve?

Back 46

It will shift the curve up and to the left.

Front 47

Treppe (staircase phenomenon)

Back 47

Type of temporal summation. Increase in hrt rate can result in increased contractility due to lack of full relaxation of ventricular myocytes.

Front 48

Poiseuille's Law

Back 48

Describes flow of liquid in a tube.
Radius is most important because it is to the 4th powr
RxRxRxR
2x2x2x2=16

Front 49

Intima

Back 49

single layer of endothelial cells (contraction and relaxation effects BP)

Front 50

Media

Back 50

thick concentric layers of smooth muscle and elastin

Front 51

Adventitia

Back 51

collagen fibers (important to strengthen vein walls)

Front 52

What three factors increase blood viscosity?

Back 52

Increased Hematocrit
Dehydration
Increase vessel length (fat)

Front 53

What two factors can decrease vessel radius?

Back 53

Occluding Plaques (MI/Stroke)
Contraction (normal)

Front 54

What and where is portal circulation.

Back 54

It is blood flow btwn 2 capillary beds.
Hepatic Portal
Renal Portal
Hypothalamic Hypophyseal

Front 55

Starlings Hypothesis

Back 55

Hydrostatic pressure and oncotic (draws fluid in) pressure counterbalance mvmt in capillaries.

Front 56

3 ways substances can cross endothelial boundary?

Back 56

Lipid Soluble
Trancytosis
Paracellular

Front 57

Intrinsic (Local) Control of Blood Flow (3)

Back 57

Myogenic (strech)
Metabolic (dialate 4 removal)
Endothlial (secrete factors)

Front 58

Two Extrinsic (central) Control factors of blood flow?

Back 58

Horomonal
Neural

Front 59

What is ouabain?

Back 59

A cardiac glycoside, that blocks Na/K ATPase