Cv A&p Review

Front 1

In arterioles, what do the α1 and β2 receptors mediate?

Back 1

α1 : vasoconstriction
β2 : relaxation

Front 2

Relationship of resistance to
a) Viscosity
b) Length of vessel
c) Radius

Back 2

a) directly proportional
b) directly proportional
c) indirectly proportional to 4th power (decrease in radius increases resistance X4)

Front 3

The volume a vessel can hold at a certain pressure, decreases with increasing age

Back 3

capacitance

Front 4

What separates the myocardial cells?

Back 4

Intercalated discs

Front 5

sarcolemma: defn

Back 5

plasma membrane of the heart

Front 6

Thick filaments in myofibril consist primarily of the _____

Back 6

protein myosin, held in place by titin filaments

Front 7

Thin filaments in the myofibril consist primarily of the _____

Back 7

protein actin, coiled with nebulin filaments.

Front 8

Troponin is a complex of three regulatory proteins : what are they?

Back 8

Troponin C, I, and T

Front 9

Responsible for binding of calcium

Back 9

Troponin C

Front 10

Inhibits cross-bridge formation in absence of calcium binding

Back 10

Troponin I

Front 11

Binds to protein actin to lend structural rigidity to thick filament

Back 11

Troponin T

Front 12

Inducing an increased amount of calcium to be released by the sarcoplasmic reticulum induces a ______ inotropic effect

Back 12

positive

Front 13

What induces the large stores of calcium to be released from the sarcoplasmic reticulum?

Back 13

Depolarization of the sarcolemma and T tubule system results in small release of calcium, which induces the larger release.

Front 14

When free calcium concentration increases in the cytosol it is bound by _______

Back 14

troponin C

Front 15

Induces the removal of troponin I, allowing formation of actomyosin cross-bridges

Back 15

binding of Ca2+ to troponin

Front 16

pacemaker of heart

Back 16

SA node

Front 17

collection of autonomic cells at jxn of SVC and RA

Back 17

SA node

Front 18

sits on subendocardial surface at opening of the coronary sinus into right atrium

Back 18

AV node

Front 19

Traversing of the impulse of the SA node results in depolarization of ____

Back 19

both atria

Front 20

What electrical activity does the the P wave represent?

Back 20

Depolarization of both atria

Front 21

What is the PR interval?

Back 21

Time for the AP to traverse the intra atrial pathways to the AV node and thru the His-Purk system

Front 22

What electrical activity does the the QRS complex represent?

Back 22

Depolarization of the ventricles

Front 23

What electrical activity does the the T wave represent?

Back 23

Repolarization of the ventricles

Front 24

Ventricles must contract from ___ to ___ for efficient ejection of blood

Back 24

Apex; Base

Front 25

two kinds of muscle cells in heart

Back 25

Contractile; Conducting (SA node, etc)

Front 26

What is the slowest conduction region? Why?

Back 26

AV node. Ensures the ventricles have enough time to fill with blood before they're activated to contract.

Front 27

What are the 3 criteria that must be met for normal sinus rhythm?

Back 27

1) AP must originate at SA node.
2) SA nodal impulses must occur regularly at a rate of 60-100 impulses/minute.

3) Activation must occur in the correct sequence and with the correct timing and with no delays.

Front 28

What ion primarily determines RMP of cardiac cells?

Back 28

K+

Front 29

What is an inward current?

Back 29

The net movement of positive charge INTO the cell. Makes it less negative/depolarization

Front 30

What is an outward current?

Back 30

The movement of positive charge OUT of cell. Hyperpolarizes/makes membrane potential more negative.

Front 31

2 basic mechs than can change membrane potential

Back 31

1) Change in electrochemical gradient for ion

2) Change in conductance, g, of an ion

Front 32

Where is the AP duration longest?

Back 32

Purkinje fibers

Front 33

In which cardiac tissue is the AP upstroke dependent on inward Ca2+ current?

Back 33

SA node

Front 34

What occurs in Phase 0 of the AP in ventricular, atrial, and Purkinje fibers ?

Back 34

Rapid depolarization - the Upstroke.

In ventricular, atrial, and Purkinje fibers, it's caused by a transient increase in Na+ conductance. There is an inward Na+ current. Inactivation gates on Na+ channels close in response to depoarlization.

Thus the Na+ channels open briefly and then close.

Front 35

What is dV/dT?

Back 35

The rate of rise of the upstroke in Phase 0 of the AP. Depends of RMP - the more negative, the faster it is.. Correlates with size of inward current.

Front 36

What occurs in Phase 1 of the AP in ventricular, atrial, and Purkinje fibers ?

Back 36

Initial repolarization.

Immediately follows upstroke.

There is a net outward current caused by
A) Closure of inactivation gates on Na+ channels.

B) Outward K+ current due to driving force

Front 37

What occurs in Phase 2 of the AP in ventricular, atrial, and Purkinje fibers ?

Back 37

Plateau.
Long period of relatively stable, depolarized membrane potential, especially in ventricular and Purkinje fibers.

There is a balance of inward and outward currents.

Front 38

What causes the balance of inward and outward currents during Phase 2 of the AP in ventricular, atrial, and Purkinje fibers ?

Back 38

1) There is an increase in Ca2+ conductance --> inward Ca2+ current. (aka slow inward current from L channels)

2) Outward K+ current (we saw this starting during Phase 1: initial repolarization)

Front 39

What are the L channels?

Back 39

Ca2+ channels open during the plateau (L for Long lasting).

Inhibited by Calcium Channel Blockers.

Front 40

What initiates the release of more Ca2+ from intracellular stores during excitation-contraction coupling?

Back 40

The inward Ca2+ current mediated by the L channels.

Ca2+-induced Calcium release.

Front 41

What are the Calcium Channel Blockers? (names)

Back 41

nifedipine, diltiazem, verapamil

Front 42

nifedipine, diltiazem, verapamil : what drug class

Back 42

L-type Calcium channel blockers

Front 43

What occurs in Phase 3 of the AP in ventricular, atrial, and Purkinje fibers ?

Back 43

Repolarization (rapid)

Results from
1) Decrease in g_Ca
2) Increase in g_K. This ends at the end of phase 3 because the membrane potential has been brought closer to the K+ equilibrium potential.

Front 44

What occurs in Phase 4 of the AP in ventricular, atrial, and Purkinje fibers ?

Back 44

Resting membrane potential/electrical diastole.

Inward and outward currents are equal.

RMP approaches but doesn't fully reach the K+ equilibrium potential, therefore driving force is very low.

The balancing force is Na+ and Ca2+ currents, whose conductance is very low but driving force is very high. (exact opposite of K)

Front 45

At Phase 4: RMP, the conductance of K+ is very ____ while the conductance of Ca+ and Na+ is very ____

Back 45

high (easily permeable); Low

Front 46

At Phase 4: RMP, the driving force on K+ is very ____ while the driving force on Ca+ and Na+ is very ____

Back 46

low; high

Front 47

What are the 3 features of the AP in the SA node that are different from those in the atria, ventricles, and Purkinje fibers?

Back 47

1) SA node exhibits automaticity - spontaneously generates APs

2) Has an unstable RMP

3) NO sustained plateau

Front 48

How does the ionic basis for Phase 0: Upstroke differ in the SA node?

Back 48

Results of an increase in g_Ca and an inward Ca current.

Carried predominantly by T-type Ca2+ channels (for Transient). NOT inhibited by L-type Ca channel blockers.

Front 49

Which phases are absent in the AP for the SA node?

Back 49

Phase 1: Initial Repolarization and Phase 2: Plateau

Front 50

What occurs in Phase 4: Spontaneous depolarization in the SA node?

Back 50

Accounts for automaticity of the SA nodal cells.

There is a slow depolarization produced by the opening of Na+ channels and an inward Na+ current called I_f, where the f stands for "funny" denoting that this current is different than the fast Na+ current responsible for the upstroke in other cells.

Front 51

What turns on I_f?

Back 51

Repolarization from the preceding AP

Front 52

Once I_f and subsequent slow depolarization bring the membrane potential to threshold in the SA node, what happens?

Back 52

Enters Phase 0: Upstroke by the T-type Calcium channels.

Front 53

What sets the heart rate?

Back 53

Rate of phase 4 depolarization, influenced by ANS

Front 54

What are the latent pacemakers?

Back 54

AV node, bundle of His, Purkinje fibers. Their rate of phase 4 depolarization is slower than the SA node (usually) and therefore is suppressed.

Front 55

Where is conduction velocity slowest and fastest?

Back 55

Conduction velocity speeds from fastest to slowest:

Purkinje fibers > Ventricle = Atria > AV node

Front 56

What is the AV delay?

Back 56

Conduction velocity thru the AV node, the slowest place.

Front 57

What are the cable properties of the myocardial fibers?

Back 57

Determined by cell membrane resistance and internal resitance (low because of gap junctions in myocardials cells)

Front 58

T/F Conduction velocity depends on AP duration

Back 58

F. AP duration is just the time it takes a given site to go from depolarization to complete repolarization - implying nothing about how long it takes for that AP to spread ANYWHERE.

Front 59

capacity of myocardial cells to generate APs in response to inward, depolarizing current.

Back 59

excitability

Front 60

amount of inward current required to bring a myocardial cell to threshold potential

Back 60

excitability

Front 61

chronotropic effects

Back 61

change heart rate

Front 62

What receptors of the ANS primarily mediate positive chronotropic effects?

Back 62

Sympathetic, β1 receptors.

Front 63

How are positive chronotropic effects mediated?

Back 63

increase in I_f.

Front 64

What receptors of the ANS primarily mediate negative chronotropic effects?

Back 64

Cholinergic, parasympathetic, Muscarinic, M2 receptors in the SA node.

Front 65

How are negative chronotropic effects mediated? (2 ways!)

Back 65

In SA node, M2 receptors are coupled to Gi protein called Gk that inhibits adenylyl cycle, producing <b>decrease in I_f</b>.

Also, Gk directly increases conductance of K+ channel called K+-ACH, and increases an outward K+ current called I_K+-ACH.

Front 66

What are the dromotropic effects?

Back 66

Changes in the conduction velocity

Front 67

Mech of the sympathetic ns causing an increase in conduction velocity at AV node (positive dromotropic effect)

Back 67

Increase I_Ca, which is responsible for the upstroke of the AP in the AV node.

Front 68

Mech of the parasympathetic ns causing an decrease in conduction velocity at AV node (negative dromotropic effect)

Back 68

Combo of decreased I_Ca, and increased I_K-ACh

Front 69

measurement of tiny potential difference on surfaceo f the body that reflect electrical activity of heart.

Back 69

ECG

Front 70

why is atrial repolarization not seen on the ECG?

Back 70

It is occurring at the same time as ventricle depolarization, so it gets obscured.

Front 71

time from initial depolarization of atria to initial depolarization of ventricles

Back 71

PR interval

Front 72

Which ECG segment correlates with AV node conduction?

Back 72

PR interval

Front 73

What increases and decreases the PR interval?

Back 73

Increases: sympathetic NS
Decreases: parasympathetic NS

Front 74

Why do the ventricles depolarize just as quickly as the atria, despite being much larger?
(Thus the P wave is similar in duration to the QRS complex)

Back 74

Because the Purkinje system is much faster than the atrial conducting system.

Front 75

represents the first ventricular depolarization to the last ventricular repolarization

Back 75

QT interval

Front 76

What is the R-R interval?

Back 76

Time between one R wave to the next.

Front 77

How is HR related to cycle length?

Back 77

HR = 1/Cycle length.

Cycle length is the R-R interval.

Front 78

Which heart sounds:
A) Mitral and tricuspid closure
B) Pulmonic and aortic valve closure
C) Atrial systole
D) Rapid phase of ventricular filling

Back 78

A) S1
B) S2
C) S4
D) S3

Front 79

complex adhering structures which connect single cardiac myocytes to an electrochemical syncytium and are mainly responsible for force transmission during muscle contraction.

Back 79

intercalated discs

Front 80

Intercalated discs consist of three kinds of cell-cell junctions. What are they?

Back 80

actin filament anchoring adherens junctions (fascia adherens), the intermediate filament anchoring desmosomes (macula adherens) and gap junctions. Gap junctions are responsible for electrochemical and metabolic coupling

Front 81

What is the isovolumetric contraction phase?

Back 81

When the left ventricle begins to contract and both the mitral and aortic valve are closed. There is an increase in pressure until <b> left ventricular pressure exceeds aortic pressure </b>, and the aortic valve opens.

Front 82

What happens when left ventricular pressure exceeds aortic pressure?

Back 82

The aortic valve opens, and the isovolumetric contraction phase is over.

Front 83

What is the pulmonary capillary wedge pressure indirectly measuring?

Back 83

The atrial pressure (will be a little bit higher than true atrial pressure).

Front 84

End-diastolic volume is aka

Back 84

preload

Front 85

What sets the resting tension of the intact myocardium?

Back 85

preload

Front 86

Avg cardiac output at rest

Back 86

about 5 l/min

Front 87

When does the mitral valve close?

Back 87

When LV pressure > LA pressure

Front 88

Causes S1

Back 88

closure of mitral and tricuspid valves

Front 89

Causes S2

Back 89

closure of pulmonic and aortic valves when Lv pressure falls below aortic pressure

Front 90

Causes S3

Back 90

From left ventricle filling

Front 91

Reappearance of S3 in adulthood connotes what?

Back 91

Decreasing compliance of left ventricle (heart failure)

Front 92

Causes S4

Back 92

Sound produced by column of blood moving from LA to LV during atrial systole (Just before S1)

Front 93

Direct reflection of right atrial pressure in physical exam

Back 93

cervical neck veins

Front 94

intrinsic ability of cardiac muscle to change tension development while starting from the same length

Back 94

contractility

Front 95

What are the two main peripheral vascular determinants on cardiac function?

Back 95

1) Venomotor changes that normally alter ventricular preload (End diastolic fiber length)

2) Arterial resistance changes that alter left ventricular ejection by increasing afterload

Front 96

How to measure preload?

Back 96

Pulmonary capillary wedge pressure. This estimates LA pressure.

Front 97

Major mech of compensation of heart failure

Back 97

Increase in intravascular volume, which increases venous return.

Front 98

What causes the decreased CO in acute hemorrhagic shock?

Back 98

Decreased preload due to blood volume loss.

Front 99

Two main determinants of afterload

Back 99

1) Systolic pressure (determined by impedance to flow in the aorta)

2) Ventricular radius (determined by LV volume)