Physiology Cardiac Cycle

Front 1

The binding of norephinephrine/epinephrine to a B1 receptor on a cardiac cell activates

Back 1

adenylyl cyclase which makes cAMP which phosphorylates PKA.

Front 2

PKA-p increases [Ca] i by what methods?

Back 2

Phosphorylates Ca channel in sarcolemma increasing flow of Ca

Front 3

PKA-p decreases [Ca]i by what methods?

Back 3

Phosphorylates phospholamban decreasing its inhibitory effect on SR Ca ATPase, decreasing [Ca] i

Front 4

Preload of cardiac muscle

Back 4

force that stretches the relaxed muscle fibers - force against ventricle during filling

Front 5

Afterload if cardiac muscle

Back 5

force against which the contracting muscle must act - pressure in the aorta that must be overcome to open aortic valve

Front 6

How can you increase pre-load?

Back 6

greater filling of ventricle during diastole

Front 7

Increasing pre-load has what effect on systolic pressure?

Back 7

increases systolic pressure to max and then it decreases if further increases in pre-load occur

Front 8

Changes in afterload effect systolic pressure how?

Back 8

Increases in afterload (increased aortic pressure) increases systolic pressure

Front 9

The ventricle is effected how during maximal afterload increase?

Back 9

Ventricle stretched to where it cannot create enough force to open aortic valve. - isovolumic contraction

Front 10

The first heart sound is the closure of the ?

Back 10

AV valves (tricuspid - Rt AV, mitral - L AV)

Front 11

The second heart sound is the closure of ?

Back 11

pulmonic and aortic valves

Front 12

Thin filament regulation

Back 12

The actin filament is blocked at low [Ca] and exposed during high [Ca].

Front 13

The long action potential in cardiac muslce is due to

Back 13

VG L-type Ca channel characteristics:long refractory period - prevents tetany.

Front 14

Altering the VG L-type Ca channel changes

Back 14

[Ca]i, thus changes contractility, force of contraction

Front 15

The increase in size of [Ca]i transient, and thus force of contraction is due to what type of stimulation

Back 15

sympathetic
B-adrenergic - norepi/epi

Front 16

positive inotropy

Back 16

increase in force of contraction

Front 17

positive lusitrophy

Back 17

increase in rate of muscle relaxation

Front 18

positive chronotrophy

Back 18

increase in contraction of heart - B-adrenergic

Front 19

What is a dipole?

Back 19

a separation of charge in space; orientation and magnitude of an electrical field

Front 20

What does an ECG detect?

Back 20

dipole created by depolarization of myocardium

Front 21

The dipole of the myocardium has what 2 characteristics?

Back 21

it changes over time
can be detected on the body surface

Front 22

The dipole can be described as _____ having a

Back 22

magnitude and direction

Front 23

The ECG represents the ____ of the ___ ____ of the ___.

Back 23

sum
electrical activity of the myocardium

Front 24

The ECG does or does not detect activation of the specialzed conduction system

Back 24

does not

Front 25

The ECG does or does not provide information about mechanical activity

Back 25

does not

Front 26

The ECG can or cannot see the AV node depolarization

Back 26

cannot

Front 27

Lead I of an ECG is set up how

Back 27

Right arm (-) to Left arm (+)

Front 28

Lead II of an ECG is set up how?

Back 28

Right arm (-) to Left leg (-)

Front 29

Lead III of an ECG is set up how?

Back 29

Left arm (-) to Left leg (-)

Front 30

AVR unipolar lead is set up how?

Back 30

RA as sensing electrode

Front 31

AVL unipolar lead is set up how?

Back 31

LA is sensing electrode

Front 32

AVF unipolar lead is set up how?

Back 32

LL is sensing electrod.

Front 33

automaticity of the heart is what?

Back 33

the ability to initiate its own beat

Front 34

rhythmicity

Back 34

the regularity of pacemaking activity

Front 35

The region of heart that initiates impulses at the greatest frequency is the

Back 35

SA node

Front 36

4 unique characteristics of the SA node depolarization

Back 36

RMP is less neg, upstroke less steep, plateau not sustained, repolarization is more gradual

Front 37

The SA node depolarization is not facilitated by

Back 37

fast sodium channels
No effect from fast Na channel blockers

Front 38

Both AV and SA node RMP is less negative than myocytes because

Back 38

they both lack iK channels

Front 39

The SA and AV node MP varies more from ______ than myocytes

Back 39

Equilibrium potential of K

Front 40

Pacemaker cells have a unique characteristic of phase 4

Back 40

a slow steady diastolic depolarization

Front 41

Pacemaker cell frequency can be varied by ______

Back 41

rate of phase 4 depolarization, the max neg during phase 4, or threshold potential

Front 42

To slow nodal firing

Back 42

increase threshold, make phase 4 MP more negative,

Front 43

The slow diastolic nodal depolarization is caused by what 3 things

Back 43

outward K current
inward current from hyperpolarizaiton, and inward Ca current

Front 44

The slow diastolic depolarization of the nodes is because

Back 44

K current out slows, funny channel Na current, and Ca current in.

Front 45

Ca channel antagonists do what in the nodes?

Back 45

diminish the amplitude of the action potential, and slop of the slow diastolic depolarization

Front 46

funny channels are triggered by

Back 46

hyperpolarization and are different Na channels than fast channels

Front 47

Ectopic pacemakers become pacemakers when

Back 47

their own rhythmicity is enhanced, higher order pacemakers are depressed, or conduction pathways between the higher order and ectopic are blocked

Front 48

adrenergic transmitters effect what channels

Back 48

all 3 - 1) outward K, 2) Na funny 3) Ca inward

Front 49

The bundles of His are what

Back 49

the upper portion of the specialized conduction system for the ventricles

Front 50

The AV nodal delay (time between P and QRS) allows for what

Back 50

ventricular filling

Front 51

Blocking fast Na channels effects the AV node how?

Back 51

no effect

Front 52

Ca channel antagonists have what effect on the AV node?

Back 52

decreases the amplitude and duration of the AP and depresses AV conduction

Front 53

The AV node relative refractory period ends

Back 53

well beyond complete repolarization

Front 54

1st degree AV block is what?

Back 54

abnormal prolongation of the AV conduction time.

Front 55

2nd degree AV block is what?

Back 55

Only a fraction of atrial impulses are conducted to ventricle

Front 56

2nd degree AV block may protect the heart how?

Back 56

protects the vetricles from excessive contraction frequencies to allow sufficient filling times

Front 57

Weak vagal activity does what to the AV node?

Back 57

prolong the AV conduction time. Atrium to His, A to V conduction time will be prolonged.

Front 58

Strong vagal tone does what to the AV node?

Back 58

blocks some or all of the atrial impulses

Front 59

3rd degree or complete AV block?

Back 59

none of the atrial impulses reach the ventricles

Front 60

vagal stimulation of the heart is carried out by

Back 60

the action of acetylcholine to hyperpolarize the RMP of conducting fibers in the AV node

Front 61

Sympathetic nerves ______ AV conduction

Back 61

facilitate
by decreasing AV conduction time,

Front 62

Sympathetic release of ________ on the __ ____ the amplitude and slope of upstroke of AV node

Back 62

norepinephrine
postganglionic sympathetic nerve terminals

Front 63

The bundle of His is located _____ and then divides into

Back 63

right side of interventricular septum, R & L bundle branches

Front 64

Bundle branches eventually branch into

Back 64

Purkinje fibers

Front 65

Purkinje fibers have a ____ refractory period that _____ some _____ impulses.

Back 65

long
blocks

Front 66

The refractory period of Purkinje fibers is ______ during slow heart rates

Back 66

lengthened

Front 67

The PR interval is the time between the

Back 67

onset of atrial depolarization and the onset of vetricular depolarization

Front 68

A long QRS complex indicates a

Back 68

block in the normal conduction pathways through the ventricles (L/R bundle branches

Front 69

ST represents the

Back 69

entire ventricular depolarization and is isoelectric

Front 70

The duration of the myocardial cell AP varies ______ with the heart rate

Back 70

inversely

Front 71

T waves can be __ or ____ but must be ________

Back 71

positive or negative
consistent

Front 72

The unipolar leads take two leads and _____ their values

Back 72

averages, not take the difference

Front 73

If P to R interval is longer it means what?

Back 73

AV node slow to depolarize, not that depolarization takes longer

Front 74

If the QRS complex is wide and bizarre it means

Back 74

depolarization started elsewhere from AV node, conduction system not working

Front 75

R waves are always

Back 75

positive or not present

Front 76

cholinergic stimulation of the heart (ACh) causes

Back 76

Inc K perm, hyperpol SA node, depress fun and Ca currents, slows spontaneous depolarization

Front 77

Vagal stimulation of the SA node causes the net effect of

Back 77

decreasing HR by lowering RMP and slowing diastolic depolarization

Front 78

Vagal stimulation of the AV node has the effect of

Back 78

shortening the plateau phase - weakend A contraction - not impt

Front 79

Vagal stimulation of the AV node

Back 79

increases K perm, decreases excitability, slows or stops impulse trnsimission

Front 80

Vagal stimulation of the AV nodes has the net effect of

Back 80

increasing AV nodal delay or inducing 3rd degree block

Front 81

Vagal stimulation of the ventricles causes

Back 81

not much effect

Front 82

Vagal stimulation of the heart overall effects

Back 82

HR and AV nodal delay

Front 83

Sympathetic stimulation of the SA node causes

Back 83

increase in f, and Ca > K currents,

Front 84

Sympathetic stimulation of the SA node has the net effect of

Back 84

increase spontaneous depolarization, increased HR

Front 85

Sympathetic stimulation of the AV node

Back 85

increases conduction velocity - decreased AV node delay

Front 86

Sympathetic stimulation of the AV node has the net effect of

Back 86

Increased HR and increased conduction velocity

Front 87

Sympathetic stimulation of the Atrial and ventricular contractile cells causes

Back 87

calcium load the cells

Front 88

Calcium loading of myocytes includes

Back 88

phosphorylation of Ca channels and phospholambam increasing Ca in cell and SR

Front 89

Sympathetic stimulation of the myocytes causes the net effect of

Back 89

increased strength of contraction, and rate of relaxation

Front 90

Sympathetic stimulation of myocytes increases the rate of relaxation by

Back 90

increasing CA uptake into SR, decreasing calcium sensitivity, phosphorylating troponin I

Front 91

sympathetic stimulation of the myocytes is carried out by

Back 91

cAMP

Front 92

postive lusitropic

Back 92

increased rate of relaxation

Front 93

positive inotrophic

Back 93

increased strength of contraction

Front 94

Sinus rhythm means

Back 94

SA nod starts depolarization and upright P leads to QRS

Front 95

sinus arrhythmia

Back 95

sinus rhythm with irregular R-R interval caused by changes in symp/vagal tone during respiration

Front 96

Sinus arrhythmia can't happen in animals with

Back 96

fast HR

Front 97

Sinus arrhythmia occurs in dogs with

Back 97

high vagal tone

Front 98

Baroreflex is coordination of

Back 98

vagal/sympathetic tone.

Front 99

S1 of heart auscultation associated with

Back 99

closure of AV valvem onset of systole, present in all species

Front 100

S2 of heart auscultation associated with

Back 100

closure of aortic and pulmonic valves, signals end of systole, present in all species

Front 101

S3 is during diastole and associated with

Back 101

rapid ventricular filling, not in normal dogs/cats, with heart failure, increased venous return in preg mares

Front 102

S4 is associated with

Back 102

atrial contraction, immediately precedes S1, present in horses

Front 103

Murmurs are

Back 103

abnormal sounds induced by turbulent blood flow

Front 104

Murmurs can originate from

Back 104

stenosis, relative stenosis, incompetent valve, anemia, septal defects

Front 105

Anemia causes a murmur because

Back 105

decreased PVC, decreases viscosity, causes turbulent flow

Front 106

Systolic murmurs are from

Back 106

incompetent AV valves, stenosis of pulmonic or aortic valve, sub-aortic stenosis, relative pulmonic stenosis

Front 107

diastolic murmurs are from

Back 107

incompetent pulmonic/aortic valves