Cardiac Questions-Phys

Front 1

What cell junction is only found in heart cells, and what is it composed of?

Back 1

Intercalated disc: Desmosomes(stretch), gap junctions (spread A.P.)

Front 2

How does the heart know that it needs more O2 (coronary circulation)?

Back 2

Use of ATP causes release of adenosine which causes vasodilation of coronary vessels

Front 3

What purpose does the fibrous skeleton serve and why is it important?

Back 3

Electrical insulation, need to make sure atria are thru contracting before the ventricles contract in order to ensure efficient pumping of blood

Front 4

Athletes usually have lower resting heart rates than sedentary people: 50 bpm as compared to 70 bpm. The resting CO in each of these people is the same, so how can the athlete have a much lower heart rate?

Back 4

His SV is higher, as the heart gets stronger with exercise, it can pump blood more efficiently to give a larger resting SV.

Front 5

A patient comes into the emergency room w/ an abnormally low SV. Before I have even diagnosed what the problem is, I begin administering an isotonic saline soln. Why?

Back 5

Raise b.p.= raise SV

Front 6

Which of these would not raise the SV of your heart?
A) vasoconstriction of veins B) vasoconstriction of arteries C) increased Ca++ influx into contractile cells
D) increased EDV
E) increased ESV

Back 6

ABDE

Front 7

What characteristics of the heart can we determine from an ECG?

Back 7

-Heart rate
-B.P.
-Cardiac output
-Check for murmurs

Front 8

Explain what each of the parts of the ECG represent in the heart.

Back 8

-P wave: atrial depolarization
-QRS: ventricular depolarization
-T wave: ventric. repolarization

Front 9

What is happening during the PR interval of the ECG recording?

Back 9

Atrial depolarization and AV nodal delay

Front 10

What is going on during the ST segment?

Back 10

Cardiac plateau

Front 11

What part of the ECG includes when the ventricle and atria are in diastole?

Back 11

TP interval

Front 12

Which is more serious, ventricular or atrial fibrillation, and why? What about atrial flutter and ventricular flutter?

Back 12

Ventricular-can’t pump any blood= dead, same

Front 13

Explain why hypertension (abnormally high diastolic pressure is bad for your heart.

Back 13

Your left ventricle has to work harder to overcome the high blood pressure in the aorta. The increased work load takes a toll on the heart over time

Front 14

A heart that is transplanted is taken from the chest of a donor and after the vagus nerve is cut, doctors notice that the heart is automatically beating about 55 bpm. What is wrong with this heart?

Back 14

Loss of a SA node, the AV node takes over but beats a little faster b/c parasympathetic stimulation has been taken away.

Front 15

What would happen to someone whose heart was beating at the maximum speed (stimulated at the end of each refractory period)?

Back 15

B.P. down because ventricular filling does not occur completely

Front 16

I have an ECG done, and I find that all the waves look normal, but my TP interval is abnormally long, and therefore, my heart rate is about 49 bpm. Do I have an abnormal condition, and if so, what is it called?

Back 16

Bradycardia

Front 17

How can a transplanted heart beat since doctors do not reattach nerves to the heart after implantation? How could it adjust to changing CO for the body’s needs?

Back 17

The heart does not need innervation to beat; it has pacemaker cells. It could still adjust CO through the Starling mechanism, and it would also still be able to respond to sympathetic stimulation through epinephrine (or any other hormones) to increase rate and force.

Front 18

I have been noticing an abnormality in my heart beat, so I go to the doctor. The doctor diagnoses me as having a block in my left bundle branch, even though my heart is still pumping blood. What effect would this problem cause and how did I notice it?

Back 18

My right ventricle would be completely depolarized much before my left ventricle, and therefore, it also contracts earlier. My Right AV valve would be shutting before the L one, and so my first heart sound was split into two separate sounds.

Front 19

I go in for my yearly physical and find a shocking problem. My heart rate is extremely rapid and irregular, and is much greater than the pulse rate taken at my wrist. The doctor takes an ECG on me, and finds no P waves at all. My QRS complexes are normal, but appear kind of sporadically. What is wrong with me? Is my CO going to be seriously impaired, and what is causing the pulse deficit?

Back 19

Most likely I have atrial fibrillation (rapid, irregular contraction of the atria). Impulses reach the AV node erratically, causing the sporadic QRS complexes. Ventricular filling would be affected because the atria are not contracting and on some contraction the ventricles won’t have time to fill. On some of the cycles, ventricular contractions are probably too weak to eject enough blood to produce a pulse, so the heart rate will be greater than the pulse rate. The heart can help compensate through sympathetic stimulation which increases venous return and increases heart contractility.

Front 20

During fetal life, the nonfunctioning collapsed lungs offer a tremendous amount of resistance, so the pressures in the right side of the heart are subsequently higher than the left side. A vessel known as the ductus arteriosus connects the pulmonary artery to the aorta and serves as a shunt to bypass the lungs. At birth, this structure normally closes and becomes a thin ligament, but occasionally, it will fail to close at birth. What direction would blood flow thru the patent ductus arteriosus in an adult? What are some possible consequences of this anomaly?

Back 20

In an adult, blood would flow from the aorta back into the pulmonary artery since pressure on the left side of the heart is higher after birth. The abnormal flow produces a machinery murmur that lasts throughout the entire cardiac cycle, and is more intense during systole. This could cause h.r. to rise, etc. because symp. Stimulation will be increased to compensate.

Front 21

A heart that is transplanted is taken from the chest of a donor and after the vagus nerve is cut, doctors notice that the heart is automatically beating about 102 bpm. What is wrong with this heart?

Back 21

Nothing; the heart rate with no parasympathetic stimulation is about 100 bpm.

Front 22

What causes heart sounds?

Back 22

Turbulent blood flow caused by valve closure

Front 23

Why does the heart go through a period of isovolumetric contraction?

Back 23

After AV valves close, pressure not high enough to open the aortic valve. needs to contract isometrically to raise the pressure.

Front 24

At which point is the ventricular volume greatest during the cardiac cycle?

Back 24

At the beginning of isovolumetric contraction, just prior to the opening of the aortic valves, just after the closing of the AV valves

Front 25

When does the majority of ventricular filling occur and why? What about the atria?

Back 25

Just after the AV valves open because blood has been building up in the atria during systole Atria have continuous filling except when they are contracting

Front 26

What do these numbers represent?
-120 mm Hg
-80 mm Hg
-135 ml
-70 ml
-65 ml

Back 26

-120 mm Hg (systolic b.p.)
-80 mm Hg (diastolic b.p.)
-135 ml (EDV)
-70 ml (SV)
-65 ml (ESV)

Front 27

During ventricular filling, ventricular pressure is (greater/less) than atrial pressure.

Back 27

Slightly less

Front 28

During ventricular ejection, ventricular pressure is (greater/ less) than atrial pressure.

Back 28

Much greater

Front 29

Atrial pressure is always (greater/less) than aortic pressure.

Back 29

Much less

Front 30

During isovolumetric contraction and relaxation, ventricular pressure is (greater/less) than atrial pressure and (greater/less) than aortic pressure.

Back 30

-Greater
-Less

Front 31

If I stimulated the heart (say I hit you in the chest with an erratically thrown baseball) at just the right moment on the downslope of the hump of the T wave, what could happen?

Back 31

Ventricular fibrillation, during the T wave part, some cells have repolarized and some have not. Therefore some could be restimulated, while others would still be refractory, causing uncoordinated contractions

Front 32

STROKE VOLUME=

Back 32

=EDV-ESV

Front 33

EF(%)=

Back 33

=100 X SV/EDV

Front 34

CO(ml/min)=

Back 34

=SV(ml/beat) x HR (bpm)

Front 35

CARDIAC OUTPUT:
LEFT SIDE =

Back 35

=RIGHT SIDE

Front 36

VENOUS RETURN=

Back 36

=CARDIAC OUTPUT

Front 37

NORMAL BP VALUES(mmHg)
-Central Venous (Rt. Atrial):
-Right Ventricular:
-Pulmonary Arterial:
-Left Atrial:
-Left Ventricular:
-Systemic Arterial:

Back 37

NORMAL BP VALUES(mmHg)
-0-4
-25/0
-25/12
-0-8
-120/2
-120/80

Front 38

ESTIMATE OF MAP=

Back 38

=1/3(SYSTOLIC) + 2/3(DIASTOLIC)

Front 39

PULSE PRESSURE=

Back 39

=SYSTOLIC PRESSURE - DIASTOLIC PRESSURE

Front 40

END-DIASTOLIC VOLUME

Back 40

PRELOAD

Front 41

OUTFLOW PRESSURE

Back 41

AFTERLOAD

Front 42

MYOCARDIAL CONTRACTILITY

Back 42

IONOTROPY (IONOTROPIC, IONOTROPE)

Front 43

MYOCARDIAL RELAXATION

Back 43

LUSITROPY

Front 44

HEART RATE

Back 44

CHRONOTROPY

Front 45

CONDUCTION RATE

Back 45

DROMOTROPY

Front 46

PRELOAD ESTIMATES (3)

Back 46

-END-DIASTOLIC PRESSURE
-ATRIAL PRESSURE
-VENOUS PRESSURE

Front 47

AFTERLOAD ESTIMATES (2)

Back 47

-ARTERIAL PRESSURE
-VENTRICULAR WORKLOAD

Front 48

CARDIAC PERFORMANCE IS

Back 48

CARDIAC OUTPUT

Front 49

END-DIASTOLIC VOLUME ESTIMATES (3)

Back 49

(PRELOAD)
-END-DIASTOLIC PRESSURE
-ATRIAL PRESSURE
-CVP

Front 50

STROKE WORK ESTIMATES (2)

Back 50

-SV
-CO

Front 51

LAW OF LaPlace:

Back 51

σ = Pr/w
σ - wall stress
P - pressure
r - radius
w - wall thickness

Front 52

Wall stress is proportional to

Back 52

Oxygen Consumption

Front 53

Ventricular Myocyte AP:
PHASE 0:
-Na+ Conductance:
-K+ Conductance:
-Membrane Potential:

Back 53

Ventricular Myocyte AP:
-Phase:
-Increased Na+ Conductance
-K+ Conduction Decreases
-Rapid increase in membrane potential

Front 54

Ventricular Myocyte AP:
PHASE 1:
-Na+ Conductance:
-K+ Conductance:
-Membrane Potential:

Back 54

Ventricular Myocyte AP:
-Phase:
-Na+ Conductance returns to baseline
-Increased K+ Conductance
-Brief fall in membrane potential

Front 55

Ventricular Myocyte AP:
PHASE 2 - (AKA):
-Ca2+ Conductance:
-Membrane Potential:

Back 55

Ventricular Myocyte AP:
-Phase:
-Plateau
-Increased Ca2+ Conductance
-Sustained Depolarization

Front 56

Ventricular Myocyte AP:
PHASE 3:
-Ca2+ Conductance:
-Membrane Potential:

Back 56

Ventricular Myocyte AP:
-Phase
-Decreased Ca2+ Conductance
-Rapid Fall in membrane potential

Front 57

Ventricular Myocyte AP:
PHASE 4:
-K+ Conductance:
-Na+ Conductance:
-Membrane Potential:

Back 57

Ventricular Myocyte AP:
-Phase:
-High K+ Conductance
-Low Na+ Conductance
-Resting membrane potential

Front 58

Pacemaker Cell AP:
PHASE 4:
-K+ Permeability:
-If:
-Ca2+ Permeability:
-Membrane Potential:

Back 58

Pacemaker Cell AP:
-Phase:
-Decreasing K+ permeability
-Increased If ('funny' channel; Na+); Slow Na+ influx
-Ca2+ permeability increases near the end
-Slow, spontaneous depolarization

Front 59

Pacemaker Cell AP:
PHASE 0:
-Na+ Permeability:
-Ca2+ Permeability:
-Membrane Potential:

Back 59

Pacemaker Cell AP:
-Phase:
-Decreased Na+ (If) permeab.
-Increased Ca2+ permeability
-Rapid Depolarization

Front 60

Pacemaker Cell AP:
PHASE 3:
-Ca2+ Permeability:
-K+ Permeability:
-Membrane Potential:

Back 60

Pacemaker Cell AP:
-Phase:
-Decreased Ca2+ permeability
-Increased K+ permeability
-Rapid Repolarization

Front 61

Pacemaker Cell AP:
EFFECTIVE REFRACTORY PERIOD:
-Myocyte response to stim.:
-Due to:

Back 61

Pacemaker Cell AP:
-Which Period:
-Myocyte non-responsive to stimulation
-Due to inactivation of Na+ channels

Front 62

Pacemaker Cell AP:
RELATIVE REFRACTORY PERIOD:
-Myocyte response to stimulus:

Back 62

Pacemaker Cell AP:
-Which Period:
-Myocyte responsive only to supra-normal stimulus

Front 63

AP vs MUSCLE TWITCH LENGTH:
-Prevents:

Back 63

What prevents Tetanization:

Front 64

Auto rhythmic cells make up the specialized conduction system (6):

Back 64

What type of cells/what do they make up:
-SA node
-AV node
-Bundles of His
-Right&Left bundle branches
-Purkinje fibers

Front 65

Specialized Conduction System:
-Route of AP:

Back 65

SA node->Rt. atrium-> Bachman's Bundle->Lt. atrium
Rt. atrium->AV node-> Bundle of His (AV bundle)->Left & Right bundle branches-> Purkinje fibers (species variation)->Ventricular myocytes

Front 66

Conduction of an excitation (action potential) wave is much (slower/faster) thru the specialized conduction system than thru myocardium.

Back 66

Faster
(Bundle branches & Purkinje fibers)

Front 67

CARDIAC MYOCYTES:
-Main Characteristics (7):

Back 67

-Striated muscle
-Contractile&regulatory protein arrangement comp. to Skel. m
-Network of branching linear fibers
-Intercalated discs contain gap jxns.
-Functional Syncytium
-Dense capillary network
-Sarcoplasmic reticulum

Front 68

CARDIAC MYOCYTES:
-Contractile & regulatory protein arrangement:

Back 68

-Myosin
-Actin
-Tropomyosin
-Troponin C, I, T

Front 69

CARDIAC MYOCYTES:
-Sarcoplasmic reticulum:
-Regions:

Back 69

-One region comes in contact w/ the external sarcolemma & T-Tubule system
-2nd region surrounds contractile proteins

Front 70

CARDIAC MYOCYTES:
-The energy-producing process in the heart is primarily:

Back 70

Aerobic
Oxidation

Front 71

CARDIAC MYOCYTES:
-Where does Oxidation occur (6):

Back 71

Within the Mitochondria of:
-Fatty Acids
-Ketones
-Carbohydrates
-Lactate
-Pyruvate
-Some amino acids

Front 72

CARDIAC MYOCYTES:
-Types of Oxidation (3):

Back 72

-Beta-Oxidation of Fats
-TCA Cycle (Krebs cycle)
-Oxidative Phosphorylation

Front 73

CARDIAC MYOCYTES:
-Mitochondria amount:
-Aerobic Pathways-depend:
-Glycolytic enzymes amount:

Back 73

-Mitoch. are abundant
-Aerobic pathways - dependence on a steady supply of O2 is High
-Glycolytic enyzmes are sparse

Front 74

E-C COUPLING:
-Main Events (7):

Back 74

-Depolarization of CM
-Increased Ca2+ permeability
-Inflow of Ca2+ stim. release of Ca2+ from SR via activation of RYR; Ca-induced Ca release
-Ca2+ released binds Trop.C
-Ca2+-Troponin complex interacts w/ Tropomyosin to unblock active sites btw. Actin & Myosin
-Force generated by cross-bridges propor. to ICF[Ca2+]
-Ca2+-sensitivity of contractile mech. altered by stretch

Front 75

MYOCARDIAL RELAXATION:
-Main Events (4):

Back 75

-Ca2+ influx ceases
-Ca2+ release from SR ceases
-Increased cystolic [Ca2+] stim. Ca2+ pumps in SR to increase Ca2+ reuptake in SR
-Ca2+ removed from cell across the cell memb. by Na+-Ca2+ exchange&by Ca2+pumps

Front 76

CARDIAC MYOCYTES:
-Pumps & Exchangers (4):

Back 76

-SR Ca2+ Pump
-Na+-Ca2+ Exchange
-Cell Memb. Ca2+ Pump
-Cell Memb. Na+/K+ ATPase

Front 77

CARDIAC MYOCYTES:
SR Ca2+Pump:
-Consumes ATP?

Back 77

Consumes ATP

Front 78

CARDIAC MYOCYTES:
Na+-Ca2+ Exchange:
-Consumes ATP?
-Facilitated by:
-Direction of operation:
-Allows:

Back 78

-Does not consume ATP
-Exchange facilitated by ATP
-Can operate in Both directions
-Allows rapid removal of Ca2+

Front 79

CARDIAC MYOCYTES:
-Cell Memb. Ca2+ Pump:
-Consumes ATP?

Back 79

Consumes ATP

Front 80

CARDIAC MYOCYTES:
-Cell Memb. Na+/K+ ATPase:
-Consumes ATP?
-Creates:

Back 80

-Consumes ATP
-Creates Na+ gradient for Na+-Ca2+ Exchange

Front 81

CARDIAC MYOCYTES:
-Which pumps/exchangers consume ATP?

Back 81

-SR Ca2+ Pump
-Cell Memb. Ca2+ Pump
-Cell Memb Na+/K+ ATPase

Front 82

CARDIAC MYOCYTES:
-Which Pump(s)/Exchanger(s) do NOT consume ATP:

Back 82

Na+-Ca2+ Exchanger

Front 83

Blacks, whites ,grays (and sometimes browns) are the __________ colors. You can mix these by a 50/50 mix of two complements.

Back 83

neutral

Front 84

CARDIAC MYOCYTES:
-Which pump/exchanger allows for rapid removal of Ca2+:

Back 84

Na+-Ca2+ Exchanger

Front 85

CARDIAC MYOCYTES:
-Which pump/exchanger creates Na+ gradient for Na+-Ca2+ exchange:

Back 85

Cell Memb. Na+/K+ ATPase

Front 86

CARDIAC MYOCYTES:
-Regulation of contraction & relaxation:
-Phosphorylation of (3):

Back 86

-Troponin I
-Phospholamban
-Ca2+ Channel in sarcolemma

Front 87

CARDIAC MYOCYTES:
-Regulation of contraction & relaxation:
-Effect of Phosphorylation of
Troponin I:

Back 87

Phosphorylation of:
-Inhibits Ca2+ binding to troponin C, thus decreases Ca2+ of contractile mechanisms

Front 88

CARDIAC MYOCYTES:
-Regulation of contraction & relaxation:
-Effect of Phosphorylation of Phospholamban:

Back 88

Phosphorylation of:
-Stimulates SR Ca2+ Pump

Front 89

CARDIAC MYOCYTES:
-Regulation of contraction & relaxation:
-Effect of Phosphorylation of Ca2+ Channel in sarcolemma:

Back 89

Phosphorylation of:
-increases Ca2+ conductance;
therefore more Ca2+ enters the cell during Depolarization

Front 90

Separation of charge in space; orientation & magnitude of an electrical field:

Back 90

Dipole

Front 91

Depolarization of the myocardium creates a dipole that (2):

Back 91

-changes over time
-can be detected on the body surface

Front 92

ECG:
-This dipole, at any moment in time, can be described as:

Back 92

a vector with a magnitude & direction

Front 93

ECG:
-The magnitude & direction of the dipole change as:

Back 93

the atria & ventricles depolarize

Front 94

ECG:
-Recording of:
-That reaches:
-Plotted over:

Back 94

-Electrical activity of the heart that reaches the body surface plotted over time

Front 95

ECG:
-Represents (2):

Back 95

-The Sum of the electrical activity of the Myocardium
-Voltage (potential difference) btw 2 electrodes on the body surface

Front 96

ECG:
-Does Not (2):

Back 96

-Detect activation of the Specialized Conduction Sys.
-Provide info about mechanical activity (i.e. strength of contraction, etc.)

Front 97

ECG:
-Each Lead Displays:

Back 97

Displays activity along a single axis

Front 98

Standard ECG Trace:
-Time Periods:

Back 98

R-R Interval
-Time period btw 2 QRS Complexes (Ventricular depolarizations)

Front 99

ECG:
BIPOLAR LEADS:
-I
-II
-III

Back 99

-Rt. Arm (RA) is negative electrode & LA is positive
-RA neg & LL pos
-LA neg & LL pos

Front 100

ECG:
-QRS COMPLEX:
-R WAVE:
-Q WAVE:
-S WAVE:

Back 100

-1st Positive Deflection
-Neg. Deflection B4 R Wave
-Neg. Deflection after R Wave

Front 101

ECG:
-QRS COMPLEX:
-If only Neg. Deflection:

Back 101

-(No R Wave)
-Call it Q-S Wave

Front 102

ECG:
-QRS:
-QR:
-RS:
-QS:

Back 102

-Neg-Pos-Neg
-Neg-Pos
-Pos-Neg
-Neg

Front 103

ECG:
-Unipolar Leads (3):

Back 103

-AVR
-AVL
-AVF

Front 104

ECG:
-Unipolar Leads Sensing Electrode:
-AVR:
-AVL:
-AVF:

Back 104

-RA is sensing electrode
-LA is sensing electrode
-LL(foot) is sensing electrode

Front 105

ECG:
-Chest Lead (1):

Back 105

Unipolar Leads located on the chest

Front 106

ECG:
-Categories of Leads (3):

Back 106

-Bipolar Leads
-Unipolar Leads
-Chest Leads

Front 107

READING ECGs:
1.Check:
2.Determine:
3.Determine:
4.Identify:
5.Check:
6.Is each:
7.Is each:
8:Is the shape of:

Back 107

1.paper speed&sensitivity
2.HR
3.regularity of rhythm
4.each wave independently
5.PR interval length
6.P wave followed by QRS?
7.QRS preceeded by P?
8.QRS normal&consistent?

Front 108

READING ECGs:
-What is the typical paper speed?

Back 108

1cm/mV

Front 109

READING ECGs:
-What does it mean if each QRS is NOT preceeded by a P wave?

Back 109

Depolarization didnt start at AV node

Front 110

READING ECGs:
-What can you determine based on shape of QRS?

Back 110

How long it took for the ventricle to depolarize:
-Rapidly=Narrow
-Slowly=Wide

Front 111

READING ECGs:
-Remember: EVERY QRS Complex is followed by:

Back 111

a T WAVE

Front 112

READING ECGs:
-Questions:
-1.Is __Normal?
-2.Is __Normal?
-3.Does __lead to__?
-4.Is __Normal?
-5.Does__only occur___?
-6.Does the __follow the normal path? That is, is the shape of the __normal?

Back 112

1.Ventricular Rate (R-R Int.)
2.Atrial depolarization wave
3.Atrial depolarization lead to Ventricular Depolarization
4.A-V Nodal Conduction Time
5.Ventricular Depolarization; After Atrial Depolarization
6.Ventricular Depolarization Wave; QRS Complex

Front 113

READING ECGs:
-Questions Regarding:
1.Ventricular Rate (R-R Int):
2.Atrial Depolarization Wave:
3.A-V Nodal Conduction time:
4.Ventricular Depolarization Wave:

Back 113

1.Normal?
2.Normal? Lead to Ventricular Depolarization?
3.Normal?
4.Only occur After Atrial Depolarization? Follow the normal path? Shape of QRS complex Normal?

Front 114

ECG:
QRS COMPLEX:
-Normal Shape/Consistency?
-Due to?

Back 114

-Narrow & shape is very consistent from beat to beat
-Efficient spread of depolarization wave by Specialized Conduction Sys.

Front 115

ECG:
QRS COMPLEX:
-Cause of Wide & Bizzare Shape (2)?

Back 115

-Ventricular Depolarization Wave that arises at some point other than the AV Node or finds the Normal Path Blocked does not effectively use the Specialized Conduction Sys.

Front 116

ECG:
QRS COMPLEX:
-Effect of Ventricular Depolarization Wave that arises at some point other than the AV node or finds the normal path blocked (2):

Back 116

-Does not effectively use Specialized Conduction Sys.
-QRS Complex is Wide & Bizarrely Shaped

Front 117

ECG:
-Inherent Firing Rate:

Back 117

-SA node>AV node>His bundles/Purkinje Fibers

Front 118

ECG:
-Associated with AV Nodal Delay (2):

Back 118

-Ventricular filling during Atrial contraction
-Return of A-V valves to near closed position

Front 119

ECG:
-What is the pacemaker?

Back 119

SA Node

Front 120

ECG:
-Pattern of Ventricular Depolarization (2):

Back 120

-Specialized Conduction System activates Myocytes
-The Depolarization wave spreads thru the myocardium in myocyte-to-myocyte fashion

Front 121

ECG:
-Ventricular filling during atrial contraction is associated with:

Back 121

AV Nodal Delay

Front 122

ECG:
-Return of AV Valves to near closed position is associated with:

Back 122

AV Nodal Delay

Front 123

ECG:
-Specialized Conduction System Activates:

Back 123

ECG:
-Myocytes activated by:

Front 124

ECG:
-The Depolarization Wave Spreads thru the:

Back 124

ECG:
-What spreads thru the Myocardium in myocyte-to-myocyte fashion:

Front 125

CARDIAC RATE&RHYTHM:
-Types of Parasympathetic (Cholinergic) Stimulation (5):

Back 125

-Vagal Stimulation
-SA Node
-Atrial Muscle
-AV Node
-Ventricle

Front 126

CARDIAC RATE&RHYTHM:
PS STIMULATION:
-Effects of Vagal Stim. of SA Node:
1.K+ Permeability:
2.SA Node Membrane:
3.ir & ica currents:
4.Membrane Potential:
5.Overall Effect:

Back 126

CARDIAC RATE&RHYTHM:
-Type&Site of Stimulation:
1.Increases K+ Permeability
2.Hyperpo. SA node memb.
3.Depresses ir & ica currents
4.Slows spontaneous depolar.
EFFECT: Decreases HR

Front 127

CARDIAC RATE&RHYTHM:
-What type of Stimulation Decreases Heart Rate?

Back 127

CARDIAC RATE&RHYTHM:
PS STIMULATION:
Vagal Stimulation of SA Node:

Front 128

CARDIAC RATE&RHYTHM:
PS STIMULATION:
-Effects of Stimulation of Atrial Muscle (2):

Back 128

CARDIAC RATE&RHYTHM:
Type/Site of Stimulation:
-Shortens Plateau Phase
-Weakens Atrial Contraction

Front 129

CARDIAC RATE&RHYTHM:
-What type of Stimulation Weakens Atrial Contraction?

Back 129

CARDIAC RATE&RHYTHM:
PS STIMULATION:
Stimulation of Atrial Muscle:

Front 130

CARDIAC RATE&RHYTHM:
PS STIMULATION:
-Effects of Stimulation of AV Node (4):

Back 130

CARDIAC RATE&RHYTHM:
Type/Site of Stimulation:
1.Increases K+ Permeability
2.Decreases Excitability
3.Slows or stops impulse transmission
EFFECT:Increases AV nodal delay or induces 3rd degree block

Front 131

CARDIAC RATE&RHYTHM:
-What type of Stimulation Increases AV Nodal Delay or Induces 3rd Degree Block?

Back 131

CARDIAC RATE&RHYTHM:
PS STIMULATION:
Stimulation of AV Node:

Front 132

CARDIAC RATE&RHYTHM:
PS STIMULATION:
-Effects of Stimulation of Ventricle:

Back 132

CARDIAC RATE&RHYTHM:
Type/Site of Stimulation:
-EFFECT: Not Much

Front 133

CARDIAC RATE&RHYTHM:
-What type of Stimulation has very little effect?

Back 133

CARDIAC RATE&RHYTHM:
PS STIMULATION:
-Stimulation of Ventricle:

Front 134

CARDIAC RATE&RHYTHM:
VAGAL TONE PRIMARILY AFFECTS:

Back 134

CARDIAC RATE&RHYTHM:
HR IS PRIMARILY AFFECTED BY:

Front 135

CARDIAC RATE&RHYTHM:
SYMPATHETIC (B-1) STIM.:
-Sites (3):

Back 135

CARDIAC RATE&RHYTHM:
What type of Stimulation:
-SA NODE
-AV Node
-Specialized Conduction Sys.

Front 136

CARDIAC RATE&RHYTHM:
SYMPATHETIC (B-1) STIM.:
-Effects of Stimulation of AV node (4):

Back 136

CARDIAC RATE&RHYTHM:
Type/Site of Stimulation:
1.Increases iK, ir, and ica
2.Increases ir & ica more than ik
3.Increases the rate of spontaneous depolarization
EFFECT: Increases HR

Front 137

CARDIAC RATE&RHYTHM:
-What type of Stimulation Increases HR?

Back 137

CARDIAC RATE&RHYTHM:
SYMPATHETIC (B-1) STIM:
-SA Node:

Front 138

CARDIAC RATE&RHYTHM:
SYMPATHETIC(B-1) STIM:
-Effects of stimulation of AV node (2):

Back 138

CARDIAC RATE&RHYTHM:
Type/Site of Stimulation:
-Increases Conduction Velocity
-EFFECT: Decreases AV Nodal Delay

Front 139

CARDIAC RATE&RHYTHM:
-What type of Stimulation Decreases AV Nodal Delay?

Back 139

CARDIAC RATE&RHYTHM:
SYMPATHETIC (B-1) STIM:
-AV Node:

Front 140

CARDIAC RATE&RHYTHM:
SYMPATHETIC (B-1) STIM:
-Effect of Stimulation of Specialized Conduction Sys?

Back 140

CARDIAC RATE&RHYTHM:
Type/Site of Stimulation:
-Increases Conduction Velocity