Chapter 14- Exam 3

Front 1

List the three ways cardiac muscle differs from skeletal muscle

Back 1

1. Smaller

2. Branch and contains intercalated discs

•Gap junctions allow ions to move rapidly between cells

•Acts like single-unit smooth muscl

3. Depends on extracellular calciumfor contraction

Front 2

99% of myocardium

Back 2

Contractile fibers

Front 3

Normally, do not conduct their own APs

Back 3

Contractile fibers

Front 4

Perform mechanical pumping of heart

Back 4

Contractile fibers

Front 5

Do not contract

Back 5

Conductive Fibers

Front 6

Initiate AP

Back 6

Conductive Fibers

Front 7

Describe the process of excitation-contraction coupling in cardiac muscle:

Back 7

1. AP opens L-type voltage gatedchannels (1)

2. Calcium enters cells (2/3

•Leads to opening of RyR channels via CICR

3. Increase in calcium leads tocalcium sparks that sum to create a calcium signal (4/5)

4. Contraction of muscle (6)

Front 8

How does cardiac muscle relaxation differ from skeletal muscle relaxation?

Back 8

Main difference is calcium is both stored in the SR and removed from the cell via the Na+/Ca2+ exchanger(NCX)

Front 9

Force generated by cardiac muscle is determined by concentration of ________ and ___________ of muscle at start of contraction.

Back 9

cross bridges and length

Front 10

Why are myocardial APs so long?

Back 10

Long refractory period

Front 11

How are the action potentials of cardiac muscle similar to those of skeletal muscle?

Back 11

•Rapid depolarization due to Na+ influx

•Steep repolarization due to K+ efflux

Front 12

How are the action potentials of cardiac muscle different to those of skeletal muscle?

Back 12

•Longer 300 msec vs 1-5 msec

•Requires calcium

•RMP is -90mV compared to -70mV ofskeletal muscle

Front 13

Steps of cardiac action potentials?

Back 13

•Depolarization

•Voltage-gated Na+ channels open

•Na+ influx

•Initial Repolarization

•K+ channels open – K+ efflux

•Na+ channels close

•Plateau

•AP flattens due to decreases in K+ permeability and increase in Ca2+permeability

•Slow Ca2+ channels open; fast K+ channels close

•Rapid Repolarization

•Ca2+ channels close; decreasing Ca2+

•Slow K+ channels open; increasing K+

Front 14

Myocardial action potentials use _________ cells

Back 14

Contractile

Front 15

Autorhythmic action potentials use _____ cells

Back 15

Conductive`

Front 16

Conductive cells have unstablemembrane potentials called ______________

Back 16

Pacemaker potential

Front 17

What are autorhytmic action potentials caused by?

Back 17

•Caused by If channels

•Open at -60mV cause Na+ influx to be greater than K+ efflux

Front 18

Steps of autorhythmic action potentials

Back 18

1. If channels open at -60mV

2. Cell slowly depolarizes

•If channels close

•Some Ca2+ channels open

3. At threshold voltage-gated calcium channels open

•Increase in calcium causes asteep depolarization

4. Ca2+ channels close at peak

5. Slow K+ channels open

•Cell repolarizes

•K+ channels close at -60mV

Front 19

__________ and _________ have a positive inotropic effect

Back 19

Catecholamines; digitalis

Front 20

How do catecholamines affect contractility?

Back 20

Catecholamines act by increasing the amount calcium available during calcium induced calcium release

Front 21

How do digitalis affect contractility?

Back 21

Digitalis acts by decreasing the removal of Ca2+ from the cytosol

Front 22

How is heart rate decreased by PSNS?

Back 22

•Increase K+ efflux, decrease Ca2+

•Hyperpolarizes cell

•Negative chronotropic effect decrease HR

Front 23

How is heart rate increased by SNS

Back 23

•Increases Na+ and Ca2+ influx

•Increases rate of depolarization

•Positive chronotropic effect increase HR

Front 24

What occurs during the P-wave

Back 24

Atrial Depolarization

Front 25

What happens during the QRS complex?

Back 25

Ventricular depolarization

Front 26

What happens during T-wave

Back 26

Ventricular repolarization

Front 27

What happens during P-R interval

Back 27

Atrial depolarization and systole as wellas onset of ventricular depolarization

Front 28

What happens during S-T segment

Back 28

Represents the period when the ventricles are depolarized and systole occurs

Front 29

What happens during Q-T interval?

Back 29

•Ventricular depol and repol

Front 30

What is PVC?

Back 30

Ventricles contract first before the atria

Single PVCs are normal and pose no harm

No known cause

Front 31

What causes torsades de pointes

Back 31

prolonged QT interval

Front 32

How does hypocalcemia affect the heart and an ECG

Back 32

Can lead to a decrease in HR and BP

As heart fails it will cause ventricular tachycardia

Common signs = prolonged QT interval on ECG

Front 33

S1

Back 33

S1 is heard at the end of the QRS complex as pressure rises in ventricle due to systoliccontraction

Front 34

S2

Back 34

S2 is heard toward the end of the T wave as repolarization of the ventricle completes andventricular pressure falls

Front 35

Preload

Back 35

Degree of stretch prior to contraction

Front 36

Afterload

Back 36

Combination of EDV and arterial resistance

Force used/required to overcome resistance in blood vessels

Front 37

Contractility

Back 37

Intrinsic ability of cardiac muscle cells to contract at any given fiber length

Front 38

Cardiac output

Back 38

CO = Heart rate x Stroke volume

Front 39

Stroke volume

Back 39

Stroke volume = EDV – ESV

Front 40

Frank-Starling law

Back 40

Stroke volume is proportional to EDV

The heart pumps all blood returned to it

Increase venous return = increased preload = increased EDV = increased stroke volume

Front 41

Phase 1: Atrial Systole

Back 41

AV valves open

Semilunar valves closed

Systolic contraction of atria adds final volume to ventricles (end-diastolic volume – EDV)

Front 42

Phase 2: Isovolumetric Contraction

Back 42

All valves closed (first heart sound, S1)

Pressure in ventricles increases with systolic contraction

Front 43

Phase 3: Rapid Ejection

Back 43

Semilunar valves open due to increased ventricular systolic pressure

Front 44

Phase 4: Reduced ejection

Back 44

Ventricles finish systole

Total ejection from phases 3 and 4 is approximately 2/3 of the blood volume in theventricles: stroke volume

Front 45

Phase 5: Isovolumetric Relaxation

Back 45

All valves closed (second heart sound, S2) as pressure in arteries exceeds that of ventricles

1/3 of blood left in ventricles: end-systolic volume (ESV)

Front 46

Phase 6 Rapid ventricular filling

Back 46

AV valves open due to pressure of venous blood

Both atria and ventricles fill with blood

Front 47

Phase 7: Reduced filling

Back 47

AV valves open, cardiac cycle ready to begin again

Front 48

Given to patients with high BP

Back 48

Calcium channel blockers

Front 49

Atrial fibrillation

Back 49

Most common

Can lead to stroke and other complications

Front 50

Ventricular fibrillation

Back 50

Severe, life-threatening condition

Lack of blood flow to brain  unconscious

Defibrillation used to correct

Front 51

Cardiac conduction system

Back 51

Sinoatrial (SA) node

Internodal tracts & Bachmann’s bundle

Atrioventricular (AV) node

AV bundle

Right and left bundle branches

Purkinje fibers

Front 52

Steps of myocardial action potential

Back 52

Depolarization

Voltage-gated Na+ channels open

Na+ influx

Initial Repolarization

K+ channels open – K+ efflux

Na+ channels close

Plateau

AP flattens due to decreases in K+ permeability and increase in Ca2+ permeability

Slow Ca2+ channels open; fast K+ channels close

Rapid Repolarization

Ca2+ channels close; decreasing Ca2+ Slow K+ channels open; increasing K+