Cv 03: Introduction To Ecg

Front 1

What is the resting membrane potential?

Back 1

Negative intracellular electrical potential difference across the plasma membrane (relative to extracellular fluid) varies between -55 and -90 mV

Front 2

What can preserve the resting membrane potential?

Back 2

1) Conc. gradient (or activity) across the plasma membrane for specific permeable ions
2) Relative permeability of plasma membrane for these specific ions
3) Na+/K+ ATPase - electrogenic pump that uses ATP to extrude Na+ and accumulate K+ against their gradient

Front 3

What are the intra and extracellular ion concentrations for Na+?

Back 3

Out: ~145 mM
In: ~10 mM

Front 4

What are the intra and extracellular ion concentrations for K+?

Back 4

Out: ~4.5 mM
In: 120mM

Front 5

What are the intra and extracellular ion concentrations for Ca2+?

Back 5

Out: ~1.0 mM
In: ~0.0001 mM

Front 6

What are the intra and extracellular ion concentrations for Cl-?

Back 6

Out: ~116 mM
In: ~20 mM

Front 7

What do the terms reliability and adaptability refer to for the heart beat?

Back 7

- Reliability - heart manages to beat constantly throughout entire life (hopefully!)
- Adaptability - heart can change rate due to activity/demand

Front 8

Which types of channels are used in a Cardiac AP?

Back 8

- Rapid depolarizing Na+ channels (non-nodal)
- Depolarizing Ca2+ (nodal and myocyte contraction)
- Repolarizing K+ (all myocytes)
- Funny channels (Na+/K+)

Front 9

What are the phases of the ventricular/atrial myocyte and Purkinje fiber action potentials? What ions are important for each phase?

Back 9

0) depolarization via fast Na+ channels
1) slight repolarization by K+
2) plateau phase due to Ca2+
3) repolarization by K+
4) return to resting

Front 10

What are the phases of the SA and AV nodal cell action potentials? What ions are important for each phase?

Back 10

0) depolarization via slow Ca2+ channels
3) repolarization by K+
4) hyperpolarization and return to resting potential by funny channels

Front 11

What is the resting membrane potential in atrial/ventricular myocytes and Purkinje fibers VS SA/AV nodal cells? What is the AP upstroke velocity?

Back 11

- Atrial/Ventricular myocytes and Purkinje fibers: RMP = -80 to -90 mV, AP upstroke velocity >100-500V/sec
- SA/AV nodal cells: RMP = -40 to -70 mV (more depolarized); AP upstroke velocity 1-10V/sec

Front 12

What explains why the myocytes and purkinje fibers have faster upstrokes than the pacemaker (SA/AV nodal) cells?

Back 12

Absence of fast Na+ channels in nodal cells and spontaneous opening of slow Ca2+ channels in pacemaker cells may explain why they have a slower time course and automaticity

Front 13

What is the largest current in the heart?

Back 13

Na+ current

Front 14

How are fast Na+ channels activated/inactivated?

Back 14

- At resting membrane potential channels closed
- Upon depolarization they rapidly activate
- If Vm stays positive, channels start to inactivate
- Some remain activated (or slowly inactivate) during the plateau phase

Front 15

What is the major current spreading through gap junctions? Why?

Back 15

Na+ - this allows the depolarization to spread to neighboring cells

Front 16

What kind of Ca2+ channels are important for SA and AV nodes?

Back 16

L-type Ca2+ channels primaril

Front 17

How are Ca2+ channels activated/inactivated?

Back 17

- Slow depolarization for phase 0 (upstroke) of SA and AV nodes
- Slow spread of depolarization to neighboring cells which contributes to electrical delay between SA and AV nodes
- Channels rapidly activate in atrial and ventricular cells, but slow inactivation (phase 2) which prolongs the plateau
- Ca2+ entry triggers Ca2+ induced Ca2+ release to initiate contraction

Front 18

What are the types of K+ currents?

Back 18

- Early outward K+ current (phase 1) - Ito
- Repolarizing K+ current (phase 3) - rapid (Ik and Ikr-) and slow (Iks-)
- G-protein activated K+ current (SA and AV nodes) - GIRK K+ channels
- K_ATP current - ATP sensitive K+ channels

Front 19

What is the function of the early outward K+ current? When?

Back 19

- Phase 1
- Atrial and ventricular cells activated by depolarization and rapidly inactivates
- Kv4.3 channel (Ito current)

Front 20

What is the function of the repolarizing K+ current? When?

Back 20

- Phase 3
- Two currents underlie (Ik and Ikr-) the rapid component and one undrlies (Iks-) the slow component
- Ik slowly activates, but does not inactivate

Front 21

What is the function of the G-protein activated K+ current? Where?

Back 21

- Outward K+ current mediated by GIRK K+ channels and regulated by ACh
- Prominent in SA and AV nodal cells
- Decreases pacemaker rate and slows conduction through AV Node

Front 22

What is the function of the K_ATP current?

Back 22

ATP sensitive K+ channels play a role in electrically regulating contractile behaviors

Front 23

Which kind of cells have I_f current? What kind of channel gives rise to this current?

Back 23

- Pacemaker current found in SA, AV and Purkinje fibers
- Mediated by a non-selective cation channel = HCN (Hyperpolarization activated Cyclic Nucleotide-gated)
- Conducts both K+ and Na+

Front 24

How are Funny channels (giving rise to I_f current) regulated? Function?

Back 24

- Not activated by depolarization
- Activated by hyperpolarization during phase 3
- Slow activation produces a slow inward depolarizing current and does not inactivate

Front 25

What characteristic divides cardiac cells into slow response cells and fast response cells?

Back 25

Speed of AP upstroke

Front 26

What determines cardiac function?

Back 26

Electrical excitation triggers contraction and determines cardiac function

Front 27

What is the primary intrinsic pacemaker?

Back 27

SA node

Front 28

What takes place at the SA node?

Back 28

- Spontaneous depolarization --> AP
- Fastest intrinsic pacemaker activity, therefore they are dominant
- Normal resting rates: sinus rhythm 60-100 bpm

Front 29

What takes place at the AV node? Location?

Back 29

- Slowly conducting, introduces delay between atrial and ventricular activation
- Located above AV ring, secondary pacemaker

Front 30

What takes place at the His-Purkinje Fibers?

Back 30

- Fibers originate at AV node w/ Bundle of His
- Split to form left bundle branch (conducts to LV) and right bundle branch (conducts to RV)
- Left bundle branch further divides into left anterior fascicle and left posterior fascicle
- Slow intrinsic pacemaker activity, but very rapid conduction

Front 31

What is the sequence of depolarization in cardiac tissue?

Back 31

1. Depolarize atria (starting at SA node--> spread to AV node)
2. Depolarize septum from L-->R
3. Depolarize anteroseptal region of myocardium toward apex
4. Depolarize bulk of ventricular myocardium from endocardium to epicardium
5. Depolarize posterior portion of base of LV

Front 32

What are the conduction velocities through the SA/AV nodes, atria/bundle of His/ventricles, and Purkinje fibers?

Back 32

- SA and AV nodes: ~0.05 m/sec
- Atria, Bundle of His, and Ventricles: ~0.08-1m/sec
- Purkinje fibers: ~5 m/sec (100x faster than SA and AV nodes)

Front 33

How long does it take for the AP to spread through these sites?
- SA node
- AV node
- Bundle of His
- Ant surface of RV
- Apical surface
- Posterior LV

Back 33

- SA node: 0 msec
- AV node: 66 msec
- Bundle of His: 130 msec
- Ant surface of RV: 190 msec
- Apical surface: 220 msec
- Posterior LV: 260 msec

Front 34

How does the amount of time for an AP to spread through the atria and ventricles compare? Why?

Back 34

- Both take ~130 msec for the AP to spread, but disproportionate amount of tissue
- AV node delays propagation in atria
- Purkinje fibers speed up propagation in ventricles

Front 35

Why is it important for the AV node to delay the propagation of the AP through the atria?

Back 35

To allow contraction and complete emptying of the atria

Front 36

Why is it important for the Purkinje fibers to speed up the propagation of the AP through the ventricles?

Back 36

So that there is coordinated contraction of the entire ventricular mass

Front 37

What is the normal PR interval, time between P wave (atrial depolarization) and QRS complex (ventricular depolarization)?

Back 37

0.16 seconds (4 little squares) = Normal
>0.20 seconds (5 little squares) = Prolonged

Front 38

What are 3 mechanisms to slow SA firing rate and pacemaker activity (lowering HR)?

Back 38

1. Decrease steepness of phase 4, thereby increasing time to reach threshold --> diastole is longer --> HR falls
2. Make maximum diastolic potential more negative, starting at a lower Em takes longer to reach threshold
3. Make threshold more positive, takes longer to reach threshold

Front 39

How can you decrease the ventricular rate in atrial flutter or atrial fibrillation without medication? Why is this important?

Back 39

- Valsalva maneuver = forced expiration against closed airway to raise intrathoracic pressure --> opening airway allows pressure to drop leading to a transmural pressure increase in aorta, activating aortic baroreceptors reflex --> activation of vagus nerve (releases ACh)
- OR massage carotid sinus
- The rapid atrial contraction leads to some transmission of APs to AV node that may make ventricles try to contract at a rate that leads to ineffective pumping

Front 40

What is the Valsalva Maneuver? Function?

Back 40

- Forced expiration against closed airway to raise intrathoracic pressure
- Opening airway allows pressure to drop
- Leads to a transmural pressure increase in aorta
- Activates aortic baroreceptors reflex
- Activation of vagus nerve (releases ACh)

Front 41

What is the action of ACh from the Vagus nerve on the heart?

Back 41

- ACh decreases I_f in SA node, reducing the steepness of phase 4
- Opens GIRK channels, increasing K+ to make diastolic potential more negative
- Reduces Ica2+, reducing steepness of phase 4 and moves threshold to a more positive value

*All of these things act to SLOW conduction velocity*

Front 42

What is the action of Norepinephrine on the heart?

Back 42

- From adrenal glands, it acts on beta-adrenergic receptors in SA and AV nodes
- Increases I_f --> increased steepness of phase 4
- Increase Ica2+ --> increased steepness of phase 4 and makes threshold more negative
- No effect on maximum diastolic potential

*All of these things act to QUICKEN conduction velocity*

- On atrial and ventricular cells it has an inotropic effect (increases force of contraction)
- Increases Ica2+ --> more release from SR --> more Ca2+ intracellularly to bind to troponin
- Also enhanced SR pumping by stimulating SERCA Ca2+ pumps

*All of these things act to INCREASE force of contraction*

Front 43

What is the effect of Temperature on the heart?

Back 43

- Increasing body temperature increases SA node firing by increasing the slope of phase 4
- Approx. 10 bpm increase w/ 1 deg. C elevation in temp.
- Cooling has the opposite effect (slows HR)

Front 44

What is the effect of Hyperkalemia on the heart?

Back 44

- Increased extracellular K+ results in depolarization of the membrane potentials of cells
- Depolarization opens some voltage-gated Na+ channels, but also increases the inactivation at the same time
- Since depolarization due to concentration change is slow, it never generates an action potential by itself instead, it results in accommodation
- Above a certain level of K+ the depolarization inactivates Na+ channels, opens K+ channels, thus the cells become refractory
- This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems
- Of most concern is the impairment of cardiac conduction which can result in ventricular fibrillation or asystole

Front 45

How does Hyperkalemia affect the EKG?

Back 45

- Reduction of P wave amplitude
- Widening of PR interval
- Widening of QRS complex
- Decreased force of contraction
- Accelerates repolarization, shortening duration of AP
- Shortens QT interval
*Characteristic tall T wave peaks

Front 46

What is the effect of Hypokalemia on the heart?

Back 46

- Hypokalemia causes hyperpolarization in the myocytes' resting membrane potential
- The more negative membrane potentials in the atrium may cause arrhythmias because of more complete recovery from sodium-channel inactivation, making the triggering of an action potential more likely.
- In addition, the reduced extracellular K+ (paradoxically) inhibits the activity of the IKr potassium current[13] and delays ventricular repolarization
- This delayed repolarization may promote re-entrant arrhythmias

Front 47

How does Hypokalemia affect the EKG?

Back 47

- Slowing of repolarization, prolonging AP duration
- Flattening of T wave or inversion
- Increased amplitude of P wave
- Pronounced U wave
- Prolongation of PR and QT intervals
- Can cause AV block and ventricular fibrillation

Front 48

What is the effect of Hypercalcemia on the heart?

Back 48

- Shortens the ventricular AP duration by shortening phase 2 of AP
- Shortens ST segment and QT interval

Front 49

What is the effect of Hypocalcemia on the heart?

Back 49

- Prolongs phase 2 of AP
- Prolongs ST segment and QT interval

Front 50

What is the effect of Tetrodotoxin (TTX) on the heart?

Back 50

- Blocks voltage-dependent changes in Na+ permeability
- No effect on K+ permeability

- Reduces phase 0 and slope of depolarization

Front 51

What is the effect of Tetraehylammonia (TEA) on the heart?

Back 51

- Blocks voltage-dependent changes in K+ permeability
- No effect on Na+ permeability

- Increases AP duration and extends refractory period (phase 3)

Front 52

What is Tetrodotoxin (TTX) used for?

Back 52

- Slows rate and magnitude of depolarization in non-nodal cells
* Treats tachycardia *
- Extends effective refractory period

Front 53

What is Tetraethylammonia (TEA) used for?

Back 53

- Slows repolarization and extends effective refractory period
- Extends QT interval on ECG

* Helpful in preventing tachyarrhythmias from re-entry mechanism *

Front 54

What is the molecular basis of cardiac arrhythmias?

Back 54

- Reduced K+ conductance
- Decreased Na+ channel inactivation

Front 55

What are calcium channel blockers used for? Mechanism?

Back 55

- Angina
- Hypertension
- Arrhythmias

- Mechanism: decrease entry of Ca2+ and delay depolarization of SA and AV nodes

Front 56

What are beta-blockers used for? Mechanism?

Back 56

- Hypertension (inhibits renin)
- Angina and MI
- Arrhythmias (slows rate of depol)

Mechanism: prevents Ca2+ entry into cell, decreases HR, decreases conduction velocity, decreases strength of contraction

Front 57

What is the length of the absolute refractory period in ventricles and atria? Relative refractory period?

Back 57

- Ventricles: 0.25-0.3 seconds
- Atria: 0.15 seconds

- Relative refractory period: 0.05 seconds

Front 58

How low does the membrane potential need to get before a new AP can be initiated? Why?

Back 58

< -50 mV
(because of inactivation of Na+ channels)

Front 59

What are the limb leads?

Back 59

I, II, III, aVR, aVL, aVF

Front 60

What are the precordial leads?

Back 60

V1-V6 (placed on chest)

Front 61

What do leads record?

Back 61

- Changes in voltage differences between two electrodes over time
- Each record a different angle and plane of the heart

Front 62

What plane do the limb leads assess? What plane do the precordial leads assess?

Back 62

- Limb leads: frontal plane
- Precordial leads: transverse plane

Front 63

What does lead I connect?

Back 63

- Right arm ---> + Left arm

Front 64

What does lead II connect?

Back 64

- Right arm --> + Left leg

Front 65

What does lead III connect?

Back 65

- Left arm --> + Left leg

Front 66

What does lead aVR connect? aVL? aVF?

Back 66

aVR: - Mid heart --> + Right arm
aVL: - Mid heart --> +Left arm
aVF: - Mid heart --> + Left foot

Front 67

How do you measure the heart rate from an EKG?

Back 67

Rate (BPM) = 60 (sec/min) / R-R interval (sec/beat)

Measure number of large boxes forming RR interval:
300, 150, 100, 75, 60, 50 bpm corresponds to intervals of 1, 2, 3, 4, 5, and 6 large boxes

Front 68

What are the mechanisms of arrhythmias?

Back 68

- Increased automaticity
- After-depolarizations
- Re-entry

Front 69

What causes increased automaticity?

Back 69

Decrease in time from depolarization from maximal diastolic potential to threshold potential via:
- Increased slope of phase 4
- Threshold potential is more negative
- Maximum diastolic potential is more positive

Front 70

What is an "after-depolarization"? Cause?

Back 70

- Spontaneous AP during or immediately after phase 3 repolarization
- Caused by abnormal Ca2+ influx during or after phase 3 of ventricular AP leading to premature ventricular contractions and V. Tach.

Front 71

What conditions promote after-depolarizations?

Back 71

Digoxin toxicity and conditions that prolong QT interval

Front 72

What is "re-entry"? Cause?

Back 72

- Re-excitation of a localized region of cardiac tissue by the same impulse, "circus movement"
- Occurs in presence of bifurcating conduction pathways, requiring:
1) unidirectional block
2) slow conduction through retrograde pathway, exceeding refractory period

Front 73

What can cause a unidirectional block and retrograde conduction? What is this called?

Back 73

- Ischemic tissue w/ decremental conduction
- Em is reduced, fast Na+ channels are inactivated, and conduction velocity is slowed
- Leads to unidirectional block
- Can lead to re-entry in ventricular tissue

Front 74

What is the most common mechanism causing supraventricular tachycardia?

Back 74

Re-entry in AV node

Front 75

What are the pathways of the AV node?

Back 75

- Fast pathway: long refractory period and rapid conduction velocity
- Slow pathway: short refractory period and slow conduction velocity

Front 76

What happens in re-entry of the AV node?

Back 76

- Premature atrial contraction may penetrate slow pathway in antegrade direction
- May block antegrade in still-refractory fast pathway
- Upon reaching turn-around point, if fast pathway has recovered from refractory period, impulse penetrates fast pathway in retrograde direction