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Cardiovascular > ECG Basics > Flashcards

ECG Basics Flashcards

1
Q

What are the effects of ACh from the vagus nerve on SA and AV nodes?

A

SA Node

  1. Decrease If → reduces phase 4 steepness
  2. Opens GIRK → increase IK → more (-) diastolic potential
  3. Decrease ICa → reduce phase 4 steepness, raise depolarization threshold

AV Node

  1. Main effect to decrease ICa → raise threshold, more difficult for cells to depolarize neighbors
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2
Q

What are the effects of NE from sympathetic nerves on the SA and AV nodes?

A

On both SA and AV nodes:

  1. Acts on B-adrenergic receptors
  2. Increases If → raise phase 4 steepness
  3. Increases ICa → raise phase 4 steepness and lower depolarization threshold
  4. No effect on max diastolic potential
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3
Q

What are the effects of NE from sympathetic nerves on atrial and ventricular cells?

A

Inotropic effect

  1. Increase ICa → increase Ca influx, Ca-induced-Ca release from SR
  2. Increase sensitivity of RYR
  3. Enhance SRECA pumping in SR
  4. Increases myofilament Ca sensitivity
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4
Q

How do the SA and AV nodes differ from atrial, ventricular, and Purkinje cells in their ion channels?

A

SA/AV nodes → funny channels → automaticity

Atria/ventricles → Na+ channels → fast conduction

Purkinje have all the ion channels

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5
Q

What effect does a higher body temp have on the SA node?

A

Increases SA node firing by increasing slope of phase 4, 1°C → +10 beats/min

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6
Q

What effect does cooler body temp have on the SA node?

A

Reduces SA node firing by decreasing slope of phase 4, 1°C → -10 beats/min

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7
Q

What are the membrane/channel effects of hyperkalemia?

A

Increased extracellular K+ levels result in depolarization of the membrane potentials of cells due to the increase in the equilibrium potential of K+.

This 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.

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8
Q

What are the signs on EKG of hyperkalemia?

A
  1. Reduction of P wave amplitude
  2. Wide P-R interval
  3. Wide QRS complex
  4. Shortens Q-T interval
  5. Characteristic tall T-wave peaks

Severe → disappearance of P wave, AV nodal bock, Vfib

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9
Q

What are the effects of hyperkalemia on action potential and myocyte contraction?

A

AP → slows rate of rise and amplitude, shortens duration by accelerating repolarization

Myocytes → Decreases force of contraction

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10
Q

What are the effects of hypokalemia on cell membrane, AP, and EKG?

A

Hyperpolarizes resting membrane potential

Slows repolarization → prolongs AP duration

Flattens T wave, prolongs PR and QT intervals

Severe → AV block and Vfib

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11
Q

Describe the effects of hypocalcemia and hypercalcemia in the heart.

A

Primarily affect myocardial AP

Hypercalcemia: shortens AP phase 2 → shortens ST segment and Q-T interval, widens T wave

(think of Ca2+ entry acting on myofilaments to increase speed of contraction, shortening QT and the plateau phase)

Hypocalcemia: prolongs phase 2 → prolongs ST segment and Q-T interval

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12
Q

What effect does Tetrodotoxin (TTX) have on the heart?

A

Blocks voltage-dependent Na+ channels, preventing development of APs

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13
Q

What effect does tetraethylammonium (TEA) have on the heart?

A

Blocks voltage-dependent K+ channels

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14
Q

What is the Valsalva maneuver?

A

Forced expiration against a closed airway.

Increased intrathoracic pressure impedes venous return to the heart → decreases CO and aortic pressure → increased HR due to baroreceptor-mediated sympathetics

This first phase is followed by opening of the airway → increased venous return to the heart → increase CO → increased aortic pressure → slowed HR due to baroreceptor stimulation of vagus

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15
Q

What does it mean if a cell is refractory? What are the refractory periods of the atria and ventricles?

A

Membrane potential is not sufficiently negative enough to initiate the next AP, must be below -50mV for Na+ channels to transition from inactivated → resting

Absolute refractory period

  • Ventricles → 0.25-0.3 sec
  • Atria → 0.15 sec

Relative refractory period → ARP + 0.05 sec

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16
Q

What part of the cardiac cycle does each EKG segment correspond to?

P wave

QRS complex

T wave

PR segment

QT segment

A

P wave → Atrial depolarization

Q wave → septal depolarization

R wave → bulk ventricular depolarization

S wave → upper LV depolarization

T wave → ventricular repolarization

PR → AV node conduction

QT → ventricular depolarization and repolarization

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17
Q

What are the phases 0-4 of the AP?

A

**Phase 0: **Na+ influx through fast Na+ channel (Ca2+ influx in pacemaker cells, Na+ channels inactivated)

**Phase 1: **Transient repolarization from K+ efflux

**Phase 2: **Equilibrium of Ca2+ influx and K+ efflux

Phase 3: **Rapid K+ efflux (IKr) via hERG→ repolarization, Slow K+ efflux (IKS) via KCNO1 → repolarization

Phase 4: Restored ionic balance, return to resting potential (slow depolarization via Na+/K+ influx in pacemaker cells, funny current)

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18
Q

What are the relevant dimensions and units of EKG paper?

A

EKG paper → 1x1 mm square, 5x5 mm boxes

Vertical axis → 0.1mV/mm

Horizontal axis → 0.04 sec/mm, 0.2 sec/5mm

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19
Q

How is HR measured on EKG?

A

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

ex. 60 / (3 large boxes = 0.6 sec/beat) = 100 bpm

R-R interval of 1-6 large boxes corresponds to:

  • 300-150-100-75-60-50 (bpm)
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20
Q

What is the geometric method for estimating EKG axis in the frontal plane?

A
  1. Measure net positive QRS on two leads
  2. Mark magnitude on circle of axes
  3. Draw two perpendicular lines
  4. Connect center of circle with intersection
  5. Estimate axis of new vector
21
Q

What is the inspection metod of estimating EKG axis in the frontal plane?

A
  1. Identify lead where the QRS is isoelectric
  2. Identify axis perpendicular to isoelectric lead
  3. Magnitude of QRS net positivity = vector in the perpendicular lead
22
Q

What are three mechanisms of arrhythmias?

A
  1. Increased automaticity
  2. Afterdepolarizations
  3. Reentry
23
Q

What factors increase automaticity? What conditions is it associated with?

A

Increased with shortened time from maximum diastolic potential to threshold potential→ increased phase 4 slope, more negative TP, more positive MDP

Observed with electrolyte abnormalities, hypoxia, sympathetic stimulation

24
Q

What are afterdepolarizations? What conditions are they associated with?

A

Spontaneous APs during or immediately following phase 3 repolarization

Caused by abnormal phase 3 Ca2+ influx → premature ventricular contraction → Vtach

Observed in digoxin toxicity, conditions that prolong Q-T interval (ex. quinidine therapy)

25
Q

What are the effects of increased intracellular Ca2+ on AP phases in SA and AV nodes? What is an example of a drug that works through this mechanism?

A

Digoxin - Prolong phase 0 and phase 1, slowing HR, Increases contractility of the heart

  1. Digoxin inhibits Na/K ATPase
  2. Inward Na gradient reduced
  3. Driving force for Na/Ca exchange reduced
  4. Ca2+ accumulates intracellularly
  5. Inward ICa responsible for depolarization in phases 0 and 1 is reduced
26
Q

What is reentry? What causes it?

A

Reexcitation of a localized region of cardiac tissue by the same impulse.

Bifurcation of a conduction pathway, requires unidirectional block and slow conduction through retrograde pathway so that by the time the anterograde pathway is recovered, it can be depolarized by the retrograde current.

27
Q

How does reentry differ in ventricles and atria?

A

Ventricular reentry → ischemia and hypoxia inactivate fast Na+ channels and slow conduction velocity producing unidirectional block

Atrial reentry → MC cause of supraventricular tachycardia (SVT). AV node has two pathways, premature contraction may penetrate slow pathway but be blocked by fast pathway (still refractory).

In either case, antegrade currenty can become retrograde and penetrate initial pathway if it is no longer refractory.

28
Q

What is a first-degree AV block? What does it indicate?

A

PR interval greater than 0.2 sec (5 mm large box)

Indicates slowed AV node conduction

29
Q

What are two types of second-degree AV block?

A

AVB Mobitz I (Wenkebach) → PR gradually lengthens until AV node fails for one beat, no QRS

AVB Mobitz II → PR is constant for at least 2 conducted beats, intermittent dropped beats in ratio of 3:1 (2:1 can be Mobitz I or II)

30
Q

What is bundle branch block (BBB)?

A

Conduction block in Purkinje fibers, can be RBB, LBB, or fascicles.

Results in slowed, dysynchronous depolarization of ventricles and less efficient contraction.

31
Q

What is third degree AV block?

A

Atria and ventricles are electrically disconnected, beat independently from one another.

See an atrial focus-driven rate for P waves, ventricular focus-driven rate for QRS complex

32
Q

What is WPW syndrome? What findings does it produce on EKG?

A

Wolff-Parkinson-White

Congenital abnormality → accessory pathway between atria and ventricles with no delay

  • Short PR (no AV node delay)
  • Delta wave → deflection at QRS onset (eccentric ventricular activation)
  • If both AV node and accessory pathway are functional, can have reentrant loops resulting in SVT
33
Q

What is atrial fibrillation? How does it present on EKG?

A

Chaotic, disorganized, rapid atrial activity without full atrial contraction.

  • Atrial rates > 400 bpm
  • Sawtooth EKG baseline
  • Rapid, irregularly irregular ventricular rate
34
Q

Describe the progression from ventricular tachycardia to fibrillation

A

Vtach is ventricular rate > 100 bpm

As rate accelerates, rhythm can become disorganized and chaotic → Vfib → req. emergency countershock

35
Q

What is the etiology of Torsades de pointes?

A

Congenital or acquired QT prolongation

Predisposes to polymorphic ventricular tachycardia

Change of morphology and axis from beat-to-beat, QRS complexes appear to twist around baseline

Life-threatening emergent situation

36
Q

Name the EKG finding

A

Normal Sinus Rhythm

37
Q

Name the EKG finding

A

First-degree AV block

38
Q

Name the EKG finding

A

Second-degree AV block: Mobitz I

39
Q

Name the EKG finding

A

Second-degree AV block: Mobitz II

40
Q

Name the EKG finding

A

Right bundle branch block (RBBB)

41
Q

Name the EKG finding

A

Left bundle branch block

42
Q

Name the EKG finding

A

Third-degree AV block

43
Q

Name the EKG finding

A

Delta Wave - WPW syndrome

44
Q

Name the EKG finding

A

Atrial fibrillation

45
Q

Name the EKG finding

A

Ventricular tachycardia

46
Q

Name the EKG finding

A

Ventricular fibrillation

47
Q

What are the major myocyte ion channels? What kinds of current does each conduct?

A
  • Voltage-gated Na+ channel → INa
    • Rapid depolarization
  • L-type Ca2+ channel → ICa
    • Depolarizing → nodal AP, myocyte contraction
  • hERG channel → IKr
    • Rapid repolarizing
  • KvLQT1 channel → IKs
    • Slow repolarizing
  • G-protein GIRK channel
    • ACh regulates in nodes
  • HCN channel → If
    • Conducts both K+ and Na+
48
Q

What are the impulse propagation times starting from the SA node (msec)?

A

SA node → 0

AV node → 66

Bundle of His → 130

Anterior surface of RV → 190

Apical surface → 220

Posterior LV → 260

Cardiovascular (2 decks)

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