ECG Basics Flashcards by M W

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

SA Node

Decrease I_f → reduces phase 4 steepness
Opens GIRK → increase IK → more (-) diastolic potential
Decrease I_Ca → reduce phase 4 steepness, raise depolarization threshold

AV Node

Main effect to decrease I_Ca → raise threshold, more difficult for cells to depolarize neighbors

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

On both SA and AV nodes:

Acts on B-adrenergic receptors
Increases I_f → raise phase 4 steepness
Increases I_Ca → raise phase 4 steepness and lower depolarization threshold
No effect on max diastolic potential

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

Inotropic effect

Increase I_Ca → increase Ca influx, Ca-induced-Ca release from SR
Increase sensitivity of RYR
Enhance SRECA pumping in SR
Increases myofilament Ca sensitivity

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

SA/AV nodes → funny channels → automaticity

Atria/ventricles → Na+ channels → fast conduction

Purkinje have all the ion channels

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

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

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

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

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What are the membrane/channel effects of hyperkalemia?

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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What are the signs on EKG of hyperkalemia?

Reduction of P wave amplitude
Wide P-R interval
Wide QRS complex
Shortens Q-T interval
Characteristic tall T-wave peaks

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

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

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

Myocytes → Decreases force of contraction

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

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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Describe the effects of hypocalcemia and hypercalcemia in the heart.

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

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

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

Blocks voltage-dependent K+ channels

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What is the Valsalva maneuver?

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

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

P wave

QRS complex

T wave

PR segment

QT segment

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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What are the phases 0-4 of the AP?

**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 (I_Kr) via hERG→ repolarization, Slow K+ efflux (I_KS) 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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What are the relevant dimensions and units of EKG paper?

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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How is HR measured on EKG?

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

Measure net positive QRS on two leads
Mark magnitude on circle of axes
Draw two perpendicular lines
Connect center of circle with intersection
Estimate axis of new vector

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

Identify lead where the QRS is isoelectric
Identify axis perpendicular to isoelectric lead
Magnitude of QRS net positivity = vector in the perpendicular lead

What are three mechanisms of arrhythmias?

Increased automaticity
Afterdepolarizations
Reentry

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

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

What are afterdepolarizations? What conditions are they associated with?

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)

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?

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 I_Ca responsible for depolarization in phases 0 and 1 is reduced

What is reentry? What causes it?

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.

How does reentry differ in ventricles and atria?

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.

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

PR interval greater than 0.2 sec (5 mm large box) Indicates slowed AV node conduction

What are two types of second-degree AV block?

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)

What is bundle branch block (BBB)?

Conduction block in Purkinje fibers, can be RBB, LBB, or fascicles. Results in slowed, dysynchronous depolarization of ventricles and *less efficient contraction*.

What is third degree AV block?

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

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

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

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

Chaotic, disorganized, rapid atrial activity without full atrial contraction. * Atrial rates \> 400 bpm * Sawtooth EKG baseline * Rapid, irregularly irregular ventricular rate

Describe the progression from ventricular tachycardia to fibrillation

Vtach is ventricular rate \> 100 bpm As rate accelerates, rhythm can become disorganized and chaotic → Vfib → req. emergency countershock

What is the etiology of Torsades de pointes?

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

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Normal Sinus Rhythm

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First-degree AV block

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Second-degree AV block: Mobitz I

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Second-degree AV block: Mobitz II

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Right bundle branch block (RBBB)

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Left bundle branch block

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Third-degree AV block

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Delta Wave - WPW syndrome

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Atrial fibrillation

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Ventricular tachycardia

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Ventricular fibrillation

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

* Voltage-gated Na+ channel → I_Na * Rapid depolarization * L-type Ca²⁺ channel → I_Ca * Depolarizing → nodal AP, myocyte contraction * hERG channel → I_Kr * Rapid repolarizing * KvLQT1 channel → I_Ks * Slow repolarizing * G-protein GIRK channel * ACh regulates in nodes * HCN channel → I_f * Conducts both K+ and Na+

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

SA node → 0 AV node → 66 Bundle of His → 130 Anterior surface of RV → 190 Apical surface → 220 Posterior LV → 260