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72 Cards in this Set
- Front
- Back
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What are the conducting cells?
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SA and AV node cells; atrial internodal tracts, bundle of His and Purkinje system cells
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What are contractile cells?
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Bulk of cardiac wall; interconnected through gap junctions
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What is the SA node?
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The source of the initial electrical impulse and accounts for "normal" sinus rhythm
The pacemaker of the heart |
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What is overdrive suppression?
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The SA node preempts and thus suppresses all other conducting cells from spontaneously firing
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What effect does forcing a cell to depolarize more often than its intrinsic discharge rate have on automaticity?
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Decreases automaticity
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What causes depolarization of the right and left atrium?
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The depolarizing wave from the SA node spreading to the internodal/interatrial fibers
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Why can't electrical impulses freely pass from the atria to the ventricles?
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B/c the annulus fibrosis blocks their propagation
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What is the only way the depolarizing wave can reach the ventricles?
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By passing through the AV node on the atrial side of the annulus fibrosus
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What is the importance of the electrical delay that is caused by forcing the depolarization wave to pass through the AV node?
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Permits atrial contraction before ventricular contraction begins, optimizing ventricular filling time
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What region of the heart does the depolarization wave enter after leaving the AV node?
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The bundle of His
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What allows the electrical stimulus to pass from the atrium to the ventricle by penetrating the annulus fibrosus?
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The bundle of His
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What does the depolarization wave enter after leaving the bundle of his?
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the Purkinje fibers
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Where in the heart is conduction slowest? fastest?
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Slowest in the AV node
Fastest through the Purkinje fibers |
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What is automaticity?
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The ability of a cell to generate its own action potential
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What is rhythmicity?
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The ability to generate these potentials in a regular repetitive manner
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What structure allows the heart to behave as a functional syncytium? (as if it were one large cell)
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Gap junctions
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Where does the fast response action potential occur?
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In normal atrial and ventricular cardiomyocytes and specialized conducting fibers (Purkinje fibers)
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Where does the slow response action potential occur?
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SA and AV nodes
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What is phase zero of the cardiac AP? what channels open? what ions move?
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"fast upstroke"
Nav channels open! Leading to an influx of Calcium |
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What is phase 1 of the cardiac AP? what channels open/close? what ions move?
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"partial repolarization"
Nav channels inactivate, rapid opening and closing of Kv channels. Initial efflux of K+ out of the cell accounts for partial repolarization |
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What accounts for the partial repolarization in a cardiac AP after phase 0?
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Opening of Kv channels
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What is phase 2 of the cardiac AP? what channels open/close? what ions move?
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"plateau"
Results from opening of Cav channels, allowing influx of Ca, counterbalanced by slow efflux of K through Kv channels |
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What is phase 3 of the cardiac AP? what channels open/close? what ions move?
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"repolarization"
Due to inactivation of Cav channels and efflux of K via Kv channels |
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What corrects the excess Na inside the cell, and excess K outside the cell?
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The Na/K ATPase
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What is phase 4 of the cardiac AP? what channels open/close? what ions move?
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"resting membrane potential"
Characterized by background Na influx and K efflux through K leak channels (Kir channels) |
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What precedes phase 0 of the cardiac AP?
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A suprathreshold stimulus from a pacemaker cell that abruptly changes the resting membrane potential to a critical threshold value ~-65mV
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What gates control Na influx?
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The activation gate which is closed at rest but opens w/ depolarization
The inactivation gate which is open at rest but has a delayed closure from depolarization |
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Do Ca channels only open on phase 2 of the cardiac AP?
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No a small Ca influx begins at ~-50mV as a result of cell depolarization
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What is the purpose of the fast-response AP in atrial and ventricular cardiac muscle?
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AP leads to calcium influx and contraction of cardiac muscle cells
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What is the sequence of excitation-contraction coupling?
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Calcium enters cell => Ca binds to troponin C => Troponin C interacts w/ tropomyosin => tropomyosin shifts exposing the actin and myosin active sites => cross-bridge cycling => contraction
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What happens if K efflux exceeds Ca influx during phase 2 of the cardiac AP?
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Plateau duration will be short and final repolarization begins early
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What is the importance of L-type Ca channels?
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Ca channels are voltage-regulated time-dependent channels that activate and inactivate slowly making a current that is long lasting
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What is the effective refractory period?
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Similar to absolute refractory period in nerve/skeletal muscle; cell will not respond to any electrical stimulus
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What is the relative refractory period?
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SOME sodium channels are excitable (inactivation gates have opened) allowing a large electrical stimulus to produce an AP but a smaller one than usual
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What is the importance of the "refractoriness" of the heart?
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Provides the heart w/ a measure of electrical safety b/c it prevents extraneous pacemakers from triggering ectopic beats
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What phase of the cardiac AP is responsible for the diastolic potential or pacemaker potential of the cardiac cell?
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phase 4
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What ions are moving during phase 4 of the cardiac AP?
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1. Decreasing potassium efflux: due to inactivation of Kv channels
2. Increasing sodium influx: Sodium enters cell through HCN cation channel 3. Spontaneous local Ca release from the SRER 4. Increased Ca influx as membrane passes -50mV |
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What is the effect of a combined increase in sodium influx and a decrease in potassium efflux?
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A gradual depolarization of the membrane during phase 4 of the AP
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What phase of the cardiac AP does the HCN channel open at?
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early phase 4
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What channel opens at -50mV of the cardiac AP?
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L-type Calcium channels
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What channels contribute to the upstroke of phase 0 of the SA AP?
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L-type Ca channels
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Why is the upstroke in the SA AP slower than the normal upstroke?
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B/c the inward current source is calcium
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What channel do SA and AV node cell membranes lack?
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fast-response voltage-gated sodium channels
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What will diminish the slow of phase zero and amplitude of the AP?
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Low extracellular calcium or presence of calcium channel antagonists
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What are the differences b/e the slow and fast response APs?
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1. unstable phase 4 (early and late diastolic phase)
2. slower upstroke in phase 0 b/c inward ion is Ca 3. Absent phase 1: no early repolarization 4. Absent phase 2: no plateau due to early activation of Kv channels => early repolarization leading to an AP of shorter duration |
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Why is there no plateau in slow response APs?
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B/c of early activation of Kv channels
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What effect does binding of epinephrine/norepinephrine to beta-1 adrenergic receptors have?
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Increases the heart rate by activating adenylyl cyclase and increasing intracellular [cAMP]
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What does cAMP do?
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Phosphorylates cAMP dependent protein kinase which phosphorylates HCN and voltage-gated calcium channels, increasing their "open probability"
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What is the effect of phosphorylation of HCN and Cav channels?
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1. Increases sodium influx through HCN channels (I-f), increasing the steepness of the phase 4 pacemaker potential
2. Increases Calcium influx through Cav channels, which steepens phase 4 pacemaker potential |
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What is the effect of ACh binding to M2 cholinergic receptors?
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Decreases HR by inhibiting adenylyl cyclase/cAMP
1. Decreased sodium influx through HCN channels, which reduces steepness of phase 4 2. Decreased calcium influx through voltage-gated Ca channels |
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What opens the GIRK channel?
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ACh opens the G-protein activated inwardly rectifying potassium channel
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What effect does opening of the GIRK channel have?
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Increases potassium efflux during phase 3 and 4 of the AP => hyperpolarization of phase 4 pacemaker potential => increases time required to reach threshold
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What are the two effects of catecholamine stimulation of beta-1 adrenergic receptors on fast-response APs?
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1. Inotropic effect
2. Lusitropic effect |
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What is the inotropic effect of catecholamine stimulation of beta-1 adrenergic receptors?
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"increased cardiac contractility"
1. Increased calcium influx through L-type Cav channels (greater CICR) 2. Increased sensitivity of SR calcium release channels to cytoplasmic calcium -> more calcium is released by the SR making more Ca available for binding of troponin 3. Enhanced SR Ca ATPase activity => increased Calcium stores for later release |
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What is the lusitropic effect of catecholamine stimulation of beta-1 adrenergic receptors?
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"Accelerated speed of ventricular and atrial muscle relaxation"
1. cAMP and PKA phosphorylate (inhibit) phospholambam 2. PKA phosphorylates Troponin I, destabilizing actin-myosin cross-bridges |
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What is the function of phospholambam?
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Inhibits SR Ca ATPase, the SR pump that returns Ca back into SR
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What is the effect of phosphorylation of phospholambam?
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Removes the inhibitory effects of phospholambam => pumping activity of SR Ca ATPase increases => Ca removed from intracellular space more rapidly => this accelerates the speed of cardiac muscle relaxation
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What are the effects of beta-1 adrenergic receptor activation in the SA and AV node? atrial muscle? ventricular muscle?
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SA/AV node: inc. conduction velocity, inc. pacemaker rate
Atrial muscle: inc. contractility Ventricular muscle: inc. contractility |
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What is the effect of M2, cholinergic, receptor activation on the SA and AV node? Atrial muscle? Ventricular muscle?
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SA/AV node: dec. conduction velocity, dec. pacemaker rate
Atrial muscle: little effect Ventricular muscle: little effect |
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What causes the P wave of the EKG? how long does it last?
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Caused by sequential activation (depolarization) of the right and left atria; lasts ~0.08s
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What is the PR interval of the EKG?
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The time from the beginning of the P wave to the start of the QRS complex, represents the amount of time the AP takes to travel from the SA node to the AV node
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How will an inhibition of conduction through the AV node be reflected in a EKG?
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A lengthening of the PR interval
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Why is atrial repolarization not seen on an EKG?
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B/c atrial repolarization is too slow and too diffused to register
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Why is SA and AV node depolarization not seen on an EKG?
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B/c of decreased nodal mass
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What causes the QRS complex? how long does it last?
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Right and left ventricular depolarization, ~0.1s or less
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How will a longer QRS complex be reflected in the EKG?
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By a longer QRS complex
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What is the ST segment? what causes it?
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An isoelectric segment that coincides w/ the plateau of the fast response ventricular AP and the rapid ejection phase of the cardiac cycle
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Why is the ST segment isoelectric?
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B/c the ventricles are uniformly depolarized
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If a part of the myocardium is damaged how will that be reflected in an EKG?
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A shift on the level of the ST segment
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What does the T wave mark? why is it upright?
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Ventricular repolarization
Upright b/c repolarization occurs in reverse sequence to depolarization |
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What is the QT interval?
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The duration of ventricular depolarization and repolarization
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What happens to the QT interval if ventricular repolarization is delayed?
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The QT interval is prolonged
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