Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
57 Cards in this Set
- Front
- Back
Normal sinus rhythm: defn
|
1) Originates in SA node
2) HR is 60-100 bpm and regular 3) Excitation occurs in normal sequence and with normal timing |
|
Normal sequence of cardiac activation
|
1) SA Node
2) Atria (R then L) 3) AV Node (with AV delay) 4) His-Purkinje system 5) Ventricles |
|
The endocardium is depolarized (before, after) the epicardium
|
Before
|
|
The endocardium is repolarized (before, after) the epicardium
|
After
|
|
An increase in HR causes an (increase, decrease) in APD.
|
Decrease. (also vice versa)
|
|
Why does prolongation of AP duration favor dysrhythmias?
|
Due to early afterdepolarizations
|
|
Where are Ca2+ channels responsible for the upstroke (phase 0)?
|
SA node, AV node.
Note that I<sub>Ca</sub> in these areas is much smaller in amplitude than I<sub>Na</sub> in atria, ventricles, or Purkinje system. |
|
How does increase K+ or Ca2+ affect AP duration and Effective refractory period?
|
Shortens AP duration and ERP
|
|
Why does increase K+ or Ca2+ Shorten AP duration and ERP?
|
Causes increased K+ conductance and therefore increased K+ efflux during phase 2 and 3, which acts to decrease APD
|
|
What does increased serum/extracellular K+ due to the membrane potential?
|
Depolarizes Em
|
|
Why does elevated interstitial K+ during ischemia slow conduction?
|
It causes Na+ channels to inactivate, reducing dV/dt
|
|
Why do small increases in serum K+ increase conduction velocity?
|
Bring the cell closer to threshold potential.
|
|
Automaticity: defn
|
Intrinsic ability of specialized cells to spontaneously depolarize and initiate action potential.
|
|
What is termed a "membrane stabilizer"?
|
Ca2+
|
|
Why is Ca2+ termed a "membrane stabilizer"?
|
Hypercalcemia makes it more difficult for membrane depolarization to open Na+ channels.
If this is the case, the myocyte must further depolarize to open a sufficient number of Na+ channels to generate an AP. This means threshold potential shifts positive. |
|
Increased serum Ca2+ (reduces, increases) excitability. Why?
|
Reduces. Threshold potential is shifted positively.
Vice versa is also true. |
|
How does K+ affect threshold potential and excitability?
|
it alters Em. Depolarization causes inactivates of Na+ channels, and with fewer Na+ channels, the cell must further depolarize to open a sufficient number, threshold potential shifts positively. Excitability is reduced.
|
|
T/F Ectopic, latent, and subsidiary pacemakers include the AVN and His-Purkinje system.
|
T
|
|
What is the affect of increasing the rate of diastolic (Phase 4) depolarization?
|
Increasing phase 4 depolarization brings the cell to threshold potential faster, and thus increases the HR.
|
|
what is the affect of shifting threshold potential closer to maximum diastolic potential?
|
Shifting threshold potential closer to maximum diastolic potential makes it easier to generate an AP (requires less positive charge), thus increasing the spontaneous rate of firing.
|
|
what is the affect of shifting maximum diastolic potential lower?
|
Makes it harder for the cell to reach threshold potential and fire an AP, slows HR.
|
|
Catecholamines (Increase, Decrease) Normal Automaticity
|
Increase
|
|
β1 receptor activation (Increases, Decreases) Normal Automaticity
|
increases
|
|
Hyperkalemia and hypercalcemia (Increases, Decreases) Normal Automaticity
|
decreases
|
|
Anti-dysrhythmic drugs (Increases, Decreases) Normal Automaticity
|
decreases
|
|
What are early afterdepolarizations?
|
Oscillations of membrane potential that arise during the plateau phase (2) or in phase 3.
|
|
What are delayed afterdepolarizations?
|
Oscillations of membrane potential that arise during diastole (Phase 4)
|
|
What initiates early afterdepolarizations? (EADs)
|
Enhancing I<sub>Na</sub> or I<sub>Ca</sub>, depressing I<sub>K</sub>. In some cases, the depolarization reaches threshold potential and fires an AP.
|
|
How does prolongation of AP duration (eg, in Long QT syndrome) favor early afterdepolarizations? (EADs)
|
Allows more time for recovery of both the Calcium current and the Sodium current.
|
|
What initiates delayed afterdepolarizations? (DADs)
|
Spontaneous release of Ca from overloaded sarcoplasmic reticulum. This increase in [Ca] causes both an after-contraction and a transient depolarization that sometimes reaches threshold and fires an AP.
|
|
What is triggered activity and why is it called this?
|
Abnormal automaticity (the DADs and EADs) because the oscillation is triggered by the preceding AP.
|
|
What type of afterdepolarization does increased heart rate favor?
|
DADs - enhances Ca2+ influx and the SR to become overloaded with Ca2+.
|
|
What are boundary currents?
|
normal cells depolarized by surrounding disease cells that aren't repolarizing normally.
|
|
____ are commonly caused by drug-induced
block of K currents or enhancement of Ca or Na current |
EADs
|
|
The sodium current is much (less than, greater than) the calcium current.
|
Greater than.
|
|
What are the 2 main determinants of conduction velocity?
|
1) Size of the inward current (either Na or Ca, depending on the site).
2) Passive properties: membrane resistance, capacitance, cell to cell resistance. |
|
Why does ischemia slow conduction velocity?
|
Cell-to-cell resistance is increased by elevated [Ca2+] and intracellular acidosis during ischemia.
In the extreme case, cells become electrically uncoupled and can't communicate with the rest of the heart. |
|
Reflects the amount of current required to initiate an AP
|
Excitability.
|
|
If recovery of excitability is delayed, what happens to the effective refractory period and relative refractory period?
|
They're prolonged.
|
|
Why is a recovery period at a more negative potential required following depolarization?
|
To reprime G<sub>Na</sub> and enable channels to again open on depolarization. Channels move from inactivated to closed state.
|
|
dV/dt: defn
|
rate of rise of the upstroke of the action potential
|
|
dV/dt is roughly proportional to what?
|
I<sub>Na</sub>
|
|
As membrane potential gets more negative, max dV/dt (increases, decreases).
|
Increases
|
|
How do Disease & Antidysrhythmic Agents affect the responsiveness relationship between max dV/dt and membrane potential?
|
They lower it, making it so that max dV/dt is less than normal at the same membrane potential.
|
|
Time when Action potential cannot be elicited
|
Absolute refractory period
|
|
Can elicit AP.
Increased current required. Conduction slow or fails. |
relative refractory period.
|
|
Time when Cannot elicit conducted AP.
|
effective refractory period
|
|
How does effective refractory period (ERP) change with increasing HR?
|
Shortens
|
|
Where are the longest AP duration and ERP?
|
Terminal purkinje fibers
|
|
conduction defect that results in impulse formation
|
reentry, reentrant excitation or circus movement
|
|
What happens in Reentry?
|
The impulse is initially blocked at some location, travels slowly over an alternate route, excites tissue distal to the block, and then can re-excite the same tissue one or more times.
|
|
What are the requirements for a reentrant circuit?
|
1) Unidirectional block
2) Functional loop in the conduction pathway 3) Total conduction time around the loop must exceed ERP of tissue proximal to the region of block. |
|
Therapeutic Approaches to Terminate Reentry: Depression of conduction. What happens?
|
Convert unidirectional block to bidirectional block
|
|
Therapeutic Approaches to Terminate Reentry: Improve conduction. What happens?
|
Convert unidirectional block to a region of slow conduction.
The APs collide and terminate excitation. |
|
Therapeutic Approaches to Terminate Reentry: Slow conduction. What happens?
|
Next sinus beat interrupts the reentry process.
|
|
What is the "slow response?"
|
When depolarized atria, ventricles, and Purkinje fibers generate an AP based on Ca2+ channels.
|
|
Characteristics of the slow response
|
Slow maximum upstroke velocity
Conducts very slowly responds to Ca channel blockers instead of Na channel blockers (because it's based on a calcium current). |