Pathophysiology and Pharmacology of Arrythmias Flashcards
What are phases 0-4 of cardiac muscle action potential?
0- rapid depolarization due to Na influx
1- Na channels inactivate and there is transient outward K
2- Ca slow acting channels allow Ca to enter the cells, while K moves out (plateau phase)
3- K channels repolarize the cell
4- rest phase (modulated by Na/K pump (2K in and 3 Na out)
Na channels are maintained at the resting state only at the _________ membrane potential present in resting cells (_____mV)
Ath the negative membrane potential Na channels are closed.
Cell resting potential is -85mV which is maintained by Na/K ATPase pump
What channels are responsible for phase O depolarization?
Na channels. As the cell begins to depolarize, local currents cause the membrane potential to raise by a few mV to reach a threshold after which the Na channels rapidly switch from closed to open states.
The Na current in phase 0 depolarization is brief because the channels switch to ______ at membrane potential raises from ________ to _____ mV.
inactive state as the membrane raises from -75 to -55 mV.
When do Na channels switch from inactive to closed/resting state?
once the membrane starts to repolarize during phase 3.
It is inactive throughout the whole plateau phase (phase 2)
What is the switch from inactive Na channels to closed/resting Na channels called?
Recovery- an AP can fire in a region of myocardium where enough Na channels have recovered (switched from inactive to closed/resting).
Which channels are closed at cell resting membrane potential?
Na, K and Ca
The Na/K ATPase pump is at work though
What channels are responsible for the phase 2 plateau of cardiac myocyte AP?
When do the channels open? How fast?
Ca channels- they open as the membrane depolarizes but open at a more + membrane potential than Na channels.
They open fairly quickly (but slower than Na) and inactivate slowly so the channels are open for a long time
When do Ca channels switch from inactive back to resting/closed state?
During phase 3 depolarization
What channels play the largest role in impulse conduction at the SA and AV nodes?
Ca channels
What channels are responsible for phase 3 depolarization? When do they open?
K delayed-rectifiers are responsible for phase 3 depolarization. They open slowly during phase 2 and more from inside the cell to outside of the cell causing repolarization.
They do NOT inactivate but return to resting/closed state as the membrane nears resting potential (-85mV)
Which type of channels have inactive states? Which channels go directly to resting/closed?
K= directly to resting/closed
Na, Ca= inactive states
What is threshold?
What is the most important factor that determines the “threshold potential”?
What is the effect of antiarrhythmic drugs on AP?
The amount of depolarization necessary to elicit an AP. It is an all-or-none process.
The number of available channels determines the threshold potential. This is why antiarrhythmic drugs block Na or Ca channels. Fewer channels are available so the depolarization needed to induce an AP increases.
What is the effective refractory period?
What cell membrane potential usually has enough channels recovered to fire another AP?
Once cardiac tissue has been depolarized, the cells cannot excite again until they have recovered from inactivation.
Minimum # of channels must be available before an AP can be generated (threshold). This usually occurs at about -50mV
What are the two main forms of abnormal impulse generation?
- enhanced automaticity- increased spontaneous firing from normal pacemaker tissue (SA, AV) or from ectopic sites (atrial myocytes, ventricular myocyte)
- triggered activity- occur after a depolarization which triggers them. Early after-depolarization and delayed after-depolarization are the 2 types .
What is the mechanism by which delayed afterdepolarization (triggered activity) occurs?
What are the major causes?
What phase of depolarization do they occur in?
They occur in phase 4 depolarization and are associated with Ca overload (digoxin toxicity or metabolically stressed cells).
SR becomes overloaded with Ca and leaks it immediately following repolarization.
Na/Ca exchanger pumps excess Ca out in exchange for Na influx which can generate depolarization. If threshold is reached, another AP can fire.
How does a reentry pathway excite the rest of the heart (instead of just the myocytes in its path?
They send off daughter impulses that spread to the rest of the heart.
What is the difference between an anatomically defined reentry circuit and a functionally defined reentry circuit?
Give examples.
Anatomically defined reentry is when the conduction circles around an electrical dead spot. An example would be conduction around the tricuspid valve or an accessory pathway.
Functionally defined reentry is when the interior of the pathway is constantly depolarized by the daughter impulses of the reentry circuit CREATING an electrical dead spot