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77 Cards in this Set

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Ventricular AP:
Phase 4
*RMP (-85mV)
*IR-K+ open, K+ exits cell
Ventricular AP:
Phase 0
*rapid depolarization
*V-Na+ channels open, Na+ rushes into cell
*IR-K+ channels close
*triggered by AP from neighboring cell which opens enough V-Na+ to reach threshold (-65mV)
Ventricular AP:
Phase 1
*partial repolarization
*V-Na+ channels are inactivated
*I-to channels open, K+ exits cell
*VOCC begin to open and allow an influx of Ca++
Ventricular AP:
Phase 2
*plateau
*I-to channels open, K+ exits
*VOCC open, Ca++ enters and triggers contraction
*Em = 0mV
*I-to channels begin to close
*DR-K+ channels begin to open
*VOCC begin to close
Ventricular AP:
Phase 3
*repolarization
*Ca++ channels mostly inactivated
*DR-K+ channels open, K+ enters cell
Ventricular AP:
Phase 4 (transition)
*transition to rest
*DR-K+ channels close
*IR-K+ channels open, K+ exits cell
*V-Na+ and VOCC recover from inactivation
Ventricular AP:
Absolute refractory period
*lasts from onset of rapid depolarization (phase 0) to midpoint of repolarization (phase 3)
*a new AP cannot be triggered
*V-Na+ are either all open or inactivated
*VOCC either all open or inactivated
Ventricular AP:
Relative refractory period
*lasts from midpoint of repolarization (phase 3) to RMP (phase 4)
*a new AP can be triggered with a larger stimulus
*V-Na+ still inactivated
*enough VOCC have recovered to allow a slow Ca-mediated AP to take place
SA node AP:
Phase 4
*Slow, spontaneous depolarization
*few IR-K+ channels (GIR-K+)
*DR-K+ channels closed
*I-f channels allow Na+ and K+ to cross membrane
*some VOCC open
*Na+ and Ca++ cause slow depol.
SA node AP:
Phase 0
*depolarization
*once threshold (-55mV) is reached, all VOCC open
*Ca++ mediated AP is much slower
SA node AP:
MDP
*maximum diastolic potential
*the lowest Em attained by repolarization
* -60 - -70mV
How is conduction delayed at the AV node?
*slow Ca-mediated depolarization
*fewer gap junctions between cells
What sets the ARP in ventricular myocytes?
It is determined by the rate of DR-K+ activation and VOCC inactivation.
What sets the RRP in ventricular myocytes?
The beginning of the RRP is determined by the rate at which VOCC a recover from inactivation. The end is determined by the rate of V-Na+ recovery from inactivation.
Why are V-Na+ non-functional in the SA and AV nodes?
Em is never repolarized enough to permit recovery from inactivation.
What sets the threshold at the SA node?
VOCC
Would VOCC blockers affect conduction at the AV node?
Yes - b/c VOCC are responsible for depolarization at the AV node. Blockage of VOCC would increase RRP and thus delay conduction.
T/F:
Na+ channels and Ca++ channels are responsible for Phase 0 in SA node cells.
False: only VOCC
T/F:
DR-K+ are responsible for the large negative RMP in ventricular myocytes.
False: IR-K+ set RMP.
T/F:
I-f channels are partially responsible for the slow depolarization in phase 4 at the SA node.
True: paucity of IR-K+, closing of DR-K+, and the opening of a few VOCC are also involved.
T/F:
K+ influx through IR-K+ is responsible for the initiation of repolarization at the end of Phase 4 in ventricular myocytes.
False: IR-K+ maintains RMP in phase 4, DR-K+ cause repolarization at the end of phase 3.
T/F:
It is impossible for cardiac myocytes to fire AP during the RRP.
False: a slow Ca-mediated AP can be generated during the RRP.
Why does the heartbeat propagate thru the heart?
Each myocyte is electrically connected to its neighbors via gap jxns
What channels are responsible for the RMP in atrial and ventricular myocytes?
IR-K+
What determines threshold in ventricular myocytes?
Activation of V-Na+.
Why doesn't Em go all the way to E-Na during Phase 0?
V-Na+ inactivate after they open and I-to open.
Why doesn't Em go all the way to E-Ca during phase 2 of the ventricular AP?
I-to and later DR-K+ are open.
Why is a cardiac AP longer than a neural AP?
VOCC open and close much slower.
What are the three general mechanisms for controlling HR at the level of the SA?
1. Change rate of phase 4 depolarization.
2. Change magnitude of MDP
3. Change magnitude of threshold
How can the rate of SA phase 4 depolarization be changed? (3 ways)
1. Change activity of I-f channels
2. Change rate of DR-K+ closing
3. Change VOCC activity
How can the MDP be made less negative? (2 ways)
What effect does this have?
*Close DR-K+ channels sooner (i.e. decrease their activity)
*Decrease the activity of GIR-K+
*this will increase HR
How can the MDP be made more negative? (2 ways)
What effect does this have?
*Increase the activity of DR-K+ (i.e. delay their closing)
*Increase GIR-K+ activity
*this will decrease HR
How can the threshold of SA cells be made less negative? (1 way)
What effect will this have?
*decrease the activity of VOCC
*this will decrease HR
How can the threshold of SA cells be made more negative? (1 way)
What effect will this have?
*increase VOCC activity
*this will increase HR
How does B-1 stimulation affect VOCC activity in SA cells?
What effects does this have?
*VOCC activity is increased
*threshold is made more negative
*Phase 4 depolarization is faster
*the end result is increased HR
*also, increased [Ca++] results in increased CTY
What effect does B-1 stimulation have on I-f activity?
What effects does this have?
*I-f activity is increased
*Phase 4 depolarization is faster
*HR is increased
What effect does B-1 stimulation have on DR-K+ activity?
What effects does this have?
*rate of opening and closing of DR-K+ is increased
*this makes MDP more negative, but the effect is negated by increased VOCC and I-f activity
*decreases duration of plateau
*allows ample diastole for the heart to fill
What effect does B-1 stimulation have on Ca++ sequestration?
It increases the rate which permits quicker relaxtion and ample diastole for filling.
What effect does muscarinic stimulation have on VOCC?
What effect does this have?
*reduces VOCC activity
*this decreases rate of phase 4 depolarization
*this also make threshold less negative
*end result = decreased HR
What effect does muscarinic stimulation have on I-f activity?
What effects does this have?
*decreases I-f activity
*this decreases phase 4 depolarization
*end result = slow HR
What effect does muscarinic stimulation have on GIR-K+ activity?
What effect does this have?
*increases GIR-K+ activity
*this causes a more negative MDP
*slows phase 4 depolarization
*end result = slower HR
What is the PR interval?
The PR segment?
*Interval = start of P to start of QRS
*segment = end of P to start of QRS
What is the purpose of refractory periods in ventricular myocytes?
They allow ample diastole for filling of the ventricles.
How does a ECG lead detect a parallel vector in the same direction?
As positive.
How does an ECG lead detect a perpendicular vector?
As zero.
How does an ECG lead detect a parallel vector in the opposite direction?
As negative.
Using a clock face as a model, give position of leads I, II, III, aVR, aVL,and aVF.
I - 3:00 (0 degrees)
II - 5:00 (60 degrees)
III - 7:00 (120 degrees)
aVR - 10:00 (-150 degrees)
aVL - 2:00 (-30 degrees)
aVF - 6:00 (90 degrees)
What effects would a B-1 antagonist have on HR? Specifically on the channels and AP.
*inhibit I-f, which would slow phase 4 depol
*inhibit VOCC which would slow phase 4 depol and raise threshold
*end result = slower HR
What effect would vagal stimulation have on AV conduction?
What channel(s) would be affected?
*inhibit VOCC activity
*threshold is raised
*phase 0 depol. slowed
*end result = slower conduction
What effects would vagal stimulation have on ventricular CTY?
None - the ventricles do not receive parasympathetic innervation. Tricky!
T/F:
Sympathetic stimulation will increase the duration of ventricular AP's.
False: SNS stim. will increase activity of DR-K+ channels so plateau will actually be shorter.
What is occuring during the ST segment?
The heart is in mechanical systole. No signal is picked up b/c at this point there is complete depolarization of the ventricles.
What marks the QT interval and what does it define?
*start of QRS to end of T
*the duration of ventricular systole
What generates the P wave?
The spread of depolarization through the atria.
What does the PR interval represent?
What is a normal value for it?
What does a value above normal mean?
*Conduction through the AV node
*normal = 0.12 - 0.20 sec.
*PR > 0.20 indicates 1st degree AV block
Describe the spread of excitation that yields the QRS.
IV septum - apex - left ventricular free wall
What does the T wave represent?
Ventricular repolarization.
T/F:
The spread of ventricular depolarization is from epicardium to endocardium.
False. Vice versa.
What does the MEA represent? What is a normal range?
*the direction of the vector of early ventricular depolarization
* 0 to 90 degrees
*correlated with the R wave
What does the Q wave represent?
Septal depolarization
Describe sinus brachycardia.
Where is its basis?
What are some causes?
*Abnl slow HR (<60bpm)
*basis in SA node
*causes: physical conditioning, SA node damage, sick sinus syndrome
How does sinus brachycadia appear on the ECG?
Everything looks normal other than being slow.
Describe sinus tachycardia.
Where is its basis?
What are some causes?
How does the ECG look?
*abnl fast HR (>120 bpm)
*based in SA node
*causes: stress, drugs, fever, CHF
*ECG is nl except for being fast
What is a PAC?
A heartbeat triggered in the atria somewhere other than the SA node.
How does a PAC appear on the ECG?
Normal P waves interspersed with abnormal, absent, or inverted P waves. Nl QRS follow all P waves.
How does retrograde transmission through a heterogenous conduction block occur?
The AP hits the area of worst damage at full velocity and is able to "jump" this to propagate through the area of milder damage (slow conduction) back upstream. It's important that the cells in the area of mild damage have recovered from the refractory period.
What is a PAT?
What causes it?
How does the ECG appear?
*Paroxysmal Atrial Tachycardia
*due to a re-entry circuit in the atrial wall
*P waves absent or inverted, QRS complexes fairly normal
What is atrial flutter?
How does it look on the ECG?
*an atrial tachycardia
*regular oscillations of base line, no defined P wave
What is atrial fibrillation?
What does the ECG look like?
*major arrhythmia of atria
*chaotic baseline with occasional QRS complexes
What is a benefit of an AV block?
In a patient with atrial flutter or fibrillation, it can prevent ventricular tachycardia.
What is a 1st degree AV block?
ECG?
*AV conduction is slower than normal
*PR interval >0.2 sec
What is a 2nd degree AV block?
ECG?
*AV conduction worsens until a ventricular beat is missed
*PR interval increases until there is a P wave not followed by a QRS
*expressed as a ratio of atrial beats to ventricular beats
What is 3rd degree AV block?
ECG?
*there is no conduction at all through the AV node
*ventricular rhythym set by ectopic pacemaker, usually distal AV node or Bundle of His
*nl QRS that appear independent of P waves
*ventricular beat ~60bpm
Why do B-adrenergic blockers cause sinus brachycardia?
The balance between sympathetic and vagal stimulation may be upset, leading to excessive vagal stim.
Why is sinus tach a sign of CHF?
In CHF CO falls due to CTY...to compensate the HR is increased through sympa stim.
What is a PVC?
ECG?
*premature ventricular contraction
*a ventricular beat is triggered by an ectopic pacemaker or a re-entry circuit
*prolonged, bizarre QRS that is not preceded by a P wave
What causes ventricular tach?
A re-entry circuit in the ventricular wall...can lead to sudden cardiac death