Exam 1 lecture 3 Flashcards
Phase 4 of ventricular action potentials
resting potential. membrane is permeable t potassium through leak channels, outward flow of potassium ions generate the Ik2p current. Inward rectifer outward potassium current Iir. Em approx. for potassium (-96mv)
Phase 0
rapid opening of voltage gated sodium channels and inward sodium current, driving membrane potential in direction of sodium (+52)
Phase 1
closing of voltage gated sodium channels, coupled with voltage gated transient outward potassium current (Ito). Pulls membrane potential back to resting
Phase 2
Plateau, reduced outward potassium current (Ik1 or Iir) coupled with an inward calcium current (Ica (l)) through L type voltage gated calcium channels
Phase 3
repolarization. closure of L-type calcium channels, an increase in outward potassium current (Ik1), and rapid and slow voltage-gated delayed outward rectifier potassium current (Iks and Ikr). Delay in reporlarization allows for calcium channels to reactivate
why is delayed outward rectifier Ikr for potassium important for repolarization
hERG forms the major portion of voltage gated ion channel protein involved in Ikr. mutations can delay cardiac repolarization. In ECG, effect is LONG QT INTERVAL, or congenital long QT syndrome
what can congenital long QT syndrome cause
serious ventricular tachycardia and ventricular fibrillation
What else can cause congenital long QT syndrome
mutations in sodium and calcium channels
drugs that block hERG cause
acquired long QT syndrome, antiarrhythmics, anti-psychotic agents and antibiotics
inward rectifier
channels close as the cell depolarizes, (ooposite potassium channels which close when cell depolarizes). This is why rectifier current is reduced at plateau phase of cardiac action potential and increases again as cell repolarizes
directions of rectifier current
downward deflections are inward currents and upward deflections are outward currents
effective refractory period
during plateau phase, arrival of second depolarizing impulse has no effect
what follows effective refractory period?
relative refractory period: when sodium channels in membrane are unable to open when voltage is changed (when other are reset and ready to respond)
why dont cardiac muscle experience tetanus like the muscles do?
because the effective refractory period last quite a long time
when does calcium enter myocardial cells,
phase 2, during the plateau phase, triggers a release of more calcium from SR-> calcium concentration int he sarcoplasm increases-> calcium binds troponin which causes conformational change in tropomyosin, allowing mysoin to bind actin
what increases inward trigger calcium current
by catecholamines acting via beta-1 adrenegic receptors and cAMP/protein kinase-> leads to phosphorylation of L-type calcium channels
why does triger calcuim lead to
increased cardiac inotropic state because more trigger calcium enters the myocyte, more is released from the SR
what blocks catecholamines
beta-blockers (bind beta adrenergic)
what do all cardiac cells have the capability of doing?
rhythmically and spontaneously depolarizing and repolarizing
override supression
normally SA node fires before the slower pacemaker can fire and so its depolarizes them before they can spontaneously depolarize
escape rhythm
another pacemaker taking over a defective SA node, fires at slower rate
ectopic focus
certain conditions in which there can be an isolated spontaneous depolarization of a cell or group of cells in another region of the heart, ventricular or atrial myocardium, area is referred to as eptopic focus
what is funny current
prepotential or pacemaker potential is represented by a slow depolarization of the cell, caused by If “funny current” carried mainly by sodium. ( basically sodium leaking into the cell)
how does parasympathetic affect pacemaker frequency
decreases heart rate, Ach (muscarinic receptors) causes potassium permeability of SA nod cells to increase. repolarization Em is dirve closer to Ek and rate of prepontential formation is reduced-> takes longer for prepotential to reach firing threshold-> heart is slowed
how does sympathetic affect pacemaker frequency
stimulate increase heart rate. NE (beta 1 adrenegeric) causes potassium channels that are opened at the last phase of AP to close more rapidly, reducing the time taken for prepotential to reach firing threshold-> heart rate is accelerated.
annulous fibrosis
electrical depolarization can only reach the ventricles by passing through the AV node-> electrically insulated from each other by fibrous 4 ringed skeleton of heart
why is there a delay in the AV node
allows time for atria to contract before ventricular contraction begins
P wave
depolarization of atria, indicates SA node function
P-R internval
indicative of time it takes for impulse to pass through the AV node into the ventricles (atrioventricular time) normal is .12-.2 seconds
( increases in AV block)
QRS
depolarization of the ventricles, normally .12 seconds. indicates the duration of the ventricular depolarization-> Q wave may be exaggerated following myocardial infarction
T wave
progressive repolarization of ventricles, after which they are ready to be stimulated again
(inverted or peaked in myocardial infarction or hyperkalemia)
S-T segment
when elevated above baseline, indicates the possibility of myocardial infarction, depression below baseline may indicate myocardial ischemia
Q-T interval
varies with heart rate: abnormally prolonged in long QT syndrome. Rule of thumb: for heart rates between 65-90 is that QT is normal if half preceding R-R interval
U wave
if present-> follows T wave, notable in hyperkalemia, digoxin, quindine and other conditions
J point
junction between QRS and ST segment
one complete ECG wave
PQRSTP
