Heart 2: Cardiac Conduction and EKG Flashcards
What determines internal resistance for current to flow between cells?
gap junctions (channels that electrically connect cardiac cells) …couples all cells together electrically
low resistance connections that allow current (action potentials) to conduct between cardiac cells.
1. cell membranes are very close (2-4 nanometers). 2. intracellular connections through connexon channels. 3. primary determinant of internal resistance in cardiac tissue 4. sensitive to INTRACELLULAR [Ca2+] and [H+] (pH) ions.
What is an intercalated disc?
specialized region of intercellular connections between cardiac cells. 3 types of adhering junctions within an intercalated disc
- fascia adherens (anchoring sites for actin that connect to the closest sarcomere)
- macular adherens (holds cells together during contraction by binding intermediate filaments, joining the cells together. desmosomes)
gap junctions
What is healing over?
if have area of heart that dies bc of plugged artery high Ca in those cells spills out of SR and activates and chews up everything…dont want that signal to spread so need to block it off.
an increase in internal resistance that results from a decrease in the number of open gap junctions. Caused by an increase in intracellular (cytosolic) Ca2+ and/or H+ ions (decrease pH). Clinical Application: electrical isolation of damaged tissue that results from myocardial infarction (see pt with MI with elevation of ST segment due to abnormal electrical activity then in a month it looks normal.. not healed but cells are so damaged that intercellular Ca and pH changes have closed down gap junctions between normal and damaged regions and no longer is there an injury current)
What is ischemia and why is it dangerous?
ischemia is lack of blood flow, it is not a lack of oxygen (that is annoxia) ischemia is worse.. not only lack of blood flow but also build up of metabolic waste of those tissues allowing damage to cells. new blood flow washes away metabolites. (hydrogen ions) ischemia is a lack of blood flow preventing nutrients as well as waste products from being exchanged… ischemia is reversible (get to hospital within 1 hour of heart attack) if it goes on too long you have infarct…cells die and once cells die they do not recover. and damaged tissues can generate abnormal electrical events which can screw up output.
pH goes up bc you become more acidic in those cells intracellular and that can close down gap junctions and if you close down gap junctions you can slow conduction through that tissue. (can be good or bad)
How can gap junctions contribute to arrhythmias in regards to healing over?
gap junctions are dynamic and change. if completely closed then thats great bc walled off abnormal electrical activity from rest of heart but often they just decrease a little bit and that can generate abnormal electrical activity between damaged and normal tissue which generates bad arrhythmias
Describe the structure and function of SA, AV node.
small diameter (small space constant), tapered ends, few gap junction connections, few myofibrils
(main pacemaker is SA)
function: pacemaker activity, slow conduction, weak contraction
Describe the structure/function of atrial and ventricular muscle.
medium diameter, rectangular abundant gap junction connections, abundant myofibrils
(main contracting tissue is atrial)
function: conduction, contraction
rapid conduction-strong contraction
Describe the structure/function of His bundle, bundle branches, Purkinje fibers.
large diameter (long space constant), cylindrical abundant gap junction connections, few myofibrils
(main conduction is His/P)
function: very rapid conduction, weak contraction
Discuss/draw how AP is synced up with EKG.
Slide 7
Describe space constant.
how quickly signal propagates through tissue. space constant is basically how quickly will AP progress along membrane. det. by membrane resistance…higher it is, the longer length constant and faster the propagation.
-Ri (internal resistance) you want to be low. myelinated fibers work so well bc low resistance down fiber but high resistance membrane.
How is membrane resistance related to K permeability?
inversely.
if K permeability goes up then more places for current to flow out and less chance of current flowing down so smaller space constant
if membrane resistance is high then less chance for K to flow out and more current to flow down so space constant larger
What effect does myelination have?
What type of drug is given to patients with a demyelinating disease?
raising membrane resistance bc covering up K channels so less K out and more K down and longer space constant. when demyelinate then membrane resistance goes down and easier for K to flow out and less chance of K flowing down and space constant is shorter.
if someone has demyelinating disease- is there a drug to help conduction through demyelinated axons. a K blocking agent … this is what give pt with MS. helps conduction with pt with demyelinating disease. helps function but not that much.
What does more Nexal connections result in?
less internal resistance.
(internal resistance is inversely related to number of Nexal connections. Internal resistance inversely related to cell diameter)
What two main factors determine cardiac conduction?
1) space constant
2) rate of rise and amplitude of AP
See slide 9
What will determine the rate of rise of amplitude in AP?
What would result in a decrease in the rise of amplitude?
depends on Na channels in fast response tissue. RMP can affect Na channel (det. the number of Na channels)
…if membrane is more positive then less Na channels are available, less rate of rise, less conduction (happens during infarct and hyperkalemia)
What happens as the RMP becomes more positive. Draw the diagram.
As the resting membrane potential becomes MORE POSITIVE, the number of fast Na+ channels available for activation DECREASES. As a result, the fast response action potential upstroke DECREASES and conduction slows.
(Slide 10).
Describe some conditions that influence the AP upstroke as a result of changes in the RMP.
- hyperkalemia (more positive RMP)
- premature excitation during relative refractory period (can create re-entry loop and arrhythmia…if premature beat on rel. refractory period you’re at more positive voltage? -if excitation does occur during that period then you get upstroke much slower and smaller in A … if that premature AP blocks it will throw heart into fatal arrhythmia )
- ischemia (causes depolarization of membrane bc cut off blood flow and not equilibrating K in extracellular fluid- no equilibrium with plasma/no blood to take it away so localized elevation of K) or myocardial injury
Draw the effects of elevated K on RMP and AP configuration.
K=3mM, 7, 10, 14, 16, 3
Slide 12.
What happens during ischemia or infarct?
During ischemia or infarct, intracellular K+ ions can leak out of damaged cells and accumulate in the interstitial (extracellular) fluid bathing the cells. The LOCAL concentration of K+ in the damaged region can increase to as much as 20 meq/L (normal 4 meq/L). As illustrated, an increase in extracellular [K+] makes the RMP more positive, inactivate Na+ channels (see Na+ inactivation curve), and thereby changes a fast action potential to a slow action potential because of the voltage-dependent properties of the fast Na+ channels. As a result, conduction within the damaged region can slow dramatically, setting up the conditions necessary for arrhythmias due to re-entry of excitation.
What is PR interval?
conduction time from atria to ventricular muscle
(AV nodal conduction time…tells how long it takes to get through AV node, tells about health of AV node)
…from P to beginning of QRS
(should not be longer than 200 milliseconds)
Describe QRS complex.
What would cause an abnormal QRS complex and what would it look like?
beginning of ventricular activation until the end. 100 milliseconds. this is how fast takes AP to go from endocardial to epicardial surface.
narrow because of sequence of activation from endo to epi.
long or slow QRS complex no longer from endo to epi so not all cells activated within 100 milliseconds anymore. conduction time twice as long, not all cells contracting together so force is less… slurred QRS complex indicates slowed intra-ventricular conduction (could result from hyperkalemia, ischemia, ventricular tachycardia)
Describe how the AV node protects the ventricles from abnormally high arterial rates.
can get arrhythmias high in atria that hit AV node and don’t want those to go through ventricle bc that would cause VF..AV node goes slow to filter out that stuff. AV node protects ventricles from high atrial rates (atrial fibrillations or flutters…) impulses getting through… give drug to prolong refractory period of AV node which will filter out that noise.
AV node bc of post REpolarization refractoriness doesn’t allow high atrial rates to be transmitted into ventricle
Why does AV node conduct slowly?
so blood can be transferred from atria to ventricles.
conduction delay permits optimal ventricular filling
also long refractory period that can protect ventricles … period of time where cannot conduct another AP. slow kinetics of activation/inactivation of AV node gating mechanisms..so refractory period of AV node is longer than AP duration.
Describe the AP of the AV node.
slow response due to slow inward Ca current. (upstroke dependent on slow inward Ca current so upstroke velocity and amplitude are small) charge coming in determines the speed of conduction
