Heart 2: Cardiac Conduction and EKG Flashcards Preview

FHB I - Cardiac Unit > Heart 2: Cardiac Conduction and EKG > Flashcards

Flashcards in Heart 2: Cardiac Conduction and EKG Deck (41):

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?

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


Describe atrial tachycardia.

mechanism for re-entry of excitation
bc of characteristics of AV node not all impulses in atria are transmitted to ventricle so atrial and ventricular rates are different


Describe 1st degree heart block.
Draw (slide 17)

longer than it should to get through AV node.

abnormal prolongation in P-R interval greater than 0.20 sec.

still get 1:1 conduction, PR interval just abnormally long, some block going on.


Describe 2nd degree heart block.
What is Mobitz Type I and II?
Draw (slide 17)

some atrial impulses fail to activate ventricles; not all P waves are followed by QRS complexes:

-Mobitz Type I, aka Wenckebach (defect of the AV node) “Diagnosis Wenckebach” -progressive increase in PR interval.. longer and longer of lag between ventricular and atrial event..so long that you drop a beat.

-Mobitz Type II (defect of the His-Purkinje system)

2nd degree can be regular or irregular or irregularly irregular. some impulses not coming through. not all P waves followed by QRS complex. normally atrial beat followed by ventricular beat. in 2nd degree heart block some impulses in atria not reciprocated in ventricles.


Describe 3rd degree heart block.
Draw (slide 17)

complete AV nodal block (AV node completely cut off); no consistent P-R interval.

no relationship between atria and ventricle- 2 are independent


What is ventricular conduction?

rapid conduction through His-Purkinje system:

-brings the electrical impulse to the endocardial surface, resulting in endocardial to epicardial activation of the ventricles
-results in the normally narrow QRS complex (less than 100 msec in duration)
-synchronizes ventricular activation


What would a notched QRS complex indicate?

asynchronous electrical activation of L and R ventricles (possible causes are L/R bundle branch blocks) ...lag between L and R ventricle


What would slurred QRS complex indicate?

slowed intra-ventricular conduction
(hyperkalemia (Na channels inactivated bc of high MP), ischemia-depolarizes RMP, ventricular tachycardia-re-entry impulse going around and around muscle and get fast HR but actual propagation of that wave is slower than it should be...slower than normal depolarization but HR is fast bc no rest between beats and just keeps going around and around..will slur QRS)


What is supraventricular tachycardia?

conduction through the ventricles is normal (rapid) because the impulse comes from the atria and travels through the AV node into the His-Purkinje system. Therefore the QRS duration is normal. As a result, ventricular wall motion is normal.

involves structure above like atria... involves atria and ventricle. 100 milliseconds or less. normal activation of ventricle but just very rapid so still get regular output..filling time is short so that can be a problem but not as dangerous bc narrow QRS seq of activation is normal and cardiac output is relatively normal.
rhythm is good just really fast. approx 200 beats per minute. pathological in certain conditions (not when exercising, when sleeping yes)


What is ventricular tachycardia?

conduction through the ventricles is not normal (relatively slower) because the impulse originates within the ventricular muscle. The impulse does not travel through the His-Purkinje system. Therefore the QRS duration is abnormally prolonged (slurred). As a result, ventricular wall motion is abnormal and stroke volume is compromised.

does not involve atria. this is medical emergency. QRS is prolonged. 200-300 milliseconds so impulse not conducting through His P system. not endo-to-epi but going around heart abnormally. strength of contraction v impaired. interval short. less filling of heart and abnormal wall action and cardiac output drops dramatically. dangerous bc degenerates quickly into ventricular fibrillation. bc decrease in cardiac output heart itself not being perfused. heart more and more ischemia. depolarizing more and slowing conduction more and will go into VF.


What is happening in atrial fibrillation?

A fib -signals going all diff directions in atria, hitting AV node … AV node not passing them on, not depolarizing. see irregularities often though. irregular heart beat. irregularly irregular= clinical expression to indicate not irregularity like 2 beats and rest (regular irregular) this means just kinda crazy and unexpected delays in HR, beat to beat, HR all over the place. unpredictable when impulse will be moving around and hit AV node at time when AV node excitable and able to depolarize AV node and send down to ventricles… so AV node doing its job of filtering out …ventricles still doing job.


What are the mechanisms of Acetylcholine?

acts on K channels (Ach-activated K channels) opens these channels through direct g protein mechanism, no 2nd messenger, acts through muscarinic receptor. hyperpolarizes the membrane potential away from threshold.
Increases K permeability and K leaves the cell. RMP gets more negative and this is how HR slows down.

-also inhibits adenylate cyclase and reduces cAMP syntheisis and thus reduces the slow inward Ca current (indirectly via inhibition of cAMP synthesis). if inhibit slow Ca inward current then slow conduction through any tissue using Ca channel for AP (AV node) Ach. released on AV node will inhibit Ca current responsible for upstroke and slow down conduction (NE does opposite)


Describe Ach. and its receptor.

released from parasympathetic nerves (vagus nerve) and acts on muscarinic receptors. (blocked by atropine)


What are the effects of Ach?
What effects would you see on an EKG?

directly inhibits atrial muscle, SA node and AV node
-inhibition of atrial muscle: negative ionotropic effect (contraction)
-inhibition of SA node: lengthens PP interval and RR interval
-inhibits AV node- lengthens PR interval
NO DIRECT effect on basal ventricular muscle function


What is accentuated antagoism as it relates to basal ventricular function and Ach?

although ACh has no direct effect on basal ventricular function, ACh can inhibit ventricular muscle function if the ventricular muscle is first PRE-STIMULATED by beta-adrenergic receptor stimulation (sympathetic nerve stimulation). Then ACh can exert a large inhibition of ventricular function by inhibiting sympathetic stimulation mediated by the production of cAMP.


Diagram the flow of responses starting with Vagus nerve.

Slide 24.


Describe the role and effects of norepinephrine.

-released from sympathetic nerves (adrenaline released from adrenals on kidneys)

-affects all areas of the heart
-acts primarily via beta1 adrenergic receptors to increase cAMP.
-increases slow inward Ca current.
...increases SA node rate (decrease R-R interval)
-increases AV node conduction (decreases P-R interval)
-increases atrial and ventricular muscle contraction: positive ionotropic effect


What are the implications for heart transplant patients in regards to NE release?

heart from donor into recipient have cut vagus nerve and everything that was autonomic function… if changes in circulating Epi. heart will respond to that but won’t respond to vagus action. so resting heart rate in heart transplant pt. is higher (doesn’t necessarily mean higher cardiac output) heart less well regulated. decrease in cardiac reserve. higher HR at beginning, when exercise it does go up eventually bc of E circulating and increase in blood flow have also changes in stroke volume. can response to exercise but not as big of a change from resting HR to exercise HR… opposite of athletic training where decrease Resting HR bc of high vagal tone… low resting HR.
heart transplant pt- higher resting HR, less responsive to stress, less anticipation…(HR not going up when you hear come up front to do stress test) …sick when down in bed and get light headed when stand up too quick. if sick and dehydrated get orthostatic hypotension… if think I'm going to stand up HR will go up a bit and help.