Heart 1: Cardiac Physiology Flashcards Preview

FHB I - Cardiac Unit > Heart 1: Cardiac Physiology > Flashcards

Flashcards in Heart 1: Cardiac Physiology Deck (39):

Why is cardiac arrhythmia so dangerous?

upsets the normal sequence of electrical activation (electrical activation det. mechanical activity which affects cardiac output of blood to brain and heart itself


When someone dies of a heart attack, what has happened?

don't die because muscle is damaged to extent that it can't pump blood, rather damage to heart causes electrical arrhythmia that affects whole heart and then heart can't pump blood as a result of abnormal electrical activity.


Why is the L ventricle 3x thicker than the R ventricle?

has to do with resistance.
L generates 5x more pressure than the R (L- 125 mmHg and R is 25 mmHg)...but pressure is higher bc the resistance is higher in systemic circulation than pulmonary circulation (resistance to current flow det. the amount of pressure) ... so lower resistance pathway to lungs doesn't have to generate as much pressure

..SAME amount of blood just higher resistance and that's why the wall is 3x thicker bc deals with greater resistance


What is the specialized conduction system of the heart?

Sinus node, AV node, common bundle of His, bundle branches, Purkinje fibers ... make up conduction system of heart. these tissues generate impulse and these tissues conduct impulse to muscle that actually contracts


Describe the sinus node and AV node.

depolarziations start in SA node and spread through atria.

sinus node- specialized cells for pacemaker activity. (heart beats spontaneously bc of sinus node) ...impulse generated spreads through R and L atria then funnels through AV node

AV node-at floor of R atrium. slows impulse down. (want atria to allow last bit of blood into ventricles) slows down conduction... slow down to get all blood from atria, ventricle relaxed as atrium contracting so can accept bolus of blood.. delay at AV node is regulated. (when symp. stimulation don't have to wait as long and wouldn't want to)


Describe the His-Purkinje system.

Describe Purkinje fibers.

Describe the spread of an impulse. What would happen if there was a failure in the conduction system?

v thick bundle of tissue (common bundle of His) Impulse enters from AV node.

Purkinje fibers all along the endocardial surface of both ventricles. v fast. activate all cells of ventricle at once (approx. 100 msec) tissue is rapidly conducting. rapid conduction through His-Purk. system results in activating all cells at once which synchronizes all cells to generate the maximum amount of force...allows coordinated ejection of blood

impulse spreads through syncytium (common tissue connected by gap junctions) from endocardial surface to epicardial surface along the border to activate the whole heart

if failure in conduction system then impulse only would spread through syncytium - electrical signal through gap junctions but thats slower than specialized conduction system.


What happens in ventricular fibrillation?

arrhythmia where all cells are electrically desynchronized and as a result there is no cardiac output


What is the importance of papillary muscles and chorda tendenae?

What happens if someone has an infarction that damages papillary muscle on the wall of L ventricle?

papillary muscles contract to support valve leaflets, connected by CT.

CT connect with papillary muscles and valve to hold valve in place during systole
(during ejection the heart generates a large pressure and if it weren't for CT holding to papillary muscle then blood would flow back through valve... papillary contracts and pulls on CT and holds mitral valve in closed position because want blood ejected through aortic valve not mitral valve (want blood going in one direction)

if infarction that damages papillary muscle- then during systole the pressure pops the mitral valve in wrong direction and you get regurgitation of blood back in L atria. murmur. (valve blows backward and leaks blood, exposes atrium to high pressure...which would stretch the atria) if on L side then pressure will back up into lung and this is how people get pulmonary edema


Draw/Describe the path of blood flow.

(MC Question: Which blood pathway is correct?)

Right atrium
tricuspid valve
right ventricle
pulmonary valve to pulmonary trunk
R or L pulmonary artery
R or L pulmonary V
Left atrium
mitral valve
L ventricle
aortic valve
ascending aorta


Is volume of blood pumped by L ventricle greater or less than the R ventricle?

NEITHER...its the SAME volume of blood. Closed loop!!


Describe the components of the EKG. What is it?


Which segment shows...
AV node conduction time?
ventricular depolarization?
atrial depolarization?
end of AP/plateau of AP?
upstroke of AP?
diagnostic of heart block?
used to look at infarcts/other abnormalities?
ventricular conduction time?
repolarization of AP?

EKG tells you about conduction of heart- it is not the AP (generated by the AP but really is the propagation of AP through tissue that generates the EKG... wave of depolarization through that creates vector of motion)

P-atrial depolarization, upstroke of AP

QRS- ventricular depolarization to end of depolarization. diagnostic bc tells you how quickly the signal got through the ventricles and if you're correctly going through Purkinje system or if went around muscle in a loop through gap junctions which would take much longer
(ventricular conduction time)

T- ventricular repolarization (repolarization of AP)

PR- (AV node conduction time) time between when atria depolarizes and ventricles depolarize (tell you about time to fill the ventricles) is diagnostic of heart block

ST- between QRS and beginning of repolarization. end of AP ...is plateau of AP...is used to look at infarcts and other abnormalities

(try to correlate this w seq of electrical activation heart. atria activated by sinus node. after that is atrial activation.. then AV node is activated. after that, common bundle of His, /His-Purkinje system, next is ventricular muscle then ventricular muscle recovery)


How is the Na/K pump inhibited?

by digitalis. (from foxglove plant)
digitalis- used as cardiac ionotrope -agent that increases force contractile of heart. (inhibit pump of heart and heart beats harder…why? ex. of cardiac glycoside. classic inhibitor of Na pump. given when people have heart failure. will make heart pump harder. binding to Na/K pump and inhibiting it)

-digitalis binds to Na/K ATPase pumps and inhibits their activity. This causes intracellular Na concentration to remain higher, which disrupts the Na gradient needed for Na/Ca exchange pump... greater concentration of cytosolic Ca then occurs inside the cell and allows for a greater degree of binding to troponin C and eventually myosin/acting binding thus allowing for greater force of contraction


How is the RMP determined?

mainly by K diffusion potential.

K gradient is main thing for establishing RMP- potential gradient of K


What would you give when someone was having a hemorrhage and why?

saline solution-NaCl
Na high outside and really wants to come in- strong concentration and electrical gradient... use of E of gradient to power efflux of Ca... Na/Ca exchanger (3 Na in, 1 Ca out)


What is a possible dangerous outcome if there is a high bolus of Ca released inside the cell?

high bolus of Ca inside the cell...all that Ca will get exchanged out... rush of Na in could cause depolarization of membrane and that could get to threshold and fire AP... could cause arrhythmia (looping electrical event that could ultimately result in death)


What is the function of the Na/Ca exchange pump?

normal function is to exclude Ca from the heart cell cytosol. Want Ca low during relaxation because Ca binds to thin filaments and will generate force that you don't want during relaxation. want the ventricle to fill easily with blood... at rest the pump is getting rid of Ca so low concentration of Ca inside cytosol of heart so filaments are very relaxed... this is indirectly altered by changes in Na/K pump...


Describe the consequences of physiological changes to the Na/K pump like phosphorylation or with glycoside/digitalis.

physiological changes (P) or clinically with glycoside/digitalis which inhibits pump…which makes Na gradient less strong which will extrude a little bit less Ca. so Ca sequestered into SR so larger intercellular stores of Ca so get more Ca release and get stronger contraction. that’s how cardiac glycosides work. alters extrusion of Ca. can be risky…if too much Ca then when it is released get big depolarization and can get arrhythmia.


How is intracellular Ca maintained low? Describe the mechanism under normal and abnormal conditions. What would happen if you had high Ca in cytosol?

Na/Ca exchange is the mechanism that keeps intracellular Ca low. exchanges 3 Na for 1 Ca but bc Ca has 2 charges on it - its electrogenic net inward (as opposed to Na/K which is a little bit outward) . this inward current and under abnormal conditions generates arrhythmias. under normal conditions Ca brought out of cell and maintained low in cytosol- can't have it high in cytosol bc automatically will activate actin and myosin and heart or skeletal muscles will go into contracture - cross bridges lock and don’t let go. heart stops. so want to maintain low intracellular Ca. primary mechanism is to to extrude Ca and driven by Na gradient ( Na flows in and Ca out)


Why doesn't the membrane voltage follow the Nerst potential for K+ in the heart?

Draw graph.

(remember normal range of extracellular K is between 3-5 millimolar ...intracellular is maintained at 150)
normally if low concentration of K outside cell you would get stronger gradient for K to leave quickly and you would generate a really negative potential across the membrane.

in heart K affects its own permeability- as K is reduced outside, K permeability is decreased. (Less K leaking out means less negative - when positive charge leaks out this keeps RMP negative, less positive charge leaking out will maintain the membrane potential at more positive voltages so you have leak of Na in and less K out and this will make membrane relatively positive)...inward rectification - way to conserve K, limits how much leaks out, especially at rest

Diagram Slide 12.


What happens if you raise extracellular K?

you depolarize RMP bc reduced gradient for K to leave the cell. more stays inside cell and cell becomes more positive. higher than 5 outside cell and get positive depolarization. with hypo it doesn't change as much...


What is going on with K channels during depolarization?

during upstroke K channels turn off so they don't fight the upstroke of AP... want quick upstroke.

cell more positive inside during upstroke/depolarization so K permeability closes down ...channel IK1 closes which is critical to maintain the upstroke

other K channels turn off during the plateau.


What is inward (anomalous) rectification? Draw graphs for both situations.

a decrease in K permeability (IK1) that occurs when either the electrical or chemical driving force on K is increaed
-decrease in extracellular K
-depolarization of membrane potential (see diagrams slide 13/14)


Describe what happens with K channels at plateau of AP in heart cells.

at plateau the K channels are closed... no K current leaving cell. if K flowed out as soon as inside of cell became positive then cell would repolarize just like a nerve... but cardiac muscle has an AP of 300-400 milliseconds. when cell depolarizes, instead of activating outward K current, it closes down K permeability which helps maintain the plateau.


Describe hyperkalemia.

abnormally high (above 5meq/L) extracellular (plasma) K+.
-increases membrane K permeability (only allows the gradient to do what gradient wants to do... K gradient could reach equilibrium...so even though permeability is higher less K leaves bc gradient has been reduced)
-decrease K concentration gradient across the membrane
-net effect is more positive membrane potential... neuronal consequences is slowness in nerves and in heart can generate a fatal arrhythmia


Describe hypokalemia.

low (less than 3meq/L) extracellular (plasma) K+
-decrease membrane K+ permeability (inward rectification)
-increase K gradient across membrane
-net effect- little to no change in membrane potential

(much better tolerated)


Describe the AP in sinus node.

Draw a AP graph.

Slow responses. carried by Ca. (no Na channels) and Ca is much slower so no rapid upstroke.

SA node has a sloping phase 4 found primarily in pacemaker type tissue.
sinus node - primary pacemaker sloping depolarization of phase 4 is what initiates the AP.

Slide 16

SA node has no fast depolarization, no plateau phase, no “resting” membrane potential.

This is the “clock” that sets the rhythm of the heart.

The heart beats on its own!


Describe the 4 phases of the cardiac AP.

Phase 0 - Na+ channels activate (open). Membrane potential approaches ENa.

Phase 1 - Na+ channels inactivate (close) and K+ channels (ITO) transiently open.

Phase 2 - Ca2+ channels activate (open) and background K+ conductance (IK1) decreases (inward rectification).

Phase 3 - delayed activation of K+ channels (IK) and background IK1 conductance increases again (reversal of inward rectification).

Phase 4 - background K+ conductance (IK1) high, delayed IK channels closed (deactivated), Ca2+ channels closed and Na+ channels recover from inactivation but remain closed.


What is the reason for the long plateau in heart AP?

Calcium is the cause AND the reason for the long plateau… Ca depolarizes the membrane, and is the signal for contraction, and contraction takes time.

Ca channels are like Na channels, but much slower at activation and inactivation.

Nerve cells don’t need to contract, so they only let a little Ca in, mostly at the nerve terminals.


Describe repolarization in cardiac cell AP.

Repolarization happens when the delayed rectifier K+ channel kicks in and starts bringing the membrane potential back toward the K Nernst potential.

Also, Ca is decreasing at this time because the Ca channels are becoming inactivated.


What does tetrodotoxin do?

Blocks Na channels. therefore converts fast response to a slow response ...turn it looking more like a node cell.


Draw and label diagram for conductance (g) of Na/Ca/K.

See slide 21.


When does Ca flow into cardiac cells?

During the plateau of the AP- flows through L tap Ca current and that triggers Ca release from SR. Ca induced Ca current. (not an electrical event)

that Ca current generates contraction. ...this is diff than skeletal muscle (Ca does not flow into skeletal muscle to generate contraction)


What 2 things cause the plateau of AP in heart cells?

1) decrease in K conductance (IK1 channel closing down - anamolous rectification) ... as soon as membrane depolarizes during upstroke the K conductance through IK1 closes down and less K goes out of cell. less outward current
and more inward current through Ca channel

1)more inward current through Ca channel making inside cell more positive
2) less outward current through IK1 (inward rectifier) making inside cell more positive


Compare Ca/Na channel.

Ca current turns on and off just like Na channel but its just much slower. has activation and inactivate gate but kinetics of them are much slower.

Ca channel activated at about -40 millivolts. at about -50 another K channel is activated


What causes phase 1? Focus on the K channels (IK1 and ITO when they are on/off and at what phases)

important in understanding how heart recovers…another K channel ITO (transient outward- transient small outward K current turned on when cell depolarizes during upstroke- Na channel turning off at same time) any time depolarization have more inward current and anytime REpolarization have outward current. ITO little K current causing repolarization. have IK causing final repolarization of phase 3.


Fast response action potentials (ventricular muscle, His-Purkinje fibers) activate both fast Na+ and slow Ca2+ channels during the initial upstroke depolarization. If certain abnormal conditions occur, fast responses can become slow responses. How?
What phases are changed which are unchanged?

Effect of tetrodotoxin (TTX) on Purkinje fiber action potential.
1) fast Na+ channel (phase 0) blocked by TTX.
2) slow Ca2+ channel unaffected and now responsible for phase 0 upstroke.
3) plateau (phase 2) unchanged.
4) repolarization (phase 3) unchanged.

...lose phase 0 with Na... Phase 2 unchanged bc mostly dominated by Ca.


How do you inactivate Na channel? What closes h gate?

inactivate Na channel- depolarization of RMP

a more positive RMP inactivates h gate and reduces number of Na channels and upstroke of AP.

get more positive RMP with hyperkalemia… doesn't convert fast to slow responses bc you’d be dead by then. thats why high K kills you bc can’t live with slow Ca channel pumping heart.


Describe some of the main differences of slow response and fast response characteristics.
Tissue, phases, membrane potential, threshold, upstroke, duration, conduction velocity

Slide 29.


1) What would happen if all fast response cells in heart were changed to show response action potentials?

2) What would happen if a small portion of heart muscle changed from fast to slow responses? (What would cause this?)

1) the heart could not conduct or contract normally, resulting in cardiac arrest .

2) However, if a small portion of the heart muscle changed from fast to slow responses because of local damage (infarct), conduction WITHIN THE DAMAGED REGION would slow dramatically. This SLOW CONDUCTION can result in arrhythmias caused by re-entry of excitation.