Cardio Physio

Question 1

Define Em/Vm, transmembrane electrochem gradient, equilibrium potential, conductance, ionic driving force, current

Answer 1

Em/Vm: membrane potential difference (cells at negative resting)
TEG: combo of chem and electrical potentials
Eion = (60mV/z) x log (ionout/ionin)
g = ability of ion to flow across cell membrane
IDF: Vm - Eion
Current: ionic charge carried by ion movement across membrane

Question 2

Voltage-gated channel activity dependent on ____; where can these be found and what do they generate?

Answer 2

membrane potential;
found in nerve, skeletal, cardiac muscle (CSN);
action potentials

Question 3

Three ion channel types, and three major channel conformations

Answer 3

Na (class I anti-a), K (class III anti-a), Ca (class IV anti-a);
Resting (closed), activated (open), inactivated (closed)

Question 4

For fast response AP, where does this occur and what are the phases?

Answer 4

Working myocardium: atrium, ventricle, His-Purkinje;
Phase 0 = depol (mostly INa, some ICa,T)
Phase 1 = early repol (Ito, both fast and slow; transient outward current)
Phase 2 = Plateau (ICa,L mostly)
Phase 3 = repol (IKs, IKr; important in preventing arrhythmias)
Phase 4 = resting (diastole): IK1, a NON-VOLTAGE gated ion channel that is blocked during AP generation

Question 5

For slow response AP, what are the phases and currents used? What ISN’T used?

Answer 5

SA node and AV node
Phase 0 = Ca-dependent AP upstroke (Mostly ICa,L, with some IF and ICa,T)
Phase3 = repol (IK)
Phase 4 = depol (IF);
NO IK1 OR INa!!!!!

Question 6

Primary pacemaker, secondary, and tertiary are where and what b/min?

Answer 6

1. SA node (60-90 b/min; activates atria)
2. AV node (40-60 b/min)
3. Purkinje (30 b/min; then ventricular activation);
   normally atria and ventricles WILL NOT HAVE PHASE 4 DEPOL, but Purkinje can!!

Question 7

To generate positive or negative chronotropy, what NT’s are needed and what channels are activated?

Answer 7

Pos: NE and epi (use IF, ICa,L)
Neg: ACh (IK,ACh, decreased ICa,L)

Question 8

Threshold is; what currents will determine depol vs repol?

Answer 8

amount of membrane depol needed to make AP;

if K current beats Na and Ca, membrane repols; if conductance of Na or Ca,L is greater than K, depol continues

Question 9

Excitation threshold for myocardial and nodal cells? Threshold potential is dependent on ____ and is

Answer 9

-65, -35 respectively;
Vm (resting membrane potential): hypokalemia hyperpolarizes and hyperkalemia depolarizes; also on Na current availability

Question 10

RMP directly affects

Answer 10

cardiac excitability (Na current availability and K conductances);
more depol current required to excite = increased threshold;
less depol current required to excite = decreased threshold

Question 11

RMP cannot be determined by

Answer 11

Nernst equation, but using the fact that the resting myocardial membrane is 20x more permeable to K than Na, Vm normally follows EK (Nernst potential for K)

Question 12

For ranging K levels, how does this affect excitability?

Answer 12

Hypokalemic (5.5-7.0): depolarizes Vm, decreased threshold, INCREASED EXCITABILITY;
Hyperkalemia (>7): depolarizes Vm, increases threshold because too much Na current has been turned off, DECREASES excitability

Question 13

Functional refractory period is

Answer 13

minimum time duration after AP required for threshold stimulus to produce FULL RESPONSE again;
in ERP: no AP made regardless;
in RRP: higher than normal stimulus can elicit AP with reduced amplitude and duration (aka not full)!!

Question 14

Important factors to determine conduction velocity?

Answer 14

1. rate of phase 0 depol (INa or .5 m/s in myocardium for atria, ventricles, His-Purkinje); ICa,L is .05 m/s in AV node
2. Threshold potential (less negative Vth = slower conduction; less INa, more ICa)
3. Resting membrane potential (more negative Vth, faster conduction with more INa)
4. Gap junction conductance is SECOND MOST IMPORTANT FACTOR: intercellular connectivity and site of cell-to-cell AP transfer

Question 15

AV node delay critical to ensure that

Answer 15

atrial contraction finishes before ventricular contraction begins

Question 16

If you block ICa,L; active tension dependent on

Answer 16

no cardiac contraction!!;
AP duration (APD is frequency-dependent)

Question 17

For excitation contraction coupling, describe contraction and relaxation:

Answer 17

Contraction:
1. Ca ions enter through ICa,L channel
2. Ca channels activate ryanodine receptor
3. Receptor releases Ca into cytosol and initiates contraction
Relaxation
1. Cytosolic Ca reduced to resting levels thanks to SERCA and NCX

Question 18

Cardiac contractility: increasing preload;
how do we max active tension?
example of positive and negative inotropy?

Answer 18

increases myocardial contractility;
if you stretch heart muscle, you increase sarcomere length and actin-myosin cross bridge sites maxed!!;
pos = exercise; neg = heart failure (stroke volume goes down, EDV goes up)

Question 19

Autonomic control of cardiac contractility:

Answer 19

Symp (NE, Epi): beta-1 adrenergic, works at Galphas to increase cAMP and PKA;
1. increases ICa,L, IF for positive chronotropy and increasing AV node conduction
2. increases ICa,L, SERCA for positive inotropy and increased Ca-sens of contractile filaments;
Parasymp (ACh): M2, works at Galphai to decrease cAMP and PKA, and also at Gbetagamma to activate IK,ACh

Question 20

EF =

Cardiac preload and afterload correlate with what?

Answer 20

SV/EDV (normally >55%);

preload correlates with EDV and afterload with TPR