Exam #2: Electrophysiology of the Heart Flashcards
What are intercalated discs? What is their function?
- Intercalated discs are interdigitations of sarcolemma between cardiac myocytes
- Contain gap junctions that increase the speed of signal transduction between myocytes
What are pacemaker cells?
Intrinsic rhythm generators in the heart, including nodal cells of:
- SA node
- AV node
- Purkinje fibers
How does the resting membrane potential differ from the equilibrium potential?
Resting membrane potential is the summation of the equilibrium potentials for each ion
Describe the intracellular vs. extracellular concentration of Na+, K+. Ca++, & Cl-.
Na+= high ECF
K+= high ICF
Ca++=v. high ECF
Cl-= high ECF
Describe the electrical driving forces on the basis of charge. How does this compare to the chemical driving force?
Electrical driving force:
- Cations want to move in (attracted by the negative resting membrane potential)
- Anions want to remain out of the cell (repulsed by the negative resting membrane potential)
*Chemical driving force is dependent on the concentration gradient for each particular ion.
What is resistance. Write Ohm’s Law.
Resistance is the force that impedes the flow of ions.
I= Vm-Veq/R
What maintains the Na+ & K+ concentration gradients?
Na+/K+ ATPase Pump
What ion is the cell most permeable to at rest? What is the effect of this?
- The cell membrane is most permeable to K+ at rest
- Resting membrane potential is closest to the equilibrium potential for K+
Describe the general sequence the cardiac action potential in terms of cellular permeability & ion channels.
1) Fast Na+ channels open, leading to Na+ entry & rapid depolarization
2) Slow Ca++ channels open leading to the plateau phase caused by Ca++ influx
3) Change in K+ permeability throughout the action potential leads to K+ efflux & causes repolarization
What is the resting membrane potential in a cardiac myocyte?
-90mV
What is phase 0 of the AP in a ventricular myocyte?
Depolarization due to opening of Fast Na+ channels
What is phase 1 of the AP in a ventricular myocyte?
Early repolarization when Fast Na+ channels inactivate (close) & some K+ channels open
What is phase 2 of the AP in a ventricular myocyte?
- Plateau phase where the membrane potential is approximately 0
- Due to slow Ca++ channels with Ca++ influx, BALANCED by K+ efflux
What is phase 3 of the AP in a ventricular myocyte?
Rapid repolarization as Ca++ channels are closing, & K+ channels open
What is phase 4 of the AP in a ventricular myocyte?
Resting membrane potential; only K+ channels are open
What is responsible for the absolute (effective/normal) refractory period in the ventricles? What is its duration?
- 0.25-0.3 sec
- Na+ inactivation gate is closed & Na + pore is closed
What is responsible for the absolute (effective/normal) refractory period in the atria? What is its duration?
- 0.15 sec
- Na+ inactivation gate is closed & Na + pore is closed
What is the relative refractory period? What is responsible for the relative refractory period?
More difficult to excite, but no impossible
- Na+ channel inactivation ( Na+ pore is closed but the inactivation gate open)
How does the effective (absolute) refractory period in cardiac muscle compare to skeletal muscle?
Longer effective refractory period in cardiac muscle; thus, it cannot tetanize
What happens when another action potential is stimulated during the relative refractory period in the cardiac myocyte?
Interruption of normal ion flow that may result in ventricular fibrillation
How does the nodal action potential compare to the ventricular myocyte action potential?
- Missing phases 1 &2 i.e. no rapid influx of Na+ b/c no fast Na+ channels
What happens during phase 3 in nodal cell?
Repolarization as K+ channels open
What happens in phase 4 in the nodal cell?
Slow leak of Na+, called the “funny current” slowly changes the membrane potential until threshold is reached
What is the effect of NE on pacemaker cells?
- Increases Ca++ permeability
- More positive charge enters the cell & cell reaches threshold faster
What is the effect of ACh on pacemaker cells?
Increases permeability of K+
What is the function of the SA node?
Primary pacemaker
What are the principal time-dependent & voltage dependent currents of the SA node?
Ica, Ik, & If
What is the effect of Beta-adrenergic stimulation on the SA node?
- Increased conduction velocity
- Increased pacemaker rate
What is the cholinergic effect on the SA node?
- Decreased pacemaker rate
- Decreased conduction velocity
What is the function of the atrial muscle?
Expel blood from the atria
What are the principal time-dependent & voltage dependent currents of the atria?
Ina, Ica, Ik
What is the effect of beta-adrenergic stimulation of the atria?
Increased strength of contraction
What is the effect of cholinergic stimulation on the atria?
Little effect
What is the function of the AV node?
Secondary pacemaker
What are the principal time-dependent & voltage dependent currents of the AV node?
Ica, Ik, If
What is the effect of beta-adrenergic stimulation of the AV node?
- Increased conduction velocity
- Increased pacemaker rate
What is the effect of cholinergic stimulation of the AV node?
- Decreased pacemaker rate
- Decreased conduction velocity
What is the function of the Purkinje fibers?
- Rapid conduction of action potential
- Tertiary pacemaker
What are the principal time-dependent & voltage dependent currents of the Purkinje fibers?
Ina, Ica, Ik, If
What is the effect of beta-adrenergic stimulation of the Purkinje fibers?
Increased pacemaker rate
What is the effect of cholinergic stimulation of the Purkinje fibers?
Decreased pacemaker rate
What is the function of the ventricular muscle?
Expel blood from ventricles
What are the principal time-dependent & voltage dependent currents of the ventricular muscle?
Ina, Ica, Ik
What is the effect of beta-adrenergic stimulation of the ventricular muscle?
Increased contractility
What is the effect of cholinergic stimulation of the ventricular muscle?
Little effect
Describe the sequence of depolarization in the heart.
1) SA node
2) Atria
3) AV node
4) Septum
5) Apex
6) Ventricular free walls
What is the velocity of signal conduction through the purkinje fibers?
4 m/s
What is the velocity of signal conduction through the cardiac myocytes?
- 3-0.5 m/sec
* Roughly a 1/10 of the purkinje fibers
What is the SA node?
Normal impulse generator of the heart (70-80 bpm)
How does impulse from the SA node reach the left atria?
Internodal tracts
How does the resting membrane potential of the SA node compare to the cardiac myocytes?
Less negative (-60mV vs. -90mV)
What is the function of the AV node?
Delay of impulse
- Allows for atrial contents to fill the ventricle
How does the AV node slow conduction?
Expression of fewer gap junctions
What are the branches of the left bundle branch?
1) Septal fascicle
2) Left posterior fascicle
3) Left anterior fascicle
What is the function of the purkinje fibers?
Very rapid transmission of the electrical impulse that allows for the synchronous contraction of ventricular myocytes
Outline the steps of excitation-contraction coupling in the heart.
1) Action potential spreads down T-tubule & there is an inward Ca++ movement through L-Type Ca++ channels (Dihydropyridine receptors)
2) Ca++ induced Ca++: Ryanodine receptor on SR activated to release MORE Ca++
3) Increased ICF Ca++ binds Troponin C & displaces tropomyosin from myosin-binding sites on actin
4) Cross-bridging occurs
Relaxation occurs when Ca++ is reaccumulated in the SR via Ca++ ATPase (SERCA) & out of the cell via the Ca++/Na+ exchanger
How do the concentration & electrical gradients differ for Cl-?
Cl- concentration is high on the outside of the cell; however, resting membrane potential of the cell is negative. Thus,
- Concentration gradient favors entry into the cell
- Electrical gradient favors efflux from the cell
What are the effects of increased extracellular potassium (hyperkalemia)?
1) Slows HR
2) Dilates heart
3) Can block conduction through AV-bundle
What is the effect of hypercalcemia on the heart?
Increases cardiac contraction (positive ionotrope)
What is the effect of hypocalcemia on the heart?
Decreased cardiac contraction (negative ionotrope)
What are the effects of K+ channel blockers on the heart?
1) Increased AP duration & absolute refractory period
2) Prolongation of QT interval on ECG
What are the effects of Ca++ channel blockers on the heart?
Slows the rate of conduction at the SA & AV nodes by delaying Ca++ entry
E.g. verapamil
