Heart Lecture 1: Cardiac Resting Membrane and Action Potential Flashcards
(29 cards)
Formula for cardiac output
heart rate x stroke volume
Stroke volume
amount of blood pumped per beat
Resting heart rate
72 beats per minute
Canonical conduction pathway
SA node –> internodal pathways –> AV node –> bundle of His –> bundle branches –> Purkinje fibers
Where is the most rapid conduction found?
Purkinje fibers (needs to activate all cells at once)
How long does it take to activate the whole heart, from the endocardium to the epicardium?
100ms
Which interval is referred to as the AV nodal conduction time?
PR interval
Why is the resting potential of a myocyte slightly more positive than the equilibrium potential of potassium?
Na+ leakage into the cell (makes it more positive) makes Vm = -90mV not -100mV
What maintains ionic concentrations within the cell?
1) Na+,K+-ATPase (3 Na out, 2 K in –> net outward + charge)
2) Na+/Ca++ exhange (3 Na in, 1 Ca out –> net inward + charge)
Function of digitalis?
to inhibit the Na, K-ATPase and therefore increase the contraction of the heart
Function of Na, Ca exchanger?
to keep intracellular calcium low (pumps one out, against its concentration gradient, for the passive import of 3 sodium ions into the cell)
Normal extracellular potassium levels?
3-5mM
Normal intracellular potassium levels
150mM
What is inward (anomalous) rectification?
a decrease in K+ permeability (meaning channels (like IK1) are likely shut) that occurs when the electrical or chemical driving force of K+ is increased
What two scenarios increase the driving force on K+? (Hint: one is chemical and the other is electrical)
1) decrease in extracellular [K+] (therefore increasing the gradient)
2) depolarization of the membrane potential (makes inside of cell more positive so a positive ion like K would want to get out)
What is the clinical importance of anomalous rectification?
creates a plateau when cell resting potential gets to be more positive
normally, in a nerve action potential, K+ channels immediately open and charge flows out when the membrane potential becomes more positive - not the case immediately with cardiac myocytes
Effects of hyperkalemia on action potential?
depolarizes resting membrane potential (MAKES IT MORE POSITIVE)
1) increases membrane [K+] permeability (more channels should be open)
2) decreases K+ conc gradient across membrane (fewer ions travel since extracellular environment is more similar to intracellular)
Effects of hypokalemia on action potential?
No net effect
1) decreases membrane [K+] permeability (IK1 channel shuts down)
2) increases [K+] gradient across membrane (greater motivation for K+ ions to move but they don’t)
Heart tissue that act via FAST APs
atrial and ventricular muscle
Heart tissue that act via SLOW APs
SA and AV node
Phases of Fast APs
0 = upstroke (net Na+ movement into the cell) 1 = initial repolarization (ITO K+ channel opens allowing net K+ out of cell; Na+ channels close) 2 = plateau (more Ca++ entering the cell and background conductance of K+ decreases via IK1, inward rectifier) 3 = repolarization (IK, delayed rectifier, opens and K+ flows out of the cell) 4 = resting potential achieved
Phases of Slow APs
0 = upstroke (slow upstroke due to Ca++ influx into cell) 3 = repolarization (K+ efflux from cell) 4 = resting potential sloped because these cells are always active
*no fancy initial repolarization or plateau
Why is the slow AP slower than the fast APs?
Slow tissue is calcium dependent - Ca++ channels are slower to activate than Na+
Difference between Ca++ activation in cardiac muscle and skeletal muscle?
Skeletal: Ca++ current is electrically connected to ryanodine receptor on sarcoplasmic reticulum - no net Ca++ influx into the cell
Cardiac: Ca++ flows directly into cell and induces Ca++ release from reticulum
