ECG and Cardio EP Flashcards
(87 cards)
what are the two functional types of cells in the heart? how do they differ?
Working cells: greatest in number, Atrial and ventricular muscle, abundant, organized myofibrils, strong contraction, no pacemaker activity
Specialized cells: SA, AV, HIS, and Purkinje, few in number, few poorly organized myofibrils, weak contraction, pacemaker activity
What percent of mass and cell population do the working and specialized cardiac cells make up in the heart? What other cell types exist?
80% mass, 20% cell pop; fibroblasts, epithelia etc
What ionically sets up the resting membrane potential in cardiac cells?
very sensitive to changes in K+, K+ is the main permeable molecule at rest, only molecule with concentration gradient from outside to inside, so RMP is close to equal to the K+ permeability
How do cardiac cells differ in their RMP?
SA node and AV node have Low RMP (-40 to -60mV); Atrial and ventricular working muscle HIS bundle, bundle branches and purkinje fiber are high RMP -80 to -90; then there exist transition fibers between low and high
What is conductance in terms of cardiac membranes?
measure of ease with which an ion crosses the membrane and is inversely related to resistance; g=1/R
How is RMP related to conductance? How is it altered in low RMP cells?
g=gNa/gK; large gNa/gK ratio is due to lower gK than a higher gNa
What things can change ionic conductance in the heart?
can change a a function of voltage, time, receptor ligands, or extracellular second messengers
Ionic current crossing the cell membrane is determined by what?
conductance of ions and the driving force acting on the ions; I=g(Vm-E)
What are the phases and what molecules are moving in what direction in each?
0=rapid depolarization phase, Na in; 1: early repolarization, activation of transient outward K+; 2: Plateau, Na inactivation, depolarization induced decrease in K+ (anomalous rectification), slow inward Ca2+; 3: final repolarization, inactivation of Ca2+, delayed increase in outward K+ (delayed rectifier); 4: RMP only K+ permeable
What is going on in nodal action potentials?
0: rapid influx of Ca2+; 2: Ca2+ in and decreased K+ out; 3: Just K+ ot; 4: RMP K+ open but less so starts higher, then funny channels cause slow influx of Na (open during repolarization at -60mV)
Explain excitation contraction coupling in the myocardial cell?
Ca2+ not uniformly distributed in cells 2mM EC, 0.1microM CP and 150microM in SR; so need influx of Ca2+ in plateau phase for contraction
What receptor/proteins are involved in regulation of contraction and how?
Voltage gated (L type) Ca2+ channels in sarcolemma control influx of Ca2+ from extracellular space; and Ryanodine receptor (RyR2) Ca2+ release channels in SR membrane stimulated by Ca2+ entering via L-type
What proteins and how are involved regulation of relaxation of cardiac myocytes?
SERCA (sarco-endoplasmic reticulum Ca2+ ATPase) ATP dependent pump pulls Ca2+ from ctoplasm into SR (- reg by PLB or phospholamban); PMCA (plasma membrane Ca2+ ATP-ase) ATP dependent Ca2+ pump pulls Ca2+ from cytoplasm to EC; NCX (Na+/Ca2+ exchanger) extrudes 1 Ca to EC for 3 Na down their gradient; and Na+/K+ ATPase not direct Ca2+ handling but it maintains normal Na gradient needed for NCX
What effect do Beta adrenergic receptors have? How?
enhance contraction and relaxation; phosphorylation of L-type channels increases Ca influx which increases RyR and both increase contraction strength; phosphorylation of RyR increases rate of Ca release which increases contraction; Phosphorylation of PLB increases Ca uptake by SERCA which increases rate of relaxation
What is the difference in the AP of a fast response and slow response in cardiac cells?
fast characterized by high RMP phase 0 mediated by Na influx via INa (Atrial, His-Purkinje, and Ventricle), slow response have low RMP and phase 0 mediated by Ca influx via L-type channels (Sa and AV node)
What happens to fast response under myocardial ischemia?
accumulation of EC K+, decrease RMP, deactivation of Na only Ca available for depolarization (slow response)
What is membrane responsiveness?
variation in action potential upstroke velocity as a function of membrane potential; Na channel availability for excitation is dependent on membrane voltage from which AP is initiated
What is the refractory period? Different phases?
ERP (effective) no matter how great the stimulus no AP; RRP (relative) get AP with a larger stimulus; Fast response= short RRP; Slow response = Long RRP; long ERP due to prominent plateau phase
What is the cause of the refractory periods and why do they differ in length?
channels cant open in inactivated state; Na recovery from inactivation is fast, Ca recovery from inactivated state is slow making the RRP longer in slow response cells
What is automaticity? What channels are responsible? Where are they found in hierarchy order and pace?
intrinsic property of cardiac cells where excitation is initiated in absence of external stimuli; pacemaker potential die to If channels leaking sodium into the cell; Primary:SA (70-100bpm), Secondary/Latent: Inferior RA (50-70 bpm), AV (30-50bpm), His-Purkinje (30-40bpm)
What effect does the sympathetic nervous system have on the SA Node? NT? Receptor? Changes effected how?
Norepinephrine acts on Beta receptors, increase conductance (g) of ICa and If which increases heart rate (also respond to circulating epinephrine)
What effect does the parasympathetic nervous system have on the SA Node? NT? Receptor? Changes effected how?
ACh acts on muscarinic receptor increasing conductance of Ik, decreasing conductance of If and ICa, this decreases AP frequency, also activates specific K+ channel (IK1ACh) to increase K+ conductance
Describe local circuit currents in cardiac cells.
flow passively between coupled active and resting cells through connexons which can change degree of opening and even close
Define the source and the sink in the source sink relationship. Provide examples.
source: factors generating current, active membrane properties, inward current channels underlieing depolarization (INa, ICa); sink: factors that take up current, passive properties, Rm (membrane resistance) and Ri (internal resistamce, mainly gap junctions)
