cardiac physiology Flashcards
resting poteintial of potassium calcium and sodium concentraitons
potassium high in the cell, calcium and sodium high outside the cell
resting membrane potential
-60–80
frquency of the SA, AV, and purkinje
SA: 60 b/min AV: 40 b/min purkinje: 20 b/min since SA is highest frequency, it sets the heart rate
innervation of SA node
sympathetic: vagus nerve parasympathetic: T1-T4
phases of SA node action potentials
phase 4: spontaneous depolarization (K+ out, Na+ in) phase 0: rapid depolarization (Ca+ in) phase 3: repolarization (K+ in)
phases of ventricular action potentials
phase 4: resting phase 0: upstroke of AP rapid depolarization (Na+ in) 1: rapid repolarization (K+ out) 2: plateau phase (K+ out, Ca+ in) 3: repolarization (K+ out)
how does acetylcholine affect heart rate
acetylcholine is released by parasympathetic nervous system through the vagal nerve decreases the rate of depolarization by decreasing funny current decreases maximum diastolic potential (start from more negative) by increasing K1 activity increase threshold potential by decreasing Ca activity
class I antiarrythmic drugs
sodium channel blockers reduce phase 0 peak and slope of depolarization
class III antiarrythmic drugs
potassium channel blockers increase action potential duration and effective refractory period, delay repolarization
class IV antiarrythmic drugs
calcium channel blockers L-type Ca, slows rate in SA and AV node
class V antiarrythmic drugs
Miscellaneous, various effects ex. funny channel blockers HCN selective blocker
class II antiarrythmic drugs
beta blockade block sympathetic activity, reduce rate of of conduction
What two mechanisms must antiarrythmic drugs meet in order to have desired effect
supress ectopic/abnormal pacemakers more than the SA node increase the ratio of the ERP/APD (effective refractory period/action potential duration)
time per small box in EKG
.2 seconds
mV per small box in EKG
.5 mV