Flashcards in Cardiac Physiology Deck (25):
Resting membrane potential of cardiac myocyte set by which ion?
Vm = -85 mV.
Ek = -89 mV
Phases of the ventricular action potential
0) Upstroke (inward Na current)
1) Notch (Inward Ca current)
2) Plateau (Rapid inward K, slow inward K)
3) Repolarization (rapid inward k, slow inward K)
4) Resting Potential (Inward rectifying K)
Phases of the SA nodal action potential
0) Upstroke (Inwards Ca current)
2) Plateau (inward ca current)
3) Repolarization (slow and rapid k current)
4) Slow depolarization (funny current)
Which current has faster phase 0?
Ventricle (because serious Na current)
Calcium current is much slower in SA node.
Is IK1 present in SA node?
No, only in ventricle. That's why there is a steady membrane potential.
Parasympathetic effect on heart
Decreased chronotropy, decreased dromotropy (cell-cell conduction)
Sympathetic effect on heart
Increased chronotropy, increased inotropy, increased dromotropy, increased lusitropy
How does the parasympathetic system decreased chronotropy?
Activation of acetylcholine-dependent K current.
ACh binds, GPCR BG subunit opens SA nodal K channel. K rushes out and slows the progression of the funny current (repolarizing).
How does B-stimulation increase chronotropy?
Increases cAMP, which opens up HCN channel more (which controls the funny current)
How does B-stimulation increase inotropy/lusitropy?
Activates PKA which phosphorylates L-type Ca channel, phosphorylation of PLB which increases Ca in serca.
What effect does parasympathetic stimulation have on the ventricles?
Baroreceptor reflex and its response to ie hemorrhage
Attempts to keep MAP the same when it changes.
If hemorrhage occurs, CO decreases, MAP decreases. So, baroreceptors will cause increase in HR, increase in contractility, constriction of arterioles (to increase TPR) and constriction of veins (increased preload ->increased CO).
How does the baroreceptor reflex constrict arterioles?
Alpha receptors increase IP3, which release Ca from SR.
Angiotensinogen converted to ANG I by renin (released from juxtaglomerular cells), ANG I converted to ANG II by ACE.
ANG II increases aldosterone, which increases Na+ reabsorption in kidney, which increases blood volume.
ANG II is also a potent vasocontstrictor
What two lines define the boundaries of the PV loop
How to increase preload? Effect on SV?
Increase blood volume, constrict veins. Increases SV
SV against LVEDP. Increase in LVEDP (preload) leads to increased SV.
Decreases SV by shifting up the ESPVR
How to increase afterload?
Increase TPR (arteriolar constriction), chronic hypertension, aortic stenosis.
How to increase contractility?
Sympathetic stimulation, increase in muscle mass.
Decreased by Ca2+ channel blockers, ischemia, B blockers.
As atrial pressure increases...
venous flow decreases