Cardiac Cell Regulation and ECGs Flashcards
Chronotropy, inotropy, dromotropy, lusitropy
Heart rate, contractions, cell-cell conduction, relaxation
Parasympathetic effect on heart rate
Decreases heart rate
Effects of parasympathetic inhibition vs effects of sympathetic inhibition
Administer atropine (muscarinic antagonist, block parasympathetic), heart rate rises rapidly. Administer propranolol, heart rate decreases a little. The effects of para inhibition are greater than symp inhibition.
Sympathetic vs parasympathetic stimulation. Why does this occur?
Sympathetic effects are slower and more even, parasympathetic effects are quick. Parasympathetic effects don’t require an intermediate enzyme (just BG subunit), sympathetic effects require AC to convert ATP to cAMP.
How does the parasympathetic system act on the heart?
Release of acetylcholine from the vagus binds to muscarinic receptor in SA and AV nodes only. Linked to Gi, so decrease in AC, cAMP, PKA. But more importantly, beta and gamma subunits of Gi will directly activate the acetylcholine-sensitive K current.
I (k,ACh)
Acetylcholine-sensitive K current, activated by B and G subunits of GPC muscarinic receptor. This will allow for K release from cell, repolarizing the membrane, and slowing firing rate.
How does activation of I (K, ACh) slow heart rate?
K will escape and repolarize membrane, lengthening the time required to depolarize membrane.
Where do sympathetic effects on the heart occur?
SA node, AV node, and ventricle.
How does sympathetic stimulation of the heart work in SA node?
NE or Epi binds to B receptor, which is coupled to Gs. Activates AC, cAMP, PKA. cAMP will directly activate funny current. Increased depolarizing Na+ will increase SA nodal firing rate.
HCN
Hyperpolarization activated, cyclic nucleotide gated. cAMP turns on funny current.
Sympathetic effects on ventricles. How?
Stronger contractions, faster relaxation. PKA from B adrenergic receptor activation will phosphorylate L-type Ca channels, phospholamban, Ryr, and troponin.
Effect of PKA on L type Ca channel
Increased Ca flux, higher SR Ca load, stronger contractions.
Effect of PKA on SERCA pump
Will phosphorylate phospholamban, which relieves inhibition on SERCA, pumping Ca in more efficiently.
B adrenergic activation causes shift to new steady state. How?
Increased Ca through L-type channels and increased Ca uptake into SR by SERCA. More Ca entering than exiting, more Ca uptake then release. More Ca released next few beats.
What is the structure in cardiac muscle that is key for AP propagation?
Gap Junctions
Gap Junction structure
Connexins arrenged in a connexon channel.
What determines how fast AP’s propagate?
Number of gap junctions. Also, inward current responsible for AP upstroke (Na) because the speed of the upstroke is proportional to the speed of conduction.
Difference between measuring APs and ECG
AP measures Vinside - Voutside.
With an ECG, both leads are outside and = V2 - V1
And, because voltage outside is the inverse of voltage inside, V2 - V1= AP1-AP2
Cellular basis for T wave
Epicardium depolarizes after and repolarizes before endocardium.
Epicardium has a shorter AP
Fundamental principles of electocardiography
1) Voltages outside the heart are transmitted to body surface
2) Electrodes don’t measure absolute voltages, just differences between each other
3) We only see ECG deflections when voltages in the heart and changing with respect to location
4) A depolarization wave moving towards an electrode gives a positive deflection.
5) An orthogonal depolarization or repolarization produces no signal.
6) The strength of a given signal depends not only on propagation direction, but also on the mass of tissue contributing to the signal.
7) Signals in additional directions can be derived by combining signals in the known directions accordingly.
Depolarization towards a positive electrode = ? deflection
Depolarization away from a positive electrode = ? deflection
Repolarization towards a positive electrode = ? deflection
Repolarization away from a positive electrode = ? deflection
Positive
Negative
Negative
Positive
Why no signal from orthogonal AP?
No difference in voltage between leads.
Einthoven’s Triangle
RA, LA, LL leads
Vi = ?
Vii= ?
Viii=?
Vi = LA-RA
Vii= LL-RA
Viii= LL-LA
Unipolar Leads
Six ECG leads in the frontal plane
What do the precordial leads do?
Placed in a transverse plane and provide info about activity along anterior-posterior directions
P Wave
QRS Complex
T Wave
Correspond to?
Atrial Depolarization
Ventricular Depolarization
Ventricular Repolarization
Why is there no atrial repolarization signal?
Not strong enough, small mass
QT interval events
Ventricular depolarization to repolarization (AP duration)
Typically 300ms
PR interval events
Atrial to ventricular polarization (propagation through AV node)
Typically 120-200 ms
Why is AV nodal propagation slow?
Upstrokes caused by slower L-type Ca current
Why does parasympathetic activation cause negative dromotropy?
Negative dromotropy = slower conduction through AV node.
Activation of mAChRs inhibit AC and reduce activation of PKA. L type Ca channel is not phosphorylated causing slower current and slower upstroke.
Why does sympathetic activation cause positive dromotropy?
Activation of AC through B adrenergic receptors, P of L type ca channels.
Boxes in EKGs
One small box = 40 ms
Large box = 200ms
5 large boxes = 1 s
Estimating electrical axis
To determine the dominant location that the depolarization wave travels
1) Look for maximum positive R with no negative, this is closest
2) Look for cloest QRS to zero, this is perpendicular
3) If 2 R waves are equally tall, the axis is between these
Why would electrical axis deviate?
Hypertrophy
Why does lead II QRS have multiple phases?
Narrow vs Wide QRS complexes
Narrow = depolarization through conduction system is fast
Wide= depolarization through ventricular propagation, which is slow
Wide is caused when spontaneous Ap fires in ventricles, and cannot use purkinje system to zip around ventricles.
Sinus bradycardia. Long spaces between R waves. Normally indicates dysfunction SA node
What is this?
First degree AV block. Delayed PR interval, which should be <200ms. All p waves are followed by QRS
What is this?
Second degree AV block. Some impulses fail to propagate towards ventricles
What is this?
Atrial Fibrillation
P waves are random and indistinct. R-R intervals are irregular.
What is this?
Premature ventricular contractions. Wide QRS complexes, so ventricles are exciting themselves. Also, they have difference shapes, meaning there are multiple foci of self-excitation. Caused by spontaneous ca release.
What is this?
Monomorphic Ventricular Tachycardia. Wide QRS, Complexes are similar.
