Cardiac Muscle Mechanics Flashcards Preview

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Flashcards in Cardiac Muscle Mechanics Deck (17)
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what is the functional syncytium made of?

two synctytia: atrial and ventricular


differences in cardiomycete structure from skeletal muscles

1. T-tubules only at Z lines
2. endfeet (triad) not observed, but the ryanodine receptors and L-type Ca++ channels are still associated


what does cardiac muscle use to open ryanodine receptors?

only small amount of Ca++ influx via L-type Ca++ channels, but they also open Ryanodine receptors then allow greater CICR (calcium induced calcium release) to cause muscle contraction


what phases of a cardiac AP correspond to absolute refractory period?

phases 1 and 2
1 = transient outward current
2 = L-type Ca++ current in, K+ current out


Ca++ dynamics during contraction phase

during depolarization; Ca++ enters sarcoplasm via L-type Ca++ channels (20% of twitch) and opens ryanodine receptors via CICR (80% of twitch)
-NCX may work in reverse, exchanging 1 Ca++ into the cell for 3 Na+ out


Ca++ dynamics during relaxation phase

during relaxation; as L-type Ca++ channels inactivate, SERCA (80%), NCX (normal operation; 15%) and PMCA (5%) remove Ca++ from sarcoplasm, back into sarcolemma


what does the trans-sarcolemmal influx of Ca++ mean for cardiac muscle?

much more sensitive to extracellular Ca++ than skeletal muscle
-also more sensitive to L-type Ca++ channel blockers


cardiac muscle contraction

use troponin C and tropomyosin movement to initiate crossbridge cycle (like in skeletal), BUT twitches don't have summation/tetanus or recruitment b/c of their long refractory period


how can tension of cardiac muscle be affected?

1. sarcoplasmic [Ca++] is altered (by inotropic agents)
2. Ca++ sensitivity of myofilaments is altered


how is heart rate increased and decreased?

increase: sympathetic activation via NE release
decrease: parasympathetic (vagal) activation via ACh release
both primarily realized by changing K+ conductances at SA node


why does the ejection fraction increase with ventricle filling?

NOT because of thick/thin filament overlap, b/c this happens at normal thick/thin overlap
-direct consequence of effect of increasing load on a single muscle fiber
-increases affinity of troponin C for Ca++, increasing contractile force (increase in sensitivity)


at what initial sarcomere length is maximal force generated?

2.2 micrometers (rarely exceeded in normal heart)


effects of greater initial length on cardiac muscle function

-increased Po (maximum load) at same Vmax
-velocity of shortening increases
-amount of shortening increases
-work of heart increases
-power delivered by the heat increases


what does inotropic intervention (w/ NE) do to cardiac twitch?

increases tension development and Ca++ levels
-increases contractility (force of contraction)
-shorten duration of contraction


coordinated response of heart to beta-adrenergic stimulation

increase in intracellular cAMP, causing increased influx of Ca++ across sarcolemma during AP, so increased release of Ca++ by SR
-cAMP activates protein kinase to phosphorylate phospholamban regulatory PRO in SR membrane to increase sensitivity of SR Ca++ pump, increasing Ca++ rate of uptake, to decrease duration of muscle contraction


does Po (maximum load) increase, decrease, or stay the same at all muscle lengths, and if NE is applied?

it increases in all cases


how is muscle shortening affected by NE addition?

it can be have a greater length of shortening compared to weight added
ex: if initial is 13 mm muscle, w/o NE will go to 12 mm (1 mm movement), but w/ NE will go to 11 mm (2 mm movement)

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