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555- Physiology & Pathophysilogy > Exam 5 - Myocardial Contraction > Flashcards

Exam 5 - Myocardial Contraction Flashcards

1
Q

Skeletal muscle

A
  • contraction via nervous system
  • Ach is neurotransmitter
  • long, striated w/ multiple nuclei
  • voluntary movement
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2
Q

Smooth muscle

A
  • contraction via nervous system (ANS) , hormonal stim (Epi/NE), muscle stretch
  • found in hollow organs and arterioles
  • can stimulate and inhibit contraction
  • long, spindle shaped w/ single nuclei
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3
Q

Cardiac muscle

A
  • contraction via specialized cardiac cells
  • branching, striated, fused at plasma membrane
  • single nuclei
  • function is to pump blood
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4
Q

Organization of fibers

A
  • Muscle fiber -> myofibril -> myofilaments
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5
Q

Sarcolema

A
  • plasma membrane enclosing muscle fiber
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6
Q

How many ATP needed to move 1 myosin head

A

1 ATP

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7
Q

Sarcoplasm

A
  • cardiac muscle cell cytoplasm
  • contains numerous mitochondria
  • large number of myofibrils running parallel
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8
Q

Intercalated discs

A
  • hold fibers together
  • aid in conduction
  • unique to cardiac muscle cells
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9
Q

Sarcoplasmic Reticulum

A
  • surrounds each myofibril
  • network of tubes and sac with high [Ca]
  • similar to smooth ER in other cells
  • Ca here used in plateau phase
  • HUGE in cardiac muscle cells
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10
Q

T tubules

A
  • Cross SR at right angles and communicate to outside
  • Move AP from exterior to interior
  • Fluid inside tubules is interstitial fluid
  • Bring extra cellular environment to interior of cell
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11
Q

Sarcomere

A
  • one z-line to another z-line

- fundamental unit of muscle contraction

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12
Q

I-Band

A
  • Thin actin strands alone
  • actually cuts across two adjacent sarcomeres
  • gets smaller during contraction
  • from end of myosin to next myosin
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13
Q

Z-line

A
  • Anchors actin filaments

- composed of proteins

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14
Q

A-band

A
  • overlapping myosin and actin
  • the length of the myosin filaments
  • stays same length during contraction
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15
Q

H-zone

A
  • area within A-band
  • contains only myosin filaments
  • gets smaller during contraction
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16
Q

M-line

A
  • Middle of H-zone

- connects adjacent myosin strands

17
Q

Titin molecule

A
  • framework for sarcomere
  • keeps acting and myosin aligned
  • very large protein (3,000,000 daltons)
  • one end anchored to the myosin…other to z-line
  • very springy….can change length with contraction/relaxation
18
Q

Z-line to z-line distance

A
  • 2 microns
19
Q

Anatomy of Actin

A
  • 1 micron long
  • 3 strands….2 F-actin and 1 Tropomyosin (70,000 D)
  • Basic unit of F-actin is G-actin molecule (42,000 D)
    - each G has one ADP attached…x-bridge attachment site
  • During resting phase (phase 4)…tropomyosin blocks active G sites
20
Q

Anatomy of Tropomyosin

A
  • Spaced along are 3 proteins
    - Troponin I: affinity for actin
    - Troponin T: affinity for tropomyosin
    - Troponin C: affinity for Calcium
  • I and T hold tropomyosin to actin
21
Q

Relationship of contractility and [Ca]

A
  • higher [Ca] = more x-bridges = more contractility = stronger contraction
22
Q

Anatomy of myosin

A
  • fiber = 200 myosin molecules
  • 480,000 D
  • Each head is an ATPase enzyme
  • made of 2 heavy chains / 4 light chains
    • heavy chains wrap around each other to form tail
    • at end of wrap…heavy chains fold on self to create head
    • each head gets 2 light chains on it (total of 4)
23
Q

Pre-load

A
  • volume in ventricle at end of diastole
  • more preload = better cardiac performance
  • this affects INTRINSIC contractility
  • EXTRINSIC would be like shifting starling curve
24
Q

Contraction of Sarcomere

A
  • Ca enters cells and interacts with Troponin C
  • This causes change in Troponin I…exposing binding site
  • X-bridges begin to form
  • head moves and pulls like oars on boat
25
Q

How long does each power stroke move

A
  • 5 nm
26
Q

Power stroke movement process

A
  • ATP binds to head… causing release of head and actin site
  • ATP is hydrolyzed and energy stored in head (cocking it)
    - ADP and phosphate still bound to head
  • Energy filled head form weak bond with new binding site
    - causes phosphate to be released
  • release of phosphate tightens bond and power stroke occurs
    - power stroke causes loss of bound ADP and into rigor stage
  • process will repeat if Ca present
27
Q

How Ca enters cardiac muscle cell

A
  • AP triggers release of Ca into cell through T-tubules
  • 90% of Ca that binds to Troponin C comes from SR
  • Ca entering cell from outside (10%) is just trigger Ca for SR
  • In regular muscle cells…Ca comes from outside…not SR
28
Q

How Ca removed from cardiac muscle cell

A
  • 90% pumped back into SR via ATP pump
    - Phospholamban helps with this
  • 5% pumped out of cell via Ca ATP pump
  • 5% pumped out via Na/Ca pump
  • Also a Na/K pump that helps build gradient for Na/Ca pump
29
Q

Isotonic

A
  • tension stays same…muscle length decreases
  • tension built up is only enough to move…then you get change in length
  • here you get max rate of shortening
30
Q

Isometric

A
  • length stays same….tension builds
  • can build up MAX tension
  • Pre-load determines resting muscle stretch
    • also acts as muscle antagonist (like bicep/tricep)
31
Q

Resting vs Active tension

A
  • Resting: tension created by stretching
  • Active: tension created by stimulation
    - difference between resting and peak isometric tension
    - resting tension is only one we can change
32
Q

Measured systolic pressure

A
  • Max pressure seen in systole
33
Q

Measured diastolic pressure

A
  • minimum pressure seen in diastole

- pressure that must be overcome to open aortic valve

34
Q

Two types of work the heart does

A
  • Pressure build up: to overcome aortic valve pressure and open
  • Ejection of blood: to overcome SVR
35
Q

Why we don’t develop max tension/velocity

A
  • No max tension: can’t have shortening

- No max velocity: only get minimal tension

36
Q

Length of optimal sarcomere

A
  • 2-2.2 microns
  • develops max tension and interaction of actin and myosin
  • perfect amount of overlap
37
Q

Muscle length and SV

A
  • As afterload increases…ability of muscle to shorten decreases
  • This will decrease SV
38
Q

Why cardiac muscle cells arranged circumferentially

A
  • creates twisting/ squeezing of ventricle from bottom-up
39
Q

Law of Laplace

A

T = P x r

T: wall tension
P: intraventricular pressure
r: ventricular radius

555- Physiology & Pathophysilogy (12 decks)

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