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Cardiology > Cardiac Function I, II, and III > Flashcards

Cardiac Function I, II, and III Flashcards

1
Q

Cardiac Cycle

  • P wave & QRS complex
  • Ventricular filling
  • Isovolumic contraction
  • Ventricular ejection
  • Isovolumic relaxation
A
  • P wave & QRS complex
    • P wave: atrial depolarization
    • QRS complex: ventricular depolarization
  • Ventricular filling (diastole)
    • Ventricular pressure < pulm/aortic pressure
    • Ventricular pressure < atrial pressure
    • AV valves open, pulm/aortic valves closed
  • Isovolumic contraction (systole)
    • Ventricular pressure < pulm/aortic pressure
    • Ventricular pressure > atrial pressure
    • AV & pulm/aortic valves closed
  • Ventricular ejection (systole)
    • Ventricular pressure > pulm/aortic pressure
    • Ventricular pressure > atrial pressure
    • AV valves closed, pulm/aortic valves open
  • Isovolumic relaxation (diastole)
    • Ventricular pressure < pulm/aortic pressure
    • Ventricular pressure > atrial pressure
    • AV & pulm/aortic valves closed
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2
Q

Cardiac Cycle

  • Passive filling
  • Active filling
  • End-diastolic volume (EDV)
  • End-systolic volume (ESV)
  • Stroke volume (SV)
  • Ejection fraction (EF)
A
  • Passive filling
    • Blood flowing from atria (higher pressure) to ventricles (lower pressure)
  • Active filling
    • Due to atrial contraction
  • End-diastolic volume (EDV)
    • Max ventricular volume at the end of filling
  • End-systolic volume (ESV)
    • Min ventricular volume at the end of ejection
  • Stroke volume (SV)
    • Volume ejected by teh ventricle during one cardiac cycle
    • SV = EDV - ESV
  • Ejection fraction (EF)
    • SV as a fraction of EDV
    • EF (%) = 100 * (SV / EDV)
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3
Q

Cardiac Muscle Structure

  • Intercalated disks
  • Syncytium
  • Sarcomere
  • Actin
  • Troponin & Tropomyosin
  • Myosin
  • Titin
  • Molecular motor
A
  • Intercalated disks
    • Muscle cells are interconnected by intercalated disks
    • Allow ions & electrical current to pass through
  • Syncytium
    • When one cardiac muscl cell gets excited, the AP spreads rapidly to all cell sint eh latticework
  • Sarcomere
    • Basic unit that gives a striated appearance
    • Orderly arrangements of thick & thin filaments
  • Actin
    • Comprise thin filaments
    • Globular (G) actin monomers are linked together in a chain-like structure & form 2 helically arranged polymer strands
  • Troponin & Tropomyosin
    • Regulatory proteins that regulate cardiac muscle contraction
  • Myosin
    • Comprise thick filaments
    • Dimers consisting of 2 intertwined subunits
    • Each subunit has a long tail & a protruding head called a cross-bridge
  • Titin
    • Large, elastic protein that extends along each thick filament from the M line to each Z line
    • Determine the passive mechanical properties of cardiac muscle
  • Molecular motor
    • Interaciton between actin & myosin is responsible for muscle force generation & muscle shortening
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4
Q

Thin filament activation

  • Resting condition
  • Electrical stimulation
A
  • Resting condition
    • [Ca2+]i is low
    • Myosin is blocked from interacting w/ actin
  • Electrical stimulation
    • Muscle cell depolarization
    • Influx of Ca2+ through voltage-gated Ca2+ channels in the sarcolemmal membrane triggers a large release of Ca2+ from the SR –> [Ca2+]i rises
    • Ca2+ binds to troponin C
    • Comformational change in troponin-tropomyosin complex –> it no longer blocks active sites on actin
    • Actin-myosin interaction can take place
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5
Q

Actin-myosin interaction

  • Cross-bridge cycle
  • Rigor
  • Relaxation
  • Key points
A
  • Unbinding of myosin and actin
    • ATP enters the ATPase site on myosin
    • Causes myosin that’s bound to actin to detach
  • Cocking of the myosin head
    • ATP hydrolyzed into ADP and Pi
    • Energy is captured by myosin (high-energy state)
  • Binding of myosin to actin
    • Myosin head binds to neighboring actin
    • Release of Pi from myosin ATPase site
  • Power stroke
    • Release of Pi transitions mysoin to the low-energy state
    • Myosin head pivots toward the middle of the sarcomere, pulling the thin filament along with it
    • Results in force generation and sarcomere (muscle) shortening
    • ADP is released from the myosin ATPase site
  • Rigor
    • Myosin is in the low-energy state, tightly bound to acin
    • Myosin is unable to separate until a new ATP molecule binds to the mysoin ATPase site
    • Rigor mortis: in the absence of ATP, the cross-bridge cycle gets stuck here
  • Relaxation
    • Ca2+ unbinds from troponin & is transported back to the SR via the ATP-dependent pump (Ca2+-ATPase)
    • Ca2+ is also removed from teh cell in exchange for extracellular Na+ via the Na+-Ca2+ exchanger on the sarcolemmal membrane
  • Key points
    • Contractile activity originates from the pulling of thin filaments by myosin heads bound to actin (the power stroke)
    • The energy needed for this is derived from ATP hydrolysis by myosin ATPase
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6
Q

4 ways to augment the intensity of contraction

A
  • Increasing sarcomere (cell) length
    • Alters overlap b/n thin & thick filaments
    • Increases actin-myosin interaction
    • Affects myofilament Ca2+ sensitivity
  • Increasing cytosolic Ca2+ levels
    • Cellular Ca2+ handling: higher Ca2+ levels produce greater thin filament activation, greater number of cross-bridges, & more intense contraction
  • Increasing thin filament activation
    • Changes Ca2+ binding & unbinding to troponin
    • Associated w/ cardiac cell remodeling
  • Altering kinetic rate constants of cross-bridge cycling
    • Number of cross-bridges in the post-power stroke increase
    • Associated w/ cardiac cell remodeling
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7
Q

Force-length relationship

A
  • As the initial muscle length is increased via stretching, both initial (or passive) force & peak force increase
  • Initial (passive) force: muscle is in the resting or passive condition (not stimulated)
  • Peak developed (active) force: amount of max force generated by the act of active contraction
    • Difference b/n peak force & passive force
    • Increases w/ muscle length
  • Ex. if you stretch a rubber band, you’ll generate higher forces
    • Muscle contracts more vigorously as it’s stretched during diastole
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8
Q

Peak developed (active) force-length relationship

  • Structural basis: degree of overlap b/n thin & thick filaments
  • Length-dependent Ca2+ sensitivity
A
  • Peak developed (active) force increases as muscle length increases
  • Structural basis: degree of overlap b/n thin & thick filaments
    • Muscle length changes cause sarcomere length to change
    • Alters thin-thick filament overlap & size of the pool for myosin-(cross-bridge)-actin interaction
    • Sarcomere length = 2.2-2.3: when the actin filaments fully overlap cross-bridges on each side of the myosin filaments
    • Sarcomere length > 2.2-2.3: linear decline in force until it becomes 0 at length 3.6
    • Sarcomere length < 2.2-2.3: steeper decline in force due to steric interference from double overlap of thin filaments
  • Length-dependent Ca2+ sensitivity
    • Longer sarcomere lengths –> greater Ca2+ sensitivity
    • At a given [Ca2+]i, decreased sarcomere length –> decreased active force
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9
Q

Passive force-length relationship

  • Relationship
  • Interstitial collagen
  • Intracellular titin
A
  • Amount of force needed to stretch the muscle by a certain amount increases as the muscle length is increased
  • Interstitial collagen
    • Collagen b/n muscle cells
    • Increase in collagen –> increased muscle stiffness (steeper slope)
      • Ex. myocardial infarction, excessive collagen deposition w/ hypertensive hypertrophy
    • Affects muscle stiffness at longer muscle lengths
  • Intracellular titin
    • Giant elastic protein that runs along thick filaments from Z to M lines
    • Affects muscle stiffness at shorter muscle lengths
    • Skeletal muscle isoforms are larger & more extensible than cardiac muscle isoforms
      • Relaxed cardiac muscle at shorter lengths displays greater passive stiffness than skeletal muscle
    • 2 isoforms expressed in cardiac muscle: N2B (less extensible) & N2BA (more extensible)
      • Ratio of isoforms correlates w/ cardiac muscle stiffness
    • Large forces are required to stretch cardiac muscle to optimal sarcomere length
      • Cardiac muscle normally functions on the ascending limb of the force-length relationship
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10
Q

Force-velocity relationship

A
  • Under physiological conditions, muscle shortens as it contracts
    • An increase in shortening load decreases the degree, duration, & velocity of shortening
    • Max shortening velociyt occurs at the beginning of shortening
  • Experiment
    • Stimulate muscle attached to a weight
    • Muscle increases force until the point where it lifts the weight
    • Amount of shortening decreases as you increase the weight
    • Afterload: amount of weight muscle is working against
  • Inverse relationship b/n initial velocity & shortening load
    • Higher load = lower velocity
    • Max load: isometric contraction
      • Muscle shortening & velocity = 0
      • Muscle force is greatest
    • Min load: shortening load = 0
      • Muscle shortening & velocity is greatest
      • Muscle force = 0
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11
Q

Preload, Afterload, & Contractility

A
  • Preload
    • Initial/resting muscle (sarcomere) length
    • Increased preload –> increased intensity of muscle contraction
  • Afterload
    • Force against which the muscle has to contract & shorten
    • Increased afterload –> decreased velocity & shortening
  • Contractility
    • Increased contractility –> increased intensity of muscle contraction
      • More peak active force is generated at any given length
      • Shortening velocity is higher at any given force
    • Affected by [Ca2+]i, thin filament activation, & kinetic rate constants of cross-bridge cycling
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12
Q

Physiological regulation of cardiac muscle contractility

  • Sympathetic nervous system
  • Sympathetic transmitter NE causes…
  • Net effects of NE on muscle contractility
  • Parasympathetic (vagal) innervation
A
  • Sympathetic nervous system
    • Primary physiological regulator of muscle contractility
    • NE increases [Ca2+]i –> increases HR –> increases contracitlity (staircase effect)
  • Sympathetic transmitter NE causes…
    • Increased influx of Ca2+ through voltage-dependent Ca2+ channels
    • Increased Ca2+ release from teh SR
    • Increased rate of Ca2+ uptake by the SR
    • Increased rate of cross-bridge cycling
    • Net effect: increased magnitude of muscle force + augmetned kinetic aspects –> greater muscle shortening
  • Net effects of NE on muscle contractility
    • ​Increase force
    • Increase shortening
    • Increase rate of force development & relaxation
  • Parasympathetic (vagal) innervation
    • ​Direct effect on cardiac muscle contractility
    • Indirect effect on muscle contractility through vagal influence on HR
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13
Q

Ventricular pressure-volume-flow and muscle force-length-velocity

  • Connection b/n ventricles & muscles
  • Laplace Law
A
  • Connection b/n ventricles & muscles
    • Ventricular volume ~ muscular length
    • Ventricular flow ~ muscular velocity
    • Ventricular pressure ~ muscular force
  • Laplace Law
    • σ = (P / 2h) * r = (P / 2h) * (3 / 4π)1/3 * V1/3
      • σ = muscle stress
      • P = ventricular pressure
      • h = ventricular wall thickness
      • r = ventricular chamber radius
      • V = ventricular volume
    • Stress: directly proportional to pressure & volume and inversely proportional to wall thickness
    • Dilated ventricle: increased muscle stress
    • Hypertensive hypertrophy: opposing effects of increased pressure and hypertrophy (increased wall thickness) may cancel each other
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14
Q

End diastolic pressure volume relationship (EDPVR)

A
  • Compliance curve of the relaxed diastolic left ventricle
  • Slope = contractility
    • Increased contractility: slope shifts up & to the left
    • Decreased contractility: slope shifts down & to the right
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15
Q

Ventricular Preload

  • Best measure
  • Factors that determine it
    • Venous compliance
    • Blood volume
    • Resistance to venous return (RVR)
    • Intrathoracic pressure (ITP)
    • HR via its effects on filling time
    • Ventricular passive stiffness
    • Posture
    • Activity of skeletal muscle
A
  • Best measure
    • Ventricular end-diastolic volume (EDV)
    • Determines muscle & sarcomere length
  • Factors that determine it
    • Venous compliance
      • Increase compliance –> decrease preload
    • Blood volume
      • Increase blood volume –> increase preload
    • Resistance to venous return (RVR)
      • Increase RVR –> decrease preload
    • Intrathoracic pressure (ITP)
      • Increase ITP –> decrease preload
    • HR via its effects on filling time
      • Increase heart rate –> decrease filling time –> decrease preload
    • Ventricular passive stiffness
      • Increase stiffness –> decrease preload
    • Posture
      • Supine to upright –> decrease preload
    • Activity of skeletal muscles
      • Increase activity –> increase preload
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16
Q

Ventricular Afterload

  • Best measures
  • Effect of ventricular contractile activity
  • Mechanical opposition to ejection (afterload) is determined by…
A
  • Best measures
    • Ventricular pressure during ejection
    • End-systolic ventricular pressure (ESP) ~ mean arterial pressure (MAP)
    • Total peripheral resistance (TPR)
  • Effect of ventricular contractile activity
    • Increase ventricular contractility –> increase cardiac output –> increase MAP –> increase afterload
  • Mechanical oppositoin to ejection (afterload) is determined by…
    • Extrinsic factors (ex. TPR)
    • Intrinsic factors (ex. ventricular contractility)
17
Q

Ventricular Contractility

  • Best measure
  • Following epinephrine administration
  • Alternative indices of ventricular contractility
A
  • Best measure
    • End systolic pressure volume relationship (ESPVR)
  • Following epinephrine administration
    • ESPVR slope is increased w/o changing intercept –> increased contractility
    • Ventricle produces more pressure for a given volume & generates more stroke volume for a given afterload (end-systolic pressure)
  • Alternative indices of ventricular contractility
    • Ventricular stroke volume - EDV/EDP relationship (Frank-Starling)
    • Venticualr stroke work - EDV/EDP relationsihp (ventricular function curve)
    • Ventricular max rate of pressure development - EDV relationship
      • Increased contractility shifts relationship leftward so ventricle can generate more stroke work for a given preload
18
Q

How stroke volume depends on ventricular preload, afterload, and contractility

A
  • SV = EDV - ESV
  • Increase preload –> increase EDV –> increase SV
  • Increase afterload –> increaes ESV –> decrease SV
  • Increase contractility –> increase SV
19
Q

Physiological regulation of ventricular contractility

A
  • Primary regulator: sympathetic nervous system via NE & Epi release
    • Increase SNS –> increase HR –> increase [Ca2+]i –> increase ventricular contractility (staircase effect)
    • Increase NE –> increase rate of force development –> increase shortening velocity during ejection –> increase rate of relaxation –> increase contractility
  • SNS allows heart to maintain a high cardiac output during exercise
    • Increase HR –> decrase filling period –> adversely affect EDV & stroke volume
    • However, increase HR –> increase shortening velocity to maintain or increaes stroke volume
  • Parasympathetic nervous system
    • Little direct effect on ventricular contractility
    • Release Ach –> increase PNS activity –> decrease HR –> indirectly decrease ventricular contractility
20
Q

Physiological relevance of the Frank-Starling relationship

  • Frank-starling relationship
  • If right heart output is transiently greater than left heart output
  • In a diseased heart (ex. dilated cardiomyopathy)
A
  • Frank-starling relationship
    • Increase preload –> increase contraction intensity
    • Cardiac muscle operates on ascending limb b/c shorter & less extensible cardiac titin resists myocyte overextension
    • Slope is steep so small changes in preload –> large changes in contraction intensity
      • Stroke volume is less sensitive to changes in afterload
    • Intrinsic mechanism for maintaining equal right & left ventricular outputs
  • If right heart output is transiently greater than left heart output
    • Blood pools in pulmonary circulation
    • Increase pulmonary venous pressure
    • Increase left atrial pressure
    • Increase left ventricular filling & EDV (preload)
    • Increase left heart output
  • In a diseased heart (ex. dilated cardiomyopathy)
    • ​Reduced steepness of the Frank-Starling relationship
    • Stroke volume becomes more sensitive to changes in afterload
21
Q

Similarities between ventricular and muscular mechanical behaviors

A
  • Increase in volume (muscule length) –> more intense contraction (higher pressures)
  • ESPVR ~ ventricular peak (active) pressure-volume relationship
  • EDPVR ~ ventricular passive pressure-volume relationship
  • Similar effects of changes in preload, muscle length shortening, & ejection volume (stroke volume)
  • Similar effects of increased contractility & afterload
22
Q

Ventricular passive mechanical behavior

  • Characterized by…
  • Myocardial composition
  • Ratio of EDV and ventricular muscle mass
A
  • Characterized by the end diastolic pressure-volume relationship
    • Slope: nonlinear, increases as EDV increases
  • Myocardial composition
    • Increased collagen –> leftward shift –> increased stiffness
    • Shift of titin from N2BA (more extensible) to N2B (less extensible) –> leftward shift –> increased stiffness
  • Ratio of EDV and ventricular muscle mass
    • Increased muscle mass in idiopathic hypertrophic subaortic stenosis –> increased EDP –> decreased filling –> decreased EDV
    • Coronary artery disease –> increased collagen –> increased stiffness
23
Q

Stroke Work and Myocardial Oxygen Consumption (MVO2)

A
  • Stroke work
    • Ventricle does external work during a cardiac cycle when it generates pressure to eject the stroke volume
    • SW = area enclosed by the P-V loop confined within ESPVR & EDPVR curves
      • A = end-diastole
      • B = onset of ejection
      • C = end-systole
      • D = onset of filling
      • Width = SV = EDV - ESV
      • Height = ESP - EDP = MAP - EDP
    • SW = (MAP - EDP) * SV
  • Myocardial oxygen consumption (MVO2)
    • MVO2 = input energy used to generate ATP for contractions
    • The same SW can result in different MVO2s
      • Higher MVO2: high MAP, low SV
      • Lower MVO2: low MAP, high SV
24
Q

Pressure-Volume Area (PVA)

A
  • Pressure-volume area (PVA): total mechanical energy generated by the ventricle
    • Stroke work (SW): external energy
    • End-systolic potential energy (PE): internal energy, dissipated as heat
  • Increase PVA –> increase MVO2
25
Q

Reconciling MVO2 for pressure load work and volume load work

  • Condition 1: increase EDV
  • Condition 2: increase ESV
A
  • SW for conditoin 2 = condition 1
  • PVA for condition 2 > condition 1
  • MVO2 for condition 2 > condition 1
26
Q

Factors affecting MVO2

  • Preload
  • Afterload
  • Contractiliy
  • Heart rate
A
  • Preload
    • Increaes preload (EDV) –> increase MVO2
    • Least significant effect
  • Afterload
    • Increase afterload (ESP or MAP) –> increase MVO2
    • Most significant effect
  • Contractility
    • Increase [Ca2+]i –> increase activation-related o2 consumption –> increase contractility (leftward shift in ESPVR) –> increase MVO2
    • Moderately significant effect
    • Drugs/perturbations that increase contractility w/o mobilizing more Ca2+ may not increase MVO2
  • Heart rate
    • Increase [Ca2+]i –> increase contractility –> increase HR
    • Modestly significant effect

Cardiology (40 decks)

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