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224 Cards in this Set
- Front
- Back
Non-striated muscles
|
Smooth muscle
Blood vessels; airways Innervated by autonomic nervous system |
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Striated muscles
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Skeletal muscle
Cardiac muscle |
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Skeletal Muscle in Heart Failure
|
Skeletal muscles atrophy (‘cachexia’) and lose function
Causes weakness and predisposes to fatigue Affects limbs and respiratory pump |
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Cachexia
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AKA wasting syndrome is loss of weight, muscle atrophy, fatigue, weakness and significant loss of appetite in someone who is not actively trying to lose weight
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What is the muscle fiber analogous to?
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Muscle cell (myocyte)
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What is the functional unit of the muscle?
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Sarcomere
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A muscle fiber is made up of what units?
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Myofibrils
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In a sarcomere, what is responsible for the cross-bridges?
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The myosin head
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Myosin will interact with how many actin filaments?
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6 actin filaments
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Actin will interact with how many myosin filaments?
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3 myosin filament.
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What is the myosin thick filament is a polymer of what?
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Myosin molecules which have flexible cross-bridges (myosin head)
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The flexible cross-bridges of the myosin molecule binds what (2)?
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ATP and actin
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What draws Z lines closer to each other?
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Interaction via flexion of cross bridge develops force and draws Z lines closer to each other
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What allows actin and myosin to interact?
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The rise in intracellular Ca2+
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What causes the rigor state?
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Removal of ADP and Pi from the myosin head
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What is needed to leave the rigor state?
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ATP
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ATP binding to the myosin head will cause what to occur?
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The myosin will discontinue contact with the actin
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ATP being hydrolyzed while bound to the myosin head will do what?
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Give energy to the myosin head and put it back into a position of binding.
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What happens when free Ca2+ binds to troponin C?
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Cause a conformational shift in the tropomyosin to allow for interaction between the myosin head and the active binding site on the actin filament.
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What is the duration of a muscle action potential?
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2-3 msec
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What is the sarcolema?
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A muscle-plasma membrane
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Ca2+ is released from a storage site known as what?
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Sarcoplasmic reticulum.
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What is the sarcoplasmic reticulum?
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Ca2+ is released from a storage site known as the sarcoplasmic reticulum.
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What do the transverse tubules do in regard to stimulating the release of calcium ions?
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Bring action potentials into the interior of the skeletal muscle fibers, so that the wave of depolarization passes close to the sarcoplasmic reticulum, stimulating the release of calcium ions.
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What happens in the synaptic cleft during an influx of Ca2+?
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Ach vesicles are released
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Ach vesicles being released into the synaptic cleft will ultimately allow what to happen?
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Allow for sodium entry into the cell (causes the end plate potential (EPP))
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How do the sodium channels in the synaptic cleft operate?
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These sodium channels are not voltage-gated. (the entry of sodium does allow for a depolarization of end plate region)
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What produces an AP in the muscle in regards to sodium channels?
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The depolarization from non voltage-gated sodium channels will hit the voltage gated sodium channels and allow for an inward flow of sodium into the cell (this will produce an AP in a muscle)
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What is the “final integrator”?
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The α-motor neuron
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Is there such thing as an IPSP at the motor end-plate?
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NO
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What happens to Ca2+ at the end of the action potential?
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Ca2+ is taken back in the sarcoplasmic reticulum by active transport
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By what method is Ca2+ taken back in the sarcoplasmic reticulum?
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Active transport
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What will cause a contraction of the motor unit?
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An action potential from the alpha motor unit
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You can increase the amount of work performed by muscles by doing what (in regards to motor units)?
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Increasing the amount of motor units recruited
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Can cardiac muscle recruit additional units for work?
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NO
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What happens during tetanus?
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High AP frequency leads to summation
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How is the myocardium function like a syncytium?
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If one myocyte depolarizes, then they will ALL eventually depolarize.
The heart functions as if it were one tissue due to the gap junctions between the myocytes. |
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What is passive force?
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The force displayed even though there is no contraction
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What is active force?
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The difference between peak force and passive force
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What is total force?
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Passive force + Active force
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Increasing the initial length of muscle will do what?
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Increases the tension produced during contraction.
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What is Lmax?
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The point at which increasing the initial stretch on muscle will not increase the development of active tension
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Explanation for Active Length-Tension Relationship - CLASSICAL
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sliding filament hypothesis --> at Lmax optimal overlap of the thick and thin filaments allows maximum number of tension-generating cross bridges
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Explanation for Active Length-Tension Relationship - HEART MUSCLE
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“length-dependent activation” = the fraction of the total potential cross bridges that are activated at any given free Ca2+ increases with increasing muscle length
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How is the ascending limb of the active-length relationship a homeostatic cycle?
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An increase in muscle length increases active tension, which would tend to increase shortening, and decrease muscle length.
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What effect will heart muscle shortening have?
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The more the heart muscle shortens, the more the volume will change
The amount that muscle shortens will appear as stroke volume |
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Light load
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light load / large Δ L, rapid ΔL/ Δ t (velocity)
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Heavy load
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heavy load / small Δ L, slow Δ L/ Δ t (velocity)
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What will an increase in afterload do?
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Decrease the change in length
Decrease Δ L/ Δ t |
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Po
|
There is a maximum load, P0, that the muscle can just barely lift.
|
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What will an increase in arterial BP do?
|
Decrease stroke volume
Decrease rate of ejection |
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Stroke volume
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Amount of blood ejected per beat
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Vmax
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A theoretical maximum velocity of shortening that could be obtained if the muscle did not have to lift the preload and its own weight.
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Vmax is a good indicator of what?
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Characterizes the health of a muscle ( a person in heart failure will have a low Vmax)
Indicator of contractability or ionotropic state |
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MVo2
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The metabolic demand of the myocardium – rate of oxygen consumption of the myocardium
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Vmax applied to heart
|
Vmax sets the maximum rate at which the heart can develop pressure and eject blood.
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Positive inotropic intervention
|
Norepinephrine (a sympathomimetic intervention):
Increases force w/o an increase in preload increases dF/dt Decreases the duration of contraction |
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Positive inotropic will do what to the F-V curve?
|
Shifts the F-V curve to the right so that
a) Increase Vmax b) Increase Po |
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Blood pressure
|
Force per unit area
Force units: dynes Area: cm2 Pressure = dyne/cm2 |
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Blood pressure
|
is the result of work that the heart has performed;
it is stored energy, or energy/ml of blood this energy is used - “dissipated” - in overcoming the viscous forces within blood to move blood around the circulation. |
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Kinetic energy in the heart
|
The heart also expends energy to accelerate the blood from zero velocity when inside the ventricles during diastole to peak velocity during ejection
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Mercury
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mm Hg stands for “millimeters of mercury”
Is 13.6 times more dense than blood (or water). |
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Preload is analogous to what term?
|
Jugular venous pressure
|
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In a patient with congestive heart failure a physician will note the height of what?
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The height to which his/her veins are engorged within the neck - a fluid column
|
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Right atrial pressure
|
Very low - almost, but not quite, zero mm Hg; just enough energy remains in the blood entering the heart to fill the ventricle(s) in preparation for the next beat.
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Transmural pressure
|
The difference in pressure between the inside and outside of the ventricles determines their volume, or preload
|
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Preload
|
The volume of blood inside the ventricle(s) immediately prior to the beginning of systole; a major determinant of stroke volume.
This volume is determined by the pressure inside the ventricle minus the pressure outside the ventricle (which, by the way, changes with respiration). |
|
Afterload
|
Roughly speaking, arterial blood pressure
Afterload is a major determinant of the amount of work the heart must perform (i.e., energy consumption = MVO2, the rate (e.g., ml/min) of oxygen consumption by the myocardium (M)) |
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CO
|
cardiac output (L/min)
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PAo
|
mean aortic pressure (mm Hg)
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PRA
|
right atrial pressure (almost 0 mm Hg, and often neglected in this computation)
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TPR (equation)
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Pao (equation)
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Consequences of parallel arrangement of hydraulic resistances in the circulation
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Arterial pressure can be controlled by altering the hydraulic resistance of individual vascular beds while, flow through individual vascular beds can be markedly increased or decreased without producing major changes in TPR and, thereby, mean arterial pressure.
|
|
Cost of hypertension
|
Elevated BP forces the heart to work harder even though stroke volume is not increased
Hypertension will eventually lead to myocardial hypertrophy and, finally, heart failure |
|
Ventricular Phases
0 1 2 3 4 |
Rising
Rapid Repolarization Plateau Repolarization Electrical Diastole |
|
Em
|
The AP is a trans-membrane potential difference (in ventricular muscle)
|
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Permeability
|
The permeability of a membrane to a given ion is a measure of the ease with which the ion can pass through (permeate) the membrane.
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What is the permeability of the membrane to potassium (PK) during electrical diastole?
|
High
|
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Equilibrium potential
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The voltage difference across the cell membrane that is equal in magnitude but opposite in direction to the force driving the ion down its concentration gradient.
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Ek (equation)
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Equilibrium potential for K+ during hyperkalemia/hypokalemia
|
The equilibrium potential for K+ becomes less negative/ more negative.
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Digitalis
|
Digitalis worked on the principle that by freezing the pump, you would raise intracellular sodium--> lead to a rise in intracellular calcium--> make it appear as though the heart is functioning better
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Phase 0
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A ventricular myocyte reaches threshold, stimulated by current from adjacent cell(s).
Rapid depolarization (dV/dt) is due to an influx of Na (a positively charged ion). |
|
Fast inward current
|
The sodium-selective ion channels are time and voltage dependent.
Once the membrane attains threshold a regenerative increase in PNa+ occurs. |
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At the peak of the action potential [Na+]i exceeds [K+]i
True of False |
False
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The sodium ion channel inactivates with sustained depolarization of the membrane (one feature of its time and voltage dependence). What effect does this have on conduction velocity?
|
Decrease conduction velocity
|
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Phase 1
|
The short-lived, partial repolarization following Phase 0 is due to a “transient outward current.”
The identity of this current is still debated. |
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Phase 2
|
During the plateau we can be confident that there is an outward leak of K+.
Therefore, to maintain a (relatively constant) Em there must be an inward current. |
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Slow inward Ca2+ current
|
The slow inward current during the plateau is carried primarily by calcium.
The kinetics of the calcium channel are “slow,” hence the name “slow inward current.” In particular: The rate of onset (activation) is slower than for the sodium channel the current lasts longer (inactivates more slowly) a greater depolarization is required to activate the channel |
|
L-type Ca2+ channel
|
The channel that carries the slow inward current is called the L-type Ca2+ channel.
in partially depolarized (e.g., ischemic muscle), the AP is produced by the slow inward current and conduction is slow. |
|
SA- and AV-nodal cells and Ca2+ current
|
Both the SA- and AV-nodal cells depend primarily upon a Ca2+ current for their action potential. Consequently, the dV/dt is low and the conduction velocity is slow. The latter is particularly important in AV-nodal function.
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K+ current during the plateau
|
The ion channel that is responsible for the high PK+ during Phase 4 has a very interesting property called “inward rectification;” in fact, it is called the Kir channel (among other names). Inward rectification means that the channel’s conductance decreases during the plateau phase. This saves the cell energy since the ATP-driven pumps don’t have to reclaim as much lost K.+
|
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Phase 3
|
Inactivation of the Ca2+ current (slow inward current) helps terminate the plateau phase), but this would not be enough to repolarize the cell rapidly.
Rapid repolarization also requires that an outward current assert itself. |
|
Voltage-dependent K+ channel: IK+
|
Potassium is driven to exit the cell during the plateau by both its concentration gradient and the relatively less-negative (even positive) Em.
Another (i.e., not Kir) channel carries a current called IK activates during the plateau phase. This outward current assures rapid repolarization. |
|
β-agonists
|
Increase the inward flow of trigger Ca2+
Increasing active F and dF/dt Increase the rate of re-sequestration of Ca2+ (shortening systole and speeding relaxation) |
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ERP
|
effective refractory period
The cell cannot be excited until ERP is over. |
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The importance of the long effective refractory period in cardiac muscle
|
Proper function of the heart requires sequential contraction/ejection followed by relaxation/filling. The tension produced by contraction peaks prior to the end of the ERP. Therefore, cardiac muscle cannot tetanize, which protects the heart from sustained contracture and an unremitting systole.
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The SA-node and the origin of the heart beat
|
“Pacemaker cells” in the SA-node spontaneously depolarize to threshold.
This is called the pace-maker potential, or Phase 4 depolarization. The slope (dV/dt) of the pacemaker potential determines heart rate. |
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SA-nodal action potential ECG facts
|
Em is less electro-negative during diastole than in a ventricular myocyte.
lower dV/dt Phase 0 less pronounced plateau |
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Functions of the AV-node
|
A “conduction bridge” between the atria and ventricles
Induction of a delay between atrial and ventricular depolarization A “backup” pacemaker AV-nodal block: protective or a sign of disease |
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Ohm’s law
|
Ohm’s law states that the magnitude of a current (I) flowing in a circuit equals the difference in potential (ΔE) across the circuit divided by the resistance (R) of the circuit:
I = ΔE/R |
|
Atrial repolarization
|
The atria does not have an observable repolarization. The atria are very small and there repolarization takes place during the QRS complex (hearing a mouse speak during a thunder storm)
|
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Salient points of ECG
|
The vector originates at the center of the triangle.
The deflection in any lead is proportional in magnitude of the “shadow” cast by the vector. A vector whose shadow points to the positive pole gives a positive deflection in that lead. |
|
How fast is the ECG recorded?
|
The ECG is recorded at standard paper speed (25 mm/sec.) and standard gain (1 mv/cm).
|
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Mean electrical axis
|
The mean electrical axis is a vector that depicts the average electrical activity over the entire QRS complex.
In a healthy man it should be oriented within the range -30 degrees and +90 degrees. Notice that this points toward the patient’s left side. |
|
Right ventricular hypertrophy (mean electrical axis)
|
The resulting increase in electrical activity from the right ventricle causes the vector to rotate toward the patient’s right side.
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When does the upstroke of the atrial muscle take place?
|
The upstroke of the atrial muscle action potential occurs sometime during the P wave
|
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When does the T wave place (phase)?
|
Phase 3 of an action potential from a ventricular myocyte
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Bundle of His
|
The electrical signal produced by the depolarization of the Purkinje fibers is too small to be seen in the standard ECG. However, if a physician is specifically interested in the conduction system, he/she can pass a bipolar electrode into the heart and position it very near the His bundle. This is called a Bundle of His recording
|
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P wave duration
|
< 0.12 sec
|
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P-R interval
|
0.12 - 0.20 sec
|
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QRS duration
|
0.06 - 0.10 sec
|
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Q-T interval (corrected for HR):
male |
< 0.45 sec
|
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Q-T interval (corrected for HR):
female |
< 0.47 sec
|
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First degree AV-nodal block
|
AV-nodal conduction is slowed, but all supraventricular depolarizations ultimately result in ventricular excitation. The P-R interval is prolonged
|
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Second degree AV-nodal block
|
Some, but not all, atrial signals are conducted to the ventricles.
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Third degree AV-nodal block
|
Complete electrical dissociation between atria and ventricles.
|
|
In third degree block, how are the ventricles excited?
|
A pacemaker in the junctional region of the AV-node “takes over” - this is called a junctional pacemaker.
This may lead to the implantation of a “demand pacemaker” An “excitable focus” within the ventricular myocardium acts as a ventricular ectopic pacemaker. |
|
Supraventricular rhythm
|
The heartbeat normally originates within the SA-node “above” the ventricles
|
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VEB
|
The heartbeat normally originates within the SA-node “above” the ventricles; this is called a supraventricular rhythm. In situations such as myocardial ischemia, however, the beat may originate within one of the ventricles. These ventricular beats disturb the normal rhythm of the heart (i.e., arrhythmias), and can have serious consequences including ventricular fibrillation leading to sudden cardiac death.
|
|
PVC Characteristics
|
The PVC is not preceded by a P wave
It occurs prior to the next expected sinus beat (i.e., it is premature). The shape, amplitude and duration of the QRS complex are “bizarre.”* |
|
PVC Characteristics
|
Systolic pressure is lower for the pre-mature beat; in fact, the ventricle may not develop sufficient pressure to open the aortic valve
There is a compensatory pause prior to the next sinus beat. |
|
Why is the shape of the QRS complex so strange/bizarre in PVC?
|
Because the pacemaker for this beat is ectopic, the wave of depolarization spreads through the myocardium via abnormal, often slowly conducting pathway (--> long duration of QRS). The resulting vector loop is very different, yielding a bizarre QRS.
|
|
What is responsible for the compensatory pause?
|
The next supraventricular depolarization, signaled by the P wave preceding the following beat, occurs at this time (i.e., it’s the natural time for the next atrial beat to occur).
|
|
What is the etiology of a VEB (2)?
|
1. increased automaticity
2. a re-entrant pathway |
|
Increased automaticity
|
Ischemic ventricular myocytes, in particular, may slowly depolarize during Phase 4 or they may display after depolarizations. In the latter case, Em fluctuates to more depolarized states; if Em attains threshold, another action potential may result that is then propagated to surrounding cells.
|
|
Re-entrant rhythm
|
One often sees two beats - a normal sinus beat followed by a ventricular beat - that are coupled (i.e., to each other). A re-entrant pathway is the most probable explanation for this phenomenon.
|
|
A re-entrant pathway requires two conditions (that are created by the ischemia)
|
A unidirectional block
Decremental conduction |
|
How is VF reversed?
|
Counter-shock
|
|
Essential hypertension
|
Chronically elevated arterial blood pressure of unknown etiology
|
|
Myogenic vasoconstriction
|
Local regulatory mechanism in which the small arterioles vasoconstrict in response to an increase in blood pressure. This mechanism maintains a nearly normal capillary pressure, thereby preventing edema
|
|
Stress
|
Force/Area
|
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Pressure (equation)
|
dyne/cm2 X cm/cm = (dyne X cm)/cm3
|
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Pulse pressure
|
Systolic pressure - Diastolic pressure
|
|
Mean arterial blood pressure (equation)
|
1/3(Systolic pressure - Diastolic pressure) + Diastolic pressure
|
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Delta Psystemic
|
Mean aortic BP - right atrial pressure
|
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Compliance
|
Change in volume/change in pressure
|
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Dyspnea
|
Difficulty in breathing
|
|
Gap junctions are built with what protein?
|
Connexin
|
|
How can you increase Po?
|
By increasing the preload so long as you don't exceed Lmax
|
|
Positive inotropism induced by epinephrine will have what effects (3)?
|
The active tension is significantly increased without an increase in preload
The rates of tension rise and tension fall are both markedly increased The duration of the twitch decreases |
|
Titin
|
Attaches the myosin with the Z line
Responsible for the passive characteristics of the muscle Constitutes the series elastic |
|
How are myocytes electrically coupled?
|
Intercalated discs with gap junctions between myocytes
|
|
What can you alter physiologically to affect blood pressure (2)?
|
Cardiac output
Total peripheral resistance |
|
Consequence of resistors in parallel? (think of experiment with 4 beds and valve on the fourth bed)
|
When the valve to the fourth bed is open, there will be a huge increase in that bed, but there will only be a slight decrease in beds 1-3
|
|
Where does the heartbeat originate? Why?
|
SA node; because the myoctyes in the SA node posses automaticity.
|
|
Supraventricular tachycardia
|
Atria depolarizing too fast, AV node will block
|
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Breathing and heart rate
|
Heart rate increases during respiration
Heart rate decreases during expiration |
|
Demand pacemaker
|
Has a lead going down into the heart, measuring the ecg. If heart beat doesn’t come after a certain amount of time, then it initiates a heart beat
|
|
Junctional pacemaker
|
A pacemaker in the junctional region of the AV-node “takes over” - this is called a junctional pacemaker.
|
|
Ventricular ectopic pacemaker
|
An “excitable focus” within the ventricular myocardium acts as a ventricular ectopic pacemaker.
|
|
Compensatory pause
|
Wait until you are on the right time scale for the next beat. The next beat will occur at the time that it was supposed to, so expanded pause between premature beat and the next normal beat
|
|
Flow (L/min)
|
pressure gradient/TPR
|
|
Left ventricular pressure (LVP) during diastole
|
(the muscle is relaxed),very low but it is not 0
|
|
When is the atrial kick observed
|
shortly after the P wave
|
|
LVP drops when?
|
shortly after the T wave
|
|
S1 (lub)
|
S1 results from the reverberations produced by closure of the atrio-ventricular valves.
|
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S2 (dub)
|
S2 is produced by the closure of the aortic and pulmonary valves
|
|
LVEDP
|
left ventricular end diastolic pressure, an index of preload.
|
|
LVEDV
|
left ventricular end diastolic volume, also an index of preload.
|
|
LVESV
|
left ventricular end systolic volume
|
|
SV
|
stroke volume (ml/beat) = LVEDV-LVESV
|
|
atrial blood pressure; during diastole
|
is identical to LVP
|
|
dP/dt
|
rate of development of LVP
|
|
dP/dt max
|
is used as an index of contractility
|
|
Aortic flow
|
rate of ejection of blood into the aorta; first derivative of volume = dV/dt (note units are mL/sec.)
|
|
The heart becomes less compliant (3)
|
myocardial hypertrophy
deposition of less elastic elements aging |
|
Implications of Starling’s Law:
|
The heart is a demand pump: within limits, it pumps whatever volume of blood is delivered to it.
The heart normally functions on the ascending limb of the Frank-Starling relationship. |
|
Sources of ATP
|
Creatine Phosphate
Glycolysis Oxidative Phosphorylation |
|
Transmural pressure
|
Pressure on the inside of vessel - the pressure outside of the vessel
If negative transmural pressure, then no blood flow and the vessel is collapsed Once transmural pressure rises above zero, you will have blood flow |
|
Positive Feedback with Sodium channels
|
Increase in sodium channels during conducting state --> Increase in the conductance of sodium --> Increase the current of sodium --> depolarize the cell --> Activate more sodium channels
|
|
Ventricular myocyte sodium channel after depolarization
|
One of the characteristics of the sodium ion channel is that it inactivates with sustained depolarization of the membrane (one feature of its time and voltage dependence)
|
|
What is the Em of ischemic myocardium?
|
Em of ischemic myocardium is generally significantly less negative than normoxic tissue
|
|
Sodium-Calcium Pump
|
Drives Na in
Drives Ca out |
|
Work
|
W = P x Δ V = ∫ P dV
Work = pressure x change in volume |
|
What is the venous and arterial pressure when there is no cardiac output?
|
Very close to zero
|
|
Conductance
|
1/Resistance
|
|
Phospholamban
|
also phosphorylated = requesters calcium faster = shuts off more quickly
Re-uptakes Calcium by active transport after contraction |
|
Current of injury
|
This will lead to S-T segment changes
The current of injury points toward the positive pole of III. Note that it is perpendicular to aVR, and points toward the negative pole of I |
|
When does arterial pressure hit a maximum value? A minimum value?
|
Arterial pressure peaks during systole, arterial systolic pressure.
Arterial pressure drops during diastole to a low value, arterial diastolic pressure. |
|
Atrial kick
|
the priming force contributed by atrial contraction immediately before ventricular systole that acts to increase the efficiency of ventricular ejection due to acutely increased preload.
|
|
MAP (equation)
|
DBP + 1/3(SBP - DBP)
|
|
Ejection fraction
|
- SV/ LVEDV
- Healthy man 50-60% - Anything less than 50-60 = Heart failure |
|
The majority of filling and ejection takes place when? Why?
|
The majority of blood flow will enter initially and then slowly level off to maximal levels.
This will protect against tachycardia |
|
Typical values
Resting HR |
~71 bpm (53-89 bpm, depending upon one’s age, physical condition)
|
|
Typical values
CO |
~6.5 L/min. (3.6-9.4)
|
|
Typical values
SV |
~93 ml (53-133 ml)
|
|
Typical values
PRA |
5 mm Hg (0.2 – 9)
|
|
Typical values
PLA |
7.9 mm Hg (2-12)
|
|
Typical values
PAo |
122/83 mm Hg
|
|
Typical values
PPA |
22/11 mm Hg
|
|
Diastolic dysfunction
|
If the myocardium becomes stiffer (less compliant), filling is compromised
Will observe decreased compliance (graph will move up and to the left) |
|
Why would you prescribe Beta blockers for decreasing compliance?
|
Beta blocker lengthens the filling period --> increase compliance
|
|
Work in the pressure-volume group?
|
The shaded area within the P-V loop
This determines myocardial metabolic demand |
|
ESPVR
|
End systolic pressure-volume relationship
Line shifts depending on ionotropic state |
|
Pulmonary capillary wedge pressure
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Just behind the tip of the catheter is a small balloon that can be inflated with air (~1 cc). The catheter has one opening (port) at the tip (distal to the balloon) and a second port several centimeters proximal to the balloon. These ports are connected to pressure transducers. When properly positioned in a branch of the pulmonary artery, the distal port measures pulmonary artery pressure (~ 25/10 mmHg) and the proximal port measures right atrial pressure (~ 0-3 mmHg). The balloon is then inflated, which occludes the branch of the pulmonary artery. When this occurs, the pressure in the distal port rapidly falls, and after several seconds, reaches a stable lower value that is very similar to left atrial pressure (LAP, normally about 8-10 mmHg). The balloon is then deflated. The same catheter can be used to measure cardiac output by the thermodilution technique.
The pressure recorded during balloon inflation is similar to LAP because the occluded vessel, along with its distal branches that eventually form the pulmonary veins, acts as a long catheter that measures the blood pressures within the pulmonary veins and left atrium. |
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What would happen if the stroke volume were different in the two ventricles?
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Assume 1/1000th of a ml is in right ventricle --> for every 1000 beats, 1 ml is getting removed from periphery and going to lungs. By the end of the day, all the blood is in the lungs
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How is stroke volume the same for both ventricles?
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Systemic vascular resistance exceeds pulmonary vascular resistance, so less energy (pressure = stored energy) is required to move an equal volume of blood through the pulmonary as compared to system circulations
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Effects of sympathetic stimulation on ventricular function
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Amount of work performed (energy expended) is increased.
Rate of performing work (power) is increased. Preload is the same Increase in pressure and increase in SV = increase amount of work dP/dt increased, amount of ejection increased, duration of systole decreased (ejection requires shorter amount of time) = increased rate of performing work |
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Starling’s law is a homeostatic cycle
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It helps stabilize heart volume
It is responsible for the balance of SVR and SVLV If all else fails, an increase in preload can maintain CO in a failing heart. |
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What happens to the P-V loop when you increase the preload?
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Preload was increased: EDV1 < EDV2
ESPVR delineated the end of ejection SV was significantly increased. The amount of work the heart performed was significantly increased |
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Why was the pressure produced during the premature beat lower than normal?
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Because the preload was decreased due to the shorter filling time.
Because the abnormal excitation pathway lead to less efficient contraction. |
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What happens to the P-V loop when you increase the afterload?
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Afterload was increased: DBPsolid< DBPbroken
ESPVR (still) delineated the end of ejection SV was significantly decreased. The work the heart performed/volume ejected was increased |
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Laplace’s Law (equation)
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P = 2T/r
T= tension P= pressure R= radius |
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An increase in preload will...(Starling)
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An increase in preload will increase CO via Starling’s law (but dilation does place the heart at a mechanical disadvantage);
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An increase in contractility allows...
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An increase in contractility allows the heart to perform more work, more quickly without an increase in preload (this, too, of course, has an energy cost).
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Myosin-Actin Interaction (picture)
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Steps in ECC (pic)
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Why would you want to next cycles?
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increases stability of the regulated variable
The redundancy can “hide” dysfunction in a limb of the regulatory system links physiological function in “separate” organs via the common variable |
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Intrinsic
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Heart self regulates
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Short term
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sitting to standing
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Extrinsic
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Neuronal control
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Intrinsic control of BP
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Tubular excretion which will increase urine output
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Extrinsic control of BP
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Baroreflex that will alter vasomotor tone
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Where are the afferent Vagus fibers that control HR?
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Atria
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Relationship between CO and VR
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They must equal each other. They don't have to be equal for a few beats, but after that, you will die.
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Mean circulatory filling pressure (Pms)
aka mean systemic pressure (Pms) |
is the pressure at which the blood “starts” its return trip to the heart
~7 mm Hg |
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The pressure gradient for venous return is?
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Pmc - Pra
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vascular function curve
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VR = k(Pmc - Pra)
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Vascular function and Ohms law
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V = IR is Ohms law
V = VR I = (Pmc – Pra) k = R^-1 |
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What happens when Pra is too low?
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The heart will collapse on itself
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Steady state operating point
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cardiac function and vascular function must conform to the relationship between Starlings law and vascular function curve
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How does a change in sympathetic nervous activity impact the relationship between CO and VR?
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The heart is able to perform more work w/o a (marked) increase in preload.
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