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224 Cards in this Set

  • Front
  • Back
Non-striated muscles
Smooth muscle
Blood vessels; airways
Innervated by autonomic nervous system
Striated muscles
Skeletal muscle
Cardiac muscle
Skeletal Muscle in Heart Failure
Skeletal muscles atrophy (‘cachexia’) and lose function
Causes weakness and predisposes to fatigue
Affects limbs and respiratory pump
Cachexia
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
What is the muscle fiber analogous to?
Muscle cell (myocyte)
What is the functional unit of the muscle?
Sarcomere
A muscle fiber is made up of what units?
Myofibrils
In a sarcomere, what is responsible for the cross-bridges?
The myosin head
Myosin will interact with how many actin filaments?
6 actin filaments
Actin will interact with how many myosin filaments?
3 myosin filament.
What is the myosin thick filament is a polymer of what?
Myosin molecules which have flexible cross-bridges (myosin head)
The flexible cross-bridges of the myosin molecule binds what (2)?
ATP and actin
What draws Z lines closer to each other?
Interaction via flexion of cross bridge develops force and draws Z lines closer to each other
What allows actin and myosin to interact?
The rise in intracellular Ca2+
What causes the rigor state?
Removal of ADP and Pi from the myosin head
What is needed to leave the rigor state?
ATP
ATP binding to the myosin head will cause what to occur?
The myosin will discontinue contact with the actin
ATP being hydrolyzed while bound to the myosin head will do what?
Give energy to the myosin head and put it back into a position of binding.
What happens when free Ca2+ binds to troponin C?
Cause a conformational shift in the tropomyosin to allow for interaction between the myosin head and the active binding site on the actin filament.
What is the duration of a muscle action potential?
2-3 msec
What is the sarcolema?
A muscle-plasma membrane
Ca2+ is released from a storage site known as what?
Sarcoplasmic reticulum.
What is the sarcoplasmic reticulum?
Ca2+ is released from a storage site known as the sarcoplasmic reticulum.
What do the transverse tubules do in regard to stimulating the release of calcium ions?
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.
What happens in the synaptic cleft during an influx of Ca2+?
Ach vesicles are released
Ach vesicles being released into the synaptic cleft will ultimately allow what to happen?
Allow for sodium entry into the cell (causes the end plate potential (EPP))
How do the sodium channels in the synaptic cleft operate?
These sodium channels are not voltage-gated. (the entry of sodium does allow for a depolarization of end plate region)
What produces an AP in the muscle in regards to sodium channels?
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)
What is the “final integrator”?
The α-motor neuron
Is there such thing as an IPSP at the motor end-plate?
NO
What happens to Ca2+ at the end of the action potential?
Ca2+ is taken back in the sarcoplasmic reticulum by active transport
By what method is Ca2+ taken back in the sarcoplasmic reticulum?
Active transport
What will cause a contraction of the motor unit?
An action potential from the alpha motor unit
You can increase the amount of work performed by muscles by doing what (in regards to motor units)?
Increasing the amount of motor units recruited
Can cardiac muscle recruit additional units for work?
NO
What happens during tetanus?
High AP frequency leads to summation
How is the myocardium function like a syncytium?
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.
What is passive force?
The force displayed even though there is no contraction
What is active force?
The difference between peak force and passive force
What is total force?
Passive force + Active force
Increasing the initial length of muscle will do what?
Increases the tension produced during contraction.
What is Lmax?
The point at which increasing the initial stretch on muscle will not increase the development of active tension
Explanation for Active Length-Tension Relationship - CLASSICAL
sliding filament hypothesis --> at Lmax optimal overlap of the thick and thin filaments allows maximum number of tension-generating cross bridges
Explanation for Active Length-Tension Relationship - HEART MUSCLE
“length-dependent activation” = the fraction of the total potential cross bridges that are activated at any given free Ca2+ increases with increasing muscle length
How is the ascending limb of the active-length relationship a homeostatic cycle?
An increase in muscle length increases active tension, which would tend to increase shortening, and decrease muscle length.
What effect will heart muscle shortening have?
The more the heart muscle shortens, the more the volume will change
The amount that muscle shortens will appear as stroke volume
Light load
light load / large Δ L, rapid ΔL/ Δ t (velocity)
Heavy load
heavy load / small Δ L, slow Δ L/ Δ t (velocity)
What will an increase in afterload do?
Decrease the change in length
Decrease Δ L/ Δ t
Po
There is a maximum load, P0, that the muscle can just barely lift.
What will an increase in arterial BP do?
Decrease stroke volume
Decrease rate of ejection
Stroke volume
Amount of blood ejected per beat
Vmax
A theoretical maximum velocity of shortening that could be obtained if the muscle did not have to lift the preload and its own weight.
Vmax is a good indicator of what?
Characterizes the health of a muscle ( a person in heart failure will have a low Vmax)

Indicator of contractability or ionotropic state
MVo2
The metabolic demand of the myocardium – rate of oxygen consumption of the myocardium
Vmax applied to heart
Vmax sets the maximum rate at which the heart can develop pressure and eject blood.
Positive inotropic intervention
Norepinephrine (a sympathomimetic intervention):

Increases force w/o an increase in preload

increases dF/dt

Decreases the duration of contraction
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
Blood pressure
Force per unit area

Force units: dynes

Area: cm2

Pressure = dyne/cm2
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.
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
Mercury
mm Hg stands for “millimeters of mercury”

Is 13.6 times more dense than blood (or water).
Preload is analogous to what term?
Jugular venous pressure
In a patient with congestive heart failure a physician will note the height of what?
The height to which his/her veins are engorged within the neck - a fluid column
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.
Transmural pressure
The difference in pressure between the inside and outside of the ventricles determines their volume, or preload
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))
CO
cardiac output (L/min)
PAo
mean aortic pressure (mm Hg)
PRA
right atrial pressure (almost 0 mm Hg, and often neglected in this computation)
TPR (equation)
Pao (equation)
Consequences of parallel arrangement of hydraulic resistances in the circulation
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)
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.
What is the permeability of the membrane to potassium (PK) during electrical diastole?
High
Equilibrium potential
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.
Ek (equation)
Equilibrium potential for K+ during hyperkalemia/hypokalemia
The equilibrium potential for K+ becomes less negative/ more negative.
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
Phase 0
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.
At the peak of the action potential [Na+]i exceeds [K+]i

True of False
False
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
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.
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.
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.
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.+
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)
ERP
effective refractory period

The cell cannot be excited until ERP is over.
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.
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.
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
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
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)
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).
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.
When does the upstroke of the atrial muscle take place?
The upstroke of the atrial muscle action potential occurs sometime during the P wave
When does the T wave place (phase)?
Phase 3 of an action potential from a ventricular myocyte
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
P wave duration
< 0.12 sec
P-R interval
0.12 - 0.20 sec
QRS duration
0.06 - 0.10 sec
Q-T interval (corrected for HR):

male
< 0.45 sec
Q-T interval (corrected for HR):

female
< 0.47 sec
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
Second degree AV-nodal block
Some, but not all, atrial signals are conducted to the ventricles.
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
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
Pressure (equation)
dyne/cm2 X cm/cm = (dyne X cm)/cm3
Pulse pressure
Systolic pressure - Diastolic pressure
Mean arterial blood pressure (equation)
1/3(Systolic pressure - Diastolic pressure) + Diastolic pressure
Delta Psystemic
Mean aortic BP - right atrial pressure
Compliance
Change in volume/change in pressure
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
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.
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
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.
What would happen if the stroke volume were different in the two ventricles?
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
How is stroke volume the same for both ventricles?
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
Effects of sympathetic stimulation on ventricular function
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
Starling’s law is a homeostatic cycle
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.
What happens to the P-V loop when you increase the preload?
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
Why was the pressure produced during the premature beat lower than normal?
Because the preload was decreased due to the shorter filling time.

Because the abnormal excitation pathway lead to less efficient contraction.
What happens to the P-V loop when you increase the afterload?
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
Laplace’s Law (equation)
P = 2T/r

T= tension
P= pressure
R= radius
An increase in preload will...(Starling)
An increase in preload will increase CO via Starling’s law (but dilation does place the heart at a mechanical disadvantage);
An increase in contractility allows...
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).
Myosin-Actin Interaction (picture)
Steps in ECC (pic)
Why would you want to next cycles?
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
Intrinsic
Heart self regulates
Short term
sitting to standing
Extrinsic
Neuronal control
Intrinsic control of BP
Tubular excretion which will increase urine output
Extrinsic control of BP
Baroreflex that will alter vasomotor tone
Where are the afferent Vagus fibers that control HR?
Atria
Relationship between CO and VR
They must equal each other. They don't have to be equal for a few beats, but after that, you will die.
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
The pressure gradient for venous return is?
Pmc - Pra
vascular function curve
VR = k(Pmc - Pra)
Vascular function and Ohms law
V = IR is Ohms law
V = VR
I = (Pmc – Pra)
k = R^-1
What happens when Pra is too low?
The heart will collapse on itself
Steady state operating point
cardiac function and vascular function must conform to the relationship between Starlings law and vascular function curve
How does a change in sympathetic nervous activity impact the relationship between CO and VR?
The heart is able to perform more work w/o a (marked) increase in preload.