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82 Cards in this Set

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  • Back
What is the relationship between left and right ventricular work?
Left ventricular work is about 10X as much as right
How do we evaluate ventricular work?
By looking at ventricular pressure vs volume diagrams
What is another way to evaluate the efficiency of the heart?
By looking at Ventricular output versus Atrial Pressure
What are ventricular output versus atrial pressure curves often referred to as?
Starling cardiac function curves
What does a Starling cardiac function curve show?
That as preload increases, it increases atrial pressure, which increases ventricular output.
Why is the slope of the left ventricle shifted to higher atrial pressures than the slope for the right ventricle?
Because the right atrium has lower pressures than the left due to the pulmonary pressure it's pumping into.
Normal CO:
5 L/min
What does the slope of the Starling cardiac function curve indicate?
How much ventricular output increases given a change in atrial pressure and preload
What does the plateau of the Starling cardiac function curve indicate?
The maximum permissive pumping ability of the heart.
Can the plateau change?
What changes the plateau of the heart - its max permissive pumping ability?
Autonomic nerves
What is the effect of Sympathetic stimulation of the heart?
Increased HR and SV
How much can Symp stimulation increase CO?
more than 100%
What is the effect of PNS stimulation of the heart? What nerves do this?
Decreased HR and SV - Vagal nerves
What happens if the Vagus stimulation is so strong that it stops the heart?
The heart will ESCAPE and beat at 20-40 beats per min
Where exactly does the heart get
-Sympathetic input
-Parasymp input
SNS - to left and right ventricles
PNS - to the SA and AV node
So does parasympathetic innervation really alter both HR and SV?
No; just heartrate
So what would happen if you blocked parasympathetic input in a resting individual?
Heartrate would elevate
What is the first derivative of left ventricular pressure an index of?
Cardiac contractility
What are 2 agents that increase contractility?
Isoproterenol and Atropine
What is Isoproterenol?
A beta receptor adrenergic stimulator that increases contractility
What is Atropine?
An acetylcholine receptor inhibitor that produces tachycardia
Normal cardiac output and RAP:
5 L/min at a RAP of ~0 mm HG
What does normal sympathetic stimulation do to CO?
Increases the maximum permissive pumping ability by about 30% - to about 13 L/min for the SAME right atrial pressure.
What does maximal sympathetic stimulation do to CO?
Increases the max permissive ability even more - to about 23 L/min
What does Vagal stimulation do to CO?
Decreases the max permissive pumping ability.
Where does electrical stimulation of heart pumping begin?
At the Sinus (SA) node
Why does the sinus node set the pace of the heart?
Because though all electrical tissue in the heart has the ability to spontaneously depolarize, the SA node does it fastest.
What allows for the atria to contract prior to the ventricles?
The AV node which has very SLOW propagation of electrical signals.
What are the main differences in the electrical discharge of a Sinus Node fiber vs that of a normal ventricle muscle fiber?
-No long plateau in SA node fiber
-Spontaneous discharge
-Much less negative resting Em
-Drift of Em
What is the drifting resting membrane potential of cardiac sinus nodal fibers due to?
Leak of potassium ions
What is the basis for changes in heartrate?
Changes in ionic conductance which affect the slope of the resting membrane potential drift.
What is the function of the AV node?
To delay transmission of electrical stimulation from the atria to the ventricles
What is accomplished by delaying the electrical impulse transmission from atria to ventricles?
It allows time for the atria to empty.
What would happen if there were no AV bundle fibers?
The atria and ventricles would contract at different rates.
How can the Ventricles contract without impulse transmission through the AV node/bundle?
Because all electrical tissue is capable of spontaneous depolarization, just slower.
How much time delay is there before an impulse beginning at the sinus node reaches the ventricular muscle?
0.16 seconds
Does impulse transmission through the right vs left atria or ventricles differ?
No, both atria depolarize fairly uniformly and so do the ventricles.
What would cause a difference in transmission of electrical impulse in the right heart vs the left heart?
Blockages in the Bundle branches purkinje fibers.
And how do we change the spontaneous heart rate?
By changing the rate of membrane potential drift of the SA node.
Let's talk about the ionic basis for the spontaneous depolarization of the sinus node cells
What is the membrane potential for cardiac sinus node cells?
About -50 mV
What determines the DRIFT of the membrane potential?
The balance between sodium and potassium ions
In what phase are sodium and potassium currents cause depolarization of the membrane?
Phase 4
What currents set up the increasing membrane potential and what is the result?
-Inward Funny Sodium current
-Decreasing outward K leak
-Result is the opening of Calcium channels which allow influx when threshold is reached
At what membrane potentials is the funny sodium current active?
Below -50 mV
When do calcium channels open?
At -55 mV
What restores ionic composition during phase 4?
-Na/K ATPase
-Na/2Ca antiporter
So the leak of sodium and potassium ions during phase 4 is critical in determining what?
The slope of the sinus node membrane potential, thus the heartrate.
What are the calcium channels that open at the end of phase 4 called?
Transient Fast T-type Ca channels
What phase begins when T-type calcium channels open?
Phase 0
How much calcium do the T-type calcium channels bring in?
A lot
What happens during Phase 3?
-Inward calcium channels close
-Outward K current
-Repolarization of the membrane
What is the NT from the parasymp nerves that reduces heartrate?
How does ACh reduce heartrate?
It opens potassium channels which hyperpolarizes Sinus Node cells and reduces the slope of the resting membrane potential.
How does hyperpolarization of sinus node cells make heartrate slower?
It takes longer to reach threshold and calcium influx.
What is the neurotransmitter released by sympathetic nerves to increase heartrate?
How does NE increase heartrate?
It binds and opens sodium channels which depolarizes the membrane and increases the slope of the membrane.
How does the source of calcium differ between cardiac and skeletal muscle for contraction?
Skeletal: Ca comes from SR; much more well developed
Cardiac: Ca comes from T-tubules; much more developed
Why is it significant that the T-tubules are the major source of calcium for cardiac contraction?
Because the T-tubules are in direct contact with the ECF, so changes in ECF calcium have a dramatic impact on changes in contractility.
Do changes in extracellular calcium have much of an effect on skeletal muscle?
No; it pretty much just relies on SR stores of calcium.
Since there is more interplay of cardiac muscle cells with extracellular calcium, what pumps become more important?
PMCA - for pumping calcium back out into the ECF after contraction.
What happens when an AP comes in contact with a cardiac muscle cell?
It spreads to the interior via the T-tubule system and along the SR
What happens as the AP spreads along the SR?
Calcium is released from the SR and much moreso from the T-tubules and combines with troponin C
How much bigger is the T-tubule volume in the heart myocytes compared to skeletal?
What happens when Calcium binds troponin C?
It tugs on tropomyosin and uncovers the active sites of Actin filaments for Myosin cocked heads
When ventricular myocytes contract, what ion is responsible for the depolarization?
What channels open to allow sodium influx in ventricular myocytes?
Fast sodium channels
What ion and channel are responsible for the long plateau phase of ventricular myocytes?
L-type calcium channels
What happens at the end of the plateau phase to bring the membrane potential of cardiac myocytes back down to resting?
Potassium leaks out of the myocyte and voltage-gated potassium channels open
What is the resting membrane potential of cardiac myocytes?
-90 mV
What happens to the fast sodium channels at the peak of the membrane potential during cardiac myocyte depolarization?
They become inactivated to prevent repeated stimulation
What happens to the potassium current during the plateau phase of the cardiac myocyte depolarization?
-Potassium permeability is reduced from normal nearly 5X
-Calcium current remains elevated by L-type channels
What are 2 major differences in skeletal muscle compared to cardiac myocytes w/ regard to ion currents?
-Skeletal muscle APs are via the opening of Fast Na channels which are VERY fast
-No 5X decrease in K permeability like in the cardiac plateau phase
What are 4 hormones and drugs that influence myocardial contractility?
-Catecholamines (B-agonists)
-Beta blockers
-Ca channel blockers
-Digitalis glycosides
What do beta agonists do?
Increase adenylate cyclase activity, which increases calcium influx thru the muscle cell membrane, increasing cytosolic Calcium
What do Beta-blockers do?
Decrease intracellular calcium by blocking sympathetic stimulation of calcium channels and Na/Ca exchangers
What do Calcium channel blockers do?
Block L-type Calcium channels
What does Digitalis do?
Inhibits Na/K ATPase, Ca channels, and Na/Ca exchangers
How does calcium affect myocardial contractility?
It increases the sensitivity of contractile proteins to Calcium
Can the Vmax of cardiac muscle change?
Can the Vmax of skeletal muscle change?