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82 Cards in this Set
- Front
- Back
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What is the relationship between left and right ventricular work?
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Left ventricular work is about 10X as much as right
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How do we evaluate ventricular work?
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By looking at ventricular pressure vs volume diagrams
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What is another way to evaluate the efficiency of the heart?
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By looking at Ventricular output versus Atrial Pressure
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What are ventricular output versus atrial pressure curves often referred to as?
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Starling cardiac function curves
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What does a Starling cardiac function curve show?
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That as preload increases, it increases atrial pressure, which increases ventricular output.
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Why is the slope of the left ventricle shifted to higher atrial pressures than the slope for the right ventricle?
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Because the right atrium has lower pressures than the left due to the pulmonary pressure it's pumping into.
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Normal CO:
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5 L/min
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What does the slope of the Starling cardiac function curve indicate?
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How much ventricular output increases given a change in atrial pressure and preload
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What does the plateau of the Starling cardiac function curve indicate?
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The maximum permissive pumping ability of the heart.
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Can the plateau change?
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Yes
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What changes the plateau of the heart - its max permissive pumping ability?
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Autonomic nerves
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What is the effect of Sympathetic stimulation of the heart?
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Increased HR and SV
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How much can Symp stimulation increase CO?
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more than 100%
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What is the effect of PNS stimulation of the heart? What nerves do this?
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Decreased HR and SV - Vagal nerves
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What happens if the Vagus stimulation is so strong that it stops the heart?
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The heart will ESCAPE and beat at 20-40 beats per min
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Where exactly does the heart get
-Sympathetic input -Parasymp input |
SNS - to left and right ventricles
PNS - to the SA and AV node |
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So does parasympathetic innervation really alter both HR and SV?
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No; just heartrate
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So what would happen if you blocked parasympathetic input in a resting individual?
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Heartrate would elevate
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What is the first derivative of left ventricular pressure an index of?
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Cardiac contractility
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What are 2 agents that increase contractility?
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Isoproterenol and Atropine
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What is Isoproterenol?
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A beta receptor adrenergic stimulator that increases contractility
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What is Atropine?
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An acetylcholine receptor inhibitor that produces tachycardia
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Normal cardiac output and RAP:
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5 L/min at a RAP of ~0 mm HG
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What does normal sympathetic stimulation do to CO?
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Increases the maximum permissive pumping ability by about 30% - to about 13 L/min for the SAME right atrial pressure.
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What does maximal sympathetic stimulation do to CO?
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Increases the max permissive ability even more - to about 23 L/min
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What does Vagal stimulation do to CO?
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Decreases the max permissive pumping ability.
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Where does electrical stimulation of heart pumping begin?
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At the Sinus (SA) node
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Why does the sinus node set the pace of the heart?
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Because though all electrical tissue in the heart has the ability to spontaneously depolarize, the SA node does it fastest.
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What allows for the atria to contract prior to the ventricles?
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The AV node which has very SLOW propagation of electrical signals.
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What are the main differences in the electrical discharge of a Sinus Node fiber vs that of a normal ventricle muscle fiber?
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-No long plateau in SA node fiber
-Spontaneous discharge -Much less negative resting Em -Drift of Em |
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What is the drifting resting membrane potential of cardiac sinus nodal fibers due to?
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Leak of potassium ions
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What is the basis for changes in heartrate?
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Changes in ionic conductance which affect the slope of the resting membrane potential drift.
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What is the function of the AV node?
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To delay transmission of electrical stimulation from the atria to the ventricles
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What is accomplished by delaying the electrical impulse transmission from atria to ventricles?
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It allows time for the atria to empty.
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What would happen if there were no AV bundle fibers?
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The atria and ventricles would contract at different rates.
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How can the Ventricles contract without impulse transmission through the AV node/bundle?
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Because all electrical tissue is capable of spontaneous depolarization, just slower.
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How much time delay is there before an impulse beginning at the sinus node reaches the ventricular muscle?
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0.16 seconds
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Does impulse transmission through the right vs left atria or ventricles differ?
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No, both atria depolarize fairly uniformly and so do the ventricles.
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What would cause a difference in transmission of electrical impulse in the right heart vs the left heart?
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Blockages in the Bundle branches purkinje fibers.
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And how do we change the spontaneous heart rate?
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By changing the rate of membrane potential drift of the SA node.
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Let's talk about the ionic basis for the spontaneous depolarization of the sinus node cells
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Ok
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What is the membrane potential for cardiac sinus node cells?
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About -50 mV
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What determines the DRIFT of the membrane potential?
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The balance between sodium and potassium ions
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In what phase are sodium and potassium currents cause depolarization of the membrane?
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Phase 4
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What currents set up the increasing membrane potential and what is the result?
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-Inward Funny Sodium current
-Decreasing outward K leak -Result is the opening of Calcium channels which allow influx when threshold is reached |
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At what membrane potentials is the funny sodium current active?
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Below -50 mV
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When do calcium channels open?
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At -55 mV
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What restores ionic composition during phase 4?
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-Na/K ATPase
-Na/2Ca antiporter |
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So the leak of sodium and potassium ions during phase 4 is critical in determining what?
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The slope of the sinus node membrane potential, thus the heartrate.
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What are the calcium channels that open at the end of phase 4 called?
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Transient Fast T-type Ca channels
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What phase begins when T-type calcium channels open?
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Phase 0
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How much calcium do the T-type calcium channels bring in?
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A lot
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What happens during Phase 3?
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-Inward calcium channels close
-Outward K current -Repolarization of the membrane |
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What is the NT from the parasymp nerves that reduces heartrate?
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Acetylcholine
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How does ACh reduce heartrate?
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It opens potassium channels which hyperpolarizes Sinus Node cells and reduces the slope of the resting membrane potential.
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How does hyperpolarization of sinus node cells make heartrate slower?
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It takes longer to reach threshold and calcium influx.
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What is the neurotransmitter released by sympathetic nerves to increase heartrate?
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Norepinephrine
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How does NE increase heartrate?
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It binds and opens sodium channels which depolarizes the membrane and increases the slope of the membrane.
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How does the source of calcium differ between cardiac and skeletal muscle for contraction?
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Skeletal: Ca comes from SR; much more well developed
Cardiac: Ca comes from T-tubules; much more developed |
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Why is it significant that the T-tubules are the major source of calcium for cardiac contraction?
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Because the T-tubules are in direct contact with the ECF, so changes in ECF calcium have a dramatic impact on changes in contractility.
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Do changes in extracellular calcium have much of an effect on skeletal muscle?
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No; it pretty much just relies on SR stores of calcium.
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Since there is more interplay of cardiac muscle cells with extracellular calcium, what pumps become more important?
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PMCA - for pumping calcium back out into the ECF after contraction.
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What happens when an AP comes in contact with a cardiac muscle cell?
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It spreads to the interior via the T-tubule system and along the SR
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What happens as the AP spreads along the SR?
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Calcium is released from the SR and much moreso from the T-tubules and combines with troponin C
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How much bigger is the T-tubule volume in the heart myocytes compared to skeletal?
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25X
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What happens when Calcium binds troponin C?
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It tugs on tropomyosin and uncovers the active sites of Actin filaments for Myosin cocked heads
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When ventricular myocytes contract, what ion is responsible for the depolarization?
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Sodium
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What channels open to allow sodium influx in ventricular myocytes?
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Fast sodium channels
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What ion and channel are responsible for the long plateau phase of ventricular myocytes?
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L-type calcium channels
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What happens at the end of the plateau phase to bring the membrane potential of cardiac myocytes back down to resting?
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Potassium leaks out of the myocyte and voltage-gated potassium channels open
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What is the resting membrane potential of cardiac myocytes?
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-90 mV
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What happens to the fast sodium channels at the peak of the membrane potential during cardiac myocyte depolarization?
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They become inactivated to prevent repeated stimulation
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What happens to the potassium current during the plateau phase of the cardiac myocyte depolarization?
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-Potassium permeability is reduced from normal nearly 5X
-Calcium current remains elevated by L-type channels |
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What are 2 major differences in skeletal muscle compared to cardiac myocytes w/ regard to ion currents?
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-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 |
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What are 4 hormones and drugs that influence myocardial contractility?
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-Catecholamines (B-agonists)
-Beta blockers -Ca channel blockers -Digitalis glycosides |
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What do beta agonists do?
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Increase adenylate cyclase activity, which increases calcium influx thru the muscle cell membrane, increasing cytosolic Calcium
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What do Beta-blockers do?
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Decrease intracellular calcium by blocking sympathetic stimulation of calcium channels and Na/Ca exchangers
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What do Calcium channel blockers do?
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Block L-type Calcium channels
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What does Digitalis do?
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Inhibits Na/K ATPase, Ca channels, and Na/Ca exchangers
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How does calcium affect myocardial contractility?
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It increases the sensitivity of contractile proteins to Calcium
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Can the Vmax of cardiac muscle change?
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YES
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Can the Vmax of skeletal muscle change?
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No
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