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23 Cards in this Set
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- Back
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How are cardiac cells coupled and what does that mean for AP propagation?
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Cardiac cells are electrically coupled through gap junctions, which brings neighboring cells to AP threshold when even a single cell is excited.
If one goes, they all go. This also means that summation does not occur as it does in skeletal muscle. |
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What is automaticity and what are the two primary automaticity nodes in the heart?
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Automaticity - can cause threshold w/o neural input
SA node - highest rate of spontaneous depolarization (60-100 normal). primary pacemaker. AV node - secondary pacemaker. (40-60) |
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What is the difference between diastole and systole?
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Systole - compression and emptying of heart (left ventricle) of blood
Diastole - relaxation |
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What are the two sources of contraction producing Ca++ in cardiac cells?
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(30%) EC Ca++ influx
(70%) SR Ca++ there is NO Ca++ influx in skeletal muscle cells |
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What is the mechanism for EC influx of Ca++ in cardiac muscle cells?
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L-type, voltage-gated channels allow EC Ca++ into cell.
Ca++ binds to RYRs (ryanodine receptors), which are Ca++ gated Ca++ gates on the SR to release the IC Ca++ of which binds to troponin to cause contraction. |
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How is Ca++ removed from the cytoplasm and what physiological obstacles can occur when these mechanisms are defective?
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Na/Ca ATPase is the main transporter of Ca back into SR
\/ Na/Ca ATPase /\ EC Ca++ /\ Force Na+-Ca++ exchanger handles IC to EC transfer of Ca++ |
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When is mitochondrial update of Ca++ (due to its negative interior membrane) clinically significant?
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When ATP production is reduced by hypoxia, ischemia, or other pathology, excessive Ca++ build-up in mitochondria causes inhibition of oxadative metabolism -> worsening a cardiac condition.
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Why do cardiac muscle cells not experience tetany or summation?
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L-type transport channels produce long Ca++ pulses -> long refractory periods.
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What three characteristics of cardiac muscle regulate active force and what the hell is the difference between them?
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1. preload - the potential for magnitude of active force based on the sarcomere length immediately before a contraction. /\ stretching brings actin-myosin filaments closer together and increases sensitivity to Ca++
2. afterload - essentially this is the aortic pressure, but more correctly it is the pressure against the ventricle must overcome in order to undergo systole 3. contractility - this is an inotropically controlled property of cardiac muscle |
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What happens when afterload changes?
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/\ afterload
/\ aortic pressure /\ P @ aortic valve opening for systole /\ EDP, /\ EDV, /\ ESP, \/ SV SV \/ because /\ afterload causes blood to be left over in the ventricle and combined with the new diastolic blood. the ventricular pressure will overcome, but SV will lessen |
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What does afterload look like relative to a normal PV loop?
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booyah.
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What does contractility depend on?
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By definition it is the amount of active force that can be produced at a certain preload but that is controlled by extrinsic factors. Extrinsic factors to up (+ inotropic state), contractility goes up at that preload.
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What is the main inotropic influence of contractility?
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concentration of and sensitivity to IC Ca++
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What fundamental principle does Frank-Starling Law state?
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cardiac output = cardiac input
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Where does 90% of the energy consumed by the heart come from?
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oxidation of fatty acids which is obviously HIGHLY dependent upon oxygen
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What is more critical to the heart being able to sustain contraction than oxygen from blood supply?
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ATP/ADP ratio because with a minor decrease in this ratio, free energy from hydrolysis of ATP falls sharply -> no ATP for voltage-gated Ca++ channels and cystolic and mitochondrial Ca++ rises to harmful levels
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What happens to sarcomeric segment length during systole in a normal heart compared to an ischemic heart?
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ischemic fibers cannot contract, so they lengthen (flaccid) instead of shorten (contract)
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LaPlace Relationship
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?
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Explain how beta-adrenergics effect cardiac muscle regulation.
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beta-adrenergics are related to sympathetic control of the heart, so norepi and epi attach to the beta1-adrenergic receptors and increase cAMP production which allows for pathways to be phosphorylated and IC Ca++ to increase
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Explain how parasympathetic regulation occurs for cardiac muscle cells.
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ACh binds to muscarinic receptors to inhibit the adenylyl cyclase used to produce cAMP. so it downregulates cAMP.
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Describe the pathological series that most commonly causes physiological hypertrophy.
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increased arterial hypertension -> increased afterload -> increased ventricular force -> physiological hypertrophy
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Aside from physiological hypertrophy, what other general type of ventricular parthology can occur?
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dialted left ventricular failure where the chamber size increases due to excessive stretch and walls thin like an overinflated balloon caused by a failure of ventricular contractility -> functional atrophy and thinning because of lack of active force.
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IN order of descending reliability, what is the best measure of preload?
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1. muscle fiber length
2. LV volume 3. LV diameter 4. LV EDP 5. LA pressure 6. Pulmonary capillary wedge pressure 7. Pulmonary artery pressure 8. Central venous pressure |
