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23 Cards in this Set

  • Front
  • Back
How are cardiac cells coupled and what does that mean for AP propagation?
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.
What is automaticity and what are the two primary automaticity nodes in the heart?
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)
What is the difference between diastole and systole?
Systole - compression and emptying of heart (left ventricle) of blood

Diastole - relaxation
What are the two sources of contraction producing Ca++ in cardiac cells?
(30%) EC Ca++ influx
(70%) SR Ca++

there is NO Ca++ influx in skeletal muscle cells
What is the mechanism for EC influx of Ca++ in cardiac muscle cells?
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.
How is Ca++ removed from the cytoplasm and what physiological obstacles can occur when these mechanisms are defective?
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++
When is mitochondrial update of Ca++ (due to its negative interior membrane) clinically significant?
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.
Why do cardiac muscle cells not experience tetany or summation?
L-type transport channels produce long Ca++ pulses -> long refractory periods.
What three characteristics of cardiac muscle regulate active force and what the hell is the difference between them?
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
What happens when afterload changes?
/\ 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
What does afterload look like relative to a normal PV loop?
What does contractility depend on?
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.
What is the main inotropic influence of contractility?
concentration of and sensitivity to IC Ca++
What fundamental principle does Frank-Starling Law state?
cardiac output = cardiac input
Where does 90% of the energy consumed by the heart come from?
oxidation of fatty acids which is obviously HIGHLY dependent upon oxygen
What is more critical to the heart being able to sustain contraction than oxygen from blood supply?
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
What happens to sarcomeric segment length during systole in a normal heart compared to an ischemic heart?
ischemic fibers cannot contract, so they lengthen (flaccid) instead of shorten (contract)
LaPlace Relationship
Explain how beta-adrenergics effect cardiac muscle regulation.
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
Explain how parasympathetic regulation occurs for cardiac muscle cells.
ACh binds to muscarinic receptors to inhibit the adenylyl cyclase used to produce cAMP. so it downregulates cAMP.
Describe the pathological series that most commonly causes physiological hypertrophy.
increased arterial hypertension -> increased afterload -> increased ventricular force -> physiological hypertrophy
Aside from physiological hypertrophy, what other general type of ventricular parthology can occur?
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.
IN order of descending reliability, what is the best measure of preload?
1. muscle fiber length
2. LV volume
3. LV diameter
5. LA pressure
6. Pulmonary capillary wedge pressure
7. Pulmonary artery pressure
8. Central venous pressure