Ballam 2: Cardiac Muscle Contraction Flashcards
Phase 2 plateau is the moment calcium
rushes into the muscle cell
The calcium influx from P2 causes
calcium induced calcium release from the sarcoplasmic reticulum
Trigger Ca
the influx from Phase 2 of the action potential, causes more calcium release in the cell
Magnitude of tension of myocardial cells is proportional to the amount of
intracellular calcium released
Two factors determine Ca amount in the muscle cell
the amount that rushed in during the depolarization and the amount that was stored previously and released by trigger Ca
Positive Inotropic Effects
Agents/Stimulation that causes an increase in the rate of tension and the peak tension
Negative Inotropic Effects
Agents/Stimulation that cause a decrease in the rate of tension and the peak tension of a muscle cell
Sympathetics and Inotropism
is a positive inotropic effector
uses beta 1 receptors and norepi
three important results of (sympathetic) positive inotropic effect
1) greater rate of tension
2) greater peak tension
3) faster relaxation
How fast is relaxation achieved after sympathetic agents acting as positive inotropic agents?
very fast. they use beta-1 receptors to achieve this relaxation.
two phosophrylating events that are key during the Calcium upswing
phosphorylation of the Ca channel
phosphorylation of phospholamban, a Ca ATPase in the SR, which causes Ca uptake into SR
These two events are initiated by sympathetic inotropic effect
Parasympathetic Nervous System has what kind of effect
negative inotropic effect
Parasympathetic Nervous System have negative inotropic effect on the
atria, and mediated by muscurinic receptors, which have the Gi couple protein adenyl cyclase: inhibits Ca release
how does the Parasympathetic Nervous System negative effect tension?
2 ways:
1) ACh decreases Calcium inward current
2) Increases potassium inward current, thereby shortening the plateau phase
these together decrease trigger calcium and calcium release from the SR
How does an increased heart rate increase contractility?
heart contractility is proportional to intracellular Ca2+
thus, increasing the heart rate increases the number of AP’s/min, increasing the amount of trigger Ca2+ released
if heart rate is increased because of beta-1 adrenergic stimulation or by catecholamines, these too will increase intracellular Ca (Trigger Ca)
2) more inward Ca2+ means more will be stored for the next round.
Positive Staircase effect
Also called the Treppe or Bowditch’s Staircase
this is when the heart rate doubles because the contractility increases with each increase in calcium from a previous action potential
the very first beat after the increase in heart rate shows no increase in tension because extra Ca hot not accumulated
tension increases stepwise
Postextrasystolic Potentiation
this occurs because of an anomalous extra beat generated by a latent pacemaker, the tension builds so the next beat is greater than normal
the extrasystolic beat itself is weak, but the very next beat will be generated because of the added calcium
Cardiac Glycosides: how they work
class of drugs that act is positive inotropic agents these drugs are derived from extracts of the foxglove plant
these drugs inhibit Na-K ATPase at the extracellular-K binding site.
When the Na-K ATPase is inhibited, less Na is pumped out of the cell, increasing intracellular Na concentration
Na intracellularly increases —> causes decrease in the Ca-Na pump (one of the mechanisms of purging calcium and pulling sodium in): as this pump begins to halt, the intracellular calcium increases because none of it is leaving, thus the calcium increases
Digoxin
Cardiac Glycoside, positive inotropic agent
inhibits Na-K ATPase located in the cell membrane of the myocardial cell.
used in congestive heart failure
Length-Tension: three effectors
1) the amount of overlap between thick and thin filaments
2) increasing muscle length causes increased troponin C sensitivity to calcium
3) increasing muscle length increases Ca release from SR
maximal length of a typical myocardial cell is
2.2 micrometers, L(max)
Frank Starling Relationship
Systolic tension is a function of “end-diastolic volume”
this relationship states that the volume of blood ejected by the ventricles depends on the volume present in the ventricle at the end of diastole
in turn, end diastolic volume depends on venous return (how much it receives from the venous system)
The upward slope of the diastole curve on the Frank-Starling curve indicates that
that as the ventricles fill, the passive tension increases as well. this reflects stretching muscle fibers.
Preload of the left ventricle.
Left-ventricular end diastolic volume . or end diastolic fiber length
Afterload of the left ventricle
is aortic pressure
When is cardiac muscle’s shortening velocity “maximal”
when afterload is zero
Stroke volume
volume of blood ejected by the ventricle on each beat
difference between volume of blood before and after ejection, typically, 70 mL
Ejection fraction
fraction of the end diastolic volume ejected in each stroke volume
cardiac output
total volume ejected by ventricle/time
total volume of blood ejected per unit of time.
stroke volume x heart rate
Ejection Fraction
The effectiveness of the ventricles ejecting blood, so its the fraction of the end-diastolic volume ejected in one stroke volume, usually around 55%
stroke volume/end diastolic volume
