19 Regulation Of The Heart Flashcards
what is the frank starling mechanism?
it states: an increase in preload will lead to increased force of contraction and stroke volume.
What causes the increase in force of contraction with increased preload?
The stretch of the muscle fibers themselves result in a more forceful contraction.
what is the staircase phenomenon?
contractility increases with increases in heart rate.
This is caused by 1) increased numbers of action potentials 2) more Ca+ per action potential.
what is extrasystole?
aka PVC (pre ventricular contraction)
T/F a PVC results in an immediate large contraction?
False, it results in a premature weak contraction followed by a large strong contraction.
Why is the beat that follows the PVC (contraction A) so large?
more time to fill (preload)
more calcium is ready for contraction B
(It is also important to note that contraction C is also a little larger)
How do the sympathetics work on the heart?
1) stellate ganglia (periphery)
2) release norepi which targets the B1 receptors of the SA node, AV node, and atria.
How do the parasympathetics work on the heart?
1) vegus nerve
2) release acetylcholine which activates the muscarinic (M2) receptor on the AV node, SA node, atria, and very little on ventricles.
Once the B1 receptor is stimulated, what is the pathway?
B1 are coupled to G-proteins, activation of adenylate cyclase, ATP to cAMP, activation of PKA, phosphorylation of proteins.
Once the M2 receptor is stimulated, what is the pathway?
M2 (muscarinic receptors) are coupled to a G-protein. The G-protein inhibits PKA activation through cAMP.
what is the nodose ganglia? where signals synapse?
cell bodies of afferent neuronal fibers from the heart that sense discomfort. Remember that the cell bodies are in the nodose gangia but that they synapse in the nucleus tractus solitari (NTS) that follow.
where are the cell bodies located for the afferent fibers picking up chemical irritation (pain) form the heart?
Dorsal root ganglia
what is the net effect with stimulation of the B1 receptor on the heart?
increased contractility
decrease the duration of contraction
Once PKA has become activated from the sympathetics, what does it do?
phosphorylates phospholamban
phosphorylates troponin 1
phosphorylates Ca+ channel
What effect does phosphorylation of the Ca+ channel have?
increased Ca+ influx and increased contractility.
what effect does phosphorylation have on troponin 1?
troponin 1 increases the off-rate of calcium from troponin C which allows for a more speedy relaxation and a decreased duration of contraction.
what is the effect of phosphorylating phospholamban?
(Phospholamban normally inhibits SERCA.) By phosphorylating it, SERCA can work faster allowing for quicker reuptake of Ca+ into the SR resulting in increased speed of relaxation, and decreased duration of contraction.
What is inotropy?
Increased contractility
T/F Sympathetic stimulation causes shortening of diastole and lengthening of systole?
False, just the opposite
what does increased contractility do to your diastolic ventricular pressure?
reduces it.
Increased contractility causes?
1) increased peak pressure
2) increased velocity of contraction
3) shortening of systole and lengthening of diastole
4) decreased ventricular diastolic pressure
5) decreased end systolic ventricular volume because of a higher ejection fraction.
T/F the parasympathetics work of the ventricles directly?
True, but only very little. Most of the effects of the parasympathetics are on the AV and SA nodes.
If all of the autonomics are blocked, what would be the new heart rate?
about 100 beats per minute
what is atropine?
a muscarinic (M2) receptor antagonist. Therefore it will cause blockage of the parasympathetics and speed the heart up.
what is propranolol?
a beta adrenergic receptor antagonist. Therefore it will cause blockage of the sympathetics and slow down the heart. (AKA beta blocker)
Are the parasympathetics fast or slow?
very fast, they can regulate the heart on a beat to beat basis.
T/F At rest, the sympathetics are active?
True, but just a little bit. The majority of innervation is from the parasympathetics. This was shown by giving propranolol which blocks beta receptors and seeing a slight drop in heart rate.
Which of the two, sympathetics or parasympathetics, affect the heart more quickly?
parasympathetics. Sympathetics are still relatively fast.
T/F Hypocalcemia and hyperkalemia both cause muscles to twitch easily?
True.
Ca+ = threshold
K+ = resting membrane potential
how do the parasympathetics control the Nodal cells? 4 ways
1) The acetylcholine activates a G protein that releases a heterodimer that opens the inward rectifier K+ channels (GIRK). This causes phase 4 to be more negative which takes longer to reach threshold.
2) decreasing the steepness of phase 4
3) moving threshold to a more positive value.
4) slowing conduction through AV node
T/F during exercise, the sympathetic nervous system takes over the majority of the bodily functions?
True, so it increases heart rate.
What would cause an increase in the slope of phase 4 nodal cells?
Increasing permeability of funny channels (cations)
increasing permeability of Ca+ channels.
Decreasing permeability of K+ channels
What activates the renin-angiotensin pathway?
1) decreased blood flow to kidneys (due to decreased C.O. or increased peripheral resistance)
2) juxtaglomerular cells release renin
3) renin converts angiotensin 1 to angiotensin 2
4) Angiotensin 2 causes the release of aldosterone, ADH, and increases sympathetic activity.
How is it possible that cardiac transplant patients can increase their heart rates without the sympathetic innervation?
By the release of Epinephrine from the adrenal medulla.
