Human Anatomy, Physiology, and Medicine. Anything human!
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1. I'm not sure contracitlity is a word, but if you expand I can try and help.
2. CO binds irreversibly to haemoglobin in red blood cells and so prevents them from carrying oxygen around the body. Not sure how F+F would affect this.
3. Is PNS peripheral nervous system here? If not you've lost me - try to expand acronyms!
4. Enervated simply means that nerves are attached, so in this case both parasympathetic and sympathetic nervous fibres are linked to the sino-atrial node. The nervous system uses action potentials to pass on signals, and these pass on the signals to effectors (such as cardiac muscle) via neuromuscular junctions so any chance in the potential of the node will affect the action of the muscle.
Therefore Ach (acetylcholine) is a neurotransmitter that's inhibitory in this situation and slows down heart rate by slowing the rate of action potentials that are fired, thus slowing the overall speed of contractions. Likewise norepinephrine/noradrenaline speed up the firing of APs and so speed heart beating. The last bit's just telling you that norepinephrine can also be produced in places other than the nerve terminals in the SA node, and these will amplify the effects by binding to the post-synaptic terminal as well.
Thanks for the quick reply. ^_^
1) Contractility is defined as the ability of the muscles of the heart to contract in the presence of a stimulus. Now I'm trying to understand why that would increase or decrease SV (how much blood gets pumped out?) [/b]
2) In the book it mentions HR is affected by both. I was wondering if SV was effected by either of them.
PNS - Parasympathetic (Rest)
SNS - Sympathetic (FF)
I found this great link that explains HR but I'm not understanding the specific sentences explaining why HR increases and why it decreases. (I know you explained it 4 but the website seems explained something called vagus tone?)
"activation of the vagus nerve innervating the SA node" and
"There is both a withdrawal of vagal tone and an activation of sympathetic nerves innervating the SA node."
4) Thanks for the great explanation. Few questions xD
- Does the SA node sends a signal to the heart to contract?
- Action potential effects muscles by sending signals so any change in AP effects muscles?
- ACH slows down actional potential, which slows down contractions, which lowers HR?
- Epinephrine increases AP signals which increase in heart rate?
Okay I'll do the 4. questions first because I'm relatively sure I can answer them correctly. The SA node sends a signal via the atrial-ventricular node (AV) down the purkinje fibres in the centre of the heart, causing it to contract from the bottom upwards (so the ventricles can empty themselves before the atria contract to fill them up again). The SA node's also known as the pacemaker since it sets the rate at which the whole system moves. (Incidentally it's one of the few parts of the nervous system that works completely independently of the brain).
I don't know how much you know about nerve signal transmission! Suffice to say if a sufficient amount of ion movement is caused by whatever stimulus it launches an action potential, and this will cause the muscle to contract. The AP is an absolute value (it's either ON or OFF) so there's no change. The muscle contracts simple if it's switched on.
ACh (small 'h' so not to get confused with adrenocorticohormone!) slows down the RATE of APs - so how many times it's switched on in a given period of time. Otherwise all correct, and just the reverse for epinephrine.
1. Stroke volume in the amount of blood pumped from a single ventricle and so is entirely dependent on the size of the ventricle and nothing else! Over time obvious a greater number of contractions would pump more, but this would be cardiac output rather than SV.
2. See above
3. Okay well the heartbeat is regulated by both PNS and the SNS. The PNS is associated with autonomic functions (so ones we don't think about like breathing in and out) and via the vagus nerve controls the baseline heartrate of about 60-80. However during exercise etc. this needs to speed up to supply more oxygen and at this point a sympathetic function takes over and allows the HR to rise.
So the conclusions I came up from #4 are right? xD Yay
I can't tell from number 2 answer from above. I get SV is depend on the size, so a larger size would mean higher SV. But is SV effected by PNS or SNS? (So many abbreviations!)
Does vagus nerve only effect autonomic functions? Or does it effect both PNS and SNS?
And how does it effect it? Does it send a signal?
My book says increased temperature increases heart rate.
Wouldn't hypothermia (low temperature) increase your HR because your heart would be pumping more blood to warm itself up?
Yes congratulations on 4!
I'm afraid I don't really know for 2. Contractions in the atria at a basal level are caused by the SA node (which is part of neither system), but it is affected by parasympathetic from the vagus to slow it down, and sympathetic to speed it up. To the best of my knowledge the vagus nerve is only involved in autonomic functions. Sorry I can't be more help here :s
Heart rate increases when the body's trying to combat change. So you're quite correct in thinking that heart rate will increase in the cold as the body tries to warm itself (especially when shivering) but it's also worth noting that it also withdraws blood supply from extremities to conserve heat.
There are two ways to look at cold: firstly the heart rate should slow along with all metabolic processes since it's these that generate the majority of our heat. However the peripheral blood vessels all dilate to let blood closer to the surface to cool us off (hence we go red in the face when we're overheating). This lowers blood pressure and means the heart has to take up the slack by pumping more. I think you're going to have to use judgement here because it's going to depend on the severity of the cold!
Except for decreasing the heart rate and the force of contraction, PNS also reduces the conduction velocity of cardiac muscle fibers. Parasympathetic stimulation can also result in increased activity by glands that control bronchial secretions.
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