Naked Science Forum
Life Sciences => Physiology & Medicine => Topic started by: nilmot on 24/03/2004 13:25:28
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In college we've learnt that there is a delay between the atrio-systole and ventricular-systole because this allows the atrium to contract longer so as much blood can enter the ventricle as possible.
Say if the heart rate is significantly increased (from 75 to 160)is there still a delay between the two contraction?
Tom
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I would think so. The delay would be very very short.
Angel
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yes, if there was no delay there'd be no point for your heart to keep beating at that point. Remember that when you count pulse you count each SET of beats. So even though your over all rate is speeding up, I wopuld imagine that the pause in the midle doesn't speed up, at least not as much.
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The delay is there, but the rate is so fast that the heart doens't have time to fill properly so the cardiac output decreases.
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yes, if there was no delay there'd be no point for your heart to keep beating at that point. Remember that when you count pulse you count each SET of beats. So even though your over all rate is speeding up, I wopuld imagine that the pause in the midle doesn't speed up, at least not as much.
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The delay is there, but the rate is so fast that the heart doens't have time to fill properly so the cardiac output decreases.
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Sorry it's taken me a little time to get to this one...
The delay in the various phases of the heart beat is produced by the rate at which the depolarisation is conveyed through the heart's conducting system.
The sino-artial node (the heart's natural pacemaker) located up in the top of the right atrium initially triggers the atrium to contract. The wave of depolarisation spreads across the atrium at about 0.5 metres per second to the atrioventricular (AV) node, essentially a relay station within the centre of the heart.
The AV node is a bit like a resistor. It dramatically slows the electrical signals travelling through it (to less than 0.05 metres per second). The purpose of slowing down the electrical signals is to ensure that the atria have finished contracting before the ventricles begin to contract.
The AV node transmits the electrical signal down the bundle of His which then splits into 3 branches - 1 supplies the right side of the heart and the other 2 supply the left. In these tissues the cardiac action potential travels quickly - at about 2 metres per second - and initiates ventricular contraction.
So, to answer the original question, there is always a gap between atrial and ventricular contraction as the impulses are delayed through the AV node. But as the heart speeds up this delay becomes slightly shorter.
Chris
"I never forget a face, but in your case I'll make an exception"
- Groucho Marx
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Some say that you should exercise for your heart to work, but making the heart work harder won't this shorten it's life and make it fatigue easier?
Also the shorten delay means less blood flows to the ventricles, is that why if you have an unhealthy heart you get itre quicker because less blood is pumped to the lungs for gas exchange?
Tom
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The exercise keeps the muscle (the heart) toned, and a muscle always functions better when it's toned.
The delay in conduction is only slightly shorter and wouldn't effect adequate filling of the ventricles. When I was talking about less cardiac output, I was referring to the rate of 160. It's hard to get adequate output when the rate goes that high. With exercise, the rate increases to keep up with the oxygen demand of the body, thus producing more cardiac output. Anything that effects the hearts ability to pump more or pump faster, will cause you to feel tired with exertion because the heart can't supply adequate oxygen to the tissues.
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Thanks for the explaination Chris and bezoar.
Tom
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Cardiac output is the total pumped volume in a minute. It is given by the equation CO (cardiac output) = heart rate x stroke volume
The stroke volume is the amount of blood that is ejected with each beat. When you exercise the metabolic demands of the body rise. This is satisfied by an increased in cardiac output achieved partly by increasing heart rate and secondly by increasing the amount of blood that each heart beat pumps.
With training the heart muscle can strengthen (like any other body muscle) meaning that it can develop more force and eject more blood. That's partly why a trained athlete has a resting pulse rate of about 40 beats per minute - because with each beat the trained heart is ejecting much more blood than a 'normal' heart.
Interestingly, the maximum achievable heart rate of an olympic athlete is slower than that of an untrained individual. That's because filling becomes the limiting factor in cardiac output. The heart cannot pump any faster or it would be pumping dry because blood quite literally cannot enter it quickly enough.
Cardiovascular physiology is one of my favourite topics...
Chris
"I never forget a face, but in your case I'll make an exception"
- Groucho Marx
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I've hear that having a good cardio-vascular system is essential. In most surgery if you are to under go general anastaeti..blah,blah (still can't spell it). You need to have a good cardio-vascular system, or else the surgery could be dangerous.
Tom
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Since we're on the topic of cardiovascular function, maybe Chris or bezoar can tell me why diabetics are at a greatly increased risk of heart attack. Does the high blood glucose increase the risk of blockages/clots, or does it mess with the solute concentrations around the heart that keep it pumping correctly?
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The impact of diabetes on blood vessels is multifactorial. Diabetes compromises renal function frequently leading to hypertension (high blood pressure) which damages the vasculature. Diabetics are often also dyslipidaemic (they have high cholesterol and triglyceride levels) because the insulin deficiency makes the body think that it is starving (because cells run low on glucose) and this triggers fat mobilisation. Again, this is bad news for blood vessels.
Also, chronically elevated blood glucose levels favour the formation of advanced glycation end products (sugar aducts) which glue themselves onto the endothelium (which lines blood vessels) causing injury and dysfunction, compounding the problem.
chris
"I never forget a face, but in your case I'll make an exception"
- Groucho Marx
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Thanks Chris. I thought maybe it was related to neuropathy, but I guess it's not. [:p]
What can a diabetic do to maintain a healthy circulatory system, aside from keeping blood sugar consistently low? My girlfriend is late onset type I diabetic and her doctors are having trouble getting her glucose levels under control. They've tried just about every oral medication and 4 different kinds of insulin, and still fluctuates from 250 to 400 every day. In the last month, she's had maybe 3 days where she was under 150 at some point in the day.
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Neuropathy occurs partly as a consequence of the microvascular damage and partly as a consequence of the metabolic effect of hyperglycaemia on schwann cells (the supporting cells that ensheath nerve axons). In hyperglycaemia schwann cells accumulate glucose and metabolise it to sorbitol. This is leads to metabolic dysfunction of the cell and secondarily impacts on the integrity of the nerve fibre. Hence, if anything, neuropathy occurs secondary to vascular disease rather than the other way around.
to address your other question,
Are you sure you mean type 1 diabetes? If your girlfriend is a type 1 diabetic, then oral hypoglycaemics are not appropriate as this is an autoimmune disorder characterised by an absolute insulin deficiency.
In general, the evidence suggests you should maintain good control over sugar, maintain a good diet which is low in fats and high in vegetables, take regular exercise, regular monitoring of renal function (to check for proteinuria) and regular monitoring of blood pressure (to check for hypertension).
Ace inhibitors, for blood pressure and proteinuria, have been shown to be beneficial to preserving long term renal function. Lipid levels can be controlled with a statin. Older diabetics should also be on aspirin (75 mg per day).
Chris
"I never forget a face, but in your case I'll make an exception"
- Groucho Marx
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Well, her last 2 doctors told her she was type I and that it came on later in life (she's 28), which is quite unusual but possible. Now, her latest rounds of testing show that her body IS making insulin (she was told otherwise by the last 2 docs she saw), so it's type II, but she didn't respond to any of the oral medications like glucophage. (she tried one other for insulin resistance that didn't seem work either) They've also changed her type of insulin 5 times since she was diagnosed, and it never quite seems to get the job done. The latest change has put her blood sugars back into the 350-500 range.
Coincidentally, her diabetes was onset by a cortisone shot in the knee. Her doctors all agree that was the trigger, so I'm curious what the mechanism might be for that? I knew cortisone affected the immune system because of it's blocking of inflammation, but to have it suddenly create insulin resistance in an otherwise healthy person? Does it affect the transport proteins that carry gluconated insulin across the cell membrane?
Anyway, she's a weird medical case. She's had 2 extremely rare conditions before the age of 23, a 14 lb. tumor in her colon at age 20 (rare at that age let alone in a woman) and pulmonary hemosiderosis, which thankfully only expressed symptoms once and has not recurred. All that, plus diabetes that doesn't respond to anything and chronic arthritis. She's one for the medical books. I'm going to make her my thesis when I'm doing my graduate work.
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