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Contents 1 pulsus 2 Negative pressure 3 Venous return & heart rate 3.1 Reply 4 Cause of pulsus paradoxus 4.1 Reply

[edit] pulsus

pulsus paradoxus is a clinical sign of cardiac tamponade.On measuring the blood pressure<systoic>during expiration and inspiration, a difference of more than 10 mm Hg is observed in conditions like cardiac tamponade.Many theories have been postulated for its mechanism but is still not clear, but probably due to impaired left ventricular filling and hence decreased stroke volume.--202.79.51.59 16:51, 27 July 2006 (UTC)sridevi beriwal

[edit] Negative pressure

There is no doubt in my mind, that i completely understand what you mean with negative pressure, nevertheless in my opinion such a thing does not exist. Negative pressure means a pressure lower than normal air/atmospheric pressure.

Reply:

-ve pressure in lung refers to lower pressure in comparison to atmospheric pressure. -ve absolute pressure does not exist, that is correct Ignatius Eric Hadinata 13:41, 3 May 2007 (UTC)

[edit] Venous return & heart rate

I read your edit on Pulsus Paradoxus

The previous edition was correct. Increased heart rate is due to baroreflex to reduced blood pressure (i.e. cardiac output). On inspiration, the intrathoracic pressure is reduced and releases some of the pressure on the pulmonary veins. This causes the veins to dilate and retains more blood. This causes less venous return to the left atrium, in turn causes lower ventricular end diastolic volume and hence reduces cardiac output. This in turn causes a lowering of blood pressure and activation of baroreflex, causing vasoconstriction and increased heart rate. If you have any objection to this, please make an entry in my talk page. Please do not mislead people by reversing key words in the article. Ignatius Eric Hadinata 08:57, 25 April 2007 (UTC)

[Above was copied from my talk. Nephron  T|C (see [1])]

You assumed I was referring to pulmonary venous return. Pulmonary venous return, I agree, is decreased with inspiration.[2]

Above said, the heart rate does increase with increased (systemic) venous return:

In the resting animal with sinus arrhythmia, inspiration increased heart rate and flow in the vena cava,[emphasis added] and to a lesser extent, in the pulmonary vein.

Circulation Research. 1967;20:381. -- http://circres.ahajournals.org/cgi/content/abstract/circresaha;20/4/381

Most people refer to the systemic venous return when they say venous return.{ref} I don't think the way I had written it was wrong per se-- it was just a bit ambiguous. The way you re-wrote it is also ambiguous (or wrong if you assume it's the systemic venous return).

In any case, I'm doubtful about your reasoning (in relation to why the HR increases) and I'd be interested in seeing a reference if you have one. The pulmonary vasculature is isolated from the systemic pressure through the valves; when the mitral valve is open the aortic is closed and vice versa. In other words, the baroreceptors in the carotid sinus & arotic arch (which drive the baroreflex) are isolated from the left atrium.

If your reasoning is correct... I suppose a person with a heart transplant would have a fixed heart rate (with respiration) --as they don't have vagal innervation of the heart. I tend to think the increased HR comes from the increased stretch of the RV due to the increased (systemic) venous return. Nephron  T|C 23:28, 25 April 2007 (UTC)

I was pretty busy last week. So, I didn't have enough time to take a close look at this. I re-examined this today and found a paper that backs-up my position.[3] I think your reseasoning in good. That said, it doesn't quite work 'cause the left and right side of the heart aren't totally independent. I changed things back, as I believe your changes were in error. If you continue to believe that I am wrong after looking at my references-- cite some references/explain how I might have misinterpreted the references to back-up your analysis/understanding. Also, we can get another opinion-- say from User:Dlodge or with a post to WP:CLINMED. Nephron  T|C 19:56, 28 April 2007 (UTC)

[edit] Reply

First of all: I do not appreciate you deleting a whole section on the article. I do not think your edit was justified and a replacement of the information that you deleted was not found in the article. However, I'm not going to worry about that now, I'm going to re-do what you deleted in a more organised style (hopefully very soon). Now, about your comments:

I agree to what you are saying. I think we both misunderstood the information because it was written in an ambiguous manner. Now that you have clarified your statement. I totally agree. As for the reduced pulmonary venous return and heart rate, this is the explanation (I got this off the lecture notes prepared by Prof. Stephen Harrap, Professor of Physiology, The University of Melbourne, but I'm sure its also in many physiology and clinical medicine book - my physiology book does not cover this unfortunately): The valves separates the pulmonary and systemic circulation and there is no direct physical relationship between the two pressures - CORRECT. That there is no effect of reduced pulmonary venous return to systemic arterial blood pressue - INCORRECT. When I wrote thos comment on your talk page, I assumed that you have an understanding of the blood pressure regulation and baroreflexes - otherwise you wouldn't have edited the entry. Hence, I didn't bother putting in every step of the mechanism. You ended up misinterpretting my explanation. So here is the full explanation:

The reduced pulmonary venous return will cause less volume at the atrium at the end of systole (that is when the tricuspid valve is still closed, but is about to open to prepare for diastole). Less volume here will cause reduced left ventricular filling at diastole (when the tricuspid valve is open to allow ventricular filling and aortic valve is closed).

I have the impression you mean bicuspid valve aka (mitral valve)-- the one between the LV and LA. Nephron  T|C 17:06, 18 May 2007 (UTC)

At the end of diastole (when both of the valve is closed - one of the isovolumetric states of the ventricle), the volume is called the end diastolic volume, which will determine how much blood can be pumped out by the ventricular contraction. From here, the reference is Rhoades et al, Human Physiology 4th ed, Brooks/Cole Thomson Learning Inc 2003 (pardon my referencing style - in a hurry, can't remember how to do it properly, if you have time, please fic it). The Frank-Starling law of the heart (page 577, figure 18-21), which is basically an adaption of the law applied to any other muscles says that the contraction force is strongest when there is optimal sacromere length. In heart, the resting sacromere length of the cardiomyoctes (which is determined by the stretch on the muscle, and hence the end diastolic volume) is less than the optimal sacromere length. Hence a decrease in their resting length (i.e. decreased stretcha and decreased end diastolic volume) will cause a decrease in the rate and force of contraction of the heart. A combination of less volume to be pumped and a lower force of contraction causes a decrease in left ventricular output to the Aorta and hence a fall in systemic arterial blood pressure, which is sensed by the baroreceptors, for example in the carotid sinus. This will cause an decrease in the firing of baroreceptors, which is sensed by the brain and causes a decrease in parasympathetic and an increase in sympathetic activity, which then causes a reflex tachycardia, which causes an increase in cardiac output and restores blood pressure. See baroreflex - I did not make that page, so that counts as third party opinion "Baroreceptors include those in the auricles of the heart and vena cavae, but the most sensitive baroreceptors are in the carotid sinuses and aortic arch" was found on the page.

I don't think it is absolutely clear why it happens-- sympathetic vs. parasympathetic (see bit below). I didn't manage to find a ref. that seems to cover it well-- with the exception of the Italian one. Unfortunately, I can't read Italian. Nephron  T|C 17:06, 18 May 2007 (UTC)

As for the receptors in the right ventricle, they are low pressure baroreceptors. They are useful in detecting low blood pressure due to volume depletion, but essentially works the same way as the one in carotid sinus (By the way, all of this can be found in Kumar and Clark, Clinical Medicine, Elseiver publication - its a medicine textbook). Again, you are saying the opposite facts. In fact, if the venous return is low enough to activate these receptors, you get tachycardia because the body is volume depleted and it has to maintain cardiac output by heart rate. Increased venous return will not in fact increase heart rate. Increased volume in tha atrium means that there is increased volume in the ventricle and increased stretch on the cardiomyocytes, which increase their resting length (closer to optimal length) and increase the force of contraction.

I suppose that I can agree with this. Also, I suppose the increased cardiac output in exercise (which is due to both increased HR and stroke volume) is multifactorial-- arteriolar dilation + incr. venous return. That said, I think it may be interesting to consider what a transplanted heart does. Does it accelerate... with exercise from its higher baseline heart rate? Nephron  T|C 17:06, 18 May 2007 (UTC)

This will cause an increase in blood pressure and the body will not increase heart rate, because the homeostasis mechanism is a negative feedback. Increased blood pressure will not make increased heart rate because then, this will be positive feedback. The body's main aim in regards to circulation is to maintain blood pressure at relatively constant level.

Its 11.15 pm now my time (Australian Eastern Daylight Saving Time) and I have examination coming tomorrow and I have no time to copy this to your talk page or the clinmed page, so if you think this should be on any other page, please feel free to copy and paste. I hope the above explanation is clear enough. I look forward to your reply at my talk page (I don't check this page often) and hope to see more of your submissions. Ignatius Eric Hadinata 13:19, 3 May 2007 (UTC)

I haven't got back to this 'til now on account of an exam. I have to look at this a bit more closely. I found a reference that I think covers it in dogs (PMID 6477728). Annoying about the abstract is-- it doesn't neatly separate the four groups mentioned when discussing results. Also, I'm not quite sure it isn't an apples and oranges comparison-- 'cause vagal and sympathetic tone influence the heart rate.

You wrote:

It was meant to be the normal mechanism by which the blood pressure is reduced during inspiration.

The reason I deleted is: the article is about PP not the physiology of respiration and cardiac function. Beyond that, I wasn't fond of the textbook citation... it is a secondary source. (I much prefer free (as in GPL/GFDL) and open access resources. IMHO, the primary literature (i.e. MEDLINE publications) -- is the best way to go.) Beyond that, your explanation was focused on the capacity of the lungs... that is only one physiologic aspect of the phenonmenon. I have the impression a Kussmaul's sign will give a PP (if other things are normal, i.e. no restrictive lung disease)-- but I have to read a bit more on that. Nephron  T|C 03:37, 13 May 2007 (UTC)

[edit] Cause of pulsus paradoxus

I have the impression that the cause of PP is not the pooling of blood in the lungs per se (as this normally happens physiologically). The problem appears to be that the heart cannot keep up with the increased demand, i.e. a person with PP has demand driven heart failure. Indicative of this is that PP is often accompanied by a Kussmaul sign. Guntheroth et al.[4] seems to support this contention:

Cardiac tamponade invariably caused tachycardia and a marked decrease in cardiac output, arterial pressure, pulse pressure, and stroke volume; venous pressure and diameter increased.

Also, I found a paper that seems to support this idea:

Frey B. Pulsus paradoxus indicating heart failure in paroxysmal supraventricular tachycardia: easy detection by pulse oximetry. Intensive Care Med. 1999 Mar;25(3):333-4. PMID 10229176.

Nephron  T|C 20:57, 28 April 2007 (UTC)

[edit] Reply

I agree, what I was trying to say was that the pooling of blood in lung is the NORMAL mechanism. In pathological conditions, there are many mechanisms of pulsus paradoxus (I got this from lectures last week again by Prof. Harrap. I'll try to reference it properly soon. Its too late at night now).

One of them is the increased intrathoracic change in pressure more than normal such as in obstructive lung disease. Others include volume depletion where the volume of blood is reduced and I agree with you: a failing heart, althought I'm not sure about the mechanism of the last one (the former two relies on the pooling of blood in lung). I'll try to get back to you on the last point (which is the same as what you've written above), but remember that the most common mistakes in medicine is assuming that only one mechanism is valid for a certain condition. If a mechanism can explain a phenomenon (such as pulsus paradoxus), it does not necessarily mean that any other mechanism is incorrect. This seems to be your problem in understanding or accepting my explanations. I'll try to get a properly written and referenced summary soon (need to do this for exam anyway) and then publish it. When I do, I can guarantee that the information is correct. Ignatius Eric Hadinata 13:30, 3 May 2007 (UTC)