aRnonymous

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I'm not sure that I completely understand the physiology behind pulsus paradoxus. For something like cardiac tamponade, my understanding was that fluid accumulation around the heart causes external "pressure" on the heart via fluid, which causes the pressure in all chambers to equalize. Now, with inspiration the pulmonary arteries dilate and intrathoracic pressure decreases, thereby increasing venous return to the right side of the heart. When this occurs, the path of "least resistance" for the right ventricle is not outwards against the fluid, but rather into the left ventricle. As a result, this reduces preload as well as output of the left ventricle which causes the effect of pulsus paradoxus. Hopefully this is right.

Now, I'm not completely understanding how this effect works with something like an airway obstruction or superior vena cava obstruction. My best guess is that an airway obstructive will cause pulmonary hypertension due to shunting of blood as a result of hypoxia, which will therefore increase right ventricular pressure, and this as a result compresses the left ventricle? Although I'm not understanding why it wouldn't just go outwards, is it because pressure outside the heart due to an obstruction actually means it requires less effort to go into the left ventricle? What about something like SVC obstruction? Wouldn't that just decrease venous return?

Maybe I'm just being picky, but I'd rather understand stuff than just memorize it! Thanks everyone!
 
Jul 6, 2011
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This is a good question and I don't have a complete understanding of it either. I agree that that in airway obstruction (or asthma), the increased PVR causes increased RV afterload, and this pressure is also reflected into the LV, causing increased left ventricular afterload. That may explain for the decreased stroke volume, and resultant pulsus paradoxus. This article seems to suggest that, but doesn't quite explain it (or maybe just over my head).

http://jap.physiology.org/content/45/4/598.abstract

SVC obstruction is associated with a decreased venous return (preload) but I'm not sure why it would cause blood pressure to increase with exhalation.
 

nitpick

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In asthma due to hyperinflated lungs there is increased afterload for the RV and hence it press on LV, apart from that there is decreased preload to the LV, which ultimately cause inspiratory fall in systolic BP more than 10mmHg.

In SVC obstruction/PE or any type of shock, I think decreased preload to LV contributes to the pulsus.
 
May 17, 2011
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Asthma, emphysema and other interstitial lung diseases (like sarcoidosis) increase pulmonary vascular pressure by a) physical obstruction secondary to
air (emphysema, asthma...) or fibrosis (sarcoidosis) and b) hypercapnia and metabolic acidosis induced bronchial vasoconstriction secondary to decreased respiratory rate (Asthma). Like the above posters said, increased pulmonary pressure increases right ventricular afterload causing a space occupying shift of the right ventricle into the left ventricle. This becomes apparent with inspiration because as you increase venous return but maintain pulmonary resistance the right ventricle will expand, not pump as effectively, and push against the left ventricle.

The following article confirms http://circ.ahajournals.org/content/66/4/887.full.pdf "Mechanism of Paradoxic Pulse in Bronchial Asthma"

Superior Vena Cava syndrome induced neck edema can decrease the lumen of the trachea and cause dyspnea. It's possible that the increased airway resistance is keeping more air in the lungs which physically obstructs pulmonary vasculature in a manner similar to Asthma. However I don't think this is the case, as superior vena cava syndrome is considered "Non-pulmonary and non-cardiac" according to wikipedia. If anyone can shed light on this issue it'd be much appreciated!
 
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ChessMaster3000

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Asthma, emphysema and other interstitial lung diseases (like sarcoidosis) increase pulmonary vascular pressure by a) physical obstruction secondary to
air (emphysema, asthma...) or fibrosis (sarcoidosis) and b) hypercapnia and metabolic acidosis induced bronchial vasoconstriction secondary to decreased respiratory rate (Asthma). Like the above posters said, increased pulmonary pressure increases right ventricular afterload causing a space occupying shift of the right ventricle into the left ventricle. This becomes apparent with inspiration because as you increase venous return but maintain pulmonary resistance the right ventricle will expand, not pump as effectively, and push against the left ventricle.

The following article confirms http://circ.ahajournals.org/content/66/4/887.full.pdf "Mechanism of Paradoxic Pulse in Bronchial Asthma"

Superior Vena Cava syndrome induced neck edema can decrease the lumen of the trachea and cause dyspnea. It's possible that the increased airway resistance is keeping more air in the lungs which physically obstructs pulmonary vasculature in a manner similar to Asthma. However I don't think this is the case, as superior vena cava syndrome is considered "Non-pulmonary and non-cardiac" according to wikipedia. If anyone can shed light on this issue it'd be much appreciated!
does the increase thoracic pressures in asthma and copd also compress the heart itself? I thought that was what caused the pulsus, rather than the increase in pulmonary vasc resistance
 

Tuloste

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My understanding was, as far as asthma and COPD go, that the high intrathoracic volume forced the person to generate excessively negative intrapleural pressures to expand their lungs (as the end-expiratory lung volume remains high, and the distensibility of the lungs at those volumes very poor) and that this negative pressure was transmitted to the pericardium causing an excacerbation of normal physiology (a healthy person can also generate a pulsus paradoxus by drawing overtly deep breaths). Also it is thought that the hyperinflated lungs may compress the heart in a manner similar to tamponade.

ps. Stridor and croup can cause pulsus paradoxus, apparently with a similar mechanism of highly negative intrapleural pressures. (similar to Müller's maneuver)
pps. Inspiratory intrapleural pressures can get so negative as to cause non-cardiogenic pulmonary edema (http://journal.publications.chestnet.org/article.aspx?articleid=1148921) :O
ppps. According to the articles I looked at, the pathophysiology of pulsus paradoxus accompanying respiratory disorders is complex and in many parts unclear. We'll have to wait for a definitive answer I guess.
 
Mar 5, 2014
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^the above wouldnt make sense for emphysema, as with emphysema you decrease your elasticity, and increase compliance of the lungs, so you achieve higher long volumes, with negligible changes of intrapleural pressures.
 

Mad Jack

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^the above wouldnt make sense for emphysema, as with emphysema you decrease your elasticity, and increase compliance of the lungs, so you achieve higher long volumes, with negligible changes of intrapleural pressures.
Remember that emphysema is ultimately a functionally obstructive process- due to the poor elasticity of the lungs, higher pressures must be generated by contraction of the chest wall muscles during exhalation to force air out of the lungs. This is how you end up with the stereotypical pink puffer in emphysema- they are actively exhaling every breath to keep breathing, using enormous energy and force to compensate for what should normally be a passive process. Essentially they have normal inspiratory intrathoracic pressures, but elevated expiratory pressures due to muscular compression of the chest wall and abdomen.
 
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To my understanding, there are two main mechanisms by which pulsus paradoxus can be generated, although due to the complex physiology of the heart and lungs I don't think these two mechanisms are the only rational explanations.

The first mechanism has already been described by OP in the first paragraph and deals with equal pressure in the R and L ventricles in the context of cardiac tamponade.

The second mechanism is due to increased negative intra-thoracic pressures required to maintain both proper ventilation and perfusion in certain disease states. Remember, this increased negative pressure helps the lungs to function at a higher point in the pressure-volume curves (theoretically leading to better ventilation) to compensate for a disease state. In doing so, this pressure also has a greater physiological effect on the L ventricle than the R ventricle - this is due to the fact that with inspiration there is increased venous return to the R ventricle but decreased venous return to the L ventricle. When this occurs the transmural pressure of the L ventricle (pressure in L ventricle - pressure outside of L ventricle) will get larger, increasing the amount of tension generation required by the myocardium to maintain the same ejection fraction (increasing the afterload). An increased afterload has the potential to lead to a decrease in stroke volume which could lead to a systolic pressure drop > 10 mmHg during inspiration, pulsus paradoxus.

To answer your question about SVC syndrome, it is my understanding that decreased return to the RV will ultimately lead to decreased LV preload, which is further exacerbated by inhalation and a subsequent increased pulmonary vessel compliance. Pulsus paradoxus is just a definition to describe the drop in pressure, it can be contingent upon strength of the patients heart, their TPR, their LV preload, and a host of other factors. Based on your rational in your first post I think you have sufficient understanding of the physiology but you were looking at things through too narrow a lens - thinking that you HAVE to have R ventricle bulging into the L ventricle in order to cause pulsus paradoxus and overlooking the volume/preload components.