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Causes of pulsus paradoxus
Cardiac causes
1. Cardiac tamponade
2. Pericardial effusion
3. Constrictive pericarditis
4. Restrictive cardiomyopathy[4]
5. Pulmonary embolism
6. Acute myocardial infarction
7. Cardiogenic shock
Extracardiac pulmonary causes
1. Bronchial asthma
2. Tension pneumothorax
Extracardiac non-pulmonary causes
1. Anaphylactic shock (during urokinase administration)[5]
2. Volvulus of the stomach[6]
3. Diaphragmatic hernia[6]
4. Superior vena cava obstruction[4]
5. Extreme obesity
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thnx
can u please tel me why it occurs--i know what occurs---but why???
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Found a source for ur question.
The pericardium consists of two layers: the outer layer is the parietal pericardium and the inner layer is the visceral pericardium. In the space between these layers is a small amount of pericardial fluid which acts as lubrication between the layers. Normally the two layers are quite compliant, and allow the heart to expand, or to grow as it does during CHF. Since the sac surrounds the heart, any process that causes fluid to fill in the sac will cause the heart to be restricted from expanding properly before it contracts. These processes include:
Acute pericarditis, due to infection of the pericardium, a dissecting aneurysm, collagen vascular disease, drugs, trauma, etc.
Effusive pericardial disease, i.e., effusions of transudate, exudate, or serosanguinate.
Cardiac tamponade, the major complication of pericardial effusion.
Constrictive pericarditis (pericardial thickening and fibrosis occurring after an acute episode of pericarditis).
When the patient inspires, blood is normally drawn back into the right ventricle(RV) because of the negative pressure in the thorax. In the restricted heart, the blood distends the right ventricle(RV), which can only expand into the space the left ventricle(LV) uses, making the left ventricle(LV) smaller. With a smaller LV, less blood can fill it and be ejected into the systemic circulation, making the systemic blood pressure fall (> 10mm Hg). When the patient expires, less blood will come back to the RV, allowing more room for the LV to fill and therefore more blood to be ejected into the systemic circulation.
Other causes of pulsus paradoxus occur for a similar reason: the air-trapping that occurs to give patients barrel chests in emphysema and asthma also restricts the room the normal expansion of the heart.
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So Generally. Anytime U affect expansion of Heart for whatever reason = Pulsus P can occur
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Revankar I am glad u asked this question b/c I did not give the correct answer to ur question on asthma before, and now I know it too!
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Under normal conditions, arterial blood pressure fluctuates throughout the respiratory cycle, falling with inspiration and rising with expiration.
The changes in the intrathoracic pressures during breathing are transmitted to the heart and great vessels. During inspiration, the right ventricle distends due to increased venous return, the interventricular septum bulges into the left ventricle reducing its size (reversed Bernheim effect), and increased pooling on blood in the expanded lungs decreases return to the left ventricle, decreasing the stroke volume of the left ventricle. Additionally, negative intrathoracic pressure during inspiration is transmitted to the aorta. The relatively higher negative pressure in the pulmonary circulation compared to the left atrium in patients with pericardial pathology causes back flow of blood from the left atrium into the pulmonary veins during inspiration.[2]
Therefore, during inspiration the fall in the left ventricular stroke volume is reflected as a fall in the systolic blood pressure. The converse is true for expiration. During quiet respiration, the changes in the intrathoracic pressures and blood pressure are minor. The accepted upper limit for fall in systolic blood pressure with inspiration is 10 mmHg.
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ndr please in simplified words explain increased pooling of blood in lung due to? Geeting stuck on negative pressure in Lungs?
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i just found out that 2 mech of pulsus is due to inc venous return and pooling of blood leading to a dec in the lv vol, reg the exact mech sorry cant explain it further
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as a result of -ve intrathoracic pressure venous return to Rt atrium increases which pushes the interventricular septum hence decreasing the Lt ventricular volume ===> decrease in CO which will altimately lowers the systolic pressure ------that how i see it correct me if understood it wrong
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Yes I definetlt get that and knew it as well just having a problem w/ what's going on in pulmonary vasculature in regards to pressures in pulm and left heart, which according to nrd citation also contributes to decr in CO, but not quite undertand the physiology of pressure diffrence?
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