Pulsus paradoxus

Last updated

Pulsus paradoxus
Synonyms Paradoxic pulse
LOINC 8452-5

Pulsus paradoxus, also paradoxic pulse or paradoxical pulse, is an abnormally large decrease in stroke volume, systolic blood pressure (a drop more than 10 mmHg) and pulse wave amplitude during inspiration. Pulsus paradoxus is not related to pulse rate or heart rate, and it is not a paradoxical rise in systolic pressure. Normally, blood pressure drops less precipitously than 10 mmHg during inhalation. Pulsus paradoxus is a sign that is indicative of several conditions, most commonly pericardial effusion. [1]

Contents

The paradox in pulsus paradoxus is that, on physical examination, one can detect beats on cardiac auscultation during inspiration that cannot be palpated at the radial pulse. [1] It results from an accentuated decrease of the blood pressure, which leads to the (radial) pulse not being palpable and may be accompanied by an increase in the jugular venous pressure height (Kussmaul's sign). As is usual with inspiration, the heart rate is slightly increased, [2] due to decreased left ventricular output. [3]

Mechanism

During inspiration, the negative intra-thoracic pressure results in an increased right venous return, filling the right atrium more than during an exhalation. The increased blood volume dilates the right atrium, reducing the compliance of the left atrium due to their shared septum. Lower left atrial compliance reduces the left atrium venous return and as a consequence causes a reduction in left ventricular preload. This results in a reduction in left ventricular stroke volume and will be noted as a reduction in systolic blood pressure in inspiration. Pulsus paradoxus is therefore an exaggeration or an increase in the fall of systolic BP beyond 10 mmHg during inspiration. [4]

Normally during inspiration, a person's systolic blood pressure decreases by ≤10 mmHg [1] and heart rate slightly increases. This is because inspiration decreases intra-thoracic pressure relative to atmospheric pressure, which increases blood flow (systemic venous return) to the right atrium of the heart by reducing pressure on the veins, particularly the venae cavae. However, the decrease in intra-thoracic pressure and stretching of the lungs during inhalation also expands the compliant pulmonary vasculature so that blood pools in the lungs and decreases pulmonary venous return to the left atrium. Also, the increased systemic venous return to the right side of the heart expands the right heart and directly compromises filling of the left side of the heart by slightly bulging the septum to the left, reducing maximum volume. Reduced left-heart filling leads to a reduced stroke volume which manifests as a decrease in systolic blood pressure, leading to a faster heart rate due to the inhibition of the baroreceptor reflex, which stimulates sympathetic outflow to the heart. [5]

Under normal physiologic conditions the large pressure gradient between the right and left ventricles prevents the septum from bulging dramatically into the left ventricle during inspiration. However such bulging does occur during cardiac tamponade where pressure equalizes between all of the chambers of the heart. [6] As the right ventricle receives more volume, it pushes the septum into the left ventricle further reducing its volume in turn. This additional loss of volume of the left ventricle that only occurs with equalization of the pressures (as in tamponade) allows for the further reduction in volume, so cardiac output is reduced, leading to a further decline in BP. However, in situations where the left ventricular pressure remains higher than the pericardial sac (most frequently from coexisting disease with an elevated left ventricular diastolic pressure), there is no pulsus paradoxus. [7]

Although one or both of these mechanisms may occur, a third may additionally contribute. The large negative intra-thoracic pressure increases the pressure across the wall of the left ventricle (increased transmural pressure, equivalent to [pressure within ventricle] - [pressure outside of ventricle]). This pressure gradient, resisting the contraction of the left ventricle, causes an increase in afterload. This results in a decrease in stroke volume, contributing to the decreased pulse pressure and increased heart rate as described above. Pulsus paradoxus occurs not only with severe cardiac tamponade but also with asthma, obstructive sleep apnea and croup. The mechanism, at least with severe tamponade, is likely very similar to those of hypertrophic and restrictive cardiomyopathies (diastolic dysfunction), where a decrease in Left Ventricular (LV) filling corresponds to an increasingly reduced stroke volume. In other words, with these cardiomyopathies, as LV filling decreases, ejection fraction decreases directly, yet non-linearly and with a negative concavity (negative first and second derivatives). Similarly, with tamponade, the degree of diastolic dysfunction is inversely proportional to the LV end-diastolic volume. So during inspiration, since LV filling is lesser relative to that during expiration, the diastolic dysfunction is also proportionally greater, so the systolic pressure drops >10 mmHg. This mechanism is also likely with pericarditis, where diastolic function is chastened.[ citation needed ]

Measurement

Pulse pressure is quantified using a blood pressure cuff and stethoscope (Korotkoff sounds), by measuring the variation of the systolic pressure during expiration and inspiration. [8]

To measure the pulsus paradoxus, place a blood pressure cuff on the patient's arm and very slowly deflate the cuff while listening for brachial pulsations. Note the pressure that you first hear with pulsations during expiration (which will be the highest). Repeat the process, and record the pressure of pulsations heard during inspiration (which will be the lowest). [9]

If the pressure difference between the two readings is >10mmHg, it can be classified as pulsus paradoxus. [10]

Causes

Pulsus paradoxus can be caused by several physiologic mechanisms. Anatomically, these can be grouped into: [1]

Considered physiologically, PP is caused by:[ citation needed ]

List of causes

Cardiac:

Pulmonary:

Non-pulmonary and non-cardiac:

PP has been shown to be predictive of the severity of cardiac tamponade. [12] Pulsus paradoxus may not be seen with cardiac tamponade if an atrial septal defect or significant aortic regurgitation is also present.[ citation needed ]

See also

Related Research Articles

<span class="mw-page-title-main">Systole</span> Part of the cardiac cycle when a heart chamber contracts

Systole is the part of the cardiac cycle during which some chambers of the heart contract after refilling with blood.

<span class="mw-page-title-main">Ventricle (heart)</span> Chamber of the heart

A ventricle is one of two large chambers located toward the bottom of the heart that collect and expel blood towards the peripheral beds within the body and lungs. The blood pumped by a ventricle is supplied by an atrium, an adjacent chamber in the upper heart that is smaller than a ventricle. Interventricular means between the ventricles, while intraventricular means within one ventricle.

<span class="mw-page-title-main">Cardiac tamponade</span> Buildup of fluid around the heart

Cardiac tamponade, also known as pericardial tamponade, is a compression of the heart due to pericardial effusion. Onset may be rapid or gradual. Symptoms typically include those of obstructive shock including shortness of breath, weakness, lightheadedness, and cough. Other symptoms may relate to the underlying cause.

<span class="mw-page-title-main">Afterload</span> Pressure in the wall of the left ventricle during ejection

Afterload is the pressure that the heart must work against to eject blood during systole. Afterload is proportional to the average arterial pressure. As aortic and pulmonary pressures increase, the afterload increases on the left and right ventricles respectively. Afterload changes to adapt to the continually changing demands on an animal's cardiovascular system. Afterload is proportional to mean systolic blood pressure and is measured in millimeters of mercury.

<span class="mw-page-title-main">Diastole</span> Part of the cardiac cycle

Diastole is the relaxed phase of the cardiac cycle when the chambers of the heart are refilling with blood. The contrasting phase is systole when the heart chambers are contracting. Atrial diastole is the relaxing of the atria, and ventricular diastole the relaxing of the ventricles.

<span class="mw-page-title-main">Mitral stenosis</span> Heart disease with narrowing of valve

Mitral stenosis is a valvular heart disease characterized by the narrowing of the opening of the mitral valve of the heart. It is almost always caused by rheumatic valvular heart disease. Normally, the mitral valve is about 5 cm2 during diastole. Any decrease in area below 2 cm2 causes mitral stenosis. Early diagnosis of mitral stenosis in pregnancy is very important as the heart cannot tolerate increased cardiac output demand as in the case of exercise and pregnancy. Atrial fibrillation is a common complication of resulting left atrial enlargement, which can lead to systemic thromboembolic complications such as stroke.

<span class="mw-page-title-main">Pericarditis</span> Medical condition

Pericarditis is inflammation of the pericardium, the fibrous sac surrounding the heart. Symptoms typically include sudden onset of sharp chest pain, which may also be felt in the shoulders, neck, or back. The pain is typically less severe when sitting up and more severe when lying down or breathing deeply. Other symptoms of pericarditis can include fever, weakness, palpitations, and shortness of breath. The onset of symptoms can occasionally be gradual rather than sudden.

Kussmaul's sign is a paradoxical rise in jugular venous pressure (JVP) on inspiration, or a failure in the appropriate fall of the JVP with inspiration. It can be seen in some forms of heart disease and is usually indicative of limited right ventricular filling due to right heart dysfunction.

<span class="mw-page-title-main">Jugular venous pressure</span> Blood pressure in a vein of the neck

The jugular venous pressure is the indirectly observed pressure over the venous system via visualization of the internal jugular vein. It can be useful in the differentiation of different forms of heart and lung disease. Classically three upward deflections and two downward deflections have been described.

<span class="mw-page-title-main">Beck's triad (cardiology)</span> Medical condition

Beck's triad is a collection of three medical signs associated with acute cardiac tamponade, a medical emergency when excessive fluid accumulates in the pericardial sac around the heart and impairs its ability to pump blood. The signs are low arterial blood pressure, distended neck veins, and distant, muffled heart sounds.

<span class="mw-page-title-main">Preload (cardiology)</span> Heart muscle stretch at rest

In cardiac physiology, preload is the amount of sarcomere stretch experienced by cardiac muscle cells, called cardiomyocytes, at the end of ventricular filling during diastole. Preload is directly related to ventricular filling. As the relaxed ventricle fills during diastole, the walls are stretched and the length of sarcomeres increases. Sarcomere length can be approximated by the volume of the ventricle because each shape has a conserved surface-area-to-volume ratio. This is useful clinically because measuring the sarcomere length is destructive to heart tissue. It requires cutting out a piece of cardiac muscle to look at the sarcomeres under a microscope. It is currently not possible to directly measure preload in the beating heart of a living animal. Preload is estimated from end-diastolic ventricular pressure and is measured in millimeters of mercury (mmHg).

Venous return is the rate of blood flow back to the heart. It normally limits cardiac output.

The following outline is provided as an overview of and topical guide to cardiology, the branch of medicine dealing with disorders of the human heart. The field includes medical diagnosis and treatment of congenital heart defects, coronary artery disease, heart failure, valvular heart disease and electrophysiology. Physicians who specialize in cardiology are called cardiologists.

Obstructive shock is one of the four types of shock, caused by a physical obstruction in the flow of blood. Obstruction can occur at the level of the great vessels or the heart itself. Causes include pulmonary embolism, cardiac tamponade, and tension pneumothorax. These are all life-threatening. Symptoms may include shortness of breath, weakness, or altered mental status. Low blood pressure and tachycardia are often seen in shock. Other symptoms depend on the underlying cause.

<span class="mw-page-title-main">Split S2</span>

A split S2 is a finding upon auscultation of the S2 heart sound.

The E/A ratio is a marker of the function of the left ventricle of the heart. It represents the ratio of peak velocity blood flow from left ventricular relaxation in early diastole to peak velocity flow in late diastole caused by atrial contraction. It is calculated using Doppler echocardiography, an ultrasound-based cardiac imaging modality. Abnormalities in the E/A ratio suggest that the left ventricle, which pumps blood into the systemic circulation, cannot fill with blood properly in the period between contractions. This phenomenon is referred to as diastolic dysfunction and can eventually lead to the symptoms of heart failure.

Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another.

A plot of a system's pressure versus volume has long been used to measure the work done by the system and its efficiency. This analysis can be applied to heat engines and pumps, including the heart. A considerable amount of information on cardiac performance can be determined from the pressure vs. volume plot. A number of methods have been determined for measuring PV-loop values experimentally.

<span class="mw-page-title-main">Heart failure with preserved ejection fraction</span> Medical condition

Heart failure with preserved ejection fraction (HFpEF) is a form of heart failure in which the ejection fraction – the percentage of the volume of blood ejected from the left ventricle with each heartbeat divided by the volume of blood when the left ventricle is maximally filled – is normal, defined as greater than 50%; this may be measured by echocardiography or cardiac catheterization. Approximately half of people with heart failure have preserved ejection fraction, while the other half have a reduction in ejection fraction, called heart failure with reduced ejection fraction (HFrEF).

<span class="mw-page-title-main">Pathophysiology of heart failure</span>

The main pathophysiology of heart failure is a reduction in the efficiency of the heart muscle, through damage or overloading. As such, it can be caused by a wide number of conditions, including myocardial infarction, hypertension and cardiac amyloidosis. Over time these increases in workload will produce changes to the heart itself:

References

  1. 1 2 3 4 Khasnis, A.; Lokhandwala, Y. (January–March 2002). "Clinical signs in medicine: pulsus paradoxus". Journal of Postgraduate Medicine. 48 (1). Mumbai - 400 012, India: 49: 46–9. ISSN   0022-3859. PMID   12082330 . Retrieved 21 March 2010. The "paradox" refers to the fact that heart sounds may be heard over the precordium when the radial pulse is not felt.{{cite journal}}: CS1 maint: location (link)
  2. ↑ Guntheroth W, Morgan B, Mullins G (1967). "Effect of respiration on venous return and stroke volume in cardiac tamponade. Mechanism of pulsus parodoxus". Circ. Res. 20 (4): 381–90. doi: 10.1161/01.res.20.4.381 . PMID   6025402. Abstract Archived 1 February 2009 at the Wayback Machine
  3. ↑ Soucek M, Kára T, Jurák P, Halámek J, Spinarová L, Meluzín J, Toman J, Rihácek I, Sumbera J, Frána P (2003). "Heart rate and increased intravascular volume". Physiological Research. 52 (1): 137–40. doi: 10.33549/physiolres.930259 . PMID   12625819. Free Full Text.
  4. ↑ Van Dam M, Fitzgerald B (2024). "Pulsus Paradoxus". National Center for Biotechnology Information, U.S. National Library of Medicine. PMID   29493917 . Retrieved 11 July 2021.
  5. ↑ Van Dam M, Fitzgerald B (2024). "Pulsus Paradoxus". National Center for Biotechnology Information, U.S. National Library of Medicine. PMID   29493917 . Retrieved 11 July 2021.
  6. ↑ Reddy, PS; Curtiss, EI; Uretsky, BF (1990). "Spectrum of hemodynamic changes in cardiac tamponade". American Journal of Cardiology. 66 (20): 1487–91. doi:10.1016/0002-9149(90)90540-H. PMID   2251997.
  7. ↑ Reddy, PS; Curtiss, EI; O'Toole, JD; Shaver, JA (1978). "Cardiac tamponade: hemodynamic observations in man". Circulation. 58 (2): 265–72. doi: 10.1161/01.cir.58.2.265 . PMID   668074.
  8. ↑ Van Dam M, Fitzgerald B (2024). "Pulsus Paradoxus". National Center for Biotechnology Information, U.S. National Library of Medicine. PMID   29493917 . Retrieved 11 July 2021.
  9. ↑ Van Dam M, Fitzgerald B (2024). "Pulsus Paradoxus". National Center for Biotechnology Information, U.S. National Library of Medicine. PMID   29493917 . Retrieved 11 July 2021.
  10. ↑ Van Dam M, Fitzgerald B (2024). "Pulsus Paradoxus". National Center for Biotechnology Information, U.S. National Library of Medicine. PMID   29493917 . Retrieved 11 July 2021.
  11. ↑ Talreja, DR; Nishimura, RA; Oh, JK; Holmes, DR (22 January 2008). "Constrictive pericarditis in the modern era: novel criteria for diagnosis in the cardiac catheterization laboratory". Journal of the American College of Cardiology. 51 (3): 315–9. doi: 10.1016/j.jacc.2007.09.039 . PMID   18206742.
  12. ↑ Curtiss EI, Reddy PS, Uretsky BF, Cecchetti AA (February 1988). "Pulsus paradoxus: definition and relation to the severity of cardiac tamponade". Am Heart J. 115 (2): 391–8. doi:10.1016/0002-8703(88)90487-5. PMID   3341174.{{cite journal}}: CS1 maint: multiple names: authors list (link)
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.