Clinical signs in medicine: pulsus paradoxus.
A Khasnis, Y Lokhandwala
Departments of Medicine and Cardiology, Seth G. S. Medical College and K. E. M. Hospital, Parel, Mumbai - 400 012, India., India
Departments of Medicine and Cardiology, Seth G. S. Medical College and K. E. M. Hospital, Parel, Mumbai - 400 012, India.
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Khasnis A, Lokhandwala Y. Clinical signs in medicine: pulsus paradoxus. J Postgrad Med 2002;48:46-9
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Khasnis A, Lokhandwala Y. Clinical signs in medicine: pulsus paradoxus. J Postgrad Med [serial online] 2002 [cited 2019 Jun 18 ];48:46-9
Available from: http://www.jpgmonline.com/text.asp?2002/48/1/46/153
Pulsus paradoxus, a physical sign of tremendous diagnostic and prognostic significance can be seen in a variety of cardiac and extra-cardiac conditions. This article will discuss the mechanism, pathophysiology, detection and management of patient with pulsus paradoxus.
The reduction in pulse volume during inspiration was first described by Lomer in 1669 in constrictive pericarditis. A similar finding was described by Floyer and later by William in 1850 in bronchial asthma. Adolf Kussmaul (Freiberg, Germany) coined the term “pulsus paradoxus” in 1873 in three patients with constrictive pericarditis. The “paradox” was: (1) the discrepancy between the absence of the pulse and present corresponding heart beat and (2) Amidst this irregularity, the regularity with which the pulse disappeared during inspiration.
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.
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.
The “paradox” refers to the fact that heart sounds may be heard over the precordium when the radial pulse is not felt. This is due to an exaggeration of the normal mechanisms mentioned above. Moreover, the clinical method of assessment of this “pulse” is by measurement of the “systolic blood pressure”. The mechanisms in various pathologies are discussed below.
1. Cardiac tamponade
2. Pericardial effusion
3. Constrictive pericarditis
4. Restrictive cardiomyopathy
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)
2. Volvulus of the stomach
3. Diaphragmatic hernia
4. Superior vena cava obstruction
5. Extreme obesity
As a general guideline, pulsus paradoxus will be a result of the following mechanisms operating alone or in combination:
1. Limitation in increase in inspiratory blood flow to the right ventricle and pulmonary artery
2. Greater than normal pooling of blood in the pulmonary circulation
3. Wide excursions in the intrathoracic pressure during inspiration and expiration
4. Interference with venous return to either atrium especially during inspiration
In this review the pathophysiology underlying only the major causes will be discussed.
Pulsus paradoxus has great diagnostic significance in pericardial disease. The following mechanisms are proposed to operate:
1. Tense fluid accumulation within the pericardial sac impairs left ventricular filling causing an exaggerated reduction in systolic blood pressure during inspiration. Katz and Gauchat found that with pericardial tamponade, intrapericardial pressure did not fall during inspiration. As a result, the pulmonary venous pressure would fall more than the left atrial pressure during inspiration tending to cause a fall in the left ventricular filling during inspiration due to incomplete transmission of the inspiratory fall of intrathoracic pressure to the left atrium. This has been documented in other studies as well. Dock proposed that the inspiratory traction by the diaphragm and mediastinum upon the taut pericardium further increased intrapericardial pressure thus interfering with cardiac filling. Shabetai found that both vena caval and pulmonary arterial blood flow velocity fail to increase normally during inspiration in patients with constrictive pericarditis.
2. Fowler et al showed that there is a persistence of the normal inspiratory increase of the filling of the right side of the heart during cardiac tamponade. If this was prevented, paradoxical pulse did not develop, however severe the tamponade. Guntheroth et al proposed that the normal respiratory variations of a reduced right ventricular stroke volume are responsible for the exaggerated respiratory variations in blood pressure during cardiac tamponade.
3. Pulsus paradoxus may be caused by pooling of blood in the pulmonary circulation and competition of the ventricles for filling within a relatively fixed pericardial space. Few reports have highlighted abnormal movement of the interventricular septum during inspiration contributing to decreased LV volume., Similar respiratory changes in mitral and septal motions and the similar respiratory interaction between the right and left ventricles have been observed during the Mueller manoeuvre. These observations suggest decreased left ventricular filling and left ventricular end-diastolic volume during inspiration in the presence of pulsus paradoxus. Large pericardial fluid collections may affect left ventricular function even in the absence of clinical manifestations.
4. One of the other principal causes for pulsus paradoxus is underfilling of the left ventricle during the preceding diastole. This is the most likely cause of this combination of events.
The pulsus paradoxus in this condition results from right ventricular dysfunction secondary to acute right ventricular dilation and excessive pooling of blood in the lungs in inspiration.
Pulsus paradoxus in acute myocardial infarction can result from right ventricular infarction, cardiogenic shock or cardiac tamponade. However, it has been described in uncomplicated myocardial infarction due to the differences in the compliance of the left atrium, left ventricle and pulmonary circulation that is further exaggerated by an increase in the left ventricular stiffness due to myocardial ischaemia.
Pulsus paradoxus is one of the ominous signs in acute exacerbation of bronchial asthma. This is the most common extra-cardiac cause of this physical sign. The main mechanism operational in respiratory disease is the unusually great fluctuations in intrathoracic pressures that are transmitted to the aorta. The following theories have been proposed:
1. During increased airway resistance, there is an exaggeration in the inspiratory-expiratory difference in stroke volume mediated primarily by the effects of intrathoracic pressure on ventricular preload. Shim et al found that patients of asthma with pulsus paradoxus had greater airflow obstruction than patients without. Also, it was often present in mild obstruction and absent in severe obstruction. In acute exacerbation of childhood asthma, pulsus paradoxus often correlates with both the severity and response to bronchodilators.
2. Hyperinflation of the chest due to air trapping is also plays a role in pulsus paradoxus. Factors other than hyperinflation also contribute to the fall in systolic pressure that occurs at full inflation of the lungs. This is also observed in patients with chronic stable obstructive airway disease.
Hypovolaemia may precipitate pulsus paradoxus in critically ill patients. Its occurrence may aid in the clinical recognition of the common syndrome of occult hypovolaemia in patients with shock and no obvious blood loss.
The patient should be instructed not to breathe too deeply (enough to make the chest movements easily visible). The sphygmomanometer cuff is inflated above systolic pressure. Korotkoff sounds are sought over the brachial artery while the cuff is deflated at rate of approximately 2 to 3 mm Hg per heartbeat. The peak systolic pressure during expiration should first be identified and reconfirmed (when Korotkoff sounds are heard only during expiration). The cuff is then deflated slowly to establish the pressure at which Korotkoff sounds become audible during both inspiration and expiration (when the Korotkoff sounds are heard during both inspiration and expiration). When the differences between these two levels exceeds 10 mm Hg during quiet respiration, a paradoxical pulse is present.
Usually, palpation of the central pulses (carotid) is recommended for the evaluation of the character of the pulse. However, pulsus paradoxus is better appreciated in the peripheral pulses (radial). When the pulsus paradoxus is severe, it may be possible to palpate a fall (reduction in the pulse volume) during the phase of inspiration and rise during the expiratory phase.
Arterial waveform analysis
In the intensive care setting, where the arterial waveform is available, pulsus paradoxus can be diagnosed by visualising changes in the systolic blood pressure tracing during the inspiratory and expiratory phases of respiration.
Pulse oximetry waveform analysis,
This technique has been found useful in the neonates with cardiac tamponade. In patients with obstructive airway disease since pulse oximetry is available in ICUs and emergency departments, it is a useful non-invasive means of continually assessing pulsus paradoxus and air trapping severity.
Reversed pulsus paradoxus, a rise in systolic blood pressure during inspiration, was first described by Massumi et al in patients with idiopathic hypertrophic subaortic stenosis, isorhythmic ventricular rhythm and patients of left ventricular failure on positive pressure ventilation. A rise in peak systolic pressure on inspiration by more than 15 mm Hg is considered significant. In a mechanically ventilated patient, positive pressure ventilation displaces the ventricle wall inward during systole to assist in ventricular emptying causing a slight rise in the systolic pressure during mechanical inspiration. A reverse pulsus paradoxus in mechanically ventilated patients is a sensitive indicator of hypovolaemia.
Salel et al described a patient of complete heart block who was misdiagnosed to have pulsus paradoxus. This was the result of forfituous synchronism of inspiration with the cyclic intermittent properly timed atrial contribution to ventricular filling characteristic of atrioventricular dissociation in this condition. This is termed pseudopulsus paradoxus. This error can be avoided by strictly adhering to the guidelines for pulsus paradoxus laid down by Gauchat and Katz: (1) The pulse must be felt in all the accessible arteries (2) There is no need for deep inspiration and (3) There must be no irregularity of cardiac action.
All cases of cardiac tamponade are not accompanied by pulsus paradoxus. The reasons for this are not clear in all cases, but it is likely that other compensatory mechanisms are brought into play in order to maintain a normal systemic blood pressure. The following are such conditions:
1. Aortic regurgitation (AR): In the presence of AR, the left ventricle can fill from the aorta during inspiration. Therefore, if aortic dissection produces both AR and tamponade, pulsus paradoxus may be absent.
2. Large atrial septal defect: The normal increase in systemic venous return on inspiration is balanced by a decrease in the left to right shunt, resulting in minimal change in the right ventricular volume.
3. Isolated right heart tamponade: This entity has been described in patients of chronic renal failure on hemodialysis
4. Elevated left ventricular diastolic pressures
5. Severe rheumatoid spondylitis or disease of the bony thorax: Wide changes in intrathoracic pressure prevented by the relative immobility of the chest wall.
6. Coexistent condition producing “reversed pulsus paradoxus”
Kussmaul’s sign is a paradoxical increase in the peripheral venous distension and pressure during inspiration. The major mechanism is a change in the shape of the pericardium with a resulting increase in the intrapericardial pressure and obstruction to the venous return to the heart. Compare this with the marked exaggeration of the normal expiratory increase in venous pressure that accompanies patients with pulmonary disease. Note that pulsus paradoxus may be present in both groups of patients.
Rule out common, important and life threatening causes first.
1. Careful history of the illness
2. Haemodynamic status of the patient
3. Meticulous examination of the jugular venous pulse – do not forget Kussmaul’s sign and abdominojugular reflux
4. Look for Beck’s triad (distended jugular veins, hypotension and muffled heart sounds) – suggestive of cardiac tamponade
5. Detailed evaluation of the respiratory and cardiovascular systems
6. X-ray chest and ECG may provide diagnosis or rule out some of the causes
7. Emergent pericardiocentesis if large pericardial effusion
8. Aggressive management of asthma, exacerbation of obstructive pulmonary disease, intercostal tube insertion/needle insertion for tension pneumothorax
9. Thrombolysis for myocardial infarction or massive pulmonary embolism
10. The other causes should be treated on their own merit
Although pulsus paradoxus is a valuable physical sign, it has its limitations. The use of the term is not uniform and as it is an exaggeration of a normal phenomenon, a cut-off value is difficult to provide. In patients of cardiac tamponade, studies have shown that when right ventricular diastolic collapse on echocardiography and pulsus paradoxus were compared, right ventricular diastolic collapse was more sensitive and more specific than pulsus paradoxus in detecting increases in intrapericardial pressure during euvolaemia and hypervolemia whereas the two tests were equally valuable in hypovolaemic states., As with other clinical signs, pulsus paradoxus must not be considered in isolation but in conjunction with the patient’s clinical state and with other indices of the severity of asthma. Finally, the absence of pulsus paradoxus does not rule out the presence of a significant pericardial effusion. However, this important bedside sign must be elicited in indicated patients, foregoing which life threatening and potentially treatable causes are likely to be missed by the examining physician.
|1||Wagner HR. Paradoxical pulse: 100 years later. Am J Cardiol 1973:91-2.|
|2||Golinko RJ, Kaplan N, Rudolph AM. The mechanism of pulsus paradoxus in acute pericardial tamponade. J Clin Invest 1963; 249–57.|
|3||Peter Mills. Examination of the cardiovascular system. In: Hutchinson’s Clinical Methods 20th Ed. p.169|
|4||Hurst JW, Schlant RC. Examination of the arterial pulse. In The Heart – Arteries and Veins 3rd Ed. p.177 – 78|
|5||Ward GL, Heiselman DE, White LJ. Pulsus paradoxus in anaphylactic shock due to urokinase administration. Chest 1992;101:589.|
|6||Hooper TL, Lawson RA. Volvulus of the stomach—an unusual cause of pulsus paradoxus. Postgrad Med J 1986;62:377-9.|
|7||Dock W. Inspiratory traction on the pericardium: the cause of pulsus paradoxus in pericardial disease. Arch Intern Med 1961;108:837.|
|8||Shabetai R, Fowler NO, Fenton JC, Masangkay M. Pulsus paradoxus. J Clin Invest 1965;44:1882-98.|
|9||Fowler NO. Pericardial disease. In The Heart – Arteries and Veins 3rd Ed. Pg 1388|
|10||Shabetai R, Fowler NO, Guntheroth WG. The hemodynamics of cardiac tamponade and constrictive pericarditis. Am J Cardiol 1970;26:480. |
|11||Cosio FG, Martinez JP, Serrano CM, de la Calada CS, Alcaine CC. Abnormal septal motion in cardiac tamponande with pulse paradoxus. Echocardiographic and hemodynamic observations. Chest 1977; 71: 787-8.|
|12||Anno Y, Matsuzaki M, Sada K, Sasada T, Fukagawa K, Sasaki T, et al. Echocardiographic findings of pulsus paradoxus: cardiovascular changes due to respiration. J Cardiogr 1981;11:147-60.|
|13||Wayne VS, Bishop RL, Spodick DH. Dynamic effects of pericardial effusion without tamponade. Respiratory responses in the absence of pulsus paradoxus. Br Heart J 1984;51:202-4.|
|14||Fitchett DH, Sniderman AD. Inspiratory reduction in left heart filling as a mechanism of pulsus paradoxus in cardiac tamponade. Can J Cardiol 1990;6:348-54.|
|15||Constant J. Arterial pulses and pressures. In Bedside Cardiology 4th Ed. Pg 63.|
|16||Esteban A, Gomez-Acebo E, de la Cal MA. Pulsus paradoxus in acute myocardial infarction. Chest 1982;81:47-50.|
|17||Shim C, Williams MH Jr. Pulsus paradoxus in asthma. Lancet 1978;1:530-1.|
|18||Gluck JC, Busto R, Marks MB. Pulsus paradoxus in childhood asthma—its prognostic value. Ann Allergy 1977;38:405-7.|
|19||Blaustein AS, Risser TA, Weiss JW, Parker JA, Holman BL, McFadden ER. Mechanisms of pulsus paradoxus during resistive respiratory loading and asthma. J Am Coll Cardiol 1986;8:529-36.|
|20||Cohn JN, Pinkerson AL, Tristani FE. Mechanism of pulsus paradoxus in clinical shock. J Clin Invest 1967;46:1744-55.|
|21||Tamburro RF, Ring JC, Womback K. Detection of pulsus paradoxus associated with large pericardial effusions in pediatric patients by analysis of the pulse-oximetry waveform. Pediatrics 2002;109:673-7.|
|22||Chadwick V, Pearce S, Taylor B, Galland BC. Continuous non-invasive assessment of pulsus paradoxus. Lancet 1992 22;339:495-6.|
|23||Massumi RA, Mason DT, Vera Z, Zelis R, Otero J, Amsterdam EA. “Reversed pulsus paradoxus”. N Engl J Med 1973; 1272–75.|
|24||Salel A, Amsterdam EA, Zelis R. Pseudopulsus paradoxus. Chest 1973;64:671-2.|
|25||Henkind SJ, Benis AM, Teichholz LE. The paradox of pulsus paradoxus. Am Heart J 1987;114(1 Pt 1):198-203.|
|26||Cogswell TL, Bernath GA, Wann LS, Hoffman RG, Brooks HL, Klopfenstein HS. Effects of intravascular volume state on the value of pulsus paradoxus and right ventricular diastolic collapse in predicting cardiac tamponade. Circulation 1985 ;72:1076-80.|
|27||Klopfenstein HS, Schuchard GH, Wann LS, Palmer TE, Hartz AJ, Gross CM, et al. The relative merits of pulsus paradoxus and right ventricular diastolic collapse in the early detection of cardiac tamponade: an experimental echocardiographic study. Circulation 1985;71:829-33.|
|28||Lewis BS, Goldberg RB, Kew MC. Pulsus paradoxus in the bedside assessment of patients with bronchial asthma. S Afr Med J 1976 17;50:1210-3.|