Pulmonary vein blood flow velocity in pulsus paradoxus.

The effect of inspiration on pulmonary vein blood flow velocity and forward pressure gradient from pulmonary vein to left atrium was studied in seven patients with chronic constrictive pericarditis, five of whom had clinically obvious pulsus paradoxus. Compared to patients without pericardial disease, where inspiration produced no change, patients with pericardial disease showed an inspiratory fall in the forward pressure gradient and forward blood flow velocity in the pulmonary veins on inspiration. The mechanism of pulsus paradoxus in these patients can be explained by incomplete transmission of the inspiratory fall of intrathoracic pressure to the left atrium.     

Mechanisms of pulsus paradoxus during resistive respiratory loading and asthma

To determine the mechanisms of pulsus paradoxus during asthma, six subjects known to have cold air bronchial hyperreactivity were studied while in a quiescent phase of their disease. All were free of significant airway obstruction at the time of study. After placement of an esophageal balloon to estimate intrathoracic pressure, the subjects were assessed during quiet breathing, resistive airway loading and then during a stable period of airway obstruction induced by cold air. Steady state left ventricular volume and performance were measured using radionuclide ventriculography; right ventricular volume was calculated from the stroke volume ratio and right ventricular ejection fraction. Cardiac cycles were segregated according to their occurrence in inspiration or expiration using a flow signal from a pneumotachograph. Combined inspiratory and expiratory resistance produced pulsus paradoxus and changes in esophageal pressure that were similar to those during asthma and significantly greater than those during quiet breathing. These changes were accompanied by decreases in left ventricular diastolic volume and stroke volume during inspiration, and increases in these variables during expiration; right ventricular volume and stroke volume demonstrated changes reciprocal to those seen in the left ventricle. These data indicate that during periods of increase in airway resistance, abnormal pulsus paradoxus results from an exaggeration in the normal inspiratory-expiratory difference in stroke volume mediated primarily by the effects of intrathoracic pressure on ventricular preload.     

Velocity of contractile element shortening in constrictive pericarditis and the effect of pulsus paradoxus.

Force-velocity curves were constructed in nine patients with CP from a high-fidelity LV pressure tracing and its simultaneously recorded first derivative. Vmax and peak Vce (Vpm) were calculated using the 2-element (Hill) or Voigt model; the curves were also constructed and Vmax measured using the 3-element Maxwell model. The measurements were compared with those in a group of four patients with CMO and with two control subjects. Measurements of the celerity of ventricular contraction--peak LVdp/dt, Max d/IP and Vmax (2-element model)--were reduced in CP and greatly reduced in CMO. The effect of beat-to-beat variations in preload during pulsus paradoxus on the indices of ventricular celerity was studied. Peak LVdp/dt and Vpm varied with the change in LVEDP: the change in Vmax was negligible using the 2-element (Hill) or Voigt model. The 3-element (Maxwell) model failed to discriminate between the three groups of patients and seems to be invalid at high LV end-diastolic pressures.     

Absence of pulsus paradoxus in a patient with cardiac tamponade and coexisting pulmonary artery obstruction

Pulsus paradoxus is a key physical finding in patients with cardiac tamponade. This report describes a 38-year-old woman with metastatic adenocarcinoma who had cardiac tamponade confirmed by cardiac catheterization. Pulsus paradoxus was notably absent. No evidence could be found for an atrial septal defect, significant aortic regurgitation, elevated left ventricular diastolic pressure, or localized tamponade, previously described disorders in which pulsus paradoxus may not be seen when tamponade occurs. The lack of pulsus paradoxus in this case was attributed to right ventricular pressure overload due to mechanical obstruction of the pulmonary artery.     

Analysis of physician ability in the measurement of pulsus paradoxus by sphygmomanometry

CONTEXT: Measurement of pulsus paradoxus (PP) is one of several measures previously advocated in the National Heart, Lung, and Blood Institute asthma management guidelines: a pulsus of > 12 mm Hg warranted hospital admission. It is one of only a few measures that is not effort dependent and therefore important in the evaluation of patients with asthma. OBJECTIVE: Determination of physician accuracy in measuring PP. DESIGN: A model of induced PP in a trained healthy subject without respiratory disease was constructed with a fixed inspiratory resistance with measurement of inspiratory air pressure and beat-to-beat BP noninvasively. SETTING: Laboratory. PARTICIPANTS: Attending physicians from emergency medicine and critical care disciplines who served as consecutive examiners of the trained reference subject generating known PP. INTERVENTIONS: A total of 19 attending physicians were assessed for ability in measuring PP by sphygmomanometry and by palpation. The reference subject generated 4 degrees of PP sequentially, with each examiner blinded to the value of negative inspiratory pressure and PP. Examiners first assessed PP qualitatively by palpation, followed by its measurement within 2 min. Main outcome measure: Proximity of physician-measured PP (PPm) to true PP (PPt). RESULTS: At inspiratory pressures of - 10, - 15, - 20, and - 25 mm Hg, PPt was 13.7, 16.2, 19.1, and 20.7 mm Hg, respectively (F = 14.8, p < 0. 0001; analysis of variance [ANOVA]). At the same pressures, PPm was 13.1, 17.5, 17.7, and 18.0 mm Hg (p > 0.10; ANOVA). Linear regression of PPm against PPt for each examiner revealed a slope (SE) of 0.53 (0.23), and not a 1:1 relationship. CONCLUSIONS: Past and present guidelines do not account for the challenges in measuring PP, especially in tachypneic patients. Sphygmomanometric determination of PP should be augmented by new aids developed through technological innovation.     

Diagnostic value and pathophysiologic basis of pulsus paradoxus in infants and children with respiratory disease

The purpose of the study was to analyze the respiratory-dependent intraarterial blood pressure variations (pulsus paradoxus, PP) in intensive care unit patients with obstructive and restrictive pulmonary disease, and to evaluate the usefulness of PP for assessment of disease severity. One-minute paper recordings of arterial blood pressures, left atrial pressures (LAP, 16 patients), breathing cycles, and electrocardiograms (ECG) were taken in 54 nonintubated children. There was a close relationship between systolic and diastolic blood pressure variations (r = 0.92). The mean coefficient of variation of PP was 18.4% (SD 11.6%). The relationship between respiratory dependent LAP fluctuations (Delta LAP) and PP was logarithmic. PP correlated significantly with a respiratory severity score (RSS: wheeze, oxygen requirement, heart rate, arterial partial pressure of carbon dioxide) in a subgroup of 16 asthmatics (r = 0.66, P = 0.005); wheeze score was the only true independent determinant of RSS (multiple regression). In the nonasthmatics with restrictive lung disease, the correlation coefficient for the association between PP and RSS was 0.34 (P = 0.08), with a significant univariate correlation between PP and wheeze score (r = 0.62, P = 0.001). We conclude that PP correlates significantly with wheeze in obstructive and restrictive disease. PP is a valuable clinical sign of disease severity in patients with wheeze as clinical manifestation of obstructive airway disease. The relationship between Delta LAP and PP confirms the finding that an increase in PP is associated with a rise in left atrial transmural pressure.     

Dynamic effects of pericardial effusion without tamponade. Respiratory responses in the absence of pulsus paradoxus.

Fourteen patients with pericardial effusions without clinical signs of tamponade (pulsus paradoxus or other cardiac and circulatory abnormalities) showed inspiratory reductions in echocardiographic left ventricular internal diastolic diameter which correlated directly with the exaggerated respiratory changes in systolic time intervals (both pre-ejection period and left ventricular ejection time). Excessive pericardial fluid affects left ventricular function even in the absence of clinical manifestations.     

Dynamic effects of pericardial effusion without tamponade. Respiratory responses in the absence of pulsus paradoxus

Fourteen patients with pericardial effusions without clinical signs of tamponade (pulsus paradoxus or other cardiac and circulatory abnormalities) showed inspiratory reductions in echocardiographic left ventricular internal diastolic diameter which correlated directly with the exaggerated respiratory changes in systolic time intervals (both pre-ejection period and left ventricular ejection time). Excessive pericardial fluid affects left ventricular function even in the absence of clinical manifestations.     

Pectus excavatum with inspiratory inferior vena cava compression: a new presentation of pulsus paradoxus

A 29-year-old man with pectus excavatum presented with exercise intolerance, pulsus paradoxus, and paradoxically split S2. Chest computed tomography (CT) showed the heart shifted leftward and a pectus severity index of 7.18. Cardiopulmonary exercise study showed reduced VO2max, anaerobic threshold, and oxygen pulse. Echocardiography revealed a decline in mitral and tricuspid valve inflow, and stroke volume during inspiration. Cardiac extrinsic compression and anatomic cardiac abnormalities were not present. Dynamic magnetic resonance imaging (MRI) demonstrated inspiratory inferior vena cava (IVC) compression at the diaphragm. We discuss IVC compression by the diaphragm as a source of patient symptoms and as a mechanism for pulsus paradoxus associated with pectus excavatum.     

Inspiratory reduction in left heart filling as a mechanism of pulsus paradoxus in cardiac tamponade

Pulsus paradoxus occurs in cardiac tamponade because the output of the left ventricle falls during inspiration. The principal cause for this is reduced filling of the left ventricle during the preceding diastole. The present study examines whether this reduced filling of the left ventricle on inspiration is due to compression by the right heart or due to reduced venous return to the left heart. The effect of pericardial tamponade on hemodynamics and left ventricular and atrial volumes was determined in six experimental animals. The data demonstrate that from the outset pericardial fluid reduces left ventricular end diastolic volume, although initially left ventricular end systolic volume decreases as well. By contrast, pulsus paradoxus is a relatively late phenomenon occurring with severe tamponade and associated with an inspiratory decrease in left atrial and ventricular volumes in the face of a drop in left ventricular filling pressure. Underfilling of the left heart is the most likely cause of this combination of events.     

Echocardiogram in pulsus paradoxus. Respiration dependent cyclic changes in mitral and aortic valve motion: a case report

The mechanism of production of pulsus paradoxus was echocardiographically studied in a 74-year-old male with subacute effusive-constrictive pericarditis which developed to constrictive pericarditis under the observation. Echocardiography disclosed the following phenomena during inspiration: 1) mitral valve did not open until the atrial systole, probably because of the lack of antegrade mitral flow during rapid filling phase (the E wave was not observed), 2) concomitantly, aortic valve opening decreased markedly in its grade, and 3) left ventricular ejection time (LVET) decreased and pre-ejection period (PEP) increased, resulting in a higher PEP/LVET ratio (up to 1.32). The opposite was true during expiration (PEP/LVET ratio was 0.40). This is probably the first case, in which the mechanism of pulsus paradoxus was investigated by aortic and mitral valve echograms.     

Usefulness of right ventricular diastolic collapse in diagnosing cardiac tamponade and comparison to pulsus paradoxus

To compare the sensitivity, specificity and predictive value of right ventricular (RV) diastolic collapse and pulsus paradoxus as signs of cardiac tamponade, 21 consecutive patients with pericardial effusion and suspected cardiac tamponade underwent prospective hemodynamic and echocardiographic evaluation. Simultaneous hemodynamic and echocardiographic data were obtained in all patients before and after pericardiocentesis. Cardiac tamponade was considered present when there was diastolic equilibration of the intrapericardial, right atrial and pulmonary capillary wedge pressures and elevation of these pressures to more than 10 mm Hg. RV diastolic collapse was 93% sensitive and 100% specific in diagnosing cardiac tamponade, whereas pulsus paradoxus was only 79% sensitive and 40% specific. The positive and negative predictive values of RV diastolic collapse (100% and 83%) were considerably better than pulsus paradoxus (81% and 40%) and demonstrate that RV diastolic collapse is more sensitive, specific and predictive of cardiac tamponade than is pulsus paradoxus. Serial simultaneous hemodynamic and echocardiographic observations at multiple points during pericardiocentesis in a smaller subgroup (5 patients) also suggest that the hemodynamic effects of RV diastolic collapse in cardiac tamponade are mediated by an increase in intrapericardial pressure.     

Use of pulse oximetry to recognize severity of airflow obstruction in obstructive airway disease: correlation with pulsus paradoxus

STUDY OBJECTIVES: The purpose of this cross-sectional study was to confirm the observation that pulse oximetry tracing correlates with pulsus paradoxus, and is therefore a measure of the severity of air trapping in obstructive airway disease. DESIGN: Cross-sectional survey. SETTING: The ICU in a tertiary care academic hospital. PATIENTS: Twenty-six patients consecutively admitted to the ICU with obstructive airway disease, either asthma or COPD. MEASUREMENTS AND RESULTS: Forty-six percent of the study patients required mechanical ventilation, and 69% had an elevated pulsus paradoxus. We defined the altered pulse oximetry baseline tracing as the respiratory waveform variation (RWV). The RWV was measured in numerical form as the change in millimeters from the baseline. Pulsus paradoxus was significantly correlated with the RWV of the pulse oximetry tracing (p < 0.0001). An analysis of the respiratory variations in the pulse oximetry waveforms in obstructive lung disease patients reflects the presence and degree of auto-positive end-expiratory pressure (auto-PEEP; p < 0.0001). CONCLUSIONS: We describe the characteristic alterations in the pulse oximetry tracings that occur in the presence of pulsus paradoxus and auto-PEEP. Since pulse oximetry is available universally in ICUs and emergency departments, it may be a useful noninvasive means of continually assessing pulsus paradoxus and air trapping severity in obstructive airway disease patients.     

Continuous noninvasive measurement of pulsus paradoxus complements medical decision making in assessment of acute asthma severity

BACKGROUND: Pulsus paradoxus (PP) is a pathophysiologic parameter that is indicative of asthma severity. The ability of PP to categorize acutely asthmatic patients in accordance with the earlier National Asthma Education and Prevention Program (NAEPP) expert panel report 1 guidelines was determined. METHODS: An arterial tonometric BP monitor, which was interfaced to an analog-digital converter, executed a periodic amplitude analysis algorithm, which computed PP in real time. The PP measurement was compared to the criterion standard of emergency physicians in determining the hospital admission vs hospital discharge disposition following the NAEPP standardized treatment. Receiver operating characteristics (ROCs) were calculated, and the PP threshold, which maximized sensitivity and specificity, was identified. In a separate laboratory investigation, PP was induced in a healthy volunteer by inspiration through a fixed resistance. Plethysmographic waveform changes, induced by PP, were measured by a second analog-to-digital converter that was connected to a pulse oximeter. RESULTS: A total of 79 patients were enrolled in the study, of whom 63 met a priori inclusion criteria and had uninterrupted data acquisition. The mean PP for patients who were appropriately discharged from the hospital was 9.1 mm Hg (95% confidence interval [CI], 7.3 to 10.9 mm Hg) and differed from the PP of 17.6 mm Hg (95% CI, 13.5 to 21.8; p < 0.001) for patients admitted to the hospital/relapsed. The sensitivity and specificity for physician disposition were 0.83 and 0.89, respectively, and for PP values were 0.78 and 0.78, respectively. The Wilcoxon area under the ROC curve was 0.82 (95% CI, 0.64 to 0.99) following treatment. The risk ratio was 5.32 for hospital admission among patients with a PP of > 11.3 mm Hg. Changes in the photoplethysmography peak height were correlated to PP from the BP monitor by a regression line with a slope of 0.01 V/mm Hg. CONCLUSIONS: Continuous PP can aid in determining disposition among emergency department (ED) patients with acute asthma. ED physicians equipped with a PP monitor would be able to objectify the work of breathing and would more closely adhere to NAEPP guidelines. The possibility that a PP detection algorithm could reside in a pulse oximeter warrants further investigation.