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Occasionally, a prominent P wave is encountered in a life insurance applicant's electrocardiogram. Prominent P waves may be normal variants or alert the medical director to prognostically significant structural heart or pulmonary disease. This case study reviews the commonly used criteria for the ECG pattern of right atrial abnormality and some of the pitfalls associated with its use.
The authors measured in a group of 30 patients invasively the pressure in the right atrium and at the same time or within 60 minutes the diameter of the interior vena cava and its changes in conjunction with respiration. They revealed a statistically significant relationship between all parameters of the diameter of the interior vena cava assessed by echocardiography and the mean right atrial pressure. The closest correlation was found in the index of the inspiration diameter of the inferior vena cava (p = 0.01; r = 0.824). A critical value of the index of the inspiration diameter of the inferior vena cava greater than or equal to 10 mm revealed patients with a pathologically elevated pressure in the right atrium with a 100% sensitivity and 88.9% specificity. Measurement of the diameter of the inferior vena cava and its respiratory variations is a suitable method for estimation of the mean right atrial pressure.
To restore sinus rhythm in the remaining heart chambers of six adult patients with atrial septal defect and chronic or paroxysmal atrial fibrillation, electrical, right atrial isolation associated with surgical correction of the defect was performed. All but one patient was free from atrial fibrillation without medication 2-25 months after operation. The isolated right atrial appendages showed intrinsic rhythmical activity in five patients and no electrical activity in one. Right atrial isolation is a safe and effective procedure that abolishes atrial fibrillation in patients with arrhythmia after surgical correction of atrial septal defect.
The problem of the efficacy of right-ventricular protection with retrograde coronary sinus cardioplegia is studied. Sixty patients undergoing myocardial revascularization were prospectively assigned to receive cold St. Thomas' Hospital cardioplegia into the aortic root (30 patients) or retrogradely in the coronary sinus (30 patients). The two groups were similar concerning preoperative and operative data. The hemodynamic recovery postoperatively was good in both groups, the increase of the heart rate, the decrease of the mean aortic pressure and the right-ventricular stroke-work index were not significantly different in the two groups. However, right atrial pressure increased significantly (p less than 0.001) in patients who received cardioplegia anterogradely and decreased, but not significantly, in the retrograde group. The data suggest that the decrease of the right-ventricular stroke-work index in the anterograde group is related to a depressed contractility and in the group with retrograde delivery of cardioplegia to a decreased preload. There were no differences between the groups with respect to clinical outcome. We conclude that retrograde delivery of cardioplegia results in an excellent protection of the right-ventricular function in elective myocardial revascularization.
PURPOSE: The purpose of this study was to determine whether the pattern of respiratory variation in right atrial pressure (Pra) predicts the cardiac output response to positive end-expiratory pressure (PEEP). MATERIALS AND METHODS: We studied 18 patients with a variety of cardiac and pulmonary disorders requiring ventilatory support. A pulmonary artery flotation catheter was in place as part of their routine management. Changes in PEEP were made from 0 to 14 cm H2O to determine the level of PEEP, which increased PO(2) without decreasing cardiac output (ie, assessment of best PEEP). Static lung compliance and auto-PEEP were obtained from the pressure signal on the ventilator. The change in Pra with a spontaneous inspiratory effort (ie, triggered breath) was used to determine whether patients had a restrictive (ie, operating on the flat part of the Starling curve), or nonrestrictive pattern (acting on the ascending part of the Starling curve) as previously described. RESULTS: Cardiac output decreased 0.7 +/- 0.8 L/min (change from baseline P <.05) in the group with an inspiratory decrease in Pra and -0.04 +/- 1.50 L/min (P = NS) in the group without an inspiratory decrease in Pra. The groups were not significantly different. However, the variance in cardiac output was large and, in contrast to our hypothesis, two patients in the group with an inspiratory decrease in Pra did not have a decrease in cardiac output. Pra and pulmonary artery occlusion pressure after the PEEP trial were greater than before, indicating that reflex circulatory adjustments occurred in response to the PEEP. CONCLUSIONS: The inspiratory pattern in Pra does not predict the response to cardiac output to PEEP in individual patients. This is most likely because of reflex adaptations in the circuit that occur with the application of PEEP. The response of a patient to PEEP is affected by the patient's volume reserves, filling status of the right atrium, and neurosympathetic activity.
Since the technique of thermodilution (TD) cardiac output measurements per se causes haemodynamic alterations, the authors examined whether the alterations elicited by iced injectate are augmented in the presence of myocardial ischaemia (MI) or pulmonary oedema (PE), compromised conditions frequently associated with critically ill patients. MI (N = 7) or PE (N = 7) was induced by clamping the anterior descending coronary artery or by a slow infusion of oleic acid into the right atrium, respectively, in anaesthetized dogs. Injection of iced injectate, 3 ml, caused similar changes in heart rate, mean systemic and pulmonary arterial pressures, pulmonary blood flow, right ventricular dP/dt, and right atrial pressure in dogs with and without MI or PE. Cardiac output estimated by TD correlated closely with pulmonary blood flow measured by electromagnetic flowmeter in both MI and PE (r > 0.9). No profound alterations in haemodynamics were observed at any injection during TD cardiac output measurements under MI or PE. These results indicate that TD cardiac output determination does not cause serious haemodynamic alterations, and can estimate right ventricular output accurately under MI and PE.
BACKGROUND: Increased mortality in patients with chronic pulmonary hypertension has been associated with elevated right atrial (RA) pressure. However, little is known about the effects of chronic right ventricular (RV) pressure overload on RA and RV dynamics or the adaptive response of the right atrium to maintain RV filling. METHODS AND RESULTS: In 7 dogs, RA and RV pressure and volume (conductance catheter) were recorded at baseline and after 3 months of progressive pulmonary artery banding. RA and RV elastance (contractility) and diastolic stiffness were calculated, and RA reservoir and conduit function were quantified as RA inflow with the tricuspid valve closed versus open, respectively. With chronic pulmonary artery banding, systolic RV pressure increased from 34+/-7 to 70+/-17 mm Hg (P<0.001), but cardiac output did not change (P>0.78). RV elastance and stiffness both increased (P<0.05), suggesting preserved systolic function but impaired diastolic function. In response, RA contractility improved (elastance increased from 0.28+/-0.12 to 0.44+/-0.13 mm Hg/mL; P<0.04), and the atrium became more distensible, as evidenced by increased reservoir function (49+/-14% versus 72+/-8%) and decreased conduit function (51+/-14% versus 28+/-8%; P<0.002). CONCLUSIONS: With chronic RV pressure overload, RV systolic function was preserved, but diastolic function was impaired. To compensate, RA contractility increased, and the atrium became more distensible to maintain filling of the stiffened ventricle. This compensatory response of the right atrium likely plays an important role in preventing clinical failure in chronic pulmonary hypertension.
BACKGROUND: The origin and magnitude of the back pressure opposing diastolic coronary inflow remain controversial. The arterial pressure at which coronary inflow stops during a prolonged diastole, ie, "zero-flow pressure," is higher than coronary venous pressure. However, because of capacitive discharge as distending pressure falls, flow at the microcirculatory level exceeds inflow, and coronary outflow ceases later than inflow. If coronary arterial pressure continues to exceed venous pressure at the point of venous flow cessation, zero-flow pressure cannot be an artifact of capacitive discharge. METHODS AND RESULTS: Coronary inflow and outflow, arterial pressure, and right atrial pressure have been measured during long diastoles in closed-chest dogs chronically instrumented with volumetric flow probes on the great cardiac vein or coronary sinus as well as the circumflex artery. Although venous outflow continued for 1 to 4 seconds after arterial inflow ceased, coronary artery pressure at the point of venous flow cessation (Pfv = 0) always exceeded right atrial pressure (13 +/- 1.3 mm Hg [SEM] vs 6 +/- 0.7 mm Hg, P < .001). When vasomotor tone was augmented using vasopressin, the diastolic pressure-flow relation shifted to the right, with Pfv = 0 increasing to 21 +/- 2.4 mm Hg despite an unchanged right atrial pressure (6 +/- 0.5 mm Hg). CONCLUSIONS: Transcoronary pressure differences persist when venous outflow stops and are larger when vasomotor tone is augmented. Measurements of zero-flow pressure that exceed venous pressure cannot be considered an artifact of continuing capacitive discharge after the cessation of arterial inflow. Diastolic coronary back pressure exceeds right atrial pressure and is tone dependent.
BACKGROUND AND AIM OF THE STUDY: The study aim was to examine tissue expression of the adhesion molecules E-selectin and P-selectin on atrial, valvular and atrial myocardial blood vessel endothelium in patients with rheumatic mitral stenosis, and to investigate whether such expression was correlated with hemodynamics. METHODS: Thirteen patients (eight women, five men; mean age 51 +/- 10 years) with severe rheumatic mitral stenosis who underwent mitral valve replacement surgery were examined on preoperative day 1, using cardiac catheterization and echocardiography. Specimens from the mitral valve and left atrium of each patient were evaluated for CD 62E and CD 62P expression using indirect immunoperoxidase and immunofluorescence techniques RESULTS: A great majority of patients presented E and/or P selectin expression of variable intensity on atrial, valvular and atrial myocardial blood vessel endothelium. A more diffuse and stronger reaction for CD 62P was noted compared to that for CD 62E. The left ventricular end-diastolic diameter and left atrial diameter were positively correlated with endocardial CD 62P and CD 62E expression. Right atrial pressure was also strongly and positively correlated with endocardial expression of CD 62E (r = 0.80, p 0.03) and CD 62P (r = 0.8, p = 0.02). CONCLUSION: Marked tissue expression of CD 62E and CD 62P was identified on atrial, valvular and atrial myocardial blood vessel endothelium. Moreover, the degree of expression of adhesion molecules was significantly correlated with the left atrial and left ventricular chamber diameters, as well as right atrial pressure.
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BACKGROUND: The purpose of this study was to characterize the circuit of macroreentrant right atrial tachycardia (MacroAT) in patients after surgical repair of congenital heart disease (SR-CHD). METHODS AND RESULTS: Sixteen patients with atrial tachycardia (AT) after SR-CHD were studied (atrial septal defect in 6, tetralogy of Fallot in 4, and Fontan procedure in 6). Electroanatomic right atrial maps were obtained during 15 MacroATs in 13 patients, focal AT in 1 patient, and atrial pacing in 2 patients without stable AT. A large area of low bipolar voltage (</=0.5 mV) involved most of the free wall in all patients and contained 2 to 7 dense scars or lines of double potentials, forming 29 narrow channels (width </=2.7 cm) between scars in all but 1 patient, who had a single scar and only focal AT. All 15 MacroATs were propagated through narrow channels. Ablation within the channel eliminated all 15 MacroATs with 1 to 3 (median 1) radiofrequency applications. Ablation was performed in 9 other channels identified during MacroAT (5 patients) and in 5 channels identified during atrial pacing (2 patients). Conduction block was obtained across 28 of 29 channels. After ablation, reproducible sustained right AT was not induced in any patient. During follow-up (median 13.5 months), new MacroATs, atrial fibrillation, or palpitations occurred in 3 of 16 patients. CONCLUSIONS: MacroAT after SR-CHD requires a large area of low voltage containing >/=2 scars forming narrow channels. Ablation within the channels eliminates MacroAT.
The most important goal of this study is to enhance our understanding of the crucial functional relationships that determine the behavior of the systemic circulation and its underlying physiological regulatory mechanisms with minimal modeling. To the present day, much has been said about the indirect hydraulic effects of right atrial pressure (PRA) via cardiac output (CO) on arterial pressure (Pa) through the heart and pulmonary circulation or the direct regulatory effects of PRA on Pa through the cardiopulmonary baroreflex; however, very little attention has been given to the hydraulic influence that PRA exerts directly through the systemic circulation. The experimental data reported by Guyton et al. in 1957 demonstrated that steady-state PRA and the rate at which blood passes through the systemic circulation are locked in a functional relationship independent of any consequence of altered PRA on cardiac function. With this in mind, we emphasize the analytic algebraic analysis of the systemic circulation composed of arteries, veins, and its underlying physiological regulatory mechanisms of baroreflex and autoregulatory modulation of total peripheral resistance (TPR), where the behavior of the system can be analytically synthesized from an understanding of its minimal elements. As a result of this analysis, we present a novel mathematical method to determine short-term TPR fluctuations, which accounts for the entirety of observed Pa fluctuations, and propose a new cardiovascular system identification method to delineate the actual actions of the physiological mechanisms responsible for the dynamic couplings between CO, Pa, PRA, and TPR in an individual subject.
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Growing recognition of the contribution of right heart function to cardiac output in a variety of pathologic conditions lends a new outlook to cardiac assessment, especially when cardiac output is inadequate for physiologic needs. Signs and symptoms of right heart dysfunction made by physical assessment can be validated by radiologic techniques as well as a newly available bedside method of thermodilution determination of right ventricular ejection fraction and right ventricular end-diastolic and end-systolic volumes. Assessment of right ventricular function can aid clinical decision making when pressure readings obtained by usual hemodynamic monitoring techniques are altered by changes in intrathoracic pressure or ventricular compliance. This article reviews physical assessment of right heart function, signs and symptoms of right heart dysfunction, radiographic evaluations and their limitations and introduces the thermodilution evaluation of right ventricular performance. Clinical examples are presented to illustrate the utility of this new technique along with selected nursing diagnoses and outcome criteria.
Clinical estimates of right atrial pressure from the jugular venous pulse were accurate when right atrial pressure was normal, but systematically underestimated elevated right atrial pressures. Because the increased distance from the mid-right atrium to the sternal angle is not accounted for, apparently normal right atrial pressure estimates by this technique do not reliably exclude elevated right atrial pressure in patients with congestive heart failure.
The inferior vena cava diameter and its respiratory response are used to estimate right atrial pressures in spontaneously breathing patients but its value in patients receiving mechanical ventilation is unvalidated. Forty-nine patients undergoing mechanical ventilation were prospectively evaluated in the intensive or coronary care units with two-dimensional echocardiography of the inferior vena cava and simultaneous measurements of mean right atrial pressures by central venous or pulmonary artery catheter. Correlation between inferior vena cava diameter at expiration and mean right atrial pressure was only 0.58. The correlation between inspiratory change in inferior vena cava diameter and mean right atrial pressure was poor (r = 0.13). Despite these correlations, an inferior vena cava diameter of < or = 12 mm predicted a right atrial pressure of 10 mm Hg or less 100% of the time, but sensitivity was only 25%. An inferior vena cava diameter > 12 mm had no predictive value for right atrial pressure.
Identification of atrial capture during pacing from right atrial appendage is frequently difficult. Electrocardiograms of forty five patients implanted with AAI/DDD pacemakers (thirty unipolar, fifteen bipolar) were analysed to characterize the specific morphology of paced P waves. Compared to sinus P waves, atrial pacing resulted in atrial depolarization of lower amplitude (0.16 +/- 0.05 mv vs 0.11 +/- 0.032 mv, P less than 0.005) but increased duration (0.07 +/- 0.009 sec vs 0.08 +/- 0.017 sec, P less than 0.005). P wave morphology was similar in unipolar and bipolar pacing units. It was positive in lead I (80%), II (71.11%), III (80%) and aVF (75.55%). In lead aVL, paced P waves were usually diphasic with an initial negative deflection (35.55%). Precordial leads showed paced atrial depolarization of small amplitude and did not help in identification of atrial capture. In unipolar pacing P waves were best seen in lead III because of small pacing spike in this lead. Lead II was suitable for identification of paced P waves in bipolar pacing. Thus careful examination of standard ECG leads for paced P waves of low amplitude, prolonged duration and specific morphology can help in confirming atrial capture following pacing stimulus from right atrial appendage.
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