Prediction of pulmonary arterial pressure in adults by pulsed doppler echocardiography

doi:10.1016/0002-9149(86)90911-2

The American Journal of Cardiology

Volume 57, Issue 4, 1 February 1986, Pages 316-321

https://doi.org/10.1016/0002-9149(86)90911-2 Get rights and content

Abstract

Doppler echocardlography was used to estimate pulmonary artery (PA) pressure in 45 AN patients with various kinds of heart disease and the patterns were compared with those of 32 normal control subjects. Doppler signals obtained in the right ventricular (RV) outflow tract just proximal to the pulmonary valve and electrocardiogram were recorded simultaneously. Doppler velocity time Intervals were measured as follows: RV preejection period, acceleration time from the onset of the RV ejection flow velocity to the peak, and RV ejection time. Thirty patients had PA hypertension and 16 patients had a low cardiac index. The best correlation with PA pressure was achieved by the RV preejection perlod/acceleration time index (r = 0.89 vs mean PA hypertension were 93 %p and 97 %r respectively. Acceleration time correlated best with the logarithm of PA mean pressure (r = −0.88). Patients were separated into 2 groups according to cardiac index. In those patterns with a cardiac index of <2.5 liters/min/m², both RV preejection period/acceleration time and acceleration time were significantly correlated with PA mean pressure (r = 0.87) and log (PA mean pressure) (r = −0.87), respectively. However, the slope of the regression line for acceleration time and log (PA mean pressure) was significantly steeper than that for patients with a cardiac index of ≥ liters/min/m² (p <0.05), whereas the relation between RV preejection period/acceleration time and PA mean pressure In the 2 groups could not be differentiated statistically from each other. Other Intervals and ratios were less quantitative because of late systolic turbulent flow and individual variability. Thus, RV preejection period/acceleration time is a new, highly quantitative and convenient predictor of PA pressure even in the presence of a low cardiac output state.

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Pulmonary embolism (PE) and pulmonary hypertension (PH) are potentially fatal disease states. Early diagnosis and goal-directed management improve outcomes and survival. Both conditions share several echocardiographic findings of right ventricular dysfunction. This can inadvertently lead to incorrect diagnosis, inappropriate and potentially harmful management, and delay in time-sensitive therapies. Fortunately, bedside echocardiography imparts a few critical distinctions.
This narrative review describes eight physiologically interdependent echocardiographic parameters that help distinguish acute PE and chronic PH. The manuscript details each finding along with associated pathophysiology and summarization of the literature evaluating diagnostic utility. This guide then provides pearls and pitfalls with high-quality media for the bedside evaluation.
The echocardiographic parameters suggesting acute or chronic right ventricular dysfunction (best used in combination) are: 1. Right heart thrombus (acute PE) 2. Right ventricular free wall thickness (acute ≤ 5 mm, chronic > 5 mm) 3. Tricuspid regurgitation pressure gradient (acute ≤ 46 mmHg, chronic > 46 mmHg, corresponding to tricuspid regurgitation maximal velocity ≤ 3.4 m/sec and > 3.4 m/sec, respectively) 4. Pulmonary artery acceleration time (acute ≤ 60-80 msec, chronic < 105 msec) 5. 60/60 sign (acute) 6. Pulmonary artery early-systolic notching (proximally-located, higher-risk PE) 7. McConnell’s sign (acute) 8. Right atrial enlargement (equal to left atrial size suggests acute, greater than left atrial size suggests chronic).
Emergency physicians must appreciate the echocardiographic findings and associated pathophysiology that help distinguish acute and chronic right ventricular dysfunction. In the proper clinical context, these findings can point towards PE or PH, thereby leading to earlier goal-directed management.
The soluble guanylate cyclase stimulator, 1-nitro-2-phenylethane, reverses monocrotaline-induced pulmonary arterial hypertension in rats
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We examined the effects of treatment with 1-nitro-2-phenylethane (NP), a novel soluble guanylate cyclase stimulator, on monocrotaline (MCT)-induced PAH in rats.
At day 0, male adult rats were injected with a single subcutaneous (s.c.) dose of monocrotaline (60 mg/kg). Control (CNT) rats received an equal volume of monocrotaline's vehicle only (s.c.). Four weeks later, MCT-treated rats were treated orally for 14 days with NP (50 mg/kg/day) (MCT-NP group) or its vehicle (Tween 2%) (MCT-V group). At the end of the treatment period and before invasive hemodynamic study, rats of all experimental groups were examined by echocardiography.
With respect to CNT rats, MCT-V rats showed significant; (1) increases in pulmonary artery (PA) diameter, RV free wall thickness and end-diastolic RV area, and increase of Fulton index; (2) decreases in maximum pulmonary flow velocity, PA acceleration time (PAAT), PAAT/time of ejection ratio, and velocity-time integral; (3) increases in estimated mean pulmonary arterial pressure; (4) reduction of maximal relaxation to acetylcholine in aortic rings, and (5) increases in wall thickness of pulmonary arterioles. All these measured parameters were significantly reduced or even abolished by oral treatment with NP.
NP reversed endothelial dysfunction and pulmonary vascular remodeling, which in turn reduced ventricular hypertrophy. NP reduced pulmonary artery stiffness, normalized the pulmonary artery diameter and alleviated RV enlargement. Thus, NP may represent a new therapeutic or a complementary approach to treatment of PAH.
What are the echocardiographic findings of acute right ventricular strain that suggest pulmonary embolism?
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Citation Excerpt :
However, when pulmonary hypertension is present, the flow will demonstrate a transient decrease in velocity during the pulmonary arterial systolic flow cycle, resulting in the appearance of biphasic flow (Fig. 9b). This is referred to as pulmonary artery mid-systolic notching [88–93]. This finding has been hypothesized to be caused by impedance of flow against elevated PAP [92,94,95], in that the reflected pressure waves return prematurely due to their faster propagation in the non-compliant pulmonary vessels [96].
Pulmonary embolism (PE) is a potentially fatal disease encountered in the hospital setting. Prompt diagnosis and management can improve outcomes and survival. Unfortunately, a PE may be difficult to diagnose in a timely manner. Point-of-care ultrasound (POCUS) can assist in the evaluation for suspected PE by assessing for acute right ventricular strain. Physicians should thus be aware of these echocardiographic findings.
This manuscript will review ten echocardiographic findings of right ventricular strain that may suggest a diagnosis of PE. It will provide a description of each finding along with the associated pathophysiology. It will also summarize the literature for the diagnostic utility of echocardiography for this indication, while providing reference parameters where applicable. Along with labeled images and video clips, the review will then illustrate how to evaluate for each of the ten findings, while offering pearls and pitfalls in this bedside evaluation.
The ten echocardiographic findings of right ventricular strain are: increased right ventricle: left ventricle size ratio, abnormal septal motion, McConnell’s sign, tricuspid regurgitation, elevated pulmonary artery systolic pressure, decreased tricuspid annular plane systolic excursion, decreased S’, pulmonary artery mid-systolic notching, 60/60 sign, and speckle tracking demonstrating decreased right ventricular free wall strain.
Physicians must recognize and understand the echocardiographic findings and associated pathophysiology of right ventricular strain. In the proper clinical context, these findings can point toward a diagnosis of PE and thereby lead to earlier initiation of directed management.
Imaging of the Heart and the Pulmonary Circulation in Pulmonary Hypertension
2021, Encyclopedia of Respiratory Medicine, Second Edition
Pulmonary Hypertension (pH) is currently defined by mean pulmonary artery pressure (mPAP) ≥ 25 mmHg at right heart catheterization. Thus the definite hemodynamic diagnosis of PH requires direct measurement of the pulmonary artery pressure. As right heart catheterization is an invasive test with a small but definite risk of morbidity and mortality, diagnostic algorithms have been devised that combines clinical history and examination, cardio-respiratory assessment by non-imaging and imaging techniques in patients suspected of having PH. The aim of these initial investigations is to establish a tentative diagnosis of PH. These investigations also help to identify the underlying etiology. Subsequently, the diagnosis of PH must be confirmed by right heart catheterization. The initial tests will provide information regarding disease severity especially altered pulmonary vascular and cardiac function and subsequently will be used to monitor disease progression and response to treatment. Advancing imaging techniques may also help us to understand the cellular and molecular mechanisms responsible for the pathophysiology of PH in the pulmonary circulation and the right ventricle (RV). Although a disease of the pulmonary circulation and the RV, there is now evidence demonstrating left ventricular (LV) abnormalities in PH. Further to this, the atrial chambers offer valuable information when measuring cardiac function as well as in identifying the etiology of PH. In this article we will discuss the use of echocardiography, plain chest radiography, computed tomography, ventilation-perfusion scanning, cardiac magnetic resonance imaging and positron emission tomography in PH.
Pulmonary Hypertension and Pulmonary Artery Acceleration Time: A Systematic Review and Meta-Analysis
2018, Journal of the American Society of Echocardiography
Citation Excerpt :
The flowchart of the screening process is presented in Figure 2. Eventually, 21 articles published between 1983 and 2016, representing a total of 1,280 patients, were included in our systematic review.4,13,16-33 The main characteristics of the trials included in the systematic review and retained for meta-analysis are summarized in Table 1 and Supplemental Table 1 (available at www.onlinejase.com).
Measuring mean pulmonary artery pressure by right-heart catheterization is the gold standard for pulmonary hypertension (PH) diagnosis. However, its invasiveness and complication leads to its limited use. The aim of this study was to determine whether echocardiography-derived pulmonary artery acceleration time (PAAT) possesses adequate diagnostic performance for PH, using right-heart catheterization as a reference standard.
MEDLINE, Embase, PubMed, and the Cochrane Central Register of Controlled Trials were searched through July 2016 for studies evaluating PAAT for the diagnosis of PH. Methodologic quality was assessed using the Quality Assessment of Diagnostic Accuracy Studies tool. For each study, the sensitivity, specificity, and diagnostic odds ratio, along with 95% CIs, were calculated to determine the diagnostic accuracy of PAAT. Meta-regression was conducted to evaluate the impact of potential confounding factors.
Of 430 articles, 21 studies (1,280 patients) were identified, including three studies that used transesophageal echocardiography and 18 studies that used transthoracic echocardiography. The pooled sensitivity across studies was 0.84 (95% CI, 0.75–0.90), the pooled specificity was 0.84 (95% CI, 0.78–0.89), and the pooled diagnostic odds ratio was 28 (95% CI, 16–49). The arrhythmia ratio in the population did not affect the specificity of PAAT's diagnostic performance and increased the sensitivity of PH detection.
The results of this study suggest that PAAT is useful for PH detection.
Advanced imaging tools rather than hemodynamics should be the primary approach for diagnosing, following, and managing pulmonary arterial hypertension
2015, Canadian Journal of Cardiology
Pulmonary hypertension (PH) is currently defined based on invasive measurements: a resting pulmonary artery pressure ≥ 25 mm Hg. For pulmonary arterial hypertension, a pulmonary arterial wedge pressure ≤ 15 mm Hg and pulmonary vascular resistance > 3 Wood units are also required. Thus, right heart catheterization is inevitable at present. However, the diagnosis, follow-up, and management of PH by noninvasive techniques is progressing. Significant advances have been achieved in the imaging of pulmonary vascular disease and the right ventricle. We review the current sensitivities and specificities of noninvasive imaging of PH and discuss its role and future potential to replace hemodynamics as the primary approach to screening, diagnosing, and following/managing PH.
L’hypertension pulmonaire (HP) est actuellement définie selon des méthodes effractives de mesure : une pression artérielle pulmonaire ≥ 25 mm Hg au repos. Pour définir l’hypertension artérielle pulmonaire, une pression artérielle pulmonaire d’occlusion ≤ 15 mm Hg et une résistance vasculaire pulmonaire > 3 unités Wood sont également requises. Par conséquent, le cathétérisme cardiaque droit est inévitable pour le moment. Malgré cela, le diagnostic, le suivi et la prise en charge de l’HP par des techniques non effractives évoluent. L’imagerie des maladies vasculaires pulmonaires et du ventricule droit a connu d’importants progrès. Nous passons en revue la sensibilité et la spécificité actuelles de l’imagerie non effractive de l’HP, et discutons de ses rôles et de son potentiel futur de remplacement de l’hémodynamique comme principale approche en matière de dépistage, de diagnostic, de prise en charge/suivi de l’HP.

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Prediction of pulmonary arterial pressure in adults by pulsed doppler echocardiography

Abstract

Am Heart J

Am J Cardiol

Am J Cordial

Echocardiographic evaluation of pulmonary hypertension

Circulation

Echocardiographic patterns of pulmonic valve motion with pulmonary hypertension

Circulation

Assessment of pulmonary valve echogram in normal subjects and in pulmonary arterial hypertension

Br Heart J

The echocardiographic assessment of pulmonary artery pressure and pulmonary vascular resistance

Circulation