دورية أكاديمية

Using a human cardiovascular-respiratory model to characterize cardiac tamponade and pulsus paradoxus.

التفاصيل البيبلوغرافية
العنوان: Using a human cardiovascular-respiratory model to characterize cardiac tamponade and pulsus paradoxus.
المؤلفون: Ramachandran D; Department of Electrical and Computer Engineering, Rice University, Houston, Texas 77005, USA. dpr2@rice.edu, Luo C, Ma TS, Clark JW Jr
المصدر: Theoretical biology & medical modelling [Theor Biol Med Model] 2009 Aug 06; Vol. 6, pp. 15. Date of Electronic Publication: 2009 Aug 06.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: BioMed Central Country of Publication: England NLM ID: 101224383 Publication Model: Electronic Cited Medium: Internet ISSN: 1742-4682 (Electronic) Linking ISSN: 17424682 NLM ISO Abbreviation: Theor Biol Med Model Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : BioMed Central, 2004-2021
مواضيع طبية MeSH: Models, Cardiovascular*, Arrhythmias, Cardiac/*complications , Arrhythmias, Cardiac/*physiopathology , Cardiac Tamponade/*complications , Cardiac Tamponade/*physiopathology , Respiratory System/*physiopathology, Blood Pressure ; Blood Volume ; Gases/metabolism ; Heart/physiopathology ; Heart Ventricles/physiopathology ; Humans ; Pericardial Effusion/complications ; Pericardial Effusion/physiopathology ; Respiration ; Stroke Volume/physiology ; Time Factors
مستخلص: Background: Cardiac tamponade is a condition whereby fluid accumulation in the pericardial sac surrounding the heart causes elevation and equilibration of pericardial and cardiac chamber pressures, reduced cardiac output, changes in hemodynamics, partial chamber collapse, pulsus paradoxus, and arterio-venous acid-base disparity. Our large-scale model of the human cardiovascular-respiratory system (H-CRS) is employed to study mechanisms underlying cardiac tamponade and pulsus paradoxus. The model integrates hemodynamics, whole-body gas exchange, and autonomic nervous system control to simulate pressure, volume, and blood flow.
Methods: We integrate a new pericardial model into our previously developed H-CRS model based on a fit to patient pressure data. Virtual experiments are designed to simulate pericardial effusion and study mechanisms of pulsus paradoxus, focusing particularly on the role of the interventricular septum. Model differential equations programmed in C are solved using a 5th-order Runge-Kutta numerical integration scheme. MATLAB is employed for waveform analysis.
Results: The H-CRS model simulates hemodynamic and respiratory changes associated with tamponade clinically. Our model predicts effects of effusion-generated pericardial constraint on chamber and septal mechanics, such as altered right atrial filling, delayed leftward septal motion, and prolonged left ventricular pre-ejection period, causing atrioventricular interaction and ventricular desynchronization. We demonstrate pericardial constraint to markedly accentuate normal ventricular interactions associated with respiratory effort, which we show to be the distinct mechanisms of pulsus paradoxus, namely, series and parallel ventricular interaction. Series ventricular interaction represents respiratory variation in right ventricular stroke volume carried over to the left ventricle via the pulmonary vasculature, whereas parallel interaction (via the septum and pericardium) is a result of competition for fixed filling space. We find that simulating active septal contraction is important in modeling ventricular interaction. The model predicts increased arterio-venous CO2 due to hypoperfusion, and we explore implications of respiratory pattern in tamponade.
Conclusion: Our modeling study of cardiac tamponade dissects the roles played by septal motion, atrioventricular and right-left ventricular interactions, pulmonary blood pooling, and the depth of respiration. The study fully describes the physiological basis of pulsus paradoxus. Our detailed analysis provides biophysically-based insights helpful for future experimental and clinical study of cardiac tamponade and related pericardial diseases.
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معلومات مُعتمدة: T15 LM007093 United States LM NLM NIH HHS; 5T15LM07093 United States LM NLM NIH HHS
المشرفين على المادة: 0 (Gases)
تواريخ الأحداث: Date Created: 20090807 Date Completed: 20100113 Latest Revision: 20211020
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC2736922
DOI: 10.1186/1742-4682-6-15
PMID: 19656411
قاعدة البيانات: MEDLINE
الوصف
تدمد:1742-4682
DOI:10.1186/1742-4682-6-15