Right ventricular adaptation in the critical phase after acute intermediate-risk pulmonary embolism

2020 ◽  
pp. 204887262092525 ◽  
Author(s):  
Mads Dam Lyhne ◽  
Jacob Gammelgaard Schultz ◽  
Anders Kramer ◽  
Christian Schmidt Mortensen ◽  
Jens Erik Nielsen-Kudsk ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Arterial Pressure ◽  
Right Ventricular ◽  
Acute Pulmonary Embolism ◽  
Pulmonary Arterial Pressure ◽  
Intermediate Risk ◽  
Right Ventricular Afterload ◽  
Mean Pulmonary Arterial Pressure ◽  
Ventricular Afterload ◽  
Pulmonary Arterial

Background The haemodynamic response following acute, intermediate-risk pulmonary embolism is not well described. We aimed to describe the cardiovascular changes in the initial, critical phase 0–12 hours after acute pulmonary embolism in an in-vivo porcine model. Methods Pigs were randomly allocated to pulmonary embolism ( n = 6) or sham ( n = 6). Pulmonary embolism was administered as autologous blood clots (20 × 1 cm) until doubling of mean pulmonary arterial pressure or mean pulmonary arterial pressure was greater than 34 mmHg. Sham animals received saline. Cardiopulmonary changes were evaluated for 12 hours after intervention by biventricular pressure–volume loop recordings, invasive pressure measurements, arterial and central venous blood gas analyses. Results Mean pulmonary arterial pressure increased ( P < 0.0001) and stayed elevated for 12 hours in the pulmonary embolism group compared to sham. Pulmonary vascular resistance and right ventricular arterial elastance (right ventricular afterload) were increased in the first 11 and 6 hours, respectively, after pulmonary embolism ( P < 0.01 for both) compared to sham. Right ventricular ejection fraction was reduced ( P < 0.01) for 8 hours, whereas a near-significant reduction in right ventricular stroke volume was observed ( P = 0.06) for 4 hours in the pulmonary embolism group compared to sham. Right ventricular ventriculo–arterial coupling was reduced ( P < 0.05) for 6 hours following acute pulmonary embolism despite increased right ventricular mechanical work in the pulmonary embolism group ( P < 0.01) suggesting right ventricular failure. Conclusions In a porcine model of intermediate-risk pulmonary embolism, the increased right ventricular afterload caused initial right ventricular ventriculo–arterial uncoupling and dysfunction. After approximately 6 hours, the right ventricular afterload returned to pre-pulmonary embolism values and right ventricular function improved despite a sustained high pulmonary arterial pressure. These results suggest an initial critical and vulnerable phase of acute pulmonary embolism before haemodynamic adaptation.

Inhaled nitric oxide has pulmonary vasodilator efficacy both in the immediate and prolonged phase of acute pulmonary embolism

2020 ◽  
pp. 204887262091871 ◽  
Author(s):  
Anders Kramer ◽  
Christian Schmidt Mortensen ◽  
Jacob Gammelgaard Schultz ◽  
Mads Dam Lyhne ◽  
Asger Andersen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Embolism ◽  
Right Ventricular ◽  
Acute Pulmonary Embolism ◽  
Porcine Model ◽  
Inhaled Nitric Oxide ◽  
Intermediate Risk ◽  
Ventricular Afterload ◽  
Pulmonary Vasodilator ◽  
Acute Pe

Background Inhaled nitric oxide (iNO) effectively reduces right ventricular afterload when administered in the immediate phase of acute pulmonary embolism (PE) in preclinical animal models. In a porcine model of intermediate-risk PE, we aimed to investigate whether iNO has pulmonary vasodilator efficacy both in the immediate and prolonged phase of acute PE. Methods Anesthetized pigs ( n = 18) were randomized into three subgroups. An acute PE iNO-group ( n = 6) received iNO at 40 ppm at one, three, six, nine and 12 hours after onset of PE. Vehicle animals ( n = 6) received PE, but no active treatment. A third group of sham animals ( n = 6) received neither PE nor treatment. Animals were evaluated using intravascular pressures, respiratory parameters, biochemistry and intracardiac pressure-volume measurements. Results The administration of PE increased mean pulmonary artery pressure (mPAP) (vehicle vs sham; 33.3 vs 17.7 mmHg, p < 0.0001), pulmonary vascular resistance (vehicle vs sham; 847.5 vs 82.0 dynes, p < 0.0001) and right ventricular arterial elastance (vehicle vs sham; 1.2 vs 0.2 mmHg/ml, p < 0.0001). Significant mPAP reduction by iNO was preserved at 12 hours after the onset of acute PE (vehicle vs iNO; 0.5 vs –3.5 mmHg, p < 0.0001). However, this response was attenuated over time ( p = 0.0313). iNO did not affect the systemic circulation. Conclusions iNO is a safe and effective pulmonary vasodilator both in the immediate and prolonged phase of acute PE in an in-vivo porcine model of intermediate-risk PE.

Evaluation of Pulmonary Arterial Pressure in Acute Pulmonary Embolism

Angiology ◽  
1994 ◽  
Vol 45 (2) ◽  
pp. 149-154 ◽  
Author(s):  
Hiroyuki Shimizu ◽  
Junko Tanaka ◽  
Norikazu Yamada ◽  
Takahiro Ohnishi ◽  
Mashio Nakamura ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Arterial Pressure ◽  
Acute Pulmonary Embolism ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Terlipressin Increases Systemic and Lowers Pulmonary Arterial Pressure in Experimental Acute Pulmonary Embolism

2020 ◽  
Vol 48 (4) ◽  
pp. e308-e315 ◽  
Author(s):  
Jacob Schultz ◽  
Asger Andersen ◽  
Mads D. Lyhne ◽  
Daniel D. R. Arcanjo ◽  
Benedict Kjaergaard ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Arterial Pressure ◽  
Acute Pulmonary Embolism ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Oxygen Therapy Lowers Right Ventricular Afterload in Experimental Acute Pulmonary Embolism

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Mads Dam Lyhne ◽  
Jacob Valentin Hansen ◽  
Simone Juel Dragsbæk ◽  
Christian Schmidt Mortensen ◽  
Jens Erik Nielsen-Kudsk ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Right Ventricular ◽  
Oxygen Therapy ◽  
Acute Pulmonary Embolism ◽  
Right Ventricular Afterload ◽  
Ventricular Afterload

scholarly journals Pulmonary vasodilation in acute pulmonary embolism – a systematic review

2020 ◽  
Vol 10 (1) ◽  
pp. 204589401989977 ◽  
Author(s):  
Mads Dam Lyhne ◽  
Jeffrey Allen Kline ◽  
Jens Erik Nielsen-Kudsk ◽  
Asger Andersen
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Embolism ◽  
Right Ventricular ◽  
Acute Pulmonary Embolism ◽  
Mechanical Obstruction ◽  
Humoral Factors ◽  
Pulmonary Vasodilation ◽  
Right Ventricular Afterload ◽  
Pulmonary Vasoconstriction ◽  
Ventricular Afterload

Acute pulmonary embolism is the third most common cause of cardiovascular death. Pulmonary embolism increases right ventricular afterload, which causes right ventricular failure, circulatory collapse and death. Most treatments focus on removal of the mechanical obstruction caused by the embolism, but pulmonary vasoconstriction is a significant contributor to the increased right ventricular afterload and is often left untreated. Pulmonary thromboembolism causes mechanical obstruction of the pulmonary vasculature coupled with a complex interaction between humoral factors from the activated platelets, endothelial effects, reflexes and hypoxia to cause pulmonary vasoconstriction that worsens right ventricular afterload. Vasoconstrictors include serotonin, thromboxane, prostaglandins and endothelins, counterbalanced by vasodilators such as nitric oxide and prostacyclins. Exogenous administration of pulmonary vasodilators in acute pulmonary embolism seems attractive but all come with a risk of systemic vasodilation or worsening of pulmonary ventilation-perfusion mismatch. In animal models of acute pulmonary embolism, modulators of the nitric oxide-cyclic guanosine monophosphate-protein kinase G pathway, endothelin pathway and prostaglandin pathway have been investigated. But only a small number of clinical case reports and prospective clinical trials exist. The aim of this review is to give an overview of the causes of pulmonary embolism-induced pulmonary vasoconstriction and of experimental and human investigations of pulmonary vasodilation in acute pulmonary embolism.

A computed method for noninvasive MRI assessment of pulmonary arterial hypertension

2004 ◽  
Vol 96 (2) ◽  
pp. 463-468 ◽  
Author(s):  
Eric Laffon ◽  
Christophe Vallet ◽  
Virginie Bernard ◽  
Michel Montaudon ◽  
Dominique Ducassou ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Cross Sectional Area ◽  
Physical Parameters ◽  
Sectional Area ◽  
Biophysical Parameters ◽  
Cross Sectional ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
The Mean

The present method enables the noninvasive assessment of mean pulmonary arterial pressure from magnetic resonance phase mapping by computing both physical and biophysical parameters. The physical parameters include the mean blood flow velocity over the cross-sectional area of the main pulmonary artery (MPA) at the systolic peak and the maximal systolic MPA cross-sectional area value, whereas the biophysical parameters are related to each patient, such as height, weight, and heart rate. These parameters have been measured in a series of 31 patients undergoing right-side heart catheterization, and the computed mean pulmonary arterial pressure value (PpaComp) has been compared with the mean pressure value obtained from catheterization (PpaCat) in each patient. A significant correlation was found that did not differ from the identity line PpaComp = PpaCat ( r = 0.92). The mean and maximal absolute differences between PpaComp and PpaCat were 5.4 and 11.9 mmHg, respectively. The method was also applied to compute the MPA systolic and diastolic pressures in the same patient series. We conclude that this computed method, which combines physical (whoever the patient) and biophysical parameters (related to each patient), improves the accuracy of MRI to noninvasively estimate pulmonary arterial pressures.

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