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

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.

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.

scholarly journals Case Report: Successful revascularization in massive pulmonary embolism with a large protruding thrombus and dilated cardiomyopathy

F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 13
Author(s):  
Hendri Susilo ◽  
Rerdin Julario ◽  
Citrawati Dyah Kencono Wungu
Keyword(s):  
Pulmonary Embolism ◽  
High Risk ◽  
Right Ventricular ◽  
Dilated Cardiomyopathy ◽  
Acute Pulmonary Embolism ◽  
Systolic Function ◽  
Vena Cava ◽  
Massive Pulmonary Embolism ◽  
Left Ventricular ◽  
Ventricular Afterload

Pulmonary embolism is a potentially life-threatening condition. Despite advances in diagnostics, lack of consensus and delays in determining the diagnosis of pulmonary embolism are still important problems. We report the diagnosis and management of a 37-year-old man suffering from massive pulmonary embolism, a large protruding thrombus, and dilated cardiomyopathy. Echocardiography showed dilatation of all cardiac chambers, a large protruding thrombus in the right atrium to the inferior vena cava, impaired left and right ventricular systolic function, and global hypokinetic of the left ventricle with eccentric left ventricular hypertrophy. A thoracic computerized tomography scan showed pulmonary embolism with infarction. The patient’s blood pressure was 60/40 mmHg and heart rate was 110 bpm. The patient was diagnosed with high-risk acute pulmonary embolism. We gave him hemodynamic support and reperfusion therapy with a loading dose of 250,000 units of Streptokinase followed by 100,000 units/hour for 24 hours. After revascularization, the patient's hemodynamic condition improved. The diagnosis of acute pulmonary embolism is based on clinical symptoms, hemodynamic changes, or radiological examination. Unstable hemodynamic underlies high-risk stratification. Hypotension or shock results from obstruction of the pulmonary artery which causes increased right ventricular afterload and acute right ventricular dysfunction. Reperfusion with thrombolysis therapy could provide good outcomes in this patient. Prolonged anticoagulation should be given to prevent the recurrence of venous thromboembolism.

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.

scholarly journals Case Report: Successful revascularization in massive pulmonary embolism with a large protruding thrombus and dilated cardiomyopathy

F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 13
Author(s):  
Hendri Susilo ◽  
Rerdin Julario ◽  
Citrawati Dyah Kencono Wungu
Keyword(s):  
Pulmonary Embolism ◽  
High Risk ◽  
Right Ventricular ◽  
Dilated Cardiomyopathy ◽  
Acute Pulmonary Embolism ◽  
Systolic Function ◽  
Vena Cava ◽  
Massive Pulmonary Embolism ◽  
Left Ventricular ◽  
Ventricular Afterload

Pulmonary embolism is a potentially life-threatening condition. Despite advances in diagnostics, lack of consensus and delays in determining the diagnosis of pulmonary embolism are still important problems. We report the diagnosis and management of a 37-year-old man suffering from massive pulmonary embolism, a large protruding thrombus, and dilated cardiomyopathy. Echocardiography showed dilatation of all cardiac chambers, a large protruding thrombus in the right atrium to the inferior vena cava, impaired left and right ventricular systolic function, and global hypokinetic of the left ventricle with eccentric left ventricular hypertrophy. A thoracic computerized tomography scan showed pulmonary embolism with infarction. The patient’s blood pressure was 60/40 mmHg and heart rate was 110 bpm. The patient was diagnosed with high-risk acute pulmonary embolism. We gave him hemodynamic support and reperfusion therapy with a loading dose of 250,000 units of Streptokinase followed by 100,000 units/hour for 24 hours. After revascularization, the patient's hemodynamic condition improved. The diagnosis of acute pulmonary embolism is based on clinical symptoms, hemodynamic changes, or radiological examination. Unstable hemodynamic underlies high-risk stratification. Hypotension or shock results from obstruction of the pulmonary artery which causes increased right ventricular afterload and acute right ventricular dysfunction. Reperfusion with thrombolysis therapy could provide good outcomes in this patient. Prolonged anticoagulation should be given to prevent the recurrence of venous thromboembolism.

scholarly journals Changes in the Pulmonary Artery Wave Reflection in Dogs with Experimentally-Induced Acute Pulmonary Embolism and the Effect of Vasodilator

Animals ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1977
Author(s):  
Tomohiko Yoshida ◽  
Ahmed S. Mandour ◽  
Katsuhiro Matsuura ◽  
Kazumi Shimada ◽  
Hussein M. El-Husseiny ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Right Ventricular ◽  
Ventricular Function ◽  
Right Ventricular Function ◽  
Acute Pulmonary Embolism ◽  
Evaluation Method ◽  
Function Parameter ◽  
Vasodilator Therapy ◽  
Ventricular Afterload ◽  
The Right

Pulmonary hypertension (PH) is a complex syndrome that has been frequently diagnosed in dogs and humans and can be detected by Doppler echocardiography and invasive catheterization. Recently, PAWR attracts much attention as a noninvasive approach for the early detection of PH. The present study aims to investigate the PAWR changes in acute pulmonary embolism (APE) and highlight the response of PAWR variables to vasodilator therapy in dogs. For this purpose, anesthesia and catheterization were performed in 6 Beagle dogs. After that, APE was experimentally conducted by Dextran microsphere administration, followed by vasodilator (Nitroprusside; 1μg/kg/min/ IV) administration. The hemodynamics, echocardiography, PVR and PAWR variables were evaluated at the baseline, after APE and after administration of nitroprusside. The result showed a significant increase in PVR, PAP, tricuspid regurgitation (TR) as well as PAWR variables following APE induction compared with the baseline (p < 0.05). Vasodilation caused by administration of nitroprusside reduced the mean atrial pressure, PVR and PAWR parameters. There were a significant correlation and linear regression between PAWR indices and PVR as well as right ventricular function parameters. In conclusion, PAWR is not only correlated with PVR but also the right ventricular function parameter, which indicates that PAWR may be useful as a new evaluation method in PH, considering that PAWR can assess both right ventricular afterload and right ventricular function.

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