Pulmonary vascular resistance versus pulmonary artery pressure for predicting right ventricular remodeling and functional tricuspid regurgitation

2018 ◽  
Vol 35 (11) ◽  
pp. 1736-1745 ◽  
Author(s):  
Francisco Gual-Capllonch ◽  
Albert Teis ◽  
Elena Ferrer ◽  
Julio Núñez ◽  
Nuria Vallejo ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricular ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Tricuspid Regurgitation ◽  
Ventricular Remodeling ◽  
Artery Pressure ◽  
Functional Tricuspid Regurgitation ◽  
Right Ventricular Remodeling

scholarly journals Comparison of cardiovascular and psychological profile of young military men after COVID-19 with and without pneumonia

2021 ◽  
Vol 26 (2) ◽  
pp. 4321
Author(s):  
E. I. Yaroslavskaya ◽  
D. V. Krinochkin ◽  
I. R. Krinochkina ◽  
N. E. Shirokov ◽  
E. P. Gultyaeva ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Tricuspid Regurgitation ◽  
Psychological Profile ◽  
Artery Pressure ◽  
Mean Pulmonary Artery Pressure ◽  
Experimental Group ◽  
Peak Gradient

Aim. To compare the cardiovascular and psychological profile of young military population after coronavirus disease 2019 (COVID-19) with/without pneumonia.Material and methods. We examined 26 military men under 30 years of age (22,3±3,7 years/21,0 [19,8; 24,3] years) with documented COVID 19 (3 months±2 weeks after two virus-negative polymerase chain reaction tests). The participants were divided into 2 groups: experimental group (n=16) — those with COVID-19 pneumonia; comparison group (n=10) — those without pneumonia. All subjects underwent a complex of clinical and diagnostic tests.Results. Military men with COVID-19 pneumonia were significantly older (23,0 [20,5; 28,5] years vs 19,5 [19,0; 20,0] years, p=0,001). They had a prolonged PQ interval (154,5 [140,0; 163,5] ms vs 137,0 [134,0; 144,0] ms; p=0,014). According to echocardiography, the following parameters were significantly larger in experimental group: anteroposterior right ventricular dimension (26,0 [24,5; 27,5] mm vs 23,5 [22,0; 25,0] mm, p=0,012), right atrium length (48,0 [46,0; 51,5] mm and 45,5 [44,0; 47,0] mm, p=0,047), tricuspid regurgitation peak gradient (18,0 [15,5; 22,0] mm vs 14,0 [12,0; 20,0] mm, p=0,047), pulmonary artery systolic pressure (PASP) (30,3 [27,6; 34,0] mm Hg vs 23,0 [20,5; 30,5] mm Hg, p=0,038), mean pulmonary artery pressure (20,3 [18,9; 22,7] mm Hg vs 16,8 [14,5; 20,6] mm Hg, p=0,038). The estimated pulmonary vascular resistance was significantly higher in the study group (1,50 [1,2; 1,8] Wood units vs 1,17 [1,1; 1,2] Wood units, p<0,001). The groups did not differ significantly in terms of symptoms of stress (perceived stress scale score of 10) and anxiety and depression disorders (GAD7 and PHQ9 questionnaires), quality of life (SF-36 survey).Conclusion. In young military personnel, COVID-19 pneumonia in the long term after the disease is associated with longer PQ interval, older age and larger right heart sizes on echocardiography, as well as with a higher tricuspid regurgitation peak gradient, PASP, mean pulmonary artery pressure, and pulmonary vascular resistance. In this category of population, no association was found between the severity of COVID-19 and psychological status parameters.

The peculiarities of pulmonary macro- and microhemodynamics changes after treatment with agonists and blockers of cholinoceptors

2021 ◽  
Vol 20 (4) ◽  
pp. 35-44
Author(s):  
Vadim I. Evlakhov ◽  
Ilya Z. Poyassov ◽  
Tatiana P. Berezina
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Venous Return ◽  
Filtration Coefficient ◽  
Artery Pressure ◽  
Capillary Filtration ◽  
Capillary Filtration Coefficient ◽  
Pulmonary Microcirculation

Background. The pulmonary arterial and venous vessels are innervated by parasympathetic cholinergic nerves. However, the studies, performed on the isolated rings of pulmonary vessels, can not give answer to the question about the role of cholinergic mechanisms in the changes of pulmonary circulation in full measure. Aim. The comparative analysis of the changes of the pulmonary macro- and microhemodynamics after acetylcholine, atropine, pentamine and nitroglycerine treatment. Materials and methods. The study was carried out on the anesthetized rabbits in the condition of intact circulation with the measurement of the pulmonary artery pressure and flow, venae cavae flows, cardiac output, and also on isolated perfused lungs in situ with stabilized pulmonary flow with measurement of the perfused pulmonary artery pressure, capillary hydrostatic pressure, capillary filtration coefficient and calculation of the pulmonary vascular resistance, pre- and postcapillary resistances. Results. In the conditions of intact circulation after acetylcholine, pentamine and nitroglycerine treatment the pulmonary artery pressure and flow decreased, the pulmonary vascular resistance did not change as a result of decreasing of pulmonary artery flow and left atrial pressure due to diminution of venous return and venae cavaе flows. On perfused isolated lungs acetylcholine caused the increasing of pulmonary artery pressure, capillary hydrostatic pressure, pulmonary vascular resistance, pre- and postcapillary resistance and capillary filtration coefficient. After M-blocker atropine treatment the indicated above parameters of pulmonary microcirculation increased, on the contrary, after N-blocker pentamine treatment they decreased. Nitroglycerine infusion caused less decreasing of the parameters of pulmonary microcirculation in comparison with effects of pentamine, but capillary filtration coefficient decreased to a greater extent. These data indicate that nitroglycerine decreases endothelial permeability of pulmonary microvessels. Conclusion. After activation or blockade of cholinergic mechanisms in the condition of intact circulation the calculated parameter of pulmonary vascular resistance is depended from the ratio of the pulmonary artery pressure and flow and left atrial pressure, which are determined by the venous return. The different character of the changes of pulmonary microcirculatory parameters after M-blocker atropine and N-blocker pentamine treatment is evidence of reciprocal relations of M- and N-cholinoceptors in the nervous regulation of the pulmonary microcirculatory bed.

Effects of Acutely Induced Changes in Arterial pH on Pulmonary Vascular Resistance during Normoxia and Hypoxia in Awake Dogs

1972 ◽  
Vol 42 (3) ◽  
pp. 277-287 ◽  
Author(s):  
O. G. Thilenius ◽  
Carol Derenzo
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Main Pulmonary Artery ◽  
Compensatory Mechanisms ◽  
Artery Pressure ◽  
Arterial Ph ◽  
Small Rise

1. Awake dogs with chronically implanted catheters (pulmonary artery, left atrium, aorta) and electromagnetic flow probe (main pulmonary artery) underwent five types of experiments in succession: (1) slow infusion of 0·4 m-hydrochloric acid; (2) rapid infusion of 1·0 m-sodium bicarbonate; (3) exposure to 30 min of hypoxia (10% O2); (4) exposure to hypoxia after arterial pH had been lowered to 7·30; (5) exposure to hypoxia after pH had been increased to 7·55. Intravascular pressures, pulmonary vascular resistance, cardiac output, arterial gas tension and pH were studied. 2. Acute acidosis (pH 7·21) resulted in a small rise in pulmonary artery pressure, cardiac output and pulmonary vascular resistance, associated with a decrease in Pa,co2. Acute alkalosis (pH 7·61) was accompanied by a small rise in pulmonary artery pressure, marked increase in cardiac output, a fall in pulmonary vascular resistance and mild elevation in Pa,co2. During acidosis hypoxia resulted in a more pronounced rise in pulmonary vascular resistance than during alkalosis (P < 0·01). 3. The study provides evidence that in the intact, awake dog with its compensatory mechanisms acute alkalosis decreases pulmonary vascular resistance by decreasing vascular tone and/or recruitment of pulmonary vascular channels; it diminishes the vasoconstrictive response to hypoxia; conversely, mild acidosis increases the pulmonary vascular resistance slightly and enhances vasoconstriction during hypoxia to a small extent.

scholarly journals Regional Right Ventricular Abnormalities Implicate Distinct Pathophysiological Conditions in Patients With Chronic Thromboembolic Pulmonary Hypertension

2020 ◽  
Vol 9 (21) ◽  
Author(s):  
Hidenori Moriyama ◽  
Takashi Kawakami ◽  
Masaharu Kataoka ◽  
Takahiro Hiraide ◽  
Mai Kimura ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Area Change ◽  
Thromboembolic Pulmonary Hypertension ◽  
Rv Function

Background Right ventricular (RV) dysfunction is a prognostic factor for cardiovascular disease. However, its mechanism and pathophysiology remain unknown. We investigated RV function using RV‐specific 3‐dimensional (3D)‐speckle‐tracking echocardiography (STE) in patients with chronic thromboembolic pulmonary hypertension. We also assessed regional wall motion abnormalities in the RV and chronological changes during balloon pulmonary angioplasty (BPA). Methods and Results Twenty‐nine patients with chronic thromboembolic pulmonary hypertension who underwent BPA were enrolled and underwent right heart catheterization and echocardiography before, immediately after, and 6 months after BPA. Echocardiographic assessment of RV function included both 2‐dimensional‐STE and RV‐specific 3D‐STE. Before BPA, global area change ratio measured by 3D‐STE was significantly associated with invasively measured mean pulmonary artery pressure and pulmonary vascular resistance ( r =0.671 and r =0.700, respectively). Dividing the RV into the inlet, apex, and outlet, inlet area change ratio showed strong correlation with mean pulmonary artery pressure and pulmonary vascular resistance before BPA ( r =0.573 and r =0.666, respectively). Only outlet area change ratio was significantly correlated with troponin T values at 6 months after BPA ( r =0.470), and its improvement after BPA was delayed compared with the inlet and apex regions. Patients with poor outlet area change ratio were associated with a delay in RV reverse remodeling after treatment. Conclusions RV‐specific 3D‐STE analysis revealed that 3D RV parameters were novel useful indicators for assessing RV function and hemodynamics in pulmonary hypertension and that each regional RV portion presents a unique response to hemodynamic changes during treatment, implicating that evaluation of RV regional functions might lead to a new guide for treatment strategies.

Pulmonary vasodilation by acetazolamide during hypoxia is unrelated to carbonic anhydrase inhibition

2007 ◽  
Vol 292 (1) ◽  
pp. L178-L184 ◽  
Author(s):  
Claudia Höhne ◽  
Philipp A. Pickerodt ◽  
Roland C. Francis ◽  
Willehad Boemke ◽  
Erik R. Swenson
Keyword(s):  
Carbonic Anhydrase ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Low Dose ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Artery Pressure ◽  
Pulmonary Vasoconstriction ◽  
Mean Pulmonary Artery Pressure

Acute hypoxic pulmonary vasoconstriction can be inhibited by high doses of the carbonic anhydrase inhibitor acetazolamide. This study aimed to determine whether acetazolamide is effective at dosing relevant to human use at high altitude and to investigate whether its efficacy against hypoxic pulmonary vasoconstriction is dependent on carbonic anhydrase inhibition by testing other potent heterocyclic sulfonamide carbonic anhydrase inhibitors. Six conscious dogs were studied in five protocols: 1) controls, 2) low-dose intravenous acetazolamide (2 mg·kg−1·h−1), 3) oral acetazolamide (5 mg/kg), 4) benzolamide, a membrane-impermeant inhibitor, and 5) ethoxzolamide, a membrane-permeant inhibitor. In all protocols, unanesthetized dogs breathed spontaneously during the first hour (normoxia) and then breathed 9–10% O2 for the next 2 h. Arterial oxygen tension ranged between 35 and 39 mmHg during hypoxia in all protocols. In controls, mean pulmonary artery pressure increased by 8 mmHg and pulmonary vascular resistance by 200 dyn·s·cm−5 ( P <0.05). With intravenous acetazolamide, mean pulmonary artery pressure and pulmonary vascular resistance remained unchanged during hypoxia. With oral acetazolamide, mean pulmonary artery pressure increased by 5 mmHg ( P < 0.05), but pulmonary vascular resistance did not change during hypoxia. With benzolamide and ethoxzolamide, mean pulmonary artery pressure increased by 6–7 mmHg and pulmonary vascular resistance by 150–200 dyn·s·cm−5 during hypoxia ( P < 0.05). Low-dose acetazolamide is effective against acute hypoxic pulmonary vasoconstriction in vivo. The lack of effect with two other potent carbonic anhydrase inhibitors suggests that carbonic anhydrase is not involved in the mediation of hypoxic pulmonary vasoconstriction and that acetazolamide acts on a different receptor or channel.

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