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.

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.

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.

scholarly journals P1529 Impact of the new PH guidelines on echocardiographic definition leading to double demand of right heart catheterization

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
C Fauvel ◽  
O Raitiere ◽  
J Burdeau ◽  
N Si Belkacem ◽  
F Bauer
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Tricuspid Regurgitation ◽  
Peak Velocity ◽  
Right Heart Catheterization ◽  
Heart Catheterization ◽  
Right Heart ◽  
Artery Pressure ◽  
Mean Pulmonary Artery Pressure ◽  
Definition Of

Abstract Background Doppler echocardiography is the most widespread and well-recognized technique for the screening of patients with pulmonary hypertension (PH). When tricuspid regurgitation peak velocity (TRPV) ≥3.4 m/s, right heart catheterization is requested to confirm mean pulmonary artery pressure &gt;25 mm Hg. In the proceedings from the 6th world symposium on pulmonary arterial hypertension recently released, the new definition of PH has been lowered to mean pulmonary artery pressure &gt; 20 mm Hg. Purpose The purpose of our work was twofold : i) to determine a new cut-off value for TRPV to accommodate the new hemodynamic definition of PH, ii) to investigate the impact on the demand of right heart catheterization (RHC) from our echo CORE lab. Methods We extracted and analyzed both the haemodynamic and echocardiographic records of 130 patients who underwent investigations the same day. Tricuspid regurgitation peak velocity was measured in apical-4 chamber view using continuous-wave doppler modality and compared to mean pulmonary artery pressure recorded from fluid-filled catheter. Results Tricuspid regurgitation peak velocity has a weak correlation with mean pulmonary pressure (y = 9.2x-2.2, r² = 0.22, p &lt; 0.01). Targeting a mean pulmonary pressure on right heart catheterization of 20 mm Hg for the definition of PH, receiver operating characteristic curve analysis demonstrated a good association between TRPV and PH diagnosis (area under the curve, 0.78 ; p &lt; 0.001). The cut-off value obtained for TRPV was 3.0 m/s (Se = 0.78, Sp = 0.37). From 01/01/18 to 31/12/18, 2539 out of 6215 had TRPV recorded from which 283 had TRPV ≥ 3.0 m/s (24,1%) and 615 had TRPV ≥ 3.4 m/s (11,1%). When applied to a community population the new TRPV cutoff &gt; 3m/s used as surrogate for mean pulmonary artery pressure &gt; 20 mm Hg may produce a 111% increase of right heart catheterization demand. Conclusions The new definition of pulmonary hypertension (invasive mean pulmonary artery pressure &gt; 20mm Hg) necessitates revisiting tricuspid regurgitation peak velocity &gt; 3 m/s as a screening test leading to more than twice RHC demand.

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.

Stability of pulmonary artery pressure during emboli-induced pulmonary edema in dogs

1965 ◽  
Vol 208 (6) ◽  
pp. 1263-1266
Author(s):  
H. Weisberg ◽  
R. T. Jortner ◽  
I. K. Kline ◽  
A. Ellis ◽  
L. N. Katz
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Edema ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Pressure Rise ◽  
Vascular Effects ◽  
Artery Pressure ◽  
Pressure Changes

Changes in some facets of cardiovascular hemodynamics occurring after acute unilateral pulmonary starch embolization were studied in the anesthetized closed-chest dog. While bilateral pulmonary edema and reduced cardiac output occurred in starch-embolized dogs, these phenomena were not seen in control animals. Pulmonary arterial pressure changes were not significant during the present experiments, but the consistent rise in pulmonary vascular resistance after embolization indicates that the latter may be a better index of pulmonary vascular effects of emboli than are pressure changes. The fall in cardiac output was of sufficient magnitude to more completely neutralize the pulmonary artery pressure rise usually expected with increased pulmonary vascular resistance following pulmonary embolization.

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