scholarly journals Blood circulation changes associated with switching to non-invasive ventilation in COVID-19 patients

2021 ◽  
Vol 6 (6-2) ◽  
pp. 51-57
Author(s):  
D. S. Shilin ◽  
Yu. K. Shapovalov ◽  
K. G. Shapovalov
Keyword(s):  
Blood Pressure ◽  
Bacterial Pneumonia ◽  
Oxygen Therapy ◽  
Left Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Respiratory Support ◽  
Prone Positioning ◽  
Non Invasive ◽  
Left Ventricular Outflow

Background. Various methods of respiratory support in combination with prone positioning have been used during the COVID-19 pandemic. The effects of combination of these two factors on hemodynamics are of interest for clinical practitioners.The aim: to evaluate the effect of prone positioning on hemodynamics in COVID-19 patients depending on the method of respiratory support.Materials and methods. The study included 17 patients of both sexes diagnosed with COVID-19-associated community-acquired polysegmental viral and bacterial pneumonia with progressive respiratory failure. The study consisted of two stages. During the first stage, the patients were receiving respiratory support with humidified oxygen (3–7 liters per minute). The second stage was initiated after switching to noninvasive ventilation (NIV). The measurements were performed using a technique of volumetric compression oscillometry on a non-invasive hemodynamic monitoring system KAP CGosm-Globus (Russia).Results. The study showed that prone positioning in patients with severe COVID-19 when switching from oxygen therapy to NIV resulted in a change in the diastolic blood pressure difference module from 2.5 (1.0; 8.2) to 8.0 (5.7; 14.0) (p = 0.016). Escalation of respiratory support led to the changes in the left ventricular outflow tract velocity difference module from 11.5 (9.5; 34.2) to 31.0 (15.7; 42.0) (p = 0.049).Conclusions. Patients with community-acquired polysegmental viral and bacterial pneumonia associated with COVID-19 demonstrated changes in diastolic blood pressure and left ventricular outflow tract velocity as a result of prone positioning following switching from oxygen therapy to NIV.

scholarly journals Norepinephrine-associated left ventricular outflow tract obstruction and systolic anterior movement

2019 ◽  
Vol 12 (12) ◽  
pp. e225879 ◽  
Author(s):  
Warner Mbuila Mampuya ◽  
Jonathan Dumont ◽  
Francois Lamontagne
Keyword(s):  
Blood Pressure ◽  
Left Ventricular Outflow Tract ◽  
Myocardial Hypertrophy ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Increase Blood Pressure ◽  
Ventricular Outflow Tract Obstruction ◽  
Left Ventricular Outflow ◽  
Systolic Anterior Movement

In the perioperative setting, norepinephrine is used to increase blood pressure, an effect mediated mostly via arterial and venous vasoconstriction. Thus, norepinephrine is, allegedly, less likely to cause or worsen left ventricular outflow tract obstruction (LVOTO) than other inotropes. We report a case of norepinephrine-associated dynamic LVOTO and systolic anterior movement in a predisposed patient. This report highlights that unrecognised dynamic LVOTO may worsen shock parameters in patients treated with norepinephrine who have underlying myocardial hypertrophy.

Cardiac output response and peripheral oxygen extraction during exercise among symptomatic hypertrophic cardiomyopathy patients with and without left ventricular outflow tract obstruction

Heart ◽  
2014 ◽  
Vol 100 (8) ◽  
pp. 639-646 ◽  
Author(s):  
Christopher H Critoph ◽  
Vimal Patel ◽  
Bryan Mist ◽  
Perry M Elliott
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Hypertrophic Cardiomyopathy ◽  
Cardiac Index ◽  
Left Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Non Invasive ◽  
Left Ventricular Outflow ◽  
Oxygen Difference

ObjectiveReduction of left ventricular outflow tract obstruction (LVOTO) often improves symptoms in hypertrophic cardiomyopathy (HCM), but the correlation between exercise performance and measured LVOT gradients is weak. We investigated the relationship between LVOTO and cardiorespiratory responses during exercise.MethodsThe study cohort included 70 patients with HCM (32 with LVOTO, 55 male, age 47±13) attending a dedicated cardiomyopathy clinic and 28 normal volunteers. All underwent cardiopulmonary exercise testing with simultaneous non-invasive haemodynamic assessment using finger plethysmography. Main outcome measures were peak oxygen consumption, cardiac index and arteriovenous oxygen difference.ResultsWhen compared with controls, patients had reduced peak exercise oxygen consumption (22.4±6.1 vs 34.7±7.7 mL/kg/min, p<0.0001) and cardiac index (5.5±1.9 vs 9.4±2.9 L/min/m2, p<0.0001). At all workloads, stroke volume index (SVI) was lower and arteriovenous oxygen difference greater in patients. During all stages of exercise, LVOTO in patients was associated with failure to augment SVI and higher oxygen consumption; cardiac reserve (4.4±2.7 vs 6.3±3.6 L/min, p=0.025) and peak mean arterial pressure (104±16 vs 112±16 mm Hg, p=0.033) were lower. Multivariable predictors of cardiac output response were age (β: −0.11; CI −0.162 to −0.057; p<0.0001), peak LVOT gradient (β: −0.018; CI −0.034 to −0.002; p=0.031) and gender (β: −2.286; CI −0.162 to −0.577; p=0.01). Within the obstructive cohort, different patterns of SV response were elicited in patients with similar clinical features.ConclusionsCardiac reserve is reduced in HCM because of failure of SV augmentation. LVOTO exacerbates this abnormal response, but haemodynamic responses vary significantly. Non-invasive exercise haemodynamic assessment may improve understanding of symptoms and help tailor therapy.

scholarly journals Miocardiopatía de y movimiento sistólico anterior de válvula mitral

2020 ◽  
Vol 49 (4) ◽  
pp. 481-485
Author(s):  
Emilia Schlack ◽  
Fernando Aranda
Keyword(s):  
Left Ventricular Outflow Tract ◽  
Ventilatory Support ◽  
Ventricular Outflow Tract ◽  
Initial Therapy ◽  
Left Ventricular ◽  
Transthoracic Echocardiogram ◽  
Vasopressor Therapy ◽  
Non Invasive ◽  
Volume Expander ◽  
Left Ventricular Outflow

Cardiomyopathy associated with left ventricular outflow tract obstruction (LVOT) is a rare cause of persistent perioperative hypotension. One of the causes of this association is the systolic anterior motion (SAM) of the mitral valve. We report a case of a 67-year-old woman who, after undergoing liver segmentectomy because of metastasis, presents post-operative hypotension that is difficult to manage. Upon evaluation with a transthoracic echocardiogram, the diagnostic suspicion of syndrome associated with LVOT obstruction secondary to SAM was raised. As initial therapy, a volume expander, in association with propanolol and phenylephrine were administred, achieving partial hemodynamic response. Later, she evolved with signs of heart failure and was transferred to the intensive care unit for management. In this unit, non-invasive ventilatory support, diuretic and vasopressor therapy were required, achieving favorable results on the second post-operative day. Echocardiography was essential to make the differential diagnosis against a persistent post-operative hypotension.

Abstract 2958: Perindopril Reduces Large Artery Stiffness and Left Ventricular Outflow Tract Diameter in Patients with Marfan syndrome

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Anna A Ahimastos ◽  
Anuradha Aggarwal ◽  
Kellie D’Orsa ◽  
Melissa Formosa ◽  
Anthony White ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Marfan Syndrome ◽  
Aortic Stiffness ◽  
Left Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Aortic Dilatation ◽  
Left Ventricular Outflow

Introduction: Aortic stiffness is elevated in Marfan syndrome (MFS) contributing to aortic dilatation and rupture, the major cause of premature death in this population. Excessive signalling by the transforming growth factor-β(TGFβ) plays a crucial role in the development of aortic dilatation. Hypothesis: Given the known beneficial effects of angiotensin converting enzyme (ACE) inhibitors on arterial stiffness, we hypothesised that perindopril therapy would reduce aortic stiffness and attenuate aortic dilatation in MFS patients, possibly through effects on TGFβ signalling. Methods: 17 MFS patients (aged 33 ± 5) on standard β-blocker therapy were randomised to also receive perindopril (8mg od, n=10) or placebo (n=7) for 24 weeks in a double blind study. Indices of arterial stiffness were assessed globally via systemic arterial compliance (SAC) and augmentation index (AIx), and regionally via central (PWVc) and peripheral (PWVp) pulse wave velocity. Left ventricular outflow tract (LVOT) diameter was assessed via a transthoracic echocardiogram. Venous blood samples were analysed for latent and active TGFβ levels using ELISA. Results: Perindopril reduced arterial stiffness as indicated by increased SAC (perindopril 62 ± 11% vs placebo -4.30 ± 1%, p<0.0001), reduced AIx (perindopril -23.50 ± 3% vs placebo 3 ± 1%, p<0.0001), reduced PWVc (perindopril -21 ± 2% vs placebo 5 ± 2%, p<0.0001) and PWVp (perindopril -20 ± 2% vs placebo 2 ± 1%, p<0.0001). In addition, perindopril significantly reduced LVOT diameter (perindopril -2.8 ± 0.4mm vs placebo 1.1 ± 0.3mm, p<0.0001). While perindopril marginally reduced mean arterial blood pressure (perindopril -1.3 ± 0.2mmHg vs placebo 0.2 ± 0.5mmHg, p=0.004), importantly, the observed changes in both stiffness (p=0.001– 0.006) and LVOT diameter (p<0.001) remained significant when mean blood pressure was included as a covariate. Finally, perindopril reduced latent TGFβ levels by -14.0 ± 4.5ng/ml when compared to placebo (2.0 ± 2.3ng/ml, p=0.01), and active TGFβ levels by -4 ± 1ng/ml (placebo 3 ± 1 ng/ml, p=0.02). Conclusions: In conclusion, ACE inhibition reduces aortic stiffness and LVOT diameter in MFS patients possibly through attenuation of TGFβsignalling, and may potentially protect against aortic rupture.

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