BACKGROUND: The dominant feature of COVID-19-associated ARDS is gas exchange impairment. Extravascular lung water index is a surrogate for lung edema and reflects the level of alveolocapillary disruption. The primary aim was the prediction of extravascular lung water index by the alveolar-arterial oxygen difference. The secondary aims were in determining the relationship between the extravascular lung water index and other oxygenation parameters, the [Formula: see text], end-tidal oxygen concentration, pulmonary oxygen gradient ([Formula: see text] minus end-tidal oxygen concentration), and [Formula: see text]. METHODS: This observational prospective single-center study was performed at the Department of Anaesthesiology and Intensive Care, The University Hospital in Ostrava, The Czech Republic, during the COVID-19 pandemic, from March 20, 2020, until May 24, 2021. RESULTS: The relationship between the extravascular lung water index and alveolar-arterial oxygen difference showed only a mild-to-moderate correlation (r = 0.33, P < .001). Other extravascular lung water index correlations were as follows: [Formula: see text] (r = 0.33, P < .001), end-tidal oxygen concentration (r = 0.26, P = .0032), [Formula: see text] minus end-tidal oxygen concentration (r = 0.15, P = .0624), and [Formula: see text] (r = -0.15, P = .01). CONCLUSIONS: The alveolar-arterial oxygen difference does not reliably correlate with the extravascular lung water index and the degree of lung edema in COVID-19-associated ARDS.
- Klíčová slova
- ARDS, COVID-19, alveolar gas equation, alveolar-arterial difference, end-tidal O2, extravascular lung water index, hypoxemia,
- MeSH
- COVID-19 * komplikace patofyziologie MeSH
- dospělí MeSH
- extravaskulární plicní voda * metabolismus MeSH
- kyslík * metabolismus MeSH
- lidé středního věku MeSH
- lidé MeSH
- plicní alveoly * metabolismus patofyziologie MeSH
- plicní edém etiologie patofyziologie MeSH
- prospektivní studie MeSH
- senioři MeSH
- syndrom dechové tísně * patofyziologie etiologie MeSH
- výměna plynů v plicích MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- pozorovací studie MeSH
- Geografické názvy
- Česká republika epidemiologie MeSH
- Názvy látek
- kyslík * MeSH
AIMS: Patients with structural heart disease (SHD) undergoing catheter ablation (CA) for ventricular tachycardia (VT) are at considerable risk of periprocedural complications, including acute haemodynamic decompensation (AHD). The PAINESD score was proposed to predict the risk of AHD. The goal of this study was to validate the PAINESD score using the retrospective analysis of data from a large-volume heart centre. METHODS AND RESULTS: Patients who had their first radiofrequency CA for SHD-related VT between August 2006 and December 2020 were included in the study. Procedures were mainly performed under conscious sedation. Substrate mapping/ablation was performed primarily during spontaneous rhythm or right ventricular pacing. A purposely established institutional registry for complications of invasive procedures was used to collect all periprocedural complications that were subsequently adjudicated using the source medical records. Acute haemodynamic decompensation triggered by CA procedure was defined as intraprocedural or early post-procedural (<12 h) development of acute pulmonary oedema or refractory hypotension requiring urgent intervention. The study cohort consisted of 1124 patients (age, 63 ± 13 years; males, 87%; ischaemic cardiomyopathy, 67%; electrical storm, 25%; New York Heart Association Class, 2.0 ± 1.0; left ventricular ejection fraction, 34 ± 12%; diabetes mellitus, 31%; chronic obstructive pulmonary disease, 12%). Their PAINESD score was 11.4 ± 6.6 (median, 12; interquartile range, 6-17). Acute haemodynamic decompensation complicated the CA procedure in 13/1124 = 1.2% patients and was not predicted by PAINESD score with AHD rates of 0.3, 1.8, and 1.1% in subgroups by previously published PAINESD terciles (<9, 9-14, and >14). However, the PAINESD score strongly predicted mortality during the follow-up. CONCLUSION: Primarily substrate-based CA of SHD-related VT performed under conscious sedation is associated with a substantially lower rate of AHD than previously reported. The PAINESD score did not predict these events. The application of the PAINESD score to the selection of patients for pre-emptive mechanical circulatory support should be reconsidered.
- Klíčová slova
- Acute haemodynamic decompensation, Catheter ablation, Mechanical circulatory support, PAINESD score, Risk assessment, Ventricular tachycardia,
- MeSH
- hemodynamika * MeSH
- hypotenze etiologie patofyziologie diagnóza MeSH
- jizva patofyziologie MeSH
- katetrizační ablace * škodlivé účinky MeSH
- komorová tachykardie * chirurgie patofyziologie etiologie diagnóza MeSH
- lidé středního věku MeSH
- lidé MeSH
- plicní edém etiologie diagnóza patofyziologie MeSH
- pooperační komplikace etiologie diagnóza MeSH
- retrospektivní studie MeSH
- rizikové faktory MeSH
- senioři MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
INTRODUCTION: Neurogenic pulmonary oedema (NPE) is avery rare complication of epileptic seizures, which could potentially increase mortality. MATERIAL AND METHODS: The case of a66-year-old male patient with NPE caused by repeated epileptic seizures is reported. Rapid resolution of pulmonary oedema is well documented by X-ray and computed tomography images. CONCLUSIONS: Neurogenic pulmonary oedema could potentially increase mortality, and thus, it is important to perform achest X-ray in all patients presenting with seizures and dyspnoea.
- Klíčová slova
- epilepsy, neurogenic pulmonary oedema, seizure,
- MeSH
- centrální nervový systém patofyziologie MeSH
- hemodynamika fyziologie MeSH
- lidé MeSH
- nemoci centrálního nervového systému patologie patofyziologie MeSH
- plicní edém patologie patofyziologie MeSH
- senioři MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- Publikační typ
- časopisecké články MeSH
- kazuistiky MeSH
INTRODUCTION: Circadian variation of in-hospital acute cardiogenic pulmonary oedema (CPE) with the highest occurrence in the early morning has been reported repeatedly. However, no study evaluating circadian variation of CPE in the field has been published. Therefore, we decided to evaluate the circadian variation of CPE in the Central Bohemian Region of the Czech Republic in the patients treated by regional emergency medical service (EMS) and analyse its association with baseline blood pressure in the field. METHODS: We extracted all dispatches to CPE cases from EMS database for the period from 1.11.2008 to 30.6.2014 and analysed for circadian variation. We identified the patients presenting with CPE coupled with arterial hypertension (systolic blood pressure >140mmHg) and hypotension (systolic blood pressure <90mmHg) and compared the subgroups (both subgroups include 2744 subjects). RESULTS: In 4747 episodes of CPE, maximal occurrence was detected in the ninth hour in the morning, representing 7.7% of all CPE episodes (p<0.05). While CPE with hypertension (2463 subjects) reached maximal occurrence also in the ninth hour (7.4% of all cases, p<0.05), CPE with hypotension (281 patients) was most frequent in the fourteenth hour (8.6% of all cases, p<0.05). CONCLUSION: The highest occurrence of CPE was observed in the ninth hour in the morning in our study. Moreover, differences in circadian variation between CPE with hypertension and hypotension were identified. Knowledge of these patterns may have an impact on the logistic of prehospital emergency care and on preventive measures in the patients who have previously undergone CPE.
- Klíčová slova
- Cardiogenic pulmonary oedema, Circadian variation, Prehospital,
- MeSH
- cirkadiánní rytmus fyziologie MeSH
- hypertenze patofyziologie MeSH
- hypotenze patofyziologie MeSH
- krevní tlak MeSH
- lidé středního věku MeSH
- lidé MeSH
- plicní edém patofyziologie MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- urgentní zdravotnické služby MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Geografické názvy
- Česká republika MeSH
Non-cardiogenic pulmonary edema is a clinical syndrome manifested by rapidly progressive respiratory distress leading, without therapy, to severe respiratory insufficiency and subsequent multiorgan failure. The pathophysiological causes are: the change in the pressure gradients in the pulmonary capillaries, the impaired membrane permeability of the alveolocapillary in the lungs, and impaired lymphatic drainage. Unlike in cardiogenic pulmonary edema, cardiac disease is not a cause, and there is no increase in wedge pressure (< 18 mm Hg). The aetiological base is diverse and includes more clinical pathological factors. The diagnosis and evaluation are usually very difficult due to the rapidly deteriorating clinical condition of the patients. A decisive, quick and comprehensive approach, using all available invasive and non-invasive methods is necessary. The basic steps of treatment are: the use of different types of ventilatory support in order to achieve adequate oxygenation, dealing with possible hemodynamic instability, and, when needed, other specific procedures. It is always important to keep in mind that this is a very serious condition with a high mortality rate. And there is a need for fast and efficient access to the best specialized clinic.
- Klíčová slova
- non-cardiogenic pulmonary edema - acute respiratory distress syndrome - protective ventilatory support - extracorporeal membrane oxygenation.,
- MeSH
- akutní nemoc MeSH
- kapilární permeabilita fyziologie MeSH
- kapiláry patofyziologie MeSH
- lidé MeSH
- lymfa fyziologie MeSH
- multiorgánové selhání diagnóza etiologie patofyziologie MeSH
- péče o pacienty v kritickém stavu MeSH
- plíce MeSH
- plicní alveoly krevní zásobení MeSH
- plicní edém diagnóza etiologie patofyziologie terapie MeSH
- progrese nemoci MeSH
- syndrom dechové tísně diagnóza etiologie patofyziologie terapie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
AIMS: The goal of the study was to examine the prognostic impact, haemodynamic and clinical features associated with lung congestion in patients with chronic heart failure (HF). METHODS AND RESULTS: HF patients (n = 186) and HF-free controls (n = 21) underwent right heart catheterization, echocardiography, pulmonary function testing and chest radiography that was blindly scored for the presence and severity of lung oedema. Lung congestion correlated directly with pulmonary vascular resistance (PVR, P = 0.004) and inversely with pulmonary artery (PA) compliance (P < 0.001) and the diffusion limit for carbon monoxide (DLCO , P = 0.009). Compared with dry lung HF, wet lung HF patients (congestion score > median) had 25% lower PA compliance and 25-35% higher PVR, transpulmonary gradients and PA pressures (40 vs. 32 mmHg, P < 0.001) despite marginally higher PA wedge pressure (PAWP; 22 vs. 19 mmHg, P = 0.002). Wet lung HF patients displayed more right ventricular (RV) dilatation and dysfunction, more restrictive ventilation and greater reduction of DLCO . The strongest correlates of lung congestion were NT-proBNP, haemoglobin, albumin, and glomerular filtration, all surpassing PAWP. After a median of 333 days (interquartile range 80-875), 59 patients (32%) died. Lung congestion was associated with reduced survival (P < 0.0001), even after adjusting for PAWP, NT-proBNP, anaemia, CAD and renal dysfunction. CONCLUSION: Interstitial lung oedema is associated with pulmonary vascular disease, RV overload and dysfunction and increased mortality in HF. These data reinforce the importance of aggressive decongestion in HF and suggest that novel agents aimed at reducing lung water may help to deter progression of pulmonary vascular disease and biventricular HF.
- Klíčová slova
- Congestion, Haemodynamics, Heart failure, Pulmonary oedema, Pulmonary vascular resistance, Right heart,
- MeSH
- analýza přežití MeSH
- cévní rezistence * MeSH
- dysfunkce pravé srdeční komory patofyziologie MeSH
- echokardiografie metody MeSH
- lidé středního věku MeSH
- lidé MeSH
- plíce diagnostické zobrazování MeSH
- plicní edém * krev diagnóza etiologie mortalita patofyziologie MeSH
- plicní hypertenze * diagnóza etiologie patofyziologie MeSH
- prognóza MeSH
- radiografie MeSH
- respirační funkční testy metody MeSH
- retrospektivní studie MeSH
- rizikové faktory MeSH
- senioři MeSH
- srdeční katetrizace metody MeSH
- srdeční selhání * komplikace diagnóza patofyziologie MeSH
- statistika jako téma MeSH
- stupeň závažnosti nemoci MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Geografické názvy
- Spojené státy americké MeSH
Neurogenic pulmonary edema (NPE) is a life-threatening complication of central nervous system (CNS) injuries. This review summarizes current knowledge about NPE etiology and pathophysiology with an emphasis on its experimental models, including our spinal cord compression model. NPE may develop as a result of activation of specific CNS trigger zones located in the brainstem, leading to a rapid sympathetic discharge, rise in systemic blood pressure, baroreflex-induced bradycardia, and enhanced venous return resulting in pulmonary vascular congestion characterized by interstitial edema, intra-alveolar accumulation of transudate, and intra-alveolar hemorrhages. The potential etiological role of neurotransmitter changes in NPE trigger zones leading to enhanced sympathetic nerve activity is discussed. Degree of anesthesia is a crucial determinant for the extent of NPE development in experimental models because of its influence on sympathetic nervous system activity. Sympathetic hyperactivity is based on the major activation of either ascending spinal pathways by spinal cord injury or NPE trigger zones by increased intracranial pressure. Attenuation of sympathetic nerve activity or abolition of reflex bradycardia completely prevent NPE development in our experimental model. Suggestions for future research into NPE pathogenesis as well as therapeutic potential of particular drugs and interventions are discussed.
- Klíčová slova
- baroreflex-induced bradycardia, blood pressure rise, blood volume redistribution, central nervous system, neurogenic pulmonary edema, spinal cord injury, sympathetic nervous system,
- MeSH
- centrální nervový systém zranění MeSH
- lidé MeSH
- plicní edém etiologie patofyziologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
The pronounced activation of sympathetic nervous system is a necessary prerequisite for the development of neurogenic pulmonary edema (NPE) in rats with balloon compression of spinal cord. In this study we examined whether this is a consequence of rapid activation of spinal pathways leading to sympathetic venoconstriction, blood pressure rise, and reflex bradycardia. We found that NPE development can be prevented by epidural upper thoracic anesthesia or by transection of the upper spinal cord. This indicates an important role of spinal pathways activation. NPE development can also be prevented by moderate blood loss, supporting the role of blood redistribution to pulmonary circulation. In rats developing NPE the catecholamine surge following spinal cord compression involved not only a dramatic increase of circulating norepinephrine but also of epinephrine levels. The pretreatment of rats with α-1 adrenoceptor blocker prazosin, α-2 adrenoceptor blocker yohimbine, or calcium channel blocker nifedipine prevented NPE development, whereas the effect of β-adrenoceptor blockade with propranolol was less convincing. In conclusion, considerable activation of thoracic spinal pathways, followed by marked catecholamine secretion, play a major role in the development of NPE in spinal cord-injured rats. Enhanced α-adrenergic nifedipine-sensitive vasoconstriction is responsible for observed blood pressure changes, subsequent baroreflex bradycardia, and blood volume redistribution, which represent major pathogenetic mechanisms of NPE development.
- MeSH
- adrenalin krev MeSH
- biologické markery krev MeSH
- bradykardie krev patofyziologie MeSH
- hrudní obratle MeSH
- krevní tlak fyziologie MeSH
- krysa rodu Rattus MeSH
- noradrenalin krev MeSH
- plicní edém krev etiologie patofyziologie MeSH
- poranění míchy krev komplikace patofyziologie MeSH
- potkani Wistar MeSH
- sympatický nervový systém fyziologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- adrenalin MeSH
- biologické markery MeSH
- noradrenalin MeSH
Neurogenic pulmonary oedema is a complication of severe central nervous system injury. The centre of neurogenic pulmonary oedema is assumed to be a group of dorsal ventrolateral medulla nuclei, which are activated by a combination of afferent pathway hyperactivity and a sudden increase of intracranial pressure. The sympathetic system plays a crucial role in the pathogenesis of neurogenic pulmonary oedema by activating a rapid cascade of processes, leading to interstitial and intraalveolar oedema, together with important haemorrhage. For the diagnosis of neurogenic pulmonary oedema, physical examination and chest X-ray are crucial. The differential diagnosis is not easy, but the chances of proper diagnosis are increased when the relation between the central nervous system injury and the pulmonary problems is considered. Targeted curative treatment of neurogenic pulmonary oedema does not exist yet; thus, the treatment options are mainly supportive and symptomatic. The most important ones are continuous patient monitoring, posture and ventilation and oxygenation support. There are several experimental models that can be used for studying the etiopathogenesis or treatment of neurogenic pulmonary oedema. The main goal of experimental studies is to elucidate a preventive and therapeutic approach that is able to prevent or treat neurogenic pulmonary oedema. In this context, the most promising agent is atropine.
Neurogenic pulmonary edema (NPE), which is induced by acute spinal cord compression (SCC) under the mild (1.5 %) isoflurane anesthesia, is highly dependent on baroreflex-mediated bradycardia because a deeper (3 %) isoflurane anesthesia or atropine pretreatment completely abolished bradycardia occurrence and NPE development in rats subjected to SCC. The aim of the present study was to evaluate whether hypertension-associated impairment of baroreflex sensitivity might exert some protection against NPE development in hypertensive animals. We therefore studied SCC-induced NPE development in two forms of experimental hypertension - spontaneously hypertensive rats (SHR) and salt hypertensive Dahl rats, which were reported to have reduced baroreflex sensitivity. SCC elicited NPE in both hypertensive models irrespective of their baroreflex sensitivity. It is evident that a moderate impairment of baroreflex sensitivity, which was demonstrated in salt hypertensive Dahl rats, does not exert sufficient protective effects against NPE development.
- MeSH
- baroreflex MeSH
- hypertenze komplikace patofyziologie MeSH
- komprese míchy komplikace patologie MeSH
- krevní tlak MeSH
- krysa rodu Rattus MeSH
- neurony metabolismus MeSH
- plicní edém etiologie patofyziologie prevence a kontrola MeSH
- potkani inbrední Dahl MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
