Literature DB >> 12145473

ECG changes during septic shock.

Mark M Rich1, Mike L McGarvey, James W Teener, Lawrence H Frame.   

Abstract

We have previously found that skeletal muscle becomes electrically inexcitable in septic patients. Work in an animal model suggests that a decrease in the available sodium current underlies the loss of electrical excitability. We examined ECGs from patients during periods of septic shock to determine whether there were any ECG abnormalities that might suggest a similar loss of excitability in cardiac tissue during sepsis. Fourteen out of 17 patients had low or significantly decreased QRS amplitudes during septic shock; 8 of 17 had long or increased QRS duration with or without bundle branch block. The mean decrease in QRS amplitude in septic patients was 41%, significantly higher than in controls where no consistent decrease in QRS amplitude was found (p < 0.01). In patients who recovered from septic shock, the QRS amplitude and the increased QRS duration both returned to normal. We conclude that there is a loss of QRS amplitude during septic shock that may be due to altered cardiac excitability. Copyright 2002 S. Karger AG, Basel

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Year:  2002        PMID: 12145473     DOI: 10.1159/000063120

Source DB:  PubMed          Journal:  Cardiology        ISSN: 0008-6312            Impact factor:   1.869


  17 in total

1.  Hyperpolarized shifts in the voltage dependence of fast inactivation of Nav1.4 and Nav1.5 in a rat model of critical illness myopathy.

Authors:  Gregory N Filatov; Mark M Rich
Journal:  J Physiol       Date:  2004-07-14       Impact factor: 5.182

Review 2.  Dysregulation of sodium channel gating in critical illness myopathy.

Authors:  James W Teener; Mark M Rich
Journal:  J Muscle Res Cell Motil       Date:  2006-07-28       Impact factor: 2.698

3.  Usefulness of Trends in Continuous Electrocardiographic Telemetry Monitoring to Predict In-Hospital Cardiac Arrest.

Authors:  Duc H Do; Alan Kuo; Edward S Lee; David Mortara; David Elashoff; Xiao Hu; Noel G Boyle
Journal:  Am J Cardiol       Date:  2019-07-17       Impact factor: 2.778

Review 4.  The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill.

Authors:  O Friedrich; M B Reid; G Van den Berghe; I Vanhorebeek; G Hermans; M M Rich; L Larsson
Journal:  Physiol Rev       Date:  2015-07       Impact factor: 37.312

Review 5.  Role of complement C5a and histones in septic cardiomyopathy.

Authors:  Fatemeh Fattahi; Lynn M Frydrych; Guowu Bian; Miriam Kalbitz; Todd J Herron; Elizabeth A Malan; Matthew J Delano; Peter A Ward
Journal:  Mol Immunol       Date:  2018-06-18       Impact factor: 4.407

Review 6.  Critical illness myopathy and polyneuropathy.

Authors:  Shawn J Bird; Mark M Rich
Journal:  Curr Neurol Neurosci Rep       Date:  2002-11       Impact factor: 5.081

Review 7.  Complement and sepsis-induced heart dysfunction.

Authors:  Fatemeh Fattahi; Peter A Ward
Journal:  Mol Immunol       Date:  2016-12-05       Impact factor: 4.407

8.  Reduced motor neuron excitability is an important contributor to weakness in a rat model of sepsis.

Authors:  Paul Nardelli; Jacob A Vincent; Randall Powers; Tim C Cope; Mark M Rich
Journal:  Exp Neurol       Date:  2016-04-24       Impact factor: 5.330

Review 9.  Mechanisms of neuromuscular dysfunction in critical illness.

Authors:  Jaffar Khan; Taylor B Harrison; Mark M Rich
Journal:  Crit Care Clin       Date:  2008-01       Impact factor: 3.598

10.  Inhibition of NADPH oxidase 2 (NOX2) prevents sepsis-induced cardiomyopathy by improving calcium handling and mitochondrial function.

Authors:  Leroy C Joseph; Dimitra Kokkinaki; Mesele-Christina Valenti; Grace J Kim; Emanuele Barca; Dhanendra Tomar; Nicholas E Hoffman; Prakash Subramanyam; Henry M Colecraft; Michio Hirano; Adam J Ratner; Muniswamy Madesh; Konstantinos Drosatos; John P Morrow
Journal:  JCI Insight       Date:  2017-09-07
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