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Books on the topic 'QRSd'

Author: Grafiati
Published: 28 June 2021
Last updated: 2 February 2022

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1

Billings, Ginny. The Billings rollography: Player piano music from 1917 to 1934. Belmont, CA (1518 Sunnyslope Ave., Belmont 94002): Rock Soup, 1990.

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2

Quaker Social Responsibility and Education. Dream or nightmare?: The closure of long-stay mental hospitals and community care : a report of a QRSE ad hoc group, October 1989. London: QRSE, 1989.

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3

Projects at Warp-Speed with QRPD. Global Brain, 1998.

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4

JR, JOSE APOLINARIO. QRD-RLS Adaptive Filtering. Springer, 2010.

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5

QRD-RLS Adaptive Filtering. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-09734-3.

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6

Heidbuchel, Hein, Mattias Duytschaever, and Haran Burri. Narrow versus wide QRS. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198766377.003.0003.

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7

Heidbuchel, Hein, Mattias Duytschaever, and Haran Burri. Which narrow QRS tachycardia? Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198766377.003.0031.

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8

Heidbuchel, Hein, Mattias Duytschaever, and Haran Burri. From narrow to wide QRS tachycardia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198766377.003.0046.

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9

Heidbuchel, Hein, Mattias Duytschaever, and Haran Burri. An APC during wide-QRS tachycardia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198766377.003.0053.

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10

Dacanay, Lev. 20 Covid-19 Poems: QRST Keys to Get You Through the Pandemic. Independently Published, 2020.

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11

A, Villani James, Wingrove Earl R, and Langley Research Center, eds. Aviation System Analysis Capability (ASAC) Quick Response System (QRS) report server. Hampton, Va: National Aeronautics and Space Administration, Langley Research Center, 1997.

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12

A, Villani James, Wingrove Earl R, and Langley Research Center, eds. Aviation System Analysis Capability (ASAC) Quick Response System (QRS) report server. Hampton, Va: National Aeronautics and Space Administration, Langley Research Center, 1997.

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13

Projects at Warp-Speed with Qrpd--: The Definitive Guidebook to Quality Rapid Product Development. 9th ed. Global Brain, Inc., 2005.

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14

Jones, Michael, Norman Qureshi, and Kim Rajappan. Atrioventricular nodal re-entrant tachycardia. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0114.

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Atrioventricular nodal re-entrant tachycardia (abbreviated as AVNRT) is one of the five subtypes of supraventricular tachycardia, manifesting most commonly as a regular, narrow QRS complex tachycardia, rate 150–250 min−1 (usually 160–180 min−1), occurring paroxysmally, with P waves either not apparent, or seen to follow the QRS complexes.
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15

Ltd, ICON Group. QRS CORP.: Labor Productivity Benchmarks and International Gap Analysis (Labor Productivity Series). 2nd ed. Icon Group International, Inc., 2000.

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16

McCloskey, Scott. The Miracle Of QRS: The Solution To Fix America's Broken Federal Government. Scott D. McCloskey, 2018.

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17

Ltd, ICON Group. QRS CORP.: International Competitive Benchmarks and Financial Gap Analysis (Financial Performance Series). 2nd ed. Icon Group International, Inc., 2000.

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18

Katritsis, Demosthenes, and A. John Camm. Atrial fibrillation and supraventricular arrhythmias. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0056.

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This chapter discusses the acute management of patients presenting with tachyarrhythmias suggestive of regular supraventricular tachycardias (SVT) and/or atrial fibrillation (AF). A classification of narrow- and wide-QRS tachycardias is presented, and the differential diagnosis of narrow- and wide-QRS tachycardias is discussed. Principles of acute therapy are presented either in the context of acute therapy before establishing a definitive diagnosis or for particular arrhythmia entities with an established diagnosis of a regular SVT or AF.
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19

Katritsis, Demosthenes, and A. John Camm. Atrial fibrillation and supraventricular arrhythmias. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0056_update_001.

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This chapter discusses the acute management of patients presenting with tachyarrhythmias suggestive of regular supraventricular tachycardias (SVT) and/or atrial fibrillation (AF). A classification of narrow- and wide-QRS tachycardias is presented, and the differential diagnosis of narrow- and wide-QRS tachycardias is discussed. Principles of acute therapy are presented either in the context of acute therapy before establishing a definitive diagnosis or for particular arrhythmia entities with an established diagnosis of a regular SVT or AF.
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20

Katritsis, Demosthenes, and A. John Camm. Atrial fibrillation and supraventricular arrhythmias. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0056_update_002.

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This chapter discusses the acute management of patients presenting with tachyarrhythmias suggestive of regular supraventricular tachycardias (SVT) and/or atrial fibrillation (AF). A classification of narrow- and wide-QRS tachycardias is presented, and the differential diagnosis of narrow- and wide-QRS tachycardias is discussed. Principles of acute therapy are presented either in the context of acute therapy before establishing a definitive diagnosis or for particular arrhythmia entities with an established diagnosis of a regular SVT or AF.
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21

Burri, Haran. Differential diagnosis of supraventricular tachycardias. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0479.

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This chapter overviews the electrocardiographic diagnosis of various aetiologies of narrow complex tachycardia, as well as the criteria for distinguishing aberrant conduction from ventricular tachycardia in cases of wide QRS tachycardia. Clinical investigations for diagnosis of supraventricular tachycardia are also covered.
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22

Katritsis, Demosthenes G., Bernard J. Gersh, and A. John Camm. Ventricular arrhythmias. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199685288.003.1275_update_004.

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Ventricular arrhythmias are classified, and their pathophysiology is presented. The differential diagnosis of wide QRS tachycardias is summarized. Risk stratification tests for patients with ventricular arrhythmias and acute and chronic management of these conditions are discussed. Ventricular arrhythmias are also discussed in the context of relevant clinical settings, and specific recommendations about management are provided. ACC/AHA and ESC guidelines that refer to ventricular arrhythmias and indications for ICD therapy have been tabulated.
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23

Drew, Barbara Jean. VALUE OF MCL(1), MCL(6), AND SELECTED LEADS IN THE DIAGNOSIS OF WIDE QRS COMPLEX TACHYCARDIA (MCL, CORONARY CARE). 1990.

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24

Jones, Michael, Norman Qureshi, and Kim Rajappan. Atrioventricular re-entrant tachycardia. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0115.

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Atrioventricular (AV) re-entrant tachycardia (AVRT) is a type of supraventricular tachycardia, manifesting most commonly as a regular, narrow-QRS-complex tachycardia. It is usually a paroxysmal tachycardia, and is dependent upon the presence of an accessory electrical connection located between the atria and the ventricles (distinct and separate from the AV node–His–Purkinje system) and which is capable of atrioventricular (antegrade) or ventriculoatrial (retrograde) electrical conduction (or both). This pathway, together with the AV node–His–Purkinje system and the atrial and ventricular myocardia, forms a macro-re-entrant circuit which enables AVRT to occur.
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25

Henry, Mark, and Robert J. Deegan. Cardiac Dysrhythmias. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0007.

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This chapter presents a systematic approach to the diagnosis and acute management of hemodynamically significant dysrhythmias and pulseless arrest states. An overall approach to the unstable patient is reviewed with a specific focus on cardiac conduction and the effects of hemodynamics. By undertaking assessment of the pulse and clinical stability of the patient, the rate and regularity of the rhythm, and the QRS morphology, the clinician can make rational assessments to guide evidence-based therapeutic interventions and avoid the risks of inappropriate treatments. Furthermore, this chapter discusses the transition from stable to unstable to pulseless rhythms and the appropriate treatment for each.
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26

Jones, Michael, Norman Qureshi, and Kim Rajappan. Multifocal atrial tachycardia. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0113.

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Multifocal atrial tachycardia (MAT) is an atrial arrhythmia arising in the left or right atrium, or both, with multiple different P wave morphologies (at least three), with an atrial rate usually faster than 100 min−1. The atrial rhythm may be irregular; however, the defining difference between MAT and atrial fibrillation is the presence of a P wave prior to each QRS complex in MAT (but the absence of P waves in atrial fibrillation). MAT may be compared to sinus rhythm with very frequent polymorphic atrial ectopic beats, and in fact similar pathophysiologic mechanisms underlie both conditions; thus, differentiating one from the other may be difficult—the principle difference is the lack of a single dominant sinus pacemaker in MAT.
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27

Jones, Michael, Norman Qureshi, and Kim Rajappan. Ventricular tachyarrhythmias: Ventricular tachycardia and ventricular fibrillation. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0118.

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Ventricular tachyarrhythmias are abnormal patterns of electrical activity arising from the ventricular tissue (myocardium and conduction tissue). Ventricular tachycardia (VT) is an abnormal rapid heart rhythm originating from the ventricles. The rhythm may arise from the ventricular myocardium and/or from the distal conduction system. The normal heart rate is usually regular, between 60 and 100 bpm, and there is synchronized atrial and ventricular contraction. In VT, the ventricles contract at a rate greater than 120 bpm and typically from 150 to 300 bpm, and are no longer coordinated with the atria. There is still organized contraction of the ventricles in VT, with discrete QRS complexes. It is a potentially life-threatening arrhythmia, with the risk of degenerating into ventricular fibrillation and resulting in sudden cardiac death. It is characterized by a broad-complex tachycardia on ECG.
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28

Frise, Matthew C., and Jonathan B. Salmon. Disorders of potassium in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0251.

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Plasma potassium levels are maintained in health between 3.5 and 5.0 mmol/L, and reflect total body potassium only in stable states at normal pH. Most true hyperkalaemia results from renal insufficiency. The goals of therapy are myocardial protection and return of plasma potassium to a safe level. Measures are commonly initiated above 5.5 mmol/L; above 6.5 mmol/L, aggressive measures should be adopted and calcium salts given if there are cardiac dysrhythmias or QRS-broadening. Glucose-insulin infusions and beta-2-agonists promote potassium shifts into cells. Diuretics and sodium bicarbonate may be helpful, but persistent hyperkalaemia is an indication for renal replacement therapy. Hypokalaemia may lead to dangerous arrhythmias, skeletal muscle weakness, ileus, and reduced vascular smooth muscle contractility. Rapid replacement should only be undertaken for severe hypokalaemia or in the context of arrhythmias. Once the extracellular deficit is corrected, there will usually be a continuing need for potassium supplementation to replenish intracellular stores.
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29

Esen, Figen. Disorders of magnesium in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0252.

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Plasma potassium levels are maintained in health between 3.5 and 5.0 mmol/L, and reflect total body potassium only in stable states at normal pH. Most true hyperkalaemia results from renal insufficiency. The goals of therapy are myocardial protection and return of plasma potassium to a safe level. Measures are commonly initiated above 5.5 mmol/L; above 6.5 mmol/L, aggressive measures should be adopted and calcium salts given if there are cardiac dysrhythmias or QRS-broadening. Glucose-insulin infusions and beta-2-agonists promote potassium shifts into cells. Diuretics and sodium bicarbonate may be helpful, but persistent hyperkalaemia is an indication for renal replacement therapy. Hypokalaemia may lead to dangerous arrhythmias, skeletal muscle weakness, ileus, and reduced vascular smooth muscle contractility. Rapid replacement should only be undertaken for severe hypokalaemia or in the context of arrhythmias. Once the extracellular deficit is corrected, there will usually be a continuing need for potassium supplementation to replenish intracellular stores.
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30

Barold, S. Serge. Atrioventricular conduction abnormalities and atrioventricular blocks: ECG patterns and diagnosis. Edited by Giuseppe Boriani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0453.

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The diagnosis of first-degree and third-degree atrioventricular (AV) block is straightforward but that of second-degree AV block is more involved. Type I block and type II second-degree AV block are electrocardiographic patterns that refer to the behaviour of the PR intervals (in sinus rhythm) in sequences (with at least two consecutive conducted PR intervals) where a single P wave fails to conduct to the ventricles. Type I second-degree AV block describes visible, differing, and generally decremental AV conduction. Type II second-degree AV block describes what appears to be an all-or-none conduction without visible changes in the AV conduction time before and after the blocked impulse. The diagnosis of type II block requires a stable sinus rate, an important criterion because a vagal surge (generally benign) can cause simultaneous sinus slowing and AV nodal block, which can resemble type II block. The diagnosis of type II block cannot be established if the first post-block P wave is followed by a shortened PR interval or by an undiscernible P wave. A narrow QRS type I block is almost always AV nodal, whereas a type I block with bundle branch block barring acute myocardial infarction is infranodal in 60–70% of cases. All correctly defined type II blocks are infranodal. A 2:1 AV block cannot be classified in terms of type I or type II block, but it can be AV nodal or infranodal. Concealed His bundle or ventricular extrasystoles may mimic both type I or type II block (pseudo-AV block), or both
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31

Jones, Michael, Norman Qureshi, and Kim Rajappan. Atrial flutter. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0117.

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Atrial flutter is the term given to one of the four types of supraventricular tachycardia; in it, atrial activation occurs as a consequence of a continuous ‘short circuit’: a defined and fixed anatomical route, resulting in a fairly uniform atrial rate, and uniform atrial flutter waves on the ECG. The ventricles are not a part of this arrhythmia circuit, and ventricular activation is variable, dependent on atrioventricular (AV) nodal conduction. Given that the atrial rate is essentially uniform (e.g. 300 min−1), ventricular activation tends to be regular (i.e. 150 min−1, 100 min−1, 75 min−1, etc., if the atrial rate is 300 mins−1), or regularly irregular if changes are occurring in the fraction of conducted impulses to the ventricles. When AV nodal conduction permits only 4:1 conduction or less, atrial flutter is usually obvious, but when ventricular rates are higher (150 min−1 or more) the flutter waves can be obscured by the QRS complexes, making diagnosis more difficult. Atrial flutter is of two types, typical and atypical. Typical atrial flutter is a right atrial tachycardia, with electrical activation proceeding around the tricuspid valve annulus. This arrhythmia is dependent on a zone of slow electrical conduction through the cavotricuspid isthmus (the tissue lying between the origin of the inferior vena cava and the posterior tricuspid valve). The resulting circuit can be either anticlockwise (activation proceeds up the inter-atrial septum, across the atrial roof, down the free wall, and then through the cavotricuspid isthmus to the basal septum) or clockwise (down the inter-atrial septum and around the circuit in the opposite direction). Anticlockwise typical atrial flutter is more common. Atypical atrial flutter refers to all other atrial flutters, and this includes other right atrial flutters (e.g. pericristal flutter), left atrial flutters, post-ablation or post-surgical flutters, and pulmonary vein flutters. The feature common to all types of flutter and which differentiates flutter from other types of supraventricular tachycardia is the presence of a macro-re-entrant anatomical circuit around which the electrical impulse travels continuously and repeatedly, thereby generating the flutter. Even though typical atrial flutter has a fairly obvious and specific appearance on the ECG, atypical flutters do not, and often it is only possible to differentiate atypical flutter from atrial tachycardias by invasive electrophysiology studies, as the ECG alone may be insufficient.
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