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1
Phenylephrine-induced electrophysiological changes in cultured neonatal rat ventricular myocytes. 1995.
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Phenylephrine-induced electrophysiological changes in cultured neonatal rat ventricular myocytes. 1995.
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Phenylephrine-induced electrophysiological changes in cultured neonatal rat ventricular myocytes. 1995.
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Phenylephrine-induced electrophysiological changes in cultured neonatal rat ventricular myocytes. 1995.
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Kassiri, Zamaneh. Reduction of transient outward K+ current and hypertrophy in neonatal rat ventricular myocytes: Role of calcium-dependent signaling pathways. 2002.
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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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Padmanabhan, Rajagopala, and Penny Sappington. Ventricular Assist Devices (DRAFT). Edited by Raghavan Murugan and Joseph M. Darby. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190612474.003.0021.
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Ventricular assist devices (VADs) have become a cornerstone of therapy in the management of end-stage heart failure, both as a means of bridging to cardiac transplantation and as destination therapy for long-term quality of life improvement. Responding to medical emergencies in patients with VADs poses numerous challenges to rapid response team (RRT) providers. Managing these patients requires basic understanding of VAD function and physiology and the multitude of complications that follow their implantation. Most healthcare professionals lack exposure to VADs, and although it may seem daunting, this chapter will provide a systematic approach of how to identify, troubleshoot, diagnose, and manage VAD-associated complications and provide emergency care for the VAD patient.
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Jones, Michael, Norman Qureshi, and Kim Rajappan. Atrial fibrillation. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0116.
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Atrial fibrillation is a tachycardia arising in the atria, with atrial electrical activity occurring chaotically and continuously, without any effective atrial contraction occurring. The effects of this are an irregular ventricular rate, loss of the atrial contribution to ventricular filling, and the pooling of blood in the atria, thus increasing the risk of thrombus formation. The ventricular rate may be fast, slow, or of normal speed, depending on the state of the patient’s atrioventricular conduction. Atrial fibrillation is classified as paroxysmal (self-terminating within 7 days), persistent (lasting longer than 1 week, or requiring cardioversion to terminate) or permanent (cardioversion unable to terminate durably to sinus rhythm).
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Bauer, Robert, and Raghavan Murugan. Portable Monitor and Defibrillators (DRAFT). Edited by Raghavan Murugan and Joseph M. Darby. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190612474.003.0031.
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Portable monitors with the capability of defibrillation, synchronized cardioversion, and transcutaneous pacing are frequently used by the rapid response teams (RRTs) in several acute care facilities to provide quick information and to treat lethal arrhythmias in critically ill and unstable patients. Portable monitors are used on lethal arrhythmias such as ventricular fibrillation (VF), monomorphic ventricular tachycardia (VT), or polymorphic ventricular tachycardia, also known as Torsades de pointes (TdP). Properly identifying lethal arrhythmias and knowing how to use the portable monitor/defibrillator is essential to positive patient outcomes. In this chapter, we review the use of portable monitors for monitoring and detection of cardiac arrhythmias as well as outline the procedure for defibrillation, synchronized cardioversion, and transcutaneous pacing in the setting of RRT activation.
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Schneider, Antoine, and Rinaldo Bellomo. Atrial Fibrillation and Other Cardiac Arrhythmias (DRAFT). Edited by Raghavan Murugan and Joseph M. Darby. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190612474.003.0005.
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Cardiac arrhythmias are common in hospitalized patients, with their incidence increasing in older patients and those with comorbidities. Cardiac arrhythmias represent a trigger for approximately 10% of rapid response team (RRT) activations. Of those, atrial fibrillation (AF) is the most commonly observed. Other common cardiac arrhythmias in the in-hospital setting include supraventricular tachycardia, atrial flutter, ventricular tachycardia, and bradycardias. Members of the RRT should be skilled in the diagnosis and management of these common arrhythmias. This chapter presents an overview of cardiac arrhythmias that RRT members are likely to encounter, discussing their incidence and significance, as well as their immediate management.
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Tourneau, Thierry Le, Luis Caballero, and Tsai Wei-Chuan. Right atrium. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0024.
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The right atrium (RA) is located on the upper right-hand side of the heart and has relatively thin walls. From an anatomical point of view, the RA comprises three basic parts, the appendage, the vestibule of the tricuspid valve, and the venous component (superior and inferior vena cava, and the coronary sinus) receiving the deoxygenated blood. The RA is a dynamic structure dedicated to receive blood and to assist right ventricular (RV) filling. The three components of atrial function are the reservoir function during ventricular systole, the conduit function which consists in passive blood transfer from veins to the RV in diastole, and the booster pump function in relation to atrial contraction in late diastole to complete ventricular filling. Right atrial function depends on cardiac rhythm (sinus or atrial fibrillation), pericardial integrity, RV load and function, and tricuspid function. Right atrial dimension assessment is limited in two-dimensional (2D) echocardiography. Right atrial planimetry in the apical four-chamber view is commonly used with an upper normal value of 18-20 cm2. Minor and major diameters can also be measured. Three-dimensional (3D) echocardiography could overcome the limitation of conventional echocardiography in assessing RA size. Right atrial function has been poorly explored by echocardiography both in physiological and pathological contexts. Although tricuspid inflow and tissue Doppler imaging of tricuspid annulus can be used in the exploration of RA function, 2D speckle tracking and 3D echocardiography appear promising tools to dissect RA function and to overcome the limitations of standard echocardiography.
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Walkey, Allan J., and Jared Magnani. Therapeutic strategy in tachyarrhythmias. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0156.
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The therapeutic approach to tachyarrhythmias in the critically-ill patient involves rapid diagnosis and haemodynamic assessment. Patients who become haemodynamically unstable due to tachyarrhythmia warrant direct current cardioversion. Effects of direct current cardioversion during critical illness are often transient unless the underlying arrhythmia precipitant is eliminated and longer-acting rate- or rhythm-controlling medications are instituted. Atrial fibrillation often responds favourably to a rate-control strategy and treatment of the underlying precipitants. After initial clinical stabilization, clinical management involves elimination of potential arrhythmogenic triggers and administration of appropriate rate or rhythm control medications. Assessment of the QT interval in patients with polymorphic ventricular tachycardia is important in determining the underlying aetiology and treatment strategy. This chapter presents an evidence-based review of the therapeutic approach to tachyarrhythmias.
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Rajappan, Kim. Bradyarrhythmias. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0119.
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A bradyarrhythmia is defined as a rhythm disturbance that results in a heart rate of less than 60 bpm. It is important to note that many healthy people have a resting heart rate that is less than 60 bpm, most commonly due to sinus bradycardia (i.e. a rhythm arising from the sinus node but with a ventricular rate less than 60 bpm). Other forms of bradyarrhythmia are sinus node disease, sick sinus syndrome, first-degree atrioventricular (AV) block, second-degree AV block (which can be characterized as Möbitz type I (Wenckebach phenomenon) or Möbitz type II), and third-degree AV block (also known as complete heart block). This chapter discusses the bradyarrhythmias, focusing on their etiology, symptoms, demographics, diagnosis, prognosis, and treatment.
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Waldo, Albert L. Rate versus rhythm control therapy for atrial fibrillation. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0511.
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Based on data from several clinical trials, either rate control or rhythm control is an acceptable primary therapeutic strategy for patients with atrial fibrillation. However, since atrial fibrillation tends to recur no matter the therapy, rate control should almost always be a part of the treatment. If a rhythm control strategy is selected, it is important to recognize that recurrence of atrial fibrillation is common, but not clinical failure per se. Rather, the frequency and duration of episodes, as well as severity of symptoms during atrial fibrillation episodes should guide treatment decisions. Thus, occasional recurrence of atrial fibrillation despite therapy may well be clinically acceptable. However, for some patients, rhythm control may be the only strategy that is acceptable. In short, for most patients, either a rate or rhythm control strategy should be considered. However, for all patients, there are two main goals of therapy. One is to avoid stroke and/or systemic embolism, and the other is to avoid a tachycardia-induced cardiomyopathy. Also, because of the frequency of atrial fibrillation recurrence despite the treatment strategy selected, patients with stroke risks should receive anticoagulation therapy despite seemingly having achieved stable sinus rhythm. For patients in whom a rate control strategy is selected, a lenient approach to the acceptable ventricular response rate is a resting heart rate of 110 bpm, and probably 90 bpm. The importance of achieving and maintaining sinus rhythm in patients with atrial fibrillation and heart failure remains to be clearly established.
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Bowker, Lesley K., James D. Price, Ku Shah, and Sarah C. Smith. Cardiovascular. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198738381.003.0010.
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This chapter provides information on the ageing cardiovascular system, chest pain, stable angina, acute coronary syndromes, myocardial infarction, hypertension, treatment of hypertension, presentation of arrhythmias, management of arrhythmias, atrial fibrillation, rate/rhythm control in atrial fibrillation, stroke prevention in atrial fibrillation, bradycardia and conduction disorders, common arrhythmias and conduction abnormalities, heart failure assessment, acute heart failure, chronic heart failure, dilemmas in heart failure, heart failure with preserved left ventricular function, valvular heart disease, peripheral oedema, preventing venous thromboembolism in an older person, peripheral vascular disease, gangrene in peripheral vascular disease, and vascular secondary prevention.
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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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Sabharwal, Nikant, Parthiban Arumugam, and Andrew Kelion. Introduction to nuclear cardiology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759942.003.0001.
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The cardiologist of the early twenty-first century takes for granted the wide range of imaging modalities at his/her disposal, but it was not always so. At the beginning of the 1970s, invasive cardiac catheterization was the only reliable cardiac imaging technique. Subsequently, nuclear cardiology investigations led the way in the non-invasive assessment of cardiac disease. This chapter covers the history of nuclear cardiology, including important milestones in the development of nuclear medicine. It details the relation of nuclear cardiology to other imaging modalities, covering the common imaging modalities used to evaluate left ventricular function and coronary artery disease, and the challenges of multislice X-ray computed tomography.
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Jones, Michael, Norman Qureshi, and Kim Rajappan. Focal (ectopic) atrial tachycardia. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0112.
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Focal atrial tachycardia is an atrial arrhythmia arising in either the left or the right atrium, usually faster than 100 min−1 and regular, with a P-wave morphology that is different from the normal P-wave morphology associated with sinus rhythm—the difference in morphology being more pronounced the further away the focus lies from the sinus node. The ventricular rate is generally fast also, dependent on the nature of the atrioventricular conduction (AV); 1:1 conduction may be seen, especially in younger patients or patients with accessory pathways capable of very rapid antegrade conduction; alternatively, 2:1, Wenckebach-type, or higher-grade AV block may be seen.
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Dilsizian, Vasken, Ines Valenta, and Thomas H. Schindler. Myocardial Viability Assessment. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199392094.003.0021.
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Heart failure may be a consequence of ischemic or non-ischemic cardiomyopathy. Etiologies for LV systolic dysfunction in ischemic cardiomyopathy include; 1) transmural scar, 2) nontransmural scar, 3) repetitive myocardial stunning, 4) hibernating myocardium, and 5) remodeled myocardium. The LV remodeling process, which is activated by the renin-angiotensin system (RAS), stimulates toxic catecholamine actions and matrix metalloproteinases, resulting in maladaptive cellular and molecular alterations5, with a final pathway to interstitial fibrosis. These responses to LV dysfunction and interstitial fibrosis lead to progressive worsening of LV function. Established treatment options for ischemic cardiomyopathy include medical therapy, revascularization, and cardiac transplantation. While there has been continuous progress in the medical treatment of heart failure with beta-blockers, angiotensin-converting enzyme (ACE) inhibition, angiotensin II type 1 receptor (AT1R) blockers, and aldosterone to beneficially influence morbidity and mortality, the 5-years mortality rate for heart failure patients remains as high as 50%. Revascularization procedures include percutaneous transluminal coronary artery interventions (PCI) including angioplasty and endovascular stent placement and coronary artery bypass grafting (CABG). Whereas patents with heart failure due to non-coronary etiologies may best benefit from medical therapy or heart transplantation, coronary revascularization has the potential to improve ventricular function, symptoms, and long term survival, in patients with heart failure symptoms due to CAD and ischemic cardiomyopathy.
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Farmakis, Dimitrios, John Parissis, George Papingiotis, and Gerasimos Filippatos. Acute heart failure. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0051_update_001.
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Acute heart failure is defined as the rapid development or change of symptoms and signs of heart failure that requires urgent medical attention and usually hospitalization. Acute heart failure is the first reason for hospital admission in individuals aged 65 or more and accounts for nearly 70% of the total health care expenditure for heart failure. It is characterized by an adverse prognosis, with an in-hospital mortality rate of 4–7%, a 2–3-month post-discharge mortality of 7–11%, and a 2–3-month readmission rate of 25–30%. The majority of patients have a previous history of heart failure and present with normal or increased blood pressure, while about half of them have preserved left ventricular ejection fraction. A high prevalence of cardiovascular or non-cardiovascular comordid conditions is further observed, including coronary artery disease, arterial hypertension, atrial fibrillation, diabetes mellitus, renal dysfunction, chronic lung disease, and anaemia.
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Cameli, Matteo, Partho Sengupta, and Thor Edvardsen. Deformation echocardiography. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0004.
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Echocardiographic strain imaging, also known as deformation imaging, has been developed as a means to objectively quantify regional and global myocardial function. First introduced as a post-processing feature of tissue Doppler imaging velocity converted to strain and strain rate, strain imaging has more recently also been derived from speckle tracking analysis. Tissue Doppler imaging yields velocity information from which strain and strain rate are mathematically derived whereas two-dimensional speckle tracking yields strain information from which strain rate and velocity data are derived. Data obtained from these two different techniques may not be equivalent due to limitations inherent with each technique. Speckle tracking analysis can generate longitudinal, circumferential, and radial strain measurements and left ventricular twist. Although potentially useful, these measurements are also complicated and frequently displayed as difficult-to-interpret waveforms. Strain imaging is now considered a robust research tool and has great potential to play many roles in routine clinical practice. This chapter explains the fundamental concepts of deformation imaging, the technical features of strain imaging using tissue Doppler imaging and speckle tracking, and the strengths and weaknesses of these methods.
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Steinberg, Alexis, and Bradley J. Molyneaux. Acute Stroke (DRAFT). Edited by Raghavan Murugan and Joseph M. Darby. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190612474.003.0019.
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The development of a stroke is an acute neurologic emergency that requires rapid evaluation as any delay in treatment worsens outcome. There are two main types of strokes, hemorrhagic and ischemic, each requiring specific rapid assessment and interventions. If an acute ischemic stroke is suspected, then a decision regarding thrombolytic therapy and endovascular thrombectomy has to be made quickly. A hemorrhagic stroke demands rapid medical management of blood pressure, reversal of coagulopathy, and early neurosurgical consult for possible external ventricular drain (EVD) placement and hemorrhage evacuation. This chapter expands on the indicated work-up in a suspected stroke patient in the setting of the rapid response team (RRT) calls, different imaging modalities, management options in the acute and subacute periods, and post-stroke complications.
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Swanson, Karen L. Neoplastic and Vascular Diseases. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0618.
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Neoplastic and vascular disorders are reviewed. Lung cancer is the most common malignancy and cause of cancer death in both men and women worldwide. The incidence of new lung cancers has continued to decrease in men and increase in women. The risk factors include cigarette smoking, other carcinogens, cocarcinogens, radon exposure, arsenic, asbestos, coal dust, chromium, vinyl chloride, chloromethyl ether, and chronic lung injury. Genetic and nutritional factors have been implicated. Among vascular disorders, pulmonary embolism is most common. Pulmonary embolism (PE) is the cause of death in 5% to 15% of hospitalized patients who die in the United States. In a multicenter study of PE, the mortality rate at 3 months was 15% and important prognostic factors included age older than 70 years, cancer, congestive heart failure, COPD, systolic arterial hypotension, tachypnea, and right ventricular hypokinesis.
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Kreit, John W. Cardiovascular–Pulmonary Interactions. Edited by John W. Kreit. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.003.0003.
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Intramural pressures within a tube or circuit determine the rate and direction of flow, whereas the transmural pressure of an elastic structure determines its volume. In Chapter 1, we applied these principles when talking about the pressure needed to overcome viscous forces and elastic recoil during ventilation. In this chapter, we use them to explain changes in blood flow between two portions of the circulatory system and changes in the volume and size of the heart chambers. Cardio–Pulmonary Interactions provides an overview of essential cardiovascular physiology as well as an in-depth discussion of how and why changes in pleural, alveolar, lung transmural, and intra-abdominal pressure during spontaneous and mechanical ventilation can alter right and left ventricular preload, afterload, and stroke volume, cardiac output, and blood pressure. The chapter also reviews the beneficial and detrimental effects of positive end-expiratory pressure (PEEP) on cardiovascular function.
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Deakin, Charles D. Defibrillation and pacing during cardiac arrest. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0063.
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Defibrillation is the passage of electrical current across the myocardium to allow synchronized repolarisation and return of a perfusing rhythm. It is now an established intervention for patients in shockable rhythms during cardiac arrest and is administered every 2 minutes during resuscitation until return of spontaneous circulation. Modern biphasic waveforms are more effective than older monophasic waveforms, achieving first shock success rate of approximately 90%. For ventricular fibrillation in adults, the initial shock should be delivered at 150 J, and if further shocks are required, escalating energy is probably more effective than a fixed energy strategy. All paediatric shocks should be delivered at 4 J/kg. Although it is important to stand clear of the patient when the shock is delivered, defibrillation should be administered with minimal interruption to resuscitation, ideally resulting in a pause to chest compressions of no more than 5 seconds. External pacing may be life-saving in patients refractory to pharmacological support of bradyarrhythmias, but is ineffective for asystole.
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Brady, Peter A. Evaluation and Treatment of Arrhythmias. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0043.
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Abnormal cardiac arrhythmias may be due to reentry, abnormal automaticity, or triggered activity. Reentrant rhythms may be microreentrant or macroreentrant. Ambulatory (Holter) monitoring is useful for the evaluation of both symptomatic and asymptomatic rhythm disturbances and their relationship to daily activity. Treadmill exercise testing is very useful in the evaluation of patients who present with bradycardia and symptoms of palpitations because it allows both documentation of the adequacy of heart rate response to exercise and the recording of the cardiac rhythm during exercise in a controlled setting with ECG monitoring. An electrophysiologic study is useful for assessing sinus node function and the cardiac conduction system and for attempting to induce atrial or ventricular arrhythmias that could explain the clinical presentation. Electrophysiologic study requires placement of electrode catheters in the heart to record and to stimulate heart rhythm. Several therapeutic options are available for heart rhythm disorders, including drug therapy, radiofrequency ablation, and device therapy.
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Whitworth, Caroline, and Stewart Fleming. Malignant hypertension. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0216.
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Malignant hypertension (MH) is recognized clinically by elevated blood pressure together with retinal haemorrhages or exudates with or without papilloedema (grades III or IV hypertensive retinopathy); and may constitute a hypertensive emergency or crisis when complicated by evidence of end-organ damage including microangiopathic haemolysis, encephalopathy, left ventricular failure, and renal failure. Though reversible, it remains a significant cause of end-stage renal failure, and of cardiovascular and cerebrovascular morbidity and mortality in developing countries.MH can complicate pre-existing hypertension arising from diverse aetiologies, but most commonly develops from essential hypertension. The absolute level of blood pressure appears not to be critical to the development of MH, but the rate of rise of blood pressure may well be relevant in the pathogenesis. The pathogenesis of this transformation remains unclear.The pathological hallmark of MH is the presence of fibrinoid necrosis (medial vascular smooth muscle cell necrosis and fibrin deposition within the intima) involving the resistance arterioles in many organs. Fibrinoid necrosis is not specific to MH and this appearance is seen in other conditions causing a thrombotic microangiopathy such as haemolytic uraemic syndrome, scleroderma renal crisis, antiphospholipid syndrome, and acute vascular rejection post transplant. MH can both cause a thrombotic microangiopathy (TMA) but can also complicate underlying conditions associated with TMA.The pathophysiological factors that interact to generate and sustain this condition remain poorly understood. Risk factors include Afro-Caribbean race, smoking history, younger age of onset of hypertension, previous pregnancy, and untreated hypertension associated with non-compliance or cessation of antihypertensive therapy.Evidence from clinical studies and animal models point to a central role for the intrarenal renin–angiotensin system (RAS) in MH; there is good evidence for renal vasoconstriction and activation of the renal paracrine RAS potentiating MH once established; however, there may also be a role in the predisposition of MH suggested by presence of increased risk conferred by an ACE gene polymorphism in humans and polymorphisms for both ACE and AT1 receptor in an animal model of spontaneous MH. Other vasoactive mediators such as the endothelin and the inflammatory response may be important contributing to and increasing endothelial damage. There have been no randomized controlled trials to define the best treatment approach, but progressive lowering of pressures over days is considered safest unless made more urgent by critical clinical state. It seems logical to introduce ACE inhibition cautiously and early, but in view of the risk of rapid pressure lowering some recommend delay.
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Farmakis, Dimitrios, John Parissis, and Gerasimos Filippatos. Acute heart failure: epidemiology, classification, and pathophysiology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0051.
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Acute heart failure is defined as the rapid development or change of symptoms and signs of heart failure that requires urgent medical attention and usually hospitalization. Acute heart failure is the first reason for hospital admission in individuals aged 65 or more and accounts for nearly 70% of the total health care expenditure for heart failure. It is characterized by an adverse prognosis, with an in-hospital mortality rate of 4-7%, a 2-3-month post-discharge mortality of 7-11%, and a 2-3-month readmission rate of 25-30%. The majority of patients have a previous history of heart failure and present with normal or increased blood pressure, while about half of them have a preserved left ventricular ejection fraction. A high prevalence of cardiovascular or non-cardiovascular comordid conditions is further observed, including coronary artery disease, arterial hypertension, atrial fibrillation, diabetes mellitus, renal dysfunction, chronic lung disease, and anaemia. Different classification systems have been proposed for acute heart failure, reflecting the clinical heterogeneity of the syndrome; the categorization to acutely decompensated chronic heart failure vs de novo acute heart failure and to hypertensive, normotensive, and hypotensive acute heart failure are among the most widely used and clinically relevant classifications. The pathophysiology of acute heart failure involves several pathogenetic mechanisms, including volume overload, pressure overload, myocardial loss, and restrictive filling, while several cardiovascular and non-cardiovascular causes or precipitating factors lead to acute heart failure through a single of these mechanisms or a combination of them. Regardless of the underlying mechanism, peripheral and/or pulmonary congestion is the hallmark of acute heart failure, resulting from fluid retention and/or fluid redistribution. Myocardial injury and renal dysfunction are also involved in the precipitation and progression of the syndrome.
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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