Veins pulmonary

Pulmonary perfusion rate Volumetric flow rate within the pulmonary veins. 

Abnormal initiation of electrical impulses occurs as a result of abnormal automaticity. If the automaticity of the SA node increases, this results in an increased rate of generation of impulses and a rapid heart rate (sinus tachycardia). If other cardiac fibers become abnormally automatic, such that the rate of initiation of spontaneous impulses exceeds that of the SA node, other types of tachyarrhythmias may occur. Many cardiac fibers possess the capability for automaticity, including the atrial tissue, the AV node, the Purkinje fibers, and the ventricular tissue. In addition, fibers with the capability of initiating and conducting electrical impulses are present in the pulmonary veins. Abnormal atrial automaticity may result in premature atrial contractions or may precipitate atrial tachycardia or atrial fibrillation (AF) abnormal AV nodal automaticity may result in junctional tachycardia (the AV node is also sometimes referred to as the AV junction). Abnormal automaticity in the ventricles may result in ventricular premature depolarizations (VPDs) or may precipitate ventricular tachycardia (VT) or ventricular fibrillation (VF). In addition, abnormal automaticity originating from the pulmonary veins is a precipitant of AF. 

O Atrial fibrillation may be caused by both abnormal impulse formation and abnormal impulse conduction. Traditionally, AF was believed to be initiated by premature impulses initiated in the atria. However, it is now understood that in many patients AF is triggered by electrical impulses generated within the pulmonary veins.20 These impulses initiate the process of reentry within the atria, and AF is believed to be sustained by multiple reentrant wavelets operating simultaneously within the atria.21 Some believe that, at least in some patients, the increased automaticity in the pulmonary veins may be the sole mechanism of AF and that the multiple reentrant wavelet hypothesis may be incorrect.21 However, the concept of multiple simultaneous reentrant wavelets remains the predominant hypothesis regarding the mechanism of AF. 

The semilunar valves separate the ventricles from their associated arteries. The pulmonary valve is found between the right ventricle and the pulmonary artery and the aortic valve is found between the left ventricle and the aorta. These valves prevent backward flow of blood from the pulmonary artery or the aorta into their preceding ventricles when the ventricles relax. The semilunar valves also have three cusps. There are no valves between the venae cavae or the pulmonary veins and the atria into which they deliver blood. The closure of the valves causes the "lub-dub" associated with the heart beat. Tire first heart sound, or the "lub," occurs when the ventricles contract and the AV valves close. The second heart sound, or the "dub," occurs when the ventricles relax and the semilunar valves close. 

The value for Cc o2 cannot be calculated in this way very easily as a sample is technically difficult to take without a catheter in the pulmonary vein. It is, therefore, assumed to be in equilibrium with the Pao2, which, in turn, is given by the alveolar gas equation. 

First level of thoracic vessels Aorta, pulmonary trunk, ductus arteriosus, atria, bronchus, pulmonary vein and arteries, and vena cava (see Note 11). 

Although heart disease commonly affects the entire myocardium, congestive heart failure is sometimes divided into left and right heart failure (Fig. 24—2). In left heart failure, the left atrium and ventricle are unable to adequately handle the blood returning from the lungs. This causes pressure to build up in the pulmonary veins, and fluid accumulates in the lungs. Consequently, left heart failure is associated with pulmonary edema (see Fig. 24—2 A). 

The lungs are covered extensively by a vast network of blood vessels, and almost all the blood in circulation flows through lungs. Deoxygenated blood is supplied to the lungs by the pulmonary artery. The pulmonary veins are similar to the arteries in branching, and their tissue structure is similar to that of systemic circulation. The total blood volume of the lungs is about 450 mL, which is about 10 percent of total-body blood volume.118... 

Diagnostic supraventricular or ventricular induction Endocavitary ablation procedure (including pulmonary vein isolation)... 

The treatment of AF entered a new era after the publication of the landmark observations of Haissaguerre et al (19). Both segmental ostial catheter ablation (20) and left atrial encircling ablation of the pulmonary veins (PVs) (21) have been reported to be successful in the treatment of AF Radiofrequency (RF) ablation is a highly effective therapeutic approach in the treatment of typical isthmus- dependent AFL (22). 

Haissaguerre M, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med 1998 339(I0) 659 666. 

Haissaguerre M, et al. Mapping-guided ablation of pulmonary veins to cure atrial fibrillation. Am J Cardiol 2000 86(9 Suppl l) K9-KI9. 

Pappone C, et al. Atrial electroanatomic remodeling after circumferential radiofrequency pulmonary vein ablation efficacy of an anatomic approach in a large cohort of patients with atrial fibrillation, Circulation 2001 104(21) 2539—2544. 

Kok LC, et al, Cerebrovascular complication associated with pulmonary vein ablation. J Cardiovasc Electrophysiol 2002 ... 

Marrouche Np et al, Phased-array intracardiac echocardiography monitoring during pulmonary vein isolation in patients with atrial fibrillation impact on outcome and complications. Circulation 2003 107(21 ) 2710-271 6. 

Made L, et al, Electrophysiologically guided pulmonary vein isolation during sustained atrial fibrillation. J Cardiovasc Electrophysiol 2003 14(3) 255-260. 

Pappone C, et al. Circumferential radiofrequency ablation of pulmonary vein ostia A new anatomic approach for curing atrial fibrillation. Circulation 2000 102(21 ) 261 9-2628. HohnloserSH, Kuck KH, LilienthalJ. Rhythm or rate control in atrial fibrillation—Pharmacological Intervention in Atrial Fibrillation (PIAF) a randomised trial. Lancet 2000 356(9244) 1789-1794. 

Kaneta S, Satoh K Kano S, et al. All hydrophobic HMG-CoA reductase inhibitors induce apoptotic death in rat pulmonary vein endothelial cells. Atherosclerosis, 2003, 170, 237-243. 

Cardiac output can be measured using dye- or thermal-dilution techniques or by placement of an electromagnetic flow probe around the pulmonary artery. Insertion of a pressure transducer or fluid-filled catheter into the pulmonary artery and pulmonary vein allows for the calculation of pulmonary vascular resistance. The measurement of flow through the proximal aorta may also be useful but does not include coronary blood flow and as such is not equivalent to... 

Q3 The red cell moves from the inferior vena cava to the right atrium, into the right ventricle and through the pulmonary artery into the arteries, capillaries and veins of the lung. From the lung it re-enters the heart via the pulmonary vein and travels through the L atrium and L ventricle before entering the aorta. 

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