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Electrophysiology
Published in A. Bakiya, K. Kamalanand, R. L. J. De Britto, Mechano-Electric Correlations in the Human Physiological System, 2021
A. Bakiya, K. Kamalanand, R. L. J. De Britto
The cardiopulmonary system consists of blood vessels that carry nutrients and oxygen to the tissues and removes carbon dioxide from the tissues in the human body (Humphrey & McCulloch, 2003; Alberts et al., 1994). Blood is transported from the heart through the arteries and the veins transport blood back to the heart. The heart consists of two chambers on the top (right ventricle and left ventricle) and two chambers on the bottom (right atrium and left atrium). The atrioventricular valves separates the atria from the ventricles. Tricuspid valve separates the right atrium from the right ventricle, mitral valve separates the left atrium from the left ventricle, pulmonary valve situates between right ventricle and pulmonary artery, which carries blood to the lung and aortic valve situated between the left ventricle and the aorta which carries blood to the body (Bronzino, 2000). Figure 3.9 shows the schematic diagram of heart circulation and there are two components of blood circulation in the system, namely, pulmonary and systemic circulation (Humphrey, 2002; Opie, 1998; Milnor, 1990). In pulmonary circulation, pulmonary artery transports blood from heart to the lungs. The blood picks up oxygen and releases carbon dioxide at the lungs. The blood returns to the heart through the pulmonary vein. In the systemic circulation, aorta carries oxygenated blood from the heart to the other parts of the body through capillaries. The vena cava transports deoxygenated blood from other parts of the body to the heart.
Pruned Tree and Leafless Tree Signs
Published in Michael E. Mulligan, Classic Radiologic Signs, 2020
This angiographic finding described by Evans has also been applied to plain chest radiographs. It is now used to describe the findings of pulmonary artery hypertension from any cause. Evans’ said, ‘It is opined here that the same mechanism is operating in most examples of gross pulmonary hypertension.’ The pruned-tree sign should not be confused with the bronchographic ‘leafless-tree’ sign of bronchioloalveolar cell carcinoma2.
Pulmonary Hypertension in Pregnancy
Published in Afshan B. Hameed, Diana S. Wolfe, Cardio-Obstetrics, 2020
If pulmonary hypertension is suspected, an echocardiogram is indicated. Echocardiography can estimate pulmonary artery pressures. Additional findings on echocardiogram related to severe pulmonary hypertension include right ventricular enlargement and tricuspid regurgitation. However, it is important to recognize that echocardiography is a screening tool and does not definitively diagnose pulmonary hypertension. It may especially have a higher false positive rate in detecting pulmonary hypertension in pregnant patients [11,12]. This may be related to the increased blood volume and decrease in systemic vascular resistance that are associated with pregnancy. This may lead to an increase in size of the inferior vena cava, thus exaggerating the estimated right atrial pressure and pulmonary artery systolic pressure. Right heart catheterization is required for definitive diagnosis of pulmonary hypertension and to accurately determine the severity. However, cardiac catheterization is an invasive procedure that carries a 1%–5% risk of complications including pneumothorax, bleeding, and infection [11]. Therefore, the indications for right heart catheterization are based on initial echocardiographic findings. If echocardiogram shows findings suggestive of pulmonary hypertension (elevated peak tricuspid regurgitation velocity, flattening of the interventricular septum, increased pulmonary artery diameter, etc.), then further investigation of pulmonary hypertension with right heart catheterization is indicated [3,10].
Management of congenitally corrected transposition from fetal diagnosis to adulthood
Published in Expert Review of Cardiovascular Therapy, 2023
Congenitally corrected transposition of the great arteries (ccTGA) is a complex congenital heart disease first described from an autopsy by a Bohemian pathologist working in Vienna, Karl von Rokitansky, in 1875 [1]. The anomaly is characterized by atrioventricular and ventriculo-arterial discordance [2]. Deoxygenated blood from the right atrium flows through the mitral valve into the morphological left ventricle, which gives rise to the pulmonary artery. Then, oxygenated blood flows into the left atrium that communicates with the morphological tricuspid valve and right ventricle, that is connected to the aorta. The aorta is located usually anterior and to the left. Consequently, the double discordance results in hemodynamic compensation, but the morphologically right ventricle works as systemic ventricle (systemic right ventricle, sRV). The most common anomalies are ventricular septal defect, pulmonary or subpulmonary stenosis, and systemic atrioventricular (morphological tricuspid) valve abnormalities [3] (Table 1). Additionally, cardiac malposition (dextrocardia or mesocardia) occurs in up to one-third of the patients. Associated malformations, especially the Ebstein-like anomaly of the systemic atrioventricular valve, have a significant impact on the clinical course of the disease. Conduction disturbances, including complete atrio-ventricular block, are another common cause of increased morbidity in ccTGA patients and might be the first manifestation of the disease.
Data-driven monitoring in patients on left ventricular assist device support
Published in Expert Review of Medical Devices, 2022
Lieke Numan, Mehran Moazeni, Marish I.F.J. Oerlemans, Emmeke Aarts, Niels P. Van Der Kaaij, Folkert W. Asselbergs, Linda W. Van Laake
In addition to noninvasive tools, invasive or implantable devices may be used to remotely monitor LVAD patients. Although not frequently used in combination with LVADs, the safety and feasibility of the CardioMEMS (Abbott Inc, Atlanta, GA, USA) in LVAD patients have been demonstrated [54]. The CardioMEMS, which measures pulmonary artery pressure, provides daily insight into a patient’s fluid status, enabling optimization of patients prior to LVAD implantation. In addition, pulmonary artery pressure lowering medication can be monitored. Several complications such as tamponade, aortic valve regurgitation, pump thrombosis, right heart failure or significant hemodynamic arrhythmias will lead to either congestion or reduced pulmonary artery pressure, which may be detected using the CardioMEMS sensor [55]. Likewise, it allows for telemonitoring after LVAD implantation. Zhou et al. incorporated a pressure sensor into the LVAD inlet in an experimental set-up. This enables a direct measure of the left ventricle function during LVAD support [56]. They stated that this is the start of a closed loop speed control based on left ventricular pressure. Although pressure sensors or flow probes may provide valuable information, durability, and reliability should be tested extensively in-vivo. The more components a device includes, the more prone it is to malfunction and failure. Future studies are warranted to prove its added value. Noteworthy, cost-effectiveness is not touched upon yet, and we may need to focus on more accessible and noninvasive telemonitoring tools first.
Pulmonary tumor thrombotic microangiopathy: A systematic review of the literature
Published in Canadian Journal of Respiratory, Critical Care, and Sleep Medicine, 2021
L. V. Morin-Thibault, D. Wiseman, P. Joubert, R. Paulin, S. Bonnet, S. Provencher
Furthermore, the mechanisms underlying the development of severe fibrocellular intimal proliferation in only a subset of patients with cancer and pulmonary tumor emboli remain elusive. However, in addition to mechanical occlusion of the pulmonary arterial bed, the increased pulmonary vascular resistance is thought to result from the dysregulation of signaling pathways leading to vascular remodeling. Intriguingly, apart from the presence of tumor cells and the variable degree of thrombus, the distal pulmonary artery remodeling resembles histologic findings documented in idiopathic pulmonary arterial hypertension (PAH).29 In addition, the overexpression of VEGF, PDGF and osteopontin, reported to be involved in the pathogenesis of PTTM,30 have repeatedly been observed in PAH, these pathways being involved in the pathophysiology of its development and progression.29,31–33 Pulmonary vascular cells in PAH also share numerous similarities with cancer cells, including a pro-proliferative and antiapoptotic phenotype and metabolism favoring an anaerobic metabolism (i.e. Warburg effect), fueling the cancer theory of PAH.34 Activation of local thrombotic and inflammatory cascades are also observed in both conditions.35 Whether these conditions share common pathophysiologic pathways, however, has yet to be confirmed.