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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.
The patient with acute respiratory problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Oxygen delivery to rapidly metabolising cells must be optimised if cellular demand (VO2) is to be met. It is useful to think of the steps facilitating O2 delivery as connecting links in a chain (see Figure 5.1). The first link is at the pulmonary level, where external respiration with gaseous exchange takes place. Additional links include the haemoglobin, which carry O2 molecules, cardiac function, which must maintain the systemic circulation, and the integrity of the microcirculation, which must facilitate gaseous exchange at cellular level. If any link is weak, then O2 delivery may well be reduced.
Basic medicine: physiology
Published in Roy Palmer, Diana Wetherill, Medicine for Lawyers, 2020
The heart is the muscular pump that drives blood around the body. It has long been known that blood will spurt from a cut artery under high pressure, but it was thought to oscillate to and fro until William Harvey showed that blood circulates from small arterial branches through tiny vessels in the tissues (capillaries) before being collected by veins and returned to the heart The dynamo behind this circulation is the heart, which contracts 60–80 times per minute throughout an individual’s life. The heart contains four chambers and is responsible for two separate circulatory systems (Figure 1.1). The systemic circulation supplies all the organs in the body with oxygenated blood, while the pulmonary circulation delivers exhausted blood to the lungs where it is replenished with oxygen. The heart chambers comprise two atria which collect the blood and pass it through valves into the two ventricles, which contract forcefully to distribute blood throughout the body. The cardiac cycle consists of diastole, the phase of filling, and systole in which contraction of the atria is immediately followed by contraction of the ventricles.
Neurologic conditions in Hereditary Hemorrhagic Telangiectasia with pulmonary arteriovenous malformations: Database study
Published in Canadian Journal of Respiratory, Critical Care, and Sleep Medicine, 2023
Chester Lau, Joel Agarwal, Ben Vandermeer, W. Ted Allison, Thomas Jeerakathil, Dilini Vethanayagam
An estimated 35–40% of HHT subjects have pulmonary arteriovenous malformations (PAVMs), consisting of abnormal connections between the feeding artery(ies) and draining vein(s).9 These fragile and dilated vessels allow blood contents from the pulmonary circulation to bypass capillary beds and travel toward the systemic circulation, preventing gas exchange.9,12 PAVMs result in the physiologic consequence of intrapulmonary right-to-left shunt (RLS), causing air and/or particulate emboli to traverse through the bloodstream into the cerebral vessels.13 This may lead to a plethora of neurological conditions, including migraines, seizures, ischemic (embolic) stroke, transient ischemic attack (TIA) and cerebral abscess.14 These neurologic conditions may also be dependent on PAVM shunt grade.9,13,15–17 Other clinical features of PAVMs include clubbing, dyspnea and hypoxemia; however, many patients with PAVMs are asymptomatic.12
Right Ventricular-Pulmonary Arterial Coupling and Outcomes in Heart Failure and Valvular Heart Disease
Published in Structural Heart, 2021
Bahira Shahim, Rebecca T. Hahn
Compared with the systemic circulation, pulmonary circulation has a much lower vascular resistance, greater pulmonary artery distensibility, and a lower peripheral pulse wave reflection coefficient.12 Pulmonary vascular impedance reflects the opposition to pulsatile flow, and determines, together with pulmonary vascular resistance (PVR), the RV afterload.9 RV afterload is reflected by arterial elastance (Ea), a load-independent measure of “total” ventricular afterload (both pulsatile and resistive components). It is measured as RV end-systolic pressure divided by stroke volume.24 PVR is a measure of the resistance of both capillaries and veins and is calculated as the difference between the mean pulmonary arterial pressure and pulmonary capillary wedge pressure, divided by the cardiac output. In the normal RV, mean pulmonary artery pressure is a reasonable approximation of end-systolic pressure. Thus, in the normal RV Ea could be estimated as PVR x heart rate.25 Although PVR represents only the resistive component of Ea, and pulmonary arterial compliance represents the pulsatile component, the latter contributes only ~23% to total afterload26 in normal patients and those with arterial pulmonary hypertension (PH) and support the use of the simplified formula. However, if post-capillary PH is present, the pulsatile component of Ea increases27 and stroke work is significantly reduced.28 Taking into account both resistive and pulsatile components of Ea may then be more important.
Serum heart-type fatty acid-binding protein as a predictor for the development of sepsis-associated acute kidney injury
Published in Expert Review of Molecular Diagnostics, 2019
Daishan Jiang, Mengzhu Shen, Xiaoyu Yuan, Meng Wang, Shanfeng Li, Wei Jiang, Zhongxia Zhou, Peipei Xi, Ting Wang, Yan Shen
Preceding studies have validated that the level of HFABP increased in sepsis, but the mechanisms remain unclear [22]. Myocardial injury and cardiac dysfunction, which are common complications of sepsis, with an incidence of about 50% in septic shock patients may cause the elevation of HFABP [23]. Besides the direct myocardial damage caused by bacterial toxins, the abnormal hemodynamics and changes of myocardial blood flow caused by sepsis are well established [24]. Additionally, HFABP elevation might be caused by mechanical stretching such as ischemic stress on account for cardiogenic shock. Moreover, glycogen and lipid decomposition in sepsis patients can directly increase the level of free fatty acids, while lipid disorders and free radical release can also lead to an increase of HFABP levels [25]. In addition to the rise of HFABP caused by the change of production and release, decreased renal function will inevitably decline HFABP excretion and increase its plasma concentration [26]. As an essential component of the systemic circulation, kidney usually suffers dysfunction accompanied by diseases of other systems multiple organ failure such as severe cardiovascular insufficiency. Heart and kidney, as vital organs in the circulatory system, often interact as both cause and effect which is manifested as type V ‘cardiorenal syndrome’.