The transport and exchange systems: respiratory and cardiovascular
Nick Draper, Helen Marshall in Exercise Physiology, 2014
The SA node, situated on the right atrial wall, stimulates autorhythmic contraction of the heart. This means that even without nervous stimulation from the autonomic nervous system the SA node, as the heart’s pacemaker, propagates contraction of the heart at rate of around 100 beats per minute. Nervous stimulation of the SA node via the parasympathetic division slows the natural rhythm of the SA node to around 70–75 beats per minute and the effects of the sympathetic nervous system and the release of the hormone adrenalin during exercise can increase SA node rhythm to an individual’s maximum heart rate. The SA node triggers an action potential through the muscle fibres of the atria causing them to contract and eject blood into the ventricles of the heart. The spread of the action potential through the atria reaches the AV node and this triggers the release of an action potential through the atrioventricular bundle (bundle of His) to the Purkinje fibres. The Purkinje fibrespropagate the action potential to the ventricular cardiac muscle initiating contraction from the apex of the heart. The location of the Purkinje fibres and the nature of cardiac muscle fibres result in a twisting-squeezing contraction by the ventricles, ejecting blood from within. The steps involved in the spread of stimula-tion across the heart are illustrated in Figure 6.19a.
Renal, Cardiovascular, and Pulmonary Functions of Dopamine
Nira Ben-Jonathan in Dopamine, 2020
The cardiovascular system is composed of the heart and the circulatory system. The heart, composed of ventricles and atria, works as a pump that pushes blood to organs, tissues, and cells. The blood delivers oxygen and nutrients to every cell in the body and removes the carbon dioxide and waste products made by those cells. The muscle mass of the heart, the myocardium, shares structural and functional characteristics of both smooth and skeletal muscle. The cardiomyocytes are rather small cells that form the highly branched network of the functional syncytium, which acts together mechanically and electrically. The atrial and ventricular muscle tissue are structurally similar but differ in their electrical properties. In addition to these, the heart has conducting tissue (Purkinje fibers) which is adapted for rapid and efficient conduction of action potential as well as sinoatrial and atrioventricular nodes that are involved in the initiation and conduction of the heartbeat.
Cardiovascular System and Muscle
George W. Casarett in Radiation Histopathology: Volume II, 2019
The endocardium, the thin layer of the heart wall, is analogous to the inner or intimai layer of blood vessels. It is lined at the lumenal surface by simple flat epithelium (ordinary vascular endothelium) continuous with the endothelium of the blood vessels entering and leaving the heart. The endothelium usually rests on a thin subendothelial layer of loose connective tissue, which in turn lies on a thick connective tissue layer containing numerous elastic elements and, in some places, in the peripheral parts of the layer, some smooth muscle fibers as well. Except for regions of papillary muscles and cordae tendinae, there is also a subendocardial layer of loose connective tissue between the endocardium and the myocardium. This subendocardial layer contains blood vessels, nerves, and branches of the heart’s conduction system; the Purkinje fibers, a net of atypical muscle fibers of the impulse-conducting system, are found here, especially in the regions of interventricular septa.
De Winter electrocardiographic pattern in a young patient with acute myocardial infarction
Published in Baylor University Medical Center Proceedings, 2023
De Winter et al suggested different explanations for this ECG pattern. The presence of an anatomical variant of the Purkinje fibers, with endocardial conduction delay, could be a mechanism. Alternatively, ischemic ATP depletion may lead to lack of activation of sarcolemmal ATP-sensitive potassium channels, which can explain the lack of ST segment elevation, as has been shown in KATP knockout animal models of acute ischemia.3 Verouden et al suggested that the area of transmural ischemia might be so large that the injury current is directed toward lead aVR and away from the precordial leads.4 Some patients exhibiting the de Winter’s pattern who are not immediately reperfused may go on to develop overt ST elevation as well as Q waves.5–7 Many patients show a static pattern until the time of reperfusion despite ongoing ischemia for prolonged periods of time. This suggests that this pattern may lie somewhere along the continuum of ischemic ECG changes between subendocardial ischemia and the transmural infarction associated with ST elevation.7
Predicting the cardiac toxicity of drugs using a novel multiscale exposure–response simulator
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2018
Francisco Sahli Costabal, Jiang Yao, Ellen Kuhl
the L-type calcium current 1, right, illustrates the single-cell action potential for human Purkinje cells. Figure 2 shows the distribution of the Purkinje fiber network across the endocardial wall.
Histopathology of the Conduction System in Long QT Syndrome
Published in Fetal and Pediatric Pathology, 2022
Alexandra Rogers, Rachel Taylor, Janet Poulik, Bahig M. Shehata
The examination of the conduction system follows a specific protocol at our institution. Following IRB approval for this study, we used this standard procedure to examine section(s) from the SA node, AV node, and internodal tracts from the superior aspect to inferior aspect. We evaluated the bundle of His and Purkinje fibers from routine sections obtained from the right and left ventricles. All sections were stained with H&E and Masson Trichrome. The matched controls with comparable age, sex, and ethnic background who died of extracardiac causes were evaluated using the same methods. Depending on the size of a heart, between one to two blocks of the SA node can normally be evaluated. Here, we were able to section one block of the SA node which contained two to three fragments of tissue. Two blocks from the AV node containing three to four pieces of tissue were also evaluated. The thickness and amount of fibrosis of the conduction system fibers from the LQTS patients were compared to controls. Fibrosis was quantified by pathologist visualization of increased Trichrome distribution in the three LQTS patients compared to controls. Comparison of fiber size (atrophy) was performed with an eyepiece containing a microscale. Four measurements were taken from each photographed section of cardiac tissue. The number four was selected due to limitation of the amount of cardiac fibers in the internodal tracts. One-sided student’s t-tests were performed to determine statistical significance of fiber size in our LQTS patients against control patients. With degrees of freedom = 3, statistical significance with a p-value of 0.05 is proven with a t-test value less (more negative) than −3.182.
Related Knowledge Centers
- Endocardium
- Histology
- Membrane Potential
- Ventricle
- Heart
- Cardiac Muscle
- Mitochondrion
- Cardiac Action Potential
- Cardiac Conduction System
- Cardiac Rhythmicity