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Right atrium

Placement of vascular access ports is similar to that of a long-term indwelling arterial catheter. A small incision is made over the selected vein and a second incision is made lower in the anterior chest to create a pocket to house the port. The catheter is tuimeled subcutaneously from its entry point into the vein with the tip inside the right atrium. The final position of the catheter is verified by fluoroscopy, secured with sutures, and the subcutaneous pocket is closed. The port septum is easily palpable transcutaneously, and the system may be used immediately. A surgeon typically inserts the vascular access port in an outpatient setting. [Pg.184]

Catheter tip should not be extended into the right atrium ° Maximum rate is 40 mEq/h... [Pg.164]

The sinoatrial (SA) node is located in the wall of the right atrium near the entrance of the superior vena cava. The specialized cells of the SA node spontaneously depolarize to threshold and generate 70 to 75 heart beats/ min. The "resting" membrane potential, or pacemaker potential, is different from that of neurons, which were discussed in Chapter 3 (Membrane Potential). First of all, this potential is approximately -55 mV, which is less negative than that found in neurons (-70 mV see Figure 13.2, panel A). Second, pacemaker potential is unstable and slowly depolarizes toward threshold (phase 4). Two important ion currents contribute to this slow depolarization. These cells are inherently leaky to sodium. The resulting influx of Na+ ions occurs through channels that differ from the fast Na+ channels that cause rapid depolarization in other types of excitable cells. Toward the end of phase... [Pg.169]

An internodal conduction pathway also extends from the SA node and transmits the impulse directly to the atrioventricular (AV) node. This node is located at the base of the right atrium near the interventricular septum, which is the wall of myocardium separating the two ventricles. Because the atria and ventricles are separated from each other by fibrous connective tissue, the electrical impulse cannot spread directly to the ventricles. Instead, the AV node serves as the only pathway through which the impulse can be transmitted to the ventricles. The speed of conduction through the AV node is slowed, resulting in a slight delay (0.1 sec). The cause of this AV nodal delay is partly due to the smaller fibers of the AV node. More importantly, however, fewer gap junctions exist between the cells of the node, which... [Pg.171]

Figure 13.3 Route of excitation and conduction in the heart. The heart beat is initiated in the sinoatrial (SA) node, or the pacemaker, in the right atrium of the heart. The electrical impulse is transmitted to the left atrium through the interatrial conduction pathway and to the atrioventricular (AV) node through the intemodal pathway. From the AV node, the electrical impulse enters the ventricles and is conducted through the AV bundle, the left and right bundle branches, and, finally, the Purkinje fibers, which terminate on the true cardiac muscle cells of the ventricles. Figure 13.3 Route of excitation and conduction in the heart. The heart beat is initiated in the sinoatrial (SA) node, or the pacemaker, in the right atrium of the heart. The electrical impulse is transmitted to the left atrium through the interatrial conduction pathway and to the atrioventricular (AV) node through the intemodal pathway. From the AV node, the electrical impulse enters the ventricles and is conducted through the AV bundle, the left and right bundle branches, and, finally, the Purkinje fibers, which terminate on the true cardiac muscle cells of the ventricles.
In addition to serving as blood reservoirs, veins help to regulate cardiac output (CO) by way of changes in venous return (VR). Venous return is defined as the volume of blood that flows from the systemic veins into the right atrium per minute. As discussed in Chapter 14 (cardiac output), a healthy heart pumps all of the blood returned to it. Therefore, CO is equal to VR ... [Pg.214]

Right atrium Right ventricle Right coronary artery Inferior vena cava Marginal branch... [Pg.144]

Elementary students are taught to think of the heart as a pump built according to a single straightforward pattern any variations from the pattern which might exist would be trifling, except, of course, in "abnormal" cases. That such is far from the case is shown by the twelve variations in the right atrium of the heart (Fig. 8). The forms of the valves of the inferior vena cava vary so much and the detailed structures are so different in size and contour as to make one almost doubt that the hearts are from the same species. [Pg.48]

The c wave This results from the bulging of the tricuspid valve into the right atrium during ventricular contraction. [Pg.151]

Right atrium (RA) The pressure waveform is identical to the CVP. The normal pressure is 0-5 mmHg. [Pg.153]

Depolarisation of the membrane of the cardiomyocyte, resulting from the action potential, initiates contraction in cardiac as in skeletal muscle. This depolarisation arises in the sinoatrial node, a small group of cells in the right atrium, and then spreads through the heart causing, first, the muscles in the atria to contract and then the muscles in the ventricles to contract. [Pg.525]

Rump CL, Bohmann C, Schaible U, Schollhorn J, Limberger N (1995) ajc-Adrenoceptor-modulated release of noradrenaline in human right atrium. Br J Pharmacol 116 2617-2624... [Pg.184]

Fig. 4. Preparation of the fixed heart for visceral examination. Cut 1 Ventral view Open the right ventricle along the septum in baso-apical direction going trough the aorta and the truncus pulmonalis (cross pulmonary valve) dorsal view open right ventricle near the septum from the heart apex towards the right atrium (through tricuspidal valve). Cut2 Ventral view Open the left ventricle along the septum from the heart apex into the left atrium (through bicuspidal valve) dorsal view cut the wall of left ventricle from the heart apex towards the left atrium. Fig. 4. Preparation of the fixed heart for visceral examination. Cut 1 Ventral view Open the right ventricle along the septum in baso-apical direction going trough the aorta and the truncus pulmonalis (cross pulmonary valve) dorsal view open right ventricle near the septum from the heart apex towards the right atrium (through tricuspidal valve). Cut2 Ventral view Open the left ventricle along the septum from the heart apex into the left atrium (through bicuspidal valve) dorsal view cut the wall of left ventricle from the heart apex towards the left atrium.
Early evidence that prejunctional histamine H3-receptors may modulate the sympathetic nerve activity on the heart was provided by Luo et al., (1991). These authors clearly stated that the selective H3-agonist (R)a-methylhistamine attenuates the inotropic response induced by transmural stimulation of the adrenergic nerve terminals in the isolated right atrium, without affecting basal contractile force of the preparation or the positive inotropic effect elicited by exogenous noradrenaline. The effect of (R)a-methylhistamine, which is not modified by Hi and H2-receptor blockade, was reversed by the specific H3-receptor antagonist thioperamide, at concentrations which do not influence the inhibitory activity mediated by other presynaptic receptors, like a2-adrenoceptors. [Pg.78]

Guinea pig Right atrium Adrenergic nerves Neurogenic inotropic response inhibition Luo et al., 1991... [Pg.82]

Right atrium Left atrium Adrenergic nerves Neurogenic chronotropic response Neurogenic inotropic response NA release (ES-evoked) inhibition inhibition inhibition Endou et al., 1994... [Pg.82]


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See also in sourсe #XX -- [ Pg.165 ]

See also in sourсe #XX -- [ Pg.4 , Pg.64 ]




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Atria

Guinea pig right atria

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