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Most of these tumors spread by lymphatic spread to the para-aortic lymph nodes [1 ] best purchase for ponstel quad spasms after acl surgery. Pancreatic Cancer Pancreatic cancer is the second most common gastrointestinal malignancy and is the fifth leading cause of cancer-related death order 500 mg ponstel otc back spasms 8 weeks pregnant. The majority of cases are ductal adeno- carcinomas (exocrine ductal epithelium buy ponstel with a visa muscle relaxant for children, 95 % of cases). Lymph node metastases are common in pancre- atic and duodenal cancer and they carry a poor prognosis [31, 32]. Lymphatic Spread and Nodal Metastasis 83 Lymphatic Spread and Nodal Metastasis Lymphatic drainage of the head of the pancreas is different from that of the body and tail (Table 3. The head of the pancreas and the duodenum share similar drainage pathways by following arteries around the head of the pancreas [32, 33]. They can be divided into three major routes: the gastroduodenal, the inferior pancreaticoduodenal, and the dorsal pancreatic: 1. Around the head of the pancreas, multiple lymph nodes can be found between the pancreas and duodenum above and below the root of the transverse mesocolon and anterior and posterior to the head of the pancreas. Although many names are used for these nodes such as the inferior and superior pancreaticoduodenal nodes (see Fig. The gas- troduodenal route collects lymphatics from the anterior pancreaticoduodenal nodes (see Figs. The inferior pancreaticoduodenal route also receives lymphatic drainage from the anterior and posterior pancreaticoduodenal nodes by following the inferior pancreaticoduodenal artery to the superior mesenteric artery node. Occasionally, they may also drain into the node at the proximal jejunal mesentery. It collects lymphatics along the medial border of the head of the pancreas and follows the branch of the dorsal pancreatic artery to the superior mesenteric artery or celiac node. The lymphatic drainage of the body and tail of the pancreas follows the dorsal pancreatic artery, the splenic artery, and vein to the celiac lymph node. The lymphatic drainage of the body and tail of the pancreas follows the dorsal pancreatic artery, the splenic artery, and vein to the celiac lymph node. Because of the lack of accu- racy, peripancreatic lymph nodes and the nodes along the gastroduodenal artery and inferior pancreaticoduodenal artery are included in radiation field, and they are rou- tinely resected at the time of pancreaticoduodenectomy. However, it is important to note when an abnormal node, such as one with low density and/or irregular border, is detected beyond the usual drainage basin and outside the routine surgical or radia- tion field, such as in the proximal jejunal mesentery or at the base of the transverse mesocolon, as these can be the site of recurrent disease [1]. Noninvasive detection of clinically occult lymph- node metastases in prostate cancer. Prognostic significance of lymph node invasion in patients with metastatic renal cell carcinoma: a population-based perspective. Stage-specific effect of nodal metastases on survival in patients with non-metastatic renal cell carcinoma. Renal cell carcinoma with retroperitoneal lymph nodes: role of lymph node dissection. Prognostic relevance of lymph node ratio following pancreaticoduodenectomy for pancreatic cancer. Pelvic Lymph Nodes 4 A good basic understanding of the anatomy and nomenclature of the inguino-pelvic nodal groups is essential for accurate staging of male and female urogenital pelvic neoplasms. Lymph nodes are not only crucial for staging and management but are also important factors in prognosticating the disease. Classification and Anatomical Location of Pelvic Lymph Nodes Common Iliac Nodal Group The common iliac nodal group consists of three subgroups: lateral, middle, and medial (see Fig. The lateral subgroup is an extension of the lateral chain of external iliac nodes located lateral to the common iliac artery (see Figs. The medial subgroup occupies the triangular area bordered by both common iliac arteries from the aortic bifurcation to the bifurcation of common iliac artery into external and internal iliac arteries. The middle subgroup is located in the lumbosacral fossa (the area bordered posteromedially by the lower lumbar or upper sacral vertebral bodies, anterolaterally by the psoas muscle, and anter- omedially by the common iliac vessels) and between the common iliac artery and common iliac vein [1 ] M. Schematic shows the common iliac nodal group, which consists of three chains: (1) the lateral chain, which is located lateral to the common iliac artery and forms an extension from the lateral external iliac nodal chain; (2) the medial chain, which occupies the triangular area bordered by both common iliac arteries and includes nodes at the sacral promontory; and (3) the middle chain, which consists of nodes within the lumbosacral fossa. The lateral subgroup includes nodes that are located along the lateral aspect of the external iliac artery (see Fig. The middle sub- group comprises nodes located between the external iliac artery and the external iliac vein (see Fig. The medial subgroup contains nodes located medial and posterior to the external iliac vein. Schematic shows the external iliac nodal group comprising the lateral chain, positioned laterally along the external iliac artery; the middle chain, situated between the external iliac artery and external iliac vein; and the medial chain (also known as obturator nodes), positioned medial and posterior to the external iliac vein Fig. These are, as depicted, the lateral (big purple) chain, the middle (small purple ) chain, and the medial (orange) chain Classification and Anatomical Location of Pelvic Lymph Nodes 93 Fig. Among the nodes of this group, the junctional nodes are located at the junction between the internal and external iliac nodal groups [2 ]. Schematic shows the chains of internal iliac lymph nodes that accompany the visceral branches of the internal iliac vessels. The central location of the sacral nodes within the pelvis and the position of the junctional nodes between the internal and external iliac arteries are clearly visible Classification and Anatomical Location of Pelvic Lymph Nodes 99 a b Fig. The superficial inguinal nodes, which are located in the subcutaneous tissue anterior to the inguinal ligament, accompany the superficial femoral vein and the saphenous vein (see Figs. The sentinel nodes for the superficial subgroup are those situated at the saphenofemoral junction, where the great saphenous vein drains into the common femoral vein. Deep iliac circumflex artery Superficial illiac circumflex artery Inferior epigastric artery Superficial inguinal nodes Deep inguinal nodes Saphenofemoral node Fig. Schematic show the locations of the superficial and deep inguinal nodes in relation to the common femoral artery, common femoral vein, and saphenous vein. The sentinel nodes in the superficial inguinal group are those located at the saphenofemoral junction Classification and Anatomical Location of Pelvic Lymph Nodes 101 Fig. The anatomical landmarks that mark the boundary between the deep inguinal nodes and the medial chain of the external iliac nodes are the inguinal ligament and the origins of the inferior epigastric and circumflex iliac vessels [2 ]. Generally, nodes larger than 10 mm in short-axis diameter are considered enlarged for the iliac nodes and 15 mm for inguinal nodes. Shape and Margin Ovoid lymph nodes with a fatty central hilum favor a benign etiology. It has also been shown that nodes with an irregular margin are more likely to be metastatic [4 ]. Mucinous primary tumors can be associated with subtle calcification within metastatic lymph nodes. Nodal Staging It is important to note whether the nodes involved are regional or nonregional for the particular organ as lymphatic pathways and N staging varies for different tumor origins. Gynecologic Malignancies Lymph nodes, either locoregional or distant, are common sites of metastatic disease in gynecologic tumor and the nodal status is the single most important prognostic factor in most gynecologic malignancies. The upper vagina, cervix, and lower uterine body drain laterally to the broad ligament, obturator, internal and external iliac nodes, and posteriorly to the sacral nodes. The ovaries and fallopian tubes drain along the ovarian artery to the para-aortic nodes, with the lower uterine drainage, or along the round ligament. Less frequently drainage from the upper uterine body is to the iliac nodes and inguinal nodes (Table 4.

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This enzyme is absent in most somatic cells purchase ponstel without prescription xanax muscle relaxer, and hence they suffer progressive loss of telomeres cheap ponstel 500mg free shipping spasms coughing. Telomerase activity and maintenance of telomere length are essential for the maintenance of replicative potential in cancer cells order 500 mg ponstel amex muscle spasms zinc. This group includes both manganese-superoxide dismutase, which is localized in mitochondria, and copper-zinc-superoxide dismutase, which is found in the cytosol. Methenamine silver (Ref: Harsh Mohan 6/e p474) The appropriate stain is methenamine silver. The cysts, when stained with methenamine silver, have a characteristic cup or boat shape; the trophozoites are diffcult to demonstrate without electron microscopy. This defciency results in recur- rent infections with catalase-positive organisms, such as S. Key fndings in chronic granulomatous disease include lymphadenitis, hepatosplenomegaly, eczematoid dermatitis, pulmonary infltrates. Caspase-1 along with closely related caspase-11 also lead to death of the infected cell. It involves sequestration of cellular organelles into cytoplasmic autophagic vacuoles (autophagosomes) that fuse with lysosomes and digest the enclosed material. The autophagosome formation is regulated by more than a dozen proteins that act in a coordinated and sequential manner. It can be: • Acute infammation: It is of shorter duration (seconds, minutes, few hours) • Chronic infammation: It is of longer duration (weeks, months and years) The changes seen in infammation can be in the blood vessels (called vascular changes) and in the cells (called cellular changes). Vasoconstriction: It is the frstQ change in the blood vessels which is transient in nature. Vasodilation: Second change in the blood vessels lasting for a longer duration is increased vascular permeability vasodilation. It results in increased blood fow leading to redness (rubor) and the is the hallmark of acute infam- sensation of warmth (color). Increased permeability: It is the hallmark of acute infammationQ caused by separation of the endothelial cells resulting in movement of fuid, cells and proteins out of the blood vessels (collectively called as exudate). The exudate is a protein rich fuid which is responsible for the swelling (tumor) associated with an injury. The various mechanisms of increased vascular permeability are explained below: MechanisMs of increased Vascular PerMeability Mechanism caused by affected blood Properties of vessels response 1. Formation of Vasoactive mediators like Venules Rapid; endothelial gaps histamine, leukotrienes, Reversible; short (Immediate transient bradykinin and contraction of lived (15 to 30 responseQ) endothelial cell cytoskeleton minutes) 2. Direct endothelial Toxins, infections, burns, Venules, Fast and may be injury (immediate chemicals causing endothelial capillaries and long lived sustained cell necrosis and detachment arterioles responseQ) 3. Cytoskeletal Due to cytokines and hypoxia Mostly venulesQ; Reversible, reorganisation capillaries may delayed and (endothelial cell be also involved prolonged retractionQ) 4. Delayed prolonged Thermal and radiation injury Venules and Delayed and leakage induced endothelial cell damage capillaries long lived 5. Leukocyte mediated Activated leukocytes causing Venules (mostly); Late and long endothelial injury endothelial injury or detachment pulmonary and lived glomerular capillaries 6. The loss of fuid results in concentration of red cells in small vessels and is the commonest mechanism for increased permeability. Cellular Changes selectins are responsible for The sequence of events in the journey of leukocytes from the vessel lumen to the “rolling” of neutrophils. Margination: Movement of the leukocytes which are normally moving in the centre of the blood vessel towards the periphery of the blood vessel is called as margination. Rolling: It is the process of transient adhesion of leukocytes with the endothelial cells. They interact Endothelial cell expression of with the complementary molecules resulting in transient adhesion. P selectin (cd 62P) – Present on platelets and endothelial cells and interacts with sialyl lewis X receptor on leukocytes. So, these patients have recurrent bacterial infections involving skin, oral and genital mucosa, respiratory and intestinal tract; persistent leukocytosis because cells don’t marginate and a history of delayed separation of umbilical cord stumpQ is present. Patients have recurrent bacterial infections, platelet disfunction short stature, bombay blood groupQ and mental retardation. Transmigration: The step in the process of the migration of the leukocytesQ through the endothelium is called transmigration or diapedesis. Neutrophils predominate in the 32 Infammation infammatory infltrate during the frst 6 to 24 hours, then are replaced by monocytes in 24 to 48 hours (except in Pseudomonas infection in which neutrophils leukocyte diapedesis, similar predominate over 2 to 4 days). Chemotaxis: It is unidirectional movementQ of the leukocytes towards antigens/ ability, occurs predominantly in bacteria in response to certain chemicals. These chemicals are called chemotactic the venules (except in the lungs, where it also occurs in capillaries). Other actin-regulating proteins likeflamin, gelsolin, proflin, andcalmodulinalso interact Example of opsonins include antibodies, complement proteins with actin and myosin to produce contraction and cellular movement. Opsonisation: Coating of the bacteria so that they are easily phagocytosed by the white blood cells is known as opsonisation. Chemotaxis: It is unidirectional or targeted movement of the *Mnemonic corollary – friends I believe all of you have had waterballs or golgappe at some leukocytes towards antigens/ point of time in your life, u can have them both with and without water but in which condi- bacteria. Bruton’s disease is a defect Some serum proteins (like fbrinogenQ, mannose binding lectinQ and C reactive proteinQ) in maturation of the B cells in which there is absence of 7. Phagocytosis: It is the process by which bacteria are killed/eaten up by the white immunoglobulin. Mannose receptors: These bind to mannose and fucose residues of glycoproteins in microbial cell wall. Engulfment: There is formation of phagolysosome (due to fusion of the lysosomes polymerization of actin fla- ments whereas in contrast, pino- and the phagosome containing the microbe) inside the leukocytes. This is followed cytosis (cell drinking) and recep- by degranulation of leukocytes. The clinical signifcance of phagolysosome formation is appreciated in an autosomal recessive dis- order known as Chediak-Higashi syndrome. It is characterized by reduced transfer of lysosomal en- zymes to phagocytic vacuoles in phagocytes, defective degranulation, and delayed microbial killing causing increased susceptibility to infections. The polymorphs also exhibit defective random move- ments and have defective chemotaxis. Clinical features: It includes neutropenia (decreased numbers of neutrophils), albinism (due to abnor- malities in melanocytes), nerve defects, nystagmus and bleeding disorders (due to defect in neurons The leukocytes in chediak- and platelets respectively). Killing and degradation: Final step in phagocytosis is the killing of infectious organism within the leukocytes. Oxygen dependent killing mechanism There is production of microbicidal reactive oxygen species within phagocytic vesicles by the following mechanism: The fnal step in the microbial killing is due to reactive oxygen species called as ‘respiratory burst’. The initial step in this process involves the one- by the name of respiratory burst oxidase. Superoxide then undergoes a further series of reactions to produce products such as peroxide, hydroxyl radical and hypochlorite.

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The volume loss would reduce ventricular volumes and cardiopulmonary stretch receptor activity in the atria and vena cava cheap generic ponstel canada muscle relaxants yahoo answers. The splanchnic circulation is one of the key components of increased vascular resistance and recruitment of blood in the veins as part of the neural reflex defense against hypotension buy ponstel master card muscle relaxant renal failure. Sodium nitroprusside is a powerful arterial vasodilator used in cardiovascular emergencies such as acute heart failure discount ponstel on line spasmus nutans treatment. Decreased stroke volume with decreased myocardial oxygen demand The correct answer is A. A powerful arterial dilator will cause a sudden drop in arterial pressure, which, in turn, will activate the baroreceptor reflex. This reflex will result in activation of sympathetic nerves to the heart and blood vessels and a suppression of vagal activation to the heart. The result, following the initial effect of the nitroprusside, is to increase heart rate, myocardial contractility, and stroke volume. Together, these effects attenuate the initial drop in blood pressure caused by the drug. Depending on the balance between myocardial stimulatory effects on rate and contractility versus the final level of blood pressure, myocardial oxygen consumption may actually increase 1 to 2 minutes after administration of nitroprusside. An older form of treatment for severe chronic hypertension was to use combined pharmacological alpha- and beta-receptor blockade. In this condition, blood pressure regulation in the patient becomes extremely dependent on: A. Blockade of all adrenergic receptors in the body by combined drug therapy results in a “chemical” sympathectomy. Blood pressure in patients on this therapy becomes exquisitely dependent upon blood volume. Therefore, factors that affect salt and water balance in the body have profound influence over blood pressure (e. The neural arms of the chemoreceptor and central nervous system ischemic reflexes would not function well, if at all, in an individual with chemical sympathectomy. Adrenal or any other catecholamines would have limited effect on the cardiovascular system in which adrenergic receptors were blocked (although the diminution of response would depend on the level of the blockade and the magnitude of catecholamine concentration). The effect of vascular resistance on blood pressure would be markedly blunted by alpha blockade. She is given this drug as a skin patch, which is to be worn during the day and which releases small amounts of this vasodilator into her circulation continuously through the skin. She is also given nitroglycerin tablets to be taken in case of an anginal attack or as a prophylaxis against angina in anticipation of physical exertion beyond normal daily activities. During one morning, a couple of hours after applying her nitroglycerin skin patch, she takes a nitroglycerin tablet in anticipation of doing some gardening but decides to lie down for a few moments before starting work. Within 10 minutes of lying down, the patient bolts from her supine position to answer her telephone. However, within seconds of rising from the supine to the standing position, she becomes light-headed and dizzy. Her heart rate starts to increase rapidly and she can feel her heart pounding in her chest. Within a couple of steps, her vision narrows and blackens and she collapses onto the floor unconscious. Shortly after this episode, the patient regains consciousness and is able to stand only after slowly arising. What cardiovascular phenomenon is most likely responsible for the loss of consciousness in this patient? What changes in blood volume distribution normally occur immediately when one moves from a supine to a standing position? What immediate effects do these have on cardiac output and arterial blood pressure? What reflex mechanisms are brought into play in response to these changes in blood pressure? Nitroglycerin is a rapidly absorbed, quick-acting direct vasodilator that relaxes smooth muscle in veins more than arteries. How does this selective effect of nitroglycerin relate to the responses of the patient suddenly standing? Loss of consciousness can result from numerous factors, but the most likely related to the cardiovascular system is a sudden severe drop in blood pressure below the autoregulatory limit of the cerebral circulation. This would cause a drop in blood flow and oxygen supply to the brain that would likely induce neurological effects such as darkening vision, dizziness, and fainting. Upon changing from the supine to the standing position, blood tends to fall toward the lower extremities due to the influence of gravity. Blood vessels are compliant with veins being much more compliant and distensible than arteries. Consequently, upon standing, blood tends to pool in the veins of the lower extremities, effectively translocating blood volume away from the central circulation. This causes a sudden drop in ventricular filling and cardiac output along with a drop in arterial pressure. Normally, cardiovascular reflexes activate sympathetic nerves to veins and arteries resulting in venous and arteriolar constriction in response to this initial drop in arterial pressure. Venous constriction helps move blood from the lower extremities into the central circulation and thus supports cardiac output. Stimulation of cardiac output helps prevent any drop in arterial blood pressure when rising to a standing position. Blood pressure is further supported by increased vascular resistance from reflex sympathetic–mediated constriction of systemic arteries in all vascular beds except the heart and brain. This support of blood pressure, along with strong autoregulation of blood flow in the brain, prevents any significant drop in cerebral blood flow that would otherwise occur should the body not be able to compensate for the drop in blood pressure that occurs upon standing against gravity. By directly relaxing smooth muscle in veins and arteries, nitroglycerin antagonizes any constrictor effect on those blood vessels. Because this agent relaxes veins more than arteries, there is a greater reduction in venous than arterial compliance and blood tends to pool more easily in the veins than normal. In addition, the actions of nitroglycerin blunt any reflex sympathetic vasoconstriction of veins in response to standing, preventing those reflexes from counteracting pooling of blood away from the central circulation and into the lower extremities. The action of nitroglycerin on arteries also antagonizes reflex arterial vasoconstriction during standing. As a result, a patient on nitroglycerin can experience a significant, precipitous drop in arterial pressure when moving suddenly from a supine to a standing position such that blood supply to the brain may become inadequate. Nitroglycerin does not have any direct effect on cardiac or skeletal muscle contraction. Therefore, the drop in arterial pressure seen upon standing while on nitroglycerin will activate neurogenic reflexes that will increase heart rate and myocardial contractility. Therefore, the patient in this study also experienced tachycardia and palpitations upon standing. Explain why alveolar ventilation measures the amount of fresh air that enters the lung.

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Left ventricular hypertrophy rotates the direction of the major dipole associated with ventricular depolarization more to the left than usual (i buy ponstel with visa spasms during period. Hyperkalemia alters potassium conductance in phase 3 of the cardiac action potential and thus affects repolarization patterns in the ventricles order ponstel without a prescription spasms right side, resulting in a characteristic spiking or “mountain” characteristic of the T wave (Fig ponstel 500 mg on line muscle relaxant lyrics. In the case of patients with coronary artery disease, the oxygen demand of the heart at rest may be within the ability of the compromised coronary artery system to deliver oxygen to the tissues (see Chapters 15 and 16 for more details). However, should the oxygen demands of the heart increase from increased physical activity or emotional stress in the patient, the heart’s diseased arterial system may not be able to meet the new, higher oxygen demand and the heart will become ischemic. Isometric stress (handgrip), dynamic (aerobic) stress (such as bicycle or treadmill ergometry), or combinations of the two are used to increase oxygen demand in the heart and in the body as a whole. The response of the patient as well as the response of the heart to this increased demand is monitored and analyzed. Extensive clinical guidelines for using and interpreting exercise stress testing have been developed and are continually updated by the American Heart Association and other professional cardiopulmonary or sports medicine groups. Exercise testing has long been used for the diagnosis of the hemodynamic consequences, or severity, of obstructive coronary artery disease. The use of exercise stress testing to reveal this “silent coronary artery disease” is invaluable to the clinician. Similarly, many antiarrhythmic drugs exert their effects by either increasing or decreasing the electrical refractory period in the ventricles. One of the first signs of ischemia in the heart is an inversion of the T wave, as shown in Figure 12. With myocardial ischemia, the cells in the ischemic region partially depolarize to a lower resting membrane potential because of a lowering of the potassium ion concentration gradient, although they are still capable of firing action potentials. After depolarization (during the action potential plateau), all areas are depolarized and true zero is recorded. Such deviations in activation can result in erratic and insufficient mechanical activation of the heart such that blood flow output to peripheral organs is compromised. The diagnosis of cardiac arrhythmias is aided greatly by detailed analyses using the electrocardiogram. Many drugs that modify cardiac electrical processes have been employed for the control and management of arrhythmias. Although these drugs can often be proarrhythmic and come with many other side effects, they are still used extensively as pharmacotherapy for many types of arrhythmias. These drugs have different, diverse, effects on electrical properties of cardiac cells. Type I agents are called sodium channel antagonists because they impair the fast sodium channel kinetics in myocardial cells. Type I agents slow phase 0 of the myocardial action potential and thereby slow conduction of action potentials through the myocardium. By impairing sodium channel operation, they tend to raise the effective action potential threshold in atrial and ventricular cells and thereby reduce cell excitability. Their salutatory effect is to convert unidirectional conduction blocks in damaged myocardium into bidirectional blocks thereby quashing reentry arrhythmias. Quinidine (a derivative of quinine), procainamide, and disopyramide belong to this subclass. Although these agents can be used to treat various atrial and ventricular arrhythmias as well as reentry tachycardias, they are so fraught with undesirable autonomic and other side effects that they are generally reserved for acute treatment of life-threatening arrhythmias. Quinidine, in particular, is so cardiotoxic that it has to be discontinued in roughly 50% of patients after just a single use. Their primary beneficial + effect is that they enhance K conductance in Purkinje fibers without altering the resting membrane potential. This enables these cells, which are often prone to form ectopic foci, to more easily counteract depolarizing stimuli that could otherwise create an ectopic foci. These agents gain access to the fast sodium channel in the active and inactive state so they are especially effective in rapidly cycling or partially depolarized tissue. For this reason, they reduce conduction velocity in ischemic tissue but not normal myocardium and are especially effective in reducing ectopic-based tachycardias. Lidocaine is the prototypical drug in this class, which are the agents of choice in the acute treatment of sustained ventricular tachycardia and the prevention of ventricular fibrillation. Flecainide was one of the early drugs developed in this category, which also includes the agent propafenone. These agents however tend to be actually proarrhythmic in many instances and are therefore rarely used. The complex effects and side effects of Class I agents make them difficult to use in the long-term management of arrhythmias. For this reason, current clinical management utilizes surgical and medical device modalities for the long-term treatment of arrhythmias. Implantable, programmable, cardiac pacemaker/defibrillator units are now being used as a surgical solution to both abnormal bradyarrhythmias (pacemaker capability) as well as sudden emergent ventricular tachycardia or fibrillation (automatic fibrillation detection and electrical defibrillation). Specialized nodal tissue cells exhibit the properties of automaticity and rhythmicity. Gap junctions at nexus between adjacent cells allow the heart to behave as a functional syncytium. Opening of voltage-gated sodium and calcium channels and the closing of voltage-gated potassium channels initiate action potentials in cardiac muscle cells. Action potentials in atrial and ventricular muscle cells have an extended depolarization plateau that creates an extended refractory period in the cardiac muscle cell. Cardiac muscle cells are repolarized following the depolarization phase by the closing of voltage- gated calcium channels and the opening of voltage-gated and ligand-gated potassium channels. A recycling decay and resetting of potassium conductance in the nodal cell membrane create recycling pacemaker potentials in the sinoatrial node. Norepinephrine increases pacemaker activity and the speed of action potential conduction, whereas acetylcholine decreases pacemaker activity and the speed of action potential conduction. Electrical activity initiated at the sinoatrial node spreads preferentially in sequence across the atria, through the atrioventricular node, through the Purkinje system, and to ventricular muscle. The atrioventricular node delays the entry of action potentials into the ventricular system. Purkinje fibers transmit electrical activity rapidly into the inner layers of the ventricular myocardium. The conduction of electrical activity through the myocardium is a function of the amplitude of action potentials and the rate of rise of depolarization of action potentials in phase 0. An electrocardiogram is a recording of the time-varying voltage differences between repolarized and depolarized regions of the heart. The electrocardiogram provides clinically useful information about the rate, rhythm, pattern of depolarization, and mass of electrically active cardiac muscle. Changes in cardiac metabolism and plasma electrolytes as well as the effects of medicinal drugs on the electrical activity of the heart can be detected by an electrocardiogram.

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