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LO Dadarp

1. Proses penghantaran impuls fisio anat: simpatis parasimpatis potensial aksi SSO (dari berbagai sumber dan web digabung2in *plak , ada yang bilang dari ganong sama sherwood menurut dafpus webnya ya udah sebut itu aja, kalo di ganong aku gak tau persis apa gak tapi di sherwood hampir persis kok *plak)
Didalam otot jantung terdapat jaringan khusus yang menghantarkan aliran listrik, jaringan tersebut mempunyai sifat-sifat yang khusus, yaitu sebagai berikut : Otomatisasi : kemampuan menghasilkan impuls secara spontan Ritmisasi : pembangkitan impuls yang teratur Konduktifitas : kemampuan untuk menyalurkan impuls Daya rangsang : kemampuan untuk menanggapi stimulasi Komponen-komponen eksitasi dari jantung secara urut terdiri dari: 1.Nodus sinoatrium (SA), daerah kecil khusus di dinding atrium kanan dekat lubang vena kava superior. 2.Nodus atrioventrikel (AV), sebuah berkas kecil sel-sel otot jantung khusus di dasar atrium kanan dekat septum, tepat di atas pertautan atrium dan ventrikel. 3.Berkas HIS (berkas atrioventrikel), suatu jaras sel-sel khusus yang berasal dari nodus AV dan masuk ke septum antar ventrikel, tempat berkas tersebut bercabang membentuk berkas kanan dan kiri yang berjalan ke bawah melalui seputum, melingkari ujung bilik ventrikel dan kembali ke atrium di sepanjang dinding luar. 4.Serat Purkinje, serat-serta terminal halus yang berjalan dari berkas HIS dan menyebar ke seluruh miokardium ventrikel seperti ranting-ranting pohon.

1) 2) 3) 4)

Potensial Aksi Terdiri dari 5 fase elektrofisiologi: 1. Fase istirahat- fase 4: pada keadaan istirahat bagian dalam sel relative negative sedangkan bagian luar relative positif. Membrane sel akan lebih permeable terhadap kalium dibandingkan natrium, karena itu sejumlah kecil ion K akan merembes keluar(dari kadar yang tinggi ke kadar yang rendah K). dengan hilangnya ion K dari intrasel maka bagian dalam sel menjadi relative negative. 2. Depolarisasi cepat- fase 0(upstroke): depolarisasi sel adalah akibat permebilitas membrane terhadap natrium sangat meningkat. Na diluar sel akan mengalir cepat masuk ke dalam sel

melalui saluran cepat sehingga mengubah muatan negative di sepanjang membrane sel, bagian luar menjadi negative dan bagian dalam menjadi positif. 3. Repolarisasi parsial-fase 1 (spike): segera sesudah depolarisasi maka terjadi sedikit perubahan mendadak dari kadar ion dan timbul suatu muatan listrik relative. Tambahan muatan negative di dalam sel menyebabkan muatan positif nya agak berkurang. Sebagai efeknya sebagian sel itu mengalami repolarisasi. Terjadi inaktifasi dari saluran cepat Na. 4. Plateu-fase 2: suatu plateu yang sesuai dengan periode refarkter absolute miokardium. Pada fase ini tidak terjadi perubahn muatan listrik melalui membaran sel. Jumlah ion yg keluar masuk dalam posisi keseimbangan. Plateu terutama disebabkan oleh aliran ion kalsium kedalam sel secara perlahan dibantu juga oleh gerakan ion Na sedikit demi sedikit melalui saluran lambat. Gerakan muatan positif ke dalam ini diimbangi oleh gerakan ion K ke luar. 5. Repolarisasi cepat-fase 3(downstroke): selama repolarisasi cepat maka aliran muatan kalsium dan natrium ke dalam sel di inaktifkan dan permeabilitas membrane terhadap kalium sangat meningkat, kalium keluar sel dengan demikian mengurangi muatan positif didalam sel. Bagian dalam sel akhirnya kembali ke keadaan negative dan bagian luar relative positif. Distribusi ion pada keadaan istirahat dipulihkan kembali melalui kegitan kontinyu pompa NaK yang dengan aktif memindahkan kalium ke dalam sel dan Natrium ke luar sel.

Sistem Saraf Otonom : Simpatik dan Parasimpatik Kecepatan denyut jantung dan volume darah dipengaruhi oleh sistem saraf simpatis dan parasimpatis. Saraf aferen dari saraf glosofaringeal dan saraf vagus membawa pesan dari reseptor sensori sinus karotikus dan arkus aorta menuju medula oblongata sebagai pusat regulasi jantung, saraf simpatis dan saraf parasimpatis keluar dari batang otak kemudian memberikan stimulus pada jantung dan melakukan fungsi regulasi saraf simpatis yang lain. Pusat kardiovaskular di otak berada di formasio retikularis dan terletak di medula oblongata bagian bawah dan pons. Impuls yang berkaitan dengan tekanan darah diintegrasikan di sini. Apabila terjadi perubahan tekanan darah, maka pusat kardiovaskular mengaktifkan sistem saraf otonom, sehingga terjadi perubahan stimulasi simpatis dan parasimpatis ke jantung dan selanjutnya akan terjadi perubahan stimulasi simpatis ke seluruh sistem pembuluh darah. Saraf simpatik dan parasimpatik mengendalikan detak jantung dan kepekaan reseptor cardiopulmonary setelah denervasi karotis dan aorta secara selektif. 3 Saraf simpatis berjalan di dalam traktus saraf spinalis torakalis menuju korteks adrenal dengan melepaskan neurotransmiter norepinefrin ke sirkulasi untuk membantu aksi regulasi jantung ke nodus SA. Norepinefrin berikatan dengan reseptor spesifik yang disebut reseptor adrenergik B1 yang terdapat di sel-sel nodus SA. Setelah berikatan, terjadi pengaktifan sistem perantara kedua menyebabkan peningkatan kecepatan lepas muatan nodus dan peningkatan denyut jantung. Kecepatan denyut jantung akan menurun apabila

pengaktifan saraf simpatis dan pelepasan norepinefrin berkurang. Peningkatan atau penurunan kecepatan denyut jantung disebut efek kronotropik positif atau negatif. saraf simpatik, yang memiliki peran yang dominan dalam kontrol kardiovaskular karena pengaruh mereka untuk meningkatkan laju jantung dan kontraktilitas, menyebabkan penyempitan arteri dan vena, penyebab dari pelepasan katekolamin adrenal, dan mengaktifkan sistem renin-angiotensin-aldosteron. 4 Saraf simpatis juga mempersarafi sel-sel di seluruh miokardium menyebabkan peningkatan gaya dari setiap kontraksi pada setiap panjang serat otot tertentu. Hal ini menyebabkan peningkatan pada SV dan disebut efek inotropik positif. Saraf parasimpatis berjalan ke nodus SA dan ke seluruh jantung melalui saraf vagus. Saraf parasimpatis melepaskan neurotransmitter asetilkolin yang memperlambat kecepatan depolarisasi nodus SA sehingga terjadi penurunan kecepatan denyut jantung yang disebut efek kronotropik negatif. Perangsangan parasimpatis ke bagian-bagian miokardium lainnya tampaknya menurunkan kontraktilitas dan volume darah, menghasilkan suatu efek inotropik negatif.4 Impuls di saraf simpatis noradrenik yang menuju jantung meningkatkan frekuensi denyut jantung (efek kronotropik) dan kekuatan kontraksi jantung (efek inotropik). Impulsimpuls ini juga menghambat efek stimuli vagus, mungkin melalui pelepasan neuropeptida Y, yakni suatu kotransmiter di ujung simpatis. Impuls dalam serabut kolinergik vagus jantung mengurangi frekuensi denyut jantung. Pada keadaan istirahat, terdapat pelepasan impuls tonik di saraf simpatis jantung dalam jumlah sedang, tetapi pada manusia dan hewan besar lainnya terdapat pelepasan impuls tonik dari vagus (tonus vagus) yang cukup besar. Bila vagus hewan percobaan dipotong, frekuensi denyut jantung akan meningkat, dan setelah obat parasimpatolitik seperti atropin diberikan, frekuensi denyut jantung manusia meningkat dari 70, yaitu nilai istirahat normal, menjadi 150-180 denyut/menit karena tidak ada yang melawan tonus simpatis. Pada manusia dengan hambatan di sistem noradrenergik dan kolinergik, frekuensi denyut jantungnya menjadi 100. 7 Sistem saraf simpatis mengontrol tekanan darah melalui mekanisme peningkatan curah jantung dan mempengaruhi tahanan embuluh perifer. Tujuan utama pengontrolan ini adalah :7 1. Mempengaruhi distribusi darah sebagai respons terhadap peningkatan kebutuhan bagian tubuh yang lebih spesifik akan darah. Misalnya saat melakukan olahraga maka distribusi darah ke sistem pencernaan dialihkan ke bagian tubuh yang terlibat dalam aktivitas tersebut seperti otot rangka dan kemudian panas tubuh dikeluarkan melalui dilatasi pembuluh darah kulit. 2. mempertahankan tekanan arteri rata-rata yang adekuat dengan mempengaruhi diameter pembuluh darah. Sedikit perubahan pada diameter pembuluh dara dapat menyebabkan perubahan yang bermakna pada tekanan darah. Penurunan volume darah dapat menyebabkan konstriksi pembuluh darah di seluruh tubuh kecuali pembuluh darah yang memperdarahi jantung dan otak. Tujuannya adalah untuk mengalirkan darah ke organ-organ vital sebanyak mungkin.

2. Faktor yg mempengaruhi denyut jantung


1) Sex. Women have a slightly faster pulse rate than men. (2) Age. The pulse rate gradually decreases from birth to adulthood then increases with advancing old age. (3) Body temperature. The pulse rate generally increases 7-10 beats for each degree of temperature elevation. (4) Digestion. The increased metabolic rate during digestion will increase the pulse rate slightly. (5) Pain. Pain increases pulse rate.

(6) Emotion. Fear, anger, anxiety, and excitement increase the pulse rate. (7) Exercise. The heart must beat faster during exercise to meet the increased demand for oxygen. (8) Blood pressure. In general, heart rate and blood pressure have an inverse relationship. When the blood pressure is low, there is an increase in pulse rate as the heart attempts to increase the output of blood from the heart (cardiac output). Sumber: http://armymedical.tpub.com/md0917/md09170024.htm What Causes High Pulse Rate There are several causes of this condition. Although, most reasons for high pulse rate are temporary in nature, a few other factors may elevate the pulse rate for a longer time. Heart Diseases Most people who complain of high or rapid pulse rate, often suffer from some or the other heart disease. Heart ailments such as coronary heart diseases, high blood pressure, pericarditis etc., are likely to give rise to high pulse rate. The hardening of arteries or the faulty heart valves lead to difficulty in pumping, thereby increasing the pulse rate. Thyroid Malfunction Overactive thyroid gland is known to have some relation with the elevation of pulse rate. Thyroid gland is responsible for controlling the metabolism, in the body. Hence, its over performance often interferes with the normal metabolism of the body. This, in some way causes the heart to increase its pumping rate, which eventually leads to a higher pulse rate. Other metabolism related disorders are also likely to cause higher pulse rate. Faulty Upper Heart Chamber Microscopic irregularities or any kind of damage in the upper chamber of the heart, results in higher pulse rate. These irregularities weaken the muscles of the upper heart chambers, thereby putting a lot of strain on the heart. Prolonged consumption of alcohol also causes the upper chamber of heart to beat at an abnormally higher rate. Emphysema Emphysema or chronic obstructive pulmonary disease (COPD) is yet another cause of high pulse rate. In emphysema, the tissues of lungs become non - elastic, which affects the normal pumping capacity of the heart. This eventually results in rapid heart beating. Smoking is a prime cause of emphysema and other respiratory diseases. Read more at Buzzle: http://www.buzzle.com/articles/high-pulse-rate-causes-of-high-pulserate.html What Affects the Heart Rate? There are a number of different factors that affect the control and response of heart rate. But, what controls the beat of the heart? Neural and Hormonal Affects There are two different factors involved in heart rate management: intrinsic and extrinsic controls. Intrinsic regulation of heart rate is the result of the unique nature of cardiac tissue it is self-regulating and maintains it's own rhythm without direction. Extrinsic controls are those that come from both hormonal responses as well as the commands from the nervous system: the central nervous system and the autonomic nervous system. Extrinsic regulation can cause the heart rate to change rapidly because of chemicals that circular in the blood or by direct action of nerves that go to the heart. A good example of this is to measure heart rate changes when certain words or emotions are said or felt without a muscle contracting. Say the words, "we are going to have a surprise test today" and watch heart rate extrinsically increase. Put on a heart rate monitor and sitting

completely still watch a movie and watch heart rate jump during a car chase or action thriller. There is no cardiovascular or cardio respiratory change as a result of this change in heart rate; it's simply the affect on the heart of chemicals and nerves responding to an external experience. The cardiovascular control center for the body is located in the ventro-lateral medulla. Here heart rate slows if activated by the cardio inhibitory center in the medulla or speeds up if activated by the cardio accelerator. From this site, the two channels of the autonomic nervous system originate the sympathetic and parasympathetic components. The sympathetic components increase heart rate by releasing the neural hormone catecholamines - epinephrine and norepinephrine. These hormones are cardio accelerators. Acceleration of the heart rate is called tachycardia. The parasympathetic nervous system located in the brain stem and upper or sacral portion of the spinal cord slows heart rate. The parasympathetic components decrease heart rate. These neurons release the neurohormone acetylcholine, which inhibits heart rate. The slowing of heart rate is called bradycardia. The combination of the neural and chemical components regulates heart rate and other heart functions. When you begin to exercise in heart zones 1-3, heart rate increases because parasympathetic (cardioinhibitory) stimulation stops. During more strenuous exercise, heart zones 3-5, the heart rate increase occurs by direct activation of the sympathetic cardioaccelerator nerves. Exercise excites the relationship between the sympathetic accelerators and the parasympathetic depressor neurons. This change in the balance in their activity called tonic activity leads to more involvement of the vagus nerves. The vagus nerves carry about 80% of the parasympathetic fibers, those responsible for slowing heart rate. With increased vagal dominance, heart rate values change and slow. One of the training effects is the slowing of resting and ambient heart rates. This is the result of the effect of fitness on the tonic activity and the favoring of greater activity by the vagus nerves to slow heart rate. These adaptations following zone 1-3 or aerobic training occur to those who are sedentary and begin and exercise program as well as those who maintain one. This is one of the benefits of training, a significant resting bradycardia. The central nervous system plays the greatest role in control over heart rate during exercise. When you start a movement pattern, the central nervous system sends impulses through the cardiovascular center in the medulla. There is a coordinated and quick response of both the heart and the blood vessels to change blood pressure, tissue perfusion to respond to the requirements. A good example of the central command involvement is with anticipatory heart rate. Before an event begins, if the individual anticipates with excitement and enthusiasm the event, heart rate increases dramatically without any muscular involvement. Anticipatory heart rate or your heart rate immediately before exercising in one experiment averaged 148 bpm when the announcer started giving starting commands to a group of sprinters. In this experiment, heart rates increased 140% in anticipation of the starting of this 60-yard dash. In fact, the body that the body increases heart rate in anticipation is good because it provides for the rapid mobilization of it's bodily reserves by revving the body's engine. Research shows that the longer the event, the lower the anticipatory heart rate changes. Internal Body Changes Almost any substance taken into the body affects the equilibrium of the comanism. Heart rate is one of the quickest changes that occur as a direct reflection of this change that results in disequilibrium. For example, beta blockers (Inderal, Propranolol, Lopressor, etc.) cause bradycardia or the heart rate to drop. Similarly, the antiarrhythmic agents (Cardioquin, Procaine, Quinidine, etc.) given to patients to improve cardiac function also causes a decrease in heart rate. Pulmonary bronchodilator drugs such as the sympathomimetics (Isoproterenol, Ephedrine, Bronkosol, etc.) cause tachycardia or increase in heart rate values. Drugs that act as stimulants such as caffeine, nicotine, methamphetamines, cocaine, PCP cause tachycardia and drugs that are depressants, barbiturates, tranquilizers, alcohol

and quaaludes cause bradycardia. Some drugs like inhalants can cause either a quickening or depressing of heart rate and respiration. Other changes can cause changes in heart rate. Lack of sleep, irritability, rapid changes in blood chemistry such as blood sugar levels, reactions to different types of ingested foods can both lower and raise resting and exercising heart rates. Emotions play a large role in heart rate response. Anger, fear, and anxiety cause tachycardia while depression usually results in lowering of heart rate. Feelings of love, compassion, happiness usually result in braycardia. Emotional stress causes heart rate to stay elevated. Environment Stresses Heart rate is affected by external stresses on the body such as heat, humidity, cold, wind, and altitude and air quality. With each stress, the human heart is affected and different compensatory changes occur, one of those being adjustment in the beat of the heart. Triathletes racing at the Hawaiian Ironman face most of these conditions simultaneously while racing in one of the most strenuous events in the world. As a result, a heart rate monitor can help provide them with key information on how their body is responding to the conditions and the duration of this high intensity racing throughout the event. The following chart shows the affects on heart rate of certain environmental stresses: Type of Specific Heart Rate Explanation Stress Stress Changes Changes in heart rate are the result of changes in the core Thermal Heat body temperature. Dressing appropriately is the most Elevated Stress gain* important consideration to maintain the bodies core temperature. Dehydration causes heart rate to increase. Thermoregulation adjustments result in improved exercise capacity to heat exposure but minimally to cold stress. This generally takes about 10 days. Shivering can increase the Heat loss Lowered heart rate significantly to increase core temperature. Considerable water can be lost from the respiratory tract during cold exposure when exercising which results in elevated heart rates (dehydration effect on heart rate). The water content in the ambient air affects the amount of water lost through sweating. In dry air, sweating can be profuse and decrease in blood volume from dehydration Humidity Dry Air Elevated substantial. Each 1 pound of body weight loss corresponds to 15 ounces (450 mL) of dehydration. Hot dry climates are easier than humid ones because evaporation of sweat, which cools the skin, can be achieved. Exercising in high humidity challenges the thermoregulatory system because the large sweat loss contributes little to Highly evaporative cooling. Sweat does not cool the skin; evaporation Elevated moist air of sweat cools the skin. Heart rate response is to increase blood flow to the skin for sweating therefore increasing heart rate. Wind caused by physical movement or air movement magnifies heat loss as the warmer insulating air on the skin is Wind Lowered and continually replaced by cooler, ambient air. Wind causes heat Wind Chill Elevated to decrease and hence heart rate to stay lower. Wind chill factor is an index that shows the effect of wind velocities on bare skin for different temperatures. There is a progressive reduction in the amount of oxygen and Lowered its partial pressure as altitude increases. As a result, the heart maximum and Altitude High beats faster to compensate for less oxygen per breath. training heart Maximum heart rate drops with increases in altitude rates approximately one beat per 1,000 feet of gain. There is some

relief from the acclimatization process, which result in improved tolerance to altitude hypoxia. * Same response to thermic effect of food Genetics The genes that you inherited are responsible for much in our lives. They too affect heart rates. It appears that the effect of your genetic makeup accounts for about 50% of the value of your maximum heart rate. This means that if your parents both have a low maximum heart rate, the odds are favorable that you will as well. Protection from the degenerative process of heart disease The state of fatigue or rest of the individual also affects heart rate. If a student is physically tired from over-exercising there is a decline in physiological performance. Overtraining is a complex series of conditions which can include nutrient-fatigue, muscle-fatigue, and neuromuscular-fatigue. Heart rate is affected differently by different kinds of fatigue. Heart rate is not affected by body composition. It's not affected by body type. It is affected by heart size with smaller hearts typically having higher resting and ambient heart rates. Fitness Level The fitter you are the less often your heart contracts thus saving heartbeats. Getting fitter is like putting money into your saving account, it's putting heartbeats into your physiological saving account. Through the phenomenon of the training effect, ambient and resting heart rates drop, by as much as 20-30 bpm. When extended over a lifetime, this can equate to hundreds of millions of heartbeats. The athlete's heart as the fit cardiac muscle is sometimes referred to is different than the sedentary individuals cardiac pump. There are structural and dimensional changes to the hearts of athletes, which reflect the specific training demands. The effects of getting a fit heart leads to cardiac hypertrophy, a muscle adaptation as a result of increased work capacity. That is, there is a moderate increase in heart size and anatomies regardless of age as the result of an aerobic and anaerobic training program. Here's a list of changes that happen to the fit, athletic heart muscles: Improved cardiac output Lower resting and ambient heart rates Increased stroke volume Enlarged ventricular chamber Thickening of the heart walls Improved coronary blood flow Improved mitochondria mass Increase number of respiratory enzymes in the myocardium Mode of Exercise Many factors affect maximum and training heart rates. The type of exercise is singularly one of the most significant. Maximum heart rate is mode specific. Anaerobic threshold heart rates are also mode specific. The greater the quantity of muscle mass that is used for the exercise, the higher the training heart rates attained. The highest heart rate numbers are those from sports which use both lower and upper muscle groups simultaneously such as cross country skiing. The lowest are those in which the body is in a horizontal position or in cool temperatures such as swimming. Heart rate and changes in heart rate are affected by many factors. Each can result in heart rate variability depending multiple factors that might be simultaneously interacting. For example, a student might be on medication, fatigued, doing a different form of exercise, after not sleeping, just eating a big complex carbohydrate meal, suffering from stress, deconditioned, living at altitude, in high relative humidity, and it's the day before their birthday and they just returned from a long trip. In combination, these factors can make a big day-today variation in heart rate. That's even more of a reason to use a heart rate monitor. It's a management tool. The heart muscle takes all of these situations and conditions into account when it sets the frequency of the beat. Both the heart muscle and the heart monitor are powerful - use them both, together. http://www.heartmonitors.com/exercisetips/changing_heartrate.htm

3. Fungsi denyut jantung lebih cepat