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)
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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.

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 Na-K 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.
Altitude
High
Lowered
There is a progressive reduction in the amount of oxygen and
maximum and its partial pressure as altitude increases. As a result, the heart

beats faster to compensate for less oxygen per breath.

Maximum heart rate drops with increases in altitude
training heart
approximately one beat per 1,000 feet of gain. There is some
rates
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