The document describes the anatomy and electrical activity of the heart. It notes that the heart is located in the chest, protected by membranes called the pericardium. The heart wall contains three layers - the epicardium, myocardium, and endocardium. The myocardium is the thick muscular layer and contains two types of cells - pacemaker cells that initiate electrical signals to trigger contractions, and contractile cells that make up the bulk of the heart muscle and contract in response to these signals. Pacemaker cells have an unstable membrane potential that causes them to spontaneously generate electrical impulses, while contractile cells remain at rest until stimulated by the pacemaker cells.
regulation of cardiac activity is given in brief along with the cardiac diseases. For diseases, just pictures are added you need to go through the explanation separately so that pictures will make you to explain it easily.
HEART RATE
REGULATION OF HEART RATE
VASOMOTOR CENTER – CARDIAC CENTER
MOTOR (EFFERENT) NERVE FIBERS TO HEART
FACTORS AFFECTING VASOMOTOR CENTER
for all medical & health care students
Topics included :- Steps involved in generation and conduction of cardiac impulse; Electrocardiogram; arrthymia - symtoms and it's types - bradycardia and tachycardia; Factors affecting heart's rhythm,
regulation of cardiac activity is given in brief along with the cardiac diseases. For diseases, just pictures are added you need to go through the explanation separately so that pictures will make you to explain it easily.
HEART RATE
REGULATION OF HEART RATE
VASOMOTOR CENTER – CARDIAC CENTER
MOTOR (EFFERENT) NERVE FIBERS TO HEART
FACTORS AFFECTING VASOMOTOR CENTER
for all medical & health care students
Topics included :- Steps involved in generation and conduction of cardiac impulse; Electrocardiogram; arrthymia - symtoms and it's types - bradycardia and tachycardia; Factors affecting heart's rhythm,
Cardiac output (The Guyton and Hall Physiology)Maryam Fida
The volume of blood pumped by each ventricle per minute is called cardiac output
Cardiac output = Stroke Volume X Heart Rate
Normal value = 5 Liters /Minute
Cardiac output = Stroke Volume X Heart Rate
The factors which regulate stroke volume and Heart rate are basically regulating Cardiac output
Volume of blood ejected by each ventricle in single systole; Normal Value = 70 ml/beat
Stroke Volume = End diastolic Volume – End Systolic Volume
So stroke volume is mainly controlled by
EDV
ESV
VENOUS RETURN: What ever blood volume returns to the heart, same is pumped forward through the Frank’s Starlings Law. According to this law 13- 15 liters of blood volume can be pumped out without cardiac stimulation.
DURATION OF DIASTOLE OR FILLING TIME: ventricular filling occurs during diastole, so there must be adequate ventricular filling time.
DISTENSIBILITY OF THE VENTRICLES: Normally ventricles are distensible to accommodate adequate blood volume. Infarction decreases the distensibility which decreases the EDV.
ATRIAL CONTRACTION: There must be adequate atrial contraction to have adequate EDV. If atrial function is not adequate then EDV will decrease.
E.S.V is basically CONTROLLED BY MYOCARDIAL CONTRACTION
FORCE OF MYOCARDIAL CONTRACTION: It depends upon the initial length of muscle fibers according to frank’s starlings law.
PRELOAD: The effect of EDV on initial length is called preload. So EDV also effects the ESV.
AFTER LOAD: Force of contraction is also dependant upon the resistance against which the ventricles have to pump
CONDITION OF THE MYOCARDIUM : It also effects the force of contraction.
AUTONOMIC NERVES : Sympathetic stimulation increases and parasympathetic stimulation decreases force of contraction
HORMONES: Catecholamines, thyroxine, glucagon, digitalis, calcium, increased temp, caffeine, theophyline increase the force.
Force decreases by hypoxia, acidosis, barniturates, procainamide and quinidine decrease the force of contraction.
Parts of the Electrical System
Electrical activity of the heart
Electrical Signals and Blood Flow
Four Steps of Cardiac Conduction
Spread of Excitation Through theHeart Muscle
Cardiac output (The Guyton and Hall Physiology)Maryam Fida
The volume of blood pumped by each ventricle per minute is called cardiac output
Cardiac output = Stroke Volume X Heart Rate
Normal value = 5 Liters /Minute
Cardiac output = Stroke Volume X Heart Rate
The factors which regulate stroke volume and Heart rate are basically regulating Cardiac output
Volume of blood ejected by each ventricle in single systole; Normal Value = 70 ml/beat
Stroke Volume = End diastolic Volume – End Systolic Volume
So stroke volume is mainly controlled by
EDV
ESV
VENOUS RETURN: What ever blood volume returns to the heart, same is pumped forward through the Frank’s Starlings Law. According to this law 13- 15 liters of blood volume can be pumped out without cardiac stimulation.
DURATION OF DIASTOLE OR FILLING TIME: ventricular filling occurs during diastole, so there must be adequate ventricular filling time.
DISTENSIBILITY OF THE VENTRICLES: Normally ventricles are distensible to accommodate adequate blood volume. Infarction decreases the distensibility which decreases the EDV.
ATRIAL CONTRACTION: There must be adequate atrial contraction to have adequate EDV. If atrial function is not adequate then EDV will decrease.
E.S.V is basically CONTROLLED BY MYOCARDIAL CONTRACTION
FORCE OF MYOCARDIAL CONTRACTION: It depends upon the initial length of muscle fibers according to frank’s starlings law.
PRELOAD: The effect of EDV on initial length is called preload. So EDV also effects the ESV.
AFTER LOAD: Force of contraction is also dependant upon the resistance against which the ventricles have to pump
CONDITION OF THE MYOCARDIUM : It also effects the force of contraction.
AUTONOMIC NERVES : Sympathetic stimulation increases and parasympathetic stimulation decreases force of contraction
HORMONES: Catecholamines, thyroxine, glucagon, digitalis, calcium, increased temp, caffeine, theophyline increase the force.
Force decreases by hypoxia, acidosis, barniturates, procainamide and quinidine decrease the force of contraction.
Parts of the Electrical System
Electrical activity of the heart
Electrical Signals and Blood Flow
Four Steps of Cardiac Conduction
Spread of Excitation Through theHeart Muscle
The peer-reviewed International Journal of Engineering Inventions (IJEI) is started with a mission to encourage contribution to research in Science and Technology. Encourage and motivate researchers in challenging areas of Sciences and Technology.
http://www.surfacetreatments.it/thinfilms
Automatic Electropolishing (Vanessa Rampazzo - 15')
Speaker: Vanessa Rampazzo - Legnaro National Laboratories of INFN | Duration: 15 min.
Abstract
Electropolishing is an electrochemical process adopted in order to reduce the internal surface roughness. The process involves a special equilibrium between the reagents and the products, that creates a differential electrical resistance through the micrometric peaks and valleys of surface. This regime is detected collecting the current in function of voltage. Observing dinamically the changes of the characteristic curve during the process it’s possible to ensure the best electropolishing setting.
The Dynamic Control of the best electropolishing point int I-V Plane is done by an automatic program, that collects continuoulsy the voltage and current and calculates in real time the best setting. Roughness smoothing is accompanied by the removal of anomalies on the surface, as pitting and stratches. The automatic program is written in Labview language and works on a industrial computer, a PLC.
The six different physiographical features of India are:
1. The Himalayas,
2. The Northern Plains,
3. The Peninsular Plateau,
4. The Coastal Plains,
5. The Indian Desert, and
6. The Islands
Cartographie des réseaux de transport d'énergie - 11/2015François Lacombe
Supports de la présentation faite au TUBA à Lyon lors de la session TUBAXPerts #7.
Deux parties : le contexte puis quelques cas très généraux d'utilisation
Cardiac muscle (The Guyton and Hall Physiology)Maryam Fida
In the heart there is Atrial muscle and Ventricular muscle which are separated from each other by the fibrous AV Rings containing Valves.
ATRIAL MUSCLE: thin walled. There are two sheets, superficial and deep sheet. Superficial sheet is common over both atria. Deep sheet is separate for each atrium. Muscle fibers in the deep sheet are at right angle to the muscle fibers in the superficial sheet.
FUNCTIONS OF THE ATRIUM:
1. Receive venous blood from large veins. So atria act as reservoir.
2. Conduct the blood into the ventricles.
3. Atrial contraction is responsible for last 25 % of ventricular filling.
4. In the right atrium there is SA Node(Pace maker) and AV node.
5. In the wall of the atria, there are low pressure stretch receptors and these are involved in various reflexes like brain bridge reflex and left atrial reflex.
6. Atria also produce a hormone i.e. Atrial Natriuretic Hormone. Whenever NaCl increases in ECF, it causes release of ANH which causes natriuresis.
VENTRICULAR MUSCLE:
Much thicker than atrial muscle. Thickness of right ventricle wall is 3-4 mm and thickness of left ventricle is 8 – 12 mm.
1.Involuntary
2.Has cross striations
3.Each cardiac muscle fiber consists of a number of cardiac cells, united at ends in series. Where as in skeletal muscle each muscle fiber is individual cell.
4.Cardiac muscle cells are branching and interdigitate.
5.Single central nucleus in each cell.
6. Atrial muscle and ventricular muscle act as separate functional syncytium and impulses from atria are conducted to ventricles through the AV Node and AV Bundle.
7. Sarcoplasmic system is present. In skeletal muscle triad is at the junction of A and I bands. In cardiac muscle T Tubules are much large and thus in cardiac muscle if we take a section it may form a diad or a triad. And these diads and triads are present at the level of Z Disks.
8.Between adjacent cardiac cells there are side to side and end to end connections and these are the intercellular junctions. These junctions are Gap Junctions. Or intercalated discs
9.When one part of myocardium is excited the whole muscle is excited.
10.Whole myocardium obeys all or none law as a whole.
11.No spike potential but action potential with plateau.
12.Has got long refractory period.
Absolute refractory period in ventricular muscle is 250 – 300 milli sec.
In atrial muscle Absolute refractory period is 150 milli sec
Because of long refractory period cardiac muscle cannot be tetanized.
Cardiac muscle has three types of membrane ion channels that play important roles in causing the voltage changes of the action potential. They are (1) fast sodium channels, (2) slow sodium-calcium channels, and (3) potassium channels
Depolarization: First, the action potential of cardiac muscle is caused almost entirely by sudden opening of large numbers of so-called fast sodium channels that allow tremendous numbers of sodium ions to enter the cardiac muscle fiber from the extracellular fluid. These channels are called “fast” channels because they remain open for only a few thousandths of a second and then abruptly close. After depolarization, there's a brief repolarization that takes place with the efflux of potassium through fast acting potassium channels.
Plateau: Secondly, another entirely different population of slow calcium channels, which are also called calcium-sodium channels. This second population of channels differs from the fast sodium channels in that they are slower to open and, even more important, remain open for several tenths of a second. During this time, a large quantity of both calcium and sodium ions flows through these channels to the interior of the cardiac muscle fiber, and this maintains a prolonged period of depolarization, causing the plateau in the action potential.
Repolarization: When the slow calcium-sodium channels do close at the end of 0.2 to 0.3 second and the influx of calcium and sodium ions ceases, the membrane permeability for potassium ions also increases rapidly; this rapid loss of potassium from the fiber immediately returns the membrane potential to its resting level, thus ending the action potential.
This presentation elaborates the economic crisis in Sri Lanka. It explains the causes of economic instability in Sri Lanka and the factors worsening it. Such miserable economic situation is presenting valuable lessons for other sister asian countries to counter their economic instability. Pakistan, a sister country of Sri Lanka is facing severe political and economic instability these days. Pakistan is learning from the Sri Lankan economic situation and tending to improve its economy but the extreme political instability is hurdling and exacerbating the economic crisis. However, policies are underway to counter the economic crisis and more probably Pakistan will escape the Sri Lankan experience.
2. Heart Anatomy
size of your fist
Location
Superior surface of diaphragm
Left of the midline
Anterior to the vertebral column, posterior to the
sternum
2
3. Coverings of the Heart:
Anatomy
Pericardium – a double-walled sac around
the heart composed of:
1. A superficial fibrous pericardium
2. A deep two-layer serous pericardium
a. The parietal layer lines the internal surface of the
fibrous pericardium
b. The visceral layer or epicardium lines the surface
of the heart
They are separated by the fluid-filled pericardial
cavity
3
4. Heart Wall
Epicardium – visceral layer of the serous
pericardium
Myocardium – cardiac muscle layer forming
the bulk of the heart
Fibrous skeleton of the heart – crisscrossing,
interlacing layer of connective tissue
Endocardium – endothelial layer of the inner
myocardial surface
4
5. Myocardial Thickness and Function
Thickness of myocardium varies according to the function of the
chamber
Atria are thin walled, deliver blood to adjacent ventricles
Ventricle walls are much thicker and stronger
right ventricle supplies blood to the lungs (little flow resistance)
left ventricle wall is the thickest to supply systemic circulation
Chapter 18, Cardiovascular System 5
6. THE MYOCARDIUM
Two specialized types
of cardiac muscle cells:
Each of these 2 types
of cells has a distinctive
action potential.
7. Cardiac cells contract without
Nervous Stimulation.
• Cardiac muscle, like skeletal muscle & neurons, is an excitable tissue
with the ability to generate action potential.
• Most cardiac muscle is contractile (99%), but about 1% of the
myocardial cells are specialized to generate action potentials
spontaneously. These cells are responsible for a unique property of
the heart: its ability to contract without any outside signal.
• The heart can contract without an outside signal because the signal
for contraction is myogenic, originating within the heart itself.
• The heart contracts, or beats, rhythmically as a result of action
potentials that it generates by itself, a property called auto
rhythmicity (auto means “self”).
• The signal for myocardial contraction comes NOT from the nervous
system but from specialized myocardial cells also called auto
rhythmic cells.
• These cells are also called pacemaker cells because they set the rate
of the heart beat.
8. Electrical Activity of the
Heart
• Myocardial Auto
rhythmic cells (1%) –
These cells are smaller
and contain few
contractile fibers or
organelles. Because
they do not have
organized sarcomeres,
they do not contribute
to the contractile
force of the heart.
• Myocardial
Contractile cells
(99%) -Contractile
cells which include
most of the heart
muscle
– Atrial muscle
– Ventricular muscle
These cells contract and
are also known as the
Working Myocardium.
9. Action Potential of the
Autorrythmic cardiac cells
• The auto rhythmic cells do not have a stable
resting membrane potential like the nerve
and the skeletal muscles.
• Instead they have an unstable membrane
potential that starts at – 60mv and slowly
drifts upwards towards threshold.
• Because the membrane potential never rests
at a constant value, it is called a Pacemaker
Potential rather than a resting membrane
potential.
10.
11. What causes the membrane
potentials of these cells to be
unstable?• Auto rhythmic cells contain channels different
from other excitable cells.
• When cell membrane potential is at -60mv,
channels are permeable to both Na and K.
• This leads to Na influx and K efflux.
• The net influx of positive charges slowly
depolarizes the auto rhythmic cells. This leads to
opening of Calcium channels.
• This moves the cell more towards threshold.
When threshold is reached, many Calcium
channels open leading to the Depolarization
phase.
12. IONIC BASIS OF
ACTION POTENTIAL
OF AUTORRYTHMIC
CELLS
Phase 1: Pacemaker Potential:
•Opening of voltage-gated Sodium
channels called Funny channels (If or f
channels ).
•Closure of voltage-gated Potassium
channels.
•Opening of Voltage-gated Transient-type
Calcium (T-type Ca2+
channels) channels .
Phase 2: The Rising Phase or
Depolarization:
•Opening of Long-lasting voltage-gated
Calcium channels (L-type Ca2+
channels).
•Large influx of Calcium.
Phase 3: The Falling Phase or
Repolarization:
•Opening of voltage-gated Potassium
channels
•Closing of L-type Ca channels.
•Potassium Efflux.
13. ACTION POTENTIAL OF A CONTRACTILE
MYOCARDIAL CELL:A TYPICAL VENTRICULAR CELL
Unlike the membranes of the autorrythmic
cells, the membrane of the contractile cells
remain essentially at rest at about -90mv
until excited by electrical activity propagated
by the pacemaker cells.
14. ACTION POTENTIAL OF A CONTRACTILE
MYOCARDIAL CELL:A TYPICAL VENTRICULAR CELL
• Depolarization
- Opening of fast voltage-gated Na+ channels.
- Rapid Influx of Sodium ions leading to rapid depolarization.
• Small Repolarization
-Opening of a subclass of Potassium channels which are fast channels.
-Rapid Potassium Efflux.
•Plateau phase
- 250 msec duration (while it is only 1msec in neuron)
- Opening of the L-type voltage-gated slow Calcium channels & Closure of the Fast K+
channels.
-Large Calcium influx
-K+
Efflux is very small as K+
permeability decreases & only few K channels are open.
• Repolarization
-Opening of the typical, slow, voltage-gated Potassium channels.
-Closure of the L-type, voltage-gated Calcium channels.
-Calcium Influx STOPS
-Potassium Efflux takes place.
15.
16. Summary of Action Potential of
a Myocardial Contractile Cell
Depolarization= Sodium Influx
Rapid Repolarization= Potassium Efflux
Plateau= Calcium Influx
Repolarization= Potassium Efflux
Editor's Notes
1. Contractile cells, which are 99% of the cardiac muscle cells, do the mechanical work of pumping. These working cells normally do not initiate their own action potentials.
2. In contrast, the small but extremely important remainder of the cardiac cells, the auto rhythmic cells, do not contract but instead are specialized for initiating and conducting the action potentials responsible for contraction of the working cells..
Spanish explorers in the New World wrote of witnessing human sacrifices in which hearts that had been torn from the chest of living victims and held outside the body continued to beat for minutes.