1 in the name of god 2 by: mahnaz.bayat ph.d where is the heart in our body? left arm right arm...

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In the name of God

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By: Mahnaz .Bayat Ph.D

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Where is the heart in our body?

Left armRight arm

Right shoulder Left shoulder

Neck

Lungs

Can you feel your heart?

The heart is located in the mediastinum, which is the central sub-division of the thoracic cavity. The mediastinum also contains other structures, such as the esophagus and trachea, and is flanked on either side by the right and left pulmonary cavities; these cavities house the lungs

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Apex is located posterior to the 4th to 5th intercostal space just medial of the left mid-clavicular line. PMI point of maximal impulse

The true base of the heart is somewhat quadrilateral. It faces back and to the right within the mediastinal cavity. It is formed mainly by the Left atrium and only partly by the posterior aspect of the right atrium.

Where are the location of the apex and the base of the heart?

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The heart has two sides!

In normal adults, the mass of the heart is 250–350 grams (9–12 oz), but an extremely diseased heart can be up to 1000 g (2 lb) in mass due to hypertrophy

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• The heart is actually two separate pumps: a right heart that pumps blood through the lungs, and a left heart that pumps blood through the peripheral organs.

• two-chamber pump composed of an atrium and a ventricle.

• The ventricles then supply the main pumping force that propels the blood either (1) through the pulmonary circulation by the right ventricle or (2) through the peripheral circulation by the left ventricle.

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http://www.innerbody.com/anatomy/cardiovascular/upper-torso/heart-posterior

http://en.wikipedia.org/wiki/Cardiac_muscle

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Physiology of Cardiac Muscle

• The heart is composed of three major types of cardiac muscle:

1) Atrial muscle fiber2) ventricular muscle fiber3) specialized excitatory and conductive muscle

fibers

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Syncytium

• The heart actually is composed of two syncytiums:

• the atrial syncytium that constitutes the walls of the two atria,

• the ventricular syncytium that constitutes the walls of the two ventricles.

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The atria are separated from the ventricles by fibrous tissue that surrounds the atrioventricular (A-V) valvular openings between the atria and ventricles.

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Cardiac muscle

• cardiac muscle is striated in the same manner as in typical skeletal muscle. cardiac muscle has typical myofibrils that contain actin and myosin filaments almost identical to those found in skeletal muscle

• Cardiac fiber are branched• the duration of contraction of Cardiac Muscle is much

longer• Cardiac fiber has one or two pale nucleus in center • as a Syncytium • The dark areas crossing the cardiac muscle fibers are called

intercalated discs; they are actually cell membranes that separate individual cardiac muscle cells from one another.

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Striated and branched

Cardiac fiber has one or two pale nucleus in center

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intercalated discs

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Plasma membranes of adjacentcardiac muscle fibers

Desmosome

Gap junction

Intercalated disc

Actionpotential

AP velocity in: myelin nerve= 120 m/sSkeletal muscle= 5 m/sCardiac muscle= 0.5 m/s

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What is the difference between Epicardium and Pericardium?

Pericardium visceral ( Epicardium ) parietal

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It is enclosed in a double-walled sac called the pericardium. The pericardium's outer wall is called the parietal pericardium and the inner one the visceral pericardium. Between them there is some pericardial fluid which functions to permit the inner and outer walls to slide easily over one another with the heart movements.

Outside the parietal pericardium is a fibrous layer called the fibrous pericardium which is attached to the mediastinal fascia.[6] This sac protects the heart, anchors it to the surrounding structures, but has no effect on ventricular hemodynamics in a healthy person.

The outer wall of the human heart is composed of three layers. The outer layer is called the epicardium, or visceral pericardium since it is also the inner wall of the pericardium. The middle layer is called the myocardium and is composed of contractile cardiac muscle. The inner layer is called the endocardium and is in contact with the blood that the heart pumps.[8] Also, it merges with the inner lining (endothelium) of blood vessels and covers heart valves

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http://www.sumanasinc.com/webcontent/animations/content/humanheart.html

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Tricuspid

Aortic

Pulmonary

Mitral

Cardiac valves

the high pressures in the arteries at the end of systole cause the semilunarvalves to snap to the closed position, in contrast to the much softer closure of the A-V valves. Second, because of smaller openings, the velocity of blood ejection through the aortic and pulmonary valves is far greater than that through the much larger A-V valves. Also, because of the rapid closure and rapid ejection,the edges of the aortic and pulmonary valves are subjected to much greater mechanical abrasion than are the A-V valves

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Mitral valve

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S1,S2

S1

S2

S1 = M1,T1

S2 = A2,P2

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Atrioventricular Valves.

• The A-V valves (the tricuspid and mitral valves) prevent backflow of blood from the ventricles to the atria during systole

• the semilunar valves (the aortic and pulmonary artery valves) prevent backflow from the aorta and pulmonary arteries into the ventricles during diastole

• close and open passively.• The papillary muscles contract when the ventricular walls

contract

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• http://www.audiosparx.com/sa/display/sounds.cfm/sound_group_iid.410

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Cardiac function

The cells of the heart, like neurons, are excitable and generate action potentials. These action potentials initiate contraction and thus determine the heart rate.

Electrical properties and generate AP Cardiac contraction

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http://highered.mcgraw-hill.com/sites/0072495855/student_view0/chapter22/animation__conducting_system_of_the_heart.html

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S-Anode

0.09 s

1m/s

0.04

The velocity of conduction of the excitatory action potential signal along both atrial and ventricular muscle fibers is about 0.3 to 0.5 m/sec

The velocity of conduction in the specialized heart conductive system—in the Purkinje fibers—is as great as 4 m/sec

The conduction velocities of the slow response in the SA and AV nodes are about 0.02 to 0.1 m/sec

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1 2

3 4

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Depolarization and repolarization in ventricles

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During depolarization the impulse is carried from endocardium to epicardium, and during repolarization the impulse moves from epicardium to endocardium.

Endocardium

Epicardium

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The conduction velocities of the slow response in the SA and AV nodes are about 0.02 to 0.1 m/sec.

1-The fast-response conduction velocities are about 0.3 to 1 m/sec for myocardial cells and 1 to 4 m/sec for the specialized conducting (Purkinje) fibers in the ventricles.2-Resting membrane potential more negative3-opening of fast voltage Na channel in phase 0 4-more overshot 5-high amplitude of AP is caused more conduction speed6-RRP is completed in phase 3

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transient outward current (ito)

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4

0

3

Pacemaker potential

Antiarrhythmic agent

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Class I agents interfere with the sodium (Na+) channel.

Class II agents are anti-sympathetic nervous system agents. Most

agents in this class are beta blockers.

Class III agents affect potassium (K+) efflux.

Class IV agents affect calcium channels and the AV node.

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prevention from tantalization in cardiac muscle by Long Action Potential and the Plateau

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Heart rate

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Control of the Heart by the Sympathetic andParasympathetic Nerves

S2,S3,S4

3,7,9,10 cranial nerve

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sympathetic and parasympathetic stimulation has a basic activity

in the heart

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By Hyperpolarizing

By Decrease slope

By increase threshold

Decrease in heart rate

Na Ca T

k

Pacemaker potential

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Ach hyperpolarized the RMP by opening of K channel

k

Hyperpolarization

M M

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Ach Decreased pacemaker slope by closing of T-calcium channel

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Ach have negative ionotropic effect by closing of L-calcium channel

cAMP

MM

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How norepinephrine can increase HR ?

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Epi have positive ionotropic effect by increasing of conductance in L-calcium channel

Drug and Sodium-potassium pumps

Digoxin (digitalis) and ouabain

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3:1 3:2

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Effect of Potassium and Calcium Ionson Heart Function

• Excess potassium in the extracellular fluids causes the heart to become dilated and flaccid and also slows the heart rate

• An excess of calcium ions causes effects almost exactly opposite to those of potassium ions, causing the heart to go toward spastic contraction.

• Conversely, deficiency of calcium ions causes cardiac flaccidity, similar to the effect of high potassium.

• Hyperkalemia = hypocalcemia

HypercalcaemiaHypercalcaemia (British English) or hypercalcemia (American English) is an elevated calcium (Ca2+) level in the blood. (Normal range: 9–10.5 mg/dL or 2.2–2.6 mmol/L). It can be an asymptomatic laboratory finding, but because an elevated calcium level is often indicative of other diseases, a workup should be undertaken if it persists. It can be due to excessive skeletal calcium release, increased intestinal calcium absorption, or decreased renal calcium excretion.

Symptoms are more common at high calcium blood values (12.0 mg/dL or 3 mmol/l). Stones (renal or biliary)Bones (bone pain) (abdominal pain, nausea and vomiting)Depression 30-40%, anxiety, cognitive dysfunction, insomnia, coma)Other symptoms can include fatigue, anorexia, and pancreatitis.Abnormal heart rhythms can result, and ECG findings of a short QT interval and a widened T wave suggest hypercalcaemia. Significant hypercalcaemia can cause ECG changes mimicking an acute myocardial infarction.Hypercalcaemia can increase gastrin production, leading to increased acidity so peptic ulcers may also occur.Severe hypercalcaemia (above 15–16 mg/dL or 3.75–4 mmol/l) is considered a medical emergency: at these levels, coma and cardiac arrest can result.

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• the high levels of calcium ions decrease neuronal excitability, which leads to hypotonicity of smooth and striated muscle.

• This explains the fatigue, muscle weakness, low tone and sluggish reflexes in muscle groups. In the gut this causes constipation. The sluggish nerves also explain drowsiness, confusion, hallucinations, stupor and / or coma.

Hypercalcaemia decrease neuronal excitabilityWhy?

Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers, increased calcium raises the threshold for depolarization.

The neuromuscular symptoms of hypercalcemia are caused by a negative bathmotropic effect due to the increased interaction of calcium with sodium channels.

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Hyperkalemia depolarized the membrane

Fast response

Slow response Slow response

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Hypokalemia: more negative K+ equilibrium -> more force pushing K+ out of the cell -> faster repolarization

Hyperkalemia: less negative K+ equilibrium -> less force pushing K+ out of the cell -> slower repolarization

Normal serum potassium levels are between 3.5 and 5.0 mEq/L; about 98% of the body's potassium is found inside cells, with the remainder in the extracellular fluid including the blood. Membrane potential is maintained principally by the concentration gradient and membrane permeability to potassium with some contribution from the Na+/K+ pump.

When arrhythmias occur, or when potassium levels exceed 6.5 mmol/l, emergency lowering of potassium levels is mandated.

Cardiac arrest in diastole in sever Hyperkalemia Cardiac arrest in systole in sever hypercalcaemia

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hypokalemia hyperkalemia

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Effect of Temperature on Heart Function

• Increased body temperature, as occurs when one has fever, causes a greatly increased heart rate, sometimes to as fast as double normal.

• Decreased temperature causes a greatly decreased heart rate, falling to as low as a few beats per minute when a person is near death from hypothermia

• Contractile strength of the heart often is enhanced temporarily by a moderate increase in temperature but prolonged elevation of temperature exhausts the metabolic systems of the heart and eventually causes weakness.

• an increase of approximately 10 beats per minute per degree centigrade

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Cardiac contraction

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Z

the sarcoplasmic reticulum of cardiac muscle is less well developed than that of skeletal muscle

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Difference between heart and skeletal muscle

• The AP in ventricular muscle have a plateau and 15 times as long as skeletal muscle

• Velocity of Signal Conduction in atrial and ventricular Muscle is about 0.3 to 0.5 m/sec, or about 1/10 the velocity in skeletal muscle

• T tubules of cardiac muscle have a diameter 5 times as great as that of the skeletal muscle tubules, which means a volume 25 times as great

• Inside the T tubules is a large quantity of mucopolysaccharides that are electronegatively charged and bind an abundant Ca

• In cardiac fiber T tubule is located in Z line and each sarcomer has one T tubule The strength of contraction of cardiac muscle depends to a great extent on the

concentration of calcium ions in the extracellular fluids.

contraction in cardiac fiber depending to extracellular concentration of Ca

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T tubule is located in Z line and each sarcomer has one T tubule

Z

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Excitation-Contraction Coupling—Functionof Calcium Ions and the Transverse Tubules

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This protein is an inhibitor of cardiac muscle sarcoplasmic reticulum Ca++-ATPase ( SERCA ) in the unphosphorylated state, but inhibition is relieved upon phosphorylation of the protein. The subsequent activation of the Ca++ pump leads to shorter intervals between contractions, thereby contributing to the lusitropic response elicited in heart by beta-agonists. The protein is a key regulator of cardiac diastolic function . Mutations in this gene are a cause of inherited human dilated cardiomyopathy with refractorycongestive heart failure.[3]

When phospholamban is phosphorylated by PKA its ability to inhibit the sarcoplasmic reticulum calcium pump (SERCA) is lost. Thus, activators of PKA, such as the beta-adrenergic agonist epinephrine (released by sympathetic stimulation), may enhance the rate of cardiac myocyte relaxation. In addition, since SERCA is more active, the next action potential will cause an increased release of calcium, resulting in increased contraction (positive inotropic effect). When phospholamban is not phosphorylated, such as when PKA is inactive, it can interact with and inhibit SERCA. The overall effect of phospholamban is to decrease contractility and the rate of muscle relaxation , thereby decreasing stroke volume and heart rate, respectively.[5]

What is phospholamban?

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DHP receptor is as L type Ca channel in cardiac muscle

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Cardiac cycle

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http://www.nhlbi.nih.gov/health//dci/Diseases/hhw/hhw_pumping.html

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Cardiac cycle

end-diastolic volume 120 milliliters stroke volume 70 milliliters, end-systolic volume. 50 millilitersThe fraction of the end-diastolic volume that is ejected is called the ejection fraction—usually equal to about 60 per cent.Cardiac output= SV × HR

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Preload

Preloadamount of blood coming into the heart from

superior and inferior vena cava

In the same way, the more powerful the ventricle, then the faster the blood will be ejected

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Afterloadthe resistance that the ventricles have to

overcome to pump out the blood through the aorta.

A high BP means that the ventricle is pushing uphill!

High viscosity and vasoconstriction mean hard work for the ventricle.

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Ventricular Pressure- volume loophas 4 stages

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S4

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Relationship of the Heart Sounds to Heart Pumping

• S1 (M1-T1) When the ventricles contract, one first hears a sound caused by closure of the A-V valves.

• S2 (A2-P2) When the aortic and pulmonary valves close at the end of systole, one hears a rapid snap This sound is called the second heart sound.

• S3 (diastolic ventricular gallop)in rapid filling phase

• S4 in atrial contraction

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Pressure Changes in the atria and jugular vein —The a, c, and v Waves

The a wave is caused by atrial contraction. The c wave occurs when the ventricles begin to contract

The v wave occurs toward the end of ventricular contraction; it results from slow flow of blood into the atria from the veins while the A-V valves are closed

Venous pulse

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Dicrotic wave in aortic pressure curve

(Incisura)

Dicrotic wave

Aortic valve closed

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Frank –starling law

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BP>160 decreased cardiac output

at normal systolic arterial pressures (80 to140mmHg),the cardiac output is determined almost entirely by the ease of blood flow through the bodyístissues, which in turn controls venous return of blood to the heart.

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What is cardiac muscle:A. a mass of independent muscle bundlesB. a syncytium of muscle cellsC. muscle cells separated by collagen bundlesD. none of the above the depolarization time in ventricular muscle is:0. 2 sec 0. 4 sec 0. 3 sec 0. 6 sec the depolarization time in atrial muscle is:0. 2 sec 0. 4 sec 0. 3 sec 0. 6 secthe long plateau of cardiac action potential is related to:Na ca k Mg the T tubules are rich in:Na ca k Mg with rise in heart rate which phase is shortened more:Systole diastole both of the above non of the above The contribution of atrial contraction to ventricular filling

in:100% 50 % 75 % 25 %

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the peak pressure of atrial contraction is:4-8 mmHg8-15 mmHg15-20 mmHg20-25 mmHgBlood ejected into pulmonary and systemic circulation during

rapid ejection period is:50% 70 90 100The pulmonary valve opens when right ventricular pressure

exceeds:8 mmHg 15 mmHg 20 mmHg 25 mmHgThe normal end-diastolic volume is :75ml 110-120ml 100ml 130-150mlThe normal end-systolic volume is:40-50 ml 50-60 ml 60-70 ml 75-85 ml The maximally achievable systolic pressure by left ventricle is:200 300 400 500 mmHg The end-diastolic pressure is around:10 8 5 2 mmHg

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The maximum efficiency of a normal heart is: 75-80 20-25 50-60 10-15 % what is true of frank-starling principle:Within limits, greater the stretch more the force of contractionHigher the stretch less the velocity of contractionWithout any limitation, increased stretch produces better and more vigorous contraction All are false

the dp/dt is a measure of ventricular:Relaxation contraction automaticity none of the aboveThe resting potential of sinus node fiber is:-90 -60 -80 -40

The action potential changes in sinus node is dependent upon:a) Fast sodium channels b) Potassium channels c) Slow ca-Na channelsd) b , c The action potential changes in purkinje fibers dependent upon:e) Fast sodium channels f) Potassium channels g) Slow ca-Na channelsh) All

The velocity of conduction in atrial muscle is:1 0.3 0.5 0.1 m/secThe AV nodal delay is:0.09 0.05 0.02 0.01 sec

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Vagal effect on AV node is mediated by:Na channel K channel Ca channel None of the

aboveThe conduction velocity in AV node is:0.1 0.5 0.05 0.2 m/sec

The intrinsic rhythmicity rate of purkinje fibers is :70-80 40-60 15-40 none of the above

Carotid sinus stimulation causes:Bradycardia hypotension tachycardia only A+B

The beginning of ventricular systole is when blood flowing back toward the relaxed ventricles causes the semilunar valves to close. A)True B)False

The atria never need to contract due to passive ventricular filling. A)True B)False

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• When the pressure in the ventricles becomes lower than the pressure in the atria...

A)the ventricles contract.B)blood flows into the pulmonary trunk.C)blood flows into the aorta.D)the atrioventricular valves open.E)the semilunar valves open.

the steps of the cardiac cycle in sequence are...

A)isovolumic contraction, isovolumic relaxation, ejection, passive ventricular filling, active ventricular filling.

B)isovolumic relaxation, isovolumic contraction, ejection, passive ventricular filling, active ventricular filling.

C)isovolumic contraction, ejection, isovolumic relaxation, passive ventricular filling, active ventricular filling.

D)isovolumic contraction, ejection, isovolumic relaxation, active ventricular filling, passive ventricular filling.

E)ejection, isovolumic relaxation, passive ventricular filling, isovolumic contraction, active ventricular filling.

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1. The Duration of ventricular contraction is 15 times greater than skeletal muscle2. Immediately after the onset of the action potential, potassium ions decreases about

fivefold3. Slow ca-Na channels closed after 0.3 to 0.5 s

4. signal velocity along both atrial and ventricular muscle fibers(0.3 to 0.5 m/sec) is 1/250 large nerve fibers and about 1/10 the skeletal-

5. energy in cardiac muscle is derived mainly from oxidative metabolism of fatty acids

6. Hyperkalemia can block conduction of the cardiac impulse from the atria to the ventricles through the A-V bundle

7. Elevation of potassium concentration to only 8 to12 mEq/L - two to three times the normal value –can cause such weakness of the heart and abnormal rhythm that this can cause death

8. Spontaneous depolarization in phase 4 SAnode is produced by K channel closing and increase in gNa ,gCa (T type)

9. Cause of the Slow Conduction in transitional fiber,AVN,Avbundle (penetrating portion) are: decrease in gap junction , derease in RMP, decrease in fiber diameter .decrese in AP amplitude

Important key point

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1. Cause of the fast Conduction in purkinje are all of the following: a. increase in gap junction numberb. high negativity in RMP, c. large diameter .d. large AP amplitude e. Decrease in myofibril

The ends of the Purkinje fibers penetrate about one third the way into the muscle mass and finally become continuous with the cardiac muscle fibers

the total time for transmission of the cardiac impulse from the initial bundle branches to the last of the ventricular muscle fibers in

the normal heart is about 0.06 second.

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http://en.wikipedia.org/wiki/Myocardial_infarction