A & P Ii - Heart

Front 1

4 Chambers

Back 1

R & L atria (sing., atrium)..receiving chambers. Thin-walled, superior position. Separated by interatrial septum.
R & L ventricles…pumping chambers, muscular, inferior, form apex. Separated by interventricular septum.

Front 2

atrioventricular (AV) valves

Back 2

Prevent backflow into the atria when the ventricles are contracting. Called the tricuspid (on the right side) and the bicuspid (on the left side.)

Front 3

Blood flow through the heart.

Back 3

Low O2 blood enters the right atrium through 3 vessels, the superior vena cava, the inferior vena cava and the coronary sinus (draining blood from the myocardium itself). The coronary sinus is in the coronary sulcus. Blood goes from the right atrium into the right ventricle via the tricuspid valve. It then goes from the right ventricle to the pulmonary trunk via the pulmonary semilunar valve. The blood then goes to the lungs via R & L pulmonary arteries. From the lungs, the high O2 blood returns to the heart via the right and left pulmonary veins. There are usually four of these. Blood goes from the left atrium through the bicuspid valve into the left ventricle and out into the aorta via the aortic semilunar valve. The left side of the heart is higher in pressure as it has to pump blood throughout the body. The loop through the lungs is the pulmonary (or heart-lung) circuit. The systemic circuit is throughout the rest of the body (so take systemic BP)

Front 4

The Cardiac Cycle

Back 4

Start with all four chambers relaxed. The AV valves are open. The semilunar valves are closed. Blood enters both atria at the same time and passively flows down into the ventricles due to the force of venous pressure. This is a period of time known as “passive filling”. This gets the ventricles 70% filled. Next, both atria contract at the same time, from the top downward, and this completely fills the ventricles—“active filling”. A tenth (0.1 sec) of a second later, after the atrial contraction, the ventricles start to contract. Contract from the apex (bottom tip) upward. As start to contract, the AV valves close (there is a brief period of time when all the valves are closed). Then the semilunar valves open and blood is pumped out into the “great arteries”—aorta and pulmonary trunk. About 0.3 seconds later, the ventricles start to relax, the semilunar valves close, the AV valves open and go back to the start.

Front 5

Systole

Back 5

contraction of the heart—specifically the ventricles.

Front 6

Diastole

Back 6

when the ventricles are relaxed

Front 7

heart sounds

Back 7

sound like “LUB –DUP,” also known as S1 and S2. LUB or S1 is caused by the closing of the AV valves and marks the beginning of systole. DUP or S2 is caused by the closing of the semilunar valves and marks the end of systole or beginning of diastole.

Front 8

Electrical system of the heart

Back 8

The cardiac muscle is unique. The heart muscle has its own electrical system (vs. skeletal muscle that needs a nerve impulse). The intercalated discs help spread the electrical signal. There are specialized cardiac cells involved in the electrical system of the heart. These are SA node (sinoatrial), AV node (atrioventricular nodes), the bundle of His, bundle branches, and Purkinje fibers. The SA nodes are the “pacemaker” of the heart because they establish the basic heart rate. They are found in the upper posterior wall of the right atrium. Has the ability to self-depolarize on a rhythmic basis (meaning it has an action potential or firing). In the absence of autonomic input, this occurs ~70-80x/minute. Every time it fires, it starts the next cardiac cycle. So the SA node sends out an action potential to both atria causing the atria to contract. The AV node is located near the floor of the right atria, near the septum. Impulses from the SA stimulate the AV. AV node has a 0.1 second delay built in and then it fires. The AV node then fires and the action potential travels along the bundle of His which travels to the septum and divides into bundle branches which travel down the septum to the apex. As the branches approach the apex, the branches give rise to the Purkinje fibers which branch out through the walls of both ventricles. They cause the ventricles to start contracting.

Front 9

SA node (sinoatrial)

Back 9

The “pacemaker” of the heart because they establish the basic heart rate. They are found in the upper posterior wall of the right atrium. Has the ability to self-depolarize on a rhythmic basis (meaning it has an action potential or firing).

Front 10

AV node (atrioventricular nodes)

Back 10

Located near the floor of the right atria, near the septum. Impulses from the SA stimulates it. Has a 0.1 second delay built in and then it fires. When it fires and the action potential travels along the bundle of His which travels to the interventricular septum and divides into bundle branches which continue to travel down the interventricular septum to the apex.

Front 11

the bundle of His

Back 11

Located in the superior part of the interventricular septum. The only electrical connection between the atria and ventricles.

Front 12

bundle branches

Back 12

The bundle of His splits into two pathways of this, which course along the interventricular septum toward the heart apex.

Front 13

Purkinje fibers

Back 13

Long strands of barrel-shaped cells with few myofibrils, they complete the pathway through the interventricular septum, penetrate into the heart apex, and then turn superiorly into the ventricular walls.

Front 14

Electocardiography (EKG or ECG)

Back 14

Can measure electrical changes of the heart by putting electrodes on the skin, which generates an electrocardiogram.

Front 15

P wave

Back 15

represents atrial depolarization—SA node firing

Front 16

QRS complex

Back 16

ventricular depolarization

The atria repolarize when the ventricles depolarize so atrial repolarization is obscured by this.

Front 17

T wave

Back 17

ventricular repolarization

Front 18

R—R interval

Back 18

rate or beats per minute (bpm)

Front 19

PQ interval (really the P-R)

Back 19

length of atrial contraction (~0.1 sec)

Front 20

QT (RT) interval

Back 20

length of systole (contraction of ventricles)

Front 21

Average resting heart rate

Back 21

72 bpm which converts to 0.8 seconds/cardiac cycle.

Front 22

Cardiac output

Back 22

the volume of blood pumped out of one ventricle per minute. (usually measure the systemic (L) side, but same amount is pumped out of right ventricle during that minute).

=heart rate (bpm) x stroke volume (mls)

Front 23

aortic valve

Back 23

Guard the bases of the large arteries issuing from the ventricles and prevent backflow into the associated ventricles. Each semilunar valve is fashioned from three pocketlike cusps, each shaped roughtly like a cresent moon.

Front 24

semilunar valves (pulmonary and aortic)

Back 24

Guard the bases of the large arteries issuing from the ventricles and prevent backflow into the associated ventricles. Each is fashioned from the three pocketlike cusps, each shaped roughly like a cresent moon.

Front 25

Stroke volume

Back 25

the amount of blood pumped out of the left ventricle during each systole.

So at rest, basically all the blood in the body goes through the heart every minute. Anything altering heart rate or stroke volume with affect cardiac output.

= end diastolic volume (EDV) - end systolic volume (ESV).

Front 26

6 factors affecting heart rate:

Back 26

1. Autonomic control—controlled by ANS. Increased sympathetic or adrenergic = increased
Increased parasympathetic stim or cholinergic or vagal stim = decreased
2. Chemicals and hormones. Epinephrine (increases). Hypernatremia (increased [Na+] or Hyperkalimia (increased [K+] will decrease. Hypercalcemia will slow and increase strength of contraction.
3. Temperature—core temp. increased core temp of heart will increase
4. Age—infants and children have faster
5. Sex—females have higher resting
6. Physical condition—athletes have lower resting. Condition the heart to be more efficient.

Front 27

end diastolic volume (EDV)

Back 27

During diastole, the ventricles relax. This is the ventricular filling time. So they are most filled at the end of filling time. The volume of blood in ventricle just before it contracts.

Front 28

end systolic volume (ESV)

Back 28

The volume of blood remaining in a ventricle after it has contracted.

Front 29

Ejection fraction

Back 29

Stroke Volume (SV)/ End Diastolic Volume (EDV)
Ex. 100/150 = 67%. Average is around 50%.

Front 30

Two Factors Determine End Diastolic Volume (EDV):

Back 30

1. Venous pressure—veins drain blood into heart. Filling pressure. Increase the venous pressure, then will increase volume.
2. Length of diastole—how long does it take to fill. With all else equal, longer diastole will result in increased volume.

Front 31

Two factors Determine End Systolic Volume (ESV):

Back 31

1. Arterial pressure—pressure exerted against the inside of the arterial walls is the same as the pressure on the semilunar valves. If there is higher arterial pressure, the higher (Ex. 120/80) . The more pressure, the harder the push and so more blood pushed out.
2. Strength of ventricular contraction. Increase strength causes decreased in blood remaining.

Front 32

Starling’s law of the heart or the Frank-Starling effect

Back 32

Within limits, the greater the stretch of the ventricle wall, the greater the strength of the contraction. If there is a low EDV, then need a small contraction. Increased EDV, need more forceful contraction. This effect helps make sure both sides of the heart pump an equal volume over the course of time. (CHF is result if volumes are not equal over time).

Front 33

Pericardium

Back 33

The double-walled sac that encloses the heart.