Chapter 20 - The Heart

Front 1

Describe the base and apex of the heart

Back 1

Base: superior pole that connects to great vessels
Apex: inferior pole (pointed tip) on the left ventricle

Front 2

Describe cardiac skeleton

Back 2

4 dense bands of elastic tissue that encircles the heart, stabilizes the position of valves & muscles, and electrically insulates the heart

Front 3

Describe the pericardium (layers and spaces)

Back 3

Pericardium is a dense layer of collagen fibers lined by serous membrane.

-visceral pericardium: surface of the heart

-parietal pericardium: lines inner surface of pericardial sac

-pericardial cavity: in between the 2 layers filled with pericardial fluid

Front 4

What's serous fluid? Where's it found/what's it for?

Back 4

A membranous fluid found lining the fibrous pericardium to reduce friction

Front 5

Describe the 3 layers of the heart

Back 5

epicardium: external layer, mesothelium

myocardium: middle layer, cardiac muscle tissue, blood vessels & more

endocardium: internal layer, continuous with the endothelium of blood vessels

Front 6

Describe the atria (location, size, vessels attached to each)

Back 6

Right atrium - receives blood from coronary sinus & vena cava. Smaller than left and has the fossa ovale (which replaced foramen ovale)

Left atrium - receives blood from pulmonary circuit (L&R pulmonary veins) after oxygenation. Larger/thicker than right atrium.

Front 7

Describe the fossa ovalis

Back 7

a shallow depression that was formerly the foramen ovalis before our lungs were developed

Front 8

Describe the foramen ovalis

Back 8

a foramen that exists only in the fetal heart that allows communication between the left and right atria

Front 9

Describe the ventricles (size, location, major vessels)

Back 9

Right ventricle: below the right atrium, contains moderator band. Vessels-pulmonary trunk (start of pulmonary circuit)

Left ventricle: holds same amount of blood as left but it larger/thicker walls because it pumps blood further into systemic circuit. Vessels-aeorta

Front 10

What structures are found in the intraventricular sulci?

Back 10

fat & vessels

Front 11

Compare/contrast the pulmonary circuit

Back 11

pulmonary: short, , carries deoxygenated bloodblood to & from the gas exchange surfaces of the lungs

systemic: large, long, transports oxygenated blood to the rest of the body

Front 12

List the main structures of the coronary circulation

Back 12

right atrium, ventricles, conducing system

Front 13

What vessels give coronary arteries their blood?

Back 13

marginal artery & posterior interventricular artery

Front 14

Where does blood drain before returning to the right atrium?

Back 14

the coronary sinus

Front 15

trace a drop of blood

Back 15

DEOXYGENATED: vena cava - right atrium - tricuspid valve - right ventricle - pulmonary valve - pulmonary artery/trunk - lungs

OXYGENATED: pulmonary veins - left atrium - bicuspid valve - left ventricle - aeortic valve - aeorta - body

Front 16

List & describe the heart valves

Back 16

AV VALVES: tricuspid (right atrium & ventricle) & bicuspid (left atrium & ventricle) have chordae tendinae that pull them open and their function is to prevent backflow

SEMILUNAR VALVES: pulmonary & aeortic, don't have muscular braces to pull them open because they're pushed by pressure from ventricles contracting. They prevent blood backflow into the ventricles

Front 17

What is the importance of heart valves?

Back 17

so oxygenated blood and deoxygenated blood don't mix and so the blood keeps flowing in the right direction instead of going backwards or not moving.

Front 18

Describe chordae tendinae and papillary muscles. Why are they important?

Back 18

When ventricles contract, the papillary muscles tense the chordae tendinae which stops the cusps of the AV valves from swinging into the atria and prevents backflow of blood back into atria.

Front 19

What's a heart murmur?

Back 19

the sound the heart makes when passing through all the valves

Front 20

Describe contractile fibers

Back 20

most of the muscle cells in the heart that help contract the heart by receiving impulses from the conduction system (purkinje fibers). They depolarize, plateau, then repolarize again.

Front 21

what are the resting potentials of contractile fibers (mV)?

Back 21

for a ventricular cell: -90 mV

for an atrial cell: -80 mV

Front 22

describe how refractory period of cardiac muscle compares to skeletal muscle & why it's important to heart function

Back 22

cardiac action potential/refractory period is 250-300 msecs, which is 30x longer than skeletal muscle. Long refractory periods prevent summation and tetany.

Front 23

Diagram & explain electrical conduction system (pages 4-6 in notes)

Back 23

[SA node activity & atrial activation begins - 0 msec] --> [stimulus stretches across atria & reaches AV node - 50 msec] --> [100 msec delay at AV node then atrial contraction begins - 150 msec] --> [impulse travels along interventricular septum within the AV bundle & bundle branches to the purkinje fibers, then to moderator band, then papillary muscles then right ventricle muscles - 175 msec] --> [impulse is distributed by purkinje fibers & relayed through myocardium. Ventricular contraction begins - 225 msec]

Front 24

how does direction and timing of electrical conduction affect contractions & heart's ability to pump blood?

Back 24

timing of the SA node sets the rhythm of the heart. direction change would change the order of the cardiac cycle and the contractions.

Front 25

what's an EKG/ECG & what info does it give about the heart?

Back 25

electrocardiogram - records electrical events in the heart and can recognize abnormal patterns so damage can be diagnosed.

Front 26

describe what happens during P-wave, QRS complex, and T-waves

Back 26

P-WAVE: atria depolarizes

QRS COMPLEX: ventricles depolarize

T-WAVE: ventricles repolarize

Front 27

compare/contrast systole and diastole

Back 27

SYSTOLE: contraction of the heart, BP rises and is shorter than diastole.

DIASTOLE: relaxtion of the heart after contraction. BP falls and process lasts longer than contraction.

Front 28

why are atrial & ventricular diastole & systole seperate events?

Back 28

because the AV & semilunar valves must open/close at seperate times. It they both opened at the same time, there would be no pressure in the heart and bloodflow would stop/slow down

Front 29

define tachycardia & bradycardia

Back 29

TACHYCARDIA: abnormally fast heart rate

BRADYCARDIA: abnormally slow heart rate

-both are abnormal pacemaker functions

Front 30

what's the cardiac cycle?

Back 30

the period between the start of one heartbeat & the beginning of the next

Front 31

what are the phases of the cardiac cycle & what happens during each phase?

Back 31

1. atrial systole begins: small amount of blood goes into the ventricles

2. atrial systole ends, atrial diastole begins

3. ventricular systole, 1st phase: ventricular contraction pushes AV valves closed, semilunar valves are still closed.

4. ventricular systole, 2nd phase: pressure rises & semilunar valves open, blood's ejected into arteries

5. ventricular diastole, early: ventricles relax, pressure drops, blood flows against the cusps and closes semilunar valves, blood flows into relaxed atria

6. ventricular diastole, late: all chambers are relaxed and ventricles fill passively

Front 32

define isovolumetric contraction

Back 32

blood volume's the same when contracting

Front 33

define isovolumetric relaxation

Back 33

blood volume's the same when relaxing

Front 34

define ventricular ejection

Back 34

ventricles eject blood in systole when the pressure is high

Front 35

define end-diastolic volume

Back 35

the amount of blood in the ventricles at the end of diastole

Front 36

define stroke volume

Back 36

the amount of blood ejected by a ventricle in one minute, mL per beat

Front 37

define contractility

Back 37

the amount of force produced during a contraction

Front 38

List the four heart sounds & describe what happens with each

Back 38

S1 - AV valves closing

S2 - "dupp" of semilunar valves closing

S3 - faint sount of blood flowing into ventricles

S4 - faint sound of atrial contraction

Front 39

define cardiac output

Back 39

the amount of blood pumped by each ventricle in one minute

Front 40

what 2 factors does cardiac output depend on?

Back 40

heart rate & stroke volume

Front 41

what are the equations for cardiac output and stroke volume?

Back 41

CO = HR x SV

SV = EDV - ESV

Front 42

define heart rate

Back 42

beats per minute

Front 43

what's the average heart rate and stroke volume in adults at rest?

Back 43

Heart rate: 70 beats/min

Stroke volume: 70 ml/beat

Front 44

If the ESV is 50 mL, EDV is 120 mL, what's the stroke volume?

Back 44

120-50=70 mL

Front 45

If the HR is 75 beats/min & SV is 70 mL/beat, what's the cardiac output?

Back 45

75 x 70 = 5,250 ml/min

Front 46

What's the effect of increased sympathetic activity on heart rate & stroke volume? How does it affect cardiac output?

Back 46

Increased sympathetic activity = increased HR, increased SV = higher cardiac output

Front 47

what's the effect of increased parasympathetic activity on heart rate & stroke volume? How does it affect cardiac output?

Back 47

Increased parasympathetic activity = SV reduced, HR goes down = lower cardiac output

Front 48

What's the effect of sudden blood loss on heart rate?

Back 48

blood pressure falls, heart rate rises, and vasoconstriction occurs to compensate for fallen blood pressure

Front 49

What are baroreceptors & chemoreceptors?

Back 49

baroreceptors: receptors in cardiac centers of cardiac reflexes that monitor blood pressure

chemoreceptors: monitor ateriol contractions of dissolved oxygen and carbon dioxide

Front 50

Why is preload in end-diastolic volume important?

Back 50

It's important because it affects the ability of muscle cells to produce tension

Front 51

what factors increase and decrease contractility?

Back 51

INCREASE: positive inotropic action = increased calcium entry into cardiac muscle cells = increased force & duration of contraction

DECREASE: negative inotropic action = calcium entry's blocked = decreased force of contraction

Front 52

which hormones are known to have a positive inotropic effect on cardiac contractility?

Back 52

epinephrine, norepinephrine, glucagon, thyroid hormone

Front 53

what are some positive & negative inotropic factors?

Back 53

ANS activity, hormones, changes in extracellular ion concentration

Front 54

what's an afterload?

Back 54

the amount of tension the contracting ventricle must produce to force open the semilunar valve & eject blood

Front 55

if afterload increases, does stroke volume increase or decrease?

Back 55

increase

Front 56

which hormones increase heart rate?

Back 56

epinephrine, norepinephrine, thyroid hormone

Front 57

EDV is affected by what two factors?

Back 57

filling time & venous return

Front 58

what's the Frank-Starling principle?

Back 58

the degree to which cardiac muscles are stretched increases the force of contraction

more in = more out

Front 59

ESV is affected by what factors?

Back 59

preload, contractility of ventricle, and afterload

Front 60

Which drugs increase & decrease BP, CO, SV, etc.?

Back 60

INCREASE: isoproterenol, dopamine, dobutamine, digitalis

DECREASE: nifedipine, verapamil, propanol, timolol, metrolol, atenolol

Front 61

What do isoproterenol, dopamine and dobutamine do?

Back 61

mimic epinephrine and norepinephrine

Front 62

What does digitalis do?

Back 62

elevates the intracellular calcium concentration

Front 63

What do nifedipine and verapamil do?

Back 63

they block calcium channels so there's less calcium in the heart

Front 64

what do propanolol, timolol, meropolol, atenolol, and labetalol do?

Back 64

they block beta receptors and/or alpha receptors & prevent sympathetic stimulation