Exsc 224

Front 1

Pericardium

Back 1

Sac which surrounds the heart, serious membrane, only surrounds the heart

Front 2

serious membrane

Back 2

membranes that surrounds organs, not open to the outside

Front 3

outermost pericardial layers of the heart

Back 3

fibrous connective tissue layers that is very though

Front 4

inner pericardial layers of the heart

Back 4

2: parietal layers and visceral layers

Front 5

parietal and visceral layers of pericardial layers of the heart

Back 5

connected to each other, 2 parts of the same sack
made up of connective tissue and squamous epithelial cells that line the interior of the cell

Front 6

epithelial cells of the heart

Back 6

produce a fluid and its job is to act as a lubricant

Front 7

what happens when the heart is at rest

Back 7

it fills with blood

Front 8

when does the heart get smaller

Back 8

when the heart contracts and pumps blood out

Front 9

friction in the heart

Back 9

heart is changing sizes which causes friction, the lubricating agent reduces friction

Front 10

pericartis

Back 10

inflammation of the pericardium not having lubricating fluid, so there is increased friction and eventually it hurts
-can be treated with antibiotics

Front 11

myocardium

Back 11

surrounds each muscle cell found in the atria and the ventricle

Front 12

properties of the myocardium

Back 12

-it makes up the majority of the mass of the heart and much of what we think of as at the function of the heart
-does not receive oxygen from blood inside the champed itself

Front 13

endocardium

Back 13

layer of connective tissue with epithelial cells that lines the internal cavities of each chamber

Front 14

what cuts of the blood of each chamber

Back 14

endocardium

Front 15

cardiac muscle bundles

Back 15

fibers in the heart move in many different directions

Front 16

what is the shape of the ventricle

Back 16

an inverted cone

Front 17

why is the ventricle in the shape of an inverted cone

Back 17

in order to pump from the bottom up there needs to be contraction forces coming from all over the heart

Front 18

left ventricle

Back 18

actually an inverted cone, has a very thick myocardium (forces high)

Front 19

right ventricle

Back 19

looks like it was tacked onto the heart structure later

Front 20

right ventricle connection

Back 20

starts connecting at the left atrium and ends back connection the left atrium

Front 21

new 4th chamber of the heart

Back 21

can separate things:
-pump blood to the lungs
-pump blood to the rest of the body independently
-allows us to not circulate mixed venus blood

Front 22

right ventricle myocardium

Back 22

has little myocardium (forces low)

Front 23

right ventricle and pumping

Back 23

can't pump against high pressures for sustained periods of time

Front 24

what does the amount of muscle show

Back 24

the amount of resistance perceived

Front 25

how much thicker is the left ventricle than the right ventricle

Back 25

3 times

Front 26

what type of shape does the right ventricle have

Back 26

crescent

Front 27

what type of shape does the left ventricle have

Back 27

cylindrical

Front 28

coronary circulation

Back 28

-atrial
-venous

Front 29

atrial

Back 29

-coronary arteries all branch off the aorta right above the aortic valve
-right side has its own branch and the left side has 2 branches

Front 30

venous

Back 30

returns the blood to the vena cava

Front 31

where do all blood vessels sit

Back 31

on the outside of the heart

Front 32

blood vessels on the outside of the heart

Back 32

-doesn't constrict blood flow to these large coronary vessels
-branch off and turn into capillaries very quickly to provide oxygen to the myocardium
-maximizes delivery of blood
-easy access to bypass

Front 33

when does coronary artery bypass graft occur

Back 33

when you have a blockage in a coronary blood vessel

Front 34

blockage in a coronary blood vessel

Back 34

-decrease flow to that part of the heart that the blood supplies
-if blockage in blood vessel, you will have attack

Front 35

process of coronary artery bypass graft

Back 35

go in and take a vein and hide in one of the blood vessels going off the aorta and tie it into the coronary artery below the blockage
-now blockage won't stop blood from getting to that area of the heart

Front 36

coronary stent

Back 36

-fine mesh wire that has been tightly rolled up that can be filled through the arteries and when they get to where the blockage is they can allow the stent to open and push the inside of the artery for blood can pass through
-very affective
-increased risk of heart attack first 24hrs after

Front 37

ballon angioplasty

Back 37

-feed in a cathatdor into artery and expand a ballon and it ruptures the blockage in the wall, opens up blood vessel
-problem, increased risk for heart attack after

Front 38

cardiac muscle is

Back 38

specialized striated muscle

Front 39

properties of cardiac muscle

Back 39

-no neuromuscular junctions
-automaticity
-conduction propagated by gap junctions
-long refractory period
-O2 dependent on product ATP
-have sarcoplasmic reticulum
-consistent with skeletal muscle,
-SR isn't the only source of calcium
-myofibrils
-doesnt like anaerobic metabolism
-cardiac muscles cells tend to be small
-cardiac muscle cells can branch
-cardiac muscle fiber connect to each other end to end
-intercalated discs
-

Front 40

automaticity

Back 40

don't tell the heart when to beat

Front 41

long refractory period of cardiac muscle

Back 41

about 300 mili secs to contract and relax

Front 42

O2 dependent on product ATP of cardiac muscle

Back 42

-lactic acid
-cant produce and survive but loves to consume as a fuel source
-glucose
-fatty acids

Front 43

sarcoplasmic reticulum of cardiac muscle

Back 43

-store calcium
-release calcium
-sequester calcium

Front 44

cardiac muscle is consistent with skeletal muscle in that __________

Back 44

has t tubule

Front 45

what is the other source of calcium in cardiac muscle

Back 45

SR isn't only source of calcium, also have proteins in the membrane which collect calcium form the extracellualar fluid

Front 46

what happens if the heart has to undergo anaerobic metabolism

Back 46

produce lactic acid = heart attack

Front 47

how many nuclei does cardiac muscle cells have

Back 47

1-4 nuceli (1000nds in skeletal)

Front 48

cardiac muscle fiber connect to each other end to end

Back 48

origin and insertion on a cardiac myosites

Front 49

intercalated discs of cardiac muscle

Back 49

-desmosomes- cell cell adhesion proteins
-gap junctions- pores that connect one cardiac myosin to the next, help with the stress but primary job is to allow sodium and potassium to flow through

Front 50

sliding filament theory

Back 50

during contraction the thin filaments slide past the thick filaments so that actin and myosin overlap to a greater degree

Front 51

how do the filaments slide

Back 51

cross-bridge cycling

Front 52

cross-bridge cycling

Back 52

1. myosin head attaches to the actin myoflilament, forming a cross bridge
2. inorganic phosphate generated in the previous contraction cycle is released, initiating the power (working) stroke. the myosin head pivots and bends as it pulls on the actin filament, sliding it toward the M line. then ADP is released
3. as new ATP attaches to the myosin head, the link between myosin and actin weakens, and the cross bridge detaches
4. as ATP is split into ADP and Pi, the myosin head is energized (cocked into the high-energy conformation)

Front 53

what is the primary function of the heart

Back 53

to pump blood through the pulmonary and systemic circulatory systems

Front 54

cardiac output (L/min) = Q

Back 54

= heart rate x stroke volume

Front 55

heart rate

Back 55

contractions/min

Front 56

stroke volume

Back 56

mL/contraction

Front 57

what is the avg adult resting cardiac output per min

Back 57

5L of blood

Front 58

do the left and right side pump the same amount of blood

Back 58

yes

Front 59

can we alter cardiac output

Back 59

yes, according to our needs

Front 60

regulation of cardiac heart rate

Back 60

-intrinsic
-extrinsic

Front 61

intrinsic (regulation of cardiac heart rate)

Back 61

-automaticity
-Sinoatrial node (SA node)
-atrioventriculuar node (AV node)
-purkinje fibers
-cardiomyocytes

Front 62

SA node in intrinsic regulation of heart rate

Back 62

-right atrium next to the superior vena cava
-pace maker because it have the highest intrinsic depolarizing rate aka depolarizes faster than other tissue

Front 63

AV node in intrinsic regulation of heart rate

Back 63

-backup to SA node
-slower than SA node

Front 64

what is the slowest in intrinsic regulation of heart rate

Back 64

cardiomyocytes

Front 65

purkinje fibers

Back 65

essentially long strands of barrel-shaped cells with few myofibrils

Front 66

where is the purkinje network more elaborate and why

Back 66

on the right side of the heart because it is larger

Front 67

extrinsic regulation of heart rate

Back 67

-autominc NS
-PNS
-SNS
-Beta one receptors are in the SA node, and the AV node and the ventricular myocardium and increases heart rate, this is different than the parasympathetic system, stimulates everything

Front 68

PNS in extrinsic regulation of heart rate

Back 68

-slows down your heart rate
-Ach
-muscarinic receptor (M2)
-decrease heart rate

Front 69

SNS in extrinsic regulation of heart rate

Back 69

-Ne and Epi
-adrenergic receptor (beta 1)
-increases heart rate

Front 70

SA node location

Back 70

sits on top of right atrium, pace maker

Front 71

what happens when the tissues of the SA node depolarizes

Back 71

its going to tell all the muscles in the atrium to contract

Front 72

where is the SA node connected and how

Back 72

connected to atrial myosin by gap junctions

Front 73

are atrial muscles and ventricle muscles attached

Back 73

no, so depolarization form one to the other does not spread

Front 74

who tells the AV node what to do

Back 74

SA node

Front 75

bundle branches

Back 75

-R and L
-pukinje fibers come off R and L bundle branches
-where we make a connection to the cardiac muscle

Front 76

what are conduction fibers important for

Back 76

determining the rate of the heart. this conduction tissue also determines the pattern of contraction

Front 77

what is the first to depolarize

Back 77

the intraventricular wall

Front 78

heart excitation related to ECG

Back 78

-SA node generates impulse; atrial excitation begins (P)
-impulse delayed at AV node
-impulses passes to heart apex; ventricular excitation begins-ventricular excitation complete

Front 79

why don't we see atrial re-polarization

Back 79

because covered by QRS complex

Front 80

automaticity

Back 80

the ability to generate an action potential without external stimuli

Front 81

what happens at threshold (cardiac intrinsic conduction)

Back 81

open up calcium channels

Front 82

once reach a positive value, calcium channels close, potassium channels open (cardiac intrinsic conduction)

Back 82

sudden depolarization (calcium rushing into the cell from outside the cell, become electrically positive)

Front 83

what is the slowest tissue to depolarize within the heart itself

Back 83

ventricular myocyte

Front 84

what happens during phase 0 of ventricular myoctye

Back 84

(membrane depolarization)
-opening of fast Na+ channels
-entry of sodium into the cell, raise membrane potential and if surpasses threshold we will have depolarization and will become electrically positive

Front 85

what happens during phase 1 of ventricular myocyte

Back 85

(brief phase, absolute refractory period)
-closure of fast Na+ channels
-opening of K+ channels
-when become temporarily positive
-very brief
-start to re-polarize, then we stop

Front 86

what happens during phase 2 of ventricular myocyte

Back 86

(plateau, prolonged absolute refractory period)
-closure of K+channels
-opening of Ca2+ entry through L-type Ca2+ channels
-maintain depolarized state
-whole point is to prevent another polarization to soon
-prolong the absolute refractory period
-cell can't depolarize again

Front 87

what happens during phase 3 of ventricular myoctye

Back 87

(repolariztion)
-closure of Ca2+ channels
-reopening of K+ channels
-restore electrically negative membrane potential

Front 88

what happens during phase 4 of ventricular myoctye

Back 88

(re-establish Na+/K+ gradients)
-pump 3 Na+ for every 2 K+
-fairly stable (relative to SA node)
-wait for re-polarization again
-still have leaky sodium channels, just don't have very many
-relatively spewing stable membrane potential

Front 89

nerve or skeletal muscle, action potential duration

Back 89

3-4 mili secs

Front 90

action potential of cardiac muscle

Back 90

300 mili secs

Front 91

cardiac muscle and phase 2

Back 91

plateau phase prolongs active state (phase 2)

Front 92

plateau phase prolongs the active state (phase 2)

Back 92

-responsible for 300 mili sec period

Front 93

advantages of prolonged active state

Back 93

-enhances contractility of myocardium
-prevents retrograde transmission of action potential

Front 94

what prevents retrograde transmission

Back 94

phase 2 prevents retrograde transmission, prevents signal from first cell flowing back into second cell telling it to contract

Front 95

extrinsic innervation of the heart

Back 95

sympathetic- cardioaccelertory
parasympathetic- cardioinhibitory
-affects only SA node and AV node

Front 96

how does the ANS modulate heart rate

Back 96

via slow leaky channels

Front 97

intrinsic property automaticity

Back 97

beats on its own

Front 98

how do we have average pace of 100 beats per min

Back 98

because parasympathetic is dominant, causing heart rate to be reduced

Front 99

fewer depolarizations =

Back 99

slower the heart rate

Front 100

what enhances the leakiness

Back 100

sympathetic nervous system

Front 101

enhanced leakiness

Back 101

sodium rushes in faster, reach threshold sooner, have an action potential

Front 102

what happens by increasing the rate of leakiness

Back 102

allows us to reach threshold more times per minute therefore higher heart rate

Front 103

parasympathetic in ANS modulates HR of slow leaky sodium channels

Back 103

slows down

Front 104

sympathetic in ANS modulates of HR of slow leaky sodium channels

Back 104

speeds up

Front 105

what are the 2 phases of the cardiac cycle

Back 105

-systole
-diastole

Front 106

systole

Back 106

-contraction phase
-spend about .3s in at rest (75 beats per min)
-spend about .2s during heavy exercise (180 beats per min)

Front 107

contraction phase

Back 107

-phase in which we pump blood, active phase
-first number when we take blood pressure

Front 108

diastole

Back 108

-relaxation phase
-ventricles fill with blood
-spend about .5s in at rest
-spend about .13s in during heavy exercise

Front 109

relaxation phase

Back 109

muscle relaxed

Front 110

ventricles fill with blood during diastole

Back 110

most of this filling is passive

Front 111

spend about .5s in at rest during diastole

Back 111

prolonged filling time

Front 112

spend about .13s during heavy exercise diastole

Back 112

as sympathetic nervous system increases heart rate, dramatically decrease amount of time spent in diastole

Front 113

stroke volume

Back 113

volume of blood we pump per contraction or per beat

Front 114

how do we calculate stroke volume?

Back 114

-based on 2 volumes of blood in the heart
- EDV (end diastolic volume) - ESV (end systolic volume)
-amount of bolo in heart at the end of of diastole (end of filling phase)
-volume of blood in the heart after contraction, after you've pumped blood out of the heart
-difference is the volume of blood effected from the heart, pumped out

Front 115

normal stroke volume

Back 115

-70mL of blood per contraction
-goes up with exercise

Front 116

ejection fraction (%)

Back 116

-the percentage of the EDV that you pump out
-calculated as (EDV-ESV)/EDV
-refers to fraction of blood pumped
-allows some volume after each stroke volume, don't pump all of the blood out of the system

Front 117

what happens when ejection fraction falls below 60%

Back 117

indicator or pathology-this heart is not in good state

Front 118

hear failure (ejection fraction)

Back 118

-below 40%
-heart to weak to pump blood effectively

Front 119

most of the filling of ventricles is ___________

Back 119

passive

Front 120

atria and ventricle with diastole or systole

Back 120

atria enter systole then re-enter diastole while the ventricle is still in diastole

Front 121

can the atria and ventricle be in systole at the same time

Back 121

no, shouldn't be

Front 122

when SA node depolarizes, what tissue depolarizes immediately after during the cardiac cycle

Back 122

atria tissue

Front 123

atrial contraction adds about what percent of final EDV of the ventricle

Back 123

20%

Front 124

what will happen following atrial relaxation during the cardiac cycle

Back 124

we will have ventricular contraction

Front 125

what happens when ventricles start to contract during the cardiac cycle

Back 125

increase in pressure in the ventricles

Front 126

increase in pressure in ventricles during the cardiac cycle

Back 126

-when the pressure increases, the AD valve will close
-represent EDV

Front 127

what happens when the ventricle begins to contract during the cardiac cycle

Back 127

close AD valve, AD valve is still closed, no shortening of myosytes

Front 128

isovolumetric contraction

Back 128

no change in volumes, all valves are closed

Front 129

what happens during isovolumetric contraction during the cardiac cycle

Back 129

-steep rise in pressure
-still haven't pumped any blood

Front 130

follow diametric pressure during cardiac cycle

Back 130

enter ejection phase

Front 131

ejection phase of cardiac cycle

Back 131

-pump blood out of ventricle
-during ejection phase aortic valve is opened

Front 132

what happens when the ventricle begins to relax during the cardiac cycle

Back 132

pressures begin to fall off, eventually pressure in this ventricle becomes lower in pressure in aorta and the aorta valve closes and we enter a third phase (isovolumetric relaxation phase)

Front 133

isovolumetric relaxation phase during cardiac cycle

Back 133

-all valves are closed, pressure falls way down
-remains until pressure in ventricle is lower than pressure in atrium

Front 134

ventricle in systole during cardiac cycle

Back 134

isovolumetric contraction phase

Front 135

ventricle in diastole during cardiac cycle

Back 135

when pressure falls below aorta

Front 136

pressures in aorta during cardiac cycle

Back 136

-have a very compressed range (120mmHg peak - 70mmHg at lowest)

Front 137

does the aorta always have blood in it during the cardiac cycle

Back 137

yes

Front 138

when does the aorta open during the cardiac cycle

Back 138

open at the end of isodiametric contraction in ventricle, opens aortic valve, pressure at lowest

Front 139

what happens when ventricle pressure starts to fall off to the pressure in aorta during the cardiac cycle

Back 139

pressure starts to decrease

Front 140

what happens when pressure in the aorta is greater than pressure in the ventricle during the cardiac cycle

Back 140

aortic valve closes

Front 141

_____ and ______ are closely tied of opening of aortic valve during the cardiac cycle

Back 141

ESV and EDV

Front 142

dicrotic notch during cardiac cycle

Back 142

is a result of pressure hitting the valve bouncing off the valve then going out towards the body (elasticity of aorta contracts, sends in both directions-balloon thing)

Front 143

blood pressure during cardiac cycle

Back 143

trying to estimate amount of pressure in aorta

Front 144

hypertension

Back 144

heart working harder, pressure around 140

Front 145

what is the pressure the heart has to work against top open aortic valve

Back 145

diastolic blood pressure

Front 146

diastolic pressure of 100mmHg effects on the heart

Back 146

effects the heart in that heart has to work harder to perform to eject blood

Front 147

factors that affect stroke volume

Back 147

-preload
-contractility
-afterload

Front 148

preload

Back 148

volume of blood returning to the heart

Front 149

venous return to the heart, when measure

Back 149

measure blood returning to vena cava (right side of heart)

Front 150

how does body posture effect venus return

Back 150

-when standing, venus return is limited
-lying down increases

Front 151

ventricular filling during venus return to the heart during preload

Back 151

ventricular filling during diastole (passive phase 80%)

Front 152

what happens when you decrease venous return

Back 152

decrease ventricular filling, decreases end diastolic volume

Front 153

increase/decrease EDV during venous return during preload

Back 153

increase EDV increase stroke volume, increase ventricular filling same with decrease, decrease EDV decrease stroke volume

Front 154

contractility

Back 154

-intrinsic (from within)
-extrinsic (from outside)

Front 155

intrinsic

Back 155

has to do with the fact that heart is elastic

Front 156

when increase volume of blood returning to heart and increase diastolic volume during intrinsic contractility what is the result

Back 156

resulting in increase in EDV have an increase in contractility

Front 157

laying down __________ venous return

Back 157

increases

Front 158

elastic qualities of intrinsic and contractility

Back 158

elastic qualities assist the muscle in shortening back to original shape so when increase EDV we increase contractility

Front 159

intrinsic influence on EDV and ESV

Back 159

doesn't influence EDV directly influences ESV directly

Front 160

properties during intrinsic and contractility

Back 160

-pump a larger volume of blood out
-preload influences stroke volume and influences contractility of the heart
-increase blood volume increase venus return, decrease blood volume decrease venus return

Front 161

extrinsic and contractility is regulated by

Back 161

autonomic nervous system

Front 162

parasympathetic nervous system, extrinsic and contractility

Back 162

associated with heart rate, also associated with force

Front 163

parasympathetic nervous system and heart rate, extrinsic and contractility

Back 163

heart rate goes down, tend to decrease contractility (chromatropic effect)

Front 164

sympathetic nervous system, extrinsic and contractility

Back 164

associated with an increase contractility of the heart

Front 165

sympathetic nervous system and increase in contractility

Back 165

stimulates an increase in contractility by increasing the calcium within the muscle
-more calcium more contractility

Front 166

what triggers the release of norepinephrine

Back 166

sympathetic nervous system

Front 167

norepinephrine and heart rate

Back 167

increases heart Ca2+ (binding to beta 1)

Front 168

how does increased intracellular Ca2+ affect contractility

Back 168

1. membrane Ca 2+ channels
2. SR Ca 2+ channels
3. SR Ca 2+ pumps

Front 169

membrane Ca 2+ channels

Back 169

gets some of the Ca from the interstitial fluid
-NE binding to beta 1 increases this
-we also stimulate release of Ca from the SR

Front 170

SR Ca 2+ pumps

Back 170

activation of the beta 1 receptors stimulates to pump faster
-allows us to contract forcefully, but still relax

Front 171

afterload, extrinsic and contractility

Back 171

resistance to blood leaving the ventricle

Front 172

when is afterload high

Back 172

when we are relaxing
-when we stand up from sitting, afterload will decrease

Front 173

what is the point of afterload

Back 173

to regulate stroke volume

Front 174

when afterload is high

Back 174

resistance to blood leaving the heart is high, we decrease stroke volume

Front 175

how do we get resistance to blood leaving the heart high, decrease in stroke volume

Back 175

by soaking up some of the contractility, larger ESV

Front 176

afterload high

Back 176

stroke volume high

Front 177

diastolic blood pressure (DBP) and afterlaod

Back 177

-ventricle has to exceed pressure on the other side of the valve (cannot open aortic valve until we exceed diastolic blood pressure, can't have ejection)
-increase diastolic blood pressure, the heart has to work harder to pump blood out
-increase diastolic blood pressure increase after load

Front 178

total peripheral resistance (TPR) and afterlaod

Back 178

-refers to state of concentration or dilation of blood vessels
-high peripheral resistance when sitting
-decrease TPR when stand up
-get more blood to systemic portion of body