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EKG & Physiology > Cardio Phys > Flashcards

Flashcards in Cardio Phys Deck (137):
1

systole

heart contraction (atrial and ventricular)

2

diastole

heart relaxation

3

cardiac muscle tissue
-cell shape
-appearance

-branching chains of cells
-uninucleate, striations
-intercalated discs

4

microanatomy of cardiac muscle

-sarcolemma: plasma membrane
-sarcoplasm: cytoplasm
-sarcoplasmic reticulum: ER
-t tubules: unique to cardiac muscle
-myofibrils
-myofiliaments

5

What are the 2 myofilaments

-myosin
-actin

6

What is the thick filament?

-myosin

7

myosin characteristics

-A band
-made up of a globular head and tail
-has ATPase binding site
-has actin binding site

8

what is the thin filament?

-actin

9

actin characteristics

-globular actin (G): individual subunits of protein that forms fibrous actin (F)

10

tropomyosin

double stranded filament that winds around actin

11

troponin
-what does it bind

-TnI: binds actin
-TnT: bind tropomyosin
-TnC: binds Ca++

12

Cardiomyocyte contractile cycle:
step 1

-Ca++ binds TnC
-conformational change
-tropomyosin displaced from actin binding sites

13

Cardiomyocyte contractile cycle:
step 2

-crossbridge formation occurs through hydrolyzation of ATP

14

Cardiomyocyte contractile cycle:
step 3

-power stroke moves actin filament toward center of sarcomere
-ADP released from myosin heads

15

Cardiomyocyte contractile cycle:
step 4

-actin release w/ ATP binding myosin
-myosin heads cocked back

16

Cardiomyocyte contractile cycle:
step 5

-cycle continues until cellular Ca++ levels decrease b/c Ca dissociates from troponin
-tropomyosin returns to original conformation that blocks actin binding site

17

summary of cardiac muscle contraction

-sarcomeres shorten
-myosin crossbridges bind actin
-draws actin to center of sarcomere
-requires Ca++

18

What is the condition of the sarcomere during the relaxed state?

-low ICF Ca++
-tropomyosin blocks actin/myosin from binding

19

depolarization wave in contraction (function of Ca++)

-Ca++ released to ICF
-Ca++ binds troponin (TnC)
-conformational change removes tropomyosin from actin to reveal myosin binding site
-myosin crossbridge binds actin

20

How do the filaments slide during cardiac muscle contraction?

-ATPase activity of myosin head hydrolyzes ATP to release energy to pivot head
-slides filaments together
-multiple attach and release phases shorten sarcomere

21

When does filament sliding end?

when the stimulation ends

22

What 2 main things are needed to have sliding filaments/contraction?

-Ca++
-ATP

23

properties of a cardiac myocyte

-striations
-actin and myosin
-involuntary control
-autonomic
-hormonal control through epi

24

What are the two different heart cell types?

-contractile myocytes
-nodal cells

25

contractile myoctes

-bulk of the heart
-act as a syncytium d/y attachment and intercellular communication

26

nodal cells

-modified myocytes
-non-contractile
-initiate and conduct electrical impulse from atria to ventricles to stimulate myocardial contraction

27

2 pathways involved with the SA node

-Intra-atrial pathways
-internodal pathways (SA to AV)

28

intra-atrial pathways (2)

1. Bachmann bundle
2. atrial myocytes

29

internodal pathways (3)

1. anterior tract
2. Wenckebach tract
3. Thorel tract

30

bundle of His

-pathway through the septum
-branches into LBB and RBB
-LBB: anterior & posterior fascicle
-RBB

31

Purkinje fibers

retrograde system that travel back up the heart walls

32

What is unique to the action potential in ventricular cardiac myocytes?

-depolarization is prolonged
-not just a spike like normal action potentials

33

What is the point of the prolongation/plateau in the cardiac myocyte action potential? And what causes it?

-to sustain the contraction of the ventricles
-Ca++ channels open and some K channels close to allow the prolongation

34

What characteristic is unique to the SA and AV nodes?

-prepotential aka pacemaker potential

35

What causes repolarization?

-influx of K+

36

SA node
-location
-rate

-RA at junction w/ SVC
-60-100 BPM

37

AV node
-location
-rate

-RA at posterioinferior area of interatrial septum
-40-60 BPM

38

Purkinje fibers and ventricular myocytes
-location
-rate

-throughout the ventricles
-20-40 BPM

39

What part of the nervous system controls the heart?

ANS

40

PSNS vs SNS outflow originations

-PSNS: craniosacral
-SNS: thoracolumbar

41

PSNS neurotransmitter

ACh

42

Ach acts on what types of receptors?

-cholinergic

43

What are the 2 types of cholinergic receptors?

-muscarinic
-nicotinic

44

SNS neurotransmitter
-from the preganglionic
-from the postganglionic

-preganglionic: Ach
-postganglionic: norepinephrine

45

norepinephrine activates what receptors?

adrenergic

46

Adrenergic receptor types

-alpha 1
-alpha 2
-beta 1
-beta 2

47

What receptor is found on cardiac muscle?

-beta 1

48

SA node is under PSNS control through what?

Vagus N.

49

AV node is under PSNS control through what?

Vagus N.

50

What is vagal stimulation

-Ach to (M2) muscarinic receptors
-Decreases Ca++ channels prevents depolarization
-Increase K+ channels to hyperpolarize mb
-firing rate decreases

51

Which has a greater effect on the heart, PSNS or SNS?

-SNS

52

SNS control of the heart

-fibers innervate nodes
-release norepinephrine to beta-1 receptors
-increases L channel opening and Ca++ influx
-increases rapidity of depolarization
-SNS drives heart rate

53

In the spread of cardiac excitation, what happens when the SA node depolarizes?

-spreads radially through atria
-converges on AV node
-takes about .1 seconds

54

What is the nodal delay at the AV node?

0.1 seconds

55

what is the cardiac cycle

-all of the events associated w/ blood flow through the heart during 1 complete heart beat
-divided into systole and diastole

56

blood flows through the heart based on __________?

pressure changes

57

AV valves

-tricuspid
-mitral

58

AP valves

-aortic
-pulmonic

59

During late diastole:
-valves
-pressure
-blood filling
-% of filling

-AV valves open
-AP valves closed
-pressure is low
-blood fills chambers
-70% of ventricular filling

60

During atrial systole
-valves
-atria
-pressure

-AV valves open
-AP valves closed
-atria contract (p wave), atrial pressure rises propelling blood to ventricles
-aortic pressure is around 80mm Hg = diastolic pressure

61

During ventricluar systole:
-valves
-path
-phases

-AV valves open
-AP valves closed
-begins at QRS
-as atria relax, vent. systole begins
-biphasic
-isovolumetric ventricular contraction phase

62

during isovolumetric ventricular contraction phase, what shuts the AV valves?

-ventricular pressure rises

63

S1 "LUB" is created by what?

-AV valves shutting (AP valves still shut)

64

pressure during isovolumetric ventricular contraction

-blood is contained in ventricles
-remains until the pressure exceeds that of aorta and pulmonary artery
-aortic pressure is around 90mm Hg

65

Ventricular systole:
-valves
-phase

-AV valves closed
-AP valves closed
-ventricular ejection phase

66

ventricular ejection phase

-ventricular pressure exceeds great arteries
-AV leaflets are pressed up, increasing arterial pressure
-AP valves open, ventricular blood is ejected
-aortic pressure is at peak - 120mm Hg
-i.e peak systolic pressure

67

two parts of early diastole

-protodiastole
-isovolumetric diastole

68

protodiastole

-ventricular pressures fall
-AP valves flap closed

69

what creates the S2 ("DUB") sound?

AP valves flap closed

70

isovolumetric diastole

-ventricular pressures continue to fall
-ends when arterial pressure exceeds ventricular pressure
-AV valves sucked open
-enter ventricular filling phase

71

Length cardiac cycle

-cardiac cycle: .8 sec

72

length of atrial and ventricular systole

-atrial systole: .1 sec
-ventricular systole: .3 sec

73

length of diastole

-diastole: .4 sec

74

end-diastolic ventricular volume (EDV)

-at the end of relaxation, AV valves open, ventricles have filled
-EDV is this volume

75

end-systolic volume (ESV)

volume after contraction

76

stroke volume (SV)

how much was moved during the contracted stroke

77

SV equation

SV = EDV - ESV

78

ejection fraction

-%EDV ejected per stroke
-good indicator of ventricular function

79

ejection fraction equation

EF = SV/EDV

i.e: EF = EDV - ESV/EDV x 100%

80

ejection fraction equation in word form

amount of blood pumped out of the ventricle divided by the total amount of blood in the ventricle

81

ejection fraction values:
-normal
-below normal
-low

-normal: 50-65%
-below normal: 36-49%
-low: 35%

82

if EF is normal:

the heart is pumping normally and can deliver an adequate supply of blood to the body and brain

83

if EF is below normal:

could indicate that the heart is not pumping well enough to meet the body's needs

84

if EF is low:

-indicates a weakened heart muscle and poorly pumping heart
-low EF number increases the risk of sudden cardiac arrest

85

cardiac cycle

she gave various charts to review the overall cycle. slides 36-38

86

arterial pulse is felt during what part of the cardiac cycle?

-ventricular systole: it creates the highest systolic pressure which travels along the arteries

87

nl arterial pulse

60-100 bpm

88

nl newborn (0-3 mo.) pulse

100-150

89

nl infant pulses

-3-6 mo: 90-120
-6-12 mo: 80-120

90

nl children (1-10yrs) pulse

70-130

91

Dicrotic notch

-vibrations caused as aortic valve snaps shut
-at end of ventricular systole (DUB)
-secondary upstroke in descending part of pulse
-measurable but not palpable

92

jugular venous pressure (JVP)

-indirectly visualized by observing jugular pulse
-atrial pressure increases during atrial systole and through isovolumetric phase of V systole
-falls when AV valves open
-atrial pressure changes are transmitted to great viens (jugular)

93

what can be a cause of JVD

heart failure

94

S1 LUB sound

-AV valve closure
-onset of V systole
-louder, longer, more resonant
-.15 sec
-25-45 mHz

95

S2 DUB sounds

-semilunar valve closure
-beginning of V diastole
-shorter and sharper sound
-.12 sec
-50 mHz

96

S3 heart sound

-1/3 of the way through diastole
-"kentucky"
-nl in young d/t rush of vent. filling
-abnl in mitral regurg or heart failure

97

S4 heart sound

-immediately before S1
-abnl
-high atrial pressure or ventricular stiffness

98

mitral valve closes slightly before what?

tricuspid

99

aortic valve closes just before what?

pulmonary

100

what is the physiological split of S2?

-you hear A before P during deep inspiration

101

bruit

-abnl sounds auscultated over a blood vessel

102

carotid bruit

-might be innocent
-lumen is reduced d/t atherosclerosis
-can cast emboli and result in cerebral ischemia
-carotid endarterectomy if >50%

103

CO =

amount of blood in L pumped out by each ventricle in 1 min.

CO = HR x SV

104

stroke volume =

vol. of blood ejected by V per contraction

105

what is the approximate blood vol in the cardiovascular system?

5 L

106

cardiac reserve

-ability of heart to push its CO above nl to meet needs

107

what is nl cardiac reserve?

4 X CO
(20L)

-athletes can be 35L

108

changes in CO are accomplished by what?

-regulation of HR and or SV

109

SV equation

SV = EDV - ESV

110

EDV

-length of ventricular diastole
-venous pressure

111

ESV

-arterial blood pressure
-force of vent. contraction

112

Frank-Starling Law

-energy of contraction is proportional to the initial length of the cardiac muscle fiber
-layman terms: the more you can stretch, the more you can contract

113

in Frank Starling law, the length of the muscle fiber is proportional to what?

EDV

114

the most important factor in stretch is what?

-venous return increasing EDV
-AKA preload*

115

anything increasing EDV also increases what?

-SV
-CO

116

frank starling curve

-shows relationship b/w ventricular SV and EDV

117

increasing CO in frank starling curve

-slow HR
-exercise

118

decreasing CO in frank starling curve

-high HR
-blood loss
-heart dz

119

____ is the single most important factor affecting SV, and therefore CO.

EDV

120

factors that can affect EDV

-healthy pericardium
-atrial systole
-vent. compliance
-blood vol.
-venous constriction
-systolic dysfunction
-diastolic dysfunction

121

afterload

-pressure on the wall of the left vent. during ejection
-end load or pressure against which the heart contracts to eject blood (resistance)

122

what increases afterload?

-HTN
-aortic stenosis
(b/c vent. has to work harder)

123

contractility

-ability of the heart muscle to contract
-the effect of sympathetic stimulation on heart
-usually increases Ca++ availability to myocardium, promoting crossbridge activity and therefore stroke
-increases conduction as well

124

what is the most important extrinsic factor affecting SV?

contractility

125

contractility is what effect?

-ionotropic
-think change in ions

126

positive ionotropic effects

-increase contractility
-SNS via catecholamines (E, NE, dopamine)
-caffeine
-theophylline
-digitalis
-insulin

127

negative ionotropic effects

-decrease contractility
-vagal stimulation
-hypercapnia
-hypoxia
-acidosis
-agents used to decrease cardiac workload
-beta blockers
-Ca++ channel blockers
-quinidine
-procainamide

128

factors affecting HR

-autonomic innervation
-hormones
-fitness level
-age

129

factors affecting SV

-heart size
-fitness level
-gender
-contractility
-duration of contraction
-preload (EDV)
-afterload (resistance)

130

chronotropy

HR

131

dromotropy

conduction

132

ionotropy

-contractility (beta 1)
-pre and after load (beta 2)

133

lusitropy

diastolic relaxation

134

myocardial oxygen consumption correlation with what?

ventricular work

135

myocardial O2 is based on what?

-SV
-mean arterial pressure

136

what causes greater O2 consumption, pressure work or volume work?

pressure work

137

what causes greater O2 consumption, afterload or preload?

afterload