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EKG & Physiology > Cardio Phys > Flashcards

Cardio Phys Flashcards

1
Q

systole

A

heart contraction (atrial and ventricular)

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2
Q

diastole

A

heart relaxation

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3
Q

cardiac muscle tissue

  • cell shape
  • appearance
A
  • branching chains of cells
  • uninucleate, striations
  • intercalated discs
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4
Q

microanatomy of cardiac muscle

A
  • sarcolemma: plasma membrane
  • sarcoplasm: cytoplasm
  • sarcoplasmic reticulum: ER
  • t tubules: unique to cardiac muscle
  • myofibrils
  • myofiliaments
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5
Q

What are the 2 myofilaments

A
  • myosin

- actin

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6
Q

What is the thick filament?

A

-myosin

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7
Q

myosin characteristics

A
  • A band
  • made up of a globular head and tail
  • has ATPase binding site
  • has actin binding site
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8
Q

what is the thin filament?

A

-actin

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9
Q

actin characteristics

A

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

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10
Q

tropomyosin

A

double stranded filament that winds around actin

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11
Q

troponin

-what does it bind

A
  • TnI: binds actin
  • TnT: bind tropomyosin
  • TnC: binds Ca++
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12
Q

Cardiomyocyte contractile cycle:

step 1

A
  • Ca++ binds TnC
  • conformational change
  • tropomyosin displaced from actin binding sites
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13
Q

Cardiomyocyte contractile cycle:

step 2

A

-crossbridge formation occurs through hydrolyzation of ATP

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14
Q

Cardiomyocyte contractile cycle:

step 3

A
  • power stroke moves actin filament toward center of sarcomere
  • ADP released from myosin heads
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15
Q

Cardiomyocyte contractile cycle:

step 4

A
  • actin release w/ ATP binding myosin

- myosin heads cocked back

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16
Q

Cardiomyocyte contractile cycle:

step 5

A
  • cycle continues until cellular Ca++ levels decrease b/c Ca dissociates from troponin
  • tropomyosin returns to original conformation that blocks actin binding site
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17
Q

summary of cardiac muscle contraction

A
  • sarcomeres shorten
  • myosin crossbridges bind actin
  • draws actin to center of sarcomere
  • requires Ca++
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18
Q

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

A
  • low ICF Ca++

- tropomyosin blocks actin/myosin from binding

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19
Q

depolarization wave in contraction (function of Ca++)

A
  • Ca++ released to ICF
  • Ca++ binds troponin (TnC)
  • conformational change removes tropomyosin from actin to reveal myosin binding site
  • myosin crossbridge binds actin
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20
Q

How do the filaments slide during cardiac muscle contraction?

A
  • ATPase activity of myosin head hydrolyzes ATP to release energy to pivot head
  • slides filaments together
  • multiple attach and release phases shorten sarcomere
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21
Q

When does filament sliding end?

A

when the stimulation ends

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22
Q

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

A
  • Ca++

- ATP

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23
Q

properties of a cardiac myocyte

A
  • striations
  • actin and myosin
  • involuntary control
  • autonomic
  • hormonal control through epi
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24
Q

What are the two different heart cell types?

A
  • contractile myocytes

- nodal cells

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25
Q

contractile myoctes

A
  • bulk of the heart

- act as a syncytium d/y attachment and intercellular communication

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26
Q

nodal cells

A
  • modified myocytes
  • non-contractile
  • initiate and conduct electrical impulse from atria to ventricles to stimulate myocardial contraction
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27
Q

2 pathways involved with the SA node

A
  • Intra-atrial pathways

- internodal pathways (SA to AV)

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28
Q

intra-atrial pathways (2)

A
  1. Bachmann bundle

2. atrial myocytes

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29
Q

internodal pathways (3)

A
  1. anterior tract
  2. Wenckebach tract
  3. Thorel tract
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30
Q

bundle of His

A
  • pathway through the septum
  • branches into LBB and RBB
  • LBB: anterior & posterior fascicle
  • RBB
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31
Q

Purkinje fibers

A

retrograde system that travel back up the heart walls

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32
Q

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

A
  • depolarization is prolonged

- not just a spike like normal action potentials

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33
Q

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

A
  • to sustain the contraction of the ventricles

- Ca++ channels open and some K channels close to allow the prolongation

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34
Q

What characteristic is unique to the SA and AV nodes?

A

-prepotential aka pacemaker potential

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35
Q

What causes repolarization?

A

-influx of K+

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36
Q

SA node

  • location
  • rate
A
  • RA at junction w/ SVC

- 60-100 BPM

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37
Q

AV node

  • location
  • rate
A
  • RA at posterioinferior area of interatrial septum

- 40-60 BPM

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38
Q

Purkinje fibers and ventricular myocytes

  • location
  • rate
A
  • throughout the ventricles

- 20-40 BPM

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39
Q

What part of the nervous system controls the heart?

A

ANS

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40
Q

PSNS vs SNS outflow originations

A
  • PSNS: craniosacral

- SNS: thoracolumbar

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41
Q

PSNS neurotransmitter

A

ACh

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42
Q

Ach acts on what types of receptors?

A

-cholinergic

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43
Q

What are the 2 types of cholinergic receptors?

A
  • muscarinic

- nicotinic

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44
Q

SNS neurotransmitter

  • from the preganglionic
  • from the postganglionic
A
  • preganglionic: Ach

- postganglionic: norepinephrine

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45
Q

norepinephrine activates what receptors?

A

adrenergic

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46
Q

Adrenergic receptor types

A
  • alpha 1
  • alpha 2
  • beta 1
  • beta 2
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47
Q

What receptor is found on cardiac muscle?

A

-beta 1

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48
Q

SA node is under PSNS control through what?

A

Vagus N.

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49
Q

AV node is under PSNS control through what?

A

Vagus N.

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50
Q

What is vagal stimulation

A
  • Ach to (M2) muscarinic receptors
  • Decreases Ca++ channels prevents depolarization
  • Increase K+ channels to hyperpolarize mb
  • firing rate decreases
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51
Q

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

A

-SNS

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52
Q

SNS control of the heart

A
  • fibers innervate nodes
  • release norepinephrine to beta-1 receptors
  • increases L channel opening and Ca++ influx
  • increases rapidity of depolarization
  • SNS drives heart rate
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53
Q

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

A
  • spreads radially through atria
  • converges on AV node
  • takes about .1 seconds
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54
Q

What is the nodal delay at the AV node?

A

0.1 seconds

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55
Q

what is the cardiac cycle

A
  • all of the events associated w/ blood flow through the heart during 1 complete heart beat
  • divided into systole and diastole
56
Q

blood flows through the heart based on __________?

A

pressure changes

57
Q

AV valves

A
  • tricuspid

- mitral

58
Q

AP valves

A
  • aortic

- pulmonic

59
Q

During late diastole:

  • valves
  • pressure
  • blood filling
  • % of filling
A
  • AV valves open
  • AP valves closed
  • pressure is low
  • blood fills chambers
  • 70% of ventricular filling
60
Q

During atrial systole

  • valves
  • atria
  • pressure
A
  • 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
Q

During ventricluar systole:

  • valves
  • path
  • phases
A
  • AV valves open
  • AP valves closed
  • begins at QRS
  • as atria relax, vent. systole begins
  • biphasic
  • isovolumetric ventricular contraction phase
62
Q

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

A

-ventricular pressure rises

63
Q

S1 “LUB” is created by what?

A

-AV valves shutting (AP valves still shut)

64
Q

pressure during isovolumetric ventricular contraction

A
  • blood is contained in ventricles
  • remains until the pressure exceeds that of aorta and pulmonary artery
  • aortic pressure is around 90mm Hg
65
Q

Ventricular systole:

  • valves
  • phase
A
  • AV valves closed
  • AP valves closed
  • ventricular ejection phase
66
Q

ventricular ejection phase

A
  • 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
Q

two parts of early diastole

A
  • protodiastole

- isovolumetric diastole

68
Q

protodiastole

A
  • ventricular pressures fall

- AP valves flap closed

69
Q

what creates the S2 (“DUB”) sound?

A

AP valves flap closed

70
Q

isovolumetric diastole

A
  • ventricular pressures continue to fall
  • ends when arterial pressure exceeds ventricular pressure
  • AV valves sucked open
  • enter ventricular filling phase
71
Q

Length cardiac cycle

A

-cardiac cycle: .8 sec

72
Q

length of atrial and ventricular systole

A
  • atrial systole: .1 sec

- ventricular systole: .3 sec

73
Q

length of diastole

A

-diastole: .4 sec

74
Q

end-diastolic ventricular volume (EDV)

A
  • at the end of relaxation, AV valves open, ventricles have filled
  • EDV is this volume
75
Q

end-systolic volume (ESV)

A

volume after contraction

76
Q

stroke volume (SV)

A

how much was moved during the contracted stroke

77
Q

SV equation

A

SV = EDV - ESV

78
Q

ejection fraction

A
  • %EDV ejected per stroke

- good indicator of ventricular function

79
Q

ejection fraction equation

A

EF = SV/EDV

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

80
Q

ejection fraction equation in word form

A

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

81
Q

ejection fraction values:

  • normal
  • below normal
  • low
A
  • normal: 50-65%
  • below normal: 36-49%
  • low: 35%
82
Q

if EF is normal:

A

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

83
Q

if EF is below normal:

A

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

84
Q

if EF is low:

A
  • indicates a weakened heart muscle and poorly pumping heart
  • low EF number increases the risk of sudden cardiac arrest
85
Q

cardiac cycle

A

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

86
Q

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

A

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

87
Q

nl arterial pulse

A

60-100 bpm

88
Q

nl newborn (0-3 mo.) pulse

A

100-150

89
Q

nl infant pulses

A
  • 3-6 mo: 90-120

- 6-12 mo: 80-120

90
Q

nl children (1-10yrs) pulse

A

70-130

91
Q

Dicrotic notch

A
  • 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
Q

jugular venous pressure (JVP)

A
  • 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
Q

what can be a cause of JVD

A

heart failure

94
Q

S1 LUB sound

A
  • AV valve closure
  • onset of V systole
  • louder, longer, more resonant
  • .15 sec
  • 25-45 mHz
95
Q

S2 DUB sounds

A
  • semilunar valve closure
  • beginning of V diastole
  • shorter and sharper sound
  • .12 sec
  • 50 mHz
96
Q

S3 heart sound

A
  • 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
Q

S4 heart sound

A
  • immediately before S1
  • abnl
  • high atrial pressure or ventricular stiffness
98
Q

mitral valve closes slightly before what?

A

tricuspid

99
Q

aortic valve closes just before what?

A

pulmonary

100
Q

what is the physiological split of S2?

A

-you hear A before P during deep inspiration

101
Q

bruit

A

-abnl sounds auscultated over a blood vessel

102
Q

carotid bruit

A
  • might be innocent
  • lumen is reduced d/t atherosclerosis
  • can cast emboli and result in cerebral ischemia
  • carotid endarterectomy if >50%
103
Q

CO =

A

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

CO = HR x SV

104
Q

stroke volume =

A

vol. of blood ejected by V per contraction

105
Q

what is the approximate blood vol in the cardiovascular system?

A

5 L

106
Q

cardiac reserve

A

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

107
Q

what is nl cardiac reserve?

A

4 X CO
(20L)

-athletes can be 35L

108
Q

changes in CO are accomplished by what?

A

-regulation of HR and or SV

109
Q

SV equation

A

SV = EDV - ESV

110
Q

EDV

A
  • length of ventricular diastole

- venous pressure

111
Q

ESV

A
  • arterial blood pressure

- force of vent. contraction

112
Q

Frank-Starling Law

A
  • 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
Q

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

A

EDV

114
Q

the most important factor in stretch is what?

A
  • venous return increasing EDV

- AKA preload*

115
Q

anything increasing EDV also increases what?

A
  • SV

- CO

116
Q

frank starling curve

A

-shows relationship b/w ventricular SV and EDV

117
Q

increasing CO in frank starling curve

A
  • slow HR

- exercise

118
Q

decreasing CO in frank starling curve

A
  • high HR
  • blood loss
  • heart dz
119
Q

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

A

EDV

120
Q

factors that can affect EDV

A
  • healthy pericardium
  • atrial systole
  • vent. compliance
  • blood vol.
  • venous constriction
  • systolic dysfunction
  • diastolic dysfunction
121
Q

afterload

A
  • pressure on the wall of the left vent. during ejection

- end load or pressure against which the heart contracts to eject blood (resistance)

122
Q

what increases afterload?

A

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

123
Q

contractility

A
  • 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
Q

what is the most important extrinsic factor affecting SV?

A

contractility

125
Q

contractility is what effect?

A
  • ionotropic

- think change in ions

126
Q

positive ionotropic effects

A
  • increase contractility
  • SNS via catecholamines (E, NE, dopamine)
  • caffeine
  • theophylline
  • digitalis
  • insulin
127
Q

negative ionotropic effects

A
  • decrease contractility
  • vagal stimulation
  • hypercapnia
  • hypoxia
  • acidosis
  • agents used to decrease cardiac workload
  • beta blockers
  • Ca++ channel blockers
  • quinidine
  • procainamide
128
Q

factors affecting HR

A
  • autonomic innervation
  • hormones
  • fitness level
  • age
129
Q

factors affecting SV

A
  • heart size
  • fitness level
  • gender
  • contractility
  • duration of contraction
  • preload (EDV)
  • afterload (resistance)
130
Q

chronotropy

A

HR

131
Q

dromotropy

A

conduction

132
Q

ionotropy

A
  • contractility (beta 1)

- pre and after load (beta 2)

133
Q

lusitropy

A

diastolic relaxation

134
Q

myocardial oxygen consumption correlation with what?

A

ventricular work

135
Q

myocardial O2 is based on what?

A
  • SV

- mean arterial pressure

136
Q

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

A

pressure work

137
Q

what causes greater O2 consumption, afterload or preload?

A

afterload

EKG & Physiology (3 decks)

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