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A&P II > Ch 20 Heart Physiology > Flashcards

Ch 20 Heart Physiology Flashcards

1
Q

Cardiac muscle tissue

A

Sarcomere- striated

Intercalated disc, one nuclei, lots of mitochondria ( ATP) , sarcolemma, no tendons- intercalated discs

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2
Q

Contractile cells - heart muscle cell

A

99% of cardiac muscle cells
Mechanical work, pumping
Do not initiate own action potential

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3
Q

Auto rhythmic cells- cardiac muscle

A

Do not contract
Initiating and conducting action potential responsible for contraction of working cells
No sarcomeres- no actin or myosin
Generate and discharge electrical impulse

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4
Q

Autorhythmicity

A

Heart beats rhythmically as a result of action potential it generates
Contract on its own, don’t need nervous system

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5
Q

Intercalated disc

A

Allow electrical impulse to travel quick to contract as unit

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6
Q

Structural elements of contractile cells

A

Sarcolemma, sarcoplasm, within plasm- myofibrils ( actin myosin), sarcoplasmic riticulum ( Swiss cheese) ,transverse tubule

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7
Q

Sarcomere

A

Basic contractile unit of cardiac ( and skeletal) muscle

Composed of long fibrous proteins that slide past each other when muscle contracts/relaxes- sliding filament

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8
Q

Part of sarcomere- myosin

A

Thick filament

Long fibrous tail and globular head, binds to actin

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9
Q

Part of sarcomere- actin

A

Thin filament

Thanks

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10
Q

Two additional proteins present in sarcomere

A

Trope in and tropomyosin

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11
Q

Sarcomere has boundary line on left and right

A

Z disc (line) made of actin and myosin ( in between actin)- made of

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12
Q

Thin (actin) made of 3 proteins

A

Actin
Tropomyosin- regulatory protein
Troponin- regulatory protein

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13
Q

Thick (mysosin) made up of

A

Myosin

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14
Q

Regulate interaction between actin and myosin

A

Tropomyosin

Troponin

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15
Q

Excitation contraction coupling mechanism

A

Motor neuron sends action potential down, releasing AcH in junction

Sodium generates electrical current- travels over sarcolemma, finds transverse tubules then to sarcoplasmic reticulum- opens pores allowing Ca to exit reticulum

Ca binds to troponin- cross bridge firmed- myosin heads will move actin

Ca is coupling agent

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16
Q

Excitation contraction coupling

A

AP over cardiac muscle membrane— reaches interior through T tubules—- t tubule AP acts on longitudinal sarcoplasmic reticulum—- release of Ca ions into sarcoplasm— Ca ions catalyze sliding of actin-myosin filaments

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17
Q

Cardiac and skeletal share mechanism of contraction but

A

They don’t work the same- skeletal takes less time from contraction to relaxing- bell shape

Cardiac elongated contraction- sustained contraction( plateau phase) - 250-300 millisecond -

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18
Q

Everything of heart is made to

A

Maximize cardiac output with least number of beats

More efficient to hold contraction

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19
Q

Action potential of skeletal muscle is caused by opening fast sodium channels

A

Action potential in cardiac muscle is caused by fast sodium channels and slow calcium channels

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20
Q

Troponin

A

3 polypeptide found in striated muscle fibers

One peptide binds to actin (Tnl) another binds to tropomyosin (TNT) a third binds to calcium (Tnc)

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21
Q

When____ ions bind to troponin, the troponin change shape forcing tropomyosin away from actin filaments. This allows myosin cross-bridges to attach onto actin enabling contraction

A

Calcium

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22
Q

Troponin holds on to ____ in cardiac muscle, giving longer contraction

A

Calcium

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23
Q

Cardiac troponin serves as a potent and specific marker for

A

Cardiac disease

Heart attack- cell membranes rupture- release of cardiac troponin into blood stream.

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24
Q

Cardiac muscle does not go in to

A

Tetany

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25
Q

Heart muscle in tetany is called what

A

Cardiac flutter and fibrillation- later can lead to death

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26
Q

Tetany is a condition where

A

A muscle cell goes into elongated contraction (spasm)

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27
Q

In order for the heart to pump it has to

A

Fill with blood

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28
Q

The heart can only fill with blood when it is

A

Relaxed

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29
Q

Refractory period is what

A

Time where cell is stimulated but doesn’t react

Refractory period is very short in skeletal

Resting period- longer than contraction in cardiac muscle

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30
Q

When sarcomere shorten they use

A

ATP, producing carbon dioxide (acting like an acid) .

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31
Q

Properties of cardiac muscle

A

Auto excitable- capability of contract even in the absence of neural control

Autorhythmic- heart beats are extremely regular

Prolonged contraction- hold contraction for longer period

Does not fatigue ( go into tetany), does not get tired

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32
Q

Cardiac cycle

A

Cardiac events that occur from beginning of one heart beat to the beginning of the next

Each initiated by spontaneous generation of action potential in sinus node

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33
Q

Cardiac cycle

A

Electrical pressure and volume change in a functional heart between successive heart beats

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34
Q

Diastole

A

Cardiac cycle phase when myocardium is relaxed

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35
Q

Systole

A

Phase of cardiac cycle when myocardium contracts

Atrial systole- when atria contract
Ventricular systole when ventricles contract

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36
Q

Fluids move from high pressure to- pressure gradient

A

Low pressure

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37
Q

Three things happen simultaneously in systolic phased

A

High pressure phase
Contraction
Emptying - fluid leaving(high pressure to low pressure) volume decreasing

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38
Q

Diastolic has 3 simultaneous events

A

Low pressure
Muscle relaxed
Filling up( volume increases)

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39
Q

When atrial are in systole ventricles are in

A

Diastole

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40
Q

End diastolic volume

A

Volume of blood that fills in ventricles at end of diastolic phase

120-150 ml

41
Q

Stroke volume

A

Volume of blood pumped by a ventricle per beat

SV= end diastolic volume minus end systolic volume

70 ml

42
Q

End systolic volume

A

Amount of blood remaining in a ventricle after contraction

43
Q

Ejection fraction

A

% of edv that is pumped by ventricle

Stroke volume/end diastole volume x100%- should be about 55-60% higher

44
Q

Ventricular systole

A

Contraction
High pressure
Fluid leaving (ventricles empty)

45
Q

Atrial systole opens

A

Bicuspid and tricuspid valves

Aortic and pulmonary closed

46
Q

S1- sound 1- lub

A

Bicuspid and tricuspid close during ventricular systole

Pulmonary and aortic are open

47
Q

S2- sound 2- dub

A

Aortic and pulmonary valves closing occurs during atrial systole.

48
Q

Lub

A

Recoil of blood against closed AV valve

49
Q

Dub

A

Recoil of blood against semilunar valves

50
Q

Murmur

A

Defect causing hissing sound when stream of blood squirts backward through valve

51
Q

Cardiac output

A

Volume of blood ejected from heart ( left ventricle) every minute

52
Q

CO= HRxSV =5000 ml/min (5liters)

SV= stroke volume

This is a resting measure

A

This is our entire volume of blood pumped every min at rest

A drop would be congestive heart failure

53
Q

Cardiac reserve

A

Difference between maximum cardiac output and resting cardiac out put

54
Q

Normal cardiac reserve as a percent

A

Normal cardiac reserve = 15-20L/min= 200-400%- cardiac reserve of 2-4

Endurance athlete= 35mL=600% - cardiac reserve of 7 times in a min

55
Q

Cardiac index

CI= cardiac output(CO) /body surface area BSA

Remember CO= HRxSV

A

Relates cardiac output to the size of the individual

Normal range of CI is 2.6-4.2 L/min per square meter

If CI falls below 1.8 L/min the patient may be in cardiac shock

56
Q

What are the factors of cardiac output

A

Inotropic- strength of contraction (stroke volume)

Chronotropic- the heart rate

57
Q

Cardiotropy is based on

A

Cardiac muscle properties

58
Q

Cardiac muscle properties that effect cardiotropy

A

Chronotropic ( HR)*

Inotropic ( contractility)- stroke volume*

Dromotropic ( conduction velocity)- sends impulse- pace maker surgery

Bathmotropic ( excitability)- electrical field- ions, Na, K— electrolyte embalance, pH balances

Lusitropic ( relaxation)*- heart fills

Any issue will decrease cardiac output

59
Q

Primary impact on chronotropic factor (HR control)

A

Autonomic nervous system

60
Q

Baroreceptors

A

Monitor heart activity by monitoring BP

Monitor HR through BP

61
Q

Vagus (x) - (parasympathetic)and glassopharyngeal (IX)

A

Sensory neurons- electrical impulse CI to medulla-into cardiovascular (CV) integration area—- cardiac inhibitory center or cardiac acceleration center

Reflex circuit-

62
Q

Reflexes have 5 basic parts

A 
Receptors
Sensory neuron
Integration center
Motor neuron
Effector
63
Q

ANS controls

A

HR

64
Q

Speed HR up with_____ slow it down with______

A

Sympathetic(epinephrine), parasympathetic ( uses acH)

65
Q

Positive chronotropic

A

Any chemical that raises HR

Epinephrine
Caffeine is

66
Q

Negative chronotropic

A

AcH

67
Q

Stroke volume - 3 variables effect

A

Preload-

Contractility

After load

68
Q

Preload

A

Volume that stretches the LV( left ventricle) just before contraction ( enters during diastole- end diastolic volume)

Measured by CVP for RV and pAWP for LV

Measures preload of the LV or LVEDP= wedge or paw

69
Q

Greater the preload the greater the stroke volume and the greater the cardiac….

A

Output

70
Q

Ventricular preload is the

A

End diastolic volume, generally dependent on ventricular filling

71
Q

Relationship between cardiac output and ventricular end diastolic volume is known as

A

Starlings law of the heart

72
Q

Increase end diastolic volume

A

Cardiac wall now stretches, stronger contraction- starling law

73
Q

Sterling law (sling shot analogy)

A

Greater the length of cardia fibers, the greater the strength of contraction

Describes how heart changes it’s force of contraction, stroke volume, in response to venous blood return

74
Q

Greater Venus blood return results in an increase in ventricular filling and preload . In turn

A

Length of cardiac muscle fibers increases- stretch as heart fills with blood, resulting in greater strength of contraction

75
Q

If preload increases so does

A

Cardiac output CO

76
Q

More sarcomere the _____

A

Stronger the contraction

77
Q

Increase stretch increases contraction which increases….

A

Stroke volume

78
Q

Left and right must pump the ____ amount of fluid

A

Same

79
Q

Factors increasing end diastolic volume

A 
Respiratory pump
Cardiac pump
Muscle pump
Blood volume
Sympathetic discharge
Standing body position 
Resistance to venous return
80
Q

Cardiac output

A

Preload -starling
Contractility-starling mech.
After load
Chronotropic

81
Q

Contractility

A

Intrinsic ability of the myocardium to pump in the absence of changes to preload or after load

Can be altered by neural, humoral, pharmacological influences-

Sympathetic nervous system activity normally has the most important effect on contractility

82
Q

Myocardial contractility is depressed by anoxia, acidosis, depletion of catecholamine stores within heart and loss of functioning muscle mass as a result of ischemia or infarction

A

Most anesthetic and anti arrhythmic agents are negative inotropes ( they decrease contractility )

83
Q

Contractility

A

Intrinsic ability of cardiac muscle

Inotropism, inotropy

Related to intracellular ca2+

Force generated by myocardium when ventricular muscle fibers shorten

84
Q

Inotropic agents

A

Positive: increase contractility - epinephrine

Negative: decrease contractility-AcH

How much calcium in muscle cells- increase Ca, increase strength and vice versa

85
Q

Increase sarcomere numbers that increase

A

Increase contraction strength

86
Q

Contractility is affected by

A

Drugs
Oxygen levels within myocardium
Cardiac muscle damage
Electrolyte imbalance

87
Q

After load

A

Amount of resistance the heart must pump against when ejecting blood

88
Q

3 components that affect stroke volume

A

Preload- increase this, increase SV

Contractility- increase this, increase SV

After load - resistance LV runs into when pushing blood in sorta, main resistance is aortic valve

89
Q

Opening aortic valve

  1. 90 units
  2. Additional 20 units
  3. Contract with additional 10 units of pressure strength

120/80- becomes blood pressure

A

Normal valve has back pressure ( 80 units)- keeps valve closed. LV has to open valve, 79 units won’t open valve. Has to contract over 80 units. ( usually 90’units) to open as far as it will

Large volume of blood through small opening- additional 20 units to pump into aorta

Push far enough in to aorta to give valve time to close- kinetic (velocity) energy

90
Q

Preload that LV has to work against is the diastolic ( bottom-80)

A

Pressure of BP against the valve

Higher pressure, more work on LV

91
Q

Decrease after load

A

That will increase stroke volume

92
Q

Top number systolic is function of

A

Diastolic- bottom increase, top increase vice versa

93
Q

Pulse pressure (40)

A

Difference between systolic (120) and diastolic (80)

94
Q

Heart will try to keep systolic (top)

A

50% higher than bottom

95
Q

Treating hypertension

A

Get bottom number to drop, top number will follow

96
Q

LV tries to keep pulse pressure

A

50% of bottom number

97
Q

Pre load

A

Always is a volume

98
Q

After load

A

Pressure (BP)

99
Q

Decrease after load to increase

A

Stroke volume

A&P II (11 decks)

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