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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
Heart muscle in tetany is called what
Cardiac flutter and fibrillation- later can lead to death
26
Tetany is a condition where
A muscle cell goes into elongated contraction (spasm)
27
In order for the heart to pump it has to
Fill with blood
28
The heart can only fill with blood when it is
Relaxed
29
Refractory period is what
Time where cell is stimulated but doesn’t react Refractory period is very short in skeletal Resting period- longer than contraction in cardiac muscle
30
When sarcomere shorten they use
ATP, producing carbon dioxide (acting like an acid) .
31
Properties of cardiac muscle
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
32
Cardiac cycle
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
33
Cardiac cycle
Electrical pressure and volume change in a functional heart between successive heart beats
34
Diastole
Cardiac cycle phase when myocardium is relaxed
35
Systole
Phase of cardiac cycle when myocardium contracts Atrial systole- when atria contract Ventricular systole when ventricles contract
36
Fluids move from high pressure to- pressure gradient
Low pressure
37
Three things happen simultaneously in systolic phased
High pressure phase Contraction Emptying - fluid leaving(high pressure to low pressure) volume decreasing
38
Diastolic has 3 simultaneous events
Low pressure Muscle relaxed Filling up( volume increases)
39
When atrial are in systole ventricles are in
Diastole
40
End diastolic volume
Volume of blood that fills in ventricles at end of diastolic phase 120-150 ml
41
Stroke volume
Volume of blood pumped by a ventricle per beat SV= end diastolic volume minus end systolic volume 70 ml
42
End systolic volume
Amount of blood remaining in a ventricle after contraction
43
Ejection fraction
% of edv that is pumped by ventricle Stroke volume/end diastole volume x100%- should be about 55-60% higher
44
Ventricular systole
Contraction High pressure Fluid leaving (ventricles empty)
45
Atrial systole opens
Bicuspid and tricuspid valves Aortic and pulmonary closed
46
S1- sound 1- lub
Bicuspid and tricuspid close during ventricular systole Pulmonary and aortic are open
47
S2- sound 2- dub
Aortic and pulmonary valves closing occurs during atrial systole.
48
Lub
Recoil of blood against closed AV valve
49
Dub
Recoil of blood against semilunar valves
50
Murmur
Defect causing hissing sound when stream of blood squirts backward through valve
51
Cardiac output
Volume of blood ejected from heart ( left ventricle) every minute
52
CO= HRxSV =5000 ml/min (5liters) SV= stroke volume This is a resting measure
This is our entire volume of blood pumped every min at rest A drop would be congestive heart failure
53
Cardiac reserve
Difference between maximum cardiac output and resting cardiac out put
54
Normal cardiac reserve as a percent
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
Cardiac index CI= cardiac output(CO) /body surface area BSA Remember CO= HRxSV
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
What are the factors of cardiac output
Inotropic- strength of contraction (stroke volume) Chronotropic- the heart rate
57
Cardiotropy is based on
Cardiac muscle properties
58
Cardiac muscle properties that effect cardiotropy
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
Primary impact on chronotropic factor (HR control)
Autonomic nervous system
60
Baroreceptors
Monitor heart activity by monitoring BP Monitor HR through BP
61
Vagus (x) - (parasympathetic)and glassopharyngeal (IX)
Sensory neurons- electrical impulse CI to medulla-into cardiovascular (CV) integration area—- cardiac inhibitory center or cardiac acceleration center Reflex circuit-
62
Reflexes have 5 basic parts
``` Receptors Sensory neuron Integration center Motor neuron Effector ```
63
ANS controls
HR
64
Speed HR up with_____ slow it down with______
Sympathetic(epinephrine), parasympathetic ( uses acH)
65
Positive chronotropic
Any chemical that raises HR Epinephrine Caffeine is
66
Negative chronotropic
AcH
67
Stroke volume - 3 variables effect
Preload- Contractility After load
68
Preload
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
Greater the preload the greater the stroke volume and the greater the cardiac....
Output
70
Ventricular preload is the
End diastolic volume, generally dependent on ventricular filling
71
Relationship between cardiac output and ventricular end diastolic volume is known as
Starlings law of the heart
72
Increase end diastolic volume
Cardiac wall now stretches, stronger contraction- starling law
73
Sterling law (sling shot analogy)
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
Greater Venus blood return results in an increase in ventricular filling and preload . In turn
Length of cardiac muscle fibers increases- stretch as heart fills with blood, resulting in greater strength of contraction
75
If preload increases so does
Cardiac output CO
76
More sarcomere the _____
Stronger the contraction
77
Increase stretch increases contraction which increases....
Stroke volume
78
Left and right must pump the ____ amount of fluid
Same
79
Factors increasing end diastolic volume
``` Respiratory pump Cardiac pump Muscle pump Blood volume Sympathetic discharge Standing body position Resistance to venous return ```
80
Cardiac output
Preload -starling Contractility-starling mech. After load Chronotropic
81
Contractility
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
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
Most anesthetic and anti arrhythmic agents are negative inotropes ( they decrease contractility )
83
Contractility
Intrinsic ability of cardiac muscle Inotropism, inotropy Related to intracellular ca2+ Force generated by myocardium when ventricular muscle fibers shorten
84
Inotropic agents
Positive: increase contractility - epinephrine Negative: decrease contractility-AcH How much calcium in muscle cells- increase Ca, increase strength and vice versa
85
Increase sarcomere numbers that increase
Increase contraction strength
86
Contractility is affected by
Drugs Oxygen levels within myocardium Cardiac muscle damage Electrolyte imbalance
87
After load
Amount of resistance the heart must pump against when ejecting blood
88
3 components that affect stroke volume
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
Opening aortic valve 1. 90 units 2. Additional 20 units 3. Contract with additional 10 units of pressure strength 120/80- becomes blood pressure
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
Preload that LV has to work against is the diastolic ( bottom-80)
Pressure of BP against the valve Higher pressure, more work on LV
91
Decrease after load
That will increase stroke volume
92
Top number systolic is function of
Diastolic- bottom increase, top increase vice versa
93
Pulse pressure (40)
Difference between systolic (120) and diastolic (80)
94
Heart will try to keep systolic (top)
50% higher than bottom
95
Treating hypertension
Get bottom number to drop, top number will follow
96
LV tries to keep pulse pressure
50% of bottom number
97
Pre load
Always is a volume
98
After load
Pressure (BP)
99
Decrease after load to increase
Stroke volume

A&P II (11 decks)

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