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HLSC 126 - Human Physiology I > Chapter 9 > Flashcards

Chapter 9 Flashcards

1
Q

Components of the Circulatory System

A

-heart: pump
-blood vessels: passageways
-blood: transports dissolved materials

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2
Q

Cardiac Muscle

A

-striated
-branched
-intercalculated discs: desmosomes + gap junctions
-consist of myosin, actin, troponin, tropomyosin
-have well developed SR and large T-tubules
-SR and ECF are the source of calcium
-deep red colour results from high oxygen blood and myoglobin
-high amounts of mitochondria for energy

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3
Q

Pulmonary Circulation

A

-closed loop of vessels carrying blood between heart and lungs
-low pressure and low resistance system

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4
Q

Systemic Circulation

A

-circuit of vessels carrying blood between heart and other body systems
-high pressure and high resistance system

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5
Q

Embryonic Development of the Heart

A

-day 25 is a single tube
-day 28 it forms a duct/sac like structure
-by birth it is fully functioning with 4 compartments

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6
Q

Base

A

part at the tip that tapers to a tip

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7
Q

Apex

A

-bottom of the heart
-directed to left side of the chest

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8
Q

The pump

A

-right and left sides of the heart function as two separate pumps even though they make up one organ

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9
Q

Atria

A

-divided into right and left halves
-superior chambers of the heart

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10
Q

Right Atrium

A

-where venous blood enters from superior and inferior vena cava (systemic veins)

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11
Q

Left Atrium

A

-where blood reenters heart via pulmonary veins after being reoxygenated in the lungs

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12
Q

Ventricles

A

-divided into right and left halves
-inferior portion

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13
Q

Right Ventricle

A

-blood flows here from right atrium and then goes to lungs via pulmonary arteries

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14
Q

Left Ventricle

A

-blood flows here from left atrium then heads to rest of the body via aorta then systemic arteries

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15
Q

Septum

A

-continuous muscular partition that prevents mixture of blood from the two sides of the heart

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16
Q

Lungs

A

-contain pulmonary capillaries that exchange nutrients (O2) and waste (CO2)

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17
Q

Veins

A

-carry blood from tissues to the atria
-not necessarily only carry deoxygenated blood

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18
Q

Arteries

A

-carry blood away from ventricles to tissues
-not necessarily only carry oxygenated blood

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19
Q

Which side of the heart is stronger?

A

-the left side
-pumps at a higher pressure into a longer system

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20
Q

Valves

A

-ensure blood flows in a linear/uni direction
-laminar flow
-blood can’t come backwards (turbulent flow)

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21
Q

Right Atrioventricular (AV) Valve

A

-aka tricuspid valve (has 3 regions)
-from right atrium to right ventricle

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22
Q

Left Atrioventricular (AV) Valve

A

-aka bicuspid/mitral valve (has 2 regions)
-between left atrium and left ventricle

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23
Q

Mitral Stenosis

A

-hardened/not working valve

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24
Q

Semilunar valves

A

-have 3 cusps/half moons
-Aortic SL Valve: from left ventricle to aorta
-Pulmonary SL Valve: from right ventricle to R and L pulmonary arteries

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25
Q

Chordae Tendinae

A

-though thin fibrous/tendon tissues that fasten the AV Valve leaflets
-prevent valves from being everted

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26
Q

Papillary Muscles

A

-extensions of the chordae tendinae cusp
-nipple shaped
-pull down chordae tendinae when ventricles contract
-keep valve tightly sealed
-anchor; prevent back flow

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27
Q

Heart Wall

A

-consists of 3 layers

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28
Q

Endocardium

A

-an extension of the endothelium that lines the entire circulatory system
-the thinner inner layer
-prone to endocarditis (infection)

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29
Q

Myocardium

A

-the cardiac muscle layer
-constitutes the bulk of the heart
-middle layer arrangement of spiral cardiac muscle

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30
Q

Epicardium

A

-thin external layer that covers heart

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31
Q

Action Potentials

A

-some cardiac cells can initiate own action potentials
-electrical impulse spread by gap junctions
-allow cells to contract as a single functional syncytium (atria and ventricles contract as separate units within this system)

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32
Q

Pericardium

A

-encloses heart
-2 layer outer sac:
1. tough, fibrous covering
2. secretory lining; secretes pericardial fluid that lubricates and prevents friction

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33
Q

Pericarditis

A

-results in a painful friction rub between the two layers when there is an infection

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34
Q

Autorhythmicity

A

-the heart contracts rhythmically as a result of action potentials that is generates itself

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35
Q

Contractile Cells

A

-constitute 99% of cardiac muscle cells
-do mechanical work of pumping
-normally do not initiate own action potentials

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36
Q

Autorhythmic Cells

A

~1% of cardiac muscle cells
-do not contract
-specialized for initiating and conducting action potentials responsible for contraction of working cells

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37
Q

Non-contractile Cell Locations

A

-SA node
-AV node
-Bundle of His
-Purkinje Fibres

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38
Q

Sinoatrial (SA) Node

A

-located in the right atrial wall near superior vena cava opening
-the normal pacemaker
-70-80 action potentials/minute

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39
Q

Atrioventricular (AV) Node

A

-located at the base of the right atrium near the septum
-40-60 action potentials/minute

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40
Q

Bundle of His

A

-originated at the AV node and enters the interventricular septum
-divides to form L and bundle branches which travel down the septum then curve up at the tip of the ventricles towards atria
-20-40 action potentials/minute w/ purkinje fibres

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41
Q

Purkinje Fibres

A

-spread through the ventricles
-extend from bundle of his
-twigs from the tree branch
-20-40 action potentials/minute w/ Bundle of His

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42
Q

Internodal Pathway

A

-from SA node to AV node
-100 milliseconds?

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43
Q

Interatrial Pathway

A

-from SA node to left atrium
-30 milliseconds?

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44
Q

Bundle of His/Purkinje Pathway

A

-30 milliseconds

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45
Q

Total Contraction time of the heart

A

160 milliseconds

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46
Q

AV Nodal Delay

A
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47
Q

Pacemaker Potential

A

-autorhythmic cells don’t have a defined resting membrane potential
-instead have pacemaker activity: membrane slowly depolarizes between action potentials until threshold is reached and ap is generated

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48
Q

Electrical Activity of the Heart

A

slides 24-31

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49
Q

Electrocardiogram (ECG)

A

-the sum of multiple action potentials
-records overall speed of activity throughout heart during depolarization and repolarization (not single action potential)
-has 3 major waves
-provides heart rate, rhythm, conduction of signals
-record at any given time represents the sum of electrical activity
-both electrodes are recording the same potential so no difference in potential is recorded

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50
Q

Leads

A

-ECG has 12 electrode system
-each pair of electrodes is called a lead; there are 6 between limbs and chest

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51
Q

P Wave

A

-represents atrial depolarization

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52
Q

QRS Complex

A

-represets ventricular depolarization
-atria is repolarizing simultaneously

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53
Q

T Wave

A

-ventricular repolarization

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54
Q

PR Segment

A

-AV Nodal Delay

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55
Q

ST Segment

A

-time during which ventricles are contracting and emptying
-not a record of contractile activity

56
Q

TP Interval

A

-time during which ventricles are relaxing and filling
-heart is repolarized and at rest

57
Q

Why is there no wave for SA nodal depolarization?

A

-not enough electrical activity is generated
-P wave is then the first to be recorded when wave of depolarization spreads across atria

58
Q

Why is the P wave smaller than the QRS complex?

A

-atria have much smaller muscle mass than ventricles and generate less electrical activity

59
Q

What ECG can measure?

A

-electrical activity triggers mechanical activity so abnormal electrical patterns are usually accompanied by abnormal contraction
-tells us about 3 main deviations:
1. abnormalities in rate
2. abnormalities in rhythm
3. cardiac myopathies

60
Q

Abnormalities in Rate

A

-determined from the distance between two consecutive QRS complexes

61
Q

Tachycardia (rate)

A

-rapid heart rate of more than 100bpm

62
Q

Bradycardia (rate)

A

-slow heart rate of fewer than 60bpm

63
Q

Arrhythmias (Abnormalities in Rhythm)

A

-variation from normal rhythm and sequence of excitation

64
Q

Atrial Flutter (rhythm)

A

-rapid but regular sequence of atrial depolarizations
-200-380bpm

65
Q

Atrial Fibrillation (A-Fib) (rhythm)

A

-rapid but irregular atrial depolarizations with no definite P waves
-QRS complexes occur sporadically
-no definite P waves

66
Q

Ventricular Fibrillation (V-Fib) (rhythm)

A

-ventricular musculature exhibits uncoordinated, chaotic contractions
-emergency state
-saw edge reading
-need to shock heart to reset SA node
-brain won’t get enough blood and systems will start to fail

67
Q

Heart Block (rhythm)

A

-defects in the cardiac conducting system
-only every second or third atrial impulse is passed to the ventricles
-2:1 or 3:1 block
-complete block: complete disassociation between atrial and ventricular activity

68
Q

Cardiac Myopathies

A

-damage of the heart muscle

69
Q

Myocardial Ischemia (myopathies)

A

-inadequate delivery of oxygenated blood to heart tissue

70
Q

Necrosis (myopathies)

A

-actual death of hear muscle cells

71
Q

Acute Myocardial Infarction (myopathies)

A

-occurs when supplying blood vessels becomes blocked or ruptured
-aka heart attack

72
Q

Cardiac Cycle

A

-assumes SA node is normal
-consists of: contraction and emptying, relaxation and filling, changes in blood flow
-all brought about by rhythmic changes in electrical activity

73
Q

Diastole

A

-relaxation and filling

74
Q

Systole

A

-contraction and emptying

75
Q

Systole and Diastole

A

-refer to ventricle activity, unless otherwise stated

76
Q

Mid Ventricular Diastole

A

-atrium is also still in diastole
-TP interval of ECG
-AV valves open
-passive filling (no pressure)
-volume slowly increases till full

77
Q

Late Ventricular Diastole

A

-atrial contraction
-P wave
-80% full
-AV valves are about to close

78
Q

End of Ventricular Diastole

A

-ends at the onset of contraction
-atrial contraction and ventricular filling have completed
-volume of blood in the ventricle at the end of diastole is called: End-Diastolic Volume (EDV) = maximum filling ~135mL

79
Q

Onset of Ventricular Systole

A

-QRS complex = ventricular excitation, which induces contraction
-ventricular pressure sharply increases after QRS, signalling systole
-AV valve closes

80
Q

Isovolumetric Ventricular Contraction

A

-ventricular pressure must continue to increase to open aortic valve
-constant volume cause both valves are closed

81
Q

Ventricular Ejection

A

-ventricular pressure exceeds aortic pressure
-aortic valve is forced open and ejection of blood begins

82
Q

Stroke Volume

A

-amount of blood pumped out each ventricle with each contraction
-usually 70mL

83
Q

End of Ventricular Systole

A

-does not empty completely
-usually only half leaves
-amount of blood left is the ESV: end-systolic volume which is usually 65mL

84
Q

Calculating stroke volume

A

EDV-ESV=SV

85
Q

Relaxation

A

-aortic valve closes but AV valve has not yet opened
-no blood can enter ventricle from atrium
-all valves closed for a brief period

86
Q

Heart Sounds

A

1st: low pitched, soft “lub”
2nd: higher pitch “dup”

87
Q

Lub

A

-first
-slow
-low pitch
-end of diastole
-closure of AV valves

88
Q

Dup

A

-second
-faster
-higher pitch
-end of systole
-closure of SL valves

89
Q

Murmurs

A

-should be no extra sounds in healthy heart

90
Q

Stenotic Valve (whistle)

A

-stiff/narrowed valve
-doesn’t open completely
-blood is squeezed out
-turbulence
-whistle sounds

91
Q

Insufficient Valve (swish)

A

-leaky valve
-flaps don’t fit properly
-turbulence
-swish sound

92
Q

Systolic Murmur Timing

A

-murmur happens between sounds
-ie. lub murmur dup

93
Q

Diastolic Murmur Timing

A

-murmur occurs at end of cycle
-ie. lub dup murmur

94
Q

Murmur Variations

A

-combination of type of murmur and timing

95
Q

Lub-whistle-dup

A

-stenotic (whistle)
-systolic (middle)
-SL valve doesnt open completely

96
Q

Lub-dup-whistle

A

-stenotic (whistle)
-diastolic (end)
-AV valve doesnt open

97
Q

Lub-swish-dup

A

-insufficient (swish)
-systolic (middle)
-AV valve doesnt close

98
Q

Lub-dup-swish

A

-insufficient (swish)
-diastolic (end)
-AV valve doesnt close

99
Q

Rheumatic Fever

A

-caused by bacteria
-can cause heart infection
-usually mitral valve stenosis
-heart failure or death possible

100
Q

Cardiac Output

A

-the amount of blood that comes out of each ventricle per minute
-determined by:
1.assuming SA node is setting hr
2. heart rate
3. stroke volume

101
Q

Stroke Volume and Cardiac Output

A

-determined by the extent of the venous return and sympathetic activity
-influenced in intrinsic and extrinsic controls
-both factors increase sv by increasing the strength of heart contraction

102
Q

Calculating Cardiac Output

A

-heart rate x stroke volume (EDV-ESV)
-ie. 70bpm x (135-65) = 4900 mL/minute

103
Q

Cardiac Reserve

A

-difference between cardiac output at rest and at maximum exercise

104
Q

Intrinsic and Extrinsic Control of Stroke Volume

A

-in the sympathetic nervous system

105
Q

Intrinsic Control

A

-increase venous return, increase EDV, increase contraction, increase stroke volume

106
Q

Extrinsic Control

A

-increase contraction, increase stroke volume

107
Q

Innervation

A

-by sympathetic and parasympathetic nervous system
-controlled by medulla

108
Q

Parasympathetic Stimulation

A

-will decrease heart rate
-controlled by vagus nerve (CN X)
-ACh is released to increase permeability of the SA node to K+ by slowly closing K+ channels
-rate at which action potentials are initiated is reduced
-ACh binds to muscanaric G Protein receptor and reduced cAMP activity
-leads to 4 outcomes to decrease cardiac output:

109
Q
  1. SA Node (parasympathetic)
A

-increased permeability to K+
-gets hyperpolarized
-reduces If current
-decreased rate of threshold
-decreases heart rate

110
Q
  1. AV Node (parasympathetic)
A

-decreases excitability
-increases AV Nodal delay

111
Q
  1. Atrial Muscle (parasympathetic)
A

-decreases and weakens contraction
-depolarizes slowly

112
Q
  1. Ventricular Muscle (parasympathetic)
A

-decreases and weakens contraction
-depolarizes slowly

113
Q

Sympathetic Stimulation

A

-thoracolumbar branch
-intends to increase heart rate
-norepi and epi released and bind to adrenergic B1 receptor
-increases cAMP activity
-4 outcomes to increase cardiac output:

114
Q
  1. SA Node (sympathetic)
A

-increases rate of depolarization to threshold
-increases heart rate

115
Q
  1. AV Nodal Delay (sympathetic)
A

-increases excitability
-delay is decreased

116
Q
  1. Atrial Muscle (sympathetic)
A

-increases and strengthens contraction

117
Q
  1. Ventricles (sympathetic)
A

-increases and strengthens contraction

118
Q

Frank-Starling Law

A

-states that “heart normally pumps out during systole the volume of blood returned to it during diastole”
-the greater the diastolic filling (muscles stretched) the larger the EDV

119
Q

Heart Failure

A

-the inability of the cardiac output to keep pace with the bodys demands for supplies and removal of wastes
-inadequate cardiac output to reach brain and organs

120
Q

Prime Defect

A

-a decrease in cardiac contractility
-weakened cardiac muscle contracts less effectively
-heart operates at a lower length-tension curve
-pumps out a smaller SV

121
Q

Compensatory Measure

A

-sympathetic activity is increased for a limited time
-sympathetic nerves: increase SV and cardiac output
-kidneys: retain more salt, water follows, this increases plasma/blood volume, in turn sv and cardiac output are increased

122
Q

Decompensated Heart Failure

A

-compensatory measures failed
-forward failure: heart can’t pump adequate blood to the tissues
-backward failure: lungs are backed up with blood
-congestive heart failure

123
Q

Systolic Failure

A

-decrease in cardiac contraction (as previously described)

124
Q

Diastolic Failure

A

-ventricles do not fill normally
-less blood pumped out with each contraction

125
Q

Nourishing Heart Muscle

A

-supplied with blood and nutrients via coronary circulation

126
Q

Coronary Circulation

A

-most blood received during diastole
-like a garden hose: during systole coronary vessels are compressed by the contracting muscle

127
Q

Coronary Vessels

A

-branches off aorta to supply heart

128
Q

Dicrotic Notch

A

-closure of the aortic valve produces a disturbance/ notch

129
Q

Role of Adenosine

A

-adenosine is formed from ATP during cardiac metabolic activity
-when heart uses more ATP = more adenosine
-heart needs more oxygen
-adenosine vasodilates coronary vessels to increase O2
-important cause heart can’t get enough ATP through anaerobic metabolism

130
Q

Coronary Artery Disease (CAD)

A

-blocking of the coronary vessels so oxygen isn’t supplied to the heart
-can lead to heart attack
-3 mechanisms:

131
Q
  1. Vascular Spasm
A

-is reversible
-abnormal spastic contraction that narrows coronary vessels
-early stages of CAD
-not enough oxygen = endothelium releases platelet activating factor

132
Q
  1. Atherosclerosis
A

-plaques form in heart vessels
-by oxidized cholesterol

133
Q

Angina

A

-chest pain
-treated with nitrogylcerine (vasodilator)

134
Q

Embolus

A

-floating plaque causes clot
-immediate death

135
Q

Thromboembolism

A

-when a blood clot forms in a vein

HLSC 126 - Human Physiology I (5 decks)

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