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(PA school) Human Physiology > Lecture 6 > Flashcards

Lecture 6 Flashcards

Cardiovascular system

1
Q

What does the circulatory system transport?

A

Nutrients and oxygen

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2
Q

What are the 3 Components of the circulatory system?

A

Heart
Blood vessels
Blood

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3
Q

1) What does blood travel through?
2) Where do these originate and terminate?

A

1) Two separate vascular loops
2) Originate and terminate at the heart

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4
Q

Name the two vascular loops blood travels through, and where they go

A

1) Pulmonary circulation: between heart and lungs
2) Systemic circulation: between heart and body

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5
Q

1) Where is the heart?
2) What happens when the heart beats forcefully?
3) What is the heart divided into?

A

1) In thoracic cavity between sternum and vertebrae
2) Apex “thumps” against left chest wall
3) 4 chambers separated by the septum

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6
Q

True or false: The outputs of R and L heart are independent.

A

False; they’re interdependent

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7
Q

1) What does the right atrium receive? Through what?
2) What valve does this then go through?
3) What does the right ventricle do? Through what?

A

1) O2 depleted blood via SVC and IVC
2) Tricuspid valve
3) Pumps this blood into pulmonary circulation via the pulmonary artery

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8
Q

1) What occurs in pulmonary circulation?
2) What type of transport is this?

A

1) Gas exchange
2) Diffusion; passive +

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9
Q

1) What does the left atrium receive? Through what?
2) What valve does this then go through?
3) What does the left ventricle do? Through what?

A

1) O2 rich blood via pulmonary veins
2) Mitral (bicuspid) Valve
3) Pumps this blood into systemic circulation via the aorta

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10
Q

List the 3 general principles of blood flow

A

1) Both sides simultaneously pump equal amounts of blood
2) Pulmonary circulation is low-pressure, low-resistance
3) Systemic circulation is high-pressure, high-resistance

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11
Q

Pulmonary circulation is _________pressure, __________resistance

A

low-pressure, low-resistance

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12
Q

1) What is the purpose of valves?
2) How many cardiac valves are there? What do they do?

A

1) Ensure correct direction of blood flow
2) 4 cardiac valves that open and close passively due to pressure differences

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13
Q

1) Where are the (atrioventricular) AV valves?
2) When do they open?

A

1) Between atrium and ventricle; one each side of heart
2) Open when atrial pressure exceeds ventricular pressure

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14
Q

What are the left and right AV valves called?

A

Right: tricuspid valve
Left: bicuspid/mitral valve

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15
Q

1) When do the SL (semilunar) valves open?
2) What are the names of each?

A

1) With ventricular contraction
2) Aortic and pulmonary SL valves

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16
Q

1) What are the chordae tendineae?
2) What do they do?
3) Where do they attach? What does this structure do?

A

1) Thin, tendinous chords
2) Prevent valves from everting
3) Attach to papillary muscles, which contract with ventricles and pull on the chordae tendineae

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17
Q

1) What is the fibrous skeleton made of?
2) What does it do?
3) What does it separate?

A

1) Dense connective tissue
2) Surrounds and anchors the valves (fibrous rings)
3) Separates atria from ventricles

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18
Q

What are the 3 distinct layers of the heart wall?

A

1) Endothelium/endocardium
2) Myocardium
3) Epicardium

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19
Q

What is the pericardium?

A

Double-walled membranous sac [around the heart]

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20
Q

True or false: All cardiac cells are coupled electrically and mechanically

A

True

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21
Q

1) How would you describe the structure of cardiac muscle?
2) How are adjacent cells joined?

A

1) A functional syncytium
2) At specialized structures called intercalated discs

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22
Q

What 2 things do the intercalated discs contain? Describe each

A

1) Desmosomes: adhering junction, tolerates mechanical stress
2) Gap junctions: low electrical resistance, AP’s spread; important for synchronous contraction

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23
Q

What is important for synchronous contraction of the heart?

A

Gap junctions

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24
Q

Describe what makes the atria and ventricles separate units (2 things)

A

1) No gap junctions between atrial and ventricular contractile cells
2) Fibrous skeleton is also nonconductive

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25
Q

How do the atria and ventricles coordinate pumping?

A

Due to specialized conduction system

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26
Q

1) What causes autorhythmicity/automaticity of the heart?
2) What occurs for this to happen?

A

1) Heart contracts rhythmically due to action potentials it generates by itself
2) Action potentials spread across muscle cell membranes, trigger cardiac muscle contraction

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27
Q

What are the two specialized types of cardiac muscle cells? Describe each

A

1) Autorhythmic cells: do not contract; initiate and conduct AP’s
2) Contractile: 99% of cardiac muscle cells; do the mechanical work, don’t initiate AP’s

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28
Q

True or false: Cardiac autorhythmic cells do not have “resting potentials. Explain your answer

A

True; instead, they have pacemaker potentials

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29
Q

Pacemaker activity is due to what 3 things?

A

1) Increased inward Na+
2) Decreased outward K+
3) Increased inward Ca+

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30
Q

1) What are the Funny channels of pacemaker activity?
2) When do they open?
3) What does this lead to?

A

1) Unique voltage-gated Na+ channels
2) Opens on hyperpolarization (rather than depolarization)
3) Slow depolarization (pacemaker potential)

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31
Q

1) What happens after the Funny channels open and depolarization starts?
2) What does this cause?

A

1) K+ channels slowly close
2) Gradually diminishes K+ outflow, causing further depolarization

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32
Q

1) What open before threshold potential, but after K channels slowly close?
2) What does this cause?

A

1) Ca+ channels open before threshold potential
2) Ca+ influx, further depolarization

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33
Q

1) What happens once threshold potential is reached?
2) What does this cause?
3) How is this different in nerves and skeletal muscle, compared to cardiac muscle?

A

1) Long-lasting voltage gated Ca+ channels open
2) Large influx of Ca+
3) It’s Na+ instead in nerves and skeletal muscle

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34
Q

1) What happens at the peak of depolarization?
2) What two things allow for things to be reset after?

A

1) Voltage gated K+ channels open, K+ efflux
2) Ca+ reuptake via SERCA pump, and the Na-K pump

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35
Q

Once an AP is generated in any cardiac muscle cell, what happens?

A

It propagates via gap junctions and conduction system

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36
Q

Autorhythmic (noncontractile) cells are found in what 4 places? Describe where each is

A

1) Sinoatrial (SA) node: of the RA near SVC
2) Atrioventricular (AV) node: of RA base near septum
3) Bundle of His (AV bundle): originates in AV node
-Enters septum between ventricles
4) Purkinje fibers: originate from Bundle of His
-Spread through ventricular myocardium

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37
Q

True or false: Autorhythmic cells in different areas have differing rates of slow depolarization

A

True

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38
Q

What is the pacemaker? Why?

A

SA node is the pacemaker because it is the fastest

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39
Q

In what two ways are all cardiac cells coupled?

A

Electrically and mechanically

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40
Q

Where does the bundle of His (AV bundle) originate? Where does it enter?

A

1) Originates in AV node
2) Enters septum between ventricles

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41
Q

Why can’t other cells resume their slower rates?

A

They are triggered at the rate of the SA node

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42
Q

If there is SA node damage, what takes over?

A

AV node

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43
Q

1) If there is blocked conduction between atria and ventricles, what happens?
2) What can be used to help?

A

1) Then coordination breaks down; Complete heart block
2) Artificial pacemaker can be used in these cases

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44
Q

What does an artificial pacemaker do?

A

Rhythmically generates impulses typically 70bpm

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45
Q

1) Define ectopic focus
2) What does it lead to?
3) What can cause this?

A

1) Area of the heart becomes more excitable and depolarizes faster than SA node
2) Premature action potential = premature ventricular contraction
3) Heart disease,anxiety, caffeine, lack of sleep, sometimes genetic

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46
Q

What are the 3 steps of electrical activity?

A

1) Atrial excitation and contraction completes before onset of ventricular contraction (160ms)
2) Cardiac muscle fibers must be coordinated
3) Atrial and ventricular pairs contract simultaneously

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47
Q

Atrial excitation and contraction completes when?

A

Before onset of ventricular contraction (160ms)

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48
Q

1) What cannot pump blood?
2) What can?
3) What can help with coordination?

A

1) Contraction of isolated muscle fibers cannot successfully pump blood
2) Smooth rhythmic contraction
3) Fibrillation

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49
Q

When the atrial and ventricular pairs contract simultaneously, what is happening?

A

Synchronized pumping of blood into pulmonary and systemic circulations

50
Q

1) Where is the interatrial pathway?
2) What happens here?

A

1) Extends from SA node to left atrium
2) AP’s spread quickly through left atrium (LA),atria contract simultaneously

51
Q

1) Where is the internodal pathway?
2) What is it the only point of?
3) What happens?

A

1) SA node to AV node
2) Only point of electrical communication between atria and ventricles
3) Sequential contraction of ventricles after atria

52
Q

1) When does the action potential arrive at the AV node?
2) Where does it conduct slowly?
3) What is this called and why does this happen?

A

1) 30ms after SA node firing
2) Throughout AV node (100ms)
3) AV nodal delay; allows time for atria to contract and fill ventricles

53
Q

What is the only point of electrical communication between atria and ventricles?

A

Internodal pathway

54
Q

1) What happens after a signal reaches the AV node?
2) Where does it go after that?

A

1) Travels rapidly down septum via bundle of His
2) Travels throughout ventricular myocardium via Purkinje fibers

55
Q

True or false: APs in contractile cells differ in shape and ionic mechanisms

A

True

56
Q

Describe the K+ channels of cardiac conduction

A

Several types of K+ channels; highly leaky at rest, causing resting potential –90mV

57
Q

What happens at threshold potential?

A

1) Rapid polarity reversal on activation
2) Fast Na+ influx

58
Q

What happens at the peak? What about the plateau?

A

1) Peak: K+ channels open, fast efflux
2) Plateau: Ca+ channels open

59
Q

What happens after K+ channels open and the plateau phase?

A

Another type of K+ channel opens, causingrapid falling phase of action potential

60
Q

1) Describe the refractory period of skeletal muscle
2) Describe the refractory period of cardiac muscle
3) Explain why the cardiac muscle refractory period is like this

A

1) In skeletal muscle, the refractory period is very short compared to the duration of the contraction
2) In cardiac muscle,the refractory period is long because of the plateau phase (almost as long as the contraction)
3) In cardiac muscle it’s almost as long as the contraction and cannot be restimulated until it is over to allow time for filling

61
Q

1) How long is the refractory period of cardiac muscle?
2) Can it be restimulated during this time?
3) What does this allow for?

A

1) Almost as long as the contraction
2) Cannot be restimulated until it is over
3) Time for filling

62
Q

1) What primarily facilitates the refractory phase?
2) When can these return to opening conformation?

A

1) Na+ channels
2) When membrane repolarizes to resting potential

63
Q

1) What is an ECG?
2) What does it measure?
3) What is it an indirect recording of?
4) What does it measure the difference between?

A

1) Electrocardiogram
2) Measures electrical activity of body fluids that reach the surface
3) Cardiac electrical activity
4) The voltage detected by electrodes, not the actual potential

64
Q

1) What does an ECG measure the sum of? What is it not a recording of?
2) What does an ECG depend on?
3) What are the ECG electrodes like?

A

1) Measures sum of electrical activity in all cardiac muscle cells
-Not the recording of a single action potential
2) Depends on orientation of the electrodes
3) “Eyes” that view the same activity from different vantage points

65
Q

For common basis for comparison, what is used for ECGs?

A

The same electrode arrangements

66
Q

Specific arrangements of a pair of electrodes is called a what?

A

Lead

67
Q

Commonly, a ___ lead EKG is performed

A

12

68
Q

1) What is a limb lead?
2) What does each lead record?

A

1) A view from a particular angle
2) Wave configurations

69
Q

What are the 3 distinct waveforms seen on ECGs?

A

1) P wave: atrial depolarization
2) QRS complex: ventricular depolarization
3) T wave: ventricular repolarization

70
Q

1) Can you see an SA node on the EKG?
2) What about atrial repolarization?

A

1) Does not generate enough activity to reach the body surface, not seen on EKG
2) Masked by QRS complex

71
Q

Why is P smaller than QRS on an EKG?

A

Atria have smaller muscle mass than ventricles

72
Q

1) What does the PR segment show?
2) What about the ST segment?

A

1) AV nodal delay
2) Ventricular plateau phase

73
Q

What are the 3 types of EKG abnormalities?

A

1) Rate
2) Rhythm
3) Myopathies

74
Q

Tachycardia is ______bpm, bradycardia is ______bpm

A

100bpm; 60bpm

75
Q

What are the 3 types of rhythm you can see on an EKG?

A

1) Flutter: rapid, regular
2) Fibrillation: Rapid, irregular
3) Block: ventricles occasionally fail to be stimulated

76
Q

What are the two types of myopathies that can be seen on an EKG? Define each

A

1) Ischemia: lack of O2/blood
2) Infarction: Necrosis due to lack of O2/blood

77
Q

1) What is the cardiac cycle?
2) What two things does it consist of? Define each

A

1) Cycle of mechanical events
2) Systole: ventricular contraction and emptying
Diastole: ventricular relaxation and filling

78
Q

1) What is mid-ventricular diastole?
2) What is pressure like during this phase?
3) What valve is open (if any)?

A

1) Time between ventricular repolarization and another atrial depolarization
2) Atrial pressure slightly exceeds ventricular pressure due to venous return
3) AV valve open, blood flows passively into ventricles

79
Q

1) What is late ventricular diastole?
2) What happens?

A

1) SA node reaches threshold and fires, atria contract (P wave)
2) Blood squeezed into ventricles

80
Q

1) What marks the end of ventricular diastole?
2) What is the end-diastolic volume (EDV)? What is this?
3) When does this stage end?

A

1) Ventricular filling complete
2) About about 135mL. Maximum amount of blood.
3) At ventricular contraction

81
Q

What is the EDV?

A

135ml

82
Q

1) What happens at the onset of ventricular systole?
2) Where is pressure higher? Are the AV valves open or closed?

A

1) Ventricular contraction.
2) Ventricular pressure exceeds atrial pressure, closing AV valves

83
Q

1) When does isovolumetric ventricular contraction occur? What happens?
2) Define isovolumetric

A

1) After AV valves close, ventricular pressure rises until it exceeds aortic pressure; there is a moment where AV valves close before aortic valve opens
2) All valves are closed, no blood enters or leaves

84
Q

1) What happens during ventricular ejection?
2) Define stroke volume (SV)

A

1) Aortic valve forced open, blood ejects
2) Amount of blood pumped out of ventricle with each contraction

85
Q

1) At the end of ventricular systole, does the ventricle completely empty?
2) What is the end-systolic volume (ESV)
3) What is the SV?

A

1) Does not empty completely during ejection
2) Averages 65mL
3) EDV – ESV; around 70mL

86
Q

1) What happens at the onset of ventricular diastole?
2) Is the AV valve open? Why?
3) What is this called?

A

1) Ventricle starts to relax, pressure falls below aortic pressure and aortic valve closes
2) AV valve not open yet because still exceeds pressure in atria
3) Isovolumetric ventricular relaxation

87
Q

1) What causes ventricular filling?
2) What happens at the end of this?

A

1) Ventricular pressure falls below atrial pressure, AV valves open, filling occurs
2) SA node fires again in late ventricular diastole,cardiac cycle starts again

88
Q

1) How long does the cardiac cycle last?
2) How long is each section?

A

1) 800ms
2) Systole: 300ms, diastole: 500ms

89
Q

1) When heart rate is rapid, what is shortened?
2) What does this cause?
3) At what heart rate does this become a problem?

A

1) Diastole is shortened more than systole
2) Reduced time for filling
3) >200bpm: diastole too short for adequate filling

90
Q

1) Define cardiac output
2) What variations exist?

A

1) Volume of blood pumped by each ventricle per minute
2) Minor beat-to-beat variations exist

91
Q

True or false: Pulmonary circulation volume is the same as systemic circulation volume

A

True

92
Q

1) What is the formula for cardiac output (CO)?
2) What is the average?
3) What is the total blood volume average?

A

1) CO = HR X SV
2) SV 70mL, HR 70bpm, average CO = 4900mL / minute
3) 5 - 5.5L

93
Q

Each half of the heart pumps what portion of blood every minute?

A

Almost the entire volume of blood

94
Q

Define cardiac reserve

A

Difference between resting CO (cardiac output) and maximum CO

95
Q

True or false: Nervous stimulation is not required, but can influence rate and strength

A

True

96
Q

1) The nervous system can influence what two aspects of the heart beat?
2) What primarily determines heart rate?

A

1) Rate and strength
2) Autonomic influence on SA node

97
Q

How does the ANS influence the SA node? (2 ways)

A

1) Acetylcholine released from vagus nerve binds to muscarinic receptors
2) Norepinephrine binds with B1 adrenergic receptors

98
Q

What is the Frank-Starling Law?

A

The heart normally pumps out during systole the volume of blood returned to it during diastole
(ie: increased venous return increases stroke volume)

99
Q

True or false: Different activities result in differences in venous return

A

True

100
Q

1) Define preload
2) What determines cardiac muscle fiber length?

A

1) Preload: stretching of cardiac muscle before contraction
2) EDV (end diastolic volume)
-Pulling ends of a spring, farther you pull, the greater the force of the spring snapping back

101
Q

1) What does greater EDV (greater filling) do to cardiac fibers and contraction force?
2) What does it do to SV?

A

1) Causes longer cardiac fibers, causing greater force of contraction
2) Increased EDV will increase SV

102
Q

1) How many heart sounds are normally in one cardiac cycle?
2) What causes these sounds?

A

1) 2
2) Vibrations in the ventricles and major arteries, not by the snapping of the valves

103
Q

What are the two heart sounds?

A

1) S1: First heart sound (“lub”)
2) S2: Second heart sound (“dub”)

104
Q

1) What is S1?
2) What does it sound like?
3) What is being closed?
4) What stage is occurring?

A

1) First heart sound (“lub”)
2) Low-pitched, soft, long
3) AV valves
4) Ventricular systole

105
Q

1) What is S2?
2) What does it sound like?
3) What is being closed?
4) What stage is occurring?

A

1) Second heart sound (“dub”)
2) Higher pitch, shorter, sharper
3) Closure of semilunar valves
4) Ventricular diastole

106
Q

1) Blood normally flows in what way? Can you hear it?
2) What does turbulent blood flow cause?

A

1) Laminar fashion (smooth layers); does not produce sound
2) Blood flow to be heard (murmur)

107
Q

What is the most common cause of turbulence?

A

Valve malfunction

108
Q

Name, define, and describe the two types of valve malfunction

A

1) Stenotic valve: stiff, narrowed, doesn’t open completely
-Blood forced through, produces whistling sound
2) Insufficient/incompetent valve: cannot close completely
-Backflow causes turbulent blood flow (regurgitation)
-Gurgling swishing sound

109
Q

1) What can help identify a defective valve?
2) What is the first heart sound? What can occur after?
3) What is the second heart sound? What can happen after?

A

1) Timing, character, and location of murmur can help identify defective valve
2) First heart sound is the onset of ventricular systole
-Systolic murmur: occurs between first and second
3) Second heart sound is the onset of ventricular diastole
-Diastolic murmur: occurs between second and first

110
Q

A whistling systolic murmur could be what?

A

Aortic/pulmonary stenosis

111
Q

1) Define rheumatic fever
2) What happens?
3) What does this cause?

A

1) Autoimmune disease triggered by streptococcus bacterial infection
2) Antibodies against these bacteria interact with body tissues, especially heart valves
3) Fibrous lesions form,causing valve to become stiff and thick (stenotic, insufficient, or both)

112
Q

What is it important to treat strep throat with?

A

Antibiotics

113
Q

1) Ventricles must contract hard enough to do what?
2) Define afterload

A

1) To open semilunar valves
2) Work imposed on heart after contraction has begun

114
Q

1) What causes the ventricle to need to generate more pressure to eject blood?
2) What increases the workload of the heart?

A

1) If arterial blood pressure is chronically elevated or if exit valve is stenotic.
2) High blood pressure

115
Q

1) How does the heart compensate for a higher workload?
2) What can a sustained increased workload cause?

A

1) Via hypertrophy of cardiac muscle fibers
2) Pathological changes leading to heart failure

116
Q

1) Define heart failure
2) Define systolic heart failure.
3) When can it happen?

A

1) Inability of CO to keep pace with demands
2) Difficulty pumping
3) Heart muscle weakened from damage (heart attack) or chronic afterload (HTN)
(also many other causes)

117
Q

1) What happens during systolic HF?
2) How does the body compensate?
3) What does it become less responsive to? What else happens to this molecule?

A

1) Contractility decreases, smaller EDV, lower CO
2) With sympathetic stimulation to maintain SV
3) NE; also NE stores in heart nerve terminals deplete

118
Q

What do the kidneys do to compensate during systolic HF?

A

Kidneys retain water to expand blood volume and increase SV

119
Q

What happens during decompensation during HF? (3 things)

A

1) Contractility further deteriorates
2) SV does not keep pace with venous return
3) Blood gets “backlogged” leading to venous congestion (“congestive heart failure”)

120
Q

1) Define coronary artery disease (atherosclerosis)
2) What does it do to blood flow?
3) What is it the underlying cause of? Why?

A

1) Pathological changes within coronary artery walls
2) Causes diminished blood flow
3) 50% of deaths, causes myocardial ischemia and infarction by 3 mechanisms

121
Q

What are the 3 mechanisms that cause myocardial ischemia and infarction? Describe each

A

1) Vascular spasm
-Early-stage CAD, transient constriction from cold, exertion, anxiety
2) Atherosclerosis
-Narrowing and eventual occlusion from atherosclerotic plaque
3) Thromboembolism
-Plaque can trigger clot formation which can travel and block blood vessels

(PA school) Human Physiology (35 decks)

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