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HSC1007 A&P > CVS Physiology > Flashcards

CVS Physiology Flashcards

1
Q

Describe the general function of the heart.

A

Major function is to service the metabolic needs of tissues
- Provide nutrients, O2
- Remove waste

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2
Q

How is the general function of the heart achieved?

A

Achieved by ensuring adequate exchange of fluids at the capillaries:
- Sufficient pressure (from heart) & output
- Integrity of vessels (cannot be ruptured/narrowed & must be able to take the bld. pressure)

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3
Q

What is the electrical activity of the heart?

A

It is the intrinsic electrical network of the heart that ensures coordinated contraction and relaxation.

The heart generates own action potential & contracts intrinsically

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4
Q

How are the autorhythmic cells responsible for the function of the heart?

A

Autorhythmic cells (aka pacemaker cells) initiate & conduct AP responsible for contraction of working cells

Ensures heart is pumping at a steady rate –> supply nutrients & O2 to all cells/all parts of the body. Ensures wastes in blood is pumped to the respective organs for removal (e.g. lungs, liver, etc)

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5
Q

How is cardiac excitation coordinated for efficient cardiac function?

A

The pair of atria and the pair of ventricles are fully coordinated.
This ensures that both members of the pair contract simultaneously. This ensures that each heart chamber contracts as a unit to pump efficiently

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6
Q

How can heart rate be controlled by the nervous system?

A

Heart rate can be controlled by:

Sympathetic NS:
Increases HR

Parasympathetic NS:
Decreases HR

Note that both sympathetic & parasym will be present, just at different amounts (e.g. resting conditions: S and P both active but P predominates)

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7
Q

What does the ECG do?

A

Record of electrical events in the heart from the surface of the body
Provide info on the cardiac rate, rhythm, pattern of depolarizaation, presence of cardiac ischemia/infarction

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8
Q

How is the 12-lead ECG derived?

A

Two electrodes placed on the limbs at each time
Each lead forms an axis in the vertical/horizontal plane
Each lead looks at electrical events in the heart from a unique vantage point

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9
Q

How does a normal ECG waveform relate to the events of the cardiac cycle?

A

In a normal heartbeat:

  1. P wave: Atrial depolarization
  2. PR segment: AV nodal delay
  3. QRS complex: Ventricular depolarization
  4. ST segment: Ventricles contracting & emptying
  5. T wave: Ventricular repolarization
  6. TP segment: Ventricles relaxing & filling
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10
Q

How is homeostasis maintained in the body?

A

The body:
1. detects deviations from normal
2. integrates this info with other info
3. makes adjustments to restore the factor to normal

Negative feedback loop because (e.g. body detects high temp & adjustment is to lower temp)

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11
Q

What are the two cardiac muscle cells?

A

Contractile cells:
- 99% of cardiac muscle cells
- receives electrical signals
- does the mechanical work of pumping

Autorhythmic cells:
- Minority = ~1%
- AKA pacemaker cells
- Initiates the electrical activity
- Sets the pace of heartbeat
- Conducts the action potentials responsible for contraction of contractile cells
- SA node, AV node, Bundle of His, Purkinje fibres

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12
Q

What sets the original pace of the heart?

A

Controlled by autorhythmic cells
NOT controlled by nerves/nervous system

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13
Q

What is the normal pacemaker of the heart?

A

Sinoatrial node (SA node)

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14
Q

Where are the pacemaker cells located in the heart?

A

SA node: R atria waall near opening of superior vena cava
AV node: Junction b/w atria & ventricles (near opening of coronary sinus)
Bundle of His: originates from AV node & travels down interventricular septum
Purkinje fibers: terminal fibers that spread through the myocardium

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15
Q

What does the electrically nonconductive fibrous tissue between the Atria and Ventricles do?

A

Prevents cardiac excitation from the SA node to pass through

This means the cardiac excitation can only pass through the AV node & bundle of His

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16
Q

Describe the impulse conduction through the heart

A
  1. SA node fires
  2. electrical activity spreads across atrial surfaces and reaches the AV node
  3. There is a 100msec delay at the AV node, then atrial contraction begins (squeeze blood to next area)
  4. electrical activity will travel along the interventricular septum through the AV node, bundle of His & Purkinje fibers to the ventricles
  5. Ventricular muscles contract
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17
Q

What is the
- resting membrane potential
- threshold potential?

A

Resting membrane potential: -60

Threshold potential: -40

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18
Q

What does the funny channel (I f) do?

A

Channel allows Na+ to move through which brings the membrane potential up (less -ve)

Needed for depolarization

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19
Q

What is depolarization?

A

When the membrane potential moves from resting to the threshold potential

i.e. moves form -60 to -40 mV

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20
Q

Briefly outline the action potential in autorhythmic cells. (6 points)

A
  1. Resting membrane potential at -60 mV
  2. Funny channel allows Na+ to move into the cell & Ca2+ moves into the cell too (not by I f) = inc. the mbn potential
  3. Causes slow depolarization (mbn potential inc. from -60 to -40) - aka pacemaker potential
  4. Once threshold potential crossed (-40 mV), spike in mbn potential - this is the action potential (AP spreads across the heart)
  5. Action potential caused by Ca2+ moving into the cell (spike up)
  6. Spike down (dec. in mbn potential) caused by K+ moving out of the cell
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21
Q

What is the rate of action potential generation for SA node?

A

70 - 80 AP per min
Translates to 70 - 80 heartbeat/min
Fastest rate, therefore sets the pace

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22
Q

What is the rate of action potential generation for AV node?

A

40 - 60 AP per min

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23
Q

What is the rate of action potential generation for Bundle and Purkinje?

A

20 - 40 AP per min

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24
Q

What does action potential cause?

A

Once an AP occurs in any cardiac muscle cell, it moves throughout the myocardium
Causes contractin

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25
Q

What happens if one of the nodes (SA/AV) are nonfunctional?

A

The next functional node/autorhythmic cell will takeover.

E.g. SA node nonfunctional; AV node takes over pacemaker activity = rate of AP generation will be 40 - 60 AP/min

E.g. AV node nonfunctional; Purkinje fiber ends up driving the ventricles

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26
Q

What happens is the atria and ventricles pump at the same time?

A

All the valves will close!

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27
Q

Why must the excitation of cardiac muscle fibers be coordinated?

A

To ensure that each heart chamber contracts as a unit to pump efficiently

Both atria and both ventricles should be fully coordinated so that both members of the pair contract simultaneously (i.e. R & L atria contract at same time; R & L ventricles contract at same time)

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28
Q

What must be complete before ventricular contraction starts?

A

Atrial excitation and contraction must be complete before ventricular contraction.

This primes the ventricles (main pumps) by fully filling them before they pump

Slight delay at AV node allows this to happen

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29
Q

Briefly describe what affects the heart rate through the cardiovascular control center and how.

A
  1. Pain, chemoreceptors (detect change in chemicals in bld), respiratory center, baroreceptors (detect change in bld. pressure) send signals to the cardiovascular control center in medulla
  2. The cardiovascular control center sends nerves down to heart to control heart rate
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30
Q

How does epinephrine (aka adrenaline), temperature, etc affect the heart rate?

A

They act directly on the SA node INDEPENDENT of the autonomic nervous system (ans)

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31
Q

How does the autonomic nervous system affect the heart rate?

A

Sympathetic nervous system: Inc. HR; flight or fight

Parasympathetic nervous system: dec HR; rest & relax

Both sympathetic & parasympathetic nervous system acts on the SA node

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32
Q

Which autonomic nervous system is active at resting conditions?

A

Both sympathetic & parasympathetic are active but parasympathetic predominates

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33
Q

An increase in HR is caused by _________ in sympathetic and __________ in parasympathetic

A

An increase in HR is caused by increase in sympathetic and decrease in parasympathetic

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34
Q

A decrease in HR is caused by _________ in sympathetic and __________ in parasympathetic

A

A decrease in HR is caused by decrease in sympathetic and increase in parasympathetic

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35
Q

What is an electrocardiogram (ECG) used to diagnose?

A

Cardiac ischemia (dec blood flow)
Cardiac infarction (heart attack)

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36
Q

What is an ECG?

A

Record of electrical events in heart from the SURFACE of the body

Provides info on cardiac rate, rhythm, pattern of depolarization & presence of cardiac ischemia/infarction

Overall spread of electrical activity throughout heart during depolarization & repolarization

Sum of electrical activity

Differential recording = poptential diff b/w 2 electrodes

(NOT direct recording of actual electrical activity of heart)

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37
Q

What is the 12 lead ECG also known as?

A

Einthoven triagle

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38
Q

12 Lead ECG

Lead I:
Lead II:
Lead III:
Lead IV:
Lead V:
Lead VI:

A

Lead I: Right arm to left arm
Lead II: Right arm to left leg
Lead III: Left arm to left leg
aVF: Left leg up
aVL: Left arm down diagonal
aVR: Right arm down diagonal

aVR/aVL/aVF = aV = augmented voltage

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39
Q

How many leads on the chest?

A

6 leads

6 leads from the limb electrodes + 6 chest electrodes = 12 leads

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40
Q

Which lead gives indication of the left ventricle?

A

Lead II
Located directly at the apex of the left ventricle

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41
Q

12 Lead ECG

A

Each lead forms an axis in vertical/horizontal plane

Each lead looks at electrical events in the heart from a unique vantage point (spatial location)

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42
Q

What can 12 lead ECG help with?

A

Can help to find the site of infarction (obstruction of blood supply) bc each lead looks at the heart from diff spatial location

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43
Q

What does P represent in a typical lead II ECG waveform?

A

Atrial depolarisation

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44
Q

What does QRS represent in a typical lead II ECG waveform?

A

Ventricular depolarisation
(atria repolarizing simultaneously but hidden by QRS complex bc atrium smaller than ventricles)

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45
Q

What does T represent in a typical lead II ECG waveform?

A

Ventricular repolarisation

46
Q

What does the RR interval represent?

A

1 heartbeat

47
Q

What does the PR segment represent?

A

AV nodal delay

48
Q

What does the ST segment represent?

A

Time during which ventricles are contracting & emptying

49
Q

What does the TP segment represent?

A

Time during which the ventricles are relaxing & filling

50
Q

Does the SA node generate sufficient electrical activity to reach the body surface?

ECG

A

No, so the firing of the SA node is not recorded.

The first wave to be sensed is the P wave –> impulse spreads through the atria

51
Q

Where is the wave for atrial repolarisation?

ECG

A

Same time as ventricular depolarization

but it is masked by QRS

52
Q

Why is the P wave smaller?
ECG

A

Because atria have smaller muscle mass than ventricles

53
Q

What are the 3 occasions where there is no electrical activity?

A
  1. PR: AV node delay
  2. ST: ventricles completely depolarised, & cardiac cells undergoing plateau phase
  3. TP: heart muscles at rest, ventricles filling
54
Q

How long is the PR interval?

A

~0.16s
aka AV node delay

55
Q

Why is there an AV node delay?

A

Time for signal to travel from the SA node to the AV node, AV node delay then travel to bundle of His
Bulk of time is the AV node delay (therefore called as such)

56
Q

How to count heart rate if the patient has an abnormal heart rate/rhythm?

A

Count the number of QRS complex within (e.g.) 20 seconds

57
Q

What is ventricular fibrillation?

A

Rapid and chaotic contraction of the many individual cardiac muscle fibres in ventricle

NOT coordinated (firing on their own), no blood (or vv little) is being pumped out of the ventricles

58
Q

What does a complete heart block look like on an ECG?

A

2 P waves, followed by QRS

59
Q

What is the plateau phase and what does it ensure?

A

Membrane potential is maintained close too this peak positive level for several hundred milliseconds

Makes sure that heart contracts AND relaxes

Prevents tetanic contraction

60
Q

What is responsible for the plateau part of the action potential?

A

Ca2+ entry from the extracellular fluid –> induces a much larger Ca2+ release from the sarcoplasmic reticulum

Opening of the L-type Ca2+ channels results in the slow, inward diffusion of Ca2+

Continued influx of positively charged Ca2+ prolongs the positivity inside the cell and is primarily responsible for the plateau part of the action potential

61
Q

What is responsible for the long period of cardiac contraction? What does cardiac contraction ensure?

A

Extra supply of Ca2+ release + slow Ca2+ removal –> responsible for long period of cardiac contraction

Increased contraction ensures adequate time to eject the blood fully

62
Q

What are the key phases of the cardiac cycle?

A

The key phases of the cardiac cycle are:

  1. Atrial systole (contraction of the atria)
  2. Isovolumetric contraction (ventricles begin to contract, but no volume change)
  3. Ventricular ejection (blood is pumped out of the ventricles)
  4. Isovolumetric relaxation (ventricles relax, but no volume change)
  5. Ventricular filling (ventricles fill with blood)
63
Q

What is the role of atrial systole in the cardiac cycle?

A

Atrial systole occurs when the atria contract –> push blood into ventricles –> complete ventricular filling (active filling).

It follows passive filling during diastole and ensures that the ventricles are fully loaded with blood.

64
Q

What is isovolumetric contraction? AKA ventricular systole - first phase

A

Ventricles begin to contract –> causing an increase in pressure, but the volume of blood in the ventricles X change bc the heart valves are closed

65
Q

During which phase does ventricular ejection occur, and what happens?

A

Ventricular systole - second phase

Ventricular ejection occurs during the phase where ventricular pressure exceeds the pressure in the arteries, leading to the opening of the aortic and pulmonary valves. Blood is then pumped out of the heart into the systemic and pulmonary circulation.

66
Q

What happens in the ventricular diastole phase (early)?

A

As ventricles relax, pressure in the ventricles drops
Blood flows back against the cusps of semilunar valves & forces them closed
Blood flows into the relaxed atria

67
Q

What happens in the ventricular diastole (late) phase?

A

All chambers are relaxed, AV valves are open, ventricles fill passively

68
Q

What causes the heart sounds ‘lub’ and ‘dub’?

A

first heart sound (‘lub’): closure of the atrioventricular (AV) valves (tricuspid and mitral valves) at the beginning of ventricular systole.

second heart sound (‘dub’): closure of the aortic and pulmonary valves at the beginning of ventricular diastole.

69
Q

What are the main factors influencing cardiac output (CO)?

A

Cardiac output is influenced by:

  1. Heart rate (HR)
  2. Stroke volume (SV), which depends on preload, afterload, and contractility.
70
Q

Revise page 12 to 15 of CVS physio 2 (because pictures and graphs)

A

Have you revised it?

71
Q

How to calculate cardiac output?

A

CO = HR x SV

HR: heart rate
SV: stroke vol
E.g. 70 beats/min x 70 ml/beat
= 4900 ml/min = 5L/min

72
Q

Define preload, afterload, and contractility.

A

Preload: The degree of stretch of the heart muscle before contraction, primarily determined by the volume of blood returning to the heart (venous return)

Afterload: The resistance the heart must overcome to eject blood, primarily influenced by arterial pressure

Contractility: The inherent strength of the heart’s contraction, independent of preload and afterload

73
Q

Effect of parasympathetic & sympathetic stimulation on:
1. SA node *
2. AV node
3. Ventricular conduction pathway
4. Atrial muscle
5. Ventricular muscle *
6. Veins *

A
  1. Para: Dec. rate of depolarizaiton to threshold + dec HR; Sym: opp
  2. Para: Dec. excitability + inc AV nodal delay; Sym: opp
  3. Para: no effect; Sym: inc excitability + hastens conduction thru bundle & purkinje
  4. Para: dec. contractility + weakens contraction; Sym: opp
  5. Para: no effect; Sym: inc contractility + strengthen contraction
  6. Para: No effect; Sym: inc venous return = inc strength of cardiac contraction (thru intrinsic control
74
Q

What is the Frank-Starling law of the heart?

A

The Frank-Starling law states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end-diastolic volume), due to the stretching of the ventricular walls.

Basically, the heart pumps whatever it receives

75
Q

What is stroke volume determined by?

A
  1. Intrinsic control: related to extent of venous return
  2. Extrinsic control:
    related to the extent of sympathetic stimulation of the heart
76
Q

How does heart rate affect cardiac output?

A

Cardiac output is the product of heart rate (HR) and stroke volume (SV).

An increase in heart rate increases cardiac output, but if the heart rate is too high, it may reduce stroke volume due to insufficient filling time.

77
Q

The frank-starling law of the heart is an intrinsic relationship between _____ and ______

A

Intrinsic relationship between EDV (end-diastolic vol) and SV

Increased EDV = increased SV

Inc. diastolic filling = inc. EDV = inc. stretching of the heart = inc. length of cardiac muscle fibers before contraction = inc. force on subsequent cardiac contraction = inc. SV

BASICALLY, if pull a rubberband softly, it snaps back softly; if pull a rubberband taut, it snaps back harder

78
Q

What happens during isovolumetric relaxation?

A

During isovolumetric relaxation, the ventricles relax, and the pressure in the ventricles drops. Both the aortic and pulmonary valves are closed, and there is no change in the volume of blood within the ventricles.

79
Q

How do pressures change within the heart during the cardiac cycle?

A

During the cardiac cycle, atrial pressure increases during atrial systole. Ventricular pressure increases during isovolumetric contraction and ventricular ejection. Ventricular pressure drops during isovolumetric relaxation, allowing for ventricular filling.

80
Q

Why does ventricular pressure increase during ventricular systole?

A

Ventricular pressure increases during systole because the ventricles contract, pushing blood against the closed valves and preparing to eject blood into the aorta and pulmonary artery.

81
Q

What changes occur in the volumes of blood in the heart chambers during the cardiac cycle?

A

Blood volume in the ventricles decreases during ventricular ejection, reaches a minimum during isovolumetric relaxation, and increases during ventricular filling as blood returns from the atria.

82
Q

How does the ECG relate to the cardiac cycle?

A

The ECG represents electrical activity in the heart:

  • P wave: Atrial depolarization (just before atrial systole)
  • QRS complex: Ventricular depolarization (before ventricular contraction)
  • T wave: Ventricular repolarization (during ventricular relaxation)
83
Q

Why does the QRS complex have a larger amplitude than the P wave on an ECG?

A

The QRS complex has a larger amplitude because ventricular depolarization involves more muscle mass than atrial depolarization, generating a stronger electrical signal.

84
Q

What heart sounds are heard during the cardiac cycle?

A

Two main heart sounds are heard:

  1. First sound (S1): Closure of the AV valves (lub)
  2. Second sound (S2): Closure of the aortic and pulmonary valves (dub)
85
Q

Why does an excessively high heart rate reduce cardiac output?

A

At excessively high heart rates, diastolic filling time is reduced, which decreases stroke volume and thus reduces overall cardiac output.

86
Q

How does heart rate affect cardiac output?

A

Cardiac output increases with an increase in heart rate, provided stroke volume remains constant or also increases.

87
Q

How does stroke volume change with the strength of ventricular contraction?

A

Increased strength of ventricular contraction (contractility) increases stroke volume, resulting in greater cardiac output.

88
Q

How does the sympathetic nervous system affect the strength of ventricular contraction?

A

The sympathetic nervous system enhances contractility by increasing calcium availability in the cardiac muscle cells, which strengthens ventricular contraction.

89
Q

What is the role of the parasympathetic nervous system in cardiac regulation?

A

The parasympathetic nervous system primarily reduces heart rate by affecting the SA node, with minimal effect on ventricular contractility.

90
Q

How does parasympathetic stimulation affect the SA node?

A

Dec rate of depolarization threshold (-40) = dec. HR

91
Q

How does sympathetic stimulation affect the SA node?

A

inc ratet of depolarization to threshold (-40) = inc HR

92
Q

How does parasympathetic stimulation affect the veins?

A

no effect

93
Q

How does sympathetic stimulation affect the veins?

A

Inc venous return = inc strength of cardiac contraction via intrinsic control

94
Q

What is the Frank-Starling law of the heart?

A

The Frank-Starling law states that the heart will pump more blood as more blood fills it (increased end-diastolic volume), due to the stretch of cardiac muscle fibers.

95
Q

Why is the Frank-Starling mechanism important in balancing the output of the two ventricles?

A

The Frank-Starling mechanism ensures that the volume of blood ejected by the ventricles is matched to the volume received, preventing blood from accumulating in either circulation (systemic or pulmonary).

96
Q

How does the Frank-Starling mechanism regulate stroke volume?

A

Stroke volume increases as preload (venous return) increases, due to the stretching of the ventricular walls, which enhances the force of contraction.

97
Q

How does sympathetic stimulation increase stroke volume?

A

Inc. contractility of the heart = defined as a change in the work performed by the heart, X brought about by change in initial fiber length

X the same as Frank-starling law bc X change in muscle fiber length

98
Q

How to calculate stroke volume?

A

SV = EDV - ESV
EDV: end diastolic vol
ESV: end systolic vol

99
Q

What is the ejection fraction?

A

Fraction of blood ejected from a ventricle with each heartbeat
Measure of cardiac contractility (pumping efficiency of the heart)

100
Q

How to calculate ejection fraction?

A

EF = SV/EDV x 100%

SV: stroke vol
EDV: end diastolic vol

Normal = 55-75%
If <40%, may be indicative of heart failure

101
Q

How does sympathetic activity affect cardiac output? (3 points)

A
  1. Directly increases heart rate = inc CO
  2. extrinsic control on stroke vol = inc. stroke vol = inc. CO
  3. Inc. venous return = inc. end-diastolic vol = inc stroke vol = inc CO
102
Q

What is cardiac output?

A

Vol of blood pumped out by each ventricle per min

103
Q

When does cardiac failure occur?

A

When CO is insufficient to service the metabolic requirements of the body’s tissues

104
Q

What are the compensatory measures of systolic heart failure?

A
  1. Sympathetic stimulation
  2. Retention of salt & water by kidneys to expand bld vol
105
Q

How does the kidney compensate in cardiac failure?

A

Kidney detects low bld flow & retains H2O to inc bld vol
bld vol is artificially high = help weak heart to pump enough bld
stretches cardiac muscle

but even with compensation by kidney, heart still X pump enough bld
So much bld vol = congestion of bld = edema

106
Q

Where does the heart receive most of its blood supply from?

A

Coronary circulation during diastole (~70%)

During diastole, closed aortic valve exposes coronary arteries
During systole, muscles contract & PARTIALLY block coronary arteries

107
Q

What is a common presenting symptom of coronary artery disease (CAD)

A

Sensatioon of chest pain (epigastric region, neck, shoulder, etc) due to myocardial ischemia

108
Q

What is acute myocardial infarction (MI)?

A

AKA heart attack
irreversible death (necrosis) of part of the heart muscle secondary to ischemia

109
Q

Cause of coronary artery disease (CAD)?

A

Atherosclerosis - aka formation of plague

progressive, degenerative, arterial disease
leads to occlusion of affected vessels, reducing blood flow through them

110
Q

What can CAD cause?

A

Rupture of artery (bc. clot is hard)
Thrombus
Embolus
Thromboembolism

111
Q

What are each of this:
Thrombus
Embolus
Thromboembolism

A

Thrombus - abnormal clot in vessel wall
Embolus - abnormal particle floating in the bld vessel
Thromboembolism - obstruction of bld vessel by blood clot dislodged form another site

112
Q

Which blood vessel has the most:
1. Endothelium
2. Elastin Fibers
3. Smooth muscle
4. Collagen fibers

A
  1. All around the same amount (capillary only has this; doesn’t have the rest)
  2. Artery; vein has a little bit
  3. Artery has the most; arterioles & veins roughly the same amt but less than artery
  4. Vein; followed by artery, then arteriole

HSC1007 A&P (8 decks)

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