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Organic Chemistry Lab > Cardiac Physiology > Flashcards

Cardiac Physiology Flashcards

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1
Q

Heart

A

Organ that pumps blood, supplies oxygen and nutrients to tissues, and removes CO2 and other wastes; pumped in parallel

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2
Q

Composition of circulatory system

A
  1. Heart - pump that provides pressure to drive blood throughout the circulation
  2. Blood Vessels - passageways in which the blood is directed to organs and tissues
  3. Blood - transport medium, allows materials to be transported over body (ex: O2, CO2, nutrients, waste, electrolytes, hormones)
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3
Q

Composition of blood

A
  • Separated into formed elements and plasma
  • RBCs - carry O2, hemoglobin
  • WBCs - defense
  • Platelets - clotting; low platelets results in hemophilia (bleeding out)
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4
Q

Types of Circulatory Pathways

A
  1. Pulmonary Circulation
  2. Systemic Circulation
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5
Q

Pulmonary Circulation

A

Pumps blood between heart and lungs; shorter circuit with less pressure

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6
Q

Systemic Circulation

A

Pumps blood to all other body systems, tissues, etc.; longer circuit with more pressure; parallel pathway with portions of the blood going to several different regions of body, this means that blood flow is not in series and doesn’t go from one organ to next

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7
Q

Where will oxygenated and deoxygenated blood mix?

A

Womb

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8
Q

Pericardium

A

Coverings of the heart
- Fibrous pericardium = outermost
- Parietal pericardium
- Visceral pericardium = innermost

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9
Q

Serous Pericardium

A

Consists of visceral and parietal, separated by cavity filled with pericardial fluid

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10
Q

What happens when there is too much pericardial fluid?

A

Cardiac tamponade

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11
Q

Walls of the heart

A
  1. Epicardium (same layer as visceral pericardium) = outermost
  2. Myocardium = excited cells, myocytes (muscle cells), thick layer
  3. Endocardium = innermost, smooth, continues with inner layer of blood vessels
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12
Q

What separates the right and left ventricles?

A

Interventricular septum

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13
Q

Chambers of the heart

A
  1. Right atrium
  2. Right ventricle
  3. Left atrium
  4. Left ventricle
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14
Q

Valves of the heart

A
  1. Tricuspid/right atrioventricular valve
  2. Pulmonary semilunar valve
  3. Bicuspid/left atrioventricular valve
  4. Aortic semilunar valve
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15
Q

Heart valves in ventricular contraction

A

Both AV valves remain closed to prevent flow backwards into the atria, and the semilunar valves are open

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16
Q

Heart valves in ventricular relaxation

A

Both AV valves are open, and the semilunar valves close to prevent blood that has entered the arteries from flowing back into the ventricles

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17
Q

When do valves open?

A

When pressure is greater behind the valve

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18
Q

When do valves close?

A

When pressure is greater in front of the valve, it doesn’t open in the opposite direction/one-way valve

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19
Q

Laminar Flow

A

Straight, doesn’t create sound

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20
Q

Turbulent Flow

A

Jumbled, can be heard

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21
Q

Diastole

A

Relaxation

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22
Q

Systole

A

Contract

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23
Q

Late Diastole

A

Both sets of chambers are relaxed an ventricles fill passively, start, already has 80% of ventricles filled

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24
Q

Atrial Systole

A

Atrial contraction forces small amount of additional blood into ventricles (20% active, atria push 20% into ventricles during contraction)

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25
Q

When is lub noise heard?

A

At the end of atrial systole, S1

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26
Q

Isovolumic Ventricular Contraction

A

Firs phase of ventricular contraction that pushes AV valves closed but doesn’t create pressure to open semilunar valves

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27
Q

Ventricular Ejection

A

Semilunar valves open and blood is ejected due to pressure in ventricles rising and exceeding pressure in arteries

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28
Q

When is dub noise heard?

A

At the end of ventricular ejection, S2

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29
Q

Midventricular Diastole

A

Blood flows from venous side into atrium and into ventricles

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30
Q

Isovolumic Ventricular Relaxation

A

Pressure in ventricles falls, blood flows back into cusps of semilunar valves and causes them to close

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31
Q

When is heart murmur heard?

A

Between dub and lub, means there is blood leaking back through the valves

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32
Q

What is the correlation between dilation and EDV?

A

Increased dilation = increased EDV

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33
Q

Autorhythmicity

A

Heart beats due to action potentials it creates on its own

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34
Q

Types of cardiac muscle cells

A
  1. Contractile cells
  2. Autorhythmic cells
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35
Q

Contractile Cells

A

99% of cells on heart; don’t initiate their own action potential; myocytes; don’t regenerate

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36
Q

Autorhythmic Cells

A

Do not contract, initiate action potentials for working contractile cells; pacemaker cells

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37
Q

What is Na+ responsible for?

A

Depolarization

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38
Q

What is K+ responsible for?

A

Repolarization

39
Q

What is Ca2+ responsible for?

A

Depolarization and firing of action potential

40
Q

What changes in ionic movement cause the pacemaker potential?

A
  • Increased inward Na+ current and decreased K+ current
  • Increased inward Ca2+ current
  • Increased K+ outward current
41
Q

What kind of channels are funny channels?

A

Sodium channels that hand off to transient Ca channels in order to reach threshold

42
Q

What are the types of Ca channels?

A
  1. Transient
  2. Long-lasting
43
Q

Transient Ca Channels

A

Propagate pacemaker potential to threshold

44
Q

Long-lasting Ca Channels

A

Propel action potential to overshoot where K+ permeability increases and it exits cell

45
Q

Pacemaker Potentials

A
  • Ca rising phase differs from nervous and skeletal muscle cells where Na influx causes positive potential direction instead of Ca
  • Falling phase is result of K efflux out of cell via activation of voltage gate K channels which are coupled with closure of long Ca channels
46
Q

Electrical Conduction Pathway

A

SA node to atria via interatrial pathway
SA node on internodal pathway to AV node, which breaks off into Bundle of His –> Purkinje fibers

47
Q

What will take over if SA node stops working?

A

AV node can take over and compensate because 80% of heart fills based on pressure difference alone

48
Q

Atrial Excitation

A

Actional potential from SA node spreads through the atria

49
Q

Pathways that speed up conduction in the atria

A
  1. Interatrial Pathway
  2. Internodal Pathway
50
Q

Interatrial Pathway

A

From SA node in right atrium to left atrium
- Rapidly transmits AP from right to left atrium and ensures that both atria become depolarized and contract simultaneously

51
Q

Internodal Pathway

A

SA node to AV node
- Only way that an electrical signal can pass to the ventricles (via AV node)

52
Q

How long and why is conduction slow through AV node?

A

Delayed for about 100 msec (AV nodal delay); happens so ventricles can fill

53
Q

Where does impulse go after AV nodal delay?

A

Bundle of His and then to Purkinje fibers

54
Q

Conduction System of Heart

A
  1. SA node depolarizes
  2. Electrical activity goes rapidly to AV node via internodal pathways
  3. Depolarization spreads more slowly across atria and conduction slows through AV node
  4. Depolarization moves rapidly through ventricular conducting system to apex of heart
  5. Depolarization wave spreads up from apex
55
Q

AP of Contractile Cells

A

Induced by pacemaker cells; contain different electrophysiological characteristics than pacemaker cells

56
Q

What is the resting membrane potential of cardiac contractile cells (myocytes)?

A

Around 90 mV

57
Q

Phases of AP for contractile cells

A
  1. Cell at resting potential
  2. Na+ channels open and depolarize
  3. Na+ channels close and K channels open transiently to cause small repolarization
  4. Long Ca channels open and fast K channels close (decreasing permeability), causing plateau and halts repolarization
  5. Ca channels close and K channels open causing repolarization
58
Q

What is the area under the curve known as?

A

Absolute refractory period

59
Q

Why does tetanus not occur with these contractile cells/myocytes?

A

The absolute refractory period overlaps with myocyte contraction and relaxation. This means another AP cannot fire until the cell is completely relaxed

60
Q

Excitation Contraction Coupling

A
  1. AP enters from adjacent cell
  2. Voltage-gated Ca channels open and Ca enters cell
  3. Ca induces Ca release through ryanodine receptor-channels (RyR)
  4. Local release causes Ca spark
  5. Summed sparks create Ca signal
  6. Ca ions bind to troponin and initiate contraction
  7. Relaxation occurs when Ca unbinds from troponin
  8. Ca pumped back into sarcoplasmic reticulum for storage
  9. Ca exchanged with Na by NCX antiporter
  10. Na gradient maintained by Na-K-ATPase
61
Q

Process of Ca release

A
  • Ca influx causes opening of ryanodine receptors on lateral sacs of sarcoplasmic reticulum = Ca induced Ca release
  • Incoming Ca sparks SR to release Ca
62
Q

Muscle Contraction w/ Excitation Contraction Coupling

A
  1. AP in contractile cell
  2. AP travels down T-tubules
  3. Entry of small amount of Ca from ECF through long Ca channels causes Ca induced Ca release
  4. Increased cytosolic Ca
  5. Troponin-tropomyosin complex in then filaments pulled aside
  6. Cross-bridge cycling between thick and thin filaments
  7. Thin filaments slide inward between thick filaments
  8. Contraction
63
Q

When would tetanus occur in cardiac muscle?

A

If the refractory period did not align with the muscle twitch

64
Q

Electrocardiogram (ECG)

A

Record of overall spread of electrical activity through heart
- 6 leads to chest and 6 to legs

65
Q

What is ECG recording of?

A

Recording of activity present in body fluids from cardiac impulse that reaches the body surface, not a direct recording of activity from heart

66
Q

What does ECG show?

A

Shows overall activity and not APs; at any one time it represents sum of activity. Also shows voltage comparison of two points of body surface –> exact pattern of activity depends on orientation of electrodes

67
Q

Waveforms of ECG

A
  1. P wave
  2. QRS complex
  3. T wave
68
Q

P Wave

A

Represents atrial depolarization/contraction; SA node fires

69
Q

QRS Complex

A

Represents ventricular depolarization/contraction while atria repolarize/relax

70
Q

T Wave

A

Represents ventricular repolarization/relaxation

71
Q

Why is the QRS complex so big?

A

The ventricles have more myocytes and electrical activity

72
Q

Where is the atrial relaxation on ECG?

A

It’s covered up by QRS complex

73
Q

How do mechanical events of heart correspond to electrical events?

A

They slightly lag behind them

74
Q

PR Segment

A

AV nodal delay

75
Q

ST Segment

A

Time when ventricles are contracting and emptying

76
Q

TP Interval

A

Time when ventricles are relaxing and filling

77
Q

What are the types of cardiac abnormalities?

A
  1. Rate
  2. Rhythm
  3. Cardiac Myopathies
78
Q

Rate Abnormalities

A
  1. Tachycardia
  2. Bradycardia
79
Q

Tachycardia

A

Heart rate of more than 100 bpm

80
Q

Bradycardia

A

Heart rate of less than 60 bpm

81
Q

Rhythm Abnormalities

A

Arrhythmia
- Atrial flutter
-Atrial fibrillation
- Ventricular fibrillation
- Heart block

82
Q

Atrial Fibrillation

A

Atrium contracts while other relaxes; less dangerous than V-fib because 80% of flow still occurs

83
Q

Ventricular Fibrillation

A

Ventricle contracts while other relaxes

84
Q

How are A-fib and V-fib treated?

A

Treated with defibrillation, but there must be some current to work

85
Q

Cardiac Myopathy

A

Damage of heart muscle
- Myocardial ischemia
- Necrosis
- Acute MI

86
Q

Myocardial ischemia

A

Inadequate delivery of oxygenated blood to heart tissue

87
Q

Necrosis

A

Death of heart muscle cells

88
Q

Acute MI

A

Heart attack; blood vessel supplying area of heart has been blocked or ruptured

89
Q

Second-degree block

A

Half of P waves aren’t followed by QRS complex and T wave while other half is; SA node works(contracts?) but ventricle doesn’t contract

90
Q

A-fib ECG

A

Abnormal pattern prior to QRS complexes and increased frequencies between QRS complexes

91
Q

Ventricular Tachycardia ECG

A

QRS complex has strange shape –> S dips down

92
Q

V-fib ECG

A

No normal electrical activity; very dangerous and can be lethal

93
Q

Third-degree block

A

Some impulses initiated by SA node don’t reach AV node while others do; P waves not followed by QRS complex; very rare, death occurs with no treatment

Organic Chemistry Lab (5 decks)

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