Last of notes complete questions Flashcards

1
Q

Cardiovascular Elements?

A

Heart, blood vessels, blood.

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2
Q

Main function of the cardiovascular system?

A

Delivers O₂/nutrients, removes CO₂/waste, transports hormones, regulates temperature/fluid balance, maintains acid–base balance, supports immunity.

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3
Q

Heart chambers?

A

Right atrium, right ventricle, left atrium, left ventricle.

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4
Q

Blood flow (right heart)?

A

Venae cavae → RA → RV → pulmonary valve → pulmonary arteries → lungs.

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5
Q

Blood flow (left heart)?

A

Pulmonary veins → LA → LV → aortic valve → aorta → body.

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6
Q

Why is the LV thick?

A

It pumps blood to the entire body and must generate high pressure.

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7
Q

Myocardium features?

A

Highly oxidative, dense capillaries, many mitochondria, intercalated discs for coordinated contraction.

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8
Q

Difference: Cardiac vs. Skeletal muscle?

A

Cardiac: small, branched, single nucleus, continuous involuntary contractions; Skeletal: large, long, multinucleated, voluntary intermittent contractions.

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9
Q

Coronary arteries?

A

Right coronary (supplies right heart) and left coronary (supplies left heart).

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10
Q

Intrinsic control of the heart?

A

Cardiac conduction system: SA node, AV node, AV bundle, and Purkinje fibers.

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11
Q

Intrinsic HR value?

A

Approximately 100 beats/min.

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12
Q

Role of the SA node?

A

Initiates the heartbeat with spontaneous depolarization.

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13
Q

Function of the AV node?

A

Delays the electrical signal to allow atrial contraction before ventricular contraction.

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14
Q

Purpose of Purkinje fibers?

A

Rapidly distribute impulses to ensure coordinated ventricular contraction.

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15
Q

Define the cardiac cycle.

A

The sequence of electrical and mechanical events during one heartbeat (systole and diastole).

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16
Q

Systole vs. diastole?

A

Systole: contraction/ejection phase; Diastole: relaxation/filling phase (diastole is about 2/3 of the cycle).

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17
Q

Stroke volume (SV) formula?

A

SV = EDV − ESV (e.g., 100 mL EDV − 40 mL ESV = 60 mL).

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18
Q

What is ejection fraction?

A

The ratio SV/EDV (e.g., 60 mL/100 mL = 60%).

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19
Q

Cardiac output formula?

A

CO = HR × SV (e.g., 70 bpm × 70 mL = 4900 mL/min, ~5 L/min).

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20
Q

Typical resting HR?

A

Between 60 and 100 beats/min; trained athletes may be as low as 35–40 bpm.

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21
Q

Estimated maximal heart rate?

A

220 minus age (e.g., for a 20-year-old: 220 − 20 = 200 bpm).

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22
Q

Extrinsic control: Parasympathetic NS?

A

Via the vagus nerve; decreases HR and contractility using acetylcholine.

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23
Q

Extrinsic control: Sympathetic NS?

A

Releases norepinephrine to increase HR and contractility.

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24
Q

Normal resting blood pressure?

A

Systolic: ~110–120 mmHg; Diastolic: ~70–80 mmHg.

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25
Q

Mean arterial pressure (MAP) estimate?

A

MAP ≈ (2/3 × DBP) + (1/3 × SBP).

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26
Q

Vascular resistance factors?

A

Depends on vessel length, blood viscosity, and especially radius (r⁴ relation).

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27
Q

Role of arterioles?

A

They regulate blood flow by vasoconstriction and vasodilation.

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28
Q

Local blood flow control?

A

Intrinsic mechanisms: metabolic (by-products, O₂/CO₂ levels), endothelial (NO, prostaglandins), and myogenic responses.

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29
Q

Functional sympatholysis?

A

Local reduction in sympathetic vasoconstriction in active muscles, allowing increased blood flow.

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30
Q

Mechanisms aiding venous return?

A

Venoconstriction, the skeletal muscle pump (with valves), and the respiratory pump.

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31
Q

Four steps in respiration?

A

Pulmonary ventilation, pulmonary diffusion, gas transport in blood, and capillary diffusion.

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32
Q

Air pathway through the respiratory system?

A

Nose/mouth → nasal cavity → pharynx → larynx → trachea → bronchi → alveoli.

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33
Q

Primary inspiratory muscles?

A

Diaphragm and external intercostals.

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34
Q

How does inspiration work?

A

Inspiratory muscles contract to expand the thoracic cavity, decreasing intrapulmonary pressure and drawing air in.

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35
Q

Accessory muscles for forced inspiration?

A

Scalenes, sternocleidomastoid, and pectorals.

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36
Q

Expiration process?

A

Normally passive via muscle relaxation and lung recoil; forced expiration involves active muscle contraction.

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37
Q

Muscles for forced expiration?

A

Internal intercostals, latissimus dorsi, quadratus lumborum, and abdominal muscles.

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38
Q

Pulmonary volumes measured by?

A

Spirometry (tidal volume, vital capacity, residual volume, and total lung capacity).

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39
Q

Define pulmonary diffusion.

A

Gas exchange between alveoli and blood across the alveolar-capillary membrane.

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40
Q

Alveolar-capillary membrane thickness?

A

Approximately 0.5–4 µm for efficient gas exchange.

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41
Q

Dalton’s law?

A

The total pressure equals the sum of the partial pressures of individual gases.

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42
Q

Atmospheric partial pressures?

A

At 760 mmHg: PN₂ ≈ 600.7 mmHg, PO₂ ≈ 159.1 mmHg, PCO₂ ≈ 0.2 mmHg.

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43
Q

Henry’s law significance?

A

The amount of gas dissolved in a liquid is proportional to its partial pressure.

44
Q

Fick’s law?

A

Diffusion rate ∝ (Surface area × Pressure gradient) / Membrane thickness.

45
Q

Alveolar O₂ exchange: key pressures?

A

Alveolar PO₂ ~105 mmHg, capillary PO₂ ~40 mmHg, resulting in pulmonary vein PO₂ ~100 mmHg.

46
Q

CO₂ diffusion gradient?

A

Approximately 6 mmHg (from ~46 mmHg in pulmonary arteries to ~40 mmHg in alveoli).

47
Q

Why does CO₂ diffuse efficiently?

A

Its diffusion constant is roughly 20 times greater than that of O₂.

48
Q

Main oxygen transport method?

A

> 98% of O₂ is bound to hemoglobin; <2% is dissolved in plasma.

49
Q

O₂–Hb dissociation curve in the lungs?

A

High PO₂ leads to nearly complete hemoglobin saturation.

50
Q

O₂–Hb curve in tissues?

A

Lower PO₂ causes significant unloading of O₂ from hemoglobin.

51
Q

Myoglobin’s role in muscles?

A

Stores oxygen and releases it when tissue PO₂ is very low.

52
Q

Effect of pH and temperature on O₂ release?

A

Lower pH and higher temperature shift the curve right, enhancing O₂ unloading.

53
Q

Central chemoreceptors?

A

Located in the medulla; respond to increased CO₂/H⁺ levels in cerebrospinal fluid.

54
Q

Peripheral chemoreceptors?

A

Found in the carotid and aortic bodies; sensitive to changes in PO₂, PCO₂, and pH.

55
Q

How does increased CO₂ affect breathing?

A

It raises H⁺ levels, stimulating an increase in the rate and depth of ventilation.

56
Q

Anticipatory HR response?

A

HR increases slightly before exercise due to reduced vagal tone and increased sympathetic stimulation.

57
Q

HR behavior during exercise?

A

HR increases with exercise intensity until reaching a plateau at maximal effort.

58
Q

Steady-state HR?

A

The constant HR maintained during a steady exercise intensity.

59
Q

Factors increasing stroke volume?

A

Higher preload, increased contractility, and decreased afterload.

60
Q

Frank-Starling mechanism?

A

Increased EDV stretches the heart muscle, enhancing contractility and SV.

61
Q

Example calculation of SV?

A

If EDV = 100 mL and ESV = 40 mL, then SV = 60 mL.

62
Q

Example ejection fraction?

A

SV/EDV = 60 mL/100 mL = 60%.

63
Q

Cardiac output at rest?

A

Approximately 5 L/min (e.g., 70 bpm × 70 mL ≈ 4900 mL/min).

64
Q

Oxygen carrying capacity?

A

Approximately 20 mL O₂ per 100 mL of blood.

65
Q

Max SBP during exercise?

A

May reach about 200 mmHg; trained athletes can reach 240–250 mmHg.

66
Q

Maximal stroke volume ranges?

A

Typically 60–130 mL/beat; athletes may have 160–200 mL/beat.

67
Q

Pulmonary diffusion capacity example?

A

At rest, about 21 mL O₂/min/mmHg; with an 11 mmHg gradient, ≈231 mL O₂/min.

68
Q

Role of body position on SV?

A

Supine position increases venous return and SV compared to upright posture.

69
Q

Importance of blood flow redistribution?

A

Directs more blood to active muscles and reduces flow to less active organs during exercise.

70
Q

Local control of blood flow?

A

Adjusts vessel diameter via metabolic by-products, endothelial factors, and myogenic responses.

71
Q

HR recovery significance?

A

A faster drop in HR post-exercise indicates better autonomic regulation and fitness.

72
Q

Training effects on submaximal HR?

A

Trained individuals have a lower HR at the same workload due to increased SV and efficiency.

73
Q

Maximal HR changes with training?

A

Maximal HR remains largely unchanged by training; it decreases primarily with age.

74
Q

Training impact on cardiac output?

A

Maximal CO increases (mainly due to increased SV), while resting CO stays similar.

75
Q

Pulmonary diffusion with exercise?

A

Improved lung perfusion increases diffusion capacity during maximal effort.

76
Q

Capillarization adaptation?

A

Increased capillary density improves oxygen delivery and waste removal in muscles.

77
Q

Role of the skeletal muscle pump?

A

Contractions help return blood to the heart by compressing veins.

78
Q

Role of the respiratory pump?

A

Changes in intrathoracic pressure during breathing aid in venous return.

79
Q

Definition of preload?

A

The end-diastolic volume stretching the ventricles prior to contraction.

80
Q

Definition of afterload?

A

The pressure the ventricle must overcome to eject blood.

81
Q

How is contractility increased?

A

Through sympathetic stimulation (norepinephrine/epinephrine) independent of EDV.

82
Q

Types of cardiac hypertrophy?

A

Non-pathological (exercise-induced) and pathological (due to high blood pressure).

83
Q

Intercalated discs function?

A

They connect cardiac cells for synchronized contraction.

84
Q

How do gap junctions work?

A

They enable rapid electrical communication between cardiac cells.

85
Q

Role of desmosomes?

A

They mechanically hold cardiac cells together during contraction.

86
Q

Function of the pericardium?

A

Protects the heart and reduces friction via pericardial fluid.

87
Q

Why is blood volume important?

A

It affects venous return, preload, and overall cardiac output.

88
Q

How does exercise affect blood pressure?

A

SBP increases significantly; DBP changes little, leading to a higher MAP.

89
Q

Effect of sympathetic stimulation on vessels?

A

It causes vasoconstriction, increasing resistance and blood pressure.

90
Q

Effect of local vasodilation in muscles?

A

It overcomes sympathetic constriction, increasing blood flow to active muscles.

91
Q

How does training affect plasma volume?

A

Training increases plasma volume, which enhances EDV and SV.

92
Q

Why is the O₂ diffusion gradient critical?

A

It drives the movement of O₂ and CO₂ across the alveolar-capillary membrane.

93
Q

How do alveolar and capillary PO₂ values drive O₂ uptake?

A

A high alveolar PO₂ relative to capillary PO₂ forces O₂ into the blood.

94
Q

Key gas exchange law?

A

Fick’s law: Diffusion rate ∝ (Surface Area × Pressure Gradient) / Membrane Thickness.

95
Q

How does exercise alter alveolar diffusion capacity?

A

Enhanced lung perfusion increases the effective surface area for gas exchange.

96
Q

Why does the lung have zones?

A

Zones (1, 2, 3) describe variations in blood flow and ventilation across the lung.

97
Q

Zone 3 of the lung?

A

Normal blood flow: capillary pressure exceeds alveolar pressure.

98
Q

Zone 1 of the lung?

A

No perfusion when alveolar pressure exceeds arterial pressure.

99
Q

Key aspect of respiratory regulation?

A

Maintaining homeostasis of PO₂, PCO₂, and pH.

100
Q

How do central chemoreceptors detect CO₂?

A

They sense changes in H⁺ concentration in cerebrospinal fluid.

101
Q

Where are peripheral chemoreceptors located?

A

In the carotid and aortic bodies.

102
Q

Role of afferent feedback in ventilation?

A

Muscle metabolites signal the respiratory center to adjust ventilation.

103
Q

Importance of the respiratory center?

A

It integrates signals to regulate the rate and depth of breathing.

104
Q

How does VO₂max reflect fitness?

A

It measures the maximal capacity for oxygen uptake and utilization during exercise.

105
Q

Effect of exercise on the O₂–Hb curve in tissues?

A

Lower tissue PO₂ promotes O₂ unloading for metabolism.

106
Q

Why is blood flow redistribution crucial during exercise?

A

It directs more oxygen and nutrients to active muscles while conserving flow elsewhere.