Midterm 3 Flashcards
1
Q
functions of the heart (4)
A
- generate blood pressure
- route blood - right side of heart brings blood to the lungs, left side to the rest of the body
- ensure one-way flow of blood - valves to prevent back flow
- regulate blood supply
2
Q
pathway of blood through heart
A
enter right atrium from body through superior vena cava -> goes through tricuspid (AV) valve -> moves into right ventricle -> goes through pulmonary semilunar valve -> pushed into pulmonary arteries -> travels through lungs to be oxygenated -> enter into pulmonary veins -> enters into left atrium -> goes through bicuspid valve -> moves into left ventricle -> goes through aortic semilunar valve -> out to body tissues through aorta
3
Q
conducting system of the heart
A
- autorhythmicity: heart can contract on its own without any neural or hormonal input
- achieved by the cardiac conduction system
- sinoatrial node (SA) node: group of conduction cells found in right atrium, distributes energy to network using conducting cells
- atrioventricular node (AV): group of conduction cells located in right atrium, sends signal from atrium to ventricle
- conducting cells: wires throughout the heart, responsible for sending signal from one place to another
internal pathways: pathways between SA and AV node - Purkinje fibres act as conduction pathway of signal along ventricles
- Bundle of His conducts signal to left atrium and ventricle
- maximum conduction rate at the AV node = 230 bpm
- pumping efficiency decreases at 180 bpm
- rates over 230 bpm can occur when the conduction system is damaged
- max limit is about 300-400 bpm
4
Q
sinoatrial (SA) node
A
- located in right atrium
- contains pacemaker cells that maintain rhythm of heart beat
- connected to the AV node via the internal pathways in the atrial wall
- determines resting heart rate
- changes in membrane potential of pacemaker cells in the SA node affect the heart rate, faster heart beat causes it to reach threshold (-40 mV) faster, prepotential is steeper
5
Q
atrioventricular (AV) node
A
- located in right atrium, take rhythm from SA node and sends it to ventricles
- slows impulse down, can’t have atria and ventricles contracting at the same time, giving atria time to finish contraction and blood to flow into ventricles before contracting them
- moves impulse to the atrioventricular (AV) bundle
6
Q
pathway of conduction in the heart
A
- SA node activity and atrial activation begin, time 0ms
- stimulus spreads across the atrial surfaces and reaches the AV node, top of atria squeeze first, time 50ms
- there is a 100ms delay at the AV node, atrial contraction begins, time 150ms
- impulse travels along the inter ventricular septum within the AV bundle and the bundle branches of the Purkinje fibres and, by the moderator band, to the papillary muscles of the right ventricle, time 175ms
- impulse is distributed by Purkinje fibres and relayed throughout the ventricular myocardium, atrial contraction is completed, and ventricular contraction begins, time 225ms
7
Q
AV bundle, bundle branches and Purkinje fibres
A
- AV bundle = bundle of His
- right and left bundle branches feed into left and right ventricles
- Purkinje fibres connect with muscle cells of ventricles
8
Q
electrocardiogram main waves
A
- P wave: atrial depolarization caused by SA node
- atrial repolarization but QRS complex covers it
- QRS complex: ventricular depolarization caused by AV node
- T wave: ventricular repolarization
- PR interval: time between onset of P wave and QRS complex
9
Q
arrhythmias
A
- abnormal heart rhythm
- SA node develops abnormal rhythm
- conduction pathway interrupted
- ectopic pacemaker
10
Q
atrial fibrillation (AF)
A
- the impulses move over the atrial surface at rates of up to 500 bpm, the atrial wall quivers instead of producing an organized contraction
- the ventricular rate cannot follow the atrial rate and may remain within normal limits, even though the atria are now non-functional, their contribution to ventricular end-diastolic volume is so small the condition may go unnoticed in older individuals
- blood may start to clot in atria if it stays stationary for too long, clot then falls into ventricle and is pumped into lungs or to the body
11
Q
ventricular tachycardia (VT)
A
- defined as four or more premature ventricular contractions (PVCs), arising from an ectopic source, without intervening normal beats
12
Q
ventricular fibrillation (VF)
A
- responsible for the condition known as cardiac arrest
- VF is rapidly fatal because the ventricle quiver and stop pumping blood
13
Q
heart block
A
- related to the P-R interval, measures performance of AV node
- first degree: P-R interval is extended
- second degree: P-R interval is skipped, dropped heart beat
- third degree: no AV node function, ventricles rendered useless
14
Q
the cardiac cycle
A
- beginning of one heartbeat to the beginning of the next heartbeat
- contraction (systole) phase and relaxation (diastole) phase
- blood will move from high pressure to low pressure
- pressure increases during contraction phase
- valves open and close due to pressure
1. atrial systole
2. atrial diastole
3. ventricular systole
4. ventricular diastole
15
Q
atrial systole
A
- atria begin to contract due to SA node
- pressure increases
- atria push blood into ventricle, 30% of volume of ventricle
- “topping up” ventricle
16
Q
atrial diastole
A
- atria begin to relax
- continually filling while relaxed
17
Q
ventricular systole
A
- two phases: isovolumetric ventricular contraction and ventricular ejection
18
Q
isovolumetric ventricular contraction
A
- occurs during ventricular systole
- end-diastolic volume (EDV, 120 mL), amount of blood at end of diastole
- ventricular contraction
- heart valves remain closed, pressure increases
19
Q
ventricular ejection
A
- occurs during ventricular systole
- pressure in ventricle exceeds pressure in aorta or pulmonary trunk, causes aortic and pulmonary valves to open
- valve opens, this is when arterial pressure is measured
- ventricles continue to contract
- pressure continues to increase, peaks, then decreases
- volume of blood ejected = stroke volume (SV), typically 70-80 mL, around 60% of EDV at rest
- blood remaining in ventricle at end of contraction = end systolic volume (ESV, 40 mL)
20
Q
ventricular diastole
A
- all valves closed
- isovolumetric ventricular relaxation
- ventricular pressure decreases
- AV valves open and passive filling occurs (70%)
21
Q
Wiggers diagram
A
look at it and practice labelling
22
Q
heart sounds
A
- ausculation
- “Lubb” = start of ventricular contraction, AV valve closes
- “Dupp” = start of ventricular filling, semilunar (aortic and pulmonary) valve closes
23
Q
cardiac output
A
- cardiac function over time
- cardiac output = amount of blood pumped by the left ventricle per minute
- Q (mL/min) = HR (beats/min) x SV (mL/beat)
- at rest, average Q is 6 L/min
- normal range of Q during heavy exercise is 20 L/min
- maximum for trained athletes exercising at peak levels is 40 L/min
24
Q
factors affecting cardiac output
A
- heart rate (chronotropic factors): autonomic innervation and hormones
- stroke volume (inotropic factors): EDV -ESV
25
Q
autonomic innervation and Q
A
- sympathetic (increase HR) and parasympathetic ( decrease HR) divisions
- cardiac centre in medulla oblongata:
- cardioacceleratory centre (sympathetic)
- cardioinhibitory centre (parasympathetic)
- autonomic tone: how much parasympathetic and sympathetic system are activated
- effects on SA node: affect flow of Na+ into pacemaker cells, more permeability leads to increased HR
- atrial reflex: if heart pumps faster, more blood comes back to heart, atria fills more and stretches, stretch receptors send signal to SA node to beat faster, leading to more opening of Na+ channels in SA node
26
Q
hormones and Q
A
- epinephrine, norepinephrine and thyroid hormone all affect the SA node leading to increases in heart rate by encouraging Na+ to enter SA and depolarize more frequently
27
Q
end-diastolic volume (EDV) and Q
A
- EDV is the volume of blood in left ventricle at end of filling in diastole
- can increase EDV by increasing filling time, this occurs by slowing down HR
- slower the HR, the more time it has to fill
- can increases EDV by increasing venous return, the amount of blood returning to heart after travelling through the body, exercising increases venous return
- filling time and venous return affect preload, increasing either leads to increases in preload, the initial stretching of cardiac myocytes prior to contracting
28
Q
end-systolic volume (ESV) and Q
A
- ESV is the amount of blood left in left ventricle after contraction, want it to be as small as possible
- increasing preload, decreases ESV by pumping more blood out of left ventricle, uses Frank-Starling law to generate more elastic energy for more powerful contraction
- increasing contractility of heart decreases ESV, either via autonomic activity or hormones
- increasing afterload, amount of pressure heart needs to overcome to eject blood out of LV, increases ESV, if afterload is higher more pressure is required to open the valves for ejection of blood causing the heart to work harder, vasodilation and vasoconstriction can impact afterload
29
Q
enlarged heart
A
- can exist due to hypertension as it tries to compensate for the higher arterial pressure, leads to thickening of the walls of LV, causing SV to get smaller
- can also occur due to having a stronger heart from exercise and training
30
Q
factors affecting heart rate
A
- autonomic innervation
- hormones
- fitness levels
- age
31
Q
factors affecting stroke volume (7)
A
- heart size
- fitness levels
- gender
- contractility
- duration of contraction
- preload (EDV)
- afterload (resistance)
32
Q
path of blood through blood vessels
A
- arteries -> arterioles -> capillaries -> venules -> veins
33
Q
arteries
A
- relatively thick muscular walls (contractile and elastic properties), needs to withstand high pressure blood being ejected by heart
- elasticity allows for passive changes in diameter, expand when blood volume gets pumped out of LV and when returning back to resting diameter helps continue pushing blood forward
- contractility allows for active changes in diameter
- sympathetic activity -> vasoconstriction and vasodilation
34
Q
elastic arteries
A
- aka conducting arteries
- first arteries that exit from heart, experience large changes in volume and pressure
- few smooth muscle fibres and a high density of elastic fibres
- expand during ventricular systole and recoil to original size during ventricular diastole, helps propel blood forward since heart isn’t contracting to generate pressure
- helps make blood flow continuous
35
Q
muscular arteries
A
- aka distribution arteries
- more smooth muscle fibres and fewer elastic fibres
- most arteries are muscular arteries
- distribute blood to skeletal muscle and internal organs
36
Q
arterioles
A
- aka resistance vessels
- smaller than arteries, thickness of wall smaller, thinner wall because blood pressure is much lower once it reaches arterioles
- capable of constriction and dilation
- no elastic component
- determine the pressure that is required to push blood through the vessels, creates a bottleneck to help direct blood to where it is needed
37
Q
capillaries
A
- “workhorses” of the cardiovascular system
- form network of vessel throughout the body
- thin walls allow gas exchange between blood and surrounding fluid
- blood travels slowly allowing for two-way exchange of gases
38
Q
venules
A
- collect blood from the capillary beds
39
Q
veins
A
- contain majority of blood in body at any one time (2/3)
- medium and large sized veins
- low-pressure system, important because when standing blood in legs pools and can’t get back to heart, assisted by venous valves for one way flow of blood
- venules and medium sized veins contain venous valves to prevent backflow, valve opens superior to contracting muscle and closes inferior to contracting muscle
- blood is moved up by contraction of gastrocnemius and soleus (muscular pump), once into abdomen, breathing helps return it to heart
40
Q
proportions of blood sitting in different blood vessels
A
- 64% of blood sitting in veins
- 7% in heart
9% in pulmonary circuit - 13% in arteries and arterioles
41
Q
pressure, resistance and flow
A
F = P/R
- flow is directly proportional to pressure, if pressure increases flow increases
- pressure drops dramatically once its exits arterial system, low pressure in capillaries and even lower in veins
- flow is inversely proportional to resistance, increasing resistance decreases flow
- to ensure flow, want pressure to be high and resistance to be low
- in veins, pressure is low but so is resistance
- in arteries, pressure is high but resistance is also high
42
Q
total peripheral resistance
A
- most important factor is friction between the blood and vessel walls
- friction depends on:
- vessel length: long = more resistance than if short, but length remained relatively constant, directly proportional to resistance
- vessel diameter: large has less resistance than smaller vessel, this is controlled by constriction and dilation, inversely proportional to resistant, significant effect on resistance
R = 1/r^4 - blood viscosity: thickness of a fluid, hematocrit is a measure of how many red blood cells are in blood, kidneys help maintain blood viscosity by controlling amount of fluid in blood
- blood doping increases the viscosity of blood by adding more RBCs
- turbulence: due to irregular surfaces and sudden changes in diameter, increases resistance, plaques lining vessels cause turbulence disrupting laminar flow affecting blood pressure and flow
43
Q
arterial blood pressure
A
- systolic pressure: during systole or contraction of LV, normal is 120 mmHg
- diastolic pressure: during diastole or relaxation, normal is 80 mmHg
- pulse pressure is the difference between systolic and diastolic pressure
- mean arterial pressure is the average arterial pressure throughout one cardiac cycle
44
Q
hypertension
A
- > 135/>85 mmHg
- increased workload on heart
- left ventricle gets larger
- greater demand for oxygen
- coronary ischemia when blockages occur
- stresses blood vessels, affects capillaries most, can cause them to burst
- promotes development of arteriosclerosis
- increased risk of aneurysms
45
Q
elastic rebound
A
- during diastole, continues to push blood away from heart and to arterioles
- maintains even blood flow
46
Q
venous return
A
- small pressure determines return
- posture can affect venous return via gravity
- two factors assist venous return:
- muscular compression: calf and leg muscles
- respiratory pump: once blood is in abdomen, respiratory system helps return it to heart
47
Q
arteriosclerosis
A
- thickening or toughening of the arterial wall
- focal calcification: accumulation of calcium in arterial walls, makes them stiffer and less flexible, can’t expand as well so BP increases
- atherosclerosis: when inner wall fill up with lipids and plaques, really unhealthy, tends to be linked to diet
48
Q
atherosclerosis
A
- tends to develop due to high levels of cholesterol
- changes in lining of artery leads to plaque
- can be reverse early with diet changes
- if not, plaque can grow and get more complex, some could even completely block an artery causing an occlusion
- more common in older men
- other factors: high cholesterol, hypertension, and cigarette smoking, diabetes, obesity and stress
49
Q
cardiovascular regulation
A
- control cardiac output and blood pressure, results in blood flow changes
- 3 systems:
1. autoregulation
2. neural mechanisms
3. endocrine mechanisms
50
Q
autoregulation of CV
A
- automatic ability to maintain normal resting conditions, dominates majority of CV control
- normal resting conditions, changes with posture
- cardiac output remains unchanged
- blood flow is controlled by adjusting peripheral resistance to respond to local changes, achieved by vasodilation or vasoconstriction
- vasodilators:
- decreased O2 levels or increased CO2 levels
- lactic acid (H+)
- elevated local temperature
51
Q
neural regulation of CV
A
- medullar oblongata -> brain stem, monitoring body conditions at all times, deals with HR
- cardiac centre: cardioacceleratory and cardioinhibitory centres
- vasomotor centre:
- vasoconstriction neurons and vasodilation neurons
- baroreceptor reflex: sense pressure
- carotid arteries: makes sure pressure going to brain is adequate
- aortic arch: first part of arterial system that takes blood away from heart
- wall of right atrium: monitors pressure of blood coming back to heart
52
Q
response to increased baroreceptor stimulation
A
- blood pressure is increasing, homeostasis is disturbed
- baroreceptors stimulated
- cardioinhibitory centre stimulated, cardioacceleratory centre inhibited, and vasomotor centre inhibited
- cardiac output decreases and vasodilation occurs
- homeostasis is restored and blood pressure decreases
53
Q
response to decreased baroreceptor stimulation
A
- homeostasis disturbed, decreasing blood pressure
- baroreceptors inhibited
- vasomotor centre stimulated, cardioacceleratory centre stimulated, and cardioinhibitory centre inhibited
- increased cardiac output and vasoconstriction occurs
- blood pressure increases and homeostasis restored
54
Q
endocrine regulation of CV
A
- epinephrine (E) and norepinephrine (NE) are produced by adrenal medullar
- stimulate HR, increasing it
- lead to peripheral vasoconstriction
- anti-diuretic hormone (ADH) leads to vasoconstriction and water retention to increase blood pressure and blood volume
55
Q
CV response to light exercise
A
- eg. walking, vacuuming
- extensive vasodilation to deliver more blood to working muscles
- increased venous return
- increase cardiac output
56
Q
CV response to heavy exercise
A
- eg. basketball, cycling, HIIT
- cardiac and vasomotor centres activate the sympathetic nervous system, increasing HR and BP
- cardioacceleratory centre increases cardiac output to 20-25 L/min
- vasomotor centre severely restricts blood flow to “non-essential” organs, such as digestive and excretory systems
57
Q
functions of the respiratory system (4)
A
- provide extensive surface area for gas exchange
- move air to/from exchange surfaces
- protection from allergens, cilia to project things out
- produce sound and detect smells, require air for us to smell or talk
58
Q
organization of the respiratory system
A
- upper respiratory system: everything neck up, nose, nasal cavity, sinuses, and pharynx
- lower respiratory system: larynx, trachea, bronchus, and bronchioles
- respiratory tract:
- conducting portion: everything except alveoli, bronchi, bronchioles
- respiratory portion: alveoli, where gas exchange occurs
59
Q
alveoli
A
- type I pneumocytes: thin membrane and allows gas exchange
- type II pneumocytes: produces surfactant that reduces surface tension
- if malfunctioning, can lead to respiratory distress syndrome where the surface tension on alveoli increases too much so they can’t inflate for gas exchange
- premature babies don’t yet have mature type II pneumocytes so they don’t have surfactant
60
Q
pleural cavity and pleural membrane
A
- thoracic cavity is cone-shaped
- ribs and diaphragm form walls and floor
- parietal pleura: closer to ribcage, when it moves during inhalation surface tension causes the visceral pleura to be pulled away from lungs increasing volume
- visceral pleura: closer to lungs and separates lungs from ribcage
- pleural cavity is the space between the visceral and parietal pleura, filled with pleural fluid
61
Q
external and internal respiration
A
- external respiration: exchange of O2 and CO2 between body and external environment
- internal respiration: absorption of O2 and release of CO2 by cells of the body
62
Q
external respiration
A
- pulmonary ventilation: breathing
- gas diffusion: gases diffusing across type I pneumocytes
- transport of O2 and CO2 in blood
63
Q
pulmonary ventilation
A
- moving air in and out of respiratory tract
- goal is to maintain alveolar ventilation
64
Q
Boyle’s Law
A
- air is a gas
- pressure of the air = atmospheric pressure, at sea level is 760 mmHg
- pressure can change due to: temperature, altitude, and volume changes
- for a gas in a closed container at a constant temperature pressure is inversely proportional to volume
65
Q
airflow
A
- air flows from a high pressure to a low pressure
- air flowing into the body = inspiration
- air flowing out of the body = expiration
- inspiration and expiration occurs due to the changes in lung volume and Boyle’s Law
- the volume of the thoracic cavity changes when we breathe
- during inspiration, volume increases dropping pressure so air moves in
- during expiration, volume decreases increasing pressure so air moves out
- rib cage moves up and out during inspiration, and down and in during inspiration
- diaphragm moves down during inspiration, and up during expiration
- at altitude, it is more difficult to breathe because the pressure difference between atmospheric pressure and pressure in lungs in lower
- lungs follow the movement of the rib cage and diaphragm due to the pleural cavity and its fluid (surface tension)
66
Q
compliance and aging
A
- lung tissue needs to be compliant to make it easy to breathe
- connective tissue of the lungs: as we age and connective tissue gets stiffer, makes it more difficult to fill them
- level of surfactant production: amount of type II pneumocytes drops over time, increasing surface tension
- mobility of thoracic cage: ribs don’t move as easily, diaphragm loses some strength, can’t generate as much of a pressure change
67
Q
3 important pressures
A
- atmospheric pressure
- intrapulmonary pressure (intra-alveolar pressure)
- intrapleural pressure
68
Q
atmospheric pressure
A
- pressure in air outside, changes with altitude
- at sea level is 760 mmHg
69
Q
intrapulmonary (intra-alveolar pressure)
A
- pressure inside alveoli
- want it to be less than atmospheric pressure to move air in
- to move air out, want to make pressure higher than atmospheric pressure
70
Q
intrapleural pressure
A
- pressure in pleural sac that surrounds the lung, less than intra-alveolar pressure
- if it was higher than intra-alveolar, wouldn’t be able to expand alveoli
- if it is the same as atmospheric pressure, it will not inflate or will remain deflated
- if intrapleural cavity is punctured, lose the pressure difference and lung collapses causing pneumothorax, intrapleural pressure becomes equal to atmospheric pressure restricting alveolar expansion
71
Q
breathing mechanics
A
- changing the volume of the lungs changes the pressure in the lungs (Boyle’s Law)
- pressure gradient results in air flow
- volume changes are a result of muscle contraction
72
Q
inspiration
A
- diaphragm is responsible for 75% of volume change, moves downward to increase volume
- external intercostals responsible for 25% of volume change, expand ribs to increase volume
- accessory muscles: sternocleidomastoid, serratus anterior, pectoralis minor, and scalene
73
Q
expiration
A
- passive involves no muscle contraction, turn off muscles and they return back to resting length, ribs go down and diaphragm moves up, decreasing volume of thoracic cavity
- active involves purposeful and powerful exhalation, uses internal intercostals to contract and pull rib cage down and in, and abdominal muscles to push up against diaphragm
74
Q
breathing modes
A
- eupnea - quiet breathing
- diaphragm and external intercostal muscles contract and inhalation occurs -> dorsal respiratory group inhibited -> diaphragm and external intercostal muscles relax and passive exhalation occurs -> dorsal respiratory group active
- hyperpnea - forced breathing
- muscles of inhalation contract, and opposing muscles relax, inhalation occurs -> DRG and inspiratory centre of VRG are inhibited, expiration centre of VRG is active -> muscles of inhalation relax and muscles of exhalation contract, exhalation occurs -> DRG and inspiratory centre of VRG are active, expiratory centre of VRG in inhibited
75
Q
respiratory rates and volumes
A
- respiratory rate: 12-18 breaths per minute
- minute volume (pulmonary ventilation): 6 L/min, amount of air entering body per minute, respiratory rate times tidal volume
- alveolar ventilation: how much air gets down to alveoli, BF x (TV-ADS)
- anatomic dead space (ADS): amount of air inhaled that doesn’t reach alveoli, conduction zone doesn’t carry out gas exchange, volume is about 150 mL, longer deeper breaths allow more air to get down to the alveoli
76
Q
spirometry volumes
TV, ERV, RV, IC, IRV, FRC, VC, TLC
A
- tidal volume (TV): amount of air that moves in and out of lungs in a single respiratory cycle
- expiratory reserve volume (ERV): amount of extra air that can be forcefully exhaled above normal volume
- residual volume (RV): amount of air left in lungs after maximum exhalation, 1000 mL in females and 1200 mL in males
- inspiratory reserve volume (IRV): forceful amount of air inhale after normal tidal volume
- inspiratory capacity: maximum amount of air that can be inhaled from resting expiratory level, TV+IRV
- functional residual capacity (FRC): volume remaining in lungs after normal, passive exhalation, RV+ERV
- vital capacity (VC): maximum amount of air that can be exhaled after a forceful inhalation, TV+ERV
- total lung capacity (TLC): TV+IRV+ERV+RV
- review spirometry diagram labelling
77
Q
forced expiratory volumes
A
- FEV1.0/FVC ratio measures the ratio of forced expiratory volume in the first one second to the forced vital capacity of the lungs
- used to distinguish obstructive and restrictive pulmonary disorders, normal range is above 80%
- in obstructive diseases, the ratio is less than 80%, diseases such as asthma, emphysema, bronchitis
- in restrictive disorders, the ratio may still be above 80% but the actual values of FEV1.0 and FVC are low due to restriction of lung expansion, diseases such as pulmonary fibrosis or obesity
78
Q
partial pressure of air
A
- 78.6% nitrogen
- 20.9% oxygen
- 0.05% water and other (CO2)
- atmospheric pressure is 760 mmHG
- Dalton’s law says that pressure of the individual gases contribute to the total pressure
- partial pressure is how much of the total pressure is due to a specific gas
79
Q
partial pressure of oxygen
A
- partial pressure is 159 mmHg, or 21% of total pressure
- changes when air reaches the alveoli to 100 mmHg as new air mixes with old air, heats up and mixes with moisture in airway
- at top of Everest, % of oxygen stays the same but pressure drops so PO2 also drops, body gets less oxygen out of the ar at altitude because of lower PO2
80
Q
partial pressure in lungs general
A
- pressure gradient is substantial between alveoli and blood
- distance is short due to the thin membranes of type I pneumocytes allowing O2 to travel out into blood very easily
- gases are lipid soluble so they can easily move across membrane
- total surface area is large, about half of a volleyball court
81
Q
partial pressure of oxygen in lungs
A
- in alveoli, PO2 is 100 mmHg
- in blood coming to lungs, PO2 is 40 mmHg, and blood leaving PO2 is 100 mmHg, as it travels through capillaries and into venous system PO2 starts at 95 mmHg then drops back to 40 mmHg as cells take up O2, PO2 in cells of body is 40 mmHg
- as blood enters lungs, carries oxygen but lower PO2 so oxygen moves from lungs into blood
- loading blood with oxygen from lungs until PO2 is equal to that in lungs
82
Q
oxygen transport
A
- 98.5% of oxygen is transported by the red blood cell (RBC) bound to hemoglobin (Hb)
- each Hb can carry 4 oxygen molecules
- Hb + O2 <-> HbO2
- each RBC has approx. 280 million Hb molecules, therefore each RBC can carry over a billion O2 molecules
83
Q
hemoglobin saturation
A
- affinity is how well two things like each other, how closely they can be bound
- % of Hb containing bound O2
- oxygen-hemoglobin saturation curve:
- during exercise, PO2 of venous return is lower because more O2 is entering tissues due to lower than usual PO2 in tissues
- has a sigmoid shape
- plateau allows us to shift down to lower pressures and not feel any significant consequences
- steep portion allows us to unload more O2 while exercising
- during exercise, oxyhemoglobin saturation drops down to 75% in blood coming back to lungs and 57% in tissues
- curves shifts to right with drops in pH and increases in temperature, leading tissues to get more O2 when these changes occur during exercise
84
Q
carbon monoxide
A
- found in combustion fumes
- CO competes with oxygen for spots on Hb
- very high affinity between CO and Hb
- very small amounts of CO can cause serious respiratory problems, deprives brain of oxygen and can lead to death
85
Q
carbon dioxide transport
A
- generated by metabolism in tissues, in glycolysis, and citric acid cycle
- transported in blood: 7% dissolved in plasma, 23% bound to Hb in RBC forming carbaminohemoglobin, and 70% converted to bicarbonate inside RBC
- we can buffer H+ ions to prevent accumulation and drop in pH, hemoglobin takes H+ to neutralize it
- bicarbonate reaction: CO2 + H2O <-> H2CO3 by carbonic anyhydrase <-> H+ + HCO3-
- we ask bicarbonate ion to leave, transporter moves it into plasma, need to add Cl- back into cell to balance charges, called chloride shift
- PCO2 in lungs is 40 mmHg, blood entering lungs has PCO2 of 46 mmHG, and blood leaving lungs has PCO2 of 40 mmHg
86
Q
ventilatory threshold graph from lab
A
- as we produce more CO2 with increased exercise intensity, our breathing rate goes up to get rid of CO2 because it puts stress on RBCs
- results sit inside wedge of normal breathing, as intensity increases there is a point where line of best fit separates, called ventilatory threshold, amount of CO2 being produced and breathing frequency dramatically increased causing hyperventilation, extra CO2 comes from anaerobic metabolism
- started using type I, then type II-A, next type II-B or II-X using size principle, type II-X fibres use glycogen reserved for glycolysis, produces a lot of lactic acid as a byproduct increasing the amount of H+ in the body, buffers it by binding it to HCO3- to form H2CO3, this is how we end up producing so much more CO2 once we use anaerobic metabolism
87
Q
boosting performance with blood doping
A
- athlete “donates” a pint or two of their blood
- blood is place in a tube in a centrifuge, where it spins around at high speeds
- the red blood cells, which carry oxygen, are forced to the bottom of the tube
- the liquid part of the blood is drawn off from the top of the tube and re-injected into the athlete
- the red blood cells are stored, sometimes frozen
- a day or so before the competition, the stored RBCs are re-injected into the athlete, enabling the blood to be able to carry more oxygen
- get initial massive increase in oxygen carrying capacity but gradually decreases back to normal
- blood doping increases oxygen transport capacity by increasing the number of RBCs to carry more oxygen to the tissues
- increases viscosity of blood
- test for blood doping by looking at RBC cell count and age of RBCs
- erythropoietin is released by the liver and kidneys to naturally increase the number of RBCs produced by the bone marrow
- inject EPO, synthetic form of erythropoietin to stimulate RBC production
88
Q
altitude and the body
A
- can naturally stimulate the production of RBCs by training at altitude, body adapts by creating more RBCs, won’t lead to substantial increases but small differences
- you can recreate altitude ad reduced atmospheric pressure using a hypobaric chamber
- first stage of elevation-induced illness is acute mountain sickness, sets in when body doesn’t adjust to lower oxygen levels, the blood vessels dilate to gather more oxygen which leads to swelling of the brain, other symptoms include dizziness, nausea or difficulty sleeping, with rest AMS should resolve in a day
- high altitude cerebral edema (HACE) occurs when AMS progresses, typically occurs above 13,000 ft, causes lethargy, irritability, vomiting, seizures and if untreated death, person with HACE may act drunk and confused, need to descend at least 3,000ft and receive medical care
- high altitude pulmonary edema (HAPE) occurs when blood pressures in the lungs rises due to low oxygen, occurs when pressures causes fluid to accumulate in the alveoli, begins with SOB, symptoms progress to bad cough and weakness, may feel gurgling or wheezing in the chest and must descend immediately to be treated, can lead to coma and death
89
Q
regulation of breathing
A
- change blood flow (oxygen delivery)
- change depth and rate of ventilation
90
Q
respiratory centres of the brain: medulla oblongata
A
- medulla oblongata:
- respiratory rhythmicity centre, similar to cardiac centre, sets rhythm of breathing
- dorsal respiratory group (DRG), inspiratory centre located in back of brain, sets amount of time you are inspiring, usually 2 seconds in and 3 seconds out, modifies its activities in response to input form chemoreceptors and baroreceptors that monitor O2, CO2, and pH in the blood, CSF and from stretch receptors that monitor the degree of stretching in the lungs
- ventral respiratory group (VRG), primarily responsible for expiration but also controls inspiration, located in front of brain, functions only when breathing demands increase and accessory muscles become involved
91
Q
respiratory centres of the brain: pons
A
- pons: located just above the medullar oblongata, higher up in brain has more control, can affect depth and rate, override respiratory rhythmicity centres
- apneustic centre: increases depth of inspiration by stimulating the DRG, during forced breathing, the apneustic centres adjust the degree of stimulation in response to sensory information from the vagus nerve concerning the amount of lung inflation
- pneumotaxi centre: allows you to increase expiration, inhibit apneustic centres and promote passive or active exhalation, an increase in pneumotaxic output quickens the pace of respiration by shortening the duration of each inhalation, a decrease in pneumotaxic output slows the respiratory pace but increases the depth of respiration, because the apneustic centres are more active
92
Q
respiratory centres of the brain: baroreceptors and chemoreceptors
A
- baroreceptors:
- decrease in BP -> increases respiratory rate
- increase in BP -> decreases respiratory rate
- chemoreceptors:
- peripheral in aortic bodies and carotid bodies
- central in the brain
- muscle
93
Q
respiratory performance and aging
A
- lose lung compliance reducing vital capacity
- arthritic changes and loss of flexibility reduce chest volume
- some degree of emphysema after age 50 due to chronic exposure to environmental pollutants
- in individuals who smoke respiratory performance declines at a much rapid rate, but if they quit the slope of the decline begins to match the rate of a non-smoker
94
Q
steps in an action potential
A
- Depolarization to threshold -60 mv.
- Activation of sodium channels and rapid depolarization.
- Inactivation of sodium channels and activation of potassium channels +30 mV.
- Potassium channels close greater than -70 mV.
Begins and ends with resting potential
95
Q
closing of potassium channels : AP
A
The voltage-gated sodium channels remain inactivated until the membrane has depolarized to near threshold levels. At this time, they regain their normal status: closed but capable of opening. The voltage-gated potassium channels begin closing as the membrane potential reaches about -70 mV. Until all the potassium channels have closed, potassium ions continue to leave the cell, this produces a brief hyperpolarization.
96
Q
inactivation of sodium channels and activation of potassium channels: AP
A
as the transmembrane potential approaches +30 mV, the inactivation gates of the voltage-gated sodium channels close, known as sodium channel inactivation, and it coincides with the opening of voltage-gated potassium channels. Positively charged potassium ions move out of the cytosol, shifting the transmembrane potential back toward resting levels. Repolarization now begins.
97
Q
activation of sodium channels and rapid depolarization: AP
A
When the sodium channels activation gates open, the PM becomes much more permeable to Na+. Driven by the large electrochemical gradient, sodium ions rush into the cytoplasm and rapid depolarization occurs. The inner membrane surface now contains more positive ions than negative ones and the transmembrane potential has changed from -60 mV to a positive value
98
Q
depolarization to threshold
A
The stimulus that initiates an action potential is a graded depolarization large enough to open voltage-gated sodium channels, occurs at -60mV, the threshold.
99
Q
functions of sympathetic nervous system (4)
A
- heightened alertness
- increased metabolic rate, respiratory rate, blood pressure and heart rate
- reduced digestive and urinary function
- activate of energy reserves and sweat glands
100
Q
organization of sympathetic division
A
originate at T1-L2, ganglia are located adjacent to spinal cord except for the adrenal medulla where the ganglia synapses directly onto the medulla
101
Q
organization of parasympathetic division
A
originate at brain stem and sacral vertebrae, ganglia are located very close to target organ
102
Q
functions of parasympathetic division
A
- decreased metabolic rate, heart rate and blood pressure
- increased secretion by salivary and digestive glands
- increased motility and blood flow in digestive tract
- stimulation of urination and defecation
103
Q
negative feedback loop cycle
A
set point > stimulus/change (+/-) > sensor/detector senses change > comparator/ integrator initiates correction > effector promotes the correction and back to beginning
104
Q
negative feedback in anterior pituitary
A
- hypothalamus produces regulatory hormone (thyroid regulating hormone, TRH or corticotrophin-releasing hormone, CRH) and sends it to anterior pituitary
- anterior pituitary releases stimulating hormone (TSH or ACTH)
- stimulation on target endocrine organ to release hormone which acts on target cells
- negative feedback from endocrine organ to anterior pituitary and hypothalamus
105
Q
insulin
A
- peptide hormone, so bind extracellularly and activates secondary messenger within cell, insulin-dependent cells have insulin receptor on cell membrane
- secreted by beta cells
responds to elevated blood glucose levels, above 6.0 mmol/L, normal range in >4.0 - 6.0 mmol/L - effects: increase glucose uptake and utilization and ATP generation, increased amino acid absorption and protein synthesis , stimulates glycogen formation, stimulates triglycerides formation in adipose tissue
106
Q
glucagon
A
- peptide hormone, requires second messenger inside cell
secreted by alpha cells - responds to depressed blood glucose levels, below 4.0 mmol/L
- effects: stimulate glycogen breakdown in skeletal muscle and liver cells, stimulate production and release of glucose by the liver (gluconeogenesis), stimulate breakdown of triglycerides in adipose tissue
107
Q
excitation-contraction coupling
A
- neuromuscular junction (NMJ) stimulates muscle to shorten, motor nerve that synapse on muscle, somatic nervous system
- sarcoplasmic reticulum, stores Ca2+
- troponin, tropomyosin undergo conformational change exposing active sites on actin allowing myosin heads to bind
- myosin crossbridge formation
108
Q
steps of excitation-contraction coupling
A
- ACh is released into synaptic cleft, ACH can bind to receptors on motor end plate
- action potential travels along length of axon
- action potential reaches axon terminal causing release of ACh into synaptic cleft
- ACh molecules bind to receptors on surface of motor end plate, causing increased permeability to Na+
- Na+ rush into cells causing action potential propagation along sarcolemma, ACh is broken down by AChE
- action potential travels along sarcolemma until it reaches a T tubule, where it enters muscle fibre
- action potential in muscle fibre triggers release of Ca2+ from sarcoplasmic reticulum
- contraction cycle can begin
109
Q
slow-twitch fibre
A
- type I, slow fatigue, slow twitch oxidative, red fibers
- small diameter, small glycogen reserves, many mitochondria to generate energy, rich capillary supply, myoglobin, fatigue resistant
- half the diameter of fast-twitch and three times slower to reach peak tension
110
Q
fast-twitch fibre
A
- type II-X, fast fatigue, fast-twitch glycolytic, white fibers
- able to reach peak tension very quickly
- large diameter, many myofibrils, large glycogen reserves, few mitochondria, low capillary supply, fatigue easily
111
Q
intermediate fibre
A
- type II-A, fatigue resistance, fast-twitch oxidative
- closely resembles fast-twitch in appearance
- intermediate diameter, intermediate mitochondria supply, intermediate capillary, somewhat fatigue resistant
112
Q
carbohydrate metabolism
A
- always has ratio of 1C, 2H, and 1O
- glucose C6H12O6
- used to generate new ATP
breakdown of glucose in steps releases energy that is used to convert ADP to ATP - catabolism of 1 glucose molecule = 38 ATP
113
Q
glycolysis
A
- breakdown of glucose to pyruvate
- occurs in a series of seven metabolic steps
- requires: glucose, enzymes, ATP and ADP, inorganic phosphate and NAD
- anaerobic process occurring in the cytoplasm
net gain of 2 ATP
114
Q
steps of glycolysis (7)
A
1 and 2. phosphorylation: costs the cell 2 ATP molecules
3. split: creates two 3C fragmetns
4. 2 NAD -> 2NADH
5. formation of 2 ATP molecules
6. formation of 2 H2O
7. formation of 2 ATP
end point of glycolysis is reached and 2 molecules of pyruvate are formed, 2 NADH, 2 H2O, and net 2 ATP
115
Q
pyruvate to acetyl CoA
A
- occur in mitochondrion
- results in a molecule of acetyl CoA, a CO2 and a 1 NADH
- aerobic process
116
Q
citric acid cycle
A
- also know as tricarboxylic acid cycle, TCA cycle or Kreb’s cycle
- goal is remove hydrogen atoms from molecules and transfer them to coenzymes (NAD and FAD)
- aerobic process
- 8 steps that start and end at the same place, produce 2 ATP, 6 NADH, and 2 FADH2 per acetyl CoA
- acetyl CoA is added to oxaloacetate to form citrate
117
Q
electron transport chain (ETC)
A
- series of reactions that occur in the inner mitochondrial membrane
- produces more than 90% of the body’s ATP
primarily produces ATP from NADH and FADH2, transport electrons to ETC to produce ATP - ATP generation is limited by the availability of either oxygen or electrons (NADH, FADH2)
- no oxygen -> no ATP production in the mitochondria
- each molecule of FADH produces 3 ATP while each FADH2 produces 2 ATP
118
Q
aerobic metabolism
A
- aerobic system provides long-term energy
- occurs in mitochondria
- includes citric acid cycle, and electron transport chain
119
Q
training the aerobic system
A
- aerobic training (endurance training):
- large, more numerous mitochondria in muscle
- enhanced breakdown of fat during sub maximal exercise (spares glycogen)
- enhanced ability to breakdown CHO during maximal exercise
- delays onset of blood lactate during exercises of progressively increasing intensity
- body composition and performance changes
- psychological benefits
120
Q
training the anaerobic system
A
- anaerobic training (sprint/power training):
- increases resting levels of ATP, CP, creatine and glycogen
- increases strength
- increases numbers of enzymes that control glycolysis
- increases capacity to generate high levels of lactate
121
Q
anaerobic metabolism
A
- anaerobic system (ATP-CP and LA) predominates in supplying energy for exercise lasting less than 2 minutes, continues to provide energy requirements for exercise as long as 10 minutes
