Cardio-Respiratory System Flashcards
What are the 3 coats that make up the walls of arteries and veins?
1 - Tunica externa (connective tissue) 2 - Tunica media (smooth muscle) 3 - Tunica interna -> Endothelium -> Glycoproteins/connective tissues -> Elastin
What are 2 key differences between arteries and veins?
- Arteries have more muscle
- Veins have valves
Where is most blood distributed at rest?
- Venous system
- Functions as a reservoir from which more blood can be added
Describe veins?
- Able to expand as they accumulate additional amounts of blood
- Higher compliance than arteries
- Venous pressure is too low to return blood to heart
- Veins pass between skeletal muscle groups which provide contractions to help move blood back (‘skeletal muscle pump’)
What is the average pressure in veins?
2 mmHg
What helps venous blood return to heart from abdominal and thoracic regions?
The act of breathing/contracting of the diaphram and pressure in the abdomen from breathing squeezes the veins to help move blood
How is one-way flow of blood back to the heart ensured?
Venous valves
How were venous valves discovered? By who?
- A tourniquet on an arm causes blood to collect in a bulge
- William Harvey
Describe the arteries?
- In aorta/larger arteries, there are numerous layers of elastin fibres b/n smooth muscle cells of tunica media
- Large elastic arteries expand when pressure rises as a result of ventricles’ contraction
- They recoil when blood pressure falls during relaxation of the ventricles
- Small arteries/arterioles are less elastic, so diameter changes slightly
What drives the blood forward in arteries during the diastolic phase?
- Elastic recoil
How many capillaries are in the body?
Over 40 billion
- Scarcely any cell is more than 60-80 um away from capillary
How does vasoconstriction/vasodilation affect capillaries?
- Vasoconstriction decreases blood flow to capillary bed
- Vasodilation increases it
What do capillaries consist of?
- The walls are composed of just endothelial cells
- They lack smooth muscle/connective tissue, making it easier to exchange materials
What happens at the arterial end of a capillary? The venous end?
Arterial end:
- BP forces fluid out of capillary to interstitial fluid
Venous end:
- Select fluid is drawn back into capillary by osmotic pressure
What is the formula for flow?
Flow = driving forces/resistance
What 3 factors does resistance depend on? Who determined this?
1 - Radius of tube/blood vessel
2 - Viscosity of blood
3 - Length of tube/blood vessel
-> Jean Leonard Marie Poiseuille
How does radius affect flow?
Decreased radius = increased resistance = decreased flow
- Vessel radius regulated by smooth muscle contraction
Contraction = decreased radius
How does viscosity affect flow?
Increased viscosity = increased friction = increased resistance = decreased flow
Increased hematocrit = increased interaction b/n RBC = increased clots = decreased radius
How does length affect flow?
Increased length = increased friction = increased resistance = decreased flow
Describe the pulmonary artery and vein?
Pulmonary artery: - Carries blood away from heart - Low oxygen Pulmonary vein: - Carries blood to heart - Highly oxygenated
Where does the nasal cavity lead to?
Pharynx
What is the pharynx?
A muscular passage connecting the nasal cavity with the larynx
What happens at the larynx?
- Air is diverted toward the lungs and food is directed to the esophagus to the stomach
- Contains the vocal cords (folds in lining tissue of larynx)
What are 4 physical properties of the lungs?
1 - Inspiration and compliance
2 - Expiration and elasticity
3 - Surface tension
4 - Lung volumes and capacities
What is necessary for inspiration?
Lungs must be able to expand when stretched (they must have high compliance)
What does compliance mean?
- Ease with which lungs can expand under pressure
- Change in lung volume per change in transpulmonary pressure (dV/dP)
How does lung disease affect respiration?
Lung disease reduces compliance
What happens during inspiration?
- Chest expands
- Diaphragm contracts
What happens during expiration?
- Chest contracts
- Diaphragm relaxes
What is necessary for expiration to occur?
Lungs must get smaller when tension is released (have elasticity)
What is elasticity?
Tendency of a structure to return to its initial size after being distended
What allows lungs to resist distension?
High content of elastin proteins = very elastic
What causes lungs to always be in a state of elastic tension?
Lungs are normally stuck to the chest wall
When does tension increase/decrease in the lungs?
Increase:
- During inspiration when lungs are stretched
Decrease:
- By elastic recoil during expiration
What is necessary for the lungs to inflate?
Lungs must be attached to the inner wall of the chest cavity
What happens to a person who has a chest wound on one side?
Cannot inflate the lung on the wounded side even though they continue to ventilate
What causes the chest cavity to increase in volume?
Contraction of the diaphragm and intercostal muscles
What do pleural membranes do?
- Make attachment of the outer lung surface to the inner surface of the chest cavity
- Produce a mucous-rich lubricating fluid (pleural fluid) into the pleural space between 2 membranes
What do the pleural membranes consist of?
- One membrane layer attached to the surface of the lung
- One membrane layer attached to the inner wall of the chest cavity
What does the pleural fluid do?
- Holds the two pleural membranes together - it is the ‘glue’ that holds the lungs attached to the inner wall of the thoracic cavity
- Lubricant that allows the lungs to slide easily within thoracic cavity as they inflate/deflate
What happens when the size of the thoracic cavity changes?
The volume of lungs changes consequently
What is surface tension exerted by? How?
- Fluid of alveoli
- Water molecules on the inner surface of alveoli are attracted to other molecules, acting to collapse the alveoli
What is surfactant?
- A mixture of phospholipids and hydrophobic proteins
What secretes surfactant?
- Secreted into alveoli by type II alveolar cells
What is the role of surfactant?
- Lowers surface tension in alveoli by disrupting interactions between water molecules
- Prevents alveoli from collapsing during expiration
When is surfactant produced?
Late in fetal life
What is respiratory distress syndrome?
Premature babies are sometimes born with lungs that lack sufficient surfactant and alveoli collapse
What is tidal volume?
Volume of gas inspired/expired in an unforced respiratory cycle (about 500 mL)
What is inspiratory reserve volume?
Max volume of gas that can be inspired during forced breathing in addition to tidal volume
What is expiratory reserve volume?
Max volume of gas that can be expired during forced breathing in addition to tidal volume
What is residual volume?
Volume of gas remaining in lungs after max expiration
What is total lung capacity?
Total amount of gas in lungs after max inspiration
What is vital capacity?
Max amount of gas expired after a max inspiration
What is inspiratory capacity?
Max amount of gas that can be inspired after a normal tidal expiration
What is functional residual capacity?
Amount of gas remaining in lungs after a normal tidal expiration
What is anatomical dead space?
- Where no gas exchange occurs
- Nose, mouth, larynx, trachea, bronchi, bronchioles
What is hemoglobin? What does it consist of?
- A protein present in cytoplasm of red blood cells
- Contains 4 heme groups, which each contain an iron molecule
- 2 alpha and 2 beta chains
What is the function of hemoglobin?
- Acts as an O2 shuttle from lungs to body tissues
- Iron can chemically bind O2 and release it when cells need it
- Acts as a CO2 shuttle from body tissues to lungs
What is the role of CO2 in the lungs?
CO2 from tissues diffuses from blood to alveoli and blood CO2 levels become low
- Increases pH
O2 binds Hb in what conditions?
High pH environment
What happens to pH levels in the tissues?
- Blood CO2 levels are high b/c cells produce CO2 as byproduct of metabolism
- O2 levels are low b/c it is being used by cells
- Decreases pH
What determines whether O2 binds hemoglobin or O2 is released from oxyhemoglobin?
Acidity of the plasma High acidity: - O2 is released Low acidity: - O2 binds Hb
What gas exchange by O2 occurs at the lungs?
- O2 dissolves in fluid lining of alveoli, diffuses through walls of alveoli and blood capillaries into plasma
- O2 then diffuses into RBCs and combines chemically with Hb to form oxyhemoglobin
- Oxyhemoglobin formation occurs in lungs b/c CO2 levels are low
What gas exchange by O2 occurs at the tissues?
- O2 is released from oxyhemoglobin (in RBC), and diffuses from RBC into body tissues
- Dissociation of Hb/O2 occurs at tissues b/c blood CO2 levels are high
Describe the solubility of Co2 gas?
- Low solubility
- Only very little can be carried in simple solution
What happens to CO2 when it diffuses into RBCs?
- Converted into bicarbonate ion by carbonic anhydrase
- A small amount of CO2 binds chemically to Hb to make carbamino compounds
What happens to CO2 in tissues?
- Constant production of CO2 causes bicarbonate equation to go in forward direction
What happens to CO2 in lungs?
- CO2 is being lost to alveolar air sacs
- Bicarbonate equation moves in reverse direction
If a diver goes down 10m, what happens to the partial pressures and amount of dissolved gasses in blood plasma?
- They will be twice values at sea level
What might cause serious effects to a diver’s body?
- Increased nitrogen and O2 dissolved in blood plasma
At what depth would there be permanent damage to the human lung?
30m
What is the mammalian diving reflex?
- Drop in heart rate (bradycardia)
- Vasoconstriction
- Spleen releases RBCs carrying O2
- Increased blood volume in lungs, occupying space created by compression of air in lungs and preventing collapse
What does SCUBA stand for?
Self-Contained Underwater Breathing Apparatus - air tanks
What does the gas mix in a SCUBA tank aim to do? What do they consist of?
- Avoid O2 toxicity
- Made of normal atmospheric air
- Commonly less nitrogen to reduce nitrogen narcosis and decompression sickness
What is decompression sickness?
N2 gas bubbles form in tissues and enter blood and block small blood channels producing pain and possibly more serious damage
How do divers prevent decompression sickness?
Divers ascend slowly so large amount of N2 can diffuse through alveoli and be eliminated through expiration
What is the primary treatment of decompression sickness?
- Hyperbaric oxygen therapy
- Raise blood O2 concentration
What health consequences arise 5000 ft above sea level?
Acute Mountain Sickness
- Headache (low arterial pressure stimulates vasodilation, increasing blood flow and pressure in skull)
- With hypocapnia (reduced CO2 in blood from hyperventilation) = cerebral vasoconstriction
What happens to health at 9000 ft above sea level?
Pulmonary edema
- Shortness of breath, fatigue, confusion
- Blood vessels constrict causing increased blood pressure in lungs
- As a result, fluid leaks from vessels to alveoli
What happens to health at 10000 ft above sea level?
Cerebral edema
- Confusion, incoordination, hallucinations
- Coma, death
Describe where blood comes/goes from atria/ventricles?
- Atria receive blood from venous system
- Ventricles pump blood to arterial system
About how much blood does each ventricle pump each beat?
75 mL
Which ventricle performs more work? Why? What is the result?
- LV performs greater work
- LV pumps blood further and against more pressure
- LV wall is thicker than RV
What are the right and left sides of the heart separated by?
- Septum
What are murmurs?
- Abnormal blood flow due to septal defects
What are the atria and ventricles separated by?
- Connective tissue/fibrous skeleton which contains one-way atrioventricular (AV) valves, which prevent backflow of blood from ventricles
What causes opening/closing of AV valves?
- Pressure differences b/n atria and ventricles
Describe the AV valve between the RA and RV?
- 3 flaps
- ‘Tricuspid valve’
Describe the AV valve between LA and LV?
- 2 flaps
- ‘Bicuspid valve’ or ‘Mitral valve’
What are semilunar valves? Where are they located?
- One-way
- Located at origin of pulmonary artery and aorta to prevent backflow of blood from arteries
What causes the opening/closing of semilunar valves?
- Pressure differences between ventricles and arteries
What is the cardiac cycle?
- Repeated pattern of contraction and relaxation of the heart
What are the 5 steps of the cardiac cycle?
- Both atria fill with blood
- Buildup of pressure in atria causes AV valves to open and 80% of blood flows to ventricles
- Atria contraction sends final 20% of blood to ventricles
- Simultaneous contraction of both ventricles (0.1-0.2 s later)
- RV sends blood to pulmonary system, LV sends blood to systemic system
What is systole?
- Phase of contraction
What is diastole?
- Phase of relaxation
What does systole/diastole commonly refer to? Is this always the case?
- Commonly refers to ventricles
- There is still an atrial systole and diastole separate from ventricular
What is the average cardiac rate? How long does each cycle last approximately?
- 75 bpm
- 0.8 s
What is stroke volume?
- Amount of blood pumped from ventricles in one heart beat
- Contraction of ventricles in systole ejects about 2/3 of blood they contain
What is end-systolic volume?
- 1/3 of initial amount of ventricles which isn’t pumped out
What is cardiac output?
- Volume of blood pumped by both ventricles per minute
- CO = HR x stroke volume
What facilitates the heart’s pumping ability?
- Electrical activity
Which 3 specialized regions of the heart can spontaneously generate action potentials?
- Sinoatrial node
- Atrioventricular node
- Purkinje fibers
What is the function of the SA node? Where is it located?
- Functions as pacemaker
- Located in RA, near opening of superior vena cava
Which nerve innervates the SA node?
- Vagus nerve
What is the role of specialized cells of the AV node?
- Move impulse from atria to ventricles
How does the electrical impulse travel in the heart?
1 - Originate at SA node, spread to adjacent myocytes in RA and LA (via gap junctions)
2 - AV node cells move impulse from atria to ventricles
3 - Impulse continues through AV bundle (or bundle of His)
4 - Descends through interventricular septum and divides R and L into Purkinje fibers in ventricle walls
5 - Spreads from endocardium to epicardium, causing both ventricles to contract simultaneously
Where does the bundle of His lie?
- Lies within interventricular septum
What makes purkinje fibers different from the SA/AV nodes?
- Could generate own impulses if needed
Describe the rate of conductance at each stage of electrical activity of the heart?
- Impulse starts at SA node
- Spreads quickly - Goes to AV node
- Conduction rate slows - Continues through AV bundle
- Conduction rate increases - Descends down interventricular septum, divides R and L into Purkinje fibers in ventricle walls
- Conduction rate peaks at 5m/s
What is the rapid conduction in the Purkinje fibers caused by?
- More positive resting membrane potential and many gap junctions
What is the electrocardiogram?
- Potential differences generated by heart are conducted to body surfaces where they can be recorded by electrodes placed on skin
- NOT single action potential
What will be affected on an ECG as a result of myocardial ischemia?
- ‘S-T elevation’
- Ventricles don’t relax as they should, so cannot fill with blood
What can lead to bradycardia?
- Hyperstimulation of right vagus nerve which innervates SA node (b/c vagus slows HR)
- AV node and Purkinje fibers can take over if SA node isn’t functioning properly
What are 2 other names for cardiomyocytes?
- Cardiac muscle cells
- Myocardial cells
How are cardiomyocytes arranged?
- Long, rod-shaped organelles called ‘muscle fibers’
What are muscle fibers of the cardiomyocytes made up of?
- Numerous ‘myofibril’ rods which have a distinct striated pattern of alternating light and dark bands
What are myofibrils?
- Functional unit of muscle fibers
How are myofibrils separated?
- By protein structures called ‘Z-discs’
- The section b/n Z-discs is a ‘sarcomere’
What happens to Z-discs during contraction of the cardiac muscles?
- Z-discs move closer together
- Thin and thick filaments slide past one another
What do Z-discs act as anchors for?
- Thin protein filaments called ‘actin’
What lies between the actin?
- Thicker filaments of ‘myosin’
What gives the striated pattern of myofibrils?
- Overlapping of thin/thick filaments
- Light = I-bands
- Dark = A-bands
Where do the Z-discs lie?
- Middle of I-bands
Where is the ‘H-zone’? What is it seen as?
- In the centre of the A-band
- Narrow light band
How are cardiomyocytes connected?
- Via gap junctions
- Permits electrical impulses to be conducted from cell to cell
What do the gap junctions of the cardiomyocytes look like when stained?
- Intercalated discs
What does contraction follow?
Ca2+ induced Ca2+ release
- Ca2+ enters cardiomyocyte cytoplasm through V-gated channels, then stimulates opening of the Ca2+ release channels (ryanodine receptors) in the sarcoplasmic reticulum
What does Ca2+ from voltage-gated channels serve as?
- Messenger for SR Ca2+ release channels
What must happen in order for heart muscles to relax?
- Ca2+ in the cytoplasm must be pumped back into the SR
What are the 5 steps of excitation-contraction coupling after voltage-gated calcium channels open?
1 - Ca2+ diffuses from ECF to cytoplasm
2 - Ca2+ release channels on SR open
3 - Ca2+ released from SR binds to sarcomere, stimulates contraction
4 - Ca2+ ATPase pumps calcium back into SR
5 - Myocardial cell relaxes
What does muscle contraction look like in cardiomyocytes?
- Myosin filaments have angular head at one end
- Muscle contraction is caused by head attaching to actin and swiveling, moving Z-discs closer together
Where is tropomyosin in cardiomyocytes?
- Attached to actin
What is attached to tropomyosin?
- Troponin complex of 3 subunits
What are the details of muscle contraction in myosin (3 steps)?
1 - When ATP is hydrolyzed to ADP, myosin head becomes activated and changes orientation
2 - Attachment of Ca2+ to troponin causes movement of troponin-tropomyosin complex, exposing binding sites to actin
3 - Myosin cross bridges can then attach to actin and undergo a ‘power stroke’
What is cardiovascular disease?
- Class of diseases involving heart/blood vessels
What is a major contributor to CVD? What does this lead to?
- Coronary artery disease, which leads to congestive heart failure
What is congestive heart failure?
- Heart doesn’t pump as efficiently
- Ventricles are often to blame
- Often caused by CAD and MI
- Back-up of blood in veins forces fluid into interstitial tissue (edema)
Is there a cure for congestive heart failure?
- No known cure
What is coronary artery disease?
- Occurs when you have plaque build-up in one or more of the 3 coronary arteries
- Blood flow to heart is restricted -> angina
What is plaque?
Build-up of cholesterol, immune cells, other substances
What is angina?
Chest pain
What causes a myocardial infarction?
- ‘Heart attack’
- Build-up of plaque is sufficient to severely and chronically interrupt blood flow
- Death of cardiomyocytes
What does the body do to try to compensate for congestive heart failure?
- Cardiac remodelling to try to pump better
- Worsens problem
What are some common treatments for congestive heart failure?
- Beta-blockers to help heart pump
- Diuretics to remove salts and fluids
- Late stage: surgery or heart transplant
What are two circulating catecholamines related to heart function?
1 - Epinephrine
2 - Norepinephrine
What is the role of epinephrine?
- Secreted from adrenal medulla during times of stress (exercise, emotional stress, pain, heart failure)
What is the role of norepinephrine?
- 20% of total blood norepinephrine is secreted from adrenal medulla
- Rest is spillover from sympathetic nerves innervating blood vessels
What are 2 effects of epinephrine binding to beta-adrenergic receptors?
- Increases heart rate and ionotropy (contractility)
- Vasodilation of systemic arteries and veins at low-moderate concentrations
What is the effect of epinephrine binding to alpha-adrenergic receptors?
- Vasoconstriction of systemic arteries and veins at high concentrations
What is the effect of norepinephrine binding to beta-adrenergic receptors?
- Increases heart rate and ionotropy (contractility) = increased cardiac output
What is the effect of norepinephrine binding to alpha-adrenergic receptors?
- Vasoconstriction of systemic arteries and veins at high concentrations
What is the overall cardiovascular response to increased circulating epinephrine and norepinephrine?
- Increased cardiac output and systemic vascular resistance
- Results in increased arterial blood pressure
How is heart rate affected by activation of baroreceptors?
- Decreases due to activation of baroreceptors (pressure sensors)
- Vagal-mediated bradycardia in responses to elevation in arterial pressure
What is the effect of blocking one adrenergic receptor?
- Alters cardiovascular response
- Other adrenergic receptor can still bind catecholamines
What is the predominant adrenergic receptor of heart?
- Beta 1
What treatment is most often prescribed for hypertension, angina, and heart failure?
- Beta-blockers
What occurs in chronic heart failure?
- Vicious cycle of sympathetic activation
What does treatment with beta-blockers do?
- Inhibits progressive deterioration of cardiac function (not a cure)
What does coffee do to cardiac function?
- Caffeine stimulates CNS
- Increases catecholamine secretion
- Increases heart rate, stroke volume, cardiac output, blood pressure
