circulation & respiration

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1
Arteries
Vessels that bring blood from ventricles of heart to tissues
Thick walls to manage high pressure of blood as it comes from heart, narrow lumen compared to veins
Elastic and muscle tissue in walls to help control blood flow
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Ventricles
Main pumping chambers of heart
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Tunica externa
Tough outer layer, made of connective tissue
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Tunica media
Thick layer made of smooth muscle and elastic fibers
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Tunica intima
Smooth endothelium forming lining
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Maintaining arterial blood pressure
As blood goes into arteries, pressure increases and lumen widens, storing potential energy in elastic fibers in walls. At the end of each heartbeat, the pressure falls and the stretched fibers squeeze the blood which keeps minimum pressure from becoming too low
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Vasoconstriction
Increases blood pressure (lumen gets smaller) when musles in artery walls contract
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Capillaries
Narrow blood vessels, transport blood through tissues and deliver oxygen and nutrients to tissues
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Capillary wall
One layer of thin endothelium cells coated with protein gel with pores. Very permeable, allows tissue plasma to form so cells can absorb substances and white blood cells can attack pathogens
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Veins
Transport blood from capillary network to heart
Thinner wall than arteries because blood is at lower pressure, can dilate and hold more blood
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Valves in veins
Maintain circulation of blood and prevent blood from flowing backwards
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Pulmonary circuit
Supplies blood to and from lungs because blood capillaries in lungs cannot withstand high pressures
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Systemic circuit
Supplies blood at all other parts of body, including heart muscles
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Human circulation
Closed system: blood confined to vessels, unlike arthropods and mollusks
Double circulation: blood pumped first to lungs and back to heart and then out to body
3 parts needed: pump, vessel, fluid
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Right atrium
Collects deoxygenated blood coming back from body through superior and inferior vena cava
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Right ventricle
Pumps blood through pulmonary arteries to lungs
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Left atrium
Oxygenated blood returns from lungs via pulmonary veins and collects in left atrium
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Journey of blood, right side of heart
Deoxygenated blood from body returns to collecting chamber (right atrium) via superior and inferior vena cava
When pressure in atrium is higher than in ventricle, it goes through the atrioventricular valve into the right ventricle
Contraction of right atrium empties blood into ventricle, semilunar valve is closed so blood can't go out that way yet
Right ventricle contracts, which closes AV valve and opens semilunar valve, blood leaves right ventricle and goes out pulmonary arteries
Blood goes to lungs from pulmonary arteries and exchanges CO2 for oxygen
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Journey of blood, left side
Oxygenated blood returns to heart via pulmonary veins and collects in left atrium
When pressure is higher in atrium than in ventricle, blood drains into ventricle, atrium contracts and pumps all blood into ventricle
Walls of left ventricle contract, shutting AV valve and opening semilunar valve
Blood goes out aorta to body. Ascending supplies upper body, descending supplies lower
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Blood in body
Oxygenated blood enters capillary beds where oxygen is transferred to tissues and CO2 is absorbed into capillaries as waste
Deoxygenated blood returns to RA via vena cava and cycle continues
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Heartbeat
Comes from sound of valve
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Sinoatrial node
Group of muscle cells that initiate heartbeat, membranes of cells are first to depolarize in each cardiac cycle
Sends electric signal that contracts atrium first, then ventricles 0.1 sec later, right side is slightly faster
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Purkinje fibers
Carry impulse quickly to ventricles
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Changing heart rate
Impulses from medulla of brain can increase or decrease heart rate
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Accelerator nerve
Triggered by low blood pressure, low oxygen, low pH, causes SA node to speed up heart rate
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Vagus nerve
Triggered by high blood pressure, high oxygen, high pH, causes SA node to slow down heart rate
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Epinephrine
Hormone that tells SA node to speed up heart rarte
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Atherosclerosis
Development of fatty tissue in artery walls
Low density lipoproteins accumulate and phagocytes are then attracted and engulf fats. Smooth muscle cells form a cap over the atheroma and the artery wall bulges, narrowing the lumen and impeding blood flow
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Atherosclerosis consequences
Lack of oxygen causes angima and impairs contraction
Build up of tissue can rupture and stimulate blood clots, which blocks flow further and can cause tissue death (heart attack)
Wall loses elasticity and can develop calcium deposits
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Atherosclerosis causes
High blood concentrations of LDL
Chronic high blood glucose, pressure
Genetics, age, being male, lack of exercise
Consumption of trans or unsaturated fat
Infection of artery wall with bacteria
Production of TMAO by microbes in bacteria
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Bypass surgery
Vein from another part of patient's body is grafted onto a coronary artery to bypass a coronary blockage
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Heart attack
Myocardia infarction: death of heart muscles, from blockage of 1 or more coronary arteries. Happens quickly because cardiac muscle need more oxygen
If heart stops or goes into ventricle fibrilation, can be restarted through defibrilation and blood flow can be maintained through CPR
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Stroke
Damage to or death of brain tissue from lack of oxygen from a blockage, usually from blood clots
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Ventilation
Taking in fresh air, getting out stale air to keep concentration gradient of oxygen and CO2 in lungs
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Gas exchange
CO2 diffuses in capillary to alveoli space, oxygen does opposite
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Alveoli
Air sacs clustered at tips of smallest bronchioles, add to surface area for gas exchange (100m squared)
Very thin (one cell thick) for quick gas exchange
Surrounded by capillaries for quick transport of gases
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Type 1 pneumocytes
Very thin alveolar cells adapted for gas exchange, very small distance to adjacent capillaries
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Type 2 pneumocytes
Rounded cell, makes up around 5% of alveolar surface
Secretes a solution containing surfactant with similar structure to phospholipids, prevents alveolar walls from sticking together and reduces surface tension and prevents lungs from collapsing
Moisture allows oxygen to dissolve and diffuse to blood in capillaries
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Negative pressure breathing
Diaphram contracts, lowering thoracic cavity. External intercostal muscles contract, raising rib cage. This increases volume of lungs, so pressure goes down
Negative pressure causes air to be pushed in from outside until lung pressure is at atmospheric pressure (inspiration)
Diaphram and external intercostal muscles relax, abdominal and internal contract
Volume decreases, pressure increases, air pushed out to lower pressure (expiration)
Inhaling is active (diaphram contracts), exhaling passive (diaphram relaxes)
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Antagonistic muscles
Muscles only work when contracting, shorten when contracted and lengthen when relaxed
2 muscles required for mvt in different directions
Antagonists: diaphram (contracts) and abodominals (relax), external and internal intercostal muscles
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Exercise and ventilation
Exercise can increase energy demands by 10, CO2 concentration rises and pH goes down
Cells in arteries (chemosensors) monitor oxygen and CO2 and send nerve impulses to parts of medulla that control ventilation rate
When pH is below normal, breathing centers increase rate of ventilation by sending nerve impulses to diaphram and intercostal muscles
Increases respiration helps eliminate CO2 and bring in fresh oxygen, oxygen allows aerobic respiration to continue and repay oxygen debt after anaerobic respiration
After exercise, CO2 levels fall, pH rises, breathing centers cause ventilation rate to decrease
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Ventilation rate
Number of times air is drawn in or expelled (breaths) per minute
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Tidal rate
Volume of air inspired
Measure water displaces, spirometer that measures flow rate moving in and out
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Lung cancer causes
Smoking (87%), passive smoking (5%), air pollution (5%), radon gas, asbestos, silica, other solids if inhaled as dust
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Lung cancer consequences
Difficulty breathing
Persistent coughing, coughing blood
Chest pain
Loss of appetite, weight loss
Fatigue
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Emphysema
Alveoli are broken down to become fewer and thicker walled, causing less surface area and longer distance for gases to difuse and less elasticity (less efficient gas exchange)
Phagocytes in lungs usually prevent lung infections by engulfing bacteria and making enzyme that kills bacteria (elastase)
Enzyme inhibitor A1AT keeps elastase from digesting healthy tissue
Smokers need more phagocytes, which makes more elastase
Causes low oxygen saturation in blood, loss of energy
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