Exam 2 Flashcards
What coordinates reflex control of BP and blood distribution
CNS
Medulla oblongata (brain stem)
Major integrating center
Monitors flow NOT pressure via stretch receptors
Cardiovascular Control Center (CVCC)
Receives input from central and peripheral receptors
Hypothalamus, baroreceptors (stretch) in aorta and carotid and intestinal tract
Constant monitoring and adjusting
If BP decreases what happens to symp output
Increases
Because causes vasoconstriction which will increase BP
Baroreceptor reflex regulating MAP
Stretch receptors in aorta and carotid
Send action potentials to CVCC
Change in BP = change in AP frequency
(ex: Increase BP = increased stretch = frequency of AP)
CVCC response to barorecep. alters CO and Resistance in arterioles
See diagram 15.5 slide 47
How do baroreceptors operate when we exercise?
Baroreceptors reset during exercise to regulate BP around a higher set point.
Orthostatic hypotension
AKA stand up too fast and see spots
Standing up causes blood to pool in lower body due to gravity
Decreased blood in ventricles due to decreased venous return
CO falls
BP falls
MAP increases (Baroreceptors) within 2 heartbeats
Factors that influence CV function
Peripheral chemoreceptors, respiratory control centers
Higher brain centers
Fluid balance
Peripheral chemoreceptors
Aterial O2 receptors
Respiratory control centers
Sends info to CVCC
Higher brain centers
Hypothalamus- body temp, symp activation
Cerebral cortex- learned or emotional factors (choose to hold breath, fear, surprise)
Vasovagal syncope
Fainting from strong parasymp release (drops HR and BP)
Body overreact to seeing blood or extreme distress
Fluid balance
Renal and CV systems highly integrated to regulate fluids
Capillary network
50,000 miles
Metabolic activity of tissue influences density of capillary network
Capillary structure
Single layer of flat endothelial cells (EC)
Diameter slightly larger than RBC
Cell junctions determine leakiness
Continuous capillaries
Most common
Leaky junctions (least leaky capillary tho)
Found in muscle, connective, and neural tissue except brain (blood brain barrier needs thicker capillaries to keep out bad from brain)
Fenestrated capillaries
Larger pores between ECs
Promote high volume fluid exchange
Kidney and intestine
Sinusoids
Modified capillaries
Bone marrow, liver, spleen
five times wider than normal capillaries
Allow RBC and plasma proteins to cross into blood
Why is velocity of blood lowest in arterioles, caps, and venules even tho they are skinniest?
These vessels have the largest cross sectional area so blood is spread out and therefore slower through network
Why do you want capillaries to have a slower blood velocity
Promotes exchange
Diffusion
Gradient driven exchange
Transcytosis
Larger molecules transported through EC
Paracellular
larger molecules move between EC pores
Typical endothelial cell junctions of continuous caps allow for
allow water and small dissolved solutes to pass
Absorption
Fluid moves into capillary; determined by bulk flow
Filtration
Fluid leaves capillary; determined by bulk flow
Hydrostatic pressure (BP)
lateral pressure of fluid through pores
Osmotic pressure
Determined by solute concentration of fluid; protein concentration in blood –> Colloid osmotic pressure
Fluid movement in capillary
Arteriole end: Hydrostatic pressure greater than colloid osmotic, so fluid is pushed out of cap = filtration
Venule end: colloid osmotic greater than hydrostatic, so fluid enters cap (water attracted to proteins) = absorption
Net flow out of cap (3L/day)
Why is colloid osmotic pressure constant from arteriole to venule
Because proteins aren’t moving in and out of blood
Lymphatic system
Returns the lost fluid back to the blood via emptying into venous system (Vena cava); not a closed loop
Thymus
Adaptive immune system, T-cells mature, detect if self or not
Atrophies with age because u are exposed to less new stuff
Spleen
Activation site of immune system
Recycle dead RBCs
Reservoir for RBCS
Can live without -> weak immune system
Lymphatic system interaction with other systems
CV system- returns fluid lost in capillaries
Digestive- transport of lipids to CV
Immune- recognition and destruction of foreign pathogens
Lymph Vessels
Blind ended vessels, lie close to capillaries
Thin flat endothelium
Very porous- protein, cell, bacteria can enter
Larger lymphatic vessels
Semilunar valves to prevent backflow, empty into venous subclavian and internal jugular
Lymph nodes
Activation of immune system
Fibrous bean nodes
Macrophages and lymphocytes
Antigen recognition
Other structures of lymph system
Spleen, thymus, gut-associated lymph tissue
Edema
Accumulation of fluid in interstitial space
Inadequate drainage of lymph- protein accumulation in interstitial place
Excessive capillary filtration- increased permeability of caps
Three factors that disrupt capillary filtration
- Increase capillary BP (more fluid exits and less can come back in)
- Decrease plasma protein concentration (increased fluid loss due to less absorption, cause by malnutrition and liver failure)
- Increased interstitial proteins (Increased capillary permeability, cause by infection/damage)
Components of blood
Plasma (Fluid)- water, ions, organic molecules, elements, vitamins, gases
Cellular elements (White & red blood cells, platelets)
Plasma
ECM
Majority water (92%)
7% protein, 1% dissolved organic substances
Similar to Interstitial fluid but with proteins
Proteins increase osmotic pressure
Plasma proteins
Albumin (largest component)
Globulins (antibodies)
Fibrinogen
Transferrin
RBCs
Erythrocytes
Lack mitochon, ER, and nucleus so there is more room for gasses to transport
only energy source is glucose via glycolysis
Can’t replicate –> short life
White blood cells
Leukocytes
Only fully functional blood cell
Critical for immune function/defense
5 types of WBCs
Lymphocytes, monocytes, neutrophils, eosinophils, basophils
Platelets
Thrombocytes
Critical for hemostasis
Lack nucleus
Fragments of megakaryocytes so not a living cell
NSAIDs knock out platelets
Hematopoietic Stem Cell
Found in bone marrow (primarily long bones)
Pluripotent- can develop into RBC, WBC, or platelets
Hematopoiesis
Synthesis of blood cells
Occurs in embryonic and postnatal environments
Complete Blood count (CBC)
Analysis of blood components
Compare blood cell numbers to normal ranges
Indicator of health conditions
Hematocrit
Percentage of RBCs in total blood volume
40-54% Males
37-47% Females
Lower in females because of weight/BV
Hemoglobin
Oxygen carrying capacity of RBCs
Units: g Hb/dL
14-17 Males
12-16 Females
Red cell count
Count of erythrocytes as they stream through beam of light
Units: cells/uL
4.5-6.5E6 Males
3.9-5.6E6 Females
Total white cell count
Shoes overall immune response, don’t need to know #s
Shape of RBCs
Biconcave disc
Increase SA which increases gas exchange
Erythrocytes (RBCs)
Most abundant cell in blood
5 mil RBCs/uL blood
Primary role to carry O2 and CO2
Lack nucleus, ER, mitochondria
Biconcave
More flexible (to bounce around vessels
Packed with Hb
Hemoglobin (Hb)
4 heme groups bind together to create 1 Hb
Major component of RBC
Heme group
Binds O2 and CO2
Has 1 iron
Contains 70% of body’s iron
Subunit of Hb
Transferrin
Protein that transports iron in the plasma
Ferritin
cells’ storage of excess iron, mostly in liver
Extra can be toxic
Iron Transport
- iron ingested
- Fe absorbed by active transport
- Transferrin transports Fe in plasma
- Bone marrow uses Fe to make Hb as RBC synth
- RBCs live for 90-120 days
- Spleen destroys RBC and converts Hb to bilirubin
- Bilirubin and metabolites excreted in urine and feces
OR after step 3
4b. Liver stores excess Fe as ferritin
5b. Liver metabolizes bilirubin and excretes it in bile
Hyperbilirubinemia
Elevated bilirubin
Jaundice
Infants- fetal Hb accumulation (liver not fully developed)
Adults- liver disease/dysfunc.
Anemia
Hb count too low
Causes:
Blood loss, Hemolysis (RBCs explode), Acquired (infection, drugs, disease), Radiation, low Fe folic acid or B12 intake, Low erythropoietin levels
Thrombocytes (Platelets)
Cell fragments of megakaryocytes
Critical for reducing blood loss, lack a nucleus, contain granules that contain cytokines and growth factors (many proteins and chemicals), live ~10 days
Challenges to the repair process
Can’t occlude the entire vessel because nutrients and gasses need to get downstream
Blood is under pressure so the repair must be strong to withstand the shear stress
Repair can’t be permanent cuz clots affect MAP
3 stages of Hemostasis
Vasoconstriction
Formation of platelet plug
Coagulation (clot formation)
*But all really happen at the same time
Vasoconstriction for vessel damage
Happens instantly, local response
Vessel releasees vasoconstrictors (seratonin & thromboxane A2)
Reduces flow and pressure to wound area, attempting to reduce blood loss
Formation of platelet plug
Damaged vessel attracts platelets
Platelets stick to the exposed collagen and platelets stick to each other because initially stuck ones release cytokines which activate other platelets (Positive feedback loop)
Cytokine
Chemicals released by blood and immune cells
Why is platelet plug not enough?
Not strong enough to withstand the shear stress that comes from blood flow pressure
Coagulation
formation of fibrin clot over platelet plug
1. damaged cells express tissue factor and collagen which trigger coagulation cascade
2. Divided into intrinsic and extrinsic pathways which converge at common
Thrombus
Permanent clot (too strong coagulation response)
Embolism
Clot breaks off and gets stuck
Pulmonary (capillary bed of lungs) or venous (typically lower legs)
Coagulation cascade
Series of enzymatic reactions
Once it starts it can’t be stopped
KNOW WHOLE PATHWAY, slide 33
Plasmin
Breaks down fibrin
activated by thrombin and tissue plasminogen activator (tPA)
Fibrinolysis
the break down of fibrin and thus breakdown of clot
4 major functions of respiratory system
- exchange of gases between atmosphere and blood
- Homeostatic regulation of blood pH (since CO2 is an acid)
- Protection from inhaled pathogens and irritating substance (epithelium traps and destroys)
- Vocalization (air moving across vocal cords)
Minor functions of Respiratory system
Water and heat regulation
Both released in exhale
Bulk flow of Air
Air moves from high to low pressure
Muscular pump creates pressure gradients
Resistance to air flow is due to diameter of tube
External respiration
Movement of gases between environment and cells
Exchange between atm and lungs
Exchange between lungs and blood
Transport of gas into blood
Exchange between blood and cells
Internal respiration
Cellular respiration: intracellular reactions that use glucose to produce ATP, CO2, and water
3 major anatomical components of Respiratory system
Conducting system
Alveoli
Bones and muscles
Conducting system
Passages that lead from external environment to surface of lungs
Upper and lower resp. tract
NO gas exchange
Alveoli
Small, interconnected sacs with their associated pulmonary capillaries that form exchange surfaces
Gas exchanged
Bones and muscles
Thorax and abdomen; muscular pump
Muscles of inspiration
Sternocleidomastoid, scales, external intercostals, diaphragm
Pull top of lungs up and bottom down to expand volume
Muscles of expiration
Internal intercostals and abdominal muscles
Muscles used in quite breathing
NONE!
Quiet breathing is passive and does not use muscles, just passive recoil
Trend of diameter through lower respiratory tract
Decreases as the air moves down/through
Trend of Cross-sectional area through lower respiratory tracts
Increases as air moves down/through
Extensive branching
Structures with no smooth muscle (cartilage only)
Trachea, primary bronchi, small bronchi, bronchioles
Structures with no cartilage (SM only)
Respiratory bronchioles and Alveoli
SM allows for change in diameter
Pleural sacs
Ensure right and left lungs don’t interact
Surrounds each lung like a water balloon filled with pleural fluid
Reduces friction, holds lungs close to thoracic wall to maximize volume
Thorax
Sealed cavity
Lungs and heart
Three membranous sacs within it (pericardial and R/L pleural)
Upper respiratory tract function
Warms air, humidifies air, filters foreign particles
Goblet cells
Secrete mucins to help with trapping
Epithelial cells
Ciliated (beat and move things along) and secrete Cl- to create saline and loosen mucus
Creation of saline
- NKCC brings Cl- into epithelial cell from ECF (K and Na are transported back out)
- Apical anion channels like CFTR allow Cl- to enter lumen
- Na+ goes from ECF to lumen via paracellular pathway moving down the electrochemical gradient
- NaCl movement from ECF creates CG so water flows into lumen
NaCl and water is saline
Defective receptor in CF patients
CFTR –> can’t properly make saline for mucus, also present in other organs
Lower respiratory tract
Exchange of gases
Promoted by alveoli cells surrounded by pulmonary capillaries
Type 1 Alveoli cells
95%, thin large cells that promote diffusion of gas
Type 2 alveoli cells
5%, secrete surfactant and increase compliance of lungs by decreasing surface tension
Pulmonary circulation
Blood going to get oxygenated
High flow, low pressure (25/8)
Receives entire CO of RV
Pulmonary hypertension
> 25 mmHg
leads to RV failure
Fatal condition because low pressure system and RV is less muscular
Atmospheric pressure
Air exerts a pressure
Sea level 760 mmHg (decreases with altitude)
Boyle’s law
P1V1 = P2V2
As pressure increases, volume decreases
Dalton’s law
Total pressure exerted by a mixture of gases is the sum of the pressures exerted by the individual gases
Partial Pressure (Pgas)
Pressure of a single gas in a mixture
Determined by abundance not molecular size
Pgas = Patm*(% of gas in atm)
Surface tension
Hydrogen bonds of H2O molecules attract one another, so fluid wants to shrink into smallest SA possible
Surface tension affect on alveoli
Increases pressure of alveoli because they are covered in fluid and this would oppose gas flow
Surfactant
Released by epithelial cells to decrease surface tension
Smaller alveoli produce more to equal pressure of larger alveoli to get equal air which means most efficient for overall gas exchange (Law of LaPlace)
Resistance of Alveoli
Length and viscosity constant so diameter determines resistance
Bronchioles provide most resistance because of SM under neural and hormonal control
Neural control of bronchioles
NO SYMP.
Para symp fibers –> bronchoconstriction
Acts as a reflex
Hormonal control of bronchioles
Primarily during high demand
Epi- bind B2 receptors of SM and causes bronchodilation
ex: Albuterol
Paracrine control of bronchioles
Most dominant most the time
High CO2 - dilation, relax SM
Histamine - constriction, produced by immune cells
Allergic reaction
Immune cells produce too much histamine which causes too much constriction
Total pulmonary ventilation
TPV = (Ventilation rate)*(tidal volume)
Vent. rate is 12-20 breaths per min
Tidal V: 500 mL
Why does not all air reach alveoli
Anatomical dead space (upper airways have no gas exchange and not all air reaches exchange area)
~150 mL don’t make it
Alveolar ventilation
Air actually reaching alveoli
Alveolar ventilation = (ventilation rate)*(Tidal volume - dead space volume)
Short rapid breaths decrease volume that reaches alveoli
Long deeper breath increase volume
Eupnea
Normal quiet breathing
Hyperpnea
Increased resp. rate and/or volume in response to increased metabolism
Hyperventilation
Increased resp. rate and/or volume without increased metabolism
Increases air to alveoli which leads to low CO2, Increase pH, dizzy/weak/faint/seizure
Hypoventilation
Decreased alveolar ventilation
shallow breathing, asthma, etc
Decrease air leads to low O2 and decrease blood pH
More rapid change of PO2 and PCO2
Tachypnea
Rapid breathing, increase resp. rate with decreased depth
Dyspnea
Difficulty breathing due to pathology or obstruction
Apnea
Stop breathing
Ventilation-perfusion matching
Lungs match air flow to blood flow in alveoli which promotes efficiency
If alveoli receives less air its cap will collapse (High CO2 constricts cap), reversible if alveolar ventilation resumes
Uniqueness of pulmonary capillaries
Collapsible: collapse diameter to reduce blood flow
Recruitable: recruit dif capillaries based on activity (start at bottom of lungs)
PCO2 increase
Dilates bronchioles and systemic arteries (strong)
Constricts Pulmonary arteries (weak)
PO2 Increase
Constrict bronchioles (weak) and systemic arteries (strong)
Dilate pulmonary arteries (stronger)
Primarily a PO2 decrease constricts pulmonary arteries
Respiratory cycle
One single inspiration followed by a single expiration
Tidal Volume
Quiet breathing, at rest
Around 500 mL
Vt
Inspiration reserve volume
Max inhale after quiet exhale
Around 3000 mL
Expiratory reserve volume
Max exhale after quiet exhale
Around 1100 mL
Residual volume
Air that remains in lungs after max exhale
Prevents alveoli collapse
Factors that affect differences in volumes
Gender, age, height, weight, etc
Inspiratory capacity
= Vt + IRV
See graph
Vital capacity
= Vt + IRV + ERV
Most physiologically relevant
See graph
Total lung capacity
= Vt + IRV + ERV + RV
See graph
Functional residual capacity
= ERV + RV
Amount of airs in lungs after quiet exhale
See graph
What is the pump creating respiratory pressure
Muscles of the thorax
Primarily diaphragm
Inspiration
Increases volume of thorax
Diaphragm drops 60-75%
Other muscles pull thorax up 25-40%
Active process (muscles contracting, energy used)
Expiration
Decrease volume of thorax
Muscles relax and recoil thorax
Normally a passive process unless exercising
Pressure gradients during ventilation
Atm pressure
Alveolar (Always greater than intrapleural)
Intrapleural
Partial pressure of gases in blood
Partial pressure of gases in tissues
Pneumothorax
Collapsed lung
Intrapleural pressure is lower than atm pressure
You can survive with a collapsed lung
gas that primarily controls bronchioles
CO2 has stronger effect
Gas the primarily controls arterioles
O2 has stronger effect
What happens when interpleural pressure becomes greater than alveolar?
Air tries to move down its pressure gradient and would collapse the lung. Therefore alveolar pressure must always be greater than interpleural
Penetrating chest trauma
Opens interpleural cavity to the atmosphere, air rushes in down its pressure gradient and collapses the lung
Compliance
The ability of the lungs to stretch
Too high of compliance leads to low elastance
Elastance
Elastic recoil, the resistance to stretch
Lungs should return to resting volume
Emphysema
Disease that destroys the elastin fibers in the lungs, stretch easily but does not recoil to normal volume, so must use muscle to expire
PO2 in dry air, alveoli, arterial blood, cells, and venous blood
Dry air: 160 mmHg
Alveoli: 100 mmHg
Arterial blood: 100 mmHG
Cells: < 40 mmHg
Venous blood: < 40 mmHg
PCO2 in dry air, alveoli, arterial blood, cells, and venous blood
Dry air: 0.25 mmHg
Alveoli: 40 mmHg
Arterial blood: 40 mmHg
Cells: 46 mmHg
Venous blood: > 46 mmHg
Why does PO2 drop drastically from arterial blood to cell
Because in the cell the O2 is getting used up in the ETC
Hypoxia
Low O2
Hypercapnia
High CO2
3 blood parameters that must be monitored
O2 (aerobic resp.), CO2 (High CO2 depresses CNS), pH (low will denature proteins)
Hypoxic hypoxia
Low arterial PO2
Caused by altitude (air comp.), hypoventilation, decreased lung diffusion, abnormal ventilation-perfusion
Anemic Hypoxia
Decreased total amount of O2 bound to Hb
Caused by blood loss, anemia, Carbon monoxide posion
Ischemic hypoxia
Reduced blood flow
Caused by heart failure, shock, thrombosis
Histotoxic hypoxa
Cells can’t use the O2 that is delivered to them
Caused by Cyanine or other metabolic poisons
Low alveolar PO2 caused by
Composition of inspired air and and alveolar ventilation
Composition of inspired air (affecting low alveolar PO2)
Humidity–> high water vapor reduced PO2
Altitude –> PO2 decreases with an increase in altitude because atm pressure decreases.
Not because there is less O2 but because there is a smaller pressure gradient for O2 so every breath you take has less O2 in it.
Alveolar ventilation affecting low alveolar PO2
Rate and depth of breathing (hypo)
Decreased compliance and increased resistance
CNS depression
Factors affecting gas diffusion between alveoli and blood
Surface area, diffusion distance
Fick’s law of diffusion, alveolar perfusion (physical block), and other factors like solubility of gas (CO2 more soluble than O2)
Surface area affect on alveoli-blood exchange
Total # of alveoli
Increase SA, greater exchange
Alveloi don’t regenerate
Diffusion distance affect on alveoli-blood exchange
Increase distance = slower gas exchange
Barrier thickness (build up of scar tissue or fibrotic lung disease increase thickness)
Amount of fluid (b/w capillary and alveoli). more fluid leads to greater distance
Fluid in interstitial space (pulmonary edema)
Fick’s Law of Diffusion
Diffusion rate proportional to:
(SA* CG* Barrier permeability) /distance
Mass flow
RATE
flow = [O2] * CO
Units: [O2] mLO2/L blood
CO: L/min
Flow: mLO2/min
Mass balance
Arterial O2 - venous O2 = oxygen consumption (QO2)
Units: mLO2/min
Takes into account how much O2 tissues are using
Fick’s equation
QO2 = CO* (arterial O2 - venous O2)
Transport of O2
<2% dissolved in plasma
98% bound to Hb (HbO2)
Oxygen obeys mass action (amount in blood = amount going to tissues)
Plasma O2 goes to tissues first
Hb sponge
At rest tissues only require 250 mLO2/min
But at rest at saturation Hb delivers 1000 mLO2/min
Hb acts as sponge reservoir of O2 for when demand increases
Blood without Hb only has 15 mLO2/min
2 factors influence amount of O2 bound to Hb
Partial pressure O2 (PO2) in plasma
Number of potential Hb binding sites (decreases with things like Anemia)