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Peripheral venous disease (PVD)
varicose veins
dilated and twisted superficial vessels (causes weakened vessel walls)
commonly found in lower extremities
How many people have PVD
10-20% of the population
Who is more affected by PVD
women are affected 2-3 X more than men
often a genetic thing
older adults (due to sarcopenia)
Where are varicose veins normally found
the inside of the leg because that’s where the saphenous vein is
causes of PVD
intrinsic weakness of vessel walls
increased intraluminal pressure
congenital defects in venous valves (the valves fail to prevent retrograde flow which causes blood to build up and cause excess pressure or bulging)
Primary PVD
originates in the superficial system due to factors like pregnancy (because of increased venous volume), prolonged standing (gravity is pulling the blood down and the vein has difficulty stopping it), and obesity
Secondary PVD
occurs due to abnormalities in the deep venous system, deep vein thrombosis (DVT, blood flow is slowed and is more prone to clotting), and inflammation
what is a concern with DVT
the thrombus can break loose and turn into an embolism
Symptoms of PVD
many cases are asymptomatic
symptoms - dull ache, heaviness, or pressure sensations in the legs after prolonged standing
Complications of PVD
superficial venous insufficiency - swelling and skin ulceration (usually around the ankle)
stasis of blood can lead to superficial vein thrombosis or rupture, causing a hematoma
PVD diagnosis
physical exam and medical history
Conservative treatment for PVD
the aim is to counterbalance increased venous hydrostatic pressure
elevation of legs while supine, avoid prolonged static standing (locking knees out slows blood flow, and moving around increases pressure and pushes the blood back up due to muscular contractions), wear compression stockings (TED hose)
Advanced PVD treatment
symptomatic or venous insufficiency varicose veins may require advanced treatment
sclerotherapy - intravenous administration of chemical agents to fibrose varicose veins (causes the vein to become fibrotic/stiff and becomes non-functional)
thermal ablation - laser or radiofrequency catheters used to obliterate varicose viens
surgical therapy (vein stripping) - direct vein litigation and removal (for severe cases)
Ventilation
filters, warms, and humidifies incoming air
air goes in and out
air goes to the alveoli (already body temp and cleaned by then)
Nose
serves as an entry point for air into the respiratory system (along with the mouth)
during exercise, you cannot get enough air in through the nose
lined with respiratory epithelium
goblet cells - mucus producing cells that line the nasal passage
ciliated cells - have finger-like projections, the cilia move back and forth and prevent foreign substances from entering
filters, warms, and humidifies the inspired air
protects lung tissues from harmful particles and pathogens
Pharynx
AKA throat
once air comes in through the nose or mouth, it enters the pharynx
nasopharynx - where the nasal passage meets the pharynx
oropharynx - where the oral cavity meets the pharynx
laryngopharynx - right above the trachea and esophagus
serves as a common pathway for both food and air
contains a flap of cartilage called the epiglottis (prevents food from entering the trachea during swollowing)
Larynx
just below the pharynx
AKA voice box
during swallowing, the epiglottis protects the trachea against aspiration
during breathing, the larynx opens and closes
during voice production, the vocal cords vibrate as air passes through
the vestibular folds are another mechanism to keep foreign objects out
Trachea
AKA windpipe
rigid tube with C shaped cartilage rings
the rings provide support and prevent collapse during inhalation
the C shaped rings allow for more flexibility and the ability to expand if needed
extends from the larynx and branches into the right and left main bronchi
inner lining is epithelium with goblet cells (warms, humidifies, and filters air)
Bronchial tree
branching airways that conduct air into the lungs
right and left main, breaks into secondary, tertiary, bronchioles, terminal bronchioles, and respiratory bronchioles
as the tree branches, the cartilage rings get smaller and are eventually replaced by smooth muscle in the bronchioles
the bronchioles can vasodilate and vasoconstrict
Alveoli
bronchiles → terminal bronchiole → respiratory bronchiole →alveoli
tiny, grape-like sacs at the terminal ends of the bronchial tree
surrounded by a network of pulmonary capillaries
estimated 300 million alveoli (same surface area as a tennis court)
lined with two types of pneumocytes
Type 1 pneumocytes
flat shape that abuts the pulmonary capillary wall
optimizes gas diffusion between alveoli and pulmonary capillary
Type 2 pneumocytes
produces surfactant which reduces surface tension
keeps alveolar walls from sticking together and prevents alveolar collapse
alveoli are surrounded by fluid and have a tendency to collapse (type 2 pneumocytes combat this)
Pulmonary surfactant
production begins at 24 weeks gestation but isn’t adequate until 32 weeks
newborn surfactant deficiency (surfactant replacement therapy significantly increases survival)
what’s one of the main issues in premature babies
lung development
they inject surfactant through a tube into the lungs
they also put the baby on oxygen and a ventilator since they do not have the muscle mass to breathe (sustained oxygen delivery can cause blindness)
most babies born before 34 weeks will not survive
Lung anatomy
cone-shaped organs located in the thoracic cavity on either side of the mediastinum
rest on the diaphragm and extend to just above the clavicles
the right lung is larger (3 lobes) and the left lung is smaller (2 lobes) to accommodate the heart
lung coverings
covered with a double-layered serous membrane called the pleura
visceral pleura adheres to the lung surface
parietal pleura lines the inner surface of the thoracic cavity
pleural cavity lies between the layers and contains pleural fluid (reduces friction during breathing)
Blood supply in the lungs
the lungs receive blood from the bronchial circulation via the bronchial arteries
arises from branches of the descending thoracic aorta just distal to the left subclavian artery
courses posteriorly along the trachea and main bronchi to reach the lungs
Resting pressures
gasses move from high pressure to low pressure
atmospheric pressure (Patm) = 760 mmHg
intrapleural pressure (Pip) = 754 mmHg (pressure in the intrapleural cavity)
intrapulmonary pressure (Palv) = 760 mmHg (pressure in the alveoli/lungs)
Inspiration - muscular contraction
diaphragm contracts downwards and the external intercostal muscles contract (lifts the ribs up and out)
expands the volume of the thoracic cavity in vertical and lateral dimensions
Inspiration - pressure changes
expansion of the thoracic cavity decreases Pip to 754 mmHg?
Palv decreases to 757 mmHg becoming lower than Patm
this creates a pressure gradient and air moves from the atm to the lungs
Expiration - muscular relaxation
primarily a passive process relying on the relaxation of the diaphragm, external intercostals, and the elastic recoil of lung tissues
thoracic volume decreases
Expiration - pressure changes
Pip = 755 mmHg
Palv = 763 mmHg
Patm = 760 mmHg
creates a pressure gradient of +3 and air moves from lungs to the atm
Gas exchange and transport
available oxygen from the ambient air depends on two factors
concentration - oxygen = 20.93%, CO2 = 0.03%, nitrogen = 79.04%
pressure - relative to sea level (760 mmHg)
Dalton’s law of partial pressure
total pressure of a gas mixture is equal to the sum of the partial pressure that each gas exerts independently
ambient air
oxygen = 20.93% X 760
CO2 = 0.03% X 760
nitrogen = 79.04% X 760
tracheal air
100% saturated air
760 - 47 = 713
oxygen = 20.93% X 713
CO2 = 0.03% X 713
nitrogen = 79.04% X 713
alveolar air
100% saturated air
760 - 47 = 713
mixed with alveolar gases
oxygen = 14.5% X 713
CO2 = 5.5% X 713
nitrogen = 80% X 713
Gas diffusion
gasses move from one area to another based on pressure (driving pressure, the greater the pressure the greater the force)
gas moves into a fluid based on the solubility
temperature and pressure dependent (faster at a warmer temp)
solubility coefficients
ability of gasses to dissolve in a solution
oxygen = 2
CO2 = 57
nitrogen = 1.3
Blood
men have 5.0-5.5 L (testosterone produces more RBC)
women have 4.5-5.0 L
Formed elements (45% of your blood)
RBC (99+% of the formed elements, transports O2)
buffycoat (<1%, WBC and platelets, sits between RBC and plasma)
plasma (55% of your blood)
90% water
10% solutes
hematocrit
fraction of RBC in blood
hematocrit/3 gives a pretty good estimate of hemoglobin levels
Gas exchange between alveoli and blood
inspired air = PO2 - 159, PCO2 - 0.3
trachea = PO2 - 149, PCO2 - 0.3
alveoli = PO2 - 100, PCO2 - 40
venous blood = PO2 - 40 (O2 comes out of alveoli to venous blood), PCO2 - 46 (CO2 goes into alveoli)
arterial blood = PO2 - 100, PCO2 - 40
skeletal muscle = PO2 - 40, PCO2 - 46
systemic artery = PO2 - 100, PCO2 - 40
systemic vein = PO2 - 40, PCO2 - 46
pulmonary vein = PO2 - 100, PCO2 - 40
pulmonary artery = PO2 - 40, PCO2 - 46
Oxygen transport
blood carries oxygen in two forms
dissolved
relatively poor solubility
0.3 mL is dissolved per deciliter (100 mL)
3 mL per liter
average blood volume = 5 L, so total dissolved = 15 mL
bound with hemoglobin
primary way to carry O2 in the blood
contains 4 iron containing subunits
can carry 4 oxygen at a time
males = 13.5-17 g/dL
women = 5-10% less
1 g Hb can reveribly combine with 1.34 mL O2
what does reversibly combine mean
at the lungs, Hb can load up with O2, and at the tissues it releases O2 (only releases however much is needed)
Oxygen transport math stuff
it’s rare to have 100% Hb saturation (normally 97-98%)
concentration of Hb X 1.34 X Hb saturation, then add dissolved O2 to get the mL O2/dL
Anemia and O2 transport
5% of women are anemic
anemia is low Hb, so people with anemia get less O2/dL
Mt. Everest values
pH = 7.5
arterial PO2 = 25 mmHg
arterial PCO2 = 13.3 mmHg
alveolar PO2 = 30 mmHg
lactate = 2 mM
Hb = 19 g/dL
O2saturation = 50%
Mt everest
10-11 months out of the yesr, it is physiologically impossible to climb
when at that altitude, you’re basically missing around 75% of normal arterial PO2
VO2 max is gonna be 25% of normal
28,000 feet is called the death zone
why is the pH elevated at high altitudes
when you go to high altitudes, you hyperventilate and blow off more CO2
blowing off more CO2 decreases the acidity and pH begins to rise
carbonic anhydrase converts carbonic acid into CO2 and H2O (and the other way around)
diamox (acetazolamide) forces the kidneys to excrete bicarbonate which increases acidity and inhibits carbonic anhydrase
phange in pH can result in cerebral or pulmonary edema
EPO is a hormone released from the kidney in response to low O2 levels and it stimulates RBC formation