A&P- Final Flashcards
Forced Mid-Expiratory flow or FEF 25-75 test
A lower FEF 25-75% value (not as a ratio but as an absolute flow rate) suggests obstruction in the smaller airways.
Really bad asthma somewhere between 500-1000mL/s is thought of as a good number
If we have a lung that has a smaller than normal inward recoil, what happens to the pleural pressure?
Then that would lead to larger lung volumes- so lose elastance in the lungs- the result is higher lung volumes.. And a more positive pleural pressure, less force pulling in (or less negative)..
CSF pH and CO2
CSF pH should be 7.31 (lower than arterial), and CSF PCO2 is 50 mmHg (higher than arterial)
Take care of 85% of blood gas management
CO2 is diffusing into the CSF that is driving up the protons through dissociation.
Peripheral Chemoreceptors
Two pairs of carotid bodies, just above the bifurcation of the internal/external carotid arteries.. info sent to glossopharyngeal CN 9 to medulla (brainstem)
3-5 aortic bodies sensory info back to brainstem via Vagus nerve (CN X)… peripheral chemoreceptors looking at H+, CO2, and O2.. Capable of sensing all three but mainly looking at the most is for large changes in O2.. So Peripheral is O2 and central chemoreceptors is CO2 and H+..
What PO2 do peripheral chemoreceptors start to ramp up vent..
80mmHg and a lot at 60mmHg
if high really wont depress vent
Perfusion increase is second response to low PaO2.. what happens to BP?
large O2 drop, BP will increase.. If we go the opposite direction, decrease in PCO2 or H+.. CO is reduced and BP comes down..
End Tidal CO2 is 48, how is BP
High.. (normal 38-40)..
If CO2 is low, how is Ca+?
CO2 is low, CO is low, BP is Low, then Ca+ is low
binding more to protiens
Sternocleidomastoid
connects with top of sternum and helps keep the ribcage from pulling down during normal breathing.. Anchor point at mastoid process on the skull behind the ear.. Contract during inspiration opposes the ribcage from getting pulled down, stabilizing muscle- helps with regular breathing.
Opening that allows for drainage from the middle ear called
pharyngotympanic tube or Estuacian canal
Nasal Vasculature
Superficial (inferior) branches coming from external carotid.. Internal branches lay in top of nose via ophthalmic a which is what connects branches to the internal carotid (internal is an even more protected circulation – very hard to stop a bleeder
concha
inferior: maxilla
middle:ethmoid
superior: ethmoid
Crista Galli - connects falx cerebri
tonsils: name 3
lingual tonsils.. Under side of tongue
Pharyngeal tonsils at the back of nose..
Palatine tonsils off to side of palate
Salivary glands
One under front of tongue is the sublingual gland (red).. Gleeking.. Submandibular farther back right under mandible (blue).. Parotid is largest.
Trigeminal nerve..
CN5 is very large.. Side of head w/ 3 divisions.. V1: very top part (ophthalmic branch- eyes and forehead sensory).. V2: middle maxillary roof of mouth and nose (middle face).. V3: mandibular division. Lower jaw mandible
Trachea Length:
Length is 11-13 cm for a normal adult.. Vast majority is inside thorax.. 2-4 cm is extra-thoracic to connect to the larynx
Ligaments that connect the 20 tracheal rings
annular ligaments
Angle Between the Main Stems:
The angle that is formed between the 2 is a combined angle of 70 degrees
The right is about 25 degree curve and the left is a 45 degree angle
ETT limitations:
The narrowest part of upper airway is the cricoid cartilage (neonates).. That is what limits size of ETT tube (if bigger then won’t go in)..
In adults or persons older than 14 then that is the opening in-between the cords (trans glottic space- green line) are most narrow space.
Mt. Everest
29,000ft (8400m) at the summit. PB: 250mmHg
0.21(250-47) => PIO2 of 43mmHg
Diving Pressure:
Sea level is 1 atm.. 30 feet under the surface is twice that at 2 atm.. For every 30 feet the pressure increases by a factor of 1 atm..
Volumes Percent of arterial blood
In arterial blood 20 mL O2 for / 100mL blood.. So 20 %
How many mL’s of O2 will give us a PO2 of 100mmHg
PO2 is about 100 when we have 0.3 mLs of O2
As lung O2 pressures increase.. From 100mg to 1000mmHg we would expect ? mL O2 in the dissolved state..
3mL O2
10X increase from normal
linear increase
30min at 2 atm will give O2 pressure around ? mmHg
1560mmHg. - upper limit of Oxygen poisoning .. O2 causes oxidative, free radical stress
O2- Superoxide
Can combine with nitric oxide (NO) to form really toxic compound OONO- (peroxynitrite) , destroys DNA, kills cells, and replication, causes cancer, anti-cancer genes don’t work well..
Hydrogen Peroxide:
H2O2: free radical or oxidizing compound.. Not good to have excess
Peroxidase
can destroy or make peroxide.. Catalyze interacts w/ hydrogen peroxide.. Acetylcysteine: scavenge free radicals scavenger NAC (liver problems) detox liver..
Fundraiser for Polio
“March a Dime”
demylenating disease
Age Formula:
(Age + 10)/4
The older the lower PaO2
PAO2 = off arterial PaCO2
[(PB-PH20)*FIO2] - (PaCO2/R)
or PIO2 – (PaCO2/ R )
normal R is 0.8
R =
RQ= Respiratory Quotient: the amount of CO2 produced/ O2 used
normal O2 used is 250mL/min and the CO2 produced is about 225mL/min => 0.8
RQ with just fats
0.7
RQ with just carbs
1
Fats for ATP is ? CO2 production
Less
CO2 gets used of by formation of water with the metabolism of fats.
If burning carbs
If burning carbs, being combined with carbons without excess H+ being produced..
Fats release H+ (somehow form water with O2)
RQ for proteins
0.8
respiratory exchange ratio (RER)
Measuring gases coming off patient for RQ referred to as respiratory exchange ratio (RER) is actual measurement of gas going in and out of patient. Same thing just different term.
Should be about 400mL of O2 in between breaths in the lungs –
(104/760) x 3000mL.. Close to a 2 min supply of oxygen .. We burn 250mL O2/min.. No big deal if don’t take a breath for 2 min..
If move our lung volume down to 1L-paralytics
that means we only have 130mL of oxygen (104/760) x 1000mL => 136.84 … which is less than 1 min of O2 reserve
High CO2 then ?
increase in BP and CO
Normal arterial pH
7.4
Normal Venous pH
7.35
What is the proton concentration dissolved in arterial blood
0.00004 mEq/L
H+ concentration vs Na+ concentration
Na+ is 142 mEq/L so H+ concentration is 3.5 million times less then Na+ concentration in the blood
ammonia
NH3 buffer - not extracellular, renal tubular
Ammonium
NH4+ buffered the H+ ion, renal tubular
KOH
alkaline metal, lithium
Strong bases
pH is a logarithmic change in the concentration of H+
Each 1 of pH unit change the H+ concentration changes by a factor of ten, pH goes down then H+ increase by factor of 10
concentration in mmol/L
pK
the neg log of the dissociative constant for a particular acid/base
ASA
Acetylsalicylic Acid (metabolic acidosis)
pK of HCO3-
6.0
main extracellular buffer
HPO4-
Phosphate compound.. good buffer inside cells, turn things on or off, phosphorylation/dephosph things the cell does to control activity- urinary buffer as well
Lowest urinary pH
4.5
body makes 1mL urine/min
Other Chemical Buffers:
Larger proteins are also buffers bc of the neg charges within them.. (fastest, works in microseconds- chemical buffers)
second fast- resp
third - renal
Normal bicarb
24 mmol/L
book said 20-24 was within normal
Compensation:
Respiratory will never fully correct metabolic acidosis
but kidneys can do a pretty good job of mitigating chronic resp acidosis like seen with COPD.
Resp can correct at best 50-75% of the variance in the pH of the problem.. Kidneys can get it closer, very powerful.
Hemorrhage
If missing proteins (hemorrhage) not as much buffering capacity w/ low Hb
as we loose blood (Hb) the bicarb level will rise to offset the loss of Hb buffering capacity to maintain a neutral pH as best as possible.
Chronic Resp Acidosis
pH low- normal
PCO2 high
bicarb: high- compensating
Acute Resp Acidosis
pH: Low
PCO2: high
bicarb: normal range 22-26- no time to compensate
Acute resp alkalosis
pH: High
PCO2: Low
bicarb: normal - low
cannot really correct, panic attack, at some point pass out from constricting blood flow to brain
Chronic Resp Alkalosis:
pH: high-normal
CO2: Low - not as low as acute
bicarb: low- compensating
Metabolic Acidosis
pH: low
PCO2: Low- compensating
Bicarb: Low
lungs good compensator
Metabolic Alkalosis
pH: high
PCO2: high- compensating
Bicarb: high
too much tums
Resp compensation for alkalosis is much less because hypoxemia trigger breathing
Accessory Muscles for breathing
Below C5 control the accessory muscles- (phrenic is C3-C5).. Above C3 you remove all motor output for breathing- accessory muscles (resp acidosis)
Resp Alkalosis
Overdose with aspirin (Salicylates) stimulates breathing
progesterone
over ventilating..
everything else resp acidosis.. fucking up gas exchange or output controllers, obstructions
Methanol
Metabolic acidosis
converts into formic acid
ASA
note that this can cause metabolic acidosis as well.. so look at labs
Pancreatic fistula
metabolic acidosis
cannot change that pH 2 stomach acid
Intestines
Large intestine > alkaline than small
Metabolic alkalosis
vomit
diuretic therapy
steroids-
mineral-corticoids (so aldosterone)- creates too much ANG 2
Cortisol looks like aldosterone -> so can stimulate the ANG-2 receptor
Ang 2
increase levels: lose H+ (alkalotic)
decrease levels: hoDL H+ (acidotic)
Diuretics
distal tubule
■ The more Na+ that H+/Na+ exchanger sees, the more H+ they exchange. (secrete)
metabolic alkalosis
exacerbated by feedback mechanism of increasing ANG II: and reabsorbing more HCO3- and loosing more H+
Intercalated Cells- manage acid/base in distal tubule
A-cell: acid (if you are acidotic- how I remember) - reabsorb bicarb
B-cell: base (if your a basic bitch) - secrete bicarb
Normal chloride
108
normal Gap = 12
Pec Minor
Attached to Scapula and shoulder bone, keeps ribcage from pulling down
Serratus Anterior
wrap around the front side of ribcage and pull the chest outwards on inspiration (makes chest a larger cavity),
Tucked behind pec minor
Connection between the superior and inferior laryngeal n.
Galen’s anastomosis
Pharyngeal Constrictors
Superior Pharyngeal constrictors: S1-S4 (suprahyoid)
Middle: M1 & 2 (M1 looks to be suprahyoid)
Inferior: I1 and I2 (infrahyoid)
Diagastric Anterior/posterior Belly
central tendon called intermediate tendon (separates bellies), goes through a connective tissue sling on the hyoid bone..
Posterior: connected to mastoid process.
Anterior: connected to mandible
Stylohyoid Muscle
Connected to the styloid process and hyoid bone
Mylohyoid
it extends from the top of the hyoid bone to the floor of the mouth. (makes up the muscular floor of the mouth)
connecting hyoid bone and mandible
Geniohyoid
Sitting ontop the mylohoid, running different orientation
Both are located on the floor of your mouth and attaches to the hyoid bone and the jaw
if any muscles contract the larynx moves up
Omohyoid (infrahyoid muscle)
Connects hyoid bone to shoulder, has central/intermediate tendon as well looped over on rib 1
Superior Belly
Inferior Belly
Sternohyoid m.
6 (sternohyoid m.)
Connects top sternum with hyoid bone
SternoThyroid
7
connects sternum and throid cartilage
shorter than sternohyoid
Thyrohoid m.
Connects thyroid to hyoid bone
separate m. from the sternothyroid
hyoid bone horns
2 sets, greater and lesser horns
Neutrophil Elastase
is inhibited by alpha1 antitrypsin (protease).. Neutrophil Elastase - will break down elastin molecules and lead to emphysema
Chronic Infection
Lungs get smaller if don’t clear crap out of lungs, lose alveoli (look emphysematous at some point)
pneumonia vs atelectasis (1 lung) blood gas
Pneumonia 1/2: 97%, 1/2: 60% => 78%.. no HPV, shunted blood (larger barrier to diffuse)
Atelectasis: 5/6: 97%, 1/6: 60% => 91%.. HPV.. can just be a lobe
Pneumonia > problem
Irritant receptor
Vagus Nerve CN 10
J receptor
juxtaposition to capillaries
located in alveoli- too much blood in lungs (heart failure or pneumonia).. doesn’t do shit, just makes you feel like it.
Pulmonary stretch receptors
Once Vt hits 1.5 - 2L of air they kick in and stop inspiration.
● Cheyne-Stokes breathing
Cheyne-Stokes breathing is a type of abnormal breathing pattern characterized by cyclical changes in breathing rate and depth. It usually involves periods of gradual increases in deep breathing followed by periods of apnea (no breathing). 40-60 second cycling time.. This pattern can arise from two main situations:
Delayed Oxygen Delivery to the Brainstem: If oxygenated blood takes longer than usual to reach the brainstem due to a cardiovascular issue (like a heart attack or severe blood loss), the brainstem’s response to the blood oxygen levels is delayed. This results in prolonged activation of the breathing drive, leading to abnormal breathing patterns as the brainstem continues to adjust to outdated blood gas levels.
Brain Damage: Conditions like severe head injuries or the effects of a heart attack can directly damage the brain areas responsible for controlling breathing. This damage can disrupt the normal breathing regulation, leading to the irregular breathing patterns seen in Cheyne-Stokes respiration.
In essence, Cheyne-Stokes breathing reflects issues with either the delivery of oxygen to the brainstem or direct damage to the neural centers that regulate breathing. This results in a distorted respiratory drive, causing the typical cyclic breathing pattern of deep breaths followed by periods of apnea.
Airflow when paralyzed and supine
Going to go more anterior.. wider gradient.. More neg anterior and more positive posterior gradient, and really low lung volume, not going to get good V/Q ratio (similar to low breathing at RV scenario)..
PEEP to fix
Last PFT: Body Plethysmography
Boyles law - P1V1 = P2V2
best at estimating trapped gas
