A&P Exam 2 Flashcards
Larynx
Thelarynxis located in the anterior compartment of theneck, suspended from the hyoidbone, and spanning between C3 and C6
Apertures Anterior to Posterior
Most anterior: Caval Aperture
Middle: Esophageal Aperture
Posterior: Along T & L spine is Aortic Aperture
Phrenic Nerve
C3, C4, C5 Keep the diaphragm alive, similar path as Vagus nerve
Scalene Muscles: Inspiration
5: Anterior, C3-C6, rib-1
6: Middle, C3-C7, rib-1
7: Posterior, C5-C7, rib 2 - most lateral and lowest
Let’s consider normal values first:
Hemoglobin (Hb) concentration: 15 g/dL (grams per deciliter)
Oxygen saturation (SaO2) of hemoglobin: 97%
Arterial PO2: 100 mmHg
Each gram of fully saturated hemoglobin can carry approximately 1.34 mL of oxygen (O2).
Total O2 content = (Hb concentration x SaO2 x 1.34) + (PO2 x 0.003)
Assuming normal conditions: O2 content = (15 g/dL x 0.97 x 1.34 mL O2/g) + (100 mmHg x 0.003 mL O2/mmHg/dL)
This roughly equals 19.14 mL O2/dL + 0.3 mL O2/dL = 19.44 mL O2/dL.
Now, let’s assume the arterial PO2 falls to 60 mmHg (hypoxemia):
If the fall in PO2 leads to a decrease in SaO2 to 90% (as less oxygen is available to bind to hemoglobin):
New O2 content = (15 g/dL x 0.90 x 1.34 mL O2/g) + (60 mmHg x 0.003 mL O2/mmHg/dL)
This equals 18.09 mL O2/dL + 0.18 mL O2/dL = 18.27 mL O2/dL.
Each Lobe has Segments
Can be removed instead of entire lobe, have own airway and blood supply
Right Main stem bronchus
Wider and not as sharp of a turn, wider bc lung is bigger
Trachea
Gen 0
Piece of cartilage that fastens the larynx on the top of the trachea
Cricothyroid or Cricoid cartilage- connected by cricotracheal ligament
Membrane that connects hyoid bone to larynx
thyrohyoid membrane
Vocal Cords- connected to
thyroid cartilage anteriorly and posteriorly in the arytenoid cartilage..
He said connected to corniculate cartilage, and anteriorly at the cricoid Cartilage?
where the vocal fold is within the laryngeal anatomy
Ligament Connecting Hyoid bone to epiglottis
Hyoepiglottic Ligament
Recurrent Laryngeal Nerve
Comes off CN-X vagus nerve
Airway Zones
Conducting Zone: 0-16, trachea-0, bronchi-(1-3), bronchioles-4, terminal bronchioles-(5-16)
Transitional Zone: 17-19, Respiratory bronchioles- (17-19)
Respiratory Zone: 20-23, alveolar ducts-(20-22), alveolar sacs-23
Alveolar surface Area
70 m^2 (tennis court).. Sacs # 8 x 10^6
Cyanosis
DeoxyHb of >5 gm/dL
In our veins we usually have a little less than 5 gm/dL deOxyHb… cyanosis is what happens when we exceed 5 gm/dL of deoxyHb- Hgb without oxygen attached
Hypoxia: Tissue- local- low O2 level
Hypoxemia: widespread in the arteries –systemic.. if one exists then likelihood for the other
Compliance:
Elastance:
Compliance: delta V/ delta P – if can only put a little volume in the system and lots of pressure then low compliance
Elastance: delta P / Delta V – inverse of compliance, if something has high compliance then it has low elastance
PTP
PTP = PA - PIP
IRV + VT + ERV
VC = IRV(2.5L) + VT(500mL) + ERV(1.5L) => 4.5L
IC + ERV
VC = IC (3.0L) + ERV(1.5L) => 4.5L
VC (working capacity) + RV
TLC (6.0L)= VC (4.5L) + RV (1.5L)
IC + FRC
TCL
ERV + RV
FRC
PIP at greatest airflow into the lungs- 1 sec into inspiration or expiration..
-6.5 cm H2O roughly for both inspiration -0.5L/sec flow at an alveolar P of -1cm H2O and also for expiration with an airflow of +0.5L/sec at an alveolar P of +1cm H2O
Fastest when the pressure difference is the most, between the alveoli and the outside environment
Alveolar Resistance
Alveolar Resistance = Extraalveolar Resistance at FRC
PVR
Combination of the dotted lines should add up to the number of the blue line (Total Pulmonary Vascular resistance).
At high lung volumes Total PRV is elevated bc alveolar BV resistance is elevated (stretched out_
At low lung volumes Total PRV is elevated bc extraalveolar resistance is elevated (compressed by more positive pleural P)
Pressure to get to TLC
PIP somewhere around -25 cm H2O
Passive Influences on PVR
PVR Active
Deoxygenated venous blood: PO2 = ?
Venous Carbon Dioxide: PCO2 = ?
Arterial blood: PaO2 = ?
Arterial blood: PaCO2 = ?
Deoxygenated venous blood (pulm art): PO2 = 40 mmHg
Venous Carbon Dioxide(Pulm Art): PCO2 = 45 mmHg
Arterial blood: PaO2 = 100 mmHg
Arterial blood: PaCO2 = 40 mmHg
Pulmonary Venous PO2:
Mixed Venous PO2:
Pulmonary Venous PO2: Blood after passing through the lungs
Mixed Venous PO2 (Pulm Art): blood Returning from the tissue
Pulmonary capillary hydrostatic pressure: Pcap
Pulmonary capillary oncotic pressure: (pie)cap
Pulmonary capillary hydrostatic pressure: 7 mmHg (lower than systemic of 17.3)- elevate by same as LAP elevation above normal
Pulmonary capillary oncotic pressure: 28 mmHg
If PAO2 is higher or PACO2 is lower than normal, we may have this reaction
Airway constriction.. (could be caused by a blood clot in the pulm art)
This is nowhere near as strong as the vascular response (HPV) to changes in alveolar gas.. Secondary to HPV
Interstitial capillary hydrostatic pressure: Pis
Interstitial capillary oncotic pressure: (pie)is
Interstitial capillary hydrostatic pressure: -8 mmHg
Interstitial capillary oncotic pressure: 14 mmHg (higher than in systemic circ)
Pulm Edema: factors
Hypoxic Pulmonary Vasoconstriction (HPV)
decreased PAO2, increase PACO2
From constricted or spasm airway, a blocked airway, or a mucus plug
Transmural Pressure gradient of the lung
Higher gradient at the top of the lung than the base.
Ventilation at FRC:
Top of lung: PIP = -8.5 , PTP = +8.5 (60% of TLC)
Base of Lung: PIP = -1.5, PTP= +1.5 (higher Pressure) - (25% of TLC)
Average PIP = -5
if talking in terms of PTP: pressure is greater at the top of the lung.
The distending Pressure is greater at the top of the lung- refers to PTP
Takes 1.5-2 cm H2O added to PTP in base of lung to add 15% more volume
Ventilation at RV
Top of lung: PIP = -2.2 , PTP = +2.2 (30% of TLC)
Base of Lung: PIP = +4.5, PTP= -4.5 (higher Pressure) - (20% of TLC)
Average PIP = +2cm H2O
Ff talking in terms of PTP: pressure is greater at the top of the lung. So top of lung still has the highest distending pressure.
All the way until hit something like a +1 (looks higher than that to me) for PTP, to get air in the base of the lung, up until that point we are applying pressure but not getting any air into this portion of the lungs.
Need a pressure increase of greater than 5 to open up the base of the lungs.
Emphysema
High PVR bc missing blood vessels, bad for right heart
Alpha1 antitrypsin
inhibits neutrophil elastase (protease) -( Elastase is an enzyme which destroys elastic fibers)
Also genetic conditions where not correct gene for antitrypsin.. If not treated then results in emphysema by age of 30.
Alcoholic- liver failure.
Cystic fibrosis: chloride pump..
Restrictive lung disease volumes
(asbestosis, sarcoidosis, fibrosis) : bc of increased PER people have a lower RV than normal, ERV and VT are lower than normal- across the board.. IRV may be low to normal.. Everything else is lower- so relates to Lower then normal TLC, IC, FRC, and VC
Obstructive Lung disease volumes
loss of elastic tissue or PER, large increase of TLC, large chunk is from increase RV- air that we can’t get out bc we don’t have enough help.. Depending on severity of disease, VC will start off normal, as disease gets worse VC will decrease as result of IRV going away.. RV keeps going up further, which compresses the ERV and the IRV, until you don’t have any excess capacity to inspire deeper or expire to low lung volumes on your own. Loss of elastic recoil eventually eats away at all of these excess volumes..
IRV is typically only used for exercise and don’t normally go to below ERV.. But could if we had to.. As COPD gets worse ERV and IRV are just lower and lower.. Eventually IRV and ERV goes away and just left with Vt – which ends up being breathing at VC if someone has real bad COPD.. If you think someone has bad lungs.. Ask them to voluntarily expire from RV and if they can’t do much.. Then probably obstructive lung disease. They have a barrel chest and hollow hyper resonance on tapping chest wall.
If VT is all the way up at TLC then we are basically filling the lung all the way up with every breath. Not a lot of fresh air coming in and there’s not a lot of leeway with these kind of reserve volumes (IRV & ERV) that get depleted with late stage obstructive lung disease.
Pulmonary Surfactant
Proteins (10%) and lipids (90%).. 4 proteins abbreviated SP- Surfactant Protein- (ABCD).. Proteins A and D are hydrophilic .. B and C are hydrophobic – situated more in the air..
Dipalmitoylphosphatidylcholine (31%) or phosphatidylcholine (31%) make up 62% of surfactant phospholipids
Position Change Capacities
Supine: FRC 2 L
Supine ERV is reduced (reducing the FRC)- squeezed out from the gastric contents pushing up.. So lower FRC if on back.. For anesthesia, that means less working room.. Less air/oxygen in the lungs, so the sorter amount of time someone would be able to tolerate not breathing. FRC is functional bc it’s a gas reservoir- plenty of O2 in there- so if I don’t take in a fresh breath of air, its not as big of a deal bc have some in the reservoir… Gives us less working time in our job
Note that the IRV and IC are increased in the supine patient but VC seems to be the same (VC could go down though according to research).. But he mentioned are working capacity is less
lower FRC means “less working room” under anesthesia is correct. This lower FRC in the supine position means there’s less oxygen reserve
Lung Compliance over normal breath
Delta V/ Delta P (compliance) and normal is 500mL/ 2.5 cm H2O (change in pressure required to drive that change in volume). => 200mL/cm H2O pressure
Concentration Formula
[gas] = PP gas/ total pressure
To get the Partial Pressure
Take concentration x Total gas Pressure (probably 713mmHg)
