Random APEX Flashcards
Normal anatomical shunt
-Thesbian (drain left heart)
-Bronchiolar (drain bronchial circulation)
-Pleural (drain bronchial circulation)
What increases zone 1 in the lungs?
Hypotension (no blood thru lungs)
PE (blocks blood from coming in contact with alveoli)
Excessive airway pressure (too much V not enough Q)
How does the body combat west zone 1?
Bronchioles constrict in OVER? perfused alveoli
How does the body combat west zone 3?
Hypoxic Pulmonary Vasoconstriction reduces blood flow to under ventilated alveoli
What causes west zone 4?
- increased volume: mitral stenosis, fluid overload
- Fluid is pulled d/t a decrease in pleural pressure: laryngospasm, mullers maneuver (bite tube and breathe in)
What causes Increased Aa gradient? O2 or CO2?
O2
Aging (higher closing capacity)
Vasodilators (prevent HPV which hinders VQ match)
RL shunt (from atelectasis, pna, bronchial intubation, intercardiac defect)
Diffusion limitation
Alveolar gas equation (partial pressure of alveolar oxygen)
[fio2-(ATM-H20)]-(PCO2/RQ)
Estimation of shunt % per Aa gradient
1% for ever 20mmHg of Aa
What increases FRC
OLD- asthma, copd
Older age- longer sigh bc wisdom, sighing
Prone/ sitting
PEEP
What decreases FRC
RLD- obesity, pregnancy, pulmonary edema
General anesthesia
Supine
Fluid overload
Normal FRC value
35ml/kg
How can we measure FRC
Nitrogen washout
Helium wash in
Body pleth
How to determine time to desaturation?
FRC/ VO2
Where FRC is (100% O2= 2300x1.0)- 2300
Where FRC is (21%O2= 2300x.21)
Where VO is 250
In the first- 9.2 minutes
In the latter is 1.9 minutes
Do you want a high or low FRC?
How do you do it?
High! Gives more time before desaturation
To increase- PEEP, prone/sitting/lateral, old age, sigh, fio2 <.8, asthma, COPD
Do we want closing volume high or low?
LOW!!!!
What increases closing volume?
CLOSE-P
COPD
LV failure
Obesity
Surgery
Extremes of age (young or old)
Pregnancy
Normal relation between FRC and CC
FRC should always be bigger!
If CC is bigger than FRC, alveoli will collapse during normal Vt
CC>FRC-> shunting, hypoxemia
How would you increase FRC in relation to CC?
PEEP
How does age effect CC/FRC?
30-CC=FRC during anesthesia
44-CC=FRC when supine
66- CC=FRC when standing
So, CC increases as we age, making it easier for airway to collapse
What decreases SvO2
Shivering
Fever
Pain
Thyroid storm
Anemia
What increases SvO2
Hypothermia
Sepsis (makes CO2, cant accept O2)
Increased CO, HGB, PaO2
Cyanide toxicity binds HGB up
How does hypercapnea affect the body
Myocardial depressant
PVR increased
K, CA increased
Increased IOP/ ICP
What drug, action, and clinical situation increase minute ventilation?
Aspirin
Surgical stimulation
Hypoxemia
Peripheral vs central chemoreceptors locations
Central- medulla- primary detector of CO2
Peripheral- carotid bodies, transverse aortic arch- secondary detector of CO2
Can increased CO2 ever depress breathing?
Yes
80-100mmHg
Which drugs cause left shift on CO2 ventilatory response?
L shift- makes u breathe more
Aspirin
Norepi
Aminophylline
Doxapram
Which drugs cause right shift on CO2 ventilatory response?
R shift- stops u from breathing
Opioids
Paralytics
Volatile anesthetics
CO2 ventilatory response- surgical stimulation vs carotid endarectomy
SS L shift- makes u breathe!
Except for carotid endarectomy, blunts baroreceptors in carotid, prevents u from breathing
Apneustic vs Pneumotaxic center
Apneustic- stimulates DRG to inspire
Pneumotaxic- Inhibits the DRG (stimulates the end of inspiration)
Pneumotaxic- strong signal-> shallow but rapid breaths, weak signal-> slow deep breaths (normal)
DRG vs VRG
DRG- inspiration rate and rhythm
VRG- expiration, but also inspiration to a lesser degree
Location of DRG and VRG
DRG- Medulla (nucleus tractus solitarius)
VRG- Medulla (nucleus ambiguous/retroambiguus)
Location of Pneumotaxic and apneustic?
“PA” = PONS
Upper pons
Lower pons
Can CO2 of H+ cross the BBB?
Only CO2
Primary stimulus at the central chemoreceptor
H+
Hypercarbia and hypoxemia to a lesser extent
Peripherl chemoreceptor job and location
Transverse aortic arch, carotid body
Respond to PaO2 <60
How do volatile anesthetics influence peripheral chemoreceptors?
.1 MAC-> decreased hypoxemic ventilatory drive
What stimulates J receptor?
PE
CHF
What inhibits HPV?
Volatile anesthetics 1-1.5 MAC
Dobutamine
Vasodilators
Vasoconstrictors may constrict well ventilated units and cause shunt
PDE inhibitors
Excessive PEEP
Large Vts
NOT INHIBITED FROM TIVA
Will shunt respond to O2?
NO
5 types of hypoxemia and their Aa gradient
Normal Aa- reduced fio2, hypoventilation
Increased Aa- shunt, VQ mismatch, diffusion limitation
What impairs hypoxemic respiratory drive?
Anemia and CO poisoning
Normal enough PaO2
COPD and dead space relationship
Direct positive
“venous admixture” ??
SHUNT
“small airway diseases”??
Obstructive
What things increase risk for PPC?
Old age >60
COPD
CHF
ASA >2
Ciagrette >40 pack yrs
Aortic>thoracic>upper abdominal
GA
Duration >2H
Albumin <3.5
What does NOT increase risk of PPC?
mild/moderate asthma
PFT
ABG
Absorption atelectasis
Keep fio2 under .8
Causes shunt
Drugs bad for asthma pts
-Histamine releasing drugs- Sux, Atracurium, Morphine, Meperdine
-Ketamine causes bronchodilation BUT increases secretions
-Ketorolac increases airway resistance
-Antiholinesterases
-Nonselective BB
Drugs good for asthmatics
All volatile agents reduce airway resistance/ dilate the airway, sevo can also reduce coughing
Sevo best, then iso, des
Propofol surpresses airway reflexes
Lidocaine surpresses airway reflexes
IV hydration to thin secretions
How to treat bronchospasm
Fio2 1.0
Deepen anesthetic (volatile agent, propofol, ketamine, lidocaine)
Albuterol
Ipratropium (anticholinergic)
EPI 1mcg/kg IV
Hydrocortisone 2-4mcg/kg IV
Aminophylline (methylxanthine, theophylline cant work acutely)
Some causes of COPD
Aplha 1 antitrypsin deficiency (emphysema only)
Smoking (bronchitis mostly)
Environmental pollutants
Respiratory infections