An Old Example Flashcards
This was a deck made last time we took the FP-C. It's def not all-inclusive and isn't divided by categories, but figured we'd throw it up anyways and will add a better situation for you all one of these days :-)
Altitude Zones
Physiologic - sea level to 10k’
Physiologic deficient - 10k’ to 50k’
Space equivalent - 50k’ to 250k’
Space - >250k”
Posterior Wall MI
RCA occlusion
Assoc’d with inf. wall MI and RVI
*super unlikely to happen, but a really high RCA occlusion can cause AV node infarction and lead to lots of funky EKG changes
Fast Flush Test
Normal is 2-5 down bounces :)
*note that 2-5ml/hr (same digits) run from pressure bag in to systemic circulation with invasive line monitoring
Overdamped - not enough squiggles
Underdamped - too many squiggles
Gay Lussac’s Law
Temperature and pressure are directly proportional
[P1/T1 = P2/T2]
Example: oxygen tank pressure throughout the day
Effective Performance Time (EPT)
Amount of time crew can perform useful flying duties in an inadequately oxygenation environment
Time of Useful Consciousness (TUC)
Time from exposure to oxygen deprived environment to point where deliberate function is lost
1/2T with explosive decompression (vs controlled)
Henry’s Law
The amount of gas dissolved in a liquid is directly proportional to the partial pressure of that gas in equilibrium within that liquid (temperature constant)
[Cx=(Px)(k)]
“Henry’s Heinekin”
Applications
Oxygenation: higher partial pressure of oxygen in the alveoli than in the blood (and opposite happens with explosive decompression, that’s why loss of consciousness happens right away)
Decompression sickness
Secondary Buffering Systems
Protein Buffering System: most potent system due to large amounts of proteins (RBCs, albumin, globulin, etc.), majority of this buffering occurs inside cells themselves (i.e. the H+ within Hbg is contained in order to not effect pH in the blood); though potent, can be easily overwhelmed
Phophate Buffer System: uses H2PO4 and HPO4-; easiest to overwhelm, very weak system; primarily occurs in the kidneys, but chronic acidosis can pull critical phophates from bones
Read more: https://opentextbc.ca/anatomyandphysiology/chapter/26-4-acid-base-balance/
Law of Mass Action
Principle that the rate of a chemical reaction is proportional to the concentrations of the reacting substances
Coronary Vessels
LCA –> LAD & LCX
LAD: L ant. wall, ant. 2/3 septum
LCX: L lat. wall (and the “LC dominant” folks have LCX feed AV node too)
RCA –> (SA nodal artery to SA node) –> PDA
Marginal branch: AV node (“RCA dominant”)
Terminal PDA: L post ventricle, L inf. ventr.
Supply in order: SA node, RV, AV node, L post. wall, L inf. wall
*Sick Sinus Syndrome comes from plaque at SA nodal artery
*70% RCA dominant, 20% co-dominant, 10% LCA
Cardiomyopathies
Dilated (systolic failure) - secondary to volume overload, not pressure; weakened walls and contractile dysfunction; tx is cardiac glycosides (digoxin), inotropes (dop or dobut), diuretics (lasix)
Hypertrophic (disatolic failure) - secondary to pressure overload, not volume; sacrifice of ventricular volume for increased muscle mass; tx is beta blockers, ca-channel blockers, amiodarone (get a longer fill/ diastole, add fluids to increase preload also)
Restrictive (systolic failure) - secondary to ischemic tissue fibrosis with decreased dynamics; tx with diuretics, anticoagulation, cardiac glycosides
(and all of these can be either primary or secondary; restricted and dilated may be secondary to pulmonary stuff)
Stages of Hypoxia
Indifferent - slight increase in both HR and RR, decreased night vision
Compensatory - increased BP, impairment of task performance
Disturbance - dizzies, sleepies, tunnel vision, cyanosis
Critical - marked mental confusion and incapacitation
Stressors of Flight
Decreased partial pressure of oxygen Barometric pressure Thermal changes Decreased humidity Noise Vibration Fatigue G-forces
Metabolic Acidosis
pH <7.4, HCO3- <22
Can be ID’d without ABGs or lactate using Anion Gap
AG = Na - Cl - TCO2
or AG = Na + K - Cl - TCO2
(Total CO2 is eseentially equivalent to HCO3-)
AG >20 = metabolic acidosis (and higher gap means worse case)
Normal AG as above = 8-16
Normal AG with K factored in = 10-20
Consider causes in algorithmic fashion:
- Lactic acidosis: lactate level? decreased CO? decreased UOP? altered LOC? consider 4 types of hypoxia
- DKA: high BGL? spilling ketones?
- Renal failure: high BUN and Crt? (note that Crt is a better indicator than BUN)
- Toxin: EtOH and heavy metals?
Consider MUDPILES or GOLDMARK to work thru causes
Treatment based on cause
- Lactic acidosis: oxygenation, increase CO
- DKA: control glucose and correct acidosis slowly (consider K shifts, watch osmolality; drop BGL <100/hr, esp. with kiddos)
- Renal failure: ID treatable etiologies (such as dehydration, poor CO, etc.)
- Toxins: stop intake, look for antidotes, treat symptoms
Pulmonary Embolus
Shunt = blood passing thru lungs w/o being oxygenated
(vs V/Q mismatch which will respond to oxygen)
Classic risk factors: smokers, females on birth control, surgical pts, bedridden folks
Other ones: cancer, preggos, obese
Tx considerations: early intubation to maximize oxygenation, heparin or LMWH to prevent further clots, consider thrombolytics, surgery consult
Greenfield filter at vena cava = hypercoagulopathy and risk for PE
S&S: acute resp distress and low SpO2 that doesn’t respond (and A-a gradient >20 with positive d-dimer)
Normal ABG and VBG Ranges
Arterial pH 7.35-7.45 PaCO2 35-45 HCO3- 22-26 PaO2 80-100 SaO2 >95% BE -2-2
Venous pH 7.31-7.41 PaCO2 40-50 HCO3- 22-26 PaO2 35-40 SaO2 70-75% BE -2-2
CHF CXR
cardiomegaly, “shaggy border” at heart margins/ pulmonary tree; kerly A and B lines = vessels engorged with fluid, more so at bases
Lactate and Shock
Shock is inadequate tissue perfusion
Inadequate tissue perfusion means anaerobic metabolism –> lactic acid –> metabolic acidosis
Therefore best “test” for shock would be lactate level
[normal is 1 +/- 0.5, >2 is significant]
Body normally has some level of anaerobic metabolism, as all vascular beds are in a state of flux; when lactic acid is released, body responods by releasing NO to cause local vasodilation
Pneumo on a Vent
Vent makes pneumo more likely
S&S maybe tough to ID
Vent –> increased PIP
1st intervention: take them off the vent! (and don’t bag them!)
2nd: decompress it
Patient has a few minutes to desat, so tx that first (“don’t ventilate that pneumo until you get it under control”)
Golden Rules of ABG
- Change of 10mmHg CO2 = change of pH 0.08 in opposite direction
- Change of 10mEq HCO3- = change of pH 0.15 in same direction
- Replacing bicarb: (kg/4) x BD = mEq of bicarb needed
(half as push, half over an hour; this is currently out of vogue…)
Atmospheric Pressure Things
At sea level, weight of a one inch squared column of air extending to the edge of space = 1ATM (or 14.7PSI or 760mmHg/ Torr)
0.5ATM or 380mmHg at 18000’ (but note that the atmosphere is not uniform in density, so greater changes lower to sea level)
33’ under water is = 1ATM
How to Determine Capture with Pacing
Electrical: each spike should have a wide QRS AND T wave of opposite polarity
Mechanical: heart tones
Buffering Systems
Carbonic Acid-Bicarbonate Buffer System: occurs primarily in the blood, lungs and kidneys; normal relationship of HCO3- to H2CO3 is 20:1; fastest regulation, but easily overcome; “second to second”
The Lungs: can adjust the amount of H2CO3 by blowing off or holding on to CO2; Law of Mass Action drives the equation; respiratory system eliminates roughly 2.5L of HCl every day; “minute to minute”
Kindeys: can reabsorb, create or excrete HCO3- or H+ as needed; secretion of H+ requires “primary active ransport” and takes energy; only the kidneys can excrete fixed acids (vs volatile acids); “hours to days”
Dalton’s Law
Total pressure of a gas mixture is the sum of all the partial pressures
[Pt=P1+P2+P3+etc.]
Factors that Exacerbate Stressors of Flight
Drugs (to include OTCs) Exhaustion Alcohol Tobacco Hypoglycemia
(think “DEATH”)
Respiratory Acidosis
pH <7.4, CO2 >45
Problem: failure to remove CO2 (from plasma, therefore from lungs, therefore a MV problem)
Fast causes: failure to get CO2 to the lungs (decreased CO)***, failure to get CO2 out of the lungs (decreased MV)
Slow causes: bronchospasm and COPD (resp alkalosis in acute asthma, this would be a late sign!); VQ mismatch (small PE, ARDS, pneumonia, poor CO, bad vent settings, poor positioning); pulmonary edema (CO2 moves across H20 better than O2, therefore resp alkalosis early on, then resp acidosis)
Treatment: remove CO2 by increasing Va (alveolar minute ventilation)
Va = (TV - Vd) x f
Vd (dead space) roughly .33TV or 1ml/lb IBW
Strategy here should be to increase volume before rate (“never give up lung”); consider that when a part of the lung gets insufficient oxygen it vasoconstricts to shunt blood to where it is needed; increase TV until you see change in PIP/ Pplat above range (this indicates that lungs are “filled up”)
***verify this
