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
COPD, Asthma, Chronic Bronchitis
All have similar patho, issue is breathing out (vs in)
Try to avoid intubation (will be difficult ot get them off)
Tx: B2 agonists, anticholingergics, ketamine, MgSO4, Steroids
- 2/3 neb’d meds go to gut, h/e atrovent can cross lipid layers and thus extra just goes to GI system
- asthma CXR: flat diaphragm, blunted costophrenic angles, lots of black, thin/ compressed heart
- mag: most useful with COPD, not much research with pedis
Treatment for Hypokalemia
Raising serum K+ 1mEq/L will require 100-200mEq of K
You should administer K+ at 10-20mEq/hr; for sure don’t exceed 1mEq/kg/hr
Morale: you can’t fix this fast, so don’t let it happen!
Right Shift
on the oxygen hemoglobin dissociation curve
Bohr Effect (releases O2)
Raised acidosis
Raised temp
Raised 2-3 DPG (chronic lungers like COPD in both its forms and smokers have increased levels)
Reduced oxygenation
[think all the “R” things]
Aortic Dissection
Debakey Classifications
Type 1 - ascending aorta and extends distally beyond arch; worst case, can impede coronary artery bloodflow –> AMI :(
Type 2 - limited to ascending aorta (jet erosions and Marfans)
Type 3 - distal to origin of left subclavian and extends towards belly, most survivable one
“Widened mediastinum” & “diffuse infiltrates” = AAA
Tx: SBP 100-110 (Nipride), B-blockers to decrease HR and decrease EF (esmolol), relieve pain aggressively! (fentanyl prefered, b/c it won’t fuck with hemodynamics as much)
ACS Treatment
in addition to the clot stuff and confirmed MI stuff…
Nitrates: increase coronary blood flow via smooth muscle relaxation, venous pooling decreases preload and LVEDP [Ntg at 5-200mcg/min]
Morphine: decreases preload, decreased sympathetic tone (which decreased myocardial oxygen demand) [2-4mg q 5-15min]
*Morphine > Fentanyl r/t histamine dump –> preload reduction; unless we are worried about BP!
Graham’s Law
Gasseus diffusion, small gasses diffuse faster
Application: O2 vs CO2 - O2 is smaller and moves thru air easier, however CO2 is more soluble and moves better for thru liquid
Considerations at the alveoli: surface area, diffusion gradient, molecule size, solubility
Sidenote: heliox maximizes surafce area (doesn’t necessarily function via a diffusion mechanism)
Read more on this: https://teachmephysiology.com/respiratory-system/gas-exchange/gas-exchange/
Bohr Effect
Change in the structure of Hbg as it releases O2; this change increases its affinity for CO2
(also consider the “Reverse Bohr Effect” - when the new Hbg releases CO2, it goes back to that shape that better recruits O2)
MUDPILES Mnemomic
for causes of metabolic acidosis
Maybe add CAT to the start…
Cyanide* and CO* Poisoning
Arsenic
Toluene
Methanol (& Metformin) Uremia DKA Paraldehyde Isoniazide* & Iron* Lactate Ethylene Glycol Salicylate
*indirect via lactic acidosis
extra stuff from https://www.ncbi.nlm.nih.gov/books/NBK482146/
Charles’ Law
Volume is directly proportional to temperature (pressure constant)
[V1/T1 = V2/T2]
“Charles Centigrade Volume”
100m up = 1 degree C in temp change
Clot Prevention/ Lysis with AMI
ASA, GIIb/IIIa - prevention, inhibit platelet aggregation
*ASA is good 8-11 days, the lifespan of a platelet; IIb/IIIa works on receptors (so not as long)
Heparin, LMWH - prevention; inactivates thrombin & factors IX, X, XI, XII; prevents conversion of fibrinogen (1) to plasmin (stops in process)
Fibrinolytics: activates plasminogen to plasmin, result is thombolysis
PaCO2 vs EtCO2
They should be similar, however will never be the same (+/- 3-5 in healthy patients, bigger gap = sicker); that said, they do both move together
EtCO2 entirely dependent on movement of air; leaks, fast flows, low TV will all affect reading, therefore check waveform
PaCO2 is measured in sample of blood, so will be more reliable
For EtCO2 to accurately reflect PaO2, a few things are necessary:
CO2 production must occur at the tissue level and diffuse in to the blood
Cardiac output must be adequate to move CO2 to the lungs
CO2 must diffuse from blood to alveoli following a concentration gradient
TV and alveolar minute volume must move the CO2 to the EtCO2 sensor
Read more: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5330081/
BUN & Crt
BUN normally around 10
Crt normally around 1
BUN : Crt normall about 10:1
Increased BUN –> dehydration
Increased Crt –> decreased UOP/ clearance or dysfunction
Septal Wall MI
LAD occlusion
Assoc’d with ant. wall MI (both LAD supply)
Also assoc’d with RBB and LAFHB (also both LAD supply)
Conduction System
SA Node –> (3 intranodal pathways, Bachman’s bundle is major one) –> AV node (sits at crux of heart where four septums come together) –> Bundle of HIS –> LBB & RBB –> purkinje network
LBB –> LAF (ant. 2/3 septum, LAD) & LPF (wide, ribbon-shaped; 3x blood supplies [LAD, RCA x2])
RBB: anterior 2/3 septum, LAD
- think 3 primary pathways from bundle of his
- LAF and RBB are single filament, thin & ropelike, one blood supply (LAD); consider them as “delicate twins”
ARDS
Causes include any major insult…
Patho: hyper-permeable pulmonary capillaries; proteins move in to alveoli, pulls fluid in there also –> capillary bed separates from the alveoli and shunt exists; causes derecruitment
Tx: PEEP (& increase freq, decrease TV; permissive hypercapnea)
CXR: patchy, diffuse infiltrates, “ground glass” appearance; patches of healthy lung
Pneumonia
Tends to be localized (therefore consolidation, infiltrate, etc “lobular”)
VAP & CAP; viral or bacterial (and fungal too…)
*avoid VAP with HoB up to get gunk down esophagus vs trachea
Tx: O2, IV abx (w/i 4hrs), oral care, HoB up, supportive tx
*“high-low” ETT with sxn built in
Oxygen Adjustment Calculation
(FiO2 starting x P1)/P2 = FiO2 at altitude
PaO2 decreases roughly 5mmHg per 1000’ increase in altitude
Cardiac Enzymes
Myoglobin - 1st to peak, non-specific [1hr, 4-12hrs, immediate]
CK-MB - (BB from brain, MM from muscle, MB from heart) - fairly specific [4-9, 24ish hrs, 48-72hrs]
Troponin 1 - elevates late, very cardiac specific, stays elevated for a while [6-8hrs, 12-24hrs, 7-10days]
[elevation, peak, return to baseline]
Treatment for Hyperkalemia
To redistribute potassium: fix the underlaying acid-base issue first!, CaCl (to raise action potential threshold in the heart), NaHCO3 (raises pH, electrical gradient manipulated), D50 (to big to move into cells alone, uses a transport protein and the process also moves K+ intracelularly), Insulin (5-10u per Amp D50), Beta-2 agonists
To treat true hyperkalemia: Lasix with NaCl infusion (requires intact kidneys, so make sure a foley is in), Kayexalate (cation-binding resin, will cause diarrhea)
Treatment of Hypoxia
- Ensure adequate VA (alveolar minute volume) by looking at TV and rate
- Maximize FiO2
- Add PEEP
- Invert I:E ratio
Potassium and Acidosis
K exists in all compartment, however is primarily in the ICF
Electrical gradient and Law of Mass Action both apply, H+ follows the same principle (however H+ has a stronger electrical force than K+)
Drop in pH –> increase in H+ –> more H+ enters the ICF –> electrical polarity forces K+ to ISF –> result is that we see K+ in the blood with acidosis
For every 0.1 change in pH, K+ changes 0.6mEq/L in the opposite direction
For every 10mmHg change in PaCO2, K+ changes 0.5mEq/L in the same direction
[ICF = intracellular fluid, ISF = interstitial fluid]
Q Waves
Pathological: scar tissue! (“old, dead heart”), 0.4s wide or >/= 1/3 of QRS
Physiological: Q waves are abnormal in all leads, h/e may be seen for lots of reasons (to include shitty lead placement)
Read more: https://litfl.com/q-wave-ecg-library/
Progression of an Infarct
Coronary arteries lie outside the heart, but perfuse thru the myocardium so that endocardial wall is perfused by terminal ends of these vessels; that means endocardium is the first place to get ischemic; MIs begin at subendocardial surface and become transmural
Consider the fingernail principle: we need to release pressure at subendocardial wall; RV perfused mostly at systole, LV mostly at diastole; therefore drop diastolic BP/ reduce preload (Ntg and Morphone) –> drop intraventricular diastolic pressure (LVEDP or PWCP)
Damage limited with non-transmural/ subendocardial; with transmural, h/e, damage is thru all of the heart muscle and there is greater risk of adverse function
Non-transmural/ subendocardial = Non-STEMI = Non Q Wave MI
High Pressure Alarm Mnemonic
Suction Connections Obstructions Pneumothorax ETT displaced (SCOPE)
Also: small tube
Note that it only takes 1-2 breaths on a vent to cause a pneumo!
PaO2 Stuff
Reflects partial pressure of O2 in the plasma
Defines oxygenation
Normal is 80-100 on room air
Rule of Thumb: PaO2 = FiO2 x 5
Equation to Conceptualize Acid Base
CO2 + H2O H2CO3 H+ +HCO3-
Carbon Dioxide + Water Carbonic Acid Hydrogen Ion + Bicarbonate Ion
Types of Hypoxia
Hypoxic hypoxia - deficiency in alveolar oxygen exchange
Stagnant hypoxia - decreased cardiac output or pooling of blood (CHF, PE, shock; tourniquet at arm)
Histotoxic hypoxia - failure of tissue’s ability to use oxygen (toxins like cyanide)
Hypemic hypoxia - decrease in oxygen carrying capacity of the blood (anemia, hemorrhage, CO poisoning)
SaO2 vs SpO2
SaO2 - partial pressure of arterial oxygen
SpO2 - measure of Hbg saturation (infrared) at the capillaries
Normally they will be comparable
Metabolic Alkalosis
pH >7.4, HCO3- >26
HCO3- or too little H+, think electrolyte disorder
“worst of the worst” b/c its hard to treat (and also difficult to get in to)
Causes: GI loss of acid (H+) r/t NG/OG suction or N/V; GI loss of electrolytes (K+) r/t diarrhea
Consider role of gastric parietal cells in all of this
Treatment: give elctrolytes (K, MG, Ca)
MI Treatment
in addition to the ACS stuff, not including clot stuff
goal is to decrease HR and myocardial O2 demand (MPO2)
Beta blockers: to tx “unnecessary tachycardia” - rule out hypotension and treat pain first!
metoprolol 5mg, repeat q 10min, max x3; carvedilol for alpha and beta + antioxidant stuff
Ca-channel blockers: dilate coronary arteries and collateral vessels along with cost of decrease in myocardial conduction and contraction; don’t give along with beta blockers! (and consider pt’s home med list too)
hydralazine is most common one
Inferior Wall MI
RCA occlusion (distal)
Assoc’d w/ post. wall MI and RVI (with higher occlusion)
Look for AV nodal involvement with higher occlusion
*super unlikely to happen, but a really high RCA occlusion can cause AV node infarction and lead to lots of funky EKG changes
Respiratory Alkalosis
pH >7.4, CO2 <35
Problem: removal of too much CO2 (alveolar hyperventilation)
Causes: tissue hypoxia secondary to poor supply (think of those four types of hypoxia) or excessive demand (such as gram-neg sepsis in warm state, hyperthermia, early salicylate poisoning, mechanical hyperventilation, anxiety)
Treatment: consider the “why?” (i.e. hypoxia, too much CO2, anxiety, etc - consider giving an anxiolytic to make this distinction: will help with anxiety, but won’t fix O2 or CO2), decrease alveolar ventilation starting with rate first (then TV)
Anterior Wall MI
LAD occlusion
Assoc’d with Septal Wall MI (both LAD supply)
Anticipate papillary muscle involvement (mitral valve) –> acute pulm. edema from incompetant or regurgitant valve
Smoking and Night Vision
Normal loss of night vision is at about 5000’
Loss of night vision for smokers is at about 1000’
Rods (at periphery) provide night vision, that’s why we teach to scan at night
Mechanism for decreased night vision with smokers: carboxybemoglobin (normal 7-10% with smokers) affects retina and rods
Also: rods are most susceptible area in the body to hypoxia (in decompression chambers vision stuff happens first)
Left Shift
on the oxygen hemoglobin dissociation curve
Holds O2 (rather holds H+ than O2, h/e in this case no H+ is available)
Alkalosis
Low Temp
Low 2-3 DPG (organophosphate-like enzyme produced by RBCs in response to low O2 states, think of it as the crowbar that pries off oxygen afetr it saturates; caused by mutliple transfusions, as PRBCs packed with citrate to prevent clotting and citrate destroys 2-3 DPG))
Lots of Carbon Monoxide (CO changes the shape of Hgb to hold on to both CO and O2)
[think of all the “L” things]
Boyle’s Law
Volume of a gas inversely proportional to pressure (constant temperature)
[P1V1 = P2V2]
“Boyle’s Balloon”
Applications:
Barotitis media - air in middle ear (descent problem)
Barodontalgia - air trapped under dental work (ascent problem)
Barosinusitis - gas trapped in sinuses (ascent problem)
Barobariatrauma - gas trapped in tissue, then released; refers mostly to Nitrogen, as it absorbs in adipose tissue well; occurs with rapid ascent –> N bubbles released; prevent with “nitrogen washout” prior to lift (also ascent problem)
GI Complication - air in the gut, treat with NG/OGT
Equipment stuff - ETTs, IV bags, MAST, casts (bivalave them if over 7 days old), IABPs, chest tubes, NGTs, foleys, etc.
A-a Gradient
PAO2 = alveolar pressure of oxygen
PaO2 = arterial pressure of oxygen (and comes from the ABG)
A-a Gradient = PAO2 - PaO2
Normal is 5-20 (higher with older age
>10 and I need to look for issues
>20 and a shunt exists
Normal PAO2 is 101.73 (sea level, room air, perfect CO2, etc)
PAO2 = FiO2 (Pbar - PH2O) - 1.2(PaCO2)
= .21 (760 - 47) - 1.2 (40)
=101.73 torr
Lateral Wall MI
LCX occlusion
May be assoc’d with ant. wall or septal wall MI (r/t LAD supply)
Valvular Disease & Murmur Stuff
Stenosis - doesn’t want to open, stuck closed
Regurgitant (aka incompetent) - floppy, wants to open when it should be shut
Mitral and aortic issues are most common and have worst prognosis
Primary cause of multi-valvular disease is rheumatic fever
Simple way to asses tones:
Systolic = “lub murmur dub”
Diastolic = “lub dub mumur”
VSD Murmur - mostly systolic, h/e some diastolic; louder - smaller defect; loudest at apices of heart
Factors of Oxygen Delivery
Delivery (FiO2 with diffusion in to plasma across alveolar membrane)
Carrying capacity (02 “saturates” Hbg)
Ability to move oxygen in to the cells (function of diffusion gradients [very large: mitochondrial P02 is 1-5mmHg, PCO2 is 48mmHg] & Bohr effect)
Ability of the cells to use the oxygen
Types of Angina
Stable - onset with exertion, 1-5min and relived by rest, predictable
Unstable - changes in freq, quality, duration, intensity; >10min with rest and/ or Ntg
Variant - spontaneous CP assoc’d with circadians (i.e in the am) and relived by Ntg
Silent - obj. evidence of ischemia, but no symptoms
Mixed - combo of stable and variant
