1 Flashcards
artery that supplies heart conducting system
RCA
How purkinje fibers depolarize ventricles
base to apex
RCA supplies what
RA/RV, part of inferior wall LV
right dominant circulatory means what
RCA gives rises to PDA. 85%
PDA supplies what in heart
posterior-superior interventricular septum and inferior wall of LV
LMCA supplies what
LA, most of inter ventricular septum, LV(septal, anterior and lateral walls)
what supplies bundle of his
PDA and LAD
CO to heart
5%, 250mL/min
extraction ratio of heart
65%
EKG inferior MI
II, III, aVF
EKG lateral MI
I, aVL, V5-V6
EKG anterior MI
V3-4
EKG septal MI
V1-2
EKG lead most sensitive for ischemia
5, 75% sensitivity to detect ischemia
TEE view to detect ischemia
trans gastric short-axis because you can visualize all 3 major coronary territories
valve w/ 2 flaps
mitral
normal area aortic valve
2.5-4.5cm2
mitral valve normal area
4-6cm2
sympathetic innervation to heart
cardioaccelerators T1-4 travel via stellate ganglion
parasympathetic input to heart
from nucleus ambiguous in medulla
sidedness of heart ANS
R to SA node. L to SV node
transplanted heart connections
no parasympathetic(vagus), no cardioaccelerator T1-4 and no baroreceptor reflexes. dependent on SV to change CO
what transplanted heart responds to for bp
isoproterenol, epi, dopamine and dobutamine aka sympathomimetic amines
myocyte AP
Na voltage gated channel open going in cell. then K open out of cell then Ca open influx
actions potential length in myocyte
200msec
pacemaker cell action potential channel
Ca first not Na
intrinsic rate of SA, AV and purkinje
SA 70-80, AV 40-60 and P 15-40
lusitropy
rate of relaxation after cardiac contractile. dependent on phospholamban which inhibits reuptake of Ca into sarcoplasmic reticulum
heart rate regulation in brain
medulla
ANS receptor in heart
b1-2 sympathetic. M2 parasympathetic
percent atrial kick adds
20-30% of ventricular filling
atrial pressure wave a
end of Atrial contraction
atrial pressure wave c
rv Contraction, triCuspid bulge
atrial pressure x
atrial relaXation
atrial pressure v
Venous filling
atrial pressure y
rapid emptYing of atrium
a fib on atrial pressure wave
loss of a wave and prominent c wave
AV dissociation on pressure wave
cannon a wave
tricuspid regurg on atrial pressure wave
tall c-v wave. no x descent
RV ischemia on atrial pressure wave
tall a and v waves. steep x and y descents
cardiac tamponade on atrial pressure wave
dominant x decent and attenuated y descent
s1 and s2
s1 close AV. s2 close Aortic and pulmonic
s3
reverberation of blood rapidly filling ventricle(benign in youth, athlete or preggo)
S4
blood filling stiff ventricle
normal SVR
900-1500
normal PVR
50-150
which chamber of the heart is more sensitive to dysfunction in increased afterload
RV
E/A ratio
early diastole filling to atrial kick phase measured on doppler
E/A ratio normal
.8-1.2, low= impaired relaxation.
when E/A isn’t predictive of diastolic fxn
heart valve problems or operator error
primary determinant of myocardial oxygen demand
heart rate
ohm’s law
change in pressure = force x resistance
parasympathetic receptor on arteries
m3
Reynold’s number
over 2000 means turbulent flow
blood volume in venous circulation
64%
carotid baroreceptor nerve
IX glossopharyngeal nerve called hearing’s nerve
aortic baroreceptor nerve
vagus
bainbridge reflex
increased right atrial pressure from more blood back so then tachycardia. common after baby delivery
behold jarisch reflex
hypotension, bradycardia and coronary artery dilation in response to sympathetic overactivity causing contraction of an underfilled ventricle
Cushing reflex
elevated ICP- hypertension, bradycardia and abnormal breathing
coronary blood flow ewquation
(art dp-LVEDP)/coronary resistance
normal blood flow to brain
50cc/100gm /min
what can be used to prevent SVT in WPW
droperidol. WPW is pre-excitation abnormality. contraindicated verapamil and digoxin because they suppress normal conduction and enhance abnormal. drop- suppresses antero and retrograde conduction to stabilize HR
digoxin moa
blocks Na/K pump so up Ca(contractility), decreases AV node conduction(b/c down K). give for CHF, a-fib.flutt,
digoxin toxicity
tachydysrhythmias, decreased nodal conduction leads to Brady and AV block. potentiated by abnormal K(diuretic). can see hockey stick EKG
treatment of digoxin toxicity
lidocaine to increase AV conductance, phenytoin, amio, K,
adenosine moa
suppress AV nodal conduction used to treat WPW and other supra ventricular tachycardia(narrow complex). antagonized by caffeine, amio and theophylline
classes of antiarrhythmics
I: Na channel blocker. 2 b blockers. 3 K channel blockers and 4 Ca blockers
class IV anti-arrhythmics
Ca blockers verapamil and diltiazem
amiodarone
depresses SA/AV nodal conduction. SE: hypotension, Brady, heart block, depression of contractility, thyrotoxicosis, pulm fibrosis, up LFT, blue skin
QT prolonging meds
antiarrhythmics, antipsychotics(haloperidol/reiperidone), anti fungal(ketoconazole, fluconazole), abx(bacterium, erythromycin), antidepressants(TCA), GI(zofran)
alpha 1 receptor
vasoconstriction of bv, smooth muscles and gluconeogenesis. Gq protein
alpha 2 receptor
feedback mechanism inhibits insulin release, stimulates glucagon release, inhibits NE release. Gi protein
b1 receptor
up chronotropy, dromotropy(impulse conduction), up EF. Gs protein
b2 receptor
smooth muscle relaxation of bronchus, uterus, inhibits glucose release, stimulate gluconeogenesis, lipolysis, Gs protein
med to avoid in MAOI
ephedrine because indirect sympathetic and can cause exaggerated effect in MAOI
dobutamine
.b1, b2 to up CO good for cariogenic and septic shock. avoid in hypotension, arrhythmogenic and can cause tachyphylaxis
dopamine low dopamine agonist, high a1, a2, b1
up CO and mild increase SVR good for neuro, septic and cardiogenic shock
Epi
a1-2, b1-2. up HR, SVR and CO. for hypotension, bronchospasm, anaphylaxis(stabilize mast cells directly), can cause hyperglycemia
NE
a1, b1, b2 agonist. vasoconstriction
phenylephrine
a1 agonist to up SVR good for sepsis
vasopressin
V1, V2 agonist. vasoconstriction and water reabsorption for sepic shock. good in setting of acidosis. can cause lactic acidosis, abdominal cramp, bronchoconstriction
isoproterenol
synthetic catecholamine to b1-2. up HR, CO, contractility, down after load and PVR
milrinone
inhibit PDE so up cAMP. leads to ionotropy, lucitropy, dromotropy, chronotropy. up HR, CO. down SVR and PVR
nitroglycerine
direct vasodilator(v over a).
nitroprusside
decomposes to NO to relax smooth muscle. forms cyanide. give thiosulfate to tx
hydralazine
activates K channels on vascular smooth. muscle to cause depolarization/relaxation. causes tachycardia. good for preggo. can cause lupus like syndrome or agranulocytosis
ca blockers
down bp. verapamil/dilt also treat tachyarrhythmias. nifedipine only smoother muscle dilation
what not to give with verapamil
b blocker. too much hypotension
ace and arb words
ace- pril. arb (sartan)
hypercalcemia signs
groans, moans, bones, stones, and psychic undertones. short qt and bradycardia.
which prostaglandin increases GFR
E2. also ANP, dopamine
major function of proximal tubule
Na resorption and water follows.
what molecules enhance Na reabsorption in the pro tubule
angiotensin II and NE
what activates D1 receptor
dopamine and fenoldopam which decrease prop reabsorption of Na in kidney
what percent does proximal tubule reabsorb
75
amount of bicarb reabsorbed in kidney
90
cell types in collecting duct
principal cells that secrete K and participate in aldosterone-mediated Na reabsorption
Intercalated cells which help w/ acid/base regulation
site of ADH action
medullary collecting duct. V2 receptor activation causes open of aquaporin to reabsorb water
where is renin
juxtaglomerular apparatus
renin story
renin released to blood and turns angiotensinogen (liver) to angiotensin I. Lung’s ACE makes angiotensin II. it acts in prox tubule to up sodium reabsorption
CO of kidney
25%
part of kidney vulnerable to ischemia
medulla
GFR percent of renal. plasma flow
20%
what is a good measure of GFR
inulin because completely filtered but not secreted or absorbed
normal GFR
120 men, 100 cc/min women
creatinine clearance and GFR comparision
creatinine clearance over estimates GFR because it is also secreted
when does GFR stop
under 40 MAP
adenosine on kidney
local release causes dilation of afferent arteriole and inhibits renin release
ANP on kidney
dilate afferent, maybe constrict efferent so up GFR. inhibits renin and aldosterone too
plamsa osmolality equation
2Na + BUN/2.8 + glucagon/18
osmol gap cause
ethanol, mannitol, methanol, ethylene glycol, isopropyl alcohol, glycine(TURP),
fluid compartments
intracellular 2/3 of TBW. extracellular 1/3—75% interstitial and 25% intravascular
diuretic that causes hyper K
thiazide
osmotic diuretic example and other effects
mannitol. it’s also a free radical scavenger, can cause pulm edema
loop diuretic MOA and SE
inhibit Na and Cl reabsorption in thick ascending loop. reversible hearing loss
where thiazides work and SE
inhibit Na reabsorption in distal tubule. hypoK. metabolic alkalosis, hyperglycemia
where K sparing diuretics work, example and SE
collecting tubules. spironolactone(aldosterone receptor blocker). High K and metabolic acidosis, gynecomastia
fenoldopam
selective Dopamine 1 receptor agonist. decreases PVR, up renal blood flow and diuresis. good for cardiac/aaa repair because of antihypertensive and renal sparing properties
extraction ratio equation
intrinsic hepatic clearance / hepatic blood flow
flow dependent drug elimination characteristics
high extraction ratio, most eliminated first pass, rapid metabolism
capacity limited drug elimination characteristics
dose dependent, zero order, hepatic elimination determined by plasma concentration, when dosing exceeds liver capacity, plasma level rises
drugs with poor extraction ratio from liver
acetaminophen, asa, clinda, diazepam, digoxin, ethanol, phenytoin, warfarin
cup inducers
anesthetics, anticonvulsants, insecticide, sedative, steroid, HAART, st John wort
crossmatch
45min. donor and recipient blood. 1-rechecks ABO/lewis. 2-at 37C in albumin checks Rh
most labile coagulation factor
7
indications for FFP
correction of factor deficiency when don’t have recombinant. PT/PTT over 1.5x normal. correction of microvascular bleeding during massive transfusion, urgent reversal of warfarin
how long do platelets last
5 days
indications for platelets
under 50 with ongoing bleeding or DIC or needs invasive procedure. if drops under 10
platelet change for 1u whole blood, 1 u apheresis,
10k, 30-50k
blood product most likely to spread virus
platelets. short life so can’t test for nucleic acids
blood product you don’t need ABO compatibility on
platelets. desirable but not absolutely required. need Rh though for female childbearing age. also cryo
what blood product not to give through warmer
platelets
cryo indications
fibrinogen under 100, ppx for hemophilia A, vWD, congenital dysfibrinogenemias, bleeding due to uremia not responsive to DDAVP
factors in cryo
8, 13, vWF, fibrinogen
who gets anaphylaxis to blood products
IgA deficient patients. reacting to donor IgA.
mild allergic run blood most common
ffp
febrile ran blood
pt antibody against donor wbc. 1 degree up in 4 hours
when does trali occur and tx
6 hours after transfusion. non cariogenic pulmonary edema, fever/chill, b/l infiltrates on CXR. mechanical ventilation, strict fluids, pulm hygiene, nebulizer
least common cause of TRALI
pRBC (least amount of plasma in it)
coagulopathy of blood transfusion
1.5x blood volumes, fibrinogen decreases. 2x Factor 2,5 8 down. 2.5 x then platelets decrease
stored pRBC pH
7.0 secondary to lactate and CO2 accumulation
4 platelet steps
adhesion via vWF/GP1B. 20 shape change/mediator release(thromboxane, prostaglandin, histamine. 2- aggregation Gp2B-3A. emergence of PF3 on platelet where coagulation cascade starts
abciximab moa
GP2B3A inhibitor so no platelet aggregation
point of coagulation cascade
make thrombin which turns fibrinogen to fibrin
what protein. and S do
degrade factor 5 and 8
factor 13 job
cross link fibrin together
tap moa
degrades fibrin
txa job. aminocaproic acid
promote fibrinogenesis. stabilize clot
factors tested in INR
extrinsic. 1, 2, 5, 7, 10
aPTT normal but long PT means what
factor 7 because shortest half life
PTT tests what factors
1, 2, 5, 8, 9, 10, 11, 12 (not 7 and 13)
normal ACT
90-120 sec
“poor man’s PTT”
ACT
give heparin and act doesn’t prolong then what
antithrombin 3 deficiency so give FFP
decreased amplitude on TEG
decreased platelet activity
end slope of TEG
give TPA if goes down fast. too much fibrinolysis
asa moa
irreversible plt cox inhibitor which prevents txa2 a potent plt pro-coagulant
cox2 inhibitor
celecoxib to mediate pain/inlammation while not causing gastric damage, decreased renal blood flow and inhibit plt txa2
calcium level for tetany/arrhythmia
less than o.5
high calcium sign
over 1.7 is coma. otherwise stones, bones, grones and psychic over tones
secreted from adrenal medulla
80% epi, 20% ne and little dopamine
nicotinic vs muscarinic
N: ion channel. receptor is everywhere
M: G protein membrane protein. in parasympathetic system so used to counteract nicotinic side effects of reversal
pressure needed for jet ventilation
15psi
highest pH IVF
albumin at 7.4 and plasmalyte
T1/2 of NS
30min
lithium and anesthesia
d/c b/c prolongs NMBA
valproate and anesthesia
interferes with platelet function
carbamazepine and anesthesia
induces p450
why procaine is bad for spinal
short(less than hour), more nausea, high anesthetic failure rate, slower recovery time PACU, but better because less back/leg pain than iidocaine
spinal w/ lido length
1.5 hours
adhesive arachnoiditis cause
chlorprocaine but because of the preservative so since changed and ok.
ropivicaine vs bupivicaine
ropi is half as potent but safer cardiac but less motor block
why neuraxial neostigmine is bad
nausea
2 MOA that occur when anticholinesterases are given neuraxial
inhibits acetylcholinesterase so more ach around to mitigate nociception. also increase concentration of NO. which is good in spinothalamic tract
specific gravity of CSF
1.0069
what influences peak block height of a spinal
patient height, site of injection, csf volume, baricity of med, dose of med, posture of patient
2 chloroprocaine onset and duration epidural w/ epi
10-15min and lasts 60-90min
lido onset and duration epidural w/ epi
15min, lasts 120-180min
bupivacaine onset and duration epidural w epi
20min and 3-4hours
ropivacaine onset and duration epidural w/ epi
15-20min and 2-3 hours
sodium bicarb on epidural
1mEq addition to 10 mL 1.5% lido makes significantly faster onset and better spread
sympathectomy level w/ neuraxial
epidural same level. spinal 2 levels above sensory
volume for blood patch
20cc
why isn’t chlorpromazine used for iV anessthesia
causes phlebitis
local that causes mehemoglobinemia
prilocaine
how long does the turniquet have to be up for bier
at least 25min
protein binding molecules in plasma
albumin binds acidic drugs. alpha-1 glycoprotein binds basic drugs
meds that can have tachyphylaxis
ephedrine, opioids, nitroglycerine, ddavp, hydralazine, reglan, ranitidine, local anesthetics
risk factors for ulnar neuropathy
head rotation away, excess arm abduction, arm pronation, male, extremes of body habitus
saphenous nerve compression surgery location
medial tibial condyle from leg holder
femoral nerve injury surgery
kinked under inguinal ligament from extreme flexion and abduction of thighs
foot drop nerve
common peroneal
when to draw tryptase
within 5 hours after anaphylaxis
sublingual to core temp
sublingual 0.5C under
meperidine metabolism
to normeperidine in liver. can cause myoclonus and seizures
morphine metabolism
in liver to m6glucoronide(more potent than morphine) and m3g(inactive)
hydromorphone metabolism
to hydromorphone3glucuronide may cause cognitive dysfunction and myoclonus
where to epidural opioids exert their effect
substantia gelatinosa in dorsal horn
volatiles on icp and cmro2 and cbf
all up cbf and icp. nitrous oxide up cmro2, others down
nitrous toxicity things
megaloblastic hematopoiesis from marrow failure, subacute combined degeneration of spinal cord(numb/falls/weak), immunosuppression(impaired chemotaxis), teratogenic(skeletal and limb, situs inverus),..prolonged exposure
ppm numbers
nitrous 25, volatiles are 2
most IV anesthetic targets
gaba potentiation except ketamine…NMDA block
when to avoid barbiturates
hemorrhagic shock because significant myocardial depressant
ALA synthetase
induced by barbiturates so causes acute porphyria attack
intra artery inject of what is bad and how to treat
barbiturates. treat with papaverine/lidocaine, heparizination and consider regional techniques for pain
long acting benzo
diazepam
intermediate acting benco
lorazepam
when prolonged propofol infusion
over 4mg.kg.hr for 48 hours. metabolic acidosis, fatty liver, rhabdo, mitochondrial dysfunction, refractive bradycardia
common SE etomidate
pain at injection site/thrombophlebitis and a lot of n/v
phobicity of fentanyl vs morphine and why it matters spinal
f lipophilic. m hydrophilic. hydro slower onset, stays in csf longer so spreads higher and lasts longer
opioid receptor euphoria
m1
m2 opioid receptor job
hypoventilation, constipation, dependence
opioids histamine
morphine and meperidine most
mu receptor where spinal
substantia gelatinosa which inhibits release of substance P
methadone moa and loa
mu agonist and nmda antagonist. T1/2 15-60hours, variable due to cup variation
meperidine difference
atropine like structure so can have vagolytic effects. good for shivering. can cause serotonin syndrome
serotonin syndrome effects
headache, agitation, hallucination, coma, shiver, sweat, up T, tachycardia, nausea, myocolus, tremor
more allergenic locals
esters
locals with the “I”
amides
onset local based on what
pKa. lower means higher fraction of neutral drug so faster onset. only de protonated can cross
potency of local based on what
hydrophobicity. which improves transit across membrane
duration of locals based on what
protein binding
procaine different
methemoglobinemia, less likely TNS, high n/v
benzocaine different
paba allergic, methemoglobinemia
chlorprocaine different
quick onset, arachnoiditis from EDTA, decreased clearance in hepatic/renal dysfunction
tetracaine different
longer duration of action and motor, TNS risk
percent occupied if TOF
up to 70% still
nerve stimulator orbicularis occult vs adductor pollicis
eye mimics laryngeal mm. adductor pollicis comes back after laryngeal
o2. cylinder
700L gas at 2200psi
n2o cylinder
1600 L max pressure 750 psi
type of system mapleson is
semi closed
mapleson spontaneous best
All Dingos Can Breathe
abg and co2
down T then more CO2 dissolved in blood. pH up and pO2 down
bp only carotid pulse
systolic 60
bp carotid and femoral pulse
sup 70
radial pulse bp
80 if feel
pulse pressure by body part
more farther from heart
ohms law
V=IR
which current is more harmful
AC is x3 more dangerous
where needle goes for cervical plexus block
posterior border of SCM at its midpoint
stellate ganglion block location
medial to carotid pulse, anterior to c6 transverse process(vertebral artery protected)
brachial plexus nerves
C5-T1
brachial artery canulation can hurt what nerve
median
what sciatic splits to
common peroneal and tibial n
ankle block nerves
4/5 from sciatic: post tibial, sural, superficial and deep peroneal. other is saphenous from lumbar plexus
henry
concentration of gas dissolved in a solution is proportional to the partial pressure x solubility
