9 Fluids Flashcards
Body water distrib
60/40/20(15/5). Water 60L. Intracellular (28l), extracellular (14), interstitial 11L, plasma 3
Major intracellular ions
K, mg, phosphate
Major extracellular ions
Na, ca, cl, hco3
Net filtration pressure
(Cap hydrostatic - interstitial oncotic) - (capillary oncotic - interstitial hydrostatic )
Osmolarity v osmolality
Osmolarity= osmoles per L of solvent. Osmolality= osmoles per kg of solvent
Nml plasma osmolarity. How to calc
280-290. 2NA + glu/18 + bun/2.8
Most imp determinant of osmolarity
Na
Ex of hypotonic solutions
D5w (253) and 0.45% NaCl 154
Isotonic solutions
LR, 0.9% NaCl, 5% albumin
Hypertonic solutions
3% nacl, d5 nacl 0.9%, d5 nacl 0.45%, d5lr, dextran 10
Side effect of albumin. Side effects of synthetic colloids
Albumin: hypocalcemia. Synthetics: risk of renal injury, coagulopathy (dextran the most). Anaphylactic potential highest w dextran
Loss of DTR most likely from
Hypermagnesemia
Hypokalemia: presentation, ekg changes
Muscle cramps to weakness. Short pr, long qt, flat t wave, u wave
Hyperkalemia: presentation, ekg changes, tx
Cv rhythm changes. Early: long pt, t wave, peaked and short qt. Mid: flat p wave wide QRS. Late: QRS to sine wave to VF
Tx hyperkalemia
Ca, insulin and d50, hyperventilation, hco3, bicarb, albuterol, k wasting diuretics, dialysis
Hyponatremia: ex, presentation
Siadh, CHF, cirrhosis, turp syndrome, cushings. Nv, skel weakness, mental changes, sz, coma, cerebral edema
HypernatremiaL ex, CM
DI, impaired thirst, bicarb admin. Thirst, mental changes, sz, coma, cerebral dehydration
Hypercalcemia: when, causes, presentation, ekg
<8.5. Hypoparathyroidism, pancreatitis, sepsis. Cramps, parasthesia, chvostek and trousseaus, laryngospasm, sz. Long QT.
Hypercalcemia: when, causes, presentation, ekg, tx
> 10.5. Hyperparathyroid, cancer, thyrotoxicosis, thiazide diuretics. Nausea, abd pain, htn, psychosis. Short QTi. 0.9% nacl and loop diuretic
Hypomag: when, causes, ekg
<1.3. Etoh abuse, diuretics, hypokalemia. Skel weakness and arrhythmias. Dont change until v low then long qt.
Hypermag: when, presentation, ekg, tx
> 2.5. Renal failure or adrenal insuff. Lose DTR, then resp dep, then cv arrest. If v high then heart block. Cacl
Acidosis fx on other systems
Inc p50, dec contractility, inc sns tone, inc dysrhythmias, inc CBF and ICP, inc PVR, high k
Alkalosis negative fx
Dec p50, dec Coronary bf, inc dysrhythmias, dec cbf and ICP, dec PVR, low k and ca
How acute v chronic resp acidosis changes pac02 and ph
CO2 inc 10 in both. Ph dec 0.08 in acute, dec 0.03 in chronic
Most common causes of metabolic alkalosis
Vomiting and MTP
Anion gap acidosis: definition, etiology
<7.35 and gap >14. MUDPILES: methanol, uremia, DKA, paraldehyde, isoniazid, lactate, ethanol/ethylene glycol, salicylates
Non gap acidosis: definition and etiology
<7.35 but gap <14. Hardup: hypoaldosteronism, acetazolamide, renal tubular acidosis, diarrhea, ureterosigmoid fistula, pancreatic fistula. And large resusc w nacl sol
How much resp compensation changes paco2 per hco3 change
1-1.5 dec paco2 per hco3 decrease of 1
How paco2 changes for inc hco3
0.5-1 inc per 1 hco3 inc
Preop eras components
Fluid and carb loading, fasting 2 hr clea 6 hr solids, abx, no premeds, selective use of bowel prep, thromboprophylaxis
Intraop eras components
Mid thoracic epidural, short acting drugs, goal directed fluids, normothermia, ponv prophylaxis, not using surgical drains
Postop eras components
Mid thoracic epidural, opioid sparing, judicious fluids, ponv prophylaxis, not using NGT or OGT, encouraging gut motility, early oral intake, early Catheter removal and ambu Latino
Plt function inhibited by what 2 things
Prostaglandin I2 and NO
Which substance adheres plt to damaged vessel
VWF
Activated platelets release what, role of this
Adp and txa2 to activate nearby plt. Txa2 also vasoconstricts
Pneumonic for remembering 13 factors
Foolish people try climbing long slopes after Christmas some people have fallen
Factors 1-4
Fibrinogen, PT, TF, calcium
Factors 5-9
Labile factor, (no 6), stable factor, antihemophilic factor, Christmas factor
Factors 10-13
Stuart prower factor, plasma thromboplastin antecedent, hageman factor, fibrin stabilizing factor
Final common pathway factors
10, 5, 2, 1
Intrinsic factors
12, 11, 9, 8 (ptt)
Extrinsic pathway factors
Pt, 3, 7
When intrinsic v extrinsic pathways are activated
Extrinsic= coag initiated outside of intravascular space. Intrinsic= inside
Extrinsic pathway steps
Tissue trauma liberates TF (3) which activates extrinsic. TF activates 7. 7 activates 10 in presence of 4. Prothrombin activator and plts activate 2.
Factors specific to the intrinsic pathway
8 9 11 12
Steps of intrinsic pathway
Blood trauma, exposure to collagen activates 12. 12a activates 11. 11a activates 9. 9a and 8 activate 10.
Steps that are the same in both pathways
Prothrombin activator and tissue phospholipids activate thrombin, 2a
Where final common pathway begins
When prothrombin activator changes II to IIa (prothrombin to thrombin)
Mnemonic for final common pathway
Five and dime store for 1 or 2 dollars on the 13th of the month
Extrinsic pathway pneumonic, what it can be inhibited by, what its measured with
Can be bought for 37 cents. Inhib: Coumadin. Measure: pt and inr
Intrinsic pathway pneumonic, inhib by, measured by
If you cant buy it for 12$ you can buy it for 11.98. Inhib by heparin, measured by ptt and act
Which mechanisms limit the size of the clot q
Vasodilation to wash out adp and txa2. Antithrombin to inactivate thrombin. TF pathway inhibitor neutralizing TF. Protein c and s inhibiting factors II, V, and VIII
Methods of clot breakdown
Plasminogen converted by tpa or urokinase into plasmin. Fibrin cleaved by plasmin into FDPs
How fibrinolysis is turned off
Tpa inhib stops conversion of plasminogen into plasmin. Alpha 2 antiplasmin inhib action of plasmin on fibrin
What happens in coag cascade initiation phase
Factor 3 and 7 activate factor 10/final common pathway to make IIa/Thrombin.
What happens in amplification phase of coagulation
Small amt of thrombin amplifies response by activating plt, factor 5, and factor 11
What happens in coag propagation phase
Factor 10 avtiv by factor 4, 8, and 9 on plt surface. Positive feedback makes enough thrombin to activate fibrin
Aptt: which pathways, which drugs, normal
Intrinsic and common. Heparin (not LMWH). 25-32
Pt/inr: pathways, drug, nml
Extrinsic and common. Warfarin. 12-14
Bleeding time: monitors what, normal
Plt function. 2-10 min. Prolonged by asa and nsaids
Act: nml, CPB nml, when to measure
90-120 sec. >400. After 3 min then every 30 min after
TEG: R time- def, nml, problem area, tx
Time to begin clot formation, 6-8 min, coag factors, ffp
TEG: k time- def, nml, problem area, tx
Time until clot has achieved fixed strength. 3-7 min. Fibrinogen. Cryo
TEG: alpha angle - def, nml, problem area, tx
Speed of fibrin accum. 50 degrees. Fibrinogen. Cryo
TEG: max amplitude- def, nml, problem area, tx
Measures clot strength. 50mm. Plt. Plt or ddavp
TEG: amplitude after 60 min- def, nml, problem area, tx
Ma-5. Excess fibrinolysis. TXA or Aca
Act is affected by what
Hypothermia, thrombocytopenia, and deficiency of fibrinogen, factor 7, or factor 12
Protamine dose, SE
1mg per 100u of heparin in system. Hypotension, pulm htn, allergic rxn
What does warfarin inhibit
2, 7, 9, 10, and proteins c and s
Warfarin reversal for non emergent and emergent situations
Vit k 10-20 mg if non emergent. If emergent 1-2u FFP, factor 7a, or PT complex concentrate
Implications for giving vitamin k
Can be given po/I’m/iv. Try to avoid iv (anaphylaxis association). But if have to give slower then 1 mg/min
How txa and aca work
Plasminogen activation inhibitor (antifibrinolytic)
Types of vwf
1= mild reduction in amt. 2= vwf made doesnt work well. 3= severe reduction in amt
Lab changes in vwf
Increased ptt and bleeding Time
Desmopressin: moa, SE, works in which vwf
Type 1. Stim endog vwf and factor 8 activity. Hypotension
Vwf: which can treat all 3 types, tx for type 3
Cryo. Type 3: purified factor 8-vwf concentrate
Hemophilia a: deficiency of what, anesthesia implic, lab changes
Factor 8. Ptt prolonged in severe disease, only s;lightly in mild. Type and cross for any procedure. Factor 8 prior to surgery and after. Ffp and cryo can be used. Ddavp if only mild
Hemophilia b: deficiency of what anesthesia implic, lab changes
Factor 9. Prolonged ptt. Factor 9 concentrate.
Lab changes in dic
Inc pt and ptt, inc d dimer. Dec plt and fibrinogen
Dic supportive tx
Fluids. Ffp, plt, and cryo. IV heparin or LMWH
Antithrombin deficiency: pt implication, tx
Unresponsive to heparin. AT concentrate and ffp
Type I hit: patho, precip by, when, plt ct, morbidity, tx
Plt agg. After large heparin dose, 1-4d after. <100k. Minimal. Resolves spontaneously
Type 2 hit: patho, precip by, onset, plt ct, morbidity, tx
IgG attack factor 4 leading to plt agg. After any heparin dose 5-14d after. <50k.high risk of amputation or death.tx: dc heparin, give a direct thrombin inhibitor
Protein c and s deficiency: what it leads to, tx
Deficiency of either inc risk of thrombosis. Heparin to warfarin
Factor V Leiden mutation: what it leads to, tx
Resistance to anticoagulant effect of protein c. Anticoag only for pts with a clot.
Which blood type has no recipient rbc antigens, which has no recipient plasma antibodies
No rbc:O. No plasma: AB
Rh compatibility
RH pos can get pos or neg. Rh neg can only get neg
Rh implication w pregnancy
Rh neg mom w Rh pos fetus needs rhogam to not develop antibodies against it
Universal donors: rbc and plasma
Rbc O neg, plasma AB pos
Universal acceptors: rbc and plasma
Rbc Ab pos, plasma o neg
Diff b/w type, screen, crossmatch. Which takes longest
Type= abo and Rh d antigens. Screen= antibodies. Cross: actual blood. Type= 5 min, rest = 45 min
W acute bleed, most to least favorable typing options if no time for crossmatch
Type and partially crossmatched —> type specific uncrossmatched —> o neg uncrossmatched (only if not woman of childbearing age w no prev transfusion)
When ffp indicated
Pt or ptt >1.5x nml, acute warfarin reversal, at 3 def, mtp, dic, c1 esterase def
Cryo contains what
Fibrinogen, factors 8 and 13, vwf
Cryo indications
Fibrinogen <80, vwf disease, hemophilia
Blood vol: premie, neonate, infant, adult
100, 90, 80, 70 ml/kg
Acceptable blood loss calc
Ebv x (start - target hgb)/start hgb. Can also use hct
PRBCs: hct, what it raises levels by, why its stored in cold temp
70%, 2-3%, to slow rate of glycolysis
Consequences of rbc preservation
Dec 2,3 DBP/curve shifted left, anaerobic metab, dec ph, inc k, cant change shape, hemolysis, inc proinflammatory mediators
Leukoreduction reduces risk of what
Hla alloimmunization, febrile nonhemolytic rxns, cmv transmission
Washing blood does what
Removes remaining plasma and antigens (not rbc antigens). Prevents anaphylaxis if Iga deficient
Irradiation does what to blood
Prevents GVHD if immunocompromised. Good if leukemia, lymphoma, stem cell transplant, DI George syndrome
How a hemolytic rxn occurs from blood transfusion
Complement activated in recipients blood, plasma antibodies attack antigens on donor blood cell membranes
Results of acute hemolytic rxn
Renal failure, dic, and hypotension
S/s of acute hemolytic rxn: under anesthesia v masked by anes
Under: hemoglobinuria, hypotension, bleeding. Masked: fever, chills, chest pain, dyspnea, nausea, flushing
Treatment of acute hemolytic rxn
Stop transfusion. UOP to 100 ml/hr w fluids, mannitol, and last resort lasix. Sodium bicarb. Urine and hgb samples to lab. Check plt, pt, and fibrinogen. Send unused blood to blood bank.
What is trali and who is most at risk
Non cardiogenic pulm edema. Critically ill (sepsis, post burn, post CPB)
Trali caused by what within it, what contains highest conc of it
Hla and neutrophil antibodies in donor plasma. Ffp and plt
Donor groups most likely to give products that will cause trali
Multiparous women, hx blood transfusion or organ transplant
Trali dx
<6hrs after transfusion, bilateral infiltrates on cxr, pao2 <300 or spo2 <90 on rm air. Normal paop
Trali mgmt
Maximize peep, low tv, avoid overhydration
Taco: what it is
Vol overload from expanding plasma vol beyond compensatory ability
Taco s.s
Pulm edema, lv dysfunc, mitral regurg, inc paop, inc bnp
SE of mtp
Alkalosis, hypothermia, hgyperglycemia, hypocalcemia, hyperkalemia
Lethal triad in trauma
Acidosis, hypothermia, coagulopathy
When intraop blood salvage is indicated
Ebl >1l or 20% ebv. Cardiac, vascular, trauma, liver trans, or ortho sx. Jehovas or preex anemia
Contraindications to intraop blood salvage
Sickle cell, thalassemia, topical drugs in field like abx or chg, infected site, oncologic procedures
