9 Fluids Flashcards

(117 cards)

1
Q

Body water distrib

A

60/40/20(15/5). Water 60L. Intracellular (28l), extracellular (14), interstitial 11L, plasma 3

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2
Q

Major intracellular ions

A

K, mg, phosphate

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3
Q

Major extracellular ions

A

Na, ca, cl, hco3

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4
Q

Net filtration pressure

A

(Cap hydrostatic - interstitial oncotic) - (capillary oncotic - interstitial hydrostatic )

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5
Q

Osmolarity v osmolality

A

Osmolarity= osmoles per L of solvent. Osmolality= osmoles per kg of solvent

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6
Q

Nml plasma osmolarity. How to calc

A

280-290. 2NA + glu/18 + bun/2.8

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7
Q

Most imp determinant of osmolarity

A

Na

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8
Q

Ex of hypotonic solutions

A

D5w (253) and 0.45% NaCl 154

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9
Q

Isotonic solutions

A

LR, 0.9% NaCl, 5% albumin

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10
Q

Hypertonic solutions

A

3% nacl, d5 nacl 0.9%, d5 nacl 0.45%, d5lr, dextran 10

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11
Q

Side effect of albumin. Side effects of synthetic colloids

A

Albumin: hypocalcemia. Synthetics: risk of renal injury, coagulopathy (dextran the most). Anaphylactic potential highest w dextran

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12
Q

Loss of DTR most likely from

A

Hypermagnesemia

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13
Q

Hypokalemia: presentation, ekg changes

A

Muscle cramps to weakness. Short pr, long qt, flat t wave, u wave

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14
Q

Hyperkalemia: presentation, ekg changes, tx

A

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

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15
Q

Tx hyperkalemia

A

Ca, insulin and d50, hyperventilation, hco3, bicarb, albuterol, k wasting diuretics, dialysis

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16
Q

Hyponatremia: ex, presentation

A

Siadh, CHF, cirrhosis, turp syndrome, cushings. Nv, skel weakness, mental changes, sz, coma, cerebral edema

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17
Q

HypernatremiaL ex, CM

A

DI, impaired thirst, bicarb admin. Thirst, mental changes, sz, coma, cerebral dehydration

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18
Q

Hypercalcemia: when, causes, presentation, ekg

A

<8.5. Hypoparathyroidism, pancreatitis, sepsis. Cramps, parasthesia, chvostek and trousseaus, laryngospasm, sz. Long QT.

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19
Q

Hypercalcemia: when, causes, presentation, ekg, tx

A

> 10.5. Hyperparathyroid, cancer, thyrotoxicosis, thiazide diuretics. Nausea, abd pain, htn, psychosis. Short QTi. 0.9% nacl and loop diuretic

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20
Q

Hypomag: when, causes, ekg

A

<1.3. Etoh abuse, diuretics, hypokalemia. Skel weakness and arrhythmias. Dont change until v low then long qt.

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21
Q

Hypermag: when, presentation, ekg, tx

A

> 2.5. Renal failure or adrenal insuff. Lose DTR, then resp dep, then cv arrest. If v high then heart block. Cacl

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22
Q

Acidosis fx on other systems

A

Inc p50, dec contractility, inc sns tone, inc dysrhythmias, inc CBF and ICP, inc PVR, high k

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23
Q

Alkalosis negative fx

A

Dec p50, dec Coronary bf, inc dysrhythmias, dec cbf and ICP, dec PVR, low k and ca

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24
Q

How acute v chronic resp acidosis changes pac02 and ph

A

CO2 inc 10 in both. Ph dec 0.08 in acute, dec 0.03 in chronic

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25
Most common causes of metabolic alkalosis
Vomiting and MTP
26
Anion gap acidosis: definition, etiology
<7.35 and gap >14. MUDPILES: methanol, uremia, DKA, paraldehyde, isoniazid, lactate, ethanol/ethylene glycol, salicylates
27
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
28
How much resp compensation changes paco2 per hco3 change
1-1.5 dec paco2 per hco3 decrease of 1
29
How paco2 changes for inc hco3
0.5-1 inc per 1 hco3 inc
30
Preop eras components
Fluid and carb loading, fasting 2 hr clea 6 hr solids, abx, no premeds, selective use of bowel prep, thromboprophylaxis
31
Intraop eras components
Mid thoracic epidural, short acting drugs, goal directed fluids, normothermia, ponv prophylaxis, not using surgical drains
32
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
33
Plt function inhibited by what 2 things
Prostaglandin I2 and NO
34
Which substance adheres plt to damaged vessel
VWF
35
Activated platelets release what, role of this
Adp and txa2 to activate nearby plt. Txa2 also vasoconstricts
36
Pneumonic for remembering 13 factors
Foolish people try climbing long slopes after Christmas some people have fallen
37
Factors 1-4
Fibrinogen, PT, TF, calcium
38
Factors 5-9
Labile factor, (no 6), stable factor, antihemophilic factor, Christmas factor
39
Factors 10-13
Stuart prower factor, plasma thromboplastin antecedent, hageman factor, fibrin stabilizing factor
40
Final common pathway factors
10, 5, 2, 1
41
Intrinsic factors
12, 11, 9, 8 (ptt)
42
Extrinsic pathway factors
Pt, 3, 7
43
When intrinsic v extrinsic pathways are activated
Extrinsic= coag initiated outside of intravascular space. Intrinsic= inside
44
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.
45
Factors specific to the intrinsic pathway
8 9 11 12
46
Steps of intrinsic pathway
Blood trauma, exposure to collagen activates 12. 12a activates 11. 11a activates 9. 9a and 8 activate 10.
47
Steps that are the same in both pathways
Prothrombin activator and tissue phospholipids activate thrombin, 2a
48
Where final common pathway begins
When prothrombin activator changes II to IIa (prothrombin to thrombin)
49
Mnemonic for final common pathway
Five and dime store for 1 or 2 dollars on the 13th of the month
50
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
51
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
52
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
53
Methods of clot breakdown
Plasminogen converted by tpa or urokinase into plasmin. Fibrin cleaved by plasmin into FDPs
54
How fibrinolysis is turned off
Tpa inhib stops conversion of plasminogen into plasmin. Alpha 2 antiplasmin inhib action of plasmin on fibrin
55
What happens in coag cascade initiation phase
Factor 3 and 7 activate factor 10/final common pathway to make IIa/Thrombin.
56
What happens in amplification phase of coagulation
Small amt of thrombin amplifies response by activating plt, factor 5, and factor 11
57
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
58
Aptt: which pathways, which drugs, normal
Intrinsic and common. Heparin (not LMWH). 25-32
59
Pt/inr: pathways, drug, nml
Extrinsic and common. Warfarin. 12-14
60
Bleeding time: monitors what, normal
Plt function. 2-10 min. Prolonged by asa and nsaids
61
Act: nml, CPB nml, when to measure
90-120 sec. >400. After 3 min then every 30 min after
62
TEG: R time- def, nml, problem area, tx
Time to begin clot formation, 6-8 min, coag factors, ffp
63
TEG: k time- def, nml, problem area, tx
Time until clot has achieved fixed strength. 3-7 min. Fibrinogen. Cryo
64
TEG: alpha angle - def, nml, problem area, tx
Speed of fibrin accum. 50 degrees. Fibrinogen. Cryo
65
TEG: max amplitude- def, nml, problem area, tx
Measures clot strength. 50mm. Plt. Plt or ddavp
66
TEG: amplitude after 60 min- def, nml, problem area, tx
Ma-5. Excess fibrinolysis. TXA or Aca
67
Act is affected by what
Hypothermia, thrombocytopenia, and deficiency of fibrinogen, factor 7, or factor 12
68
Protamine dose, SE
1mg per 100u of heparin in system. Hypotension, pulm htn, allergic rxn
69
What does warfarin inhibit
2, 7, 9, 10, and proteins c and s
70
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
71
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
72
How txa and aca work
Plasminogen activation inhibitor (antifibrinolytic)
73
Types of vwf
1= mild reduction in amt. 2= vwf made doesnt work well. 3= severe reduction in amt
74
Lab changes in vwf
Increased ptt and bleeding Time
75
Desmopressin: moa, SE, works in which vwf
Type 1. Stim endog vwf and factor 8 activity. Hypotension
76
Vwf: which can treat all 3 types, tx for type 3
Cryo. Type 3: purified factor 8-vwf concentrate
77
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
78
Hemophilia b: deficiency of what anesthesia implic, lab changes
Factor 9. Prolonged ptt. Factor 9 concentrate.
79
Lab changes in dic
Inc pt and ptt, inc d dimer. Dec plt and fibrinogen
80
Dic supportive tx
Fluids. Ffp, plt, and cryo. IV heparin or LMWH
81
Antithrombin deficiency: pt implication, tx
Unresponsive to heparin. AT concentrate and ffp
82
Type I hit: patho, precip by, when, plt ct, morbidity, tx
Plt agg. After large heparin dose, 1-4d after. <100k. Minimal. Resolves spontaneously
83
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
84
Protein c and s deficiency: what it leads to, tx
Deficiency of either inc risk of thrombosis. Heparin to warfarin
85
Factor V Leiden mutation: what it leads to, tx
Resistance to anticoagulant effect of protein c. Anticoag only for pts with a clot.
86
Which blood type has no recipient rbc antigens, which has no recipient plasma antibodies
No rbc:O. No plasma: AB
87
Rh compatibility
RH pos can get pos or neg. Rh neg can only get neg
88
Rh implication w pregnancy
Rh neg mom w Rh pos fetus needs rhogam to not develop antibodies against it
89
Universal donors: rbc and plasma
Rbc O neg, plasma AB pos
90
Universal acceptors: rbc and plasma
Rbc Ab pos, plasma o neg
91
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
92
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)
93
When ffp indicated
Pt or ptt >1.5x nml, acute warfarin reversal, at 3 def, mtp, dic, c1 esterase def
94
Cryo contains what
Fibrinogen, factors 8 and 13, vwf
95
Cryo indications
Fibrinogen <80, vwf disease, hemophilia
96
Blood vol: premie, neonate, infant, adult
100, 90, 80, 70 ml/kg
97
Acceptable blood loss calc
Ebv x (start - target hgb)/start hgb. Can also use hct
98
PRBCs: hct, what it raises levels by, why its stored in cold temp
70%, 2-3%, to slow rate of glycolysis
99
Consequences of rbc preservation
Dec 2,3 DBP/curve shifted left, anaerobic metab, dec ph, inc k, cant change shape, hemolysis, inc proinflammatory mediators
100
Leukoreduction reduces risk of what
Hla alloimmunization, febrile nonhemolytic rxns, cmv transmission
101
Washing blood does what
Removes remaining plasma and antigens (not rbc antigens). Prevents anaphylaxis if Iga deficient
102
Irradiation does what to blood
Prevents GVHD if immunocompromised. Good if leukemia, lymphoma, stem cell transplant, DI George syndrome
103
How a hemolytic rxn occurs from blood transfusion
Complement activated in recipients blood, plasma antibodies attack antigens on donor blood cell membranes
104
Results of acute hemolytic rxn
Renal failure, dic, and hypotension
105
S/s of acute hemolytic rxn: under anesthesia v masked by anes
Under: hemoglobinuria, hypotension, bleeding. Masked: fever, chills, chest pain, dyspnea, nausea, flushing
106
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.
107
What is trali and who is most at risk
Non cardiogenic pulm edema. Critically ill (sepsis, post burn, post CPB)
108
Trali caused by what within it, what contains highest conc of it
Hla and neutrophil antibodies in donor plasma. Ffp and plt
109
Donor groups most likely to give products that will cause trali
Multiparous women, hx blood transfusion or organ transplant
110
Trali dx
<6hrs after transfusion, bilateral infiltrates on cxr, pao2 <300 or spo2 <90 on rm air. Normal paop
111
Trali mgmt
Maximize peep, low tv, avoid overhydration
112
Taco: what it is
Vol overload from expanding plasma vol beyond compensatory ability
113
Taco s.s
Pulm edema, lv dysfunc, mitral regurg, inc paop, inc bnp
114
SE of mtp
Alkalosis, hypothermia, hgyperglycemia, hypocalcemia, hyperkalemia
115
Lethal triad in trauma
Acidosis, hypothermia, coagulopathy
116
When intraop blood salvage is indicated
Ebl >1l or 20% ebv. Cardiac, vascular, trauma, liver trans, or ortho sx. Jehovas or preex anemia
117
Contraindications to intraop blood salvage
Sickle cell, thalassemia, topical drugs in field like abx or chg, infected site, oncologic procedures