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Apex Pt 2 > 9 Fluids > Flashcards

9 Fluids Flashcards

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
Q

Most common causes of metabolic alkalosis

A

Vomiting and MTP

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26
Q

Anion gap acidosis: definition, etiology

A

<7.35 and gap >14. MUDPILES: methanol, uremia, DKA, paraldehyde, isoniazid, lactate, ethanol/ethylene glycol, salicylates

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27
Q

Non gap acidosis: definition and etiology

A

<7.35 but gap <14. Hardup: hypoaldosteronism, acetazolamide, renal tubular acidosis, diarrhea, ureterosigmoid fistula, pancreatic fistula. And large resusc w nacl sol

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28
Q

How much resp compensation changes paco2 per hco3 change

A

1-1.5 dec paco2 per hco3 decrease of 1

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29
Q

How paco2 changes for inc hco3

A

0.5-1 inc per 1 hco3 inc

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30
Q

Preop eras components

A

Fluid and carb loading, fasting 2 hr clea 6 hr solids, abx, no premeds, selective use of bowel prep, thromboprophylaxis

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31
Q

Intraop eras components

A

Mid thoracic epidural, short acting drugs, goal directed fluids, normothermia, ponv prophylaxis, not using surgical drains

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32
Q

Postop eras components

A

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

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33
Q

Plt function inhibited by what 2 things

A

Prostaglandin I2 and NO

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34
Q

Which substance adheres plt to damaged vessel

A

VWF

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35
Q

Activated platelets release what, role of this

A

Adp and txa2 to activate nearby plt. Txa2 also vasoconstricts

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36
Q

Pneumonic for remembering 13 factors

A

Foolish people try climbing long slopes after Christmas some people have fallen

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37
Q

Factors 1-4

A

Fibrinogen, PT, TF, calcium

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38
Q

Factors 5-9

A

Labile factor, (no 6), stable factor, antihemophilic factor, Christmas factor

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39
Q

Factors 10-13

A

Stuart prower factor, plasma thromboplastin antecedent, hageman factor, fibrin stabilizing factor

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40
Q

Final common pathway factors

A

10, 5, 2, 1

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41
Q

Intrinsic factors

A

12, 11, 9, 8 (ptt)

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42
Q

Extrinsic pathway factors

A

Pt, 3, 7

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43
Q

When intrinsic v extrinsic pathways are activated

A

Extrinsic= coag initiated outside of intravascular space. Intrinsic= inside

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44
Q

Extrinsic pathway steps

A

Tissue trauma liberates TF (3) which activates extrinsic. TF activates 7. 7 activates 10 in presence of 4. Prothrombin activator and plts activate 2.

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45
Q

Factors specific to the intrinsic pathway

A

8 9 11 12

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46
Q

Steps of intrinsic pathway

A

Blood trauma, exposure to collagen activates 12. 12a activates 11. 11a activates 9. 9a and 8 activate 10.

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47
Q

Steps that are the same in both pathways

A

Prothrombin activator and tissue phospholipids activate thrombin, 2a

48
Q

Where final common pathway begins

A

When prothrombin activator changes II to IIa (prothrombin to thrombin)

49
Q

Mnemonic for final common pathway

A

Five and dime store for 1 or 2 dollars on the 13th of the month

50
Q

Extrinsic pathway pneumonic, what it can be inhibited by, what its measured with

A

Can be bought for 37 cents. Inhib: Coumadin. Measure: pt and inr

51
Q

Intrinsic pathway pneumonic, inhib by, measured by

A

If you cant buy it for 12$ you can buy it for 11.98. Inhib by heparin, measured by ptt and act

52
Q

Which mechanisms limit the size of the clot q

A

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
Q

Methods of clot breakdown

A

Plasminogen converted by tpa or urokinase into plasmin. Fibrin cleaved by plasmin into FDPs

54
Q

How fibrinolysis is turned off

A

Tpa inhib stops conversion of plasminogen into plasmin. Alpha 2 antiplasmin inhib action of plasmin on fibrin

55
Q

What happens in coag cascade initiation phase

A

Factor 3 and 7 activate factor 10/final common pathway to make IIa/Thrombin.

56
Q

What happens in amplification phase of coagulation

A

Small amt of thrombin amplifies response by activating plt, factor 5, and factor 11

57
Q

What happens in coag propagation phase

A

Factor 10 avtiv by factor 4, 8, and 9 on plt surface. Positive feedback makes enough thrombin to activate fibrin

58
Q

Aptt: which pathways, which drugs, normal

A

Intrinsic and common. Heparin (not LMWH). 25-32

59
Q

Pt/inr: pathways, drug, nml

A

Extrinsic and common. Warfarin. 12-14

60
Q

Bleeding time: monitors what, normal

A

Plt function. 2-10 min. Prolonged by asa and nsaids

61
Q

Act: nml, CPB nml, when to measure

A

90-120 sec. >400. After 3 min then every 30 min after

62
Q

TEG: R time- def, nml, problem area, tx

A

Time to begin clot formation, 6-8 min, coag factors, ffp

63
Q

TEG: k time- def, nml, problem area, tx

A

Time until clot has achieved fixed strength. 3-7 min. Fibrinogen. Cryo

64
Q

TEG: alpha angle - def, nml, problem area, tx

A

Speed of fibrin accum. 50 degrees. Fibrinogen. Cryo

65
Q

TEG: max amplitude- def, nml, problem area, tx

A

Measures clot strength. 50mm. Plt. Plt or ddavp

66
Q

TEG: amplitude after 60 min- def, nml, problem area, tx

A

Ma-5. Excess fibrinolysis. TXA or Aca

67
Q

Act is affected by what

A

Hypothermia, thrombocytopenia, and deficiency of fibrinogen, factor 7, or factor 12

68
Q

Protamine dose, SE

A

1mg per 100u of heparin in system. Hypotension, pulm htn, allergic rxn

69
Q

What does warfarin inhibit

A

2, 7, 9, 10, and proteins c and s

70
Q

Warfarin reversal for non emergent and emergent situations

A

Vit k 10-20 mg if non emergent. If emergent 1-2u FFP, factor 7a, or PT complex concentrate

71
Q

Implications for giving vitamin k

A

Can be given po/I’m/iv. Try to avoid iv (anaphylaxis association). But if have to give slower then 1 mg/min

72
Q

How txa and aca work

A

Plasminogen activation inhibitor (antifibrinolytic)

73
Q

Types of vwf

A

1= mild reduction in amt. 2= vwf made doesnt work well. 3= severe reduction in amt

74
Q

Lab changes in vwf

A

Increased ptt and bleeding Time

75
Q

Desmopressin: moa, SE, works in which vwf

A

Type 1. Stim endog vwf and factor 8 activity. Hypotension

76
Q

Vwf: which can treat all 3 types, tx for type 3

A

Cryo. Type 3: purified factor 8-vwf concentrate

77
Q

Hemophilia a: deficiency of what, anesthesia implic, lab changes

A

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
Q

Hemophilia b: deficiency of what anesthesia implic, lab changes

A

Factor 9. Prolonged ptt. Factor 9 concentrate.

79
Q

Lab changes in dic

A

Inc pt and ptt, inc d dimer. Dec plt and fibrinogen

80
Q

Dic supportive tx

A

Fluids. Ffp, plt, and cryo. IV heparin or LMWH

81
Q

Antithrombin deficiency: pt implication, tx

A

Unresponsive to heparin. AT concentrate and ffp

82
Q

Type I hit: patho, precip by, when, plt ct, morbidity, tx

A

Plt agg. After large heparin dose, 1-4d after. <100k. Minimal. Resolves spontaneously

83
Q

Type 2 hit: patho, precip by, onset, plt ct, morbidity, tx

A

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
Q

Protein c and s deficiency: what it leads to, tx

A

Deficiency of either inc risk of thrombosis. Heparin to warfarin

85
Q

Factor V Leiden mutation: what it leads to, tx

A

Resistance to anticoagulant effect of protein c. Anticoag only for pts with a clot.

86
Q

Which blood type has no recipient rbc antigens, which has no recipient plasma antibodies

A

No rbc:O. No plasma: AB

87
Q

Rh compatibility

A

RH pos can get pos or neg. Rh neg can only get neg

88
Q

Rh implication w pregnancy

A

Rh neg mom w Rh pos fetus needs rhogam to not develop antibodies against it

89
Q

Universal donors: rbc and plasma

A

Rbc O neg, plasma AB pos

90
Q

Universal acceptors: rbc and plasma

A

Rbc Ab pos, plasma o neg

91
Q

Diff b/w type, screen, crossmatch. Which takes longest

A

Type= abo and Rh d antigens. Screen= antibodies. Cross: actual blood. Type= 5 min, rest = 45 min

92
Q

W acute bleed, most to least favorable typing options if no time for crossmatch

A

Type and partially crossmatched —> type specific uncrossmatched —> o neg uncrossmatched (only if not woman of childbearing age w no prev transfusion)

93
Q

When ffp indicated

A

Pt or ptt >1.5x nml, acute warfarin reversal, at 3 def, mtp, dic, c1 esterase def

94
Q

Cryo contains what

A

Fibrinogen, factors 8 and 13, vwf

95
Q

Cryo indications

A

Fibrinogen <80, vwf disease, hemophilia

96
Q

Blood vol: premie, neonate, infant, adult

A

100, 90, 80, 70 ml/kg

97
Q

Acceptable blood loss calc

A

Ebv x (start - target hgb)/start hgb. Can also use hct

98
Q

PRBCs: hct, what it raises levels by, why its stored in cold temp

A

70%, 2-3%, to slow rate of glycolysis

99
Q

Consequences of rbc preservation

A

Dec 2,3 DBP/curve shifted left, anaerobic metab, dec ph, inc k, cant change shape, hemolysis, inc proinflammatory mediators

100
Q

Leukoreduction reduces risk of what

A

Hla alloimmunization, febrile nonhemolytic rxns, cmv transmission

101
Q

Washing blood does what

A

Removes remaining plasma and antigens (not rbc antigens). Prevents anaphylaxis if Iga deficient

102
Q

Irradiation does what to blood

A

Prevents GVHD if immunocompromised. Good if leukemia, lymphoma, stem cell transplant, DI George syndrome

103
Q

How a hemolytic rxn occurs from blood transfusion

A

Complement activated in recipients blood, plasma antibodies attack antigens on donor blood cell membranes

104
Q

Results of acute hemolytic rxn

A

Renal failure, dic, and hypotension

105
Q

S/s of acute hemolytic rxn: under anesthesia v masked by anes

A

Under: hemoglobinuria, hypotension, bleeding. Masked: fever, chills, chest pain, dyspnea, nausea, flushing

106
Q

Treatment of acute hemolytic rxn

A

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
Q

What is trali and who is most at risk

A

Non cardiogenic pulm edema. Critically ill (sepsis, post burn, post CPB)

108
Q

Trali caused by what within it, what contains highest conc of it

A

Hla and neutrophil antibodies in donor plasma. Ffp and plt

109
Q

Donor groups most likely to give products that will cause trali

A

Multiparous women, hx blood transfusion or organ transplant

110
Q

Trali dx

A

<6hrs after transfusion, bilateral infiltrates on cxr, pao2 <300 or spo2 <90 on rm air. Normal paop

111
Q

Trali mgmt

A

Maximize peep, low tv, avoid overhydration

112
Q

Taco: what it is

A

Vol overload from expanding plasma vol beyond compensatory ability

113
Q

Taco s.s

A

Pulm edema, lv dysfunc, mitral regurg, inc paop, inc bnp

114
Q

SE of mtp

A

Alkalosis, hypothermia, hgyperglycemia, hypocalcemia, hyperkalemia

115
Q

Lethal triad in trauma

A

Acidosis, hypothermia, coagulopathy

116
Q

When intraop blood salvage is indicated

A

Ebl >1l or 20% ebv. Cardiac, vascular, trauma, liver trans, or ortho sx. Jehovas or preex anemia

117
Q

Contraindications to intraop blood salvage

A

Sickle cell, thalassemia, topical drugs in field like abx or chg, infected site, oncologic procedures

Apex Pt 2 (5 decks)

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