Fluids, Blood, Acid Base Flashcards
Difference between gap and non gap metabolic acidosis
Gap = accumulation of H+ (acid gain)
→ ketoacidosis, lactic acidosis, renal failure, methanol, uremia, paraldehyde, isoniazid, salicylates
Non-gap = Loss of HC03 (bicarbonate loss) OR chloride gain
→ diarrhea, renal tubular acidosis, hypoaldosteronism, fistula, acetazolamide, excessive NS admin (excessive Cl- pushes too much HC03 out of kidneys
Major intracellular ions
K+
Mg2+
P04 (2-)
Major extracellular ions
Na+, Ca2+, Cl-, HC03-
FFP
-ALL coag factors + fibrinogen, plasma proteins
INDICATIONS: warfarin reversal, coagulopathy, AT III deficiency, massive transfusion, DIC, C1 esterase deficiency (hereditary angioedema)
Cryoprecipitate
-Fibrinogen, Factor 8, Factor 13, vWF
INDICATIONS: Fibrinogen deficiency, Hemophilia A+B, vWB disease all types
Desmopressin (DDaAVP)
Synthetic analogue of ADH
- Stimulates endogenous release of vWF
- ↑ Factor 8 activity
Dose 0.3-0.5mcg/kg IV
INDICATIONS: vWB Disease (Type 1>Type 2), mild to moderate Hemophilia A
Appropriate treatments for Hemophilia A
What will labs show
All must restore Factor 8.
-FFP, Cryo, Factor 8 Concentrate, Recombitant Factor 7
PTT prolonged, normal PT
Appropriate treatments for Hemophilia B
What will lab values show
If severe, factor 9-prothrombin concentrate, but it has serious thromboembolic risks
Prolonged PTT, normal PT
Appropriate treatments for von Willebrand’s disease
Desmopressin 0.3 mcg/kg (works well for type 1, ok for type 2, doesn’t for type 3)
Cryo (can be used for all types)
Purified VIII-vWF concentrate for type III
Maximum ABL
EBV x [(Start Hct - allowed Hct)/Start Hct]
Change of Hgb/Hct one can expect with PRBC admin
How do you guesstimate Hct from Hgb?
-For each 1 unit PRBC given….
——Hgb should ↑ 1g/dL
——Hct should ↑ 2-3%
-Hgb can be estimated as 1/3 of Hct
Signs of hypercalcemia, TX
HTN Shortened QT Hypotonia Kidney stones Polyuria Dehydration Bone pain NV ABD pain, pancreatitis Cognitive dysfunction
TX: 0.9%NS and LOOP diuretic
Which hematocrit level (high) is a threat to life
60% → impaired organ perfusion
Warfarin reversal options
Non urgent: Phytonadione
Urgent: FFP, Recombitant Factor 7, prothrombin complex concentrate
Reversal agent for dabigatran (Pradaxa)
Idarucizumab
Determinants of plasma osmolarity
Sodium, glucose, BUN
280-290mOsm/L
Sodium is most important determinant
Hyperglycemia and uremia can ↑
Presentation of hypermagnesemia
Loss of deep tendon reflex = 10mg/dL or 4mEq/L
Resp depression = >18mg/dL or 6.5mEq/L
Cardiac arrest =>25mg/dL or 10 mEq/L
Where are platelets formed? Where are they metabolized?
- formed by megakaryocytes in bone marrow
- cleared by macrophages in the reticuloendothelial system and spleen
What does injured tissue initially express to attract platelets?
Tissue factor and vWF
12 factors
1 Fibrinogen 2 Prothrombin 3 Tissue factor 4 Calcium 5 Labile factor 7 Stable factor 8 Anti Hemophilic Factor 9 Christmas factor 10Stuart-Prower factor 11 Plasma thromboplastin antecedent 12 Hageman factor 13 Fibrin stabilizing factor
Extrinsic pathway
3, 7
Activated by vascular injury (tissue factor release)
Fast, only about 15 seconds
Measured by PT/INR
Inhibited by Coumadin
Intrinsic pathway
8, 9, 11, 12
Activated by blood injury or exposure to collagen
Measured by PTT and ACT
Longer, about 6 mins
(Not 11.98, but 12)
Inhibited by heparin
Final common pathway
1, 2, 5, 10, 13
Think of dollar denominations
Describe fibrinolysis
Plasminogen is a proenzyme synthesized by liver.
(TPA/urokinase) turns plasminogen into plasmin, which is a proteolytic enzyme that degrades fibrin into FDP
Heparin MOA
Inhibits intrinsic and final common pathways
ATIII is a naturally occurring anticoagulant that circulates in plasma but heparin binds to it and makes it 1000x more powerful
Normal ACT
90-120 seconds
Should be >400 seconds before CPB
Heparin and protamine CPB doses
Heparin =300-400units/kg
Protamine = 1mg for q 100 u heparin predicted to be in circulation
Reasons for hypercalcemia
Cancer, Hyperparathyroidism, Thyrotoxicosis, Thiazide diuretics, immobilization
TX: loop diuretics, NS.
N/V, ABD pain, mental status change, HTN, shortening QT
Reasons for hyponatremia
Cushing’s, SIADH, CHF, cirrhosis, TURP syndrome
Platelet membrane glycoproteins
Repelled by healthy endothelium, attach to injury
- GpIb → platelet to vWF
- GpIIb-IIIa complex → links platelets together
Possible SE of protamine
Hypotension (histamine release, give >5 mins) Pulmonary HTN (TxA2 and serotonin release) Allergic RXN (fish allergy, vasectomy, previous NPH insulin use)
ADP receptor inhibitors and when to stop before procedure
Plavix 7 days
Ticlodipine 14 days
Prasugrel 3 days
Ticagrelor 2 days
GIIB/IIIa receptor antagonists
Abciximab 3 days
Eptifibatide 1 day
Tirofiban 1 day
Thrombin inhibitors
Hirudin
Argatroban
Bivalirudin
All <8 hr stop time before surgery
Pts who have antithrombin III deficiency who are heparin non responders or who have HIT get these drugs
Factor X inhibitor
Fondaparinux
Stop 4 days before surgery
Lab values seen with vWF disease
↑ bleeding time, PTT
Others normal
Labs seen with DIC
↑ PT/PTT
↑ d-dimer
↓ platelets
↓ fibrinogen
Eccymosis, petechaie, mucosal bleeding, can happen in OB
Patients at risk for DIC
Sepsis
OB (preeclampsia, placental abruption, AFE)
Malignancy (↑ risk: adenocarcinoma, leukemia, lymphoma)
TX: IVF, FFP, platelets, Cryo, heparin or lovenox for severe microvascular thrombosis
Universal acceptors
AB blood can accept all types
Plasma O negative
O has no erythrocyte antibodies because it doesn’t have A or B in it so it can go anywhere
Universal donors
Blood O
Plasma AB +
Because 85% of the population is Rh-positive, O+ can be used as emergent in acute bleed if the patient is not a woman of child bearing age and has not received a prior transfusion
What Rhogam does
Prevents Rh-negative mom from being sensitized against Rh-positive fetus, if this didn’t happen a subsequent pregnancy could trigger erythroblastosis fetalis
Most common infectious complication of transfusion
CMV, leukoreduction greatly ↓ risk so anyone immunocompromised should get leukoreduced blood
CMV > Hep B > Hep C > HIV
Most common cause of transfusion related mortality in US
TRALI
Critically ill, sepsis, burns, post CPB at high risk
