• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/88

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

88 Cards in this Set

  • Front
  • Back
INTRA-OP GOAL URINE OUTPUT
0.5 - 1 cc/kg/hr
change in urine output does not occur until 20% of blood is lost
ICF
2/3 of body water
40% of weight
primarily K+ organic anions and proteins
EQUATION FOR TOTAL BODY WATER DEFICIT
TBW (L) = (WT in kg X % water)
TBW males = 60%
TBW females = 50%
TBW infants = 80%
HYPONATREMIA
Na+ req. (mmol) =
Na+ req. (mmol) = TBW x (desired Na+ - serum Na+)
RATE OF INFUSION FOR SODIUM REPLACEMENT
Rate of Infusion (Na+) cc/hr = Na+ req. (mmol) x 1000 / infusate Na+ (mmol/L) x time (hrs)
EFFECTS OF K+ AND CA++
K+ effects resting membrane potential
Ca++ determines threshold potential
HYPERNATREMIA
-secondary to lack of water (not too much salt)
-Hallmark sign - peripheral edema
-Tx crystalloids
HYPONATREMIA
Neurologic systems occur below 120 mEQ/L
- associated with alcoholism, liver failure, severe burns, hemodialysis, and sepsis
(COMA SEIZURES, H/A, CEREBRAL EDEMA, N/V, CRAMPS, AND WEAKNESS)
TYPE OF HYPOTONIC HYPONATREMIA
(SERUM OSMO < 280)
HYPOVOLEMIC HYPONATREMIA
causes - diuretics, ketonuria, 3rd spacing, adrenal insufficiency, and N/V.
HYPOTONIC HYPONATREMIA
^ water in serum (hypotonic) --> decrease in osmolarity < 280 --> decrease in solutes in serum (decrease in osmo b/c of dilution) -->
PSEUDOHYPONATREMIA
A.K.A. isotonic hyponatremia
osmo 280-285
causes- hyperlipidemia, hyperproteinemia, infusion of ISOTONIC non electrolytes
ex- glucose, mannitol, and glycine
HYPOVOLEMIC HYPONATREMIA
-decrease in TBW and Na+ with a relatively greater decrease in Na+
-causes- diuretics, ketonuria, 3rd spacing, adrenal insufficiency, and N/V
TX- 0.9%NS regardless whether Urine Na+ >20 or < 10
ISOTONIC HYPONATREMIA
Increase in TBW with a near normal total body Na+
-causes- diuretics, barbs, adrenal insufficiency, hypothyroid, SIADH, increase in uptake of fluids, ESRD, and ARF
TX Urine Na+ >20 treat with water restriction
Urine Na+ <10 tx with hypertonic saline, fluid restriction, -/+ loop diuretic
HYPERVOLEMIC HYPONATREMIA
Increase in Na+ with a relatively greater increase in TBW
-causes- nephrotic syndrome, CHF, and cirrhosis
treatment with Sodium and Water restriction, diuretics
HYPONATREMIA CORRECTION
-rapid causes demyelinating lesions in brain (pontine myelonitis)
-mild sx 0.5mEQ/L/Hr
-mod sx 1 mEQ/L/Hr
-severe sx 1.5 mEQ/L/Hr
SEVERE HYPONATREMIA WITH SX AND SEIZURES
3% hypertonic saline
-fluid restriction
-furosemide
correction to Na+ > 130 safe for GA
HYPERKALEMIA EFFECTS
-prolonged PR interval
-widening QRS complex
-peaked T wave
ACUTE HYPERKALEMIA... WHAT HAPPENS AND HOW DO YOU TREAT?
-resting membrane potential is less neg
-cell depolarizes and resting potential moves TOWARD threshold
-paralysis, and EKG changes
-TX sodium bicarb (~50mEQ promotes cellular uptake of K w/in 15 min, beta agonists, glucose 30-50 gm + 10 units of insulin --> can take up to an hour, hyperventilation, hemodialysis
ACUTE HYPOKALEMIA... WHAT HAPPENS AND HOW DO YOU TREAT?
-resting membrane potential becomes MORE neg
-cell hyperpolarizes, RMP moves away from threshold
-cell becomes more excitable, harder to reach threshold
-palpitations, cramping, parasthesias, hallucinations
-
NMBD AND HYPOKALEMIA?
NMBD should be reduced 25-50% since hypokalemia causes increased sensitivity
HYPOCALCEMIA
-skeletal muscle spasm including laryngospasm
-decreased myocardial contractility
-***avoid hyperventilation
0.1 decrease in arterial pH can increase ionized Ca <> by 0.16 mg/dL
ACUTE HYPOCALCEMIA
-increase in nerve and muscle excitability
-tingling in lips and hands due to increasing of firing
-twitches and tetany
-parathyroidectomy- tetany laryngospasm
-hyperventilation
-prolonged QT interval and t wave inversion
-trousseaus's and chvosteks sign
TX OF ACUTE HYPOCALCEMIA
-symptomatic hypoCa is a true medical emergency
-CaCl2 300-500 mg or cal gluconate 100 - 200 mg
-check a Mg and consider giving 1 gm
HYPERCALCEMIA
-causes- hyperparathyroidism, malignancy (bone), renal failure, thiazide diuretics, excess Ca
- signs- HTN, dysrhythmias, shortened QT, sedation, polyuria, anorexia, pancreatitis
ACUTE HYPERCALCEMIA
-threshold potential shift away from resting potential
-threshold becomes less neg
-cells become less excitable
-excessive urination, constipation, renal failure, death
TX - rehydration with NS followed by brisk diuresis with LOOP diuretic to accelerate Ca excretion
HYPOMAG
causes- starvation, chronic alcohol, diarrhea, insulin
-chosvteks, trouseaus, cardiac changes simlar to hypo Ca.
TREATMENT FOR HYPER MG
-rehydration with D5 1/2 NS and loop diuretic
-monitor for vasodilation and negative inotropic effects
-decrease NMBD by 25-50%
PROLONGED FASTING CAN CONTRIBUTE TO ...?
hypoglycemia, hypovolemia, and anxiety
PEDIATRIC NPO GUIDELINES
-up to 2 hours pre-op can have clear liquids
-breast milk up to 4 hours pre op
-formula, nonhuman milk, light meal up to 6 hours pre op
-full meal carbonated bev up to 8 hours pre op
-
NPO DEFECIT
# hours NPO x Hourly maintenance
give 50% first hour
give 25% second hour
give 25% third hour
TYPICAL DAILY OUTPUT
Urine 1500 ml
insensible/ evaporation 800ml
(resp 400ml, skin 400ml)
sweat glands 100ml
stool 100ml
INTRA-OP FLUID SHIFTS
fluid shift into 3rd space
-small incision/ minimal trauma 2-4 cc/kg/hr
-mod incision/ mod trauma 4-6
-large incision/ large trauma 6-8
-major vascular case 8-10
CRYSTALLOIDS
-contain electrolytes dissolved in water or dextrose in water
-isotonic- 0.9% NS, LR
-NS contains more Cl than ECF
COLLOIDS
-natural or synthetic molecules, impermeable to vascular membrane
-determine the colloid osmotic pressure that balances the distribution of water b/t intravascular and interstitial spaces
-albumin, 6% hydroxyethyl starch (hespan, hextend)
IV FLUIDS
-NaCl 0.9%- renal patients, blood admin
-Plasmalyte- Mg, acetate, gluconate
-LR- Na, Cl, K, Ca
-D5W- 5g dextrose/L
-dextran, hetastarch- volume expansion
-
INTRA-OP FLUID SHIFT
-small incision/minimal trauma 2-4 cc/kg/hr
-moderate incision/mod trauma 4-6 cc/kg/hr
-large incision/ severe trauma 6-8 cc/kg/hr
-major vascular case/ extreme trauma 8-10 cc/kg/hr
LACTATED RINGERS
-dextrose, K, Ca, Na, lactate
-concerns for patients with renal and hepatic disease
-diabetics
-blood transfusion
CRYSTALLOIDS
-contains more chloride than the ECF can cause hyperchloremic induced metabolic acidosis
-good choice for renal and diabetic patients
-can cause hyponatremia in brain injury patients
-
DEXTROSE CONTAINING SOLUTIONS
-prevention of hypoglycemia
-especially for pediatric, insulin infusion
-hyperglycemia is associated with increased risk of ischemic neurologic injury
CRYSTALLOID ADVANTAGES
-inexpensive * promotes urinary flow * restores third space loss * used for extracellular repletion * used for initial resuscitation
CRYSTALLOID DISADVANTAGES
-dilutes plasma proteins * causes reduction of capillary osmotic pressure * has transient effect * potential for pulmonary edema
COLLOID ADVANTAGES
-sustained increase in plasma volume * requires smaller volume for resuscitation * less peripheral edema * tends to remain intravascular * more rapid resuscitation * useful in conditions of altered vascular permeability
COLLOID DISADVANTAGES
* expensive * can cause coagulopathy (dextran > hetastarch > hextend) * can cause anaphylactic reaction (dextran) * decreases Ca (albumin) * can cause renal failure (dextran) * can cause osmotic diuresis * can cause impaired immune response (albumin)
HYPERTONIC SALINE
-2%/3%
-beneficial in fluid resuscitation from shock/trauma and major surgical losses
-INDICATIONS
-major surgical procedures, aortic, radical cancer sx
-shock
-slow correction of hyponatremai
-TURP syndrome
-reduction in perioperative edema
-reduction in ICP
HYPERTONIC SALINE EFFECTS
-hypernatremia, hyperosmolarity, hyperchloremia, hypokalemia, ^CO, decreased SVR/PVR, improved microcirculatory flow, decreased ICP, increased solute to kidneys
EBV FOR PEOPLE
-premature- 95ml/kg
-term neonates- 85ml/kg
-infants and child- 80ml/kg
-adult males- 75ml/kg
-adult females- 65ml/kg
ESTIMATED BLOOD LOSS FROM OR TOWELS
4 x 4 soaked = 10ml blood
lap sponge soaked = 100ml blood
WHEN TO TRANSFUSE CALCULATION
MABL = (Body weight in kg x EBV) x (existing Hct - Desired Hct) / existing Hct
FACTORS THAT AFFECT O2 DELIVERY
-inability to increase CO
-shifts in the oxyhemoglobin curve
-inadequate oxygenation
-abnormal Hgb
O2 EXTRACTION RATIO (SvO2) mixed venous
-what fraction of the total O2 delivered is consumed or extracted by the tissues
-ER = O2 consumption / O2 delivery
- (VO2 / DO2) = 250 / 1000 = 25%
which means a normal mixed venous saturation is 75%
PRBC WILL INCREASE Hgb AND Hct BY WHAT?
-Hgb 1 g/dL
-Hct 2-3 %
* 3ml/kg increases Hgb by 1
* 10 ml/kg increases Hct by 10%
ALBUMIN
-pooled plasma in saline
-highly soluble, globular protein, accounting for 70-80% of the colloid osmotic pressure of plasma
-5% rapid intravascular volume expansion
-25% hypoalbuminemia
-has an intravascular 1/2 life of > 24 hours
CRYSTALLOIDS WHY DO YOU HAVE TO ADMIN MORE THAN COLLOIDS
-most perioperative volume deficits are ECF
-crystalloids will eventually equilibrate between plasma and interstitial space therefore more is needed to maintain intravascular volume
ALBUMIN AND PLASMA DERIVATIVES
-no possibility of transfer of diseases because of how heated
-no coag factors
-associated with increased mortality in critically ill patients
DEXTRAN
-synthetic plasma expander
-intravascular 1/2 life 6 hours
-can cause anaphylaxis, volume overload, pulm edema, cerebral edema, platelet dysfunction, renal failure, and patients with diabetes, renal insufficiency are at an increased risk
SYNTHETICS HETASTARCH
-HETASTARCH, VOLUVEN - non-ionic starch derivatives
SYNTHETICS HEXTEND AND HESPAN
HEXTEND (6% in HES and LR)
HESPAN (6% in HES and NS)
-synthetic polymers
-contains Na, Ca, K, and Mg
-intravascular 1/2 life > 24 hours
-Infuse no more than 1000 ml
-higher volumes can result in bleeding complications due to decreased factor VIII/ vWBf, platelet defects, fibrin clots
-anaphylactoid rxns have been reported with both dextran and hetastarch but much less freq with hetastarch
WHY IS ROUTINE BLOOD TYPING DONE?
To identify antigens on the on the erythrocyte membranes (A, B, Rh)
WHAT ARE ANTIBODIES
Anti A or Anti B
they are formed whenever membranes lack A and/or B antigens
-these antibodies are capable of causing rapid intravascular destruction of erythrocytes that contain the corresponding antigens
ABO SYSTEM
-chromosomal locus produces 3 alleles
A, B, O
-each represent an enzyme that modifies a cell surface glycoprotein producing a different antigen
EBV FOR PEOPLE
-premature- 95ml/kg
-term neonates- 85ml/kg
-infants and child- 80ml/kg
-adult males- 75ml/kg
-adult females- 65ml/kg
ESTIMATED BLOOD LOSS FROM OR TOWELS
4 x 4 soaked = 10ml blood
lap sponge soaked = 100ml blood
WHEN TO TRANSFUSE CALCULATION
MABL = (Body weight in kg x EBV) x (existing Hct - Desired Hct) / existing Hct
FACTORS THAT AFFECT O2 DELIVERY
-inability to increase CO
-shifts in the oxyhemoglobin curve
-inadequate oxygenation
-abnormal Hgb
PaO2
-partial pressure of oxygen in the plasma phase of arterial blood
SaO2
-percentage of all the available heme binging sites saturated with O2
CaO2
(arterial O2 content)
-how much oxygen is in the blood ml O2/dL
VO2
-rate at which oxygen is used by tissues
-product of CO and the difference between arterial and venous content
-Normal O2 consumption is 250ml/min
DO2
-quantity of O2 made available to the body in one min is known as the oxygen delivery
- CO x arterial O2 content (CaO2)
= 1000 ml O2/min
O2 EXTRACTION RATIO (SvO2) mixed venous
-what fraction of the total O2 delivered is consumed or extracted by the tissues
-ER = O2 consumption / O2 delivery
- (VO2 / DO2) = 250 / 1000 = 25%
which means a normal mixed venous saturation is 75%
ALBUMIN
-pooled plasma in saline
-5% rapid intravascular volume expansion
-25% hypoalbuminemia
--highly soluble, globular protein, accounting for 70-80% of the colloid osmotic pressure of plasma
-has an intravascular 1/2 of > 24 hours
DEXTRAN
-composed of polymerized glucose molecules
- intravascular 1/2 6 hours
-anaphylaxis, pulm edema, cerebral edema, plt dysfunction, pts with diabetes or renal failure increases the risk
ALTERNATIVES TO TRADITIONAL BLOOD THERAPY
-normovolemic hemodilution
-cell saver - 50-60% Hct (intra op salvage)
-oxygen carrying substitutes- bovine petroleum based therapies
-autologous donation (pre op)
-complete circuit (jehovahs witness)
-post op salvage in chest tube (complications are reinfused anticoagulants, dilutional coagulopathy, air embolism)
DILUTIONAL COAGULOPATHY
-seen with massive transfusions (> 1 EBV, > 10 units)
-microvascular bleeding
-hematuria
-bleeding at IV sites
-clinically oozing
-increased PT/PTT
-decreased platelets
TREATMENT
-sugically control the bleeding
-keep the patient warm
-maintain perfusion and euvolemia
-don't over hydrate and dilute the patient
-consider FFP/ plt
-consider vitamin K, DDAVP (enhances plt adhesiveness)
SYMPTOMS OF CITRATE INTOXICATION
-occurs from the addition of CDP as preservative for stored blood, and can occur with rapid tranfusion, >150ml/min
-hypocalcemia
-hypotension
-increased LVEDP
-increased CVP
-prolonged QT interval
-hypomagnesemia (tacharrythmias, torsades, refractory VF
TREATMENT
-calcium and mag
-citrate will be metabolized quickly in krebs cycle so may be over before it needs to be treated
BIOCHEMICAL CHANGES IN STORED BLOOD
-progressive acidosis
-Increased K, ^CO2, ^lactate, decreased glucose, decreased 2,3 DPG, destroyed plt, decreased factor V (15%) and factor VIII (50%)
TRALI
-transfusion related acute lung injury
-noncardiogenic form of pulm edema associated with blood product admin (RBC, FFP, plt)
-appearance similar to ARDS
-usually begin within 6 hours of transfusion
-pt develops dyspnea, cyanosis, fever, chills, hypotension and noncardiogenic pulm edema
-treatment largely supportive
-
WHAT TO DO IF TRANSFUSION REACTION IS SUSPECTED
-stop the transfusion
-treat hypotension with fluids and vasopressors, consider steroids
-send unused donor blood and sample from patient to blood bank to be recrossmatched
-test pt for free Hgb, haptoglobin, Coombs test, and DIC screening
-preserve renal with brisk urine output, ivf, lasix, mannitol
COMPLICATIONS OF BLOOD TRANSFUSIONS
-infection, TRALI, hyperkalemia, acidosis, hypothermia
CRYOPRECIPITATE
-fraction of plasma that precipitates after FFP thawed
-has high <> of factor VIII for hemophilia
-high <> of fibrinogen to treat hypofibrinogemia
PLATELETS
-thrombocytopenia <50,000
- 1 unit replaces 5-10,000
-each unit contains about 50ml of plasma which increases the risk of reaction
FFP
-contains plasma and clotting factors
-no platelets
-utilized in coag deficiencies, reversal of warfarin therapy, and microvascular bleeding
-1 unit of FFP will increase clotting factors by 3 %
-hypernatremia can occur from massive transfusion of FFP
WHOLE BLOOD
-40% Hct
-used primarily in hemorrhagic shock >25 % EBV
-contains all factors, increased likelihood of reaction
PRBC
contains rbc, wbc, and plt, reduced plasma
-Hct 70%
-cold storage destroys plat
-
EMERGENCY TRANSFUSIONS
-O is universal donor
-if > 2 units are given must screen patient blood for antibodies before give their own blood to them
-above remains true only for whole blood >10 units give only O blood for 3-4 months (life of RBC)
-can give O+ just not to women of child bearing age
TYPE AND CROSS
-always want to use this type compatibility 99.95%
-if in emergency use type specific uncrossmatched blood
-last resort O-
ABO BLOOD GROUPIN
A - anti A
B - anti B
AB - no antibodies
O - anti A and anti B
RH SYSTEM
-involves antigen D
-80-85% of caucasian have the D antigen
-people LACKING this are considered Rh NEGATIVE and usually develop antibodies against the D antigen after exposure to previous Rh positive transfusion or pregnancy (Rh negative mother delivering an Rh positive baby)