Fluids & Blood Flashcards
Fluid Compartments
60% 70 kg
TBW 42L
1. Intracellular 40% 28L
2. Extracellular 20% 14L
a. Interstitial 15% 11L
b. Plasma 5% 3L
↑TBW
Neonates
↓TBW
Females
Elderly
Obese
Intracellular Ions
K+
Mg2+
Phosphate
Extracellular Ions
Na+
Ca2+
Cl¯
HCO3¯
Net Filtration Pressure
Starling forces
(Pc - Pif) - (πc - πif)
Pc = capillary hydrostatic
Pif = interstitial hydrostatic
πc = capillary oncotic
πif = interstitial oncotic
OsmolaRity
Osmoles per LiteR solution mOsm/L
OsmolaLity
Osmoles per kg solvent mOsm/kg H2O
Plasma Osmolarity
Normal 280-290 mOsm/L
= 2[Na+] + (Glucose/18) + (BUN/2.8)
NaCl 0.9%
ISOtonic
Hyperchloremic metabolic acidosis
Na+ 154 mEq/L
Cl¯ 154 mEq/L
↑Cl¯ load → kidneys excrete HCO3¯ to maintain electroneutrality → non-gap metabolic acidosis
IVF Na+ Concentration
NaCl 154 mEq/L
Plasmalyte 140 mEq/L
LR 130 mEq/L
Crystalloid Replacement
3:1 ratio
Plasma volume ↑20-30 minutes
Dilutional effects
Albumin
Only colloid derived from human blood products
1:1 ratio
Anti-inflammatory properties
Binds Ca2+ → hypocalcemia
Synthetic Colloids
*Renal injury risk (FDA black box warning)
Dextran 40
Hetastarch
Hextend
Voluven
Dextran 40
Synthetic colloid
↓blood viscosity → improves microcirculation
1° coagulopathy
Dextran > Hetastarch > Hextend
Anaphylaxis risk
Hetastarch
Synthetic colloid
2nd highest coagulopathy risk
Hextend
Synthetic colloid
Do NOT exceed 20 mL/kg
3rd highest coagulopathy risk
Hyperkalemia
Definition & Causes
K+ > 5.5 mEq/L
↑RMP (closer to threshold potential)
Causes include PRBCs, renal failure, NSAIDs, acidosis, Succinylcholine, β blockers, cellular injury (tumor lysis, hemolysis, burns, crush injury, & rhabdomyolysis )
Hyperkalemia
Cardiac Dysrhythmias S/S
5.5-6.5 peaked T waves
6.5-7.5 P wave flattening + PR prolongation
7.0-8.0 QRS prolongation
> 8.5 QRS → sine wave → Vfib
What is the most common electrolyte abnormality?
Hypokalemia
K+ < 3.5 mEq/L
Hyperpolarizes RMP
Hyperkalemia
Treatment
Ca2+ IV
- Central 20 mEq/hr
- Peripheral 10 mEq/hr
Insulin + D50
Hyperventilation
HCO3¯
β2 agonists
Elimination - diuretics, Kayexalate, & dialysis
Hypokalemia
Causes
GI loss - vomiting/diarrhea, NG suction, Zollinger-Ellison syndrome, JG bypass
Renal loss - diuretics or metabolic alkalosis
Redistribution into cells (hyperkalemia treatment)
Hypokalemia
S/S
Skeletal muscle cramps → weakness → paralysis
Worsens dig toxicity
EKG prolonged PR & QT intervals
Flat T wave
U wave present
What maintains the intracellular K+ distribution?
Na-K+ ATPase pump
K+ Supplementation
Do NOT administer > 0.5-1 mEq/kg/hr
Hypernatremia
Causes
↓total body Na+ content
Osmotic diuresis, N/V, adrenal insufficiency
Normal Na+
DI, renal failure, diuretics
↑total body Na+
Hyperaldosteronism ↑Na+ intake
Hypernatremia
S/S
Na+ > 145 mEq/L
Based on serum osmolality normal range 280-290 mOsm/L
350-375 HE, agitation, confusion
376-400 weakness, tremors, ataxia
401-430 hyperreflexia & muscle twitching
> 430 seizures, coma, death
Hyponatremia
Causes
↓total body Na+ content
Diuretics, salt-wasting, hypoaldosteronism
Normal Na+
SIADH, hypothyroid, H2O intoxication, periop stress
↑total body Na+
CHF or cirrhosis
Hyponatremia
S/S
Mild 125-129 N/V & malaise
115-124 HE, lethargy, & altered LOC
< 115 seizures, coma, cerebral edema, & respiratory arrest
Hyper/hyponatremia
Treatment
Dependent on cause*
Na+ restriction
IVF selection based on tonicity
Diuretics
What mechanisms maintain Na+ homeostasis?
GFR, RAAS, & ANP (BNP)
Na+ Supplementation
NaCl 3% 1-2 mL/kg/hr
↑ < 1-2 mEq/L per hour
What occurs when hyponatremia corrected too quickly?
Osmotic demyelination syndrome or central pontine myelinolysis
- Mental status changes
- Seizures
- Spastic quadriplegia
- Pseudobulbar palsy
- Encephalopathy
- Coma & death
Calcium
Normal Serum Levels
Total 8.5-10.5 mg/dL
Ionized 4.6-5.2 mg/dL
What is the most abundant electrolyte?
Calcium
2nd messenger, neurotransmitter release, & muscle contraction
Hypercalcemia
S/S
Nausea, abdominal pain, HTN, psychosis, mental status changes, seizures, & shortened QT interval
Hypercalcemia
Treatment
NS
Loop diuretic
Calcium Storage
1° bones
Albumin = intravascular Ca2+ reservoir
Hypocalcemia
Causes
Hypoparathyroidism
Vitamin D deficiency
Renal osteodystrophy
Pancreatitis
Sepsis
Hypocalcemia
S/S
Skeletal muscle cramps
Nerve irritability → paresthesia & tetany
Laryngospasm
Mental status changes → seizures
Chvostek or Trousseau signs
Prolonged QT interval
Hypocalcemia
Treatment
Calcium
Vitamin D
Chvostek Sign
Tapping on the jaw angle (facial nerve/masseter muscle) causes facial contraction on the ipsilateral side of the
Trousseau Sign
Upper extremity BP cuff inflated above SBP 3 minutes
Hand & forearm muscle spasms
Magnesium
Normal plasma Mg2+ 1.7-2.4 mg/dL or 1.5-3 mEq/L
Antagonizes Ca2+ effects
Parathyroid Hormone & Calcitonin
PTH ↑serum Ca2+
Parathyroid gland releases PTH → osteoclasts release Ca2+ from bone storage + ↑Ca2+ renal reabsorption & Ca2+ absorption in the small intestine
Calcitonin ↓serum Ca2+
↑Ca2+ → thyroid releases calcitonin → osteoclast activity inhibited + ↓Ca2+ reabsorption
Hypercalcemia
Causes
Hyperparathyroid
Cancer
Thyrotoxicosis
Thiazide diuretics
Immobilization
Magnesium 1° Location
Muscle & bone
1% ECF
0.3% plasma
Where is Mg2+ reabsorbed?
Renal tubules
Magnesium Clinical Uses
Pre-E 4G load over 10-15 min then 1G/hr infusion
Opioid-sparing techniques (ERAS)
Acute bronchospasm
Cardiac rhythm disturbances - symptomatic PVCs or Torsades de pointe
Hypermagnesemia
Causes
Excessive admin
Renal failure
Adrenal insufficiency
Hypermagnesemia
S/S
Not significant unless extremely high
Heart block
Potentiates NMBs (Succinylcholine & non-depolarizing)
No Hypermagnesemia S/S
2.5-5 mg/dL
2.1-4.2 mEq/L
What serum magnesium level are diminished deep tendon reflexes noted?
5-7 mg/dL
4.2-5.8 mEq/L
Lethargy, drowsiness, flushing, N/V
When are deep tendon reflexes lost?
Serum Mg2+ 7-12 mg/dL
5.8-10 mEq/L
HoTN, EKG changes, somnolence
When does respiratory depression occur?
Serum Mg2+ > 12 mg/dL
> 10 mEq/L
Apnea, complete heart block, cardiac arrest, coma, paralysis
Hypermagnesemia
Treatment
Calcium chloride or gluconate
Hypomagnesemia
Causes
Poor intake, alcohol abuse, diuretics, critical illness, hypokalemia
Hypomagnesemia
S/S
Not significant unless extremely low
Prolonged QT
Mg2+ level when tetany & dysrhythmias present
< 1.2 mg/dL
< 1 mEq/L
Tetany, seizures, dysrhythmias
Mg2+ level when neuromuscular irritability present
1.2-1.8 mg/dL
1-1.5 mEq/L
Neuromuscular irritability, hypokalemia, hypocalcemia
Hypomagnesemia
Treatment
Magnesium sulfate supplementation
Acid-Base
Respiratory Compensation
CO2 = volatile acid
Acid-Base
Renal Compensation
Reabsorb filtered HCO3¯
Remove titratable acids (non-volatile)
Ammonia formation
Acidosis
CNS/Pulmonary/Cardiac Effects
↑CBF/ICP
↑PVR
↑P50 (R shift)
↑SNS tone ↑dysrhythmias risk
↓contractility
Hyperkalemia H+/K+ pump
Alkalosis
CNS/Pulmonary/Cardiac Effects
↓CBF/ICP
↓PVR
↓P50 (L shift)
↓Coronary blood flow
↑dysrhythmias risk
Hypokalemia
↓ionized Ca2+
Respiratory Acidosis
Causes
↑CO2 production
↓CO2 elimination ↑Vd
Rebreathing
What is the most common respiratory acidosis cause?
Hypoventilation
ACUTE
Respiratory Acidosis
Every 10 mmHg > 40 ↓pH 0.08
Chronic
Respiratory Acidosis
Every 10 mmHg > 40 ↓pH 0.03
What causes non-anion gap acidosis?
Metabolic acidosis
Normal anion gap 8-12 mEq/L
HCO3¯ loss
HARDUP
- Hypoaldosteronism
- Acetazolamide
- Renal tubular acidosis
- Diarrhea
- Uretosigmoid fistula
- Pancreatic fistula
Non-Anion Gap Acidosis
Treatment
Admin sodium bicarbonate
What causes an anion gap acidosis?
Metabolic acidosis
Add +acid
Anion gap > 12 mEq/L
MUDPILES
- Methanol
- Uremia
- DKA
- Paraldehyde
- Isoniazid
- Lactate ↓DO2, sepsis, cyanide poison
- Ethanol or ethylene glycol
- Salicylates → inhibit Krebs cycle
Anion Gap Acidosis
Treatment
Lactic acidosis = IVF, O2, cardiopulmonary support
DKA = IVF + insulin
Uremia or drug-induced = dialysis
Metabolic Acidosis
Respiratory Compensation
↑minute ventilation ↓PaCO2
PaCO2 ↓1-1.5 mmHg ↓HCO3¯ 1 mEq/L
What causes metabolic alkalosis?
HCO3¯ addition = massive transfusion
Loss non-volatile acid = NG suction, vomiting, loop diuretics, acid loss via urine, ECF depletion ↑Na+ reabsorption H+/K+ excretion to maintain electroneutrality
Antacids
↑mineralocorticoid activity = Cushing or hyperaldosteronism
Metabolic Alkalosis
Respiratory Compensation
↓minute ventilation ↑PaCO2
PaCO2 ↑0.5-1 mmHg ↑HCO3¯ 1 mEq/L
Shock Stage
I
Blood loss < 15% or < 750 mL
Pulse < 100
BP normal
Pulse pressure normal
RR 14-20
UOP > 30 mL/hr
Fluid management = crystalloid
Shock Stage
II
Blood loss 15-30% or 750-1,500 mL
Pulse 100-120
BP normal
↓pulse pressure
RR 20-30
UOP 20-30 mL/hr
Fluid management = crystalloid
Shock Stage
III
Blood loss 30-40% or 1,500-2,000 mL
Pulse 120-140
↓BP ↓pulse pressure
RR 30-40
UOP 5-15 mL/hr
Fluid management = crystalloid + blood
Shock Stage
IV
Blood loss > 40% or > 2L
Pulse > 140
↓BP ↓pulse pressure
RR > 40
Minimal/absent UOP
Fluid management = crystalloid + blood
Universal Donor
RBCs O ¯
Plasma AB +
Universal Recipient
RBCs AB +
Plasma O ¯
O ¯
Contains NO RBC antigens
Anti-A & anti-B plasma antibodies
O +
85% population Rh-D positive (+)
O + an acceptable emergency transfusion RBC type when patient NOT childbearing age & has not received a previous transfusion
Rh
Rh+ RBC antigen D present
No plasma antibodies
Rh+ able to receive (+) OR (-)
Patient w/ Rh¯ + exposure to Rh+ blood → develops antibodies to Rh antigen (anti-D)
Rh & Pregnancy
Fetus receives Rh+ antigen from father
Maternal Rh¯& fetal blood Rh+ do not mix during pregnancy
Rh+ antigen able to cross the placenta during delivery
Mother sensitized when Rh+ antigen crosses the placenta during delivery
Develops antibodies to Rh+ antigen (anti-D)
Subsequent pregnancy w/ Rh+ fetus → erythroblastosis fetalis
Erythroblastosis Fetalis
Hemolytic disease that affects the newborn d/t Rh incompatibility
Who & when to administer Rhogam?
Rh immune globulin
Pregnant Rh¯ mothers
Starting at 28 weeks gestation to prevent sensitization
Protects the fetus during delivery
Type
Determines ABO & Rh-D antigens in the recipients blood
5 minutes
0.2% probability incompatibility reaction
Screen
Determines most clinically significant antibodies present
45 minutes
0.06% probability incompatibility reaction
Crossmatch
Provides the most accurate compatibility
Mixes the recipient plasma w/ blood in the actual unit to be transfused
45 minutes
0.05% probability incompatibility reaction
Emergency PRBCs Transfusion
- Type-specific partially crossmatched blood
- Type-specific uncrossmatched blood
- Type O ¯ uncrossmatched blood
*After 2 units type O blood transfused must continue to use type O despite patient’s blood type!
PRBCs
Hgb 6-10 g/dL ?
Hgb < 6 g/dL TRANSFUSE
↑CaO2
1 unit 300 mL Hct 70%
↑Hgb 1 g/dL or Hct 2-3%
Platelets
1 pack per 10 kg
Do NOT use filter or warm
Stored at room temp 5 days
↑bacterial contamination risk → sepsis
FFP
All coagulation factors, fibrinogen, & plasma proteins
↑factor concentration 20-30%
Factor VII 1/2 life 3-6 hours
Complete infusion w/in 24 hours thawing
FFP Indications
Coagulopathy 10-20 mL/kg
Warfarin reversal 5-8 mL/kg
Antithrombin deficiency
Massive transfusion
DIC
C1 esterase deficiency
Hereditary angioedema
Cryo
Contains fibrinogen, factor VIII & XIII, vWF
Dose 5 bag pool
↑fibrinogen 50 mg/dL
Complete infusion w/in 6 hours thawing
EBVs
Adult 70 mL/kg
Child 70 mL/kg
Infant 75-80 mL/kg
Full term 80-90 mL/kg
Premature 90-100 mL/kg
Stored Blood Additives
Citrate (anticoagulant) inhibits Ca2+ → hypocalcemia
Phosphate (buffer combats acidosis) → alkalosis
Dextrose (1° glycolysis substrate) → hyperglycemia
Adenine (substrate helps RBCs re-synthesize ATP) extends storage 21 → 35 days
What temperature is blood stored at?
1-6° C
Extents lifespan via slowing glycolysis
RBC Storage Lesion
↓2,3 DPG → shifts oxyhemoglobin curve L
↓ATP
↓pH ↑lactic acid
↑K+
Impaired ability to change shape → impacts capillary flow
Hemolysis
↑proinflammatory mediators production
Leukoreduction
Removes WBCs
Leukocytes (WBCs) responsible HLA alloimmunization, febrile non-hemolytic transfusion reactions, & CMV transmission
HLA Alloimmunization
Body develops antibodies against non-self antigens (human leukocyte antigens)
The body attacks HLA proteins present on the platelet surface
Most common cause platelet refractoriness
Washing
Washing blood products w/ saline removes any plasma & antigens in the donor RBCs
RBC antigens are not removed
Prevents anaphylaxis in IgA deficient patients
Irradiation
Exposes blood to gamma radiation
Disrupts WBC DNA in the donor cells & destroys donor leukocytes
Prevents graft-vs-host disease in immunocompromised patients
GVHD → donor leukocytes attach recipient bone marrow → pancytopenia, fever, hepatitis, & diarrhea
When to administer irradiated blood?
1st/2nd degree relative blood donors
Leukemia
Lymphoma
Hematopoietic stem cell transplants
DiGeorge syndrome
Blood Transfusion Infectious Complications
CMV
Hepatitis B
Hepatitis C
HIV
Acute Hemolytic Reaction
S/S
Occurs when patient receives incompatible blood product
Hemoglobinuria, HoTN, & bleeding
- Fever/chills
- Chest pain
- Dyspnea
- Nausea
- Flushing
Acute Hemolytic Reaction
Treatment
- Stop the transfusion
- Maintain UOP > 75-100 mL/hr (IVF, Mannitol 12.5-25 g, Furosemide 20-40 mg)
- Alkalinize the urine HCO3¯
- Send urine & plasma Hgb samples to blood bank
- Check platelets, PT, & fibrinogen
- Send unused blood to the blood bank to double-check cross-match
- Support hemodynamics
Non-Hemolytic Transfusion Reaction
Fever most common
Presentation includes fever, chills, HE, nausea, & malaise
Non-Hemolytic Transfusion Reaction
Treatment
Supportive
Acetaminophen
Allergic Transfusion Reaction
Rarely severe
Present w/ urticaria & facial swelling
Allergic Transfusion Reaction
Treatment
Antihistamines
TRALI
Transfusion-related ALI non-cardiogenic pulmonary edema
Most common cause transfusion related mortality
Cause: HLA human leukocyte antigens & neutrophil antibodies present in the donor plasma
Donor antibodies cause neutrophil activation → endothelial injury → capillary leak → pulmonary edema → impaired gas exchange → hypoxemia → acidosis & death
Donor populations /w high antibodies concentration
Multiparous women
Blood transfusion history
Organ transplant
Blood products w/ highest TRALI incidence
Blood products containing plasma
Platelets or FFP
HLA & neutrophil antibodies present in donor plasma
Recipients at increased risk to develop TRALI
Critical illness
Sepsis
Burns
Post- CPB
TRALI S/S
Onset < 6 hours after transfusion
Bilateral infiltrates on CXR
PaO2/FiO2 < 300 mmHg
SpO2 < 90% on RA
Normal PAOP
TRALI Management
1° supportive
Maximize PEEP
LPV low VT
Avoid overhydration
TACO
Transfusion-associated circulatory overload
Volume overload cause by expanding the patient plasma volume beyond compensatory ability
TACO S/S
Pulmonary edema
Hypervolemia
LV dysfunction
Mitral regurgitation
↑PAOP
↑BNP
TACO Management
Supportive
Massive Transfusion
Alkalosis - citrate metabolizes HCO3¯
Hypocalcemia
Hypothermia
Hyperglycemia (dextrose)
Hyperkalemia - stored RBCs the cell membrane become dysfunctional & allows K+ to leak; reduce risk by admin washed or fresh cells < 7 days old
Trauma Lethal Triad
Acidosis (hypoperfusion)
Hypothermia
Coagulopathy
- Acidosis impairs hemostasis
- PT & PTT prolonged < 34°C
- Massive volume resuscitation causes dilutional coagulopathy
Intraop Blood Salvage
Indications
EBL expected > 1L or 20% EBV
Pre-existing anemia
Patient refuses allogenic blood products
How much volume required to admin 250 mL (1 unit) saline diluted RBCs?
500-750 mL 2-3x
Hct 50-60%
What blood products are not returned to the patient w/ intraop blood salvage?
Platelets & coagulation factors
Dilutional coagulopathy
How does salvaged blood compared to blood bank?
↑O2 carrying capacity
Better maintain concave shape
Intraop Blood Salvage
CONTRAINDICATIONS
Sickle cell anemia
Thalassemia
Oncologic procedures
Topical drugs (antibiotics) in the sterile field
Infected surgical site
C-section controversial d/t theoretical amniotic fluid embolism risk
