Hematology Flashcards
Calculation for arterial O2 content
CaO2 = SaO2(Hgb x 1.39) + PaO2(0.003)
1.39 = O2 bound to hemoglobin SaO2= saturation of hemoglobin with O2 PaO2= arterial partial pressure of oxygen 0.003 = dissolved oxygen ml/mmHg/dl Normal O2 capacity is 16-20 mL/dL
Normal value for O2 content / capacity
16-20mL/dL
O2 carrying capacity is defined by the presence of
hemoglobin
More hemoglobin = more O2 carrying capacity
Causes of anemia
1. Acute • Acute blood loss 2. Chronic • Nutritional deficiency • Hemolytic anemia • Aplastic anemia • Manifestation of another disease • Abnormal structure of RBC • Sickle cell, thalassemias
Compensatory mechanisms involved in anemia
– Increased cardiac output
– Increased red blood cell 2,3-diphoshoglycerate (DPG)
– Increased P-50 (partial pressure of O2 at which Hgb is 50% saturated with O2)
– Increased plasma volume
– Decreased blood viscosity
– Decreased SVR (larger BV diameter allows more blood to flow through it)
– RIGHTWARD shift of Oxygen-Hemoglobin dissociation curve
– Redistribution of blood flow to organs with higher extraction ratio (ER) –> cardiac and brain cells
A shift to the right in the Hgb dissociation curve is associated with
- Facilitates release of O2 from
Hgb to tissues
- Hgb variants with O2 affinity
- Due to Acidosis
- Exercise
- Hypermetabolism and fever
- Increased 2,3 diphosphoglycerate (2,3-DPG)A shift to the left in the Hgb dissociation curve is associated with
- Inhibits release of oxygen from HGB to tissues
- Alkalosis
- Hbg variants that increase O2 affinity (carbon monoxide)
- Hypothermia
- Decreased 2,3 diphosphoglycerate (2,3-DPG)
Anemia is suspected in these values for men and women
– <12.5g/dl (males) hct 40%
– BUT, remember that Hgb and Hct are relative measurements (think about their context→ hemodilution, bleeding, pregnant, etc.)
What is the most effective treatment of anemia?
Treat the cause!
Remember that anemia is almost always the manifestation of another disease process
General anesthesia management for chronic anemia
- Maximize O2 delivery
– Consider ↑ FiO2
– Transfuse If necessary - Avoid drug-induced ↓ in C.O.
– Selection of induction agent (etomidate)
– Anesthetic technique (↑ opioid)
– Hydrate, if tolerated; avoid hypovolemia - Avoid conditions that favor a leftward shift of the oxyhemoglobin dissociation curve
– Avoid respiratory alkalosis, hypothermia, etc. - Consider your volatile anesthetics
– May be less soluble in plasma of anemic patient (b/c volatile anesthetics cling to the lipid layer of RBCs)
• This is more theoretical than actual, but may need to decrease your IA dose
– Consider that this decrease in solubility may be offset by the impact of increased cardiac output
Causes of iron deficiency anemia
o Disorder of hemoglobin resulting in reduced or ineffective erythropoiesis and microcytic RBCs
o Most common form of nutritional deficiency in children and infants
o In adults- reflects depletion of iron stores from chronic blood loss, which may be from:
• Gastrointestinal tract
• Menorrhagia
• Cancer
S/S of Pernicious Anemia and Anesthetic Considerations
S/S:
• Bilateral peripheral neuropathy (assess for this pre-op!)
• Loss of proprioceptive and vibratory sensations in lower extremities
• Decreased deep tendon reflexes
• Unsteady gait
• Memory impairment and mental depression
Anesthesia:
• Avoid regional blocks due to neuropathies
• Avoid nitrous oxide (b/c it inhibits methionine synthase –> necessary for mylin formation)
• Maintain oxygenation
• Emergency correction for imminent surgery is with red cell blood transfusions
S/S of Folic Acid (B9) Deficiency anemia and anesthetic considerations
S/S • Smooth tongue • Hyperpigmentation • Mental depression • Peripheral edema • Liver dysfunction • Severely ill patients
Anesthesia
• Note thorough airway exam →Oral manifestations may make airway management challenging due to changes in tongue texture, etc.
• Have an alternate airway management plan!
These are the 4 hereditary hemolytic anemias
- Hereditary spherocytosis
- Paroxysmal nocturnal hemoglobinuria
- Glucose-6-Phosphate Dehydrogenase Deficiency
- Pyruvate Kinase Deficiency
Hereditary spherocytosis
o Hereditary disorder affecting red cell membrane skeletal structure
o Lifelong hemolytic anemia
o Most common red cell membrane defect-disorder of membrane skeletal proteins -> cell more rounded, fragile, shortened circulation half-life (destroyed in spleen)
o Splenomegaly, fatigability, risk of episodes of hemolytic crisis, often precipitated by infections; risk of gallstones/ jaundice
Paroxysmal nocturnal hemoglobinuria (description and anesthetic considerations)
o Hereditary disorder of RBC structure
o Clonal disorder that arises in hemotopoietic cells with a reduction in membrane protein in RBCs
o Poor prognosis once diagnosed (8-10 years)
• Preoperative hydration and prophylactic administration of RBCs have been advocated
Glucose-6 Dehydrogenase Deficiency (description and anesthetic considerations)
o Disorder affecting red cell metabolism
o Most common enzymopathy- African Americans, Asians, Mediterranean populations-> G6PD activity decreases-> susceptible to damage by oxidation
o ↑ rigidity of membrane & accelerates clearance
• Affects approximately 10% of black males in U.S.
• Acute and chronic episodes of anemia
Anesthesia:
• Need to avoid exposure to oxidative drugs (methylene blue, IAs, benzos, etc)
• Avoid hypothermia, acidosis, hyperglycemia, infection
Pyruvate Kinase Deficiency
o Disorder affecting red cell metabolism
o Deficiency of glycolic enzyme which converts glucose to lactate & is primary pathway for ATP production->results in K+ leak-> ↑ rigidity & accelerates destruction
o Accumulations of 2.3-DPG in the RBCs cause right shift oxy-Hbg curve
Anesthetic Considerations for Hemolytic Anemias***
o ↑ risk of tissue hypoxia
o If previous splenectomy may have ↑ risk of perioperative infection
o Increased risk venous thrombosis due to activation of coagulation
o Erythopoietin is often prescribed for 3 days preoperatively
o Preop hydration and prophylactic administration of RBCs have been advocated
o Acute drops in Hb below < 8 g/dl and chronic reductions to below 6 g/ dl should be considered for transfusion
o Caution Methylene Blue administration
Patho of sickle cell disease
Mutant hemoglobin (S) due to valine substitution for glutamic acid on B-globulin chain-> Hgb aggregates & forms a polymer when exposed to low O2 concentrations
This can cause small vessels to be occluded
Lifespan of a RBC is sickle cell disease
12-17 days
Is sickle cell TRAIT, the patient is heterozygous for the gene, and __% of their Hgb is S, and __ % is normal Hgb A
40% = S 60% = Normal
Most patients are asymptomatic and does not pose risk for surgery or anesthesia.
In sickle cell DISEASE, the patient is homozygous for the gene and __% of their Hgb is Hgb (S) form
70-98%
Sickle Cell patients are at high risk for these complications peri-operatively d/t hemolysis and vasoocclusion
– Stroke – Heart failure – MI – Hepatic or splenic sequestration – Renal failure
Anesthetic Considerations for Sickle Cell Disease
**** Avoid all situations leading to…
1. Hypoxemia
2. Hypovolemia
3. Stasis
4. Hypothermia
5. Acidosis
• Look for evidence of organ damage, cardiac dysfunction, concurrent infection
• May benefit from conservative transfusions with high risk surgery
– ASA recommends pre-operative transfusion to increase HCT to 30%
• Goal of transfusion is to decrease Hgb S to less than 30% (Want to increase Hgb A levels) However, low risk procedures normally don’t need transfusion.
• Give Supplemental O2
• Preoperative hydration for 12 hours prior to surgery (decrease likelihood of hypovolemia/sickling)
• Pre-medication
o Avoid respiratory depression that can lead to hypoxia and acidosis
• Regional anesthesia is fine, although:
o Concern with hypotension
o Stasis of blood flow
o Compensatory vasoconstriction
• Aggressive pain management
• Avoid infections
What is sickle cell crisis and how is it managed?
• Life threatening complication
• As a result of hypoxia, Hgb S forms an insoluble globulin polymer
– Acute episodic vaso-occlusive crisis
– Ischemia / infarction of organs the danger
– Pain, stroke, renal failure, liver failure, splenic sequestration, PE
– Very painful
• Acute chest syndrome-can be fatal (typically 2-3 days postop)
– Pleuritic chest pain, dyspnea, fever, acute pulmonary hypertension
Anesthetic Management of Sickle Cell Crisis:
– Transfusion or exchange transfusion to hct of 30%
– Supplemental 02
– Antibiotics (to avoid infections)
– Inhaled bronchodilators (for the acute chest syndrome)
– Aggressive pain management
