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
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
A shift to the left in the Hgb dissociation curve is associated with
Anemia is suspected in these values for men and women
–
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
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
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