Hematology Flashcards

1
Q

Calculation for arterial O2 content

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Normal value for O2 content / capacity

A

16-20mL/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

O2 carrying capacity is defined by the presence of

A

hemoglobin More hemoglobin = more O2 carrying capacity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Causes of anemia

A
  1. Acute • Acute blood loss 2. Chronic • Nutritional deficiency • Hemolytic anemia • Aplastic anemia • Manifestation of another disease • Abnormal structure of RBC • Sickle cell, thalassemias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Compensatory mechanisms involved in anemia

A

– 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

A shift to the right in the Hgb dissociation curve is associated with

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

A shift to the left in the Hgb dissociation curve is associated with

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Anemia is suspected in these values for men and women

A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the most effective treatment of anemia?

A

Treat the cause! Remember that anemia is almost always the manifestation of another disease process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

General anesthesia management for chronic anemia

A
  1. Maximize O2 delivery – Consider ↑ FiO2 – Transfuse If necessary 2. Avoid drug-induced ↓ in C.O. – Selection of induction agent (etomidate) – Anesthetic technique (↑ opioid) – Hydrate, if tolerated; avoid hypovolemia 3. Avoid conditions that favor a leftward shift of the oxyhemoglobin dissociation curve – Avoid respiratory alkalosis, hypothermia, etc. 4. 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Causes of iron deficiency anemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

S/S of Pernicious Anemia and Anesthetic Considerations

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

S/S of Folic Acid (B9) Deficiency anemia and anesthetic considerations

A

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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

These are the 4 hereditary hemolytic anemias

A

• Hereditary spherocytosis • Paroxysmal nocturnal hemoglobinuria • Glucose-6-Phosphate Dehydrogenase Deficiency • Pyruvate Kinase Deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hereditary spherocytosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Paroxysmal nocturnal hemoglobinuria (description and anesthetic considerations)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Glucose-6 Dehydrogenase Deficiency (description and anesthetic considerations)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Pyruvate Kinase Deficiency

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Anesthetic Considerations for Hemolytic Anemias*******

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Patho of sickle cell disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Lifespan of a RBC is sickle cell disease

A

12-17 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Is sickle cell TRAIT, the patient is heterozygous for the gene, and __% of their Hgb is S, and __ % is normal Hgb A

A

40% = S 60% = Normal Most patients are asymptomatic and does not pose risk for surgery or anesthesia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

In sickle cell DISEASE, the patient is homozygous for the gene and __% of their Hgb is Hgb (S) form

A

70-98%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Sickle Cell patients are at high risk for these complications peri-operatively d/t hemolysis and vasoocclusion

A

– Stroke – Heart failure – MI – Hepatic or splenic sequestration – Renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Anesthetic Considerations for Sickle Cell Disease

A

****** 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is sickle cell crisis and how is it managed?

A

• 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Characteristics of Thalassemia Major

A

• Inability to form beta-globin chains of hemoglobin • Hepatosplenomegaly • Dyspnea and orthopnea • Infection risk • Arrhythmias, CHF • Skeletal malformations • Growth failure and osteoporosis • Hemothorax • Spinal cord compression • Mental retardation • Very sensitive to digitalis • Increased RBC production • Jaundice

28
Q

Iron overload may cause

A

Endocrine: Impaired growth, hypogonadism, infertility, hypoparathyroidism, DM Heart: CM and CHF Liver: cirrhosis

29
Q

Considerations for thalassemia

A

• Potential difficult airway 2° to maxillary deformities o Consider awake fiberoptic intubation • Complications of iron loading from chronic therapy o Diabetes (Blood glucose monitoring) o Adrenal insufficiency (↓ response to vasopressors) o Liver dysfunction & Coagulation abnormalities o Hypothyroidism & hypoparathyroidism o Arrhythmias (ECG) o Right-sided Heart failure (ECHO) • CHF common with severe anemia • Cardiac arrhythmias due to heart failure • Hemodynamic compromise with induction agents if low cardiac reserve-use cardiac sparing drugs • Very sensitive to the effects of digitalis • Hepatosplenomegaly • Coagulopathy (? Regional Anesthesia) • Hypersplenism can result in thrombocytopenia and ↑ risk of infection

30
Q

Cause of aplastic anemia

A

– Marrow Damage from: • Drugs • Radiation • Infectious process

31
Q

Anesthetic Considerations for Aplastic Anemia

A

– May need pre-op transfusion – Patients on immunosuppressive therapy • Steroid “stress” dose should be considered – Reverse isolation due to thrombocytopenia and increased risk of infection – Prophylactic antibiotics due to neutropenia – Hemorrhage (GI & Intracranial) – LV dysfunction 2° high output state and fluid overload – Co-existing congenital abnormalities • Fanconi anemia is the peds version • Cleft palate; cardiac defects – Difficulty cross-matching blood products after multiple transfusions – Preinduction/induction**** • Consider transfusions before induction • Airway hemorrhage possible with DVL • Avoid nasal intubation • Regional Anesthesia • Labile hemodynamic response to induction – Maintenance**** • PEEP will facilitate use of ↓ FiO2 • Avoid nitrous oxide • Maintain normothermia – Extubation and Postoperative period**** • Period with greatest O2 demands • Monitor coagulation status

32
Q

What is methemoglobin?

A

Hemoglobin is normally Fe+2, but is now Fe+3

33
Q

Methemoglobin will shift the curve to the

A

left

34
Q

These factors can cause methemoglobinemia

A

• Nitrate poisioning • Toxic reactions to drugs such as local anesthetic prilocaine • Hurricane spray

35
Q

Anesthetic Considerations for Methemoglobinemia

A

• Can influence the accuracy of pulse oximetry as methhemoglobin absorbs light equally in both red and infrared. • At Sa02 of >85% underestimates the true value • At Sa02 of

36
Q

S/S of acute blood loss with 20% and 40% of EBV

A

20% EBV Loss - Orthostatic hypotension - Decreased CVP - Tachycardia 40% EBV Loss - Hypotension - Tachycardia - Tachypnea - Oliguria - Acidosis - Restlessness - Diaphoresis

37
Q

What is the first fluid we go for to replace blood loss?

A

Crystalloids

38
Q

What is the definition of a massive transfusion?

A

– Transfusion of > 10 units of RBC in 24 hour period – Replacement of at least one blood volume in 24 hour period – Replacement of 50% blood volume in 6 hour period

39
Q

Complications of massive transfusion

A

– Hypothermia – Volume overload – Dilutional coagulapathy – Decreased in 2,3 DPG – Hyperkalemia – Citrate toxicity (binds calcium)

40
Q

Polycythemia usually isn’t a problem until Hct >

A

55%

41
Q

Hemophilia A is from a deficiency of factor ___, and causes a prolonged ____

A

VIII PTT (However, PT will be normal)

42
Q

Anesthetic Considerations for Hemophilia A

A

Factor VIII must be brought to near normal levels before the procedure. Can achieve this with Factor VIII infusion and DDAVP

43
Q

Hemophilia B is from a deficiency of factor ___, and causes a prolonged ____

A

IX PTT (again, PT will be normal)

44
Q

Anesthetic Considerations for Hemphilia B

A

Factor IX replacement

45
Q

Characteristics of VonWillebrand’s disease

A

• Lack of vWF, which is needed for plt adhesion • Platelet count normal • Bleeding time is markedly prolonged (normal is 3-10minutes) • May have prolonged PTT • Skin and mucus membrane bleeding common

46
Q

Anesthetic considerations for vWD

A

Replace vWF with Cryo or DDAVP

47
Q

Medications that interfere with plt function

A

ASA (COX inhibitor that blocks the formation of thromboxane A2, which inhibits platelet aggregation) Antibiotics (big impact on critically ill pts) Volume expanders like hetastarch and dextran

48
Q

Besides medications, these factors can also inhibit plt function

A

– Hypothermia (

49
Q

Treatment for altered plt function

A

Replace vWF (Cryo or DDAVP) Transfuse plts

50
Q

Platelet count >____ needed for major surgery to control bleeding and > _____ for intracranial procedures

A

50,000 for major surgery 100,000 for intracranial procedures

51
Q

Surgical hemorrhage causes release of ____ from hepatic stores

A

Fibrinogen

52
Q

Lab tests associated with DIC

A

– Rapid decrease in platelet count

53
Q

Treatment of DIC

A

– Treat whatever triggered the DIC – Transfusion of platelets, FFP, fibrinogen, Anti-thrombin III – Heparin administration to block thrombin formation which blocks consumption of the other clotting factors and allows hemostasis to occur. – Hemodynamic/ respiratory support

54
Q

Anesthetic Considerations for those on long-term anticoagulation

A

– Hold Coumadin 5 days (we want the INR to be less than 1.8) • Measure INR one day pre-op and if INR >1.8 give 1mg Vitamin K SQ – If high risk without anticoagulation- – Start IV or SQ heparin 3 days after stopping Coumadin – Turn off heparin 6 hours prior to surgery – Surgery can be safely performed if INR is

55
Q

This infection can cause hemolysis

A

Malaria

56
Q

Overall in anemia, our goal is to avoid disruption of the compensatory mechanisms of anemia. These may include:

A

Increased CO Decreased blood viscosity Increased plasma volume Increased 2,3-DPG Increased P-50 (PaO2 when SaO2 is 50%) Shift to the right of the dissociation curve Redistribution of blood flow to organs with higher extraction ratios

57
Q

Normal O2 carrying capacity is

A

16-20mL/dL

58
Q

General anesthesia management goals for the patient with chronic anemia

A

1) Give enough O2 - FiO2 - Possible transfusion 2) Avoid drugs that will decrease CO - Avoid propofol on induction - Avoid hypovolemia 3) Avoid things that will shift the curve to the left (alkalosis, hypothermia, decreased 2,3-DPG) 4) Consider your volatile anesthetics (lower Hgb means lower solubility and decreased dose, but may be offset somewhat by higher CO)

59
Q

Two origins or acquired hemolytic anemias

A

1) Immune mediated - Drug induced (PCN reaction) - Transfusion reaction - Hypersplenism 2) Infection - Malaria

60
Q

Methemoglobin causes a marked shift to the

A

LEFT

61
Q

These 3 things can cause methemoglobinemia

A

• Nitrate poisioning • Toxic reactions to drugs such as local anesthetic prilocaine • Hurricane spray

62
Q

This is the emergency treatment for toxic methemoglobinemia

A

1 to 2 mg/kg of intravenous methylene blue as a 1% solution in saline infused over 3 to 5 minutes. • may be repeated after 30 minutes.

63
Q

Massive blood transfusion will have this effect on 2,3-DPG

A

It will decrease 2,3-DPG levels

64
Q

Treatment of DIC

A

– Transfusion of platelets, FFP, fibrinogen, Anti-thrombin III – Heparin administration to block thrombin formation which blocks consumption of the other clotting factors and allows hemostasis to occur. – Hemodynamic/ respiratory support

65
Q

We hold warfarin (coumadin) for __ days pre-op and we want INR to be less than ____

A

5 days 1.8 If not less than 1.8, we give 1mg of vitamin K SQ

66
Q

If our patient can’t be taken off anticoagulation prior to surgery, how do we manage that?

A

– Start IV or SQ heparin 3 days after stopping Coumadin – Turn off heparin 6 hours prior to surgery – Surgery can be safely performed if INR is