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Co-Existing & Basic Principles 2016 * > Anemia & Blood disorders > Flashcards

Anemia & Blood disorders Flashcards

1
Q

What are some questions you might want to ask in regards to hematology?

A
  • Have you ever had a blood problem?
  • Anemia? Leukemia?
  • Any clotting problems?
  • Lots of bleeding from cuts, nosebleeds, surgery, dental work?
  • Have you ever required a blood transfusion?
  • Has a family member/blood relative ever had a serious bleeding condition or clotting problem?
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2
Q

What common medications would make you concerned in terms of possible hematological problems?

A
  • Aspirin/NSAIDS
  • Vitamin E,
  • Ginseng, Gingko, Garlic, Saw Palmetto.
  • How often, how much, and last dose?
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3
Q

Anemia Pathology

A
  1. Can be either Acute or Chronic
    • Acute = Acute blood loss
    • Chronic = Nutritional Hemolytic, Aplastic, Manifestation of another disease, Abnormal RBC structure (Sickle cell, Thalassemia)
  2. ​​​Disease state related to
    1. ​abnormal low concentration of hemoglobin (RBCs)
    2. Abnormal structure of hemoglobin
  3. Clinical manifestation of decreased oxygen carrying capacity and delivery
    1. ​Hemoglobin Defines oxygen carrying capacity
    2. Anemia decreases o2 carrying capacity
  4. ​Care must inclued treatment of the underlying disease as well as the state of anemia
  5. MUST avoid disruption of compensatory mecheanisms
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4
Q

Calculation of arterial blood oxygen content

A

CaO2 = (Hgb x 1.39) SaO2 + 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 = 16-20 mL/dL
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5
Q

Compensatory mechanisms for anemia

A
  1. Increase CO
  2. Increase 2,3-DPG
  3. Increased P50
  4. Increase plasma volume
  5. Decreased blood viscosity = increased CO
  6. Decreased SVR
  7. Blood shunting to organs with higher extraction ratios
  8. Kidneys release EPO
  9. RIGHTWARD shift in ox-hem disassociation curve
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6
Q

Oxyhemoglobin disassociation curve shifts to the right with:

A

Think of anything that increases metabolism → RBC will want to drop off Oxygen at the tissues

  • Increased CO
  • Acidosis = Decreased pH
  • Increased 2-3 DPG
  • Exercise
  • Increased temeperature (sepsis)
  • Hgb variants with decreased oxygen affinity (Sickle cell)
    *
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7
Q

Oxyhemoglobin disassociation curve shifts to the left with:

A

Think anything that decreases metabolism →tissue does not need as much oxygen

  • Decreased CO2
  • Alkalosis = Increased pH
  • Decreased 2/3 DPG
  • Decreased temperature - hypothermia
  • High oxygen affinity Hgb variants (Fetal Hgb)

(a leftward shift on someone that is dependent on a rightowrd shift may be a problem - we do this from hyperventilation and decreaseing temperature)

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8
Q

Changes that could interefere with oxygen delivery to the tissues

A
  1. Decreased CO
  2. LEFTWARD shft in oxy-heme disassociation curve
    1. Respiratory alkalosis
      1. hyperventilation/decreased PaCO2
      2. Hypothermia
      3. Abnormal Hgb such as fetal hemoglobin and carboxyhemoglobin
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9
Q

Anemia Basic Anesthetic management

A
  1. Know your pts preoperative Hgb and HCT
    • anemia suspected if hemoglobin
      • <11.5 g/dl (females); hct <36%
      • <12.5 g/dl (males); hct <40%
  2. Hgb and HCT are RELATIVE measuremants

Treating the underlying cause

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10
Q

Anesthesia management and considerations for chronic anemia

A

Goal = AVOID disruptions of compensatory mechhanisms that are aimed at maintinging O2 delivery to the tissues!

  1. Indentify and treat underlying disease if possible
  2. Maximize O2 delivery- High FiO2
  3. Avoid drug induced decreases in CO
    • consider etomidate induction
    • may want to use high opioid technique
    • hydrate/avoid hypovolemia
    • AVOID propofol, high amounts of IAs, STP
  4. AVOID leftward shifts of the oxyhemoglobin disassociation curve
    • no hyperventilation/respiratory alkalosis
    • no hypothermia
  5. Consder volitile anesthetics may be LESS soluble in plasma
    • may have a faster induction, however, often OFFSET by the fact that these patients have and increased CO
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11
Q

Anemia and the decision to transfuse

A

Goal of transfusion therapy = Increase O2 carrying capacity and/or correct a coagulation disorder

  • There is NO tranfusion trigger and the decision to transfuse is based on:
    • The clinical judgment that the oxygen carrying capacity MUST be increased to prevent oxygenconsumtion(VO2) from being greater thanoxygendelivery (DO2)
  • A drop in Hgb from 15 to 10 = 33% decrease in arterial oxygen content!
    • it is also manifested by a RIGHT shift in the poxthemoglobin disassociation curve
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12
Q

2006 ASA guidelines regurding blood transfusion

A
  1. Rarely indicated if Hgb > 10 g/dL
  2. Almost ALWAYS indicated if Hgb
  3. If Hgb is 6-10: transfusion is based on the patients risk for complication and inadequate oxygenation
  4. Use of a transfusion trigger of Hgb is NOT RECOMMENDED
  5. Where apprropriate use of autologous blood, cell save or acute normovolemic hemodilution and measures to decrease blood loss (deliberate hypotension)
  6. Indications for transfusion are more liberal for autologous blood than blood from the blood bank
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13
Q

How do you know when to transfuse?

A
  1. You calculate the allowable blood loss for your surgical case
    • ABL = EBV x (patients Hct - Allowable Hct)

​​ patients Hct

  1. Know that:
    • 1 unit of RBCs will increase Hct 3-5%;
    • ​​or it will increase Hgb ~1 g/dL
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14
Q

Nutritional anemias

A
  • Iron deficiency
  • Folic acid deficiency
  • B12 deficiency
  • Chronic illness (infections, cancer, RF, DM, AIDS, connective tissue disorders)
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15
Q

Iron deficiency anemia- RBCs are? Common causes in adults?

A
  • Nutritional Anemia
  • Ineffective erythropoesis and Microcytic RBCs
  • In adults, depletion of iron stores is caused by chronic blood loss
    • GI bleed
    • menorrhagia
    • cancer
  • Most common form of nutritional anemia in infants and children
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16
Q

B12-def. anemia - RBCs are? May result in? Anesthesia considerations?

A

Macrocytic (Megaloblastic bone marrow morphology)

B12 deficiency may result in pernicious anemia

  • Bilateral peripheral neuropathy
  • Loss of proprioception/vibratory sensation in lower limbs
  • Decreased deep tendon reflexes
  • Unsteady gait
  • Memory impairment/mental depression

Anesthesia considerations:

  • Avoid regional blocks (neuropathys)
  • Avoid N2O (binds B12)
  • Maintain oxygenation
  • Emergency correction for imminent surgery is RBC transfusion
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17
Q

Causes hemolytic anemias

A

Acquired Hemolytic Anemias

  • Drug induced (High dose PCN, alpha- methyldopa)
  • Disease/infection induced (malaria, epsteen Barr)
  • Sensitization of RBCs (Maternal/fetal)

(particals released durring hemolysis can result in <strong>DIC</strong> and <strong>hypersplenism</strong>)

Hereditary hemolytic anemias

  1. Hereditary spherocytosis
  2. Paroxysmal nocturnal hemoglobinuria
  3. Glucose 6 Phospahete dihydrogenase deficiency
  4. Pyruvate Kinase Deficiency
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18
Q

Folic acid deficiency anemia- RBCs are? May result in? Anesthesia considerations?

A

Macrocytic (Megaloblastic bone marrow morphology)

Folic acid deficiency may result in penicious anemia

  • Smooth tongue (difficult intubation)
  • Hyperpigmentation
  • Mental depression
  • Peripheral edema
  • Liver dysfunction
  • Severely ill patient

Anesthesia considerations:

  • Thorough airway assessment
  • Have an alternative airway plan in place
  • often have difficult airways d/t tongue texture!
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19
Q

Glucose-6-Phosphate dehydrogenase deficiency What is it? Who does it affect? What should you avoid?

A

Disorder affecting RBC metabolism

Form of hemolytic anemia

  • Most common enzymopathy; decreased G6PD activity leaves RBCs susceptible to damage by oxidation.
  • Cell membranes have increased rigidity of membranes and there is accelrated RBC clearance
  • Acute and chronic episodes.
  • Most prevalent in: Blacks, Asians, Mediterranean populations

Anesestetic consideratons:

  • AVOID: oxidative drugs (LAs, N2O, Meth. Blue)
  • AVOID: hypothermia, acidosis, hyperglycemia, infection
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20
Q

Peri-op risks and concerns for hemolytic anemia

A

Hemolytic anemia risks:

  • Increased tissue hypoxia
  • Increased infection risk if prior splenectomy
  • Increased risk of venous thrombosis

To offset these risks preop planning should include:

  • EPO given for 3 days pre-op
  • Consider for transfusion if:
    • Hgb acutely < 8 g/dl or
    • Hgb chronically 6 g/ dl
  • Adequate pre-op hydration and prophylactic RBC transfusions
  • Caution with Methylene Blue - can increase hemolysis!!!
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21
Q

Sickle cell anemia patho

A

Cellular Pathology

  • Inherited
  • Defects in a Single AA substitution in the ß-globin chains of hgb
    • →valine substituted for a glutamic acid
  • Hgb aggregates & forms polymers when there is low O2 concentrations
  • Hemoglobin S has a shorter life span
    • ​12-17 days vs 120 days normal
  • the sicke cells obstructs and occlude small vessels

Sickle cell trait vs. disease

  • trait = heterozygus carriers (asymptomatic)
    • 8% African Americans are Heterozygous carriers (hemoglobin genotype AS
    • Usually are asymptomatic & Do NOT need Rx
    • 40% of their Hgb is S
    • 5% at some time have: hematuria, difficulty concentrating urine, and do not require pre-op transfusions
  • disease = Homozygus (have the disease)
    • Hgb S - 70-98%
    • Anemia is well-tolerated – pts have compensatory RIGHT shift of oxyhemoglobin dissociation curve to provide adequate O2 delivery to tissues
    • These pts have a 30% overall complication rate: stroke, HF, MI, hepatic or splenic sequestration, RF
    • Avoid all situations leading to: Hypoxemia, Hypovolemia, Stasis
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22
Q

Explain a Sickle cell crisis

A
  • Life threatening
  • Acute vaso-occlusive crisis (Deoxygenation causes Hgb S to form insoluble globulin polymers​)
  • Ischemia and organ infarcts
  • very painful
  • Can cause stroke, renal failure, liver failure, splenic sequestration, PE and acute chest syndrome
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23
Q

Periop planning for Sickle cell anemia

A
  • O2
  • 12 hours hydration
  • Pre-op exchange transfusons (HCT to 30% Hgb S )
  • Caution with pre-med
    • ​avoid respiratory depression that can lead to acidosis
  • USE Regional!
  • AGGRESSIVE pain management
  • Strict aseptic technique, must avoid infections
  • Avoid tourniquets

AVOID ALL SITUATIONS LEADING TO

  • Hypoxemia
  • Hypovolemia
  • Stasis
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24
Q

What are the signs and symptoms of acute chest syndrome and how is it managed?

A

Signs and symptoms of acute chest syndrome due to pumonary vascular occlusion

  • Pleuritic chest pain
  • dyspnea
  • fever
  • acute pulmonary HTN

Treatment:

  • Transfuse to Hct 30%
  • give oxygen
  • antibiotics
  • inhaled bronchodilators
  • aggressive pain management
25
Q

Thalassemia major

patho and signs and symptoms

A
  • Inability to form alpah or beta-globin hemoglobin chains

​Signs and symptoms:

  • Hepatosplenomegaly
  • Dyspnea &orthopnea
  • Infection risk
  • CHF, dysrhythmias
  • Bone malformations (Overgrown maxillae - difficult intubation!!!)
  • Hemothorax
  • Spinal compression (No epidurals or spinals)
  • Mental Retardation
  • Digitalis sensitivity
  • Increased RBC production
  • Jaundice
  • Iron overload
26
Q

thalassemia

Perioperative risks and concerns

A
  1. Difficult airway (maxillary deformities), consider awake fiber optic
  2. Complications of iron loading d/t chronic therapy
    1. ​​Arrythmias, CHF, Right heart failure, cardiomyopathy
      • Get an EKG and ECHO
      • also note: VERY sensitive to the effects of digitalis
    2. Adrenal Insufficiency
      • Decreased vasopressor response
    3. Hemodynamic compromise with induction agents
      • ​if low cardiac reserve use cardiac sparing drugs
    4. Diabetes → monitor blood glucose
    5. Liver Dysfunction→ coagulopathy
      • ​AVOID regional
    6. Hepatosplenomegaly
      1. thrombocytopenia
      2. increased infection risk
    7. Hypothyroid and hypoparathyroid
27
Q

Aplastic anemia is caused by

A
  1. Bone marrow failure characterized by destruction of rapidly growing cells
  2. Marrow damage from:
    1. Drugs (all kinds)
    2. Radiation
    3. Chemotherapy
    4. Infectious diseases
  3. CBC values extremely low
    • ​​Remember: usually see spontaneously bleeding with plt counts of <50-75K; these pts may need pre-op transfusion
  4. Know the pt’s pre-op medications and therapies. They will typically be on steroids, chemo, Rad tx
28
Q

Aplastic anemia

perioperative risks and concerns

A
  • Often on immunosuppression
    • may need “stress dose” steroids
  • Reverse isolation
  • Prophylactic antibiotics d/t neutropenia
  • Hemorrhage (GI and intercranial)
  • LV dysfunction due to high output state
  • Difficulty in cross-matching
    • (have had multiple transfusions)
  • Co-existing congenital abnormaliities
    • (Fanconi anemia - peds- cleft palate and cardiac defects)
29
Q

Co-existing congenital abnormalities with aplastic anemia

A

Fanconi anemia in peds

  • Cleft lip/palate
  • Cardiac defects
30
Q

aplastic anemia

Induction

A
  • Consider preop transfusion
  • Airway Hemorrhage possible with DVL
  • Avoid nasal intubation
  • Consider Regional if coags allow
  • Will have labile hemodynamic response to induction
31
Q

aplastic anemia

Maintenance

A
  • PEEP will allow for lower FiO2
  • Avoid nitrous (immunosupression)
  • Maintain normothermia
32
Q

aplastic anemia

Emergence

A
  • Extubation and post-op perioid are the periods with greatest oxygen demands
  • Monitor coagulation status
33
Q

Methemoglobinemia

What is it?

What casues it?

A
  1. Formed when iron in Hgb is oxidized from the ferrous to the ferric state (2+ to 3+)
  2. LEFT shift = little oxygen delivery to the tissues
  3. Normal blood level = 1%
  4. At 30-50% methemoglobinemia there will be signs of oxygen deprivation→​​BROWN blood
  5. Over 50% can lead to coma and death

Causes:

  • Nitrate poisoning (SNP)
  • Toxic drug reactions
    • such as from prilocaine (throat spray)
34
Q

Anesthesia considerations for metHgb

A
  1. Makes the pulse ox inaccurate
    • MetHgb absorbs red and infrared light equally
      • at SaO2 over 85% → true value is underestimated
      • at SaO2 under 85%→ true value is overestimated

(just think the OVER/UNDER RULE!!!)

  1. Toxic Methemoglobinemia requires emergent treatment
    1. Oxygen
    2. Methylene Blue 1% solution: 1-2 mg/kg over 3-5 minutes
      • Mary repeat after 30 minutes
35
Q
  • Clinical Signs of acute blood loss
A

20% acute blood loss:

  • Tachycardia
  • Orthostatic hypotension
  • CVP changes

40% acute blood loss

  • Tachycardia
    • (may have EKG chnages d/t change in O2 carrying capacity)
  • hypotension
  • tachypnea
  • oliguria
  • acidosis
  • restlessness
  • diaphoresis
36
Q

Acute blood loss

Treatment

A
  1. Restore intervascualr volume
    • (crystalloids, colloids, blood products)
  2. Monitor Labs
    1. Coagulation
      • CBC (Hgb/HCT, platelets), PT, PTT, INR, fibrinogen
    2. ​Calcium and potassium
    3. ABGs (persistant metabolic acidosis reflects hypovolemia and inadequate oxygen delivery to the tissues)
  3. Hemodynamic monitoring
    1. CVP, A-line, +/- PA
    2. do they have adequate urine output? Hematuria?
37
Q

Blood loss

Induction, maintinence and Post op

A
  1. Induction: Ketamine/Etomidate
  2. Maintinence
    • May too unstable for ANY Inhaled anesthetics
    • trauma cocktail = scopolamine, benzo, opioid mix
    • Keep warm
    • use pressors sparingly→not treating the problem!
    • watch surgical field for non-clotting blood
  3. Post-operative
    • May need post op ventilation
    • Risk for Pulmonary edema and ARDS
38
Q

Definition massive transfusion

what are consiquences of massive transfusion?

A

Definition

  • More than 10 units PRBCs in 24 hour period
  • Replacement of at least one blood volume in 24 hours
  • 50% blood volume replacement in 6 hours

Consiquences

  • Hypothermia
  • Volume overload
  • Dilutional coagulopathy
  • Decreased 2,3-dpg
  • Hyperkalemia
  • Citrate toxicity (hypocalcemia)→hypotension
  • Tissue hypoperfusion and lactic acidosis
39
Q

Polycythemia

What is it?

Problem?

A

Increased Hct and high RBC mass → caused by:

  • dehydration
  • Excess RBC production (polycythemia vera)
  • Chronic hypoxia

Increased blood viscosity poses risk for:

  • Thrombosis leading to CAD, pulm HTN, CNS disorders
  • Hct > 55% is problematic
40
Q

Hemophilia A

Anesthesia considerations

A
  1. Factor VIII (8 deficiency)
  2. Increased PTT NORMAL PT
    • Severe→ (VIII 1%) childhood diagnosis → spontaneous hemorrhages; joints, muscles, organs
    • Moderate→ (VIII1-5%)high bleeding risk in surgery→ Have less joint bleeding problems
    • Mild→ (VIII = 6-30%)→adultdiagnosis→bleeding risk inMAJOR surgery
  3. ​Anesthesia considerations:
    • Pre-op factor VIII​ →start at 100% then mintain at >50%
    • IV: 50-60 U/kg loading then 25-30 U/kg q8-12 hours
    • E1/2 = 12 hours
    • May need for two weeks post op.
    • DDAVP is also effective at correcting for surg
41
Q

Hemophilia B- Severe, moderate, mild

A

Congenital Factor IX deficiency

Increased PTT normal PT

  • Severe (factor IX 1%)→ severe bleeding
  • Moderate(factor IX = 1-5%)
  • Mild (factor IX = 5-40%)

Anesthesia Considerations

  • GIVE factor IX prior to surgery!!!
  • 7000 Units (70kg) = 100 U/kg
  • Half life is 18-24 hours, so 50% of original dose needs to be given every 12-24 hours to keep levels about 50%.
  • Treatment can result in increased thromboembolic events
42
Q

von Wilibrand disease

Anesthesia considerations

A

Von Wilibrand Disease

  • Dysfunctional platelets (NORMAL plt count)
  • prolonged Bleeding time (>10 minutes)
  • Increased PTT
  • Bleed from mucus membranes
    • ​epistaxis, bruising, menorrhagia, gingival and GI bleeding

Anesthesia Considerations

  • Avoid messing with the nose (intubation/trumpets)
  • Desmopressin (DDAVP) IV or intranasal
    • IV: 0.3mcg/kg in 30-50ml NS over 10-20 minutes
    • Intrnasal = 300mcg divided between each nostril
    • (can produce tachycardia and hypotension)
  • Cryo for severe bleeding or surgical prophylaxis
43
Q

Compare Labs and Treatment

Hemophelia A, Hemophelia B and von Wilibrand disease

A
45
Q

Platelet Dysfunction

Causes and Treatment

A

Drugs

  1. Asprin/NSAIDS
    • Inhibits aggregation for life of the platelet
    • bleeding time = 2-3x longer within 3 hours of ingestion
    • 72 hours = returns to normal
    • Aggregation inhibited up to 10 days
  2. ​Antibiotics
    • Interferes with platelet adhesion and activation
    • Biggest impact on critically ill
  3. Volume expanders
    • dextran = platelet inhibition
    • hespan = dilutional thrombocytopenis​

Other Factors

  1. Hypothermia
  2. Acidosis (pH
  3. Uremea and liver disease

​Treatment

  1. vWF in Cryo
  2. Desmopressin DDVAP
  3. Platelet transfusion
46
Q

Thrombocytopenia

what is it?

signs and symptoms

goals and treatment

A
  • Low platelet count
  • approximately 1/3 of platelets sequestered in spleen
  • Signs:
    • Petechial rash
    • nose bleeds
    • GI bleeds
    • bruising
  • Need >50,000 for major surg
  • A six pack of platelets should increase platelets by about 50,000
47
Q

Most common intra-op coagulopathy

A
  • Dilutional thrombocytopenia or coagulopathy
    • occurs when blood loss replaced with crystalloid, colloid or PRBCs
    • dilution of platelets and clotting factors
    • occurs with massive transfusion (more than 10 units)
  • Surgical hemorrhage also causes fibrinogen release from hepatic stores
48
Q

Acquired defects in platelet production

A
  • Radiation
  • Chemo
  • Toxic chemicals
  • Thiazides,
  • ETOH,
  • estrogen
  • Cancer
  • Viral hepatitis
  • B12/folate deficiency
49
Q

Tests of Coagulation

Lab Values

Clotting factors

A
50
Q

DIC

What is it?

what is it associated with?

Clinical symptoms?

Labs

Treatmetn

A

DIC = diseminated intravascular coagulation

  1. Classified as a Consumptive coagulopathy
    • Bleeding, microemboli, consumption of platelet and clotting factors, fibrin deposits and impaired fibrin degredation
  2. Associated with:
    • sepsis, trauma, cancer, immune disorders
    • OB complications, vascular disorders
  3. Clinical symptoms d/t thrombosis and bleeding:
    • microemboli accumulation in the pulmonary system
    • organ damage
  4. ​​​​No single lab test diagnostic
    • ​Rapid decrease in PLT to
    • Prolonged PT/PTT
    • Presence of split fibrin degridation products
    • Normal Fibrinogen levels
    • Low plasma Antithrombin III
  5. ​Treamtment = manage casue and coagualtion process
    • ​PLT, FFP, Fibrinogen, Antithrombin III
    • Heparin (Blocks thrombin and faciltates hemostasis)
    • Hemodynamic and respiratory support
52
Q

Vitamin K deficiency

A
  1. Vitamin K is needed for formation of factors
    • II, VII, IX, X
  2. Causes:
    • Malnutrition/malabsorbtion
    • Antibiotic induced elimination of intestinal flora
    • Liver Disease/obstrucyive jaundice
  3. Lab profile:
    • Prolonged PT, NORMAL PTT
  4. Treatment:
    • Vitamin K (takes 6-24 hours for effect)
    • FFP for acute bleeding
53
Q

Hypercoagulability Disorder

Causes

Anesthesia considerations

A

Causes of Hypercoaguability disorders

  • Malignancies, Pregnancies, Oral contraceptives
  • Lupus, Nephrotic syndrome

Anesthesia considerations

  1. Prevent thrombus, PE, DVT, blood clots
    • Early ambulation
    • SubQ heparin
    • Compression devices
    • ASA
    • IVC filter
    • Regional anesthesia is beneficial, but contraindicated if pt on LMWH
54
Q

What is long-term anticoagulation therapy used for

A

​Long term anticoagulation used for:

  • A-fib, Venous thrombosis and heart valves
  • Hereditary hypercoagulable states
  • Cancer

(Threapy poses a problem at the time of surgery → MUST evaluate the risk of thrombosis with the risk of bleeding)

55
Q

Antiplatelet therapy is indicated periop for what conditions? Which meds are commonly used?

A

Antiplatelet therapy indicated for:

  • Pts at high risk for CVA, MI, vascular thrombosis complications

Medication used

  • ASA, PDE inhibitors, ADP receptor antagonists
56
Q

Warfarin

Anesthesia considerations

A
  • Mechanism
    • Competes with vitamin K →inhibits formation of vitamin K dependent clotting factors
    • factor II, VII, IX, and X
  • Lab tests: PT/INR
  • Reversal: Vitamin K, FFP, 4 factor PCCs
  • Holding Warfarin prior to surgery:
    • At least 5 days
    • check INR ONE day preop,
      • if > 1.8→ give 1 mg vitamin K subQ
  • If they are high risk and cannot go without anticoagualtion
    • Start heparin 3 days after stopping warfarin
    • Stop heparin 6 hours prior to surg
    • surgery can be safely performed if INR
    • (regional??? I wouldn’t)
57
Q

Heparin

Anesthesia connsiderations

A

Mechanism

  • INDIRECTLY inhibits thrombin and Xa by binding to antithrombin III

Lab tests: PTT or ACT

Reversal: Protamine

Complication: HIT (thromboembolic complication)

58
Q

What is P50

A
  • the partial pressure at which 50% of hemoglobin is saturated
  • Usually around 26-28%
  • A right shift needs a higher partial pressure to sarurate 50% (left shift = lower PP)
59
Q

Relative partial pressures and oxygen saturation

A

At 40 mmHg 70% of hemoglobin will be saturated

At 60 mmHg 90% of hemoglobin will be saturated

60
Q

Explain the steep part of the oxyhemoglobin disassociation curve

A
  • there is a rapid unloading of O2 in response to a small change in the partial pressure of O2
61
Q

Treatment for acute blood loss

A
  1. Restore intervascualr volume first!!!
    • Colloid
    • crystalloid
    • Blood products (O2 carrying capacity)
  2. Monitor coagulation
    • (blood loss decreases clotting factors)
    • PT, PTT, INR, CBC, PLT
    • If you see oozing in the surgical field CHECK FIBRINOGEN!!!
  3. Monitor serum calcium and potassium levels
    1. citrate binds to calcium
    2. blood products have high potassium and will have a higher contenct as the cells degrade
    3. Hypotension? may need some calcium!
  4. ABGs
    • persistent metabolic acidosis reflects reflects hypovolemia and decreased oxygen delivery to the tissues

Co-Existing & Basic Principles 2016 * (21 decks)

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