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!!!!! Co-Existing Disease !!!!! > Anemia > Flashcards

Anemia 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

Types of amenia

A
  1. Acute = Acute blood loss
  2. Chronic
    1. Nutritional Hemolytic
    2. Aplastic
    3. Manifestation of another disease
    4. Abnormal RBC structure (SS, Thalassemia)
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4
Q

What are the CLINICAL manifestations of amenia

A

Decreased oxygen carrying capacity and the accompanying decreased tissue oxygen delivery

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5
Q

What defines O2 carrying capacity

A

Hgb.

Anemia decreases it.

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6
Q

Bonus- What are the B/G coefficients of the common volatile agents?

A
  • N20- 0.47
  • Halothane- 2.3
  • Enflurane- 1.8
  • Isoflurane- 1.4
  • Sevoflurane- 0.69
  • Desflurane- 0.42
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7
Q

In anemia treatment, what two things must be considered

A

Treatment of the underlying cause, as well as the state of anemia itself

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8
Q

Calculation of arterial blood oxygen content

A

CaO2 = (Hgb x 1.39) SaO2 + PaO2 (0.003)

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9
Q

Compensation 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
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10
Q

In anemia, the oxy-hemoglobin dissociation curve…

A

Shifts to the RIGHT

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11
Q

Methemoglobin resembles a shift to

A

the LEFT

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12
Q

Curve shifts to the right are seen 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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13
Q

Curve shifts to the left are seen 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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14
Q

Suspicion of anemia begins around

A

Hgb

(<11.5 g/dL in females)

(<12.5 in males)

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15
Q

What is the most effective treatment for anemia

A

Treating the underlying cause

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16
Q

Bonus- What are the maximum doses for Bupivacaine and Lidocaine?

A
  • Bupivacaine- 2.5mg/kg
  • Lidocaine- 4mg/kg (7 with epi)
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17
Q

In managing a pt with chronic anemia, what do we really want to avoid?

A

Disrupting their compensation methods.

For example, most don’t do well with alkalosis, hypothermia, or decreased CO (propofol)

Will intererfere with O2 delivery

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18
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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19
Q
  • How do volatile agent kinetics change in a patient with anemia?
  • In an anemic patient, what often offsets the lower B/G coefficient in regards to inhaled agents
A
  • Lower B/G coefficient
  • faster on/off,
  • may need less gas

Often offset by:

  • Increased CO
  • That’s Pharm and Coexisting colliding…
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20
Q

The decision to transfuse is based on:

A
  • The clinical judgment that the oxygen carrying capacity must be increased to prevent oxygen consumtion (VO2) from outstripping oxygen delivery (DO2)
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21
Q

What are the two possible goals of transfusion therapy?

A
  • Increase O2 carrying capacity
  • Correct a coagulation disorder
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22
Q

1 unit of RBCs will increase Hct by how much

A

3-5%

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23
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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24
Q

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

A
  • Microcytic (also hypochromic, right?)
  • In adults, depletion of iron stores is caused by chronic blood loss
    • GI bleed
    • menorrhagia
    • cancer
  • Most common form of nutritional anemia in children
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25
Q

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

A

Macrocytic (Megaloblastic bone marrow morphology)

May result in:

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

Anesthesia considerations:

  • Avoid regional blocks (neuropathys)
  • Avoid N2O (binds B12)
  • Maintain oxygenation
  • Emergency correction for surgery is RBC transfusion
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26
Q

Causes of acquired hemolytic anemias

A

Immune Hemolysis and Infection

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

(particals released durring hemolysis can result in DIC and hypersplenism)

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27
Q

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

A

Macrocytic (Megaloblastic bone marrow morphology)

May result in:

  • 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
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28
Q

Anesthesia considerations for folic acid def. anemia

A
  • Thorough airway assessment-
  • Have an alternative airway plan in place, often have difficult airways
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29
Q

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

A

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, Benzos, Meth. Blue) AVOID: hypothermia, acidosis, hyperglycemia, infection
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30
Q

Pyruvate kinase deficiency

A

Hemolytic anemmia

  • Deficiency of glycolic enzyme→ which converts glucose to lactate→ it is the primary pathway to ATP production →
  • leads to K+ leak→ results in rigid RBC and accelerated destruction
  • 2,3-dpg accumulates, causes right shift
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31
Q

Peri-op risks for hemolytic anemia

A
  • Tissue hypoxia
  • Increased infection risk if prior splenectomy
  • Increased risk of venous thrombosis
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32
Q

Pre-op planning for hemolytic anemia

A
  • EPO often given for 3 days pre-op
  • Hgb acutely less than 8 or chronically less than 6 should be considered for transfusion
  • Ensure pre-op hydration, prophylactic RBC transfusions
  • Caution with methylene Blue - can increase hemolysis!!!
    *
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33
Q

Sickle cell anemia patho

A
  • Inherited Single AA defect in the ß-globin chains
  • Mutant S hemoglobin →valine substituted for a glutamic acid
  • Hgb aggregates and forms polymers when exposed to low O2 concentrations
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34
Q

Sickle cell anemia trait

A
  • Carriers
  • 1 normal, 1 abnormal gene
    • 40% is S Hgb, 60% is normal
  • Usually non-symptomatic,
  • about 5% will have hematuria and difficulty concentrating urine.
  • No treatment needed.
  • 8% of african americans have the trait
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35
Q

SS disease

A
  • Homozygous for SS trait
  • 70-98% Hgb S
  • Chronic hemolysis, low O2 situations can lead to vaso-occlusive crisis
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36
Q

Pts with SS disease typically display what type of shift in the O-Hgb dissociation curve?

A

Right shift

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37
Q

Complications associated with SS disease

A
  • Stroke
  • heart failure
  • MI
  • Hepatic/Splenic sequestration
  • renal failure
  • High rate of peri-op complications
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38
Q

Sickle cell anemia crisis

A
  • Life threatening
  • Deoxygenation causes Hgb S to form insoluble globulin polymers
    • Acute vaso-occlusive crisis
    • Ischemia and organ infarcts
    • very painful
    • Stroke, renal failure, liver failure, splenic sequestration, PE
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39
Q

Anesthetic concerns for Sickle cell anemia

A
  • Assess for organ damage,
  • cardiac dysfunction,
  • current infections
  • Possible benefit from conservative transfusions preoperatively if having a high risk surg→ decrease Hgb S to less than 30% (diluted with Hgb A)
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40
Q

3 things that must be avoid in Sickle cell anemia

A
  1. Hypoxia
  2. Hypovolemia
  3. Blood stasis
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41
Q

Periop planning for Sickle cell anemia

A
  • O2
  • 12 hours hydration
  • Caution with pre-med
    • ​avoid respiratory depression that can lead to acidosis
  • Regional
  • AGGRESSIVE pain management
  • Strict aseptic technique, must avoid infections
  • Avoid tourniquets
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42
Q

Is regional a good idea in SS?

A
  • Yes! = advocated for!
  • But must keep in mind:
    • Hypotension
    • Blood stasis
    • Compensatory vasoconstriction
43
Q

What is a potentially fatal post-op complication in Sickle cell crisis?

A

Acute chest syndrome.

It typically occurs 2-3 days postop

44
Q

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

A

Signs and symptoms of acute chest syndrome

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

Treatment:

  • Transfuse to Hct 30%
  • give O2
  • antibiotics
  • inhaled bronchodilators
  • aggressive pain management
45
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
46
Q

Iron overload in thalassemia leads to

A
  • Pituitary: Impaired growth, infertility
  • Hypothyroidism & Hypoparathyroidism
  • Adrenal insufficiency (decreased response ot vasopressors)
  • Heart: Cardiomyopathy, Heart Failure, Arrhythmias and Rt sided heart failure
  • Liver: Hepatic cirrhosis/coagualtion abnormalities
  • Pancrease: DM (monitor blood glucose)
  • Gonads: Hypogonadism
47
Q

Some periop concerns with thalassemia

A
  • Difficult airway due to maxillary deformities, consider awake fiber optic
  • Adrenal insufficiency→ decreased vasopressor response
  • Diabetes → monitor blood glucose
  • Liver dysfunction→ coagulopathy and throbocytopenia
    • AVOID regional
    • (also note: they are VERY sensitive to the effects of digitalis)
  • Arrhythmias→ EKG Right sided failure → ECHO
48
Q

Aplastic anemia is caused by

A
  1. Bone marrow failure
  2. Which may be cased by:
    1. Drugs (all kinds)
    2. Radiation
    3. Chemotherapy
    4. Infectious diseases
49
Q

What does a CBC look like in aplastic anemia

A

RBCs < 3.5 x million/mcL

WBCs < 2.5 billion/L

Neutrophils <200 cells/mcL

Platelets <100,00/mcL

50
Q

Aplastic anemia periop 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)
51
Q

Co-existing congenital abnormalities with aplastic anemia

A

Fanconi anemia in peds

  • Cleft lip/palate
  • Cardiac defects
52
Q

Induction in aplastic anemia

A
  • Consider preop transfusion
  • Airway Hemorrhage possible with DVL
  • Avoid nasal intubation
  • Consiter Regional
  • Labile hemodynamic response to induction
53
Q

Maintenance in aplastic anemia

A
  • PEEP will allow for lower FiO2
  • Avoid nitrous (immunosupression)
  • Maintain normothermia
54
Q

Emergence in aplastic anemia

A
  • Period with greatest O2 demands
  • Monitor coags post-op
55
Q

Methemoglobinemia

A
  1. Formed when iron in Hgb is oxidized from the ferrous to the ferric state (2+ to 3+)
  2. This creates a marked LEFT shift
  3. Normal level is 1%
  4. At 30-50% pt will display signs of oxygen deprivation
    • ​​brownish colored blood
  5. Over 50% can lead to coma and death
56
Q

Methemoglobinemia can be caused by

A
  • Nitrate poisoning
  • Toxic drug reactions
    • such as from prilocaine (throat spray)
57
Q

Anesthesia considerations for metHgb

A
  • Messes with pulse ox- 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 UNDER/OVER RULE!!!)

58
Q

Emergency treatment for metHgb

A
  • O2
  • Methylene Blue 1% solution: 1-2 mg/kg over 3-5 minutes
  • Mary repeat after 30 minutes
59
Q
  • Signs of 20% acute blood loss?
  • 40% 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
60
Q

What kind of anesthetic technique might be required in someone with massive blood loss?

A
  1. Ketamine/Etomidate induction
  2. May be unable to tolerate any IA
    • may need scopolamine, benzo, opioid mix (trauma cocktail)
  3. Keep warm
  4. use pressors sparingly
    • (not treating the problem!)
  5. watch surgical field for non-clotting blood
61
Q

Post-op, what would be a concern is a pt that received massive volume resuscitation

A
  • May need post op ventilation
  • Risk for Pulmonary edema and ARDS
62
Q

Define massive transfusion

A
  • 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
63
Q

Consequences of massive transfusion

A
  • Hypothermia
  • Volume overload
  • Dilutional coagulopathy
  • Decreased 2,3-dpg
  • Hyperkalemia
  • Citrate toxicity (hypocalcemia)→hypotension
  • Tissue hypoperfusion and lactic acidosis
64
Q

Whats polycythemia

A
  • Expanded red cell mass and increased Hct, caused by-
    • Reduced volume (dehydration)
    • Excess RBC production (polycythemia vera)
    • Chronic hypoxia
65
Q

What problems can polycythemia cause? At what Hct does it become a major problem?

A

Increased blood viscosity poses risk for:

  • Thrombosis leading to CAD, pulm HTN, CNS disorders
  • Hct > 55% is problematic
66
Q

Hemophilia A- Severe, moderate, mild

A

Increased PTT NORMAL PT …….. FACTOR VIII

  • Severe-
    • Factor VIII less than 1%
    • diagnosed in childhood
    • freq. spontaneous hemorrhages; joints, muscles, organs
  • Moderate
    • Factor VIII 1-5%,
    • less severe, but still increased risk of bleeding in surg, fewer joint problems
  • Mild-
    • Factor VIII 6-30%,
    • often undiagnosed until adulthood,
    • increased bleeding risk in major surgery
67
Q

Hemophilia A anesthesia considerations

A
  • Must bring factor VIII levels to near normal (100%)
  • 3500-4000U given: 50-60 U/kg IV initially,
  • half life of 12 hours.
  • 25-30 U/kg every 8 to 12 hours as maintenance to keep the plasma levels of factor VIII . 50%
  • May need to continue up to two weeks post up.
  • DDAVP is also effective at correcting for surg
68
Q

Hemophilia B- Severe, moderate, mild

A

Increased PTT NORMAL PT ……… FACTOR IX

  • Severe
    • factor IX less than 1%
    • associated with severe bleeding
  • Moderate
    • factor IX 1-5%
  • Mild
    • factor IX 5-40%
69
Q

Hemophilia B anesthesia considerations

A
  • 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
70
Q

vWB disease patho and signs

A
  • Dysfunctional platelets (NORMAL plt count)
  • Bleeding time is markedly prolonged (normal = 3-10 minutes)
  • may also have increased PTT
  • Commonly bleed from mucus membranes-
    • ​epistaxis
    • easy bruising
    • menorrhagia
    • GI
    • gingival
71
Q

vWB disease anesthesia considerations

A
  • Avoid messing with the nose
  • DDAVP 0.3mcg/kg in 30-50ml NS over 10-20 minutes
    • (can produce tachycardia and hypotension)
  • Can also give 300mcg nasally divided between each nostril
  • Cryo more reliable for severe bleeding or surgical prophylaxis
72
Q

What does ASA do to platelets

A
  • Inhibits aggregation for life of the platelet,
  • prolongs bleeding time 2-3x within 3 hours of ingestion
  • Aggregation can be abnormal for up to 10 days
73
Q

What other drugs can cause platelet dysfunction

A
  • Antibiotics- affect aggregation and adhesion
  • Volume expanders- dextran, hespan
  • NSAIDS
74
Q

Conditions that cause platelet dysfunction

A
  • Hypothermia < 35˚C
  • Acidosis < 7.3
  • Uremia(renal disease)
  • Liver disease
75
Q

Thrombocytopenia- what is it, signs and symptoms

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
76
Q

Most common intra-op coagulopathy

A
  • Dilutional- platelets/coagulation factors
    • get diluted with fluids or PRBCs (more than 10 units)
  • Surgical hemorrhage also causes fibrinogen release
77
Q

Acquired Platelet defects can be caused by

A
  • Radiation
  • Chemo
  • Toxic chemicals
  • Thiazides,
  • ETOH,
  • estrogen
  • Cancer
  • Viral hepatitis
  • B12/folate deficiency
78
Q

DIC What is it? what is it associated with? Clinical symptoms?

A
  • Destruction of platelets??
  • Excessive deposits of fibrin/ impaired fibrin degradation
  • Bleeding results from microemboli formation that consumes clotting factors
  • Associated with:
    • sepsis
    • trauma
    • cancer
    • OB complications
    • vascular disorders
    • immune disorders
  • Clinical symptoms are a consiquence of thrombosis and bleeding:
    • microemboli accumulation in the pulmonary system
    • organ damage
79
Q

DIC lab profile

A
  • Rapid decrease in platelet count <50,000
  • Prolonged PT/PTT
  • Presence of ELEVATED split fibrin degredation products
  • LOW plasma concentrations of Antithrombin III
  • NORMAL fibrinogen levels
80
Q

DIC management

A
  • Transfuse:
    • platelets
    • FFP
    • fibrinogen
    • antithrombin III
  • Give heparin to block thrombin formation → STOPS the consumption of clotting factors
  • Hemodynamic and respiratory support
81
Q

What factors is PT sensitive to?

A

I, II, V, VII, X

(normal 10-12 secs)

82
Q

What factors is PTT sensitive to?

A

I, II, V, VII, X

IX, XI, XII

(normal 25-35 secs)

83
Q

What factors is ACT sensitive to?

A

I, II, V, VII, X

IX, XI, XII

(normal 90-120 secs)

84
Q

What factors is Thrombin time sensitive to?

A

I, II

(normal 9-11 secs)

85
Q

What is a normal fibrinogen?

A

160-350

86
Q

What’s a normal bleeding time?

A

3-10 minutes

87
Q

Vitamin K is needed for formation of which factors?

A

II, VII, IX, X

88
Q

What is the lab profile for vitamin K deficiency? Treatment?

A
  • Prolonged PT
  • NORMAL PTT

Treatment:

  • Vitamin K (takes 6-24 hours for effect)
  • FFP for acute bleeding
89
Q

Anesthesia considerations for hypercoagulability

A

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
90
Q

What is long-term anticoagulation therapy used for

A
  • Venous thrombosis
  • Hereditary hypercoagulable states
  • Cancer
  • Mechanical heart valves
  • A-fib
91
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
92
Q

How does warfarin work

A
  • Competes with vitamin K →inhibits formation of vitamin K dependent clotting factors
  • factor II, VII, IX, and X
93
Q

What lab tests are needed for warfarin monitoring

A

PT/INR

94
Q

How does heparin work

A

INDIRECTLY inhibits thrombin and Xa by binding to antithrombin III

95
Q

What lab tests are needed for heparin monitoring

A

PTT or ACT

96
Q

Heparin can be reversed with

A

Protamine

97
Q

How many days should warfarin be held pre-op and what should be checked

A
  • At least 5 and check an INR ONE day preop,
  • if greater than 1.8→ give 1 mg vitamin K subQ
98
Q

What should be done for someone on warfarin, but is very high risk for clotting

A
  • Start heparin 3 days after stopping warfarin
  • Then stop heparin 6 hours prior to surg
  • surgery can be safely performed if INR < 1.5
99
Q

what changes can interefere with O2 delivery to the tissues, or with compensatory mechanisms of an anemic patient?

A
  1. Anything that shifts the curve to the left
    • decreasing CO (Propofol causes BP to go down and can be detrimental in an anemic patient
    • Respiratory alkalosis (hyperventilation /decreased PaCO2)
    • Hypothermia
    • Abnormal hemoglobin - fetal Hgb and carboxyhemoglobin (smokers))
100
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)
101
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

102
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
103
Q

What is acute 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
104
Q

How is warfarin reversed?

A

Vitamin K

4-factor PCCs

FFP

!!!!! Co-Existing Disease !!!!! (15 decks)

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