Apex Unit 9 FLuid / Blood Flashcards
What is the plasma volume of a 70-kg male?
3 liters
5 liters
7 liters
9 liters
Three liters
On a question like this, many students expect to be asked about blood volume. We tried to be a bit tricky and asked about plasma volume instead. It’s always a good idea to reword the question in your mind before moving on to the answer choices.
In a 70 kg adult, the total blood volume is ~ 5 L, while the plasma volume is ~ 3 L.
Whenever you’re confronted with a body water question, we want you to remember: 60/40/20 (15/5)
In the average 70 kg male, classic teaching suggests that water represents 60 percent of the total body weight. This equals 42 L.
The total body water (TBW) can be divided into:
1. Intracellular volume = 40 percent of total body weight or 28 L
2. Extracellular volume = 20 percent of total body weight or 14 L
The ECV can be further divided into:
1. Interstitial fluid = 16 percent of total body weight or 11 L
2. Plasma fluid = 4 percent of total body weight or 3 L
*If it’s easier to remember 15 percent and 5 percent instead of 16 percent and 4 percent, that’s okay. Either way, you would’ve arrived at the same answer.
Match each term with its definition.
Osmosis
Osmolality
Osmolarity
Osmosis + Movement of water across a semipermeable membrane
Osmolality + Number of osmoles per kilogram of solvent
Osmolarity + Number of osmoles per liter of solution
Calculate the plasma osmolarity.
Sodium = 150 mEq/L Glucose = 108 g/dL BUN = 14 mg/dL
(Enter your answer as mOsm/L and round to the nearest whole number)
311 mOsm/L
Plasma osmolarity = (Na+ x 2) + (Glucose / 18) + (BUN / 2.8)
(2 x 150) + (108 / 18) + (14 / 2.8)
300 + 6 + 5 = 311 mOsm/L
We made the math easy. You’re welcome.
The normal plasma osmolarity is 280 - 290 mOsm/L. In this patient, hypernatremia is responsible for the hyperosmolar state.
Rank the tonicity for each fluid. high to low
NaCl 3%
D5W
Albumin 5%
D5 + NaCl 0.45%
NaCl 3% + 1
D5 + NaCl 0.45% + 2
Albumin 5% + 3
D5W + 4
Hypotonic solutions have an osmolarity lower than the plasma.
Isotonic solutions have an osmolarity roughly equal to the plasma.
Hypertonic solutions have an osmolarity higher than the plasma.
Choose the statements that MOST accurately describe colloids. (Select 3.)
They are proinflammatory.
Colloids are associated with better outcomes than crystalloids.
Dextran reduces blood viscosity.
Albumin causes hypocalcemia.
Albumin can cause hyperchloremic metabolic acidosis.
Hetastarch dose should not exceed 20 mL/kg.
Hetastarch dose should not exceed 20 mL/kg
Albumin causes hypocalcemia
Dextran reduces blood viscosity
Some synthetic colloids (hetastarch and dextran but not voluven) increase the risk of coagulopathy. Their dose should not exceed 20 mL/kg.
Albumin binds calcium and can contribute to hypocalcemia.
Dextran reduces blood viscosity. It is used to improve microcirculatory flow during some vascular surgeries.
Sodium chloride (not albumin) can cause hyperchloremic metabolic acidosis, although you should also keep in mind that most colloids are prepared with NaCl.
Albumin has anti-inflammatory (not pro-inflammatory) properties.
When comparing colloids to crystalloids, outcomes are the same (not better).
Loss of deep tendon reflexes is MOST likely a consequence of:
hypomagnesemia.
hypermagnesemia.
hypocalcemia.
hypercalcemia.
Hypermagnesemia
One of the first clear signs of magnesium toxicity is loss of deep tendon reflexes. Think about this in the patient being treated for preeclampsia.
Loss of DTR tends to occur when serum Mg+2 is either:
4 – 6.5 mEq/L
10 – 12 mg/dL
Indeed, different books use different units of measurement. You should know both
Match each acid-base disturbance with its arterial blood gas.
pH 7.30, PaCO2 = 50, HCO3 = 24
pH 7.21, PaCO2 = 36, HCO3 = 17
pH = 7.50, PaCO2 = 31, HCO3 = 26
pH = 7.49, PaCO2 = 41, HCO3 = 28
Respiratory acidosis + pH 7.30, PaCO2 = 50, HCO3 = 24
Metabolic acidosis + pH 7.21, PaCO2 = 36, HCO3 = 17
Respiratory alkalosis + pH = 7.50, PaCO2 = 31, HCO3 = 26
Metabolic alkalosis + pH = 7.49, PaCO2 = 41, HCO3 = 28
Which acid-base disorder is MOST likely to occur in response to untreated pain in the postanesthesia recovery unit?
Respiratory alkalosis
Metabolic acidosis
Respiratory acidosis
Metabolic alkalosis
Respiratory alkalosis
Untreated pain leads to hyperventilation and respiratory alkalosis.
Complications of respiratory alkalosis include:
Dysrhythmias
Decreased cerebral blood flow
Decreased P50 (oxyhemoglobin dissociation curve shifts to left)
Decreased serum calcium (muscle spasm or tetany if severe)
The MOST likely etiologies of metabolic alkalosis include: (Select 2.)
large volume resuscitation with NaCl.
massive transfusion.
vomiting.
diabetic ketoacidosis.
Vomiting
Massive transfusion
Metabolic alkalosis is characterized by a pH > 7.45. It is caused by increased bicarbonate and/or a loss of nonvolatile acids.
Vomiting produces H+ loss from the stomach.
Massive transfusion can produce metabolic alkalosis, because the liver converts citrate to bicarbonate.
Diabetic ketoacidosis and large volume resuscitation with NaCl produce metabolic acidosis. This explains why we don’t use large volumes of NaCl in the trauma patient.
Identify the components of the enhanced recovery after surgery program that are believed to improve postsurgical outcomes. (Select 2.)
Insertion of nasogastric tube
Carbohydrate drink two hours before surgery
Avoidance of premedication
Isoflurane instead of desflurane
Carbohydrate drink two hours before surgery
Avoidance of premedication
The primary objective of ERAS is to enhance postsurgical outcomes with a standardized approach to perioperative care.
Match each mediator with its primary function in the blood.
von Willebrand factor
Protein C
tPA
Plasminogen activation inhibitor
Procoagulant
Antifibrinolytic
Fibrinolytic
Anticoagulant
von Willebrand factor + Procoagulant
Protein C + Anticoagulant
tPA + Fibrinolytic
Plasminogen activation inhibitor + Antifibrinolytic
The blood contains factors that favor clot formation (procoagulants) and those that hinder clot formation (anticoagulants).
The blood also contains factors that break down clot (fibrinolytics) and those that impair the clot break down process (antifibrinolytics).
Platelets contain all of the following components EXCEPT:
actin.
adenosine diphosphate.
calcium.
deoxyribonucleic acid.
Deoxyribonucleic acid
Platelets don’t have a nucleus; therefore, they don’t contain DNA and they can’t undergo cell division.
Platelets are produced by megakaryocytes in the bone marrow.
Which substance is responsible for adhering the platelet to the damaged vessel?
Tissue factor
von Willebrand factor
Thromboxane A2
ADP
von Willebrand factor
Primary hemostasis describes the formation of the platelet plug. This process requires that the platelet adhere, activate, and aggregate at the site of vascular injury.
You should associate platelet adhesion with von Willebrand factor.
You should associate platelet activation and aggregation with ADP and thromboxane A2.
Match each coagulation factor with its pathway.
Tissue factor
Hageman factor
Prothrombin
Calcium
Extrinsic pathway
Affects all of the pathways
Final common pathway
Intrinsic pathway
Tissue factor + Extrinsic pathway
Hageman factor + Intrinsic pathway
Prothrombin + Final common pathway
Calcium + Affects all of the pathways
Which factors are specific to the classical intrinsic pathway? (Select 3.)
IV VI VII VIII IX XI
VIII
IX
XI
Factors specific to the intrinsic pathway include: VIII, IX, XI, XII (8, 9, 11, 12)
Factors specific to the extrinsic pathway include: III, VII (3, 7)
Calcium (factor IV) is a cofactor in both coagulation pathways.
There is no factor VI.
Place the events of the final common pathway in the correct sequence.
1st event
2nd event
3rd event
Prothrombin activator activates thrombin
Activated fibrin stabilizing factor crosslinks fibrin
Thrombin activates fibrin monomer
1st event + Prothrombin activator activates thrombin
2nd event + Thrombin activates fibrin monomer
3rd event + Activated fibrin stabilizing factor crosslinks fibrin
Identify the true statements regarding fibrinolysis. (Select 2.)
Alpha-2 antiplasmin inhibits the action of plasmin on fibrin.
Plasminogen is synthesized in the endothelium.
tPA inhibitor inhibits the conversion of fibrinogen to fibrin.
D-dimer measures fibrin split products.
D-dimer measures fibrin split products
Alpha-2 antiplasmin inhibits the action of plasmin on fibrin
Plasminogen is synthesized in the liver (not the endothelium). It is converted to plasmin by tPA, and plasmin converts fibrin to fibrin degradation products. These are measured by D-dimer.
Alpha-2 antiplasmin inhibits the action of plasmin on fibrin.
tPA inhibitor inhibits the conversion of plasminogen to plasmin (not fibrinogen to fibrin).
Match each phase of the contemporary model of coagulation with its key event.
Initiation
Amplification
Propagation
A large quantity of thrombin is produced
The TF/VIIa reaction activates the final common pathway
Platelets are activated
Initiation + The TF/VIIa reaction activates the final common pathway
Amplification + Platelets are activated
Propagation A large quantity of thrombin is produced
Identify the BEST predictor of bleeding during surgery.
Bleeding time
PT/INR
History and physical
Thromboelastogram
History and physical
History and physical is the best predictor of bleeding during surgery.
Heparin inhibits the:
extrinsic pathway.
intrinsic pathway.
extrinsic and final common pathway.
intrinsic and final common pathway.
Intrinsic and final common pathway
Heparin inhibits the intrinsic and final common pathways.
Heparin binds to antithrombin and accelerates the anticoagulant ability of AT by 1,000.
The heparin-AT complex neutralizes thrombin and factors X, XII, XI, and IX. It also inhibits platelet function.
Warfarin inhibits:
factors III and X.
factors II, VII, IX, X.
factors II, VII, IX, X and protein C.
factors II, VII, IX, X and protein C and S.
Factors II, VII, IX, X and protein C and S
Warfarin is a vitamin K antagonist, so it inhibits production of all the vitamin K dependent factors (II, VII, IX, and X). It also inhibits protein C and S.
Match each medication with its mechanism of action.
Clopidogrel + ADP receptor antagonist
Abciximab + GIIb/IIIa receptor antagonist
Warfarin + Vitamin K antagonist
Enoxaparin + Antithrombin catalyst
A patient scheduled for coronary revascularization is diagnosed with type III von Willebrand disease. What is the BEST treatment for this patient?
DDAVP
Platelets
vWF/factor VIII concentrate
Cryoprecipitate
vWF/factor VIII concentrate
There are three types of Von Willebrand disease:
Type I: Mild-moderate reduction in the amount of vWF produced.
Type II: The wWF that is produced doesn’t work well.
Type III: Severe reduction in the amount of vWF produced.
Since this patient has type III disease, giving DDAVP will have no effect. DDAVP would’ve been the correct answer if the patient has type I disease. It does not pose a risk of transfusion-related infection.
The rest of the answers are suitable choices, but they’re not the best. Platelets and cryoprecipitate contain vWF, however they also carry the risk of transfusion related infection.
Which coagulopathies present with a prolong PTT and normal PT? (Select 2.)
Factor II deficiency
Hemophilia A
Hemophilia B
Factor X deficiency
Hemophilia A
Hemophilia B
Even if you didn’t know that hemophilia A is factor 8 deficiency and hemophilia B is factor 9 deficiency, you should be able to use other pieces of the stem and answer choices to guide you down the right path.
PT measures the classical extrinsic (tissue factor) pathway.
PTT measures the classical intrinsic pathway.
Both pathways arrive at the final common pathway.
Factors II and X are part of the final common pathway. Therefore, a deficiency of factor II and X will prolong both PT and PTT.
Since hemophilia A and B affect the intrinsic, but not the extrinsic pathway, these coagulopathies will prolong the PTT only.
A septic patient undergoing exploratory laparotomy has developed bleeding from the wound and around his IV sites. He has a platelet count of 40,000 mm3, fibrinogen of 95, and an elevated D-dimer. What is the BEST treatment for this patient?
Heparin infusion
Fresh frozen plasma
Tranexamic acid
Albumin
Fresh frozen plasma
DIC is characterized by disorganized clotting and fibrinolysis that lead to the simultaneous occurrence of hemorrhage and systemic thrombosis. Definitive treatment of DIC is reversal of the cause, which in this case is sepsis. In the meantime, treatment is supportive.
Although some consider it “feeding the beast,” failure to replace platelets, FFP, and cryoprecipitate will lead to diffuse coagulopathy and hemorrhage.
A patient with a history of type II heparin induced thrombocytopenia requires anticoagulation for cardiopulmonary bypass. What is the BEST treatment?
Heparin test dose
Bivalirudin
Enoxaparin
Warfarin
Bivalirudin
Heparin is contraindicated in the patient with type II HIT, so a test dose shouldn’t be given. Remember that the immune response is a process of amplification. Think of the child with a peanut allergy, even a single peanut can yield devastating consequences.
Bivalirudin is a direct thrombin inhibitor that can be used as an alternative to heparin. In this context, it is a suitable alternative for cardiopulmonary bypass.
Enoxaparin is a low molecular weight heparin and can’t be used for CPB.
Warfarin requires 36 - 72 hours to achieve anticoagulation, so it isn’t used for CPB.
Triggers of sickle cell crisis include: (Select 2.)
hyperthermia.
dehydration.
alkalosis.
pain.
Pain
Dehydration
Sickle cell disease is an inherited disorder that affects erythrocyte geometry. Understanding the triggers helps you plan your anesthetic. Triggers include:
Pain Dehydration Hypoxemia Acidosis (not alkalosis) Hypothermia (not hyperthermia)
Match each donor blood group to the recipient(s) who can receive it.
O + A, B, AB, O
A + A, AB
B + B, AB
AB + AB
Type and screen:
takes five minutes.
mixes the recipients plasma with donor blood.
tests for ABO and Rh-D compatibility only.
tests for ABO, Rh-D compatibility, and most clinically significant antibodies.
Tests for ABO, Rh-D compatibility, and most clinically significant antibodies
Typing determines the presence of ABO and Rh-D antigens in the recipient’s blood. This takes five minutes.
Screening determines the presence of the most clinically significant antibodies. This takes 45 minutes.
Crossmatching provides the most accurate determination of compatibility by mixing the recipients plasma with blood in the actual unit that will be transfused. This takes 45 min.
Which blood product contains the HIGHEST concentration of fibrinogen?
Whole blood
Fresh frozen plasma
Packed red blood cells
Cryoprecipitate
Cryoprecipitate
Although whole blood and FFP contain fibrinogen, cryoprecipitate contains the highest concentration of fibrinogen.
A five bag pool is expected to increase fibrinogen by 50 mg/dL.
What is the maximum allowable blood loss in a 70-kg patient with a hemoglobin of 12 g/dL? The transfusion trigger is a hemoglobin of 6 g/dL.
(Enter your answer as a whole number in mL)
2275 – 2625
The maximum allowable blood loss calculation requires you to determine the estimated blood volume and then use this value in the MABL equation. Since this patient is 70 kg, we can estimate that his blood volume is 4900 mL (70 mL/kg).
MABL = EBV x (Starting hgb - Target hgb) / Starting Hgb = 2275 - 2625.
We took a range of answers to account for the fact that some books say adult blood volume is 65 - 75 mL/kg.
Match each blood additive with its function.
Citrate + Anticoagulant
Dextrose + Substrate for glycolysis
Phosphate + Buffer
Adenine + Substrate for ATP synthesis
Rank each infectious complication of transfusion from MOST common to LEAST common.
(One is most common, and four is least common)
Cytomegalovirus + 1
Hepatitis B + 2
Hepatitis C + 3
HIV + 4
A patient with O blood received AB blood during surgery. Within five minutes, you observe hemoglobinuria, hypotension, and increased surgical bleeding. What actions should you perform at this time? (Select 2.)
Give a crystalloid bolus.
Slow the rate of transfusion.
Send an AST/ALT to the lab.
Administer sodium bicarbonate.
Give a crystalloid bolus
Administer sodium bicarbonate
This patient is experiencing an acute transfusion reaction after receiving AB blood. Remember, that O blood contains anti-A and anti-B antibodies.
Immediate treatment includes stopping (not slowing) the transfusion.
Free hemoglobin obstructs the renal tubules, which can cause acute tubular necrosis. Increasing UOP with a fluid bolus helps move things through the renal tubules.
Sodium bicarbonate alkalizes the urine, which reduces hemoglobin precipitation.
You should send a serum hemoglobin, platelets, PT, fibrinogen, and a urine sample to the lab. A liver panel does nothing to aid in the treatment of this patient.
Fresh frozen plasma from which donor population imparts the HIGHEST risk of transfusion-related acute lung injury?
Jehovah witness
Creutzfeldt Jakob
Organ recipient
Multiparous female
Multiparous women
TRALI is believed to result from HLA and neutrophil antibodies present in donor plasma. Some donor populations possess a higher concentration of antibodies, and blood products from these populations increase the likelihood that the recipient will develop TRALI.
Donors that increase risk: multiparous women, history of blood transfusion, organ recipient
Recipients at greatest risk: critical illness, sepsis, burns, post-CPB
Jehovah witness patients will not accept blood transfusion.
Creutzfeldt Jakob disease (mad cow) is a prion disease that can be spread through infected blood products.
Consequences of massive transfusion include all of the following EXCEPT:
alkalosis.
hypercalcemia.
hyperkalemia.
hyperglycemia.
Hypercalcemia
Citrate intoxication is a complication of massive transfusion. As you’ll recall, citrate binds calcium and this can cause myocardial depression, coagulopathy, and impair nerve transmission.
