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38 Cards in this Set

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  • Back
What factors effect the delivery of transdermal fentanyl

a. Dermal blood flow, presence of fur, obesity, hypothermia, hypovolemia, and proximity to an external heat source. It takes 12 to 24 hours after application of the patch for steady-state plasma fentanyl concentrations to be achieved. The patch lasts approximately 72 hours in the dog and up to 5 days in the cat.
53
How does Thromboelastography (TEG) work

a. Viscoelastic analyzers measure changes in the viscosity or elasticity of a blood sample as it turns from liquid to a fibrin clot during coagulation. The use of whole blood is ideal to re-create the physiology of coagulation ex vivo because it summates the contribution of each individual component (e.g., platelets, red blood cells, plasma factors) to hemostasis.
b. The machine contains a rotating plastic cylindrical cuvette (the cup) with a stationary suspended piston (the pin) that is lowered into the center of the cuvette. As clot formation progresses, the fibrin that is generated physically links the pin to the cup. As this connection strengthens , the rotation of the cup is transmitted to the pin and this torque is translated into the TEG tracing by the torsion wire.
54
Does TEG generally correlate with PT/PTT

a. Reaction time generally reflects coagulation factor levels but does not always correlate with prothrombin time (PT) and activated partial thromboplastin time (aPTT).
55
What is the r time

a. The R-time is the time in minutes from when that blood is placed in the TEG until initial fibrin formation.
56
What is the k time

a. The K-time measures in minutes the time it takes from initiation of clot to a predetermined amount (20 mm) of clot strength.
57
What is the alpha angle

a. The α-angle measures in degrees the rate of fibrin buildup and cross-linking as a function of amplitude and time.
58
What is MA

a. The maximum amplitude (MA, measured in mm), the widest part of the TEG tracing, is a direct result of fibrin production and platelet function and represents the final clot strength.
59
What affects the k time and the alpha angle

a. Fibrinogen levels, platelet number, and factor XIII
60
What else does TEG measure

a. The TEG also demonstrates fibrinolysis as a percentage and this indicates clot strength
61
An animal that is hypercoagulable will demonstrate what with TEG

a. A a shorter R-time, a steeper α-angle (corresponding to more rapid clot formation), and a greater MA than the reference range. Some animals may display all these characteristics and some only an increased α-angle and MA.
62
An animal that is hypocoagulable will show what

a. A prolonged R-time if they have a decrease in coagulation factors. If animals are hypocoagulable due to thrombocytopenia, the R-time remains normal (because it is determined by plasma proteins), but the α-angle and MA will be significantly decreased.
63
What studies have shown TEG to be clinically useful

a. Studies involving dogs with Parvovirus, dogs with metastatic neoplasia, dogs with DIC, consistent with traditional clotting tests in an ICU setting, protein-losing nephropathies, enteropathies (where tendencies toward hypercoagulability were identified), hyperadrenocorticism (where affected dogs did not have TEG parameters different from a control group), and immune-mediated hemolytic anemia (where affected dogs also displayed hypercoagulability).
64
What things can influence the accuracy of TEG

a. Anemia: As Hct drops, the tracing appears progressively hypercoagulable, with both a steeper angle and a larger MA.
b. Thrombocytopenia: Patients with thrombocytopenia less than 50 to 75 × 103 platelets/ µL generate a hypocoagulable tracing. The TEG tracing (specifically MA) is also directly correlated to the patient's fibrinogen concentration.
65
What are some limitations of TEG

a. TEG is very sensitive to heparin , and even subtherapeutic levels result in significantly prolonged assay times and may not generate a tracing.
b. In both dogs with hemophilia and those with factor VII deficiency the TEG demonstrated hypocoagulability. The TEG can presumably be used to monitor dogs that have other factor deficiencies as they are addressed therapeutically, although the value of a TEG analysis versus standard coagulation testing (e.g., PT, aPTT) in this context is debatable.
c. Subject to user error and there are no designated operating protocols in veterinary medicine
66
What describes a respiratory acid base disorder

a. Respiratory acid-base disorders occur whenever there is a primary change in PCO2,
67
What describes a metabolic acid base disorder

a. Metabolic acid-base disorders occur whenever SID (strong ion difference) or Atot are changing primarily.
68
What is the definition of strong ion difference

a. The SID is the difference between all strong cations and all strong anions. Strong ions are fully dissociated at physiologic pH and therefore exert no buffering effect. However, strong ions do exert an electrical effect because the sum of completely dissociated cations does not equal the sum of completely dissociated anions. Because strong ions do not participate in chemical reactions in plasma at physiologic pH, they act as a collective positive unit of charge
69
What are the strong ions

a. The quantitatively most important strong ions in plasma are Na +, K +, Ca2+, Mg2+, Cl −, lactate, β-hydroxybutyrate, acetoacetate, and SO4.
70
What changes from an ion standpoint to increase SID

a. An increase in SID (by decreasing Cl − or increasing Na +) causes a strong ion (metabolic) alkalosis, a decrease in albumin
71
What changes to decrease SID

a. A decrease in SID (by decreasing Na + or increasing Cl −, , or organic anions), increases in phosphorus causes a strong ion (metabolic) acidosis.
72
How does one calculate anion gap

a. AG = (Na + + K +) – (Bicarb- + Cl–)
73
How do you calculate strong anion gap

a. SIG = [albumin] × 4.9 – AG (for dogs)
b. SIG = [albumin] × 4.58 – AG + 9 (for cats)
74
What things cause an increased anion gap

a. Acidosis caused by addition of unmeasured anions (lactic acidosis, ketoacidosis, renal failure, poisonings) • Hyperphosphatemia (hyperphosphatemic acidosis)
75
What things cause a decreased anion gap

a. Hypoalbuminemia (hypoalbuminemic alkalosis)
76
Describe chloride gap

a. Increases in chloride lead to metabolic acidosis by decreasing SID, whereas decreases in chloride cause metabolic alkalosis by increasing SID.
77
Describe A-a gradient as it applies to a clinical patient:

a. If the (A − a) O 2 gradient is increased, a component of the hypoxemia results from ventilation-perfusion mismatching, although it may be increased in some patients with extrapulmonary disorders . Clinically, a normal gradient excludes pulmonary disease and suggests some form of central alveolar hypoventilation or an abnormality of the chest wall or inspiratory muscles.
78
Describe causes of respiratory alkalosis

a. Respiratory alkalosis occurs whenever the magnitude of alveolar ventilation exceeds that required to eliminate the CO 2 produced by metabolic processes in the tissues. Common causes of respiratory alkalosis include stimulation of peripheral chemoreceptors by hypoxemia (Right-to-left shunting • Decreased FiO2 (e.g., high altitude) • Congestive heart failure • Severe anemia), primary pulmonary disease (Pulmonary diseases with ventilation-perfusion mismatch • Pneumonia • Pulmonary thromboembolism • Pulmonary fibrosis • Pulmonary edema • Acute respiratory distress syndrome), direct activation of the brainstem respiratory centers (Liver disease • Hyperadrenocorticism • Gram-negative sepsis • Drugs • Corticosteroids • Central neurologic disease • Heatstroke), overzealous mechanical ventilation , and situations that cause pain, anxiety, or fear
79
When might one see clinical abnormalities in patients with respiratory alkalosis

a. When PCO2 is less than 25 mmHg, cerebral vasoconstriction
80
What causes acute respiratory acidosis

a. Acute respiratory acidosis usually results from sudden and severe primary parenchymal (e.g., fulminant pulmonary edema), airway (Aspiration (e.g., foreign body, vomitus) • Mass (e.g., neoplasia, abscess) • Tracheal collapse • Asthma • Obstructed endotracheal tube • Brachycephalic syndrome • Laryngeal paralysis/ laryngospasm) pleural, chest wall (•Diaphragmatic hernia • Pleural space disease (e.g., pneumothorax, pleural effusion) • Chest wall trauma/ flail chest; neurologic (e.g., spinal cord injury), or neuromuscular (e.g., botulism) disease. Cardiopulmonary arrest • Heatstroke
81
What causes chronic respiratory acidosis

a. Chronic respiratory acidosis results in sustained hypercapnia and has many causes including alveolar hypoventilation, abnormal respiratory drive, abnormalities of the chest wall and respiratory muscles, and increased dead space; small and large airway diseases
82
At point is it dangerous for a patient to be hypercapneic

a. Clinically, the effects of hypercapnia on the central nervous system (CNS) can result in signs ranging from anxiety, restlessness, and disorientation to somnolence and coma, especially when PCO2 approaches 70 to 100 mm Hg. Cerebral vasodilation.
83
Why is it potentially dangerous to supplement oxygen to patients with chronic respiratory acidosis

a. Chemoreceptors less sensitive to changes in PCO2 and more responsive to oxygen so supplementing with oxygen can decrease ventilation drive and make respiratory acidosis worse
84
Hypoalbuminemia causes what change to pH

a. Presence of hypoalbuminemia complicates identification of increased unmeasured anions (e.g., lactate , ketoanions) because hypoproteinemia not only increases pH but also decreases AG. Thus the severity of the underlying disease leading to metabolic acidosis may be underestimated if the effects of hypoalbuminemia on pH, , and AG are not considered
85
Hyperphosphatemia causes what

a. Hyperphosphatemia, especially if severe, can cause a large increase in Atot, concentration leading to metabolic acidosis.
86
Describe how changes in strong ion difference occur and what their effect on pH are:

a. A decrease in SID is associated with metabolic acidosis, whereas an increase in SID is associated with metabolic alkalosis. There are three general mechanisms by which SID can change: (1 ) a change in the free water content of plasma, (2) a change in Cl −, and (3) an increase in the concentration of other strong anions.
87
Things that cause SID to increase (increases in sodium or decreases in chloride) include what

a. Pure water loss
i. Inadequate access to water (water deprivation) • Diabetes insipidus
b. Hypotonic fluid loss
i. Vomiting • Nonoliguric renal failure • Postobstructive diuresis
88
What things cause hypochloremic alkalosis

a. Excessive gain of sodium relative to chloride; Sodium bicarbonate administration
b. Excessive loss of chloride relative to sodium
i. Vomiting of stomach contents • Therapy with thiazides or loop diuretics
89
What are three general mechanisms that cause decreases in SID

a. Three general mechanisms can cause SID to decrease, resulting in SID acidosis:
b. (1) a decrease in Na +,
i. With hypervolemia (gain of hypotonic fluid) • Severe liver disease • Congestive heart failure • Nephrotic syndrome
ii. Normovolemia
1. • Psychogenic polydipsia • Hypotonic fluid infusion •
iii. With hypovolemia (loss of hypertonic fluid) • Vomiting • Diarrhea • Hypoadrenocorticism • Third-space loss • Diuretic administration
c. (2) an increase in Cl –
i. Excessive loss of sodium relative to chloride
1. Diarrhea •
ii. Excessive gain of chloride relative to sodium • Fluid therapy (e.g., 0.9% saline, 7.2% saline, KCl-supplemented fluids) • Total parenteral nutrition •
iii. Chloride retention
1. Renal failure • Hypoadrenocorticism
d. (3) an increased concentration of other strong anions (e.g., L-lactate, β-hydroxybutyrate).
i. Uremic acidosis • Diabetic ketoacidosis • Lactic acidosis • Toxicities, ethylene glycol toxicity, salicylate toxicity