Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Critical Care > CVT Critical Care > Flashcards

CVT Critical Care Flashcards

1
Q

What is Virchow’s Triad?

A

endothelial damage, alterations in blood flow, hypercoagulability

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

What occurs with arterial thrombosis?

A

High shear = Large # platelets, held by fibrin strans (Tx: Inhibit further arterial thrombogenesis)

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

What occurs with venous thrombosis?

A

Low shear = Fibrin and RBCs (Tx: Anti-coagulants)

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

What is the MOA of Aspirin?

A

irreversible acetylation of platelet COX site = decreased TxA2 synthesis ? TxA2 (produced by activated platelets) ? platelet aggregation and stimulates activity of new platelets via increased GPIIb/IIIa expression on platelet membranes
? Permanent effects lasting the lifetime of platelets (7-10days)

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

What is the MOA of clopidogrel?

A

? Thienopyridines: ADP receptor antagonists
? Irreversible inhibition of ADP binding to specific ADP receptors (P2Y12) on platelet membranes
? Impairs platelet release reaction and ADP-mediated activation of GPIIb/IIIa

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

What is the MOA of Fibrinogen receptor antagonists?

A

? Glycoprotein GPIIb/IIIa Blockers: fibrinogen receptor antagonists
? Abciximab (monoclonal Ab that binds to receptor) and eptifibatide (competitive memetic of fibrinogen)
? Abciximab + aspirin in cats = decreased thrombus formation compared to aspirin alone
? Eptifibatide causes circulatory failure and death in cats = BAD
? Activation of GPIIb/IIIa final common pathway of platelet aggregation (regardless of the initiating stimuli)
? Inhibit fibrin binding to GPIIb/IIIa

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

What is the goal of an anticoagulant?

A

Inhibit generation of fibrin

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

What is the MOA of warfarin?

A

Coumadin ? Vitamin K antagonist altering synthesis of K-dependent coagulation factors (II, VII, IX, X, protein C and S
? Interferes with hepatic reductase activity = impaired post translational carboxylation
? Delayed anticoagulant activity (4-5 days)
? Inactive clotting factors replacing previous functional counterparts
? Rapid inhibition of protein C and S = transient period of hypercoagulability in humans (not documented in vet med)

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

How do you measure warfarin tx?

A

Measure PT and calculate INR (International Normalized Ratio)
Goal: INR = 2-3

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

Why do you need to administer heparin when starting warfarin?

A

With rapid inhibition of Protein C and protein S = hypercoagulbility but other vit k dependent coag factors not affected for 4-5 days - thus heparin to prevent hypercoagulability that may be seen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which 2 factors are most responsive to inhibition by antithrombin?

A

Iia (thrombin) and Xa

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

How does heparin bind to antithrombin?

A

Via high affinity pentasaccharide sequence

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

What is unfractionated heparin?

A

Glycoaminoglycan that binds to antithrombin and then bind to inactivate factor Xa and about 1/3 are able to bind to and inactivate thrombin (Iia)

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

What are the effects of unfractionated heparin and how are they monitored?

A 
Unpredictable effect!  Binds to plasma proteins
Check PTT (1.5-2.5X baseline PTT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is low molecular weight heparin?

A

Depolymerization of unfractionated heparin = Smaller

100% binds to antithrombin and that binds to and inactivates factor Xa (DOES NOT bind to thrombin)

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

What are the effects of low molecular weight heparin and how are they monitored?

A

More predictable

Check with Anti-Xa levels

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

Name the 5 types of shock.

A

? Hypovolemic: decreased circulating blood volume
? Hemorrhage, dehydration, trauma
? Can include ?relative hypovolemia? = GDV, tamponade
? Cardiogenic: decreased forward flow
? Congestive heart failure, arrhythmias, tamponade, drug OD
? Distributive: loss of systemic vascular resistance
? Sepsis, obstruction, anaphylaxis
? Metabolic: deranged cellular metabolism
? Hypoglycemia, cyanide, mitochondrial dysfunction, cytopathic hypoxia of sepsis
? Hypoxemic: decreased O2 content in arterial blood
? Anemia, severe pulmonary disease, CO toxicity, methemoglobinemia

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

What are considered to be the 3 stages of shock?

A

Compensatory, Early Decompensatory, Late Decompensatory

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

Why do some cats in shock present with respiratory dysfunction?

A

The lungs are the shock organ in the cat

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

What is SvO2?

A

Mixed venous O2 saturation = Assessmen of global tissue oxygenation

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

What is ideal to maintain SvO2 (from jug cath)?

A

About 70%

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

How do hypertonic solutions work?

A

? Hypertonic Solutions: 7% NaCl: osmotic shift of water from extracellular to intracellular
? Transient volume expansion (<30 mintes), follow with crystalloids
? 5ml/kg over 5-10 minutes
? ?endothelial swelling, ?cardiac contractility, mild peripheral vasodilation, ?ICP

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

What are the labile coag factors that are not present in FFP?

A

Factor V, VIII, vWB (also no platelets)

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

What is the MOA of epinephrine?

A

? Potent pressor: mixed a/b activity
? Beta effects are variable between patients, but more potent compared to norepi
? May impair splanchnic blood flow = strong vasoconstriction in regional vasculature
? Inhibits mast cell and basophil degranulation= good for anaphylaxis

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

What is the MOA of norepinephrine?

A

? Mixed alpha and beta receptor agonist, preferential alpha effects
? Mild increase in HR/contractility and better pressor effects in those with normal CO
? Sepsis = cardiac insufficiency and vasodilation = diminished cardio effects of norepi
? In combo with dobutamine (potent b) to avoid increasing afterload in the face of diseased myocardium
? in combo with Dopa/Dobutamine may ?urine output and creatinine clearance
? Renal blood flow may improve when arterial BP normalizes
? Hypovolemia = norepi causes deleterious renal vasoconstriction
? Enhanced splanchnic DO2

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

What pressor can result in seizures in cats?

A

Dobutamine

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

What is the MOA of vassopressin?

A

On vascular smooth m via V1 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the best time to use vasopressin?

A

During the late stages of shock since you have depleted your endogenous stores in hypothalamus = Esp in patients that are vasodilated and not responding to catecholamines = Enhances sensitivity to catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is relative adrenal insufficiency?

A

Adrenal insufficiency of critical illness (decreased glucocortcoid synthesis or peripheral resistance to glucocorticoids) = Leading to refractory hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Name a pure mu agonist.

A

Fentanyl, hydromorphone, morphine

31
Q

How is remifentayl metabolized?

A

BY plasma esterases

32
Q

Name a partial mu agonist.

A

Buprenorphone

33
Q

Name a kappa agonist and mu antagonist.

A

Butorphanol

34
Q

What drug can be used to reverse opiods?

A

Naloxone

35
Q

Which opiod can result in hyperthermia in cats?

A

Hydromorphone

36
Q

Which drug can be used to reverse alpha-2 agonists?

A

Atipamezole

37
Q

What is the MOA of ketamine?

A

NMDA antagonist - Blocks wind up and central sensitization

38
Q

What is the MOA of tramadol?

A

Weak mu opioid and noepi/serotonin reupatke inhibitor

39
Q

What channel can be over expressed in chronically inflammed tissue (esp nervous tissue)?

A

Na+ channel - May consider lidocaine (Na+ channel blocker)

40
Q

In critically ill patients what is the problem with over feeding (over RER)?

A

GI intolerance, hepatic dysfunction, increased CO2 production

41
Q

What is the equation for calculating RER?

A

? >25 kg: RER= 70x(BW in kg) 0.75

? 3-25 kg: RER = (30xBW in kg) +70

42
Q

Which drugs can be given through an endotracheal tube?

A

naloxone, atropine, vasopressin, lidocaine, epinephrine ? NEVER Na bicarb, norepi, calcium salts, isoproterenol

2x IV dose, diluted in 5-10 mls saline, followed by saline flush

43
Q

What should be administered if KCL bolused!?

A

Calcium gluconate

44
Q

What determines cerebral perfusion?

A

CPP = MAP - ICP

45
Q

When is it most concerning for compromised cerebral blood flow?

A

When autoregulation mechanisms may not be working after traumatic brain injury = more susceptible to ischemia when MAP falls

46
Q

What is the Cushing’s reflex with increased ICP?

A

? Systemic hypertension with bradycardia
? Increased ICP = acute drop in CPP = dramatic increase in sympa tone = systemic vasoconstritction and increased CO = significant increase in MAP

Baroreceptors in aorta/carotid sinus trigger reflex bradycardia

47
Q

What system is used to assess neurologic status after traumatic brain injury?

A

Modified Glasgow Coma Scale

48
Q

What happens to ICP during hypoventilation?

A

? Hypoventilation = hypercapnia can cause significantly increased ICP

49
Q

What happens to ICP during hyperventilation?

A

Hypocapnia can cause cerebral vasoconstriction and decrease CBF

50
Q

Why is a CRI of mannitol not recommended in traumatic brain injury?

A

? Increases permeability of BBB, when mannitol present for prolonged periods it can cross into cerebral parenchyma and worsen edema

51
Q

What is the incidence of seizures after traumatic brain injury?

A

54% post trauma (can be immediate, early, or late)

52
Q

What has been correlated with outsome in SA with traumatic brain injury?

A

Modified Glasglow Coma Scale

53
Q

How is dehydration named in the body?

A

Based on the fluid that is left in the body

54
Q

In metabolic acidosis, when the HCO3- drops what do cats do with pCO2?

A

NO change in pCO2 when HCO3- drops in cats

55
Q

What is the equation for anion gap?

A

(Na + K) - (HCO3 + CL)

56
Q

What is the equation for Aa gradient?

A

A/a = 150 ? 1.25(pCO2) ? pO2
Normal values usually less than 15
Increased (>25 mmHg)in pulmonary disease (V/Q mismatch, right to left shunt)

57
Q

What is hetastarch made up of?

A

Hydroxyethyl starch

58
Q

What is a potential complication with hetastarch?

A

Coagulopathies: Affect vWF and Factor VIII

59
Q

Which hydroxyethyl starch can be used that has a reduced risk of coagulopathy and prolonged half life?

A

Voluven

60
Q

What effects may hydroxyethyl starch have on endothelial surface?

A

HES may also down-regulate endothelial surface adhesion molecules (decreasing inflammation, endothelial injury, and leukocyte migration into the interstitium)
HES may be able to reverse changes in microvascular premeability secondary to free radical damage in reperfusion injury

61
Q

In general, the use of a colloid will typically allow for what reduction in the amount of crystalloids that are used?

A

About a 40-60% reduction

62
Q

What is the COP of whole blood?

A

About 20 mmHg

63
Q

What is the COP of frozen plasma?

A

About 20 mmHg

64
Q

What is the COP of 25% Human albumin?

A

About 200 mmHg

65
Q

What is the COP of hetastarch?

A

About 30 mmHg

66
Q

What is the term when large volumes of fluid increase the abdominal pressure?

A

Adbominal compartment syndrome

67
Q

Which small dog breed is over-represented for GDV?

A

Dachshunds

68
Q

What are 3 prognostic indicators for GDV?

A

? Lactate>6 mmol/L
? Gastric Resection
? Splenectomy

69
Q

What is the diagnostic of choice for GDV?

A

Right lateral rad = ? pylorus is gas-filled and located cranial and dorsal to the fundus
? Compartmentalization line between pylorus and fundus, where their walls contact one another

70
Q

What is the mortality rate of GDV that are surgically managed?

A

About 15-18%, but increased if gastric resection, splenectomy, or arrhythmias at presentation

71
Q

What organism causes about 50-60% of osteomyelitis in fracture cases?

A

Staphylococcus = Think cefazolin or fluoroquinolone if Gram -

72
Q

What is the shock triad in cats?

A

Hypotension - Bradycardia- Hypothermia

73
Q

At what level is the COP considered to be clincially significant?

A

Less than 14 mHg

74
Q

What machine is used to measure colloid osmotic pressure?

A

Colloid osmometry

Critical Care (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions