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Uncategorized > Winter- Final Exam > Flashcards

Winter- Final Exam Flashcards

1
Q

a 5-10% increase in CO can raise a MAP from 100 mmHg to ______ mmHg?

A

150 mmHg

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2
Q

name 4 things that affect the rate of filtration of water and salt through the kidneys

A

MAP
Renal BF
Pressure in Glomerular capillaries
Oncotic pressire in Glomerular capillaries

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3
Q

name 3 things that affect the rate of reabsorption of water and salt through the kidneys

A

Concentration of Angiotension II, Aldosterone and Antidiuretic Hormone
*All of these increase rate of reabsorption

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4
Q

describe the steps of the renin-angiotensin system when there is a decrease in MAP

A
  1. Prorenin splits into renin which is released into the afferent arterioles and circulates to the rest of the body
  2. Renin circulates in the blood for 30-60min where it acts on angiotensinogen to release angiotensin 1
  3. Angiotensin 1 is carried to the lungs where angiotensin converting enzyme converts it to angiotensin 2
  4. Angiotensin 2 lasts for 1-2min before being deactivated by andiotensinases
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5
Q

Renin start out as inactive Prorenin. Where is Prorenin produced/stored?

A

juxtaglomerular cells (walls of afferent arterioles) of the kidneys

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6
Q

what does Angiotensin 1 do

A

it is a mild vasoconstrictor (produces minimal changes in vascular constriction)

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7
Q

what does Angiotensin 2 do

A

it is a potent vasoconstrictor of arterioles and a mild vasoconstrictor of veins. It also increases water and salt reabsorption AND causes the adrenal gland to secrete Aldosterone which also increases water and salt reabsorption (net affect is an increase in MAP)

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8
Q

What creates a bigger increase in CBV: increased water intake or increased salt intake?

A

increased salt intake

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9
Q

what are 4 characteristics of essential HTN

A

Increased CO
Increased sympathetic activity (kidneys)
Increased levels of angiotensin 2 and aldosterone
Impaired renal function

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10
Q

how do small arteries/arterioles and veins each control MAP

A

small arteries/arterioles are able to change resistance and flow while veins are able to change volume

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11
Q

name 8 mechanisms for controlling BP

A 
Aldosterone (hormonal)
Renin-Angiotensin (hormonal)
Renin Blood Volume Pressure Control (Kidneys)
Baroreceptors (Nervous)
Chemoreceptors (Nervous)
CNS Ischemic Response (Nervous)
Capillary Fluid Shift (Physiologic)
Stress/Relaxation (Physiologic)
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12
Q

what are baroreceptors and where are they located?

how do carotid and aortic baroreceptors send impulses?

A

they are stretch receptors located in the walls of most large arteries in the neck and thorax.

  • Carotid baroreceptors send impulses via Herings nerves to the Glossopharyngeal nerves and then to the sensory area of the vasomotor center
  • Aortic baroreceptors send impulses via the Vagus nerve to the vasomotor center
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13
Q

when are carotid and aortic baroreceptors stimulated?

A 
Carotid= 60 mmHg
Aortic= 90 mmHg
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14
Q

if the MAP increases or decreases, how long does it take for the baroreceptors to reset to the new pressure

A

1-2 days

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15
Q

what are chemoreceptors and where are they located

A

they are sensitive to a lack of O2 and an excess of CO2 and hydrogen ions. when stimulates they excite nerves through Herings and Vagus nerves to the vasomotor center which increases or deceases BF. they are located a carotid and aortic bodies

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16
Q

what is the CNS ischemic response

A

a direct response to the vasomotor center due to ischemia (increasing CO2). Very powerful response- will re-direct flow to higher priority organs.

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17
Q

at what pressure is the CNS ischemic response initiated and what pressure can it raise the MAP too

A

initiated when BP falls below 60 mmHg

can raise MAP to 250 mmHg

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18
Q

For a healthy resting adult, what is the:

  • average CO
  • average weight
  • average BSA
  • average CI
A
  • average CO: 5 LPM
  • average weight: 70 kg
  • average BSA: 1.7 m2
  • average CI: 3 L/Min/m2
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19
Q

what 2 substances do endothelial cells release to either vasodilate or vasoconstrict?

A

Nitric Oxide= direct vasodilator

Endothelin= potent vasoconstrictor

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20
Q

describe why endothelial cells release Nitric Oxide, how it affects the body, and its half life

A
  • released due to chemical stimuli (increase Ca++ or andiotensin II) and physical stimuli (increased flow)
  • Acts on larger vessels- so when flow through capillaries increases, nitric oxide is released to dilate larger vessels
  • half life is 6 seconds
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21
Q

describe why endothelial cells release Endothelin and its affects on the body

A

released by damaged endothelial cells/ small quantities produce significant vasoconstriction- it can close arterial vessels as large as 5 mm in diameter

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22
Q

what are the 3 vascular endothelial growth factors that promote new vessel growth from existing vessels

A
  1. Vascular Endothelial Growth Factor
  2. Fibroblast Growth Factor
  3. Angiogenin
    * *a decrease in tissue oxygenation leads to production of these growth factors by the effected cells
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23
Q

what are the 2 Anti-andiogenic substances that BLOCK the growth of new vessels

A
  1. Angiostatin
  2. Endostatin
    * *being researched for anti-cancer agents
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24
Q

Name the 4 Vasoconstrictor agents released within the body

A
  1. Nor-Epi (potent constrictor- released via ANS and adrenal medullae)
  2. Epinepherine (not as potent as Nor-Epi)
  3. Angiotensin II (very potent)
  4. Antidiuretic Hormone [aka Vasopressin] (more potent than andiotensin II- released from posterior pituitary)
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25
Q

Name the 2 vasodilator agnets released within the body

A
  1. Bradykinin (activated by damage to blood/inflammation- causes powerful dilation and increased capillary permeability)
  2. Histamine (released by mast cells and basophils located in damaged/inflamed tissue- causes dilation and increased capillary permeability- can result in edema formation- common in allergic reactions)
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26
Q

what happens with increased concentrations of:

  1. Calcium
  2. Potassium
  3. Magnesium
  4. Hydrogen
  5. Acetate/Citrate
A
  1. Calcium: smooth muscle contraction (vasoconstriction)
  2. Potassium: inhibits smooth muscle contraction (vasodilation)
  3. Magnesium: inhibits smooth muscle contraction (significant vasodilation)
  4. Hydrogen: (vasodilation)
  5. Acetate/Citrate: (mild vasodilation) [in banked blood]
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27
Q

what is an osmole

A

way of measuring total concentration of particles in solution. 1 osmole= 1 mole of particles (6.02x10^23)
[1 mOsm= 1/1000 of an osmole]
-Osmolality= osmoles/kg water
-Osmolarity= osmoles/liter water

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28
Q

For each mOsm of solute that cannot cross the membrane, how much osmotic pressure is generated

A

19.3 mmHg per mOsm
(So if an RBC has an intracellular osmolarity of 300mmHg and the cell is placed in water, the osmotic gradient created across the membrane is 5790mmHg)

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29
Q

How do isotonic solutions such as 0.9% NS effect the osmotic balance btwn intra and extracellular compartemtns

A

Same osmolarity so no water shifts and the osmotic balance is not disrupted

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30
Q

what are 6 metabolic waste products removed from the body by the kidneys

A
  1. Urea (amino acid metabolism)
  2. Creatinine (from muscle creatine)
  3. Uric Acid (from nucleic acids)
  4. Bilirubin (end products from hemoglobin breakdown)
  5. Hormone metabolites
  6. Toxins/Foreign substances (drugs/pesticides/food additives)
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31
Q

how much muscle creatine is converted to creatinine each day to serve as an energy source for production of ATP in muscle?

A

1-2%

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32
Q

how do the kidneys contribute to acid-base regulation

A

they control hydrogen ion and bicarb concentration and they also remove sulfuric and phosphoric acid

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33
Q

how do the kidneys contribute to erythrocyte (RBC) production

A

they secrete erythropoitin which stimulates RBC production- hypoxia (low O2) stimulates release of erythropoietin- **patients with severe renal disease will also develop severe anemia due to lack of erythropoietin production

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34
Q

what are the 3 renal processes for excretion

A
  1. Glomular filtration (out of body to urine)
  2. Tubular Secretion (out of body to urine)
  3. Tubular Reabsorption (back to the body)
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35
Q
  • what is the normal glomular filtration rate per day?
  • what is the normal glomular filtration rate per minute?
  • how many times is the complete volume of plasma filtered a day?
A

180 L/day
125 ml/min
plasma volume is filtered 6x a day

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36
Q

how does increased and decreased glomular oncotic pressure effect GFR

A

increased glomular oncotic pressure= decreased GFR

decreased glomular oncotic pressure= increased GFR

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37
Q

how does increased plasma protein concentration in arterial blood effect GFR

A

it will increased the glomular oncotic pressure which will decrease GFR

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38
Q

what happens when you increase the filtration fraction (fraction of plasma being filtered)

A

more plasma is filtered and as the blood becomes more concentrated- the glomular oncotic pressure gradually increases and then the GFR decreases.

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39
Q

equation: filtration fraction

A

GFR/ RBF

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40
Q

How does increased hydrostatic pressure (mean arterial pressure) effect GFR

A

increased MAP= increased GFR

decreased MAP= decreased GFR

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41
Q

how does renal O2 consumption and blood flow compare to the brain

A

O2 consumption is 2x that of the brain

Blood Flow is 7x that of the brain

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42
Q

when blood enters the renal artery, how is it distributed within the kidney

A

98% goes to the renal cortex

2% goes to the renal medulla

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43
Q

do the kidneys have sympathetic or parasympathetic innervation

A

sympathetic

when activated, the vessels constrict and decreased GFR and RBF

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44
Q

how does angiotensin II (vasoconstrictor) interact with the kidneys

A

decreased GFR and RBF and increases tubular reabsorption during times of decreased MAP or volume depletion

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45
Q

how does nitric oxide (vasodilator) interect with the kidneys

A

helps maintain dilation of renal vessels which increased GFR and RBF

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46
Q

how do the kidneys react to increased extracellular osmilarity?

A

the posterior pituitary releases ADH so the kidneys hold on to water so that the osmolarity is diluted

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47
Q

how do the kidneys react to decreased extracellular osmilarity?

A

the posterior pituitary stops releasing ADH so the kidneys excrete more water so that the osmilarity becomes concentrated

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48
Q

what portion of the kidney does ADH act on in order to reabsorb water

A

late distal tubule and collecting duct

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49
Q

describe the proximal tubule of the kidney

A

filters out electrolytes and water

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50
Q

describe the descending loop of the kidney

A

high permeability to water

low permeability to Na+, Cl- and Urea

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51
Q

describe the thin ascending loop of the kidney

A

NO permeability to water

Little reabsorption of Na+, Ca++ and Cl-

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52
Q

describe the thick ascending loop of the kidney

A

NO permeability to water

Active reabsorption of Na+, Cl-, Ca++ and K+

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53
Q

describe the early distal tubule of the kidney

A

NO permeability to water

Active reabsorption of Na+, Cl- and K+

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54
Q

describe the late distal and cortical collecting tubules of the kidney

A

water reabsorption based on ADH concentration

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55
Q

describe the medullary collecting tubules of the kidney

A

water reabsorption based on ADH concentration

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56
Q

how does insulin interact with potassium

A

insulin moves potassium (and glucose) into cells

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57
Q

how does Aldosterone interact with potassium

A

increased potassium concentration stimulated aldosterone secretion (aldosterone will increase Na+ reabsorption [in the body] and increase K+ secretion [out of the body]) *the increased Na+ will increase BP

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58
Q

how does an increase in hydrogen concentration effect potassium secretion

A

increased [H+] (causes acidosis) will decrease K+ secretion

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59
Q

what is the normal Ca++ concentration? what does hypocalcemia and hypercalcemia cause?

A

2.4 mEq/L or 1.2 mmol/L
Hypo= increased muscle and nerve excitability (tetany)
Hyper= depressed neuromuscular excitability (can lead to cardiac arrhythmia’s

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60
Q

where is Ca++ stored in the body and what happens if plasma concentration of Ca++ increases or decreases

A

99% stored in bone (other 1% in intracellular space)
if plasma concentration drops then Ca++ is moved from the bone and if the concentration rises then Ca++ is moved back to the bone

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61
Q

what is the most important regulating agent for Ca++ concentrations

A 
Parathyroid Hormone (PTH)
-an increase in PTH will stimulate bone to release Ca++ and increase reabsorption
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62
Q

can Ca++ be secreted from the kidneys

A

No. It can only be filtered and reabsorbed

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63
Q

in what portion of the kidney does filtration occur

A

glomerulus

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64
Q

in what portions of the kidney do reabsorption and secretion occur

A

proximal tubule
loop of henle
distal tubule
collecting tubule

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65
Q

what is the reabsorption transport maximun for glucose

A

375 mg/min

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66
Q

describe the passive reabsorption of water in the kidneys? (what is it driven by and how does it change through the different portions of the kidney)

A
  • driven by osmotic differences created by the movement of solute (mainly Na+)
  • Proximal tubule is highly permeable to water. Solvent drag occurs (water carries electrolytes with it)
  • Loop of Henle has a low permeability to water (so little water movement occurs)
  • Distal Tubule/Collecting Tubules has variable permeability that depends on the amount of ADH
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67
Q

what mainly occurs if the proximal tubule

A

65% of water and Na+ is reabsorbed

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68
Q

what mainly occurs in the loop of henle

A

thin descending= highly permeable to water and some solutes
thin ascending= impermeable to water
thick ascending= impermeable to water but able to reabsorb solutes

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69
Q

what mainly occurs in the distal tubule

A
  • provides feedback control for GRF and renal BF
  • impermeable to water
  • permeable to solutes
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70
Q

what mainly occurs in the collecting tubule

A
  • impermeable to urea
  • Na+ and K+ reabsorption is controlled by aldosterone
  • secretes H+
  • water permeability is controlled by ADH
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71
Q

name the 2 K+ sparing diuretics that are Aldosterone Antagosits and describe the mechanism

A

Spironolactone and Eplerenone

- they are aldosterone and mineralocorticoid receptor antagonists. So they inhibit Na+ reabsorption and K+ secretion

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72
Q

name the 2 K+ sparing diuretics that are Na+ Channel Blockers and describe the mechanism

A

Amiloride and Triamterene

-they inhibit entry of Na+ into the cell which reduces the amount of Na+ transported by Na-K ATPase

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73
Q

what mainly occurs in the medullary collecting duct

A
  • determines final concentration of urine
  • water permeability is controlled by ADH
  • can reabsorb solutes
  • can secrete H+ (like the collecting tuble)
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74
Q

where is Aldosterone secreted and what does it regulate

A
  • secreted by the zona glomerulosa cells in the adrenal cortex
  • regulated Na+ reaborption and K+secretion
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75
Q

what does Angiotensin II do

A

it is the most powerful Na+ retaining hormone- increased production is caused by low BP or low ECF volume

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76
Q

where is ADH (aka Vasopressin) made and what does it do

A
  • made in the hypothalamus

- controls water permeability in the distal tubule and collecting tubule/duct

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77
Q

where is Atrial Natiuretic Peptide secreted from and what does it do?

A

-secreted from cardiac atrial cells when the atria become distended by volume overload
-causes direct inhibition of Na+ and water reabsorption and inhibits renin secretion (and thus Angiotensin II also)
(important for heart failure patients)

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78
Q

what does parathyroid hormone do

A

it is the most important hormone for regulating Ca++

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79
Q

Protamine:

  • describe its chemical structure
  • describe its chemical tendencies
  • where is it derived from
A
  • its a polycationic polypeptide protein thats 67% arginine
  • its strongly alkaline with numerous positive charges
  • derived from salmon sperm (now made via recombinant technology)
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80
Q

what is the current theory for how heparin-protamine complex is cleared from the body

A

reticuloendothelial system (AKA the mono-nuclear phagocyte system)

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81
Q

what is the reticuloendothelial system (AKA the mono-nuclear phagocyte system)?

A

“Diffuse” part of the immune system (responsible for clearing stuff)
-consists of monocutes. macrophages, tissue histiocytes and Kupffer cells (located in the liver, spleen and lymph nodes)

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82
Q

when can protamine act as a mild anticoagulant

A

when over 3x the amount needed for heparin neutralization is given

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83
Q

what can an overdose of protamine cause

A

platelet dysfunction that can last for several hours

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84
Q

describe the adverse reactions to protamine for:

  • Classification 1 Type 1:
  • Classification 1 Type 2a:
  • Classification 1 Type 2b:
  • Classification 1 Type 2c:
  • Classification 1 Type 3:
A
  • Classification 1 Type 1: Mild hypotension due to histamine release (from rapid infustion)
  • Classification 1 Type 2a: True anaphylaxis thats IgE mediated (loose pressures)
  • Classification 1 Type 2b: Immediate Anaphylactoid thats mediated by thromboxane (everything constricts)
  • Classification 1 Type 2c: delayed Anaphylactoid (post-op pulmonary edema)
  • Classification 1 Type 3: catastrophic pulmonary vasoconstriction
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85
Q

if you experience protaine reaction classification 1 type 1, what can you do to correct it

A

give cromolym sodium
–its a mast cell membrane stabilizer that helps to prevent mast cell degranulation before its occurrence
(remember that Classification 1 Type 1 is Mild hypotension due to histamine release)

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86
Q

describe the adverse reactions to protamine for:

  • Classification 2 Type A
  • Classification 2 Type B
  • Classification 2 Type C
A
  • Classification 2 Type A: Pharmacologic histamine release
  • Classification 2 Type B: True anaphylaxis
  • Classification 2 Type C: Anaphylactoid reaction with pulmonary vasoconstriction
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87
Q

if you see a protamine reaction begin, what do you do

A

stop protamine
go back on bypass
then give intra-aortic or just let it wear off

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88
Q

what is the primary activator of fibrinolysis during heart surgery and when is there a large surge of it

A

Tissue Plasminogen Activator (TPA)

-Large surge after protamine is given

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89
Q

Thrombin is produced throughout CPB. When are there large surges of thrombin

A

termination of CPB

after protamine is given

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90
Q

what regulates Tissue Palsminogen Activaor (TPA)

A

Plasminogen Activator Inhibitor 1 (PAI-1)

- therefore TPA must overcome circulating PAI-1 to initiate fibrinolysis

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91
Q

Name 3 Antifibrinolytic Agents

A

Aminocaproic Acid (Amicar) [lysing analog]
Tranexamic Acid [lysing analog]
Aprotinin

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92
Q

how does Aminocaproic Acid (Amicar) work

A

-inhibits cleavage of plasminogen to plasmin
prevents plasmin from binding to fibrinogen
(treated excessive bleeding from hyperfibrinolysis)

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93
Q

how does aprotinin work

A

-inhibits plasmin directly

its a non-specific serine protease inhibitor (especially trypsin) - prevents excessive blood loss

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94
Q

what is the half life of lysine analogs such as Amicar or Tranexamic Acid

A

1-2 hours

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95
Q

what is normal UOP on CPB

A

0.5- 1 ml/kg/hr

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96
Q

how do flow rates for peds and adults compare

A

Peds have a higher flow (3.0-3.4 CI) because they have a higher O2 demand and metabolic rate

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97
Q

how much will K+ drop immediately post CPB

A

about 1.0 mEq/L

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98
Q

what are 4 risks of blood transfusions

A

HIV
Hepatitis
Bacterial Infection
Fever/Chills

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99
Q

what is TRALI (Transfusion Related Acute Lung Injury)

A
  • Occurs w/in 6 hrs of transfusion
  • Symptoms similar to ARDS (Hypotension/Fever/Tachycardia/Pulmonary Edema)
  • Treatment: Ventilator support for ~96 hrs
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100
Q

what is an Autologous Donation

A

a blood donation to ones self prior to surgery

  • requires a HCT of 33%
  • whole blood can be split into PRBC/FFP/Platelets
  • contraindications= recent MI, CHF, AS, TIAs,HTN
  • may not be cost effective
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101
Q

what is Prebypass Autologous Normovolemic Hemodilution

A

used to remove blood (500-1000ml) from the patient before CPB and save it for during the case. The volume is replaced with crystalloid.

  • reqires a hct of 35%
  • an anticoagulant is placed in the bag
  • contraindication: COPD, CHF, CAD, AS, RI
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102
Q

who discovered heparin? year?

A

McLean in 1916

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103
Q

what is heparins chemical structure

A
  • highly sulfated glycosaminoglycan
  • highly negatively charged molecule (remeber protamine is positive)
  • poor lipid solubility (safe for BBB and Placenta)
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104
Q

how does heparin work

A

via potentiation of AT3 to neutralize circulating thrombin and other activated serine proteases such as
Factors 7, ,9, 10, 11, 12 KNOW

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105
Q

describe unfractionated heparin

A
  • contains heparin molecules of varying lengths

- longer chains have a higher MW and bind better with AT3 and thrombin

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106
Q

describe mucosal heparin

A
  • lower MW
  • higher dose requires for same response (30% less)
  • works via Factor 10 inhibition (not completely reversed by protamine)
  • more expensive
  • less likely to cause HIT
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107
Q

describe lung heparin

A 
higher MW
greater potency= lower dose required
more protamine requires due to more AT3 interactions
cheaper
more likely to cause HT
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108
Q

what is the half life for heparin at:
100 u/kg
200 u/kg
400 u/kg

A

100 u/kg= 60 min
200 u/kg= 90 min
400 u/kg= 120 min

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109
Q

how odes hypothermia effect the half life of heparin

A

hypothermia delays heparin clearance and increases the half life. (the concentration can remain constant for 40 min at 25C)

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110
Q

how much is AT3 activity increased in the presence in heparin

A

1000- 10,000x

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111
Q

when can you conclude your patient is heparin resistant

A

when more than 600 u/kg is given and the ACT in

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112
Q

name 3 things that can cause heparin resistance

A 
AT3 deficiency
Extreme thrombocytosis (Platelet count over 500,000 
Septicemia
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113
Q

describe Familial/Congenital AT3 Deficiency

A

Autosomal dominant
AT3 is less than 50% normal
Presents with low limb venous thrombosis or pulmonary embolism
Treated with life long antithrombic therapy

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114
Q

describe Aquired AT3 Deficiency

A
  • Occurs when pts are on heparin pre-op or have DIC
  • AT3 is only 60% normal
  • Treated with Recombinant AT3 (Thrombate or ATryn) or FFP
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115
Q

How can heparin lead to HIT

A

can cause platelet dysfunction by binding to platelets and releasing PF4 and activating GPIIb/IIIa

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116
Q

what does the platelet count fall to in HIT patients

A

below 100,000 or 50% below baseline

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117
Q

Describe HIT Type 1

A
  • NOT immune mediated
  • Apprears w/in first 2 days of heparin exposure
  • Mild Platelet count drop that normalizes w/ continued heparin therapy
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118
Q

Describe HIT Type 2

A

IMMUNE MEDIATED
-Appears 4-14 days after exposure to Heparin
-Moderate/Severe platelet count drop that does NOT normalize with continued heparin therapy
Life threatening

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119
Q

What are the 4 HIT Antibody Diagnostic Tests and what do they measure

A
  1. ELISA assay: measures antibodies to the heparin/PF4 complexes (initial screening test)
  2. HIPA assay: measures the presence of antibodies to the heparin /PF4 complexes (confirmation test)
  3. C-SRA: measures serotonin released by platelets activated by the HIT antibodies (Gold Standard test)
  4. PaGIA: uses polysytryene particles that are coated with PF4-heparin complexes to which patient serum is added and compared to the standard (Newest Test)
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120
Q

how can you diagnose HIT

A
  • Thrombocytopenia (absolute drop from platelet baseline)
  • THROMBOSIS (deep vein thrombosis, MI, strokes, ect)
  • Greinacher scoring system
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121
Q

How can you treat HIT

A

Anticoagulation via DTIs (Direct Thrombin Inhibitors) or Factor 10a Inhibitors

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122
Q

what should you definitely not give a HIT patient

A

Warfarin. (because it streal vit-K from factors that need to activate protein C- so it temporarily acts as a pro-coagulant

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123
Q

Name the 3 DTIs (Direct Thrombin Inhibitors)

A

Lepirudin (Refludan)
Bivalirudin (Angiomax)
Argatroban

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124
Q

Lepirudan (Refludan) [Direct Thrombin Inhibitor]

  • Half life:
  • Clearance mechanism:
  • How is it measured:
A
  • Half life: 80 min (can be up to 48 hrs if pt has renal issues)
  • Clearance mechanism: renal excretion
  • How is it measured: aPTT or ECT
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125
Q

Bivalirudin (Angiomax) [Direct Thrombin Inhibitor]

  • Half life:
  • Clearance mechanism:
  • How is it measured:
A
  • Half life: 25 min (3 hrs if pt has renal issues)
  • Clearance mechanism: renal excretion
  • How is it measured: aPTT or ECT
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126
Q

Argatroban [Direct Thrombin Inhibitor]

  • Half life:
  • Clearance mechanism:
  • How is it measured:
A
  • Half life: 50 min
  • Clearance mechanism: hepatic clearance
  • How is it measured: aPTT or ACT
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127
Q

name the Factor Xa Inhibitor that can treat HIT

A

Fondaparinux (Arixtra)

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128
Q 
Fondaparinux (Arixtra) [Factor Xa Inhibitor]
-Half life:
-Clearance mechanism:
-How is it measured:
how does it work?
A

-Half life: 20 hrs
-Clearance mechanism: renal excretion
-How is it measured: Anti-Xa assay or ACT
binds to AT3 but does not directly inhibit thrombin

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129
Q

with HIT patients, when you use a cell saver- what do you have to be careful of

A

don’t use heparin- use citrate based anticoagulants

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130
Q

How can you prepare for a HIT case

A
  • get a hematologist involved
  • discontinue heparin before anesthetizing the patient
  • Non-heparinize everythin
  • choose an anticoagulant (a DTI or FXaI)
  • No stasis (keep circuit circulating)
  • Discontinue anticoagulant 30 min prior to termination
  • MUF
  • Recirculate the pump with added anticoagulant and drain circuit ASAP
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131
Q

describe ACT

A

Activated Clotting Time

  • Whole blood clotting time accelerated by using celite or koalin activator (XI and XII)
  • Normal = 90-120 seconds
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132
Q

describe aPTT

A

Activated Partial Thromboplastin Time

  • Tests INTRINSIC pathway (VIII, IX, XI)
  • Normal = 25-40 seconds
  • Very sensitive to heparin- not useful during CPB
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133
Q

describe PT

A

Prothrombin Time

  • Tests EXTRINSIC pathway (VII)
  • Normal = 10-13 seconds (Large institutional variances occur so an INR is used to standardize PT)
  • Less sensitive to heparin
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134
Q

describe TT

A

Thrombin Time

  • Tests COMMON pathway
  • Normal = less than 17 seconds
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135
Q

what are the 2 physiological systems that regulate body temperature

A
  1. Hypothalamus (Vascular regulation and Skeletal muscle activity)
  2. Endocrine (Metabolic regulation and Stress response)
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136
Q

what is the temperature range for mild hypothermia

A

32-35

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137
Q

what is the temperature range for moderate hypothermia

A

28-31

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138
Q

what is the temperature range for deep hypothermia

A

18-27

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139
Q

what is the temperature range for profound hypothermia

A

below 18

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140
Q

name 4 reasons why hypothermia is important during CPB

A
  • reduces metabolic rate
  • reduces oxygen consumption
  • reduces excitatory neurotransmitter release
  • preserves high-energy phosphate stores
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141
Q

what are the appropriate cardiac index flows for temps:

  • 34-37C=
  • 30-34C=
  • 25-30C=
  • 18-20C=
  • below 18C=
A
  • 34-37C= 2.4 L/min/m2
  • 30-34C= 2.0 L/min/m2
  • 25-30C= 1.8 L/min/m2
  • 18-20C= 1.5 L/min/m2
  • below 18C= 1.0 L/min/m2
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142
Q

do you see more or less bleeding when cooling the patient

A

more bleeding

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143
Q

what is the Q10 Principle

A

for every decrease in temp by 10C, the patients METABOLIC RATES will decrease by 50%

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144
Q

what is the Q7 Principle

A

for every decrease in temp by 7C, the patients OXYGEN CONSUMPTION will decrease by 50%

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145
Q

how is gas solubility effected by temperature change

A

Inverse relationship. When you warm the patient, the partial pressure decreases because more gas is dissolved. When you cool the patient, the partial pressure increases because the gas becomes less soluble. [content of the gas itself does not change- only the amount dissolved].

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146
Q

what is the recommended cooling and warming rate

A 
cooling= 1C per min
warming= 1C per 3-5 min
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147
Q

what is the max temp gradient for adults and peds

A 
adults= below 10C
peds= below 8C
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148
Q

describe DHCA

A

Deep Hypothermic Circulatory Arrest
Cool to 18-20C
Turn off pump for 30-60 min
-Keep recirculating circuit through shunts

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149
Q 
What are the safe arrest times at:
37C=
28C=
22C=
16C=
10C=
A 
37C= 5 min
28C= 10 min
22C= 20 min
16C= 40 min
10C= 80 min
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150
Q

Describe HILFB

A

Hypothermic Intermittent Low Flow Bypass

Use flows for for 1-2 min every 15-20 min

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151
Q

Describe HLFB

A

Hypothermic Low Flow Bypass

Continuous low flows during whole surgery

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152
Q

What 2 drugs can you give during DHCA cases to increase ischemic tolerance of the brain

A

Thiopental (Short acting barbituate)

Solumedrol (Anti-inflammatory/Cell membrane stabilizer)

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153
Q

what is the Henrys Law equation for O2 and CO2

A 
O2= 0.003* Partial Pressure
CO2= 0.06* Partial Pressure
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154
Q

what is the equation for Partial Pressure

A

PP= Content / Solubility

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155
Q

what is the relationship btwn temperature and pH

A

Inverse. Increase in temp will decrease pH

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156
Q

what are the 3 acid-base buffering systems

A

bicarb
protein
phosphate

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157
Q

describe Alpha-State management

A

pH and CO2 (non-corrected temp) O2 (corrected temp)
maintain constant CO2 content w/ temp changes
-pH changes when temp changes (Inverse)
-During hypothermia, the patients auto-regulation of BF is maintained

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158
Q

describe pH-State management

A

pH/CO2/O2 all temp corrected to patients temp
maintain constant pH w/ temp changes
-adjust CO2 content w/ changes in temp to keep pH constant
-During hypothermia pt is more acidic but increased CO2 increases cerebral BF

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159
Q

at what temperature do we loose auto-regulation of cerebral blood flow

A

below 20C

- flow becomes pressure dependent at this point

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160
Q

what is the best acid-base strategy for:

  • regular adult CPB:
  • profound hypothermia w/ arrest for adult CPB:
  • pediatric CPB:
A
  • regular adult CPB: Little hypothermia = No difference. Mild/Moderate hypothermia= Alpha-Stat might be better
  • profound hypothermia w/ arrest for adult CPB: Use pH while cooling (better cerebral BF) and then switch to alpha (to remove acidosis)
  • pediatric CPB: pH-State (better cerebral BF)
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161
Q

whats the difference btwn naturally occurring anticoagulant and procoagulant factors in the body

A
  • anticoagulant factors= released by vascular endothelial cells (ex: prostacyclin or vascular plasminogen activator)
  • procoagulant factors= released from vascular lining when it gets disrupted (ex: platelets or plasma proteins)
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162
Q

what is the intrinsic pathway

A
  • activated by collagen/platelets or high MW Kinin

- 12/ 11/ 9+8/ 10+5/ 2/ 1+13

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163
Q

what is the extrinsic pathway

A
  • activated by tissue factor

- 7/ 10+5/ 2/ 1+13

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164
Q

what is the cell based coagulation pathway

A
  • activated by Factor 7 and Tissue Factor
  • 7+TF Complex/ 9+10/ 10+5 (Prothrombinase Complex)/ 2(small amount)/ 5+8+11+1/ Platelets recruited/ 11 binds to platelets/ 9/ 9+8 (pH Tenase Complex)/ Prothrombinase Complex/ 2 (big burst)/ 1 (clot forms)/ 13 (clot stabilizes)
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165
Q

what factors are Ca++ and vitK dependent

A

2, 7, 9, 10

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166
Q

whats the difference btwn how does the body naturally respond to clotting off arteries and veins

A 
arteries= rapid response by platelets followed by fibrin formation
veins= slower response by thrombin generation
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167
Q

what type of agents are used to prevent coronary thrombosis and deep vein thrombisis

A

coronary thrombosis= antiplatelet agents

deep vein thrombosis= antithrombin agents

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168
Q

what are the 4 steps for platelet activation

A
  • platelet loses discoid shape
  • GP2b/3a undergoes confrontational change (Ca++ dependent)
  • GP2b/3a binds to vWF
  • Subendothelial collagen binds to platelet GP1a/2a and GP4 receptors
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169
Q

after platelets are activated, what 3 platelet agonist are released to recruit additional platelets

A
  • thromboxane (platelet agonists and vasoconstrictor)
  • serotonin (platelet agonists and vasoconstrictor)
  • ADP (platelet agonists)
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170
Q

how is a platelet plug formed

A

fibrinogen and vWF form bonds btwn platelets to form a tight matrix

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171
Q

what is the name for clotting Factor 1

A

Fibrinogen

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172
Q

what is the name for clotting Factor 2

A

Prothrombin

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173
Q

what is the name for clotting Factor 3

A

Tissue thromboplastin

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174
Q

what is the name for clotting Factor 4

A

Calcium

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175
Q

what is the name for clotting Factor 5

A

Proaccelerin

Labile Factor

176
Q

what is the name for clotting Factor 6

A

there is no factor 6

177
Q

what is the name for clotting Factor 7

A

Proconvertin

Stable Factor

178
Q

what is the name for clotting Factor 8

A

Antihemophilic Factor A

179
Q

what is the name for clotting Factor 9

A

Antihemophilic Factor B
Plasma thromboplastin component
Christmas Factor

180
Q

what is the name for clotting Factor 10

A

Stuart Factor

Stuart Power

181
Q

what is the name for clotting Factor 11

A

Antihemophilic Factor C

Plasma thromboplastin antecedent

182
Q

what is the name for clotting Factor 12

A

Antihemophilic Factor D

Hageman Factor

183
Q

what is the name for clotting Factor 13

A

Fibrin Stabilizing Factor

Laki-Lorand Factor

184
Q

what 4 autologous anticoagulants helps control the spread of coagulation activation

A

Protein C
Protein S
Tissue Factor Pathway Inhibitor
Antithrombin III

185
Q

how does protein C and S block the clotting cascade

A

They are activated by thrombin generation then Protein S activates Protein C which then inhibits Factors 5 and 8 and then activates plasmin

186
Q

what are proteins C and S dependent on

A

vit K

187
Q

how does AT3 block the clotting cascade

A

it inhibits thrombin and Factors 10, 9, 11 and 12

188
Q

describe fibrinolysis

A

when thrombin generation begins (Factor 2), plasmin formation begins to degrade fibrin clots

189
Q

how is plasmin formed

A

plasmin is the product of plasminogen activation by uPA and tPa

190
Q

what happens when plasmin degrades/cleaves fibrin

A

fibrin split product are formed. they can be measured to determine how much fibrinolysis is occurring

191
Q

define antigen

A

foreign things that enter the body and bind to antibodies and/or receptors on T or B cells
(ex: bacteria, viruses, fungi, yeasts, malignant cells

192
Q

define immunogen

A

any substance that can stimulate an immune response.

-all are antigenic in nature (so they can bind to antibodies) [that doesnt mean that all antigens are immunogens]

193
Q

define pathogen

A

an antigen with the ability to cause disease (ex: toxin or microorganism)

194
Q

what are the 3 main categories of WBCs and their sub-catagories

A
  1. Granulocytes (most numerous)= Neutrophils, Basophils, and Eosinophils
  2. Monocytes= macrophages in body tissues
  3. Lymphocytes= T and B cells
195
Q

where are neutrophils made? what is the main function

A

made in hematopoietuc marrow

main function is phagocytosis

196
Q

where are eosinophils made? what is the main function?

A

made in hematopoietic marrow

main function is allergic reactions- release major basic protein

197
Q

what is the main function of basophils

A

chemotaxis and phagocytic activity
- they release heparin (to prevent blood clotting) and histamine (vasodilation) in areas of foreign invasion so that other WBCs can continue to circulate and kill the antigen

198
Q

where are monocytes/macrophages made? what is the main function?

A

made in bone marrow

main function is phagocytosis

199
Q

where do T-cells mature? what is the main function

A

mature in thymus

main function is to recognize foreign matter, bind to the antigen and release cytokines/interleukins

200
Q

what are the 5 classes of antibody molecules

A

IgG, IgM, IgD, IgA, IgE

most are IgG or IgM

201
Q

what are the 2 specific receptors on the membrane surface of phagocytic cells

A

Fc receptor: binds with antibody

C3 receptor: binds with complement

202
Q

describe how the immune system lysis’s cells

A

complement activation leads to production of membrane attack complex (MAC) which will then lyse the antigen membrane

203
Q

describe the IgM antibody class

A
  • main function is to activate the complement system
  • can cause antigen agglutination
  • Anti-A and Anti-B antibodies are IgM
204
Q

what is the first antibody produced against an antigen and the first antibody produced by the fetus

A

IgM

205
Q

what type of antibody are released during allergic and parasitic infections? how do they function?

A

IgE

they bind with basophils and mast cells and stimulate them to release histamine

206
Q

what is the most important and potent antibody?

A

IgG

Produced in greatest amounts on the second exposure to an antigen

207
Q

what is the only antibody that can cross the placenta

A

IgG

  • Provides protection for the fetus
  • Rh antibody is an IgG antibody
208
Q

what are the functions of the 4 subgroups of IgG antibody

A 
IgG1= protects against bacteria
IgG2= destroys bacteria that are in a saccharide coat
IgG3= activates complement proteins
IgG4= produces potent vasodilators
209
Q

what antibody is present in body fluids and mucous secreted by mucous membranes

A

IgA

-binds to the antigen to immobilize it

210
Q

what are the 3 phases of the immune response when the antigen stimulates activation of T and B cells

A
  1. Cognitive Phase= antigen interacts with T cells
  2. Activator Phase= T cells release cytokines which stimulate the proliferation of T and B cells
  3. Effector Phase= granulocytes/macrophages/complement are activated and the antigens are destroyed
211
Q

what 3 ways can you further categorize T cells

A

Cytotoxic
Helper
Suppressor

212
Q

describe Cytotoxic T cells

A

destroys virally infected cells, malignant cells and allogentic cells (organ transplant)

213
Q

describe Helper T cells

A

releases cytokines to recruit other cells
can convert inactive T cells into cytotoxic T cells
activates B cells

214
Q

describe Suppressor T cells

A

activated to stop the immune response after the antigen is destroyed

215
Q

describe B cells

A

produces antibodies in response to antigens (called humoral immunity)

216
Q

at what point does the classical and alternative pathway of the complement system merge

A

C3 convertase

217
Q

what is the difference btwn the classical and alternative pathways of the complement system

A
  • Classical: Activated by surface contact activation of Factor 7, heparin-protamine complexes and blood-air interfaces
  • Alternative: Activated by contact with foreign surfaces and suction blood
218
Q

what 2 parts of the complement system are the big neutrophil agonists

A

C5a and kallikrein

219
Q

describe Terumos X-Coating circuit

A

Poly-2-Methoxyethylacrylate (PMEA) [no heparin]

220
Q

describe Medtronics Carmeda circuit

A

heparin coating- covalent bonded

221
Q

describe Medtronics Trillium circuit

A

heparin coating- covalent bonded

222
Q

describe Medtronics Balance Biosurface circuit

A

hydrophilic polymer coating (no heparin)

223
Q

describe Maquets Bioline circuit

A

Albumin and heparin coating

224
Q

describe Maquets Softline circuit

A

hydrophilic and hydrophobic polymer coating (no heparin)

225
Q

describe Sorins Phisio circuit

A

synthetic phosphorylcholine (no heparin)

226
Q

what are oxygen free radicals

A
  • they are created an O2 molecule looses an electron
  • they attack and steal energy from other cells
  • antioxidants donate electrons to free radicals to neutralize them
227
Q

define anoxia

A

total depletion of oxygen

228
Q

define hypoxia

A

lack of oxygen (insufficient supply)

229
Q

define ischemia

A

restriction of blood supply to an organ

230
Q

what can reperfusion of circulation cause

A

inflammation

-results in oxidative damage through inducing oxidative stress rather than restoration of normal function

231
Q

describe the 4 things that reperfusion injury can cause

A
  1. Free O2 Radicals
  2. Myocyte Hypercontracture
  3. Mitochondrial Dysfunction
  4. Activation of coagulation
232
Q

what abrupt biochemical and metabolic changes occur during reperfusion injury

A
  1. Mitochondrial reenergization
  2. Generation of free O2 radicals
  3. Intracellular Ca++ overload
  4. Rapid restoration of pH
  5. Inflammation
233
Q

how does cell death occur from reperfusion injury

A

results from the opening of mitochondrial permeability transition pore and induction of cardiac myocyte hyper-contraction

234
Q

what 4 factors determine the amount of O2 Free Radicals that are produced

A
  1. Severity of ischemic injury
  2. Activation/recruitment of neutrophils to myocardium
  3. Level of O2 in cardioplegia
  4. Presence of endogenous scavengers/inhibitors
235
Q

what is the mitochondrial permeability transition pore

A

a non-selective protein channel that is closed during ischemia and open during reperfusion
(also opens in response to Ca++ overload, oxidative stress and ATP depletion)

236
Q

what 3 things can we preemptively do to prevent/decrease O2 Free radicals

A
  1. Give drugs that inhibit formation (anesthetics)
  2. Give drugs that scavenge them (Mannitol)
  3. Give anti-neutrophil drugs
237
Q

during reperfusion, Ca++ overload may occur- how does this cause injury

A

it depletes high-energy phosphate stores (ATP) which decreases the cells ability to contract

238
Q

what 5 things can cause myocardial edema

A
  1. Increased intracellular or interstitial osmotic pressure
  2. Increased microvascular permeability
  3. High cardioplegia delivery pressure
  4. Hyopthermia changes in Na/K pump
  5. Disruption of Na+ or Cl- electrical potentials across the cell membrane (if it accumulates in the cell it will attract water)
239
Q

what 4 clinical results do we see from reperfusion injury

A
  1. Arrhythmia’s (PVCs, V-Fib)
  2. Systolic dysfunction (Stroke Vol, Contractile Function)
  3. Dystolic dysfunction (Impaired filling)
  4. Myocardial necrosis
240
Q

name 2 points during CPB that the heart is prone to fibrillate

A

post XC

cooling

241
Q

what are the consequences of fibrillation

A

distention/overfilling

muscular/cellular damage

242
Q

what happens to myocardial metabolism when ischemia begins to occur

A

metabolism switches to anaerobic metabolism and lactic acid is produced, pH decreases and Ca++ overload occurs (which then decreases ATP stores and cellular contractile ability)

243
Q

without cardioplegia, how long would it take for irreversible ischemic injury to the myocardium to occur

A

20 min

244
Q

what phase of the cardiac action potential does potassium cardioglegia disrupt

A

Phase 3 (K+ efflux/repolarization)

245
Q

how does potassium cardioplegia arrest the heart

A

when blood K+ levels reach 8-10mEq/L (normal is 3.5-5mEq/L), the cells cannot repolarize and Na+ remains inside the cell.
-After XC removal, the extra K+ is washed out and the cells can begin to repolarize

246
Q

what is the flow range of antegrade CPG and the target root pressure range

A

flow= 250-400 ml/min
root pressure= 50-100 mmHg
(**line pressure depends on pressure drop of cannula used)

247
Q

name pros and cons of antegrade CPG

A

Pro: Left and Right distribution, quick arrest
Con: Requires competent AV

248
Q

what is the flow range of retrograde CPG and the target coronary sinus pressure range

A

flow: 150-200 ml/min

CS pressure: 40 mmHg

249
Q

name pros and cons of retrograde CPG

A

Pro: Good for AV regurg, can run continuously
Con: Bad right heart protection, possible sinus rupture

250
Q

what is the flow range of vein graft CPG and the target infusion pressure range

A

flow: 50-100 ml/min

infusion pressure: 50 mmHg

251
Q

what is Custodial Cardioplegia (HTK) and What does HTK stand for

A

it is an intracellular CPG solution made of low Na+, histidine, tryptophan and manniol
HTK= Histidine Tryptophan Ketoglutarate

252
Q

what is Del Nido CPG

A

instead of regular 4:1 ratio, Del Nido is 1:4

253
Q

in regards to myocardial protection, what is the action of K+ when added to a CPG solution

A

electromechanical arrest

254
Q

in regards to myocardial protection, what is the action of Na+ when added to a CPG solution

A

decrease edema and intracellular Ca++ buildup

255
Q

in regards to myocardial protection, what is the action of Ca++ when added to a CPG solution

A

membrane stabilization

256
Q

in regards to myocardial protection, what is the action of bicarb when added to a CPG solution

A

increase pH

257
Q

in regards to myocardial protection, what is the action of THAM when added to a CPG solution

A

increase pH

258
Q

in regards to myocardial protection, what is the action of glucose when added to a CPG solution

A

increase osmolarity

decrease edema

259
Q

in regards to myocardial protection, what is the action of mannitol when added to a CPG solution

A

increase osmolarilty

decease edema

260
Q

define conventional ultrafiltration (CUF)

A

using a hemoconcetrator to remove plasma water and low MW solutes by using hydrostatic pressure forces across a semipermeable membrane

261
Q

define zero balance ultrafiltration (ZBUF)

A

using a hemoconcentrator to maintain a controlled input and output on CPB

  • Used on CPB to lower K+ levels
  • Remeber to add bicarb to Saline
262
Q

define slow continuous ultrafiltration (SCUF)

A

using a hemoconcentrator in a slow/steady manner during CPB

263
Q

define modified ultrafiltration (MUF)

A

using a hemoconcentrator AFTER CPB

264
Q

how does blood and effluent flow through a hemoconcentrator

A

blood flows inside the fibers

effluent flows outside the fibers

265
Q

how does hemoconcentration differ from dialysis

A
  • hemoconcentration lets the hydrostatic pressure gradient push body water to the effluent side
  • dialysis uses a dialysate solution on the effluent side to control precise solute excretion
266
Q

how does a hemococentrator work

A

works via diffusion- solutes move from a higher concentration on the blood side to a lower concentration on the effluent side- trying to make concentrations on both sides equal

267
Q

what does the rate of hemoconcentration depend on

A

flow rate and transmembrane pressure

268
Q

what does the ability of a solute to be filtered through a hemoconcentrator depend on

A

sieving coefficient (MW of the solute compared to the pore size [daltons] of the filter)

269
Q

what does a sieving coefficient of zero and 1 mean?

A 
zero= no solute will pass (large MW)
1= solute concentrations will equilibrate on both side of the membrane
270
Q 
What are the sieving coefficients of:
K+:
Mg++:
Ca++:
Heparin:
A

K+: 1 [will eqilibrate]
Mg++: 1 [will eqilibrate]
Ca++: 0.55 [will dilute systemic Ca++]
Heparin: 0.2 [will decrease ACT]

271
Q

what is the max transmembrane pressure for a hemoconcentrator per the IFU

A

500 mmHg

pink effluent is an indicator that the TMP is too high

272
Q

what is the max MW for the pore size of a hemoconcnetrator per the IFU

A

65,000 Daltons

273
Q

when looking at lab values, how can you diagnose renal failure

A 
decrease in GFR (normal is 125 ml/min)
increased creatinine (normal is less than 1.5mg/dl)
increased BUN (normal is 10-20mg/dl)
274
Q

what complications can renal failure present during CPB

A 
low blood volume
metabolic acidosis
high K+ levels
hematuria (blood loss in urine)
proteinuria (protein loss in urine)
275
Q

what does SIRS stand for

A

Systemic Inflammatory Response

common systemic response to CPB

276
Q

name 4 possible signs of SIRS (only 2 of the 4 have to be present to diagnose SIRS)

A
  1. Temp above 38C or below 36C
  2. HR over 90 bpm
  3. Respiratory Rate over 20/min
  4. Leukocyte count over 12,000
277
Q

how is the nervous system broken down (subdivisions)

A
  1. CNS (Brain+Spinal Cord)

2. PNS (Afferent/ Efferent [Somatic/ Automatic (Enteric/Parasympathetic/Sympathetic)]

278
Q

of the Peripheral Nervous System: what is the difference btwn Afferent and Efferent subdivisions

A
  1. Afferent: (At the nerves) sends signal from the body to the brain and spinal cord
  2. Efferent: (Exits nerves) sends signals from the brain and spinal cord to the body
279
Q

of the Peripheral Nervous System: what is the difference btwn Automatic and Somatic subdivisions

A
  1. Automatic: Involuntary- controls cardiopulmonary and digestive systems. Further divided into sympathetic and parasympathetic
  2. Somatic: Voluntary- controls skeletal muscle under conscious control. Cholinergic: ACh is the neurotransmitter
280
Q

the ANS and edocrine system work together to regulate bodily functions- what is the difference btwn the 2

A

ANS: uses electrical impulses
Endocrine: uses hormonal signals

281
Q

whats the difference btwn parasympathetic and sympathetic pre/post ganglionic fibers

A
  1. Parasympathetic: Long preganglionic fiber w/ ACh neurotransmitter- Short postganglionic fiber w/ ACh neurotransmitter
  2. Sympathetic: Short preganglionic fiber w/ ACh neurotransmitter- Long postganglionic fiber w/ NE or ACh neurotransmitter
282
Q

of the Autonomic Nervous System: what is the difference btwn parasymathetic and sympathetic subdivisions

A
  1. Parasympathetic: ‘rest and digest’. Cholinergic subdivisoins (Muscarinic and Nicotinic)
  2. Sympathetic: ‘Fight and Flight’. Adrenergic subdivisions (Alpha, Beta, Dopaminergic)
283
Q

of the Parasymathetic Nervous System: what is the difference btwn Muscarinic and Nicotinic subdivisions

A
  1. Muscarinic: postganglionic receptors for parasympathic organs (“Feed and Breed”)
  2. Nicotinic: postganglioic receptors for somatic (muscle) reseptors
284
Q

of the Autonomic Nervous System: what does the Enteric Nervous System do

A

its a semiautonomous in the GI tract- has to subdivisions (Myenteric plexus and Submucous plexus)

285
Q

blood pressure is almost exclusively controlled by what subdivisions of the CNS

A

sympathetic nervous system

286
Q

whats the difference btwn cholnergic and adrenergic neurons

A
  1. Cholinergic (aka Parasympathetic): muscarinic or nicotinic receptors
  2. Adrenergic (aka Sympathetic): Alpha 1, Alpha 2, Beta 1, Beta 2 or Dopaminergic receptors
287
Q

what is the #1 cardiovascular variable your body seeks to auto-regulate

A

MAP

288
Q

what is the difference btwn inotrope and chronotrope

A
  1. Inotrope= contractile force

2. Chronotrope= heart rate

289
Q

what is another name for the vagus nerve

A

cranial nerve 10

290
Q

what are the 3 catagories of anticholinergic drugs? give an example of each

A
  1. Antimuscarinic (EX: Atropine- stabilize HR)
  2. Ganglionic Blocker (EX: Trimethophan [Arfonad]- blocks PNS and SNS- used for HTN crisis or dissecting aortic aneurysm [causes hypotension])
  3. Neuromuscular Blocker
    - (Non-Depolarizing: EX: Vecuronium- used during intubation)
    - (Depolarizing: EX: Succinylcholine- used during intubation)
291
Q

what are 2 bad side effects of succinylcholine (a depolarizing neuromuscular blocker)

A
  1. Hyperkalemia (bc K+ pumps are locked open)

2. malignant hyperthemia- when used with the gas anesthetic Halothant [Fluothane]

292
Q

what is the difference btwn norepinepherine and epinephrine

A

both adrenergic (catecholamines) and part of the SNS

  • NE is the main SNS neurotransmitter
  • Epi is released from the adrenal medulla as a hormone when stimulated by the SNS
293
Q

what do alpha 1 receptors innervate

A

smooth muscle (blood vessels)

294
Q

what do alpha 2 receptors do? give an example of a drug

A

located on preganglionic nerves and are used to create negative feedback loops
EX: Precedex- (A2 agonist) anesthetic sedative

295
Q

what do beta 1 receptors mainly innervate

A

heart

296
Q

what do beta 2 receptors mainly innervate

A

lungs

297
Q

how does epinephrine work

A

pos inotrope and chronotrope

  • increases SBP and decreases DBP
  • constricts vessels to gut/skin and dilates vessels to liver and skeletal muscles
  • causes hyperglycemia
298
Q

what is the CPR dose of epinepherine

A

1mg IV/IO every 3-5 minutes

299
Q

how does norepinephrine work? what is its drug name?

A

pos inotrope
vasoconstriction w/o vasodilating
-increases SBP and DBP
Drug name? Levophed

300
Q

what are the low/medium/high doses for dopamine and what are the effects at each dose

A
  1. Low= 2mcg/kg/min: vasodilates kidney/brain/viscera
  2. Med= 2-10 mcg/kg/min: increases CO
  3. High= >10 mcg/kg/min: arterial/venous vasoconstriction
301
Q

name 4 instances when dopamine would be the drug of choice

A
  1. cardiogenic/septic shock
  2. renal failure
  3. hypotension
  4. congestive HF
302
Q

what is the drug name for the synthetic analog of dopamine? how is it different? what does it do? when would it be used during CPB?

A
  • dobutamine (dobutrex)
  • its a beta 1 selective agonists- so it works mainly on the heart
  • increases SV so it increases CO
  • short term support to help wean from CPB
303
Q

how does phenylephrine (Neo-Synephrine) work? what does it do

A

Alpha 1 selective agonist

  • vasoconstrictor
  • increases SBP and DBP
  • used on CPB to increase SVR and MAP
304
Q

what arrhythmia can phenylephrine (neo-synephrine) treat

A

supraventricular tachycardia

305
Q

what are the cardiovascular effects of beta blockers (in general)

A

treats HTN
neg inotrope and chronotrope
decrease CO
decrease SA and AV node conduction

306
Q

define pharmacodynamics

A

what a drug does to the body

307
Q

define pharmacokinetics

A

what the body does to a drug

308
Q

what are the 5 steps of pharmacokinetics

A

“LADME”
L= Liberation (released from capsule/tablet)
A= Absorption (moving into plasma)
D= Distribution (dissemination of the drug throughout body compartments [plasma/tissue])
M= Metabolism (biotransformation into secondary compounds)
E= Excretion (remove drug from body)

309
Q

what is the main enzyme in the liver that metabolizes/oxidizes drugs

A

Cytochrome P-450 (aka CYP-450)

310
Q

what is first pass metabolism

A

drug enters systemic circulation through the portal vein after loosing a fraction of its concentration

311
Q

how do agonists work

A

they bind to and activate a receptor to bring about an effect

312
Q

how do antagonists work

A

they bind to a receptor and prevent effects from happening

313
Q

how do partial agonists work

A

they bind to receptor but only allow lower responses

314
Q

define a drugs therapeutic index

A

TD50/ED50
the ratio of the drug dose that produces a toxic effect in 50% of the population vs the dose that produces a therapeutic effect in 50% of the populaiton

315
Q

define a drugs bioavailability

A

the fraction of an administered drug that reaches systemic circulation

316
Q

besides a drugs sieving coefficient, what other factor effects if a drug can pass through a hemoconcentrator

A

the degree of protein binding

- too much protein binding=drug will not fit through the hemoconcentrator

317
Q

define first order kinetics

A

a constant proportion of the drug is metabolized per unit time (down-ward slope)

318
Q

define zero order kinetics

A

a set amount is metabolized over times (plateaued slope)

319
Q

what is the difference btwn systolic and diastolic heart failure

A

systolic: thin walled LV- decreased EF and contractility
diastolic: thick walled LV- decreased CO and filling

320
Q

name the 5 main causes of heart failure

A 
ischemia
immune mediated
idiopathic
viral
HTN
321
Q

what are the 6 classes of QALY improving drugs for heart failure

A
  1. positive inotropes (catecholamines/glycosides/bipyridines)
  2. diuretics
  3. renin angiotensin blockers
  4. primary vasodilators
  5. beta blockers
  6. aldosterone antagonists
322
Q
  1. positive inotropes (catecholamines/glycosides/bipyridines) are used for heart failure. Give an example of each subcategory and what it does
A
  1. Catecholamines (EX: Epi, NE, Dopamine: B1 stimulant)
  2. Glycosides (EX: Digitalis [Digoxin]) blocks Na/K Pump
  3. Bipyridines (EX: Milrinone [Primacor]: Phosphodiesterase Inhibitor- increase contractility)
323
Q

diuretics can be used for heart failure. what is the main one used to treat symptoms of excessive venous pressure and what are the net effects

A

Furosemide [Lasix]

-decreased afterload and preload= decreased myocardial O2 demand/consumption

324
Q

renin angiotensin blockers (aka ACE Inhibitors) are used for heart failure. What sufix do the drug names end in? how do they work?

A

drugs end in -PRIL
they decrease circulating levels of angiotensin 2 which will decrease preload and afterload by decreasing retention of Na and water

325
Q

primary dilators can be used for heart failure. give an example and describe how it works

A

Nitrates (Isosorbide [Isordil])

they decrease preload, afterload and SVR

326
Q

beta blockers can be used for heart failure. how do they work

A

they block the SNS stimulation which contributes to cardiomyocyte apoptosis (cell death) and mitogentic remodeling. The neg chronotrope component decreases the myocardial O2 demand

327
Q

aldosterone antagonists can be used for heart failure. give an example and describe how they work

A

Spironolactone [Aldactone]

they prevent Na and water retention which will decrease preload, afterload and myocardial O2 demand

328
Q

what are the 6 classifications of antiarrhythmics and what do they do

A 
1A= Na+ Blocker- Slows phase 0
1B= Na+ Blocker- Shortens phase 3
1C= Na+ Blocker- Really slows phase 0
2= Beta Blocker- Inhibits phase 4 depolarization
3= K+ Blocker- Prolongs phase 3
4= Ca++ Blocker- Inhibits the action potential in the SA and SV nodes
329
Q

what antiarrhythmic classification does lidocaine fall under

A

1B (Na+Blocker)

330
Q

what arrhythmias can Beta Blockers treat

A
  • atrial tachyarrhythmias (including AV nodal re-entrant tachyarrythmias
  • ventricular arrhythmias (post MI)
331
Q

Amiodarone is a common antiarrhythmic. What is its classification and what arrhythmia does it reat

A

3 (K+ Blocker)

treats A-Fib

332
Q

what antiarrhythmic is used to treat SVT

A

Adenosine

333
Q

what drug is used to treat digoxin-induced arrhythmias

A

magnesium sulfate

334
Q

what are 4 treatments for anemia

A
  1. Iron
  2. vit B12
  3. vit B9 (Folic Acid)
  4. Epogen (synthetic erythropoietin)
335
Q

what type of anemia does iron deficiency cause

A

hypochromic, microcytic anemia

336
Q

what type of anemia does vit B9 (folic acid) deficiency cause

A

megaloblastic anemia

337
Q

what type of anemia doe vit B12 deficiency cause

A

pernicious anemia (can also cause megaloblastic anemia)

338
Q

give an example of a sickle cell drug and describe how it works

A

Hydroxyurea [Hydrea, Droxia]

causes HgS to get diluted by HgF

339
Q

name the 4 indirect thrombin inhibitors (both drug names if applicable)

A
  1. Unfractionated Heparin
  2. Low MW Heparin [Lovenox]
  3. Warfarin [Coumadin]
  4. Fondaparinux [Arixtra]
340
Q

name the 3 direct thrombin inhibitors

A
  1. Lepirudin [Refludan]
  2. Bivalirudin [Angiomax]
  3. Argatroban
341
Q

is heparin acidic or basic

A

very acidic

-because of the carboxyl and sulfate groups

342
Q

how is heparin cleared from the body

A

its cleared by binding to macrophages and being depolymerized and desulfonated in the liver and then the metabolites are excreted in the urine

343
Q

what is the difference btwn unfractionated and low MW heparins half life

A

unfractionated heparin half life= 1 hour ish

low MW heparin half life= 3-7 hours ish

344
Q

what is the drug name for the synthetic Low MW heparin. describe it

A

Fondaparinux [Arixtra]

345
Q

how does warfarin [coumadin] work

A

inhibits vit K- so vit K stores are eventually depleted- and vit K is required to produce clotting factors 2, 7, 9, 10 and Protein C and S

346
Q

what are the other names for factors 2, 7, 9 and 10

A

2: Prothrombin
7: Proconvertin
9: Plasma Thromboplastin Component
10: Stuart-Power Factor

347
Q

what test is used to monitor warfarin activity? whats the normal value

A

PT (Prothrombin Time)

normal is 10-15 seconds

348
Q

how does Lepirudin [Refludan] work

A

direct thrombin inhibitor
cleared by the kidneys
NO reversal agent
half life is 1 hour

349
Q

how does Bivalirudin [Angiomax] work

A

direct thrombin inhibitor
only 20%renal clearance
can be removed by a hemoconcentrator
half life is 25 min

350
Q

how does Argatroban work

A

direct thrombin inhibitor
cleared by the liver
half life is 40 min

351
Q

how does aspirin work

A

irreversibly binds to COX1 and COX2 for the entire life of the plt- this inhibits the release of ADP, Thromboxane A2 and Prostaglandin E2

352
Q

what dose of aspirin will cause complete platelet inactivation

A

160 mg

353
Q

what kind of drug is Clopidogrel [Plavix]

A

Thienopyidine (Blocks plt aggregation like aspirin does)

354
Q

describe how naturally occurring antithrombin works and where it is made

A

mild anticoagulant effect on thrombin and factors 9 and 10- its effects are multiplied exponentially by heparin
small protein made in the liver

355
Q

what are the 2 forms of AT3 available and their drug names

A
  1. Made from human plasma= Thrombate

2. Made from milk of genetically modified goats= Atryn

356
Q

is protamin cationic or anionic? acidic or basic?

A

cationic
basic
(heparin is the opposite)

357
Q

how does protamine ‘reverse’ the effects of heparin

A

it binds with heparin at a 1:1 ratio (so for 100 units of heparin, 1mg of protamine will reverse it. The h/p complex does not interact with AT3 so the coagulation pathway proceeds unimpeded

358
Q

protamine by itself is a mild anticoagulant- how does it work

A

it decreases thrombin generation by inhibiting factor 5

359
Q

since protamine binds with heparin at a 1:1 ration, why do some protocols call for a 1:3 ratio

A

because protamine is eliminated from the plasma faster than heparin

360
Q

what is the difference in how protamine reverses unfractionated heparin and low MW heparin

A

protamine only partially reverses low MW heparin

361
Q

name 3 ways you can minimize protamine reactions?

A

slow administration
intra-aortic administration
administration with steroids and antihistamines

362
Q

what are 4 signs that your patient is having a protamine reaction

A 
extreme hypotension
pulmonary hypotension
anaphylaxis
cardiovascular collapse
--may have to crash back on CPB
363
Q

name the 2 antifibrinolytics that are lysine analogs

A 
aminocapronic acid (Amicar)
tranexamic acid
364
Q

which antifibrinolytic, aminocapronic acid (Amicar) or tranexamic acid, is more potent? by how much?

A

tranexamic acid is 10x more potent than amicar

365
Q

how do antifibrinolytics (aminocapronic acid (Amicar)

and tranexamic acid) work? how are they cleared from the body?

A
  • prevents plasminogen activation which inhibits fibrinolysis (prevents clot breakdown)
  • cleared by the kidneys
366
Q

what type of drug is aprotinin? how does it work

A

serine protease inhibitor
blocks plasmin to prevent post-op bleeding
(pulled from the market in 2007)

367
Q

what type of drug is desmopressin? how does it work? what diseases is it useful for?

A

a synthetic form of antidiuretic hormone (ADH aka Vasopressin). much less potent

  • causes plt adhesiveness to increase
  • useful for mild hemofilia A and von Willebrands Disease
368
Q

what does FFP contain? when is it typically used

A

contains Factors 1, 2, 5, 7, 9, 10, 11 and 13, AT3 and proteins C and S
-used for post op bleeding

369
Q

20 ml/kg of FFP will raise a patients AT3 levels by what %

A

20%

370
Q

what does cryoprecipitate contain? what is it derived from?

A

contains Factors 1 and 8 and von Willebrands

-derived from the precipitate that forms after FFP is thawed and centrifuged

371
Q

how much fibrinogen (factor 1) is in 1 unit of cryo

A

250-350 mg

372
Q

what are the 2 functions of the pancreas? describe each

A
  1. Exocrine: digestive enzymes and bicarb

2. Endocrine:produces insulin (signals ‘fed’ state) and glucagon (signals ‘hungry’ state)

373
Q

what are the 3 types of cells that the endocrine system of the pancreas? describe each

A
  • Alpha cells: secretes glucagon (increases BG)
  • Beta cells: secretes insulin (decreases BG)
  • Delta cells: secretes somatosatin
374
Q

what are the 2 types of diabetes? describe each

A
  1. Diabetes Insipidus: kidneys don’t respond to or produce ADH (you pee a lot)
  2. Diabetes Mellitus: absolute deficiency of insulin (4 subtypes)
375
Q

describe the 4 subtypes of diabetes mellitus

A
  • Type 1: Insulin Dependent (absolute insulin deficiency)
  • Type 2: Non-Insulin Dependent (relative insulin deficiency)
  • Type 3: ‘Other’
  • Type 4: Gestational DM [extreme insulin resistance during 3rd trimester]
376
Q

besides decreasing blood glucose levels, what else can insulin treat during CPB

A

-Hyperkalemia: drives K+ intracellularly

side note: you can also ZBUF or give Bicarb to decrease K+ levels

377
Q

what is the difference btwn primary (essential) and secondary HTN

A
  • Primary (essential)= blend of nature/nuture, generally idiopathic, most common form (90%)
  • Secondary= caused from a specific etiology, less common (10%)
378
Q

what are the 2 ways you can decrease BP

A

decrease CO or SVR

PQR

379
Q

CO and SVR are generally controlled by what 3 things

A

SNS
Baroreceptors
Renin/Angiotensin system

380
Q

what are the 8 drug categories that can be used to treat HTN? describe each

A
  1. Diuretics (decreases blood volume)
  2. Beta Blockers (decreases CO, SNS tone and [renin])
  3. ACE Inhibitors (decreases [angiotensin 2] which decreases Na and water retention)
  4. Angiotensin 2 Receptor Blockers (ARBs): (just like ACE inhibitors except they don’t cause bradykinin release)
  5. Renin Inhibitors (prevents angiotensinogen from converting to angiotensin 1)
  6. Ca++ Channel Blockers (decreases contractile force)
  7. Alpha 1 Blocker (Blocks A1 receptors so smooth muscles can relax)
  8. Alpha 2 Agonists (decreases SNS outflow firing by increasing neg feedback loop transmission)
381
Q

are ACE inhibitors or ARBs more effective at blocking angiotensin

A

ARBs are more effective bc there are other chemicals that can convert angiotensin 1 into angiotensin 2

382
Q

what are the 3 ways you can decrease HTN on CPB

A
  1. decrease flow
  2. increase gas anesthetic
  3. give vasodilating drugs
383
Q

what drugs can you give on CPB to decrease HTN? describe each

A
  1. Hydralazine [Apresoline]: causes endothelial cells to release nitric oxide and dilate smooth muscles
  2. Nitroglycerin: low doses cause venous dilation and high doses cause arterial dilation
  3. Nipride/Nitropress: potent arterial dilator
384
Q

what is a bad consequence of using nitroprusside

A

it has a toxic metabolite called thiocyanate and its half life is many days (it causes cellular metabolism to shut down)

385
Q

define classic angina

A

fixed coronary artery obstruction

-pain relieved by rest or nitroglycerin

386
Q

define unstable angina

A

pain at rest or w/ increasing duration/severity

- pain is NOT relieved by rest or nitroglycerin

387
Q

define prinzmetal angina

A

pain is episodic and unrelated to exertion

-treated with nitroglycerin or Ca++ blockers

388
Q

define acute coronary syndrome

A

an atheromatous plaque ruptures and inflammatory cells are activated, then the thrombus forms and vasoconstriction occurs, the cardiac muscle begins to die and MI markers are released

389
Q

define mixed angina

A

a fixed obstruction combined with vasospasm and/or endothelial disruptions
-pain during exertion and rest

390
Q

what are the 2 angina treatment stratagies

A

increase O2 delivery

decrease O2 demand

391
Q

does venous or arterial tone determine diastolic wall stress

A

venous tone
-because venous tone determines how much blood can be stored in the venous blood delivery system before its returned to the heart

392
Q

how do nitrated/nitrites help treat angina

A

causes a rapid decrease in myocardial O2 demand

393
Q

what condition causes blood to turn chocolate brown? how do you treat it? what does it mean if the patient does not respond to these treatments? how do you treat?

A

methemoglobinemia

  • blood with an oxidized heme group (oxidized iron)
  • Treat it with methylene blue at 1-2 mg/kg IV over 3-5 minutes (max out at 50 mg), ascorbic acid and pure O2
  • Unresponsive= Glucose-6-phosphate Dehydrogenase (G6PD) deficient. Treat w/ exchange transfusion and hyperbaric oxygen
394
Q

how do Na+ channel blockers work

A

they allow less Ca++ the enter the cell which decreases cardiac workload- and they switch cardiac metabolism from fatty acids to carbs which require less O2 to metabolize

395
Q

how do opioids work? How do they effect the cardiovascular and respiratory system? what are 2 adverse effects? name a common opioid. what drug would you give for an opioid overdose or adverse rxn?

A

they prevent presynaptic release of neurotransmitters, particularly excitation afferent neurotransmitters= decreased perception of pain

  • decreased HR, respiratory rate and tidal volume
  • histamine release (allergic rxn) and increased intracranial pressure
  • common opioid is Morphine
  • Narcan (opioid antagonist)
396
Q

how do barbiturates work? name a common barbiturate.

A

sedative that mimics the inhibitory neurotransmitter GABA and causes CNS depression and loss of consciousness
-common barbiturate is thiopental (anes intubation)
(Propofol killed michael jackson)

397
Q

how do benzodiazepines work? name 3 common drugs (both names for each)

A

tranquilizer that mimics the inhibitory neurotransmitter GABA and causes decreased anxiety

  1. Diazepam [Valium]
  2. Lorazepam [Ativan]
  3. Midazolam [Versed]
398
Q

how do inhaled anesthetics work? name the 3 used for CPB (both names for each)

A

Liquid anesthetic that is vaporized and mixed w/ the oxygen-blend gas. The mixture goes into the oxygenator and diffuses into the blood stream. Diffusion rate is dependent on the concentration gradient and lipid solubility.

  1. Isoflurane [Forane]
  2. Desflurane [Suprane]
  3. Sevoflurane
399
Q

what are the physiological effects of inhaled anesthetics while on CPB? what are the adverse effects

A

Cardiovascular, Respiratory and CNS Depression
Adverse effects: increased intracranial pressure in patients with head trauma or brain tumors, decreased BP and renal BF, CO2 retention (acidosis)

400
Q

how can inhaled anesthetics cause ‘coronary steal syndrome’

A

causes arteriolar dilation of normal/healthy vessels which diverts blood away from stenotic areas

401
Q

define vapor pressure (in regards to inhaled anesthetics). Do inhaled anesthetics have a high or low vapor pressure?

A

the tendency of an inhalation anesthetic to vaporize to its gaseous state- determines how readily it will evaporate in the machine vaporizer
-All have a high vapor pressure

402
Q

define Blood:Gas Partition Coefficient (in regards to inhaled anesthetics). what is the difference btwn a high and low B:G Coefficient

A

Measures the solubility of an inhaled anesthetic in blood compared to alveloar gas- describes induction speed and recovery

  • Low= agent is less soluble in blood and has a fast induction and recovery
  • High= agent is more soluble in blood and has a slow induction and recovery
403
Q

define minimum alveolar concentration (MAC). what is the difference btwn a low and high MAC

A

the concentration of anesthetic vapor in the alveoli that is required to prevent a motor response in 50% of patients- measures potency

  • Low= more potent=low setting
  • High= less potent=high setting
404
Q

name somethings that can alter MAC per individual

A

age, metabolic activity, body temp, disease, pregnancy, obesity, other drugs
-thats why the MAC ‘setting’ has to be tailored to the individual

405
Q

what inhaled anesthetic is no longer used in the USA

A

Halothane

  • it is partially metabolized and produces hepatotoxic byproducts
  • it can contribute to malignant hyperthemia
406
Q

Describe Isoflurane [Forane]

  • Vapor Pressure:
  • B:G Coefficient:
  • MAC:
A
  • Vapor Pressure: High
  • B:G Coefficient: Low
  • MAC: 1
407
Q

which inhaled anesthetic in the most common and has the fewest adverse cardiovascular effects

A

isoflurane [forane]

408
Q

Describe Sevoflurane

  • Vapor Pressure:
  • B:G Coefficient:
  • MAC:
A
  • Vapor Pressure: High
  • B:G Coefficient: Low
  • MAC: 2
409
Q

how are inhaled anesthetics removed from the body

A

lungs

410
Q

Describe Desflurane [Suprane]

  • Vapor Pressure:
  • B:G Coefficient:
  • MAC:
A
  • Vapor Pressure: High
  • B:G Coefficient: Low
  • MAC: 6
411
Q

which inhaled anesthetic has the lowest B:G Coefficient

A

Desflurane [Suprane]

known as ‘one breath anesthesia’- in one breath your asleep and in one breath your awake

412
Q

in regards to antibiotics: define minimum inhibitory (MIC) and minimum bacteriocidal concentration (MBC)

A 
MIC= lowest antibiotic dose that inhibits bacterial growth
MBC= lowest antibiotic dose that kills 99.9% of the bacteria
413
Q

what are the 3 major pathogen categories? describe each

A
  1. Gram Positive Bacteria: cell wall is unprotected (easier to kill)
  2. Gram Negative Bacteria: cell wall is protected (harder to kill)
  3. Fungi:
414
Q

describe Beta-Lactam antibiotics. name 2 antibiotic categories that are Beta-Lactam

A

they prevent enzymatic rxns necessary for a stable cell wall- so newly produced bacterial cell walls are weak and fall apart
-Penicillins and Cephalosporins: they are cidal (=kill)

415
Q

what are first generation penicillins effective against

A

Gram Pos Bacteria (particularly Strep)

Gram Neg Cocci (particularly Staph)

416
Q

what broad spectum penicillin is the drug of choice for pre-cardiac surgery dental prophyllaxis

A

Amoxicillin

417
Q

what are the main open heart infection culprits

A

Staph and Strep infections

418
Q

name 2 cephalosporin antibiotics that may be used on CPB

A
  • Cefazolin (Kefzol)

- Cefuroxime (Zinacef)

419
Q

describe how Vancomycin work and what it is reserved for ? what are they limited too?

A

Similar to pens/cephs (B-Lactam atibiotics) but they make the cell wall fall apart by preventing lipid polymerization- Cidal

  • used for MRSA and MRSE and Enterococcal Infections
  • Limited to Gram Pos Bacteria
420
Q

how do aminoglycoside antibiotics work? what are the limited to? what is important to remember about them?

A

they are derived from fungi- they bind to the bacteria’s ribosomal 30S subunit and therefore interfere further protein synthesis- Cidal

  • Limited to Gram Neg Bacteria (such as E. Coli)
  • All of them cross the placenta and concentrate in fetal tissue
421
Q

how do glucocorticoid steriods work? name a common one

A

they promote gluconeogenesis, protein catabolism and lipolysis which decreases inflammation (immunosuppressive)
-Prednisolone

422
Q

what do naturally occurring glucocorticoids do

A

“stress hormone”- causes vasoconstriction and glucose release (therefore its a strong insulin antagonists), decreases WBCs

423
Q

what diseases are HYPO and HYPER adenocortico diseases

A 
Hypo= Addisons Disease (too little glulcocorticoids)
Hyper= Cushings Syndrome (too much glucocorticoids)
424
Q

what are the 5 major classes of immunosuppressives (such as anti-rejection)? what do they each do?

A
  1. Glucocorticoids: Suppress T cells
  2. Calcineurin Inhibitor: Inhibits T cell activation
  3. mTOR Inhibitor: Prevents maturation and proliferation of T cells
  4. Antiproliferative Agents: Prevents T and B cells from multiplying
  5. Monoclonal Antibodies: Contains 1 specific antibody derived from a single cloned B cell (targets specific cells)
425
Q

define malignant hyperthermia (physiology of it)

A

its an autosomally dominant disorder of skeletal muscles- the Ca++ that’s stored in skeletal muscles is released inappropriately causing the muscles to contract and stiffen simultaneously
(Fluminant MH is the most common)

426
Q

when do symptoms of malignant hyperthermia typically appear? what age groups are most often affected?

A
  • symptoms occur w/in 1 hour

- mostly occurs in children and young adults (

427
Q

what drugs can cause malignant hyperthermia

A

inhaled anesthetics in combination with succinylcholine

428
Q

name 5 clinical signs of malignant hyperthermia

A 
profound hyperthermia
muscle rigidity
increase in CO2
Acidosis (metabolic and respiratory)
Hyperkalemia
429
Q

how do you treat malignant hyperthermia on CPB

A
  1. stop inhaled anesthetics and succinylcholine
  2. hyperventilate with 100% oxygen
  3. give Dantrolene (2.5mg/kg)
  4. correct acidosis (give bicarb) and electrolytes
  5. cool patient
430
Q

how does Dantrolene work

A

blocks the release of Ca++ from skeletal muscles sarcoplasmic reticulum

431
Q

what are the 4 categories of diuretics

A

loop diuretics
thiazides
K+ sparing
osmotic diuretics

432
Q

how do loop diuretics work? name a common one? whats the dose?

A

they act on the ascending loop of henle and block the transport of Na+, K+ and Cl- back into circulation. (Non-K+ sparing so watch K+ levels. Also depletes Ca++)
-Furosemide (Lasix) 2.5-5 mg [pump dose]

433
Q

what type of diuretics are the most efficacious

A 
loop diuretics (work w/in minutes when given IV)
-called yellow zipper diuretics
434
Q

how do thiazide diuretics work? name a common one? whats the dose?

A

they act on the cortical region of the ascending loop of henle and block the transport of Na+ and Cl- back into circulation (also Non-K+ sparing), Also decrease SVR and promote the reabsorption of Ca++
-Chlorothiazide (Diuril) 500 mg [pump dose]

435
Q

how do K+ sparing diuretics work? name a common one

A

they act on the collecting tubules to prevent Na+ reabsorption and K+ excretion
-Spironolactone (Aldactone)

436
Q

how do osmotic diuretics work? name a common one? whats the dose

A

they work on the proximal tubule and the descending loop of henle -osmotic molecules that are filtered through the glomerulus and osmotically carry water with them
-Mannitol (Osmitrol) 12.5g [causes profound transient hypotension due to skeletal muscle vasodilation]

437
Q

what is the anesthetic stage and plane for surgical anesthesia

A

Stage 3 Plane 2

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