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Anesthesiology > Anesthesia > Flashcards

Anesthesia Flashcards

1
Q

Prerenal values for: Na meq/L FENA % UOsm mosm/L U/P osm BUN/Cr

A

Prerenal Na meq/L FENA 1 percent UOsm400 mosm/L U/P osm >1.8 BUN/Cr >20

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2
Q

Intrinsic Renal pathology Na meq/L FENA U Osm mosm/L U/P osm BUN/Cr

A

renal Na meq/L >40 FENA >3 UOsm 250-300 mosm/L U/P osm <20

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3
Q

Chemotherapeutic that causes pulmonary fibrosis

A

Bleomycin

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4
Q

innervation and function of cricothyroid muscle

A

External laryngeal branch of superior laryngeal nerve Tensor of vocal cords

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5
Q

Internal laryngeal branch of superior laryngeal nerve

A

Sensation above vocal cords

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6
Q

recurrent laryngeal nerve innervation

A

sensation below vocal cords motor control to all laryngeal muscles except cricothyroid

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7
Q

during performance of axillary nerve block, needle passes through wall of axillary artery. the nerve most likely encountered is

A

radial

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8
Q

anatomy axillary block

A

…………………. median ………………… ax art ……..ax vein…..ax art bone ax vein uln. n. radial n. bone ax vein

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9
Q

Radial nerve block

A

between biceps tendon and brachioradialis muscle at level of elbow joint

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10
Q

Wrist nerve and artery anatomy

A

N-A-/N-/A-N lateral to medial, radial n, radial art, median nerve, ulnar artery, ulnar nerve

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11
Q

Ulnar nerve block

A

At elbow, between olecranon and medial epicondyle of humerus At writst, just medial to ulnar artery

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12
Q

Median nerve block

A

At elbow, just medial to brachial artery between two heads of pronator teres In wrist, between flexor carpi radialis and palmaris longus

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13
Q

Ankle block

A
  1. Superficial peroneal nerve (sciatic)- field block from medial to lateral malleolus- sensation top of foot and toes 2. Deep peroneal block (sciatic)- lateral to ex. hallicus- innervates flexors of toes, sensation web 3. Sural (sciatic)- posterior to lateral malleolus, sensory to posterolateral leg, lateral foot, 5th toe 4. posterior tibial (sciatic)- posterior to medial malleolus, sensory to sole of foot, plantar surface of foot 5. saphenous (femoral)- anterior to medial malleolus, sensory to anteromedial side of leg and medial side of foot
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14
Q

gasserian ganglion block

A

trigeminal nerve block- ipsilateral face, cornea, sclera, anterior tongue, middle cranial fossa, can produce total spinal

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15
Q

superficial cervical plexus block

A

first four cervical nerves, superficial at lateral border of SCM, horners syndrome and hoarsness (RLN)

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16
Q

celiac plexus block

A

thoracic sympathetic ganglion and greater and lesser splanchnic nerves. located at L1 -hypotension, diarrhea, shoulder pain

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17
Q

Sciatic nerve block

A

lateral position, hip and knee flexed, line drawn between posterior superior iliac spine and greater trochanter, at midpoint of line perpendicular line should be drawn 3 cm down.

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18
Q

Side effects cimetidine

A

bradycardia, heart block, cardiac arrest increased airway resistance confusion, agitation, hallucinations, seizures slows metabolism and excretion of digitalis, diazepam, inderal, meperidine, pentazocine, aminophylline, verapamil, lidocaine

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19
Q

Reversal of urokinase in a hemorrhaging patient requiring surgery

A

cryoprecipitate

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20
Q

Diseases associated with Prolonged PTT

A

hemophilia A, B and von Willebrand’s disease

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21
Q

Vit K dependent factors

A

2, 7, 9, 10

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22
Q

all procoagulants synthesized in liver except

A

factor VIII, which is synthesized in the reticuloendothelial system.

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23
Q

Hemophilia A: Coag tests treatment

A

prolonged PTT, normal PT factor VIII concentrate

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24
Q

Hemophilia B coag tests treatment

A

Factor IX (males only) prolonged PTT and normal PT. treatment hyman purified and recombinant factor IX as well as FFP

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25
Q

von Willebrand disease

A

decreased concentration of factor VIII, prolonged PTT. Best tx:DDAVP if responsive (see types of VWD), factor VIII concentrate if not responsive cryo is less effective (40 units/kg) monoclonal antibody factor VIII does not work bc of missing platelet factor platelet transfusion ineffective. regional contraindicated unless factor levels above 30%

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26
Q

Heparin mechanism

A

Antithrombin III cofactor, inactivates thrombin preventing it’s action on fibrinogen. t1/2 1 hour. Heparin is a strong acid, protamine a strong base, protamine neutralizes heparin 1mg protamine for 100 units of heparin

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27
Q

Fibrinolytic system cascade

A

factor XII -> plasminogen -> plasmin -> fibrin -> fibrin split products

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28
Q

Tranexamic acid and aminocaproic acid mechanism

A

competitive inhibitor of plasminogen activation, inhibiting the breakdown of clot.

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29
Q

Aprotinin mechanism and effect

A

trypsin inhibitor, which inhibits plasmin’s fibrinolytic activity and has been shown to reduce perioperative blood loss.

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30
Q

most likely cause of anaphylactic reaction in a patient who has been previously transfused

A

Recipient IgA deficiency (reaction to donor IgA, washed cells may be beneficial)

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31
Q

FFP indications

A

replacement of isolated factor deficiencies Antithrombin III deficiency deficiency of factor V or VIII TTP

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32
Q

Donor PRBCs Recipient Plasma O A B AB

A

O, A, B, AB A, AB B, AB AB

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33
Q

True/false: an A+ patient who has received 10 units of O negative RBCs can still safely receive A neg and A pos RBCs.

A

True. Group O Rhneg blood may lead to hemolysis if multiple units of Group O WHOLE BLOOD are administered bc of the antibodies therein, therefore, one should not switch back to pt’s blood type after WHOLE blood. The passively transfused anti-A and anti-B antibodies are seldom a problem after group O RBCs are transfused.

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34
Q

fluid replacement in burns

A

4ml/kg per percent body burned (Arm- 9%, trunk -36%, leg-18%, head- 9%)

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35
Q

V fib algorithm

A

Please: precordial thump Shock : shock 200J or 2J/kg EVerybody: epi or vaso Shock: 200J or 2J/kg And :amiodarone 300 mg Make: mag if torsade Patients : procainamide 100mg Better: buffers (bicarb in protracted code)

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36
Q

Nitroprusside

A

Dose titrated to 10mcg/kg/min toxic if 1mg/kg in 3 hours CYANIDE toxicity: unexplained metabolic acidosis treatment is sodium nitrate and thiosulfate

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37
Q

Verapamil is contraindicated in

A

V TACH Indications: second line for supraventricular tachyarrhythmias

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38
Q

left shift of CO2 response curve (increased sensitivity)

A

arterial hypoxemia metabolic acidemia increased ICP, anxiety, fear, cirrhosis drugs: doxapram, strychnine, picrotoxin

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39
Q

right shift of CO2 response curve (alveolar ventilation v PCO2)

A

aminophylline salicylates catecholamines opioids metabolic alkalemia, denervation of chemoreceptors, normal sleep, drugs, hypothermia

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40
Q

hypoventilation/hypercarbia

A

A RIPE acidosis, arrythmias right shift of oxhemoglobin dissociation curve intracerebral steal PA pressure increase Epi-norepi release

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41
Q

hyperventilation/hypocarbia

A

AVCO apnea, alkalosis, airway constriction V/Q mismatch decreased CO, cerebral blood flow, coronary blood flow, calcium oxy-Hb dissociation curve shifted to left

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42
Q

Frank starling curve

A

Stroke volume vs left ventricular filling pressure

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43
Q

right ventricular perfusion depends on ____ arterial pressure, left ventricular perfusion depends on ____ arterial pressure

A

systolic diastolic

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44
Q

Drugs that increase uterine tone

A

(PEOKA) PGF2alpha Ergots Oxytocin Ketamine Amide local anesthetics

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45
Q

Drugs that decrease uterine tone

A

BEMP Beta-2 agonists Ethanol Magnesium sulfate methylxanthines Potent volatile anesthetics

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46
Q

Effect of lidocaine in atrial fibrillation

A

Lidocaine markedly increases A-V conductance and may lead to accelerated ventricular response

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47
Q

Digitalis toxicity- level and cause, should you cardiovert?

A

Toxicity >3ng/ml Causes: Renal failure hypokalemia (note: this is the mechanism for loop diuretics increasing the potential for dig toxicity) hypothyroidism hypomagnesemia hypocalcemia CARDIOVERSION may result in V FIB

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48
Q

Thiazide mechanism

A

Inhibits Na and Cl reabsorption in cortical portion of the ascending loop of Henle and distal convoluted tubule

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49
Q

Loop diuretic mechanism

A

inhibit Na and Cl reabsorption in the medullary portion of the ascending loop of Henle

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50
Q

Acetazolamide mechanism

A

inhibits carbonic anhydrase, which inhibits reabsorption of bicarb and prevents secretion of H+- leading to hypokalemic, hyperchloremic acidosis

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51
Q

catecholamine biosynthesis, release, and metabolism

A

phenylalanine -> tyrosine ->dopa (by tyrosine hydroxylase), ->dopamine by dopa decarboxylase. Dopamine enters storage granules, where it is converted to norepinephrine After action potential, influx of calcium causes vesicles to fuse, releaase norepi into synaptic cleft; 2/3s of norepi is removed from synaptic cleft by reuptake into nerve terminals The remainder is metabolized by MAO in cytoplasm Norepi in the circulation is metabolized by MAO and COMT Norepi is converted to epi in the adrenal medulla by phenylethanolamine-n-methyltransferase (PNMT)

52
Q

IV agents associated with myoclonus

A

Etomidate - 1/3 of patients during induction Normeperidine Opioid- 2/2 depression of inhibitory neurons methohexital Propofol thiopental tx: valproate and clonazepam

53
Q

Local anesthetic characteristics Potency depends on ____ Onset depends on ____ Duration depends on ___

A

Potency - lipid solubility onset - pKa duration - protein binding

54
Q

Alfentanil onset duration volume of distribution metabolism

A

rapid onset due to low pKa (90% in unionized form- onset 1-2 min) short duration due to low VoD and extensive hepatic metabolism- in cirrhotics, elimination t1/2 is 200 min lower lipid solubility and greater protein binding than morphine repeated doses do not result in significant cumulative effect

55
Q

Magnesium effect on acetylcholine

A

decreases release of ach from nerve terminal, decreases sensitivity of the end-plate to the effects of Ach.

56
Q

Drugs prolonging neuromuscular blockade

A

Lithium Sodium Magnesium antibiotics botulinum procaine decreased Ca+ decreased K+

57
Q

Ketorolac: contraindications and complications

A

Contraindications: Bronchospasm angioedema- associated anaphylactic reactions nasal polyps- associated anaphylactic reactions concurrent use of NSAIDs known allergy or intolerance to aspirin h/o GI bleeding complications: GI bleeding, ulceration, perforation acute renal failure, nephritis hemorrhage hypersensitivity: anaphylaxis, bronchospasm, angioedema

58
Q

Phenytoin metabolism drug interactions- cause increase sensitivity to phenytoin_____ cause decreased sensitivity to phenytoin____ Phenytoin decreases effectiveness of _____

A

metabolism: hepatic cimetidine and diazepam cause increased sensitivity to phenytoin barbiturates, theophylline, and antacids cause decreased sensitivity to phenytoin phenytoin decreases effectiveness of nondepolarizing muscle relaxants, steroids, lasix, and dopamine *Is useful as an antiarrythmic in refractory V tach or digoxin induced arrythmias

59
Q

Alprostadil: -Effects -side effects

A

vasodilation inhibition of platelet aggregation stimulation of intestinal and uterine smooth muscle marked relaxation of ductus arteriosus Side effects apnea bradycardia hypotension fever

60
Q

Echothiophate

A

Inhibitor of plasma cholinesterase - avoid succinylcholine, ester local anesthetics

61
Q

pseudocholinesterase increased in _____ decreased in _____

A

increased in obesity and goiter decreased in pregnancy, liver disease, burns, organophosphates, echothiophate, malnutrition

62
Q

sodium nitroprusside adverse effects

A

cyanide and thiocyanate toxicity rebound hypertension intracranial hypertension blood coagulation abnormalities increased pulmonary shunting in normal patients leading to hypoxemia hypothyroidism

63
Q

Dibucaine number

A

homozygous normal: 70-85 heterozygous: 30-65 fluoride resistant: 34 homozygous atypical: 16-25 silent: 0 Patients with no pseudocholinesterase activity must rely on GFR to clear sux Homozygous atypical: 2-3 hours of respiratory insufficiency

64
Q

macroshock vs microshock

A

the amount of current applied to the outside or inside of body Macroshock 1mA perception 10mA “let go” 100 mA V fib Microshock 10uA rec max leakage 100uA V fib

65
Q

Line isolation monitor: threshold, what to do if it alarms

A

alarm at 2mA if before a procedure begins, postpone or move the procedure if during a procedure, unplug systematically starting with most recently plugged in item

66
Q

Replacement of K

A

0.2-0.5 meq/kg/hr if urine output adequate

67
Q

PTH

A

bone: reabsorption, increased Ca and increased phosphate kidney: decrease ca++ excretion, increase phosphate excretion gut: increases GI absorption of ca++ and phosphate

68
Q

calcitonin

A

net effect: hypocalcemia and hypophosphatemia by decreasing bone reabsorption, increasing renal excretion, and decreasing GI absorption of each

69
Q

Vit D

A

net effect hypercalcemia and hyperphosphatemia potentiates PTH and in large amoutns causes bone and GI reabsorption of calcium

70
Q

Hypercalcemia treatment

A

maintain or expand volume status lasix calcitonin etidronate disodium plicamycin

71
Q

Causes of tetany

A

hypocalcemia - tetany, circumoral paresthesias, neuromuscular excitability, laryngospasm, seizures, ST or QT prolongation, TW inversion, +trousseau or chvostek hypomagnesemia- muscle fasciculations, tremor, muscle spasticity, tetany, +trousseau or chvostek uremia tetanus

72
Q

manifestations of hypo/hyperphos

A

hypo: CHF NM blockade/respiratory failure, rhabdo, hyporeflexia, seizures, AMS Nausea/vomiting Hyperphos: ectopic calcification and signs and symptoms of hypocalcemia ie. seizures, tetany, laryngospasm

73
Q

SIADH treatment

A

fluid restriction demeclocycline - antagonizes effects of ADH on renal tubules sodium chloride infusion 100-400 meq/day hypertonic saline to raise plasma concentration 0.5meq/hr if acute symptomatology

74
Q

Timeframe for symptoms following inadvertent removal of parathyroid glands during thyroidectomy?

A

Symptoms of hypocalcemia in 24-72 hours

75
Q

Hyperaldosteronism ( ____’s Disease)

A

Conn’s disease leads to hypertensioon and a hypokalemic, metabolic alkalosis

76
Q

Causes of increased aldosterone secretion:

A

increased potassium decreased sodium, decreased intravascular volume or hypotension ACTH and angiotensin II

77
Q

Addison’s disease

A

Adrenal hyposecretion: acute adrenal insufficiency -hypotension, fluid depletion, hyperkalemia, hyponatremia risk of cardiovascular collapse treatment is cortisol

78
Q

Roizen criteria for pheochromocytoma preparation BP control: EKG criteria:

A

BP: No inhospital BP >/ 165/90 No orthostatic BP /< 80/40 EKG: no ST segment changes x 2 weeks /< 5 PVCs in a 5 minute period

79
Q

What kind of lesion will cause a decrement in the inspiratory portion of a flow-volume loop

A

An extrathoracic lesion, ie. an obstructive tumor

80
Q

What kind of lesion will cause a decrement in the expiratory portion of the flow-volume loop?

A

An intrathoracic problem, such as COPD or mediastinal mass

81
Q

Effect of acetazolamide on the eye

A

Carbonic anhydrase is important in the synthesis of aqueous humor in the eye. Acetazolamide diminishes production.

82
Q

Agents that decrease intraocular pressure

A

volatile anesthetics, most IV anesthetic agents, nondepolarizers, lidocaine

83
Q

Agents that increase intraocular pressure

A

succinylcholine, nitrous oxide. Atropine has no effect, scopolamine has greater mydriatic effect -> less area for drainage->more of an effect.

84
Q

Relationship between ketamine and intraocular pressure

A

Unknown what effect it has on IOP- it’s controversial. However, ketamine does cause blepharospasm and nystagmus.

85
Q

How long must NO2 be avoided after intraocular sulfur hexafluoride injection?

A

10 days. Sulfur hexafluoride has a very low water solubility and is included in the air mixture which is injected to restore pressure following vitreous surgery.

86
Q

oculocardiac reflex arc

A

trigeminal-vagal reflex Afferent limb: sensed ->ciliary ganglion -> Gasserian ganglion (via ophthalmic division of trigeminal nerve) -> sensory nucleus of 4th ventricle Efferent limb: sensory nucleus of 4th ventricle respnds via vagus nerve -> hypotension, bradycardia, PVCs.

87
Q

Retrobulbar block

A

Ptosis, akinesia of globe, anesthesia of globe, temporary blindness Akinesia of EOM: III, IV, VI Anesthesia of conjunctiva, cornea, uvea: ciliary nerve blockade orbicularis oculi is not blocked (VII-closes eye), therefore, partial blockade of VII is helpful

88
Q

Classic signs and symptoms of carcinoid

A

Hormone release: histamine, kinins, serotonin Bronchospasm: avoid morphine, tx w H1 and H2 blockers preop, tx w volatiles, steroids, benadryl, somatostatin hypotension: 2/2 hormones, volume depletion. avoid succinylcholine (histamine release). Avoid catecholamines, give angiotensin instead hypertension: due to serotonin release. tx with SNP or TNG SOMATOSTATIN controls diarrhea, flushing, and wheezing in 75% of cases. cutaneous flushing

89
Q

Electrolyte disturbance in nausea/vomiting

A

hypokalemic, hypochloremic metabolic alkalosis

90
Q

tx of opioid induced sphincter of oddi spasm

A

naloxone or glucagon (1-3 mg)

91
Q

Precipitating factors for crisis in sickle cell disease

A

hypoxia (O2 sat <40 w sickle cell trait) hypothermia hypotension hypovolemia infection dehydration acidosis venostasis

92
Q

Indications for preoperative exchange transfusion (sickle cell disease, including for sickle cell trait)

A

goal HgAA 50-70%, Hg 8-12g/dl potential severe hypoxic stress: Thoracotomy CP bypass cerebral aneurysm clipping induced hypotension

93
Q

Normal size of mitral valve

A

4-6 cm^2

94
Q

Normal size of aortic valve

A

2.5-3.5cm^2

95
Q

% of CO accounted for by atrial kick in Mitral stenosis

A

35%

96
Q

Three types of indirect apnea monitors

A

impedance pneumography- electrodes on each side of thoracic cavity with low intensity current passing between them pressure sensitive pad, the transducers sense body motion caused by breathing and convert to electrical signal pneumatic abdominal sensor- pressure changes by expansion and contraction of abdomen during respiration are detected as breaths

97
Q

three types of direct apnea monitors

A

thermisters placed in front of mouth and nose detect cool air on inspiration, warm air on expiration proximal airway pressure sensors at mouth or nose infrared CO2 sensors

98
Q

100% saturated hemoglobin corresponds to ___ nm wavelength, 50% saturated Hg corresponds to ___nm wavelength

A

940 660 oxygenated Hg absorbs less red light than deoxyHg, accounting for it’s red color. Carboxy Hg is viewed by the pulse ox as OxyHg.

99
Q

Effect of underdamped system on systolic and diastolic blood pressures

A

Systolic increased, diastolic decreases

100
Q

Factors leading to underdamped (hyperresonant) system

A

Small tubing, ID 1.5m stiff tubing big catheter (18g in radial art)

101
Q

factors leading to an overdamped waveform

A

high viscosity soft, high compliance tubing bubbles in the system

102
Q

Definition of critical damping

A

The optimal damping in a pressure system

103
Q

Conversion: 1mmHg = ___ cmH20

A

1.36

104
Q

Complications of cannulation of temporal artery

A

cerebral emboli via carotid artery system

105
Q

CVP waves

A

All College eXams Vary Yearly A: atrial contraction c: closure of tricuspid x descent: atrial relaxation V: filling of RA during systole y descent: TV opens

106
Q

Causes of cannon “a” waves

A

junctional rhythm tricuspid stenosis RVH pulmonary stenosis pulmonary hypertension

107
Q

Pathophysiology of myasthenia gravis

A

Decreased available acetylcholine receptors at the postsynaptic site of NMJ due to destruction by circulating antibodies.

108
Q

How to distinguish between myasthenic crisis from cholinergic crisis

A

Edrophonium (tensilon) test: myasthenic crisis: strength improves cholinergic crisis: weakness worsens

109
Q

pathophysiology of myasthenic syndrome

A

AKA Eaton Lambert syndrome. Decreased acetylcholine release following nerve stimulation (presynaptic)

110
Q

Hallmark of Eaton Lambert

A

Strength with exercise IMPROVES. No improvement following acetylcholinesterase administration. Marked sensitivity to nondepolarizers and depolarizers. may be seen in patients with thyroid disease and SLE

111
Q

characteristics of myotonic dystrophy

A

Prolonged muscle contraction and delayed muscle relaxation following stimulation. -Atrophy and weakness are key features -facial, pharyngeal, and sternocleidomastoid are typically involved

112
Q

Myotonia dystrophica

A

Most common, most serious form of myotonic dystrophy Respiratory muscle weakness cardiac abnormalities including cardiomyopathy, cardiac dysrhythmias, cardiac conduction abnormalities myocardial depression from volatiles Succinylcholine causes sustained muscle contraction, hyperkalemia, and should be avoided. Nondepolarizers acceptable in decreased doses.

113
Q

What is the most common type of pathogen causing bacterial meningitis after spinal?

A

Mouth flora

114
Q

Morphine metabolite with action at mu opioid receptor, responsible for respiratory depression

A

morphine 6-glucuronide

115
Q

True or false: In a patient taking suboxone (buprenorphine/naloxone), opioid requirements are increased primarily due to the naloxone.

A

False. Naloxone is very poorly absorbed when taken orally and is only present in the formulation to prevent IV abuse of the drug. Buprenorphine is a mu agonist/kappa antagonist. Opioid naive patients experience buprenorphine as a profound analgesic. Opioid dependent patients may experience withdrawal with buprenorphine as it has a high affinity for the mu receptor and will displace other opioids, but activates the receptor less strongly than a pure opioid agonist. Patients on buprenorphine may demonstrate high levels of opioid tolerance and buprenorphine may antagonize pure opioid agonists such as morphine.

116
Q

SSEP Increase latency: decrease amplitude: Decrease latency: increase amplitude:

A

Increase latency: opioids, benzos, volatiles, hemodilution, ETOMIDATE decrease amplitude: hypoxia, hypo/hyperthermia, hypotension, volatiles, nitrous, benzos, opioids, Increase amplitude: Ketamine, etomidate ETOMIDATE INCREASES LATENCY AND AMPLITUDE. No agents identified that decrease latency.

117
Q

Changes in CBF with : 1mmHg change in PaCO2? PaO2 < __mmHg? Change in CMRO2 with change in temp?

A

1-2ml/100g/min for each 1 mmHg change in PaCO2 CBF increases dramatically if Pa O2 <50mmHg CMRO2 decreases 7% for each 1 *C decrease in temp.

118
Q

Agents that increase CBF: Agents that decrease CBF: Agents that increase/decrease CMRO2

A

Increase CBF: volatiles, Nitrous oxide, ketamine decrease CBF: all other IV anesthetics Decrease CMRO2: volatiles, IV anesthetics Increase CMRO2: Nitrous oxide, ketamine **Note: all IV agents decrease CBF and CMRO2, except ketamine, which increase both! (Like Nitrous) Volatiles DECOUPLE CBF and CMRO2– hence increasing CBF and decreasing CMRO2.

119
Q

Glasgow coma scale

A

Eye opening 4 spontaneous 3 to speech 2 to pain 1 none Best verbal response 5 oriented 4 confused conversation 3 inappropriate words 2 incomprehensible sounds 1 none Best motor response 6 obeys 5 localizes 4 withdraws 3 abnormal flexion 2 extensor 1 none

120
Q

EEG Delta waves theta alpha beta

A

Delta waves: 0-4 deep sleep, deep anesthesia, hypoxia, tumors theta: 4-8 sleep, anesthesia, hyperventilation alpha: 8-13 resting, alert, awake beta: 13-30 mental concentration, barbiturates, benzos volatiles: sub mac increase to beta, then slow, able to produce silence barbiturates: initially low voltage, fast, then to high amplitude delta and theta, burst suppression, silence ketamine: high amplitude theta and beta opioids: slow alpha, then delta, never silence Progression: increased frequency decreased frequency, increased amplitude, decreased frequencey, decreased amplitude silence

121
Q

A machine calibrated at sea level and taken to a higher elevation delivers a higher or lower concentration that dialed in?

A

It delivers a higher concentration. Since the VP/BP ratio increases, the delivered concentration is higher.

122
Q

Second gas effect

A
123
Q

The second gas effect

A

Administration of a high concentration of a gas such as N20, will facilitate the rise in alveolar concentration of a second gas given with it. The first is by an increase in tracheal inflow caused by the uptake of gases in the alveolus that creates a void, drawing more gas down the trachea. The second is the concentration effect, where by the uptake of N20 reduces the volume of the alveolus, concentrating the remaining gases in a smaller volume.

124
Q

Indications for SBE prophylaxis

A

  1. Prosthetic cardiac valve or prosthetic material used for valve repair 2. history of infective endocarditis 3. CHD: -unrepaired cyanotic congenital heart disease, -including palliative shunts/conduits -repaired congenital heart disease with persistent defect -completely repaired CHD with prosthetic material in first 6 months after the procedure -repaired CHD with prosthetic materials and persistent defect adjacent to the repair (inhibits endothelialization) 4. Cardiac transplantation recipients with valvulopathy
125
Q

What effect does V/Q mismatching have on anesthetic induction with volatile anesthetics?

A

The effect of V/Q mismatching on uptake of volatile anesthetics is dependent on the solubility of the anesthetic agent (see Anesthetic uptake: Solubility coefficient, also see classic manuscript [Eger and Severinghaus. Anesthesiology 25: 620, 1964; FREE Full-text at Anesthesiology]). Using endobronchial intubation as an example - for relatively insoluble agents (ex. desflurane [blood gas solubility coefficient 0.42, MAC 6-7.3%]), the rate of rise of arterial partial pressure of agent is slower for a given inspired concentration (despite the fact that the alveolar partial pressure of desflurane in the intubated lung rises more rapidly). For relatively soluble agents, for which rate of uptake is dependent on minute ventilation (ex. isoflurane [blood gas solubility coefficient 1.46, MAC 1.15%]), the rate of rise of arterial partial pressure of agent in the ventilated lung increases for a given inspired concentration, because the ventilated lung receives an effectively doubled minute ventilation - this higher partial pressure allows more anesthetic agent to transfer to the blood stream, and partially attenuates the effect of the essentially unventilated lung.

125
Q

What is the mechanism of tirofiban?

A

Reversible antagonist of fibrinogen, GPIIbIIIa receptor

125
Q

What are the following prostaglandins? PGE1: PGE2: PGI2: PGI2 Analog:

A

PGE1: maintains ductus patency at 0.1 ug/kg/min. Can diagnose duct-dependent lesion (see Hallidie-Smith KA, below) PGE2: maintains ductus patency at in utero (PGE2 not available as a drug) PGI2: epoprostenol/Flolan PGI2 Analog: iliprost/Ventavis

Anesthesiology (11 decks)

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