Anesthesia Flashcards
Prerenal values for: Na meq/L FENA % UOsm mosm/L U/P osm BUN/Cr
Prerenal Na meq/L FENA 1 percent UOsm400 mosm/L U/P osm >1.8 BUN/Cr >20
Intrinsic Renal pathology Na meq/L FENA U Osm mosm/L U/P osm BUN/Cr
renal Na meq/L >40 FENA >3 UOsm 250-300 mosm/L U/P osm <20
Chemotherapeutic that causes pulmonary fibrosis
Bleomycin
innervation and function of cricothyroid muscle
External laryngeal branch of superior laryngeal nerve Tensor of vocal cords
Internal laryngeal branch of superior laryngeal nerve
Sensation above vocal cords
recurrent laryngeal nerve innervation
sensation below vocal cords motor control to all laryngeal muscles except cricothyroid
during performance of axillary nerve block, needle passes through wall of axillary artery. the nerve most likely encountered is
radial
anatomy axillary block
…………………. median ………………… ax art ……..ax vein…..ax art bone ax vein uln. n. radial n. bone ax vein
Radial nerve block
between biceps tendon and brachioradialis muscle at level of elbow joint
Wrist nerve and artery anatomy
N-A-/N-/A-N lateral to medial, radial n, radial art, median nerve, ulnar artery, ulnar nerve
Ulnar nerve block
At elbow, between olecranon and medial epicondyle of humerus At writst, just medial to ulnar artery
Median nerve block
At elbow, just medial to brachial artery between two heads of pronator teres In wrist, between flexor carpi radialis and palmaris longus
Ankle block
- 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
gasserian ganglion block
trigeminal nerve block- ipsilateral face, cornea, sclera, anterior tongue, middle cranial fossa, can produce total spinal
superficial cervical plexus block
first four cervical nerves, superficial at lateral border of SCM, horners syndrome and hoarsness (RLN)
celiac plexus block
thoracic sympathetic ganglion and greater and lesser splanchnic nerves. located at L1 -hypotension, diarrhea, shoulder pain
Sciatic nerve block
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.
Side effects cimetidine
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
Reversal of urokinase in a hemorrhaging patient requiring surgery
cryoprecipitate
Diseases associated with Prolonged PTT
hemophilia A, B and von Willebrand’s disease
Vit K dependent factors
2, 7, 9, 10
all procoagulants synthesized in liver except
factor VIII, which is synthesized in the reticuloendothelial system.
Hemophilia A: Coag tests treatment
prolonged PTT, normal PT factor VIII concentrate
Hemophilia B coag tests treatment
Factor IX (males only) prolonged PTT and normal PT. treatment hyman purified and recombinant factor IX as well as FFP
von Willebrand disease
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%
Heparin mechanism
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
Fibrinolytic system cascade
factor XII -> plasminogen -> plasmin -> fibrin -> fibrin split products
Tranexamic acid and aminocaproic acid mechanism
competitive inhibitor of plasminogen activation, inhibiting the breakdown of clot.
Aprotinin mechanism and effect
trypsin inhibitor, which inhibits plasmin’s fibrinolytic activity and has been shown to reduce perioperative blood loss.
most likely cause of anaphylactic reaction in a patient who has been previously transfused
Recipient IgA deficiency (reaction to donor IgA, washed cells may be beneficial)
FFP indications
replacement of isolated factor deficiencies Antithrombin III deficiency deficiency of factor V or VIII TTP
Donor PRBCs Recipient Plasma O A B AB
O, A, B, AB A, AB B, AB AB
True/false: an A+ patient who has received 10 units of O negative RBCs can still safely receive A neg and A pos RBCs.
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.
fluid replacement in burns
4ml/kg per percent body burned (Arm- 9%, trunk -36%, leg-18%, head- 9%)
V fib algorithm
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)
Nitroprusside
Dose titrated to 10mcg/kg/min toxic if 1mg/kg in 3 hours CYANIDE toxicity: unexplained metabolic acidosis treatment is sodium nitrate and thiosulfate
Verapamil is contraindicated in
V TACH Indications: second line for supraventricular tachyarrhythmias
left shift of CO2 response curve (increased sensitivity)
arterial hypoxemia metabolic acidemia increased ICP, anxiety, fear, cirrhosis drugs: doxapram, strychnine, picrotoxin
right shift of CO2 response curve (alveolar ventilation v PCO2)
aminophylline salicylates catecholamines opioids metabolic alkalemia, denervation of chemoreceptors, normal sleep, drugs, hypothermia
hypoventilation/hypercarbia
A RIPE acidosis, arrythmias right shift of oxhemoglobin dissociation curve intracerebral steal PA pressure increase Epi-norepi release
hyperventilation/hypocarbia
AVCO apnea, alkalosis, airway constriction V/Q mismatch decreased CO, cerebral blood flow, coronary blood flow, calcium oxy-Hb dissociation curve shifted to left
Frank starling curve
Stroke volume vs left ventricular filling pressure
right ventricular perfusion depends on ____ arterial pressure, left ventricular perfusion depends on ____ arterial pressure
systolic diastolic
Drugs that increase uterine tone
(PEOKA) PGF2alpha Ergots Oxytocin Ketamine Amide local anesthetics
Drugs that decrease uterine tone
BEMP Beta-2 agonists Ethanol Magnesium sulfate methylxanthines Potent volatile anesthetics
Effect of lidocaine in atrial fibrillation
Lidocaine markedly increases A-V conductance and may lead to accelerated ventricular response
Digitalis toxicity- level and cause, should you cardiovert?
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
Thiazide mechanism
Inhibits Na and Cl reabsorption in cortical portion of the ascending loop of Henle and distal convoluted tubule
Loop diuretic mechanism
inhibit Na and Cl reabsorption in the medullary portion of the ascending loop of Henle
Acetazolamide mechanism
inhibits carbonic anhydrase, which inhibits reabsorption of bicarb and prevents secretion of H+- leading to hypokalemic, hyperchloremic acidosis
catecholamine biosynthesis, release, and metabolism
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)
IV agents associated with myoclonus
Etomidate - 1/3 of patients during induction Normeperidine Opioid- 2/2 depression of inhibitory neurons methohexital Propofol thiopental tx: valproate and clonazepam
Local anesthetic characteristics Potency depends on ____ Onset depends on ____ Duration depends on ___
Potency - lipid solubility onset - pKa duration - protein binding
Alfentanil onset duration volume of distribution metabolism
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
Magnesium effect on acetylcholine
decreases release of ach from nerve terminal, decreases sensitivity of the end-plate to the effects of Ach.
Drugs prolonging neuromuscular blockade
Lithium Sodium Magnesium antibiotics botulinum procaine decreased Ca+ decreased K+
Ketorolac: contraindications and complications
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
Phenytoin metabolism drug interactions- cause increase sensitivity to phenytoin_____ cause decreased sensitivity to phenytoin____ Phenytoin decreases effectiveness of _____
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
Alprostadil: -Effects -side effects
vasodilation inhibition of platelet aggregation stimulation of intestinal and uterine smooth muscle marked relaxation of ductus arteriosus Side effects apnea bradycardia hypotension fever
Echothiophate
Inhibitor of plasma cholinesterase - avoid succinylcholine, ester local anesthetics
pseudocholinesterase increased in _____ decreased in _____
increased in obesity and goiter decreased in pregnancy, liver disease, burns, organophosphates, echothiophate, malnutrition
sodium nitroprusside adverse effects
cyanide and thiocyanate toxicity rebound hypertension intracranial hypertension blood coagulation abnormalities increased pulmonary shunting in normal patients leading to hypoxemia hypothyroidism
Dibucaine number
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
macroshock vs microshock
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
Line isolation monitor: threshold, what to do if it alarms
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
Replacement of K
0.2-0.5 meq/kg/hr if urine output adequate
PTH
bone: reabsorption, increased Ca and increased phosphate kidney: decrease ca++ excretion, increase phosphate excretion gut: increases GI absorption of ca++ and phosphate
calcitonin
net effect: hypocalcemia and hypophosphatemia by decreasing bone reabsorption, increasing renal excretion, and decreasing GI absorption of each
Vit D
net effect hypercalcemia and hyperphosphatemia potentiates PTH and in large amoutns causes bone and GI reabsorption of calcium
Hypercalcemia treatment
maintain or expand volume status lasix calcitonin etidronate disodium plicamycin
Causes of tetany
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
manifestations of hypo/hyperphos
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
SIADH treatment
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
Timeframe for symptoms following inadvertent removal of parathyroid glands during thyroidectomy?
Symptoms of hypocalcemia in 24-72 hours
Hyperaldosteronism ( ____’s Disease)
Conn’s disease leads to hypertensioon and a hypokalemic, metabolic alkalosis
Causes of increased aldosterone secretion:
increased potassium decreased sodium, decreased intravascular volume or hypotension ACTH and angiotensin II
Addison’s disease
Adrenal hyposecretion: acute adrenal insufficiency -hypotension, fluid depletion, hyperkalemia, hyponatremia risk of cardiovascular collapse treatment is cortisol
Roizen criteria for pheochromocytoma preparation BP control: EKG criteria:
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
What kind of lesion will cause a decrement in the inspiratory portion of a flow-volume loop
An extrathoracic lesion, ie. an obstructive tumor
What kind of lesion will cause a decrement in the expiratory portion of the flow-volume loop?
An intrathoracic problem, such as COPD or mediastinal mass
Effect of acetazolamide on the eye
Carbonic anhydrase is important in the synthesis of aqueous humor in the eye. Acetazolamide diminishes production.
Agents that decrease intraocular pressure
volatile anesthetics, most IV anesthetic agents, nondepolarizers, lidocaine
Agents that increase intraocular pressure
succinylcholine, nitrous oxide. Atropine has no effect, scopolamine has greater mydriatic effect -> less area for drainage->more of an effect.
Relationship between ketamine and intraocular pressure
Unknown what effect it has on IOP- it’s controversial. However, ketamine does cause blepharospasm and nystagmus.
How long must NO2 be avoided after intraocular sulfur hexafluoride injection?
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.
oculocardiac reflex arc
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.
Retrobulbar block
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
Classic signs and symptoms of carcinoid
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
Electrolyte disturbance in nausea/vomiting
hypokalemic, hypochloremic metabolic alkalosis
tx of opioid induced sphincter of oddi spasm
naloxone or glucagon (1-3 mg)
Precipitating factors for crisis in sickle cell disease
hypoxia (O2 sat <40 w sickle cell trait) hypothermia hypotension hypovolemia infection dehydration acidosis venostasis
Indications for preoperative exchange transfusion (sickle cell disease, including for sickle cell trait)
goal HgAA 50-70%, Hg 8-12g/dl potential severe hypoxic stress: Thoracotomy CP bypass cerebral aneurysm clipping induced hypotension
Normal size of mitral valve
4-6 cm^2
Normal size of aortic valve
2.5-3.5cm^2
% of CO accounted for by atrial kick in Mitral stenosis
35%
Three types of indirect apnea monitors
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
three types of direct apnea monitors
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
100% saturated hemoglobin corresponds to ___ nm wavelength, 50% saturated Hg corresponds to ___nm wavelength
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.
Effect of underdamped system on systolic and diastolic blood pressures
Systolic increased, diastolic decreases
Factors leading to underdamped (hyperresonant) system
Small tubing, ID 1.5m stiff tubing big catheter (18g in radial art)
factors leading to an overdamped waveform
high viscosity soft, high compliance tubing bubbles in the system
Definition of critical damping
The optimal damping in a pressure system
Conversion: 1mmHg = ___ cmH20
1.36
Complications of cannulation of temporal artery
cerebral emboli via carotid artery system
CVP waves
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
Causes of cannon “a” waves
junctional rhythm tricuspid stenosis RVH pulmonary stenosis pulmonary hypertension
Pathophysiology of myasthenia gravis
Decreased available acetylcholine receptors at the postsynaptic site of NMJ due to destruction by circulating antibodies.
How to distinguish between myasthenic crisis from cholinergic crisis
Edrophonium (tensilon) test: myasthenic crisis: strength improves cholinergic crisis: weakness worsens
pathophysiology of myasthenic syndrome
AKA Eaton Lambert syndrome. Decreased acetylcholine release following nerve stimulation (presynaptic)
Hallmark of Eaton Lambert
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
characteristics of myotonic dystrophy
Prolonged muscle contraction and delayed muscle relaxation following stimulation. -Atrophy and weakness are key features -facial, pharyngeal, and sternocleidomastoid are typically involved
Myotonia dystrophica
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.
What is the most common type of pathogen causing bacterial meningitis after spinal?
Mouth flora
Morphine metabolite with action at mu opioid receptor, responsible for respiratory depression
morphine 6-glucuronide
True or false: In a patient taking suboxone (buprenorphine/naloxone), opioid requirements are increased primarily due to the naloxone.
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.
SSEP Increase latency: decrease amplitude: Decrease latency: increase amplitude:
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.
Changes in CBF with : 1mmHg change in PaCO2? PaO2 < __mmHg? Change in CMRO2 with change in temp?
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.
Agents that increase CBF: Agents that decrease CBF: Agents that increase/decrease CMRO2
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.
Glasgow coma scale
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
EEG Delta waves theta alpha beta
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
A machine calibrated at sea level and taken to a higher elevation delivers a higher or lower concentration that dialed in?
It delivers a higher concentration. Since the VP/BP ratio increases, the delivered concentration is higher.
Second gas effect
The second gas effect
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.
Indications for SBE prophylaxis
- 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
What effect does V/Q mismatching have on anesthetic induction with volatile anesthetics?
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.
What is the mechanism of tirofiban?
Reversible antagonist of fibrinogen, GPIIbIIIa receptor
What are the following prostaglandins? PGE1: PGE2: PGI2: PGI2 Analog:
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
