Anesthesiology (ABA) Oral Boards – Flashcards

1. D/c triggering agents 2. Call for help 3. 100% FiO2; high flow; hyperventilate 4. Dantrolene: 2.5 mg/kg IV every 5 min to max 10 mg/kg or until symptoms subside 5. Collect labs: blood gases, electrolytes, calcium, LFT's, CK 6. Treat hyperkalemia: hyperventilate, dextrose + insulin 7. Active cooling: ice to groin and axilla, ice lavage of stomach 8. Maintain >2 ml/kg/hr urine output with fluids, lasix and mannitol; insert foley

<35 degrees celsius: platelet dysfunction <33 degrees celsius: decreased synthesis of clotting factors <30 degrees celsius: arrhythmias

Beta blockers (esmolol, propranolol, inhalational agents) Phenylephrine to increase SVR Increase venous return (push/lift legs to chest)

Kinked ET tube (most common) Endobronchial intubation Pulmonary edema Left heart failure Amniotic fluid embolism Bronchospasm Aspiration Thrombo-embolic phenomenon *!Not all wheezing is asthma!*

*Glossopharyngeal Nerve* Provides sensory innervation to the posterior third of the tongue, the vallecula, the anterior surface of the epiglottis (lingual branch), the walls of the pharynx (pharyngeal branch), and the tonsils (tonsillar branch). *Block Method*: It can be blocked using one of three methods: topical spray application, direct mucosal contact of soaked pledgets, or direct infiltration by injection. *Superior Laryngeal Nerve* Innervates the base of the tongue, posterior surface of the epiglottis, aryepiglottic fold, and the arytenoids. *Block method*:Direct infiltration is accomplished at the level of the thyrohyoid membrane inferior to the cornu of the hyoid bone. A reliable block with a definite endpoint is effected by retracting the needle marginally after contacting the greater cornu and injecting 2mL of local anesthetic after negative aspiration. Less invasive blockade can be accomplished by placing anesthetic-soaked cotton pledgets into the pyriformfossae bilaterally. *Recurrent Laryngeal Nerve* Provides sensory innervation to the trachea and vocal folds. *Block method*: trans-tracheal

*Neuro* Stroke, bleed, seizure *Airway/Resp* Edema (manifesting as voice change) Pulmonary edema (endothelial dysfunction) Decreased FRC *Cardiac* Volume depleted, increased SVR

Normal Values: *FEV1* 80-120% *FVC* 80-120% The test is interpreted as within normal limits if both the VC and the FEV1/VC ratio are in the normal ranges. *OBSTRUCTIVE ABNORMALITY* The test is interpreted as showing obstructive abnormality when the FEV1/VC ratio is below the normal range. The severity of the abnormality might be graded as follows: *Mild*: Predicted FEV1 <100% and ≥70% *Moderate*: Predicted FEV1 <70% and ≥60% *Moderately severe*: Predicted FEV1 <60% and ≥50% *Severe*: Predicted FEV1 <50% and ≥34% *RESTRICTIVE ABNORMALITY* Reduction in the VC without a reduction of the FEV1/VC ratio

Decreased intra-incisor distance Inability to prognath jaw Limited neck mobility Decreased thyromental distance Neck circumference >16 inches H/o radiation therapy Change of voice, stridor Mallampati III or higher *Hx of difficult intubation*

Increased Body Mask Index (BMI >45) Snoring/Obstructive Sleep Apnea Presence of Beard Lack of dentition Age > 55 years Mallampati III or higher Male Gender Airway masses/tumors

*Pathophysiology* dynamic outflow obstruction, because the degree of obstruction is variable and is dependent on the loading conditions (ventricular filling and arterial blood pressure) and the contractility state of the left ventricle. *Anesthetic goals* -myocardial depression, often with volatiles -preload full, afterload increased (e.g. phenylephrine) -rate normal, rhythm sinus -beta blockers are first line treatment

2 or more of the following: -temp >38 degrees celsius or 90 bpm -RR > 20/min or PaCO21200 or 10% immature bands Sepsis=SIRS criteria + documented infection

1) High risk surgery (major vascular, abdominal, thoracic or ortho surgery) 2) H/o ischemic heart disease (risk of re-infarction is high for 2 months after an MI) 3) H/o CHF 4) H/o cerebrovascular disease 5) H/o preoperative use of insuline 6) Pre-op serum creatinine >2.0 7) Active cardiac conditions: -unstable coronary syndromes (unstable angine, MI within last 2 months) -decompensated heart failure -significant arrhythmias -significant valvular disease

1. Vagal maneuvers: Valsalva 2. Adenosine 3. If SVT persistent despite prior therapy OR if patient hemodynamically unstable: cardioversion

C.I. 2-4 PCWP 6-12 PA Pressure 25/10

-BP >140/90 -Proteinuria >3 gm/day -generalized edema after 12 hr bed rest or >5 lb wt gain/week

-SBP>160 or DBP>110 -proteinuria >5 gm/day -H/A, blurred vision, altered mental status -pulmonary edema -epigastric or RUQ pain -HELLP syndrome -impaired liver function

+Continuing pain that is disproportionate to any inciting event. +At least 1 symptom reported in at least 3 of the following categories: *Sensory*: Hyperesthesia or allodynia *Vasomotor*: Temperature asymmetry, skin color changes, skin color asymmetry *Sudomotor/edema*: Edema, sweating changes, or sweating asymmetry *Motor/trophic*: Decreased range of motion, motor dysfunction (eg, weakness, tremor, dystonia), or trophic changes (eg, hair, nail, skin) +At least 1 sign at time of evaluation in at least 2 of the following categories: *Sensory*: Evidence of hyperalgesia (to pinprick), allodynia (to light touch, temperature sensation, deep somatic pressure, or joint movement) *Vasomotor*: Evidence of temperature asymmetry (>1°C), skin color changes or asymmetry *Sudomotor/edema*: Evidence of edema, sweating changes, or sweating asymmetry *Motor/trophic*: Evidence of decreased range of motion, motor dysfunction (eg, weakness, tremor, dystonia), or trophic changes (eg, hair, nail, skin) +No other diagnosis better explaining the signs and symptoms

Evaluate with hx and exam. -smoking history -use of inhalers -productive cough -baseline symptoms

Monitors the power lines of an isolated power system. It continuously samples the difference between both lines of an ungrounded power system and alarms when a short circuit that has the potential to allow 5 mA of current flow to ground to develop. Just because LIM alrams, does not mean there is an actual shock hazard, which would only be the case if a 2nd fault were also present.

*Early Decels* Due to vagal compression of fetal head of stretching of neck *Late Decels* Smooth reduction in FHR after peak contraction due to uteroplacental insufficiency *Variable Decels* Abrupt and variable changes in FHR due to umbilical cord compression

*Criteria for CRPS I*: 1)The presence of an initiating noxious event or a cause of immobilization 2)Continuing pain, allodynia (perception of pain from a nonpainful stimulus), or hyperalgesia (an exaggerated sense of pain) disproportionate to the inciting event 3)Evidence at some time of edema, changes in skin blood flow, or abnormal sudomotor activity in the area of pain 4)The diagnosis is excluded by the existence of any condition that would otherwise account for the degree of pain and dysfunction. *Criteria for CRPS II (causalgia)*: 1) The presence of continuing pain, allodynia, or hyperalgesia after a nerve injury, not necessarily limited to the distribution of the injured nerve 2)Evidence at some time of edema, changes in skin blood flow, or abnormal sudomotor activity in the region of pain 3)The diagnosis is excluded by the existence of any condition that would otherwise account for the degree of pain and dysfunction.

1) Physical therapy 2) TCA's, gabapentin, mild opioid (to aid with tolerance of PT) 3) Diagnostic sympathetic block 4) Somatic block, if sympathetic block fails 5) Spinal cord stimulator 6) Intrathecal medications

1) Prerenal -hypovolemia -hypotension -decreased CO -increase in renal vascular resistance 2) Renal -nephrotoxins -intrinsic disease -ischemia -confirm ATN with FENa>2 3) Post-renal -urethral obstruction/disruption -ureteral obstruction/disruption

Cardiac: r/o CHF secondary to anemia, hypoxia, hemochromatosis Pulm: intra pulmonary shunting, acute chest syndrome Neuro: deficits from stroke or seizures GU: renal function specifically concentrating ability of kidneys Endo & hepatic: possible effects of iron overload

LR -hypotonic -small amount of K+ -large amounts may produce met alkalosis (lactate-->HCO3) 0.9 NS -slightly hypertonic -large amounts may produce hypernatremia and hyperchloremic met acidosis Plasmalyte -isotonic -contains Mag, acetate & gluconate

Type specific blood: 2/1000 Type & Screen: 6/10000 Type & Cross: 5/10000 T/C prevents 1/10000 more acute hemolytic reactions than just a T/S

Estimated blood volume x (Starting HCT-target HCT)/starting HCT

MOTOR RESPONSE 6-To command 5-Localizes to pain 4-Withdraws to pain 3-Decorticate posture 2-Decerebrate posture 1-None VERBAL RESPONSE 5-Oriented 4-Confused 3-Inappropriate 2-Incomprehensible 1-None EYE MOVEMENTS 4-Spontaneous 3-To command 2-To pain 1-None

Tests coagulation cascade, platelet fxn, platelet fibrin interaction and fibrinolysis to determine etiology of coagulopathy. R: time for clot to form MA: strength of clot K: speed of clot formation

a. First, I would confirm the BP value by palpating the pulse at 2 separate sites and repeat the NIBP reading. b. At the same time, I would look at his other vital signs, including HR, saturation, ETC02, and temperature. Depending on my findings, I may consider chest auscultation and examination. c. Then, I would look for a specific cause. ■ I would look at the ECG for heart rate rhythm, and ST segment changes. ■ I would examine the surgical field for signs of bleeding or IVC compression. ■All drugs given to the patient and relevant history should be reviewed. ■ If present, invasive monitors should be checked for filling pressures and CO. d. Critically low BPs should be treated acutely with epinephrine or ephedrine if there is bradycardia and phenylephrine if there is tachycardia. e. An initial fluid bolus may also be indicated unless it is strongly suspected that fluid will worsen CHF. f. CPR is necessary for life-threatening hypotension.

Loop diuretic that inhibits chloride resorption in thick ascending loop of henle

1. Neuroleptic malignant syndrome 2. Thyroid storm (no rigidity) 3. Pheochromocytoma (no rigidity) 4. Cocaine (no severe acidosis) 5. Sepsis (no HTN or hypercarbia)

1. hypoxia 2. hypovolemia 3. hypothermia 4. hyper/hypokalemia 5. hypoglycemia 6. hydrogen ions (acidosis) 1. Toxins (inhalational agents!) 2. Trauma 3. Tension PTX 4. Thrombosis: coronary, pulmonary 5. Tamponade-cardiac

The diseases that are known to be linked with MH susceptibility are invariably also caused by mutations on chromosome 19 in the same region as that which encodes for ryanodine. 1. central core myopathy 2. multiminicore myopathy 3. King-Denborough syndrome 4. Native American myopathy 5. (possibly) hypokalemic periodic paralysis.

Hyperkalemia Hypoxia Mechanical stimulation from a central line

*a. ABCs* • Hypoxia • Hypercarbia (C02 narcosis) • Hypocarbia (insufficient C02 stimulus) *b. Medication effect* • Premedications (sedatives, scopolamine, droperidol, benzodiazepines) •Central anticholinergic syndrome (atropine, scopolamine, organophosphates, TCA) • Neuromuscular blocker •Anesthetic (inhaled, intravenous) • Usual medications (narcotics, sedatives, tranquilizers, lithium, reserpine, clonidine, alpha-methyldopa, steroids, amphetamines, etc.) • Substance abuse (alcohol, cocaine, LSD, heroin, etc.) *c. Endocrinologic/metabolic* • Hyponatremia • Hypocalcemia • Hypoglycemia • Hypermagnesemia • Hypothermia • DKA • Hepatic encephalopathy • Renal encephalopathy • Hypothyroidism • Addison's Disease • Cushing's Disease *d. Neurologic* • Ictal or post-ictal state • CVA (ischemic, thrombotic, embolic, hemorrhagic) • Cerebral edema *e. Baseline condition*

a. Low inspired 02 concentration b. Hypoventilation -Central or obstructive causes with spontaneous ventilation - Mechanical causes with controlled or spontaneous ventilation c. Shunt-V/Q mismatch -Atelectasis -Mucous plugs -Pneumo-/hemo-/chylothorax -Pleural effusion -Pulmonary contusion -Endobronchial intubation -Pulmonary edema -Pneumonia/pneumonitis -Aspiration -Bronchospasm -Pulmonary embolism -Inhibition of hypoxic pulmonary vasoconstriction -Decreased MV02 -Intracardiac shunt -Pulmonary arterio-venous fistulae -During one-lung ventilation d. Increased diffusion barrier e. Baseline condition

Decreased protein binding Increased permeability of BBB Decreased drug elimination Increased sensitivity to drugs

1) duration of disease for 6 years or longer 2) chronic comorbid pulmonary disease 3) pyridostigmine dose >750 mg/d 4) VC <2.9L 5) Other indicators include preoperative use of steroids, and previous episode of respiratory failure.

CO x SVR CO is dependent on preload, afterload, contractility and HR. SVR determined by arteriolar tone and blood viscosity

Ability of heart to increase cardiac output in response to increase in preload. E.g. Giving fluid bolus in order to increase blood pressure(CO)

Demand: -Heart rate -Wall tension (dependent on preload and afterload) -Contractility Supply -Coronary perfusion pressure -Heart rate -O2 content (decreased by anemia, hypoxia) -coronary artery diameter

-chest pain -exercise tolerance -syncope -palpitations -orthopnea -episodes of CHF -hospitalizations -medications -old records

1. Bleeding (adjacent arterial injury, hematoma formation, airway compromise, or cardiac tamponade) 2. Pneumothorax, hemothorax, and chylothorax 3. Nerve injury 4. Infection (bacteremia, sepsis, endocarditis) 5. Venous thromboembolism 6. Venous (and paradoxical) air embolism

-patients presenting in cardiogenic shock -patients with acute hemodynamic instability -possibly for coronary bypass surgery in otherwise stable patients

1) Filling pressures 2) Cardiac output 3) Calculated hemodynamic indices -CI -SVR -PVR -stroke volume -stroke index -LV stroke work index 4) MVO2

Symptom triad: angina, syncope, CHF Severe AS: pressure gradient>50 mm Hg, valve area <0.7 cm^2

1) Avoid tachycardia (and severe brady) 2) Normal SR (defibrillate if AF or SVT occurs) 3) Avoid and aggressively treat hypotension

80(MAP-CVP)/CO

80(PA-PCWP)/CO *Causes of Increased PVR* Hypercarbia/Acidosis Hypoxia Light anesthesia Catecholamine surge Hypothermia

1) sepsis 2) cirrhosis 3) hypothermia 4) nitroprusside (cyanide) toxicity 5) Inadvertently wedged PAC that samples pulm. cap. blood

*SYMPTOMS* LV CHF from chr. atrial distension, a fib, pulm edema, inadequate CO and eventually PHTN and RV failure *Pathophysiology* When the mitral valve area goes below 2 cm2, the valve causes an impediment to the flow of blood into the left ventricle, creating a pressure gradient across the mitral valve. This gradient may be increased by increases in the heart rate or cardiac output. As the gradient across the mitral valve increases, the amount of time necessary to fill the left ventricle with blood increases. Eventually, the left ventricle requires the atrial kick to fill with blood. As the heart rate increases, the amount of time that the ventricle is in diastole and can fill up with blood (called the diastolic filling period) decreases. When the heart rate goes above a certain point, the diastolic filling period is insufficient to fill the ventricle with blood and pressure builds up in the left atrium, leading to pulmonary congestion *GOALS* 1) *Avoid LA overloading* -avoid tachycardia -aggressively treat tachydysrhythmias 2) *Avoid dropping the LA pressures* -fluids to maintain BP & CO -PAC to follow PCWP trends 3) *If pulm HTN present avoid exacerbations* by avoiding hypoxia, acidosis and hypercarbia

Goals (fast, full & forward) -keep HR high -keep preload high to maintain SV -low SVR to reduce regurgitation fraction

1) Repeat non-inv reading and/or flush A line 2) Verify oxygenation and ventilation (pulse ox, color and capnograph) 3) Check EKG for dysrhythmias, brady/tachy 4) Treat cause: hypoxia, hypercarbia, pain, fluid overload or unintended pressor administration with nitroglycerine, nitroprusside, labetolol, nifedipine, or nicardipine

a. ABCs: patient's color, pulse oximeter, HR, BP, temp, & capnogram b. Meds: neuromuscular blockers (twitch stimulator), residual inhalational agent (sampling exhaled gases), intraoperative drugs (type and dose of narcotics, benzodiazepines, and ones continuously infused), and premedications (like scopolamine and droperidol). c. Examine his pupils and review the chart for conditions that could affect mental status, such as seizures, or a stroke (embolic, ischemic, hemorrhagic, or thrombotic). d. If no diagnosis were apparent, I would consider metabolic causes and consider obtaining an ABG, electrolytes, glucose, e. If all else failed, I may consider a head CT and/or a neurologic consult. f. In the mean time, the patient may need to have his airway controlled and protected, and ventilation controlled or assisted.

Gives indication of tubular resorptive capabilities for sodium and the GFR. FENa1%: renal azotemia (from tubular injury causing inability of tubules to resorb sodium)

Contains: Fibrinogen Factor VIII Factor XIII vWF

*Central Venous Pressure (CVP)*: 2-6 mm Hg *PA pressure* Systolic: 20-30 mm Hg End diastolic: 8-12 mm Hg *Pulmonary Wedge Capillary Pressure (PCWP)/ Pulmonary Artery Occluded Pressure (PAOP)* 4-12 mm Hg *Cardiac Output* 4-8 L/min *Cardiac Index* 2.5-4 L/min *Mixed Venous Oxygen Saturation (Svo2)* 60-80% *Systemic Vascular Resistance (SVR)* 800 -1200 dynes/sec/cm-5 *Pulmonary Vascular Resistance (PVR)* 37-250 dynes/sec/cm-5 *Stroke Volume (SV)* 60-120 ml/beat *Ejection Fraction (EF)* 55-70%

*Pancuronium* Vagolytic effects (increased HR, MAP and CO) Hepatic metabolism and renal elimination *Cisatracurium* Offer cardiovascular stability Metabolized by Hoffmann degradation Preferred paralytic for ICU infusion Ideal for use in patients with renal failure *Rocuronium* Eliminated via biliary excretion Prolonged action in biliary dysfunction and renal failure *Vecuronium* Hepatic metabolism and biliary excretion

Warm, dry, stimulate, Clear airway *If HR <100 bpm*: PPV, SpO2 monitoring *If HR <60 bpm*: consider intubation+ epinephrine and chest compressions