Board Prep Flashcards
(158 cards)
Decreased ETCO2
Hypothermia Hypothyroidism Increased Dead Space (COPD) Hyperventilation Decreased Cardiac Output Decreased CO2 production Circuit leak or Occlusion Pulmonary Embolism (air, thrombus, gas, fat, marrow, amniotic) Increased muscle relaxation Increased depth of anesthesia Surgical manipulation of the heart or thoracic vessels Wedging of the PA Catheter
Increased ETCO2
Increased CO2 production (MH, thyrotoxicosis, hyperthyroidism) Hyperthermia Shivering or convulsions Sepsis Rebreathing (valve prolapse, failed CO2 absorber) Hypoventilation Depression of the respiratory center Reduction of ventilation Increased or improving Cardiac Output Right to left intracardiac shunt Excessive catecholamine production Administration of blood or bicarbonate Release of aortic clamp/arterial clamp or tourniquet Glucose in the IV fluid Parenteral hyperalimentation CO2 insufflation Subcutaneous epinephrine injection
Minimal to zero ETCO2 or Sudden Drop
Equipment Malfunction ETT disconnect, obstruction, or total occlusion Bronchospasm No Cardiac Output Cardiac Arrest Bilateral PTX Massive PE Esophageal intubation Application of PEEP Cricoid pressure occluding tip of ETT Sudden, severe hypotension
Determining source of decreased ETCO2
Call for help
Assess vital signs
Feel for a pulse
Take patient off ventilator and handbag listening for breath sounds
EKG interpretation
Rhythm Regularity P wave (2.5 mm long and high) (Best viewed in Lead II) PR interval (No longer than 0.2 seconds) Q wave QRS complex (up to 0.12 seconds) (R & R prime in V1 = RBBB, R & R prime in V6 = LBBB) ST segment (V5 most sensitive lead) T wave Axis
ASA recommendations for preoperative EKG
Age >50 yo (good for one year if 50-69, good for 6 months if >69)
History of cardiovascular disease or HTN (mandatory if changes in symptoms)
History of DM (required if >40 yo or has had DM >10 years)
Central nervous system disease
Standard ASA Monitors
Oxygenation (pulse ox)
Ventilation (ETCO2, respiratory volumes, disconnect alarms)
Circulation (EKG, blood pressure, HR - every 5 minutes)
Temperature
Indications for arterial line
Continuous real time blood pressure monitoring
Planned pharmacological or mechanical cardiovascular manipulation
Repeated blood sampling (ABG, Hgb, Glucose)
Failure of indirect BP measurement
Supplementary diagnostic information from the arterial waveform (PPV)
Patient with end organ disease
Patient with large fluid shifts
Arterial line complications
Distal ischemia (thrombosis, proximal emboli) Pseudoaneurysm AV fistula Hemorrhage Hematoma Infection Skin necrosis Peripheral neuropathy Misinterpretation of data Cerebral air embolism from retrograde flow from flushing
Indications for central line
CVP monitoring Transvenous cardiac pacing Pulmonary Artery Catheter Temporary hemodialysis Drug administration (vasoactive, hyperalimentation, chemotherapy, prolonged antibx) Rapid infusion of fluids Major surgery with large fluid shifts Aspiration of a venous air embolus Inadequate peripheral access Sampling site for repeated blood testing
PA Catheter measurements
Cardiac Output and Index (CO/CI) Pulmonary Artery Pressure (PAP) Central Venous Pressure (CVP) Calculation of oxygen delivery Assessment of cardiac work Mixed Venous Oxygen Saturation (MVO2) Pulmonary Capillary Wedge Pressure (PCWP) Systemic Vascular Resistance (SVR)
Indications for PA Catheter
Cardiac (CHF, low EF, left sided valvular dz, CABG, aortic cross clamp)
Pulmonary (COPD, ARDS)
Complex fluid management (shock, burns, acute renal failure)
High risk obstetrical care (eclampsia, placental abruption)
Neurological (sitting craniotomy, venous air embolus)
Causes of Hypernatremia
Inadequate intake of fluid
Renal loss of hypotonic fluid (diuretics, DI, intrinsic renal disease)
Extrarenal (nonrenal loss of H20)
Primary Na gain (hypertonic tube feeds or fluids)
Clinical features of Hypernatremia
Altered mental status Lethargy Confusion Coma Seizures Pleural effusion Ascites Peripheral edema Heart Failure Thirst Nausea and Vomiting Neuromuscular irritability
Treatment of Hypernatremia
Determine volume status (diuresis if hypervolemic) (Free H2O deficit = {(plasma Na/140)-1} x kg x 0.6, replace half of water deficit in first 24 hours, then remainder over 2-3 days, use 5% dextrose in water or 0.45% NaCl)
Rate of Na correction should not exceed 0.5 mEq/L per hour
Treatment of Central Diabetes Insipidus
DDAVP (IV 2-4 mcg)(Nasal Spray 10-40 mcg)
Low Na Diet
Low dose thiazide diuretic
Carbamazepine (enhances vasopressin secretion)
NSAIDs
Treatment of Nephrogenic Diabetes Insipidus
Treat underlying cause
Treat symptomatic polyuria (Low Na diet, thiazide diuretic)
Causes of hypovolemic hyponatremia
Non renal (GI losses, integumentary losses, third spacing, cerebral salt wasting)
Renal (Diuretics, osmotic diuresis, hypoaldosteronism, salt wasting nephropathy, post obstructive diuresis, non-oliguric acute tubular necrosis, acute and chronic renal failure)
Causes of euvolemic hyponatremia
Polydipsia (psychogenic, exercise induced, medications)
Administration of hypotonic IV fluids
Beer potomania
SIADH (neurologic, pulmonary disease, malignant tumors, major surgery, pharmacologic)
Causes of hypervolemic hyponatremia
Renal (acute or chronic failure) Non renal (heart failure, hepatic cirrhosis, nephrotic syndrome) Redistributive hyponatremia (hyperglycemia, mannitol) Pseudohyponatremia (hyperlipidemia, hyperproteinemia, glycine solutions) Endocrine disorders (adrenal insufficiency, hypothyroidism)
Causes of hyperkalemia
Pseudohyperkalemia (hemolysis, prolonged use of tourniquet, marked leukocytosis)
Endogenous K (tumor lysis, rhabdomyolysis, exercise induced, burns)
Exogenous K (increased intake, transfusions)
Renal (insufficiency, chronic failure, oliguria, nephropathy)
Acidosis (metabolic raises K 0.7/0.1 pH, resp raises K 0.1/0.1 pH, diabetic ketoacidosis)
Drugs (succinylcholine, Beta blocker, digitalis, ACEI, heparin, cyclosporine,
spironolactone, amiloride, triamterene)
Endocrine (primary adrenal insufficiency, pseudohypoaldosteronism)
Hyperkalemic periodic paralysis (excitement, cold, fasting, stress, infection, GA)
Chronic hyperkalemia (decreased renal excretion)
Clinical features of hyperkalemia
Weakness, tingling, parathesias Flaccid paralysis Hypoventilation Cardiac toxicity (increased T waves, flattened P wave, AV conduction delay, QRS widening, v fib/flutter)
Treatment of hyperkalemia
Non emergent (reduce K intake, increase K output, IV loop and thiazide diuretics,
consider dialysis)
Emergent (calcium chloride centrally or calcium gluconate peripherally, sodium bicarb,
D50 plus insulin, albuterol)
Causes of hypokalemia
Redistribution of K into cells Metabolic alkalosis (decrease K 0.3/0.1 pH) Medications (insulin, epi and selective beta2 agonists) Hypokalemic periodic paralysis Potassium depletion Decreased dietary intake Extra renal (diarrhea, laxatives, intestinal bypass or fistula, vomiting and gastric suction) Renal (diuretics, steroids, PCN derivatives, renal tubular acidosis, diabetic keto, mineralocorticoid excess - hyperaldosteronism)