WillWallace Adv Pt DX Wilkens 7 and 18, whites 7, westgard
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| Quality control | creating a measurement and documentation system to confirm accuracy and reliability
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| Accuracy | aka precision, that measured value is true physiologically value
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| Reliability | high degree of confidence that measured value is truly actual physiological value
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| Quality assurance | broader term that means not only are values accurate and reliable but clinically useful, by written policy and procedure manual, record keeping, equip maint, staff train, error correcting
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| Calibration | sets the accuracy of the instrument (usually 2 points)
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| quality control materials | materials used to calibrate electrodes in blood gas analyzers
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| aqueous buffers | water based for PH and CO2
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| Precision gases for PO2 | 0, 12, 20, 20.95 (from room air), 21 and 100%
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| Precision gases for CO2 | 0, 5, 10, and 12%
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| tonometered liquids | exposed in lab to known O2 and CO2 levels, 3 types, human or animal serum, or whole blood
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| what tonometer is considered most accurate for for PO2 and CO2? | whole blood
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| tonometered bovine blood | since human blood cannot be used, bovine is best choice for O2, Co2 and Ph for tonometered liquids
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| Assayed liquids | non water based liquids pretomonetered by manufacturer for PO2, CO2 and Ph, good for speed and accuracy
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| Oxygenated fluorocarbon based emulsions | aka preflourinated compounds, accurate as whole blood, but less risk, good for PO2, CO2, Ph
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| Levy-Jennings charts | quality control charts used to record calibrations
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| Westgard rules | used to determine when analyzer is not working and applied to L-J chart.
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| Why is L-J and Westgard rules used for ABG's? | guarantees 95% accuracy, includes random errors and systematic errors
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| random errors | 1-2S, 1-3S and R4S, imprecision, unpredictable aboration of QC material, need to rerun control
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| systematic errors | 2-2S, 4-1S, 10X, accuracy problem, must be investigated, corrected and documented, contaminated buffers, incorrect gas concentration or incorrect procedures, mach problem
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| S | standard deviation, amount of difference from the mean that is used to measure in Westgard rules, can be plus or minus from the mean
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| Mean | average of total quality control tests on a specific machine, mean and deviation are set when testing is done on ABG's
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| 12S rule | Westgard random error rule, where if 1 control measurement is more than 2 standard deviations from the mean, it will be rejected or warned, depending on preset rules
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| 13S rule | Westgard random error rule, where if 1 control measurement is more than 3 standard deviations from the mean, it is considered “out of control” and will be rejected
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| R4S rule | random error rule, if 2 consecutive measurements are 4 standard deviations or more apart, they will be rejected (control 1 is up or down 2 and control 2 is up or down in opposite direction)
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| 22S rule | systematic error, 2 consecutive are above or below 2 standard deviations and will be rejected
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| 41S rule | systematic error
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| 10X rule | aka 10 mean, rejects when 10 consecutive are on one side of the mean
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| “out of control” | single or series is outside of the established limit (two standard deviations)
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| Ph high/low calibration | 6.84-7.38
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| PCO2 high/low calibration | 5-12%
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| PaO2 high/low calibration | 0-10%
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| what is the accuracy of the 12S rule | 95%
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| ABG samples provide what | precise measurement of Acid-Base balance and lungs ability to oxygenate the blood and remove CO2
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| Accurate interpretation of ABG require what | knowledge of pt total clinical picture including any TX receiving
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| where are mixed venous blood samples drawn | rt atrium or pulm artery
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| what is mixed venous blood sample used for | evaluate overall tissue oxygenation
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| why not venous samples | only give metabolic rates so little value, exposed to peripheral vascular beds
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| normal ABG values for arterial blood is | Ph 7.35-7.45, PaO2 80-100 mmHg, PaCO2 35-45 mmHg, HCO3 22-26, BE +-2
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| Normal ABG for mixed venous blood is | Ph 7.34-7.37, PaO2 38-42 mmHg, PaCO2 44-46, HCO3 24-30
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| Prior to ABG draw, what should RT review for in Pt chart | low platelet count or increased bleeding time (meds etc)
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| Preferred site of ABG arteriotomy (needle into artery) | radial artery
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| Sites for ABG arteriotomy in adult are | radial artery, brachial artery, dorsalis pedis, or femoral artery.
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| What must be evaluated prior to a radial stick | collateral circulation of the hand, via modified Allens test
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| how is modified Allens test performed | have pt make tight fist, RT compress both radial and ulnar artery, instruct pt to open hand and relax, RT release ulnar
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| what is a positive Allens test | hand pinks w/in 10-15 seconds after release of ulnar artery, means circulation is adequate for puncture site
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| what should RT do if Allen test is negative | try other arm then try brachial
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| what should RT do for pt who needs frequent ABG's | insert indwelling arterial catheter (only in ICU)
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| what do bubbles in sample do | may equilibriate w/blood and cause bad sample-need to remove bubbles immediately after draw
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| How should RT handle sample after draw | remove bubbles, store in ice water to stop metabolism, analyze with in 1 hr
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| room temp samples must be analyzed how soon | 10-15 mins
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| how long should pressure be applied to stick wound | 3-5 mins or longer if clotting problem
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| ABG and VGB samples are used to evaluate what | acid-base balance (Ph, PaO2 PaCO2, HCO3 BE), oxygenation status (PaO2, SaO2, CaO2, PvO2), and adequate ventilation (PaCO2)
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| What does PaO2 reflect | O2 in plasma of arterial blood, reflects ability of lungs to transfer O2 into blood
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| Predicted PaO2 is dependent on what | pt age, FIO2, PIO2 (Pb and altitude)
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| effects of age on PaO2 | 103.5-(.42xage)+- 4, so if old fart like Jeff and age is 60 then 103-(.42x60) is 78.3 so normal range of PaO2 for Jeff is 74-82
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| hypoxemia | PaO2 less than normal predicted range, at any age, for pt breathing room air or PaO2 <65mmhg, severe <40mmHg (any age) in pt with increased FIO2
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| Does hypoxemia exist if pt is on >FIO2 and his PaO2 is normal? | NO, hypoxemia is only a <PaO2 lower than predicted regardless of FIO2
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| Hypoxia | inadequate tissue oxygenation
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| how are hypoxemia and hypoxia related | hypoxemia may result in hypoxia in pts with <CO, but they are not synonymous
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| most common cause of hypoxemia is | >V/Q mismatch, in pts with lung disease
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| increased V/Q mismatch | decrease in V/Q matching, perfusion is god, but ventilation is not, mucus plugging, secretions, bronchospasm, in specific portions of the lung
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| decreased V/Q matching is what | (has been on last two Vent tests), an increase in V/Q mismatch
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| causes of hypoxemia | >V/Q mismatch, diffusion defects, >CO2 from hypoventilation, Drug OD (>CO2), <PIO2 (altitude), equip failure
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| SaO2 | norm >95%, O2 saturation, actual amount of O2 bound to Hb expressed as a %
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| how is SaO2 determined | can be calculated, but true SaO2 must be can only be gotten from co-oximeter
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| Oxyhemoglobin disassociation curve | shows the effects of O2 loading and unloading in relationship to Hb
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| Left shift in HbO2 disassociation curve | >Ph, >SaO2, >Hb affinity, <temp, <CO2, <fetal Hb, <2,3 DPG, (increased affinity makes unloading at tissue more difficult)
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| Right shift in HbO2 disassociation curve | <Ph, <SaO2, <Hb affinity, >temp, >CO2, >fetal Hb, >2,3 DPG, (decreased affinity makes unloading at tissue easier)
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| Ph and Hb affinity for O2 | as Ph changes Hb affinity for O2 is directly affected (Bohr effect), Ph up, Hb affinity also up, Ph down Hb affinity also down
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| 2,3 DPG | organic phosphate in RBC, stabilizes deoxygenated Hb, reducing its affinity for O2, without it Hb would never unload O2 at the tissue
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| what >2,3DPG | Alkalosis, chronic hypoxemia, anemia
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| what <2,3DPG | acidosis
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| Shunt | V/Q is equal to 0, perfusion with no ventilation, alveoli blocked, refractory to O2
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| decreased V/Q mismatch | shunt effect, perfusion in excess of ventilation, non-refractory to O2, partial obstruction, hypoventilation, COPD, interstitial disease
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| Normal V/Q matching | .8
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| increased V/Q matching | ventilation in excess of perfusion, deadspace effect, regional hyperventilation, often seen in PPV and <CO
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| Deadspace | ventilation no perfusion, increased PaO2 with a decreased CO2 (usually less than 40) emboli
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| CaO2 | (Hb x 1.34)xSaO2+(PaO2x.003), norm 16-20 vol%, O2 bound to Hb and O2 in plasma, very important because of influence to tissue oxygenation
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| how is CaO2 measured | can only truly accurate w/co-oximeter
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| decreased CaO2 | anemia (normal PaO2 & SaO2 with <Hb), polycythemia (<PaCO2 & SaO2 w/normal CaO2), Hb bound by another gas (co-monoxide, metho)
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| P(A-a)O2 | norm 10-15 mmHg on room air, or 25-65on 100%, predicted dependent on age and FIO2, increase is resp defect, every increase of 50 is 2% shunt above normal of 2-3%
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| Can A-aDo2 be calculated on nasal canulla? | no, FIO2 must be known, never calc on low flow devices
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| A-aDO2 for old pt | (age x 0.4), old fart like Jeff at age 70 x .4 equals 28 mmHg on room air
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| When might you see hypoxemia w/normal A-a diff | hypoventilation or <PIO2
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| A-a DO2> 350 on 100% is what | indication for mech ventilation w/refractory hypoxemia
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| PvO2 | norm 38-42, mixed venous, must be drawn from pulmonary artery
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| Oxygen delivery is a function of what? | CO and CO2
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| PaO2, SaO2 and CaO2 evaluate what | respiratory component
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| how is tissue oxygenation assessed | PvO2
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| decreased PvO2 | <35 most often from impaired circulation, hypovelemia, PPV, LHF
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| normal or increase PVO2 in a very sick pt is usually caused by | tissue hypoxia still exists, PVO2 is unreliable-mechanism is unknown
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| C(a-v)O2 | norm 3.5-5 vol%, increased w/stable VO2 indicates perfusion to organs is decreasing
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| a-v diff >6vol% | cardiovascular decompensation and tissue oxygenation is inadequate
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| a-v diff <3.5 vol% | perfusion exceeds normal (if steady VO2), if VO2 is down then hypothermia
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| HbCO | norm .5%, carboxyHb, carbon monoxide poisoning, must use co-oximeter, 200-250 x greater affinity than O2 for Hb
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| increased HbCO causes what | tissue hypoxia, inhibits unloading of O2 at tissue, >of 5-10% w/smokers, >40-60% causes visual disturbances, myocardial toxicity, LOC, eventual death
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| S&S of increased HbCO | headache, dyspnea, nausea, tachycardia, tachypnea
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| what effect does HbCO have o PaO2 and SaO2 | if co-oximeter is not used, both will be normal
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| significance of PAO2 + PaO2 (on room air) | 110-130 is hypoxemia due to hypoventilation, <110 is hypoxemia due to lung defect, >130 is pt on >FIO2 or error
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| First sign of hypoxemia is | short of breath especially on exertion
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| clinical manifestations of hypoxemia are | tachycardia, tachypnea, hypertension, cyanosis, confusion
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| severe hypoxemia may result in | tissue hypoxia, met acidosis, bradycardia, hypotension, coma
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| In ICU pt, how do we identify tissue hypoxia | PvO2 <35 and a-v diff >5 vol%
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| lungs remove CO2 by | ventilation
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| kidneys role in acid-base balance is what | remove small quantities of acid, restore buffer capacity of fluids by replenishing HCO3
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| Ph | hydrogen ion concentration in blood, reflects acid-base balance
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| acid | solutions capable of donating H+
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| bases | solutions capable of accepting H+
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| PaCo2 | respiratory component of acid-base balance, identifies degree of ventilation in relation to metabolic rate
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| hypercarbia mot often results from | hypoventilation, CO2 >45
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| hypocarbia is usually caused by | hyperventilation, CO2 <35
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| How is uncompensated resp acidosis identified | ⬆Ph,⬇CO2, with normal HCO3 and normal BE
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| what is fully/completly compensated resp acidosis? | ⬆HCO3 enough to bring Ph within normal range
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| What is the most reliable measurement of pt ventilation | CO2, and should be interpreted in light of a normal VE w/CO2 or >VE w/normal CO2
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| HCO3 | bicarb, norm is 22-26 mEq/L, primary metabolic component of acid-base balance, regulated by renal system, usually requires 12-24 hrs for compensatory response
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| A decrease in CO2 (to the left in O2 curve) reduces HCO3 how much | CO2 <5mmHg will <HCO3 by 1
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| An increase in CO2 (to the right) will increase HCO3 how much | CO2 >10-15 will >HCO3 by 1
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| BE+- | base excess base deficit, standard deviation of HCO3 that takes buffering of RBC's into account. Calculated with Ph, CO2 and Hematocrit and is a more complete analysis of metabolic buffering capability
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| Base excess | positive value indicates either base has been added or buffer removed, larger the number the more sever the metabolic component
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| what is the importance of BE | allows analysis of pure metabolic components of acid-base balance, changes in met components alter acid-base, respiratory components do not
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| do changes in CO2 effect BE? | NO, only metabolic changes alter BE
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| Simple respiratory acidosis is | inadequate ventilation, elevated CO2
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| common causes of resp acidosis | acute upper airway obstruction, severe diffuse airway obstruction (acute or chronic), massive pulm edema
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| Common non-respiratory problems that cause resp acidosis | drug OD, spinal cord injury, neuromuscular diseases, head trauma, trauma to thoracic cage
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| How is acute resp acidosis compensated | none, renal changes are to slow
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| How is chronic resp acidosis compensated | kidneys increase absorption of HCO3
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| How is uncompensated resp acidosis identified | ⬆Ph,⬇CO2, with normal HCO3 and normal BE
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| What is partially compensated resp acidosis | ⬆HCO3, but Ph is not yet w/in normal limits
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| what is fully/completely compensated resp acidosis? | ⬆HCO3 enough to bring Ph within normal range
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| How is degree of compensating determined in resp acidosis | acute-HCO3⬆1 for every 10-15 ⬆in CO2, chronic- HCO3⬆4 for every 10 ⬆CO2
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| If expected level of HCO3 compensation is not occurring for acute or chronic acidosis what should RT suspect? | complicating metabolic disorder is also present
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| neuromuscular disease or obstructive disorder w/resp acidosis, pt will RR will be what | short of breath and ⬆RR
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| Drug OD or impaired resp center pt w/ resp acidosis pt RR will be what | reduced
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| what effect does acute elevation of CO2 and acidosis have on CNS | anesthetic, confused, semi-conscious and eventually coma
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| in acute resp acidosis how high does CO2 get for Pt to reach coma | around 70 mmHg
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| because ⬆CO2 causes systemic vasodilation, what cardiac manifestations should be expected? | warm flush skin, bounding pulse, arrhythmias
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| because ⬆CO2 causes cerebral vasodilation, what might be expected | ⬆ICP, retinal venous distension, papilledema, headache
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| when HCO3 levels are up, what happens to chloride levels | if ⬆ result of renal compensation, then chloride will be ⬇
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| resp Alkalosis | abnormal condition in which there is an increase in ventilation relative to the rate of CO2
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| How does RT identify resp alkalosis in ABG | PaCO2 below expected level indicating ventilation is exceeding the normal level, hyperventilation
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| what are the common causes of resp alkalosis | hyperventilation caused by pain, hypoxemia (PaO2 55-60), acidosis, anxiety
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| how do the kidneys compensate for resp alkalosis | excrete HCO3
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| What is the expected compensation for acute resp Alkalosis | none, ⬆Ph, ⬇PaCO2, normal HCO3
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| What is the expected compensation for partially compensated resp Alkalosis | ⬆Ph, ⬇HCO3
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| What is the expected compensation for fully compensated resp Alkalosis | normal Ph, ⬇HCO3
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| Expected compensation is not present for HCO3 in resp alkalosis, what should RT suspect | complicating metabolic disorder is also present
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| In resp alk what is the advantage of a ⬇PaCO2 | an⬆ PAO2 and therefor less chance of hypoxemia being present, or if present it will be better than if CO2 is up.
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| Clinical S&S associated w/ resp alkalosis | tachypnea, dizziness, sweaty, tingling in fingers and toes, muscle weakness and spasms
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| when does RT need to be cautious not to induce resp alkalosis? | during IPPB and mech vent
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| simple met acidosis | HCO3 or BE falls below normal, caused when buffers are not produce in enough quantity (high Gap), or when buffers are lost (normal Gap)
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| Anion Gap | normal 11 (8-16 mEq/L), when fixed acids accumulate in the body, H+ reacts to HCO3 causing it to ⬇,leading to a ⬇ anion gap
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| Causes of met acidosis with high anion gap can be divided into two categories what are they | metibolicy produced acid gains or ingestion of acids
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| High anion gap met acidosis from metabolicy acid gains | lactic acidosis (hypoxia, sepsis), ketoacidosis (diabetes, starvation, lack of glucose), renal failure (retained sulfuric acid)
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| High anion gap metabolic acidosis from ingestion of acids | salcylate poisoning (aspirin), methanol, ethylene glycol
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| normal anion gap metabolic acidosis (hyperchloremic acidosis) from loss of HCO3 is caused by | diarrhea or pancreatic fistula
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| normal anion gap met acidosis from failure to reabsorb HCO3 is most often caused by | renal failure
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| normal anion gab met acidosis from ingestion may be caused by | ammonium chloride or IV nutrition
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| what signs may be present w/renal disease | ⬆blood urea, nitrogen and creatinine, ⬇urine output
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| How does the body compensate for met acidosis | ⬇CO2(hyperventilation)
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| If normal or ⬆PaCO2 is present w/met acidosis what should RT suspect | resp defect is also present (combination resp/met acidosis)
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| What is the predicted compensation of PaCO2 for met acidosis | PaCO2 eqs (1.5xHCO3)+8+-2, if PaCO2 is not at predicted level based on calc, resp abnormality is present
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| what is the most common and obvious sign of met acidosis | Kussmaul's breathing
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| what is Kussmaul's respiration | very rapid, very deep ventilation
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| S&S and Pt complaints w/severe met acidosis | dyspnea, headache, nausea, vomiting followed by confusion and stupor. Vasoconstriction, pulm edema, arrhythmias (if severe enough)
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| simple met alkalosis | above normal HCO3
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| most common causes of met alk | hyperkelemia, hypochloremia, ng suction (⬇acid), vomiting (⬇acid), post hypercapnic disorder, diuretics, steroids or to much bicarb therapy
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| how does body compensate for met alkalosis | hypoventilation to ⬆ PaCO2
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| fully compensated met alk is identified by | ⬆ in PaCO2 enough to return Ph to normal (hypercarbia may be present and may appear as resp acidosis)
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| when should RT suspect a mixed acid base disorder | normal or near normal Ph w/severe abnormal HCO3 or PaCO2
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| where should RT look for clues of mixed acid base disorders | pt hx, physical exam, lab tests, knowing primary disorders, expected compensations
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| expected compensation for acute resp acidosis | PaCO2⬆15-HCO3 ⬆1
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| expected compensation for chronic resp acidosis | PaCO2⬆10-HCO3 ⬆4
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| expected compensation for acute resp alkalosis | PaCO2⬇5-HCO3 ⬇1
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| expected compensation for chronic resp alkalosis | PaCO2⬇10-HCO3 ⬇5
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| expected compensation for met acidosis | PaCO2 eqs (1.5xHCO3)+8+-2 (shortcut is last two digits of Ph is equal to PaCO2) or HCO3 ⬆1-PaCO2⬆.6
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| mixed/combined resp met acidosis | ⬆PaCO2 ⬇HCO3
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| why is combined resp/met acidosis so easy to identify | hypercapnia and low HCO3 work synergistically to significantly reduce Ph, often resulting in profound acidosis
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| common causes of resp/met acidosis are | cardio pulm resuscitation, COPD and hypoxia, poisoning and drug OD
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| cardio pulm resuscitation and resp/met acidosis | heart stops-blood circulation stops, apnea causes resp acidosis, and hypoxia causes lactic acidosis (metabolic)
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| COPD and hypoxia w/resp met acidosis | chronic COPD w/compensated resp acidosis suddenly gets met disturbance like hypotension or renal failure, causing hypoxia and lactic acidosis
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| mixed/combined met resp alkalosis | ⬆HCO3 w/below normal PaCO2-additive effects may result in severe alkalosis
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| When met alk is super imposed on resp alk, why does it become so severe | when superimposed there is no compensation
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| what clinical situation will RT most likely see met/resp alkalosis | hypoxemia, hypotension, neuro damage, to much mech vent, anxiety, pain, or any of above in combo
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| What pts most often get combined met resp alkalosis | chronic COPD w/elevated HCO3, suddenly reduction in PaCo2 from mech vent will cause resp alk onto the met alk pt already has
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| Mixed met acidosis with resp alkalosis are difficult to recognize because | either abnormality usually compensates for the other
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| met acidosis with Paco2 lower than predicted for degree of acidosis | resp alk is also occurring simultaneously, Ph will be just above 7.4 (appearing to compensate for for resp alk)
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| what is the prognosis for met acidosis on resp alkalosis | poor, most likely seen in critically ill
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| sleep related breathing problems occur in what % of adults | 5% (more often in men)
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| incidence of sleep-related problem ⬆ to what after age 60 | 37%
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| two basic types of sleep are | non-rem and rem
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| NREM and REM cycle | every 60-90(book) minutes (Karel says 70-90)
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| NREM | non-rapid eye movement, the beginning of sleep, 4 stages
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| Stage 1 | NREM, beginning of sleep, large eye rolls/low amp waves, drowsiness, lasts only minutes
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| Stage 2 | NREM, sleep spindles (12-14 Hz), w/large K complexes (77uV), deeper sleep, lasts 20-30 mins, PREDOMINANT STAGE OF SLEEP IN ADULTS
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| Stage 3 & 4 | NREM, slow wave sleep, difficult to rouse, high amp waves (75 UV), increase (time) with age and pathological state
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| Stage 4 | aka Delta
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| NREM & ventilation | RR slows and becomes irregular (becomes more regular as in Delta), PaCO2⬇(in early stages), BP⬇ 5-10% in stages 1-2% and 8-14% in Delta
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| REM begins | 60-90 mins after sleep begins
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| Dreams | NREM-dreamlike, REM-dreaming
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| REM per night | 4-5, getting progressively longer and more intense during the night
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| 1st REM episode of the night lasts how long | 5 mins
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| REM toward morning is how long | 30-60 mins
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| % of REM sleep in a lifetime | 20-25%
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| % of REM sleep in an infant | 55-80, tapers till meeting adult % at 6 months
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| Physical changes of REM | partially paralyzed, resp effort is chaotic, diminished response to hypercapnia & hypoxemia, ⬇upper airway tone
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| sleep continuity theory | as sleep interruption goes up, daytime alertness goes down
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| does the amount of time spent in any sleep stage 1234 or REM predict performance or degree of sleepiness? | no, only interruption of sleep
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| sleep apnea | cessation of airflow for at least 10 seconds during sleep, 3 types obstructive, central and mixed
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| OSA | obstructive sleep apnea, airflow reduction >70%, in the presence of resp effort
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| CSA | central sleep apnea, 10 seconds or more of apnea w/no effort to breath, intermittently normal
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| Mixed sleep apnea | periods of OSA & CSA during the same night of sleep
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| hypopnea | OSA w/30% reduction of airflow and >4% ⬇in SaO2 during sleep, results in hypoxemia-causes temp arousal from sleep
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| what can cause temp arousal from sleep during sleep? | hypopnea and OSA
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| UARS | upper airway resistance syndrome, ⬆neg intrathoracic press from⬆WOB (but no O2 desaturation)
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| what can disturb ventilation during sleep | apnea, hypopnea and UARS
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| why don't UARS pts remember be awaken from apnea episodes in the night? | usually just arouse to lighter stage not fully awake
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| best way to determine exact type and severity of of sleep disorder | PSG-polysomnogram
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| RDI | resp disturbance index, positive if >5 (incidences in a night)
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| RDI measures | obstructive apnea's, hypopnea's, central apnea's per hour
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| RDI for infants | >1 per hr, SaO2 <95%, end VT CO2 >53 during apnic episode
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| REM behavior disorder | people who act out in dreams
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| % of people w/sleep disorders | 15%
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| SDC | sleep disorder criterion, RDI 5-20 mild, 20-40 moderate, >40 severe
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| what is the difference between UARS and OSA | UARS do not become hypoxic during sleep, (they have excessive sleepiness from poor continuity of sleep)
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| Best TX for UARS | CPAP (nasal)
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| What are the most common forms of SDB in adult | OSA and hypopnea
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| cause of OSA | upper airway occlusion during sleep
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| causes of hypopnea | partial closure of the airway
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| anatomical abnormalities that may lead to OSA/hypopnea | micrognathia (sm lower jaw), large tongue, large tonsils/adenoids, retrognathia (under developed mandible), deviated septum
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| most common site of obstruction in OSA/hypopnea | pharynx (soft pallet to glottic inlet)
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| pathophysiology of an upper airway obstruction during sleep | airway relaxes, narrows or occludes, causing ⬆WOB causing ⬆intrathoracic press to overcome obstruction, causing narrowing airway
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| what does upper airway obstruction cause | hypoxemia and sleep arousal
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|
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| what % of pts w/sleep apnea are obese? | 60-90%
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| what is the most dangerous symptom of OSA? | excessive daytime sleepiness
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| EDS | excessive daytime sleepiness, impairs cognitive and psycho-motor function
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| typical Hx of OSA pt | obese middle age male, loud snoring, excessively sleepy, stops breathing at night
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| hallmark of OSA | loud snoring
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|
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| cardinal symptoms of OSA | 3S rule-Snore (loud, habitual), Spousal (reports apnic episodes), Sleepiness (daytime, excessively)
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|
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| clinical features of OSA | snores, EDS, morning headaches, fragmented sleep, memory loss, confused awakenings, personality changes, impotence, night sweats, dysrrhthmias, ⬆BP, CHF, enuresis (bed wetting)
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|
||||
| airway features of OSA may include | nasal obstruction, low soft palate, large uvula, enlarged tonsils/adenoids, macroglosia, large neck (>17.5)
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|
||||
| %of OSA w/hypertension | 50%
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|
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| what is the biggest risk factor of OSA in children | obesity
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|
||||
| cardiac changes w/OSA | bradycardia during apnic episodes, then tachycardia follow, PVC's and CHF
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|
||||
| what % of OSA have PVC's | 20, asystole 10%
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|
||||
| TX for OSA | CPAP
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|
||||
| what is the Hallmark symptom of OSA in children | snoring
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|
||||
| % of sleep apnea that is CNA | 10%
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|
||||
| CSA | cessation of airflow resulting from lack of movement of the diaphragm-loss of vent drive
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|
||||
| when afferent input of vent drive is absent during sleep | CSA
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|
||||
| what factors may play a role in /csa in children | cardiac, hematologic, metabolic, neurologic, gastro, or nuero abnormalities
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|
||||
| most significant difference between OSA and CSA pts | body size, smaller in CSA and fewer daytime daytime side effects
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|
||||
| SIDS | leading cause of death in children under age 1, unknown cause, peaks at 2-4 months
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|
||||
| ALTE | apparent life threatening event, child appears to be dying because of apnea (pallor and cyanosis)
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|
||||
| best way to prevent SIDS | supines sleeping position, decreases by 50%, parental non smoking and removal of soft bedding
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|
||||
| RT should observe sleeping pt for what if they notice a pause in pts breathing | time episodes, sleeping position, presence/absence cyanosis, note breathing effort
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|
||||
| primary tool to evaluate sleeping disorders | PSG
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|
||||
| what is used to determine sleep stage | EEG, electroencephalogram
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|
||||
| EOG | electrooculogram
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|
||||
| Chin EMG | chin muscle activity, also used to detect REM
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|
||||
| Tools of PSG | EEG(stage), EOG, Chin EMG and leg EMG (REM), 1 lead ECG (arrhythmias), electrodes for respiration, snoring microphones and pulse ox
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|
||||
| can pulse ox be used for diagnosis of UARS | not reliable, need cooximeter
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|
||||
| what is the gold standard for diagnosing sleep apnea | PSG (polysomnogram)
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|
||||
| MSLT | multiple sleep latency test, recommended for pts who's reported sleepiness is more than his/her level of SDB indicates
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|
||||
| sleep latency | amount of time required to fall asleep
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|
||||
| what is the most reliable and valid test of daytime sleepiness | MSLT, 4-5 daytime naps
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|
||||
| what is the normal time for a person to fall asleep for a nap if they have severe sleepiness | 5-8 mins (norm 15)-no specific disorder, can be any
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|
||||
| what % of men have sleep related problems | 5%
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|
||||
| what is the predominant stage of NREM | 2
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|
||||
| T/F breathing tends to be irregular during early stages of NREM? | T
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|
||||
| T/F BP tends to⬇ during initial stages of sleep? | T
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|
||||
| T/F During REM sleep, sleeper is partially paralyzed? | T
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|
||||
| T/F breathing is chaotic/irregular during REM in most sleepers | T
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|
||||
| what is the key concept in central sleep apnea | intermittent absence of respiratory effort
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|
||||
| hypopneas are most closely related to what? | OSA
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|
||||
| all of the following are believed responsible for the onset of OSA | relaxation of the upper airway, big ⬆in resistance, more forceful contraction of insp muscles, significant ⬆ static compliance
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|
||||
| all of the following clinical feature are typical for adult pts w/OSA | excessive daytime sleepiness, loud snoring, impaired cognitive function
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|
||||
| most common arrhythmia seen in OSA | PVC's (20%)
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|
||||
| all of the following are seen in children w/OSA | daytime sleepiness, hyperactivity, aggressive behavior
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|
||||
| peak onset for SIDS | 2-3 months
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|
||||
| all of the following are monitored during polysomnogram | EEG, ECG, leg emg
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|
||||
| what test is for measuring daytime sleepiness | MSLT
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|
||||
| how long are naps during MSLT | min 20 minutes, max 35 mins
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|
||||
| actigraphy | wristwatch like device worn for several days
🗑
|
||||
| tx mild osa | lose weight, oral devicem avoid alcohol and caffeine
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|
||||
| moderate sleep apnea tx | CPAP
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|
||||
| tx of severe sleep apnea | bilevel, surgical procudures UPPP, LAUP
🗑
|
||||
| caution of CPAP with OSA | can cause central sleep apnea is some cases
🗑
|
||||
| tritrating CPAP | 30 day trial, set up at 4epap, up 1 for 20 breaths until stable
🗑
|
||||
| TX of mild OSA | lose weight, sleep on one side, oral mouth guard, avoid alcahol and caffeine
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|
||||
| TX of moderate OSA | CPAP, set at 4 and adjust up in incriments of 1 until obstruction relieved
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|
||||
| why do we repeat polysomnogram in 30 days after start of CPAP in OSA? | to make sure CSA is not underlying issue
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|
||||
| TX for severe OSA | Bilevel, or surgury (UPPP, LAUP or tracheostomy)
🗑
|
||||
| TX for CSA | Auto-SV (bipap w/auto backup) or CPAP (infants only)
🗑
|
||||
| what is Auto-SV | records and targets pt peak flow and RR over a 4 minute period, adjusts press down as pt peak press rises (similar to CPAP+press support), automatically increases press if breathing stops and lowers it again if breathing is normal
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|
||||
| Initial settings for Auto-SV | Epap-4, Ipap-same as E or max of 10, RR set to pt with minimum 10, re-evaluate in 20 mins
🗑
|
||||
| Hypopnea TX | CPAP or BIpap, set at 2 ipap, increase at 1 until relief found, set back up at 1.2 second IT
🗑
|
||||
| primary hypoventilation syndrom | CSA
🗑
|
||||
| what SA is frequently associated with heart disease | CSA
🗑
|
||||
| types of CSA | primary and cheynes-stokes
🗑
|
||||
| primary CSA | mostly in premies, cause unkown
🗑
|
||||
| Cheyne stokes CSA | caused by heart failure, stroke, or kindney failure, drug OD
🗑
|
||||
| length of breath absence in cheyne-stokes id's disease | 50-70 sec heart failure, 20-40 sec altitude, neuro disease, renal failure
🗑
|
||||
| ASV | adaptive servo-ventilaltion, new tx for CSA, records pt breathing pattern and then uses data to normalize breathing as necessary
🗑
|
||||
| CCHS | congenital central hypoventilation, very rare CSA children get, have no hypoxic drive while sleeping, have to trached and mech vented at night
🗑
|
||||
| what neurvous system regulates HR and BP | autonomic
🗑
|
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