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Adv PT DX test 1
WillWallace Adv Pt DX Wilkens 7 and 18, whites 7, westgard
| Question | Answer |
|---|---|
| Quality control | creating a measurement and documentation system to confirm accuracy and reliability |
| Accuracy | aka precision, that measured value is true physiologically value |
| Reliability | high degree of confidence that measured value is truly actual physiological value |
| 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 |
| Calibration | sets the accuracy of the instrument (usually 2 points) |
| quality control materials | materials used to calibrate electrodes in blood gas analyzers |
| aqueous buffers | water based for PH and CO2 |
| Precision gases for PO2 | 0, 12, 20, 20.95 (from room air), 21 and 100% |
| Precision gases for CO2 | 0, 5, 10, and 12% |
| tonometered liquids | exposed in lab to known O2 and CO2 levels, 3 types, human or animal serum, or whole blood |
| what tonometer is considered most accurate for for PO2 and CO2? | whole blood |
| tonometered bovine blood | since human blood cannot be used, bovine is best choice for O2, Co2 and Ph for tonometered liquids |
| Assayed liquids | non water based liquids pretomonetered by manufacturer for PO2, CO2 and Ph, good for speed and accuracy |
| Oxygenated fluorocarbon based emulsions | aka preflourinated compounds, accurate as whole blood, but less risk, good for PO2, CO2, Ph |
| Levy-Jennings charts | quality control charts used to record calibrations |
| Westgard rules | used to determine when analyzer is not working and applied to L-J chart. |
| Why is L-J and Westgard rules used for ABG's? | guarantees 95% accuracy, includes random errors and systematic errors |
| random errors | 1-2S, 1-3S and R4S, imprecision, unpredictable aboration of QC material, need to rerun control |
| 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 |
| 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 |
| Mean | average of total quality control tests on a specific machine, mean and deviation are set when testing is done on ABG's |
| 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 |
| 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 |
| 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) |
| 22S rule | systematic error, 2 consecutive are above or below 2 standard deviations and will be rejected |
| 41S rule | systematic error |
| 10X rule | aka 10 mean, rejects when 10 consecutive are on one side of the mean |
| “out of control” | single or series is outside of the established limit (two standard deviations) |
| Ph high/low calibration | 6.84-7.38 |
| PCO2 high/low calibration | 5-12% |
| PaO2 high/low calibration | 0-10% |
| what is the accuracy of the 12S rule | 95% |
| ABG samples provide what | precise measurement of Acid-Base balance and lungs ability to oxygenate the blood and remove CO2 |
| Accurate interpretation of ABG require what | knowledge of pt total clinical picture including any TX receiving |
| where are mixed venous blood samples drawn | rt atrium or pulm artery |
| what is mixed venous blood sample used for | evaluate overall tissue oxygenation |
| why not venous samples | only give metabolic rates so little value, exposed to peripheral vascular beds |
| 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 |
| Normal ABG for mixed venous blood is | Ph 7.34-7.37, PaO2 38-42 mmHg, PaCO2 44-46, HCO3 24-30 |
| Prior to ABG draw, what should RT review for in Pt chart | low platelet count or increased bleeding time (meds etc) |
| Preferred site of ABG arteriotomy (needle into artery) | radial artery |
| Sites for ABG arteriotomy in adult are | radial artery, brachial artery, dorsalis pedis, or femoral artery. |
| What must be evaluated prior to a radial stick | collateral circulation of the hand, via modified Allens test |
| 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 |
| 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 |
| what should RT do if Allen test is negative | try other arm then try brachial |
| what should RT do for pt who needs frequent ABG's | insert indwelling arterial catheter (only in ICU) |
| what do bubbles in sample do | may equilibriate w/blood and cause bad sample-need to remove bubbles immediately after draw |
| How should RT handle sample after draw | remove bubbles, store in ice water to stop metabolism, analyze with in 1 hr |
| room temp samples must be analyzed how soon | 10-15 mins |
| how long should pressure be applied to stick wound | 3-5 mins or longer if clotting problem |
| 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) |
| What does PaO2 reflect | O2 in plasma of arterial blood, reflects ability of lungs to transfer O2 into blood |
| Predicted PaO2 is dependent on what | pt age, FIO2, PIO2 (Pb and altitude) |
| 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 |
| 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 |
| 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 |
| Hypoxia | inadequate tissue oxygenation |
| how are hypoxemia and hypoxia related | hypoxemia may result in hypoxia in pts with <CO, but they are not synonymous |
| most common cause of hypoxemia is | >V/Q mismatch, in pts with lung disease |
| 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 |
| decreased V/Q matching is what | (has been on last two Vent tests), an increase in V/Q mismatch |
| causes of hypoxemia | >V/Q mismatch, diffusion defects, >CO2 from hypoventilation, Drug OD (>CO2), <PIO2 (altitude), equip failure |
| SaO2 | norm >95%, O2 saturation, actual amount of O2 bound to Hb expressed as a % |
| how is SaO2 determined | can be calculated, but true SaO2 must be can only be gotten from co-oximeter |
| Oxyhemoglobin disassociation curve | shows the effects of O2 loading and unloading in relationship to Hb |
| 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) |
| Right shift in HbO2 disassociation curve | <Ph, <SaO2, <Hb affinity, >temp, >CO2, >fetal Hb, >2,3 DPG, (decreased affinity makes unloading at tissue easier) |
| 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 |
| 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 |
| what >2,3DPG | Alkalosis, chronic hypoxemia, anemia |
| what <2,3DPG | acidosis |
| Shunt | V/Q is equal to 0, perfusion with no ventilation, alveoli blocked, refractory to O2 |
| decreased V/Q mismatch | shunt effect, perfusion in excess of ventilation, non-refractory to O2, partial obstruction, hypoventilation, COPD, interstitial disease |
| Normal V/Q matching | .8 |
| increased V/Q matching | ventilation in excess of perfusion, deadspace effect, regional hyperventilation, often seen in PPV and <CO |
| Deadspace | ventilation no perfusion, increased PaO2 with a decreased CO2 (usually less than 40) emboli |
| 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 |
| how is CaO2 measured | can only truly accurate w/co-oximeter |
| decreased CaO2 | anemia (normal PaO2 & SaO2 with <Hb), polycythemia (<PaCO2 & SaO2 w/normal CaO2), Hb bound by another gas (co-monoxide, metho) |
| 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% |
| Can A-aDo2 be calculated on nasal canulla? | no, FIO2 must be known, never calc on low flow devices |
| A-aDO2 for old pt | (age x 0.4), old fart like Jeff at age 70 x .4 equals 28 mmHg on room air |
| When might you see hypoxemia w/normal A-a diff | hypoventilation or <PIO2 |
| A-a DO2> 350 on 100% is what | indication for mech ventilation w/refractory hypoxemia |
| PvO2 | norm 38-42, mixed venous, must be drawn from pulmonary artery |
| Oxygen delivery is a function of what? | CO and CO2 |
| PaO2, SaO2 and CaO2 evaluate what | respiratory component |
| how is tissue oxygenation assessed | PvO2 |
| decreased PvO2 | <35 most often from impaired circulation, hypovelemia, PPV, LHF |
| normal or increase PVO2 in a very sick pt is usually caused by | tissue hypoxia still exists, PVO2 is unreliable-mechanism is unknown |
| C(a-v)O2 | norm 3.5-5 vol%, increased w/stable VO2 indicates perfusion to organs is decreasing |
| a-v diff >6vol% | cardiovascular decompensation and tissue oxygenation is inadequate |
| a-v diff <3.5 vol% | perfusion exceeds normal (if steady VO2), if VO2 is down then hypothermia |
| HbCO | norm .5%, carboxyHb, carbon monoxide poisoning, must use co-oximeter, 200-250 x greater affinity than O2 for Hb |
| 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 |
| S&S of increased HbCO | headache, dyspnea, nausea, tachycardia, tachypnea |
| what effect does HbCO have o PaO2 and SaO2 | if co-oximeter is not used, both will be normal |
| 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 |
| First sign of hypoxemia is | short of breath especially on exertion |
| clinical manifestations of hypoxemia are | tachycardia, tachypnea, hypertension, cyanosis, confusion |
| severe hypoxemia may result in | tissue hypoxia, met acidosis, bradycardia, hypotension, coma |
| In ICU pt, how do we identify tissue hypoxia | PvO2 <35 and a-v diff >5 vol% |
| lungs remove CO2 by | ventilation |
| kidneys role in acid-base balance is what | remove small quantities of acid, restore buffer capacity of fluids by replenishing HCO3 |
| Ph | hydrogen ion concentration in blood, reflects acid-base balance |
| acid | solutions capable of donating H+ |
| bases | solutions capable of accepting H+ |
| PaCo2 | respiratory component of acid-base balance, identifies degree of ventilation in relation to metabolic rate |
| hypercarbia mot often results from | hypoventilation, CO2 >45 |
| hypocarbia is usually caused by | hyperventilation, CO2 <35 |
| How is uncompensated resp acidosis identified | ⬆Ph,⬇CO2, with normal HCO3 and normal BE |
| what is fully/completly compensated resp acidosis? | ⬆HCO3 enough to bring Ph within normal range |
| 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 |
| 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 |
| A decrease in CO2 (to the left in O2 curve) reduces HCO3 how much | CO2 <5mmHg will <HCO3 by 1 |
| An increase in CO2 (to the right) will increase HCO3 how much | CO2 >10-15 will >HCO3 by 1 |
| 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 |
| Base excess | positive value indicates either base has been added or buffer removed, larger the number the more sever the metabolic component |
| 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 |
| do changes in CO2 effect BE? | NO, only metabolic changes alter BE |
| Simple respiratory acidosis is | inadequate ventilation, elevated CO2 |
| common causes of resp acidosis | acute upper airway obstruction, severe diffuse airway obstruction (acute or chronic), massive pulm edema |
| Common non-respiratory problems that cause resp acidosis | drug OD, spinal cord injury, neuromuscular diseases, head trauma, trauma to thoracic cage |
| How is acute resp acidosis compensated | none, renal changes are to slow |
| How is chronic resp acidosis compensated | kidneys increase absorption of HCO3 |
| How is uncompensated resp acidosis identified | ⬆Ph,⬇CO2, with normal HCO3 and normal BE |
| What is partially compensated resp acidosis | ⬆HCO3, but Ph is not yet w/in normal limits |
| what is fully/completely compensated resp acidosis? | ⬆HCO3 enough to bring Ph within normal range |
| 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 |
| If expected level of HCO3 compensation is not occurring for acute or chronic acidosis what should RT suspect? | complicating metabolic disorder is also present |
| neuromuscular disease or obstructive disorder w/resp acidosis, pt will RR will be what | short of breath and ⬆RR |
| Drug OD or impaired resp center pt w/ resp acidosis pt RR will be what | reduced |
| what effect does acute elevation of CO2 and acidosis have on CNS | anesthetic, confused, semi-conscious and eventually coma |
| in acute resp acidosis how high does CO2 get for Pt to reach coma | around 70 mmHg |
| because ⬆CO2 causes systemic vasodilation, what cardiac manifestations should be expected? | warm flush skin, bounding pulse, arrhythmias |
| because ⬆CO2 causes cerebral vasodilation, what might be expected | ⬆ICP, retinal venous distension, papilledema, headache |
| when HCO3 levels are up, what happens to chloride levels | if ⬆ result of renal compensation, then chloride will be ⬇ |
| resp Alkalosis | abnormal condition in which there is an increase in ventilation relative to the rate of CO2 |
| How does RT identify resp alkalosis in ABG | PaCO2 below expected level indicating ventilation is exceeding the normal level, hyperventilation |
| what are the common causes of resp alkalosis | hyperventilation caused by pain, hypoxemia (PaO2 55-60), acidosis, anxiety |
| how do the kidneys compensate for resp alkalosis | excrete HCO3 |
| What is the expected compensation for acute resp Alkalosis | none, ⬆Ph, ⬇PaCO2, normal HCO3 |
| What is the expected compensation for partially compensated resp Alkalosis | ⬆Ph, ⬇HCO3 |
| What is the expected compensation for fully compensated resp Alkalosis | normal Ph, ⬇HCO3 |
| Expected compensation is not present for HCO3 in resp alkalosis, what should RT suspect | complicating metabolic disorder is also present |
| 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. |
| Clinical S&S associated w/ resp alkalosis | tachypnea, dizziness, sweaty, tingling in fingers and toes, muscle weakness and spasms |
| when does RT need to be cautious not to induce resp alkalosis? | during IPPB and mech vent |
| 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) |
| 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 |
| 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 |
| High anion gap met acidosis from metabolicy acid gains | lactic acidosis (hypoxia, sepsis), ketoacidosis (diabetes, starvation, lack of glucose), renal failure (retained sulfuric acid) |
| High anion gap metabolic acidosis from ingestion of acids | salcylate poisoning (aspirin), methanol, ethylene glycol |
| normal anion gap metabolic acidosis (hyperchloremic acidosis) from loss of HCO3 is caused by | diarrhea or pancreatic fistula |
| normal anion gap met acidosis from failure to reabsorb HCO3 is most often caused by | renal failure |
| normal anion gab met acidosis from ingestion may be caused by | ammonium chloride or IV nutrition |
| what signs may be present w/renal disease | ⬆blood urea, nitrogen and creatinine, ⬇urine output |
| How does the body compensate for met acidosis | ⬇CO2(hyperventilation) |
| If normal or ⬆PaCO2 is present w/met acidosis what should RT suspect | resp defect is also present (combination resp/met acidosis) |
| 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 |
| what is the most common and obvious sign of met acidosis | Kussmaul's breathing |
| what is Kussmaul's respiration | very rapid, very deep ventilation |
| 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) |
| simple met alkalosis | above normal HCO3 |
| most common causes of met alk | hyperkelemia, hypochloremia, ng suction (⬇acid), vomiting (⬇acid), post hypercapnic disorder, diuretics, steroids or to much bicarb therapy |
| how does body compensate for met alkalosis | hypoventilation to ⬆ PaCO2 |
| 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) |
| when should RT suspect a mixed acid base disorder | normal or near normal Ph w/severe abnormal HCO3 or PaCO2 |
| where should RT look for clues of mixed acid base disorders | pt hx, physical exam, lab tests, knowing primary disorders, expected compensations |
| expected compensation for acute resp acidosis | PaCO2⬆15-HCO3 ⬆1 |
| expected compensation for chronic resp acidosis | PaCO2⬆10-HCO3 ⬆4 |
| expected compensation for acute resp alkalosis | PaCO2⬇5-HCO3 ⬇1 |
| expected compensation for chronic resp alkalosis | PaCO2⬇10-HCO3 ⬇5 |
| 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 |
| mixed/combined resp met acidosis | ⬆PaCO2 ⬇HCO3 |
| 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 |
| common causes of resp/met acidosis are | cardio pulm resuscitation, COPD and hypoxia, poisoning and drug OD |
| cardio pulm resuscitation and resp/met acidosis | heart stops-blood circulation stops, apnea causes resp acidosis, and hypoxia causes lactic acidosis (metabolic) |
| 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 |
| mixed/combined met resp alkalosis | ⬆HCO3 w/below normal PaCO2-additive effects may result in severe alkalosis |
| When met alk is super imposed on resp alk, why does it become so severe | when superimposed there is no compensation |
| 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 |
| 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 |
| Mixed met acidosis with resp alkalosis are difficult to recognize because | either abnormality usually compensates for the other |
| 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) |
| what is the prognosis for met acidosis on resp alkalosis | poor, most likely seen in critically ill |
| sleep related breathing problems occur in what % of adults | 5% (more often in men) |
| incidence of sleep-related problem ⬆ to what after age 60 | 37% |
| two basic types of sleep are | non-rem and rem |
| NREM and REM cycle | every 60-90(book) minutes (Karel says 70-90) |
| NREM | non-rapid eye movement, the beginning of sleep, 4 stages |
| Stage 1 | NREM, beginning of sleep, large eye rolls/low amp waves, drowsiness, lasts only minutes |
| 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 |
| Stage 3 & 4 | NREM, slow wave sleep, difficult to rouse, high amp waves (75 UV), increase (time) with age and pathological state |
| Stage 4 | aka Delta |
| 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 |
| REM begins | 60-90 mins after sleep begins |
| Dreams | NREM-dreamlike, REM-dreaming |
| REM per night | 4-5, getting progressively longer and more intense during the night |
| 1st REM episode of the night lasts how long | 5 mins |
| REM toward morning is how long | 30-60 mins |
| % of REM sleep in a lifetime | 20-25% |
| % of REM sleep in an infant | 55-80, tapers till meeting adult % at 6 months |
| Physical changes of REM | partially paralyzed, resp effort is chaotic, diminished response to hypercapnia & hypoxemia, ⬇upper airway tone |
| sleep continuity theory | as sleep interruption goes up, daytime alertness goes down |
| does the amount of time spent in any sleep stage 1234 or REM predict performance or degree of sleepiness? | no, only interruption of sleep |
| sleep apnea | cessation of airflow for at least 10 seconds during sleep, 3 types obstructive, central and mixed |
| OSA | obstructive sleep apnea, airflow reduction >70%, in the presence of resp effort |
| CSA | central sleep apnea, 10 seconds or more of apnea w/no effort to breath, intermittently normal |
| Mixed sleep apnea | periods of OSA & CSA during the same night of sleep |
| hypopnea | OSA w/30% reduction of airflow and >4% ⬇in SaO2 during sleep, results in hypoxemia-causes temp arousal from sleep |
| what can cause temp arousal from sleep during sleep? | hypopnea and OSA |
| UARS | upper airway resistance syndrome, ⬆neg intrathoracic press from⬆WOB (but no O2 desaturation) |
| what can disturb ventilation during sleep | apnea, hypopnea and UARS |
| why don't UARS pts remember be awaken from apnea episodes in the night? | usually just arouse to lighter stage not fully awake |
| best way to determine exact type and severity of of sleep disorder | PSG-polysomnogram |
| RDI | resp disturbance index, positive if >5 (incidences in a night) |
| RDI measures | obstructive apnea's, hypopnea's, central apnea's per hour |
| RDI for infants | >1 per hr, SaO2 <95%, end VT CO2 >53 during apnic episode |
| REM behavior disorder | people who act out in dreams |
| % of people w/sleep disorders | 15% |
| SDC | sleep disorder criterion, RDI 5-20 mild, 20-40 moderate, >40 severe |
| what is the difference between UARS and OSA | UARS do not become hypoxic during sleep, (they have excessive sleepiness from poor continuity of sleep) |
| Best TX for UARS | CPAP (nasal) |
| What are the most common forms of SDB in adult | OSA and hypopnea |
| cause of OSA | upper airway occlusion during sleep |
| causes of hypopnea | partial closure of the airway |
| anatomical abnormalities that may lead to OSA/hypopnea | micrognathia (sm lower jaw), large tongue, large tonsils/adenoids, retrognathia (under developed mandible), deviated septum |
| most common site of obstruction in OSA/hypopnea | pharynx (soft pallet to glottic inlet) |
| pathophysiology of an upper airway obstruction during sleep | airway relaxes, narrows or occludes, causing ⬆WOB causing ⬆intrathoracic press to overcome obstruction, causing narrowing airway |
| what does upper airway obstruction cause | hypoxemia and sleep arousal |
| what % of pts w/sleep apnea are obese? | 60-90% |
| what is the most dangerous symptom of OSA? | excessive daytime sleepiness |
| EDS | excessive daytime sleepiness, impairs cognitive and psycho-motor function |
| typical Hx of OSA pt | obese middle age male, loud snoring, excessively sleepy, stops breathing at night |
| hallmark of OSA | loud snoring |
| cardinal symptoms of OSA | 3S rule-Snore (loud, habitual), Spousal (reports apnic episodes), Sleepiness (daytime, excessively) |
| 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) |
| airway features of OSA may include | nasal obstruction, low soft palate, large uvula, enlarged tonsils/adenoids, macroglosia, large neck (>17.5) |
| %of OSA w/hypertension | 50% |
| what is the biggest risk factor of OSA in children | obesity |
| cardiac changes w/OSA | bradycardia during apnic episodes, then tachycardia follow, PVC's and CHF |
| what % of OSA have PVC's | 20, asystole 10% |
| TX for OSA | CPAP |
| what is the Hallmark symptom of OSA in children | snoring |
| % of sleep apnea that is CNA | 10% |
| CSA | cessation of airflow resulting from lack of movement of the diaphragm-loss of vent drive |
| when afferent input of vent drive is absent during sleep | CSA |
| what factors may play a role in /csa in children | cardiac, hematologic, metabolic, neurologic, gastro, or nuero abnormalities |
| most significant difference between OSA and CSA pts | body size, smaller in CSA and fewer daytime daytime side effects |
| SIDS | leading cause of death in children under age 1, unknown cause, peaks at 2-4 months |
| ALTE | apparent life threatening event, child appears to be dying because of apnea (pallor and cyanosis) |
| best way to prevent SIDS | supines sleeping position, decreases by 50%, parental non smoking and removal of soft bedding |
| 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 |
| primary tool to evaluate sleeping disorders | PSG |
| what is used to determine sleep stage | EEG, electroencephalogram |
| EOG | electrooculogram |
| Chin EMG | chin muscle activity, also used to detect REM |
| Tools of PSG | EEG(stage), EOG, Chin EMG and leg EMG (REM), 1 lead ECG (arrhythmias), electrodes for respiration, snoring microphones and pulse ox |
| can pulse ox be used for diagnosis of UARS | not reliable, need cooximeter |
| what is the gold standard for diagnosing sleep apnea | PSG (polysomnogram) |
| MSLT | multiple sleep latency test, recommended for pts who's reported sleepiness is more than his/her level of SDB indicates |
| sleep latency | amount of time required to fall asleep |
| what is the most reliable and valid test of daytime sleepiness | MSLT, 4-5 daytime naps |
| 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 |
| what % of men have sleep related problems | 5% |
| what is the predominant stage of NREM | 2 |
| T/F breathing tends to be irregular during early stages of NREM? | T |
| T/F BP tends to⬇ during initial stages of sleep? | T |
| T/F During REM sleep, sleeper is partially paralyzed? | T |
| T/F breathing is chaotic/irregular during REM in most sleepers | T |
| what is the key concept in central sleep apnea | intermittent absence of respiratory effort |
| hypopneas are most closely related to what? | OSA |
| 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 |
| all of the following clinical feature are typical for adult pts w/OSA | excessive daytime sleepiness, loud snoring, impaired cognitive function |
| most common arrhythmia seen in OSA | PVC's (20%) |
| all of the following are seen in children w/OSA | daytime sleepiness, hyperactivity, aggressive behavior |
| peak onset for SIDS | 2-3 months |
| all of the following are monitored during polysomnogram | EEG, ECG, leg emg |
| what test is for measuring daytime sleepiness | MSLT |
| how long are naps during MSLT | min 20 minutes, max 35 mins |
| actigraphy | wristwatch like device worn for several days |
| tx mild osa | lose weight, oral devicem avoid alcohol and caffeine |
| moderate sleep apnea tx | CPAP |
| 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 |
| TX of moderate OSA | CPAP, set at 4 and adjust up in incriments of 1 until obstruction relieved |
| why do we repeat polysomnogram in 30 days after start of CPAP in OSA? | to make sure CSA is not underlying issue |
| 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 |
| 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 |
Created by:
williamwallace
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