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Adv PT DX test 1

WillWallace Adv Pt DX Wilkens 7 and 18, whites 7, westgard

QuestionAnswer
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