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WillWallace ABG's

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 decompensasion 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
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
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
Created by: williamwallace