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ABG's
WillWallace ABG's
| Question | Answer |
|---|---|
| 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
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