WillWallace ABG's
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| ABG samples provide what | precise measurement of Acid-Base balance and lungs ability to oxygenate the blood and remove CO2
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| Accurate interpretation of ABG require what | knowledge of pt total clinical picture including any TX receiving
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| where are mixed venous blood samples drawn | rt atrium or pulm artery
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| what is mixed venous blood sample used for | evaluate overall tissue oxygenation
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| why not venous samples | only give metabolic rates so little value, exposed to peripheral vascular beds
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| normal ABG values for arterial blood is | Ph 7.35-7.45, PaO2 80-100 mmHg, PaCO2 35-45 mmHg, HCO3 22-26, BE +-2
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| Normal ABG for mixed venous blood is | Ph 7.34-7.37, PaO2 38-42 mmHg, PaCO2 44-46, HCO3 24-30
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| Prior to ABG draw, what should RT review for in Pt chart | low platelet count or increased bleeding time (meds etc)
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| Preferred site of ABG arteriotomy (needle into artery) | radial artery
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| Sites for ABG arteriotomy in adult are | radial artery, brachial artery, dorsalis pedis, or femoral artery.
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| What must be evaluated prior to a radial stick | collateral circulation of the hand, via modified Allens test
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| how is modified Allens test performed | have pt make tight fist, RT compress both radial and ulnar artery, instruct pt to open hand and relax, RT release ulnar
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| what is a positive Allens test | hand pinks w/in 10-15 seconds after release of ulnar artery, means circulation is adequate for puncture site
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| what should RT do if Allen test is negative | try other arm then try brachial
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| what should RT do for pt who needs frequent ABG's | insert indwelling arterial catheter (only in ICU)
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| what do bubbles in sample do | may equilibriate w/blood and cause bad sample-need to remove bubbles immediately after draw
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| How should RT handle sample after draw | remove bubbles, store in ice water to stop metabolism, analyze with in 1 hr
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| room temp samples must be analyzed how soon | 10-15 mins
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| how long should pressure be applied to stick wound | 3-5 mins or longer if clotting problem
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| ABG and VGB samples are used to evaluate what | acid-base balance (Ph, PaO2 PaCO2, HCO3 BE), oxygenation status (PaO2, SaO2, CaO2, PvO2), and adequate ventilation (PaCO2)
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| What does PaO2 reflect | O2 in plasma of arterial blood, reflects ability of lungs to transfer O2 into blood
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| Predicted PaO2 is dependent on what | pt age, FIO2, PIO2 (Pb and altitude)
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| effects of age on PaO2 | 103.5-(.42xage)+- 4, so if old fart like Jeff and age is 60 then 103-(.42x60) is 78.3 so normal range of PaO2 for Jeff is 74-82
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| hypoxemia | PaO2 less than normal predicted range, at any age, for pt breathing room air or PaO2 <65mmhg, severe <40mmHg (any age) in pt with increased FIO2
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| Does hypoxemia exist if pt is on >FIO2 and his PaO2 is normal? | NO, hypoxemia is only a <PaO2 lower than predicted regardless of FIO2
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| Hypoxia | inadequate tissue oxygenation
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| how are hypoxemia and hypoxia related | hypoxemia may result in hypoxia in pts with <CO, but they are not synonymous
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| most common cause of hypoxemia is | >V/Q mismatch, in pts with lung disease
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| increased V/Q mismatch | decrease in V/Q matching, perfusion is god, but ventilation is not, mucus plugging, secretions, bronchospasm, in specific portions of the lung
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| decreased V/Q matching is what | (has been on last two Vent tests), an increase in V/Q mismatch
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| causes of hypoxemia | >V/Q mismatch, diffusion defects, >CO2 from hypoventilation, Drug OD (>CO2), <PIO2 (altitude), equip failure
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| SaO2 | norm >95%, O2 saturation, actual amount of O2 bound to Hb expressed as a %
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| how is SaO2 determined | can be calculated, but true SaO2 must be can only be gotten from co-oximeter
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| Oxyhemoglobin disassociation curve | shows the effects of O2 loading and unloading in relationship to Hb
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| Left shift in HbO2 disassociation curve | >Ph, >SaO2, >Hb affinity, <temp, <CO2, <fetal Hb, <2,3 DPG, (increased affinity makes unloading at tissue more difficult)
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| Right shift in HbO2 disassociation curve | <Ph, <SaO2, <Hb affinity, >temp, >CO2, >fetal Hb, >2,3 DPG, (decreased affinity makes unloading at tissue easier)
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| Ph and Hb affinity for O2 | as Ph changes Hb affinity for O2 is directly affected (Bohr effect), Ph up, Hb affinity also up, Ph down Hb affinity also down
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| 2,3 DPG | organic phosphate in RBC, stabilizes deoxygenated Hb, reducing its affinity for O2, without it Hb would never unload O2 at the tissue
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| what >2,3DPG | Alkalosis, chronic hypoxemia, anemia
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| what <2,3DPG | acidosis
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| Shunt | V/Q is equal to 0, perfusion with no ventilation, alveoli blocked, refractory to O2
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| decreased V/Q mismatch | shunt effect, perfusion in excess of ventilation, non-refractory to O2, partial obstruction, hypoventilation, COPD, interstitial disease
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| Normal V/Q matching | .8
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| increased V/Q matching | ventilation in excess of perfusion, deadspace effect, regional hyperventilation, often seen in PPV and <CO
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| Deadspace | ventilation no perfusion, increased PaO2 with a decreased CO2 (usually less than 40) emboli
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| CaO2 | (Hb x 1.34)xSaO2+(PaO2x.003), norm 16-20 vol%, O2 bound to Hb and O2 in plasma, very important because of influence to tissue oxygenation
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| how is CaO2 measured | can only truly accurate w/co-oximeter
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| decreased CaO2 | anemia (normal PaO2 & SaO2 with <Hb), polycythemia (<PaCO2 & SaO2 w/normal CaO2), Hb bound by another gas (co-monoxide, metho)
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| P(A-a)O2 | norm 10-15 mmHg on room air, or 25-65on 100%, predicted dependent on age and FIO2, increase is resp defect, every increase of 50 is 2% shunt above normal of 2-3%
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| Can A-aDo2 be calculated on nasal canulla? | no, FIO2 must be known, never calc on low flow devices
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| A-aDO2 for old pt | (age x 0.4), old fart like Jeff at age 70 x .4 equals 28 mmHg on room air
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| When might you see hypoxemia w/normal A-a diff | hypoventilation or <PIO2
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| A-a DO2> 350 on 100% is what | indication for mech ventilation w/refractory hypoxemia
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| PvO2 | norm 38-42, mixed venous, must be drawn from pulmonary artery
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| Oxygen delivery is a function of what? | CO and CO2
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| PaO2, SaO2 and CaO2 evaluate what | respiratory component
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| how is tissue oxygenation assessed | PvO2
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| decreased PvO2 | <35 most often from impaired circulation, hypovelemia, PPV, LHF
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| normal or increase PVO2 in a very sick pt is usually caused by | tissue hypoxia still exists, PVO2 is unreliable-mechanism is unknown
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| C(a-v)O2 | norm 3.5-5 vol%, increased w/stable VO2 indicates perfusion to organs is decreasing
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| a-v diff >6vol% | cardiovascular decompensasion and tissue oxygenation is inadequate
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| a-v diff <3.5 vol% | perfusion exceeds normal (if steady VO2), if VO2 is down then hypothermia
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| HbCO | norm .5%, carboxyHb, carbon monoxide poisoning, must use co-oximeter, 200-250 x greater affinity than O2 for Hb
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| increased HbCO causes what | tissue hypoxia, inhibits unloading of O2 at tissue, >of 5-10% w/smokers, >40-60% causes visual disturbances, myocardial toxicity, LOC, eventual death
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| S&S of increased HbCO | headache, dyspnea, nausea, tachycardia, tachypnea
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| what effect does HbCO have o PaO2 and SaO2 | if co-oximeter is not used, both will be normal
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| significance of PAO2 + PaO2 (on room air) | 110-130 is hypoxemia due to hypoventilation, <110 is hypoxemia due to lung defect, >130 is pt on >FIO2 or error
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| First sign of hypoxemia is | short of breath especially on exertion
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| clinical manifestations of hypoxemia are | tachycardia, tachypnea, hypertension, cyanosis, confusion
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| severe hypoxemia may result in | tissue hypoxia, met acidosis, bradycardia, hypotension, coma
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| In ICU pt, how do we identify tissue hypoxia | PvO2 <35 and a-v diff >5 vol%
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| lungs remove CO2 by | ventilation
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| kidneys role in acid-base balance is what | remove small quantities of acid, restore buffer capacity of fluids by replenishing HCO3
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| Ph | hydrogen ion concentration in blood, reflects acid-base balance
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| bases | solutions capable of accepting H+
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| PaCo2 | respiratory component of acid-base balance, identifies degree of ventilation in relation to metabolic rate
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| hypercarbia mot often results from | hypoventilation, CO2 >45
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| hypocarbia is usually caused by | hyperventilation, CO2 <35
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| What is the most reliable measurement of pt ventilation | CO2, and should be interpreted in light of a normal VE w/CO2 or >VE w/normal CO2
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| HCO3 | bicarb, norm is 22-26 mEq/L, primary metabolic component of acid-base balance, regulated by renal system, usually requires 12-24 hrs for compensatory response
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| A decrease in CO2 (to the left in O2 curve) reduces HCO3 how much | CO2 <5mmHg will <HCO3 by 1
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| An increase in CO2 (to the right) will increase HCO3 how much | CO2 >10-15 will >HCO3 by 1
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| BE+- | base excess base deficit, standard deviation of HCO3 that takes buffering of RBC's into account. Calculated with Ph, CO2 and Hematocrit and is a more complete analysis of metabolic buffering capability
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| Base excess | positive value indicates either base has been added or buffer removed, larger the number the more sever the metabolic component
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| what is the importance of BE | allows analysis of pure metabolic components of acid-base balance, changes in met components alter acid-base, respiratory components do not
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| do changes in CO2 effect BE? | NO, only metabolic changes alter BE
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| Simple respiratory acidosis is | inadequate ventilation, elevated CO2
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| common causes of resp acidosis | acute upper airway obstruction, severe diffuse airway obstruction (acute or chronic), massive pulm edema
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| Common non-respiratory problems that cause resp acidosis | drug OD, spinal cord injury, neuromuscular diseases, head trauma, trauma to thoracic cage
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| How is acute resp acidosis compensated | none, renal changes are to slow
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| How is chronic resp acidosis compensated | kidneys increase absorption of HCO3
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| How is uncompensated resp acidosis identified | ⬆Ph,⬇CO2, with normal HCO3 and normal BE
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| What is partially compensated resp acidosis | ⬆HCO3, but Ph is not yet w/in normal limits
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| what is fully/completely compensated resp acidosis? | ⬆HCO3 enough to bring Ph within normal range
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| How is degree of compensating determined in resp acidosis | acute-HCO3⬆1 for every 10-15 ⬆in CO2, chronic- HCO3⬆4 for every 10 ⬆CO2
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| If expected level of HCO3 compensation is not occurring for acute or chronic acidosis what should RT suspect? | complicating metabolic disorder is also present
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| neuromuscular disease or obstructive disorder w/resp acidosis, pt will RR will be what | short of breath and ⬆RR
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| Drug OD or impaired resp center pt w/ resp acidosis pt RR will be what | reduced
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| what effect does acute elevation of CO2 and acidosis have on CNS | anesthetic, confused, semi-conscious and eventually coma
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| in acute resp acidosis how high does CO2 get for Pt to reach coma | around 70 mmHg
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| because ⬆CO2 causes systemic vasodilation, what cardiac manifestations should be expected? | warm flush skin, bounding pulse, arrhythmias
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| because ⬆CO2 causes cerebral vasodilation, what might be expected | ⬆ICP, retinal venous distension, papilledema, headache
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| when HCO3 levels are up, what happens to chloride levels | if ⬆ result of renal compensation, then chloride will be ⬇
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| resp Alkalosis | abnormal condition in which there is an increase in ventilation relative to the rate of CO2
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| How does RT identify resp alkalosis in ABG | PaCO2 below expected level indicating ventilation is exceeding the normal level, hyperventilation
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| what are the common causes of resp alkalosis | hyperventilation caused by pain, hypoxemia (PaO2 55-60), acidosis, anxiety
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| how do the kidneys compensate for resp alkalosis | excrete HCO3
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| What is the expected compensation for acute resp Alkalosis | none, ⬆Ph, ⬇PaCO2, normal HCO3
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| What is the expected compensation for partially compensated resp Alkalosis | ⬆Ph, ⬇HCO3
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| What is the expected compensation for fully compensated resp Alkalosis | normal Ph, ⬇HCO3
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| Expected compensation is not present for HCO3 in resp alkalosis, what should RT suspect | complicating metabolic disorder is also present
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| In resp alk what is the advantage of a ⬇PaCO2 | an⬆ PAO2 and therefor less chance of hypoxemia being present, or if present it will be better than if CO2 is up.
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| Clinical S&S associated w/ resp alkalosis | tachypnea, dizziness, sweaty, tingling in fingers and toes, muscle weakness and spasms
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| when does RT need to be cautious not to induce resp alkalosis? | during IPPB and mech vent
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| simple met acidosis | HCO3 or BE falls below normal, caused when buffers are not produce in enough quantity (high Gap), or when buffers are lost (normal Gap)
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| Anion Gap | normal 11 (8-16 mEq/L), when fixed acids accumulate in the body, H+ reacts to HCO3 causing it to ⬇,leading to a ⬇ anion gap
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| Causes of met acidosis with high anion gap can be divided into two categories what are they | metibolicy produced acid gains or ingestion of acids
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| High anion gap met acidosis from metabolicy acid gains | lactic acidosis (hypoxia, sepsis), ketoacidosis (diabetes, starvation, lack of glucose), renal failure (retained sulfuric acid)
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| High anion gap metabolic acidosis from ingestion of acids | salcylate poisoning (aspirin), methanol, ethylene glycol
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| normal anion gap metabolic acidosis (hyperchloremic acidosis) from loss of HCO3 is caused by | diarrhea or pancreatic fistula
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| normal anion gap met acidosis from failure to reabsorb HCO3 is most often caused by | renal failure
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| normal anion gab met acidosis from ingestion may be caused by | ammonium chloride or IV nutrition
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| what signs may be present w/renal disease | ⬆blood urea, nitrogen and creatinine, ⬇urine output
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| How does the body compensate for met acidosis | ⬇CO2(hyperventilation)
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| If normal or ⬆PaCO2 is present w/met acidosis what should RT suspect | resp defect is also present (combination resp/met acidosis)
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| What is the predicted compensation of PaCO2 for met acidosis | PaCO2 eqs (1.5xHCO3)+8+-2, if PaCO2 is not at predicted level based on calc, resp abnormality is present
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| what is the most common and obvious sign of met acidosis | Kussmaul's breathing
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| what is Kussmaul's respiration | very rapid, very deep ventilation
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| S&S and Pt complaints w/severe met acidosis | dyspnea, headache, nausea, vomiting followed by confusion and stupor. Vasoconstriction, pulm edema, arrhythmias (if severe enough)
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| simple met alkalosis | above normal HCO3
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| most common causes of met alk | hyperkelemia, hypochloremia, ng suction (⬇acid), vomiting (⬇acid), post hypercapnic disorder, diuretics, steroids or to much bicarb therapy
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| how does body compensate for met alkalosis | hypoventilation to ⬆ PaCO2
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| fully compensated met alk is identified by | ⬆ in PaCO2 enough to return Ph to normal (hypercarbia may be present and may appear as resp acidosis)
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| when should RT suspect a mixed acid base disorder | normal or near normal Ph w/severe abnormal HCO3 or PaCO2
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| where should RT look for clues of mixed acid base disorders | pt hx, physical exam, lab tests, knowing primary disorders, expected compensations
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| expected compensation for acute resp acidosis | PaCO2⬆15-HCO3 ⬆1
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| expected compensation for chronic resp acidosis | PaCO2⬆10-HCO3 ⬆4
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| expected compensation for acute resp alkalosis | PaCO2⬇5-HCO3 ⬇1
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| expected compensation for chronic resp alkalosis | PaCO2⬇10-HCO3 ⬇5
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| expected compensation for met acidosis | PaCO2 eqs (1.5xHCO3)+8+-2 (shortcut is last two digits of Ph is equal to PaCO2) or HCO3 ⬆1-PaCO2⬆.6
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| mixed/combined resp met acidosis | ⬆PaCO2 ⬇HCO3
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| why is combined resp/met acidosis so easy to identify | hypercapnia and low HCO3 work synergistically to significantly reduce Ph, often resulting in profound acidosis
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| common causes of resp/met acidosis are | cardio pulm resuscitation, COPD and hypoxia, poisoning and drug OD
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| cardio pulm resuscitation and resp/met acidosis | heart stops-blood circulation stops, apnea causes resp acidosis, and hypoxia causes lactic acidosis (metabolic)
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| COPD and hypoxia w/resp met acidosis | chronic COPD w/compensated resp acidosis suddenly gets met disturbance like hypotension or renal failure, causing hypoxia and lactic acidosis
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| mixed/combined met resp alkalosis | ⬆HCO3 w/below normal PaCO2-additive effects may result in severe alkalosis
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| When met alk is super imposed on resp alk, why does it become so severe | when superimposed there is no compensation
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| what clinical situation will RT most likely see met/resp alkalosis | hypoxemia, hypotension, neuro damage, to much mech vent, anxiety, pain, or any of above in combo
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| What pts most often get combined met resp alkalosis | chronic COPD w/elevated HCO3, suddenly reduction in PaCo2 from mech vent will cause resp alk onto the met alk pt already has
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| Mixed met acidosis with resp alkalosis are difficult to recognize because | either abnormality usually compensates for the other
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| met acidosis with Paco2 lower than predicted for degree of acidosis | resp alk is also occurring simultaneously, Ph will be just above 7.4 (appearing to compensate for for resp alk)
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| what is the prognosis for met acidosis on resp alkalosis | poor, most likely seen in critically ill
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