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by: Pallavi Battar
Pallavi Battar
GPA 3.75

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ABG's study guide for test
Nursing Interventions Lab
Esther Kawamura
Study Guide
50 ?




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This 6 page Study Guide was uploaded by Pallavi Battar on Saturday September 17, 2016. The Study Guide belongs to NURS 450 at San Francisco State University taught by Esther Kawamura in Fall 2016. Since its upload, it has received 32 views. For similar materials see Nursing Interventions Lab in NURSING at San Francisco State University.


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Date Created: 09/17/16
Lab Lecture Week 4 ABG Slide #/ Title Teacher’s/ Textbook Questions (Answers Notes Below) 1-2 1) One system compensates 1) why do we use arterial for the other (metabolic and blood to measure ABGs? respiratory) 2) Going into the artery and drawing arterial bloodheparin syringes used so that the arterial blood doesn’t coagulate 3 and 20 2) What are the 3 major acid base regulation mechanisms? 3) How do you read ABGs? 5 4) What are the normal ABG values? 5) SaO2 vs PaO2? 1) CO2  respiratory 6) ROME 7-11 > respiratory system will compensate in minutes 7) Which type of [BUT lungs can only hypo or compensation occurred hyperventilate so much] first? 2) Bicarb  Metabolic > kidneys take hours- days to compensate [BUT may over compensate for a long time and are not as limited with buffering ability] 12-13/ Respiratory 1) Can be acute or chronic; 8) What are some causes of compensatory increase in hypoventilation or Acidosis (pH<7.35 and CO2>45) plasma HCO3 obstructions that lead to hypoventilation? 2) inadequate CO2 excretion w/ inadequate ventilation 9) Other causes or results in respiratory acidosis? HYPOVENTILATION causing a drop in PaO2 10) What happens when the PaCO2 is >60 mmHg? 3) Acute hypercapnia st Acute pulmonary edema, 11) what is the 1 sign of FBAO, atelectasis, PNX, respiratory acidosis in sedative OD, sleep apnea, anesthetized patients? morbid obesity, O2 admin. to pt w/ chronic 12) what causes chronic hypercapnia, severe PNA, respiratory acidosis? ARDS 4) Clinical manifestations 13) what happens if PaCO2 (vary acute vs. chronic) is chronically greater than > suddenincrease 50 mmHg? pulse, RR, BP; confusion, HA, decreased LOC 14) how is Respiratory >severe  increased ICP acidosis treated? causing papilledema and dilated conjunctival blood vessels; hyperkalemia can result (increased [H+] overwhelms compensatory mechanism and K+ moves out to ECF) >Chronic rapid increase in PaCO2 causes increased ICP (cerebrovascular vasodilation), tachypnea, cyanosis 5) compensatory response  renal retention of metabolic carbonic acid (takes days) HCO3 6) Tx decrease PaCO2 slowly 14-15/ Respiratory 1) caused by 15) predisposing factors of Alkalosis (pH>7.45 and HYPERVENTILATION chronic respiratory (“blowing off CO2” seen alkalosis? PaCO2<35) in DKA); decrease plasma [HCO3]; Chronic chronic hypocapnia and decrease serum [HCO3] 2) causes  extreme anxiety, hypoxemia, early salicylate intoxication, gram negative bacteremia, inappropriate ventilator settings 3) S/Sx dizzy (vasoconstriction), numbness/tingling (decreased Ca2+ ionization), tinnitus, sometimes loss of consciousness, tachycardia, ventricular/atrial dysrhythmias 4) Assessment  acute: hypokalemia, hypocalcemia, hypophosphatemia; Chronic: usually asymptomatic 5) Tx depends on underlying cause, breathe slowly to allow CO2 to accumulate in closed system (breathe into paper bag), anti-anxiety agents, 16-17/ Metabolic 1) 2 types 16) S/Sx of metabolic Acidosis (pH<7.35 and a) High anion gap acidosis? HCO3<22) acidosis (acid increased to 30mEq/L or more): excess accumulation of fixed acid ketoacidosis, lactic acidosis, late salicylate poisoning, uremia, menthol or ethylene glycol poisoning, and ketoacidosis w/ starvation, sepsis, impaired renal excretion of acids, ASA b) Normal anion gap acidosis (hyperchloremic acidosis): direct loss of bicarbonate diarrhea, lower intestinal fistulas, ureterostomies, diuretic use, early renal insufficiency, excess Chloride administration, parenteral nutrition w/o bicarb, or bicarb producing solutes (lactate) 2) Assessment Cardinal feature (decreased serum bicarb levelprimary imbalance); hyperkalemia; Compensatory (hyperventilation to decrease CO2) 3) Tx acute [eliminate source of chloride; monitor EKG for hyperkalemia and subsequent hypokalemia]. Chronic st [hypocalcemia tx 1 to prevent tetany from increase in pH and decrease ionization of Ca]. Alkalizing agents, hemodialysis, or peritoneal dialysis may be done too. 18-19/ Metabolic 1) Base Bicarb Excess 17) Predisposing factors Alkalosis (pH>7.45 and (increased HCO3 of Metabolic Alkalosis? HCO3>26) primary imbalance) 18) S/Sx of metabolic 2) Causes acidosis? > Loss of Gastric Secretionsvomiting (loss of HCl), gastric suction, pyloric stenosis > alkali ingestion from bicarb containing antacids during CPR 3) 2 ways that hypokalemia causes metabolic alkalosis a) kidneys conserve K+ so H+ excretion increases b) ICF K+ moves to ECF (as K+ leave cells, H+ ions enter to maintain electroneutrality) 4) Chronic occurs w/ long term K+ wasting diuretic use, villous adenoma, gastric fluid external drainage, significant K+ depletion, CF, chronic ingestion of milk and calcium carbonate. 5) Tx (acute and chronic) correct underlying problem, monitor I/O, give chloride so kidneys can absorb Na w/ Cl to allow excretion of excess bicarb, restore fluids (NaCl fluids) b/c continued volume depletion perpetuates alkalosis, give KCl to replenish K+ and Cl- losses (hypokalemic pts), H2 receptor antagonist (cimetidine) reduces gastric HCl production (decrease metabolic alkalosis associated w/ gastric suction), and carbonic anhydrase inhibitors (for pts who can’t tolerate rapid volume expansionCHF pts.) Answers (***From Textbook***) 1) To determine acid/base status and determine oxygenation status 2) Buffers, PaCO2 (Respiratory System), HCO3/ Bicarbonate (Renal System) 3) Look at the pHacidosis or alkalosis; Look at CO2 and HCO3  respiratory or metabolic; Look at O2 Is either one compensating for the other? 4) pH 7.35-7.45 PaCO2  35-45 HCO3  22-26 Base Excess (BE)  -2 to +2 PaO2  80-100 SaO2  95%+ 5) SaO2  percentage or oxygen on each RBC; PaO2  the amount of oxygen in arterial blood 6) Respiratory Opposite (Increase CO2 = decrease pH [respiratory acidosis]; Decrease CO2 = increase pH [respiratory alkalosis]) Metabolic Equal (Increase HCO3 = increase pH [metabolic alkalosis]; decrease HCO3 = decrease pH [metabolic acidosis]) 7) pH will indicate whether the patient has primary metabolic acidosis/alkalosis with respiratory compensation or primary respiratory acidosis/alkalosis with metabolic compensation 8) Causes of hypoventilation  Narcotics, splitting due to pain, restrictive respiratory disease, wrong ventilator settings (rate may be inadequate and CO2 can be retained) Obstructions that lead to hypoventilation  Asthma, atelectasis, emphysema, pulmonary edema, pulmonary embolism 9) Diseases that cause muscle impairment muscular dystrophy, MS, Myasthenia Gravis, Guillian-Barre Syndrome 10) PaCO2 >60 mmHg cause cerebrovascular vasodilation and increased cerebral blood flow  causes HA 11) V-Fib 12) Pulmonary diseases  chronic emphysema, bronchitis, obstructive sleep apnea, and obesity. If PaCO2 doesn’t exceed body’s ability to compensate, the patient will be asymptomatic. 13) Respiratory center becomes insensitive to CO2 as a stimulant (hypoxemia becomes a major drive for respiration). Oxygen administration removes stimulus for hypoxemia and patient will develop “CO2 narcosis” (unless quickly revered). Therefore, give LOW FLOW O2. 14) Treatment improve ventilation bronchodilators, antibiotics, thrombolytics and anticoagulants, Hydration (2-3 L/day) to keep mucous membranes soft to facilitate removal of secretions, supplemental O2, mechanical ventilation (if used inappropriately may cause rapid excretion of CO2 that the kidneys are unable to get rid of excess HCO3 to prevent seizures and alkalosis), Semi-fowlers position 15) Chronic Hepatic insufficiency and cerebral tumors 16) Vary w/ severity HA, confusion, drowsiness, increased RR and depth, N/V, decreased BP, cool/clammy skin, dysrhythmias, and shock. If pH<7 (peripheral vasodilation and decreased C.O.). Chronic seen in chronic renal failure. 17) K+ loss through K+ wasting diuretic use (thiazides, furosemide) and ACTCH secretion (hyperaldosteronism and Cushing Syndrome) 18) S/Sx (acute and chronic) are r/t decreased calcium ionization tingling, dizziness, hypertonic muscles, hypocalcemia, decreased respirations (compensation by lungs), Atrial tachycardia, ventricular disturbances (as pH increases and hypokalemia develops; PVCs or U waves on EKG), decreased motility and paralytic ileus.


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