Question Answer
______ ____ analysis is the most basic test of lung function. blood gas
what does evaluation of the acid-base and oxygenation status of the body provide? important info about the function of the lungs themselves
what does anaeobic sampling involve? invasive that carries risks of blood-borne pathogens
calculating _______ _______ and the ______ ________ uses blood gas measurements to assess gas exchange as it applies to oxygenation. oxygen content; shunt fraction
____ is the negative logarithm of the hydrogen ion concentration in the blood, used as a positive number. pH
how is pH derived? converting H+ to a negative exponent of 10 and calculating its logarithm
what is the physiologic range of pH of blood in clinical practice? 6.90-7.80
what is PCO2? measures partial pressure exerted in CO2 in solution in the blood
what is the PCO2 in mixed venous blood? 40-46 mmHg
what is PO2? what is the normal mixed venous PO2? measures partial pressure exerted by O2 dissolved in blood; 37-43 mmHg
__________ _______ influences the expected arterial PO2. barometric pressures
how is blood pH measured? exposing blood to a glass electrode; light absorbance w/ optical pH indicator (anaerobic)
what temperature are pH measurements made at? 37 degrees
how is PCO2 measured? exposing blood to a modified pH electrode in jacket w/ teflon membrane at tip
what does the jacket contain? HCO3 buffer
the change in pH is measured by the electrode and is proportional to the ____. PCO2
newer blood gas analyzers use a ______________ to measure the absorbance of CO2 in the infrared portion of the spectrum. PCO2 may also be estimated using a ____________ electrode. spectrophotometer; transcutaneous
if the hemoglobin is measured or estimated, the _____ _______ can be calculated. what is the normal at a pH of 7.40? base excess; 48 mEq/L
what is BE the difference between? actual buffering capacity of the blood and expected value
what are the main buffers that affect the BE? HCO3 and Hb
how is PO2 measured? exposing whole blood to platinum electrode covered w/ polypropylene membrane
what is this type of electrode called? polarographic (clark)
what are blood gas values (pH, PCO2, PO2) influenced by? pt’s temperature
what are the technical problems with blood gas electrodes and related measuring devices? electrode-based analyzers? contamination by protein or blood products; depletion of buffers, tears/ruptures
what are common problems with spectrophotometric methods? mechanical/electrical failure, inadequate mixing
where are mixed venous samples drawn from? and what is a common problem? PAC; contamination w/ flush solution, displacement of catheter tip
venous samples from peripheral veins are not useful for assessing ___________. oxygenation
what does contamination often occur? air is left in syringe; poor fitting plungers; failure to properly cap
how long does a glass syringe sample last in ice water? within how long should plastic syringe sampled be analyzed? 1-2 hours; 30 mins
when a blood gas specimen is placed in an ice-water bath, the ________ of O2 increases, as does the affinity of Hb for O2. solubility
within how long should samples be analyzed? 15-20 mins (>20 mins – iced)
what are acid-base disorders arising from lung diseases often related to? PCO2 and its transport as carbonic acid
PaCO2 is inversely proportional to _________ __________. alveolar ventilation
________ is a common cause of hyperventilation. hypoxemia
O2 therapy is usually titrated to maintain PaCO2 values <___ mmHg without hypercapnia and acidosis. 60
what is the normal alveolar-arterial gradient? <20 mmHg
hyperventilation may increase PaO2 as high as ____ mmHg in a normal pt. 120
what can a decreased PaO2 result from? hypoventilation, diffusion abnormality, V/Q imbalance, high altitude
what does hypoxemia commonly result from? inadequate/abnormal Hb
what is the severity of impaired oxygenation indicated by? PaO2 at rest
what is PaO2 a good index of? lungs’ ability to match pulm capillary blood flow w/ adequate ventilation
_______ _______ is the most accurate way to assess O2 delivery and the probability of tissue hypoxia. oxygen content
what is the mixed venous oxygen tension (PVO2) normal range? what is the avg mixed venous O2 content? CaO2? 37-43 mmHg; 15 ml/dl; 20 ml/dl
what does PVO2 change in response to? alterations in CO and O2 consumption
what can the degree of arterial desaturation NOT be predicted from? static pulmonary function measurements
___________ refers to the measurement of Hb and its derivatives by spectroscopy. hemoximetry
O2 saturation is the ratio of oxygenated Hb to etiher…? total Hb or functional Hb (binds O2)
what are the methods of measuring O2 saturation of Hb? spectrophotometer; measure SvO2
at PaO2 values of approximately ____, Hb becomes completely saturated. 150
______ changes in PaO2 result in ______ changes in saturation. small; large
what is P50? what is the P50 of normal adult Hb? partial pressure at which Hb is 50% saturated; 27 mmHg
how is P50 determined? equilibrating blood w/ several gases at low O2 tensions; compare measured SaO2 w/ expected
what is the normal COHb? 0.5%-2% of total Hb
when COHb is elevated, arterial blood appears ______ ____. bright red
what are the 2 ways COHb interferes with O2 transport? 1. binds competitively to Hb 2. shifts the O2Hb curve to the left
removal of CO from the blood depends on the _______ __________. minute ventilation
____________ forms when iron atoms of the Hb molecule are oxidized from Fe++ to Fe+++. what is the normal level? methemoglobin; <1.5% of total Hb
what do high levels of MetHb result from? oxidizing agents
what is the avg saturation of mixed venous blood in healthy pts? 75% at a PVO2 of 40 mmHg
____ is useful in assessing cardiac function in critical care setting and during exercise. what do values <60% indicate? SvO2; cardiovascular decompensation (tissue hypoxemia)
SpO2 estimates SaO2 by analyzing absorption of light passing through a capillary bed, either by __________ or ___________. transmission; reflectance
pulse oximeters measure the light absorption of a mixture of 2 forms of Hb…? the relative absorptions at ____ nm (red) and ____ nm (near infrared) can be used to calculate the combination of the two Hb forms. 1. O2Hb 2. reduced Hb; 660; 940
what is the accuracy of pulse oximetry? +/- 2% of actual saturation (SaO2 >90%)
when is pulse oximetry most useful? shown to correlate w/ blood oximetry in pt w/ known circumstance
when is blood gas analysis required? evaluate hyperoxemia or acid-base status
_________ includes continuous, noninvasive monitoring of expired CO2 and analysis of the single-breath CO2 waveform. capnography
what are the methods used to measure exhaled CO2 gas? infrared analyzers; mass spectrometer
what is the shape of the expired CO2 curve determined by? ventilation-perfusion matching
what does the absolute concentration of CO2 at the alveolar plateau depend on? minute ventilation and CO2 production
in healthy individuals, approx __% of th eCO is shunted past the pulmonary system. 5
what disease patterns is intrapulmonary shunting common in? atelectasis or foreign body aspiration; ARDS, pneumonia
what does the accuracy of clinical shunt measurement depend on? accuracy of PO2 determinations

Question Answer
drugs that can be instilled down an ET tube LEAN lidocaine, epi, atropine, na bicarb
Lidocaine anti-arrhythmia, drug of choice for VF and VT, suppresses myocardial conduction
lidocaine dose load dose 1-1.5 mg/kg, second dose .5-.75 mg/kg max 3mg/kg
lidocaine cautions old farts, renal problems
Epinephrine B-adrenergic, drug of choice for CA w/ pulseless VT, asystole, PEA, severe <BP when pacing and atropine fail, with phosphodiesterase inhibitor like Xanthines (enzyme that breaks up CAMP), anaphylaxis, (can be used as vasopressor)
epi dose 1mg 3-5 mins during ACLS (20ml flush after each), 1mg/500ml NS for cont IV, 2-2.5 mg diluted in 10ml NS for ETT instillation
epinephrine precautions >BP, >HR
Atropine anti-cholinergic, first line for symptomatic brady, 2nd drug after epi or vasopressor in asystole or PEA,
Atropine dose brady is .5 mg 3-5 mins max .04 mg/kg or 3mg total, PEA and asystole is 1mg IV/IO, repeat 3-5 mins if needed, max 3mg, ETT instilled 2-3 mg max 9mg
atropine hazards >myocardial O2 demand (caution with MI), hypothermic brady
Na Bicarb rare used in known preexisting hyperkalemia, known preexisting metabolic acidosis (ketoacidosis, aspirin OD, cocaine), no good for hypercarbic acidosis
NA bicarb dose 1mEq/kg IV bolus
bicarb precautions adequate ventilation and CPR are ACLS buffers not bicarb, so not recommended for routine use in cardiac arrest
most important thing RT needs to know about ACLS circulation and perfusion
perfusion CO + systemic vascular resistance
anti-arrhythmic drugs (according to Karyl) LADMAA, lidocaine, amiodarone, dopamine, magnesium, adenosine, atropine
amiodarone cardiac arrest unresponsive to CPR, shocking and vasopressors, management of life-threating, recurrent VF and unstable VT that are unresponsive to other TX’s
amiodarone cautions life-threating side effects and difficult mgmt, hospitalized for loading dose
amiodarone dose ACLS 300mg IV/IO (in 20-30 mL D5W) with ONE 150 mg 3-5 mins if needed, for mgmt of VF and VT max dose per day 2.2 g, load with 150 mg, rest is complicated and doubtful on test)
adenosine ????????vasodilator, depresses AV and sinus node activity, drug of choice for stable narrow PSVT (paroxysmal aka continuous)
adenosine cautions not for OD or poison tachy or 2nd or 3rd heart block, less effective w/caffeine, PT IN MILD REVERSE TRENDELENBURG TO ADMIN DRUG!!!!!
adenosine dose trendelenburg for 6mg rapid infusion, less than 5 second half life, then elevate for 2nd and 3rd dose at 12mg, 30mg max
dopamine ???????, second line for symptomatic brady (after atropine) and hypotension <70-100 with shock
dopamine dose 2-20 ug/kg per minute, titrate to pt response
dopamine precautions correct hypovelemia with volume prior to dopamine, caution with CHF, may cause tachy or excess vasoconstriction, never mix with bicarb
magnesium sulfate cardiac arrest with torsades dede pointes, life-threating V-arrhythmias due to digitalis toxicity
magnesium precautions rapid < BP with rapid admin, caution with renal failure present.
Magnesium dose cardiac arrest due to hypo-magnesium or torsades 1-2 g (2-4ml of 50%) in 10ml of D5W over 5-20 mins, torsades with pulse 1-2 g with 50-100 ml D5W over 5-60 mins, followed by .5 to 1 g/h to control torsades
drug types that control rhythm and rate are anti-rhythmics, b-blockers and calcium channel blockers
drugs of choice for rhythm and rate are (according to book) (DVM-DANCED Kay loves vets ) dopamine, vasopressin, milrinone, dobutamine, amrinone/inamrinon, nitroglycerin, calcium, epi, digitalis)
vasopressin can be alternative to epi in shock-refractory VF, asystole and PEA, also as hemodynamic support in septic shock
vasopressin cautions potent vasoconstrictor can cause cardiac ischemia and angina, not recommended for pt w/coronary art disease
vasopressin dose 40 U IV/IO ONE TIME ONLY, only one dose for cardiac arrest, can replace epi first or second dose (epi can be give 3x during CA)
Milrinone (positive inatrope) myocardial dysfunction and increased systemic or pulmonary vascular resistance, CHF post surgery, shock w/high systemic vascular resistance
milrinone cautions very short half life(shorter than inamrinone), nausea, vomit, hypotension, may accumulate in renal failure pts
milrinone dose 50 ug/kg over 10 mins loading dose, .375-.75/min for 2-3 days
other drugs used during ACLS are (according to book) morphine, bicarb and thrombolitics
morphine narcotic analgesic/opioid (agonist), chest pain with ACS (acute coronary syndrome) unresponsive to nitrates and acute cardiogenic pulmonary edema (if blood pressure is adequate), fyi morphine is a phosphodiesterase inhibitor
Thrombolitics streptokinase and urokinase, clot-busters (FYI, was on first test and Mark got it wrong, Heparin is listed in answers and is not a clot-buster, only strepto and uro
ACLS drugs are administered via IV, IO (intraosseous-into the bone marrow of tibia, femur and iliac crest are bone of choice), instilled via ETT
Isoproterenol is sometimes used during ACLS for what a pure B-adrenergic agonist (potent inotropic and chronotropic) as vasopressor, temp if external pacer not avail for TX of symptomatic brady or refractory torsades unresponsive to magnesium, poisoning from B-blockers
Isoproterenol cautions NEVER AS A TX FOR CARDIAC ARREST, increased O2 need of myocardial may increase ischemia, never with epinephrine(causes VT/VF)
isoproterenol dosing 2-10 ug/min, titrate to adequate HR, in torsades titrate until VT is suppressed
Big 4, main drugs in ACLS are (like going to drink beer at on oxygen bar) O2+ALE. O2, atropine, lidocaine, and epi
dopamine and dobutamine are for what >CO and >BP, vasopressors
bicarb in ACLS is useful when pt has preexisting met acidosis
best drugs in ACLS for pt with frequent PVC’s and runs of VT lidocaine
ongoing CPR, pt is intubated and ventilated, pt is asystole on monitor, what is drug choice 1mg epinephrine
following resuscitation, pt in CCU cont having freq multi-focal PVC’s and runs of VT what do you recommend lidocaine 2-4 mg/min to reduce cardiac irritability
diltiazem and verpimil are calcium channel blockers for mgmt of atrial dysrrhythmias
when ACLS drugs are instilled in ETT, what is dose 2-2.5 times standard IV dose
what is O2 FIO2 for ACLS 100%
best IV solution when admin ACLS drugs via IV, in the absence of volume depletion NS or lactated ringers (use whats available, don’t let absence of volume keep you from choosing lactated ringers)
if using thrombolytic (clotbusters-urokinase and streptokinase) following MI, should be administered when? within 6 hours
MONA MI drugs, morphine, O2, Nitroglycerin, aspirin
which of the following is true about the use of magnesium in CA? 1 mg is indicated for VF/pulseless VT associated with torsades de pointe
Pt is in CA, CPR in progress, pt is intubated and IV is started, rhythm is asystole, what is first drug to administer epi 1mg or vasopressin 40 U IV
Pt is intubated, IV/IO is not available. What combo of drugs can be instilled in ETT? Hint V is Lean vasopressin, lidocaine, epi, atropine, na bicarb
Pt with acute MI with ongoing chest pain is unresponsive to 3 doses of nitroglycerin. Pt is given 4mg of morphine. Shortly after, BP is 88/60 and complains of chest pain, what do you do? give NS 250-500 mL fluid bolus
Pt has sinus brady with rate of 36, atropine has been given totaling 3mg, pt is confused and BP is 100/66, what now? start dopamine 2-20 ug/min (because BP is good)
Pt is in refractory VF and has received multiple shocks. 2Mg epi and an initial dose of lidocaine IV. A second dose of lidocaine is indicated, what is the recommended dose? .5-.75 mg/kg IV push
which of the following is contra-indicated for the administration of nitrates use of phosphdiesterase
what is the correct use of vasopressin in CA dose of 40 U IV/IO 1 time only, never instead of epi during asystole, and not for VF prior to the first shock
pt has wide complex tachycardia, rate is 138, BP 110/70 and asymptomatic, what action is recommended expert consult (pt is asymptomatic)
pt is in CA, VF and refractory to initial shock. What drug and dose should we give first epi 1mg
pt in pulseless VT, two shock and epi has been given, what is next drug and dose amiodarone 300 mg
your called to a code and CPR is ongoing, no shock is indicated and pt has asystole on monitor, what’s next establish IV or IO access, need to get drugs in
35 year old woman with palpitations, she is lite headed like Kay, stable tachycardia at 180, irregular narrow QRS, vagal manover did not work, IV is in place, what drug do you recommend to convert? adinosine (chemical cardiovert)
Pt with possible ACS, brady at 42 bpm, what is initial dose of atropine? .5mg
62 yr old male with left side weakness and difficulty speaking, what should we give him Fibrinolytic agent (TPA) (streptokinase), but not the asprin (never give asprin with TPA or heprin)
Nicotinic-2 receptor somatic (voluntary) receptor for skeletal muscle
ACH and skeletal muscle ACH is neurotransmitter for somatic nervous system at muscle/nerve junction, N2 is receptor
NE neurotransmitter of sympathetic division of nervous system, A, B1 and B2 are receptors
peripheral-acting muscle relaxants (2 classes) drugs that interact w/N2 and cause paralysis, depolarizing and non-depolarizing
depolarizing neuromuscular blockers (muscle relaxant) cause persistent depolarizing at motor so ACH cannot work, muscles twitch, but cannot respond
non-depolarizing neuromuscular (muscle relaxants) competitive inhibition aka antagonism with ACH for N2 receptor
what class of drugs are used for pt on ventilator for paralytic non depolarizing competitive antagonist
the non depolarizing muscle relaxant drugs are d-tubocurarine/curare (prototype), atracurium/tracrium and vecuronium/norcurum
d-tubocurarine/curare prototype non depolarizing, semi-synthetic muscle relax, side affects-releases histamine, bad cardio so not used anymore
atracurium/tracrium non-depolarizing peripheral muscle relaxant for surgery strong cardio probs, no histamine
vecruronium/norcuron none-polarizing peripheral muscle relaxant for surgery, metabolized in liver excreted by kidney
depolarizing muscle relaxants medication succinylcholine, competitive antagonist w/ACH met in plasma and liver, fast acting-short duration, peripheral, used mostly in ER for ET intubation
Succinylcholine hazards/precautions releases histamines, cardio probs <BP, can interact with Halothane to cause MALIGNANT HYPOTHERMIA
direct acting peripheral muscle relaxants cantrolene/Dantrium, used for muscle spasms w/ MS, CP, malignant hypothermia and spinal cord injuries
what drug can cause malignant hypothermia succs, when mixed with general anesthetics like Halothane during surgery, usually in teen males
CNS muscle relaxants aka CNS sedatives drug carisoprodol/Soma, central acting muscle relaxant, used in TX of spastic from over exertion, trauma and nervous tension
somatic nerve fiber neurotransmitter and receptor are ACH and N2
Peripheral acting muscle relaxant d-tubocurarine/Curare uses what method of action non-depolarizing
peripheral acting muscle relaxant succinylcholine uses what method of action depolarizing
peripheral acting muscle relaxant dantrolene/Dantrium uses what method of action direct-acting
CNS muscle relaxants work at the level of the spinal cord, do not affect normal function of neuromuscular junction, all of the drugs cause varying degrees of sedation, IV or ET
do antibiotics cross the blood brain barrier no
antimicrobial agents selectively toxic, kill or inhibit microorganisms
antibiotic compounds produced by living organisms that kill bacteria
antibacterial inhibit or destroy bacteria
bacteriostatic antibiotic that inhibit bacteria
bacteriocidal antibiotic that kill bacteria
antibacterial therapy fails because of insensitive to DX, mixed infection, wrong drug, developed resistance, super infection, inadequate regimin, unable to penetrate infec site, no supportive measures, toxicity or hypersensity
categories of antibiotics beta-lactams, neg-pos organisms, broad spectrum and sulfonamides
beta-lactam antibiotics drugs are penicillins, cephalosporins, carbapenams and monobactams
autolytic mechanism of action of beta-lactams, inhibit cell wall synthesis in bacteria, causing lysis of cell
natural penicillins are penicillin G and V, G is not stable in acid so IV, V is acid stable so can be PO, includes streptococci, gentococci and meningcocci
beta-lactamase inhibitors clavulanic and sulbactam, NOT AN ANTIBIOTIC, but combines to broaden antibacterial spectrum
beta-lactamase inhibitors drug Augmentin, amoxicillin combined with betalactamase inhibitor
best drug for staph and nosocomial infections aminoglycosides/gentamicin, very toxic antibiotic, tough on body, TX of pseudomonas, staph and nosocomials
adverse effects of aminoglycosides/Gentamicin ototoxicity(hearing loss), nephrotoxicity and renal dysfunction, neuromuscular blockade can result in resp paralysis
first line TB drugs are (RISE) rifampin/Rifadin, isoniazid/Nydrazid, streptomycin, ethambutol/Myambutol
best drug for TB prevention if pt has been exposed Isoniazid (Inti)
TX for TB drug combos all 4 drugs for 2-3 months, then combo of 2 for additional 9 months
anti-fungal for Candida is nystatin
amphotericin B/fungizone valley fever
ketoconazole/nizoral most common anti-fungal, TX for chronic candidiasis, bad side effects, man boobs like mark
acyclovir/zovirax antiviral, TX for cold sores, CMV, mono (Epstein-Barr)
ribavirin antiviral for RSV (need spag unit)
aerosolized antimicrobials are pentamadine (for PCPneumonia), Riboviron(RSV), Thrombomycine/TOBI (CF)
best antibiotics for for CF TOBI, 28 days on 28 off, for TX and prophylactic of P-aerafinosa, also can us gentamiocen (chronic colonization)
influenza drugs relenza, antiviral that only works if taken at first onset
bonus question, who discovered penicillin, meds biggest discovery ever? Flemming
pulm infections effectively treated with aerosol antibiotics are TB, spergilloma and coccidiomycosis
antiprotozoal method of action inhibit RNA, DNA and protein synthesis
antiprotozoal antibiotic pentamidine, used in TX of P-pneumonia (aids)
Question Answer
Correction of metabolic alkalosis may involve which of the following? D) I, II, and III I. Restoring normal fluid volume II. Administering acidifying agents III. Restoring normal K+ and Cl– levels
In order to eliminate the influence of PCO2 changes on plasma HCO3- concentrations, what additional measures of the metabolic component of acid-base balance can be used? D) Standard bicarbonate
Which organ system actually excretes H+ from the body? A) Kidneys
An ABG result shows the pH to be 7.56 and the HCO3- to be 23 mEq/L. Which of the following is the most likely disorder? D) Respiratory alkalosis
What compensates for a metabolic alkalosis? B) Hypoventilation
Based on the following ABG results, what is the most likely acid-base diagnosis? pH = 7.43, PCO2 = 39 mm Hg, HCO3- = 25.1 mEq/L A) Acid-base status within normal limits.
What explains the lack of an increased anion gap seen in metabolic acidosis caused by HCO3- loss? A) For each HCO3- ion lost, a Cl- ion is reabsorbed by the kidney.
Based on the following ABG results, what is the most likely acid-base diagnosis? pH = 7.08, PCO2 = 39 mm Hg, HCO3- = 11.8 mEq/L A) Acute metabolic acidosis
What affect does hyperventilation have on the closed buffer systems? B) Causes them to release more H+.
A patient has a confirmed metabolic acidosis with a normal PCO2. What inference can you draw from these findings? A) A ventilatory disorder must coexist.
What drives the bicarbonate buffer systems enormous ability to buffer acids? D) Ventilation continually removing CO2 from system.
Based on the following ABG results, what is the most likely acid-base diagnosis? pH = 7.38, PCO2 = 21 mm Hg, HCO3- = 11.7 mEq/L B) Fully compensated metabolic acidosis
With partially compensated respiratory alkalosis, which of the following blood gas abnormalities would you expect to encounter? D) II, III, and IV II. Decreased HCO3- III. Decreased PCO2 IV. Increased pH
Fixed acids are produced primarily from the catabolism of which of the following? C) Proteins
A patient with a measured plasma HCO3- concentration of 24 mmol/L has an episode of acute hypoventilation, with the PCO2 rising from 40 to 70 mm Hg. What do you predict will happen acutely to the plasma HCO3- concentration? B) HCO3- will rise to about 27 to 28 mmol/L.
By comparison, how much fixed acid is produced in any given period compared to the volatile acid CO2? B) Less fixed than volatile.
Which of the following clinical findings would you expect in a fully compensated respiratory acidosis? I. elevated HCO3- III. pH between 7.35 and 7.39 I. elevated HCO3- III. pH between 7.35 and 7.39 I. elevated HCO3- III. pH between 7.35 and 7.39 A) I and III
What is the primary chemical event in respiratory acidosis? C) Increase in blood CO2 levels
A patient with Kussmaul’s respirations most likely has: A) metabolic acidosis.
What is the treatment for severe metabolic acidosis? D) NaHCO3- infusion
If the blood PCO2 is high, the kidneys will do which of the following? A) Excrete more H+ and reabsorb more HCO3-
Which buffer system has the greatest capacity? A) Bicarbonate
Of what use is the Henderson-Hasselbalch equation for a clinician? D) It allows validation of the reported values on a blood gas report.
Which of the following is FALSE about the relationship between chloride (Cl-) and bicarbonate HCO3- in acid-base balance? D) Activation of the NH3 buffer system enhances Cl- gain and HCO3 loss.
What is the main compensatory mechanism for metabolic acidosis? B) Hyperventilation
The majority of the acid the body produces in a day is excreted through the lungs as CO2. What happens to the H+ ions? D) They bind to an OH-forming H2O.
What are some causes of metabolic acidosis with an increased anion gap? II. Ketoacidosis III. Lactic acidosis IV. Renal failure C) II, III, and IV
Which of the following are components of the body’s nonbicarbonate buffer system? I. Hemoglobin II. Plasma proteins III. Organic phosphates IV. Inorganic phosphates D) I, II, III, and IV
What is the limiting factor for H+ excretion in the renal tubules? C) Insufficient buffers
Based on the following ABG results, what is the most likely acid-base diagnosis? pH = 7.35, PCO2 = 68 mm Hg, HCO3- = 34.3 mEq/L C) Fully compensated respiratory acidosis
In the face of uncompensated respiratory acidosis, which of the following blood gas abnormalities would you expect to encounter? I. Decreased pH III. Increased PCO2 B) I and III
What is a normal response of the body to a failure in one component of the acid–base regulatory mechanism? B) Compensation
Which of the following are potential causes of respiratory alkalosis? I. Anxiety III. Hypoxemia IV. Pain B) I, III, and IV
Which of the following is NOT a clinical sign of acute respiratory alkalosis? B) Depressed reflexes
The primary goal of acid-base homeostasis is to maintain which of the following? C) Normal pH
Compensation for respiratory acidosis occurs through which of the following? D) Increase in blood HCO3- levels
Which of the following accurately describes compensation for acid-base disorders? A) Kidneys take hours to days to compensate for respiratory disorders.
Primary metabolic alkalosis is associated with which of the following? A) Gain of buffer base
Using the Henderson-Hasselbalch equation, determine the accuracy of the gas below. To be considered accurate, it must be within 0.03 pH unit. pH = 7.22, PCO2 = 49 mm Hg, HCO3- = 20 mEq/L B) This gas is accurate as the calculated pH is 7.23.
What is the primary buffer system for fixed acids? B) HCO3-
What condition or treatment could cause iatrogenic respiratory alkalosis? B) Mechanical hyperventilation
Using the Henderson-Hasselbalch equation, determine the accuracy of the gas below. To be considered accurate, it must be within 0.03 pH unit. pH = 7.35, PCO2 = 77 mm Hg, HCO3- = 41 mEq/L A) This gas is completely accurate.
Based on the following ABG results, what is the most likely acid-base diagnosis? pH = 7.01, PCO2 = 71 mm Hg, HCO3- = 16.3 mEq/L C) Combined respiratory and metabolic acidosis
What are the major mechanisms responsible for maintaining a stable pH despite massive CO2 production? I. Isohydric buffering III. Pulmonary ventilation D) I and III
A patient who has fully compensated respiratory acidosis becomes severely hypoxic. If her lungs are not too compromised, what might her gases now appear to be? B) Fully compensated metabolic alkalosis
The numerator of the Henderson-Hasselbalch (H-H) equation (HCO3-) relates to which of the following? C) Renal buffering and excretion of fixed acids.
Based on the following ABG results, what is the most likely acid-base diagnosis? pH = 7.43, PCO2 = 20 mm Hg, HCO3- = 12.6 mEq/L C) Fully compensated respiratory alkalosis
A patient has a bicarbonate concentration of 36 mEq and a PCO2 of 60 mm Hg. What is the approximate pH? C) 7.4
Correction of acute respiratory acidosis is accomplished by which of the following? B) Increasing alveolar ventilation
Which of the following systems is primarily responsible for the buffering of fixed acids? B) HCO3-
Question Answer
Indications for bipap Avoid intubation Relieve symptoms Improve gas exchange Improve QOL
Hazards of bipap Barotrauma from pressures Facial sores Decreased VR and CO Hyper/hypo ventilation.
Indications of Oxygen Therapy Documented hypoxemia Suspected hypoxemia Severe Trauma Acute MI (Keep alarm at 95%)
Hazards of Oxygen Therapy Depression of Ventilation (Pa02> 60) ROP (PaO2 > 80 mmHg) Nitrogen Washout (FiO2 > 50%) Oxygen Tozicity (FiO2 > 50%)
Indications for Pulse Oximetry Adequacy of arterial saturation Assess response to treatment
Hazards of Pulse Oximetry Pressure sores Electrical shocks
Indications for suctioning To remove secretions Ineffective cough
Hazards of suctioning hypoxemia dysrhythmia mucosal tears infection
Indications for SVN/MDI Deliver medications mobilize secretions Decrease WOB
Hazards of SVN/MDI Bronchospasm (allergic to med) Tachycardia, Infection Hyperventilation
Indications for IS Conditions predisposing to atelectasis (abd/thoracic sx, post-op) Treat atelectasis Patients w/Restrictive lung ds
Hazards of IS hypoxemia from removal of mask Hyperventilation, fatigue low risk of barotrauma
Indications for IPPB Lung Expansion (VC<10ml/kg, neuro,atelectasis) Short-term NIV Deliver meds (unable SVN)
Hazards of IPPB Barotrauma from pressures Decreased VR, CO Increased ICP
Indications of EzPap Prevent or treat atelectasis dec air trapping mobilize secretions Optimize med delivery
Hazards of EzPap Barotrauma from pressures Hemodynamic compromise Increased ICP Gastric Distention
Indications for CPT Mobilize secretions (>25 ml/day) Remove soft foreign bodies Atelectasis from mucus plugging Improve V/Q by turning
Hazards of CPT Hypoxemia Vomiting and aspiration Pain/injury to ribs hypoxemia
Indications for Mechanical Ventilation IVF (VC<10 ml/kg, MIP -20 cmH20, RSBI > 105, VT < 5ml/kg, RR>35) AVF (ph < 7.25, PaCO2 > 55) Apnea and Prophylactic (CHI, Smoke) Severe Oxygenation Issue (P/F < 200, PAaO2>350 on 100%)
Hazards of Mechanical Ventilation Decreased CO, VR Increased ICP Barotrauma Decreased splanich or gastric perfusion
Indications for ABG evaluate PaCO2 and A/B balance Assess response to tx Monitor severity of disease Severe SOB
Hazards of ABG Arteriospasm Hemorrhage Trauma Pain, infection
How do you treat Respiratory Acidosis? increase the RR, PS, VT or decrease the dead space Ex A/C, A, C
How do you treat respiratory alkalosis? decrease the RR, PS, VT or increase the dead space
VC-CMV Preset Vt, Preset Rate, Pressures Vary If patient overbreathes, they get preset Vt. Hazard is respiratory alk. Yu need to switch to SIMV if patient is overbreathing the ventilator and alk.
PC-CMV Preset Pressure, Preset Rate, VT varies Indicated when PIP >40 cm, Plat >30. If patient overbreathes they get preset pressure. If they don’t over breathe they get back up rate Ex: A/C, C, A
SIMV Preset Vt, Preset Rate, Pressures Vary If it is in between a mechanical breath, patient will get their own tidal volume. If it is time for a machine breath patient will get set Vt.
PSV Preset Pressure, Vts vary (2 pts) Set to achieve Vt 5-7 ml/kg and RR < 30 Only applied to spontaneous breaths Dec WOB, and Inc Spont Vt (3 pts)
CPAP/PEEP Preset pressures, Vt vary (2 pts) Indicated PaO2 is <60 on FiO2 >50%
PRVC Preset Vt, Preset Rate, Preset HPL Pressures vary Machine measures exhaled Vt. Will increase or decrease IP (PC) by 3 cmH20 to get desired Vt. The pressure stays < 5 HPL
Troubleshoot Vent: HP alarm HP alarm: kinked tubing, herniated cuff, bronchospasm, Pneumothorax, secretions
Troubleshoot Vent: LP alarm LP Alarm: loss sys press (gas, power), loss circuit pressure (ett cuff, loose humidifier, loose circuit), premature term (Ex PF)
Troubleshoot Vent: FiO2 alarm FiO2 alarm: inapp alarm or Fi02 setting, bad cell
Names and dosages for Albuterol (Proventil/Ventolin), 0.5% solution: 0.5 mL=2.5mg or 90 mcg/puff.
Receptor/MOA for Albuterol B1 and B2: B1 increases HR and myocardial contractility. B2 Relaxes bronchial smooth muscle, stimulates mucociliary activity
Hazards of Albuterol Palpitations, hypertension, nervousness, tremors, hypokalemia, hyperglycemia
Names/dosage of Xopenex Levalbuterol, 1.25mg, .63mg, .31mg
Receptor/MOA of Xopenex B1 and B2: B1 increases HR and myocardial contractility. B2 Relaxes bronchial smooth muscle, stimulates mucociliary activity
Hazards of Xopenex hypokalemia, tachycardia, hyperglycemia
Names/dosage of Atrovent Ipratropium Bromide, 0.02% solution = .5mg 18 mcg/puff
Receptor/MOA of Atrovent Muscarinic = blocks AcH from binding to M receptors allowing dilation of airways
Hazards of Atrovent Dry mouth, pupillary dilation,increased IOP, and HR
Names/dosage of Duo Neb Alubuterol + Atrovent 0.5 mg Atrovent, 3.0 mg Albuterol
Receptor/MOA of Duo Neb M, B1, B2: Muscarinic = blocks AcH from binding to M receptors allowing dilation of airways, B1 increases HR and myocardial contractility. B2 Relaxes bronchial smooth muscle, stimulates mucociliary activity
Hazards of Duo Neb Palpitations, hypertension, nervousness, tremors, hypokalemia, hyperglycemia hypokalemia, tachycardia, hyperglycemia Dry mouth, pupillary dilation, Increased IOP and HR
Names/Dosage of Intal Comolyn Sodium, 20 mg/ampule, 800 mcg/puff
Receptor/MOA of Intal Mast cells/inhibits degranulation of mast cells
Hazards of Intal Cough, wheezes
Names/dosage for Mucomyst N-Acetylcysteine, 10%=6ml, 20%=3ml
Receptor/MOA for Mucomyst Disulfide bonds/breaks up bond and replaces with sulfhydryl-thins secretions
Hazards for Mucomyst Bronchospasm, stomatitis, nausea, rhinorrhea
Names/Dosage for Singulair Montelukast, 4 mg, 5 mg and 10 mg tablets
Receptor/MOA for Singulair Blocks CysLT1 on leukotrienne receptor/blocks bronchoconstriction and mucous production
Hazards of Singulair headache, infection
Names/Dosage for Advair Serevent/Fluticasone, DPI=100mcg/50mcg, 250mcg/50mcg, 500mcg/50mcg
Receptor/MOA for Advair B2 and steroid receptor: B2=Relaxes bronchial smooth muscle, stimulates mucociliary activity, Glucocorticoid/steroid binds to receptor and helps regulate transcription of anti-inflammatory substances-↓ swelling

Question Answer
Primary organ used to metabolize medications? Liver
Primary organ used to eliminate medications from the body? Kidney
Where does an adrenergic medication work? It works on nerve fibers that are stimulated by norepinephrine (NE) or epinephrine-Nerves of the Sympathetic Branch of the CNS.
Where does a cholinergic medication work? It works on nerve fibers that are stimulated by acetylcholine (ACh)-Nerves of the parasympathetic Branch of the CNS.
How does a Sympathomimetic medication work? It enhances the adrenergic response of the sypathetic nerves.
How does a Parasympatholytic medication work? It blocks the cholinergic response of the parasympathetic nerves.
What is an Orphan drug? A drug that is developed for a rare disease that may not recover the cost of development.
What are the three phases of drug action? Pharmaceutical-Dosage/Administration Pharmacokinetic-Absorption/Metabolism/Elimination Pharmacodynamic-Targets site/Effects
What are the advantages of the inhalation route of drug administration? -Smaller doses -Fewer/less severe side effects -Rapid onset -Targeted to the respiratory sys. -Painless -Safer -Convenient
What is the Therapeutic Index? The difference between therapeutic and toxic concentrations of a drug.
What is the difference between Affinity and Efficacy? Affinity is attraction. Efficacy is the ability to produce a desired effect.
What is Tachyphylaxis? Diminishing responsiveness to a drug after routine usage.
What is a Corticosteroid? It is an anti-inflammatory drug which inhibits the activity and number of inflammitory cells. Commonly used for asthma, COPD and rhinitis.
What are the three categories of Nonsteroidal Anti-Asthma Agents? 1)Mediator Agonists-Blocks histamine/prophylactic 2)Anti-Leukotrienes-Inhibits leukotrine formation/prophylatic 3)Monoclonal Antibodies-Decreases mediators in allergic response
What is a Xanthine? Promotes bronchodilation by inhibiting the breakdown of Beta 2 agonists-allows the drug to work longer. Also increases ventilatory drive and expiratory flow rates-reduces air trapping.
What is the result of stimulating alpha receptor sites? Vasoconstriction & Increased B/P
What is the result of stimulating Beta-1 receptor sites? Increased HR & Increased force of cardiac contractions
What is the result of stimulating Beta-2 receptor sites? Bronchodilation
What three physiological changes occur in the lungs as a result of histamine release? Secretions Edema Bronchoconstriction
Name the three bronchodilators recommended for continuous nebulization? Albuterol Levalbuterol (XopenX) Terbutaline
what is meant by parenteral administration? Given intravenously (IV)
What are the possible adverse effects of sympathomimetic bronchodilators? -Tremors -Palpitations -Tachycardia -Headache -Hypertension -Nervousness -Dizziness -Nausea -Vomiting Worsening V/Q Mismatch
What is the keyhole theory? Bronchodilators begin with a catecholamine nucleus and as they progressed the amine side got longer making it look like a key.
What is the difference between “Cidal” & “Static” antimicrobial agents? Cidal-Kills the pathogen Static-Inhibits growth/spread of pathogen
What are common adverse side effect of corticosteroids? -Oral thrush (candida) -Hoarseness -Bronchoconstriction -Cough
Mucolytics should be accompanied by what companion drug? Bronchodilator
What are common side effects of of mucolytics? -Bronchospasm -Rhinorrhea -Airway obstruction
What are the clinical uses of Xanthines? -COPD -Asthma -Neonatal apnea
What are some of the possible side effects for Xanthines? -Tremors -Tachypnea -SVT -Hypotension -Diuresis
What are some of the possible complications of using diuretics? -Vol depletion -Hypokalemia -Acid-base disorders -Hyperglycemia -Ototoxicity (hearing imparement)
Acetaminophen Tn: Tylenol Cat: Non-narcotic Analgesic Ind: Anti-pyretic
Meperidine Tn: Demerol Cat: Narcotic/Opioid Ind: Pain
Morphine Tn: Cat: Narcotic/Opioid Ind: Pain Add: Vasodilator
Cefazoline Tn: Ancef Cat: Antibiotic
Ceftriaxone Tn: Rocefphin Cat: Antibiotic (broad)
Levofloxacin Tn: Levaquin Cat: Antibiotic
Tobramycin Tn: TOBI Cat: Antibiotic
Vancomycin Tn: Cat: Antibiotic Add: Tx for MRSA
Amphotericin B Tn: Fungizone Cat: Antifungal
Haloperidol Tn: Haldol Cat: Antiphsycotic
Acyclovir Tn: Zovirax Cat: Antiviral
Rifampin Tn: Cat: Anti-tuberculin Add: Tx TB
Formoterol & Budesonide Tn: Symbicort Cat: Bronchodilator & Corticosteroid
Salmeterol & Fluticasone Tn: Advair Diskus Cat: Bronchodilator & Corticosteroid
Albuterol Tn: Respolin (DPI) Aerolin (HHN) Proventil (MDI) Cat: Bronchodilator
Epinephrine Tn: Bronkaid Cat: Bronchodilator/Cardiac Add: Status Asthmaticus Cardiac arrest
Levalbuterol Tn: XopenX Cat: Bronchodilator Add: Less cardiac effects
Salmeterol Tn: Serevent Cat: Bronchodilator
Albuterol & Ipatropium Bromide Tn: Combivent (DPI) DuoNeb (SVN) Cat: Combo bronchodilator
Atropine Tn: Cat: LABD/Cardiac Add: Dysrrhythmic Agent
Ipatropium Bromide Tn: Atrovent Cat: LABD
Tiotropium Bromide TN: Spiriva HandiHaler Cat: LABD
Belcomethasone Tn: Vanceril QVAR HFA (DPI) Cat: Corticosteroid
Fluticasone Tn: Flovent Rotadisk (DPI) Flovent (MDI) Cat: Corticosteroid
Methylprednisone Tn: Solu-Medrol (IV) Cat: Corticosteroid
Chlorothaiazide Tn: Diuril Cat: Thiazide Diuretic Add: For CHF/Hypertension
Furosemide Tn: Lasix Cat: Loop Diuretic
Mannitol Tn: Cat: Osmotic Diuretic Add: Used to reduce ICP
Amiodarone Tn: Cat: Dysrrhymic Agent
Digitalis Tn: Digoxin Cat Inatropic Agent
Acetylcysteine Tn: Mycomyst Cat: Mucolytic Add: Also used for acetaminophen overdose
Atratracurium Tn: Tracrium Cat: NMBA-Paralytic Ind: Mech Ventilation
Cisatracurium Tn: Nimbex Cat: NMBA-Paralytic Ind: Mech Ventilation
Vecuronium Tn: Norcuron Cat: NMBA-Paralytic Ind: Mech Ventilation
Succinylcholine Chloride Tn: Anectine Cat: NMBA-Paralytic Ind: Intubation Add: Only Depolarizing agent avail
Cromolyn Sodium Tn: Intal Cat: NSAID Ind: Prophylaxis Add: Mediator Antagonist
Montelukast Sodium Tn: Singulair Cat: NSAID Ind: Prophlaxis Add: Leukotriene Mod.
Nedocromil Sodium Tn: Tilade Cat: NSAID Ind: Prophylaxis Add: Mediator Antagonist
Naloxone Tn: Narcan Cat: Respiratory Stimulant Ind: Drug Overdose
Diprivan Tn: Propofol Cat: Sedative/Hypnotic
Ketamine Tn: Ketanest Cat: Sedative/Hypnotic
Lorazepam Tn: Ativan Cat: Sedative/Tranquilizer Add: Benzodiazepine
Midazolam Tn: Versed Cat: Sedative/Tranquilizer Add: Benzodiazepine
Nitroglyercin Tn: NTG Cat: Vasodilator
Nitroprusside Tn: Nipride Cat: Vasodilator
Dopamine Tn: Cat: Vasopressor
Norepinephrine Tn: Levophed Cat: Vasopressor
Aminophyline Tn: Cat: Xanthine (IV) Ind: COPD, Asthma, Neonatal Apnea
Theophyline Tn: Cat: Xanthine Ind: COPD, Asthma, Neonatal Apnea
How do sympathomimetic drugs work? They stimulate adenyl cyclase to convert ATP to cyclic AMP-Bronchodilation/inhibits histamine
How do parasympatholytic drugs work? They block the guanyl cyclase which keeps GTP from becoming cyclic GMP-Bronchoconstriction/histamine release
Why can’t catecholamines be given orally? They breakdown by the enzyme COMT in the digestive tract.
Question Answer
A 6 sec capillary refill indicates what condition? Normal capillary refill is less the 3 sec. Slow capillary refill indicates decreased perfusion
A non-rebreathing mask reservoir completely deflates during a pt. inhalation. How would you forrest this? A reservoir bag should stay at least 1/3 full during breathing cycles. If if you notice collapse you should increase the flow.
Question Answer
Indications for IS are presence of atelectasis, predisposition for atelectasis ie: upper ab or thoracic surgery, or surgery to COPD pt, pt with restrictive lung defect ie: quad or diaphragm problem
Contraindications for IS unconscious, uncooperative or uncoordinated pt, inadequate VC less than 10 mL per Kg or IC less than 70 percent
Hazards and complications of IS are hyperventilation and resp alkalosis, pain, pulm barotraumas, exacerbation of bronchospasm, fatigue, ineffective unless performed as ordered, inappropriate as sole treatment for lung collapse or consolidation
The three types for Incentive spirometers are flow dependent (ball), volume displacement (bellows), photoelectric (combined flow and vol displac)
Voldyne spirometers flow dependent, 1 tube with float, slow deep breath, keep float in set range, range is 0 to 4000 mL
Triflow three tubes with floats, flow dependent, highest of the three x seconds held equals total volume
Volurex bellows volume displacement, range is to 4000 mL
Spirocare photoelectric, must have electric source and gives read out, combination volume displacement and flow dependent
SMI is sustained maximal inspiration aka incentive spirometry, mimics natural sigh, visual feedback to patient, increases pulm press and insp volume
The three phases of hyperinflation therapy are planning, implementation and follow-up
Preliminary planning for IS includes pt screening and baseline assessments, establishing explicit pt outcomes
Pt therapeutic outcomes for IS should include absence or improved atelectasis, decreased RR, norm pulse, norm or improved BS, increased SPO2, VC and PEF, restoration of FRC or VC, improved cough, normal CXR, improved P(A-a)O2
Implementation of IS includes Attainable goals with moderate effort set by RT, observation of pt performance by RT, good pt instruction
Follow-up with IS should include check to be sure pt is using IS correctly
What pt need to be screened for IS and given a baseline assessment upper ab or thoracic surgery patients
IS hold is how long 5 to 10 seconds
If pt has trouble holding 5 seconds in IS what should RT do add one way valve
If pt does not rest between maneuvers during IS, what problem may develop pt does not breath deep enough and can develop resp alkalosis
Pt monitoring during IS therapy should include frequency of sessions, breaths per session, volume and flow achieved, breath hold time maintained, spot check pt compliance, device in reach of pt, increase volumes ea day, vitals and BS, pt motivation and effort
Lung expansion therapy includes IPPB, IS, CPAP, PEP
The most common serious problems seen in pt after thoracic or abdomen surgery is atelectasis, acute resp failure and pneumonia
The two primary types of atelectasis seen in post op are reabsorption atelectasis and passive atelectasis
Reabsorption atelectasis is mucus plugs prevent ventilation, air trapped gas is absorbed into blood and alveoli then collapse
Passive atelectasis is persistent small VT causes distal alveoli to collapse from lack of ventilation
Lobar atelectasis is severe form of atelectasis seen in about 5 percent of pt usually caused by a large mucus plug in pt with low VT and excessive secretions
What is the most common cause of atelectasis in the hospital pt does not take periodic deep breath and fully expand lungs.
Indications for lung expansion therapy are post op, neuromuscular, sedation, spinal cord injury, bedridden from major trauma
During the first 48 hours post op, what happens to the lungs progressive decrease in FRC
Decreased FRC is associated with alveolar collapse in what area of the lung basal or dependent
Atelectasis causes what to happen to V/Q ventilation perfusion mismatch
What clinical signs does RT look for in pt history for atelectasis recent surgery, history of lung disease, smoking
Physical signs of atelectasis are, increased RR, fine late inspire crackles over region affected, bronchial BS, diminish BS tachycardia if hypoxemia present
How does rt confirm atelectasis CXR opacity, displaced interlobal fissures, crowded pulm vessels, air bronchograms, elevated diaphragm, tracheal shift
Lung expansion therapy increase lung volume by what increasing transpulmonary press gradient
Proper use of IPPB requires careful pt selection, indications be specifically defined, treatment porpertly administered and monitored by trained RT
IPPB is the application of inspiratory positive pressure to spontaneously breathing patients as an intermittent short term modality never as a prophylactic
How long does an IPPB treatment last 15 to 20 minutes
During an IPPB treatment, positive pressure is transmitted from the alveoli to where pleural space
Indications for IPPB need to improve lung expansion, atelectasis when IS or CPT not working, high risk for atelectasis but unable to cooperate, pt who only needs 1 therapy instead of multiple modalities, inability to clear secretions and other modes fail, short term vent
Contraindications for IPPB pneumothorax, ICP greater 15, unstable hemodynamics, active hemoptysis, tacheoesophageal fistula, recent esphogeal surgery, TB, CXR with blebs, recent surgery to face or head, hiccups, air swallowing nausea
Hazards to IPPB increased airway resistance, barotraumas, nosocomial infection, resp alkalosis (most common) pco2 down ph up, hyperoxia, impaired venous return, gastric destention if pt not alert, airtrapping psychological dependence
4 steps to administering IPPB includes 1 planning, 2 evaluating alternatives, 3 baseline assessments, 4 implementation
Preliminary planning for IPPB therapy includes determining need, base therapeutic outcome on diagnostic information and as explicit and measurable as possible, significant atelectasis, reduced VC less than 10 mL/kg,at risk pts who need assistance breathing but not mech vent
Potential outcome to IPPB therapy are improved VC, increased FEV1 or peak flow, enhanced cough, improved CXR, BS and oxygenation, favorable subjective pt response
What does RTT look for when evaluating alternatives to IPPB cheaper method available, if not, document, if so, document and change method
Baseline assessment in IPPB should include what vitals, auscultations, observation of pt appearance sensorium (LOC), include specific assessment to individual identified clinical goals
Implementation of IPPB should include what 6 steps 1 infections control, 2 equipment prep, 3 patient orientation, 4 pt position, 5 initial application, 6 adjusting parameters
An example of IPPB outcome set for a pt with post op atelectasis would be spontaneous IC of 70 percent of predicted, improved CXR, decreased late inspire crackles, reduced RR under 25 per min
Infection control in IPPB includes hand washing, CDC universal precautions (gloves), CDC TB airborne gloves gown hepamask, pt infection control posted, only sterile dilutes and meds, disinfect reusables, change nebs or disinfect 24 hrs on continuous, rinse in sterile water only
Equipment preparation for IPPB when and for what before taking to pt room, for leaks
Patient orientation in IPPB should include explain dr order, what IPPB does, how it feels, what to expect
Patient position in IPPB is semi fowler with no slouching supine if pt unable to semi fowler
Initial application of IPPB includes insert past teeth, lips seal, set machine so breath can initiate with minimal pt effort, adjust to -1 t -2 (system check) system press at 10 move slowly to 15, 6 to 8 breaths per min, 2 to 4 times longer exp than insp
What happens to IPPB if there is a leak it shuts off
99 percent of the time a leak can be fixed in IPPB with what nose clips
What should RTT do if mouth wont seal in IPPB use CPAP mask
When a CPAP mask is used in IPPB why does an NG tube need to be installed so air does not enter stomach
Post treatment assessment of IPPB includes repeat pt assessment, vitals, BS, sensorium, untoward effects and specific clinical follow up, did pt meet goals, frequency based on response to therapy
How often should acute care pt be reevaluated for IPPB on dr orders, based on pt response to therapy, every 72 hours or with any change in status
Record keeping when discontinuing IPPB should be sucking but complete, include pre and post assessment, untoward effects need to notify dr, nurse and noted
The 5 things to monitor on the machine during IPPB are 1sensitivity, 2 peak pressure, 3 flow settings, 4 fio2 and 5 I:E ratio
The 12 things to monitor on a pt during IPPB therapy are RR and VE, peak flow or FEV1/FVC, pulse and rhythm, sputum quantity, color, consistency, odor, mental function, skin color, BS, BP, SPO2 if hypoxia, ICP, CXP, subjective pt response
What do large negative pressure swings early in inspiration indicate in IPPB sensitivity or trigger setting to low, RTT should increase sensitivity
in what pt settings would IS be found critical care, acute care inpatient, extedned care and skilled nursing home, home care
Bird machine cycles prematurely 1. Most common is pt obstructing mouthpiece with tongue, 2. flow to high, 3. pressure to low
Bird machine cycles on and off rapidly aka auto cycling 1. most common is sensitivity 2. Coach pt about breathing
Bird machine aspiratory tie is to long 1. Flow is to low, 2. Leak in circuit probably pt mouthpiece or pt needs nose clips, 3. Pressure to high, 4 coach pt to take exp pause of 3 seconds at the end of each breath, this will help extend expiration
Pressure manometer indicates high negative pressure prior to inspiration adjust sensitivity
Pressure manometer hesitates or rises erratically during inspiration flow is to low
Bennet cycles prematurely pt abstracting mouthpiece or pressure set to low
Bennet cycles on and off rapidly coach pt how machine works…only cycles when it senses a breath, obstruction or kinked tube, senility to high, Rate control on? Turn off rate control.
Bennet inspiratory time to long check peak flow control is fully clockwise, check for leaks , pressure to high, coach pt to take exp pause
Bennet ventilator fails to cycle off flow to low or leak in pt circuit
The most accurate way t measure inspired volumes is volume displacement
Three methods of volume measurement used in IS are timing the duration of flow, volume displacement and photoelectric
Gas pressure is regulated in the bird vent by magnetic attraction opposing gas pressure
Gas pressure in the Bennet vent is regulated by a low-pressure reducing valve
Needle valves are an effective way to control gas flow
Which incentive spirometer operates using volume displacement volurex
Which incentive spirometer operates using photoelectric sensor spirocare
A pt using a flow-dependent IS reaches a goal of 600 mL per second and holds for 3 seconds, what would the inspired volume be 1800 mL
An IPPB ventilator fails to cycle off, you suspect a leak, what would you check first pt ability to seal mouthpiece, pt nose, all circuit connections, exhalation valve
You are using a Bennett PR2 to give an IPPB, and want to increase the delivered tidal volume what should you do increase the pressure
When giving an IPPB treatment on a Bennet the vent triggers on and off rapidly, what do you do adjust sensitivity
Your attempting an IPPB with a Mark 7 and the circuit is assembled correctly but will still not trigger on, what do you suspect is the problem? flow rate has been turned off
What controls the FIO2 delivered in a Bennett PR2 operating in the source gas setting terminal flow control
When giving IPPB therapy using a Mark 7, changes in delivered FIO2 can be attributed to what venturi gate and pressure
If an IPPB ventilator fails to cycle in exhalation (off) the problem is ALWAYS a leak
A control on the Bennett PR2 that is designed to compensate for leaks is what terminal flow control
Which IPPB vent is designed primarily for home use Bennett AP5
Which IPPB vents can be used with apneic pts PR2, Mark 7, Mark 7A, Mark 8
When a pt attempts to trigger the IPPB ventilator on, a -8 cmH2O is recorded on the press manometer, what should the RTT should do adjust the sensitivity
Mark bird machines are pneumatically powered pressure controller for IPPB therapy, can be pressure cycled or on 7A and 8 can be time controlled or press cycled
The pressure chamber on the mark is located on the right side, gas press from the gas source builds and pressurizes pt circuit for delivery
The center body of the mark is the narrow casting of aluminum alloy that seperates the ambient and press chambers, gas source on top
sensitivity control on the mark is is located on the far left and controls pt effort, range is 0 to 10 below ambient press, ideal adjustment at -1 to -2, initiates inspiration
The flow rate control on the mark is the large dial in front on the center body, controls the flow of gas, high flow is 80 L per min
The expiratory timer control on the mark is the bottom dial on the center body and is used only in apnea pts.
The inspiratory pressure control of the mark is located on the far right side and sets the insp pressure
The expiratory flow control on the mark is FOUND ONLY ON THE MARK 8,a negative press control used to vent neonates, creates peep and neep
Time press trigger control on the mark is ONLY FOUND ON THE 7A AND 8, pneumatic switch that determines if the machine operates in pressure or timed
The air mix control on the mark is unique to the 7 and is the middle knob in the center body, pulling it out is the on off switch for the venturi venturi and controls FIO2
The steps to assembling the mark IPPB ventilator circuit are after explaining to pt and taking vitals, set up nebulizer, adjust press to sensitivity 10, flow 15, insp 10, pull air mix, increase insp to 15 during exp breaths only, take BS at 15, vitals, cough and BS when done
If a mark cycles prematurely during an IPPB what is usually the cause pt obstructing mouthpiece with tongue or flow to low or to high
Autocycling in the mark during IPPB usually is caused by setting is to sensitive, adjust
Inspiratory time is to long in the mark during IPPB increase flow, check for leaks, decrease press, give pt better instructions
Manometer in mark during IPPB indicates high neg pressure during inspiration adjust sensitivity
Manometer hesitates or jumps during inspiration in mark during IPPB increase flow
What is a PR2 Pneumatic power ventilator for hospital use, needs 50 psi gas source
What is the function of the Bennet valve on the PR2 on off switch, needs only .5 cmh2o to on
What is the AP5 electric powered home use pressure triggered, flow cycled machine
On off switch for the AP5 is toggle switch located under the manometer
Pressure control on the AP5 is located on the top right and uses a spring loaded disk and is limited to 30, but augmented by venturi
With help from the venturi, the AP5 can produce press of 75 to 90 liters per min
The nebulizer control on the AP5 is on the bottom right side, it operates contiuously and is controlled by a needle valve
How does RTT set the volume on the PR2? cannot set volume, only pressure
The inspiratory pressure control in a PR2 is the center knob between the monometers and sets the pressure, it reduces the incoming 50 psi to a safe working press, single stage reducer can be set 0-45
Air dilution control in the PR2 is located on the right side, top middle knob, and determines the FIO2
A pt with a VT of 700 is put on IPPB and 1 day has PIP of 30 two weeks later PIP is 50¬タルs, what is happening to his lungs lungs are getting stiff
The negative press control on the PR2 is never used during IPPB, it ventilates neonates and evacuates gas from pt circuit, located on the side, bottom of the middle two knobs
What are the accumulators on the PR2 on the top, direct the path of gas, left determines length of exp, right determines length of insp, middle phases insp and expir
Expiration timer on the PR2 is on the front right is never used in IPPB, lengthens the expiration time when used as ventilator
Inspiration nebulizer control on the PR2 is located on the bottom right side (on the side), and nebulizes meds, adjust to half open
The expiration nebulizer control on the PR2 is located on the bottom left (on the side) and is for exhalation of meds, adjust open just enough to mist nebulizer
Sensitivity control in the PR2 is located on the side, top right knob, controls patient effort to cycle on machine, uses needle valve
Terminal flow control on the PR2 is found only on the Bennet, located on the side, top left knob, helps cycle vet of when leaks are present, can compensate up to 15 liters, dilutes FIO2
Peak flow control on the PR2 is located on the bottom shaft and delivers pressure, vent clockwise, IPPB counter clock
System Pressure manometer on the PR2 is the meter on the left and reads the pt press in circuit
The control press manometer on the PR2 is the meter on the right and reads the press in the machine or the set press
What is the significance of the PR2 having 2 manometers both control and system manometers should match, if not, adjust pressures to match by turning insp press control up or down
Factors to consider that decrease VT when using pressure limited IPPB increased RAW, decreased CL, decreased insp press, increased flow like in COPD
Factors to consider that increase VT when using pressure limited IPPB decreased Raw, increased CL, increased insp press, decreased flow or increased press
Factors that increase inspiratory time in IPPB decreased flow, increased CL, decreased raw
Factors that decrease inspiratory time in IPPB increased flow, decreased CL, increased raw
Factors to consider when using a pressure limited IPPB vent effects on fio2 using terminal
CPAP is continuous positive airway press, elevates and maintains high alveolar and airway press through out a full breathing cycle
CPAP increases PL gradient in inspiration or expiration? both
Pressure during CPAP is 5 to 20 cmH20, pt must be breathing spontaneously
How does CPAP help resolve atelectasis unknown
Although it is unknown how CPAP helps resolve atelectasis, what factors probably contribute or have beneficial effects recruit collapsed alveoli via increase in FRC, decreased WOB due to increased CL, improved ventilation, increased secretion removal
Indications for CPAP are decreased FRC, decreased CL, cardiogenic pulm edema, atelectasis should be continuous because FRC will be lost after treatment ended, PAO2 less than 60 on FIO2 greater than 60
Hazards and complications of CPAP are barotraumas aka pneumothorax, decreased CO, Venous return or urinary output, or hypoventiltation, nausea, increased ICP
Patient circuit for CPAP includes gas source, flow meter 60 to 90 L per min, humidifier, reservoir bag to increase flow, mask or t tube, high and low press alarm, end press cap
What kind of a gas source does CPAP use usually an O2 blender
A pt on a CPAP for a couple of days and suddenly his high press alarm goes off, what is the most common reason? obstruction
What is the most common reason for a low pressure alarm in CPAP disconnect
During the planning stage of CPAP, what are the desired outcomes of the therapy improved BS, improved vitals, lover RR, resolution of abnormal CXR and restoration of normal oxygenation via SPO2 or ABG
Why is a CPAP pt in danger of hypoventilation pt must be able to spontaneously breath and blow off CO2
If an infant has been doing well on CPAP but suddenly his stats are falling what might the problem be mask is loose or out of place
What is the high and low press monitored in CPAP 2 and -2
What is the most common problem in CPAP a leak in the circuit causing a loss in pressure usually the mask
What can be done to eliminate the problem of gastric insufflations and aspiration in CPAP NG tube
What is the flow for CPAP 3 to 4 times a patients minute volume, should drop to 1 to 2 on inspiration
Bilevel positive pressure or BiPAP is another type of press ventilation that can be used on incubated or non intubated
Why is BiPAP popular for COPD pts copd¬タルer are hard to wean off mechanical vents, BiPAP is 1st choice,
Indications for BiPAP are home vent for neuromuscular, sleep apnea, COPD in ventilation crisis
What are the cycle settings for apnea pts time cycled in central sleep apnea, pt cycled in obstructive sleep apnea
Pressure settings for bipap are 10 and 5 or 10 and 4, can be remembered by ¬タワI am greater¬タン IPAP is always the greater number
IPAP is what pressure support in CPAP, augments tidal volume, calculation is 7 to 10 mL per KG of body weight
EPAP is what CPAP
Criteria for BiPAP is stable hemodynamics, cooperative pt, minimal airway secretions, no need for airway protection
What is the indication the Pt has reached optimal lung volumes in IPPB listen at lung base, if you hear aeration, you hear optimal lung volume
State two parameters on the IPPB that will affect VT pressure (best) and flow
If IPPB auto cycles, what is most likely cause sensitivity needs adjusting or rate control may be on
Why do COPD do well on BiPAP it helps blow off CO2
If pt has hard time cycling off machine what are steps to fix 1. lips-use flange or mask with NG tube, 2. Nose clip, 3. Flow
IPPB machine hesitates before cycles into inspiration what is most likely cause flow is to low
Dr Margo asks you your opinion about giving IPPB to a pt with air bronchograms what to tell her air bronchograms indicate mucus plugging aka secretion problem, pt needs bronchial hygiene and humidity with IPPB
Hyperventilation causes resp alkalosis
What is the most common problem associated with lung expansion therapy resp alkalosis
Dr Chris asks your opinion for lung expansion on a post op pt on FIO2 of 60% and PaO2 of 58, what do you suggest CPAP
Dr Gails asks your opinion for lung expansion on post op pt whit 67% PaO2 and PaCO2 of 58, what do you suggest BiPAP , pt needs help blowing off co2
Pt needs lung expansion but is not alert or is unable to cooperate, what do you suggest IPPB at 10-15 with monitoring, why-need alert pt for IS, PEP or CPAP
Alert pt, no secretion problems, VC greater than 15mL/kg or IC greater than 70% of expected, what should RTT choose IS
Alert pt with secretion problem RTT should choose PEP unless atelectasis persists, then add CPAP
What is primary difference in choosing a pt for CPAP or BiPAP CPAP for pt with decreased PaO2 but normal CO2 and BiPAP for pt wit trouble blowing of CO2