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Hemo chapt 13

WilliamWallace Hemo chapt 13

CO2 bi-product of tissue metabolism, elimination is primary function of ventilation
capnometry monitoring exhaled CO2
capnography graphing CO2 measurements against time
what is the purpose of capnography to detect changes in metabolic rate, ventilator function (disconnect, apnea), efficiency of ventilation, CO2 transport and changes in perfusion
CO2 elimination depends on what QT, regional V/Q ratios, and emptying times of the lung regions
what lung area has an >V/Q ratio non dependent regions (so lower CO2)
what lung areas have a <V/Q ratio dependent lung regions, so higher co2 levels)
disease that cause >V/Q (and <CO2) pulm emboli (ventilation is good but not effective) >deadspace
disease that cause <V/Q ratio (and >CO2) atelectasis, asthma, pneumonia etc, poor ventilation in relation to blood flow cause (gas exchange is shunted)
PetCO2 end tidal CO2, exhaled CO2 is highest at end of exhalation, in normal lung is good estimate of PaCO2
what effect does mech vent, pulm disease and <perfusion have on PetCO2 >arterial-PetCO2 gradient
when is capnography used OR, ER, ETT placement, mech vent (disconnect), systemic perfusion monitoring during CPR (effectiveness)
VCO2 carbon dioxide production, CO2 over 1 minute, change provides info of metabolic rate and transport of CO2
>VCO2 fever (10% / 1C), trauma, peritonitis (25-50%), head trauma, rewarming after hypothermia, >carbs
<VCO2 <QT and <tissue perfusion, <RT vent output, <venous return, pulm emboli
VD deadspace volume, inspired volume that does not come in contact with capillary blood
VD/VT portion of VT that is wasted, 2 parts anatomic deadspace and alveolar deadspace
anatomic deadspace conducting airways, 2mL/kg IBW
alveolar deadspace alveoli that are ventilated but not perfused (emboli)
VD/VT calc (PaCO2-PetCO2)/PaCO2, normal is 25-30%
factors that >VD/VT ratio pt position (lateral or upright rather than supine), anesthesia (<VT), mech vent pts w/ >VE or <VT, emboli, hypoperfusion, or precapillary constriction
low and high flow equip problems that can lead to <oxygenation loose tube, canulla, humidifier or nipple connection, inadequate flow for pt need, blender malfunction
ventilator related problems that can lead to <oxygenation ETT malfunction, vent-circ malfunction, improper settings or modes
disease progression leading to impaired oxygenation ARDS, cardiogenic pulm edema, pneumonia, obstruction, asthma, COPD
onset of new clinical problems that lead to impaired oxygenation pneumothorax, atelectasis, aspiration, ETT (fistula, stenosis, malacia), nosocomial pneumonia, fluid overload, microatelectasis, bronchospasm, retained secretions, shock, sepsis, organ failure
interventions for impaired oxygenation suction, position changes, CPT, bronchoscopy, thorocentesis, peritoneal dialysis, hemodialysis, dx procedures, lines and tube placements
meds for impaired oxygenation bronchodilators, vasodilators, inotropic agents
DO2 oxygen delivery, norm 550-650 mL/min/m2, increased with ARDS and septic shock, decreased with <QT and <CaO2 calc (QT x CaO2 x 10)/2.2
majority of cellular oxygen is used for what? production of ATP (adenosine triphosphate), some for cell wall stability and chemical synthesis
factors that influence DO2 increased (hyperdynamic state) w/ARDS and septic shock, decreased with <CaO2, <QT,
factors that influence oxygen utilization metabolic rate (fever, disease, trauma, sepsis, nutrition), cell integrity (organ injury, sepsis), O2 availability, level of cellular toxins and byproducts (organ injury, sepsis)
how does critical pt compensate for >consumption of O2 increasing use of O2 reserve system
what are the O2 reserve systems QT and distribution, PaO2 and SaO2 value, and Hb, any 1 of the 3 is lacking, the other 2 will pick up the pace
how does tissue hypoxia occur dysfunction of 2 or more of the reserve systems
oxygen content, CaO2 total of oxygen carried in the blood, sum of O2 bound to Hb plus O2 dissolved in plasma
How much 02 is carried by Hb 99%
how much O2 is carried by the plasma 1% and is measured as PaO2
PaO2 reflects degree of Hb saturation and driving pressure of O2 between between systemic capillary tissue
CaO2 calc (Hb x 1.34)SaO2 + (PaO2 x .003), norm 16-20 vol%
mechanisms that result in inadequate oxygenation of pulm cap blood V/Q mismatch (most common), diffusion block (rare), hypoventilation, shunt (extreme <V/Q)
what is the major determinant of QT metabolism
what is the major determinant of peripheral distribution regional O2 consumption, temp, humoral agents
At what PaO2 level is QT affected <50 torr
how can RT do quick non invasive check of peripheral perfusion squeeze fingernail bed, pinks up in more than 3 seconds is indicative of PaO2<50
what is bodies protective mechanism when PaO2 falls below 50 (as with shock and sepsis or increase in sympathetic tone <blood flow to lower O2 consuming body regions like skin
ODC oxyhemoglobin dissociation curve
what is clinical significance of flat top portion of ODC changes in PaO2 have little effect on O2 content or Hb saturation when PaO2 is greater than 60 torr
what is clinical significance of S (steep) portion of ODC big effect on CaO2 and Hb saturation when PaO2 between 40-70, small changes in PaO2 cause big unload at tissue
P50 PaO2 of 27, Hb is 50% saturated
Left shift in ODC >PH, >affinity (Hb wont unload at tissue), <CO2, <23DPG, <VO2, <VCO2, caused by hyperventilation, hypothermia, hypophosphtremia
Right shift in ODC <PH, <affinity (Hb easily unloads at tissue), >CO2, >23DPG, >VO2, >VCO2
how does body normally compensate for left shift in ODC >QT
what PaO2 should assure SaO2 of >90% 60-80 torr
PaO2 >125 torr can cause what <blood flow to kidneys and brain from vasoconstriction
A-a indication of gas exchange efficiency, large value indicates resp abnormality (must know FIO2), norm is 5-10 torr on 21%, 30-60 torr on 100%, >35% is weaning indication, >350 indicates need for mech vent support (<350 weaning)
a/A ratio norm 90%, <74% is shunt (>V/Q) or diffusion defect, >35 is weaning indicator, can be used to finding FIO2 for desired PaO2
PaO2/FiO2 easy measure of oxygen efficiency, norm 350-450, <300 ALI, <200 ARDS (>200 is weaning indicator)
OI oxygen index, used as prognostic index of morbidity and mortality in infants using ECMO, advantage is it uses MAWP, >40 is 80% mortality, OI of 20-25 is mortality of 50%, OI >25 for 4 hrs rt should consider protective strategies
OI calc MAWP x FIO2 x 100/PaO2
QS/QT intrapulmonary shunt equation (intrapulmonary shunt is major cause of hypoxemia in ICU), > with atelectasis, pneumonia, ARDS, pulm edema, conj heart anomalies or arterial-venous anastomosis
classic shunt equation (QS/QT calc) (CcO2-CaO2)/(CcO2-CvO2)norm is 2-3%, or <10 if vented, 10-20 mild, 20-30 severe, >30% life threatening, <20 is weaning indicator
VO2 oxygen consumption, norm 2.86-4.29 mL/min/kg or 150-350mL/min, amount of O2 extracted at tissue at peripheral tissue in 1 minute plus uptake in lungs, used in respiratory quotiant
VO2 calc for indirect calorimetry (based on Fick principal) QT x (a-v) x 10 (measures cost of breathing)
VO2 measurements (2 ways) 1. Indirect calorimetry-hemodynamic state-O2 cost of breathing. 2. Direct calorimetry-inspired and expired gas volumes and concentrations
RQ-respiratory quotient uses VO2 to measure internal respiration, norm is .8
VO2 > hypertermia, exercise, seizures, shivering
VO2 < decrease O2 availability, <QT, <CaO2, or < use like with hypothermia cyanide poison
>DO2 for any reason means what >availability leads to >consumption as with ARDS, cardiogenic pulm edema, COPD, pneumonia
*Pvo2 norm 38-42, indication of O2 used by entire body and is affected by DO2 and VO2
<PvO2 caused by <QT, anemia, hypoxemia, affinity hypoxia (<PvO2 w/>SvO2), lactic acidosis (PvO2 <27)
PvO2 less than 27 torr is most often from what lactic acidosis
PvO2 >45 is most often caused by what bad sample, L-R shunt, septic shock, >QT, cyanide poison
where is VO2 the highest heart and brain (so PvO2 is lowest)
where is PvO2 sample drawn from pulmonary artery catheter, slowly over 1 minute for 3-5 ml's of blood
SvO2 norm 68-77%, measured from mixed venous sample (PvO2), a sensitive index of QT and tissue perfusion if VO2 is stable, small changes in PvO2 cause big changes in SvO2 and CvO2
how is SvO2 monitored fiber-optic reflective oximetry in a 5 lumen pulm artery catheter
SvO2 normals 67-77%, >77% is sepsis, L-R shunt, >QT, hypothermia, cell poison or wedged catheter, <60 is cardio decompensation, <50 lactic acidosis, <30 unconscious, <20 permanent brain damage
SvO2 with lactic acidosis <60%
factors that <SvO2 suctioning, shivering, RX, extubation, weaning, pos press therapy
<SvO2 indicates what deteriorating pulm gas exchange, >VO2 or <QT
A-V diff norm 4-6 vol%, must get simultaneous arterial and mixed venous draw
A-V >6% <QT, >VO2
A-V <4% septic shock, >QT, anemia, left shift in ODC causing >affinity
what is value of A-V diff helps determine effects of mech vent and peep on QT and evaluating the need for additional support
advantage of A-V over PvO2 reflects content difference rather than partial pressure
do pulse ox and PaO2 reflect tissue oxygenation no, only adequacy of pulm oxygenation
O2ER oxygen extraction ratio, norm 25-30%, a-v/CaO2, identifies portion of DO2 actually consumed, so indicates efficiency of circulation
principal of pulse ox spectrophotometric principal of lite absorption, red and infrared lite, measures functional saturation
co-oximeters principal detects methHb, COHb, deoxyhemoglobin and oxyhemoglobin, measures fractional saturation
conditions that cause false high pulse ox <perfusion from <QT or peripheral shunting, hypothermia, >bilirubin (>10), >COHb, >MetHb, cyanide poison (aka cardio-green) and methylene blue dye
locations for pulse ox fingers, big toe, ear lobe, forehead
when is pulse ox especially not accurate SaO2 <65, hypothermia, shock
lactic acid product of anaerobic metabolism, caused by DO2 or its use by tissue is not enough for metabolic demand and anaerobic metabolism kicks in
clinically how is lactic acidosis identified metabolic acidosis with >blood lactate concentrations (>lactate is a <O2)
blood lactate norm 1.7-2.0 mm/L, can go to 3.83 in pts w /shock, >8 is 90% mortality
beta-adrenergics affect on blood lactate increased lactate because of glycolysis
beta-blockers affect on blood lactate decreases
lactic acidosis tx bicarb, may increase lactate but because of redistribution of extracellular and intracellular lactate levels it doesn't worsen metabolic acidosis
cirrhosis and lactate because liver cant clear properly, can confirm presence of tissue hypoxia but not prognosis
REE Resting energy expenditure (24 hrs), measures metabolic rate
normometabolic with in 10% of predicted
hypometabolic <90% of predicted, from inadequate nutrition, causes muscle wasting
hypermetabolism >100% of predicted, from over nourishment, causes stress to major organs
Created by: williamwallace