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Hemo chapt 13
WilliamWallace Hemo chapt 13
| Question | Answer |
|---|---|
| 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
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