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Carbon Dioxide Physiology & Hypoxemia
Nick Ford, DO
Carbon Dioxide
Two dissimilar atoms, one carbon atom with two doubly bonded oxygen atoms
Product of cellular metabolism in mammals
Can diffuse readily across cellular membranes
20 times as easy as oxygen
TransportModes of transportation in the blood
Bicarbonate (HCO3-)
Carbamino-hemoglobin
Dissolved CO2
In physical solution
DetectionCapnography
Utilizes infrared radiation to detect the carbon and oxygen atoms
Can detect esophageal intubation,Not detect endobronchial intubation
Elements of a Waveform
A-B: respiratory baseline, begin exhalation, dead space removing CO2-free gasB-C: continued exhalation, CO2 rich + mix dead spaceC-D: represents an approach to end-exhalation “alveolar plateau” with nearly constant rich CO2 gasD: point at which during exhalation that CO2 is at the highest concentrationD-E: inspiration
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Capnogram Variations
Sudden decrease to zero: Considered equipment problem, possible disconnect
Sudden decrease but not to zero:Consider a leak or an obstruction (partial) of airway or system
Exponential decrease:Increased dead space; possible causes are PE, cardiac arrest
Sudden increase:Consider tourniquet release
Gradual increase:Consider decreased minute ventilation, prolapsed expiratory valve
Ventilatory Control
Central ResponseMedulla
CN IX (glossopharyngeal)
Afferent limb
CN X (vagus)
Efferent limb
Increased PaCO2 tensionCauses CO2 passes through blood-brain-barrier
Acid (H+) is then formed creating acidosis d/t lack of buffering
MV increased w/ depth, rate increases
PaCO2 > 100mmHg will become a respiratory depressant
Peripheral Response
Hypoxemia Triggers Response
(PaO2 < 60mmHg)
Carotid bodiesRespond via ventilation
Aortic bodiesRespond via circulatory changes
ApneaNormal PaCO2 is 36-44mmHg (sea level)
ApneaResults in a 6mmHg increase CO2 during the first minute and 3mmHg increase CO2 for each subsequent minute thereafter
ETCO2 correlation to PaCO2Difference of 5mmHg in normal patient, difference increases with increased dead space
Apneic Threshold a point in which a maximum PaCO2 level is achieved without initiating spontaneous ventilation
Approximately 5mmHg below resting PaCO2
CO2 Response Curve
Plots MV in L/min along the Y-axis and PaCO2 mmHg along the X-axis
Rightward shift or a downward and rightward shift implies suppression of ventilation
Leftward and leftward and upward implies stimulation of ventilation
Effects on the CO2 Response
CurveLeftward
Occur d/t sensitivity to CO2 secondary to causes:
Metabolic acidemia
Central (anxiety, fear, ICP, cirrhosis)
Arterial hypoxemia
Rx
Doxapram, analeptics, strychnine
Rightward
Occur d/t sensitivity to CO2 secondary to causes:
Metabolic alkalemia
Normal sleep
Hypothermia
Denervated peripheral receptors
Drugs
Catecholamines, salicylates, aminophylline
Effects on the CO2 Response
CurveDownward and to the Right
Sedatives, barbiturates, volatile anesthetics, opiates
CO2 Response Curve
Control of Breathing http://rfumsphysiology.pbworks.com/f/h12-1.bmp
Hypercarbia
Hypoventilation
compliance
respiratory drive (2nd to central anesthetic effect)
Surgical positioning
CO2 Production
O2 consumption goes hand-in-hand with CO2 production
Hyperthermia (≥40°C) and MH
Hyperthyroid
Hyperalimentation
Shivering
Catecholamine release
- arterial carbon dioxide tension > 45mmHg
Hypercarbiacontinued… Dead Space
Ventilation
(Not participant of gas exchange)
PEEP may increase Zone 1 ventilation
Anesthesia circuit system33-46% intubated patient
64% when ventilated by mask
PE, thrombosis
Rapid, shallow respirations
Inspired CO2
Direct CO2 in circuit
Exhausted CO2 absorber
Rebreathing CO2 if fresh gas flow is low
Laparoscopic procedures with CO2 insufflation
Complications of Hypoventilation-
hypercarbiaRightward shift oxy-hemoglobin dissociation curve
PA pressure (CO2 is pulmonary Vc; most other locations a Vd)
Cerebral blood flow or 1ml/100g/min for every mmHg or PaCO2 from baseline
Acidosis
Arrhythmias
Epi-norepi release resulting in Splanchnic Vc, cutaneous Vd
Sympathoadrenal system stimulation in respond to cardiac/vascular depression
Preterm infants will have smaller increases in MV
Increased uterine blood flow at PaCO2 >60mmHg
Complications of Hyperventilation-
hypocarbiaLeftward shift oxy-hemoglobin dissociation curve
V/Q mismatch
Apnea
CBF, CO, Ca, coronary BF
OxygenOxygen exists as dissolved in the blood or as bound to hemoglobin
O2 Content = (1.34 x Hb) * SaO2SaO2: percentage volume of oxygen attached to hemoglobin
[CaCO2=(1.34 * HgB * Sat) + (0.003 *PaO2)]
Final electron acceptor in electron transport chain in mitochondria, permitting life/metabolism
Oxygen DetectionSaturation
Frequently measured by pulse oximetryFalse elevations
Carboxyhemoglobin and methemoglobin (until 85%) have similar absorption spectrum as oxyhemoglobin; can be difficult to detect difference
Fluoroescent lighting
False depressionTape
Blue nail polish
Dyes- indigo carmine, methylene blue
Partial pressureABG
HypoxemiaDefined simply as decreased arterial oxygen tension in the blood below 60mmHg
Oxygen dissociation curve
*Clin
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Oxygen dissociation
P50 Parital pressure of O2 where Hgb is 50% saturated
adults = 27mmHg
Infants = 19mmHg
A : nml mixed venous
B : 90% saturation = 60mmHg
Oxygen Dissociation
CurveLeft Shift
release of O2 from HgbAlkalosis
temperature
2,3-BPG
methemoglobin
Haldane effect: Deoxygenated blood (reduced Hgb) carries more CO2 in carbamino compounds – no Δ in PaCO2
Right Shift
release of O2 from HgbAcidosis
temperature
2,3-BPG (states d/t anemia, altitude, cirrhosis)
CO2
Bohr effect:O2-Hgb curve shifts d/t Δ’s in CO2
Mixed Venous O2 levels
Sampling from Pulmonary artery
Provides insight to tissue oxygen delivery
Normal PvO2 = 35-45mmHg with SaO2 65-75%
Factors that influence PvO2Loading/unloading of O2 by Hgb
O2 utilization
Hgb present
Cardiac output
Causes of Hypoxemia
Decreased FiO2
Hypoventilation
V/Q mismatch / Shunt
Absolute shunt (V/Q=0)
Diffusion abnormality
Anemia / Poisoning
Hypovolemia
Intrapulmonary derangements
Decreased FiO2Level adjusted too low
Possible mechanical or technical failure of anesthesia machine or ventilatory apparatus
N2O washoutN2O is 35x more soluble than nitrogen
The washout occurs as N2O leaves the bloodstream faster than O2 can enter, thereby dilluting the PAO2 and creating hypoxia
HypoventilationRespiratory Depression
Drugs
Paralysis
COPD may decrease their hypercapneic ventilatory drive
Carotid bodies- may become desensitized in carotid artery disease
Habitus
Thoracic / Upper abdominal incisions
Airway obstructionAirway class
Sedation vs GA w/ airway device
EquipmentBlocked tube
Disconnect
Ventilator malfunction
V/Q Mismatch & Shunt
FRC- GA reduces by about 400ml in adult
Supine- decreases by another 800ml
Obesity, pregnancy, abdominal sx, ascites
Large FRC may cause end-expiratory volumes below closing capacity
also pulmonary compliance
closing capacity (equal to closing volume + residual volume)
w/ smoking, obesity, LVF, Age, Surgery, Chronic bronchitis
Increased airway resistance
Bronchospasm
One-lung ventilation
Surgical clamping or compression
Pneumonia
Absolute ShuntPerfused without ventilation
Does not improve with O2 delivery
Normal physiologic shunt is about 2-5% of overall CO
Diffusion abnormality
rare
HypoxemiaAnemia / Poisoning
Methemoglobinemia
Carbon Monoxide
Nitroprusside toxicity
Cytochrome oxidase binds CN-, thus inhibiting aerobic metabolism
Low Cardiac Output
Hypovolemia Blood loss
Most efficient way to improve oxygenation is to hemoglobin
High SVR
Cardiogenic Shock
Intrapulmonary Derangements
Bronchospasm
EmbolismPE
Fat embolus
Gas embolus
Pulmonary edema
Pneumothorax
Aspiration
Atelectasis
Hypoxic Pulmonary
VasoconstrictionPulmonary Vc in response to regional lung hypoxia
Minimizes shunt, flow up to 50%
Advice to Those Taking the Re-
certification ExamReview Material and Question Books
Carbon Dioxide; Clinical Arterial Blood Gas Analysis; Hypoxemia; Respiratory. Written Board P.R.E.P. Big Blue. 2003. Neils Jensen.
Review of Clinical Anesthesia. Connelly & Silverman. Lippincott Williams & Wilkins.
Appleton & Lange Board Review of Anesthesiology. Mark Dershwitz. McGraw Hill.
ReferencesUniversal Capnography. A vital asset that can improve patient care on almost any call. www.JEMS.com. Patricia A. Brandt, RN, BSN, MHR2009 Mar 1.
Control of Breathing http://rfumsphysiology.pbworks.com/f/h12-1.bmp
Carbon Dioxide; Clinical Arterial Blood Gas Analysis; Hypoxemia; Respiratory. Written Board P.R.E.P. Big Blue. 2003. Neils Jensen.
Anesthesia Secrets 2nd Edition, 2000. James Duke, MD. Haley & Belfus, Inc.