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

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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.