CAPNOGRAPHY: END TIDAL CO2 Monitoring Flashcards
is the process of supplying oxygen to the body’s cells.
Oxygenation
is the process of exchanging oxygen and carbon dioxide
Ventilation
into the body via the airway, it’s offloaded onto the red blood cells while carbon dioxide diffuses across the membrane into the alveoli and is then exhaled. You breathe in oxygen and exhale CO2.
Oxygen comes
is the body’s process of supplying oxygenated blood to the cells and is reliant on adequate cardiac output in order to be optimal
Perfusion
involves substances moving across concentration gradients from areas of higher concentration to areas of lower concentration. This is the process involved with gas exchange.
Diffusion
Ventilation and perfusion is matched
Normal:
1.Cellular metabolism of food into energy – O2 consumption & CO2 production
2. Transport O2 & CO2 between cells and pulmonary capillaries
3. Ventilation between alveoli and pulmonary capillaries
Respiration - the 30,000 foot view
Contributes to the patient’s dead space through the addition of respiratory equipment, circuit attachments, filters, etc.
Mechanical dead space:
The amount of gas that fills the conducting passages of the airway (i.e. the trachea and upper bronchi) but is not involved in gas exchange.
Anatomic dead space:
The amount of gas filling the alveoli that does not contribute to gas exchange.
May be caused by gas that reaches alveoli, but the alveolar-capillary units are either underperfused or nonperfused
Alveolar dead space:
The sum of anatomic and alveolar dead space. It represents the total volume in the airway and alveoli not participating in gas exchange.
Physiological / total dead space:
Alveoli perfused but not ventilated
Shunt perfusion
Alveoli ventilated but not perfused
Deadspace ventilation
Anything that causes the alveoli to collapse or is the alveoli is filled with fluid.
Mucous plug
ET tube in the right or left main stem bronchus
Atelectasis
Pneumonia
Pulmonary edema
What that can cause Shunt Perfusion (No exchange of O2 or CO2):
(High V/Q) Ventilation is not the problem. Perfusion IS the problem. No exchange of O2 or CO2 occurs.
Dead Space ventilation:
Assesses ventilation, which is the movement of air in and out of the lungs
Assesses CO2 in the airway
Provides breath-to-breath ventilation status
End tidal CO2 (EtCO2) monitoring is the fastest indicator of ventilatory compromise.
Capnography
Assesses oxygenation: The amount of oxygen that is bound to red blood cells (O2 saturation, SpO2)
Slow to indicate a change in ventilation
Pulse oximetry
Is there CO2 exhaled
Colorimetric
How much CO2 is expired
Capnometry
What’s the rhythm
Capnography
Normal: 35-45 mmHg
Arterial blood is drawn directly from the artery. The amount of CO2 present in the sample is the value.
ABG: arterial CO2 (PaCO2)
Normal 30-43 mmHg
Gradient: The end-tidal CO2 is 1-5mmHg below the arterial CO2 because the end-tidal CO2 is always diluted with some “dead space” gas.
The gradient will increase in the presence of a ventilation/perfusion mismatch.
Capnography: end-tidal CO2
Capnography/capnometry is an objective measurement of exhaled CO2 levels.
A measurement of ventilation
Capnometry: End tidal CO2 monitoring is represented as a number and a graph on a monitor.Top right - EtCO2 mmHg
Capnograph: The waveform that shows how much CO2 is present at each phase of the respiratory cycle. Bottom graph on monitor
Normal range: 35 – 45 mm Hg
Capnography: end tidal CO2 monitoring
Sidestream monitors rely on a separate monitor connected to the patient’s airway by a tube. Gas samples are aspirated from exhaled gas flow via the ventilator circuit and are read at the monitor. Sidestream monitors can be used with non-invasive ventilation.
Mainstream monitors have a sampling window that is inserted directly in-line with the ventilator circuit for CO2 measurement. This allows a more rapid response time and requires a smaller amount of sample gas than sidestream monitoring. But mainstream monitors increase mechanical dead space, depending on the size of the chamber used to collect a gas sample, while adding weight on the airway, and can’t be used for non-invasive ventilation.
The newest type of EtCO2 monitor is Microstream which uses molecular correlation spectrography for greater precision. The Microstream monitor has a rapid response time and may be used with both invasive and non-invasive ventilation.
Types of end tidal CO2 monitors
Critical care
Cardiac arrest
Sedation
Uses
Assess the adequacy of circulation to the lungs
Low EtCO2 with other signs of shock indicates poor systemic perfusion, which can be caused by hypovolemia, sepsis or dysrhythmias.
Confirm Endotracheal tube placement & effective ventilation.
Critical care
Used to indicate the effectiveness of chest compressions. An EtCO2 less than 10 mm Hg indicates that compressions are not fast or deep enough. If circulation is restored, a spike in EtCO2 often appears before a pulse is detected.
Confirm endotracheal tube placement & effective ventilation.
Cardiac arrest
A tool to assess ventilatory function which is usually impaired by sedative and analgesic medication
Provides early detection of respiratory compromise and timely intervention.
Sedation
When monitoring End Tidal CO2, there are 3 aspects to consider: the EtCO2 value, the waveform shape and the respiratory rate. It is fairly easy to interpret numerical values for EtCO2 & RR, however, interpretation of the waveform shape requires specific knowledge discussed below.
A normal capnogram always has the following features:
The waveform has four phases:
Interpreting end tidal CO2
The waveform shape always starts at zero and returns to zero
A maximum CO2 is reached with each breath, corresponding to EtCO2
The amplitude of the waveform depends on EtCO2 concentration
The width of the waveform depends on the expiratory time
There is a similar shape for subjects with normal lung function
A normal capnogram always has the following features:
Phase I: start of the exhalation, CO2 concentration is initially zero
Phase II: CO2 increases rapidly as alveolar gas exits the airway
Phase III: CO2 concentration is relatively constant (reflects the concentration of CO2 in the alveolar gas). This phase ends with a value of maximum CO2 concentration
Phase IV: start of inhalation, CO2 decreases to zero as atmospheric air enters the airway
The waveform has four phases:
Labeled real time: real inhalation, pause, and exhalation
Time: waveforms squished together to see trends better
Capnographic waveform
Phase 1 is inhalation. (the inspiratory baseline)
Not lot going on
CO2 nearly or at 0 because no Co2 detected - very beginning of expiration - taking in breath, pause, diaphragm relaxed, then exhale
Stays 0 for period time - exhale dead space where not reach lungs at all - not oxygenated and not carrying CO2 - stay at 0 and just barely start come up - once CO2 begins to increase - then go to phase 2
Represents the end of inspiration and the start of expiration
No CO2 is detected. The start of expiration has no CO2 because the initial gases expired originate from the dead space of the upper airway and the capnography trace remains at zero.
Since no CO2 is going out when a patient is breathing in, the baseline is usually zero, or a flat waveform
Beginning of exhalation - getting rid of dead space
Capnogram phase 1
Phase 2: The continuation of exhalation.
Rapid increase of CO2 levels
Breathe out - where O2 and CO2 exchange happened so breathing out CO2
Corresponds with exhaling
Characterized by a rapid rise in CO2 concentration as dead space gas is replaced with alveolar gas.
The speed at which the CO2 is exhaled determines the slope of this part of the curve.
Capnogram phase 2
Phase 3 is the alveolar plateau - top of flat hill
Little incline
Very end/peak: end tidal volume/CO2 reading - measure end tidal CO2 reading - pick number that corresponds with peak
After exhale and big concentration CO2 rapidly increase then levels off then this is - end is where read the value
All of the gas passing by the CO2 sensor is alveolar gas which causes the capnograph to flatten out.
The gently sloping plateau represents late expiration where alveolar gas which is rich in CO2 is detected.
The peak measurement at the end of phase 3 is the EtCO2 reading.
Capnogram phase 3
After exhale - now time inhale - rapid decline in CO2 levels until come back to baseline and start phase 1 over again
Cycle repeats self over and over
Different morphology in way shaped depending on what going on with body
Phase 4 is inspiration and marked by a rapid downward direction of the capnograph. This downward stroke corresponds to the inspiratory fresh gas which is free of carbon dioxide.
Capnogram phase 4
High end tidal CO2 - anything produces CO2
CO2 Production
Pulmonary Perfusion
Alveolar Ventilation
Mechanical
What situations would give you a high ETCO2 reading
Fever - elevated - increased metabolic demand
Recent Sodium Bicarbonate Administration
Malignant Hyperthermia - underlying disease process
Pain - elevated - increased metabolic demand
CO2 Production
Increased cardiac output - blood going through lungs and CO2 exchange occurring more frequently
Elevated blood pressure - blood going through lungs and CO2 exchange occurring more frequently
Pulmonary Perfusion
Hypoventilation - 8 breaths/min - not breathing off CO2 - not breathing it off at norm resp rate then CO2 higher; lower RR - higher CO2
Respiratory Insufficiency (ie seizures)
Respiratory Depression (ie opioids, head trauma)
Sedation - breath slower
Bronchial intubation - not intubated in correct spot - higher CO2
Alveolar Ventilation
Ventilator leak - issues with ventilator
Exhausted CO2 absorber - device measuring CO2 not working appropriately
Mechanical
Pulmonary Perfusion
Mechanical
Alveolar Ventilation
CO2 Production
What situations would give you a low ETCO2
Anything that makes circulation through lungs less/slower decreases CO2 levels - not circulating CO2 and CO2 not offloaded from RBC through cap membrane through alveoli and out through expiration
Decreased cardiac output
Hypotension/Shock
Cardiac Arrest - even if performing high quality CPR; should have ETCO2 - 10-20 mmHg (closer to 10)
Pulmonary Embolism
Sudden Hypovolemia
V/Q Mismatch
Pulmonary Perfusion
Circuit disconnection
Mechanical
Hyperventilation - breathing of too much CO2; ETCO2 = low
Apnea - absence of breathing; 2-8 secs where not breathing; not exhaling for period of time - stuck in phase 1 of capnography so low
Severe airway obstruction
Sudden Extubation
Alveolar Ventilation
Hypothermia - affects CO2 production; makes lower
Diabetic Ketoacidosis (respiratory compensation) and other aciditic states
Aspirin Overdose (respiratory compensation)
Metabolic Acidosis
CO2 Production
Must be systematic when look at it
N: Number
E: Expected:
W: Waveform:
Then determine what is going on
Assesing capnographic waveform
Is there is a number
What is value - is it within normal range
The first thing to look at is the number. Remember normal is 30-43. Is the number high? Low? Normal?
N: Number
Waveform match what expect see with patient condition/dx
Does this number match up with what I expect the patient’s PaCO2 to be? If not, then it’s important to take a pause and think about the physiology.
E: Expected:
The next 3 portions of the approach look at the waveform.
S: Shape:
T: Trend:
R: Rate:
W: Waveform:
Sharp uptake
Plateau - gradual incline then sharp decline
All phases there
Waveform come back to baseline
Is the shape normal? Does it look like a rectangle with a nice Phase III plateau and a sharp transition into Phase 4. If not, does it have any of the classic abnormal waveforms
S: Shape:
Every waveform on strip - look same
Any trends - getting bigger/smaller
Look at morphology and see if pattern
The trend relates to both the waveform and the number. Is the number or waveform getting larger? Smaller? Is there significant variation in the types of waves?
T: Trend:
regular/irregular/fast/slow
What is the frequency of the waves and are they regular or irregular?
R: Rate:
More common waveforms see in practice
Sudden loss of waveform
Decreasing EtCO2
CPR assessment
Sudden increase in ETCO2
Bronchospasm (“Shark-fin” appearance)
Hypoventilation
Hyperventilation
Decreased EtCO2
Alterations in affecting ETCO2
Just stopped breathing on me: hx of apnea, get ready to code pt
Think worst then treat patient then machine
Nice waveform then nothing
ET tube disconnected from monitor, dislodged, kinked, or obstructed
Loss of circulatory function
Sudden loss of waveform
ET tube cuff leak - get obstruction/mucous plug; been intubated awhile - nice waveform then look crepy
ET tube in hypopharynx
Partial obstruction
Decreasing EtCO2
Attempt to maintain min of 10 mmHg
Looks norm
CPR assessment
Return of spontaneous circulation (ROSC)
Best thing see in code
Care provider doing good CPR - all sudden CO2 built up exhaled because patient breathing by self
Sudden increase in ETCO2
Asthma
COPD
Bronchospasm (“Shark-fin” appearance)
Going on awhile
Steady
ETCO2 >45 mmHg
Hypoventilation
Going faster
Well below 45 mmHg
Hyperventilation
Apnea
Sedation
Decreased EtCO2