Intraoperative Monitoring
Niels F. Jensen, MD
Copyright 2007: Oral Board PREP
The Best Medicine for Your Oral Boards
Phone: 800-321-7737
Note: The choice and discussion of monitors is clearly one of the
most important aspects of the Oral examination. There are several
reasons: First, it is an area that lends itself to the kind of
organization that the examiners are testing. Second, it indicates
medical concerns. Third, it provides ample opportunity to make
both positive points as well as mistakes. Many have jeopardized
their position by either having an inadequate basic knowledge of
various monitors, failing to adequately monitor, or, perhaps most
frequent, placing a monitor that is not needed. By knowing and
clearly articulating the indications for the various monitors, you
score. The appropriate use of arterial lines and pulmonary artery
catheters is especially important.
I. Types of Monitors:
1a. Standard ASA
a. EKG (V5, if necessary)
b. BP cuff
c. T-probe
d. Oxygen monitor
e. Pulse oximeter
f. Capnograph
g. Disconnect monitor
h. Precordial stethoscope-esophageal stethoscope
1b. Invasive
a. Foley cath
b. Arterial line
c. CVP
d. PA cath
1c. Situation
a. EEG, precordial doppler, intracranial pressure
b. SSEP (see neuro)
c. TEE
d. Fetal monitoring
II. Carbon dioxide (1,2)
1. CO2 Analysis-Capnography
a. It relies upon infrared absorption. It represents an
evaluation of the CO2 waveform.
b. Carbon dioxide contains two dissimilar atoms and absorbs
infrared radiation in a spectral range that is convenient to
measure.
c. Capnography is virtually infallible in detecting
esophageal intubation and is better than a pulse oximeter
(because it is quicker) in detecting esophageal intubation or
a disconnect.
d. It is important to consider several situations applicable
to the capnograph:
THE NORMAL CAPNOGRAPH
Components of a normal waveform.
1) Segment AB represents the beginning of exhalation when tracheal
dead space empties of its CO2 free gas.
2) Segment BC represents the period of continued exhalation when
increasing amounts of CO2 rich respiratory gas mixes
with dead space gas and results in an increasing CO2
concentration.
3) Segment CD represents the near-end of exhalation, the so called
"alveolar plateau" representing nearly constant CO2 rich
alveolar gas.
4) Point D is the highest value of CO2 concentration at the end
of normal exhalation and is the PETCO2.
Causes of variation in the normal CO2 waveform.
5) A Sudden drop to zero indicates a technical defect.
6) A Sudden drop but not to zero indicates leakage or
partial obstruction.
7) An Exponential decrease should immediately raise
suspicions about increased alveolar dead space such as
occurs with a large pulmonary embolus.
8) A Sudden increase can be caused by the release of a
tourniquet.
9) A Gradual increase may indicate one of several things,
including decreased minute ventilation and prolapse of
the expiratory valve.
III. Mass Spectrometer: (3)
1. The mass spectrometer performs an analysis of molecular mass
to the charge. It is used to determine the concentrations of
oxygen, carbon dioxide, nitrogen, nitrous oxide, and the VA's.
Gases are ionized by an electric field and then accelerated into
and separated by a magnetic field according to their molecular
mass to charge. Lightest ions are deflected first
MASS SPECTROMETRY
How the mass spectrometer works:
The mass spectrometry works by an analysis of the molecular mass
to the charge. After being ionized by a beam of electrons, a gas
molecule is accelerated by an electric field and then shot into a
magnetic field where the radius of the curvature depends on the
mass of the molecule. The lightest ions are deflected first and
this provides a way to identify compounds and to measure
concentrations.
IV. Apnea Monitoring (4) (Nothing in the book is casual. Know
this!)
1. Apnea monitors detect apneic events. They sense respiration
and trigger alarms if respiratory signals aren't detected. There
are several methods to sense respiration:
a. The most common is impedance pneumography. Electrodes
are placed on each side of the thoracic cavity and low
intensity alternating current is passed between them. Small
decreases in the impedance of the chest are sensed as a
respiration.
b. A second indirect method of monitoring respiration is a
pressure sensitive pad. Transducers sense body motion caused
by breathing and convert the force to electrical signals.
c. The third major indirect monitor is the pneumatic
abdominal sensor. Pressure changes caused by the expansion
and contraction of the abdomen during respiration are
detected as breaths.
d. We have reviewed the three major indirect monitors of
respiration. There are three direct monitors as well:
thermisters, proximal airway pressure sensors, and carbon
dioxide sensors. The thermister, placed in front of the
mouth or nose, detects the cool air passing by it during
inspiration and the warm air of expiration. These
temperature changes vary electrical resistance and are
detected as breaths. Proximal airway pressure sensors are
also located at the mouth or nose. They contain pressure
sensitive switches which are sensitive to the pressure
changes during respiration. Carbon dioxide sensors measure
carbon dioxide at exhalation. These are infrared sensors.
e. The worst case is when apnea monitors fail to alarm
during apnea because they sense artifact and interpret it as
respiration. Artifacts include vibration from equipment,
heart beats, and patient movement. Impedance pneumographs
and pressure sensitive pads are most common because they are
the simplest to use. They are also the most prone to this
type of error. The impedance pneumograph sometimes
interprets heart rate as respiration or fails to detect upper
airway obstruction because it senses continued chest wall
activity as respiration. These false negatives, failure to
alarm when there is apnea are obviously of concern.
f. A more common problem is alarming without apnea.
Frequent causes: incorrect sensitivity settings, dry
electrodes, or displaced electrodes or sensors.
g. Most new apnea monitors include heart rate monitoring.
An alarm will sound with bradycardia, caused for example by
hypoxemia induced by apnea.
V. Pulse oximetry (5)
1. Pulse oximetry involves transillumination of tissue with two
frequencies of light.
One frequency is at 940 nanometers and corresponds to 100%
saturation of hemoglobin (and the absorption of less red light).
The other frequency is at 660 nanometers and corresponds to 50%
hemoglobin saturation which is also called the isobestic point
(and corresponds to the absorption of more red light).
2. Oxygenated hemoglobin absorbs less red light than deoxyHb,
accounting for its red color.
3. Basically, the pulse oximeter measures a difference between
background absorption during diastole and peak absorption during
systole.
4. It is difficult to obtain calibration data at a saturation
less than about 30%. Therefore, the accuracy of the pulse
oximeter tends to decrease during episodes of severe hypoxemia.
5. There must be a pulse to distinguish between light absorbed by
arterial blood and background associated with venous blood.
Therefore, vasoconstriction seen during hypovolemia, hypothermia,
or shock leads to unreliable readings.
6. CarboxyHb is viewed by the pulse oximeter as oxy Hb. In other
words, COHb causes an overestimation of oxygenation. A co-
oximeter must be used to distinguish COHb from oxy-Hb.
7. MetHb is seen by the pulse oximeter as a saturation of 85%.
8. Methylene blue and indocyanine green lower the sat reading for
about 10 minutes.
9. Technical limitations of Pulse Oximetry:
a. No pulse present: Low peripheral perfusion
1) Hypotension
2) Hypothermia
3) Hypovolemia
b. Hemoglobin variants present
1) Carboxyhemoglobin is treated as oxygenated hemoglobin.
2) Met-Hb and indocyanine green are treated as having a sat
of 85%.
c. Severe anemia present
1) If less than about 3-4 gm/dl the pulse oximeter doesn't
work well.
d. Venous pulsations
1) Right heart failure or tricuspid regurgitation disturb
this monitor.
VI. Transcutaneous oxygen monitoring (6)
1. It is a noninvasive way to measure tissue oxygenation.
2. TCOM is based upon the following concept: Capillary PO2 may
approximate arterial PO2 in areas of the skin where local blood
flow exceeds the amount necessary for local tissue oxygen needs.
This approximation may especially hold if the local area is
warmed. Therefore, TCOM measures the PaO2 in capillary blood
noninvasively.
3. An electrode is attached to the skin, which is warmed to 40
degrees centigrade. This provides local vasodilatation. Oxygen
from capillaries can then diffuse through the skin into a Clark
type electrode, for direct measurement.
4. Limitations:
a. Errorenous measurement in the presence of peripheral
vasoconstriction.
b. Errorenous measurement in the presence of decreased
cardiac output. Cutanuous hypoxia occurs and this creates an
artifactual decrease in measured PtcO2.
c. Errorenous measurement in the presence of thick, usually
adult, skin. In infants local blood flow to less cornified-
keratininzed skin is high, making the technique more useful.
d. Sudden decreases in PaO2 are not detected because of the
slow diffusion time of oxygen across skin. The time constant
of measurement is minutes, limiting the ability for rapid
therapeutic response. Conjunctival probes are available and
partly lessen the problem of long diffusion time across skin.
e. Skin burns can result from prolonged application. Don't
leave in place for longer than about 2-3 hours.
VII. Oxygen monitor: Two types
A. Paramagnetic analysis
1. Oxygen is paramagnetic, it is attracted to a magnetic field.
2. Most anesthetic gases are diamagnetic, they are repelled by a
magnetic field.
B. Electrochemical analysis
1. The diffusion of oxygen through an electrolyte solution
creates an electric current which is proportional to
concentration.
VIII. Arterial line: (7)
ARTERIAL LINE
1. Indication(s): An arterial line is indicated when there may
be wide swings in blood pressure where such swings may be
deleterious, such as in patients with cardiac or cerebrovascular
disease. It is also indicated when frequent blood gas analysis
will be necessary for example in a patient with severe, chronic
pulmonary disease.
a. Blood pressure swings can be threatening in the presence
of coronary artery disease or where there is a history of
cardiac failure. Hypotension decreases coronary perfusion
pressure and increases in afterload increase myocardial
oxygen consumption.
2. MAP= 1/3 SBP + 2/3 DBP.
3. When a transducer is 10 cm below the right atrium it generates
a pressure that is 10 cmH2O or 7.5 mmHg higher than actual BP.
4. Systolic pressure in the aorta is far lower than in the radial
artery. The further into the periphery one goes the greater the
systolic pressure and the lower the diastolic pressure (increase
in the pulse pressure).
5. If the blood pressure cuff is too small or is loosely wrapped,
the blood pressure reading will be too high. If the blood
pressure cuff is too large, then falsely low recordings may
result.
6. Manual blood pressure recording: (For many years, especially
in children, blood pressure was measured by Doppler ultrasound.
The Oscillometric method, embodied in the dinamap, is now the
standard for automated blood pressure recording.) How does this
work?
a. Initially the cuff is inflated above the systolic BP and
there is no oscillation
b. As the cuff is deflated, oscillations begin and this is
the mean BP.
c. Values for the systolic and diastolic pressure are
derived by using various formulas that examine the rate of
change of pulsation. (The systolic point is generally chosen
as the point at which pulsations are increasing and are 25-
50% of maximum. Diastolic pressure is commonly placed at the
point of 80% decline of pulse amplitude.)
7. The best first choices for cannulation are the radial, ulnar,
and dorsalis pedis arteries. Brachial artery catheterization is
associated with a higher incidence of thrombosis (about 10-17%)
but should be cannulated if an arterial line is needed and the
other arteries cannot be cannulated. In this case, remove the
catheter as soon as possible.
8. Contraindications to the radial arterial line:
a. Local infection
b. Pre-existing ischemia to the hand (an abnormal Allen's
test is a relative, not an absolute, contraindication.) In a
normal Allen's test color returns to normal within 5 seconds
of release of the ulnar artery. This test may not be a
reliable prognosticator of hand ischemia secondary to radial
artery cannulation.
1) The duration of the cannulation and the size of the
cannula may not influence the incidence of hand
ischemia.
2) If the Allen's test is abnormal, place a pulse oximeter
on one of the fingers distal to the cannula.
3) Cannulation of the superficial temporal artery in a child
may be associated with cerebral emboli via the carotid
artery system.
4) Spasm of an artery can cause ischemia and this is
treatable with a sympathectomy (stellate ganglion
block).
c. Raynaud's phenomenon
VIII. CVP Monitoring: (8)
1. Central venous pressure monitoring is appropriate in cases of
major surgery with major fluid shifts, either acutely or over
several hours of surgery. It is also indicated for the following:
a. Aspiration of air emboli
b. Insertion of transvenous pacing wires
c. Administration of vasoactive substances such as dopamine
2. Contraindications include local infection and placement of the
line in the surgical field. Coagulopathies are not an absolute
contraindication to the placement of central lines.
CVP WAVES
3. CVP Waves: To remember these four oscillations, think of the
following sequence: atrial contraction, atrial relaxation, atrial
filling, and atrial emptying.
a. The first elevation, the a wave, reflects the slight rise
in atrial pressure that accompanies atrial contraction. It
occurs just before the first heart sound and before the
carotid pulse.
b. The following trough, the x descent, starts with atrial
relaxation. It continues as the right ventricle, contracting
during systole, pulls the floor of the atrium downward.
c. During ventricular systole, blood continues to flow into
the right atrium from the venae cavae. The tricuspid valve
is closed, the chamber begins to fill, and the right atrial
pressure begins to rise again, creating the second elevation,
the v wave..
d. When the tricuspid valve opens early in diastole, blood
in the right atrium flows passively into the right ventricle,
and right atrial pressure falls again, creating the second
trough or y descent .
e. Remember this: The a wave is absent in atrial
fibrillation whereas cannon a waves are seen with junctional
rhythms, tricuspid stenosis, right ventricular hypertrophy,
pulmonary stenosis, and pulmonary hypertension
4. Most frequent causes of elevated CVP:
a. Volume overload and/or Right heart failure
b. Light anesthesia
5. The most frequently used veins are: brachial, cephalic,
subclavian, internal and external jugular.
a. Long arm sites are associated with a higher incidence of
failure to place centrally.
b. The subclavian vein approach is associated with a higher
incidence of pneumothorax.
c. The right internal jugular site provides a straighter and
shorter route to the SVC and is not associated with the risk
of thoracic duct injury. In addition, the left pleural apex
arises higher and the risk of pneumothorax is increased.
6. Subclavian lines: (tips for success)
a. Place the patient in a trendelenburg position with a roll
between the shoulders.
b. Line up the bevel of the large needle with the numbers.
Begin with the bevel straight up and when the vein is
entered, turn the syringe about 90 degrees. This is a key
point.
c. Error on the side of being too lateral to the sternal
angle. Aim for the notch.
d. Go into the skin perpendicular and then place left thumb
on the needle and guide it under the clavicle.
e. If possible, place the monitor with the patient awake and
breathing spontaneously.
7. Mangano (1980) noted good correlation between the CVP and the
PCWP in patients with good LV function, no wall motion
abnormality, and a resting PCWP less than 18. If these conditions
do not pertain, the correlation is not as good. In addition, the
presence of COPD and/or pulmonary hypertension also makes the
correlation less valid. In fact, in these circumstances,
the CVP and PCWP may have no correlation at all and the
direction of change may be opposite.
8. Why would a CVP ever be preferable to a PA cath? It is likely
that some of the complications seen with the PA cath (see below)
would not be seen as frequently.
IX. PA catheters: (9,10,11)
1. Indications: The pulmonary artery catheter is indicated for
patients who are undergoing major surgery with major fluid shifts
who have severe LV dysfunction (and/or cardiac failure), pulmonary
hypertension, or cor pulmonale. Thus, both the nature of the
patient and the type of surgery to be performed are important.
For example, if surgery is minimally invasive, the monitoring
needs are very much different than if it is a major vascular,
major abdominal, or thoracic case.
a. The PA catheter is primarily used to monitor both preload
and afterload in order to reduce myocardial oxygen
consumption.
b. Remember that the PA catheter is specifically
useful in obtaining cardiac outputs, obtaining mixed
venous gases, and calculating systemic vascular
resistance.
c. If the aorta is to be crossclamped, a specific indication
for the pulmonary artery catheter is to detect LV failure in
response to cross-clamping, an event which is difficult to
predict in the presence of mild to moderate left ventricular
dysfunction.
NORMAL INTRACARDIAC PRESSURES
(This is their view: You wanted it, you better know about it)
a. RA 1-5 mm Hg
b. RV 15-30/1-5 mm Hg
c. PA 15-30/5-15; mean of 10-20 mm Hg
d. PCWP 5-12 mm Hg
2. The PADP is usually 1-3 mmHg greater than the PCWP. At less
than 15 mmHg, mean PCWP correlates well with LVEDP. Read
pressures at end-expiration, since this is the closest to zero
intrathoracic pressure.
3. Large A and V waves on PA tracing indicate: Mitral
regurgitation, heart failure, and heart block.
4. An example of efficacy: The placement of a PA catheter in
patients with mitral stenosis.
a. Perform a history and physical examination. If there is
a history of dyspnea, orthopnea, PND, or poor exercise
tolerance with physical exam suggesting failure ( rales,
edema, ascites, hepatosplenomegaly ) then placement of a PA
cath should be done. If, however, the patient has a good
exercise tolerance or has no signs of cardiac failure, then a
PA catheter is not mandatory. Again, the type of surgery
being performed and particularly the anticipated blood loss
associated with it should be assessed.
b. What are the risks of a PA catheter:
1) Risks of insertion
a) Infection
b) Pneumothorax
c) Hematoma
d) Injury to major vessels such as the carotid artery
e) Air embolism
2) Arrhythmias, Heart Block, and Heart perforation
a) PA can produce a right bundle branch block. If left
bundle branch block is already present, one may
want to place a pacing Swan.
b) Perforation of the heart can lead to cardiac tamponade.
3) Valvular damage
4) Pulmonary artery perforation (the right atrium or right
ventricle can also be perforated) and/or pulmonary
infarction.
a) The incidence of pulmonary artery rupture is 0.2% and
this risk is increased in patients with pulmonary
hypertension (such as patients with MS) and
patients on anticoagulants. This is a life-
threatening emergency, associated with a very high
mortality. Signs and symptoms include the
emergence of blood from the endotracheal tube.
Treatment entails a thoracotomy with one lung
anesthesia on cardiopulmonary bypass. Interim
steps include:
i) Leave the PA catheter in place.
ii) Get the patient into the operating room.
iii) Place a double lumen endotracheal tube
iv) Lower blood pressure with nitroglycerin (unless the
patient is already in profound, hypovolemic
shock) to decrease blood loss.
b) Pulmonary infarction can occur if the balloon of the
catheter is in a permanently wedged position.
5) Thrombosis-thromboembolism/Air embolism
c. The cephalic or basilar vein approach has fewer
complications but the failure rate is higher.
5. Contraindications: PA catheter
a. Mechanical heart valves (absolute)
b. Hypercoaguable states
c. Recently inserted transvenous pacemaker, bifascicular
heart block, coagulopathy, frequent dysrhythmias, history of
pulmonary stenosis (all relative contraindications).
6. Thermodilution cardiac output is immeasurable or inaccurate in
the following situations:
T Tricuspid regurgitation
I Intracardiac shunts
A Atrial fibrillation
7. Cardiac output measurements should be made at end-expiration
with 10 cc of room temp injectate. Cold (0-4 degree cent)
injectate can be used to produce a better signal to noise ratio.
8. It is not always necessary to monitor the PA pressure for
coronary artery surgery. If LV function is very good and the
patient does not have significant COPD, then the CVP correlates
well with PCWP. If LV function is not good or significant
pulmonary hypertension exists, then the CVP does not correlate as
well with the PCWP.
9. Treating an increased PCWP. First ask the question: Is it
light anesthesia, fluid overload, a vasoactive drug, or heart
failure? If the blood pressure is up it may be light anesthesia.
If the patient is hypotensive, it is probably fluid overload.
Treatment of fluid overload:
a. Restrict fluids
b. Nitroglycerin, Lasix, and an inotrope such as dopamine
10. PCWP=LAP=LVEDP=LVEDV
11. SVR= MAP - CVP/ CO X 80 (Normal 900-1500)
12. Cardiac output: normal is 3.3-5.5
a. Steps in treatment of low cardiac output:
1) Optimize preload
2) Optimize afterload
3) Start an inotropic agent
13. If a PA line is placed for a patient having a thoracotomy:
a. Obtain a postinsertion chest X-ray to rule out a
pneumothorax
b. Consider obtaining fluoroscopy to determine in which lung
the balloon floats
14. How far should we go insert?
a. The right atrium is usually encountered at 20 cm and the
wedge position is encountered at about 50-55 cm.
b. Balloon inflation during catheter insertion is necessary
to minimize the damage to the endothelium.
15. Causes of elevated LVEDP?
a. Hypervolemia, cardiac failure
b. Vasoactive drugs (i.e. neosynephrine)
c. Light anesthesia
d. Aortic crossclamp
16. Causes of low LVEDP?
a. Hypovolemia
b. Vasodilator drugs (SNP and TNG)
c. Deep anesthesia
d. Unclamping of the aorta
e. Hypoxia or hypercarbia (secondary to increased PVR and
decreased filling)
17. Causes of pulmonary edema are the same general causes as for
edema elsewhere: (12)
a. Increased capillary pressure
1) MS
2) Heart failure
3) Retention of fluid by diseased kidney
b. Increased capillary leak
1) Aspiration
2) ARDS
3) Burn
4) Neurogenic
c. Decreased oncotic pressure caused by decreased albumin
1) Albumin loss from burn or nutritional deficiency
d. Lymphatic obstruction
1) Tumor
18. If evidence of pulmonary edema appears, one must make the
diagnosis between cardiogenic (increased capillary pressure) and
noncardiogenic (increased capillary leak, oncotic, or lymphatic
obstruction) processes. A PA catheter can be useful in this
context.
a. If cardiogenic pulmonary edema exists, the PCWP will be
high (18 mmHg) and if aspiration has occurred it will be low.
Cardiogenic pulmonary edema is also associated with bibasilar
rales, patchy infiltrates, and a pink, frothy sputum. It
often requires fluid restriction, diuretics, and inotropes.
b. Noncardiogenic pulmonary edema is associated with massive
blood transfusion, smoke inhalation, sepsis, and DIC. There
are bibasilar rales but the PCWP is not generally elevated.
It often requires fluid restriction or cautious fluid
administration.
19. Pulmonary Hypertension: The causes are from increased
pulmonary blood flow or increased pulmonary vasoconstriction. The
PA systolic BP is above 30 mm Hg.
a. PVR= mean PA - PCWP/CO X 80. Normal is less than 200.
b. Causes:
1) Increased pulmonary blood flow:
a) Left to right intracardiac shunts
2) Increased pulmonary resistance
a) Hypoxia, hypercarbia, acidosis
b) Lung disease and destruction of pulmonary vascular beds
c) Embolism: fat, amniotic, and air
3) Increased backward pressure from mitral stenosis and
mitral regurgitation
20. If a patient in cardiac failure develops the sudden onset of
supraventricular tachycardia, how should this be treated? This is
a common scenario. The treatment of SVT is adenosine, 6 followed
by 12 mg. Esmolol and verapamil can worsen heart failure and
exacerbate pulmonary hypertension. Hypotension should prompt
cardioversion.
21. Is the PCWP a reliable monitor of intra-op myocardial
ischemia?
a. This is controversial. The PA cath is a valuable tool to
monitor cardiac output and left ventricular preload.
Furthermore, studies in which ischemia was provoked with
atrial pacing or angioplasty reveal an increase in PCWP.
b. However, a recent Dutch study (Dr. Marc van Daele of the
Thoraxcenter at the University of Rotterdam) revealed that
changes in the PCWP appear to be neither a sensitive nor a
reliable indicator of intraoperative myocardial ischemia. In
fact, the 12 lead ECG appeared to be more sensitive in
identifying ischemia detected by transesophageal echo than
the wedge pressure.
X. Doppler principle
1. Some basics:
a. Frequency: Number of cycles/second
b. Wavelength: Distance travelled by sound during one cycle
c. Speed of sound: 1540 meters/second in water
d. Speed of sound (C)= Frequency (F) X Wavelength (l)
2. The Doppler principle states that frequency and wavelength
shifts will occur depending upon whether an object is moving
toward or away from an observer. If an object is moving toward an
observer reflected wavelength is shorter and frequency higher. If
an object is moving away from an observer reflected wavelength is
longer and frequency lower.
3. Example and application: When 2,000,000 Hz is reflected off
from red blood cells moving toward an observer, they send back
2,006,000 Hz. The Doppler shift is +6,000 Hz.
XI. EKG monitoring (13)
1. When the patient is awake, angina is the best sign of
myocardial ischemia. When the patient is asleep, a 1 mm ST
depression in V5 is the best sign. 90% of ST segment information
contained in a conventional 12 lead EKG is found in lead V5.
2. Many EKG machines do not have precordial leads. A modified V5
or CM5 may be used. Place the right arm electrode (negative) just
to the right of the sternum. Place the left arm electrode at the
V5 position (5th intercostal space at the anterior axillary line),
and place place the left leg electrode at any convenient position.
Now, monitor lead I.
3. CB5 might be just as good: Place the right arm (-) electrode
over the middle part of the right scapula, the left arm electrode
over the V5 position and monitor lead I.
4. What does the EKG tell us? You must be able to articulate
what you know!
a. Rate, rhythm
b. Ischemia
d. Conduction abnormalities
e. Axis and hypertrophy
5. CAD and the myocardial ischemia it can cause are regional
disease processes. An inferior lead such as lead II may be normal
while ST segment depression and T wave inversion can be evident in
precordial leads. The following specific leads look at the
following specific regions:
a. II, III, aVF RCA RA, RV
b. V3-V5 LAD Ant LV
c. I, aVL circumflex Lateral LV
6. The usual 12 lead EKG can be broken down into the following:
a. Three standard limb leads: They record the potential
difference between two points on the body.
1) Einthoven's Law: I + III= II
b. Six precordial chest leads: The chest wall electrode is
connected to the positive terminal while the negative
terminal is connected to the right arm, left arm, or left
leg. Nearness of the electrode to the heart means that small
abnormalities of the ventricle can produce marked EKG
changes. The V5 lead is so valuable because the ST segment
is a very accurate predictor of ischemia.
1) V1-V2 are mainly negative because they are at the base.
2) V2-V6 are mainly positive because they are near the apex.
c. Augmented unipolar leads: Two limbs are connected to
negative electrodes while the third is connected to the
positive electrode.
1) aVR: positive electrode is on the right arm
2) aVL: positive electrode is on the left arm
3) aVF: positive electrode is on the left leg
7. Axis: Normally about 60 degrees. I and aVF should be
positive.
a. LBBB or LVH causes left axis deviation (less than 0
degrees)
b. RBBB or RVH causes right axis deviation (greater than
100 degrees)
8. Decreased voltage is caused by:
a. Pericardial fluid
9. Q wave occurs because there is no electrical activity in the
infarcted area. Must be more than 1 mm and greater than 0.04
seconds in duration (one box in depth and one box in duration).
10. T wave inversion: see below
11. Atrial and ventricular hypertrophy:
a. Ventricular hypertrophy: Look at S in V1 and R in V5.
If they add up to greater than 35 mm (each box is 1 mm) there
is probably LVH.
b. Atrial hypertrophy: Look at V1. If the p wave is more
than 3 small squares wide and/or is biphasic one should
suspect atrial hypertrophy
12. Evaluation of preoperative or intraoperative PVC's:
A. Begin by asking several questions--Are they present on the old
EKG? What is the frequency? Are they unifocal or multifocal? Do
they occur such that there is an R wave on the T wave? What
should one do? If more than 6 per minute treat with lidocaine.
While doing so review the causes and investigate. The causes are
several and include the following: Investigations that are often
appropriate are to check the vital signs, order an ABG, EKG, and
serum electrolytes.
B. Consider the possible etiologies and treat accordingly:
a. Hypoxia, hypercarbia, pain
b. Hypotension- anemia
c. Myocardial disease: myocardial infarction, myocardial
ischemia, CHF, cardiomyopathy- myocarditis, valvular heart
disease, conduction system abnormality
d. pH abnormalities
e. Blood pressure abnormalities, either hypo or hypertension
f. Electrolyte abnormalities (K+, Ca+, and Mg+ are the most
common offenders) and/or endocrine problems (hyperthyroidism,
pheochromocytoma)
g. Temperature abnormalities
C. Is treatment necessary?
a. If they are less than 6 per minute and are unifocal, no
treatment is necessary.
b. If they are greater than 6 per minute, administer
lidocaine 1 mg/kg loading with 0.5 mg/kg administered in 5
minutes. If they persist, a 1-4 mg/min drip should be
started.
c. Vital sign check, ABG, EKG, and electrolytes. (VAE)
13. ST segment elevation/ST segment depression---T wave
inversion/Q wave abnormality---"nonspecific" changes: Treat
associated factors such as hypo or hypertension, anemia,
tachycardia while preparing nitroglycerin drip consider other
etiologies.
1) ST segment elevation:
While preparing to treat myocardial ischemia, a number of other
etiologies for ST elevation should be considered. (CEA)
Coronary artery disease
Acute myocardial infarction
Epicardial injury
Pericarditis
Myocarditis
Blunt Trauma
Post-cardioversion
Agents/Drugs
Hyperkalemia
Digitalis
Hypothermia
Carbon Monoxide-Cyanide
2) ST segment depression and/or T wave inversion (DIAL)
Myocardial ischemia and subendocardial infarction
A. Digitalis-Quinidine
Injury to the CNS
Acute cor pulmonale (pulmonary embolus)
Athletic heart syndrome
Left Bundle Branch Block
B. Filters:
a. They are in the EKG machines to filter out electrocautery
interference.
b. They lessen the fidelity of the monitor and sometimes if
there is a prominent R wave the deflection makes it appear as
if there is ST depression.
c. Therefore, if there is ST depression turn off the filter.
3) Abnormal Q waves
Hallmark of transmural myocardial infarction
Left and right ventricular hypertrophy
Left and right bundle branch block
Cor pulmonale (pulmonary embolism)
Cardiomyopathy
IHSS
Pneumothorax, emphysema
4) Nonspecific ST or T wave changes on a preoperative EKG are not
associated with increased perioperative risk.
XII. Foley Cath
1. Why use a foley cath? Urine output is a very sensitive
indicator of renal perfusion as well intravascular volume. If the
case involves significant fluid shifts, is going to be long, or is
to be performed in a patient with borderline renal function a
foley cath is indicated.
a. Morbidity from renal failure is high. Anesthesiologists
must protect the kidneys by making sure they are well
perfused.
b. Urine output should be maintained at a level of at least
0.5 cc/kg/hr.
c. See renal section for treatment of intraoperative
oliguria.
XIII. Peripheral Nerve Stimulator
1. See neuromuscular section
XIV. Transesophageal Echo
1. Two dimentional transesophageal echocardiography provides
remarkably revealing images of cardiovascular anatomy and
physiology.
a. It not surprising, given this that information derived
from TEE can dramatically alter anesthetic and surgical
management.
b. The fact that no adverse effects of ultrasound have been
demonstrated in humans obviosly adds to its risk-benefit
ratio.
2. Pizoelectric crystals are the transducers and receivers of
sound used in echocardiography.
a. These quartz crystals vibrate when electrically
stimulated to produce ultrasound.
b. Two basics: First, when ultrasound strikes the interface
of tissues of different densities a portion is reflected.
The greater the difference in tissue density, the greater the
portion reflected. Second, sound is assumed to travel at
1540 m/sec in all tissues of the body at 37 degrees
centigrade and therefore the longer the sound wave takes to
bounce back to the transducer the greater its distance from
the transducer.
3. The first echocardiograms were motion or M-mode
echocardiograms but they revealed only a small part of the heart
at once. By using multiple crystals multiple views could be
obtained and were collated into a 2 dimentional image.
4. While the current technology cannot reveal meaningful data on
coronary blood flow, the monitor does provide other important data
on the presence and extent of ischemic heart disease.
a. Specifically, segmental wall motion abnormalites have
been recorded within seconds of the onset of regional
ischemia and akinesia and dyskinesia clearly reveal regions
of old infarction.
b. Besides providing an earlier and more reliable monitor
for myocardial ischemia than ST segment changes,
echocardiography is clearly a premier tool for the assessment
of ventricular function, providing accurate assessments of
ventricular filling and ejection, wall thickness, and mass.
End diastolic volume, ejection fraction, wall stress, and
correlates of contractility can be calculated from these.
5. Advances in West Germany in 1982 made it possible to position
a phased transducer in the esophagus, making intraoperative 2D
echo practical for the anesthesiologist.
a. A typical esophageal transducer is 42 mm long and is
mounted upon a gastroscope.
b. Once the transducer has been inserted through the mouth,
advanced 30-35 cm, retroflexed with the controls of the
gastroscope to angle the beam about 10-30 degrees caudad, a
view of the left atrium, left ventricle, and left ventricular
outflow tract is clearly visible.
c. Left and right ventricular size and fuction are
demonstrable with small position changes.
d. These images can be recorded at the start and conclusion
of surgery as well as at strategic intervals such as cross-
clamping. Therefore, TEE provides the anesthesiologist with
a direct and quantitative method to assess LV preload and
ejection.
e. Will the transesophageal echo take the place of the
pulmonary artery catheter in many situations in the future?
Probably, by virtue of both costs and benefits.
6. Other uses include: diagnosis of atrial septal defects,
evaluation of especially the mitral valve, and detection of air
embolism and paradoxical air embolism. When it comes to air
embolism a recent study suggests that the TEE is more sensitive
than a precordial doppler.
7. Should you be using the TEE?
a. If you care for patients at high risk for perioperative
cardiovascular instability, you should learn how to use the
TEE.
b. The fact is though that many of us have never used this
device. Don't bluff. The basic information presented here
is important but make it very clear that you have never used
this device, if that is the case.
c. Please remember that the TEE is especially useful in
viewing the mitral valve, an important fact when there is a
failure to wean from CPB. Evaluate the mitral valve.
XV. EEG Monitoring
1. The EEG represents the summation of cortical electrical
activity generated by post-synaptic potentials, in other words
electrical activity from the cerebral cortex, voltage against
time.
a. It permits evaluation of the CNS where it is not possible
to perform a clinical exam, such as during general
anesthesia.
2. The EEG is classified on the basis of both rhythm and
frequency: Delta, Theta, Alpha, and Beta --each associated with
different physiologic states.
a. Delta (0-4 Hz): Deep sleep, deep anesthesia, hypoxia,
tumors.
b. Theta (4-8 Hz): Sleep, anesthesia, hyperventilation.
c. Alpha (8-13 Hz): Resting, alert adult. Dominant
frequency in the awake state.
d. Beta (13-30 Hz): Mental concentration.
3. In general, patterns are used as opposed to frequency analysis
and these patterns can be activated, depressed, or isoelectric.
4. Frequency is still important and many factors can alter it.
(Know in some detail.)
Increased frequency
Hyperoxia
Hypercarbia: mild
Hypoxia: initial
Seizure
Barbiturates: Small dose
Diazepam:
N2O: 30-70%
Inhalation agents < 1 MAC
Ketamine
Decreased frequency, Increased Amplitude
Hypoxia: mild
Hypocarbia: moderate to extreme
Hypothermia
Barbiturates: moderate dose
Etomidate
Narcotics
Inhalation agent > 1 MAC
Decreased frequency, Decreased amplitude
Hypoxia: marked
Hypercarbia: severe
Hypothermia
Hypotension
Barbiturates: large dose
Electrical Silence
Brain Death
Hypoxia: severe
Hypothermia: profound
Barbiturates: coma dose
Isoflurane: 2 MAC
5. For anesthesiologists, the most important thing to know is
that changes, especially decreased amplitude or slowing, may
represent CNS hypoxia.
a. Decreased amplitude or slowing of the EEG should be
treated by optimizing (usually raising) blood pressure and
ruling-out hypoxia and hypothermia.
6. Anesthetic effects: What do we need to have on the tip of our
tongue about this complex area?
a. In general, as the depth of anesthesia increases, EEG
frequency decreases until a delta or theta level is reached.
Dr. Jensen's Presentation Points Winston Churchill:
Comments to the Cabinet upon becoming Prime Minister, some of whom
were known to favor the compromise that had marked the previous five
years: "I am convinced that every man of you would rise up and tear
me down from my place if I were for one moment to contemplate parley
or surrender. If this long Island story of ours is to end at last,
let it end only when each one of us lies choking in his own blood
upon the ground." Return to Index
NOTES: 1. Swedlow, DB. ASA Refresher Course, vol 13, chapter 15, Mass
Spectrometers and Respiratory Gas Monitoring, Barash, PG, and Tinker,
JH, (eds.), Lippincott.
2. Neustein, SM, Eisenkraft, JB. One-Lung Anesthesia. Clinical
Cases in Anesthesia, Reed, AP (ed), Churchill
Livingstone, p. 48-49.
3. Swedlow, DB. ASA Refresher Course, vol 13, chapter 15, Mass
Spectrometers and Respiratory Gas Monitoring, Barash, PG, and Tinker,
JH, (eds.), Lippincott.
4. Staewen, W. Apnea Monitoring Basics. Biomedical Instrumentation
and Technology.
5. Gilbert, HC, and Vender, JS. Monitoring the Anesthetized
Patient. Clinical Anesthesia, Barash, PG, Cullen, BF, and
Stoelting, RK, (eds.), Lippincott, p. 742-743.
6. Moon, RE, and Camporesi, EM. Respiratory Monitoring.
Anesthesia, Miller, RD, (ed.), Chruchill Livingstone,
p. 1143.
7. Gabrielson, GV. Abdominal Aortic Aneurysm. Clinical Cases in
Anesthesia, Reed, AP (ed), Churchill Livingstone,
p. 167-168.
8. Bodner, N. Intracranial Mass, ICP, Venous Air Embolism,
Autoregulation. Clinical Cases in Anesthesia, Reed, AP
(ed), Churchill Livingstone, p. 69-70.
9. Reich, DL, Joffe, D. Congestive Heart Failure. Clinical Cases
in Anesthesia, Reed, AP (ed), Churchill Livingstone,
p. 23.
10. Mihm, FG. ASA Refresher Course, vol. 15, chapter 11, Analysis
of Information Pitfalls of Pulmonary Artery Catheter Monitoring,
Barash PG, and Tinker, JH, (eds.), Lippincott.
11. Gilbert, HC, and Vender, JS. Monitoring the Anesthetized
Patient. Clinical Anesthesia, Barash, PG, Cullen, BF, and
Stoelting, RK, (eds.), Lippincott, p. 752-755.
12. Murray, TR, and Marshall, BE. ASA Refresher Course, vol. 15,
chapter 12, Cause and Management of Perioperative Pulmonary Edema,
Barash, PG, and Tinker, JH, (eds.), Lippincott.
13. Stoelting, RK. Pharmacology and Physiology in Anesthetic
Practice, Lippincott, p. 707-718.
14. Cahalan, MK. ASA Refresher Course, vol. 18, chapter 5,
Transesophageal Echocardiography: Should I Be Using It?, Barash, PG,
and Tinker, JH, (eds.), Lippincott.
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