May 9, 2025 • 43 mins
Continue your journey to mastering anaesthesia—one chapter at a time.
In this episode, Dr. J.R. Decker reads and discusses Chapter 5 (Part 3) of Morgan & Mikhail’s Clinical Anesthesiology (7th Edition).
Follow as you read along to strengthen your foundations in anaesthesia, one clear and engaging session at a time.
Perfect for trainees, revision, or daily listening.
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:01):
Morgan and Michael's Clinical Anesthesiology, 7th edition,
Chapter 5, Part 3. Pulmonary artery catheterization
indications. The Pulmonary Artery
(00:24):
Pennsylvania catheter, or Swann Ganz catheter, was introduced
into routine practise in operating rooms and in coronary
and critical care units in the 1970s.
It quickly became common for sicker patients undergoing major
(00:45):
surgery to be managed with PA catheterization.
The catheter provided measurements of both Co.
That's cardiac outputs and pulmonary artery occlusion
pressures and was used to guide hemodynamic therapy, especially
(01:08):
when patients became unstable. Determination of the pulmonary
artery occlusion or wedge pressure permitted, that is in
the absence of mitral stenosis. An estimation of the left
ventricular end diastolic pressure LVEDP and depending on
(01:32):
ventricular compliance, ventricular volume.
Although the ability of the pulmonary artery catheter to
perform measurements of cardiac outputs.
Sorry, let's take it again. Through the ability of the
pulmonary artery catheter to perform measurements of cardiac
(01:55):
output, the patient, the patient's stroke volume was also
determined. Cardiac output is equals to
stroke volume times HR. That's heart rate.
Stroke volume is equals to cardiac output divided by heart
(02:19):
rate. Blood pressure is equal to
cardiac output times systemic vascular resistance.
Consequently, hemodynamic monitoring with the pulmonary
(02:39):
artery catheter attempted to discern why a patient was
unstable so that therapy could be directed at the underlying
problem. If the SVR is diminished, such
as in states of vasodialectric shock that is, sepsis, the
(03:02):
stroke volume may increase. Conversely, a reduction in
stroke volume may be secondary to poor cardiac performance or
hypovolemia. Determination of the wedge or
(03:23):
pulmonary capillary occlusion pressure, that is, PCOP by
inflating the catheter balloon estimates the LVDEP, that is the
left ventricular end diastolic pressure.
(03:45):
A decreased stroke volume in thesetting of a low pulmonary
capillary occlusion pressure divided by the LVDEP indicates
hypovolemia. Let's take it again.
(04:07):
A decreased SV in the setting ofa low CPOC, PCOP, stroke LVEDP
indicates hypovolemia and the need for volume administration.
A full heart reflected by a highCPOCPCOP stroke, LVEDP, and low
(04:34):
stroke volume indicates the needfor a positive ionotropic drug.
Conversely, a normal or increased stroke volume in the
setting of hypotension should betreated with the administration
(04:55):
of vasoconstrictor drugs to restore SVR in a vasodilated
patient. 2 Although patients canand do present concurrently with
(05:16):
hypovolemia, sepsis, and heart failure, the aforementioned
shock treatment approach using the PA catheter to guide therapy
became more or less synonymous with perioperative intensive
care and cardiac anaesthesia. However, several large
(05:44):
observational studies have shownthat patients managed with PA
catheters had worse outcomes than similar patients who were
managed without PA catheters. Other studies seem to indicate
that although PA catheter guidedpatient management may do no
(06:08):
harm, it offers no specific benefits.
Although the PA catheter can be used to guide goal directed
hemodynamic therapy to ensure organ perfusion in shock states,
(06:29):
other less invasive methods to determine hemodynamic
performance are available including trans pulmonary
thermodilution, cardiac output measurements, pulse contour
analysis of the atrial pressure waveform, and methods based on
(06:54):
bio impedance measurements across the chest.
All these methods permits calculation of the stroke volume
as a guide for hemodynamic management.
Moreover, right atrial blood oxygen saturation, as opposed to
(07:21):
mixed venous saturation that is normal is 75%, can be used as an
alternative measure to discern tissue oxygen extraction and the
adequacy of tissue oxygen delivery.
(07:43):
Despite numerous reports of its questionable utility and the
increasing number of alternativemethods to determine hemodynamic
parameters, the PA catheter is still employed perioperatively
more often in the United States than elsewhere.
(08:06):
Although echocardiography can readily determine if the heart
is full, compressed, contracting, or empty, a trained
individual is required to obtainand interpret the images.
(08:26):
Alternative hemodynamic monitorshave gained wide acceptance in
Europe and are increasingly usedin the United States, further
decreasing the use of PA catheters.
PA catheterization can be considered whenever cardiac
(08:51):
index, preload, volume status, or the degree of mixed venous
blood oxygenation need to be known.
These measurements might prove particularly important in
surgical patients at great risk of hemodynamic instability or
(09:15):
during surgical procedures associated with a greatly
increased incidence of hemodynamic complications.
However, the authors prefer trans esophageal
echocardiography in these situations.
(09:38):
Contraindications. Relative contraindications to PA
catheterization include left bundle branch block that is
because of the concern about complete heart block and
conditions associated with a greatly increased risk of
(10:03):
arrhythmias. A catheter with pacing
capability is better suited to these situations.
A PA catheter may serve as a nine dose of infection in
bacteremic patients of thromboseformation.
(10:25):
In patients prone to hypercoagulation techniques and
complications. Although various PA catheters
are available, the most popular design integrates 5 lumens into
(10:47):
a 7.5 F catheter 110 centimetreslong with a Poly vinyl chloride
body. The lumens house the following
wiring to connect the thermistornear the catheter tip to a
(11:12):
thermal dilution cardiac output computer.
An air channel for inflation of the balloon, A proximal port 30
centimetres from the tip for infusions, cardiac output
(11:33):
injections, and measurements of right atrial pressures.
A ventricular port at 20 CM for infusion of drugs and a distal
port for aspiration of mixed venous blood samples and
(11:55):
measurements of PA pressure. Next we go to Figure 5-16
talking about a balloon tipped pulmonary artery flotation
catheter, also known as the Schwann Gans catheter.
(12:23):
At the proximal lens you have the RA and proximal infusion,
and at the distal lens you have the thermistor, pulmonary
artery, distal port, proximal infusion port, right atrial
port, and balloon. Insertion of a PA catheter
(12:52):
requires central venous access, which can be accomplished using
the previously described Seldinger technique.
Instead of a central venous catheter, a dilator and sheath
are threaded over the guide wire.
(13:14):
The sheet lumen accommodates thePA catheter after removal of the
dilator and guide wire. Prior to insertion, the PA
catheter is checked by inflatingand deflating its balloon and
(13:39):
filling all three lumens with intravenous fluid.
The distal port is connected to a transducer that is zeroed to
the patient's mid axillary line.The PA catheter is advanced
(14:02):
through the introducer and into the internal jugular vein at
approximately 15 centimetres. The distal tip should enter the
right atrium and a central venous tracing that varies with
(14:22):
respiration confirms an intrathoracic position.
The balloon is then inflated with air according to the
manufacturer's recommendations. That is usually 1.5 mils to
protect the endocardium from thecatheter tip and to allow flow
(14:48):
through the right ventricle to direct the catheter forward.
The balloon is always deflated during withdrawal.
During catheter advancement, theECG should be monitored for
arrhythmias. Transient ectopy from irritation
(15:13):
of the right ventricle by the balloon and catheter tip is
common and rarely requires treatment.
A sudden increase in the systolic pressure on the distal
tracing indicates a right ventricular location of the
(15:34):
catheter tip. Entry into the pulmonary artery
normally occurs by 35 to 45 centimetres and is heralded by
sudden increase in diastolic pressure.
(16:00):
Next we get to Figure 5, hyphenating, talking about the
central line placement and passing through the tricuspid
valve and other aspects of passing the pulmonary artery
(16:24):
catheter into the heart. Take a while to study this, the
various diagrams, and the explanations associated with
them. The balloon should be deflated
and the catheter withdrawn if pressure changes do not occur at
(16:48):
the expected distances to prevent catheter.
Nothing. Occasionally the insertion may
require fluoroscopy or TEE for guidance. 4 After the catheter
(17:11):
tip enters the pulmonary artery,minimal additional advancement
results in a pulmonary artery occlusion pressure, that is,
PAOP waveform. The PA tracing should reappear
(17:34):
when the balloon is deflated, waging before maximal balloon
inflation signals an over wedgedposition and the catheter should
be slightly withdrawn, that is with the balloon deflated.
(17:57):
Because PA rupture from balloon over inflation may cause
haemorrhage and mortality, wage readings should be obtained
infrequently. PA pressure should be
continuously monitored to detectan over wedged position
(18:22):
indicative of catheter migration.
Correct PA catheter position is confirmed by a chest radiograph.
The numerous complications of pulmonary artery catheterization
include all those associated with central venous cannulation
(18:48):
plus endocarditis, thrombogenesis, pulmonary
infarction, pulmonary artery rupture and haemorrhage.
That is, particularly in patients taking anticoagulants,
older adults or female patients,or patients with pulmonary
(19:11):
hypertension. Catheter nothing, arrhythmias,
conduction abnormalities, and pulmonary valvular damage.
Even trace hemoptysis should notbe ignored because it may herald
(19:37):
PA rupture. If the latter is suspected,
prompt placement of a double lumen trachea tube may maintain
adequate oxygenation by the unaffected lung.
(19:57):
The risk of complications increases with the duration of
catheterization. Which usually should not exceed
72 hours. Clinical considerations.
PA catheters allow more precise estimation of left ventricular
(20:23):
preload than either CVP or physical examination.
That is, but not as precise as TEE.
As well as the sampling of mixedvenous blood catheters with
(20:44):
self-contained thermistors, which is discussed later in this
chapter, can be used to measure cardiac output from which a
multitude of hemodynamic values can be derived.
Some catheter designs incorporate electrodes that
(21:07):
allow intra cavitry, ECG recording and pacing.
Optional fibre optic bundles allow continuous measurements of
the oxygen saturation of mixed venous blood.
(21:28):
Next we get to Table 5-1 Hemodynamic variables derived
from pulmonary artery catheterization data.
The titles are the variable formula Normal and the units
(22:00):
variable Cardiac Index. Formula Cardiac outputs in
litres per minute divided by body surface area in metre
squared. Normal range 2.2 to 4.2 units,
(22:25):
litres per minute per metre. Square variable total peripheral
resistance formula. MEP minus CVP times 80 divided
(22:46):
by cardiac output in litres per minute.
Normal range 1200 to 1500 and units Dyne's second per CM
(23:06):
raised to the power of 5. Variable pulmonary vascular
resistance formula PA minus PAO P * 80 divided by cardiac
(23:28):
outputs in litres per minute, normal range 100 to 300 units,
Dines seconds per centimetre raised to the power of 5.
(23:50):
Variable stroke volume formula. Cardiac output in litres per
minute times 1000 divided by heart rate in beats per minute.
(24:10):
Normal range 60 to 90 units mills per beat.
Variable stroke index that is SIformula stroke volume in miles
(24:33):
per beat divided by body surfacearea in metre squared.
Normal range is 20 to 65 units is miles per beat per metre
squared. Variable right ventricular
(24:57):
stroke walk index formula is 0.0136 times PA minus CVP times
SI stroke index. Normal range is 30 to 65 units
(25:23):
is grammes metre per beat per metre squared.
Variable left ventricular strokewalk index formula 0.0136 MAP
(25:48):
minus PAOP times SI normal rangeis 46 to 60 and the units is
gramme metre per beat per metre square.
(26:11):
Stalin demonstrated the relationship between left
ventricular function and left ventricular end diastolic muscle
fibre length, which is usually proportionate to end diastolic
volume if compliance is not abnormally decreased, for
(26:41):
example, by myocardial leukaemiaoverload, ventricular
hypertrophy or pericardial tamponade.
LVEDP should reflect fibre length in the presence of a
(27:02):
normal mitral valve. Left atrial pressure approaches
left ventricular pressure duringdiastolic filling.
The left atrium connects to the right side of the heart through
(27:22):
the pulmonary vasculature. The distal lumen of a correctly
wedged PA catheter is located from right sided pressures by
balloon inflation. Its distal opening is exposed
(27:45):
only to capillary pressure, which, in the absence of high
airway pressures or pulmonary vascular disease, equals left
atrial pressure. In fact, aspiration through the
distal port during balloon inflation samples arterialized
(28:11):
blood. PAOP is an indirect measure of
LVEDP which, depending upon ventricular compliance,
approximates left ventricular end diastolic volume, whereas
(28:38):
central venous pressure may reflect right ventricular
function. A pulmonary artery catheter may
be indicated if either ventricleis marked markedly depressed,
causing disassociation of right and left sided hemodynamics.
(29:00):
CVP is poorly predictive of pulmonary capillary pressures,
especially in patients with abnormal left ventricular
function. Even the PAOP does not always
predict LVEDP, the relationship between left ventricular end
(29:31):
diastolic volume that is actual preload and pulmonary artery
occlusion pressure that is estimated preload can become
unreliable during conditions associated with changing left
atrial or ventricular compliance, mitral valve
(29:56):
function, or pulmonary vein resistance.
These conditions are commonly are common immediately following
major cardiac or vascular surgery and in critically I'll
patients who are receiving ionotrophic agents or
(30:20):
experiencing septic shock. Ultimately, the value of the
information provided by the pulmonary artery catheter is
dependent upon its correct interpretation by the patient's
caregivers. Thus, the pulmonary artery
(30:44):
catheter is only a tool to assist in goal directed
perioperative therapy. Given the increasing number of
less invasive methods now available to obtain similar
information, we anticipate that PA characterization will become
(31:07):
mostly of historical interest. Cardiac outputs.
Indications cardiac output measurements to permit
(31:29):
calculation of the stroke volumeis one of the primary reasons
for pulmonary artery catheterization.
Currently there are a number of alternative, less invasive
methods to estimate ventricular function to assist in goal
(31:51):
directed therapy techniques and complications.
A thermal dilution 5. The injection of a quantity that
(32:14):
is 2.55 or 10 meals of fluid that is below body temperature,
that is usually room temperatureor iced into the right atrium
changes the temperature of bloodin contact with the thermistor
(32:36):
at the tip of the PA catheter. The degree of change is
inversely proportional to cardiac output.
Temperature change is minimal ifthere is a high blood flow,
whereas temperature change is greater when flow is reduced.
(33:04):
After injection, one can plot the temperature as a function of
time to produce a thermal dilution curve.
Cardiac output is determined by a computer programme that
integrates the area under the curve.
(33:28):
Accurate measurements of cardiacoutput depend on rapid and
smooth injection, precisely known injectant temperature and
volume, correct entry of the calibration factors for the
specific type of PA catheter into the cardiac output
(33:49):
computer, and avoidance of measurements during
electrocutory, tricuspid regurgitation, and cardiac shunt
invalidate results because only right ventricular output into
(34:12):
the pulmonary artery is actuallybeing measured.
Rapid infusion of the Heist injectant has rarely resulted in
cardiac arrhythmias. Next we go to Figure 5-19,
(34:35):
explaining the comparison of thermodilution curves after
injection of cold saline into the superior venal cover.
You can pause the recording to, you know, take a little while to
go through this. A modification of the
(34:59):
thermodilution technique allows continuous cardiac output
measurements with a special catheter and monitor system.
The catheter contains a thermal filament that introduces small
pulses of heat into the blood proximal to the pulmonic valve
(35:25):
and a thermistor that measures changes in PA blood temperature.
A computer in the monitor determines cardiac output by
cross correlating the amount of heat input with the changes in
(35:46):
blood temperature. Trans pulmonary thermal
dilution. That is, Picosystem Worldview
system relies upon the same principles of thermal dilution,
(36:06):
but it does not require pulmonary artery
catheterization. A central line and a thermistor
equipped arterial catheter that is usually placed in the femoral
artery are necessary to perform trans pulmonary thermal
(36:27):
dilution. Thermal measurements from radial
artery catheters have been foundto be invalid.
Transpulmonary thermodilution measurements involve the
injection of a cold indicator into the superior venal cava via
(36:52):
a central line. The thermistor notes the change
in temperature in the arterial system following the cold
indicators transit through the heart and lungs and estimates
the cardiac output. Next, we get to Figure 5-20,
(37:18):
describing 2 methods combined for precise monitoring.
Pause the recording and take some time to go through it.
The two methods, Transpulmonary thermodilution, also permits the
(37:39):
calculation of both the global and diastolic volume.
GEDV and the extravascular long water EVLW.
Through mathematical analysis and extrapolation of the thermal
(38:01):
dilution curve, it is possible for the trans pulmonary thermal
dilution computer to calculate both the mean transit time of
the indicator and it's exponential decay time.
(38:21):
The intrathoracic thermal volumeITTV is the product of the
cardiac output and the mean transit time MTT.
The ITTV includes the pulmonary blood volume, that is PBV, EVLW,
(38:48):
and the blood contained within the heart.
The pulmonary thermal volume PTVincludes both the El that's EVLW
and the PBV, and it's obtained by multiplying the cardiac
(39:13):
output by the exponential decay time EDT.
Subtracting the pulmonary thermal volume from the
intratoracic thermal volume gives the GEDV, that is the
(39:39):
global end diastolic volume. The global end diastolic volume
is a hypothetical volume that assumes that all of the heart's
chambers are simultaneously fullin diastole, with a normal index
(40:02):
between 640 to 800 mils per metre squared.
The global end diastolic volume can assist in determining volume
status. An extravascular long water
index of less than 10 mils per kilogramme is normative.
(40:31):
The extravascular long water is the intratoracic thermal volume
minus the intratoracic blood volume.
The intratoracic blood volume isequal is equal to the global end
(40:54):
diastolic volume times 1.25. Next we get to Figure 5-21,
explaining the upper curve representing the classical
thermal dilution curve showing the concentration of an
indicator over time at the site of detection.
(41:18):
Take a little while to pause therecording and go through this
figure. Next we get to Figure 5-22,
explaining the assessment of global Ender's tolling volume by
Transcardio pulmonary thermal dilution.
(41:42):
Pause this recording again and spend a little while to
understand the figure. Thus, the extravascular long
water is equals to the intratoracic thermal volume
(42:07):
minus the intratoracic blood volume.
An increased extravascular long water can be indicative of fluid
overload. Through mathematical analysis of
the transpulmonary thermodilution curve, it is
(42:30):
therefore possible to obtain volumetric indices to guide
fluid replacement therapy. Moreover, these systems
calculate stroke volume variation and pulse pressure
variation through pulse contour analysis, both of which can be
(42:56):
used to determine fluid responsiveness.
Both stroke volume and pulse pressure are decreased during
positive pressure ventilation. The greater the variations over
the cause of positive pressure, inspiration and expiration, the
(43:23):
more likely the patient is to improve hemodynamic measures
following volume administration.Figure 5-23 demonstrates that
patients located on the steeper portion of the curve will be
(43:46):
more responsive to volume administration compared with
those whose volume status is already adequate.
Dynamic measures such as stroke volume and pulse pressure
variation assist in the identification of individuals
(44:07):
likely to respond to volume administration.
Next, we get to Figure 5-23, explaining that the fluid
responder located on the steep portion of the right atrial
(44:27):
pressure stroke cardiac output curve will augment the cardiac
output with minimal change in right atrial pressure when
administered a fluid challenge. Pause the recording to take some
time and go through this figure.Next we get to figure 5-24
(45:04):
explaining calculation of pulse pressure variation, and next to
it we go to Figure 5-25 explaining that pulse pressure
variation decreases as volume isadministered.
(45:25):
Take in a while to go through these figures.
Morgan and Michael's Clinical Anesthesiology, 7th edition,
Chapter 5, Part 3. Pulmonary artery catheterization
indications. The Pulmonary Artery
(00:24):
Pennsylvania catheter, or Swann Ganz catheter, was introduced
into routine practise in operating rooms and in coronary
and critical care units in the 1970s.
It quickly became common for sicker patients undergoing major
(00:45):
surgery to be managed with PA catheterization.
The catheter provided measurements of both Co.
That's cardiac outputs and pulmonary artery occlusion
pressures and was used to guide hemodynamic therapy, especially
(01:08):
when patients became unstable. Determination of the pulmonary
artery occlusion or wedge pressure permitted, that is in
the absence of mitral stenosis. An estimation of the left
ventricular end diastolic pressure LVEDP and depending on
(01:32):
ventricular compliance, ventricular volume.
Although the ability of the pulmonary artery catheter to
perform measurements of cardiac outputs.
Sorry, let's take it again. Through the ability of the
pulmonary artery catheter to perform measurements of cardiac
(01:55):
output, the patient, the patient's stroke volume was also
determined. Cardiac output is equals to
stroke volume times HR. That's heart rate.
Stroke volume is equals to cardiac output divided by heart
(02:19):
rate. Blood pressure is equal to
cardiac output times systemic vascular resistance.
Consequently, hemodynamic monitoring with the pulmonary
(02:39):
artery catheter attempted to discern why a patient was
unstable so that therapy could be directed at the underlying
problem. If the SVR is diminished, such
as in states of vasodialectric shock that is, sepsis, the
(03:02):
stroke volume may increase. Conversely, a reduction in
stroke volume may be secondary to poor cardiac performance or
hypovolemia. Determination of the wedge or
(03:23):
pulmonary capillary occlusion pressure, that is, PCOP by
inflating the catheter balloon estimates the LVDEP, that is the
left ventricular end diastolic pressure.
(03:45):
A decreased stroke volume in thesetting of a low pulmonary
capillary occlusion pressure divided by the LVDEP indicates
hypovolemia. Let's take it again.
(04:07):
A decreased SV in the setting ofa low CPOC, PCOP, stroke LVEDP
indicates hypovolemia and the need for volume administration.
A full heart reflected by a highCPOCPCOP stroke, LVEDP, and low
(04:34):
stroke volume indicates the needfor a positive ionotropic drug.
Conversely, a normal or increased stroke volume in the
setting of hypotension should betreated with the administration
(04:55):
of vasoconstrictor drugs to restore SVR in a vasodilated
patient. 2 Although patients canand do present concurrently with
(05:16):
hypovolemia, sepsis, and heart failure, the aforementioned
shock treatment approach using the PA catheter to guide therapy
became more or less synonymous with perioperative intensive
care and cardiac anaesthesia. However, several large
(05:44):
observational studies have shownthat patients managed with PA
catheters had worse outcomes than similar patients who were
managed without PA catheters. Other studies seem to indicate
that although PA catheter guidedpatient management may do no
(06:08):
harm, it offers no specific benefits.
Although the PA catheter can be used to guide goal directed
hemodynamic therapy to ensure organ perfusion in shock states,
(06:29):
other less invasive methods to determine hemodynamic
performance are available including trans pulmonary
thermodilution, cardiac output measurements, pulse contour
analysis of the atrial pressure waveform, and methods based on
(06:54):
bio impedance measurements across the chest.
All these methods permits calculation of the stroke volume
as a guide for hemodynamic management.
Moreover, right atrial blood oxygen saturation, as opposed to
(07:21):
mixed venous saturation that is normal is 75%, can be used as an
alternative measure to discern tissue oxygen extraction and the
adequacy of tissue oxygen delivery.
(07:43):
Despite numerous reports of its questionable utility and the
increasing number of alternativemethods to determine hemodynamic
parameters, the PA catheter is still employed perioperatively
more often in the United States than elsewhere.
(08:06):
Although echocardiography can readily determine if the heart
is full, compressed, contracting, or empty, a trained
individual is required to obtainand interpret the images.
(08:26):
Alternative hemodynamic monitorshave gained wide acceptance in
Europe and are increasingly usedin the United States, further
decreasing the use of PA catheters.
PA catheterization can be considered whenever cardiac
(08:51):
index, preload, volume status, or the degree of mixed venous
blood oxygenation need to be known.
These measurements might prove particularly important in
surgical patients at great risk of hemodynamic instability or
(09:15):
during surgical procedures associated with a greatly
increased incidence of hemodynamic complications.
However, the authors prefer trans esophageal
echocardiography in these situations.
(09:38):
Contraindications. Relative contraindications to PA
catheterization include left bundle branch block that is
because of the concern about complete heart block and
conditions associated with a greatly increased risk of
(10:03):
arrhythmias. A catheter with pacing
capability is better suited to these situations.
A PA catheter may serve as a nine dose of infection in
bacteremic patients of thromboseformation.
(10:25):
In patients prone to hypercoagulation techniques and
complications. Although various PA catheters
are available, the most popular design integrates 5 lumens into
(10:47):
a 7.5 F catheter 110 centimetreslong with a Poly vinyl chloride
body. The lumens house the following
wiring to connect the thermistornear the catheter tip to a
(11:12):
thermal dilution cardiac output computer.
An air channel for inflation of the balloon, A proximal port 30
centimetres from the tip for infusions, cardiac output
(11:33):
injections, and measurements of right atrial pressures.
A ventricular port at 20 CM for infusion of drugs and a distal
port for aspiration of mixed venous blood samples and
(11:55):
measurements of PA pressure. Next we go to Figure 5-16
talking about a balloon tipped pulmonary artery flotation
catheter, also known as the Schwann Gans catheter.
(12:23):
At the proximal lens you have the RA and proximal infusion,
and at the distal lens you have the thermistor, pulmonary
artery, distal port, proximal infusion port, right atrial
port, and balloon. Insertion of a PA catheter
(12:52):
requires central venous access, which can be accomplished using
the previously described Seldinger technique.
Instead of a central venous catheter, a dilator and sheath
are threaded over the guide wire.
(13:14):
The sheet lumen accommodates thePA catheter after removal of the
dilator and guide wire. Prior to insertion, the PA
catheter is checked by inflatingand deflating its balloon and
(13:39):
filling all three lumens with intravenous fluid.
The distal port is connected to a transducer that is zeroed to
the patient's mid axillary line.The PA catheter is advanced
(14:02):
through the introducer and into the internal jugular vein at
approximately 15 centimetres. The distal tip should enter the
right atrium and a central venous tracing that varies with
(14:22):
respiration confirms an intrathoracic position.
The balloon is then inflated with air according to the
manufacturer's recommendations. That is usually 1.5 mils to
protect the endocardium from thecatheter tip and to allow flow
(14:48):
through the right ventricle to direct the catheter forward.
The balloon is always deflated during withdrawal.
During catheter advancement, theECG should be monitored for
arrhythmias. Transient ectopy from irritation
(15:13):
of the right ventricle by the balloon and catheter tip is
common and rarely requires treatment.
A sudden increase in the systolic pressure on the distal
tracing indicates a right ventricular location of the
(15:34):
catheter tip. Entry into the pulmonary artery
normally occurs by 35 to 45 centimetres and is heralded by
sudden increase in diastolic pressure.
(16:00):
Next we get to Figure 5, hyphenating, talking about the
central line placement and passing through the tricuspid
valve and other aspects of passing the pulmonary artery
(16:24):
catheter into the heart. Take a while to study this, the
various diagrams, and the explanations associated with
them. The balloon should be deflated
and the catheter withdrawn if pressure changes do not occur at
(16:48):
the expected distances to prevent catheter.
Nothing. Occasionally the insertion may
require fluoroscopy or TEE for guidance. 4 After the catheter
(17:11):
tip enters the pulmonary artery,minimal additional advancement
results in a pulmonary artery occlusion pressure, that is,
PAOP waveform. The PA tracing should reappear
(17:34):
when the balloon is deflated, waging before maximal balloon
inflation signals an over wedgedposition and the catheter should
be slightly withdrawn, that is with the balloon deflated.
(17:57):
Because PA rupture from balloon over inflation may cause
haemorrhage and mortality, wage readings should be obtained
infrequently. PA pressure should be
continuously monitored to detectan over wedged position
(18:22):
indicative of catheter migration.
Correct PA catheter position is confirmed by a chest radiograph.
The numerous complications of pulmonary artery catheterization
include all those associated with central venous cannulation
(18:48):
plus endocarditis, thrombogenesis, pulmonary
infarction, pulmonary artery rupture and haemorrhage.
That is, particularly in patients taking anticoagulants,
older adults or female patients,or patients with pulmonary
(19:11):
hypertension. Catheter nothing, arrhythmias,
conduction abnormalities, and pulmonary valvular damage.
Even trace hemoptysis should notbe ignored because it may herald
(19:37):
PA rupture. If the latter is suspected,
prompt placement of a double lumen trachea tube may maintain
adequate oxygenation by the unaffected lung.
(19:57):
The risk of complications increases with the duration of
catheterization. Which usually should not exceed
72 hours. Clinical considerations.
PA catheters allow more precise estimation of left ventricular
(20:23):
preload than either CVP or physical examination.
That is, but not as precise as TEE.
As well as the sampling of mixedvenous blood catheters with
(20:44):
self-contained thermistors, which is discussed later in this
chapter, can be used to measure cardiac output from which a
multitude of hemodynamic values can be derived.
Some catheter designs incorporate electrodes that
(21:07):
allow intra cavitry, ECG recording and pacing.
Optional fibre optic bundles allow continuous measurements of
the oxygen saturation of mixed venous blood.
(21:28):
Next we get to Table 5-1 Hemodynamic variables derived
from pulmonary artery catheterization data.
The titles are the variable formula Normal and the units
(22:00):
variable Cardiac Index. Formula Cardiac outputs in
litres per minute divided by body surface area in metre
squared. Normal range 2.2 to 4.2 units,
(22:25):
litres per minute per metre. Square variable total peripheral
resistance formula. MEP minus CVP times 80 divided
(22:46):
by cardiac output in litres per minute.
Normal range 1200 to 1500 and units Dyne's second per CM
(23:06):
raised to the power of 5. Variable pulmonary vascular
resistance formula PA minus PAO P * 80 divided by cardiac
(23:28):
outputs in litres per minute, normal range 100 to 300 units,
Dines seconds per centimetre raised to the power of 5.
(23:50):
Variable stroke volume formula. Cardiac output in litres per
minute times 1000 divided by heart rate in beats per minute.
(24:10):
Normal range 60 to 90 units mills per beat.
Variable stroke index that is SIformula stroke volume in miles
(24:33):
per beat divided by body surfacearea in metre squared.
Normal range is 20 to 65 units is miles per beat per metre
squared. Variable right ventricular
(24:57):
stroke walk index formula is 0.0136 times PA minus CVP times
SI stroke index. Normal range is 30 to 65 units
(25:23):
is grammes metre per beat per metre squared.
Variable left ventricular strokewalk index formula 0.0136 MAP
(25:48):
minus PAOP times SI normal rangeis 46 to 60 and the units is
gramme metre per beat per metre square.
(26:11):
Stalin demonstrated the relationship between left
ventricular function and left ventricular end diastolic muscle
fibre length, which is usually proportionate to end diastolic
volume if compliance is not abnormally decreased, for
(26:41):
example, by myocardial leukaemiaoverload, ventricular
hypertrophy or pericardial tamponade.
LVEDP should reflect fibre length in the presence of a
(27:02):
normal mitral valve. Left atrial pressure approaches
left ventricular pressure duringdiastolic filling.
The left atrium connects to the right side of the heart through
(27:22):
the pulmonary vasculature. The distal lumen of a correctly
wedged PA catheter is located from right sided pressures by
balloon inflation. Its distal opening is exposed
(27:45):
only to capillary pressure, which, in the absence of high
airway pressures or pulmonary vascular disease, equals left
atrial pressure. In fact, aspiration through the
distal port during balloon inflation samples arterialized
(28:11):
blood. PAOP is an indirect measure of
LVEDP which, depending upon ventricular compliance,
approximates left ventricular end diastolic volume, whereas
(28:38):
central venous pressure may reflect right ventricular
function. A pulmonary artery catheter may
be indicated if either ventricleis marked markedly depressed,
causing disassociation of right and left sided hemodynamics.
(29:00):
CVP is poorly predictive of pulmonary capillary pressures,
especially in patients with abnormal left ventricular
function. Even the PAOP does not always
predict LVEDP, the relationship between left ventricular end
(29:31):
diastolic volume that is actual preload and pulmonary artery
occlusion pressure that is estimated preload can become
unreliable during conditions associated with changing left
atrial or ventricular compliance, mitral valve
(29:56):
function, or pulmonary vein resistance.
These conditions are commonly are common immediately following
major cardiac or vascular surgery and in critically I'll
patients who are receiving ionotrophic agents or
(30:20):
experiencing septic shock. Ultimately, the value of the
information provided by the pulmonary artery catheter is
dependent upon its correct interpretation by the patient's
caregivers. Thus, the pulmonary artery
(30:44):
catheter is only a tool to assist in goal directed
perioperative therapy. Given the increasing number of
less invasive methods now available to obtain similar
information, we anticipate that PA characterization will become
(31:07):
mostly of historical interest. Cardiac outputs.
Indications cardiac output measurements to permit
(31:29):
calculation of the stroke volumeis one of the primary reasons
for pulmonary artery catheterization.
Currently there are a number of alternative, less invasive
methods to estimate ventricular function to assist in goal
(31:51):
directed therapy techniques and complications.
A thermal dilution 5. The injection of a quantity that
(32:14):
is 2.55 or 10 meals of fluid that is below body temperature,
that is usually room temperatureor iced into the right atrium
changes the temperature of bloodin contact with the thermistor
(32:36):
at the tip of the PA catheter. The degree of change is
inversely proportional to cardiac output.
Temperature change is minimal ifthere is a high blood flow,
whereas temperature change is greater when flow is reduced.
(33:04):
After injection, one can plot the temperature as a function of
time to produce a thermal dilution curve.
Cardiac output is determined by a computer programme that
integrates the area under the curve.
(33:28):
Accurate measurements of cardiacoutput depend on rapid and
smooth injection, precisely known injectant temperature and
volume, correct entry of the calibration factors for the
specific type of PA catheter into the cardiac output
(33:49):
computer, and avoidance of measurements during
electrocutory, tricuspid regurgitation, and cardiac shunt
invalidate results because only right ventricular output into
(34:12):
the pulmonary artery is actuallybeing measured.
Rapid infusion of the Heist injectant has rarely resulted in
cardiac arrhythmias. Next we go to Figure 5-19,
(34:35):
explaining the comparison of thermodilution curves after
injection of cold saline into the superior venal cover.
You can pause the recording to, you know, take a little while to
go through this. A modification of the
(34:59):
thermodilution technique allows continuous cardiac output
measurements with a special catheter and monitor system.
The catheter contains a thermal filament that introduces small
pulses of heat into the blood proximal to the pulmonic valve
(35:25):
and a thermistor that measures changes in PA blood temperature.
A computer in the monitor determines cardiac output by
cross correlating the amount of heat input with the changes in
(35:46):
blood temperature. Trans pulmonary thermal
dilution. That is, Picosystem Worldview
system relies upon the same principles of thermal dilution,
(36:06):
but it does not require pulmonary artery
catheterization. A central line and a thermistor
equipped arterial catheter that is usually placed in the femoral
artery are necessary to perform trans pulmonary thermal
(36:27):
dilution. Thermal measurements from radial
artery catheters have been foundto be invalid.
Transpulmonary thermodilution measurements involve the
injection of a cold indicator into the superior venal cava via
(36:52):
a central line. The thermistor notes the change
in temperature in the arterial system following the cold
indicators transit through the heart and lungs and estimates
the cardiac output. Next, we get to Figure 5-20,
(37:18):
describing 2 methods combined for precise monitoring.
Pause the recording and take some time to go through it.
The two methods, Transpulmonary thermodilution, also permits the
(37:39):
calculation of both the global and diastolic volume.
GEDV and the extravascular long water EVLW.
Through mathematical analysis and extrapolation of the thermal
(38:01):
dilution curve, it is possible for the trans pulmonary thermal
dilution computer to calculate both the mean transit time of
the indicator and it's exponential decay time.
(38:21):
The intrathoracic thermal volumeITTV is the product of the
cardiac output and the mean transit time MTT.
The ITTV includes the pulmonary blood volume, that is PBV, EVLW,
(38:48):
and the blood contained within the heart.
The pulmonary thermal volume PTVincludes both the El that's EVLW
and the PBV, and it's obtained by multiplying the cardiac
(39:13):
output by the exponential decay time EDT.
Subtracting the pulmonary thermal volume from the
intratoracic thermal volume gives the GEDV, that is the
(39:39):
global end diastolic volume. The global end diastolic volume
is a hypothetical volume that assumes that all of the heart's
chambers are simultaneously fullin diastole, with a normal index
(40:02):
between 640 to 800 mils per metre squared.
The global end diastolic volume can assist in determining volume
status. An extravascular long water
index of less than 10 mils per kilogramme is normative.
(40:31):
The extravascular long water is the intratoracic thermal volume
minus the intratoracic blood volume.
The intratoracic blood volume isequal is equal to the global end
(40:54):
diastolic volume times 1.25. Next we get to Figure 5-21,
explaining the upper curve representing the classical
thermal dilution curve showing the concentration of an
indicator over time at the site of detection.
(41:18):
Take a little while to pause therecording and go through this
figure. Next we get to Figure 5-22,
explaining the assessment of global Ender's tolling volume by
Transcardio pulmonary thermal dilution.
(41:42):
Pause this recording again and spend a little while to
understand the figure. Thus, the extravascular long
water is equals to the intratoracic thermal volume
(42:07):
minus the intratoracic blood volume.
An increased extravascular long water can be indicative of fluid
overload. Through mathematical analysis of
the transpulmonary thermodilution curve, it is
(42:30):
therefore possible to obtain volumetric indices to guide
fluid replacement therapy. Moreover, these systems
calculate stroke volume variation and pulse pressure
variation through pulse contour analysis, both of which can be
(42:56):
used to determine fluid responsiveness.
Both stroke volume and pulse pressure are decreased during
positive pressure ventilation. The greater the variations over
the cause of positive pressure, inspiration and expiration, the
(43:23):
more likely the patient is to improve hemodynamic measures
following volume administration.Figure 5-23 demonstrates that
patients located on the steeper portion of the curve will be
(43:46):
more responsive to volume administration compared with
those whose volume status is already adequate.
Dynamic measures such as stroke volume and pulse pressure
variation assist in the identification of individuals
(44:07):
likely to respond to volume administration.
Next, we get to Figure 5-23, explaining that the fluid
responder located on the steep portion of the right atrial
(44:27):
pressure stroke cardiac output curve will augment the cardiac
output with minimal change in right atrial pressure when
administered a fluid challenge. Pause the recording to take some
time and go through this figure.Next we get to figure 5-24
(45:04):
explaining calculation of pulse pressure variation, and next to
it we go to Figure 5-25 explaining that pulse pressure
variation decreases as volume isadministered.
(45:25):
Take in a while to go through these figures.
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