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SEPTEMBER 2005
VOL 7.8
STANDARDS of CARE
Peer Reviewed
EMERGENCY AND CRITICAL CARE MEDICINE ®
F ROM
THE
P UBLISHER
OF
COMPENDIUM
MEASUREMENT OF CENTRAL VENOUS
PRESSURE IN CRITICAL PATIENTS
Mary B. Tefend, RVT, MS
Clinical Instructor, Veterinary Critical Care Nursing
Douglass Macintire, DVM, MS, DACVIM, DACVECC
Professor
Department of Clinical Sciences
School of Veterinary Medicine
Auburn University
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Now Available!
See page 5 for details.
C
entral venous pressure (CVP) is the hydrostatic
or luminal pressure in the intrathoracic vena
cava. Because CVP is affected by circulatory
mean systemic pressure and venous return and
because it affects cardiac preload, its measurement
provides valuable information about cardiac performance and intravascular volume. CVP varies throughout
both the respiratory and cardiac cycles; during inspiration, intrathoracic pressure decreases and CVP falls.
In the presence of normally functioning cardiac
valves, right ventricular cardiac preload (i.e., the
amount of blood in the ventricle at the end of diastole) is affected by right atrial pressure, which in turn
is determined by CVP. CVP therefore indirectly
reflects right ventricular preload. Monitoring cardiac
preload via CVP in critically ill patients can help
ascertain blood volume status and subsequently
direct the course of fluid therapy. It also helps clinicians interpret the cardiac response to intravenous
fluids and thus identify which patients are likely to
develop pulmonary edema, even before traditional
clinical signs of fluid overload occur. In addition,
measuring CVP can be helpful in determining the
presence of volume depletion secondary to trauma or
illness and can be used in the management of renal
dysfunction, heart disease, septic shock, or any
patient that may require administration of large volumes of intravenous fluids.
Measuring CVP is technically simple. The goal of
monitoring CVP is to provide an objective assess-
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ment of both volume status and cardiac function in
response to intravenous fluids. Monitoring CVP can
help prevent volume overload from occurring and
aid in volume resuscitation for critical hypovolemic
patients. It can provide early evidence of volume
overload in patients with suspected cardiovascular
disease, pericardial effusion, or right-sided heart
failure. Causes of elevated CVP not associated with
volume overload include pleural or pericardial effusion, pulmonary hypertension, pulmonary thromboembolism, and pneumothorax; CVP may also be
elevated in patients with poor pulmonary compliance or that are mechanically ventilated and require
increased positive end expiratory pressure or increased
mean airway pressures.
DIAGNOSTIC CRITERIA
Historical Information
Age/Gender/Breed Predispositions
• None. CVP monitoring can be used on any animal.
• CVP monitoring is particularly useful for patients at
risk of volume overload (e.g., geriatric patients,
oliguric patients with acute renal failure).
• CVP monitoring can be used to avoid volume
Also in this issue:
6 Management of Canine Paraphimosis
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SEPTEMBER 2005 VOL 7.8
overload in patients receiving colloids (such as hetastarch or Oxyglobin
[Biopure]).
• CVP monitoring can be helpful in patients with septic shock because
vasodilation contributes to hypotension despite seemingly adequate fluid
loading.
• CVP monitoring can help prevent fluid overload in patients with acute
oliguric renal failure (urine output less than 1 ml/kg/hr).
Other Historical Considerations/Predispositions
Monitoring CVP is often indicated to help assess cardiovascular function.
CVP is a measure of pressure generated in the intrathoracic vena cava as
deoxygenated blood returns to the heart. If heart rate and myocardial function are held constant as venous return decreases, CVP decreases. Similarly,
as venous return increases, CVP increases. This is of clinical importance as
the CVP is used to measure the filling pressures of the right side of the heart,
or more specifically, the right atrial and right ventricular end-diastolic pressures. Extreme elevations in CVP are seen with right-sided heart failure and
pericardial effusion. Pleural effusion can also cause abnormally high CVP in
the absence of suspected right-sided heart failure.
Monitoring CVP is useful in patients receiving large volumes of fluids,
especially when physical examination is insufficient to assess an end-point
for fluid resuscitation. Because CVP can be affected by cardiac function, CVP
should also be monitored in patients with suspected heart disease.
CVP may be high as a result of conditions associated with decreased ventricular compliance, such as hypertrophic cardiomyopathy, pericardial effusion, and right AV valvular insufficiency.
CVP, like other hemodynamic markers, can be a useful tool only when
used in combination with other parameters to assess critical patients. Note that
CVP trends are more important than a single number. Typically, normal CVP
values range from 0 to 8 cm H2O, with values less than zero indicating hypovolemia and values over 10 cm H2O suggesting volume overload.
In general, a low CVP value (less than 0 cm H2O) is consistent with hypovolemia and may indicate insufficient blood volume in the ventricle during
diastole or increased venous compliance secondary to septic shock or endotoxemia. The combination of low CVP values with tachycardia and other
physical examination findings indicating poor perfusion (e.g., poor pulse
quality or poor jugular filling, pale mucous membranes, prolonged capillary
refill time) usually indicates the need for volume replacement.
Conversely, tachycardia or jugular distention combined with elevated
CVP values may suggest fluid overload. A high CVP (greater than 8 cm H2O)
indicates volume overload, tricuspid valve insufficiency, increased pulmonary vascular resistance (afterload), pericardial effusion, or other causes of
right-sided congestive heart failure. Patients with consistently elevated CVP
readings exceeding 10 cm H2O may develop edema and/or effusions.
EMERGENCY AND CRITICAL CARE MEDICINE ®
Editorial Mission:
To provide busy practitioners with concise,
peer-reviewed recommendations on current
treatment standards drawn from published
veterinary medical literature.
This publication acknowledges that standards
may vary according to individual experience
and practices or regional differences. The
publisher is not responsible for author errors.
Compendium’s Standards of Care:
Emergency and Critical Care Medicine®
is published 11 times yearly
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© 2005, Veterinary Learning Systems.
Editor-in-Chief
Douglass K. Macintire, DVM, MS,
DACVIM, DACVECC
Editorial, Design, and Production
Lilliane Anstee, Vice President,
Editorial and Design
Maureen McKinney, Editorial Director
Cheryl Hobbs, Senior Editor
Michelle Taylor, Senior Art Director
Bethany L. Wakeley, Studio Manager
Chris Reilly, Assistant Editor
Kristin Sevick, Editorial Assistant
Andrea Vardaro, Editorial Assistant
Editorial Review Board
Mark Bohling, DVM
University of Tennessee
Harry W. Boothe, DVM, DACVS
Auburn University
Derek Burney, DVM, PhD, DACVIM
Houston, TX
Joan R. Coates, DVM, MS, DACVIM
University of Missouri
Physical Examination Findings
Associated with Abnormal CVP
Curtis Dewey, DVM, DACVIM, DACVS
Plainview, NY
• Low CVP measurements consistent with hypovolemia may accompany
physical examination findings of poor perfusion, which include:
Nishi Dhupa, DVM, DACVECC
Cornell University
KEY TO COSTS
D. Michael Tillson, DVM, MS, DACVS
Auburn University
$ indicates relative costs of any diagnostic and treatment regimens listed.
$ costs under $250
$$ costs between $250 and $500
$$$ costs between $500 and $1,000
$$$$ costs over $1,000
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— Generalized weakness; dull mentation.
— Poor peripheral pulse quality; prolonged capillary refill time.
— Pale or muddy, dry mucous membranes.
— Abnormal respiratory rate and/or effort.
— Decreased urine output.
• Increased trends or elevated CVP measurements may
indicate volume overload; clinical signs include:
— Increased heart rate.
— Increased respiratory rate.
— Harsh lung sounds.
— Chemosis.
— Clear nasal discharge.
— Increased body weight.
— Jugular vein distention.
— Peripheral edema.
— Radiographic evidence of pulmonary edema,
pleural effusion, and pulmonary venous congestion.
CHECKPOINT
— Contraindications to measuring CVP are few
and relate to placement of a central venous
catheter. Patients that may have complications
with central venous catheterization include
those with a history of:
• Coagulopathies, which may cause excessive bleeding from the venipuncture site.
• Thromboembolic diseases.
• Hyperadrenocorticism.
• Immune-mediated hemolytic anemia.
• Increased intracranial pressure (e.g.,
because of head trauma, seizures,
intracranial disease).
• Respiratory distress.
dirofilariasis, pericardial effusion or tamponade,
and restrictive pericarditis.
— Increased pulmonary vascular resistance (e.g.,
pulmonary hypertension, pulmonary fibrosis,
heartworm disease).
TREATMENT
Treatment of critical patients should not be based
solely on CVP measurements; physical examination
findings should always be weighed more significantly
than CVP readings. In addition, edema and effusion
can be secondary to other processes, such as increased
capillary endothelial permeability associated with systemic inflammation and low oncotic pressure, even in
hypovolemic patients.
• If the CVP is less than 2 cm H2O, real or functional
hypovolemia should be suspected. A fluid challenge can be administered intravenously by a 10 to
15 ml/kg bolus of a crystalloid fluid or a 3 to 5 ml/kg
bolus of a colloid solution. The CVP should be
rechecked immediately after administration of the
fluid bolus:
— Animals with hypovolemia will show little or
no change in CVP.
— Animals with normovolemia will show a transient increase in CVP of 2 to 4 cm H2O with a
return to baseline within 15 minutes.
— Animals with hypervolemia or reduced cardiac
compliance will show a sustained increase in
CVP (greater than 4 cm H2O) that continues for
more than 30 minutes.
• If the CVP exceeds 10 cm H2O, fluid therapy should
be discontinued until CVP decreases; fluid rate
should then be decreased. In some cases of volume
overload, intravenous furosemide is indicated.
Causes of elevated CVP include:
— Volume overload.
— Right-sided heart failure, tricuspid insufficiency,
Procedural Recommendations
Equipment $
• Central venous catheter (Arrow International; 18gauge for cats, 16-gauge for medium-sized dogs,
14-gauge for large-breed dogs; commercial length
typically 20 cm).
• T-port (Arrow International).
• Manometer (Allegiance or Cardinal Health).
• Extension tubing.
• Three-way stopcock.
• Saline-filled syringe.
Technique
The use of standard protocols in measuring CVP is
important to minimize infection, to promote catheter
longevity, and most importantly, to yield consistent
results. Recommended technique:
• Tip of a central venous catheter should be located in
the cranial vena cava just outside the right atrium.
• Patient should be in right lateral recumbency with
the head and neck hyperextended to avoid positional catheter issues.
• The saline-filled syringe, saline-flushed extension
set, and three-way stopcock are attached to the
manometer.
• The central venous catheter is attached to the
manometer via the extension set.
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• Placement of a multilumen catheter allows for concurrent fluid therapy, drug infusions, and/or blood
sampling as well as CVP monitoring. CVP values
should be measured through the distal port (usually the colored port) if a multilumen catheter is
used.
• In slowly evolving fluid overload with fluid therapy
(hours to days), CVP may not increase until the
capacitance veins have reached maximum distension and edema is imminent; therefore, CVP monitoring is less valuable than body weight change and
other physical findings in this setting. CVP will
change much more rapidly and unequivocally in
response to rapid fluid challenges.
• A catheter inserted into the femoral vein can also be
used to estimate CVP. The tip of the catheter should
be positioned in the abdominal vena cava, which
will provide a good estimate of right ventricular filling pressure as long as there is not increased
abdominal pressure from bladder distention, an
abdominal mass, severe abdominal pain, or an
abdominal pressure wrap.
• Sterility should be emphasized both during
catheter placement and when taking each CVP
reading. Nursing care becomes particularly important because central catheters are typically left in
place for a longer time than are peripheral
catheters. Daily inspection of insertion site, daily
bandage changes, intermittent flushing with
heparinized saline, and conscientious practice of
sterile technique during measurement readings are
of utmost importance. Excessive loops of tubing
should be avoided, Luer-lock connections should
be used to prevent fluid leakage or air boluses, and
three-way stopcocks on the catheter itself are
needed to avoid introduction of bacteria; likewise,
manometers need to be taped onto the cage or
stored with sterile caps if used intermittently.
FRONT
— CVP can be monitored continuously by
using a disposable pressure transducer
(Edwards Lifesciences) mounted on a board
or placed at the level of the patient’s heart.
The pressure transducer converts the
pressure changes generated by contraction
of the heart into an electrical signal, which
is transmitted to a monitor (Agilent
Technologies, V24CT) through a transducer
cable (Agilent Technologies). The signal is
then amplified and displayed as a pressure
waveform. Values are reported in mm Hg
instead of cm H2O; the mm Hg value is
multiplied by 1.36 to convert it to cm H2O. $
• The zero point on the manometer should be
equal with the level of the patient’s heart; the
zero point can be gauged visually by lining it up
with the manubrium (most cranial portion of the
sternum).
• The stopcock is turned off to the patient and the
manometer filled with saline. The stopcock is then
turned off to the syringe, allowing direct communication between the manometer and the catheter.
The saline column is allowed to equilibrate. Proper
placement of the catheter will result in small fluctuations of the fluid meniscus coinciding with
changes in intrathoracic pressure that occur with
respirations.
• CVP equals the level of the fluid on the manometer
less the number correlating with the zero point. For
example, if the fluid meniscus is at 15 cm H2O and
the zero point (manubrium) is at 10 cm H2O, the
CVP is estimated to be 5 cm H2O.
• Several readings should be taken before recording a
measurement.
Prognostic Criteria
Practical Tips
• Because CVP values can be affected by a patient’s
position, consistency in patient positioning is
critical.
• Incorrect catheter placement affects readings;
placement should be confirmed by radiography or
fluoroscopy.
• Changes in normal intrathoracic pressures (e.g.,
because of pneumothorax or positive pressure ventilation) will affect CVP readings, resulting in falsely
high readings.
• Undulations in fluid level that correlate to the
patient’s heartbeat may indicate excessive length of
catheter in the right atrium or right ventricle and
will result in falsely elevated CVP measurements.
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Favorable
• CVP measurements in the normal range combined
with normal urine output (more than 2 ml/kg/hr) in
patients with acute renal failure.
• CVP values returning to the normal range after discontinuation of intravenous fluids or administration of furosemide in patients showing signs of
hypervolemia.
• Negative or low CVP readings increasing to 5 to 7
cm H2O in response to fluid loading, pressor therapy, or positive inotrope therapy in patients with
vasodilatory shock.
• Decrease in CVP readings to normal range following pericardiocentesis in animals with pericardial
effusion.
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Unfavorable
• Increasing CVP in patients with acute renal failure
and anuria or oliguria is a poor prognostic indicator.
• Volume overload associated with cyanosis, respiratory distress, and pulmonary edema has a guarded
prognosis and should be corrected immediately and
the patient treated with supplemental oxygen.
• Acute increase in CVP associated with labored
breathing can be seen with pulmonary hypertension secondary to pulmonary thromboembolism.
Prognosis is guarded.
• Gradually increasing CVP and progressive dyspnea
can also be seen with accumulating pleural effusion. Thoracentesis is indicated.
RECOMMENDED READING
De Laforcade AM, Rozanski L: Central venous pressure and arterial blood pressure measurements. Vet Clin North Am Small
Anim Pract 31(6):1163–1173, 2001.
Macintire DK, Drobatz KJ, Haskins SC, Saxon WD: Manual of
Small Animal Emergency and Critical Care Medicine.
Philadelphia, Lippincott Williams & Wilkins, 2005, pp 71–74.
Silverstein D: Resuscitation versus hydration: Fluid therapy objectives. Proc IVECCS VIII:184–189, 2002.
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CRITICAL
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MEDICINE