1.
American Journal of Therapeutics 0, 000–000 (2011)
Pulmonary Hypertension: A Review of
Pathophysiology and Anesthetic Management
Ali Salehi, MD
Pulmonary hypertension is a condition that can result in serious complications in patients
undergoing any type of anesthesia during the perioperative period. By definition, pulmonary artery
hypertension is caused by a persistent rise in mean pulmonary artery pressure $25 mm Hg with
Pulmonary capillary wedge pressure # 15 mm Hg or exercise mean pulmonary artery pressure $35
mm Hg and pulmonary vascular resistance $ 3 wood unit’s. The severity of the complications
depends on the severity of the underlying condition, other comorbidities, and type of procedure,
anesthetic technique, and anesthetic drugs. In this article, we briefly review the pulmonary vascular
physiology, pathophysiology of the disease, clinical assessment and diagnosis, treatment options,
and the anesthetic management of these patients.
Keywords: pulmonary hypertension, pulmonary vasoconstriction/dilatation, nitric oxide, prostacycline, phosphodiesterase-3, phosphodiesterase-5, anesthetic agents, anesthetic management
PHYSIOLOGY
A pulmonary vascular bed is a high flow, low pressure
system. Normal PA pressure is about one-fifth of the
systemic pressure.1 It has a lower resistance compared
with systemic vasculature (40–120 vs. 800–1200
dynÁs/cm5)1 due to thinner media and less smooth
muscle. Factors that can affect the pulmonary vascular
resistance (PVR) include oxygenation, hypercarbia and
acidosis, cardiac output, lung volumes and airway
pressure, gravity, pulmonary vascular endothelium
and vascular mediators.2–4 Pulmonary vasculature
constricts in response to hypoxia (Euler–Liljestrand
reflex) and dilates in response to hyperoxia. PVR rises
as the PO2 decreases below 60 mm Hg.5
Ronald Regan UCLA Medical Center, Department of Anesthesiology, Division of Cardiothoracic Anesthesia, David Geffen School
of Medicine at UCLA, Los Angeles, CA.
Address for correspondence: Ronald Regan UCLA Medical Center,
Department of Anesthesiology, Division of Cardiothoracic Anesthesia, David Geffen School of Medicine at UCLA, 757 Westwood
Plaza, Suite 3325, Los Angeles, CA 90095-7403. E-mail: asalehi@
mednet.ucla.edu
1075–2765 Ó 2011 Lippincott Williams & Wilkins
Hypercarbia does not directly affect PVR. It increases
PVR through an increase in H+ ion and resulting acidosis.
Hypoxia and acidosis have a synergistic effect on PVR.5
Increase in cardiac output enrolls the closed blood
vessels and dilates the open vessels in the lung
resulting in a net increase in pulmonary circulation
area and hence a decrease in PVR. An increase in left
artrial (LA) pressures also has the same effect.
Clinically, the use of inotropes or enhanced blood
volume will passively decrease PVR.4
VR is maximum with small lung volumes (vasoconstriction of alveolar blood vessels) and large lung
volumes (compression of extraalveolar vessels), and it
is minimum at functional residual capacity. This results
in a ‘‘U’’ shape relationship (Fig. 1) between PVR and
lung volumes.4 High positive end expiratory pressure
(PEEP) also compresses the vasculature in the wellventilated areas of the lung and diverts the flow to less
ventilated areas resulting in [PVR and YPaO2. Hence,
in clinical practice, one should avoid hypo/hyperventilation and high PEEP in patients with pulmonary
hypertension.
Gravity increases the blood flow to the dependent
parts of the lung. This is important in patients with
unilateral lung disease. To obtain the best gas
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FIGURE 1. Relationship between lung volume and PVR.
RV, residual volume, FRC, functional residual capacity,
TLC, total lung capacity.4
exchange, these patients should be ventilated with their
diseased side up.6
There are 2 main mechanisms in the pulmonary
vascular endothelium that affect the pulmonary
vascular tone and PVR: The first mechanism initiated
in the endothelium is the activation of nitric oxide (NO)
syntase. NO syntase converts L-Argenine to L-Citrulin
and release of NO. NO diffuses to the smooth muscle
and increases the activity of the enzyme Guanylate
synthase, which converts guanosine triphosphate to
cGMP resulting in vasodilatation. Phosphodiesterase-5
(PDE-5) catalyzes the breakdown of cGMP limiting the
duration of vasodilatation (Fig. 2). The second mechanism initiated in the endothelium involves the activation of the enzyme Cyclooxygenase. This results in
production of prostacycline (PGI2) from arachidonic
acid. PGI2 diffuses to the smooth muscle and increases
the activity of the enzyme Adenylate syntase, which
converts adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP). PDE-3 catalyzes the
breakdown of cAMP (Fig. 2). These mechanisms are
stimulated by O2, shear force, ATP, and vascular endothelial growth factor.3,7 PGF2a, endothelin (ET-1), angiotensin, serotonin result in pulmonary vasoconstriction.
Pulmonary vascular response to autonomic nervous
system depends on the baseline vascular tone.
b-Receptors mediate the response when PVR is low
(vasodilatation), and a receptors mediate the response
when PVR is high (vasoconstriction).
PATHOPHYSIOLOGY
The natural history of the disease consists of 3 stages:
1. Endothelial dysfunction and vasoconstriction. In this
stage, there is a decrease in the endothelial-derived
NO and PGI2 and an increase in thromboxane
American Journal of Therapeutics (2011) 0(0)
Salehi
A2 and ET-1, which result in pulmonary vasoconstriction, smooth muscle (SM) proliferation, and
platelet aggregation. Platelet aggregation leads to in
situ thrombosis and further releases of endothelial
derived factors.1,3,8–10
2. Vascular remodeling and in situ thrombosis. Chronic
hypoxia, inflammation (due to acute respiratory
distress syndrome, chronic obstructive pulmonary
disease, and sepsis) leads to endothelial damage and
failure of these cells to eliminate the factors that
initiate SM proliferation: Angiotensin 2, ET-1,
Thromboxane A2, Superoxide radicals. SM proliferation occurs in both muscular and nonmuscular
vessels. There is also an increase in the activity of
Protein kinase C, which mediates fibroblast proliferation and collagen deposition in the adventitia
layer.1,8,9
3. The last stage is the formation of plexiform lesions
that irreversibly obliterate the pulmonary arterioles.
This is seen in late pulmonary artery hypertension
FIGURE 2. Mechanism of endothelium-dependent vasodilation in the pulmonary artery. Endothelial nitric oxide
synthase (eNOS) and cyclooxygenase (COX) are stimulated by physiologic agonists ATP and vascular endothelial
growth factor (VEGF) and directly by oxygen and shear
stress. NO and PGI2 diffuse to vascular smooth muscle,
where they activate soluble guanylate cyclase (sGG) and
adenylate cyclase, respectively, to increase the levels of
cGMP and cAMP. These cyclic nucleotides initiate smooth
muscle relaxation. Specific PDEs promote breakdown of
the cyclic nucleotides. The arginine analog, asymmetric
dimethyl arginine (ADMA), superoxide (OÀ ), and ET-1
2
decrease NO release and cause vasoconstriction. NSAID,
nonsteroidal anti-inflammatory drug; PGIS, prostacyclin
synthase.7
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3.
Pulmonary Hypertension: A Review
(idiopathic pulmonary hypertension, scleroderma,
Eisenmenger’s syn).1
There are factors that can accelerate the progression
of the disease in either acute or chronic setting. These
factors include hypoxia, acidosis, increased cardiac
output (pregnancy, obesity, anemia, hyperthyroidism). Progression of the disease increases the right
ventricular (RV) afterload and RV dilation and
eventually RV failure. The slower the rate of progression, the higher the chances for RV to adapt and
better prognosis.
CLINICAL ASSESSMENT AND
DIAGNOSIS
Pulmonary hypertension in the past was classified into
primary and secondary pulmonary arterial hypertension
(PAHTN). In 1998, the World Health Organization
introduced a new classification based upon categories
sharing similar pathophysiology, clinical presentation,
and treatment options. WHO classified PAHTN into 5
categories: (1) Pulmonary artery hypertension, (2) Pulmonary hypertension with left heart disease, (3) Pulmonary hypertension with respiratory disease, (4)
Pulmonary hypertension caused by chronic embolic/
thrombotic disease, and (5) Miscellaneous.
Symptoms vary based on the severity of the disease.
Patients could be asymptomatic in the mild form of the
disease to demonstrating fatigue, weakness, dyspnea,
leg swelling, abdominal fullness, palpitations, angina,
syncope, and cyanosis in more advanced stages.4
Frequent signs of pulmonary hypertension during
physical examination include normal to low blood
pressure (BP), jugular vein distention with prominent
‘‘a’’ wave, left parasternal heave, loud P2 with split
second heart sound, S3 and/or S4 of RV origin, crackles
3
on lung auscultation, and signs of R. heart failure
(hepatomegaly, ascites, leg edema).2
The WHO has classified patients suffering from
pulmonary hypertension based on their functional
class into 4 classes. Class I patients are those in whom
regular activity does not cause undue dyspnea, fatigue,
or chest pain; class II patients have slight limitation of
physical activity; class III patients have marked
limitations of physical activity; and class IV patients
are those who cannot carry out any physical activity
without inducing any symptoms.
A series of laboratory tests are needed to confirm the
diagnosis and assess the severity of the disease and its
underlying pathology. These include chest x-ray, electrocardiogram (ECG), complete blood count, urinalysis,
coagulation profile, Echocardiogram (presence of RV
hypertrophy and dilatation, severity of
tricuspid
regurgitation, flattening of the intraventricular septum),
pulmonary function tests, ventilation/perfusion scan,
chest computed tomography/magnetic resonance imaging, stress test, 6-minute walk test, right and left heart
catheterization including acute vasodilator response test
(administering NO at a concentration of 20–40 ppm if
the PVR decreases by 20% and CO is unchanged or
increased the patient is an acute responder),7 and liver
function tests (LFTs; Table 1).
TREATMENT
Treatment of pulmonary hypertension consists of
a general and a specific approach. General treatment
for patients with PAHTN consists of supplemental
oxygen to keep SaO2 . 90% at rest or during activity. It
has been shown that supplemental O2 can improve
survival in these patients. Diuretics are given to
prevent volume overload and treat ascites and edema.
Salt restriction is recommended. Digoxin is given to
treat heart failure. Proper nutrition is required to
Table 1. Diagnostic work-up.8
Diagnostic test
Associated condition
Echocardiogram
Chest radiography
Pulmonary function tests
V/Q scan, pulmonary angiography, spiral CT scan
Sleep study
Blood tests (CBC, chemistry panel, serology,
coagulation tests)
LFTs
Cardiac catheterization with vasodilator testing
Electrocardiogram
LV/RV dysfunction, valvular heart disease, CHD
Underlying pulmonary disease
COPD, restrictive lung disease
Chronic thromboembolic disease
Sleep apnea
Connective tissue disease,
hypercoagulable states
Portopulmonary hypertension
Arrhythmias, right axis deviation, heart block
COPD, chronic obstructive pulmonary disease; LFTs, liver function tests.
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maintain ideal body weight. Exercise is to be done as
tolerated. Anticoagulation with warfarin is recommended to prevent in situ thrombi. Goal INR is 2–3, and its
dose needs to be adjusted if used with prostacylin.
Specific treatment includes the use of the different
classes of pulmonary vasodilator medications. We
review them briefly as follows:
Calcium channel blockers
These are only used in patients with a positive
vasodilatory response. Their major side effects are
hypotension and right heart failure. Nifedipine,
Diltiazem, and Amlodipine are commonly used.2,4,7
Prostacycline analogs
These are analogs of PGI2, a product of endothelial
arachidonic acid, which causes smooth muscle relaxation
via [cAMP. They improve outcome and long-term
survival. The Most common drugs from this group are
Epoprostenol a nonselective IV PGI2 analog with a half life
of 4–6 minutes, unstable at room temperature with high
pH requiring central access for administration. Iloprost is
a selective inhaled PGI2 analog with a half life of 20–30
minutes. It has a simple delivery system and can be used
in nonintubated patients. Treprostinil is a nonselective
SQ/IV PGI2 analog with a half life of 3 hours. It was
approved for use in 2002. It is stable at room temperature
and has a neutral pH. Beraprost is an oral PGI2 analog,
which is still under investigation.2,11
Inhaled nitric oxide
Inhaled nitric oxide (INO) is a selective pulmonary
vasodilator through activation of cGMP. It is delivered to
the well-ventilated areas of the lung, thus improving
the V/Q matching and decreasing intrapulmonary
shunting. It has a half life of 2–6 minutes and is
rapidly deactivated by oxyhemoglobin and haptoglobin–
hemoglobin complexes. It produces methemoglobin in
reaction to oxyhemoglobin, so its levels should be checked
every q6 hours to keep it below 3–5%. It can be delivered
via a nasal cannula, face mask, endotracheal tube. It has
a complicated delivery system and is expensive. Its usual
dose is 10–40 ppm. High flow rates should be used during
its administration to prevent the accumulation of
Nitrogen Dioxide (toxic byproduct of INO). INO should
never be abruptly discontinued because it can result in
rebound pulmonary hypertension.2,8,11
Endothelin receptor blockers
ET-1 is a direct pulmonary vasoconstrictor by augmenting smooth muscle proliferation and fibrosis. It
has 2 receptors, ETa responsible for SM proliferation
and vasoconstriction and ETb responsible for clearance
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Salehi
of endothelin and production of NO and PGI2 from the
endothelium. This group of drugs has been shown to
improve hemodynamics, exercise tolerance, and symptoms. Bosentan is a nonselective oral Eta blocker with
a half life of 5 hours approved for patients with WHO
functional classes III and IV. It can cause hepatotoxicity;
therefore, monthly LFTs are recommended. Ambrisentan is a selective Eta antagonist approved for patients
with WHO functional classes II and III. It is administered orally and can cause hepatic toxicity and birth
defects. Sitaxsentan is under investigation in the United
States. It is 6000 times more selective for Eta than
bosentan is.8,11
Phosphodiesterase-5 inhibitors
This group of drugs inhibits phosphodiesterase-5
and thus increases the cGMP levels leading to smooth
muscle relaxation and vasodilatation. Sildenafil is
approved for treatment of pulmonary hypertension
regardless of functional class. It is safe to use with Eta
blockers, PGI2 analogs, and INO. It prolongs INO
effect and attenuates the rebound PAHTN when INO is
discontinued. Sildenafil improves functional class and
exercise tolerance in 12 weeks and 1-year follow-up
with good safety profile.12,13 It is orally administered
and can be given via a nasogastric tube intraoperatively. Its use is contraindicated with nitrates due to
high risk of developing profound hypotension.
Phosphodiesterase-3 inhibitors
By inhibiting phosphodiesterase-3, these inhibitors
increase the cAMP levels, which in return cause smooth
muscle relaxation and nonselective vasodilatation. They
also have a positive inotropic effect. Most important
drugs from this group are Amrinone and Milrinone.
Milrinone comes in both inhaled and IV forms. IV
milrinone and INO have a more pronounced effect in
reducing pulmonary artery pressure than when they are
used alone. It also attenuates the rebound pulmonary
hypertension when INO is being weaned. Inhaled
milrinone has an additive effect with inhaled PGI2. Its
most important side effect is hypotension.4,14
ANESTHETIC MANAGEMENT
Assessment of patients with pulmonary hypertension
undergoing anesthesia should include obtaining the
history and performing a thorough physical examination, obtaining the recent ECG, chest x-ray, echocardiogram, right heart catheterization, and an arterial blood
gas sample. All treatments need to be continued to the
day of surgery with few considerations. Subcutaneous
Trepostinil should be converted to IV Epoprostenol. Oral
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Pulmonary Hypertension: A Review
Anticoagulation can be converted to short acting IV
agents and be discontinued at the time of surgery. Any
sign of worsening of pulmonary hypertension or RV
function should necessitate further work up and treatment, and delay of the intended procedure if possible.8
MORTALITY AND MORBIDITY
Noncardiac surgery in patients with pulmonary
hypertension is associated with considerable morbidity
and mortality even in patients that are stable and well
managed. Ramakrishna et al15 showed a 7% mortality
and 42% morbidity in patients undergoing major
noncardiac surgery (Orthopedic, Thoracic, Vascular,
Laparoscopic, etc). The risk is even higher with
C-section and liver transplantation. Factors predicting
perioperative morbidity risk include New York Heart
Association class II or greater, history of PE, Surgery
.3 hours, Intermediate to high risk surgery. Factors
predicting perioperative mortality risk include right
axis deviation on the ECG, RV hypertrophy, RV systolic
pressure/Systolic BP $ 0.66, use of intraoperative
vasopressors, and history of PE. (Table 2).
ANESTHETIC GOALS
Formulating an appropriate anesthetic plan requires
a clear vision into the general and hemodynamic goals
for these patients. General goals include avoiding
hypoxia, hypercarbia, acidosis (respiratory or metabolic), Hypo or Hypervolemia, hypothermia, providing adequate anesthesia and pain control. Hypoxia,
hypercarbia and acidosis directly or indirectly increase
PVR, which in turn can cause a rapid rise in the PA
pressures leading to a pulmonary hypertensive crisis
and RV failure. Hypovolemia leads to systemic
hypotension and impairment of RV perfusion and
RV failure. Hypervolemia depending on the presence
or absence of left ventricular (LV) dysfunction can
result in pulmonary congestion, RV overload, elevation
of central venous pressure, and end organ congestion
(Liver, Kidney). Providing adequate anesthesia and
5
pain control are essential because pain leads to
sympathetic stimulation, which in the context of
increased pulmonary vascular tone in these patients
can result in pulmonary hypertensive crisis.
Hemodynamic goals include maintenance of preload
to maintain ventricular filling, maintaining afterload to
sustain adequate ventricular perfusion pressure, normal to high contractility to preserve cardiac output and
forward flow, maintaining sinus rhythm and normal
heart rate (avoiding extremes) to sustain adequate
ventricular filling and preserving stroke volume and
cardiac output.
PREMEDICATION
Control of anxiety is important in these patients.
Benzodiazepines should be titrated carefully to prevent
oversedation and hypoventilation, which can be
detrimental. Bronchodilators should be considered if
indicated. All pulmonary hypertension specific treatments should be continued in the perioperative period.
Specific changes may be needed as mentioned before.
MONITORING
In addition to standard American Society of Anesthesiologists monitors, selection of invasive monitors
depends on the severity of the disease and the risks
associated with the procedure (fluid shifts, blood loss,
acidosis, and swings in BP). Patients with mild
pulmonary hypertension usually do not need invasive
monitoring. In patients with moderate to severe
pulmonary hypertension, an arterial line is indicated
to monitor beat to beat BP changes and blood gas
monitoring to detect acid/base imbalances and oxygenation. Central venous pressure monitoring usually
is adequate to guide fluid management in the setting of
normal RV function. Pulmonary artery catheters are
usually indicated when the procedure is associated
with significant fluid shifts, BP swings or in patients
with compromised RV function. It should be noted that
floating PA catheters is associated with higher risk of
Table 2. Perioperative considerations.8
Predictors of morbidity
Predictors of mortality
History of PE
NYHA class II or greater
Intermediate to high risk surgery
Surgery duration . 3 hrs
History of PE
Right axis deviation
Right ventricular hypertrophy
RV systolic pressure/systolic blood pressure $ 0.66
Intraoperative vasopressor use
NYHA, New York Heart Association.
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PA rupture, and arrhythmias in this patient population.8 Transesophageal echocardiography can also be
used to assess RV and LV function, calculate PA
pressures, and cardiac output. It could be an alternative
in patients with high risk of PA rupture or arrhythmias.
Its use depends on the practitioner’s comfort in
obtaining and interpreting images.
ANESTHETIC TECHNIQUES
A Specific Anesthetic technique is less important than
the attention to the anesthetic goals and prevention of
triggers that cause PAHTN crisis. An appropriate
anesthetic technique should be based on the type of
procedure, risks associated with the procedure,
patients’ comorbidities, and severity of disease. Because any airway instrumentation can precipitate
pulmonary hypertensive crisis in patients with moderate to severe PAHTN, local anesthesia or conscious
sedation may be preferred considering that the procedure allows the use of such techniques. If conscious
sedation is chosen, end tidal carbon dioxide (ETCO2)
administered via a nasal cannula should be carefully
monitored because it reflects adequate pulmonary
blood flow and RV function, Sudden drop in ETCO2
can be a sign of increase in PVR and RV failure.
Anesthesiologists should be ready to assist or control
ventilation.14 If it is determined that the patient may
not be able to maintain adequate ventilation (morbid
obesity, sleep apnea, high anesthetic requirements)
under sedation or the procedure will not permit
spontaneous ventilation, general anesthesia with
laryngeal mask airway or endotracheal intubation
should be considered. Carmosino et al16 showed that
Incidence of complications in children with pulmonary
hypertension is independent of the method of airway
management. If mechanical ventilation is considered,
moderate tidal volumes and low PEEP should be
considered to optimize lung recruitment and pulmonary blood flow and minimize atelectasis.8
Neuraxial anesthesia and regional blocks can be used
in this patient population if not contraindicated (anticoagulation). Spinal anesthesia should be avoided due
to profound sympathetic blockade, decrease in venous
return, and bradycardia. Lumbar epidural anesthesia
with careful titration is the method of choice if
neuraxial anesthesia is considered, although the
successful use of combined spinal epidural anesthesia
during delivery has been reported.17 Thoracic epidural
anesthesia should be considered with caution because
it blocks the efferent cardiac sympathetic nerve fibers,
which results in negative inotropic response to sudden
rise of PA pressures and RV failure.18
American Journal of Therapeutics (2011) 0(0)
Salehi
ANESTHETIC AGENTS
There is conflicting evidence in the literature regarding
the effects of anesthetic agents on the pulmonary
vasculature. IV anesthetics have little effect on PVR. They
cause less intrapulmonary shunting than inhalational
agents do because they do not blunt the hypoxic vasoconstriction in the lungs.19,20 Propofol and Thiopental
decrease PVR and pulmonary artery pressure (PAP) and
mean arterial pressure and myocardial contractility,
which are not desirable. The effect of Etomidate on
pulmonary vasculature is not well studied. It has minimal
effect on the systemic hemodynamics. Benzodiazepines
and Narcotics have minimal systemic and pulmonary
hemodynamic effect. There is no consensus on the
pulmonary effects of Ketamine. It can increase PVR
and PAP depending on their baseline values with the
most profound effect when baseline PVR and PAP are
high.21 Ketamine does not increase PVR when used with
pulmonary vasodilators while maintaining its systemic
effects [maintenance of systemic vascular resistance (SVR)
and BP] which makes its use desirable in this setting.4
Inhalational agents impair hypoxic vasoconstriction
in the lungs and hence increase intrapulmonary
shunting. They cause dose-dependent depression of
myocardial contractility and decrease SVR, which may
cause RV dysfunction. Desflurane augments vasocontrictive response to a1 adrenergic activity and
increases PVR and PAP. Isoflurane and Sevoflurane are
acceptable components of a balanced anesthetic
technique. NO increases PVR in adults but has little
effect in infants with pulmonary hypertension.22
Pulmonary vascular response to N2O is dependent
on the perioperative degree of PVR.23
A balanced anesthesia technique is preferred for
general anesthesia. Combination of Midazolam, Fentanyl, low-dose Propofol, or Etomidate/low concentration
of Sevoflurane can be used for induction. Anesthesia can
be maintained with low-dose inhalational agents and
intermittent doses of narcotics. If Neuromuscular relaxation is desired, agents with low hemodynamic effects
are preferable (Rocuronium, Vecuronium).
POSTOPERATIVE CARE
These patients need a monitored bed or an intensive
care unit postoperatively to provide adequate ventilation and oxygenation, pain control, fluid management
and to monitor hemodynamics. Pulmonary vasodilatory therapies should continue in the postoperative
period. In most patients, morbidity and mortality occur
several days after surgery due to progressive [PVR,
RV dysfunction, and sudden death.
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7.
Pulmonary Hypertension: A Review
MANAGEMENT OF PULMONARY
HYPERTENSIVE CRISIS
Management of pulmonary hypertensive crisis is based
on the principles discussed before: administration of
100% O2 to increase PAO2 and PaO2 and decrease PVR;
hyperventilation to induce a respiratory alkalosis;
reduction of PAP by YPaCO214; correction of metabolic
acidosis. PVR is directly related to the H+ concentration. Management also involves starting INO or other
pulmonary vasodilators; supporting myocardial contractility and cardiac output with inotropic support.
Epinephrine and Milrinone are preferred. If systemic
hypotension and vasodilatation occur, the use of
vasopressors is recommended. Norepinephrine is preferred because of its wider ratio of systemic to pulmonary effects (more systemic vasoconstriction than
pulmonary). Adequate pain management to eliminate
noxious stimuli, which can cause an increase in PAP.14
CONCLUSIONS
In managing patients with pulmonary hypertension,
anesthesiologists face many challenges. One should
carefully assess these patients, obtain all the necessary
studies, consult with the surgeon and other specialties
involved in the care of these patients, and devise a wellthought anesthetic plan.
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