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allows for optimization of cardiac output while at the
same time maintaining balanced oxygen delivery and
consumption.
2. Heart rhythm should be ideally sinus. Patients
hypotension perioperatively, these patients are more
prone to subendocardial ischemia. erefore, the need
to avoid hypotension in patients with severe AS cannot
be overemphasized.
with AS oen develop both systolic and diastolic
dysfunction as a result of this disease. Myocardial
Management of Hemodynamic Emergencies
hypertrophy leads to a decrease in the compliance of
the le ventricle (LV) and thereby a decrease in the
passive lling of the LV during diastole. Atrial systole
normally provides 20%– 30% of the LV lling volume.
In elderly patients (when AS mostly occurs), atrial
systole can contribute up to 40% of the LV lling.
us le atrial systole is particularly important to
maintain in patients with AS. Maintenance of normal
sinus rhythm is important, and any kind of nonsinus
rhythm, such as atrial utter, atrial brillation, and
Hypotension: Immediately treat with an alphaadrenergic agonist such as phenylephrine. Vasopressin
is an alternative, especially in patients taking ACEI or
ARB preoperatively.
Hypertension: since stroke volume is very preload
dependent in AS, systemic hypertension should be
treated preferentially with arterial vasodilators, such
as short- acting calcium channel blockers, instead of
preload- reducing agents such as nitroglycerin.
other supraventricular tachycardia (SVT) can result in
loss of eective atrial systole, reduced LV lling, and
decreased cardiac output. ese arrhythmias are poorly
tolerated by this patient population. If these patients
develop an unstable or rapid arrhythmia, immediate
electrical direct current (DC) cardioversion should be
performed.
Tachycardia: if the patient is tachycardic and
hypertensive, treat underlying causes rst, such as pain
or inadequate anesthesia. If the patient is hypotensive,
treat with alpha- adrenergic agonists. If the patient
appears hypovolemic, administer an intravenous uid
bolus.
3. Preload should be adequate. Intravascular volume
should be titrated to a level that ensures adequate
cardiac output without an excessive rise in le atrial
pressure. is can be achieved with guidance from
a central venous or pulmonary artery catheter.
Monitoring LV chamber size with intraoperative
TEE may be particularly useful. Due to impaired LV
compliance, a patient with AS and apparently “normal”
lling pressures might actually be hypovolemic.
23
4. Contractility should be maintained. Most AS patients
have preserved LVEF. If EF is reduced, inotropes should
be considered but used carefully, given their propensity
to increase myocardial ischemia.
5. Aerload should be maintained at high- normal levels.
With AS and a relatively xed stroke volume, a drop
in SVR may lead to a precipitous fall in blood pressure
and a signicant drop in coronary perfusion, leading to
myocardial ischemia. In addition, in order to overcome
the narrowing of the aortic valve, le ventricular
hypertrophy develops and ventricular performance
decreases, which means individual myocytes are
forced to work harder and their contractile force for
each unit of energy burned is lessened, resulting in an
overall unfavorable oxygen supply/ demand balance.
In conjunction with a propensity of developing
Bradycardia with hypotension: treat with ephedrine,
and consider a small dose of glycopyrrolate or
atropine, with beta blocker stand- by in case the
patient becomes overly tachycardic. If the bradycardia
is refractory (e.g., due to preoperative beta blocker
administration) and this impairs hemodynamics,
consider transesophageal or transvenous pacing.
Acute atrial brillation: in unstable patients this
warrants direct current cardioversion (DCCV). If
stable, consider tight rate control with beta blocker,
calcium channel blocker, amiodarone, and so on.
Cardiac arrest: patients with severe AS do not respond
well to chest compressions due to the narrowed aortic
valve orice impairing blood ow. e key is to closely
monitor hemodynamic stability, promptly treat the
patient accordingly and thus avoid cardiac arrest. In case
cardiac arrest occurs and chest compression is proven
ineective, cardiac pacing or open chest massage should
start without delay. Percutaneous cardiopulmonary
support has also been shown to be eective to bridge
the arrested patient to surgery.24 For major noncardiac
surgery, if cardiac arrest is even a remote possibility,
external adhesive debrillator pads with percutaneous
pacing function should be applied to the chest before
surgery commences.
56 PART II. CARDIAC CRISES
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57
AORTIC REGURGITATION
PATHOPHYSIOLOGY
Mechanism
Insuciency of the aortic valve causes backow of blood
into the le ventricle during diastole, resulting in le ventricular hypertrophy, volume overload, dilation, and eventually le ventricular systolic and diastolic dysfunction.
AR, because the LV is now adapted to a large volume and
has increased diastolic compliance. Monitoring of central
venous or pulmonary pressures and size and function of the
le ventricle should be performed with invasive catheters or
echocardiography. Patients with AR are much better suited
to central neuraxial anesthetic techniques (than those with
AS) due to the attendant reduction in SVR.
Moderate- to high- risk elective noncardiac surgery with
appropriate intraoperative and postoperative hemodynamic monitoring is reasonable to perform in patients with
Etiology
Acute causes of aortic regurgitation (AR) include infective
endocarditis causing abnormal leaet closure or perforation, and acute aortic dissection causing incompetent aortic
root or annulus.8 Acute AR may also occur from iatrogenic
complications, such as following percutaneous aortic balloon dilation or TAVR or following blunt chest trauma.
Chronic causes of AR include diseases of the valve or
aortic root: rheumatic aortic valve, bicuspid aortic valve or
Marfan’s syndrome, Ehlers- Danlos syndrome, ankylosing
spondylitis, chronic aortic dissection, and Behçet’s disease.
asymptomatic severe AR and a normal LVEF.
Perioperative Hemodynamic Goals
1. Heart rate should be maintained at the high- normal
range. In AR, regurgitation occurs during diastole, so
limiting this period of the cardiac cycle will also limit
25
the extent of backward ow. A mild tachycardia allows
for both an overall increase in cardiac output and a
decrease in the amount of regurgitation.
Bradycardia results in a lower oxygen requirement for
8
each beat of the heart but allows for a longer diastolic time,
a larger regurgitant volume, and therefore a reduction in
Symptoms
Patients with acute AR usually present with heart failure
symptoms, such as dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea. Patients may also have angina
due to incompetence of the valve and reduced coronary
perfusion pressure during diastole. Patients with chronic
AR can be asymptomatic, since the LV oen has time to
adapt to the volume overload and heart failure symptoms
may not occur. However, once they become symptomatic,
patients oen deteriorate quickly.
forward cardiac output. e regurgitant ow will increase
the LVEDP, and thus increase the LV workload.
AR also leads to a precipitous drop in aortic root
pressure during diastole. is drop in pressure results
in a drop in coronary perfusion pressure and impairs
coronary blood ow. An increased heart rate and
limitation of the total diastolic interval minimize this
reduction in diastolic pressure and augment coronary
artery blood ow.
2. Rhythm should be ideally sinus. Sinus rhythm is best
tolerated by AR patients due to more ecient LV lling.
MANAGEMENT OF AORTIC REGURGITATION
Preoperative Evaluation and Anesthetic Consideration
Severe AR is dened as a central AR jet width > 65% of the
LVOT width, a vena contracta > 0.6 cm or holodiastolic
ow reversal in the descending aorta by echocardiography.
In patients with acute severe AR resulting from infective
endocarditis or aortic dissection, surgical repair or replacement should not be delayed, especially if there is hypotension, evidence of shock, or pulmonary edema.
Patients with chronic AR present with LV volume overload. A decrease in systemic aerload will augment forward
LV output and reduce the regurgitant volume. However,
preload should be maintained, particularly in chronic
SEVERE VALVULAR DISEASE 57
26,27
3. Preload should be adequate to “full.” e le ventricle
in patients with AR has normal lling during diastole
from the le atrium, but also has a variable fraction of
the forward cardiac output returning to the LV through
an incompetent aortic valve. is increase in enddiastolic volume is compensated by LV dilation. Since
the LV is used to a high preload, the patient does not
tolerate hypovolemia well, and a normal to relatively
full preload is thus recommended. However patients
with AR must not be overzealously uid resuscitated,
as this may lead to acute decompensation of the LV and
concomitant pulmonary edema.
4. Contractility should be maintained. With dilatation
of the le ventricle to accommodate the extra volume,
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the myocytes become stretched. Patients initially
will maintain contractility, however with continued
MANAGEMENT OF MITRAL STENOSIS
Preoperative Evaluation and Anesthetic Considerations
dilation, contractility decreases.28 Preoperative
echocardiography to assess LV function is very
important for management of these patients.
5. Aerload should be in the low- normal range. A
slight, controlled drop in systemic vascular resistance
promotes forward cardiac ow and a decrease in
regurgitation without compromising systemic perfusion
pressure. Uncontrolled drops in SVR or exaggerated
increases in blood pressure/ aerload can lead to
detrimental consequences however.
Severe MS is dened as mitral valve area < 1.0 cm2 or mean
gradient across mitral valve > 10 mmHg with sinus rhythm,
heart rate between 60 and 80 beats per minute.
A thorough clinical history and physical examination
provide important information regarding the severity and
progress of MS. e history should include functional status changes, heart rate at rest and exertion, palpitations and
arrhythmia, history of heart failure, and any response to
treatment.
Patients with severe MS are at increased risk for noncardiac surgery and should be managed similarly to patients
Management of Hemodynamic Emergencies
with AS. Maintenance of normal LV preload and sinus
rhythm, and avoidance of tachycardia and systemic hypo-
Hypotension associated with SVT/atrial brillation should
be promptly treated with synchronized DCCV. Persistent
bradycardia can be treated with beta- agonists and anticholinergic drugs.
tension, should be the goal in the perioperative period. Of
particular concern is judicious intravenous uid administration so as to avoid increases in le atrial pressure and
pulmonary capillary pressure that may precipitate acute
pulmonary edema. is is particularly important in patients
who do not lose much blood during surgery, in whom the
MITRAL STENOSIS (MS)
“routine” administration of several liters of IV uid may be
extremely hazardous.
PATHOPHYSIOLOGY
Mechanism
Progressive obstruction of the mitral valve orice causes
increased pressure in the le atrium and the pulmonary circulation. Atrial hypertension may cause atrial dilation and
then lead to atrial brillation. Congestion may cause pulmonary edema and pulmonary hypertension.
Patients with MS who meet standard indications for valvular intervention (open mitral commissurotomy or percutaneous mitral balloon commissurotomy) should undergo
valvular intervention before elective noncardiac surgery. If
the valve anatomy is not favorable for percutaneous mitral
balloon commissurotomy, or if the noncardiac surgery is
an emergency, then noncardiac surgery may be considered
with invasive hemodynamic monitoring and optimization
of loading conditions.
Etiology
Mitral stenosis is almost always caused by rheumatic heart
disease. It is the most common valvular heart disease of
pregnancy. Other etiologies of MS can be senile calcication and degeneration of a prosthetic valve.
Moderate- risk elective noncardiac surgery in patients
with appropriate intraoperative and postoperative hemodynamic monitoring may be reasonable to perform in
asymptomatic patients with severe MS if the valve morphology is not favorable for percutaneous balloon mitral
commissurotomy.
One particular clinical scenario is the pregnant patient
with severe MS presenting for labor and delivery. Because
Symptoms
the delivery is associated with large uid volume shis, labor
pain may trigger sinus tachycardia, SVT, or atrial brilla-
Patients frequently present with dyspnea due to uid transudate into the lungs, which reduces lung compliance and
increases the work of breathing. Pulmonary edema may occur
if the pulmonary venous pressure exceeds the plasma oncotic
pressure. is is especially likely if a large uid bolus or headdown position raises pulmonary pressure suddenly. Other
symptoms include palpitations, chest pain, and hemoptysis.
tion, pushing is associated with sudden increase in intraabdominal and intrathoracic pressure, pulmonary edema
may occur without warning.29 erefore, these patients
should have a “cardiac delivery” without active pushing in
an ICU setting with appropriate degrees of hemodynamic
monitoring (which may include placement of a PA catheter).
Cardioversion equipment should be immediately available.
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59
Perioperative Hemodynamic Goals
1. Heart rate should be maintained in the low- normal
range. Increasing the heart rate will decrease lling of
the LV due to a shortening of the diastolic time as well
as ow limitation imposed by the stenosis. However,
signicant reductions in heart rate will compromise
cardiac output. As with AS, maintaining a baseline
heart rate between 70 and 90 beats/ minute will
usually be ideal.
30,31
2. Rhythm. Maintaining these patients in sinus rhythm
at their baseline heart rate is ideal; however, due to a
chronic increase in le atrial pressure and resultant
le atrial dilation, many patients present with atrial
brillation. Atrial brillation leads to loss of atrial
kick and late diastolic LV lling, and can reduce end
diastolic volumes by up to 40%. If sinus rhythm is not
consider synchronized DCCV, biphasic, 120– 200 J,
monophasic 200 J. Since these patients might also have
chronic atrial brillation, le atrial dilation, and stretching, they may not respond to cardioversion well; then
the decision for rate control versus rhythm control is
dependent on multiple factors, including the duration of
atrial brillation, hemodynamic response to atrial brillation, le atrial size, prior episodes of atrial brillation,
and a history of embolic events. e medication of choice
will be beta blocker, calcium channel blocker, amiodarone (150 mg over 10 min as a bolus dose, then followed
by 1 mg/ min for 6 hours as maintenance) or digoxin.
Anticoagulation with heparin or coumadin is indicated
to prevent thromboembolism if there is a prior history of
thromboembolism, or if a thrombus is detected in the le
atrium. However, this has to be weighed against the risk of
bleeding in surgical patients.
achievable, tight heart rate control is essential.
3. Preload should be maintained at adequate but not
excessive levels. A xed, reduced mitral valve area
in patients with MS necessitates maintenance of
adequate preload. A drop in preload results in a drop
in le atrial pressure, a decrease in LV lling, and a fall
in cardiac output.
Acute Pulmonary Edema
Treat precipitating factors for acute pulmonary edema
such as rapid atrial brillation. Administer loop diuretics.
Positive pressure ventilation can reduce pulmonary edema,
this can be achieved by noninvasive BiPAP ventilation or
increasing PEEP if the patient is already intubated and the
hemodynamic situation allows. Avoid hypercarbia, acido-
4. Contractility should be maintained. In the early stages
of MS, le ventricle contractility is not impacted.
sis, and hypoxia, which may exacerbate pulmonary hypertension and cause right heart failure.
With progression of the disease or the presence of
multiple valvular lesions such as combined MS and AS
that occurs in rheumatic heart disease, le ventricular
MITRAL REGURGITATION
function may be impaired. Contractility should be
maintained perioperatively. e drug of choice is
digoxin, as it not only improves the contractility but
also reduces heart rate.
5. Aerload should be maintained at its baseline level.
Mitral stenosis results in a xed lesion and therefore
a xed stroke volume due to limitations in getting
blood through the le ventricle during diastole. A fall
PATHOPHYSIOLOGY
Mechanism
Insuciency of the mitral valve causes backow of blood
into the le atrium during systole, with resultant le heart
volume overload, pulmonary edema, pulmonary hypertension, and potentially right heart failure.
in aerload would not be tolerated well, because an
increase in cardiac output can only be achieved by an
Etiology
increase in heart rate. e increase in heart rate will
further limit diastolic lling and reduce stroke volume.
erefore, it is critical to avoid precipitous drops in
aerload, which will lead to tachycardia.
Acute mitral regurgitation (MR) may be due to disruption of dierent parts of the mitral valvular and subvalvular apparatus.8 Endocarditis may cause leaet perforation
or chordal rupture. Spontaneous chordal rupture may
Management of Hemodynamic Emergencies
Rapid Atrial Fibrillation
Treat underlying causes of rapid atrial brillation such as
pain or inadequate anesthesia. If the patient is unstable,
occur in patients with degenerative mitral valve disease. Rupture of one or other of the papillary muscles
may occur in patients who have an acute myocardial
infarction. is is usually a surgical emergency and is an
extremely high risk situation.
SEVERE VALVULAR DISEASE 59
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Chronic causes of MR include rheumatic fever, Marfan’s
syndrome, dilating cardiomyopathy, ischemic heart disease,
and so on.
8
Systolic anterior motion (SAM) of the mitral valve is
a paradoxical motion of the anterior mitral valve leaet
toward the le ventricular outow tract (LVOT) during
systole, causing dynamic obstruction of the LVOT. e
mitral valve leaets are distorted, causing a posteriorly
directed MR jet.
Most commonly, SAM is seen in the asymmetric septal form of hypertrophic cardiomyopathy, but it has also
been described in hypertensive heart disease, diabetes
mellitus, acute myocardial infarction, aer mitral valve
repair, and even in asymptomatic patients during pharmacologic stress with dobutamine.32 For patients without
any cardiac abnormalities undergoing general anesthesia,
absolute hypovolemia or the vasodilator eect of anesthetic agents can result in LV underlling, which reduces
the LVOT size and results in a hyperdynamic LV.33
Underlling of the LV also changes the geometry of the
ventricle to move the papillary muscles relatively anterior
and inward. is hyperdynamic state raises outow tract
velocity, increasing drag forces on the MV, and results in
LVOT obstruction.
especially true for a complete papillary muscle rupture that
causes severe MR, which is poorly tolerated. Even if there is
a partial papillary muscle rupture with hemodynamic stability, urgent surgery is indicated, because this can suddenly
progress to complete papillary muscle rupture. In cases of
ruptured chordae tendineae, mitral valve repair is usually
feasible and preferred over mitral valve replacement, and
the timing of surgery can be determined by the patient’s
hemodynamic status. If endocarditis is the cause of severe
symptomatic MR, earlier surgery is generally preferred due
to its favorable outcomes over medical therapy. It is unclear
whether or not repair is superior to replacement in patients
with ischemic heart disease (requiring revacularization)
and severe MR.
In patients with asymptomatic severe chronic MR,
moderate- risk elective noncardiac surgery with appropriate intraoperative and postoperative hemodynamic monitoring is reasonable to perform. e overall hemodynamic
goals are avoidance of both increased aerload and bradycardia by choosing the appropriate anesthetic regimen.
Invasive hemodynamic and/ or TEE monitoring provides
great value in guiding management during and aer the
operative procedure, when these patients are admitted to
an intensive care unit postoperatively.
Although SAM is not a common etiology for MR,
the treatment is very dierent from other etiologies. e
conventional treatments for MR may not only be ineective, but also possibly worsen dynamic obstruction of the
LVOT. erefore, if the etiology of MR is uncertain or
conventional treatment is ineective, echocardiography
should be performed to rule out or conrm the presence
of SAM.
Perioperative Hemodynamic Goals
1. Heart rate should be in the high- normal range. In
a manner similar to aortic insuciency, profound
bradycardia is not well tolerated, since this can lead to
increased regurgitant volume and acute le ventricular
uid overload. A mild tachycardia between 90– 110
beats/ minute is usually optimal for these patients.
Symptoms
Patients present with le heart failure symptoms, such as
dyspnea on exertion, orthopnea, and paroxysmal nocturnal
dyspnea.
2. Rhythm should be ideally sinus. With signicant
regurgitation, the le atrium becomes dilated to
accommodate the regurgitant volume. Patients are
more prone to developing atrial brillation. A rapid
ventricular response should be avoided.
MANAGEMENT OF MITRAL REGURGITATION
Preoperative Evaluation and Anesthetic Considerations
Severe MR is dened as a prominent or ail MV leaet or
ruptured papillary muscle, vena contracta > 0.7 cm with a
large central MR jet or with a wall- impinging jet of any size,
swirling in the le atrium, or systolic ow reversal in the
pulmonary veins.
If the MR is acute and the patient is symptomatic,
prompt mitral valve surgery is recommended. is is
60 PART II. CARDIAC CRISES
3. Preload should be adequate but not excessive. Patients
with MR oen maintain adequate levels of preload and
the le ventricle may be presented with higher than
normal volumes during diastole as a result of the MR.
4. Contractility should be maintained. Many patients who
present with MR also have ventricular dysfunction. A
poorly functioning ventricle leads to hypertrophy and
dilation of the mitral annulus resulting in chronic MR.
In these patients, the ventricular function is usually
depressed and further myocardial depressants can lead
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61
to decompensation. us it is important to maintain
contractility perioperatively.
5. Aerload should be kept appropriately low. e
balance between aerload and le atrial pressures
determines the fraction of regurgitant ow and forward
cardiac output. A slight reduction in systemic vascular
resistance leads to an increase in forward cardiac
output and is well tolerated by patients with MR.
Precipitous increases in aerload decrease forward
cardiac output and cause an increase in le atrial and
pulmonary capillary pressure. If this increase is too
great, pulmonary edema can result.
In advanced disease pulmonary hypertension is common. Hence avoidance of factors that increase pulmonary
artery pressure (hypoxia, hypercarbia, high inspiratory
pressures, acidosis) is important in order to avoid the development of right heart failure.
aortic pressure, IABP decreases LV aerload, increasing forward output while decreasing regurgitant volume.
Simultaneously, the IABP increases diastolic and mean
aortic pressure, thereby supporting the systemic circulation.
However, IABP is only a temporizing measure for achieving hemodynamic stability until denitive mitral surgery
can be performed.
A percutaneous circulatory assist device (Impella,
TandemHeart) may also be eective to stabilize a patient
with acute hemodynamic compromise before operation.
36,37
Systolic Anterior Motion
e management of patients with SAM is based on
understanding the pathophysiology. If SAM is conrmed
by echocardiography, the treatments steps are:
1. Stop inotrope, administer IV uid bolus in order to
increase loading conditions.
2. Vasoconstriction with a direct acting alpha- agonist.
Management of Hemodynamic Emergencies
Acute Pulmonary Edema and Cardiogenic Shock
In acute severe MR, the le atrial and pulmonary venous
3. Beta blockade to reduce contractility.
TRICUSPID REGURGITATION
pressures increase quickly, since the le atrium compliance has not adapted to the acute increase in volume, leading to pulmonary congestion and pulmonary edema. e
decreased forward ow will lead to cardiogenic shock and
hypotension. e treatments of this acute decompensation
are stepwise34:
PATHOPHYSIOLOGY
Mechanism
Insuciency of the tricuspid valve causes backow of blood
into the right atrium during systole.
First consider medical treatment:
1. Inotropes. Inotropes will increase forward ow and
improve peripheral perfusion. However, isolated use
of an inotrope without decreasing SVR may actually
worsen MR, because the resistance in the le atrium is
lower than the SVR, thus favoring regurgitant ow.
2. Decrease SVR. is is usually accomplished by infusion
of an easily titratable agent such as sodium nitroprusside
or nicardipine. However, use of vasodilators is oen
limited by systemic hypotension, which makes an
inodilator such as dobutamine more eective.
Etiology
Acute tricuspid regurgitation (TR) is usually caused
by right ventricular dilation due to volume overload or
increased aerload such as pulmonary hypertension due to
acute pulmonary embolism. Approximately 80% of cases of
signicant TR are functional in nature and related to tricuspid annular dilation and leaet tethering in the setting of
right ventricular remodeling due to pressure and/ or volume
overload.
8
Other causes include right ventricular infarction, tricus-
pid endocarditis, rheumatic fever, Ebstein’s anomaly, and
3. Diuresis. Loop diuretics are usually used. Positive
carcinoid syndrome.
8
pressure ventilation is also eective in reducing the
pulmonary edema.
Symptoms
If medical treatment is not eective and the patient deteriorates, intra- aortic balloon counterpulsation (IABP) can
be helpful to treat acute severe MR.35 By lowering systolic
SEVERE VALVULAR DISEASE 61
Patients present with symptoms of right heart failure, such
as ascites, hepatomegaly, pulsatile liver, edema, and jugular
venous distention.
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MANAGEMENT OF TRICUSPID REGURGITATION
Preoperative Evaluation and Anesthetic
Considerations
Severe TR is dened as presence of abnormal/ ail
leaet, poor coaptation/ tethering, vena contracta width
> 0.7 cm, and/ or hepatic vein systolic ow reversal on
echocardiography.
For acute severe TR, controlling the precipitating cause
is the key for management. Patients with infective endocarditis should be considered for urgent valve surgery. If acute
pulmonary embolism is the cause, then surgical thrombectomy or a thrombolytic procedure should be considered. If
the patient is acutely volume overloaded, then aggressive
diuresis will reduce the severity of TR and may improve
symptoms.
e perioperative goal is to maintain right ventricular
contractility, reduce pulmonary vascular resistance, and
avoid factors causing pulmonary hypertension.
Progressive hepatic dysfunction may occur due to
the elevated right atrial pressure, and thus assessment
of liver function is useful in patients with advanced
degrees of TR.
case of pulmonary hypertension, it can also reduce
the dilation of the annulus and thus reduce the
severity of TR.
5. Aerload should be maximally reduced without causing
systemic hypotension.
Management of Hemodynamic Emergencies
Acute Right Heart Failure
1. Inotropes. Milrilone is generally preferred
over epinephrine due to its tendency to cause
helpful pulmonary vasodilation. Its systemic
vasodilation eect can be overcome by concomitant
administration of vasopressin and/ or norepinephrine.
Of these two, vasopressin causes less pulmonary
vasoconstriction.
2. Diuresis. Patients with severe TR usually present
with signs or symptoms of right heart failure,
including peripheral edema and ascites. Diuretics
can be used to decrease volume overload in these
patients. Loop diuretics are typically provided
and may relieve systemic congestion, but their use
Perioperative Hemodynamic Goals
1. Heart rate should be in the high- normal range, 90– 110
beats per minute. is is similar for managing severe MR.
can be limited by worsening a low- ow syndrome.
Aldosterone antagonists may be of additive benet,
especially in the setting of hepatic congestion, which
may promote secondary hyperaldosteronism.
2. Rhythm should be ideally sinus. Any type of nonsinus
rhythm leads to loss of eective atrial kick and hinders
the forward stroke volume of the right ventricle and
thus reduces cardiac output.
3. Preload should be adequate. Managing preload in
3. Reduction of pulmonary artery pressures and
pulmonary vascular resistance with specic inhaled
pulmonary vasodilators may be helpful in reducing
right ventricular aerload and functional TR in
selected patients.
patient with severe TR is a true challenge. Underlling
will cause a drop in stroke volume, and thus cardiac
output and blood pressure, since the right ventricle is
adapted to a large end diastolic volume. On the other
hand, volume overload will precipitate right ventricular
dilation, annulus dilation, and an increase in the
amount of TR. us echocardiography or a PA catheter
is extremely valuable in the management of these
patients.
4. Contractility should be maintained ideally close to
normal. Since 80% of signicant TR is related to
tricuspid annular dilation and leaet tethering in the
setting of right ventricular remodeling due to pressure
and/ or volume overload, maintaining right ventricle
contractility can usually ensure forward ow. In the
SEVERE PULMONIC STENOSIS
Pulmonic stenosis (PS), also known as pulmonary stenosis,
is a dynamic or xed obstruction of ow from the right ventricle to the pulmonary artery. It is usually rst diagnosed in
childhood. It may occur in association with more complicated congenital heart disorders. Less common etiologies
include carcinoid and obstructing vegetations or tumors.
When PS is present, resistance to blood ow causes
right ventricular hypertrophy. If right ventricular failure
develops, right atrial pressure will increase, and this may
result in a persistent opening of the foramen ovale, shunting of unoxygenated blood from the right atrium into the
le atrium, and systemic cyanosis.
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63
e treatment of choice is percutaneous balloon valvuloplasty, and this is generally done when a resting peak
gradient is seen to be > 60 mmHg or a mean > 40 mmHg
is observed.
38
3. Is a preinduction arterial line indicated?
4. Is central venous access indicated? Will you place a
pulmonary artery catheter?
5. How will you induce the patient? What are your
SEVERE TRICUSPID STENOSIS
Tricuspid stenosis (TS) is a valvular heart disease that results
in the narrowing of the orice of the tricuspid valve of the
heart. It is relatively rare. It is almost always caused by rheumatic fever and is generally accompanied by MS. Other rare
causes include carcinoid syndrome, endocarditis, endomyocardial brosis, lupus erythematosus, right atrial myxoma,
and congenital tricuspid atresia.
As a result of TS, there is a persistent diastolic pressure
gradient between the right atrium and right ventricle. is
gradient increases when blood ow across the tricuspid
valve increases, as occurs with inspiration and exercise, and
decreases when blood ow decreases, such as with expira-
hemodynamic goals for induction? What will be your
induction agents of choice?
6. Assuming you proceed with combined general
anesthesia with epidural analgesia, arterial line and large
bore peripheral IV access, the patient remained stable
aer anesthesia induction. However during dissection
of the tumor, the splenic artery ruptured with sudden
blood loss of 1000 mL, the patient became hypotensive
and tachycardia. You noticed multifocal PVCs, how
will you manage this patient?
7. Assuming you successfully resuscitated the patient and
she remained stable for the rest of the case, you are
planning to emerge the patient, how will you dose the
epidural catheter?
tion. As a result, most patients with severe TS have systemic
venous congestion with jugular venous distension, ascites,
and peripheral edema.
REFERENCES
Its clinical manifestations are far overshadowed by
those attributable to the associated le- sided (particularly
mitral) valve disease. Because TS is oen not detected during bedside examination, echocardiography is essential for
diagnosis and characterization. When valve and/ or chordal
thickening and calcication are evident, additional ndings
indicative of severe TS include mean pressure gradient > 5
mmHg, pressure half- time > 190 milliseconds, valve area <
1.0 cm2 (measured by continuity equation), and associated
right atrial and inferior vena cava enlargement.
Tricuspid stenosis itself usually does not require treatment. However, if there are concurrent valvular diseases,
surgical repair or replacement must be considered. In isolated symptomatic TS, percutaneous balloon valvuloplasty
may be considered.
39
Loop diuretics may be useful to relieve systemic and
hepatic congestion in patients with severe, symptomatic
TS, although their use may be limited by worsening the
low- ow syndrome. Attention to le- sided valve disease
and AF, when present, is also important.
CASE- BASED LEARNING DISCUSSION
1. What degree of AS did this patient have?
2. Is an epidural analgesic technique indicated in this case?
What will be your major concern with epidural analgesia?
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