Download AANA Journal Course 3: Aortic stenosis: A review

3
AANA Journal Course
Update for nurse anesthetists
6 CE Credits*
Aortic stenosis: A review
David Phillips, CRNA, MSN
Wake Forest, North Carolina
2005 Student Writing Contest Honorable Mention
The prevalence of aortic stenosis has been increasing in
recent decades, and nurse anesthetists are more likely to
encounter this problem as the population ages. Fortunately,
the widespread use of echocardiography has expanded our
understanding of valvular heart disease. The purpose of this
course is to evaluate the current literature regarding aortic
stenosis with a focus on anesthetic management.
The 2 most common causes of aortic stenosis are calcific
tricuspid disease and congenital bicuspid valves. An inflammatory, atherosclerotic disease process also has been identified in aortic stenosis. Patients with aortic stenosis are at
high risk for perioperative cardiac complications. Anesthetic
management often includes invasive hemodynamic monitoring and carefully tailored anesthetic techniques.
Objectives
AVR surgeries, constituting 72% of all valve replacements that year.2 These trends suggest that anesthesia
providers are increasingly likely to care for these
patients during cardiac and noncardiac surgery.
Few cardiovascular diseases present more of a challenge to anesthesia professionals than aortic stenosis
(AS). People who live with this disease often have little or no cardiac reserve, and they may not tolerate the
stress response associated with surgery. Likewise, most
anesthetic techniques produce hemodynamic changes
that can be disastrous in the presence of significant AS.
It is estimated that 2% of elderly Americans have
AS.1 The prevalence has risen in recent decades
because of a growing elderly population and improved
diagnostic techniques. The number of patients with a
diagnosis of AS and the number of aortic valve
replacement (AVR) surgeries has climbed steadily
since 1990 (Figure 1).2 In 2002, there were 56,000
Diagnoses
AVR
100
400
80
300
60
200
40
AVR (in thousands )
Introduction
Figure 1. Increasing prevalence of aortic stenosis (AS)
Diagnoses (in thousands )
At the conclusion of this course, the reader should be
able to:
1. List the most common causes of aortic stenosis.
2. Describe the pathophysiology of aortic stenosis.
3. Differentiate mild, moderate, and severe aortic
stenosis.
4. Explain the significance of aortic stenosis in
patients undergoing noncardiac surgery.
5. Discuss the anesthetic management of patients
with aortic stenosis.
Key words: Anesthesia, anesthetic management, aortic stenosis, noncardiac surgery, risk.
100
20
0
0
90 92 994 996 998 000 002
2
1
1
19 19
2
1
Year
The number of patients discharged from hospitals with a diagnosis of
nonrheumatic AS and the number of patients undergoing aortic valve
2
replacement (AVR). Data from the National Center for Health Statistics.
* AANA Journal Course No. 26: The American Association of Nurse Anesthetists is accredited as a provider of continuing education in nursing by
the American Nurses Credentialing Center Commission on Accreditation. The AANA Journal course will consist of 6 successive articles, each with
objectives for the reader and sources for additional reading. At the conclusion of the 6-part series, a final examination will be printed in the AANA
Journal. Successful completion will yield the participant 6 CE credits (6 contact hours), code number: 28327, expiration date: July 31, 2007.
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AANA Journal/August 2006/Vol. 74, No. 4
309
Causes
Rheumatic heart disease was the primary cause of AS
in the United States before 1950. The widespread use
of penicillin and improved diagnostic criteria have led
to a decline in the prevalence of rheumatic AS.3 During the same period, calcification of a tricuspid aortic
valve emerged as a major cause of AS.3 This condition
is associated with advanced age and is more prevalent
now simply because people are living longer.
A pathologic study of surgically removed valves
demonstrated that the 2 most common cases of AS in
the United States are calcification of tricuspid valves
and congenital bicuspid valves (Figure 2).3 An estimated 1% to 2% of the general population is born with
a bicuspid aortic valve.4 Most people with bicuspid
aortic valves develop calcific changes by late middle
age that require valve replacement by the seventh
decade of life.5
Figure 2. Causes of aortic stenosis*
Calcific
bicuspid
36%
Calcific
tricuspid
51%
Other
4%
Rheumatic
9%
* Data from Dare et al. 3
Pathogenesis
Calcific tricuspid AS traditionally was thought to
result from “wear and tear” of the valve that progressively worsened with age, thus the label “degenerative” or “senile” AS. It now is recognized that calcific
AS involves an inflammatory, atherosclerotic process
similar to that in coronary artery disease.4 The risk
factors for calcific AS are remarkably similar to those
of atherosclerotic disease and include increased age,
male gender, height, smoking, hypertension, diabetes
mellitus, high low-density lipoprotein levels, and low
high-density lipoprotein levels.1,6 Indeed, people with
AS have a high prevalence of coronary artery disease
and peripheral arterial disease.7,8
Several series report similar immunohistological
changes in the lesions of atherosclerotic disease and
calcific AS.9,10 The initial injury in AS results from
mechanical stress that disrupts the valvular endothelial
basement membrane. This disruption promotes lipid
accumulation, infiltration of macrophages and T lymphocytes, and, finally, calcification. Therefore, calcific
AS is not merely a degenerative process but rather an
active and potentially modifiable disease process.
Bicuspid valves have 1 less cusp to share the workload and are prone to stenosis because of the greater
mechanical stress. After the initial injury, the same
inflammatory changes that take place in tricuspid
stenosis are seen in bicuspid valves.11 However, calcification of a bicuspid valve occurs more rapidly and
requires surgical replacement at an average of a
decade earlier than in tricuspid stenosis.5
Rheumatic heart disease remains a significant cause
of AS in the United States. This disease is initiated by
a pharyngeal infection with group A streptococci. Susceptible individuals seem to develop an autoimmune
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AANA Journal/August 2006/Vol. 74, No. 4
process that results in fibrosis of the cusps, fusion of
the commissures, and calcification. Rheumatic AS is
almost always seen with mitral stenosis.4
Pathophysiology
All of the common causes of AS eventually result in
calcification, regardless of the initial cause. Calcification of the cusps on the aortic side of the valve (Figure 3) impedes opening of the valve during systole. A
reduced valve area produces an obstruction to left
ventricular outflow. To maintain a normal stroke volume, the left ventricle compensates with concentric
hypertrophy, a process in which the myocardium
thickens without enlargement of the ventricular cavity. The myocardium hypertrophies over many years
as the obstruction becomes more severe.4
The thick myocardium produces sufficiently high
left ventricular pressures when contracting to force
blood past the valvular obstruction. A pressure gradient results between the left ventricle and the ascending aorta during systole and frequently is reported on
echocardiogram and catheterization reports. The ventricular hypertrophy maintains normal wall stress
despite the increased pressure load on the left ventricle. As a result, contractility is preserved until late in
the disease process when the obstruction becomes so
severe that the pressure load overwhelms the ability of
the ventricles to compensate. The left ventricle is the
end organ affected in AS.4
Diastolic dysfunction can occur earlier in the disease process. The left ventricle becomes less compliant. Ventricular filling is impaired due to poor diastolic relaxation and becomes increasingly reliant on
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Figure 3. Calcific aortic stenosis
Table 1. Aortic stenosis severity*
2
Severity
Valve area (cm )
Normal
3-4
Mild
>1.5
Moderate
1.0-1.5
Severe
<1.0
15
* Data from Bonow et al.
Diagnosis
A tricuspid aortic valve with large calcium nodules
(black arrow), unfused commissures (white arrow), and
a small valve area.
left atrial contraction to fill. Left ventricular end-diastolic pressures often are elevated. Left atrial enlargement and pulmonary hypertension can result.4
In a person with asymptomatic AS, cardiac output
can increase in response to stresses through an increase
in heart rate but not through an increase in stroke volume. When the heart rate accelerates, there is a
decreased systolic period during which stroke volume
is maintained by an increase in the pressure gradient,
an increased flow rate through the aortic valve, and a
slight increase in valve area. However, when the stenosis becomes severe, the leaflets become more rigid and
stroke volume cannot be maintained when the heart
rate increases. The person becomes symptomatic with
activity or stress. Heart failure is the end result.4
Clinical manifestations
The classic triad of symptoms for AS are dyspnea,
angina, and syncope. Exertional dyspnea is the most
common initial symptom and is a sign of impending
left ventricular failure. Angina is seen even in the
absence of coexisting coronary artery disease. Coronary flow is inadequate to meet the increased demands
of the hypertrophied left ventricle. Exertional syncope
is a symptom specific to AS and helps rule out other
valvular disorders. In a prospective study that looked
at 397 patients (95% were symptomatic), the incidence
of symptoms were as follows: dyspnea, 63%; angina,
51%; syncope, 42%; and other, 13%.12
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Aortic stenosis usually is detected during physical
examination by the presence of a grade 3 or 4 systolic
murmur that is heard over the right second intercostal
space. Other specific findings include a late peaking of
the murmur and a significant delay and decrease in
the carotid upstroke.13 These are useful screening
tools in asymptomatic patients; however, echocardiography is the “gold standard” for confirming the diagnosis and determining the severity of stenosis.
Echocardiography is noninvasive and cost-effective
compared with cardiac catheterization, and it provides
superior information on the morphologic features and
motion of the aortic valve.14
The aortic valve area and the aortic pressure gradient are the 2 most commonly used determinants of
stenosis severity. These parameters can be measured
with echocardiography and cardiac catheterization.
Severe AS is categorized as a valve area less than 1 cm2
(Table 1) and a pressure gradient of more than 50 mm
Hg.15 Most patients with a valve area less than 0.5 cm2
have severe hemodynamic alterations and can have
pressure gradients of more than 100 mm Hg.12
Disease course
This disease begins with a latent period that extends
over several decades. Outcome remains good in the
absence of symptoms, with few cardiac deaths
reported.16 The hemodynamic progression of the disease is rather linear, with the valve area decreasing
0.12 cm2 per year and the pressure gradient increasing
7 mm Hg per year.17 Once the valve area is reduced to
about one fourth of its original size, more rapid hemodynamic alterations occur.18
Noticeable symptoms do not usually occur until
severe stenosis is present. The average valve area at
symptom onset is 0.93 cm2, and the average pressure
gradient is 49 mm Hg17; however, there is wide individual variation. The presence of symptoms is the best
indicator of outcome. The onset of symptoms is associated with a high risk for sudden cardiac death.16 A
study of patients who refused AVR revealed that mor-
AANA Journal/August 2006/Vol. 74, No. 4
311
tality was 57% at 3 years after the onset of symptoms.19 The average age at which patients become
symptomatic depends on the cause: rheumatic disease, 39 years; bicuspid disease, 48 years; and calcific
tricuspid disease, 66 years.20
Treatment
There are no definitive medical treatments for AS
other than antibiotic prophylaxis to prevent infective
endocarditis and limitations on physical activity.15
However, there is hope for new medical therapies
because calcific aortic stenosis now is believed to
involve an active inflammatory atherosclerotic
process. For example, recent retrospective trials
demonstrated a slowing of disease progression in
patients receiving statin therapy.21,22 Randomized
clinical trials are currently evaluating this therapy.
Asymptomatic patients are evaluated with echocardiography every 1 to 5 years. Once symptoms appear,
the recommended treatment for AS is valve replacement.15 The mortality rate for AVR is 4% and, when
combined with coronary revascularization, 6%.23
After the obstruction is removed, there is symptomatic improvement and a regression in left ventricular hypertrophy.4 Ventricular wall mass returns to normal after 8 years.21 Long-term survival after the
procedure is comparable to age-related norms.24
Percutaneous balloon aortic valvuloplasy is a less
invasive procedure that is clearly inferior to valve
replacement in adult patients. Still, it can modestly
increase valve area for a few months and is recommended for some patients who are not candidates for
AVR and need temporary improvement.15 The search
for other less invasive procedures has persisted. In
2002, the first human case of a percutaneous aortic
valve replacement was reported.25 This experimental
procedure is performed under local anesthesia and
mild sedation. This new technology is being proposed
as a possible treatment for patients with severe AS
whose risk for surgery is too high due to comorbidities. Research in this area is ongoing.
Aortic stenosis and noncardiac surgery
The current guideline is for patients with severe or
symptomatic AS to undergo AVR before elective noncardiac surgery.26 This is not always possible because
the patient may be a poor candidate for AVR, the
patient may refuse AVR, or the procedure is too
urgent. If noncardiac surgery must be performed,
some patients can benefit from preoperative balloon
valvuloplasty.26
Several studies have looked at the risk associated
with AS and noncardiac surgery (Table 2). The classic
report by Goldman et al27 was the first to report an
increased risk of cardiac complications. This was followed by a few trials in the 1980s and 1990s that suggested a more modest risk.28-30 The authors attributed
these results to more aggressive monitoring and therapy. However, these studies had small samples, and
the study by O’Keefe et al28 consisted mostly of minor
procedures with sedation and local anesthesia. More
recently, Rohde et al31 found that patients with a pressure gradient or more than 40 mm Hg have 6.8 times
the risk for cardiac complications, and Kertai et al32
Table 2. Reported risk for patients with aortic stenosis undergoing noncardiac surgery*
Reference
Year
Design
No. of
cases
Outcomes
measured
108
Nonfatal MI, death
Relative risk for gradient >25
after adjustment for clinical
factors, 5.2
Reported risk
32
2004
Retrospective
31
2001
Prospective
67
Major cardiac events
Relative risk for gradient >40
after adjustment for clinical
factors, 6.8
1998
Retrospective
55
Major cardiac events
5/55 had event; 2 MI, 2 CHF,
1 VF; same risk as control
group
29
1998
Retrospective
22
Cardiac events, death
2/22 had event; 1 fatal MI, 1
noncardiac death
28
1989
Retrospective
48
Perioperative complications
1/48 had event, 1 VT
1977
Retrospective
23
Postoperative cardiac
events
Relative risk, 3.2
Kertai et al
Rohde et al
30
Raymer and Yang
Torsher et al
O’Keefe et al
27
Goldman et al
†
* MI indicates myocardial infarction; CHF, congestive heart failure; VF, ventricular fibrillation; and VT, ventricular tachycardia.
† This does not include 6 cases of hypotension included by the authors.
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reported that patients with a gradient of more than 25
mm Hg have 5.2 times the risk.
The recent studies confirm the early results by
Goldman and colleagues.27 Patients with AS are
clearly at higher risk for developing cardiac complications, including myocardial infarction, heart failure,
and ventricular arrhythmias. In the study by Rohde et
al,31 AS had the highest risk of all the echocardiographic variables studied, including mitral regurgitation. Finally, the report by Kertai et al32 indicated that
the degree of stenosis is proportional to the level of
risk. Patients with a pressure gradient of 25 to 49 mm
Hg had a 15% complication rate, whereas patients
with a gradient of more than 50 mm Hg had a 30%
complication rate.
Anesthetic management
The principles of anesthetic management for AS are
similar for cardiac and noncardiac surgery. The preoperative assessment is focused on determining the
severity of AS. Whenever possible, the patient should
be evaluated before surgery by a cardiologist and have
an echocardiogram. Routine auscultation of heart
sounds for a loud systolic murmur can identify undiagnosed patients admitted for surgery. The level of
suspicion is raised if there is a history of angina, dyspnea, syncope, rheumatic disease, or a known bicuspid valve.
Patients with AS and bicuspid valves are considered
at moderate risk for the development of bacterial
endocarditis and should receive antibiotic prophylaxis
according to the American Heart Association guidelines.33 Light premedication with anxiolytics during
the preoperative period can minimize the release of
catecholamines in anxious patients.
Intraoperative management is directed toward
maintaining hemodynamic stability and cardiac output. Patients with AS usually are vasoconstricted
before induction and easily become hypotensive with
the administration of anesthesia. Hypotension should
be treated aggressively with an alpha-adrenergic agonist such as phenylephrine to maintain coronary perfusion, which is dependent on diastolic pressure at the
aortic root.34 The ischemic cascade that follows
hypotension is illustrated in Figure 4. The ideal heart
rate ranges from 50 to 70 beats per minute.35 Tachycardia can result in ischemia and also does not allow
enough systolic time for flow across the stenotic aortic valve. Excessive bradycardia decreases cardiac output. Maintenance of sinus rhythm is important to
maintain the atrial contribution to ventricular filling.
Supraventricular tachycardias and atrial fibrillation
should be treated immediately with synchronized cardioversion.35 External defibrillators are used for
prompt conversion of ventricular fibrillation because
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Figure 4. Potential downward hemodynamic spiral
Coronary
perfusion
Blood
pressure
Cardiovascular
collapse
Myocardial
ischemia
Preload
SVR
Anesthetics
Ventricular
dysfunction
SVR indicates systemic vascular resistance.
chest compressions are not effective in pushing blood
through a stenotic valve.4 Fluid status should be optimized so the noncompliant left ventricle can maintain
stroke volume.
There is a low threshold for the placement of invasive hemodynamic monitors in patients with AS. Arterial catheters commonly are used for beat-to-beat
blood pressure monitoring. Pulmonary artery
catheters are useful for evaluating fluid status and cardiac output. Left-sided filling pressures normally are
elevated in AS because of a noncompliant ventricle,
and volume status is easily underestimated.34 Central
venous catheters are poor indicators of fluid status in
AS.34 Transesophageal echocardiography is a useful
direct measure of preload and contractility, but the
probe cannot be inserted until after the critical induction period.35 A 5-lead electrocardiogram is recommended for detection of ischemia and arrhythmias.
Close monitoring should continue into the postoperative period, especially if the surgery involves significant fluid shifts.4
Anesthetic technique
There is little research supporting one anesthetic technique over another for AS. The literature regarding
this issue consists primarily of case reports. Some
authors of anesthesia texts recommend general anesthesia over regional anesthesia because it allows
greater control over blood pressure.36,37 If general
anesthesia is chosen, the sympathetic response to
direct laryngoscopy should be attenuated to prevent
ischemia. An opioid-based technique produces minimal cardiovascular effects.33-37 Any medication that
causes significant myocardial depression, hypotension, tachycardia, bradycardia, or histamine release
should be used cautiously. Volatile anesthetics are
used in low concentrations to avoid myocardial
AANA Journal/August 2006/Vol. 74, No. 4
313
depression and nodal arrythmias.34
Some authors consider severe AS to be a contraindication to spinal and epidural anesthesia.36 The sympathectomy produced can result in rapid hypotension and
deterioration in the patient’s condition (see Figure 4).
However, epidural anesthesia results in a more gradual
decline in blood pressure and allows incremental titration of anesthetics. Epidural anesthetics have been used
at some institutions for parturients with congenital
AS.38,39 A sample of other regional anesthetic techniques used safely in case reports includes intrathecal
sufentanil for lithotripsy,40 continuous spinal anesthesia for hip replacement,41 and a combined lumbar
plexus and sciatic nerve block for hip replacement.42
Carefully planned regional techniques like these may
be an option for select patients with AS.
Summary
Nurse anesthetists will encounter more patients with
AS as the elderly population continues to grow.
Patients with AS are at substantial risk for cardiac
complications in the perioperative period. A coordinated effort is needed among surgeons, cardiologists,
and anesthesia professionals to minimize the risk.
Aggressive hemodynamic monitoring and gentle anesthetic techniques can provide the majority of these
patients with favorable outcomes.
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spinal anesthesia with invasive monitoring for surgical repair of
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AUTHOR
David Phillips, CRNA, MSN, is a staff nurse anesthetist at Franklin
Regional Medical Center, Louisburg, NC. He was a student at Duke
University Nurse Anesthesia Program, Durham, NC, when this course
was written. Email: [email protected]
ACKNOWLEDGMENT
I thank all the nurse anesthetists and anesthesiologists at Durham
Regional Hospital, Durham, NC, for sharing their wealth of knowledge
in cardiac anesthesia.
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