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fashion.8 Familiarity with the operation of local debrillator units prior to emergency situations is crucial for proper
operation and patient safety.
Successful cardioversion should not cause complacency
because, as was demonstrated in one study, up to 50% of
patients converted to sinus rhythm may subsequently revert
to SVT.31 erefore, unless a known arrhythmia trigger has
been eliminated, therapeutic serum levels of antiarrhythmics (as described under stable SVT) may also be necessary
to maintain sinus rhythm.
25
In the event of failure of adenosine to terminate the SVT,
the next treatment should consist of an IV beta blocker or
calcium channel blocker. Numerous beta blockers are available for use, although β1- selective beta blockers should be
preferentially chosen due to their decreased risk of triggering bronchospasm. Esmolol is an excellent rst choice due
to its short duration of action and quicker recovery should
hypotension occur. Metoprolol has an intermediate onset of
action and is another good choice for selective beta blockade. Nondihydropyridine calcium channel blockers (diltiazem or verapamil) can be given instead, although verapamil
Stable Regular Supraventricular Tachycardias
In the stable patient it is important to distinguish between
regular and irregular rhythms since irregular SVT is usually
atrial brillation— a disease that is typically more dicult
to treat, warranting its own algorithm for treatment.
e initial pharmacologic treatment of stable regular
SVT involves the use of adenosine, which serves as a treatment (terminating SVTs) as well as a diagnostic tool (slow-
should be avoided in patients with heart failure, due to its
greater negative inotropic eect. Amiodarone is a less desirable initial option for treatment of stable regular SVTs, due
to its long time to onset. In the marginally stable patient,
however, amiodarone may be preferable, since it is less likely
to be associated with hypotension due to its less vigorous
negative ionotropic and vasodilatory action. Doses of antiarrhythmics used to terminate tachyarrhythmias are summarized in Table 7.6.
ing ventricular rate to allow proper rhythm identication).
Administer adenosine as a 6- mg bolus: observe for ventricular response and underlying atrial rhythm. Repeat with a
12- mg bolus if there is inadequate response to the rst dose.
e conscious patient should be adequately informed that
a transient sense of impending doom is frequently experienced with this medication. e initial dose of adenosine
should be reduced to 3 mg when given through central
venous access or in patients following heart transplant. e
medication should be avoided altogether in patients with
asthma.
6
Stable Irregular Supraventricular Tachycardias
Stable irregular SVTs, atrial brillation in particular, can
be much more dicult to terminate, and therapy typically
focuses on control of the ventricular rate to a goal of <110
bpm. is decreases the risk of myocardial ischemia and
hemodynamic compromise.
Calcium channel blockers or beta blockers are rstline treatment for rate control of stable irregular SVT, on
account of their rapid time to onset. However, both these
classes are negative inotropes and their use may signicantly
ADENOSINE DOSING
impair ventricular function in patients with congestive heart
failure. Digoxin or amiodarone are the preferred choices for
6– 12 mg PIV
3 mg PIV Heart Transplant
3 mg Central line
Consistent termination with adenosine is seen with reentrant rhythms (AVNRT, AVRT). If the patient has a rhythm
dened by increased automaticity (atrial brillation, atrial
utter, or atrial tachycardia), transient slowing of the ventricular response will occur without rhythm termination.
Attention should still be paid to the underlying atrial tracing as this can facilitate precise rhythm identication.
If there is a delay in acquisition of adenosine, vagal
maneuvers, such as carotid massage, can be performed aer
conrmation of the absence of a carotid bruit. is technique
rarely leads to prolonged arrhythmia termination; hence, signicant eort should not be expended to perform it.
patients at risk for decompensation with ventricular depression, although these medications have the disadvantage of a
longer time of onset— digoxin loading may take > 24 hours.
Table 7.6 details the dosing of these rate- control agents.
In patients with atrial brillation for > 48 hours, it is
important to be cautious with the use of amiodarone.
Amiodarone can cardiovert patients to sinus rhythm, and the
initiation of organized atrial activity can dislodge recently
accumulated le atrial thrombus, causing embolic strokes.
Embolic strokes have been observed within days of cardioversion of patients in atrial brillation without appropriate
anticoagulation.32 erefore, conversion to sinus rhythm
should not be regularly attempted in patients with chronic
atrial brillation without evidence of long- term anticoagulation or echocardiographic evaluation for the absence of
le atrial thrombi. Unfortunately, in the unstable patient,
46 PART II. CARDIAC CRISES
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chemical or electrical conversion to sinus rhythm may be
the only means to prevent further hemodynamic collapse
and should not be delayed in this circumstance.
To prevent postoperative atrial brillation in patients
BOX 7.2 CAUSES OF SUPRAVENTRICULAR TACHYCARDIA IN
THE PERIOPERATIVE PERIOD
Hypoxemia
undergoing coronary artery bypass surgery, oral beta
blockers are recommended for all patients without contraindications,33 since beta blockers can reduce the risk
Hypercarbia
Pain
of this rhythm in the postoperative period. Additionally,
magnesium supplementation reduces the incidence of
post- cardiac- surgery atrial brillation.34 In the noncardiac
Inadequate anesthesia
Anemia/ Blood loss
surgery population, oral beta blocker should be continued
for those patients on a preoperative regimen, but should
not be started de novo, due to an increased risk of stroke
and death.
35
Of note, if a patient with known preexcitation syn-
drome (WPW) develops atrial brillation, AV nodal
Hypovolemia
Acidosis
Electrolyte imbalances
Cardiac ischemia
blocking agents including adenosine, beta blockers, and
calcium channel blockers must be avoided. ese medications carry the risk of inducing dangerous ventricular
Cardiogenic shock
Mechanical irritation (including central line/ wire, chest tube)
arrhythmias by increasing conduction through the accessory pathway.25 Consider the input of a cardiologist for
this rhythm if time permits, otherwise, treatment may be
Presence of structural heart disease
Anaphylaxis
attempted with amiodarone or procainamide as detailed
in Table 7.6.
Fever
WOLFF- PARKINSON- WHITE SYNDROME
NO adenosine
NO beta blockers
NO calcium antagonists
YES amiodarone
Any source of procedural stress that increases catecholamine outow can be associated with the development of
perioperative tachycardias. In addition, structural heart
disease, disturbances in myocardial ion channel func-
Malignant hyperthermia
Thyrotoxicosis
Medications (anticholinergics, milrinone, dopamine,
dobutamine, beta agonists)
SOURCES: Gabrielli A, O’Connor MF, Maccioli GA. Anesthesia advanced circulatory life
support. Comm Crit Care Med. 2008; Vanden Hoek TL, Morrison LJ, Shuster M, et al.
Part 12: Cardiac arrest in special situations: 2010 American Heart Association
Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
Circulation. 2010;122(SUPPL. 3); Balser JR. Chapter 1 Perioperative Dysrhythmias.
ASA Refresh Courses Anesthesiol. 2000;28. http:// journals.lww.com/ asa- refresher/
Fulltext/ 2000/ 28000/ Chapter_ 1_ Perioperative_ Dysrhythmias_ .2.aspx; Thompson A,
Balser JR. Perioperative cardiac arrhythmias. Br J Anaesth. 2004;93(1):86– 94.
doi:10.1093/ bja/ aeh166.
tion, and mechanical irritation of the heart can all lead to
tachydysrhythmias. Commonly cited sources of perioperative supraventricular tachycardias are listed in Box 7.2.
Patients with a known history of SVT, particularly atrial
brillation and atrial utter, are at high risk for recurrence
in the perioperative period. Proactive anesthetic planning
beginning in the preoperative period, and continuing postoperatively, is required to reduce the exposure to SVT triggers and provide protective treatment (for example, beta
blockers). However, many of the triggers (usually catecholamine mediated) are inherent to the perioperative process
itself, and preventative measures are not consistently successful. As intraoperative SVT is oen triggered or facilitated by intraoperative stimuli, such as surgical stress or
volatile anesthetics, the majority of these rhythms spontaneously resolve with the discontinuation of anesthesia and
surgical stimulus.
25
Postoperative SVT, in contrast, usually occurs on
postoperative day 2 through 4, and the most common
rhythm is atrial brillation, accounting for over 50% of
postoperative SVT cases and occurring in 4% of patients
aer major noncardiac surgery.36 Preoperative atrial
brillation, advanced age, pulmonary disease, congestive
heart failure with volume overload, and hypomagnesemia
are all known to be risk factors for development of atrial
brillation.
24
CARDIAC DYSRHYTHMIAS 47
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Supraventricular tachycardia aer noncardiac surgery
has been linked to increased morbidity, and mortality rates
of 25%– 50%. However, it is dicult to determine whether
increased mortality is caused by the SVT or whether the
association is simply correlative— arising from other
comorbidities.
As most regular SVTs resolve early in the postoperative
period,25 they oen do not require further treatment, and
assessment can be limited to routine postoperative care and
increased vigilance. However, if regular SVT continues to
recur, it is important to assess for electrolyte disturbances,
myocardial ischemia, or medication causes.
Although the rate of spontaneous conversion of postoperative atrial brillation is high (about 60%25), this rhythm
will still necessitate continued management in the form of
outpatient rate control and/ or anticoagulation medication
BOX 7.3 CAUSES OF PERIOPERATIVE BRADYCARDIA
Hypoxemia
Hypercarbia
Vagal outow (oculocardiac reex, visceral stimulation,
carotid stimulation)
Severe hypotension/ hypovolemia
Acute myocardial ischemia (usually inferior)
Drug effects: beta blockers, calcium channel blockers,
clonidine, dexmedetomidine, digitalis, local
anesthetics, amiodarone or other antiarrhythmic drugs,
phenylephrine, hypermagnesemia
Increased intracranial pressure
Hypothermia
Cardiac conduction disease— e.g., degenerative brosis of
the atrium and sinus node
in about 40% of the cases. Consultation with cardiology or
close follow- up with the surgical service will therefore be
required. Interestingly, the rate of resolution of postoperative atrial brillation is only modestly increased from 60%
to 68% with pharmacologic treatment,25 however, treatment is still warranted to reduce complications of persistent
atrial brillation.
physiologically low resting heart rate in healthy individuals. While this scenario may be less concerning than acute
bradycardia, these patients are still at risk for further decrements in heart rate that may result in clinical instability.
Acute intraoperative drops in heart rate in previously
stable patients are oen due to acute medication adminis-
CLINICAL SCENARIOS— BRADYARRYTHMIAS
tration (including phenylephrine, neostigmine, and beta
blockers) or procedural stimulation (pneumoperitoneum,
In much the same way that stable versus unstable versus
pulseless tachyarrythmias require prompt recognition and
treatment, the same applies for bradyarrhythmias. e following sections discuss various degrees of sinus bradycardia
followed by a discussion of heart block.
pressure or traction on the globe of the eye, carotid manipulation, or high spinal anesthesia). An expanded list of causes
can be found in Box 7.3. For procedures associated with
carotid bulb, ocular, or visceral manipulation, close attention should be paid to key points in the procedure during
which this manipulation is likely to happen. is will give
SINUS BRADYCARDIA
Sinus bradycardia is identied by the presence of a sinus
rhythm (1:1 association of P and QRS complexes) with a
rate of < 60 bpm. Symptomatic bradycardia involves the
presence of symptoms of end- organ malperfusion, usually with a heart rate < 50 bpm.6 Careful attention should
be paid to the possibility of the presence of a heart block,
which can be identied by a higher ratio of P- waves to QRS
complexes. Heart block is dealt with in a future section.
ample opportunity to act prior to full clinical deterioration.
Patients with limited stroke volume are particularly
susceptible to becoming symptomatic during periods of
bradycardia— this includes patients with valvar pathology
(severe aortic stenosis, aortic insuciency, or mitral insufciency), and those with depressed systolic function (RV
or LV dysfunction). Additionally, patients with prior conduction pathology or starting at a low resting heart rate are
more prone to become symptomatic with only a modest
further decrease in rate.
Sinus Bradycardia Risk Factors, Prevention
and Progression
Bradycardia that precedes an anesthetic encounter may represent the eect of chronic medication therapy (including
beta blockers), myocardial conduction disease, or even a
48 PART II. CARDIAC CRISES
Sinus Bradycardia Treatment
Asymptomatic bradycardia does not require treatment, but
should be monitored closely, given the potential for development of symptomatology. e rst goal of treatment in
symptomatic bradycardia should be cessation of the inciting
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event if it has been identied. is should entail conrmation of a patent airway with sucient oxygenation, while
simultaneously communicating with the proceduralist.
Cessation of vagotonic procedural stimulation is usually
sucient to curtail brief episodes of bradycardia if this is
the cause. In the event of profound or prolonged cardiopulmonary eect, further action is needed. Severe hemodynamic instability requires IV atropine 0.5— 1- mg bolus
every 3–5 minutes, maximum dose (0.04 mg/ kg). Atropine
is not readily titratable, as it crosses the blood- brain barrier, and low doses cause a centrally mediated paradoxical
slowing of the heart rate.37 e larger doses required to
ensure eect pose the risk of an excessive response, which
can be problematic in those with poor tolerance of tachy-
Figure 7.4 Example of a transesophageal atrial pacing catheter. The
TAPSCOPE 550F. SOURCE: Picture cour tesy CardioCommand. Copyright by
CardioCommand, Inc. 2007– 2015. Reprinted with permission.
cardia (e.g., severe aortic stenosis and myocardial ischemia).
In these settings, especially if bradycardia is less profound,
titration of IV glycopyrrolate in 0.2- mg increments up to 1
mg, may allow a more nuanced control of heart rate.
38
Limited responsiveness to the vagolytic eect of anticholinergics can be expected in those with reduced vagal tone,
such as the elderly and in the denervated heart of the transplant recipient. For the latter, it should be noted that reinnervation may occur over time, restoring the transplanted heart’s
susceptibility both to sinus arrest with neostigmine
to vagolysis with atropine and glycopyrrolate.
39,40
40
and
Alternative pharmacological interventions include β1-
agonists. ese include IV boluses of ephedrine 5– 10 mg,
and epinephrine 10– 30 mcg, or continuous infusions of
dopamine (2– 10 mcg/ kg/ min), epinephrine (2– 10 mcg/
min), or isoproterenol infusion (2– 10 mcg/ min). Be aware
that isoproterenol, due to its β2 activity, is also associated
with a decrease in blood pressure and therefore may not be
an appropriate choice if hypotension and vasodilation is
already a concern. In the unusual event of refractory bradycardia due to beta blocker overdose, treatment options also
include the administration of glucagon, high- dose insulin,
or IV calcium salts.
10
and skeletal muscle contractions may contribute to cardiac
output so that transcutaneous pacing can be more eective
than endocardial ventricular pacing.
42,43
Indeed, prophylactic transcutaneous pacing has been used eectively for
expected bradycardia during carotid stenting.
44
Transvenous pacing has the advantage of being a relatively longer- term option. It can be used on a conscious
patient and the risk of burn injury to the skin is eliminated.
Furthermore, sequential AV pacing is available only via
a transvenous method. is route, however, is limited by
the considerable time required to obtain pacing capture if
appropriate venous access is not already in place. Migration
of transvenous pacing catheters causing loss of capture is
also a common drawback of this route. Transesophageal
pacing, on the other hand, can be a rapid and relatively easy
method of temporary atrial pacing that avoids most of the
diculties outlined in this section (Figure 7.4). e limitations of this convenient method of pacing are the mild
discomfort caused to the conscious patient and the absence
of ventricular pacing.45 Transesophageal pacing will be of
no value in the patient with AV block.
In the absence of a pharmacological response, attention
should turn to electrical pacing. Transcutaneous pacing is
the fastest, easiest, and most accessible option for electrical pacing in most environments, however, it requires sedation of the aware patient to prevent discomfort and its
ecacy may be limited in patients with large body habitus,
due to high impedance and failure to capture. In the intraoperative setting, the chest may be unavailable for pacing
due to the sterile eld or patient positioning (Figure 7.3).
Furthermore, only ventricular capture can be expected,
resulting in a reduced stroke index41 because of AV dyssynchrony. On the other hand, associated diaphragmatic
Sinus Bradycardia Follow- Up Care
As most episodes of bradycardia are time- limited due to a
reversible inciting event, post- stabilization eorts should
focus on prevention of recurrence of the stimulus— securing
an unsecured airway, maintaining normothermia, improving cardiac supply/ demand, and relief of intracranial hypertension. In particular, the aerent limb of the vagal reex
can be blunted by the proceduralist through inltration of
local anesthetic around the carotid bulb or performance of
a retro/ peri- bulbar block of the eye.
CARDIAC DYSRHYTHMIAS 49
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In patients with structural injury to the conduction
system that is unlikely to resolve, plans should be made for
placement of a permanent intracardiac or epicardial pacing
device when clinically appropriate. In the meantime, care
should be taken to ensure the continued functionality of
temporary pacing methods.
HEART BLOCK
Heart Block Rhythm Identication
Heart block is a disorder of impulse conductance from the
atrium to the ventricles. First- degree block involves slowed
conduction from atria (A) to ventricles (V) (PR interval >
200 ms), second- degree block is dened by intermittent AV
conduction. Second- degree block is further divided into
two types. Mobitz type I second- degree block (also known
as Wenckebach) features progressively prolonged PR intervals until a ventricular beat is dropped— then the cycle starts
over again. As this block generally is at or proximal to the
AV node, the QRS complex is generally narrow. Mobitz
type II is oen described as a 2:1, 3:2, or 4:3 block, where
every second, third, or fourth beat respectively, is not conducted from atrium to ventricle. In type II Mobitz, the PR
interval remains a consistent length. As the block is infranodal, and there may be associated bundle- branch blocks, the
QRS is usually widened. e distinction is important, as
rst- degree block and Mobitz type I second- degree block
(Wenckebach) rarely progress, while Mobitz type II seconddegree blocks may be a precursor of third- degree block.
ird- degree block (complete heart block) is complete AV
dissociation, where no atrial activity is transmitted to the
ventricle, and ventricular activity arises from some lower
pacemaker, which may be the AV node, the His- Purkinje
system, or the ventricular myocardium itself. ird- degree
block almost always features a ventricular rate of < 60 bpm,
and oen signicantly lower. While rst- and second- degree
blocks are rarely of hemodynamic signicance, third- degree
block can present as a life- threatening emergency.
agents individually or in combination. ese include calcium channel blockers, beta blockers,46 local anesthetic,
amiodarone, or digoxin. In addition, cardiac surgery can
be a source of disruption of the conduction system that
leads to a new heart block. is is particularly true of valvar
surgeries47 (including percutaneous aortic valve replace-
48,49
ment
) and intervention for hypertrophic obstructive
cardiomyopathy.50 In this context, the majority of patients
recover AV conduction in a few days postoperatively.
Temporary pacing is therefore used initially, switching to
a permanent pacemaker only if the block fails to resolve.51
In the case of medication- induced heart block, the oending agent should be discontinued as soon as possible and
an alternative medication must be sought if available.
As with sinus bradycardia, the more benign forms of
heart block (rst- degree and Mobitz type I second- degree)
need only be treated in the event of clinical instability (presence of symptoms). Fortunately, these rst two
rhythms are oen asymptomatic. Treatment, if required,
should consist, as with symptomatic bradycardia, of IV
glycopyrrolate or atropine (see sinus bradycardia section).
Electrical pacing remains an alternative therapy if atropine
is unsuccessful.
ird- degree heart block and symptomatic Mobitz type
II second- degree block should be promptly treated with
electrical pacing (transcutaneous or transvenous). Details of
the merits and pitfalls of each are detailed in the section on
treatment of sinus bradycardia. In relation to heart block, it
is of importance to note that ventricular pacing is essential.
Since transesophageal pacing cannot activate the ventricles,
this is not an adequate approach. Transcutaneous pacing is
acceptable as it causes V- pacing, however sequential AVpacing, as available through the transvenous route, has the
additional advantage of providing enhanced ventricular
preload through atrial contraction. AV- pacing is of particular importance in the patient with le ventricular systolic or
diastolic dysfunction. If there is a delay in initiation of electrical pacing, atropine bolus (as above) can be administered
for complete heart block.
Heart Block Management
Foremost, when new- onset heart block is diagnosed, consideration should be given to the presence of an acute inferior wall MI— both the AV node/ His- Purkinje system and
inferior wall are commonly supplied by the right coronary
artery. Twelve- lead EKG can be useful in distinguishing this
secondary diagnosis.
Induced heart block in the perioperative setting can
be attributed to high vagal tone or various pharmacologic
Heart Block Follow- Up Care
First- degree and Mobitz type I block require little followup care due to the small likelihood of progression to a
more dangerous conduction abnormality. Mobitz type II
and third- degree block will require permanent pacemaker
placement prior to hospital discharge. Plans should be made
for admission to an acute/ critical care unit with appropriate monitoring until placement of permanent pacing
50 PART II. CARDIAC CRISES
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capabilities. As always, care should be taken to ensure the
continued functionality of temporary pacing methods.
CASE- BASED LEARNING DISCUSSION
1. Based on the case outlined in the beginning of the
chapter, what would be your rst steps in assessing
bradycardia in your patient receiving a laparoscopic
cholecystectomy? What information would you use
to decide whether to treat the heart rate? Suppose the
noninvasive blood pressure is 82/ 42, what steps could
you take to normalize the patient’s vital signs?
2. You are able to correct the patient’s bradycardia, and the
case appears to be proceeding uneventfully. You notice
suddenly that your patient’s heart rate is increasing
to 134 bpm. What are your next steps? e rhythm
is regular, narrow complex, and the patient’s blood
pressure is 105/ 65. What are the rst three diagnoses
on your dierential? What treatment will you pursue?
3. Despite your best eorts, the patient’s continues to
decline— the noninvasive blood pressure and your
end- tidal CO2 are now unmeasurable. You also notice
that your peak airway pressures have increased from 26
to 55 cmH2O. What are your rst steps? What root
causes might explain this situation? What would be the
appropriate treatment for each cause?
4. You are able to correct the patient’s cardiac arrest, and
the surgery is completed. e patient is delivered to the
PACU with normal vital signs. About 20 minutes later,
you receive an urgent page to the PACU to assess this same
patient. On the monitor, you notice his heart rate is 156
bpm. e rhythm is irregular with a narrow QRS complex.
What additional information would you seek at this time?
Suppose the blood pressure is 99/ 52 and the patient reports
he suddenly became short of breath. What treatments
would you initiate? What additional tests or treatments
would you consider aer stabilizing the patient?
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23. Balser JR. Chapter 1: Perioperative dysrhythmias. ASA Refresh
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Dysrhythmias_ .2.aspx.
24. Balser JR. Perioperative arrhythmias: incidence, risk assessment,
evaluation, and management. Card Electrophysiol Rev. 2002;6(1–
2):96– 99. http:// www.ncbi.nlm.nih.gov/ pubmed/ 11984026.
Accessed March 30, 2015.
25. ompson A, Balser JR. Perioperative cardiac arrhythmias. Br J
Anaesth. 2004;93(1):86– 94. doi:10.1093/ bja/ aeh166.
26. Gupta AK, akur RK. Wide QRS complex tachycardias.
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S0025- 7125(05)70315- 1.
27. Atlee JL. Cardiac arrhythmias: drugs and devices. Curr Opin
Anaesthesiol. 2001;14(1).
28. Janse MJ, Wit AL. Electrophysiological mechanisms of ventricular
arrhythmias resulting from myocardial ischemia and infarction.
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29. Barnes BJ, Hollands JM. Drug- induced arrhythmias. Crit
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CCM.0b013e3181de112a.
30. Owczuk R , Wujtewicz MA, Sawicka W, et al. e eect of intravenous
lidocaine on QT changes during tracheal intubation. Anaesthesia.
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31. Liebold A, Wahba A, Birnbaum DE. Low- energy cardioversion with
epicardial wire electrodes: new treatment of atrial brillation aer
open heart surgery. Circulation. 1998;98(9):883– 6. doi:10.1161/
01.CIR.98.9.883.
32. John Mancini G., Goldberger AL. Cardioversion of atrial brillation: Consideration of embolization, anticoagulation, prophylactic
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33. Hillis LD, Smith PK, Anderson JL, et al. 2011 ACCF/ AHA
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Association Task Force on Practice Guidelines. Developed in collaboration with the American Association for oracic Surgery,
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34. Miller S, Crystal E, Garnkle M, Lau C, Lashevsky I, Connolly
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35. Wijeysundera DN, Duncan D, Nkonde- Price C, et al. Perioperative
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36. Walsh SR, Tang T, Wijewardena C, Yarham SI, Boyle JR, Gaunt ME.
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37. Rudole RD, Bulmer FMR. Some cardiac eects of atropin. Am J
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38. Preiss D, Berguson P. Dose- response studies on glycopyrrolate
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39. Bjerke RJ, Mangione MP. Asystole aer intravenous neostigmine in
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40. Sawasdiwipachai P, Laussen PC, McGowan FX, Smoot L, Casta A.
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01.anes.0000282140.68060.fa.
41. Trigano JA, Remond JM, Mourot F, Birkui P, Lévy S. Le ventricular pressure measurement during noninvasive transcutaneous cardiac
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42. Feldman MD, Zoll PM, Aroesty JM, Gervino E V, Pasternak RC,
McKay RG. Hemodynamic responses to noninvasive external cardiac pacing. Am J Med. 1988;84(3 Pt 1):395– 400. http:// www.
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43. Murdock DK, Moran JF, Speranza D, Loeb HS, Scanlon PJ.
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44. Im S- H, Han MH, Kim SH, Kwon BJ. Transcutaneous temporary cardiac pacing in carotid stenting: noninvasive prevention of
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45. Verbeet T, Castro J, Decoodt P. Transesophageal pacing: a versatile diagnostic and therapeutic tool. Indian Pacing Electrophysiol J.
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46. Zeltser D, Justo D, Halkin A, et al. Drug- induced atrioventricular
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47. Berdajs D, Schurr UP, Wagner A, Seifert B, Turina MI, Genoni M.
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49. Khawaja MZ, Rajani R, Cook A, et al. Permanent pacemaker
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8.
SEVERE VALVULAR DISEASE
Yafen Liang and Andrew Shaw
CLINICAL CASE
for mitral valve stenosis, le ventricle for aortic valve steno-
sis) and this actually generates more workload for the heart.
A 78- year- old female with a newly diagnosed pancreatic
head mass presented for elective Whipple procedure. Past
medical history included hypertension, hyperlipidemia,
diet- controlled diabetes, colon cancer status post right colectomy 7 years ago, and moderate aortic valve stenosis with
a peak gradient of 32 mmHg, mean gradient of 14 mmHg,
and an aortic valve area of 1.1 cm2. Her preoperative echocardiogram revealed preserved le ventricular ejection
fraction of 60% with signicant concentric le ventricular
hypertrophy and stage 2 diastolic dysfunction. Her activity
level is limited due to pain from arthritic knees.
Also, in aortic stenosis, reducing downstream pressure
would lead to a dangerous reduction in le ventricular per-
fusion pressure (in a usually hypertrophied myocardium)
and is thus to be avoided.
In response to a reduction in aerload, the heart will
increase heart rate or stroke volume to maintain cardiac output and thus maintain blood pressure. As the stenotic lesion
worsens, compensatory increases in stroke volume become
limited and therefore hypotension occurs. As mentioned,
with a decrease in blood pressure, there is a reduction in cardiac perfusion leading to myocardial ischemia that further
limits cardiac output. us, maintaining aerload is crucial
KEY CLINICAL FACTORS
in aortic stenosis.
In regurgitant lesions, a rapid heart rate reduces the
time for regurgitant ow, and thus reduces the regurgita-
e pathophysiology of valvular diseases follows the fundamental principles of uid dynamics. Flow across any
orice depends on the cross- sectional valve area, the pressure gradient across the valve, and the amount of transit
time there is for blood to cross the valve. us, alteration in
any of these components translates into a change in stroke
volume, which in turn results in a change in cardiac output
(CO). Since eective ow = forward ow – regurgitant
ow, the goal is to maximize forward ow and minimize
regurgitation.
In stenotic lesions, the cross- sectional valve area is xed,
and thus in order to increase forward ow, the rst step is to
increase the amount of the time the ow transits the valve.
Hence, appropriately reducing the heart rate is preferable.
e second step is to increase the pressure gradient/ ow
velocity across the valve. Increase of the pressure gradient
can be achieved by reducing the downstream resistance
and/ or increasing the upstream pressure. Since the greatest
downstream resistance is at the stenotic valve itself, and this
is xed, increased pressure gradient can be only achieved by
increasing the pressure upstream of the lesion (le atrium
tion volume. Reducing the aerload can lead to a lower
degree of regurgitation and thus more eective forward
ow. erefore for regurgitant lesions, maintaining a high
normal heart rate and lowering aerload are the two most
important hemodynamic goals.
Broadly speaking, stenotic valvular heart diseases (aortic
stenosis and mitral stenosis) are more challenging to manage perioperatively than regurgitant valvular heart diseases.
Patients have a xed cardiac output and are unable to compensate for the reduction in systemic vascular resistance
caused by the vasodilating eect of a general anesthetic. On
the other hand, patients with regurgitant lesions generally
do better with anesthesia due to vasodilation eect of anesthetics and increased forward ow.
Conrmation of the diagnosis of valvular heart disease (VHD) is usually done with echocardiography. Twodimensional echocardiography indicates abnormal valvular
function and morphology, but does not indicate the severity of stenosis or regurgitation. Doppler echocardiography
measures velocity of ow across stenotic valves from which
pressure gradients and severity of a stenotic valve can be
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estimated. Doppler ow imaging can also provide estimates
of the severity of regurgitant valve disease.
1– 3
In addition,
echocardiography can also assess other concomitant valvular diseases and associated ventricular chamber size and
function.
However, the clinical symptoms may not correlate with
the echocardiographic ndings. A careful history is of
great importance in the evaluation of patients with VHD,
because in general decisions about treatment are based on
the presence or absence of symptoms. Due to the slow, progressive nature of many valve lesions, patients may not recognize symptoms because they may have gradually limited
their daily activity levels. If the clinician is unable to obtain
a reliable history, and imaging studies are equivocal, a func-
morphology of the valve leads to an acceleration of brocalcic deposits, and these patients tend to present with signicant aortic stenosis at an earlier age. ey also oen have
coexistent aortopathy, which may require surgical correction at time of valve replacement. Rheumatic heart disease
used to be the leading cause of AS, but has been decreasing
in frequency in the Western world.
8
Hypertension, diabetes mellitus, hyperlipoproteinemia,
and uremia all accelerate the process of aortic valve stenosis.9 In about 50% of patients who present with aortic stenosis, signicant coronary artery disease is also present, thus
evaluation of the patient with severe AS for major noncardiac surgery should include work up for presence and severity of CAD.
10
tional study is oen needed, for instance, exercise- induced
hypotension for conrmation of critical aortic stenosis.
Generally speaking, patients with severe VHD presenting for elective noncardiac surgery should have the
valve intervention performed rst if they are symptomatic,
and asymptomatic patients can have minor and moderate
risk surgery performed with close monitoring and skilled
anesthesia care. Asymptomatic patients with severe VHD
should consider valve intervention if they are to undergo
high- risk surgery. If the surgery is deemed to be emergent
or urgent, a comprehensive perioperative anesthesia management plan including preoperative assessment and optimization; intraoperative maintenance of hemodynamic
stability, appropriate monitoring, ability to recognize and
treat hemodynamic emergencies; postoperative monitoring and management of complications should be developed
preoperatively, and carried out meticulously throughout.
4– 6
Symptoms
Patients with worsening AS oen present with syncope,
angina, and dyspnea, which is abbreviated as “SAD.” e
presence and severity of symptoms are closely related to the
prognosis of this disease.
11,12
Interventions should ideally be
performed prior to the occurrence of those symptoms.
In patients with severe AS, increased oxygen consumption during exertion leads to vasodilation. However, a concomitant increase in cardiac output to overcome this drop
in systemic vascular resistance (SVR) cannot occur due
to the xed stenotic lesion, resulting in hypotension and
a decreased perfusion of the brain. If the drop in cerebral
perfusion is severe enough, syncope can occur. Syncope at
presentation indicates a worse prognosis and the 3- year
7
mortality without aortic valve replacement approaches
50% in this setting.
AORTIC STENOSIS
PATHOPHYSIOLOGY
Mechanism
Obstruction at the aortic valve orice causes increased pressure in the le ventricle (LV) and impaired ow through
the valve, with resultant le ventricular hypertrophy and
diastolic dysfunction.
Aortic stenosis leads to progressive myocardial hypertrophy in an eort to generate higher le ventricular
pressures and maintained cardiac output. Myocardial
hypertrophy necessitates a higher oxygen requirement
while AS leads to a simultaneous decrease in aortic root
pressure, the driving force behind myocardial perfusion
pressure during diastole. When the oxygen demand is not
met by the supply, an oxygen debt results in the development of angina. is becomes a vicious spiral, since
ischemia leads to myocardial dysfunction, which further
impacts le ventricular function, a drop in cardiac output,
Etiology
e main etiology for aortic stenosis (AS) is senile brocalcic degeneration leading to aortic sclerosis and stenosis (80%).8 Congenital bicuspid aortic valve is the second
most common cause for AS (30%– 40%).8 e special
and further reductions in myocardial perfusion. Patients
with AS and concomitant angina have a 5- year (uncorrected) mortality close to 50%.
Dyspnea in the presence of AS arises from the increased
le ventricular pressures required to pump blood across
the stenotic aortic valve. When the le ventricular
54 PART II. CARDIAC CRISES
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55
pressure becomes too high, the pressure is transmitted
across the mitral valve and into the pulmonary system,
thus leading to progressive systolic and diastolic dysfunction culminating in congestive heart failure and dyspnea
symptoms. When patients progress to congestive heart
failure, their prognosis becomes poor without aortic valve
replacement.
13
conditions, percutaneous balloon aortic valvuloplasty
(BAV) as a bridging strategy, and/ or transcatheter aortic
valve replacement (TAVR).
16,17
e chosen anesthetic technique should maintain aerload and avoid tachycardia in order to maintain the balance
between myocardial oxygen demand and supply in the presence of a hypertrophied le ventricle and reduced coronary
blood ow. Direct measurement of arterial blood pressure
should be routinely deployed except for very short or minor
MANAGEMENT OF AORTIC STENOSIS
Preoperative Evaluation and Anesthetic Considerations
Assessing the severity of AS is the rst step. Severe AS is
dened as a measured peak aortic valve velocity >4 m per
second, calculated aortic valve area < 1 cm2, or calculated
mean pressure gradient across the aortic valve > 40 mmHg.
In patients with severe AS, volume shis and rhythm
disturbances associated with the surgical stress and cardiovascular side eects of anesthetic medications may lead to
an unfavorable hemodynamic state. e occurrence of hypotension and tachycardia can result in decreased coronary
perfusion pressure, development of arrhythmias or ischemia,
myocardial injury, cardiac failure, and sudden death.
14,15
It is recommended therefore that patients with severe
procedures. is should be performed before induction of
general anesthesia. Careful uid balance is essential, guided
by invasive monitoring if possible (central venous catheter,
pulmonary artery catheter, and/ or TEE, if available).
Certain groups of patients with AS have a low transaortic ow rate due to either LV systolic dysfunction with a
low LV ejection fraction (LVEF) or due to a small hypertrophied le ventricle with a low stroke volume (low ow, low
gradient AS).
18– 22
is category of severe AS poses a diagnostic and management challenge distinctly dierent from
the challenges faced by the majority of patients with AS,
whose severity is well reected by high pressure gradient
and peak ow velocity. e severity of low ow, low gradient AS is also frequently overlooked due to its somewhat
paradoxical presentation.
AS who require emergency noncardiac surgery should
be managed with invasive hemodynamic or continuous
transesophageal echocardiography (TEE) monitoring
intraoperatively and remain in an intensive monitoring
setting for 48 to 72 hours postoperatively.7 Symptomatic
patients presenting for major elective noncardiac surgery
should probably undergo aortic valve replacement rst,
as they are at great risk of sudden death perioperatively
(untreated severe symptomatic stenosis has a 50% 1year survival). Asymptomatic patients for major elective
surgery with anticipated marked uid shis (thoracic,
abdominal, vascular, or major orthopedic) should, if feasible, have valve replacement considered prior to their
noncardiac surgery. Asymptomatic patients for intermediate risk or minor surgery can proceed with surgery with
usual careful anesthetic management. Great care should
be taken if spinal anesthesia is planned in the presence
of uncorrected AS, as the sudden loss of aerload with
attendant hypotension can predispose these patients to
ischemic complications.
For patients who meet indications for aortic valve
replacement (AVR) before noncardiac surgery but are considered high risk or ineligible for surgical AVR, options
include proceeding with noncardiac surgery with invasive
hemodynamic monitoring and optimization of loading
Perioperative Hemodynamic Goals
1. Heart rate should be maintained in the low- normal
range. Patients with severe AS have a relatively narrow
window with regard to heart rate. In all situations,
maintenance of the baseline resting heart rate should
be the goal. As mentioned, these patients have a poorly
compliant le ventricle and therefore require a longer
diastolic time and proportionately higher le atrial
pressures to adequately ll the LV. Since lling occurs
during diastole, an appropriate reduction in heart
rate allows adequate time to ll LV. A rapid heart rate
increases oxygen requirements while at the same time
limiting supply, placing these patients at increased risk
for ischemia, leading to further myocardial dysfunction.
A common misconception is that bradycardia would
be better for patients with aortic stenosis; however,
due to the xed lesion at the aortic valve limiting the
amount of blood ejected during each cardiac cycle
(i.e., a xed stroke volume), an excessive drop in heart
rate can signicantly limit cardiac output leading to
hypotension.
erefore, maintenance of heart rate at the patient’s
baseline level, usually between 70 and 90 beats/ minute
SEVERE VALVULAR DISEASE 55
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