Full text of DOI:10.1007/BF03020528

CARDIOTHORACIC ANESTHESIA, RESPIRATION AND AIRWAY
283
Ketamine anesthesia for pericardial window in a
patient with pericardial tamponade and severe
COPD
[La kétamine utilisée pour l’anesthésie d’une ponction péricardique chez une
patiente qui présente une tamponnade et une MPOC sévère]
Tim Aye MD CCFP FRCP, Brian Milne MD MSc FRCP
Purpose: To describe the use and concerns of ketamine anesthe-
sia for pericardial window in a patient with pericardial tamponade
and severe chronic obstructive pulmonary disease (COPD) with
CO2 retention.
de la possibilité d’une défaillance ventriculaire droite dans un ventricule
déjà altéré ne se sont pas matérialisées.
Conclusion : La kétamine utilisée dans le présent cas de tampon-
nade cardiaque, MPOC et rétention de CO2 a permis le maintien de
la ventilation spontanée, l’absence d’hospitalisation et le sevrage de la
ventilation mécanique, la bronchodilatation et la préservation relative
de la courbe de réponse du CO2. Nous n’avons pas noté d’effet nocif
sur la postcharge ventriculaire droite.
Clinical features: A 73-yr-old woman with long-standing COPD
and cor pulmonale admitted with pericardial effusion and tamponade
had surgery for a pericardial window receiving a total of ketamine 450
mg iv. Arterial pCO2 increased from 71.8 mmHg preoperatively to
96 mmHg intraoperatively postdrainage of 1000 mL of effusion.
Hemodynamic stability and SpO2 >93% were maintained.
Intubation was avoided and concerns of increased pulmonary vascu-
lar resistance and potential for right ventricular failure in an already
compromised right ventricle were not observed clinically.
NESTHESIA for pericardial window
surgery in patients with pericardial tam-
ponade can prove a challenge due to
Conclusion: In this patient with pericardial tamponade, COPD
and CO2 retention, the advantages of ketamine included maintain-
ing spontaneous ventilation, avoiding institution and weaning of
mechanical ventilation, bronchodilation and relative preservation of
the CO2 response curve. Deleterious effects on right ventricular
afterload were not observed.
A
impaired diastolic filling and decreased
stroke volume.1 Infiltration with local anesthesia, with
or without sedation, and general anesthesia have been
used for pericardiotomy in this situation.2 Ketamine,
because it increases systemic vascular resistance and
heart rate, and maintains cardiac contractility, is useful
in patients with cardiac tamponade. Kaplan et al.
reported on the use of ketamine to supplement local
anesthesia for reopening a sternotomy in a postopera-
tive cardiac tamponade patient with subsequent endo-
tracheal anesthesia.3 There is, however, a paucity of
information on the use of ketamine in patients with
cardiac tamponade. Despite the fact that clinicians will
often choose ketamine for patients with pericardial
tamponade for its beneficial effects on maintaining
systemic blood pressure, it can however have deleteri-
ous effects on right ventricular afterload. We describe
a case of a patient with cor pulmonale and chronic
Objectif : Décrire l’utilisation de l’anesthésie avec kétamine et les
craintes qu’elle suscite dans le cas d’une ponction péricardique chez
une patiente qui présente une tamponnade et une maladie pul-
monaire obstructive chronique (MPOC) sévère avec rétention de CO2.
Éléments cliniques : Une femme de 73 ans atteinte d’une MPOC de
longue date et d’un cœur pulmonaire et présentant un épanchement
péricardique et une tamponnade, a subi une ponction péricardique et a
reçu 450 mg iv de kétamine. La pCO2 artérielle a augmenté de 71,8
mmHg, avant l’opération, à 96 mmHg pendant l’opération, le
postdrainage de 1 000 mL de liquide. La stabilité hémodynamique et
la SpO2 ont été maintenues > 93 %. On a évité l’intubation et les
craintes d’une augmentation de la résistance vasculaire pulmonaire et
From the Department of Anesthesiology, Queen’s University, Kingston, Ontario, Canada.
Address correspondence to: Dr. Brian Milne, Department of Anesthesiology, Kingston General Hospital, 76 Stuart Street, Kingston,
Ontario K7L 2V7, Canada. Phone: 613-548-7827; Fax: 613-548-1375; E-mail: milneb@post.queensu.ca
Accepted for publication October 31, 2001.
Revision accepted December 12, 2001.
CAN J ANESTH 2002 / 49: 3 / pp 283–286

284
CANADIAN JOURNAL OF ANESTHESIA
obstructive pulmonary disease (COPD) who had a
pericardial window under ketamine anesthesia where
this was taken into consideration.
voltage and her chest x-ray suggested a large pericar-
dial effusion.
The patient eventually consented to needle
drainage of the pericardial effusion prior to definitive
surgery providing she was not aware. An echocardio-
gram demonstrated a very large anterior and posterior
pericardial effusion and a chronically dilated right ven-
tricle with systolic and diastolic collapse. Under echo
guidance, in the intensive care unit (ICU) in the sit-
ting position, 400 mL of chocolate coloured pericar-
dial fluid was drained. Three boluses of midazolam 0.5
mg and propofol 20 mg iv were given during the pro-
cedure. Hemodynamics remained stable throughout
the procedure and at the termination, right ventricu-
lar collapse was still present on echocardiogram. In the
operating room with continuous intra-arterial moni-
toring, automated segment lead I, II, and V analysis,
nasal O 4 L·min–1, the patient was prepped and
draped i2n the sitting position. After administration of
glycopyrrolate 0.3 mg, and midazolam 1 mg, anesthe-
sia was induced with ketamine in 25 mg increments to
a total of 100 mg. Blood pressure was 120 mmHg sys-
tolic, and heart rate 100 beats·min–1. The patient was
gradually returned to the supine position and lido-
caine 1% was infiltrated locally. Subxiphoid drainage of
1000 mL of effusion increased her blood pressure to
140 mmHg systolic. Heart rate was 100–115
beats·min– 1 and SpO2 >93% throughout. An intraop-
erative blood gas postdrainage showed a pH 7.28,
PO2 102 mmHg, pCO 96 mmHg, HCO3 44
mmoL·L– 1. A total of 4502mg of ketamine were used
during the procedure. The xiphisternum and a large
ellipse of anterior pericardium were excised along with
talc poudrage of the pericardial space. She returned to
the ICU with stable hemodyamics and had no recall of
events. There were no postoperative problems except
for a pneumothorax, which required insertion of a
left-sided chest tube, probably due to the pericardio-
centesis. She was discharged home five days postoper-
atively and analysis of the pericardial fluid was negative
for malignancy, showing only inflammatory cells.
Case report
A 73-yr-old, 72-kg woman with long-standing COPD
and cor pulmonale was admitted with pericardial effu-
sion and tamponade. Admission one month prior for
drainage of a pericardial effusion was complicated by
insertion of a pulmonary artery catheter introducer
into the carotid artery and postpericardiocentesis
intrapericardial hemorrhage. Her pulmonary artery
pressure at that time was 54/25 mmHg. She was dis-
charged home on nasal O 4 L·min– 1. Prior to the pre-
sent admission she expe2rienced increasing dyspnea,
orthopnea and peripheral edema. Other medical prob-
lems were obesity, stable angina, and hypothyroidism.
Medications included enalapril, furosemide, isosor-
bide dinitrate, ranitidine, thyroxin, salbutamol and
ipratropium bromide. She reported allergies to peni-
cillin, codeine and morphine. Blood pressure on
admission was 130/80 mmHg, heart rate 90
beats·min– 1, respiratory rate 24 breaths·min–1 and a
pulsus paradoxus of 10 mmHg. Breath sounds were
decreased bilaterally with bibasilar crackles. Her SpO
2
was 98% on nasal O 4 L·min– 1, and jugular venous
pressure (JVP) was 32cm H2O.
The following day she was in distress with increas-
ing shortness of breath. She was unable to lie down
stating she had never been this bad before. There had
been no improvement with salbutamol inhalation and
she had been started on prednisone. Her blood pres-
sure was 116/68 mmHg, heart rate 110 beats·min–1,
pulsus paradoxus 26 mmHg and SpO 93% on nasal
O2 4 L·min–1. Examination revealed2 decreased air
entry with faint wheezes, JVP 8 cm H O, with poorly
palpable peripheral pulses. The patient2refused to have
another pericardiocentesis “awake” because of her
previous experience and requested surgical drainage
be performed under a general anesthetic.
Initially a thoracoscopic pericardial window was
considered but in consultation with the attending
anesthesiologist it was decided that problems with col-
lapsing the emphysematous lung, difficulty in tolerat-
ing one lung anesthesia, and lack of an expeditious
resolution made a subxiphoid approach to the pericar-
dial window preferable. Anemia was corrected with
two units of packed cells bringing the hemoglobin
concentration to 106 mg·dL–1. Electrolytes and liver
function tests were normal, an arterial blood gas on 4
L·min–1 nasal O2 showed pH 7.38, PO2 78.9 mmHg,
PCO2 71.8 mmHg, HCO3 37.5 mmoL·L– 1. Her elec-
trocardiogram showed a sinus tachycardia with low
Discussion
Pericardial tamponade is primarily a problem of
impaired diastolic filling due to continuous elevation
of intrapericardial pressure decreasing stroke volume,
cardiac output and systemic blood pressure.1 The
choice of anesthetic in this patient had to take into
account the combined pathophysiology of pericardial
tamponade and chronic obstructive lung disease with
CO2 retention. Hypercarbia may increase right ven-
tricular afterload, and cause dysrhythmias which could
be detrimental to the failing right ventricle.2 While the

Aye et al.: KETAMINE, TAMPONADE A N D C O P D
285
use of ketamine has been deemed as potentially disas-
trous in patients with cardiac tamponade and minimal
right ventricular functional reserve,4 Kaplan reported
the use of ketamine 0.5 mg·kg–1 to supplement local
anesthesia for opening the lower end of a sternotomy
incision in a patient with postoperative tamponade.
Following this, in contrast to our case, general anes-
thesia was induced with ketamine and succinylcholine,
the trachea intubated and anesthesia maintained with
nitrous oxide, pancuronium, and morphine.3 The sole
use of local anesthesia advocated by Stanley et al.2 or
awake intubation5 was not an option due to our
patient’s desire to be “asleep”.
Although ketamine can have myocardial depressant
effects in vitro and in patients who are maximally
stressed with depleted catecholamines,6 in this case
ketamine produced no decrease in blood pressure.
The patient refused to be monitored with a pul-
monary artery catheter due to her previous experience
of an introducer having been placed into the carotid
artery. This prevented monitoring of cardiac output
and pulmonary artery pressures. The effect of keta-
mine on the pulmonary vasculature was a main con-
sideration due to COPD with associated loss of
pulmonary capillaries and arterial hypoxia leading to
pulmonary vasoconstriction. Spotoft et al. found
increases in pulmonary artery pressures mainly
through increases in pulmonary vascular resistance
in numerous ways, but the majority are associated with
direct myocardial depressant effects and decreases in
systemic vascular resistance. Inhalational agents shift the
CO2 response curve to the right and the associated
hypercarbia may be detrimental to the patient with
COPD and CO retention. Acute or chronic respirato-
2
ry acidosis may cause central nervous side effects,
increase right ventricular afterload, and cause dysrhyth-
mias, all complications which should be avoided in
patients with limited myocardial reserve. Although ket-
amine is a respiratory depressant, its’ effects are mild10,11
and even though there is no guarantee against pul-
monary aspiration, respiration is maintained with rela-
tively intact laryngeal reflexes. In humans, ketamine
alone causes mild respiratory depression similar but at a
lesser degree to that seen with narcotics in the premed-
icant or analgesic dose range in that the slope of the
ventilatory response to CO is unchanged, while the
2
response curve is shifted to the right.1 2 Maintaining
spontaneous ventilation may be better tolerated in the
patient with cardiac tamponade.1 3 Increased tracheo-
bronchial secretions may be attenuated with an antisial-
ogogue and apneic spells may be minimized by titrating
doses with slow injections.
Thus, in this patient with pericardial tamponade,
COPD and CO2 retention, the advantages of keta-
mine included maintaining spontaneous ventilation,
avoiding institution and weaning of mechanical venti-
lation, bronchodilation and relative preservation of
the CO2 response curve, lack of cardiac depression,
intense somatic analgesia, and amnesia. These advan-
tages were felt to outweigh the disadvantages of
effects on pulmonary vasculature, increased tracheo-
bronchial secretions, and emergence reactions. The
theoretical concerns of increased pulmonary vascular
resistance and potential for right ventricular failure in
an already compromised right ventricle were not
observed clinically, and we were able to avoid intuba-
tion and mechanical ventilation in our patient with
COPD and CO2 retention.
unrelated to changes in PaO2 and PaCO with keta-
2
mine.4 There was initial concern that this increase in
pulmonary vascular resistance may be greater than the
increase in systemic vascular resistance which could
cause an increase in shunt fraction. However, Rees et
al. found no increase in shunt fraction using ketamine
in humans during one lung anesthesia when compared
to enflurane.7 One of the main problems with studies
on the effects of ketamine on the pulmonary vascula-
ture is controlling for the effects of respiratory depres-
sion on partial airway obstruction. Balfors et al. found
no change in pulmonary vascular resistance during
ketamine anesthesia in adults with assisted ventila-
tion.8 Despite the effects of ketamine on pulmonary
vasculature, its beneficial bronchodilating effect which
parallels that of inhalational agents has been used in
the treatment of reactive airways.9 In our patient with
COPD, ketamine’s bronchodilating effects may also
have been advantageous.
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