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usaha herbal

Mandatory modes

The mandatory ventilation modes (S)CMV and P-CMV deliver time-cycled mandatory breaths, volume-controlled or pressure-controlled, respectively.
When the patient triggers or the user initiates a breath, the respiratory rate increases, while both the inspiratory time and the tidal volume (for (S)CMV) or respiratory pressure (for P-CMV) remains constant. The minute volume increases as a result.

Synchronized controlled mandatory ventilation ((S)CMV) mode.

The (S)CMV mode provides volume-controlled mandatory breaths only. The controls active in the (S)CMV mode are shown figure B-1. the tidal volume (Vt) setting defines the delivered volume. The rate and breath timing setting (see section 1.5) define the breath cycle timing. Breaths can be triggered by the ventilator, patient, or user.

In this mode, the user sets the Vt, the rate and the other breath timing controls, and the FlowPattern. As in all other modes, the user also set the PEEP/CPAP and Oxygen, and the pressure or flow trigger if desired.

ACID-BASE INTERPRETATION

Disorders of acid-base balance can be found in as many as nine of every 10 patients in the ICU, which means that acid-base disoders may be the most common clinical problems you will encounter in the ICU. This chapter present a structured approach to the identification of acid-base disoders based on a set of well-defined rules that can be applied to arterial blood gas (ABG) and serum electrolyte measurement.

BASIC CONCEPTS
The hydrogen ion concentration [H+] in extracellular fliud is determined by the balance between the partial pressure of carbon dioxide (PCO2) an the conceration of bicarbonate (HCO3) in the fliud. This relationship is expressed as follows.

[H+] (nEq/L) = 24 x (PCO2/HCO3)

Using a normal arterial PCO2 of 40 mm Hg and a normal serum HCO3 concentration of 24 mEq/L, the normal [H+] in arterial blood is 24 x (40/24) = 40 nEq/L


Hydrogen Ion concentration and pH

Note that the [H+] in extracellular fliud is expressed in nanoequivalents (nEq) per liter. A nanoequivalent is one-millionth of a miliequivalent, so there are millions more sodium, chloride, and oder ions measured in mEq than there are hydrogen ions. because nanoequivalents represent such as small amount, the [H+] is routinely expressed in pH units, which are derived by taking the negative logarithm of the [H+] in nEq/L.

jantung sehat

Selain dengan mengetahui makanan untuk jantung sehat, perlu juga kiranya mengenali tips-tips lainnya yang berhubungan dengan masalah jantung sehat. Ingtlah, betapa pentingnya mengenali faktor yang menyebabkan resiko terkena serangan jantung, baik teman kita atau saudara kita. Dengan demikian, kemampuan memelihara agar terhindar dari resiko serangan jantung lebih waspada. Berikut ini beberapa tips menjaga jantung sehat.


* Selalu menjaga keseimbangan berat badan dalam batas normal. Dengan berat badan normal maka daya pacu jantung akan lebih ringan.
* Lakukan olah raga secara teratur. Karena olah raga akan melatih daya pacu jantung dan peredaran darah. Pada saat olahraga peredaran darah akan berjalan cepat dan akan mengangkut semua racun yang di dalam tubuh. Lari ringan atau jalan kaki selama 30 menit yang dilakukan rutin setiap hari (10 menit yang dilakukan dalam sehari) sangat bagus untuk kesehatan jantung. jalan kaki cepat 10 menit 3 kali sehari dapat membakar jumlah kalori yang sama dengan berolah raga 30 menit, selain itu juga bsa menurunkan kolesterol jahat LDL dan menaikkan Kadar kolesterol baik HDL.
* Jaga kolesterol dalambatasan normal. Jika anda merasa ber-kolesterol tinggi maka konsultasikan dengan dokter.
* Minum jus buah. Semua Jus dengan 100% buah mengandung nutrient pelindung jantung yang sama dengan sayuran, dengan contoh jus tomat 230ml sama dengan 2 saji sayuran. Jadi apabila kita jarang mengkonsumsi sayuran bisa di gantikan dengan jus buah, pastinya lebih menyegarkan. Tapi akan lebih baik jika tetap mengkonsumsi sayur.·
* Apabila kita mengalami kurang tidur di malam hari, kita bisa menggantinya dengan tidur siang 30 menit setiap hari. Mungkin bisa di lakukan saat istirahat untuk yang bekerja. Berdasar hasil sebuah studi, tidur siang 30 menit setiap hari dapat menurunkan resiko penyakit jantung sebanyak 37% dengan menurunkan kadar hormon penyebab stres. Kalaupun tidak punya waktu sebanyak itu, tidur siang dengan waktu yang lebih singkat masih bisa menurunkan resiko penyakit jantung sekitar 12%.
* General chek up, cheklah kesehatan anda secara rutin… dengan mengkonsultasikan kesehatan anda ke dokter, maka kesehatan akan lebih terjamin.
* Melakukan rileksasi. Hal ini dimkasudkan agar detak jantung kesehariannya berjalan secara normal seperti biasa.

Referensi:
http://cozyeslife.blogspot.com/2010/01/kiat-menjaga-jantung-sehat.html
http://www.lifestyle.dnaberita.com/15%20November%202009%20Life%20Style%20Jantung.php

usaha herbal

Herbal-herbal Penurun Kolesterol

Selasa, 03 Januari 2006


Penyakit jantung koroner dua kali lebih besar mengancam orang-orang yang mempunyai kadar kolesterol 200-240 mg persen dibandingkan mereka yang kadarnya di bawah 240 mg persen.

Kolesterol adalah komponen asam lemak yang terdapat dalam darah. Zat ini sangat diperlukan oleh tubuh untuk proses-proses tertentu bagi kelangsungan hidup. Di antaranya untuk membentuk hormon, membentuk sel, dan merawat sel-sel saraf.

Tetapi, dalam jumlah berlebih kolesterol menjadi ancaman serius bagi tubuh, bahkan bisa menyebabkan kematian. Penyakit yang disebabkan kolesterol adalah aterosklerosis (penyempitan pembuluh darah), penyakit jantung koroner, stroke, tekanan darah tinggi, dan hiperkolesterolemia.

Kadar kolesterol dalam darah bisa diatasi dengan pengobatan secara tradisional dengan memakai aneka tumbuhan yang banyak hidup di Indonesia. Praktik ini sudah berlangsung dari generasi ke generasi.

Yang biasa dimanfaatkan untuk pengobatan kolesterol tinggi adalah daun jati belanda (Guazuma ulmifolia), kemuning (Murraya paniculata), dan tempuyung (Sonchus arvensis).

Daun jati belanda dipercaya bisa meluruhkan lemak dan menurunkan kadar kolesterol dalam darah. Tanaman yang berasal dari negara Amerika beriklim tropis ini tumbuh secara liar di wilayah tropis lainnya seperti di Pulau Jawa.

Jati belanda mengandung senyawa tannin, damar, triterpen, alkaloid, karotenoid, flavonoid, dan asam fenol. Selain bisa menurunkan kadar kolesterol, tanaman ini juga berkhasiat untuk melangsingkan tubuh, astrigen, sebagai obat diare dan obat batuk.

Sedangkan kemuning mengandung atsiri, damar, tannin, glikosida, dan meransin. Tanaman yang biasa tumbuh liar di semak belukar, tepi hutan, atau ditanam sebagai tanaman hias dan tanaman pagar ini bisa dipakai untuk mengobati radang buah zakar (orchitis), radang saluran napas (bronkhitis), infeksi saluran kencing, kencing nanah, keputihan, sakit gigi, dan haid tidak teratur. Juga untuk mengurangi lemak tubuh berlebihan, pelangsing tubuh, nyeri pada tukak (ulkus), memar akibat benturan, rematik, keseleo, digigit serangga dan ular berbisa, ekzema, dan luka terbuka pada kulit.

Tanaman tempuyung memiliki rasa pahit dan bersifat mendinginkan. Pada prinsipnya semua bagian tanaman ini bisa dimanfaatkan. Tapi, yang paling sering adalah bagian daunnya. Penurun kadar kolesterol tinggi dengan kandungan kimia saponin, flavonoida, politenol, alfa-lactucerol, beta-lactucerol, manitol, inositol, kalium, silika, dan taraksasterol adalah manfaat yang bisa didapatkan dari daun tempuyung.

Bila diramu, jati belanda, kemuning, dan tempuyung bisa menjadi obat herbal untuk menurunkan kadar kolesterol dalam darah. Inilah yang dilakukan oleh PT Indofarma. Ketiga herbal tadi diramu menjadi sebuah produk herbal yang diberi nama Prolipid. Sesuai dengan kandungan bahan-bahan pembuatnya, herbal ini membantu menurunkan kadar kolesterol yang tinggi dalam darah.

Hasil penelitian
Senyawa tanin dan musilago yang terkandung dalam daun Jati belanda dapat mengendapkan mukosa protein yang ada di dalam permukaan usus halus sehingga dapat mengurangi penyerapan makanan. Dengan demikian proses obesitas (kegemukan) dapat dihambat.

Hasil penelitian tentang daun jati belanda memperkuat penggunaannya secara ilmiah sebagai tanaman obat. Ekstrak daun jati belanda yang diberikan secara oral dengan konsentrasi 15 persen dan 30 persen dapat menurunkan kadar kolesterol total serum kelinci.

Sedangkan hasil penelitian pada daun kemuning menunjukkan, pemberian infus daun ini sebesar 10 persen, 20 persen, 30 persen, dan 40 persen sebanyak 0,5 ml pada mencit dapat menurunkan berat badannya secara bermakna. Ini menunjukkan telah terjadi peningkatan pembakaran lemak tubuh. Kolesterol merupakan salah satu komponen dari lemak.

Beberapa teori yang lain menyebutkan bahwa khasiat daun jati belanda dan kemuning adalah karena kandungan damarnya. Mekanismenya sebagai berikut, kolesterol yang terbentuk menjadi asam empedu berikatan dengan damar dan segera dieksresi melalui feses. Cepatnya asam empedu dieksresikan oleh tubuh akan disertai oleh cepatnya pembentukan asam empedu sehingga kolesterol dalam tubuh segera diubah menjadi asam empedu. Dengan demikian, proses ini akan mengurangi kadar kolesterol.

Sementara itu, bahan simplisia yang digunakan berkhasiat meningkatkan metabolisme tubuh sehingga pembakaran timbunan lemak dalam tubuh akan meningkat. Dengan demikian akan mengurangi kadar lemak tubuh. Ini berarti akan mengurangi terbentuknya kolesterol karena lemak merupakan faktor risiko tinggi terhadap kolesterol.

Karena merupakan bahan-bahan alami, jika digunakan secara teratur dan terukur, herbal-herbal ini bisa membantu menurunkan kadar kolesterol dalam darah.

Pentingnya Mengendalikan Kolesterol
Lipid atau lemak terdapat dalam makanan kita sehari-hari. Lemak tidak pernah larut dalam plasma darah. Kecuali bila berikatan dengan protein tertentu, ia bisa menyatu dan mengambang dalam darah.

Kolesterol, ditinjau dari sudut kimiawi, diklasifikasikan dalam golongan lipida (lemak) yang berkomponen alkohol steroid. Sebagian besar berfungsi sebagai sumber kalori dalam makanan.

Lemak sangat dibutuhkan oleh tubuh. Selain sebagai cadangan makanan dan pelarut vitamin A, D, E, dan K, lipid juga berfungsi untuk memelihara jaringan saraf dalam tubuh. Tetapi, kadar lemak berlebihan akan memberikan efek yang serius berupa kerusakan pembuluh koroner. Kolesterol berperan dalam proses pengapura dinding pembuluh darah koroner.

Menurut Product Manager PT Indofarma, Agus Kuanto, unsur lemak dalam plasma adalah kolesterol, trigliserida, fosfolipid, dan asam lemak bebas. Tiga unsur yang pertama berikatan dengan protein tertentu membentuk lipo protein. Sedangkan unsur lemak yang terakhir berikatan dengan albumin.

Lemak yang berasal dari makanan mengalami pemecahan menjadi asam lemak bebas, trigliserida, fosfolipid dan kolesterol selama proses pencernaan dalam usus karena di-assembling dan diserap ke dalam darah dalam pembentukan kilomikron.

''Menurut penelitian di Amerika Serikat, kadar kolesterol dianggap tinggi atau hiperkolesterolemia jika mencapai 240 mg persen,'' katanya.

Penyakit jantung koroner dua kali lebih besar mengancam orang-orang yang mempunyai kadar kolesterol 200-240 mg persen dibandingkan mereka yang kadarnya di bawah 240 mg persen.

Ancaman ini akan meningkat menjadi empat kali lebih besar apabila kadar kolesterolnya di atas 300 mg persen. Kadar kolesterol dalam darah dapat berubah-ubah setiap waktu tergantung pola makan. Namun, perubahan itu tidak seberapa besar.

Beberapa faktor yang mempengaruhi kolesterol adalah faktor genetik, umur, jenis kelamin, dan lingkungan. Kadar kolesterol ini cenderung meningkat pada orang-orang yang gemuk, kurang berolahraga, stres, dan perokok.

''Pola makan sehari-hari tidak dapat diabaikan begitu saja. Sebab diet merupakan salah satu faktor yang dapat mempengaruhi tinggi rendahnya kadar kolesterol dalam darah,'' ungkap Agus. (jar )


Sumber : http://www.republika.co.id/koran_detail.asp?id=229459&kat_id=150

mengapai sukses

Mungkin Anda dan saya sering menyaksikan betapa kesuksesan, puncak keberhasilan, atau tercapainya cita-cita, terkadang justru memunculkan semacam krisis eksistensi. Keberhasilan-keberhasilan memang bisa membawa seseorang ke posisi puncak dan bergelimang popularitas. Namun, tak jarang justru pada saat berada di puncak kesuksesan karir itulah seseorang mulai mempertanyakan apa sesungguhnya tujuan hidupnya yang sejati.

Memang, kesuksesan harus ditapaki dengan perjuangan, pengorbanan, konsistensi, dan kerja keras. Semua orang ingin berhasil dan tidak ada sukses yang gratis. Banyak orang salah menafsirkan dan menganggap bahwa kesuksesan tidak memiliki ekses negatif sama sekali. Ini salah! Sukses pasti memiliki ekses negatif jika diraih dengan cara-cara yang bertentangan dengan prinsip-prinsip dasar kemanusian. Misalnya, sukses diraih dengan mengorbankan orang lain atau mengingkari keyakinan kita yang paling dalam. Tetapi ingat, sukses yang diraih dengan cara-cara yang benar sekalipun bisa mendatangkan akibat-akibat negatif.

Popularitas para pesohor misalnya, selain mendatangkan kekayaan, nama besar, pemujaan, bahkan fanatisme, ternyata juga bisa mendatangkan gangguan-gangguan psikologis. Misalnya: kesepian, keterasingan, stres, depresi, neurotik, megalomania, dan ujung-ujungnya lari ke perilaku abnormal atau narkotika. Kita pasti ingat apa penyebab kematian para pesohor seperti Elvis Presley, Marlyn Monroe, John Lenon, dan Bruce Lee. Sukses spektakuler mereka ternyata diikuti pula dengan tekanan-tekanan mental yang ternyata tidak berhasil mereka kuasai. Akhirnya, sukses itu menjadi bumerang dan menghancurkan hidup mereka sendiri.

Sukses itu tidak identik dengan tercapainya semua keinginan material, berlimpahnya harta kekayaan, popularitas atau nama besar. Apa artinya sukses jika itu diraih dengan mengorbankan harga diri, mengorbankan nilai dan keyakinan yang paling dalam, mengorbankan keluarga, saudara, sahabat, atau teman-teman sendiri.

Sukses sejati adalah sukses yang membuat kita merasa bersyukur telah menjadi manusia yang seutuhnya. Sukses yang membuat kita tergerak untuk menularkan dan membantu orang lain mencapai kesuksesannya. Sukses yang membawa manfaat dan kebahagiaan bagi banyak orang. Jika saat ini kita sedang berjuang menggapai sukses, jangan pernah lupa meletakkan tujuan kemanfaatan bagi sesama itu, ke dalam fondasi rancang bangun perjuangan kita. Maka, sukses sejati pasti kita raih!

Demikian dari saya Andrie Wongso

The New England Journal of Medicine
A
DVANCES
IN
M
ECHANICAL
V
ENTILATION
M
ARTIN
J. T
OBIN
, M.D.
From the Division of Pulmonary and Critical Care Medicine, Edward
Hines, Jr., Veterans Affairs Hospital and Loyola University of Chicago
Stritch School of Medicine, Hines, Ill. Address reprint requests to Dr. Tobin
at the Division of Pulmonary and Critical Care Medicine, Edward
Hines, Jr., Veterans Affairs Hospital, Rte. 111N, Hines, IL 60141, or at
mtobin2@luc.edu.
HE chief reason that patients are admitted to
an intensive care unit is to receive ventilatory
support. In this article, I update the basic principles
of mechanical ventilation, which I reviewed in
the
Journal
in 1994,
1
and discuss recent advances.
BASIC PRINCIPLES
The indications for mechanical ventilation, as derived
from a study of 1638 patients in eight countries,
2
are acute respiratory failure (66 percent of patients),
coma (15 percent), acute exacerbation of chronic obstructive
pulmonary disease (13 percent), and neuromuscular
disorders (5 percent). The disorders in the
first group include the acute respiratory distress syndrome,
heart failure, pneumonia, sepsis, complications
of surgery, and trauma (with each subgroup accounting
for about 8 to 11 percent of the overall group).
The objectives of mechanical ventilation are primarily
to decrease the work of breathing and reverse lifethreatening
hypoxemia or acute progressive respiratory
acidosis.
Virtually all patients who receive ventilatory support
undergo assist-control ventilation, intermittent
mandatory ventilation, or pressure-support ventilation;
the latter two modes are often used simultaneously.
2
With assist-control ventilation, the most widely used
mode, the ventilator delivers a set tidal volume when
triggered by the patient’s inspiratory effort or independently,
if such an effort does not occur within a
preselected time.
Intermittent mandatory ventilation was introduced
to provide graded levels of assistance. With this mode,
the physician sets the number of mandatory breaths
of fixed volume to be delivered by the ventilator; between
these breaths, the patient can breathe spontaneously.
3
Patients often have difficulty adapting to
the intermittent nature of ventilatory assistance, and
the decrease in the work of breathing may be much
less than desired.
4
T
Pressure-support ventilation also provides graded
assistance but differs from the other two modes in
that the physician sets the level of pressure (rather
than the volume) to augment every spontaneous respiratory
effort.
5
The level of pressure delivered by the
ventilator is usually adjusted in accordance with changes
in the patient’s respiratory frequency. However, the
frequency that signals a satisfactory level of respiratorymuscle
rest has never been well defined, and recommendations
range from 16 to 30 breaths per minute.
6
New modes of mechanical ventilation are often introduced.
Each has an acronym, and the jargon is inhibiting
to those unfamiliar with it. Yet each new
mode involves nothing more than a modification of
the manner in which positive pressure is delivered to
the airway and of the interplay between mechanical
assistance and the patient’s respiratory effort. The purpose
of a new mode of ventilation may be to enhance
respiratory-muscle rest, prevent deconditioning, improve
gas exchange, prevent lung damage, enhance
the coordination between ventilatory assistance and
the patient’s respiratory efforts, and foster lung healing;
the priority given to each goal varies.
COORDINATING RESPIRATORY EFFORT
AND MECHANICAL VENTILATION
Probably the most common reason for instituting
mechanical ventilation is to decrease the work of the
respiratory muscles. The inspiratory effort expended
by patients with acute respiratory failure is about four
times the normal value, and it can be increased to six
times the normal value in individual patients.
7
Critically
ill patients in whom this increased level of effort
is sustained indefinitely are at risk of inspiratory-muscle
fatigue, which can add structural injury to already
overworked muscles.
8
It is sometimes thought that
the simple act of connecting a patient to a ventilator
will decrease respiratory effort. Yet unless the settings
are carefully selected, mechanical ventilation can actually
do the opposite.
With careful selection of ventilator settings, inspiratory
effort can be reduced to the normal range.
9
But eliminating inspiratory effort is not desirable because
it causes deconditioning and atrophy of the respiratory
muscles.
10
Surprisingly, researchers have not
attempted to determine the desirable target for reducing
inspiratory effort in patients with acute respiratory
distress. To reduce effort markedly requires that
the ventilator cycle in unison with the patient’s central
respiratory rhythm (Fig. 1). For perfect synchronization,
the period of mechanical inflation must match
the period of neural inspiratory time (the duration
of inspiratory effort), and the period of mechanical
Downloaded from www.nejm.org on July 13, 2010 . Copyright © 2001 Massachusetts Medical Society. All rights reserved.
MEDICAL PROGRESS
N Engl J Med, Vol. 344, No. 26
·
June 28, 2001
·
www.nejm.org
·
1987
inactivity must match the neural expiratory time.
12,13
Difficulties in synchronization can arise at the onset
of inspiratory effort, at the onset of flow delivered by
the ventilator, during the period of ventilator-induced
inflation, and at the switch between inspiration and
expiration.
Almost all patients who undergo mechanical ventilation
receive some form of assisted ventilation, with
the patient’s inspiratory effort triggering the ventilator.
To ensure that the ventilator does not cycle too
often, the clinician sets a threshold for airway pressure
that will trigger the ventilator. This threshold,
referred to as set sensitivity, is usually ¡1 to ¡2 cm
of water.
14
To reach this threshold, the patient must
initiate an inspiratory effort. But when the threshold
is reached, inspiratory neurons do not simply switch
off. Consequently, the patient may expend considerable
inspiratory effort throughout the machine-cycled
inflation.
15
The display of airway pressure and flow tracings
Figure 1.
Flow, Airway Pressure, and Inspiratory and Expiratory Muscle Activity in a Patient with Chronic Obstructive Pulmonary
Disease Who Received Pressure-Support Ventilation at an Airway Pressure of 20 cm of Water.
The electromyograms in the lower portion of the figure show inspiratory muscle activity in the patient’s diaphragm and expiratory
muscle activity in the transversus abdominis. The patient’s increased inspiratory effort caused the airway pressure to fall below the
set sensitivity (¡2 cm of water), and inadequate delivery of flow by the ventilator resulted in a scooped contour on the airway-pressure
curve during inspiration. While the ventilator was still pumping gas into the patient, his expiratory muscles were recruited,
causing a bump in the airway-pressure curve. That the flow never returned to zero throughout expiration reflected the presence of
auto–positive end-expiratory pressure. The broken red line shows airway pressure in another patient, who generated just enough
effort to trigger the ventilator and in whom there was adequate delivery of gas by the ventilator. Data are from Jubran et al.
6
and
Parthasarathy et al.
11
Seconds
Flow
Airway
pressure
Diaphragm
Transversus
abdominis
120
¡120
0
20
10
0
cm of water liters per minute
¡10
0 1 2 3 4 5 6 7
0 1 2 3 4 5 6 7
0 1 2 3 4 5 6 7
Downloaded from www.nejm.org on July 13, 2010 . Copyright © 2001 Massachusetts Medical Society. All rights reserved.
1988
·
N Engl J Med, Vol. 344, No. 26
·
June 28, 2001
·
www.nejm.org
The New England Journal of Medicine
on ventilator screens has increased awareness that inspiratory
effort is frequently insufficient to trigger
the ventilator. At high levels of mechanical assistance,
up to one third of a patient’s inspiratory efforts may
fail to trigger the machine.
9,16,17
Surprisingly, unsuccessful
triggering is not the result of poor inspiratory
effort; indeed, the effort is more than a third greater
when the threshold for triggering the ventilator is
not reached than when it is reached.
9
Breaths that do
not reach the threshold for triggering the ventilator
have higher tidal volumes and shorter expiratory times
than do breaths that do trigger the ventilator. Consequently,
elastic-recoil pressure builds up within the
thorax in the form of intrinsic positive end-expiratory
pressure (PEEP), or auto-PEEP.
9
To trigger the
ventilator, the patient’s inspiratory effort first has to
generate a negative intrathoracic pressure in order to
counterbalance the elastic recoil and then must reach
the set sensitivity. The consequences of wasted inspiratory
efforts are not fully known, but they add
an unnecessary burden in patients whose inspiratory
muscles are already under stress.
The inspiratory flow rate is initially set at a default
value, such as 60 liters per minute. If the delivered
flow does not meet the patient’s ventilatory needs,
inspiratory effort will increase.
15
Sometimes the flow
is increased in order to shorten the inspiratory time
and increase the expiratory time, especially in patients
with inspiratory efforts that are insufficient to trigger
the ventilator. But an increase in flow causes immediate
and persistent tachypnea, and as a result, the
expiratory time may be shortened.
18
In one study,
for example, increases in inspiratory flow from 30 liters
per minute to 60 and 90 liters per minute caused increases
in the respiratory rate of 20 and 41 percent,
respectively.
19
In studies of interactions between the patient’s
respiratory effort and mechanical ventilation, remarkably
little attention has been paid to the switch between
inspiration and expiration. With the use of pressure-
support ventilation, ventilatory assistance ceases
when the patient’s inspiratory flow falls by a preset
amount (e.g., to 25 percent of the peak flow).
5
Air
flow changes more slowly in patients with chronic
obstructive pulmonary disease than in other patients,
and patients often start to exhale while the ventilator
is still pumping gas into their chests.
6,11
In 5 of 12
patients with chronic obstructive pulmonary disease
who were receiving pressure support of 20 cm of
water, expiratory muscles were recruited during ventilator-
induced inflation.
6
IMPROVING OXYGENATION AND
PREVENTING LUNG INJURY
A primary goal of mechanical ventilation is to improve
arterial oxygenation. Improvement is achieved
partly through the use of endotracheal intubation to
ensure the delivery of oxygen to the airway and partly
through an increase in airway pressure. Satisfactory
oxygenation is easily achieved in most patients with
airway obstruction. The main challenge arises in patients
with alveolar-filling disorders, especially the
acute respiratory distress syndrome — a form of noncardiogenic
pulmonary edema resulting from severe
acute alveolar injury. It has long been recognized that
arterial oxygenation can be achieved at a lower inspired
oxygen concentration by increasing airway pressure.
The goal of using the lowest possible oxygen
concentration to achieve an arterial oxygen saturation
of approximately 90 percent has not changed in
decades. What has changed is how this goal is viewed
in relation to other factors, particularly ventilator pressures.
In recent years, there has been a growing tendency
to be more concerned about high airway pressures
than about oxygen toxicity, although this shift
has been based on a consensus of opinion rather than
on data from studies in patients and animals.
From the outset, clinicians recognized that mechanical
ventilation could rupture alveoli and cause air
leaks.
20
In 1974, Webb and Tierney showed that mechanical
ventilation could also cause ultrastructural
injury, independently of air leaks.
21
Their observations
went largely unnoticed until a decade later, when
several investigators confirmed and extended them. Alveolar
overdistention causes changes in epithelial and
endothelial permeability, alveolar hemorrhage, and
hyaline-membrane formation in laboratory animals.
22
Diffuse infiltrates on chest radiographs originally
led clinicians to infer that lung involvement was homogeneous.
But computed tomography (CT) reveals
a patchy pattern: about one third of the lung is unaerated,
one third poorly aerated, and one third normally
aerated.
23,24
A ventilator-induced breath will follow
the path of least impediment, travelling preferentially
to the normally aerated areas. As a result, these regions
are vulnerable to alveolar overdistention and the
type of ventilator-induced lung injury found in laboratory
animals
25
(Fig. 2).
A new era of ventilatory management began in
1990, when Hickling et al.
26
reported that lowering
the tidal volume caused a 60 percent decrease in the
expected mortality rate among patients with the acute
respiratory distress syndrome. In a subsequent trial,
Amato et al.
27,28
randomly assigned patients to a conventional
tidal volume (12 ml per kilogram of body
weight) or to a low tidal volume (less than 6 ml per
kilogram). Mortality was decreased by 46 percent
with the lower tidal volume. In a recent study of 861
patients, the Acute Respiratory Distress Syndrome
Network
29
confirmed this benefit: mortality was decreased
by 22 percent with a tidal volume of 6 ml per
kilogram as compared with a tidal volume of 12 ml
per kilogram. Lowering the tidal volume, however,
failed to improve the outcome in three controlled
trials.
30-32
The discrepant findings can be explained by
differences in trial design. Increased survival was de-
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1989
Figure 2.
Lung Injury Caused by Mechanical Ventilation in a 31-Year-Old Woman with the Acute Respiratory Distress Syndrome Due
to Amniotic-Fluid Embolism.
The patient had undergone mechanical ventilation for eight weeks with tidal volumes of 12 to 15 ml per kilogram of body weight,
peak airway pressures of 50 to 70 cm of water, positive end-expiratory pressures of 10 to 15 cm of water, and a fractional inspired
oxygen concentration of 0.80 to 1.00 in order to achieve a partial pressure of carbon dioxide that was less than 50 mm Hg and a
partial pressure of oxygen that was 80 mm Hg or higher. Computed tomography (CT) performed two days before the patient died
revealed a paramediastinal pneumatocele in the right lung (Panel A, arrowheads) and numerous intraparenchymal pseudocysts in
the left lung (Panel B, black arrow, open circle, and asterisk).
At autopsy, both lungs were removed and fixed by intrabronchial infusion of formalin, alcohol, and polyethylene glycol at an insufflation
pressure of 30 cm of water. Panel C shows the paramediastinal pneumatocele in the right lung (arrowheads); the horizontal
broken line is the level of the CT section. Panel D shows a 1-cm-thick section of the left lung, corresponding to the CT section. Small
pseudocysts are present (arrow), and two large pseudocysts (asterisk and open circle) have compressed and partially destroyed
the parenchyma. The development of these lesions in a patient without a history of chronic lung disease indicates the harm that
may result with the use of high tidal volumes and airway pressures. The photographs were kindly provided by Dr. Jean-Jacques
Rouby, Hôpital de la Pitié–Salpêtrière, Paris.
°.
°.
*
*
Right Lung
C
R L R L
A
D
B
Left Lung
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The New England Journal of Medicine
monstrable only when the patients undergoing conventional
ventilation had a mean pressure during an
end-inspiratory pause (the so-called plateau pressure,
a surrogate for peak alveolar pressure) that exceeded
32 cm of water.
33
The pressures pertinent to ventilatory management
are the peak inspiratory pressure, plateau pressure,
and end-expiratory pressure. Patients with airway obstruction
may have a very high peak pressure without
any increase in the plateau pressure. Indeed, the gradient
between the two is directly related to the resistance
of the airway to airflow. An increase in the peak
inspiratory pressure without a concomitant increase
in the plateau pressure is unlikely to cause alveolar
damage. The critical variable is not airway pressure itself
but transpulmonary pressure — airway pressure
during the end-inspiratory pause minus pleural pressure.
The normal lung is maximally distended at a
transpulmonary pressure between 30 and 35 cm of
water, and higher pressures cause overdistention. Patients
with stiff chest walls, such as those with the
acute respiratory distress syndrome due to a nonpulmonary
disorder (e.g., abdominal sepsis), have an elevated
pleural pressure. In such patients, the airway
plateau pressure may exceed 35 cm of water without
causing alveolar overdistention.
Clinical decisions based on plateau pressure must
take into account the relation between lung volume
and airway pressure in the individual patient. The pressure–
volume curve in patients with the acute respiratory
distress syndrome typically has a sigmoid shape
with two discrete bends, called inflection points (Fig.
3).
34
Some investigators believe that a plateau pressure
above the upper bend causes alveolar overdistention.
Reducing the tidal volume lowers the plateau
pressure, but at the cost of hypercapnia. In a study in
which 25 patients with the acute respiratory distress
syndrome underwent mechanical ventilation with a
tidal volume of 10 ml per kilogram, 20 had a plateau
pressure that was 2 to 14 cm of water above the upper
bend of the pressure–volume curve.
35
Lowering
the plateau pressure to a value that fell below the upper
bend required a 22 percent decrease in the tidal
volume, causing the partial pressure of carbon dioxide
to increase from 44 to 77 mm Hg.
35
The partial
pressure of carbon dioxide, in turn, can be decreased
by as much as 28 percent by removing tubing and
thus decreasing dead space and increasing the frequency
of ventilator-induced breaths. By virtue of
their stiff lungs, patients with the acute respiratory
distress syndrome who do not have an underlying airway
obstruction can tolerate a frequency of 30 breaths
per minute without gas trapping.
36
Severe hypercapnia
can have adverse effects, including increased intracranial
pressure, depressed myocardial contractility,
pulmonary hypertension, and depressed renal blood
flow.
37,38
The view that these risks are preferable to
the higher plateau pressure required to achieve normocapnia
represents a substantial shift in ventilatory
management.
Lowering the tidal volume is not without hazards.
In addition to the potential harm of hypercapnia,
the volume of aerated lung may be decreased,
39
with a
consequent increase in shunting and worsening oxygenation.
One means of minimizing the loss of lung
volume is the use of sighs (i.e., single breaths of large
tidal volume). In one study, increasing the plateau
pressure by at least 10 cm of water during sighs, applied
three times a minute over a period of one hour,
caused a 26 percent decrease in shunting, with a 50
percent increase in the partial pressure of oxygen.
40
It is unknown whether sighs used at this low frequency
cause injury from alveolar overdistention.
The more usual way of improving oxygenation is
through the use of PEEP with the intention of recruiting
previously nonfunctioning lung tissue. Selecting
the right level of PEEP for a given patient with
the acute respiratory distress syndrome is difficult,
because the severity of injury varies throughout the
lungs. PEEP can recruit atelectatic areas but may overdistend
normally aerated areas.
41,42
In a study involving
six patients with acute lung injury, for example, the
use of PEEP at 13 cm of water resulted in the recruitment
of nonaerated portions of lung, with a gain
of 320 ml in volume, but three patients had overdistention
of already aerated portions of lung, with
an excess volume of 238 ml.
43
Overall, about 30 percent of patients with acute
lung injury do not benefit from PEEP or have a fall in
the partial pressure of oxygen.
23,44,45
With the patient
in the supine posture, PEEP generally recruits the regions
of the lung closest to the apex and sternum.
23
Conversely, PEEP can increase the amount of nonaerated
tissue in the regions close to the spine and the
diaphragm.
23
Among patients in the early stages of
the acute respiratory distress syndrome, those with
pulmonary causes, such as pneumonia, are less likely
to benefit from PEEP than are those with nonpulmonary
causes, such as intraabdominal sepsis or extrathoracic
trauma.
46
This distinction may be related
to the type of morphologic involvement: pulmonary
causes of the syndrome are characterized by alveolar
filling, whereas nonpulmonary causes are characterized
by interstitial edema and alveolar collapse. In the later
stages of the acute respiratory distress syndrome,
remodeling and fibrosis may eliminate this distinction
between pulmonary and nonpulmonary causes.
To select the right level of PEEP, some experts
recommend bedside calculation of the pressure–volume
curve. With the ventilators currently used in the
United States, calculating the pressure–volume curve
is logistically difficult and technically demanding.
34
Yet many ventilators have a computer screen, and minor
software modifications would make it feasible to
calculate the curve in as little as two minutes — as
with the ventilators available in France.
47
Providing
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1991
this option on ventilators would increase clinicians’
experience with the use of pressure–volume curves
in ventilatory management.
Even if the pressure–volume curve is not calculated
at the bedside, it is useful to select the PEEP level according
to this conceptual framework. A level above
the lower bend in the pressure–volume curve is
thought to keep alveoli open at the end of expiration
and thus prevent the injury that can result from shear
forces created by the opening and closing of alveoli.
48-50
This level of PEEP may also prevent an increase
in the amount of nonaerated tissue and, thus,
atelectasis. However, the notion that the lower bend
signals the level of PEEP necessary to prevent endexpiratory
collapse and that pressures above the upper
bend signal alveolar overdistention is a gross oversimplification.
The relation between the shape of the
pressure–volume curve and events at the alveolar level
is confounded by numerous factors and is the subject
of ongoing research and debate.
51-55
An understanding
of this relation is also impeded by the difficulty
in distinguishing collapsed lung units from
fluid-filled units on CT.
Most patients with the acute respiratory distress
syndrome have an increase in the partial pressure of
oxygen when there is a change from the supine to
the prone position. In a study of 16 patients, for example,
12 had an increase of 9 to 73 mm Hg in the
partial pressure of oxygen, and 4 had a decrease of
7 to 16 mm Hg.
56
The mechanism responsible for
the improvement in the partial pressure of oxygen is
not clear. The attribution of this improvement to lung
recruitment has not been proved.
56
It is now posited
that a prone position causes ventilation to be distrib-
Figure 3.
Respiratory Pressure–Volume Curve and the Effects of Traditional as Compared with Protective Ventilation in a 70-kg Patient
with the Acute Respiratory Distress Syndrome.
The lower and upper inflection points of the inspiratory pressure–volume curve (center panel) are at 14 and 26 cm of water, respectively.
With conventional ventilation at a tidal volume of 12 ml per kilogram of body weight and zero end-expiratory pressure (left-hand
panel), alveoli collapse at the end of expiration. The generation of shear forces during the subsequent mechanical inflation may tear
the alveolar lining, and attaining an end-inspiratory volume higher than the upper inflection point causes alveolar overdistention. With
protective ventilation at a tidal volume of 6 ml per kilogram (right-hand panel), the end-inspiratory volume remains below the upper
inflection point; the addition of positive end-expiratory pressure at 2 cm of water above the lower inflection point may prevent alveolar
collapse at the end of expiration and provide protection against the development of shear forces during mechanical inflation.
0 2 4 6 0 10 20 30 40
1000
800
600
400
200
Seconds Pressure (cm of water) Seconds
Conventional Ventilation
Protective Ventilation
Tidal Volume (ml)
0 0
800
600
400
200
0
600
400
200
0 2 4 6
Alveolar
overdistention
Alveolar
collapse
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uted more evenly to the various regions of the
lungs,
57,58
improving the relation between ventilation
and perfusion.
59,60
DISCONTINUING MECHANICAL
VENTILATION
Because mechanical ventilation can have life-threatening
complications, it should be discontinued at the
earliest possible time. The process of discontinuing
mechanical ventilation, termed weaning, is one of the
most challenging problems in intensive care, and it
accounts for a considerable proportion of the workload
of staff in an intensive care unit.
2
When mechanical ventilation is discontinued, up
to 25 percent of patients have respiratory distress severe
enough to necessitate the reinstitution of ventilatory
support.
61,62
Our understanding of why weaning
fails in some patients has advanced considerably in recent
years. Among patients who cannot be weaned,
disconnection from the ventilator is followed almost
immediately by an increase in respiratory frequency
and a fall in tidal volume — that is, rapid, shallow
breathing
63
(Fig. 4). As a trial of spontaneous breathing
is continued over the next 30 to 60 minutes, the
respiratory effort increases considerably, reaching more
than four times the normal value at the end of this
period.
7
The increased effort is mainly due to worsening
respiratory mechanics. Respiratory resistance
increases progressively over the course of a trial of
spontaneous breathing, reaching about seven times
the normal value at the end of the trial; lung stiffness
also increases, reaching five times the normal value;
and gas trapping, measured as auto-PEEP, more than
doubles over the course of the trial.
7
Before weaning
is started, however, the respiratory mechanics in such
patients are similar to those in whom subsequent
weaning is successful.
66
Thus, unknown mechanisms
associated with the act of spontaneous breathing cause
the worsening of respiratory mechanics in patients
who cannot be weaned from mechanical ventilation.
In addition to the increase in respiratory effort, an
unsuccessful attempt at spontaneous breathing causes
considerable cardiovascular stress.
67
Patients can have
substantial increases in right and left ventricular afterload,
with increases of 39 and 27 percent in pulmonary
and systemic arterial pressures, respectively,
64
most likely because the negative swings in intrathoracic
pressure are more extreme. At the completion
of a trial of weaning, the level of oxygen consumption
is equivalent in patients who can be weaned and
in those who cannot. But how the cardiovascular system
meets the oxygen demand differs in the two
groups of patients.
64
In those who are successfully
weaned, the oxygen demand is met through an increase
in oxygen delivery, mediated by the expected
increase in cardiac output on discontinuation of positive-
pressure ventilation. In patients who cannot be
weaned, the oxygen demand is met through an increase
in oxygen extraction, and these patients have a
relative decrease in oxygen delivery.
64
The greater oxygen
extraction causes a substantial decrease in mixed
venous oxygen saturation, contributing to the arterial
hypoxemia that occurs in some patients.
64
Over the course of a trial of spontaneous breathing,
about half of patients in whom the trial fails have
an increase in carbon dioxide tension of 10 mm Hg
or more.
7
The hypercapnia is not usually a consequence
of a decrease in minute ventilation.
63
Instead,
hypercapnia results from rapid, shallow breathing,
which causes an increase in dead-space ventilation. In
a small proportion of patients who cannot be weaned,
primary depression of respiratory drive may be responsible
for the hypercapnia.
7
The discontinuation of mechanical ventilation needs
to be carefully timed. Premature discontinuation places
severe stress on the respiratory and cardiovascular
systems, which can impede the patient’s recovery.
Unnecessary delays in discontinuation can lead to a
host of complications. Decisions about timing that
are based solely on expert clinical judgment are frequently
erroneous.
68-70
Several functional measures are
used to aid decision making. The level of oxygenation
must be satisfactory before one attempts to discontinue
mechanical ventilation. Yet in many patients with
satisfactory oxygenation, such attempts fail. The use
of traditional predictors of the success or failure of
attempts — maximal inspiratory pressure, vital capacity,
and minute ventilation — frequently has false
positive or false negative results.
71
A more reliable
predictor is the ratio of respiratory frequency to tidal
volume (f/V
T
).
72
The ratio must be calculated during
spontaneous breathing; calculating it during pressure
support markedly impairs its predictive accuracy.
68
The higher the ratio, the more severe the rapid,
shallow breathing and the greater the likelihood of
unsuccessful weaning. A ratio of 100 best discriminates
between successful and unsuccessful attempts
at weaning. In a case of clinical equipoise — that is,
a pretest probability of 50 percent — an f/V
T of 80,
which has a likelihood ratio of 7.5, is associated with
almost a 95 percent post-test probability of successful
weaning.73 If the f/VT is higher than 100, the
likelihood ratio is 0.04 and the post-test probability
of successful weaning is less than 5 percent.
Several groups of investigators have evaluated the
predictive value of f/VT.74-78 Its positive predictive
value — the proportion of patients who are successfully
weaned among those for whom the ratio predicts
success — has generally been high (0.8 or higher).
The negative predictive value — the proportion of
patients who cannot be weaned among those for
whom the ratio predicts failure — has sometimes
been reported to be low (0.5 or less). Low negative
predictive values have often been reported for patients
with a high likelihood of successful extubation
— for example, patients undergoing routine postop-
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erative ventilatory assistance and patients who have
tolerated initial trials of weaning.75,76
There are four methods of weaning.79 The oldest
method is to perform trials of spontaneous breathing
several times a day, with the use of a T-tube circuit
containing an enriched supply of oxygen. Initially 5 to
10 minutes in duration, the trials are extended and
repeated several times a day until the patient can sustain
spontaneous ventilation for several hours. This
approach has become unpopular because it requires
considerable time on the part of intensive care staff.
The two most common approaches, intermittent
mandatory ventilation and pressure support, decrease
ventilatory assistance gradually by respectively lowering
the number of ventilator-assisted breaths or the
level of pressure. When a minimal level of ventilatory
assistance can be tolerated, the patient is extubated.
The minimal level of assistance, however, has never
been well defined. For example, pressure support of
6 to 8 cm of water is widely used to compensate for
the resistance imposed by the endotracheal tube and
ventilator circuit.80 A patient who can breathe comfortably
at this level of pressure support should be
able to tolerate extubation. But if the upper airways
are swollen because an endotracheal tube has been in
place for several days, the work engendered by breathing
through the swollen airways is about the same as
that caused by breathing through an endotracheal
tube.81 Accordingly, any amount of pressure support
overcompensates and may give misleading information
about the likelihood that a patient can tolerate
extubation.
The fourth method of weaning is to perform a
single daily T-tube trial, lasting for up to two hours.
If this trial is successful, the patient is extubated; if
the trial is unsuccessful, the patient is given at least
Figure 4. Tidal Volume, Pleural Pressure, and Pulmonary-Artery Pressure in a Patient Undergoing Assist-Control Ventilation and at
the Start and End of a Failed Trial of Spontaneous Breathing.
During mechanical ventilation, the patient’s inspiratory effort is in the normal range and the pulmonary-artery pressure is 45/22
mm Hg (systolic/diastolic). At the start of the trial of spontaneous breathing, the tidal volume falls to 200 ml, the respiratory frequency
increases to 33 breaths per minute, there are swings in pleural pressure of 11 cm of water, and the pulmonary-artery pressure
at the end of expiration is 60/28 mm Hg. At the end of the trial, 45 minutes later, the tidal volume and respiratory frequency
are unchanged, there are swings in pleural pressure of 19 cm of water, auto–positive end-expiratory pressure is 4 cm of water, and
the pulmonary-artery pressure is 60/31 mm Hg. The values in a healthy subject are tidal volume, 380 ml; respiratory frequency, 17
breaths per minute; pleural-pressure swings, 3 cm of water; and pulmonary-artery pressure, 18/8 mm Hg. Data are from Tobin et
al.63,64 and Jubran et al.7,65
0 2 4 6 0 2 4 6 0 2 4 6
Seconds
0 2 4 6 0 2 4 6 0 2 4 6
0 2 4 6 0 2 4 6 0 2 4 6
0
400
Tidal Volume
(ml)
800
10
0
¡10
¡20
Pleural Pressure
(cm of water)
60
30
0
0 2 4 6
Pulmonary-Artery
Pressure (mm Hg)
Mechanical
Ventilation
Failed Weaning Trial
Start End Healthy Subject
90
¡400
0 2 4 6
0 2 4 6
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The New England Journal of Medicine
24 hours of respiratory-muscle rest with full ventilatory
support before another trial is performed.82
Until the early 1990s, it was widely believed that
all weaning methods were equally effective, and the
physician’s judgment was regarded as the critical determinant.
But the results of randomized, controlled
trials clearly indicate that the period of weaning is as
much as three times as long with intermittent mandatory
ventilation as with trials of spontaneous
breathing.61,62 In a study involving patients with respiratory
difficulties on weaning, trials of spontaneous
breathing halved the weaning time as compared
with pressure support62; in another study, the weaning
time was similar with the two methods.61 Performing
trials of spontaneous breathing once a day is
as effective as performing such trials several times a
day62 but much simpler. In a recent study, half-hour
trials of spontaneous breathing were as effective as
two-hour trials.83 However, this study involved all patients
being considered for weaning, not just those
for whom there were difficulties with weaning.
A two-stage approach to weaning — systematic
measurement of predictors, including f/VT, followed
by a single daily trial of spontaneous breathing — was
compared with conventional management in a randomized
trial.69 Although the patients assigned to the
two-stage approach were sicker than those assigned
to conventional weaning, they were weaned twice as
rapidly. The rate of complications and the costs of
intensive care were also lower with two-stage management
than with conventional management.
When patients can sustain spontaneous ventilation
without undue discomfort, they are extubated. About
10 to 20 percent of such patients require reintubation.
61,62 Mortality among patients who require reintubation
is more than six times as high as mortality
among patients who can tolerate extubation.83,84 The
reason for the higher mortality is unknown; it is not
clearly related to the development of new problems
after extubation or to complications of reinserting
the tube. Indeed, the need for reintubation may simply
be a marker of a more severe underlying illness.
In a controlled trial involving patients who could
not sustain spontaneous ventilation, the patients who
were extubated and then received noninvasive ventilation
through a face mask had a shorter mean overall
period of ventilatory support (10.2 days) than those
who remained intubated and were weaned by decreasing
pressure support (16.6 days).85 Although this result
is promising, it is not clear how many such patients
or which ones could benefit from this approach.
OTHER APPROACHES TO MECHANICAL
VENTILATION
Noninvasive ventilation, an approach that is becoming
more widespread, was reviewed in the Journal
in 1997.86 Two new approaches under investigation
are liquid ventilation87 and proportional-assist
ventilation16; they have not yet been approved for general
clinical use.
CONCLUSIONS
Since my previous overview of mechanical ventilation
in the Journal, we have gained a better understanding
of the pathophysiology associated with unsuccessful
weaning and have learned how to wean
patients more efficiently. We have also learned how
ventilator settings influence survival in patients with
the acute respiratory distress syndrome. Less progress
has been made in determining how the ventilator can
best be used to achieve maximal respiratory-muscle
rest, which is the most common reason for providing
mechanical ventilation. Although further research may
lead to unexpected new insights, an important challenge
for researchers is to identify elements of our
current knowledge that can be incorporated into a
clinical management scheme to improve the outcome
for patients who require ventilatory assistance.
Supported by a Merit Review grant from the Department of Veterans
Affairs Research and Development Service.
I am indebted to Drs. Amal Jubran, Franco Laghi, and Thomas
Brack for helpful criticisms on successive drafts of the manuscript.
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