Prinsip Umum Ventilasi MekanikErwin Kresnoadi

Departemen Anestesi dan Reanimasi Fakultas Kedokteran Universitas Mataram

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ABSTRAK

Ventilasi mekanik merupakan pelayanan medis utama yang sering digunakan di intensive care unit (ICU) karena kegagalan nafas merupakan diagnosis utama yang sering memerlukan perawatan di ICU. Berbagai modifikasi ventilasi mekanik dapat menghasilkan terapi yang lebih baik dengan resiko trauma yang lebih sedikit ke paru-paru dan interaksi negatif yang lebih sedikit dengan system organ lainnya. Pada artikel ini, kiami mengeksplorasi prinsip-prinsip umum dasar ventilasi mekanis, fitur ventilator, komplikasi akut ventilasi mekanis, bentuk baru ventilasi mekanis, dan tambahan berarti untuk ventilasi mekanis.

Kata Kunci : Ventilasi Mekanik, , intensive care unit, kegagalan nafas, komplikasi.

SEJARAH

Konsep di balik ventilasi mekanis sudah ada sejak berabad-abad yang lalu. Pada bentuk pertama dari ventilasi mekanis, Paracelsus (1493-1541) menggunakan "hembusan api" yang terhubung dengan tabung yang dimasukkan ke dalam mulut pasien sebagai perangkat untuk membantu proses ventilasi pasien. Perangkat mekanis pertama dirancang khusus untuk membantu proses ventilasi bagi pasien menggunakan pompa kaki yang dikembangkan oleh Fell O'Dwyer pada tahun 1888. Generasi pertama dari ventilator mekanik difokuskan terutama pada pengiriman sebagian besar gas secara intermiten kepada pasien dengan pemantauan yang terbatas. Karena aliran gas membutuhkan gradien tekanan, ventilator mekanik harus menghasilkan gradien tekanan antara pembukaan jalan nafas dan alveoli untuk menghasilkan aliran inspirasi dan pengiriman volume gas.Tekanan negative ventilasi menhasilkan gradien tekanan (disebut gradien tekanan transairway) dengan mengurangi tekanan alveolar ke tingkat dibawah tekanan pembukaan jalan napas. Dua perangkat klasik yang menghasilkan ventilasi tekanan negatif adalah "iron lung" dan lapisan dada baja atau kerangka dada. Iron lung banyak digunakan selama wabah poliomielitis tahun 1930-an dan 1940-an. Perangkat ini membungkus pasien dari leher ke bawah dan membuat tekanan negatif pada tubuh pasien untuk mengembangkan paru-paru. Sedangkan lapisan baja dada atau kerangka dada dimaksudkan untuk meringankan masalah akses pasien dan tank shock yang terjadi karena venous pooling pada abdomen bagian bawah selama penerapan tekanan negatif yang terkait dengan iron lung. Meskipun kerangka dada meningkatkan akses pasien dan mengurangi potensi untuk tank shock ventilasi dengan perangkat ini mungkin dibatasi oleh kesulitan dalam mempertahankan segel kedap udara antara kerangka dan dinding dada pasien.

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Pada tahun 1950 jenis ventilasi ini umumnya ditinggalkan untuk ventilasi tekanan positif intermiten dengan trakeostomi tube untuk mencegah aspirasi pada pasien yang tidak dapat melindungi jalan napasnya. Perangkat ini memulai era ventilator mekanik, dan selama bertahun-tahun, mereka telah berevolusi menjadi mesin canggih yang tak pernah terpikirkan oleh pelopor awal mereka. Perbaikan dalam ventilator mekanik muncul melalui pemahaman yang diperoleh dalam memanipulasi variabel aliran dan tekanan untuk kepentingan pasien. Evolusi teknis dari ventilator termasuk kemajuan seperti ventilasi wajib intermiten, ventilasi wajib sinkron intermiten (SIMV), dan pengenalan akhir positif-tekanan ekspirasi (PEEP). Kemampuan pemantauan yang lebih baik dari generasi pertama ventilator, dan dengan mesin yang kemudian diciptakan, praktisi mampu mengubah aliran inspirasi serta tekanan melalui pola aliran yang berbeda. Mesin yang ada kini menggunakan mikroprosesor yang melayani baik dalam mekanisme operasi perangkat dan sistem pemantauan dan juga memungkinkan penyesuaian otomatis dari sebagian besar aspek nafas mekanik yang disampaikan. Perbaikan penting termasuk (1) kemampuan untuk memonitor interaksi pasien dengan ventilator, sehingga memungkinkan mode yang menggunakan umpan balik secara kontinyu, dan (2) regulasi sendiri oleh ventilator mekanik.

INDIKASI UNTUK VENTILASI MEKANIK

Ventilasi mekanis harus digunakan saat pasien tidak dapat mempertahankan ventilasi spontannya untuk memberikan oksigenasi yang memadai dan / atau pembuangan karbon dioksida. Bantuan mekanis juga mungkin diperlukan untuk mempertahankan pH, mengurangi kerja pernapasan, atau mengurangi beban kerja jantung pada keadaan adanya penurunakn kerja sistem kardiovaskular (Tabel 1). Kegagalan ventilasi akut, adanya gejala dan tanda yang mengarah ke kegagalan ventilasi, hipoksemia berat, dan dukungan ventilasi profilaksis adalah kondisi klinis yang memerlukan ventilasi mekanis. Indikator klinis seperti takikardia, aritmia, hipertensi, dan takipnea, penggunaan otot-otot bantu pernafasan, diaforesis, dan sianosis digunakan untuk mendiagnosis gangguan pernapasan.

Tabel 1 . Indikasi untuk Ventilasi Mekanik

Mekanisme Fisiologis Indikator Klinis

Rentang Normal

Nilai yang mendukung untuk kebutuhan ventilasi mekanik

Ventilasi alveolar inadekuat

PaCO2 (mm Hg) 36–44[*] Peningkatan akut dari nilai normal atau nilai baseline pasien

Ekspansii paru inadekuat

VT (mL/kg) 5–8 <4–5

VC (mL/kg) 60–75 <10-15

Respiratory rate (nafas/min)

12–20 ≥35

Kelemahan otot pernapasan

MIP (cm H2O) 80–100 <20-30

MVV (L/min) 120–180 <2 × resting VE requirement

VC (mL/kg) 60–75 <10-15

Kerja pernapasan berlebihan

VE dibutuhkan untuk menjaga PaCO2

5–10 >15-20

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Mekanisme Fisiologis Indikator Klinis

Rentang Normal

Nilai yang mendukung untuk kebutuhan ventilasi mekanik

 normal (L/min) 25–40 >60

VD/VT (%) — —

Hipoksemia P(A - a)O2 difference on FIO2 =1.0 (mm Hg)

25–65 >350

PaO2/FIO2 ratio (mm Hg) 350–400 <200Adapted from Pierson DJ, Kacmarek R: Foundations of Respiratory Care. New York, Churchill Livingstone, 1992.

FIO2, inspired oxygen fraction; MIP, maximum inspiratory pressure; MVV, maximum voluntary ventilation; P(A - a)O2, alveolar to arterial PO2 difference; VC, vital capacity; VD, dead space ventilation; VE, minute ventilation; VT, tidal volume.

PH darah umumnya merupakan indikator yang lebih baik daripada PCO2 untuk menyesuaikan ventilasi menit. Pada keadaan hypercapnia seharusnya tidak diintervensi secara agresif jika pH masih dapat diterima dan pasien tetap waspada. Konsekuensi fisiologis dari perubahan pH masih diperdebatkan dan jelas tergantung pada patofisiologi yang mendasari dan komorbiditas. Namun, pH 7,65 atau lebih besar atau kurang dari 7,10 sering dianggap cukup berbahaya dan memerlukan kontrol ventilasi menit dengan menggunakanventilasi mekanis. Dalam keadaan ekstrem ini, ambang batas untuk memulai berbagain dukungan klinis, tergantung oleh tren pH, nilai gas darah arteri, status mental, pola pernapasan, stabilitas hemodinamik, dan respon terhadap terapi.

Melengkapi FiO2 (fraksi oksigen inspirasi), menambahkan PEEP, atau mengubah pola ventilasi untuk meningkatkan tekanan udara rata-rata dan, akibatnya, menyebabkan tekanan alveolar menjadi mekanisme untuk ventilasi mekanis sehingga dapat meningkatkan oksigenasi. Sebuah keseimbangan yang lebih baik antara penghantaran oksigen dan konsumsinya dapat dicapai bila ventilasi dikendalikan, sehingga dapat membebaskan oksigen yang diperlukan untuk sistem organ lainnya. Pengamatan menunjukkan pentingnya meminimalkan kebutuhan akan ventilasi O2 selama insufisiensi jantung atau iskemia dengan mebiarkan aliran darah diafragma untuk lebih diarahkan ke organ-organ vital. Selain itu, dengan mengurangi upaya ventilasi untuk mengatasi beban kerja pernapasan yang berlebihan dapat mengurangi afterload ke ventrikel kiri. Pasien dengan asidosis metabolik mungkin memerlukan bantuan untuk proses ventilasinya untuk menghindari keadaan dekompensasi.

EFEK FISIOLOGIS DARI VENTILASI MEKANIK

Ventilator saat ini digunakan untuk perawatan orang dewasa menggunakan tekanan positif untuk membantu mengembang kan paru-paru. Meskipun tekanan positif memiliki efek menguntungkan dari ventilasi mekanik, namun tekanan postifi juga bertanggung jawab untuk banyak efek samping yang merugikan. Ventilasi mekanis dapat mempengaruhi hampir semua sistem organ dari tubuh karena interaksi homeostatis antara paru-paru dan sistem organ lainnya.

Selama pernapasan spontan yang normal, diafragma dan otot-otot pernapasan lainnya menciptakan aliran gas dengan cara menurunkan tekanan pleura, alveolar, dan saluran napas. Tekanan alveolar biasanya atmospheric pada akhir inspirasi dan ekspirasi akhir. Diafragma dan otot interkostal diaktivasi selama inspirasi normal yang menyebabkan rongga thoraks meluas dan menurunkan tekanan

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intrapleural dari -5 cm H2O ke -8 cm H2O. Tekanan alveolar berfluktuasi dari +1 cm H2O selama ekshalasi dan -1 cm H2O selama inhalasi. Tekanan intrathoracic menurun selama ekshalasi, dan aliran balik vena meningkat .Shunt mengacu pada kondisi di mana terdapat area pada paru-paru yang melakukan perfusi tetapi tidak melakukan proses ventilasi. Shunt mungkin berasal dari intracardiac (anatomi) atau intrapulmonal (kapiler). Nilai normal fraksi shunt intrapulmonal sekitar 2% sampai 5%. Ventilasi mekanis dapat meningkatkan fraksi shunt menjadi sekitar 10% pada individu normal. Ventilasi mekanis biasanya menurunkan shunt pada penyakit paru-paru akut infiltratif, meningkatkan distribusi ventilasi terutama di area paru-paru yang sebelumnya underventilated. Tekanan yang lebih besar dari tekanan pembukaan dan penutupan alveolar dapat membuka alveolus yang telah kolaps sebelumnya dan dapat mencegahnya untuk kembali kolaps. Namun, jika ventilasi tekanan positif menghasilkan overdistention, memungkinkan terjadi redistribusi aliran darah paru ke area yang mengalami unventilated, hal ini mengakibatkan hipoksemia. Dengan ventilasi mekanis, peningkatan tekanan alveolar meningkatkan resistensi pembuluh darah paru, sehingga menghambat aliran melalui paru-paru. Mean airway pressure-tekanan rata-rata dalam jalan napas selama satu siklus respirasi yang lengkap-secara langsung berkaitan dengan waktu inspirasi, laju pernapasan, tekanan inspirasi puncak, dan tekanan ekspirasi positif akhir. Hal ini harus dijaga serendah mungkin jika terdapat shunt dari kanan-ke-kiri. Dead space mengacu pada daerah paru-paru yang berventilasi tetapi tidak melakukan proses perfusi. Dead space anatomy adalah volume dari saluran nafas yang menuju ke paru-paru, berkisar sekitar 150 mL. Dead space alveolar mengacu pada alveoli yang mengalami overventilaasi relatif terhadap perfusi, hal ini diperbesar oleh kondisi apapun yang mengurangi aliran darah paru. Mechanical dead space mengacu pada volume yang kembali dihirup dari sirkuit ventilator, volume ini sama seperti perpanjangan dari anatomic dead space. Ventilasi mekanis juga dapat meningkatkan dead space anatomy dengan memperluas jalan nafas yang bersifat nonkonduksi. Speningkatan fraksi dead sace memerlukan menit ventilasi yang lebih besar untuk menjaga ventilasi alveolar dan PaCO2. Hiperventilasi menurunkan PaCO2, efek yang mungkin diinginkan ketika tekanan intrakranial meningkat tetapi sebaliknya harus dihindari karena efek yang merugikan dari overdistention. Hipoventilasi meningkatkan PaCO2, ketinggian sederhana (50-70 mm Hg) mungkin tidak terlalu merugikan dan mengurangi pH. Hal ini telah menyebabkan hiperkapnia selama ventilasi mekanis mungkin tidak merugikan.

Ventilasi tekanan positif dapat menurunkan cardiac output, mengakibatkan hipotensi dan hipoksia jaringan potensial. Tingginya resistensi vaskular paru menyebabkan afterload ventrikel kanan menjadi lebih besar, dan jika parah, menghasilkan pergeseran septum ventrikel dan penurunan fungsi ventrikel kiri. Produksi urin dapat menurun karena perfusi ginjal yang lebih rendah, hal ini berhubungan dengan berkurangnya cardiac output atau meningkatnya kadar hormon antidiuretik dalam plasma dan penurunan peptida natriuretik atrial yang terjadi dengan ventilasi mekanis. Dengan meningkatnya tekanan pleura dan tekanan juxtacardiac, ventilasi tekanan positif membantu ejeksi ventrikel kiri dan membantu memenuhi kebutuhan pada keadaan disfungsi ventrikel kiri yang parah. Pada pasien dengan cedera kepala, ventilasi tekanan positif dapat mengurangi aliran darah otak melalui dua mekanisme: (1) penurunan curah jantung akibat penurunan aliran balik vena dan (2) peningkatan tekanan vena jugularis. Ventilasi mekanis juga merupakan salah satu faktor risiko untuk terjadinya ulkus stress.

MECHANICAL BREATH GENERATION

Sebuah mode dari ventilasi mekanis mengacu pada program dimana ventilator berinteraksi dengan pasien, hubungan antara jenis pernapasan oleh ventilator, dan variabel (pemicu, batas, dan

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siklus) yang mendefinisikan inspirasi (Tabel 2). Setiap siklus pernapasan mekanik dapat dibagi menjadi empat fase berikut:

  Inspirasi adalah keadaan di mana ventilator menyebabkan katup ekshalasi menutup dan saluran gas di bawah tekanan menuju ke dada.

  Siklus adalah pergantian dari inspirasi ke ekspirasi. Siklus dapat terjadi sebagai respon terhadap waktu yang telah digunakan, volume penghantaran, atau penurunan dalam laju aliran. Setelah siklus terjadi, katup ekshalasi terbuka, inspirasi berakhir, dan ekshalasi pasif terjadi.

  

Ekspirasi dimulai ketika aliran ventilator utama dihentikan atau terhenti dan sirkuit ekshalasi dibuka untuk memungkinkan gas keluar dari paru-paru. Ekshalasi berlanjut sampai inspirasi berikutnya dimulai. Hal ini tidak didasarkan pada kembalinya volume paru-paru ke tingkat tertentu tertentu.

   Triggering adalah perubahan dari ekspirasi ke inspirasi

Table 2. Overview of Features of Selected Modes of Mechanical VentilationVentilator Mode

Control Trigger Limit Cycling Inspiratory Flow

Controlled mechanical ventilation (CMV)

Ventilator Time Flow/volume or pressure

Volume or time

Selected or decelerating

Assist volume control (AVC)

Assist Patient or time

Flow, volume Volume Square, decelerating, or sinusoidal

Assist pressure control (APC)

Assist Patient or time

Pressure, inspiratory time

Time Decelerating

Synchronized intermittent mandatory ventilation (SIMV)

Assist Patient or time

None for patient breaths

Flow for spontaneous breaths

Decelerating for spontaneous breath

      Flow/volume (VC) or pressure (PC) for ventilator breaths

Volume or time for ventilator breaths

Square (VC), decelerating (VC or PC), or sinusoidal (VC) for ventilator breaths

Pressure-regulated volume control (PRVC)

Assist Patient or time

Pressure (may vary from breath to breath)

Time Decelerating

Pressure-support ventilation (PSV)

Assist Patient None Flow Decelerating

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Semua ventilator mekanik membutuhkan beberapa sinyal dari pasien (kecuali dalam mode kontrol, di mana pasien tidak berinteraksi dengan ventilator) hal ini dibutuhkan untuk menentukan kapan inhalasi harus dimulai. Dengan tidak adanya interaksi antara pasien dengan ventilasi, penghantaran pernapasan disampaikan atas dasar waktu. Ini disebut pernapasan tanpa bantuan (unassisted breath), karena disampaikan dalam ventilasi terkontrol. Ketika pasien memicu pernapasan (napas bantuan), hal ini akan menyebabkan gangguan baik dalam tekanan udara atau aliran gas di cabang ventilasi inspirasi. Berangkat dari definisi ini, terdapat dua jenis ventilator napas, yaitu ventilator kontrol penuh, dan ventilator control parsial (assist).

Ventilator-Ventilasi Terkontrol

Pada ventilasi mekanis yang dikontrol (CMV), tidak ada trigger yang berasal dari pasien, melainkan semua pernapasan dipicu, terbatas, dan diatur siklusnya oleh ventilator. Dengan ventilator yang tersedia saat ini, mode CMV tidak dapat dipilih. Mode ini dapat digunakan ketika pasien tidak mampu berinteraksi dengan ventilator, seperti pada kelumpuhan neuromuskuler.

Partial Ventilator-Controlled (Assist) Ventilation

In assist volume control (AVC) ventilation or assist pressure control (APC) ventilation, the clinician sets a minimum rate and either tidal volume or pressure, respectively. The patient can trigger the ventilator at a more rapid rate and will receive the set volume each time. In intermittent mandatory ventilation (IMV), ventilator-limited (i.e., by volume or pressure) breaths are similarly delivered at a set (minimum) rate, but the patient can breathe spontaneously by triggering a demand valve between machine-limited breaths. With current ventilators, IMV is modified to synchronized IMV (SIMV), in which the ventilator synchronizes the timing of machine breaths with patient effort. In pressure support ventilation (PSV), flow delivery is determined by the pressure support settings and the patient may trigger all the breaths without ventilatory assistance.

Pada assist volume control (AVC) ventilation atau assist pressure control (APC) ventilation, dokter menetapkan laju minimal,serta menetapkan volume tidal atau tekanan. Pasien dapat memberikan trigger kepada ventilator pada tingkat yang lebih cepat dan akibatnya pasien akan menerima volume set setiap kali. Pada intermittent mandatory ventilation (IMV), ventilator-terbatas (terbatas oleh volume atau tekanan) penapas yang sama disampaikan pada set (minimal) tingkat, namun pasien dapat bernapas spontan dengan memicu katup permintaan antara mesin-terbatas napas. Dengan ventilator saat ini, IMV dimodifikasi untuk IMV disinkronkan (SIMV), dimana ventilator mensinkronisasikan waktu napas mesin dengan kesabaran. Dalam tekanan ventilasi dukungan (PSV), pengiriman aliran ditentukan oleh pengaturan tekanan dukungan dan pasien dapat memicu semua napas tanpa bantuan ventilasi.

MEKANISME PEMICUAN

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Proses pemicuan dapat dicapai dengan mengurangi tekanan udara di bagian proksimal sirkuit (dekat ventilator) sampai berada di ambang bawah tekanan sirkuit yang telah diset. Ketika pasien melakukan usaha inspirasi, penurunan tekanan dideteksi oleh ventilator, dan ketika tingkat dari ambang preset (biasanya disebut sebagai sensitivitas) tercapai, terjadi pemicuan untuk dilakukannya inspirasi (katup ekshalasi menutup, dan terbentuk tekanan pada sirkuit inspirasi). Ambang batas untuk memicu pernapasan (yaitu, sensitivitas set) dapat diubah sesuai sesuai kebutuhan klinis, namun, tantangan terbesar dalam ventilasi mekanis adalah menentukan tingkat di mana sensitivitas tekanan harus ditetapkan (biasanya berkisar antara -1 sampai -2 cm H2O). Jika sensitivitas diatur terlalu rendah, ventilator akan dipicu oleh setiap proses yang menyebabkan tekanan udara turun di bawah ambang batas yang ditetapkan. Proses tersebut termasuk gerakan pasien, kompresi eksternal, pengisapan lambung, dan kebocoran udara di sirkuit atau di chest tube. Sebaliknya, jika ambang yang diatur terlalu tinggi, upaya untuk melakukan pernapasan menjadi meningkat, yaitu, untuk memicu setiap pernapasan, pasien harus melakukan upaya yang signifikan untuk mencapai ambang batas agar terjadi aliran inspirasi. Pendeteksian arus telah dikembangkan sebagai alternatif untuk memicu tekanan sehingga dapat mengurangi keterlambatan respon antara sinyal yang dihasilkan oleh pasien dan penghantara sejumlah volume gas oleh ventilator.

Whereas pressure triggering requires a direct effect of a pressure drop on the inspiratory sensor, flow triggering requires pressure drop–induced disruption in a constant stream of air flow in the inspiratory circuit maintained during expiration and has been demonstrated to decrease work of breathing compared with pressure triggering. Refinement and improvement in pressure triggering, however, make these two mechanisms of triggering similar to the work of breathing. In recent years much attention has been directed at shortening the time between patient effort and initiation of the ventilator breath, thus minimizing patient effort. This inherent delay, although greatly reduced, between signal and delivery of gas can lead to significant patient-ventilator dyssynchrony and may increase the work of breathing for the patient. Although a direct cause-and-effect relationship is unlikely, trigger asynchrony has been demonstrated to be associated with worsened outcome. Ongoing research looks to define new triggers, such as esophageal pressure, inspiratory muscle signals, and direct central nervous system signals, to further reduce the delay in delivering inspiratory gas flow.

Sedangkan tekanan memicu membutuhkan efek langsung dari penurunan tekanan pada sensor inspirasi, aliran memicu membutuhkan penurunan tekanan yang disebabkan gangguan dalam aliran konstan aliran udara di sirkuit inspirasi dipertahankan selama ekspirasi dan telah ditunjukkan untuk mengurangi kerja pernapasan dibandingkan dengan tekanan memicu. Perbaikan dan peningkatan tekanan memicu, bagaimanapun, membuat dua mekanisme memicu mirip dengan kerja pernapasan. Dalam beberapa tahun terakhir banyak perhatian telah diarahkan untuk memperpendek waktu antara usaha pasien dan inisiasi napas ventilator, sehingga meminimalkan kesabaran. Ini penundaan yang melekat, meskipun sangat berkurang, antara sinyal dan pengiriman gas dapat menyebabkan signifikan pasien-ventilator dyssynchrony dan dapat meningkatkan kerja pernapasan bagi pasien.

LIMITING PARAMETERS DURING INSPIRATION

Three parameters can be programmed on ventilators in the ICU to limit inspiration: volume, pressure, and flow. In volume control mode, the limiting parameter is volume, and although this mode ensures a preselected volume, excessive inspiratory pressures may result if the patient's lung compliance decreases or airway resistance increases. In pressure-limited

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breaths, as in APC ventilation, gas flows until pressure in the patient equals pressure in the ventilator or preset inspiratory time is reached. Although this mechanism allows limitation of pressure in the lung at end-inspiration, tidal volume and minute ventilation will decrease if the patient's lung compliance diminishes, potentially leading to significant alveolar hypoventilation. In flow-limited breaths, as in traditional AVC, the ventilator-delivered breath during inspiration will not exceed the preset flow rate value.

Cycling Mechanisms

The changeover from inspiration to expiration cycling can occur in response to elapsed time, delivered volume (volume-cycled), elapsed time (pressure control), or a predetermined decrement in flow rate (pressure support). After cycling occurs, the exhalation valve opens, inspiration ends, and passive exhalation occurs.

Volume-Cycled Breaths

With volume cycling, the ventilator continues to deliver fresh gas until a preselected volume of gas is delivered. In a closed ventilator circuit, the rise of pressure is directly proportional to the volume of gas delivered, airway resistance, and lung/chest wall compliance. Volume-cycled ventilators potentially deliver a predetermined volume regardless of the airway pressure needed to deliver the volume. For this reason, these devices almost always include a pressure relief (“pop-off”) valve to protect the patient against excessive inhalation pressures during the tidal volume delivery. The pop-off pressure is selected through use of the pressure limit alarm. Under these circumstances, after the preset pressure limit is reached, the inspiratory cycle is prematurely terminated, and exhalation is allowed to proceed. This process continues until either the cause of the increased impedance is corrected or a new preset pressure limit is provided by the operator. During this period of pressure limiting, the preset volume is not being delivered, and significant alveolar hypoventilation can occur.

Time-Cycled Breaths

With time-cycled breaths (pressure-control breaths), inspiration continues for a preset interval. Cycling is therefore time dependent. Exhalation begins when this period has elapsed, regardless of whether or not the desired volume has been delivered or the preset ventilator system pressure has been achieved in the airspace. With time-cycled ventilation, the end of inspiration does not depend on the patient's lung characteristics or even on whether the ventilator is attached to the patient. As in flow-cycled breaths (pressure-support breaths, discussed later), pressure is preset in the ventilator and maintained at that constant level throughout inspiration; this yields a square pressure-over-time waveform. Assuming respiratory rate is controlled, inspiration time can be set to give a precise inhalation-to-expiration (I : E) ratio. This ratio can be adjusted, for example, from 3 : 1 to 1 : 5, depending on the needs of the patient.

The inspiratory flow during this type of breath is initially high and then tapers as the alveolar pressures rises. The delivered tidal volume at any point is not guaranteed to be

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maintained and increases or decreases with changes in airway resistance or lung elastance. The development of automatic positive end-expiratory pressure (auto-PEEP) further reduces the delivery of the tidal volume as end-expiration pressure—the downstream gradient for flow over the fixed inspiratory time—increases. Potential benefits from this type of breath are that airway pressures may be limited and that the greatest part of inspiratory volume is achieved earlier in the respiratory cycling, allowing for more uniform distribution of the tidal volume during the latter part of inspiration. As in flow-cycled breaths (discussed later), tidal volume may vary with changes in patient effort or in lung compliance and airways resistance. This mode, therefore, is not recommended in situations in which lung mechanics are rapidly changing, and monitoring of expired gas volumes over time is crucial to ensure adequate alveolar ventilation.

Flow-Cycled Breaths

With flow cycling (pressure-support breaths), when a predetermined decrement of flow is achieved (typically, a drop to 25% of initial flow), inspiration is terminated. As in pressure control, flow is achieved across a pressure gradient between a rapidly achieved ventilator system pressure and the patient. Breaths may also be terminated when excessive airway pressure is detected (e.g., coughing during inspiration) or after a preset time interval, the latter as a safety factor in case leaks in the system (such as cuff leaks) prevent proper cycling. Both time-cycled and flow-cycled breaths are “pressure-limited.” Because flow rate decreases dramatically as patient inspiratory effort decreases and then ceases, the patient exerts control not only of initiation of breath but also of its termination. Strength and duration of patient inspiratory effort influence tidal volume. This type of ventilator breath may be used as a mode of mechanical ventilation (stand-alone PSV), with SIMV to augment spontaneous breaths or with continuous positive airway pressure (CPAP), as discussed later, to overcome endotracheal tube resistance during a weaning trial.

INSPIRATORY FLOW PATTERNS

Inspiratory flow patterns may be automatically determined by the mode selection or can be selected and variable with some modes. Many mechanical ventilators allow selection of one of three different types of inspiratory flow patterns when volume-cycled breaths are used with volume control mode of ventilation or SIMV with volume limited breaths (versus selection of pressure limited breaths). These are as follows:

  ▪    A square wave (constant flow), in which the inspiratory flow rises rapidly to a preset level

and then stays at that level until cycling occurs

  ▪    A sinusoidal flow wave pattern, in which the flow first increases and then decreases during

inspiration

  ▪    A descending ramp wave, in which the flow increases rapidly to a maximum level and

then decreases gradually until the end of inhalation

Dari ketiga hal tersebut pola aliran gelombang sinusoidal paling menyerupai pola inspirasi normal. Pola alur inspirasi pada mode pressure control dan support ventilator mekanik selalu mengalami penurunan karena alirannya menurun mengikuti gradien tekanan antara

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tekanan ventilasi yang konstan dan batas tekanan yang menyempit karena peningkatan tekanan didalam paru-paru pasien. Saat berbagai macam abnormalitas terjadi pada parenkim paru atau jalan nafas, terdapat kecenderungan untuk terjadi perbedaan ventilasi (misalnya daerah yang paten terjadi overventilasi sedangkan daerah obstruksi terjadi hypoventilasi). Penelitian menunjukkan bahwa memperpanjang waktu inspirasi dapat menyebabkan dstribusi ventilasi yang lebih homogen di dlam paru-paru yang abnormal. Tehnik untuk meningkatkan distribusi udara pada daerah yang mengalami obstruksi parah termasuk menambah jeda inspirasi dan merubah pola laju inspirasi. Pada model paru-paru, distribusi ventilasi dapat berubah jika pola aliran udara berubah. Pola aliran yang deseleratif seperti kalur yang menurun menghasilkan distribusi yang paling merata bahkan pada bagian yang paling abnormal. Pola sinusoidal umumnya merupaan hasil dari pemanjangan inspirasi karena membutuhkan periode yang lebih lama untuk mengantarkan volume tidal yang diberikan saat puncak laju aliran inspirasi yang spesifik. Saat kebutuhan untuk ventilasi sangat tinggi, sangat sulit memberikan ventilasi dalam jumlah besar dengan waktu ekspirasi yang cukup hingga digunakan square wave pattern of inspiratory gas flow. Reseptor pada jalan nafas dapat bereaksi sebaliknya pada laju aliran yang tinggi yang dapat menyebabkan batuk yang tidak teratur.

The square wave pattern is also associated with the highest peak airway pressure. However, this peak is offset by a shorter inspiratory time and a longer expiratory time, allowing amelioration of hyperinflation and auto-PEEP. The square waveform is therefore preferred in patients with severe obstruction to minimize auto-PEEP. As previously stated, theoretical results have demonstrated that prolongation of inspiration at low flows in a decelerating wave pattern would result in the most homogeneous distribution of gas and may be the preferred pattern for inspiratory flow in patients with nonobstructive lung disorders. The end-inspiratory alveolar pressure, as measured by an end-inspiratory hold, is the same for a given tidal volume regardless of type of inspiratory flow pattern and associated peak inspiratory pressure.

COMMONLY USED MODES OF MECHANICAL VENTILATION

Modes of mechanical ventilation that are commonly used are AVC, APC, SIMV, pressure-regulated volume control, and PSV. CMV is less commonly used. Table 2 summarizes the features of these modes, and Table 3. lists their advantages and disadvantages.

Table 3. Potential Advantages and Disadvantages of Selected Modes of Mechanical Ventilation

Mode Advantages Disadvantages

Controlled mechanical ventilation (CMV)

Rests muscles of respiration Requires use of sedation/neuromuscular blockade

Assist volume control Reduced work of breathing Potential adverse hemodynamic

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Mode Advantages Disadvantages

(AVC) effects

Guarantees delivery of set tidal volume (unless peak pressure limit alarm is exceeded)

May lead to inappropriate hyperventilation and excessive inspiration pressures

Assist pressure control (APC)

Allows limitation of peak inspiratory pressures

Same as AVC

Potential hyperventilation or hypoventilation with lung resistance/compliance changes

Synchronized intermittent mandatory ventilation (SIMV)

Less interference with normal cardiovascular function

Increased work of breathing compared with assist control

Patient may find it difficult to adjust to two different ventilation breaths

Pressure-regulated volume control (PRVC)

Maintains similar tidal volumes with varying resistance and compliance

Same as AVC

Inspiratory pressures may vary

Pressure-support ventilation (PSV)

Patient comfort Apnea alarm is only backup

  Improved patient-ventilator interaction

Variable patient tolerance

  Decreased work of breathing  

Assist Volume Control

The AVC mode of ventilation delivers volume-limited breaths triggered by the patient or ventilator. All of the breaths are ventilator-delivered with a preset tidal volume (volume-cycled). The assist modes allow the patient to determine the number and frequency of mechanical ventilator breaths. Breaths may be assisted, unassisted, or a combination. Assisted breaths are triggered by a change in airway pressure or flow. In the assist modes, a backup rate is set to ensure a minimal number of ventilator breaths in case the patient's respiratory rate drops below the preset rate. If the patient breathes more often than the set rate, additional ventilator breaths are delivered. An inspiratory hold can be performed to obtain the plateau pressure that approximates the alveolar pressure. This maneuver is performed to approximate the static compliance of the lungs.

In most circumstances, ventilation using assist modes results in a marked diminution in the work of breathing, which in some circumstances can approximate zero. With an assisted breath, however, certain patients continue to exert significant effort throughout inspiration. [15]

Such patients can perform a considerable amount of ventilatory work in this mode. Although it is not exactly clear why this undesirable situation occurs, the reason may be the inherent delay between the triggering and onset of pressurization and volume flow through the airways by the

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mechanical ventilator. Because the respiratory drive for a given ventilation is determined by the lung mechanics and demand of the previous breath during the first 100 ms, a delay of this magnitude can result in the patient's failure to sense that the ventilator will deliver a satisfactory tidal volume. Under these circumstances, the patient's inspiratory effort continues despite adequate ventilation from the device. Evaluating the pressure-time curves of each breath may yield subtle hints that this situation is occurring (i.e., change in the shape of the inspiratory rise—the greater the patient effort, the more concave the inspiratory rise in pressure).

Assist Pressure Control

APC ventilation is a partial ventilator-controlled mode similar to AVC ventilation, in that it is an assist mode based on patient or automatic triggering and all of the breaths are ventilator-delivered. This mode provides pressure-limited, time-cycled breaths on the basis of set applied pressure limits and inspiratory time, allowing limitation of peak inspiratory. The tidal volumes delivered can vary according to the set pressure, the compliance of the lungs and chest wall, and patient effort. Although this mode may be better tolerated by the patient, greater monitoring is necessary because changes in lung compliance may lead to hyperventilation or hypoventilation.

Synchronized Intermittent Mandatory Ventilation

SIMV permits the patient to breathe spontaneously from a fresh gas source without ventilator assistance in between mechanical breaths delivered at predetermined. Some studies have shown that SIMV may reduce the need for sedation or analgesic agents, thus facilitating weaning from mechanical ventilation. This mode of ventilation was specifically created to allow the weaning of patients from mechanical ventilation when the only other modes that existed were CMV and assist control. Because SIMV is typically associated with lower intrathoracic pressure than the other modes, it has been advocated by some writers to enhance cardiac performance. The combination of PSV and SIMV allows spontaneous breaths to be increased to an acceptable tidal volume not achieved with spontaneous effort alone. A very low level of PSV may also be selected to compensate for the inherent impedances of the ventilator circuit and endotracheal tube, enabling the patient to establish a more natural breathing pattern and to have the sensation of breathing spontaneously without an endotracheal tube in place. Higher levels can be selected when respiration muscle strength or lung disease makes spontaneous breaths inadequate. A potential advantage of stand-alone PSV (discussed previously) is that all breaths are partially supported to the same degree, whereas with SIMV plus PSV, the patient receives a totally supported mechanical breath followed by one or more less supported breaths. In this regard, the patient's inherent neurologic mechanisms may find the alternating pattern disturbing.

A potential difficulty associated with the SIMV mode is the higher level of work the patient must perform to obtain a spontaneous breath. The spontaneous respiration's work is increased because the patient must overcome the impedance of the ventilatory circuit and the endotracheal tube. It is unusual for SIMV to be used without some level of pressure support to offset this increased work of breathing. Some newer ventilators automatically apply endotracheal tube compensation in the form of pressure support based on breath-by-breath estimation of airway resistance. When SIMV is used as a weaning mode, evaluation for extubation typically occurs with an SIMV rate of 4 to 6 breaths per minute.

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Pressure-Regulated Volume Control

Pressure-regulated volume control mode is a variant on APC ventilation whereby the pressure is allowed to go up or down within set limits to achieve a targeted tidal volume. This is achieved by adjusting the ventilator system pressure up or down (within preset limits) to achieve the desired tidal volume. This mode allows use of a pressure control breath and associated decelerating flow pattern while limiting the disadvantage of changing tidal volumes in response to changes in airways resistance or lung compliance.

Pressure Support Ventilation

PSV (flow-cycled breaths) was introduced in the mid-1980s to reduce the work of spontaneous breathing in the SIMV mode. It is now commonly used as the sole method of ventilation support. With PSV, as the patient inhales, the ventilator automatically adjusts the flow to provide and maintain a preset inspiratory support pressure. The ventilator's pressure support mechanism provides a variable flow but a constant pressure, allowing the patient to participate in selecting inspiratory flow rates and VT that are in tune with the inherent problem and respiratory muscle status. Pressure support levels are now available up to 100 cm H2O, depending on the ventilator model. Most ventilators also offer adjustment of the inspiratory rise in the pressure, which allows more synchrony in patients with either high or low inspiratory demands. For weaning a patient off ventilator support, pressure support is gradually diminished—2 to 5 cm H2O at a time—until the patient is tolerating 5 cm H2O of PSV, at which point extubation can be undertaken. Patients intubated with smaller endotracheal tubes, even if ready to be weaned, may not tolerate pressure support of 5 cm H2O and may require 7 or 10 cm H2O. Because PSV depends on an intact ventilatory drive, it cannot be used in patients with respiratory drive suppression. It is not ideal for patients with bronchospasm or excessive bronchial secretions because of the frequently changing airway resistance and lung compliance in these patients. A consequence of a preset pressure delivered to the patient is that any change in either airway impedance or lung compliance will result in a concomitant change in the volume the patient is able to obtain with a given level of pressure support.

Controlled Mechanical Ventilation

With CMV, the patient has no influence on mechanical ventilation, including no ability to initiate breaths or to determine characteristics of a breath. It is predominantly used for stabilizing patients with the severest respiratory compromise during the initial phase of mechanical ventilation support. After stabilization by this mode of ventilation, patients are switched to an alternative mode in which nonsupported spontaneous ventilation or partially supported spontaneous ventilation can be maintained by the patients themselves. The duration of CMV can vary from hours to days to weeks, or even to months, depending on the nature of the lung injury. Current ventilators do not have a CMV setting; this mode is achieved by selecting the AVC mode and instituting heavy sedation or paralysis so there is no patient interaction with the ventilator.

OTHER MODES OF MECHANICAL VENTILATION

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The majority of patients supported on mechanical ventilation initially receive AVC. Less frequently used modes of mechanical ventilation are bilevel ventilation, proportional assist ventilation, volume-assisted pressure support ventilation, high-frequency ventilation, and inverse ratio ventilation.

Bilevel Ventilation

Bilevel ventilation is characterized by ventilating, over time, from two system pressures, one higher (Phigh) and one lower (Plow). This mode was introduced in 1987 as airway pressure release ventilation (APRV). It initially targeted paralyzed patients with acute respiratory distress syndrome (ARDS) with no spontaneous ventilation capability, featuring brief periods of Plow to clear CO2. This mode of mechanical ventilation has evolved into one that allows not only spontaneous ventilation but also application of pressure support to spontaneous breaths. It is now also known as APRV with spontaneous breathing as well as bilevel positive airway pressure (BiPAP) (not to be confused with the brand name BiPAP ventilation by Respironics, one of many commercially available ventilators made for noninvasive ventilation).

Bilevel ventilation can be used with two different conceptual applications and settings. In both circumstances the Phigh is targeted to maintain an open lung in patients with ARDS through application of an upper pressure below the upper deflection zone (area of overinflation) of the pressure volume curve but yet high enough to open the majority of alveoli that can be recruited. In one application (APRV with spontaneous breathing), Plow is set at a level at which significant expiratory flow is still occurring but prior to the point of significant end-expiratory alveolar closure. In this circumstance the time at the low system pressure setting (T low) is brief and is not associated with capability for spontaneous breathing but is long enough to allow adequate full expiration ( Fig. 9-5A ). Spontaneous breathing occurs on Phigh with the second application (BiPAP); the Plow is set above the lower inflection point and may be maintained for a time (T low) that allows spontaneous breathing during both Phigh and Plow (see Fig. 9-5B ). Therefore, the ratio of Thigh to Tlow tends to be around 6 : 1 for APRV with spontaneous breathing and 1 : 2 for BiPAP. In both cases, the drop from Phigh to Plow is intended to allow CO2 elimination and spontaneous breathing from either Phigh alone or, in the case of BiPAP, both Phigh and Plow. This modality is intended to elicit diaphragm activity and increase dependent lung ventilation and therefore oxygen ation in the area where shunt and low/is marked. Although the application of pressure support may increase tidal volume during spontaneous breathing, it might also decrease diaphragm activity. In addition, the work of breathing at high lung pressure (Phigh) is less if the Phigh is associated with lung recruitment and improved compliance. Finally, setting Phigh at a target consistent with lung protection strategy (30 cm H2O or less) does not factor in the additional increase in transalveolar pressure associated with the negative intrathoracic pressure generated by spontaneous breathing. It has been shown that bilevel ventilation can decrease inspiratory work of breathing more than CPAP can alone. Bilevel ventilation may be used for maintenance ventilatory support of patients with ARDS to facilitate the weaning process.

Proportional Assist Ventilation

One of the shortcomings of traditional mechanical ventilation is that the ventilator cannot adjust from breath to breath to accommodate the patient's change in demand for ventilation.

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Normal individuals do not breathe spontaneously with the same inspiratory flow and VT with each inspiratory effort. Varied respiratory patterns are likely a patient preference. Proportional assist ventilation varies inspiratory support with each mechanical breath on the basis of a patient's inspiratory effort. After measurement of inspiratory resistance and lung compliance, constants are entered into the device, which then facilitate variable amplifications of the patient's effort. As the patient's demand increases, the assist from the mechanical ventilator augments proportionately; likewise, when the patient's demand decreases, the patient is assisted less by the mechanical ventilator. This type of ventilator-patient coupling may allow the patient to feel more comfortable with mechanical ventilation.

During the course of the illness, compliance and resistance of the patient's airways will change, requiring reentry of the constants used to facilitate inspiratory augmentation. Proportional assist ventilation is based on the assumption that the patient will respond in an appropriate manner to determine the optimal type of inspiratory effort, rate, and frequency that should be employed. This assumption may not always be true.

Volume-Assisted Pressure Support

Pressure support ventilation can be delivered by volume-assisted pressure support. This form of ventilation ensures a minimum PSV-delivered tidal volume. It is achieved by having two ventilators, working in parallel, within one device. If the VT falls below a preset limit, the secondary ventilator then cycles in concert to deliver the additional volume necessary to achieve the target preset VT. This form of mechanical ventilation has been demonstrated to be well tolerated, although studies are not available to document whether it offers any clinical outcome benefit.

High-Frequency Ventilation

High-frequency ventilation (HFV) employs positive-pressure ventilation with VT smaller than or equal to the anatomic dead space (VD) of the lung at typical respiratory frequencies of 60 to 150 breaths per minute or more. Ventilators that employ respiratory frequencies of between 240 and 660 breaths per minute have been designated as ultrahigh-frequency jet ventilators. High-frequency oscillatory ventilation (HFOV) uses a piston, diaphragm, or high-fidelity speaker and generates frequencies in the range of 180 to 900 breaths per minute, with VT in the range of about 5 to 80 mL. In high-frequency percussive ventilation (HFPV), gas is delivered as a pressure-limited conventional breath with oscillations superimposed on the breath. The most common approach to high-frequency ventilation used today is high-frequency oscillation.

Breaths delivered from these ventilators are time-cycled, positive-pressure breaths in which both inspiration and exhalation are actively generated by the ventilator. The method of breath delivery can be a reciprocating pump, diaphragm, or high-fidelity speaker, depending on the device. Adequacy of ventilation depends on the bias flow that is generated and passed in front of the pump or speaker, which propels the gas into the endotracheal tube. This bias flow is also used to flush out CO2 during the active expiratory phase. A significant component of bulk convection distributes gases through the large airways, at which point the distribution of gas throughout the rest of the respiratory tree is based on other physical properties. Pendelluft, or the

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movement of gas from fast-filling and fast-emptying units of the lung into slower ones, probably plays a significant role in distributing the gas within the alveoli. Taylor dispersion is the radial diffusion of gases associated with a convective process that allows molecules in the central zones, where axial velocities are higher, to diffuse into the lateral zones, where axial velocities are lower. In a theoretical model, Fredburg demonstrated that at these frequencies and velocities, augmented diffusion would play a significant role in achieving gas transport and that gas molecules enhanced with greater energy would move down concentration gradients with greater speed. Gas exchange would be better matched to perfusion because the gases are relying on concentration gradients rather than pressure gradient. The major advantage of delivering small tidal volumes is that it can be done at relatively low pressures, potentially reducing the risk of barotraumas. However, it has not been shown to be superior to conventional ventilation.

Inverse Ratio Ventilation

Typical I : E ratios for the spectrum of mechanically ventilated patients range from 1:2 to 1:5, lower ratios being used for patients with obstructive airways disease. Inverse ratio ventilation (IRV), positive-pressure ventilation with an I : E greater than 1, has been advocated by some for use in patients with severe ARDS (see Chapter 11 ). IRV can be achieved with either volume-cycled or time-cycled ventilation and has been shown to effectively increase oxygenation in patients with ARDS. Extending the inspiratory time while holding tidal volume constant increases the mean airway pressure without raising the peak alveolar pressure. IRV therefore also allows achievement of the same mean airway pressure with a lower inspiratory plateau pressure (IPP). Theoretically this has a potential advantage for patients with severe ARDS. Evidence supports a benefit to limiting IPP. The most common application of IRV is with the use of pressure-controlled (time-cycled) ventilation. The peak airway pressure remains the same, whereas inspiratory time is lengthened. In this way, mean airway pressure rises but peak inspiratory pressure, as a reflection of peak alveolar pressure, does not. Oxygenation may therefore be improved while limiting peak alveolar pressure. The bulk of the oxygenation improvement seen can be obtained at I : E ratios of 1 : 1, and further increases in I : E: ratios are not usually efficacious. Patients with significant airflow obstruction should not be treated with this mode of ventilation. Prolonged I : E ratios may raise the rate of pneumothorax, as the shortened expiratory time may not allow for complete expiration, resulting in auto-positive end-expiratory pressure (auto-PEEP). IRV remains controversial but should be considered when conventional ventilation modes leave the patient with ARDS in persistent severe hypoxemia, particularly in the presence of an IPP greater than 30 cm H2O.

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