Organ Support di Ruang ICU (Mechanical Ventilator dan Alatalat lain untuk Organ Support)

Organ Support di Ruang ICU (Mechanical Ventilator dan Alat-

alat lain untuk Organ Support)

ADE WINATA PERDATIN ACEH

2022

HIGHLIGHT

• Intensive Care Unit (ICU) suatu bagian dari rumah sakit yang mandiri dengan staf khusus dan perlengkapan yang khusus yang di tujukan untuk observasi, perawatan dan terapi pasien – pasien yang menderita penyakit akut, cedera atau penyulit - penyulit yang mengancam nyawa atau potensial mengancam nyawa dengan prognosis yang di harapkan masih reversible

• Multi Organ Dysfunction Syndrome umumnya ditemui di unit perawatan intensif (ICU) dan terjadi sekitar 40-50% kematian

• Ventilasi mekanik adalah suatu sistem alat bantuan hidup yang dirancang

untuk menggantikan atau menunjang fungsi pernapasan yang normal

Critical Care Bed Capacity in Asian Countries and Regions

DOI:

10.1097/CCM.0000000000004 222

• Pasien kritis: Pasien dgn kondisi ancaman jiwa ( yang dapat

menyebabkan kematian dalam waktu segera )

• Kegagalan organ/sistem dapat menyebabkan kondisi kritis.

• Harus dikenali secara dini, lakukan life saving (resusitasi )

Pasien Kritis

 Kesadaran menurun

 Tanda vital tidak normal ekstrem

 Nafas : Sesak nafas, sulit bernafas, nafas tidak normal, sianotik) RR < 8 atau > 30 x/mnt

 Tekanan Darah <90 Atau >200 mmHg

 Nadi < 40 Atau > 150 X/mnt

 Suhu < 35 Atau > 40 ᵒC)

TANDA –TANDA KONDISI KRITIS

………

Memerlukan penatalaksanaan yang cepat dan optimal

• Kejang (umum) atau Lethargis

• Shock (Kenali tanda-tanda shock)

• Nyeri dada (nyeri substernal)

• Aritmia dg tanda-2 shock atau EKG yang menunjukkan kegawatan jantung

• Hasil px penunjang yang eksrem (Misal : Hb < 4 g%, K

< 2,5 atau > 7, Na < 120, GDS < 30 atau > 750 mg%, Ureum > 200, Ph < 7,3, PaO2 < 50 dll.

• SEPSIS (Shock sepsis– dg ada gagal organ)

AKI, acute kidney injury; ARDS, acute respiratory distress syndrome; PAMP, pathogen-associated molecular patterns; DAMP, damage-associated

molecular patterns.

Organ failure in “series” and

“parallel.”

Shock/Hipoksia (KONSEP DELIVERY OKSIGEN)

DO

₂

⁼

Arterial Oxygen Content^{CaO2 =}

x

^Cardiac

Output

SV x HR

Preload Afterload Contractility

Syok Hipovolemik Syok Obstruktif

Syok Distributif

(Anafilaksis, Neurogenik, Septik)

Syok Kardiogenik

DO2 : 1000

ml/menit/m2

VO2 : 250

ml/menit/m2

PASIEN KRITIS

MANAJEMEN PASIEN KRITIS

Tujuan/Target (awal ) :

Mencukupkan kebutuhan

energi intrasel, dengan cara

meningkatkan hantaran O2

(oxygen delivery, DO2 ) dan

menurunkan konsumsi O2

(VO2 )

Hipoksia

DO₂

VO₂

 VO

₂

 DO₂

DO₂

VO₂

 DO₂

 VO₂

Normal balance between VO

₂

and DO

₂

Hipoksia

VO₂



DO₂

 VO2

 DO2

Method to increase DO2:

Transfusion, Volume, Inotropic and FiO2 + PEEP

Methods to reduce VO2:

Intubation and mech.ventilation, sedation, pain relief, anti-pyretic therapy

Resuscitation

Langkah-langkah sistematis tatalaksana pasien kritis:

1. Mengenali kegawatan secara dini

2. Aktivasi system emergency 3. Primary Management (Initial

survey dan resusitasi) 4. Secondary management

(secondary survey dan lanjutan resusitasi)

5. Terapi emergency sesuai penyebab

6. Monitoring dan evaluasi

7. Tatalaksana definitif dan paska

resusitasi

MULTI ORGAN FAILURE

The Complex Nature of

MODS

From Multiple Organ Support Therapy to

Extracorporeal Organ Support in Critically Ill Patients Blood Purif 2019;48:99–

105

DOI: 10.1159/000490694

PROSES TERJADINYA SAKIT KRITIS

Onset of illness

Early Sign &

Symptom

Shock Infection

Trauma

Compensation;

Preserve brain and

heart Fail/ decomp Death

Depends on;

• Age

• Severity of illness

• Preexisting disease

Tachypnea Tachycardia Hypertension

 pH Lactate

LeucocyteCRP

Bradycardia Hypotension

Alkalosis Severe Acidosis

 Normal

Where were should we?

C o m p e n s a t o r y p h a s e

Restlessness, anxiety, combativeness

MULTIPLE ORGAN SUPPORT THERAPY (MOST)

• we described the concept of identifying the possibility to provide simultaneous and combined support to different failing organ systems

• MOST includes

1. oxygenation and ventilatory support (invasive and non- invasive mechanical

ventilation [MV], veno-venous (VV) extracorporeal membrane oxygenation [ECMO]

and extracorporeal carbon dioxide removal [ECCO2R]),

2. mechanical circulatory support (intra-aortic balloon pump, veno-arterial (VA) ECMO, 3. percutaneous and surgical ventricular assist devices [VADs] and total artificial heart), 4. renal replacement therapy (RRT) and

5. extracorpo- real liver support (molecular adsorbent recirculating sys- tem, plasmapheresis and sorbent therapies)

RESPIRATO RY

SUPPORT

RESPIRATORY INJURY

PENYEBAB KEMATIAN SECARA UMUM ADALAH KARENA

APNUE

1. Hipoksia

2. Trauma

3. Infeksi

4. Reaksi

imunologis

5. Gangguan genetika

Penyebab Kematian Sel

Oxygen uptake

(VO

₂

)

Oxygen Delivery (DO

₂

)

Critical DO₂

VO

₂

tidak tergantung DO

₂

VO

²

ter ga ntu ng D O

²

Sh oc k ^{= D}

ys ox ia Normal relationship Pathologic condition

VO₂ ↑ ; catabolic state, sepsis, increased muscle activity, awakening, hyperthermia, shivering, inotrope excess, etc.

↑ Critical DO₂

VO

₂

↓ ; rest, sedation, control ventilation, hypothermia

↓ Critical DO₂

Setiap penurunan DO

₂

; ↓ Hb, ↓ SaO

₂

atau ↓ CO, tidak akan mempengaruhi uptake O

₂

dari sel, hal

ini disebabkan sel-sel mempunyai kemampuan meningkatkan ekstraksi O

₂

1000 ml/mnt

0 ml/mnt 400 600 700

O

₂

UPTAKE (VO

₂

) to O

₂

SUPPLY (DO

₂

) RELATIONSHIP

200 300

100

Ventilasi mekanik

• suatu alat bantu mekanik yang berfungsi memberikan bantuan nafas pasien dengan cara

memberikan tekanan udara

positif pada paru- paru melalui

jalan nafas buatan

Kriteria Pemasangan Ventilasi Mekanik :

1. Frekuensi napas lebih dari 35 kali per menit.

2. Hasil analisa gas darah dengan O2 masker PaO2 kurang dari 70

mmHg.

3. PaCO2 lebih dari 60 mmHg

4. AaDO2 dengan O2 100 % hasilnya lebih dari 350 mmHg.

5. Vital capasity kurang dari 15 ml / kg BB

Pontopidan (2003),

INDIKASI VENTILASI MEKANIK

1. Pasien dengan gagal nafas.

2. Insufisiensi jantung.

3. Disfungsi neurologist

4. Tindakan operasi

RENAL SUPPORT

RENAL FAILURE

• Over 50% of patients develop stage 1 AKI at some point during their ICU course, while the incidences of stage 2 and 3 AKI are considerably less, and requirement for

renal replacement therapy (RRT) is approximately 10%

• The severity of organ dysfunction is inde- pendently associated with mortality: mortality may reach 50%

when RRT is required

• pre- venting AKI by early identification of patients at risk or avoiding the progression of its severity may impact

out- come of other organs as well

(the sequential or serial sepsis theory) (40, 43, 47,56), whereby pro- and anti-infammatory media- tors are alternatively produced in high- or low- generation periods, thus leading to SIRS and/or CARS or simultaneously (the parallel sepsis theory), and SIRS and CARS may coexist in diffe rent districts or systems (46) (Fig. 3).

In intensive care medicine, blocking one mediator has not led to measurable outcome improvement in patients with sepsis (57). Possibly more clearly defined subgroups would gain from T N F-blockade treatments (58). However, antagonizing a cytokine may lead to deleterious consequences resulting in substantially higher mortality (59). A low-level T NF response seems to be necessary for the host defence to infection (60,61), while high levels need to be modulated by anti-infammatory feedback. As sepsis does not fit a simple model but shows the complex behaviour of mediator levels that change over time, neither single-mediator-directed nor one-time inter- ventions seem appropriate. T herefore, one of the major criticisms attributed to continuous blood purifica tion treatments in sepsis, its lack of specifi- city, could turn out to be a major strength. Non- specific removal of soluble mediators, bethey pro- or anti-infammatory, without completely eliminating their effec t may be the most logical and adequate approach to a complex and long-running process such as sepsis (Fig. 4).

T he issue of whether haemofil tration can remove infam matory mediators has been controversial for some time. Numerous ex vivo as well as animal and

human studies have shown that synthetic filter s can extract nearly every substance involved in sepsis to a certain degree (62). Prominent examples are com- plement factors (63,64), T N F, IL-1, IL -6 (65 ^/68), IL-8 (69) and platelet-activating factor (PAF) (70,71). Regarding plasma cytokine levels, their decrease appears minor in degree. Some studies showed no infue nce on cytokine plasma levels by CRRT (72 ^/74). However, significant clinical bene- fits in terms of haemodynamic improvement have been achieved even without measurable decreases in cytokine plasma levels (75).

T he removal of substances other than the mea- sured cytokines may have been responsible for the achieved effect. In a recent study, M ariano et al. (69) evaluated the priming activity of sera from septic patients on polymorphonuclear neutrophils. T his activity was related to ultrafiltrable mediators, among which IL -8 seemed to be important. T he results of this study further suggest that several mediators may act together to alter the functional responses of the circulating leucocytes. When the response to sepsis is viewed in anetwork perspective, absolute values seem to be less relevant than relative ones. Within an array of interdependent mediators, even small decreases could induce major balance changes. In this context, a further step in clarifying the immunological impact of CRRT has been taken by measuring an event farther downstream integrat- ing several cytokine infuenc es: monocyte respon- siveness (53, 70 ^/79).

Fig. 3. In the sequential theory, peaks of proinfammatory mediators are followed by peaks of anti-infammatory mediators. In the parallel theory, a mixture of pro- and anti-infammatory mediators coexists. SIRS: systemic infammatory response syndrome; CARS: compensated anti-infammatory response syndrome; GCSF: granulocyte ^/colony-stimulating factor; IL : interleukin; T NF: tumour necrosis factor; PAF:

platelet-activating factor.

62 C Ronco et al.

J Org Dysfunct Downloaded from informahealthcare.com by Nyu Medical Center on 01/09/15 For personal use only.

Infamatory theory

In spite of some encouraging results, the extent of achievable clinical benefit with conventional CRRT (using conventional filt ers and fow rates) in sepsis has generally been disappointing (80). Conse- quently, attempts have been made to improve the efficien cy of soluble mediator removal in sepsis by increasing the amount of plasma water exchange, i.e.

increasing ultrafiltra tion rates. Animal studies pro- vide great support to this concept. Starting in the early 1990s, several studies using differe nt septic animal models examined the effect of high ultrafil- tration rates (up to 200 ml kg ¹ h ¹) on physiolo- gical parameters and outcome. T hese studies established that a convection-based treatment can remove substances with haemodynamic effec ts re- sembling septic shock, when suffici ently high ultrafiltra tion rates are applied (81 ^/83). Several studies confirmed and refined these results. In three of them (84 ^/86), the correlation of survival with ultrafiltra tion rate was specifically examined. A direct correlation could be demonstrated. Significant improvements in cardiac function, systemic and pulmonary vascular resistance and hepatic perfusion were found (84). Another study in lambs showed significant improvements in lung function (87). Only a minority of studies identified reduced mediator plasma levels (86,88).

M ore relevant to human sepsis was the finding that ultrafiltra tion dosage is correlated to outcomein critically ill patients with ARF. In a large, rando- mized controlled study including 425 patients,

an ultrafiltra tion dosage of 35 ml kg ¹ h ¹ in- creased thesurvival rate from 41% to 57% compared with a dosage of 20 ml kg ¹ h ¹ (89). Eleven to 14% (per randomization group) of the patients had sepsis. In these subgroups there was a trend towards a direct correlation between treatment dosage and survival even above 35 ml kg ¹ h ¹, in contrast to the whole group where a survival plateau was reached. T his supports the concept of a sepsis dosage of haemofiltrati on in septic patients, in contrast to a renal dosage in critically ill patients without systemic infammation, the former being probably distinctly higher (without proven upper limit). T here was no increase in adverse effects even with the highest ultrafiltrati on dosage.

Recently, several human studies have examined the clinical effec ts of HVHF (12, 90 ^/93). T he fir st results seem to be satisfactory, especially in patients where poor survival was predicted. T hese trials need cautious interpretation with respect to their limited design, but they certainly deliver evidence of feasi- bility and efficacy to set the stage for a large-scale trial on HVH F in sepsis.

Other approaches to achieve higher mediator clearance in sepsis have been sought. Apart from increasing ultrafiltrati on rates, higher removal rates of middle molecular weight molecules could beachieved by enlarging theporesizeof membranes.

Animal data (94,95) as well as preliminary clinical data (96) demonstrate feasibility and probable superior removal rates of selected cytokines

Fig. 4. T he sequential theory leads to the conclusion that, if pro- and anti-infammatory activities could be monitored, specific therapies could be targeted for selected actions in different moments during the course of the syndrome. In the parallel theory, any therapy could be effectiv eon oneside but deleterious on another. In both theories (sequential and parallel) theconcept introduced by thepeak concentration hypothesis suggests that a non-selective control of the infammation peaks and immunoparalysis may contribute to reducing the patient’s disorder and increasing the self defences induced by nearly normal immunohomeostasis. CPFA: continuous plasmafiltration ^/adsorption;

CAST : continuous attenuation of sepsis therapy; IL: interleukin; T NF: tumour necrosis factor; PAF: platelet-activating factor.

M ultiple organ support therapy in intensivecare 63

J Org Dysfunct Downloaded from informahealthcare.com by Nyu Medical Center on 01/09/15 For personal use only.

CRRT

1.blood purification and renal support 2.temperature control

3.Acid base control 4.fuid balance control 5.cardiac support

6.protective lung support 7.brain protection

8.bone marrow protection

9.blood detoxification and liver support

10.therapy of sepsis, immunomodulation and endothelial support.

CARDIAC

SUPPORT

ECMO extracorporeal membrane oxygenation

Med Intensiva. 2019;43(2):108-120

KONTRA INDIKASI

Med Intensiva. 2019;43(2):108-120

Poor Prognosis

• Weight(<65kg or >90kg).

• Age (>53 years, above all, patients over 63).

• Hemodynamic: pulse pressure (≤20 mmHg), diastolic

• blood pressure (>40 mmHg), cardiac arrest.

• Respiratory: peak inspiratory pressure (>20 mmHg),

• mechanical ventilation (with more h less survival).

• Renal: acute renal failure, chronic renal failure, HCO3

• (<15 mmol/l).

• Other organ failure: central nervous system dysfunction,

• renal failure, liver failure.

Med Intensiva. 2019;43(2):108-120

Med Intensiva. 2019;43(2):108-120

ECMO for VENTILATORY FAILURE

Med Intensiva. 2019;43(2):108-120

ECCO2R, extracorpo- real CO² removal;

VA-ECMO, venous ar- terial extracorporeal membrane oxygen- ation;

SCUF, slow continuous ultrafiltra- tion;

CVVH, continuous veno-venous hemofiltration;

CVVHD, continuous ve- no-venous hemodialysis;

CVVHDF, con- tinuous veno-venous Hemodiafiltration;

SLED, sustained low efficiency hemodialy- sis;

PF, plasmapheresis;

PE, plasma ex- change;

HP, hemoperfusion;

AHD, albumin hemodialysis;

CPFA, continuous plas-ma filtration adsorption;

VV-ECMO, veno venous extracorporeal membrane oxygen- ation.

ECOS

techniques

KESIMPULAN

• Pada pasien kritis terjadi gangguan multi organ yang cepat bila tidak segera dikenali dan ditangani

• Organ support menjadi penting pada pasien kritis di karenakan kebutuhan akan multi organ failure yang bisa terjadi

• Dibutuhkan oragn support bukan hny di ICU tapi juga pada saat

penanganan awal pasien di IGD

TERIMA KASIH