SERBA-SERBI PERIOPERATIVE TAW

Protocol for Early Goal-Directed Therapy

Supplement O2 Endotracheal intubations

Mechanical ventilation

Central venous and arterial catheterization

Sedation, Paralysis (if intubated), or both

CVP

MAP

ScvO2

Crystalloid

Colloid

< 8 mmHg

Vasoactive agents

< 65 mmHg

> 90 mmHg

8 – 12 mmHg

65 – 90 mmHg

≥ 70%

Goal achieved

Transfusion of RC until Ht ≥ 30%

≥ 70%

< 70%

Inotropic agents

Hospital admission

YesNo

< 70%

(Rata-rata 70)

Inotrop:-dobutamin start 2.5 u/kg/mnt naikan 2.5 u/kg/mnt tiap 30 mnt turunkan jika MAP <65, HR>120

Urin > 0.5/kg/jamSaO2 > 93%

1 cm H2O = 0.7 mmHg1 mmHg = 1.3 cmH2O8 – 12 mmHg = 10 – 15 cm

-lactat > 2 = sedang tdj proses anaerob- > 5 = prolong syock (>30 mnt) mulai tjd edema sel- > 8 = irreversible prosesAerob : Glukosasiklus crebpiruvat + 32 ATPAn aerob: Glukosasiklus creblactat + 2 ATPResusitasi cairan: (max dari onset trauma = 30 mnt)Pilihan I HAES 6% atau NaCl 3 % (=1/3 kebut drpd bila pakai kristaloid)

TEHNIKINDUKSI: (pento-lido-succ=5-3-1 cc)1. pentotal 500 mg serbuk+20 cc aqua 25 mg/cc dose: 2 mg/kg utk pre intubasi saja 4 mg/kg utk pre intubasi dilanjutkan anestesia2. lidocain 2% 2cc /amp ambil 2 amp (BB 70 kg) ivtunggu 2 menit sambil lakukan baging, monitor HR3. Succinil colin 200 mg 10 ml20 mg/cc dose: 1 mg/kg iv amati fasiculasi s/d negatif (sekitar 30 dt)

TAW-BTKV

SIRS (Sistemic Inflamatory Response Syndrome) ditegakkan berdasarkan adanya 2 dari 4 kriteria dengan salah satunya harus temperatur atau leukosit abnormal.- temperatur > 38.5 atau < 36.5 0C - takikardi (heart rate > 2 SD)- takipneu (respirasi > 2 SD)- leukositosis atau leukopeni atau neutrofil immatur > 10%Kriteria organ disfunction :1. cardiovaskular disfunction:

- tekanan darah < 5 persentil - tekanan darah normal namun tergantung kepada vasoactive drug - dua dari: BE > 5 mEq, lactat > 2x N, oliguri (<0.5 ml/j), cap refill > 5 detik, gap t badan dgn t perifer > 30C

2. respiratory disfunction: - PaO2/FiO2 < 300 - PaCO2 > 65 - Butuh FiO2 > 50 untuk mencapai saturasi > 92 - Butuh ventilator

3. renal disfunction - kreatinin > 2x normal (N= 0,7 – 1,3)4. hepatic disfunction

- bilirubin total > 4 mg/dl - SGPT 2x normal (N= 5 – 23)

5. hematologic disfunction - angka trombosit < 80.000 atau turun > 50% dari nilai tertinggi dalam 3 hari terakhir

6. neurologic disfunction - GCS < 11 atau turun 3 point dari normal (misal CCS normal E4M4V3)

Severe sepsis: - cardiovascular disfunction atau respiratory disfunction atau - > 2 organ disfunction lainnya. Septic syock ditegakkan apabila ada cardiovascular disfunction.

Age group Heart rate RR Leukocyte count

(x1000/cum m)

  Tachycardia Bradycardia    

0-1 week >180 <100 >50 >34

1wk-1month >180 <100 >40 >19,5 or<5

1mo-1year >180 <90 >34 >17.5 or <5

2-5year >140 NA >22 >15.5 or <6

6-12years >130 NA >18 >13.5 or<4.5

13-< 18year >110 NA >14 >11or <4,5

FLUID CHALLENGE TESTModified 7-3 4-2 rules of Weil

Pningkatan () PAOP (PCAW)Atau Pningkatan () CVP

Cairan infus yang diberikan dlm 10 menit

< 12< 6

PAOP awal atau CVP awal

12-166-10

< 3< 2

Monitor 10 menit

> 16> 10

2 ml/kg 1 ml/kg4 ml/kg

3-72-4

> 7 > 4

PAOP < 3 atau CVP < 2

PAOP > 3 atau CVP > 2

Stop Monitor

If limits of rules exceededConsider contractility agent

1 cm H2O = 0.7 mmHg1 mmHg = 1.3 cmH2O

-CVP <7 cmH2Oloading 200 cc-7 s/d 13 H2O loading 100 cc-> 13 loading 50 ccTunggu 10 mnt:Bila naik <2 hipovolemi 2-5 normovolemi >5 hipervolemi

Analylis of Acid-Base Disorder,Koreksi elektrolit

Koreksi asidosis: bila pH < 7,2excess basa X BB X 0.3 (0.4 utk anak) berikan ½ dose pd 2 jam I sisanya dlm 22 jam kmd (utk blind Tx. 1 mEq/kg) koreksi masiftetani, deathKoreksi alkalosis (sign:tetani,hiperiritable): -Ca glukonas iv; (+) NaCl,,KCl bila K -pH>7.6: HCl mEq = (HCO3-24) X 0.5 X BB berikan ½-nya dlm 4-8 jam sisanya besok. acetazolamide 250-500 mg tiap 6 jam (5 mg/kg/hari)Koreksi hipo-K: - K mEq = K X BB X 0.3 - selesaikan koreksi dlm 6 jam - atau kecepatan 0,5 mEq/kg/jam (max 20 mEq/jam iv perifer, dlm 200 cc lar) (vena sentral: encerkan dlm 50 c lar1j) Koreksi hiper-K: 1. stabilisasi membran: Cagluk 0,5 ml/kg amp 10 ml5%,10% Ca gluk 10% + 10 cc D5 iv pelan/15’, 4x atau 4 Amp Ca gluk 10%+100 cc D5 drip dalam 2 jam, kmd: 2. 12 U RI + D10% 500 cc12 gttAtau lar GI= D40%2cc/kg + insulin 0,1 UI/kg + CaCl2 500 mg + Biqnat 1 mEq/kgAtau dialisa: K>7, BUN>200,asidosis,edem paruOr hiperventilasi, kayeksalat 1 gr/kg dlm 100 cc air, PO/jam bila hiperK tanpa ggn EKG

pH = 7.35 - 7.45 K = 3.4 – 5.4 pCO2= 35 – 45 Na=135 – 146 PO2 = 80 – 95 Cl= 95 – 108 HCO3= 22 – 26 Ca=8.1 – 10.4 BE = -3.81 – 1.81 Mg=0.8 – 1.0

Koreksi hipoNa: HiperNa: - Na mEq = DNa X BB X 0.6 defisit air =(X-140)/140 x BWx0,6=L - maintenance 1.5 (1-3) mEq/kg/24 jam Koreksi hipoCa: HiperCa: - CaCl2 10% 0,2 ml/kg iv pelan, atau NaCl 0,9% + furosemid 1-2 mg/kg - Ca glukonas 10% 0.5 ml/kg Koreksi albumin : sediaan: human Alb 200 ml, 20&25% - alb gr = Dalb X BB X 0.8 , (max alb 1 gr/kg) - habiskan dlm 4 jam, kmd lasix 0.5 mg/kg iv - anak: 0.5-1 gr/kg dlm 2-4 jam kmd lasix 1-2 mg/kg (bisa 2x/hr)

KOREKSI CAIRAN:1. Dehidrasi ringan: urin N/, 2. Dehidrasi sedang: oliguri, T agak, N agak, asidosis ringan, ext dingin, mucosa kering, turgor turun3. Dehidrasi berat : anuri, T /syok,N ,asidosis berat,

ext dingin/sianosis, mucosa kering, turgor Dehidrasi(%)(D) Maintenance (M)

Ringan: adult 4% adult: 40 cc/kg/24j anak 4-5 anak:BB: 0 – 10 kg = 100 cc/kg/24jSedang: adult 6 0 – 10 kg = 100 cc/kg/24j anak 5-10 (8) 10 – 20 kg = (1000+(50x(BB-10))/24j Berat : adult 8 20 - 30 = (1500+(20x(BB-20))/24j anak 10-15(12) (formula 100-50-20) diatas 30 kg = 2000 cc/M2 BSA

Cairan:Pemberian: 6 jam I = ½ D + ¼ M dewasa: RL 18jam kmd= ½ D + ¾ M anak 0-1 mg = N5 (D5-1/5S) 1mg-1 th=N4 (D5-1/4S) 1 th-10th=N2 (D5-1/2S)Contoh: >10th =N (D5 S)Dewasa 50 kg dehidrasi sedang: D = 6% x 50 x 1.000 = 3.000 cc M= 40 cc x 50 = 2.000 cc6 jam I = ½ D + ¼ M = 1.500 + 500 = 2.000cc 2000 x 15 = 83 gtt 6 x 60 18 j kmd= ½ D + ¾ M=3.000 cc 2000 x 15 = 42 gtt 18 x 60

SYOCK PERDARAHAN/HIPOVOLEMIA

Kelas I Kelas II Kelas III Kelas IV

Kehilangan darah

(% Volume darah)

s/d 15 % 15 - 30 30 – 40 > 40 %

Kehilantan darah(ml) s/d 750 750 – 1500 1500 – 2000 > 2000

Nadi < 100 > 100 > 120 > 140

Tekanan darah N N turun Turun

Tek nadi (S – D) N atau naik turun turun Turun

Produksi urin(ml/jam) > 30 20 – 30 5 – 15 Tak berarti

RR 14 – 20 20 – 30 30 – 40 > 35

Status mental Sdkit cemas Agak cemas Cemas.bingung Bingung, lethargy

Penggantian cairan

(hukum 3:1)

Darah hilang 30%=Hb 3

Kristaloid Kristaloid Kristaloid + darah

Kristaloid + darah

Resusitasi kristaloid:RL 2000 cc pd dewasa, 20 cc/kgBB pd anak

Estimated blood volume: neonatus : 85 c/kgBB bayi : 80 dewasa pria : 75 wanita: 65

LUKA BAKAR Kulit: 16 % BB, 1,5-1,9 M2, 5 – 5 mm

Tk. I :Hiperemi, hiperestesi IIA: basah +bula, hiperestesi B: basah+bula+keputihan, hipoestesi III: kering, putih-hitam, hipoestesi

EPIDERMIS: 5 % dr ketebalan kulit (1,5 – 5 mm), stratum-corneum: non inti, sitoplasma: keratin(skleroprotein filamentosa-lusidum : umum pd kulit tebal, garis translucen-granulosum: 3 – 5 sel poligonal gepeng, inti tengah, sitoplasma granula basofil kasar (granula keratohyalin)/ protein kaya histidin-spinosum: berkas filamen tonofibrin utk kohesi sel & lindungi dari abrasi (tebal pd daerah kulit yg selalu tergesek & tertekan)-basale/germinativum: mitosis hebat, perbaharui tiap 15 – 30 hr, kecepatan migrasi ke permukaan + 19 hr DERMIS: tebal s/d 3 mm-papiler : tipis, jar ikat longgar, pleksus subpapiler-retikuler: tebal, jar ikat padat, makin tua kolagen salingbersilangan & elastin makin jarang pleksus subdermal

KRITERIA RAWAT INAP:1.Facial burn2.Grade II sendi, perineal3.anak,ortu: grade II >10% dewasa : grade II > 15%4.Elektric burn

PATOFISIOLOGY:1.Permeabilitas kapiler yg blm mati cairan, elekt, prot ekstravasasi 1 % luas = ekstravasasi ½ - 1 % blood volum luas 20 % = blood loss 10 -20 % => syock (dlm 6 -8 jam)2.Eritrosit fragil, pecah, hemokonsentrasi trombus, hemoglobinuria, hiperK3.Barier stratum corneum rusak: evaporasi s/d 4 – 5 L/M2/24 jam 4.Jantung: MDF (miocard depresant factor): glikoprotein kulit terbakar/spt pancreas hipoksia release 16 unit pd hr I naik 2x lipat pd hr IV5.Ren : ARF via: dehidrasi; timbunan Hb, mioglobin pd glomerulus/nefron6.Cortison7.Gld tiroid 8.lambung: dilatasi akut; paralise. Hptalamuscortison ulkus kecil difus (curling ulcer)9.IgG, IgM: terendah hr I, Normal mgg III sepsis mudah pd mgg II10. HiperK temporer s/d 48 jam I, hipoK setelah hr ke III ( infus K: 80 – 160 mEq/hr)TERAPI:

1. Airway, breathing s/d intubasi ventilator 4.stress ulcer rantin 2 x 1 Amp 2. Iv line (dewasa: Tk II > 15 % luas, III, anak/ortu >10 %) 5.Nutrisi : kalori basal rumus harris benedict max 200% kalori basal formula parkland/baxter = 4 cc x BB x % luas dg distribusi KH 7,2 gr/kg/hr; prot 2 gr/kg; lemak 1.1 gr/kg ½ jumlah diberikan pd 8 jam I, ½ nya pd 16 jam kmd 6.Necrotomi debridement escharotomi cairan kristaloid, hr II kristaloid stop ( Na ) ganti glukosa, grade IIb,III dpt eksisi dini pd hr IV-XIV (bila stabil) STSG hr III baru ada tempat utk koloid (krn sebelumnya akan bocor) granulasi > 3 cm sulit utk epitelialisasi pertimb skin graft Monitor: - urin output : 1 - 2 cc/kg/jam - Hmt 45 granulasi yg meninggi kerok/fressening + kompres desinfektan - CVP + 7 cmH2O - Alb > 3,5 7.antibiotik3.Nyeri neurogenic syock pd jam-jam I (T, HR) 8.position of comfort is contracture position morfin 0,05 mg/kg iv, kepala>jantung, leher ekstensi, bahu abd 90 0 fleksi 300, siku ekstensi dg antidot naloxon 40 ugr iv (1cc Amp+10cc aqua masukkan 1 cc split, wrist netral, panggul abd 150,lutut ekstensi, kaki netral, footboard (dpt ulangi tiap 30 – 45 mnt)

KEBUTUHAN CAIRAN SELAMA OPERASI: 1. Maintenance: rumus 4 utk BB 10 kg I (Formula 4-2-1) 2 10 kg II 1 10 kg seterusnya 2. Hutang selama puasa pre ops : rumus : lama waktu puasa X MContoh: anak 2 th BB 11 kg, puasa pre ops 4 jam : M = 4 X 10 kg = 40 cc 2 X 1 kg = 2 cc 42 cc P = 4 jam X M = 4 X 42 = 160 cc cairan yg hrs masuk pd : 1 jam I durante ops= M +(0.5 P)=40 + (0.5 x 160) = 120 cc II = 0.25P = 0.25 x 160 = 40 cc III = 0.25P = 0.25 x 160 = 40 cc

EBV = estimated blood volume = BB x 8 % X 1000 = 11 x 80 = 800 cc EBL = estimated blood loose = 10 % EBV = 80 cc ( jml max blood loose yg msh dpt ditolerir, tanpa transfusi) pd syock hipovolemia, vol transf dpt beri sd 50 %EBV

Ukuran ETT : (Umur th + 16) : 4 (bila > 3 th (umur + 12):2) kedalaman insersi = ukuran ETT x 3 = cm

ANESTESI Contoh: Anak 11 kg:Premedikasi: midazolam 0.5 mg/kg, tunggu 30 mnt, kmdinduksi inhalasi : O2 70% + N2O 30% + sevoflurane 8 % - FGF = 2 s/d 3 ( 1,000 + (100 x 11)) atau = 2-3 (Minute Volume) = 4,2 s/d 6,3 Lt/mnt = 2-3 (RR X TV) (fress gas flow) = 2-3 (RR X (BB x (8 –10))

= 2-3 (20 X (11 x(8-10)) 2 (20 x 110 cc) = 4.40 L 3 (20 x 110 cc) = 6.60 L 4.40 28 s/d 6.60 Lt/mnt Nafas control: 1.5 x MV = 1.5 x (20 x 110) = 3.300 cc Reservoir bag : 1 liter

Obat intravena: - pentotal = (4 – 6) 11 = 44 – 66 mg ( 500 mg serbuk+20 cc aqua 25 mg/cc) - norcuron = 0,1 x 11 = 1,1 mg Amp 4 mg - Fentanil = (2 – 3) 11 = 22 – 33 ug Amp 2 cc ; 5 ug/cc - SA = 0,01 x 11 = 0,1 mg Amp 1 cc; 0,25 mg/cc - lidocain = 1 x 11 = 11 mg Amp 2 cc; 20 mg/cc alternatif: - trachium : 0.5 x 11 = 5.5 mgMonitor:- HR : 100 – 160 -RR : 20 – 24 -TD : 80 +(2x umur) = 80 + (2x2)= 84 diastole = 2/3 sistole = 2/3 x 84 = 56

Maintenance: sevoflurane 2-3 % Alternative block cauda spina: jarum No 23 O2 70% bupivacaine 0.2% 0.5 ml/kg ditambah N2O 30% epinefrin 1:200.000 ; 0.5 ugr/kg fentanil 2 ugr/kg hati2! Bila N > 10x/mnt (>20 %) sistole > 15 mmHg gel T > 25 % lead II

bupivacaine false trought (iv)

KEBUTUHAN ENERGIHarrison Benedict:Pria : BEE (kcal/hr) = 66.47 + 13.57 (W) + 5 (H) – 6.76 (A)Wanita: = 655.1 + 9.56 (W) + 1.85 (H) – 4.68 (A)BEE=basal energy Expenditure, Weight=kg, Height=cm, Age=thTEE=total energy exp = BEE x stress factor x 1.25Stress factor:-uncomplicated post op = 1.00 – 1.05 -malignancy = 1.10 – 1.45 -sepsis = 1.05 – 1.25 -mayor trauma/burn/severe sepsis= 1.30 – 1.55 Infant BEE = 70 kcal/kg/hr (utk pertumbuhan: tambahi 20 kcal/kg)Growing child= 30-35 kcal/kg/hr (utk tumbuh tambahi 5 – 10 kcal/kg)Umur Kebut kal Cairan Kenaikan kebut kal(%) < 1 th = 80 - 95 kcal/kg/hr, 120 – 140 cc/kg/hr demam= 12% tiap 1oC1 – 3 = 75 – 90 110 – 120 bedah 20 – 30 4 – 6 = 65 - 75 90 – 110 sepsis 40 – 50 (berat)7 – 10 th = 55 – 75 75 – 90 combustio 10011 – 18 = 45 – 55 60 – 75 heart fail 15 – 25 growth fail 50 – 100 MEP = kebut kal s/d 2x kebut basal (6 kkal/ kenaikan 1 kg BB)Kandungan kalori/gr KH=4, protein=4, lemak=9, glukosa=3.4 kkal

Kebutuhan Elektrolit:1. Na = 2 – 4 mEq/kg/hr2. K = 1 – 2 mEq/kg/hr3. Ca =4. Cl =

Karbohidrat: - minimal 130 g/hr, - max kec.4 mg/kg/mnt (critical ill), 7 mg/kg pd pasien stabil (anak: 4 mg/kg/mnt6 mgnaikkan 2 mg/hrmax 12-14 mg/kg/mnt)- bila pemberian > 24 jam: range aman 25 – 30 dextrose kcal/kg- bila akses perifer: osmolar max pakai D10 namun pd anak konsentrasi 20-25% yg tdk berefek overload cairan. Preparat D10 100 mg/ ccWater soluble vitamin(sediaan: soluvit) ditambahkan 0.5 ml ke tiap 100 ml D10

Protein : 0.8 g/kg (2.0 g/kg bila katabolism/metabolik stress) anak: mulai 0.5-1 g/kg/hr naikan 0.5-1g/hrmax 2.5 – 3 g/kg/hr preparat TPN: vamine 15 ml=1 gr. Trace element: Fed-El ditambahkan dlm dose 4 ml/30 ml vamineLemak: harus < 30% total kebut kalori (aman: 1 – 1.5 g/kg/hrnaikkan 1 g/hr) anak: 3.3 g lemak/100 kcal , max 4 g/hr dimana 300 mg dari jenis omega-6(as linoleid/n-6 as lemak) start 0.5 gr/kg/hrnaikkan 0.25-0.5/hrmax 3 g/kg/hr Preparat TPN: IL 10 ml = 1 gr fat soluble vitamin(sediaan: Vitalipid) ditambahkan 1 ml/kg(max 4) ke IL

Contoh pemberian TPN:Anak, 7 th, BB= 19 kg1. Kebut kalori = 19 kg x (55 s/d 75)= 1045 s/d 1425 kkal2. Cairan = 19 x (75 – 90) = 1425 – 1710 cc/hr3. Protein = 19 x (mulai) 1 gr = 19 gr/hr4. Na = 19 x (2 – 4) = 38 – 76 mEq/hr5. K = 19 x (1 – 2) = 19 – 38 mEq/hr

Dalam aminofusin 5% terdapat : - protein 5 gr/100 cc , kebut 19 gr/hr perlu aminofusin (19/5) x 100 = 380 cc dalam 380 cc aminofusin terdapat: - Na (380/1000) x 30 = 11.4 mEq/380 cc - K (380/1000) x 25 = 9.5 mEq/380 ccKebutuhan cairan 1425 – 1710 cc/hr diperoleh dari aminofusin 380 cc + (cairan lain 1710 – 380) 380 cc + max 1330 cc cairan lainDalam 1250 cc KaEnMG3 terdapat: - Na (1250/1000)x 50 = 62.5 mEq - K (1250/1000)x 20 = 25 mEqJadi pasien diberikan: dlm 24 jam - KaEnMg3 1250 cc - aminofusin 380 cc, dalam infus terpisah

KOMPOSISI CAIRAN TIAP LITER

  Na K Kalori Prot mOsm

D5%     200   278

D10%     400   556

NaCl 0.9 % 154       308

RL (laktat) 130 4     273

Asering (asetat) 130 4     273

RD5% 147 4 200   589

Ringer solution 147 4     310

Martos 10%     400   284

Potacol R 130 4 200   412

KaEn1B 385 4 150   285

KaEn3A 60 10 108   290

KaEn3B 50 20 108   290

KaEnMG3 50 20 400   695

PanAminG     200 27.2 507

IntraFusin 3.5% 61.5 30 240 35 790

Aminovel 600 35 25 400 50 1320

AminofusinL600 40 30 400 50 1100

Amiparen 2     100 888

Triparen2 57.5 45 1167.5   1468

Triofusin600     500   700

Triofusin E1000 80 30 1000   1600

Ivelip 20%     2000   270

Clinimix N9G15E 35 30 300 27.5 845

KOMPOSISI cairan tubuh: 70%-80% dari BBtdr dr:1. ekstra sel: 20 % BB: - 5% plasma -15 % interstitial 2. intra sel : 40% dari berat badanperbandingan ektra: intra = neonatus = 1:1 anak = 2:3Kebutuhan elektrolit:Natrium = 3-5 mEq/kgBB/hariKalium = 2-5 mEq/kgBB/hariKlorida = 4-12 mEq/kgBB/hariKalsium = 0,5- 3 mEq/kgBB/hariFosfor = 0,5- 1 mEq/kgBB/hariPenggantian cairan gastrointestinal:

cairan gaster : NS 4,5%, 20-40 mEq/L KCLcairan gaster dan duodenum : RL, 20-40 mEq/L KCLileostomi : RLdiare : RL, NS 4,5% dan KCL

aminosteril 5% sediaan 500 ml, tiap 1 L mengandung :.AA : 50 gr/L.Osmolaritas : 483 mosm/Laminosteril 10% sediaan 500 ml, tiap 1 L mengandung :.AA : 100 gr/L.Kalori : 1675 kJ/L ~ 400 kcal /L.Osmolaritas : 965 mosm/L

Amiparen 10% sediaan 500 ml, tiap 1 L mengandung :.AA : 5,9 gr/L.Na : 2 mEq/L.Acetat : 120 mEq/L

Pedialyte sediaan 500 ml, tiap 1 L mengandung :.Kalium : 10 mEq.Na : 22,5 mEq.Cl : 17,5 mEq.Citrate : 15 mEq.Dektroxe : 25 gr

Untuk Kalium < 3 mEq/L tanpa kelainan EKG 75 mg/kgBB/hari po dibagi 3 dosis Untuk Kalium < 3 mEq/L dengan kelainan EKG KCl 7,46% dosis :3-5 mEq/kgBB/hari maksimum 40 mEq

SYOCK ANAFILAKTIK1. Adrenalin 0,3 – 0,5 cc IM lar 1:1000, ulangi tiap 5-10 mnt anak-anak 0,01 mg/kg respon jelek: 3-5 cc lar 1:10,000 (1 cc lar 1:1,000 + 9 cc saline) dg dosis < pemberian I2. Posisi terlentang, kepala rendah, trendelen3. Airway clear, O2

4. Iv line perbaiki hipovolemi relatif5. Masih sesak: aminofilin 5 mg/kg encerkan dlm D5/NaCl 20 cc iv pelan (10-20 mnt) . sediaan aminofilin Amp 10cc 240mg6. lain-lain: urtikadifenhidramin (delladrylR) 5-20 mg iv sesak berkepanjangan: hidrocortison 100-250 mg iv (2 jam baru berefek)

STATUS ASMATICUS• Broncodilator: a. nebulizer b. adrenalin 1:1000 , 0,3 cc sc15 mnt0,3dst (hati2: CAD, hipertensi, hipertiroid; tdk ada efek pd asidosis). c. 2 adrenergic : metaproterenol, terbutalin, fenoterol d. aminofilin 1 Amp10 cc240 mg + 20 cc D5 iv lambat 5-10 mnt kmd drip 1,5 Amp dlm D5 500 16 gtt atau drip 20 mg/kg/hr2. Corticosteroid loading dose hidrocortison 200 – 300 mg iv maintenance 4 mg/kg/4-6 jam iv tapering 6 jam – 8 s/d 12 jam – IM – peroral 2 minggu tapering equivalen dose hidrocortison 100 mg metilprednison (solumedrol)tiamsinolon: 20 mg dexametason, betametason: 4 mg3. Antocolinergic4. Antihistamin5. Ekspectoran6. cairan, oksigen7. antibiotik

SNAKE BITE

Grade: 0 : 1 atau lebih fank mark, nyeri minimal, edema eritem 1 inci, pd 12 j I, tanpa gejala sistemik 1 : 1-5 inci, nyeri hebat, sistemik (-) 2 : 6-12 inci, sistemik (+): mal,muntah,pusing,syock, neurotoxic 3 : > 12 inci, sistemic (+), kadang ptecia general, echy fank mark 4 : sistemik, ggn ekskresi urin(uri berwarna/darah)-gagal ginjal, koma, edem meluas dari ekstremitas ke badan ipsilateral

Sabu: grade 0 – 1 = tdk perlu 2 = 3 – 4 ampul dlm 500 NaCl atau D5 3 = 5 – 15 Amp bila alergi sabu: 1 Amp sabu + 250 D5 drip dlm 90 mnt dg monitor tensi, EKG alergi muncul?adrenalin

Macam bisa ular:Polipeptida ( Enzimatik) Fosfolipase A, hialuronidase, ATP-ase,5 – nukleotidase, kolinesterase, protease, fosfomono esterase,RNA-se, dan DNA-se.E f e k : Neurotoksik, hematotoksik, trombo genik, hemolitik, kardiotoksik dll.

RABIES : Human Ig = 20 IU/kg im hari 0,3,7,14,28 Equina Ig = 40 IU

Normal Ureum = 15 – 45 Creat = 0.7 – 1.3 Urat = 3.5 – 7.2 K = 3.5 – 5.5 Na = 135 - 145

GFRClearance Creat O = (140 – usia) X BB 72 – creat plasma O = 85 % O GFR = Clearance Creat = Urin creat X Vol urin ml/mnt Plasma creatGFR 0 – 5 = gagal ginjal terminal 5 – 25 = gagal ginjal berat 25 – 75 = insuffisiensi (ggl ginjal ringan) > 75 = baikOliguria = urin output < 0.5 cc/kgBB/jam

CKD grade 5 = CRF = ESRD

Azotemia:- Uremia - Creat - Hiperurikemia - guanidin,fenol,amin, as hidroksi aromatik, indikan inhibisi enzim poten MOF

Evaluation Of Oliguria

U:P Osmolality (urine:plasma) >1.4:1 1:1

U:P Creatinine >50:1 <20:1

Urine Na (mEq/L)  <20 >80

FENa (%) fractional excretion of sodium <1 >3

RFI %  = Renal Failue Index =

Urinary Sodium

(Urinary Creatinine / Serum Creatinine)

<1% >1%

CCR (mL/min) = creatinine clearance 15-20 <10

BUN/Cr >20 <10

          ATNPre-Renal

Cascade filtrasi glomeruli:

CO 5000 ml/mnt 1200 cc 660 cc 125 cc 1.25 cc/mnt25% 55% 20% 1%

a. renalis plasma filtrat colecting

NEFROLOGI

PRsegment

PRinterval QRS

interval

STsegment

STinterval

QT interval

Jpoint

5 mm0,2 dt

0,1 mV

VATQRS RATE (HEART RATE): -Normal interval R-R (3-5) kotak = 60-100-Rumus. 1500 . jarak R-R (mm)IRAMA:-Sinus ritmik:-frek 60-100 teratur -P (-) di aVR, (+) di II -setiap P diikuti QRS-T-Aritmia (tak memenuhi syarat diatas)AXIS:POSISI:TRANSISIONAL ZONE:Lead horizon, equipoten (trans. zone) di:-V1-V2 = counterclock rotation (CCR)-V3-V4 = No rotation (NR)-V5-V6 = clockwise rotation (CR)P.: lihat di II dan V1 -durasi <3 mm (0.12 dt)-Amplitudo<3 mm (0.3 mV)-positif di II, negatif di aVRPR interval(defleksi atria s/d awal dep.vent)-3-5 mm(0.12-0.2 dt)-<3 = WPW sindrom->5 = AV block-Berubah-ubah = Wandering pacemakerQ:-durasi < 0.04 dt -Amplitudo < 2 mm -kecil,sempit di I,II,aVF,V5-6Q pat:->1 mm (0.04 dt) -dalamnya > 25% R -bila di aVR = masih normalQRS Interval (lamanya dep vent)-<3 mm (0.12 dt)-total defleksi pos-neg: I+II+III <15 =low voltage-r inisial <2 mm pd V3 =poor r wave progresive-kompleks rS di V1 = pola ventrikuler kanan- qR di V6= pola ventrikuler kiriST segmen (dari J point s/d awal T-isoelektrik atau 0.5 s/d 2 mm

T:-< 10 mm pd lead horizon -< 5 mm pd lead ventral

VAT:(ventrikuler Activation Time/QR interval) waktu impuls dr endocard ke epicard di V1-2 <0.03 dtdi V5-6 <0.05 dt

Amplitudo di Equipoten  I aVF di AXIS    III + 30positif positif aVL + 60    I + 90    aVF 0    II - 30positif negatif aVR - 60    I - 90    aVR + 120negatif positif II + 150    aVF +180negatif negatif aVL – 120     III - 150

AXIS frontal:

horizon -30 s/d -15semi horizon - 15 s/d + 15intermediet +15 s/d + 45semi vertikal +45 s/d + 75vertikal +75 s/d + 110abnormal +110 s/d + - 180right axis deviation  abnormal - 30 s/d - 90left axis deviation  extrem - 90 s/d + - 180right axis deviation  

POSISI:

0

- 30

+ 120

- 90

Kecepatan rekaman : 25 mm/dt 1 mm=1/25 dt = 0.04 dtKekuatan voltase : 10 mm = 1 mV

I+III = II = Hk.Einthoven

HIPERTROFI ATRIUM KIRI (HAki):-P width & notched (lebar & lekuk) di II (durasi > 0.11 dt) (krn waktu dep atrium ki mjd lambatjarak antar 2 komponen penyusun gel P melebarP width & notch di II-P (-) di V1 (krn komponen akhir(kedua) gel P > negHati2 notched dpt N, kec jarak antar 2 puncak > 0.04 dt

HIPERTROFI ATRIUM KANAN (HAka):-P tall & peak (tinggi & tajam) di II (Amp > 3), durasi N.-dan P (+) di V1. dua hal ini disebut pulmonal P.-Tjd gbr P ini kr dep atrium ka (yg lbh >) mendahului ki

HIPERTROFI VENTRIKEL KIRI (LVH):Frontal (lbh spesifik drpd pre kordial):-R aVL > 11 mm-R aVF > 20 mm-R I + S III > 25 mmPrekordial: S V12 > 25 mm-S V1 + (R V5 atau V6) > 26 mm R V56> 25 mm-R V5, V6 > 26 S V12 + R V56 > 35mm -S terbesar + R terbesar > 45-Segmen ST skunder:-elevasi/depresi ST

-ST concaf ke atas V1-2 & kelainan T: T berlawanan QRS misal. QRS V123 neg, ttp T pos QRS V456 pos, ttp T neg Pato: LVHdiameter serat miocard menebal iskemi & hantaran dinding vent melambat (bila 2 hal tsb ada mortalitas naik)-Onset defleksi intrinsikoid terlambat (VAT memanjang) pd V6 > 0.05 dtLVH tipe volum overload: Q V5-6, T runcing & simetris pressure : ST depress, T inverted V5-6

HIPERTROFI VENTRIKEL KANAN (RVH):Sensitif di V1Right axis deviation ( > + 110)R V1 > S V1 (R/S ratio > 1)R V1 > 7 mmS V1 < 2QR atau qRS di v1S di V56 > 7rSR’ V1 dg R’ > 10 mm rR V1 + S V5 atau V6 > 10.5RVH tipe A : overload pressure vent ka, misal stenosis pulmonumR J tipe C : overload volum, mis atria septal defek pola rSR’(ingat: pola Rsr’ = normal) tipe B : kompleks RS equifasik

HIPERTROFI BIVENTRIKULER: tjd bila pd:RVH: -dominasi R, T tinggi di V56 -Q V56 > 3 mm -devias axis ke kiri

LVH:-R or R’ pd pre cordial kanan -S V6 > normal

LEAD II

LEAD V1

HAka HAki

CORONARY ARTERY DISEASE (CAD):- Stable angina- Unstable angina pectoris (UAP) - N STE MI - ST EMI1. Chronic Stable Angina (demand ischemi) lumen coroner menyempit, masih cukup suplay, ttp saat demand transitory imbalance suplay demandiskemi2. Coroner vasospasme atau agregasi platelet/trombi akut coroner flow turun atau tak adaacut reduction O2 suplay suplay ishemibiasanya bersamaan demand acut coroner sindrome(ACS): a. Unstable Angina Pectoris (EKG & enzim tak mendukung Dx AMI) b. cardiac enzim release ….Miocard Infark NSTEMI & STEMI Troponin I & T: naik dlm 3–12 j onset pain, peak 24-48 j, N 5-14 hari. (tjd perub kadar naik > 0,2 ng/ml setelah 2 jam) CK-MB(creatine kinase-miocardband)):sensitif ,spesifik - kadar enzim naik dlm 3 s/d 12 j onset pain - peak dlm 24 j, baseline 48 – 72 j kmd. - (tjd perub kadar naik >1,5 ng/ml)

- Normal: 3 – 6 % dari total CK -Non ST Elevation Miocard Infarc (NSTEMI) -ST Elevasi Miocard Infarc (STEMI):- Non Q wave - Q wave marker lain:- myoglobin, CRP, IL-6,serum Amiloid-A - LDH (onset dlm 24 jam, peak 3-6 hr, durasi 8-12 hr TIMI-RS (Trombolisis In Miocard Infarc-Risk Score):

(1) age older than 65, (2) 3 or more cardiac risk factors (pria,tua,DM,rokok,hipertensi,

hiperkolesterol,hiperlipidemi, riwayat CVA,inherited metabolic disorder, metampetamin, ocupational stres, conective tissue ds)

(3) ST deviation,(4) aspirin use within 7 days, (5) 2 or more anginal events over 24 hours, (6) history of coronary stenosis, and (7) elevated troponin levels.

aANGINA PECTORIS:Pato: regio iskemiNa-K pump turun 1. ion K ekstrasel miokard meningkat 2. Ca influks meningkat, 1&2 berakibat area iskemi: -dep lbh terlambat QRS melebar -rep lbh duluan drpd area sehatperub ST & T -pot membran mjd kritis mudah aritmiaMisal sub endocard iskemitepat sebelum repolarisasi,Dimana area lain telah neg, area iskemi msh posarus listrikMenjauhi lead, shg akan terekam lbh neg ST depress (sebaliknya: ST elevasi bila lesi di subepicard)Ciri EKG angina: segment ST:1.ST depress (iskemi subendocard/angian pectoris)2.ST elevasi (iskemi subepicard/angina prinzmetal/ angina varian/spasme sepintas a. cor3.ST datar dg/tanpa depresi (N=ascendent gentle)Gel T:flat/bifasik/inverted arrowhead(sempit simetris,cor T wave)

INFARK MIOKARD-Infark transmural Vki: (dari sub epi s/d subendocard tjd infark) vektor insial biasa, kmd dep Vka & bag Vki yg sehat dg arah menjauhi area infarkQ dlm & lebar (pola QS)

-Infark non transmural Vki (tak seluruh ketebalan otot kena) vektor inisial biasa, kmd dep Vka & Vki yg sehat Q lbh dlm, akhirnya dep mncapai epicard superfi- cial dr area infarkdefleksi positifR terminal Q lbh dlm, R terminal (pola gel QR)

Fase Klinis Infark:1.Fase akut:-ST dg or tanpa slope elevasi -T tinggi & lebar -VAT memanjang2.Fase fully evolved / fase berkembang penuh:

-tjd pd hr 1 s/d 7 sejak infark-Q pat-ST elevasi konveks ke atas-T inverted arrowhead

3.Fase resolusi:-Q pat tetap ada (meski 10% kasus hilang)-ST mungkin sudah isoelektris-T mungkin sdh normal

Kelainan perub Lokasi Tempattampak di lead resiprokal infark sumbatan

I,aVL, V1-6   ekstensiv anterior LADV1-4   anteroseptal a.septalV4-6, I, aVL   anterolateral CxI, aVL, V5-6   lateral wall CxII, III, aVF I, aVL inferior wall RCA

  V 1,2,3Posterior wall

     

     

Anterior wall AMI

Very early AMI-I, aVL, V2-3-Resiprocal: II, III, aVF

ST remain elevated in lead anteriorbut T inverted

Complete large AMIQ in I, aVL, V1-4

Inferior wall AMI

Non spesific ST, T change

Lead II, III, aVFQ, ST elevasi, T invertedResiprocal di aVL

True posterior wall extention of inferior AMI: in V2:

R increase, ST depress, increase T

Ujung Cx,Tikungan RCAs/d desc post

BLOCK:-Sino Atrial (SA) Block-Atrio Vent (AV) Block: -Partial AV block: -Tk I: First Degree AV block -Tk II:-Second Degree AV Block/mobits tipe I (wenckebach phenomena) -Second Degree AV Block/mobits tipe II (constant block) -Advance/High grade AV block -Complete AV Block (third degree AV Block)-Ggn Konduksi Intra Ventrikuler -BBB:-RBBB:-komplet -inkomplet -LBBB:komplet/inkomplet -perifer left vent conduction defect: -left anterior fascicular block (LAF) -left posterior fascicular block (LPF) -phasic aberant ventriculer conduction -Non specific intraventriculer conduction delay -multi fascicular block

SA BLOCK:Blokade pd batas SA node dg jar atria sekitarnyaTdk ada aktifitas di atria & venttdk ada P-QRS-TGap yg kosong kompleks PQRST ini, intervalnya kelipatan dari interval N. Bila hambatan lama/permanen berakibat muncul escape beat/escape rytm.

AV BLOCK:Blokade pd batas atrium-vent pd AV junctionFIRST DEGREE AV BLOCK:Perlambatan hantaran impuls dr atria ke ventpemanjangan PR interval (>0.2 dt)

SECOND DEGREE AV BLOCKKegagalan intermiten sebagian impuls dr sinus AV utkMencapai vent (sebag PQRST N, sebag tdk N)

SECOND DEGREE AV BLOCK/Mobits tipe IFase refrakter relatif di AV node makin lama makin panjang sampai akhirnya impuls gagal utk disalurkanP-interval PR-QRST NP-interval PR memanjang-QRSTP-interval P makin memanjang-QRSTAbsen P-dilanjutkan muncul QRST, (drooped beat) kmd:P-interval PR-QRST N

SECOND DEGREE AV BLOCK/Mobits tipe IIHambatan di AV junc, periodik & tetap, shg interval PRtetap(constant) ttp scr periodik tdp gel sinus (P) yg di-Block shg tdl diikuti QRS.Mis: tiap 4 Phanya ada 3 QRSratio weckenbach: 4 : 3Causa block ini:-kelainan pd AV node -fisiologis (pd atria frek>350/mnt) (bersifat protektif)

ADVANCE AV BLOCK:-btk tipe II dg cir tambahan ada >2 impuls yg berturutan alami block pd frek denyut atrial < 150/mnt-dpt pula muncul sbg siatu aritmia agonal-sering tjd pd infark anterior-onset sering mendadak & didahului RBBB

THIRD DEGREE AV BLOCK:-kegagalan konduksi di AV node yg total & permanen atria & vent berdenyut sendiri-sendiri (Atria oleh SA node vent oleh pacemaker di bawah block (AV dissosiation)-P muncul teratur, QRS-normal (bila pacemaker tinggi/His) -notch, slurred (lebar,bila pcm di V)

GANGGUAN KONDUKSI INTRA VENTRIKULERPATO:1.iskemiAMI (trtm anterior)ggn hantaran 2.sclerodegeneratif (fasiculus distal kena tanpa keikutsertaan miocard (tenegree disease) 3.jantung rematik kalsifikasi anulus 4.degenerasi reaktif thd: -hipertensi sistemik kalsf. hantaran -deformitas kongenital (Lev disease)

BUNDLE BRANCH BLOCK (BBB):Impuls disalurkan ke cabang yg tak diblock dulu, kmdmelalui serabut miocard mengaktifkan ventrikel sisiyg diblock. Krn miocard konduktor jelek, maka impuls yg dihantarkan otot perlu waktu lamaQRS lebarSetiap QRS > 0.12 selalu pikirkan BBB.

RIGHT BUNDLE BLOCK (RBBB):-Interval QRS > 0.12 dt -Pd right chest lead (V1-2) r dan R (bila ada infark septumpd V1 rR mjd tak ada)-left chest lead (V56), I, aVL: S slurring (lebar)-ST skunder & T inverted pd V1 (krn dep vent abnormal)Incomplet RBBB: rSR” di V1, ttp QRS N N

LEFT BUNDLE BRANCH BLOCK (LBBB):-interval QRS > 0.12 dt-Q lebar & dlm di V12 (krn inisial septum dep diaktifkan oleh RBB yg arah impuls dr ka ke ki Q pat shg Dx LVH & infark sukar ditegakkan-R notch, slurring di V56, aVL-S slurring di V12-ST skunder, T inverted

LAH: left anterior hemiblockLPH: left post hemiblock

LEFT ANTERIOR FASCICULAR BLOCK (LAFB):Perjalanan impuls berbeda dari Normal, yaitu:-Impuls LBB ke left posterior fasc (ke bawah depan) ke miokardke area terakhir yi ke belakang atas (area yg biasa diurus LAF).-mean nQRS axis lbh neg 30 (deviasi kiri/CR)-rS di II, III, aVF-qR di I, aVL

LEFT POSTERIOR FASCICULAR BLOCK (LPFB):Kebalikan dari LAFB, impuls dr LBB ke LAF(atas blk)ke bawah depan (area yg biasa diurus LPF)-mean QRS axis lbh positif 110-qR di II,III, aVFrS di I, aVLLPF/ LP hemiblock jarang. Dpt di Dx bila: setelah menyingkirkan Dx RVH, Infark miokard.

PHASIC ABERANT VENT CONDUCTION:Impuls supra vent sampai ke BB ada 3 kemungkinan:1.Diblock total (impuls datang dini saat BB msh refrakter)2.Dihantarkan normal (BB sudah refrakter penuh)3.Dihantar scr aberant (satu cab BB blm refrakter penuh)Didahului P, gbr mirip RBBB, segment awal QRS samaDg seg awal QRS N, didahului RR panjang

ACCELERATED CONDUCTION:Penyaluran impuls dr atria ke vent melewati jalur lain(tdk lewat AV nodehis dst). Jalur lain ini lbh cepat-interval PR sangat pendek (<0.12)-QRS memanjang (>0.12)-terdapat DELTA WAVE-mudah diserang takiaritmia-terpenting disini:wolf parkinson wave(WPW Sindrom)-jalur lain (assesori) tsb adalah penghubung atria dg vent (jembata n kekerabatan anatomis elektrik) yg normalnya pd trisemester II telah obliterasiMacam lintasan asesori:-lintasan atrionodal (Jaines)-node ventriculer (Mahaim)-fasciculus ventrikuler (Mahaim)-tractus atrio His (Lev)

EXTRA SISTOLE /Atrial Premature Beat-Asal fokus ektopik di atrium-P abnormal & muncul prematur-Masa kompensasi (sandwich interval) tak penuh (waktu antara 2 sinus beat.Bila interval waktu ini sama dg 2X interval R-R/P-R disebut komp penuh)-konduksi di AV node N atau block tjd block krn impuls ektopik datang terlalu dini, dimana saat itu AV node masih refrakter-konduksi intra vent N atau aberant-menurut letak asal fokus ektopik: 1. low atrial prematur beat: P neg di II, pos di aVR 2. High atrial: P pos di II, neg di aVR

AV JUNGTION EXTRA SISTOLE/AV nodal prematur/ AV jungtion prematur beat-fokus ektopik di AV jungtion, impuls dilanjutkan ke atria dan atau vent-P abnormal (bila QRS pos,justru P neg bila QRS neg P positif P abnormal dpt terletak di depan atau di dlm (shg tak nampak) atau di blk kompleks QRS-sandwich interval tak penuh-konduksi intra vent N atau aberant-ada 3 tipe (menurut etak P abnormal thd kompleks QRS) 1. High AV junc Extra Sistole (P di depan QRS) 2. AV junc (P di dlm QRS shg tak nampak) 3. Low AV jung Extra Sistole (P di blk QRS)Sulit bedakan high dg low, shg disebut: Supra Vent Extr Sis

VENTRIKULER BIGEMINI/Ventrikel extra sistole/Vent prem. Beat/v. p. contraction-fokus ektopik di vent krn miokard itu konduktor jelek impuls ektopik tsb akan dihantarkan scr abnormalQRS lebar & bizare-tdk ada P didepan QRS yg dibuat oleh ektopik-QRS tsb prematur, lebar, bizare

-ST depres, T inverted-sandwich interval penuhTanda-tanda vent bigemini (VB) yg berat: -VB >5x permenit -multifokal -R on T phenomen (VB tepat jatuh pd gel T sebelumnyapemicu VT/VF -muncul post exercise -usia > 40 thVB dari 1 fokus yg sama akan mempunyai bentukdan coupling time (CT)yg samaCT = jarak antara VB dg sinus beat sebelumnya

ESCAPE BEAT (EB):-Atrial escape beat-AV node escape/AV junc rythm/idionodal rythm-Vent escape beat/Vent esc rythm/idiovent rythmPato:suatu release phenomen, yi terlepasnya potensial pacemaker dari pengaru SA node. kegagalan atau hambatan pd pcmker sinus atau hambatan konduksi impuls sinus, akan berakibat pot pcmker lain akan ambil alih (A, AV, Vent).Ciri EKG:-muncul setelah pause panjang -gambaran esc beat tiap pot pcmker adalah sesuai dg gambaran prematur beat masing2.Bila causa EB menetap, maka irama jantung akan ditent oleh pcmker yg baru: a. idionodal rythm:pcmker di AV junc, 50-60x/mnt b. idiovent rythm :pcmker di vent, 30-40 x/mnt

ABNORMAL TAKIKARDI (rate 140-250 x/mnt)Paroxismal Atrial Takikardi-fokus ektopik atria melepas impuls cepat-sederetan prematur beat/PB/ (gel ektopik) timbul cepat,berturutan,teratur-P sering tak terlihat-konduksi di AVnode & intra vent N atau aberant

Paroxismal AV Junc Takikardi-fokus ektopik di AV junc lepaskan impuls cepat-sederetan AV Junc PB-konduksi intra vent N atau aberantDUA JENIS gel diatas sulit dibedakansebut sajaParoxismal supravent takikardi

Paroxismal Vent Takikardi:-fokus ektopik vent lepaskan impuls cepat-sederetan Vent PB berturutan

ATRIAL FLUTTER: (250-350 x/mnt)-fokus ektopik atria lepaskan impuls cepat teratur -P flutter wave/F wave/saw tooth appearn/gigi gergaji-intra vent konduksi N atau aberant

ATRIAL FIBRILASI (>350 x/mnt)-cepat tak teratur > 350x/mntvent mjd irreguler-P sukar terlihat, sbg getaran pd baseline, “f” wave-konduksi di AV node disertai block-konduksi intravent N atau aberant

VENTRIKULER FIBRILASI-Defleksi sangat ireguler, bizare (dlm btk,tinggi,lebar)-biasanya mrpk stad terminal ggn cormati

WANDERING PACEMAKER:-fokus ektopik di mana saja (SA node, A, AV junc) shg gel P berubah-ubah, PR interval juga.

HIPERKALEMIA HIPOKALEMIA

PERIKARDITIS

ACLSmodified by TAW

Asses responsivenessRespon (+)

1. 0bservasi2. Tx sesuai indikasi (di bawah ini):

Respon (-)

C all: - activated EMS (Emergency Respon System) - for defibL okL istenF eel

Breath (-) 2 kali hembusan

PULSE

(+)

Positif Negatif

O2 (termasuk intubasi)I v lineM onitor (12 lead)

CPR1 seri/1mnt=100x/mnt pola 15: 2 5: 1

Monitor

VT/VFpulseles

Non VT/VF

DC : 200-300-360PEA

ASISTOLE

SirkulasiKembalispontan

Persisten VF

Observasi

ARITMIA

TAKIKARDI (>100)

BRADIKARDI

1. Serius simptom,sign2. HR >150

STABIL

AFA Fluter

PSVT VT

(<60)

Serius:-simptom:-nafas pendek - kesadaran turun - chest pain-sign:-T drop,pre/syock, -congestive pulmo -AMI,CHF

YATDK

-II0type2-III0

Klinis spt ASMA, ttp:-Retraksi (-)-Ronkhi basah s/d apec-Pucat, megap2,ala nasi lebar-EKG variatif:-sinus taki-T bisa > 140/90-PCO2 >> PO2 N<50) (N=85 – 90)

ACUTE LUNG OEDEM (ALO)

-Chest pain-Elevasi ST-dg/tanpa BBB: -QRS > 12 -Right=rsR’ di V1-V3 -left = RR’ di V5-V6

AMI

ASISTOLE

TransCutaneousPacing (TCP)

-Epinefrin 1 mg iv push (sediaan=1Amp1cc1mg lar 1:1,000) ulangi tiap 3 – 5 mnt-Atropin 1 Amp iv (sediaan=1Amp1cc 0,25 mg) ulangi tiap 3 – 5 mnt s/d total 0,04 mg/kg

Persisten Asistole VF atau lainnya

1. Cek apakah CPR sudah betul2. Atipical clinical feature present3. Support for cease-effort protocol in place

Akhiri Tx bila:1.2.

Tx sesuai kelainan

PERSISTEN VT/VF

IntubasiIv line

1 mg epuinefrin I flush 20 cc naCl elevasi (bila iv sulit: intratraceal 2,5 mg )

CPR – DC 360CPR – DC 360CPR – DC 360

1 mg Epinefrin II

CPR – DC 360CPR – DC 360CPR – DC 360

A / L / V

Amiodaro300 mg iv bolus 15 – 20 mntSediaan: Amp 150 mg

Lidocaine (Xylocard)1 – 1,5 mg/kgBBSediaan: amp 2cclar 2%=20 mg/cc

0,5 – 0,75 mg/kgBB, max 3 mg/kgBB maintenance 2 – 4 mg/mnt

Vasopresin 40 UI single doseSediaan: Amp pitresin 20 UI

PEA(Pulseless Electrical Activity)

Tentukan causa utama:1. Hypovolemia 6. Obat (OD drug, kecelakaan)2. Hypoxia 7. tamponade, cardiac3. Asidosis 8. Tension pneumothorac4. Hyper/hypokalemia 9. Thrombosis coroner, ACS5. Hypertermia 10. Thrombosis DVT, pulmonary embolism

Tx sesuai causa, dan:1. PEA HR slow : atropin 1 mg iv ulangi tiap 3 – 5 mnt

max total 0,04 mg/kg2. PEA HR tdk slow: epinefrin 1 mg iv flush ulangi tiap 3 – 5 mnt

BRADICARDIA (<60)

NO SERIUSSign & simptom

Block II0 type-2Block III0

NO

OBSERVASI

YES

- TCP- iv PACING

SERIUS:Simptom: nafas pendek, kes turun, chestpainSign: T turun, syock, ALO, CHF, AMI

Atropin 0,5 – 1 mg iv max 0,04 mg/kgBBDopamin 5 – 20 u gr/kg/mntEpinefrin 2 – 10 u gr/mnt (1 Amp + NaCl 500 1 – 5 cc/mntTCPIsoproterenol

TAKIKARDI (>100)

-Serius simptom & sign: nafas pendek, kes turun, chest pain T turun, syock, ALO, CHF, AMI- HR > 150

-O2

-iv line-Siapkan suction O2 sat monitor intubasi set-sedatif-Dg/tanpa anastesi analgesi

CARDIOVERSISincronize100200300360

Sedatif: - diazepam, - midazolam - barbiturat - ketamin - etomidat - metohexitalAnalgetik: - fentanil - morfin - meperidin

Stabil/Serius (-)

AFA Fluter

-Diltiazem-B blocker-Verapamil-Prokainamid-Quinidin-anticoagulan

PSVT

Bruit carotis (+) Bruit (-)

Vagal manouver

Adenosin 6 mg iv flush

1 – 3 mnt

Adenosin 6 mg iv flush

1 – 3 mntAdenosin 12 mg iv

Stop bila tjd Block II0

T makin turunSerius sign & simptom

Cardioversi mulai 50

T, N membaik

Verapamil 2,5 – 5 mg iv pelanSambil lihat T & HR 2-3 mnt)

15 – 30 mnt

Verapamil 5 – 10 mg iv

Pertimbangkan :-digoxin - B block

- diltiazem

VT

Lidocain 1 – 1,5 mg/kg flush

Lidocain 0,5 – 0,75 mg/kg flush max total 3 mg/kg

5 – 10 mnt

Procainamid20 – 30 mg/mnt, max 17 mg/kg

Bretilium

cardioversi

ALL ABOUT OXYGEN Cascade O2:760 ---- 149100 10 s/d 20Atmosfer-nasal-alveoli-arteri-kapiler-selIn CO 5 L/mnt, Hb 15 gr%, at rest:O2 delivery in arteriol=1000 ml/mnt which 250 ml/mnt diffusion to extravasculer(consumption) O2 in venula:1000-250=750 ml/mnt, CO2 in venula 200 ml/mntUdara atmosfer 760 mmHgFiO2 = 21 % = 760 x 21 % = 149 mmHg 20,94%21%Humifiedreduce 47 (760 – 47) x 0.2094 = 149 PAO2 = the partial pressure of oxygen in Alveoli = PIO2 – PaCO2/R = 149 – (40/0.8) = 100mmHgHenry’s law :Dissolved for each mmHg PO2 0.003 ml O2/100 ml blood if CO 5 L/mnt 0.003 x 100 x 15 ml O2/mnt suplay ini tdk cukup krn Kebutuhan at rest: 250 ml O2/mnt– utk itu perlu angkutan1 gr Hb ikat 1,34 ml O2 Hb 15 gr% 1.34 x 15 = 20 ml O2/100 ml blood CO 5 L/mnt 20 x (5.000 ml : 100 ml) = 1000 ml O2/mntThe amount of oxygen in the blood is calculated using the formula:[1.34 x Hb x (SaO2/100)] + (0.003 x PO2) = where the PO2 is 100mmHg, and the hemoglobin concentration is 15g/L [1.34 x Hb x (saturation/100)] + 0.003 x PO2 = 20.8mlHow much oxygen is delivered to the tissues per minute?The delivery of oxygen to the tissues per minute is calculated from: DO2 = [1.39 x Hb x SaO2 + (0.003 x PaO2)] x Q Q=COSo if Hb 15g/l, CO 5L, PaO2 of 100 and SaO2 of 100%,what is his oxygen delivery? DO2 = [1.39 x 15 x 100 + (0.003 x PaO2)] x Q = 1000 mlHow much oxygen is extracted per minute?Tissue oxygen extraction is calculated bysubtracting mixed venous oxygen content from arterial oxygen content. PVO2 =the partial pressure of oxygen in mixed venous blood= 47mmHgThe Fick equation :

The Fick equation :VO2 is the oxygen consumption per minute,CaO2 is the content of oxygen in arterial blood, and CvO2 is the content of oxygen in venous blood: VO2 = Q x (CaO2-CvO2) mlO2/minThe CnO2 is (1.34 x Hb x SnO2/100) + 0.003 x PnO2, where n = a or vThe major difference between the two is obviously the sat Hb:100% on the arterial side and 75% on the venous side. where Hb15g/dl: CaO2 20ml/100ml, CvO2 is 15ml/100ml: the difference is 5ml/100ml = 50 ml/l multiplied by CO a cardiac output of 5L = O2 consumption per minute is 250ml.oxyhemoglobin dissociation curvebelow a SaO2 of 90%, small differences in Hb saturation reflectlarge changes in PaO2 above 90%, the curve is flat, but below this level the PaO2 declines sharply, 75% saturation the PaO2 is about 47mmHg(Mixvein) 50% saturation the PaO2 is 26.6mmHg, 25% saturation the PaO2 is a miserable 15mmHg. a shift in the curve rightwards – releasing oxygen : heat, exercise, acidosis, hypercarbia and increased 2,3-DPGConversely: cold weather or during rest, when the tissues are cold, alkalotic, hypocarbic and low 2,3-DPG,

PaCO2 > 50 dgpH < 7.25

PaO2 < 60 pd FiO2 > 0.5

Criteria Description

Objective measurements Adequate oxygenation (eg, PO2 >60 mm Hg on FIO2 >

0.4; PEEP <5–10 cm H2O; PO2/FIO2 >150–300);

  Stable cardiovascular system (eg, HR <140; stable BP; no (or minimal) pressors)

 Afebrile (temperature < 38°C)

 No significant respiratory acidosis

 Adequate hemoglobin (eg, Hgb >8–10 g/dL)

  Adequate mentation (eg, arousable, GCS >13, no continuous sedative infusions)

 Stable metabolic status (eg, acceptable electrolytes)

Subjective clinical assessments Resolution of disease acute phase; physician believes discontinuation possible; adequate cough

Suitability for Weaning

Protokol evaluasi trauma tumpul abdomen Menurut Maingot’s

menurut peitzmanmenurut peitzman

Protokol evaluasi trauma tembus abdomen Menurut Maingot’s

menurut peitzmanmenurut peitzman

3 zona Rongga retroperitoneum(untuk tujuan eksplorasi) - Zona I : daerah sentral bagian atas retroperitoneum ( retroperitoneum sentro medial ) dari hiatus aorta dan oesophagus sampai promontorium sakralis. Struktur primernya:aorta, vena kava , vasa prox ginjal, vena porta , pancreas dan duodenum.- Zona II : pinggang kiri dan pinggang kanan ( retroperitoneum lateral) , yang berisi kedua ginjal dan ureter bagian suprapelvis, di sebelah kanan, berisi:kolon kanan dan mesokolon di sebelah kiri, berisi: kolon kiri dan mesokolon .- Zona III : terdiri dari pelvis (retroperitoneum pelvis) dan berisi kolom sigmoid dan rectum, vesika urinaria , kedua ureter segmen pelvis bagian distal.

KIDNEY Injury I -Microscopic or gross hematuria, urologic studies normal -Subcapsular hematoma, nonexpanding without parenchymal laceration II .Nonexpanding perirenal hematoma confined to renal retroperitoneam .Laceration < 1 cm parenchymal depth of renal cortex without urinary extravasation III Laceration > 1 cm parenchymal depth of renal cortex without collecting system rupture or urinary extravasation IV -Parenchymal laceration extending through the renal cortex, medulla, and collecting system -Main renal artery or vein injury with contained hemorrhage V .Completely shattered kidney .Avulsion of renal hilum which devascularizes kidney

Alur penanganan trauma hepar

Alur penanganan trauma lienGrad

eTipe Injuri Deskripsi Terapi

1 Hematom Subcapsular, <10% permukaan Tidak ada tindakan khusus

Laserasi Laserasi Capsul, kedalam <1cm

2 Hematom Subcapsular, 10%-50% permukaan ; intra parenkim <5cm

Memerlukan suture repairatau mesh untuk

Laserasi Laserasi Capsul, kedalamam 1 – 3 cm, tidakmencapai trabekula.

‘menambal’ defek pada lien

3 Hematom Subcapsular >50% permukaan ; intra parenkim > 5cm atau expanding

Laserasi Kedalaman parenkim > 3cm, atau mengenai pembuluh darah trabekula

4 Laserasi Laserasi segmental atau Mengenai pembuluh darah hilus (>25% lien)

Anatomic ressection, termasuk ligasi pembuluh

5 Laserasi Ruptur total darah lobar atau bahkan

Vascular Devascularisasi lien spleenectomy

TRAUMA DUODENUM DAN PANCREAS

Indications for Damage Control Surgery Vanderbilt University Medical Center 20051. Trauma & EGS (Emg General Surgery) Patient in extremis a. Life threatening hemorrhage requiring abdominal packing, or temporizing vascular shunts b. Bowel resection in the face of dwindling physiologic reserve requiring delayed GI reconstruction c. Mesenteric ischemia with planned re-look laparotomy d. Massive intra-abdominal contamination or visceral edema precluding primary fascial closure e. Massive volume resuscitation (>15 units pRBC & > 10 L crystalloid) –expecting significant visceral edema and the development of Abdominal Compartment Syndrome.

II. Temporizing Abdominal Closure 1. Plastic barrier (bowel isolation bag) to protect the bowels 2. Surgical towel & 2 Jackson Pratt drains brought out through the wound 3. Ioban adhesive cover.

III. Time to subsequent operative procedure. 1. Unplanned re-exploration should be done in the face of ongoing surgical bleeding 2. Re-exploration is done when patient has regained physiologic reserve (End-points to be determined by Trauma / EGS surgeon: Lactic acid, base deficit, correction of coagulopathy, normalization of temperature). 3. Time to unpacking of abdomen should not exceed 72 hours (Incidence of Intraabdominal abscess significantly increased beyond 72 hrs.) 4. Planned washouts of open abdomen should be everyday for “contaminated abdomen” and every other day for “clean-contaminated” open abdomen. 5. Abdominal washouts should be done with warm saline only.

IV. The Contaminated – Dirty Abdomen = Tertiary Peritonitis 1. Defined as gross purulent fluid in more than one quadrant (Single quadrant =Intra-abdominal abscess) 2. Irrigation to be done with warm saline only 3. Acetic Acid maybe used to soak laparotomy pads or kerlex rolls of a defined abscess cavity with planned serial washouts until visually clean.

V. Abdominal Fascial Closure 1. Primary Fascial abdominal closure should be evaluated at each laparotomy. 2. Indications for continued open abdomen a. Visceral Edema with inability for primary closure b. Contaminated – Dirty abdomen c. Significant Extra-abdominal Sepsis with Acute Lung Injury on significant ventilatory support.

VI. Planned Ventral Hernia 1. Once intra-abdominal issued have been corrected and unlikely to obtain primary fascial closure by post injury day 8, trauma / EGS surgeon must consider a planned ventral hernia course. 2. Small ventral defect (< 10 cm wide) consider AlloDerm closure with or without skin closure (with or without bipedicle flaps) 3. Large defect (> 10 cm wide) vycril mesh closure with planned STSG when granulated bed matured

ACS (Abd Comprt Syndrom): Grade I : 10-15 cm H2O

Grade II : 15-25 cm H2O Grade III : 25-35 cm H2O Grade V : greater than 35 cm H2O

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Mangled Extremity severity (MES) Scorea. Skeletal/soft tissue injury - low energy (stab, simple facture, civil gunshot) 1 - medium (open/multiple facture, dislocation) 2 - high (crush injury, militer gunshot, close range shotgun) 3b. Limb ischemia - pulse reduced or absent, but normal perfusion 1 - pulselessness, parestesia, diminished capillary refill 2 - cool, paralized, insensate, numb 3c. Shock - sistolic > 90 mmHg 1 - hipotensive transiently 2 - persistent hypotension 3d. Age - < 30 1 - 30 – 50 2 - > 50 3

Gustillo classification of open fracture I. wound < 1cm, clean, minimal injury to the musculature, no significant stripping of periosteum II. Wound > 1 cm, no significant: soft tissue damage/flap/avulsion III. a. contaminated, soft tissue injury but viable to cover: bone, neurovasculer, without muscle transfer b. masiff contaminated, cover with muscle transfer c. vasculer injury