Anestesi Pada Pasien Dengan

Penyakit Sistem Kardiovaskular

Dr. AKHYAR H NASUTION, Sp.An, KAKV

Departemen Anestesiologi dan Reanimasi

Fakultas Kedokteran
Universitas Sumatera Utara
Medan
2008
 Clinical Predictors of Increased Perioperative
Cardiovascular Risk
(myocardial infarction, heart failure, death)

Major
 Unstable coronary syndromes

- Acute of recent MI with evidence of important ischemic

by clinical symptoms or noninvasive study
- Unstable of severe angina (Canadian class III and IV)
 Decompensated heart failure

 Significant arrythmias

- High-grade atrioventricular block

- Symptomatic ventricular arrythmias is the presence of
underlying heart disease
- Supraventricular arrythmias with uncontrolled ventricular rate
 Severe valvular disease
Clinical Predictors of Increased Perioperative
Cardiovascular Risk
(myocardial infarction, heart failure, death)
Intermediate
 Mild angina pectoris (Canadian class I or II)
 Previous MI by history of pathological Q waves
 Compensated or prior heart failure
 Diabetes mellitus (particularly insulin dependent)
 Renal insufficiency

Minor
 Advanced age
 Abnormal ECG (left ventricular hypertrophy, left bundle branch block, ST-T

abnormalities)
 Rhythm other than sinus (eg, atrial fibrillation)
 Low Functional capacity (eg, inability to climb one flight of stairs with a bag of

groceries)
 History of stroke
 Uncontrolled systemic hypertension
 Shortcut to noninvasive testing
in preoperative patients
if any two factors are present
1. Intermediate clinical predictors are present
(Canadian class I or II angina, prior MI based on
history of pathological Q waves, compensated or
prior heart failure, or diabetes)
2. Poor functional capacity (less than 4 METs)
3. High surgical risk procedure (emergency major
operations, aortic repair or peripheral vascular
surgery, prolonged surgical procedures with
large fluid shifts of blood loss)
Cardiac risk stratifaction for noncardiac
surgical procedures
High (reported cardiac risk often greater than 5%)
- Emergent major operations, particularly in the elderly
- Peripheral vascular surgery
- Anticipated prolonged surgical procedures associated
with large fluid shift and/or blood loss
Intermediate (reported cardiac risk generally les than 5%)
- Carotid endarterectomy
- Head and neck surgery
- Prostate surgery
Low (reported cardiac risk generally less than 1%)
- Endoscopic procedures
- Superficial procedure
- Cataract surgery
- Breast surgery
 25 – 50% kematian setelah pembedahan non
jantung disebabkan komplikasi kardiovaskuler.
Perioperatif Infark Miokard (IM), Edema
Pulmonal, Gagal Jantung Kongestif (GJK),
Aritmia dan Tromboemboli adalah yang paling
sering tampak pada pasien dengan dengan
penyakit kardiovaskuler sebelumnya.

 Insiden kardiogenik pulmonari edema post

operative sekitar 2% pada pasien-pasien dengan
usia diatas 40 tahun, 6% pada pasien-pasien
dengan riwayat gagal jantung dan 16% pada
pasien dengan poorly compensated heart failure.
 PRE OPERATIVE
MANAGEMENT

- Riwayat penyakit, pemeriksaan fisik dan EKG harus difokuskan

untuk mengidentifikasi potensi terjadinya kardiovaskuler yang serius
(CAD, CHF, Aritmia)

- Bila ditemukan penyakit kardiovaskuler maka perlu ditentukan

resiko kardiak adalah evaluasi dasar yang meliputi keadaan umum,
usia, kelas fungsional, fakta resiko kardiak, kormodibitas penyakit
lain (diabetes mellitus, gangguan fungsi ginjal, penyakit vaskular
perifer dan penyakit paru kronik) dan jenis operasi

- Bila perlu dapat dilakukan pemeriksaan transthoracic

echocardiography (TTE) yang dapat membantu evaluasi resiko
perioperative komplikasi kardiak yang berat
Oxygen delivery = Cardiac output x Arterial oxygen content

Stroke volume x Heart rate Hemoglobin x Arterial

oxygen saturation

Preload Afterload Contractility

 INTRAOPERATIVE
MANAGEMENT
Intraoperative Predictors for PCM (Perioperative
Cardiac Morbidity)
- Diantara predictor intraoperative klasik, pembedahan emergensi,
pembedahan vaskular besar dan operasi lebih dari 3 jam pada
pembedahan abdominal atas atau torak
- Diantara prediktor dinamik, hipotensi dan takhikardi memprediksi
PCM
- Sedanngkan hipertensi masih merupakan prediktor yang
kontroversial
- Myocardial iskemia diduga sebagai prediktor
- LV end-diastolic pressure adalah pengukur yang sensitif pada
iskemia

Mangano DT. Perioperative cardiac morbidity. Anesthesiology 1990;72:153-184

INTRAOPERATIVE MANAGEMENT
Monitor the Patient

- EKG: simultaneous leads V5 and II, multiple-lead ST-segment analysis

if available
- Blood pressure: noninvasive automatic Doppler sphygmomanometric
technique
- Pulse oximeter for arterial oxygenation
- Temperature: esophageal
- Swan-Ganz catheter: PCWP, pulmonary artery diastolic pressure (PAD),
hemodynamic study only for patients with ventricular dysfunction
- Central venous pressure (CVP) line: if the patient has good LV function
- Foley catheter: urine output
- Oxygen analyzer for inspired gas mixture
- End-tidal CO2 analyzer
Hemodynamic Monitoring
 Hemo = Blood (Darah)
 Dynamic = Flow (Aliran)
 Parameter Utama:
– Invasive Blood Pressure (IBP) – tekanan darah yang
diukur
– Cardiac Output – jumlah darah yang dipompa per menit
– Contractility – kecepatan dan kekuatan kontraksi
– Vascular Resistance – hambatan aliran darah
– Fluid Level – jumlah cairan dalam tubuh/pembuluh darah
 OVERVIEW OF FACTORS AFFECTING TISSUE PERFUSSION

MYOCARDIAL CONTRACTILITY

PRE-LOAD AFTER-LOAD

STROKE VOLUME HEART RATE

CARDIAC OUTPUT PERIPHERAL RESISTANCE

VOLUME

BLOOD PRESSURE
DIAMETER

VISCOSITAS
TISSUE PERFUSSION
PRINSIP UMUM
 Sensor harus mendeteksi signal secara
akurat
 Monitoring tidak pernah sebagai terapeutik
 Evaluasi resiko – keuntungan menggunakan
monitor
 Monitoring adalah suatu tim proses
Artery Line

 Pengukuran langsung tekanan darah

 Teknik lebih akurat
 Informasi hemodinamik kontinyu
 Pengambilan multipel sampel arteri
 Pada Kondisi apa perlu
pengukuran invasive arterial
pressure ?
 Akut hipertensi atau perdarahan
 Cirulatory or cardiac arrest
 Hipertensi krisis
 Sepsis
 Neurologik injuri
 Komplikasi post operasi
 Pasien dengan vasoactive drugs
 Pasien membutuhkan pemeriksaan analisa gas
darah yang sering
Haemodynamic Monitoring

NON INVASIVE INVASIVE

Non Invasive

 Palpation
 Doppler Probe
 Auscultation
 Oscillometry
 Arterial tonometry
 100

115
110

20 cm
 Aneroid gauge

Brachial artery

Radial artery

Doppler probe

Doppler
 Air chamber
Element of
Pressure pressure sensor

Sensor

Artery Wall
Invasive

 Arterial Catheter
 Central Venous Catheter
for pressure monitoring, volume replacement, or
central drug infusion
 Pulmonary Artery (Swan-Ganz)
Catheter
Pemakaian
Hemodynamic Monitoring
 Banyak dibutuhkan di Critical Care dan
Surgery
 Fungsi:
– Memantau kondisi jantung pasien
– Menentukan perawatan yang akan diambil
 Dilakukan oleh dokter Anesthesi
 Menggunakan Swan-Ganz
 Parameter yang dibaca: PAW & TD CO
Tujuan Monitoring
Hemodinamik Invasif

Memberi informasi kuantitatif

 Homeostasis fisiologis ada atau tidak
 Mendapatkan peringatan “dini” perubahan
status pasien
 Intervensi terapeutik adekuat/ tidak dan
benar/ keliru
 INTRAOPERATIVE MANAGEMENT
 Penggunaan Pulmonary Artery Catheter
(PAC)

- Diperkirakan terjadi peningkatan fluid shifts

- CHF akibat komplikasi MI
- Pada CAD yang signifikan yang menjalani prosedur yang
berhubungan dengan stress hemodinamik yang
signifikan ; dan pada sistolik dan diastolik LV disfunction,
cardiomiopaty dan valvular disease yang menjalani operasi
dengan resiko tinggi

Eagle KA, Berger PB, Calkins H, Anesth Analg 2002;94:1052-1064

Alat yang selama ini dipakai

 Pulmonary Artery
Catheter:
– Swan Ganz / Right
Heart Catheter
– Sudah sejak >25
tahun
– Parameter:
 PA Pressure
 PA Wedging (PAOP)
 CO/CI
Lumen:
Lumen pada Swan-Ganz
1. Distal: mengukur pressure
2. Proximal: Injeksi cairan Lubang
3. Middle: pemberian obat Distal

Lubang
Proximal

Lokasi
Thermistor

Suntikan untuk Balon

Kabel Thermistor
membuka balon
Cara pemasangan
 Masuk dari vena leher
(Jugular) atau
selangkangan (femoral)
 Dorong Catheter di
jantung kanan
 Keluar dari RV ke
pembuluh utama
sebelum paru-paru
(Pulmonary Artery)
 Injeksi cairan (dingin),
thermistor mengukur
perubahan suhu darah
terhadap waktu
(Thermodilution)
Pemasangan Swan-Ganz ke
Monitor
 Tampilan di Monitor
MONITORED: CO 6.9

HR 70
MAP 86
CVP 10
PAM 18
PAW 12
WEIGHT 75.0

HEIGHT 168.0
CALCULATE BSA 1.85
D:
CI 3.7
SV 98.6
SVR 88.0
SVRI 1626
PVR 69
PVRI 128
LVSWI 53.7
RVSWI 5.8

Tetapi tidak semua monitor bisa menghitung seperti ini!

Keunggulan Swan Ganz

 Sudah populer
 Bisa mengukur Pressure PA Wedging
(PAW/PAOP)
 Pemberian obat langsung ke jantung
(melalui Middle Lumen ke jantung
kanan)
 Paling Akurat
Kelemahan Swan Ganz
 Pemasangan sulit,  Tidak semua orang bisa
tergantung skill memasang
 Data yang di baca tidak  Terlambat memberikan
continuous (hanya pada perawatan tepat karena
saat injeksi cairan) kurang data dan tidak
update
 Posisi di dalam jantung  Jika terlalu lama bisa
(RA & RV) menyebabkan aritmia
 Parameter: CO/CI, PA  Kebutuhan sekarang
pressure, PAW pressure lebih banyak parameter
 LOW PRELOAD
Hypoperfusion

RAP or CVP < 6 mmHg
PAW or LA pressure < 8 mmHg in patient without
cardiac dysfunction, or < 18 mmHg in patient with
cardiac dysfunction

Administration of fluid in attempt to increased circulating
volume  IV fluid challenges of 100 to 250 ml crystalloid
solution should be administrered over 10 minute until
evidence of improved perfusion occurs.
 HIGH PRELOAD
 Left-side filling pressure ↑  pulmonary venous pressure becomes
higher than colloid osmotic pressure surrounding the vasculature 
causes fluid to be driven from the vasculature and into surrounding
interstitial or interalveolar spaces

dyspnea PAW > 20 -22 mmHg
hypoperfusion PAW > 30 mmHg

Cardiogenic pulmonary edema

Oxygen uptake ↓  hypoxemia with increased oxygen delivery
High ventricular end diastolic pressure (measured by PAWP)  decreased
coronary collateral blood flow

Therapy  Diuretics and Ventilator

 Nitropruside and
dopamine
Nitropruside
Phentolamine
Digitalis
Cardiac output (L/min/m2)

normal
Low cardiac

Diuretics nitrates
symptoms

Heart failure
Output

Left ventricular end diastolic pressure (mmHg) Pulmonary

congestion

Ventricular function curves depicting effects of various agents used for treating heart failure.
Diuretics and nitrates lower filling pressure along the same curve and have little action on
forward cardiac output. Positive inotropic agents and arterial vasodilators shift the
ventricular function curve upward and to the left, increasing cardiac output for any left
ventricular end-diastolic pressure. The combination of an arterial vasodilator and a positive
inotropic agents (e.g, nitropruside and dopamine or amrinone) can augment cardiac output
and lower filling pressure to a greater extent.
 AFTERLOAD

Left ventricle  SVR vasoconstriction

Right ventricle PVR
vasodilatation

Myocardial Vein oxygen consumption

(MVo2)
 volume
Stoke

Wall tension

Relation ship between stroke volume and wall tension (i.e., afterload) for the
intact left ventricle. At constant preload, increase in wall tension result in a
decline in stroke volume. Increased preload or increased contractility shifts the
curve upward and to right, resulting in a greater stroke volume for any given
afterload.
 LOW
AFTERLOAD
Pressure = Flow x Resistance
SVR ↓  severe hypotension
 inadequate coronary artery perfusion
Vasopressor  vasoconstriction secondary to stimulation
of alpha receptors in vascular smooth muscle

Phenylephrine,
metaraminol,
norepinephrine, β1-stimulating
properties
ephedrine,
dopamine (> 10 to 20 µg/kg/min)
 HIGH AFTERLOAD
CO ↓ Symphatetic stimulation cause arterial
BP ↓ vasoconstriction to maintain blood pressure

Stroke volume ↑
MV02 ↓

 Arteriovasodilators  smooth muscle relaxant activate β2

adrenergic
receptor in the smooth muscle of the arterioles
(hydralazine, nitroprusside, nitroglycerine)
 Calcium channel blockers
 Alpha blockers
 Angiotensin converting enzyme (ACE) inhibitors
 Counterpulsation
 CONTRACTILITY
 Decreased contractility associated with reduced
ejection can occur with :
- Hypovolemia
- Myocardial ischemia
- Infraction
- Certain pharmacologic and anesthetic agents
 Increases in inotropism may be necessary to
maintain adequate stroke volume and oxygen
delivery
 In patient with ischemic heart disease increase in
MVo2 that accompanies increased contractility
 DECREASED CONTRACTILITY

 Studies by Shoemaker et.al. have shown that maintenance

of a stroke work index of the left ventricle > 55 g-m/beat is
associated with improved survival in the shock patients.

 Improvement in myocardial contractility can be obtained

with the use of :
- Inotropic agents catecholamins
(dopamine, dobutamine, isoproterenol, epinephrine)
 increased adenosine 3’:5’-cyclic phosphate (cyclic AMP)
- Phosphodiesterase inhibitors (amrinone and milrinone)
 inhibits the breakdown of cyclic AMP into its inactive
form
 INCREASED CONTRACTILITY

 Increase in oxygen demand

 Betablockers  inhibits stimulation of

β1 adrenergic receptors in the
myocardium (cardioselective) and β2
adrenergic receptors in the smooth
muscle in the arterioles of the lung
(nonselective)
 HEART RATE
CO = Stroke volume (SV) x Heart rate (HR)

 HR > 120 bpm may associated with decreased

in SV and CO because of decreased diastolic
filling time of the left ventricle
 HR with shortened diastolic duration also
decrease left ventricle coronary perfuasion time
and increased MVo2  causing imbalance
between myocardial oxygen supply and demand
 HEART RATE
 Beta blocker  reduce chronotropism
and calcium channel blockers to
decrease conduction
 Bradycardia with the heart rate of < 50
bpm  CO ↓ and tissue perfusion ↓

 Therapy  Atropine
Pace maker
HEMOGLOBIN

 Abnormal reduction of hemoglobin can

improve a significans threat to tissue
oxygenation has much as
aproximatelly 98 % of the oxygen is
carried by the hemoglobin molecules.
 Abnormally high hemoglobin
concentration can increase cardiac out
put secondary to increased viscosity
Arterial Oxygen
Saturation
 SaO2 can be maintaine at norma level
( >97 % ) with :
Increased
PEEP
CPAP
ACMO
 Calcium antagonists
Arterial vasodilatos
Too High
IABP
Too Low (Afterload) Alpha blockers
Vasopressors SVR/PVR ACE inhibitors
Too High Diuretics
Venous vasodilators
Too Low (Preload)
Vasopressors PAW/LA/RA
Too High Beta blockers
Positive inotropics
(Contractility) IABP
Ventricular Too Low
LVWSI/RVWSI Calcium antagonist
ossist devices
Too High
Pacemaker Beta blockers
Too Low Heart rate
Atropine Calcium antagonist
Too High
↑ FiO2
PEEP/CPAP Too Low Arterial oxygen
Hyperbaric oxygenation saturation
ECMO Too High

Blood product Too Low Hemoglobin

Hb solution
 Hemodynamic effects of commonly used cardiovascular drugs

Drugs HR Afterload Contractility Preload Coments

INOTROPIC
AGENTS
Digoxin -or ↓ ± ↑ - ↓ Ventricular rate in AF
Dopamine ± or ↑ - or ↑ ↑↑ ↑ or ↓ Effect on SVR is dose
dependent; ↑ renal blood
flow
Dobutamine - or ↑ ± ↑↑ ↓
Isoproterenol Can cause dysrythmias
↑↑ ↓↓ ↑↑ ↓
Norepinephrine ↑ or ↓ ↑↑ ↑ ↑ Can cause dysrythmias
Epinephrine Can cause dysrythmias
↑↑ ↑ or ↓ ↑↑ ↑
Methoxamine - ↑↑ - ↑
Amrinone/ - or ↑ ↓ ↑ ↓
milrinone
 Hemodynamic effects of commonly used cardiovascular drugs

Drugs HR Afterload Contractility Preload Coments

ANALGESIC
AGENTS
Morphine - ↓ - ↓

DIURETICS
(furosemide, - ↓ - ↓ May ↓ cardiac
ethacrynic acid, output if diuresis
bumetanide) excessive

ANTIDYSRHYTHMIC
- - ±↓ -
AGENTS
- - ±↓ -
Lidocaine
- - ±↓ -
Procainamide
↑ - - - or ↓
Quinidine
Atropine
 INTRAOPERATIVE MANAGEMENT
 Regional VS General Anestesia pada Pasien dengan
Penyakit Jantung
- Pasien dengan penyakit jantung telah dibandingkan efek-efek regional v
general anestesi pada insidensi infarc perioperative, disritmia dan CHF.
Pada kebanyakan penelitian telah menunjukkan tidak ada perbedaan
pada infarction rate selama general dan regional (spinal, epidural, nerve
block, lokal anestesia)
- Regional anestesi dapat menguntungkan pada pasien-pasien dengan
sebelumnya MI yang menjalani transurethral prostatectomy; reinfarction
rate pada anestesi spinal kurang dari 1% vs 2-8% pada anestesi genera
- Pemilihan anestesia yang paling baik adalah sesuai dengan kebijakan tim
perawatan anestesia, yang mana akan mempertimbangkan kebutuhan
ventilasi posoperative; efek kardiovaskular, depresi miokardial; blokade
simpatis

- Bode RH Jr, Lewis KP, Zarich SW, et al. comparison of general and regional anesthesia. Anesthesiology 1996;84:3-13
- Mangano DT. Perioperative cardiac morbidity. Anesthesiology 1990;72:153-184
- Norris EJ, Beattie C, Perler BA, et al. Anesthesiology 2001;95:1054-1067
 INTRAOPERATIVE MANAGEMENT

 INDUKSI ANESTESI

- Induksi yang baik adalah penting untuk mencegah

hipotensi, hipertensi dan takhikardi, yang mana
dapat menyebabkan iskemi miokardial
- Semua obat-obat anesthesi dapat digunakan pada
pasien penyakit jantung, kecuali ketamin karena
dapat menyebabkan hipertensi dan takhikardi

Martin DE, Rosenberg H, Aukburg SJ, et al. Lowe-dose fentanyl blunts circulatory responses to tracheal intubation.
Anest Analg 1982;61:680
 INTRAOPERATIVE MANAGEMENT
 Penggunaan Obat Anestesia

- Pada akhir pembedahan, diharapkan dapat dilakukan

ekstubasi. Digunakan N2O dan kombinasi Isoflurane dosis
rendah dan Fentanil untuk mempertahankan anestesia

- Narkotik dosis tinggi sebaiknya dicegah bila ventilasi

postoperative tidak direncanakan

- Pemakaian intermediate-acting neuromoscular blocking

agent seperti vecuronium, atracurium dan rocuronium
dapat digunakan secara aman karena tidak
menyebabkan perubahan kardiovaskular

-Fleming N.Con: the chice of muscle relaxants is not important in cardiac surgery. J Cardiothorac Vas Anesth : 1995;9:772-
774
Hudson RJ, Thomson IR. Pro: the choice of muscle relaxants is important in cardiac surgery. J Cardiothorac Vas
Anesth 1995;9:768-771
 HYPOTENSION
Remember : BP = CO x SVR
BP = (SV x HR) x SVR

1. Low SVR :
• sympathetic blockade
• vasodilators
• spinal shock
• anaphylaxis
• blood transfusion
• septic shock
2. Low HR ( see bradycardia )
3. Low Stroke Volume
4. Medicine :
• SVR lowering : nipride
• preload lowering : NTG
• contractility lowering : beta blockers
5. Surgeons disturbing baroreceptors
carotid artery surgery
 HYPERTENSION
1. Pain / Light anesthesia
2. Hypermetabolic state (fever / sepsis,
thyroid storm, MH crisis)
3. Catecholamine  (hypoxia, hypercarbia,
acidosis, awareness during surgery)
4. Medicine (eg, epinephrine injection )
5. Endocrine (pheochromacytoma, MH,
thyroid crisis)
6. Renal (parenchymal, renovascular)
7. Cushing’s reflex
8. Coarctation
9. Full bladder
 TACHYCARDIA
1. Light anesthesia / pain
2. Hypovolemic Shock
3. Hypermetabolic State :
• shivering
• fever
• MH
• thyroid
• alcohol “withdrawal”
4. Catecholamine  :
• hypoxia, hypercarbia
• acidosis
• pheochromacytoma
5. Sepsis
6. Medicine :
• atropin, gallamine
• pancuronium, ketamin
7. Arrhytmia :
• Atrial : SVT, Atrial fibrillation ,
Atrial flutter, pre-excitation
• Ventricular : VT (remember epi + halothane )
 BRADYCARDIA
1. HYPOXEMIA !!
2. Athletic heart
3. Deep anesthesia
4. Vagal Causes :
• occulocardiac
• maxillary traction
• peritoneal traction
• cervical dilatation
• laryngoscopy
5. Cushing’s reflex
6. Medicine :
• neostigmine, edrophonium,
pyridostigmine
• beta blocker
7. Arrhytmias
 OBAT INTRAVENA :

BARBITURAT * METHOHEXITONE
* THIOPENTONE

BP  ok : * CAPACITANCE VENODILATATION

PRELOAD 

* SVR 

* MYOCARDIAL CONTRACTILITY 
BENZODIAZEPIN :
* DIAZEPAM
* MIDAZOLAM

BP PENGARUHNYA TIDAK KENTARA

CARDIAC INDEX
PERUBAHAN
SVR MINIMAL
 KETAMIN :

HEART RATE 
CONTRACTILITY  BP 
SVR  O2 Consumption 

Risk MCI 

CONTRA INDICATION : Hypertension ( + )

Hyperthyroid
History of MCI
Intra Cranial Pressure 
 OPIAT
MORPHINE HIPOTENSI ( + ) , ok :
- VASOMOTOR TONE 
- CAPACITANCE VESSEL 
- HISTAMIN RELEASE 

PETIDINE HEART RATE 

- ANTICHOLENERGIC ACTION 
(PARASYMPHATOLITIC,
ATROPIN LIKE ACTION)

BLOOD PRESSURE 
- CONTRACTILITY 
- SVR 
 INHALASI
N2O  circulation effect minimal
SVR, PVR 
HALOTHANE contractility 

ENFLURANE cardiac output  BP 

SVR 

HALOTHANE provocator :
“catecholamine induced dysrhytmias”
HALOTHANE + ADRENALINE  EMERGENCY
ETHER

ISOFLURANE SYMPHATIC STIMULATION

CYCLOPROPAN

BP N @ 
RESPON KARDIOVASKULAR
TERHADAP PEMBEDAHAN DAN
ANESTESI
 TEKNIK PREANESTETIK & MONITORING

 LARINGOSKOPI & INTUBASI

 PERUBAHAN FUNGSI VENTILASI
 POSISI TUBUH
 PERDARAHAN
 STIMULASI DARI PEMBEDAHAN
 KEDALAMAN ANESTESI
 INTRAOPERATIVE MANAGEMENT
Depressi Segment ST
- Menunjukkan iskemia miokard disebabkan peningkatan
myocardial oksigen demand atau penurunan oksigen
supply. Peningkatan oksigen supply koreksi
hipotensi, hipoksemia dan anemi berat. Penurunan
oksigen demand koreksi hipertensi dan takhikardi
dengan memperdalam level anestesia atau gunakan
vasodilator, beta blockers dan kalsium channel blockers.

- Bila tidak ada perubahan haemodinamik nitrogliserin

drip, intravenous nicardipine dapat digunakan untuk
mengurangi spasme koroner

- Ishibashi Y, Shimada T, Yoshitomi H, et al. Clin Exp Pharmacol Physiol 1999;26:404-410

Mangano DT. Perioperative cardiac morbidity. Anesthesiology 1990;71:153-184
 INTRAOPERATIVE MANAGEMENT
Ekstubasi

- Ketika pasien bangun, nafas adekuat dan efek

blokade neuromuscular telah hilang

- Untuk mencegah takhikardi yang berhubungan

dengan ekstubasi dan emergensi, dapat diberikan
dosis preventif seperti 1 mg/kg lidokain atau
esmolol atau 0,1 mg/kg labetalol, diltiazem, atau
verapamil 2 menit sebelum ekstubasi

- Helfman SM, Gold MI, Delissen EA, et al. Anesth Analg 1991;72:482-486
Mikawa K, Nishina K, Maekawa N, et al. Anesth Analg 1996;82:1205-1210