1

ACUTE CORONARY SYNDROME

PRESENTASI KLINIS UAP :
 Prolonged (20 min) anginal pain at rest
0-3 : Low risk  New onset (de novo) angina (Class II or III of the Classification of the Canadian
4 :Intermediate Cardiovascular Society)
5-14 : High risk  Recent destabilization of previously stable angina with at least Canadian Cardiovascular
Society Class III angina characteristics (crescendo angina)
 Post-MI angina  dalam waktu 30 hari setelah infark
PEMBAGIAN WAKTU MI:
 Acute MI  0-7 hari
 Localized changes appearing within minutes to hours
 ST segment elevation over the area involved
 ST segment depression in the opposing leads (reciprocal changes)
 T wave maybe symmetrically peaked or deeply inverted
 Arrhytmias or conduction abnormalities may occur
 Recent MI  7-28 hari
 Localized changes remain days to weeks after the vent
0-2 : Low risk  ST segment may or may not have returned to baseline
3-4 : Intermediate  Localized Q wave or QS complexes have appeared
5-7 : High risk  T wave are symmetrically inverted in the area involved
 Old MI  > 28 hari
 Abnormal Q waves, QS complexes or regression or R wave persist indefinitely
 ST segment are isoelectric (otherwise consider ventricular aneurysm)
 Inversion of the T wave may persist indefinitely
 Abnormalities remain unchanged since month after the event

β-BLOCKER PADA ACS

 Diberikan per-oral dalam 24 jam pertama setelah masuk RS
UAP / NSTEMI  prefer CCB atau β-blocker  Kontraindikasi:
STEMI  prefer ACE-I dan β-blocker  Moderate-severe LV failure & pulmonary edema
APS  prefer β-blocker  Bradikardia  < 60 bpm
Angina Prinzmetal  akibat vasospasme, ditandai dgn adanya ST elevasi tanpa kenaikan enzim   Hipotensi  SBP < 100 mmHg
Tx: CCB  Sign of poor peripheral perfusion
 Second degree or third degree heart block
 Reactive airway disease
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 ST DEPRESI CURIGA ISCHEMIA  tipe horizontal dan downslopping TROMBOLITIK

KONTRAINDIKASI :
Absolutes
 Any prior intracranial hemorrhage
 Known structural cerebral vascular lesion (eg, AVM)
 STEMI:
 ST elevasi ≥ 1 mV dari 2 sadapan lead II, III, aVF dan I, aVL  Known malignant intracranial neoplasm (primary or metastatic)
≥ 2 mV di lead V1-V6  Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours
 LBBB baru  Suspected aortic dissection
 Active bleeding or bleeding diathesis (excluding menses)
 Significant closed head trauma or facial trauma within 3 months
 N-STEMI
Depresi ST ≥ 0,1 mV, inversi gel T > 0,2 mV yg simetris dari 2 lead yg bersebelahan
Relative
 History of chronic, severe, poorly controlled hypertension
 PENINGKATAN CARDIAC ENZIM PADA ACS
 Pemeriksaan pertama 2 x di atas nilai standar  Severe uncontrolled hypertension on presentation (SBP > 180 mmHg or
 Peningkatan 2 x atau > 50% (serial) dalam waktu 6 jam DBP > 110 mmHg)
 Rasio CKMB / total CK > 2,5%  History of prior ischemic stroke > 3 months, dementia, or known intracranial pathology not
covered in contraindications
 Traumatic or prolonged (> 10 minutes) CPR or major surgery (< 3 weeks)
 EFEKTIVITAS PCI VS TROMBOLISIS
Onset < 3 jam (usia < 75 tahun)  PCI = trombolisis  Recent (within 2 to 4 weeks) internal bleeding
Onset > 3 jam  PCI > trombolisis  Noncompressible vascular punctures
Usia > 75 tahun  PCI tdk direkomendasikan (?), trombolitik kontraindikasi relatif, pilihan  For streptokinase/anistreplase: prior exposure (> 5 days ago) or prior allergic reaction to these
mungkin konservatif (heparinisasi) agents
 Pregnancy
 Active peptic ulcer
 PENANGANAN PERTAMA ACS :
 Aspilet 320 mg (4 tablet)  Current use of anticoagulants: the higher the INR, the higher the risk of bleeding
 Plavix 300 mg (4 tablet)  jika Primary PCI tambah 300 mg dan Atorvastatin 80 mg
 Jika usia ≥ 75 thn  tidak perlu loading Aspilet dan Plavix !!! INDIKATOR KEBERHASILAN TROMBOLISIS :
 ST elevasi menurun > 50 % dari sebelumnya
 Nyeri dada berkurang (relief pain)
 PENGGUNAAN ATORVASTATIN :
 APS : 20 mg  Peak dari cardiac enzim lebih cepat tercapai
 ACS : 40 mg
 Primary PCI dan post PCI : 80 mg Keberhasilan trombolisis  evaluasi EKG dan enzim dilakukan dalam waktu 60-90 menit (dari awal
dilakukan trombolitik !!!)
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KLASIFIKASI KILLIP  disfungsi LV pada NSTEMI atau STEMI

ANTI-TROMBOTIK PADA UAP / NSTEMI (GUIDELINES AHA 2007)

CARA MERACIK STREPTASE :

Dosis: 1,5 juta unit habis dalam 1 jam
 1 vial streptase tambahkan 5 cc NaCl  bagi menjadi 2 
@ 2,5 cc, kemudian masukkan dalam syring pump 50 cc  drip 100 cc / jam

KOMPLIKASI TROMBOLISIS :
P : perdarahan
A : aritmia
H : hipotensi
A : alergi

RV INFARK
 Trias  clear lung, JVP meningkat, hipotensi
 Terapinya  loading cairan dulu !!! hati-hati penggunaan cedocard

EVOLUSI EKG PADA STEMI :

Pada kondisi tertentu: atrial fibrilasi, LV thrombus, atau cerebral, venous atau pulmonary emboli (VTE)
 warfarin + aspirin dan CPG  target INR: 2.0 – 2.5
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NSTEMI  INVASIF VS KONSERVATIF (GUIDELINES ESC 2011) GRACE RISK SCORE

In summary, timing of angiography and revascularization should be based on patient risk profile.
Patients at very high risk (as defined above) should be considered for urgent coronary angiography (<
Creatinin
2 h). In patients at high risk with a GRACE risk score of > 140 or with at least one major high risk
0,0 – 0,39
criterion, an early invasive strategy within 24 h appears to be the reasonable time window. This implies
0,4 – 0,79
expedited transfer for patients admitted to hospitals without on-site catheterization facilities. In lower
0,8 – 1,19
risk subsets with a GRACE risk score of < 140 but with at least one high risk criterion, the invasive
1,2 – 1,59
evaluation can be delayed without increased risk but should be performed during the same hospital stay,
1,6 – 1,99
preferably within 72 h of admission. In such patients, immediate transfer is not mandatory, but should
0,2 – 3,99
be organized within 72 h (e.g. diabetic patients). In other low risk patients without recurrent symptoms,
> 4,0
a non-invasive assessment of inducible ischaemia should be performed before hospital discharge.
Coronary angiography should be performed if the results are positive for reversible ischaemia.

KRITERIA HIGH RISK

Primary
 Relevant rise or fall in troponin
 Dynamic ST- or T-wave changes (symptomatic or silent)
Secondary
 Diabetes mellitus
 Renal insufficiency (eGFR <60 mL/min/1.73 m²)
 Reduced LV function (ejection fraction <40%)
 Early post infarction angina
 Recent PCI
 Prior CABG
 Intermediate to high GRACE risk score
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ATRIAL SEPTAL DEFECT & VENTRICLE SEPTAL DEFECT KRITERIA SYOK KARDIOGENIK (SHOCK TRIAL) :
 High Flow, High Resistance  Hypotension (systolic blood pressure < 90 mmHg for at least 30 min, need for vasopressors, or
Oksigenasi tes  pH reactive, ditandai dengan Qp:Qs (Flow Ratio)  dan PARI   IABP support)
masih bisa ditutup  Clinical evidence of end organ hypoperfusion
 High Flow, Low Resistance  Confirmatory hemodynamic or radiographic features: pulmonary capillary wedge pressure
 mutlak bisa ditutup (PCWP) ≥ 15 mm Hg and cardiac index ≤ 2.2 l/min/m2 (for non-anterior MI) or pulmonary
 Low Flow, Low Resistance congestion on a chest X-ray, with subsequent hemodynamic confirmation (for anterior MI)
 tidak perlu ditutup
 Low Flow, High Resistance INDIKASI TMT TEST PADA ANGINA STABIL
≈ mulai terjadi Eisenmenger  sudah terlambat untuk ditutup  Menilai optimalisasi terapi
 Menilai previous MI  ada tidaknya residual ischemia dan stratifikasi resiko
KRITERIA PDA :  Post-revaskularisasi  menilai ada tidaknya residual stenosis
 Left ventricular enlargment
 Enlargment of aorta KONTRA-INDIKASI TMT TEST
 Enlargment of pulmonal (pulmonary prominence) Absolute
 Continuous systolic murmur  Acute myocardial infarction (within 2 d)
 High-risk unstable angina
BISING SISTOLIK  Uncontrolled cardiac arrhythmias causing symptoms or hemodynamic compromise
 Symptomatic severe aortic stenosis
BISING DIASTOLIK  Uncontrolled symptomatic heart failure
 Acute pulmonary embolus or pulmonary infarction
 Acute myocarditis or pericarditis
 Acute aortic dissection

Relative
 Left main coronary stenosis
 Moderate stenotic valvular heart disease
 Electrolyte abnormalities
 Severe arterial hypertension  SBP > 200 mmHg and/or DBP > 110 mmHg
 Tachyarrhythmias or bradyarrhythmias
 Hypertrophic cardiomyopathy and other forms of outflow tract obstruction
 Mental or physical impairment leading to inability to exercise adequately
 High-degree atrioventricular block
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INDIKASI MENGHENTIKAN TMT TEST ELEKTROKARDIOGRAFI

Absolute indications
 Drop in systolic blood pressure of >10 mm Hg from baseline blood pressure despite an AKSIS JANTUNG PADA EKG
increase in workload, when accompanied by other evidence of ischemia aVL aVF Aksis
 Moderate to severe angina (+) (+) INTERMEDIATE aVL > tinggi 200
 Increasing nervous system symptoms (eg, ataxia, dizziness, or near-syncope) (liat QRS-nya) aVL = aVF 300
 Signs of poor perfusion (cyanosis or pallor) aVF > tinggi 400
 Technical difficulties in monitoring ECG or systolic blood pressure (+) (-) HORIZONTAL (+) -200
 Subject’s desire to stop (liat QRS di lead II) (-) -400 (LAHB)
 Sustained ventricular tachycardia 0 -300
 ST elevation ( ≥ 1.0 mm) in leads without diagnostic Q-waves (other than V1 or aVR) (-) (+) VERTIKAL (+) 800
(liat QRS di lead I) (-) 1000 (LPHB)
Relative indications 0 900
 Drop in systolic blood pressure of ( ≥ 10 mm Hg from baseline blood pressure despite an (+) 0 SEMI HORIZONTAL = 00
increase in workload, in the absence of other evidence of ischemia 0 (+) SEMI VERTIKAL = 600
 ST or QRS changes such as excessive ST depression ( > 2 mm of horizontal or downsloping
ST-segment depression) or marked axis shift LAHB (LEFT ANTERIOR HEMI BLOCK)
 Arrhythmias other than sustained ventricular tachycardia, including multifocal PVCs, triplets  rS di II, III, aVF
of PVCs, supraventricular tachycardia, heart block, or bradyarrhythmias  q di I, aVL
 Fatigue, shortness of breath, wheezing, leg cramps, or claudication  Aksis: LAD
 Development of bundle-branch block or IVCD that cannot be distinguished from ventricular
tachycardia
 Increasing chest pain
 Hypertensive response  SBP > 250 mmHg and/or DBP > 115 mmHg

GAMBARAN X-RAY
LVH : apex ke lateral dan bawah
RVH : apex ke lateral, terangkat ke atas
LAH : pinggang jantung hilang
RAH : double contour

LPHB (LEFT POSTERIOR HEMI BLOCK)

 rS di I, aVL
 q di II, III, aVF
 Aksis: RAD
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AV BLOCK DERAJAD II  NADI TIDAK TERATUR

Mobitz I  P-P teratur, R-R irregular, drop beat (+), P-R memanjang progresif MEMBEDAKAN VES  RVOT atau LVOT
Mobitz II  P-P teratur, R-R irregular, drop beat (+), PR memanjang tdk progresif All outflow track PVC's will have strong positive deflections in leads II, III and aVF. To distinguish if
the origin is right or left, look to the precordial leads V1 - V3. The LVOT lies posterior to the RVOT.
AV BLOCK TOTAL  NADI TERATUR To reach the positive electrodes of the first three precordial leads, the electrical wavefront must travel
 P-P teratur, R-R regular a greater distance from the LVOT than it wou ld if it originated from the RVOT. This extra distance
causes an R wave to appear in V1 or V2. The more pronounced the R wave in these leads, the more
VENTRIKEL EKSTRA-SISTOLE posterior the origin lies.
 VES frekuen  Most authors use the adjective frequent when there are 5 or more PVCs per
minute on the routine ECG or more than 10 to 30 per hour during ambulatory monitoring (Chou
et al) KRITERIA LVH
 RVOT type  LBBB pattern di V1-V3 Sokolow-Lyon Voltage Criteria
 R wave in lead I + S wave in lead III > 25 mm (2.5 mV)
 R wave in aVL > 11 mm (1.1 mV)
 R wave in V6 > 26 mm (2.6 mV)
 R wave in V6 + S wave in V1 > 35 mm (3.5 mV)
The criteria reportedly have a 49% sensitivity and a specificity of approximately 90%

Cornell Voltage Criteria

S wave in V3 + R wave in aVL > 28 mm (2.8 mV) in men or > 20 mm (2.0 mV) in women; the
sensitivity is approximately 49% and the specificity is approximately 90%

Romhilt-Estes Scoring System

 LVOT type  RBBB pattern di VI-V3  R wave in the limb leads ≥ 20 mm, S wave in lead V1 or V2 ≥ 30 mm, or R wave in lead V5
or V6 ≥30 mm = 3 points
 Negativity of P wave in V1 > 1 mm in depth with duration > 0.03 second = 3 points
 ST-T wave changes (if patient is not taking digoxin) = 3 points (if patient is taking digoxin =
1 point)
 Presence of left axis = 2 points
A score of 4 points indicates probable LVH, and a score of 5 or more points indicates LVH. The
sensitivity is approximately 30% and the specificity is approximately 90%
 8

KRITERIA RVH (GABRIEL KAHN) WOLFF-PARKINSON-WHITE (WPW)

 Right-axis deviation greater than +110 degrees  Serabut Kent
 Tall R wave in V1 ≥ 7 mm (can be a normal variant), S wave in V1 ≤ 2 mm, R/S ratio in V1  Interval PR memendek
> 1, R/S ratio in V5 or V6 ≤ 1  Ada gelombang delta
 S wave in V5 or V6 >2 mm  QRS melebar
 qR pattern in V1 (not commonly observed but increases specificity)  Tx: amiodarone, procainamide; AVOID  AV nodal blocking (CCB, β-blocker, adenosine,
digoxin) terutama pada AF + WPW
LETAK ACCESSORY PATHWAY PADA WPW
 Delta wave di lead V1 dan I, aVL LOWN-GANONG-LEVINE (LGL)
 Positif di V1 dan negatif di I, aVL  LEFT SIDE  Serabut James
 Negatif di V1 dan positif di I, aVL  RIGHT SIDE  Interval PR memendek
 Delta wave di lead III, aVF  Tidak ada gelombang delta
 Positif  anterior, anterolateral, anteroseptal  QRS tidak melebar
 Negatif  posterior, posterolateral, posteroseptal
***Untuk rencana ablasi  amiodarone perlu di stop 2 minggu, sementara digoxin atau β-blocker
cukup 5 hari

SGARBOSSA’S CRITERIA  LBBB / PACED RHYTHM

(1) ST-segment elevation > 1 mm concordant with QRS complex (Score = 5)
(2) ST-segment depression > 1 mm in lead V1, V2 or V3 (Score = 3)
(3) ST-segment elevation > 5 mm discordant with QRS complexe (Score = 2)

Score ≥ 5  sensitivitas (14%) , spesifisitas (100%) untuk diagnosa AMI pada LBBB

TERAPI PSVT
 Isoptin (verapamil) 2 x 40 mg atau Metoprolol 2 x 25 mg

KRITERIA EKOKARDIOGRAFI
 IHD (Ischemic Heart Disease) : gangguan kinetik segmental
 HHD (Hipertensive Heart Disease) : LVH konsentrik

KRITERIA BRUGADA (VENTRIKEL TAKIKARDIA)
a) Absence Of An RS Complex In All Precordial Leads
 This is essentially the same as having positive or negative concordance
 If all the precordial leads consist of either monophasic R or S waves then VT is diagnosed
 If there are any RS complexes present in V1-6 –> move on to the next step of the algorithm
Precordial R wave only  VT
b) RS Interval > 100 ms In One Precordial Lead
 If RS complexes are present in V1-6 then the RS interval is measured
 This is the time from the onset of the R wave to the nadir of the S wave
 If the RS interval is > 100 ms  VT is diagnosed
9
c) AV Dissociation
 The ECG is scrutinised for hidden P waves; these are often superimposed on the QRS
complexes and may be difficult to see.
 If P waves are present at a different rate to the QRS complexes  AV dissociation is
present and VT is diagnosed
d) Morphological Criteria For VT
Leads V1-2 and V6 are assessed for characteristic features of VT. There are two sets of morphological
criteria depending on the appearance of the QRS complex in V1 :
 If there is a dominant R wave in V1  see criteria for RBBB-like morphology
 If there is a dominant S wave in V1  see criteria for LBBB-like morphology
Broad Complex Tachycardia With RBBB Morphology
Appearance in V1-2
With a positive R wave in V1, three patterns are indicative of VT :
 Smooth monophasic R wave
 Notched downslope to the R wave — the taller left rabbit ear (= Marriott’s sign)
 A qR complex (small Q wave , tall R wave) in V1
 10

Appearance in V6 Appearance in V6
In V6, the following patterns are consistent with VT : With a LBBB-like pattern, the presence of Q waves in V6 is indicative of VT. There are two possible
 QS complex – a completely negative complex with no R wave (= strongly suggestive of VT) patterns
 R/S ratio < 1 – small R wave, deep S wave (indicates VT only if LAD is also present)  QS waves in V6 (as with RBBB-like patterns, this finding is very specific for VT)
 qR pattern = small Q wave, large R wave

Broad Complex Tachycardia With LBBB Morphology

Appearance in V1-2
With a dominant S wave in V1, the following three features are diagnostic of VT :
 Initial R wave > 30-40 ms duration
 Notching or slurring of the S wave (Josephson’s sign)
 RS interval (time from R wave onset to S wave nadir) > 60-70 ms
 11

DIGITALISASI (ACLS 2010) CEDOCARD / ISOSORBIDE DINITRATE (1 Ampul  10 ml ≈ 1 mg/ml)

Loading doses: 0,004 to 0,006 mg/kg (4-6 mcg/kg) initially over 5 minutes. Second and third boluses  1 µg/menit ≈ 0,06 mg/jam
2-3 mcg/kg to follow at 4-8 hour interval. Total loading dose 8-12 mcg/kg divided over 8-16 hour
 1 mg/jam ≈ 16,6 µg/menit
 Dosis : 2-10 mg/jam (VENO-DILATOR); dosis > 200 µg/menit (≈ 12 mg/jam) berefek
Acute Rate Control (Book: Clinical Management of AF 2011)
Initial dose: 0.25-0.5 mg IV, followed by 0.25 mg every 4 to 6 hours as required ARTERI-DILATOR
Total dose for IV digitalization: 0.75 to 1.5 mg
Onset of action: 30 to 60 minutes AMIODARONE (1 Ampul  3 cc ≈ 50 mg/ml)
Peak effect: 1 to 6 hours Drip cepat amiodarone 150 mg dalam 30 menit (100 cc/jam)
Dilanjutkan 1 mg/menit selama 6 jam (20 cc/jam)
Chronic Rate Control Dilanjutkan 0,5 mg/menit selama 18 jam (10 cc/jam)
 Rapid oral digitalization  menyebabkan fibrosis paru setelah pemakaian > 6 bulan
 Initial dose: 0.5 mg PO, followed by 0.25 or 0.5 mg every 6 hours  kombinasi digoxin + amiodarone akan memperpanjang repolarisasi (Long QT)
 Total dose for oral digitalization: 1 to 2 mg
 Follow with maintenance dose of 0.125 to 0.25 mg daily DOPAMIN (1 Vial  5 ml ≈ 40 mg/ml)
 Slow digitalization: Dosis : …. mcg/kgBB/menit
 0.125 to 0.25 mg PO daily 1 mcg = (1 x BB x 60) / 4000 = …. cc/jam
 Steady state achieved after 7 to 10 days
 Hal-life 36 to 48 hours in patients with normal kidney function DOBUTAMINE (1 Vial  5 ml ≈ 250 mg)
Dosis : …. mcg/kgBB/menit
METOPROLOL FOR RATE CONTROL OF AF 1 mcg = (1 x BB x 60) / 5000 = …. cc/jam
 Acute rate control: 2.5-5.0 mg IV over 2 minutes; may repeat every 5 minutes up to 15 mg
total ENOXAPARINE (LOVENOX)  syringe 60 mg/0,6 ml
 Chronic rate control: 50-200 mg/day PO in 2 to 3 divided doses  Usia < 75 tahun
 Peak effect: 20 minutes (IV), 1.5 to 4 hours (PO)  30 mg bolus IV diikuti 1 mg/kg SC tiap 12 jam (dosis SC pertama kali diberikan segera
 Plasma half-life 3 to 7 hours setelah bolus IV)
 Usia ≥ 75 tahun
DILTIAZEM DOSE  0,75 mg/kg SC tiap 12 jam tanpa dosis inisial bolus IV
Acute Rate Control  Impaired renal function (CCT < 30 ml/min)
 15-20 mg (0.25 mg/kg) IV over 2 minutes  1 mg/kg SC 1 x per-hari atau dapat menggunakan UFH
 May give another IV dose in 15 minutes at 20-25 mg (0.35 mg/kg) over 2 minutes
FONDAPARINUX (ARIXTRA)
Maintenance Infusion Initially 2,5 mg IV diikuti 2,5 mg SC 1 x per-hari direkomendasikan untuk pasien STEMI yang
5-15 mg / jam titrasi hingga HR yang ingin dicapai mendapatkan trombolitik (streptase) dengan crea < 3 mg/dL. Kontraindikasi: CCT < 20 ml/min)
 12

UFH  (1 Vial  5 ml ≈ 5000 iu/ml)

STEMI
 Initial bolus 60 U/kg (max bolus 4000 U)
 Continue 12 U/kg/jam, round to the nearest 50 U (max 1000 U/jam)
 Adjust to maintain aPTT 1,5-2 x control (50-70 detik) selama 48 jam or until angiography
 Check initial aPTT at 3 hours, then every 6 hours until stable, then daily
 Platelet count daily

UAP / NSTEMI
 Initial bolus 60 U/kg (max 4000 U)
 Continue 12 U/kg/jam, max 1000 U/jam

PRADAXA (DARBIGATRAN)
Dosis  tergantung HASBLED
Low risk : 2 x 150 mg
High risk : 2 x 110 mg

Dopamin
 < 2 mcg/kg/menit : dosis renal
 2-10 mcg/kg/menit : inotropik
 >10 mcg/kg/menit : vasokonstriktor
 13

REVISED CARDIAC RISK INDEX PERBEDAAN CCB

Efek Dihidropiridine Non-dihidropiridine
1. High-risk surgical procedures Vasodilator +++ (potent) + (less potent)
 Intraperitoneal Negative effect on Little or no effect Greater depressive effect
 Intrathoracic cardiac contractility
 Suprainguinal vascular Anti-ischemic + +++
2. History of ischemic heart disease
 History of myocardial infarction Little cardiac depressant activity  nicardipine, nifedipine GITS, felodipine
 History of positive exercise test No cardiac depressant activity  amlodipine, lacidipine
 Current complain of chest pain considered secondary to myocardial ischemia
 Use of nitrate therapy Nicardipine Diltiazem Verapamil
 ECG with pathological Q waves (dihidropiridine) (benzothiazepine) (phenylalkylamine)
3. History of congestive heart failure Peripheral +++++ +++ +++
 History of congestive heart failure vasodilatation
 Pulmonary edema Coronary +++++ +++ ++++
 Paroxysmal nocturnal dyspnea vasodilatation
 Bilateral rales or S3 gallop Suppression of SA + +++++ +++++
 Chest radiograph showing pulmonary vascular redistribution Node
4. History of cerebrovascular disease Supression of AV 0 ++++ +++++
 History of transient ischemic attack or stroke Node
5. Preoperative treatment with insulin
Supression of 0 ++ ++++
6. Preoperative serum creatinine > 2.0 mg/dL
Cardiac Contractility

Risk of Major Cardiac Event

KONDISI-KONDISI DIMANA TROPONIN DAPAT MENINGKAT
Points Class Risk
 Chronic / Acute Renal Dysfunction
0 I 0.4%
 Severe CHF – acute and chronic
1 II 0.9%
 Hypertensive crisis
2 III 6.6%
 Tachy- or bradyarrhytmias
3 or more IV 11%
 Pulmonary embolism, severe pulmonary hypertension
 Inflammatory disease (myocarditis), burn ( > 30% body surface area)
"Major cardiac event" includes myocardial infarction, pulmonary edema, ventricular
 Acute neurological state (stroke, SAH)
fibrillation, primary cardiac arrest, and complete heart block
 Aortic dissection, aortic valve disease or HCOM, rhabdomyolisis
 Cardiac contusion, ablation, pacing, cardioversion or endomyocardial biopsy
 Infiltrative disease (amyloidosis, sarcoidosis, haemochromatosis, scleroderma)
 Critically ill patient (respiratory failure, sepsis)

SEVERITY OF HEART FAILURE IN THE CONTEXT OF ACS
KILLIP Classifications  Designed to provide a clinical estimate of the severity of circulatory
derangement in the treatment of acute myocardial infarction
 Stage I No heart failure
No clinical signs of cardiac decompensation
 Stage II Heart failure
Diagnostic criteria include rales, S3 gallop, and pulmonary venous hypertension.
Pulmonary congestion with wet rales in the lower half of the lung fields.
 Stage III Severe heart failure
Frank pulmonary oedema with rales throughout the lung fields
 Stage IV Cardiogenic shock
Signs include hypotension (SBP < 90 mmHg), and evidence of peripheral vasoconstriction such
as oliguria, cyanosis and sweating
FORRESTER Classification  Designed to describe clinical and haemodynamic status in acute
myocardial infarction
 Normal perfusion and pulmonary wedge pressure (PCWP - estimate of left atrial pressure)
 Poor perfusion and low PCWP (hypovolaemic)
 Near normal perfusion and high PCWP (pulmonary oedema)
 Poor perfusion and high PCWP (cardiogenic shock)
14
ACE-INHIBITOR  ESC GUIDELINES 2008
Indications :
LVEF ≤ 40%, irrespective of symptoms
Contraindications :
 History of angioedema
 Bilateral renal artery stenosis
 Serum potassium concentration > 5.0 mmol/L
 Serum creatinine > 220 µmol/L (≈ 2.5 mg/dL)
 Severe aortic stenosis
Potential adverse effects :
 Worsening renal function - some rise in urea (BUN) and creatinine is expected after initiation
of an ACEI and is not considered clinically important unless rapid and substantial. Check for
nephrotoxic drugs such as non-steroidal anti-inflammatory drugs (NSAIDs). If necessary,
reduce ACEI dose or discontinue. An increase in creatinine of up to 50% from baseline or to
an absolute concentration of 265 µmol/L (3 mg/dL), whichever is lower, is acceptable. If the
creatinine rises above 265 µmol/L (3.0 mg/dL), but below 310 µmol/L (3.5 mg/dL), halve
dose of ACEI and monitor blood chemistry closely. If creatinine rises to 310 µmol/L (3.5
mg/dL) or above, stop ACEI immediately and monitor blood chemistry closely.
 Hyperkalaemia - check for use of other agents causing hyperkalaemia, e.g. potassium
supplements and potassium-sparing diuretics, e.g. amiloride, and stop. If potassium rises
above 5.5 mmol/L, halve dose of ACEI and monitor blood chemistry closely. If potassium
rises over 6.0 mmol/L, stop ACEI immediately and monitor blood chemistry closely.
 Symptomatic hypotension (e.g. dizziness) is common - often improves with time, and patients
should be reassured. Consider reducing the dose of diuretics and other hypotensive agents
(except ARB/β-blocker/aldosterone antagonist). Asymptomatic hypotension does not require
intervention.
 Cough - if an ACEI causes a troublesome cough, switch to an ARB
*** Penggunaan ACE-I pada gagal ginjal  evaluasi creatinin 2 minggu, jika terjadi peningkatan >
20%  stop ACE-I. Bisa diganti kombinasi Hidralazine + Nitrat
 15

β-BLOCKERS closely. If creatinine rises to > 310 mmol/L (3.5 mg/dL) stop spironolactone (or eplerenone)
Indications : immediately and monitor blood chemistry closely; specific treatment of renal dysfunction may
 LVEF ≤ 40% be needed.
 Mild to severe symptoms (NYHA functional class II–IV); patients with asymptomatic LV  Breast tenderness and/or enlargement - switch from spironolactone to eplerenone
systolic dysfunction after MI also have an indication for a b-blocker
 Optimal dose level of an ACEI or/and ARB (and aldosterone antagonist, if indicated)
 Patients should be clinically stable (e.g. no recent change in dose of diuretic) DIGOXIN
In patients with symptomatic HF and AF, digoxin may be used to slow a rapid ventricular rate. In patients with AF
Contraindications : and an LVEF ≤ 40% it should be used to control heart rate in addition to, or prior to a b-blocker.
 Asthma [COPD is not a contraindication]
 Second or third degree heart block, sick sinus syndrome (in the absence of a permanent Class of recommendation I, level of evidence C
pacemaker), sinus bradycardia( < 50 bpm) In patients in sinus rhythm with symptomatic HF and an LVEF ≤ 40%, treatment with digoxin (in addition to an
ACEI) improves ventricular function and patient well-being, reduces hospital admission for worsening HF, but has
no effect on survival.
Potential adverse effects :
 Symptomatic hypotension
Class of recommendation IIa, level of evidence B
 Worsening HF
Digoxin in patients with HF and atrial fibrillation
 Excessive bradycardia
 Digoxin is useful for initial control of the ventricular rate in a patient with rapid AF and may be
considered in decompensated HF patients prior to initiation of a b-blocker
ALDOSTERONE ANTAGONIST  In the longer term, a b-blocker, either alone or in combination with digoxin, is the preferred treatment
Indications : for rate control (and other clinical outcome benefits) in patients with an LVEF ≤ 40%
 LVEF ≤ 35%  While digoxin alone may control the ventricular rate at rest (target < 80 bpm), it does not usually provide
 Moderate to severe symptoms (NYHA functional class III–IV) sufficient rate control during exercise (target heart rate ≤ 110–120 bpm)
 Optimal dose of a b-blocker and an ACEI or an ARB (but not an ACEI and an ARB)  In patients with an LVEF > 40%, verapamil or diltiazem may be used alone or in combination with
digoxin to control the ventricular rate

Contraindications :
 Serum potassium concentration > 5.0 mmol/L Digoxin in patients with HF, LVEF ≤ 40%, and sinus rhythm
 Treatment with digoxin did not alter all-cause mortality but did lead to an RRR for hospital admission
 Serum creatinine > 220 mmol/L (2.5 mg/dL)
for worsening HF
 Concomitant potassium sparing diuretic or potassium supplements
 Digoxin can cause atrial and ventricular arrhythmias, particularly in the context of hypokalaemia
 Combination of an ACEI and ARB

Indications :
Potential adverse effects :
 Atrial fibrillation
 Hyperkalaemia - if potassium rises to .5.5 mmol/L, halve dose of spironolactone (or
With ventricular rate at rest > 80 bpm, at exercise > 110-120 bpm
eplerenone), e.g. to 25 mg on alternate days, and monitor blood chemistry closely. If potassium
 Sinus rhythm
rises to 6.0 mmol/L stop spironolactone (or eplerenone) immediately and monitor blood
 LV systolic dysfunction (LVEF ≤ 40%)
chemistry closely; specific treatment of hyperkalaemia may be needed.
 Mild to severe symptoms (NYHA functional class II–IV)
 Worsening renal function - if creatinine rises to> 220 mmol/L (2.5 mg/dL) halve dose of
 Optimal dose of ACEI or/and an ARB, b-blocker and aldosterone antagonist, if indicated
spironolactone (or eplerenone), e.g. to 25 mg on alternate days, and monitor blood chemistry
 16

Contraindications : PROBABLE ST
 Second- or third-degree heart block (without a permanent pacemaker); caution if suspected Clinical definition of probable ST is diagnosed after intracoronary stenting in the following cases :
sick sinus syndrome  Any unexplained death within the first 30 d
 Pre-excitation syndromes  Regardless of the time after the index procedure, any MI that is related to documented acute
 Previous evidence of digoxin intolerance ischemia in the territory of the implanted stent without angiographic confirmation of ST and
in the absence of any other obvious cause
Potential adverse effects :
 Sinoatrial and AV block POSSIBLE ST
 Atrial and ventricular arrhythmias, especially in the presence of hypokalaemia (digoxin- Clinical definition of possible ST is diagnosed with any unexplained death from 30 day after
specific Fab antibody fragments should be considered for ventricular arrhythmias caused by intracoronary stenting until the end of trial follow-up
toxicity)
 Signs of toxicity include: confusion, nausea, anorexia, and disturbance of colour vision TIME FRAME OF STENT THROMBOSIS
≤ 1 hari : Acute stent thrombosis
CATH LAB > 1 hari - 1 bulan : Subacute stent thrombosis
Proyeksi coronografi : > 1 bulan – 1 tahun : Late stent thrombosis
RAO 10 CRAN 30 : batang LAD > 1 tahun : Very late stent thrombosis
RAO 20 CAUD 20 : batang LCx
LAO 45 CRAN 25 : LAD (view lain) FAKTOR RESIKO STENT THROMBOSIS
LAO CAUD (SPIDER) : LM, pangkal LAD dan LCx Patient factors Procedural factors
LAO 30 CRAN 15 : RCA  Thickness and robustness of neointimal  Dissection
stent coverage  Incomplete stent apposition
STENT THROMBOSIS (ST)  Drug response/interactions  Stent expansion
 Gene polymorphism Lesion factors
DEFINITE ST  Left ventricular function  Vessel size
Definite stent thrombosis is diagnosed when either angiographic or pathological confirmation is present  Acute coronary syndrome  Lesion length
 Renal failure  Thrombus
Angiographic confirmation of ST  Diabetes mellitus  Plaque characteristics
The presence of a thrombus originating in the stent or in the segment 5 mm proximal or distal to the Antithrombotic and anticoagulation therapy  Bifurcation
stented region and at least one of the following criteria within a 48-h time window :  Coagulation activity Device factors
 Acute onset of ischemic symptoms at rest (typical chest pain > 20 min)  Inhibition of platelet aggregation  Stent surface
 New ischemic ECG changes suggestive of acute ischemia  Drugs
 Typical rise and fall in cardiac biomarkers  Polymer
*** Jika terjadi stent thrombosis  tanpa adanya ST elevasi (EKG)  tidak perlu reperfusi segera
Pathological confirmation of stent thrombosis  Tx: Aspilet 1 x 160 dan CPG 2 x 75, heparinisasi (bila perlu). Jika ada ST elevasi  reperfusi
Evidence of recent thrombus within the stent determined at autopsy dgn trombolitik atau PCI (seperti pada STEMI)
 17

ISR (IN STENT RESTENOSIS) PIAT (PERCUTANEOUS INTRA-ARTERIAL THROMBOLYSIS)

3 hal yang perlu dilacak : Tata cara :
 Optimalisasi terapi ??  Pendahuluan : bolus heparin 5000 unit [tidak perlu jika sudah on-heparin]
 Jenis stent ??  Streptokinase [intra arterial] dengan dosis:
 Resistensi obat yang digunakan ?? Bolus awal 200.000 unit [selama 10 menit]
FLOW RATIO [Qp/Qs] Lanjutkan maintenance 100.000 unit / jam  selama 12 jam
Metode FICK  Qp/Qs = (SAO2 – MVO2) / (PVO2 – PAO2)  Drip heparin 500 unit / jam IV  bersamaan dengan drip streptokinase
Mixed Vein  (3 SVC + 1 IVC) / 4  Post tindakan:
** Jika flow ratio ≥ 1.5  HIGH FLOW Allupurinol 3 x 1 tablet
Bicnat tablet 3 x 500 mg
PARI (PULMONARY ARTERIAL RESISTANCE INDEX)  Arteriografi evaluasi 12 jam kemudian
Rumus: {(mPA – mLA) x [(PV – PA) / 100] x Hb x 13,6} / O2 consumption
** Jika PARI ≥ 7  HIGH RESISTANCE Cara meracik Streptase :
 Ambil 1 vial streptase [1,5 juta unit]  tambahkan dgn 5 cc NaCl
WILKINS SCORE  Bagi menjadi 2 spuit dalam 3 cc @ 2,5 cc [2,5 cc ≈ 750.000]
** Jika score < 8  kandidat baik untuk dilakukan BMV  Untuk bolus awal 200.000 unit  ambil 0,65 cc [dari spuit 3 cc pertama]
 Untuk dosis maintenance 100.000 unit / jam  spuit 3 cc kedua [isi 2,5 cc ≈ 750.000 unit]
masukkan ke dalam spuit 50 cc [syring pump]  drip 6,6 cc / jam  selama 12 jam
 Untuk maintenance selama 12 jam butuh ≈ 80 cc [2 x ganti syring pump]
 Ambil 1,5 cc streptase pd spuit pertama [isi 1,5 cc ≈ 450.000 unit]  masukkan dalam spuit
50 cc [syring pump]  drip 11,1 cc / jam

Kontra-indikasi PIAT
Absolute:
 Established cerebrovascular event (including transient ischemic attacks within last 2 month)
 Active bleeding diathesis
 Recent gastrointestinal bleeding (< 10 day)
 Neurosurgery (intracranial, spinal) within last 3 month
 Intracranial trauma within last 3 month

Relative major:
 Cardiopulmonary resuscitation within last 10 day
 Major nonvascular surgery or trauma within last 10 day
 Uncontrolled hypertension: > 180 mm Hg systolic or > 110 mm Hg diastolic
 Puncture of noncompressible vessel
 Intracranial tumor
 Recent eye surgery
 18

Minor:
 Hepatic failure, particularly those with coagulopathy
 Bacterial endocarditis
 Pregnancy
 Diabetic hemorrhagic retinopathy

WELLS SCORE FOR DVT

Clinical Feature Score
Active Cancer 1
Paralysis, paresis, or recent plaster immobilization of the lower extremity 1
Recently bedridden for more than 3 days or major surgery within 4 weeks 1
Localized tenderness along the distribution of the deep venous system 1
Entire leg swollen 1
Calf swelling by more than 3 cm when compared with the asymptomatic leg 1
Pitting edema (greater in symptomatic leg) 1
Collateral superficial veins (nonvaricose) 1
Previously documented DVT 1
Alternative diagnosis as likely or more possible than that of DVT -2
Probability: High ≥ 3; Moderate 1-2; and Low < 1
PERBEDAAN ALI VS DVT
WELLS SCORE FOR PE ALI DVT
Clinical Feature Score Thrombogenesis Chronic (years) Acute (days/weeks/months)
Clinical signs and symptoms of DVT +3 Virchow triad Vessel dominance Stasis and hypercoagulability
PE is # 1 diagnosis, or equally likely +3 dominance
Heart rate > 100 +1,5 Sign 5P (pain, pale, paraesthesia, Pain, unilateral edema,
Immobilization at least 3 days, or surgery in the previous 4 weeks +1,5 pulseless, paralysis) tenderness, warmth
Previous, objectively diagnosed PE or DVT +1,5 Main treatment Anti-pletelet Anti-coagulant/heparin
Hemoptysis +1 for prevention
Malignancy with treatment within 6 month or palliative +1
Probability: High > 6; Moderate 2-6; Low < 2 Proses pembentukan trombus pada DVT dimulai pd daerah dengan alian darah vena yang lambat, di
daerah yang mengalami aliran turbulensi seperti daerah di sekitar katup vena atau daerah vena yang
langsung mengalami trauma. Trombus yang terbentuk terdiri dari fibrin, eritrosit, leukosit dan
trombosit. Trombus DVT terdiri dari dua tipe : tipe pertama, komposisinya didominasi oleh benang
fibrin dan eritrosit sehingga sering disebut sebagai trombus merah dan tipe kedua, komposisinya
didominasi oleh trombosit sehingga sering disebut sebagai trombus putih. Trombus tipe pertama lebih
sering ditemukan pada trombus yang menempel pada dinding pembuluh darah vena, sedang trombus
 19

tipe kedua lebih sering sering ditemukan di daerah yang lebih distal. Temuan tersebut memperkuat FAKTOR RISIKO VTE (TRIAS VIRCHOW)
dugaan bahwa pada trombogenesis vena aktivitas faktor prokoagulan berperan lebih besar dari pada Stasis Hiperkoagulabilitas Kerusakan endotel
faktor trombosit. Disamping itu, hal ini juga dapat menjelaskan mengapa obat-obat anti-trombosit Usia > 40 tahun Kadar estrogen tinggi Bedah
mempunyai peran yang tidak signifikan dalam mencegah atau mengobati trombus vena (JOHAN Imobilitas Kanker VTE sebelumnya
KURNIANDA) Gagal jantung kongestif Peradangan usus Pemasangan jalur vena
Stroke Sindrom nefrotik sentral
Paralisis Sepsis Trauma
Cedera spinal Merokok
Hiperviskositas Kehamilan
Polisitemia Trombofilia
PPOK berat
Anesthesia
Obesitas

TROMBOLISIS FOR PE
Streptokinase 250.000 IU as a loading dose over 30 min, followed by 100.000
IU/h over 12-24 h
Accelerated regimen: 1.5 million IU over 2 h
Urokinase 4400 IU/kg as a loading dose over 10 min, followed by 4400
IU/kg/h over 12-24 h
rtPA 100 mg over 2 h
or 0.6 mg/kg over 15 min (max dose 50 mg)

ANTIKOAGULAN UNTUK TERAPI PE (ESC GUIDELINES 2008)

 UFH
Dosis: 80 U/kg (bolus) dilanjutkan infus 18 U/kg/jam, target APTT 1,5-2,5 x kontrol. Terutama
pilihan pada gangguan ginjal (CCT < 30 ml/menit) dan high risk utk terjadi perdarahan (efek
antikoagulannya cepat reversible). Dosis UFH ini bisa digunakan juga untuk terapi DVT
 Enoxaparin
Dosis: 1.0 mg/kg atau 1.5 mg/kg tiap 12 jam
 Fondaparinux
5 mg (BB < 50 kg) 1 x sehari
7.5 mg (BB 50-100 kg) 1 x sehari
10 mg (BB > 100 kg) 1 x sehari
 20

CRITICAL LIMB ISCHEMIA STAGING UNTUK PAD

Critical limb ischaemia is the most severe clinical manifestation of LEAD, defined as the presence of Fontaine classification Rutherford classification
ischaemic rest pain, and ischaemic lesions or gangrene objectively attributable to arterial occlusive Stage Symptoms  Grade Category Symptoms
disease (ESC Guidelines 2011) I Asymptomatic  0 0 Asymptomatic
Critical limb ischemia (CLI) is a manifestation of peripheral artery disease (PAD) that describes patients I 1 Mild claudication
with chronic ischemic rest pain, foot and leg ulcers, or gangrene. CLI should only be used to describe I 2 Moderate
patients who have chronic ischemic disease, which is defined as the presence of symptoms for more II Intermittent  claudication
than 2 weeks. The chronicity of CLI distinguishes the condition from acute limb ischemia, which is claudication I 3 Severe claudication
defined as a quickly developing or sudden decrease in limb perfusion (TASC II) III Ischaemic rest  II 4 Ischaemic rest pain
pain
KLASIFIKASI KATEGORI KLINIS ALI (RUTHERFORD) IV Ulceration or  III 5 Minor tissue loss
Grade Category Sensory loss Motor deficit Prognosis gangrene III 6 Major tissue loss
I Viable None None No immediate
threat
IIA Marginally None or None Salvageable if ALGORITME MANAGEMENT ALI
threatened minimal (toes) promptly treated
IIB Immediately More than toes Mild / moderate Salvageable if
threatened promptly
revascularized
III Irreversible Profound, Profound, Major tissue loss
anaesthetic paralysis (rigor) Amputation
Permanent nerve
damage inevitable

ABI (ANKLE-BRACHIAL INDEX)

The primary non-invasive test for the diagnosis of LEAD is the ABI. In healthy persons, the ABI is >
1.0. Usually an ABI < 0.90 is used to define LEAD. For diagnosis in primary care, an ABI < 0.8 or the
mean of three ABIs < 0.90 had a positive predictive value of ≥ 95%; an ABI > 1.10 or the mean of three OBAT-OBATAN UNTUK ALI ATAU CLI
ABIs > 1.00 had a negative predictive value of ≥ 99%. The level of ABI also correlates with LEAD  Aspilet 1 x 80
severity, with high risk of amputation when the ABI is < 0.50. An ABI change > 0.15 is generally  Plavix 1 x 75
required to consider worsening of limb perfusion over time, or improving after revascularization.  Simvastatin / Atorvastatin
 Cilostazol (Pletaal) 50 mg/hari atau 100 mg/hari  Phosphodiesterase -3 inhibitor,
kontraindikasi: HEART FAILURE, karena dapat mengakibatkan aritmia letal (VT, VF)
 Disolf (Lumbrokinase) 3 x 2 tablet
 21

ACLS Lidocaine may be considered if amiodarone is not available (Class IIb, LOE B). The initial dose is 1
to 1.5 mg/kg IV. If VF/pulseless VT persists, additional doses of 0.5 to 0.75 mg/kg IV push may be
administered at 5- to 10-minute intervals to a maximum dose of 3 mg/kg.

When VF/pulseless VT cardiac arrest is associated with torsades de pointes, providers may administer
an IV/IO bolus of magnesium sulfate at a dose of 1 to 2 g diluted in 10 mL D5W (Class IIb, LOE C).

DC Shock  120-200 J (Biphasic); 360 J (Monophasic)

Amiodarone  First dose: 300 mg bolus, second dose: 150 mg
Reversible Cause  5H (Hypovolemia, Hypoxia, Hydrogen ion / acidosis, Hypo/hyperkalemia,
Hypothermia); 5T (Tension pneumothorax, Tamponade cordis, Toxins, Thrombosis pulmonary,
Thrombosis coronary)
 22

RISK SCORE IN PREGNANCY (CARPREG)

CARPREG risk score: for each CARPREG predictor that is present a point is assigned. Risk
estimation of cardiovascular maternal complications :
0 point 5%
1 point 27%
> 1 point 75%
Indikator:
 Prior cardiac event (heart failure, transient ischaemic attack, stroke before pregnancy or
arrhythmia)
 Baseline NYHA functional class > II or cyanosis
 Left heart obstruction (mitral valve area < 2 cm2, aortic valve area < 1.5 cm2, peak LV outfow
tract gradient >30 mmHg by echocardiography)
 Reduced systemic ventricular systolic function (ejection fraction < 40%)

PERIPARTUM CARDIOMYOPATHY (PPCM)

PPCM is an idiopathic cardiomyopathy presenting with heart failure secondary to LV systolic
dysfunction towards the end of pregnancy or in the months following delivery (develop during the last
month of pregnancy or within 5 months of delivery). It is a diagnosis of exclusion when no other cause
of heart failure is found. The LV may not be dilated, but the EF is nearly always reduced below 45%
(ESC Guidelines 2011)

Terapi:
During pregnancy, ACE inhibitors, ARBs, and renin inhibitors are contraindicated because of
fetotoxicity. When ACE inhibitors are needed during breast feeding, benazepril, captopril, or enalapril
should be preferred. Hydralazine and nitrates can be used instead of ACE inhibitors/ARBs for afterload
reduction. Dopamine and levosimendan can be used if inotropic drugs are needed. β-blocker treatment
is indicated for all patients with heart failure, if tolerated. β1-selective drugs (i.e. metoprolol) should be
preferred. Atenolol should not be used. Newborns should be supervised for 24–48 h after delivery to
exclude hypoglycaemia, bradycardia, and respiratory depression. Diuretics should only be used if
Synchronized Cardioversion pulmonary congestion is present since they may decrease blood flow over the placenta. Furosemide and
Initial recommended doses : hydrochlorothiazide are most frequently used. Aldosterone antagonists should be avoided.
 Narrow regular: 50-100 J Spironolactone can be associated with antiandrogenic effects in the first trimester.
 Narrow irregular: 120-200 J biphasic or 200 J monophasic
 Wide regular: 100 J
 Wide irregular: defibrillation dose (NOT synchronized)
 23

HIPERTENSI DALAM KEHAMILAN (ESC GUIDELINES 2011)

The definition of hypertension in pregnancy is based on absolute BP values (SBP ≥ 140 mmHg or
DBP ≥ 90 mmHg), and distinguishes mildly (140–159/90–109 mmHg) or severely (≥ 160/110 mmHg)
elevated BP, in contrast to the grades used by the European Society of Hypertension (ESH)/ESC or
others. Hypertension in pregnancy is not a single entity but comprises:
 pre-existing hypertension
 gestational hypertension
 pre-existing hypertension plus superimposed gestational hypertension with proteinuria
 antenatally unclassifiable hypertension

Terapi:
Women with pre-existing hypertension may continue their current medication except for ACE
inhibitors, ARBs, and direct renin inhibitors, which are strictly contraindicated in pregnancy because
of severe fetotoxicity, particularly in the second and third trimesters. α-Methyldopa is the drug of
choice for long-term treatment of hypertension during pregnancy. The α-/β-blocker labetalol has
efficacy comparable with methyldopa. If there is severe hypertension it can be given i.v. Metoprolol is
also recommended. Calcium channel blockers such as nifedipine (oral) or isradipine (i.v.) are drugs of
second choice for hypertension treatment. Diuretics should be avoided for treatment of hypertension
because they may decrease blood flow in the placenta.

SYNCOPE (ESC GUIDELINES 2009)

Syncope is a T-LOC due to transient global cerebral hypoperfusion characterized by rapid onset, short
duration, and spontaneous complete recovery.

Klasifikasi Syncope :
 Reflex (neutrally-mediated) syncope  vasovagal, situasional, carotid sinus syncope
 Syncope due to orthostatic hypotension  primary autonomic failure, secondary autonomic
failure, drug-induced orthostatic hypotension, volume depletion
 Cardiac syncope (cardiovascular)  arrhythmias (bradycardia / tachycardia), structural
disease (cardiac like AMI, tamponade, cardiac masses, etc; others like PE, acute aortic
dissection, pulmonary hypertension)
 24

PRESENTASI KLINIS ACUTE HEART FAILURE CHA2DS2-VASc

 Worsening or decompensated chronic HF  Skor untuk resiko terjadinya stroke pada AF non-valvular. Indikator :
 Pulmonary oedema Congestive Heart Failure / LV dysfunction 1
 Hypertensive HF Hypertension 1
 Cardiogenic shock Age ≥ 75 2
 Isolated right HF Diabetes mellitus 1
 ACS and HF Stroke / TIA / thrombo-embolism 2
Vascular disease 1
ATRIAL FIBRILASI Age 65-74 1
Types of AF : Sex category (female) 1
 Every patient who presents with AF for the first time is considered a patient with first
diagnosed AF, irrespective of the duration of the arrhythmia or the presence and severity of Risk category CHA2DS2-VASc Recommended anti-thrombotic
AF-related symptoms. therapy
 Paroxysmal AF is self-terminating, usually within 48 h. Although AF paroxysms may One major risk factor or ≥ ≥2 OAC (INR: 2-3)
continue for up to 7 days, the 48 h time point is clinically important - after this the likelihood 2 clinically relevant non-
of spontaneous conversion is low and anticoagulation must be considered. major risk factor
 Persistent AF is present when an AF episode either lasts longer than 7 days or requires One clinically relevant non 1 Either OAC or aspirin 75-325 mg
termination by cardioversion, either with drugs or by direct current cardioversion (DCC). major risk factor daily. Prefered: OAC rather than
 Long-standing persistent AF has lasted for ≥ 1 year when it is decided to adopt a rhythm aspirin
control strategy. No risk factor 0 Either aspirin 75-325 mg daily or
 Permanent AF is said to exist when the presence of the arrhythmia is accepted by the patient no anti-thrombotic therapy.
(and physician). Hence, rhythm control interventions are, by definition, not pursued in patients Preferred: no anti-thrombotic
with permanent AF. Should a rhythm control strategy be adopted, the arrhythmia is therapy rather than aspirin
redesignated as “longstanding persistent AF”
Major risk factor  previous stroke, TIA, or systemic embolism, age ≥ 75 years
STROKE RISK ASSESMENT IN AF (CHADS2) Clinically relevant non-major risk factor  heart failure or moderate to severe LV systolic
C - Recent Cardiac Failure 1 dysfunction (LV EF ≤ 40%), hypertension, diabetes mellitus, female sex, age 65-74 years, vascular
H - Hypertension 1 disease
A - Age ≥ 75 1
D - Diabetes 1 **patients with paroxysmal AF should receive OAC according to their risk score
S - Prior Stroke or TIA 2
Treatment: Score 0  ASA alone; Score 1  ASA or warfarin (INR 2-3); Score ≥ 2  Warfarin
(INR 2-3)
 25

HASBLED SCORE DUKE CRITERIA FOR IE

It would seem reasonable to use the HAS-BLED score to assess bleeding risk in AF patients, whereby Major Criteria
a score of ≥ 3 indicates ‘high risk’, and some caution and regular review of the patient is needed Blood cultures positive for IE
following the initiation of antithrombotic therapy, whether with VKA or aspirin.  Typical microorganisms consistent with IE from two separate blood cultures:
Viridans streptococci, Streptococcus bovis, HACEK group, Staphylococcus aureus; or
Letter Clinical charasteristic Point awarded Community-acquired enterococci, in the absence of a primary focus
H Hypertension 1  Microorganisms consistent with IE from persistently positive blood cultures:
A Abnormal renal and liver function (1 point each) 1 or 2 At least two positive blood cultures of blood samples drawn > 12 h apart; or
S Stroke 1 All of three or a majority of ≥ 4 separate cultures of blood (with first and last sample drawn at
B Bleeding 1 least 1 h apart)
L Labile INRs 1  Single positive blood culture for Coxiella burnetii or phase I IgG antibody titer > 1:800
E Elderly (e.g. age > 65 years) 1
D Drugs or alcohol (1 point each) 1 or 2 Evidence of endocardial involvement
 Echocardiography positive for IE
“Hypertension” is defined as systolic blood pressure > 160 mmHg. “Abnormal kidney function” is Vegetation – Abscess – New partial dehiscence of prosthetic valve
defined as the presence of chronic dialysis or renal transplantation or serum creatinine ≥ 200 µmol/L.  New valvular regurgitation
“Abnormal liver function” is defined as chronic hepatic disease (e.g. cirrhosis) or biochemical
evidence of significant hepatic derangement (e.g. bilirubin > 2 x upper limit of normal, in association Minor Criteria
with aspartate aminotransferase/alanine aminotransferase/alkaline phosphatase > 3 x upper limit  Predisposition: predisposing heart condition, injection drug use
normal, etc.). “Bleeding” refers to previous bleeding history and/or predisposition to bleeding, e.g.  Fever: temperature > 380C
bleeding diathesis, anaemia, etc. “Labile INRs” refers to unstable/high INRs or poor time in  Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm,
therapeutic range (e.g. < 60%). “Drugs/alcohol” use refers to concomitant use of drugs, such as intracranial haemorrhages, Janeway lesions
antiplatelet agents, non-steroidal anti-inflammatory drugs, or alcohol abuse, etc.  Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots, rheumatoid factor
 Microbiological evidence: positive blood culture but does not meet a major criterion or
ANTIBIOTIC PROPHYLAXIS FOR IE  GUIDELINES ESC 2009 serological evidence of active infection with organism consistent with IE
Antibiotic prophylaxis should only be considered for patients at highest risk of IE
 Patients with a prosthetic valve / prosthetic material used for cardiac valve repair Diagnosis of IE is:
 Patients with previous IE DEFINITE  2 major criteria, or 1 major and 3 minor criteria, or 5 minor criteria
 Patients with congenital heart disease POSSIBLE  1 major and 1 minor criteria, or 3 minor criteria
 Cyanotic congenital heart disease, without surgical repair, or with residual defects, palliative
shunts or conduits
 Congenital heart disease with complete repair with prosthetic material whether placed by
surgery or by percutaneous technique, up to 6 months after the procedure
 When a residual defects persists at the site of implantation of a prosthetic material or device
by cardiac surgery or percutaneous technique
Antibiotic prophylaxis is no longer recommended in other forms of valvular or congenital heart
disease
 26

HIPERKALEMIA What sort of conditions can lead to vagally mediated bradyarrhythmias ?

5,5 – 6,5 Tall peaked T waves Increases in vagal tone can occur secondary to physiological or pathological conditions. Extreme fitness
6,5 – 7,5 Loss of P waves can result in increased vagal tone, resulting in bradycardia. This is usually seen in elite athletes.
7,0 – 8,0 Widening of QRS complexes Pathological conditions that increase vagal tone include chronic respiratory diseases (that exaggerate
8,0 – 10 Sine wave, ventricular arrhythmias, the respiratory phasic variations in vagal tone), primary CNS disorders (brain tumors),
asystole gastrointestinal disorders, and some endocrine conditions (Addison's Disease).

What does an abnormal response to an atropine response test mean ?

There are 2 general causes for suboptimal responses to an atropine response test:
 The atropine dose was insufficient to abolish vagal tone. This could be due to technical error
(i.e., the dose was miscalculated, the dose was administered incorrectly), or the patient may have
exceedingly high vagal tone. Repeating the test is recommended if either of these situations is
suspected.
 The sinus node is diseased and cannot respond appropriately or there is atrio-ventricular block.
SA (SULFAS ATROPINE) TEST These are pathological causes of a failed atropine response test. In these cases, patients are
The atropine response test is the diagnostic administration of atropine to differentiate vagally-mediated usually classified as having intrinsic sinoatrial nodal disease, or “Sick Sinus Syndrome” or third
and non-vagal bradyarrhythmias. This is very important in cases of persistent bradycardia as non-vagal degree atrioventricular (3’ AV) block. With 3’ AV block the QRS complexes do not increase in
bradyarrhythmias, if resulting in clinical signs, usually require pacemaker implantation, where as frequency (and therefore cardiac output does not increase) but the P-wave frequency normally
vagally mediated bradycardias may be of no clinical significance or require treatment for non-cardiac increases to >140bpm. The recommended treatment for both these presentations is usually
disease. pacemaker implantation.

How do I perform an atropine response test ? DEXTROPOSISI  posisi jantung bergeser ke kanan (karena tarikan / fibrosis paru)
There are several ways of performing the atropine response but the author has had the most consistent DEXTROCARDIA  posisi jantung terbalik
results with the methods outlined below: SINUS BLOCK / SA EXIT BLOCK  pause is multiple of 2 P-P interval
Method 1 SINUS ARREST  pause is not multiple of 2 P-P interval
1. Record the ECG at baseline.
2. Administer 0.04mg/kg atropine IV ANALISIS GAS DARAH
3. Wait 15 minutes PO2 / FiO2  untuk penilaian ARDS
4. Record the ECG for at least 2 minutes (use a slow paper speed). Normal > 300 Gagal nafas tipe 1  pO2 < 50
5. If the response is incomplete, repeat steps 2-4. ALI 200-300 Gagal nafas tipe 2  pCO2 > 50
ARDS < 200
Method 2
1. Record the ECG at baseline. AaDO2 (alveoli arteriola diffusion oxygen)
2. Administer 0.04mg/kg atropine SQ Normal < 70-80
3. Wait 30 minutes Gangguan difusi > 80
4. Record the ECG for at least 2 minutes (use a slow paper speed).  Bisa akibat infiltrat (pneumonia) atau cairan (efusi / edema paru)
 27

Edema paru DOSIS ACE-I PADA ACS

Karena ARDS  peningkatan permeabilitas Trial Initial dosage Target dosage
Karena cardial  peningkatan tekanan hidrostatik GISSI-3 lisinopril 5 mg initially Up to 10 mg daily
ISIS-4 captopril 6.25 mg initially, 12.5 mg in 2 h, 25 Up to 50 mg b.i.d.
ACUTE EMBOLI VS TROMBOSIS mg at 10–12 h
Embolism Thrombosis CHINESE captopril 6.25 mg initially, 12.5 mg 2 h later Up to 12.5 mg t.i.d.
Arrhythmia No arrhythmia if tolerated
Sudden onset Sudden onset or slower onset SMILE zofenopril 7.5 mg initially, repeated after 12 h Up to 30 mg b.i.d.
No history of claudication, rest pain History of claudication, rest pain and repeatedly doubled if tolerated
No risk of atherosclerotic factors Risk of atherosclerotic factors AIRE ramipril 2.5 mg b.i.d. increased to 5 mg Up to 5 mg b.i.d.
Normal contralateral pulse exam Abnormal contralateral pulse exam b.i.d. if tolerated
Normal physical examination of chronic Diminished hair growth, thin skin, thick SAVE captopril Test of 6.25 mg, increased if Up to 50 mg t.i.d.
limb ischemia nails, ulcers tolerated to 25 mg t.i.d.
Crescent-shape occlusion at the proximal Diffuse irregular narrowing artery TRACE trandolapril Test of 0.5 mg Up to 4 mg daily
edge of the clot with distal spasm on VALIANT valsartan 20 mg initially uptitrated in four Up to 160 mg b.i.d.
angiogram steps
Multiple round filling defects on No multiple round filling defects OPTIMAAL losartan 12.5 mg Up to 50 mg daily
angiogram EPHESUS eplerone 25 mg intially Up to 50 mg daily
Normal appearing artery other than affect Present of collateral arteries
area
Lodge at arterial bifurcation Sites of chronic atherosclerotic disease MORTALITAS SETELAH REVASKULARISASI (SHOCK TRIAL)

WESTERMARK SIGN refers to dilation of the

pulmonary artery proximal to an embolism with
collapse of distal vessels (oligemia, reduced blood
volume), sometimes with a sharp cutoff
 28

OBAT UNTUK HIPERTENSI EMERGENCY STROKE ISKHEMIK AKUT (SIA)

Hypertensive emergency (crisis) is characterized by a severe elevation in blood pressure (> 180/120
mmHg) complicated by evidence of impending or progressive target organ dysfunction. Hypertensive
urgency, on the other hand, is a severe elevation in blood pressure without progressive target organ
dysfunction. The initial goal of hypertensive urgency is to reduce blood pressure to 160/110 mmHg
over several hours to days using conventional oral therapy. MAP should be reduced by no more than
25% within the first 24 hours using conventional oral therapy.
 ASA/AHA Stroke Guidelines  anti hipertensi tidak diberikan kecuali untuk pasien yang
direncanakan pemberian rt-PA
 Jangan diberi anti hipertensi kecuali TD > 220/120 mmHg
 Indikasi penurunan TD pada pasien SIA :
 AMI, CHF, Diseksi aorta, ARF, Hipertensi ensefalopati
 Akan dilakukan terapi trombolisis jika TD > 185/110 mmHg

Type of Emergency Drug of Choice Second-line Drugs DOSIS ANTI HIPERTENSI PADA SIA (AHA/ASA GUIDELINES 2007)
Neurologic Not eligible for thrombolytic therapy
Hypertensive Nitroprusside Labetalol or nicardipine  TDS ≤ 220 or TDD ≤ 120
encephalopathy Observe, unless other end organ involvement (aortic dissection, AMI, pulmonary edema,
Subarachnoid Nimodipine Labetalol or nicardipine hypertensive encephalopathy)
haemorrhage  TDS > 220 or TDD 121-140
CVA Labetalol Nitroprusside, enalaprilat  Labetalol 10-20 mg IV for 1-2 min. May repeat or double every 10 min (max 300 mg)
Renal  Nicardipine 5 mg/h IV infusion as initial dose; titrate to desired effect by increasing
Acute kidney injury Nicardipine Fenoldopam 2.5 mg/h every 5 min to max of 15 mg/h
Cardiac  Aim for a 10-15% reduction in blood pressure
Aortic dissection β-Blocker + nitroprusside Labetalol, trimethaphan  TDD > 140
Pulmonary edema Nitroglycerin Nitroprusside ± ACE  Nitroprusside 0.5 g/kg/min IV infusion as initial dose with continuous blood pressure
monitoring
inhibitor
 Aim for a 10-15% reduction in blood pressure
Cardiac ischemia Nitroglycerin ± β-blocker Nitroprusside, labetalol
Adrenergic crisis
Eligible for thrombolytic therapy (Pre-treatment)
Pheochromocytoma Nitroprusside + β-blocker Phentolamine
 TDS > 185 or TDD > 110
Cocaine
 Labetalol 10-20 mg IV for 1-2 min. May repat 1 time or nitropaste 1-2 min
Eclampsia Methyldopa Hydralazine
Magnesium sulfate (do not
CARVALLO’S SIGN
use with CCB)
Carvallo's sign is a clinical sign found in patients with tricuspid regurgitation. The pansystolic
murmur found in this condition becomes louder during inspiration; this sign enables it to be
STROKE PERDARAHAN (ISMAIL SETYOPRANOTO)
distinguished from mitral regurgitation. During inspiration, the venous blood flow into the right atrium
 Tekanan darah diturunkan 15-20% bila TDS > 180 mmHg, TDD > 120 mmHg, MAP > 130,
and ventricle are increased, which increases the stroke volume of the right ventricle during systole. As
dan volume darah bertambah
a result, the leak of blood from the right ventricle into the right atrium is larger during inspiration,
 Jika gagal jantung  TD diturunkan dgn labetalol IV dosis 10 mg ( dalam 2’) sampai 20 mg
causing the murmur to become louder. During expiration, the leak of blood backwards through the
(dalam 10’) max 300 mg; Captopril 3 kali 6,25-25 mg per-oral
tricuspid valve is lessened, making the murmur more quiet. Conversely, the murmur of mitral
regurgitation becomes louder during expiration due to the increase in venous return from the pulmonary
veins to the left heart.

IABP (INTRA AORTIC BALLOON PUMP)
The Intra-aortic balloon pump (IABP) is a mechanical device that increases myocardial oxygen
perfusion while at the same time increasing cardiac output. Increasing cardiac output increases
coronary blood flow and therefore myocardial oxygen delivery. It consists of a cylindrical polyethylene
balloon that sits in the aorta, approximately 2 centimeters (0.79 in) from the left subclavian artery and
counterpulsates. That is, it actively deflates in systole, increasing forward blood flow by reducing
afterload. It actively inflates in diastole, increasing blood flow to the coronary arteries. These actions
combine to decrease myocardial oxygen demand and increase myocardial oxygen supply. A computer-
controlled mechanism inflates the balloon with helium from a cylinder during diastole, usually linked
to either an electrocardiogram (ECG) or a pressure transducer at the distal tip of the catheter.
Indikasi :
 Cardiogenic shock when used alone as treatment for myocardial infarction. 9-22% survive the
first year
 Reversible intracardial mechanical defects complicating infarction, i.e. acute mitral regurgitation
and septal perforation
 Unstable angina pectoris benefits from counterpulsation.
 Post cardiothoracic surgery - most common and useful is counterpulsation in weaning patients
from cardiopulmonary bypass after continued perioperative injury to myocardial tissue
 Preoperative use is suggested for high-risk patients such as those with unstable angina with
stenosis greater than 70% of main coronary artery, in ventricular dysfunction with an ejection
fraction less than 35%
 Percutaneous coronary angioplasty
 In high risk coronary artery bypass graft surgery where cardiopulmonary bypass time was
shortened, as well as during intubation period and hospital stay
 Thrombolytic therapy of acute myocardial infarction
Contraindications :
Absolute contraindication
 Severe aortic valve insufficiency
 Aortic dissection
 Severe aortoiliac occlusive disease
Relative contraindication
 Prosthetic vascular grafts in the aorta
 Aortic aneurysm
 Aortofemoral grafts
29
Complications :
Since the device is placed in the femoral artery and aorta it could provoke ischemia, and compartment
syndrome. The leg is at highest risk of becoming ischemic if femoral artery it is supplied becomes
obstructed. Placing the balloon too distal from the arcus aortae may induce occlusion of the renal artery
and subsequent renal failure. Other possible complications are cerebral embolism during insertion,
infection, dissection of the aorta or iliac artery, perforation of the artery and hemorrhage in the
mediastinum. Mechanical failure of the balloon itself is also a risk which entails vascular surgery to
remove under that circumstance. After balloon removal there is also a risk of 'embolic shower' from
micro clots that have formed on the surface of the balloon, and can lead to peripheral thrombosis,
myocardial ischemia, hemodynamic decompensation, and late pseudoaneurysm.
PULSUS PARADOXUS (PATOFISOLOGI LILLY)
Pulsus paradoxus is an important physical sign in cardiac tamponade that can be recognized at the
bedside using a standard blood pressure cuff. It refers to a decrease of systolic blood pressure (more
than 10 mm Hg) during normal inspiration. Pulsus paradoxus is not really “paradoxical”; it is just
an exaggeration of appropriate cardiac physiology. Normally, expansion of the thorax during
inspiration causes the intrathoracic pressure to become more negative compared with the expiratory
phase. This facilitates systemic venous return to the chest and augments filling of the right ventricle
(RV). The transient increase in RV size shifts the interventricular septum toward the left, which
diminishes left ventricular filling. As a result, in normal persons, LV stroke volume and systolic blood
pressure decline slightly following inspiration. In cardiac tamponade, this situation is exaggerated
because both ventricles share a reduced, fixed volume as a result of external compression by the tense
pericardial fluid. In this case, the inspiratory increase of right ventricular volume and bulging of the
interventricular septum toward the left have a proportionally greater effect on the limitation of LV
filling. Thus, in tamponade there is a more substantial reduction of LV stroke volume (and therefore
systolic blood pressure) following inspiration. Pulsus paradoxus may also be manifested by other
conditions in which inspiration is exaggerated, including severe asthma and chronic obstructive airway
disease.
Measurement of Pulsus Paradoxus at the Bedside
Pulsus paradoxus is an exaggeration of the normal decline in systolic blood pressure that occurs with
inspiration. It can be measured at the bedside using a manual sphygmomanometer. First, inflate the
sphygmomanometer to a level greater than the patient’s systolic pressure. As the cuff is slowly deflated,
carefully listen for the appearance of the first Korotkoff sounds. This level marks the maximum systolic
pressure and occurs during expiration. If the pressure is held at that level (i.e., if you stop deflating the
cuff) in a patient with pulsus paradoxus, the Korotkoff sounds will drift in and out, audible with
 30

expiration, and absent with inspiration. That is, the systolic pressure will fall during inspiration to a
level below the cuff’s pressure and no sound will be heard during that time. Next, slowly deflate the
cuff and continue listening. When the cuff pressure falls to the level just below the patient’s systolic INR Tindakan
pressure during inspiration, the Korotkoff sounds stop drifting in and out (i.e., they are audible during INR > therapeutic range Withhold next dose of warfarin and resume lower dose of
both inspiration and expiration). Pulsus paradoxus is calculated as the difference between the initial but < 5.0 and NO warfarin when INR approaches therapeutic range
systolic pressure (when the intermittent Korotkoff sounds are first heard) and this pressure (when the bleeding
sounds are first audible throughout the respiratory cycle). In the presence of cardiac tamponade, this INR 5.0 – 9.0 and NO Cease warfarin. If bleeding risk high, give vitamin K, 1-2
pressure difference is > 10 mmHg. bleeding mg orally or 0,5-1 mg iv. Check INR within 24 hours.
Resume lower dose of warfarin once INR approaches
PENATALAKSANAAN PERDARAHAN KARENA WARFARIN therapeutic range
INR Tindakan INR > 9.0 Low risk Cease warfarin. Give vitamin K up to 5 mg orally or 0,5-
INR 3.0 - 6.0 (INR target 2.5) Kurangi / hentikan dosis warfarin and NO of bleed 1 mg iv. Check INR in 6-12 hours. Resume lower dose of
INR 4.0 – 6.0 (INR target 3.5) Mulai lagi warfarin jika INR < 5.0 bleeding warfarin once INR < 5.0
INR 6.0 – 8.0 Hentikan warfarin High risk Cease warfarin. Give vitamin K 1 mg iv. Consider
Tidak ada perdarahan atau Mulai lagi warfarin jika INR < 5.0 of bleed Prothrombinex-HT (25-50 units/kg) and FFP (150-300
perdarahan ringan mL). Check INR in 6-12 hours. Resume lower dose of
INR > 8.0 Hentikan warfarin warfarin once INR < 5.0
Tidak ada perdarahan atau Jika ada faktor resiko perdarahan yang lain, Any clinically SEEK SENIOR ADVICE. Cease warfarin. Give vitamin
perdarahan ringan berikan 0,5 – 2,5 mg vitamin K oral significant bleeding K 5-10 mg iv. Prothrombinex-HT (25-50 units/kg) and
Perdarahan hebat Hentikan warfarin where warfarin-induced FFP (150-300 mL). Assess INR frequently until INR < 5.0
Berikan konsentrat kompleks protrombin 50 coagulopathy considered and bleeding stops. If prothrombinex-HT is unavailable,
unit/kg atau FFP 15 mL/kg a contributing factor increase FFP dose to 10-15 ml/kg and assess INR
Berikan 5 mg vitamin K (oral atau iv) frequently until INR < 5.0 and bleeding stops.

RECOMMENDED TARGET INR RANGES

 AF, DVT, PE, and bio-prosthetic heart valve in patients with sinus rhythm for 6 weeks post-
op  INR target 2.0 - 3.0
 Mechanical prosthetic heart valves  INR target 2.5 – 3.5
 31

AMIODARONE IN THYROID HEART DISEASE ANTIDROMIC & ORTHODROMIC (AVRT)

The effects range from abnormal thyroid function test findings to overt thyroid dysfunction, which may
be either amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH).
Both can develop in apparently normal thyroid glands or in glands with preexisting abnormalities.
Amiodarone causes a wide spectrum of effects on the thyroid :
 Amiodarone inhibits type 1 5'-deiodinase enzyme activity, thereby decreasing the peripheral
conversion of T4 to triiodothyronine (T3) and reducing the clearance of both T4 and reverse T3
(rT3). Consequently, the serum levels of T4 and rT3 increase and the serum levels of T3 decrease
by 20-25%.
 Amiodarone inhibits entry of T4 and T3 into the peripheral tissue. Serum T4 levels increase by
an average of 40% above pretreatment levels after 1-4 months of treatment with amiodarone.
This, in itself, does not constitute evidence of hyperthyroidism (thyrotoxicosis).
 Inhibition of type 2 5'-deiodinase enzyme activity in the pituitary due to feedback regulation is
seen in the first 1-3 months and leads to an increase in thyroid-stimulating hormone (TSH) levels.
This is not an indication for T4 replacement in these patients. Serum TSH levels return to normal
in 2-3 months as T4 concentrations rise sufficiently to overcome the partial block in T3
production. The response of TSH to thyroid-releasing hormone (TRH) may be reduced.
 Amiodarone and its metabolites may have a direct cytotoxic effect on the thyroid follicular cells,
which causes a destructive thyroiditis.
 Amiodarone and its metabolite desethylamiodarone can act as a competitive antagonist of T3 at
the cardiac cellular level. Wolff–Parkinson–White syndrome. A. During normal sinus rhythm, the shortened PR interval, delta
wave, and widened QRS complex indicate fusion of ventricular activation via the AV node and
In summary, serum T4 levels rise by 20-40% during the first month of therapy and then gradually fall accessory pathway. B. An atrial premature beat can trigger an orthodromic atrioventricular reentrant
toward high normal. Serum T3 levels decrease by up to 30% within the first few weeks of therapy and tachycardia, in which impulses are conducted anterogradely down the AV node and retrogradely up the
remain slightly decreased or low normal. Serum rT3 levels increase by 20% soon afterward and remain accessory pathway. Retrograde P waves are visible immediately after the QRS complex. There is no
increased. Serum thyrotropin (TSH) levels usually rise after the start of therapy but return to normal in delta wave because anterograde ventricular stimulation passes exclusively through the AV node. C.
2-3 months. Antidromic atrioventricular reentrant tachycardia in which impulses are conducted anterogradely down
the accessory tract and retrogradely up the AV node. The QRS complex is very widened because the
INFERIOR VENA CAVA FILTER IN DVT ventricles are stimulated by abnormal conduction through the accessory pathway.
Used in patients with acute venous thromboembolism who have:
 Absolute contraindication to anticoagulation therapy CONCEALED WPW
 Experience recurrent VTE despite adequate anticoagulation Accessory pathways do not always result in ECG findings of ventricular pre-excitation (i.e., short PR,
delta wave). Many are capable of only retrograde conduction. In this case, during sinus rhythm, the
ventricles are depolarized normally through the AV node alone and the ECG is normal (i.e., the
accessory pathway is concealed). However, because the accessory pathway is capable of retrograde
conduction, it can form a limb of a reentrant circuit under appropriate circumstances and result in
orthodromic AVRT. Management of patients with tachycardia involving a concealed accessory
 32

pathway is the same as for patients with AVNRT. Because the reentrant circuit travels anterogradely ATRIAL TAKIKARDIA
down the AV node, vagal maneuvers and drugs that interrupt conduction over the AV node (e.g.,
adenosine, verapamil, diltiazem, and β-blockers) can terminate the tachycardia. Another option for
recurrent episodes is catheter ablation of the accessory pathway, which is curative in most patients.

AVNRT
The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which
are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located
inferiorly and slightly posterior to the AV node, often following the anterior margin of the coronary
MULTIFOCAL ATRIAL TAKIKARDIA sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways
are formed from tissue that behaves very much like the AV node, and some authors regard them as part
of the AV node. More females than males have signs of AVNRT. The ratio is approximately 3:1.
Symptoms are bouts of fast heart rates with sudden onset. Neck vein palpitations can be prominent
(the 'Frog Sign'). Termination is often possible with valsalva manouevres (blowing on wrist,
squatting, carotid sinus massage) or medication (adenosine, verapamil, diltiazem), or
electrocardioversion.
In multifocal atrial tachycardia (MAT), the ECG shows an irregular rhythm with multiple (at least
three) P-wave morphologies, and the average atrial rate is > 100 bpm. An isoelectric (i.e., “flat”)
baseline between P waves distinguishes MAT from the chaotic baseline of AF. This rhythm is likely
caused by either abnormal automaticity in several foci within the atria or triggered activity and occurs
most often in the setting of severe pulmonary disease and hypoxemia. Because patients with this rhythm
are often critically ill from the underlying disease, the mortality rate is high, and treatment is aimed at
the causative disorder. The calcium channel blocker verapamil is often effective at slowing the
ventricular rate as a temporizing measure.
 33

Typical AVNRT (Common AVNRT)  90%

In common AVNRT, the anterograde conduction is via the slow pathway and the retrograde conduction
is via the fast pathway ("slow-fast" AVNRT). Because the retrograde conduction is via the fast
pathway, stimulation of the atria (which produces the inverted P wave) will occur at the same time as
stimulation of the ventricles (which causes the QRS complex). As a result, the inverted P waves may
not be seen on the surface ECG since they are buried with the QRS complexes. Often the retrograde p-
wave is visible, but also in continuity with the QRS complex, appearing as a "pseudo R prime" wave
in lead V1 or a "pseudo S" wave in the inferior leads.

Atypical AVNRT (Uncommon AVNRT)  6%

In uncommon AVNRT, the anterograde conduction is via the fast pathway and the retrograde
conduction is via the slow pathway ("fast-slow" AVNRT). Because the retrograde conduction is via
the slow pathway, stimulation of the atria will be delayed by the slow conduction tissue and will
typically produce an inverted P wave that falls after the QRS complex on the surface ECG.

Atypical AVNRT (Slow-Slow AVNRT)  4%

The slow AV nodal pathway as the anterograde limb & left atrial fibers that approach the AV node
from the left side of the inter-atrial septum as the retrograde limb.

***Paying careful attention to the relationship between the P wave and the QRS complex during
tachycardia is also very helpful in distinguishing tachycardia mechanisms. If the retrograde P wave
falls within or just after the QRS, the most likely diagnosis is AVNRT. If the tachycardia shows a
retrograde P wave in the ST segment, AVRT is most likely. Finally, atrial tachycardia is
characterized by the presence of P waves immediately in front of the QRS (long RP tachycardia).

MITRAL VALVE PROLAPSE
Mitral valve prolapse (MVP) is a valvular heart disease characterized by the displacement of an
abnormally thickened mitral valve leaflet into the left atrium during systole. There are various types of
MVP, broadly classified as classic and nonclassic. In its nonclassic form, MVP carries a low risk of
complications. In severe cases of classic MVP, complications include mitral regurgitation, infective
endocarditis, congestive heart failure, and, in rare circumstances, cardiac arrest, usually resulting in
sudden death.
Upon auscultation of an individual with mitral valve prolapse, a mid-systolic click, followed by a late
systolic murmur heard best at the apex is common. In contrast to most other heart murmurs, the
murmur of mitral valve prolapse is accentuated by standing and valsalva maneuver (earlier systolic
click and longer murmur) and diminished with squatting (later systolic click and shorter murmur). The
only other heart murmur that follows this pattern is the murmur of hypertrophic cardiomyopathy. A
MVP murmur can be distinguished from a hypertrophic cardiomyopathy murmur by 1) the
presence of a mid-systolic click which is virtually diagnostic of MVP, and 2) the fact that hand grip
maneuver intensifies the murmur of MVP and diminishes the murmur of hypertrophic
cardiomyopathy. The hand grip maneuver also diminishes the duration of the murmur and delays the
timing of the mid-systolic click. Hand grip maneuver increases total peripheral resistance (afterload)
and therefore increases back pressure on the mitral valve resulting in a more intense murmur without
changing the timing of the systolic click. (needs clarification). Both valsalva maneuver and standing
decrease venous return to the heart thereby decreasing left ventricular diastolic filling (preload) and
causing more laxity on the chordae tendineae. This allows the mitral valve to prolapse earlier in systole,
leading to an earlier systolic click (i.e. closer to S1), and a longer murmur.
34
Terapi MVP  β-blocker, jika sudah ada MR severe  mitral valve repair atau replacement (MV
repair preferable)
SYNTAX SCORE
The SYNTAX score is a novel anatomical tool characterizing coronary vasculature. Importantly, the
SYNTAX score grades the complexity of coronary artery disease and does not consider lesion
treatment. The SYNTAX score described here predicts outcomes for patients treated with PCI but has
less predictable value for patients undergoing treatment with bypass surgery. Complex lesion anatomy
poses a greater technical challenge and, consequently, a higher risk of adverse events when treated by
percutaneous intervention. In contrast, CABG bypasses the lesion and is thus less influenced by lesion
complexity. Furthermore, the SYNTAX score is a useful tool to describe the extent of the coronary
artery disease complexity for an individual patient, allows for comparison between patients, and can be
used effectively to communicate patient disease complexity between physicians. The goal of the
SYNTAX score is to assist the clinician in selecting the optimal revascularization strategy, resulting in
the best possible outcome for the individual patient.
EuroSCORE
EuroSCORE (European System for Cardiac Operative Risk Evaluation) is a risk model which allows
the calculation of the risk of death after a heart operation.
Low Risk (0-2 points) : 0.8% in-hospital mortality
Moderate Risk (3-5 points) : 3.0% in-hospital mortality
High Risk (6 or more points) : 11.2% in-hospital mortality

Factors
Related to patient
Age
Gender
Chronic pulmonary disease
Extracardiac artery disease
Neurological dysfunction
Previous heart surgery
Serum creatinine
Active endocarditis
Critical preoperative state
Related to the heart
Instable angina
Left ventricle dysfunction
Recent myocardial
infarction
Pulmonary hypertension
Related to the procedure
Emergency
Surgeries associated to
CABG
Surgery of the thoracic aorta
Post-infarction ventricular
septal defect
35
Definition Score MARKER ACS
For 5 years or fraction > 60 years 1
female 1
Prolonged use of the bronchodilators or steroids 1
Claudication or obstruction > 50% of carotid 2
arteries or previous or planned intervention of the
abdominal aorta, carotid arteries or peripheral
arteries
Disease affecting walking or daily activities 2
Requiring opening of the pericardium 3
> 2.3 mg in the pre-operative period 2
Using antibiotics at time of surgery 3
Any of the following: ventricular tachycardia or 3
fibrillation or aborted sudden death, pre-operative
Troponin
heart massage, pre-operative ventilation before
In the case of MI, cardiac troponin serum levels begin to rise 3 to 4 hours after the onset of discomfort,
arriving in the surgery room, pre-operative
peak between 18 and 36 hours, and then decline slowly, allowing for detection for up to 10 to 14 days
inotropic support, intra-aortic balloon or pre-
after a large MI. Thus, their measurement may be helpful for detection of MI for nearly 2 weeks after
operative acute renal failure ( < 10 ml/h)
the event occurs. Given their high sensitivity and specificity, cardiac troponins are the preferred serum
biomarkers to detect myocardial necrosis.
Resting angina requiring the use of nitrates before 2
arrival in the anesthesia room
CKMB
EF 30 - 50% 1
The serum level of CK-MB starts to rise 3 to 8 hours following infarction, peaks at 24 hours, and
EF < 30% 3
returns to normal within 48 to 72 hours.
< 90 days 2
Systolic pressure of the pulmonary artery > 60 2
PERUBAHAN EKG PADA PENINGKATAN TEKANAN INTRAKRANIAL
mmHg
 Prominent U waves
 ST-T segment changes
Performed before the following day’s shift 2  Notched T waves
Another heart procedure at the same time as 2  Shortening and prolongation of Q-T intervals
CABG
Ascending aorta, aortic arch or descending aorta 3
4

KLASIFIKASI HIPERTENSI PADA KEHAMILAN  JNC VII
Chronic hypertension  BP >140 mmHg systolic or 90 mmHg diastolic
prior to pregnancy or before 20 weeks gestation
 Persists >12 weeks postpartum
Preeclampsia  BP >140 mmHg systolic or 90 mmHg diastolic
with proteinuria (>300 mg/24 hrs) after 20 weeks
gestation
 Can progress to eclampsia (seizures)
 More common in nulliparous women, multiple
gestation, women with hypertension for >4
years, family history of preeclampsia,
hypertension in previous pregnancy, renal
disease
Chronic hypertension with  New onset proteinuria after 20 weeks in a
superimposed preeclampsia woman with hypertension
 In a woman with hypertension and proteinuria
prior to 20 weeks
 gestation
 Sudden two- to threefold increase in proteinuria
 Sudden increase in BP
 Thrombocytopenia
 Elevated AST or ALT
Gestational hypertension  Hypertension without proteinuria occurring after
20 weeks gestation
 Temporary diagnosis
 May represent preproteinuric phase of
preeclampsia or recurrence of chronic
hypertension abated in midpregnancy
 May evolve to preeclampsia
 If severe, may result in higher rates of premature
delivery and growth retardation than mild
preeclampsia
Transient hypertension  Retrospective diagnosis
 BP normal by 12 weeks postpartum
 May recur in subsequent pregnancies
 Predictive of future primary hypertension
36
HYPERTENSIVE CRISES: EMERGENCIES AND URGENCIES  JNC VII
Hypertensive emergencies are characterized by severe elevations in BP (>180/120 mmHg)
complicated by evidence of impending or progressive target organ dysfunction. They require immediate
BP reduction (not necessarily to normal) to prevent or limit target organ damage. Examples include
hypertensive encephalopathy, intracerebral hemorrhage, acute MI, acute left ventricular failure with
pulmonary edema, unstable angina pectoris, dissecting aortic aneurysm, or eclampsia. Hypertensive
urgencies are those situations associated with severe elevations in BP without progressive target organ
dysfunction. Examples include upper levels of stage II hypertension associated with severe headache,
shortness of breath, epistaxis, or severe anxiety. The majority of these patients present as noncompliant
or inadequately
treated hypertensive individuals, often with little or no evidence of target organ damage.
Patients with hypertensive emergencies should be admitted to an intensive care unit for
continuous monitoring of BP and parenteral administration of an appropriate agent. The initial goal
of therapy in hypertensive emergencies is to reduce mean arterial BP by no more than 25 percent
(within minutes to 1 hour), then if stable, to 160/100–110 mmHg within the next 2–6 hours.
Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.
For this reason, short-acting nifedipine is no longer considered acceptable in the initial treatment of
hypertensive emergencies or urgencies. If this level of BP is well tolerated and the patient is
clinically stable, further gradual reductions toward a normal BP can be implemented in the next
24–48 hours. There are exceptions to the above recommendation—patients with an ischemic stroke in
which there is no clear evidence from clinical trials to support the use of immediate antihypertensive
treatment, patients with aortic dissection who should have their SBP lowered to <100 mmHg if
tolerated, and patients in whom BP is lowered to enable the use of thrombolytic agents. Some patients
with hypertensive urgencies may benefit from treatment with an oral, short-acting agent such as
captopril, labetalol, or clonidine followed by several hours of observation.
** (literatur lain) The initial goal of treatment is to reduce the mean arterial pressure by no more than
25% to reach a goal blood pressure of 160/100 mm Hg within 2 to 6 hours or to decrease diastolic blood
pressure 10% to 15% or to approximately 110 mmHg within 30 to 60 minutes.
 37

MEMBACA RONTGEN
PERTAMA
IDENTITAS foto rontgennya. Nama, umur, jenis kelamin, nomor foto, tanggal foto dan klinisnya.
Harus dipastikan supaya tidak tertukar.
KEDUA
LAYAK BACA atau tidak. Seperti misalnya, foto yang terlalu keras, yang terpotong, posisinya tidak
baik, inspirasi kurang (inspirasi cukup jika costa 6 memotong hemidiafragma di tengah)
KETIGA
POSISI FOTO. AnteroPosterior (AP) atau PosteroAnterior (PA). Foto AP berarti sinar X berasal dari
bagian depan tubuh dan film berada di belakang. Sementara foto PA berarti sinar X ada di belakang
dan film berada di bagian depan tubuh. Hal ini penting, karena semakin jauh letak organ dari film maka
gambaran foto yang didapat akan termagnifikasi (diperbesar) sehingga tidak sesuai dengan keadaan
sebenarnya. Yang lebih mendekati keadaan organ yang sebenarnya adalah foto PA (jika kita menilai
jantung dan paru, karena lebih dekat ke film). Pada foto AP clavicula akan tampak mendatar, scapula
berada di dalam lapangan paru, dan yang tampak depan adalah costae anterior. Sedangkan pada foto
PA yang tampak depan adalah costae posterior, clavicula menjungkit, dan scapula berada di luar
lapangan paru.
 Parenkim paru, keadaan hilus, corakan bronkovaskuler, dan apakah terdapat lesi atau tidak. Hilus
merupakan tempat keluar masuknya arteri dan vena pulmonalis, bronkus, dan juga saluran limfe.
Normalnya diameter hilus sama dengan diameter trakea. Pada foto rontgen, hilus memberikan
gambaran yang padat. Untuk corakan bronkovaskuler, normalnya hanya terdapat pada 1/3
lapangan paru dari central pada dewasa, sedangkan pada anak hanya 1/4 dari lapangan paru.
Corakan bronkovaskuler yang meningkat dapat menjadi suatu tanda suatu proses perandangan
paru misalnya pada bronkitis, pneumonia. Kemudian lesi pada parenkim paru. Misal pada TB
(gambaran infiltrat, fibrotik, kavitas). Bisa juga gambaran metastasis pada parenkim paru
(noduler, milier, koin)
 Jantung, nilai besar dan ukurannya, normal atau tidak. Ukuran bisa kita nilai dengan menghitung
CTR (Cardio Thoracic Ratio), normalnya pada orang dewasa adalah 48%-50%, sedangkan pada
anak-anak sebesar 52%-53%. Cara menghitungnya adalah a + b : c
 Tarik garis di linea mediana
 Tarik garis tegak lurus linea mediana
sejajar diafragma
 Ukur garis a, b dan c

KEEMPAT
Untuk membaca foto rontgen prinsipnya adalah membandingkan keadaan kiri dan kanan, jadi jika kita
melihat suatu keadaan di bagian kanan maka bandingkan dengan bagian kirinya. Selanjutnya untuk
pembacaan dapat dilakukan dari dalam ke luar atau dari luar ke dalam.  Diafragma, apakah terdapat elevasi, bagaimana bentuknya, dan permukaannya licin atau tidak.
 Soft tissuenya terlebih dahulu, apakah terdapat soft tissue swelling atau tidak. Soft tissue swelling Diafragma letak tinggi misalnya bisa disebabkan oleh desakan massa dari bawah, paralisis m.
bisa terjadi misalnya pada trauma, tumor, dll. diafragmatika atau lumpuhnya n. Phrenicus
 Tulang-tulang, intak atau tidak. Apakah ada kelainan, fraktur, destruksi, dan lainnya. Destruksi
bisa terjadi misal akibat metastasis tumor ganas ke tulang. Gambaran metastasis yang ada dapat
berupa gambaran radiolusen (hitam) atau radioopaque (putih) yang abnormal pada gambaran
tulang. Kelainan, misalnya lordosis, kifosis, atau scoliosis pada vertebrae.
 Mediastinum dinilai normal atau tidak, apakah terdapat pembesaran atau tidak. Misal, adanya
tumor pada mediastinum akan menampakkan gambaran mediastinum yang melebar atau tampak
adanya massa pada mediastinum.
 Trakea juga dapat kita nilai. Trakea yang normalnya berada di tengah, bisa mengalami pergeseran
akibat desakan atau proses-proses lain.
 Pleura, bagaimana sudut costofrenikusnya, lancip atau tumpul, normalnya lancip. Sudut
costofrenikus yang tumpul dapat menandakan suatu efusi pleura.
 38

Nama : REGURGITASI AORTA

Umur : Tanda Deskripsi
RM : Corrigan's pulse A rapid and forceful distension of the arterial pulse with a quick
Diagnosa : (Water hammer collapse secondary to the increased pulse pressure
ICCU Bed : pulse)
De Musset's sign Bobbing of the head with each heart beat
AO 20-39 LVIDd 35-52 Muller's sign Visible pulsations of the uvula
LA 15-40 LVIDs 26-36 Quincke's sign Capillary pulsations seen on light compression of the nail bed
LA / AO 1.1 IVSd 7.0-11 Traube's sign Systolic & diastolic sounds heard over femoral artery ("pistol
RV < 30 IVSs shots")
RA LVPWd 7.0-11 Duroziez's sign Gradual pressure over femoral artery leas to a systolic &
mPAP LVPWs diastolic bruit
PVAcct TAPSE > 14 Hill's sign Popliteal systolic blood pressure exceeding brachial systolic
EPSS < 10 AoVmax blood pressure by 60 mmHg or greater
EF 53-77 Simpson > 20 mmHg – mild AR
MVA > 3 cm2 > 40 mmHg – moderate AR
> 60 mmHg – severe AR
Mitral : Shelly's sign Pulsation of the cervix
Trikuspid : Rossenbach's sign Hepatic pulsations
Aorta : Becker's sign Visible pulsations of the retinal arterioles
Pulmonal : Gerhardt's sign Pulsation of the spleen in the presence of splenomegaly
(Sailer's sign)
Kinetik : Mayne's sign A decrease in diastolic blood pressure of 15 mmHg when the
Disf diastolik : arm is held above the head
Effusi : Landolf's sign Systolic contraction and diastolic dilation of the pupil
IVC : Bisferiens pulse Characterized by two systolic peaks, the percussion and tidal
waves, separated by a distinct midsystolic dip; the peaks may be
equal, or either one may be larger. This type of pulse is detected
most readily by palpation of the carotid and, less commonly,
of the brachial arteries. It occurs in conditions in which a large
stroke volume is ejected rapidly and is observed most commonly
in patients with pure aortic regurgitation or with a combination
of aortic regurgitation and stenosis