Case Presentation

Aulia Ulfah MD G991620

Arina Aulia G99172
Arum Cahyaning G99162081
Risa Darwadi G99
Rusydina FA G99
Farizca NW G99171

dr. Tuko Srimulyo, SpJP, M.Kes, FIHA

KEPANITERAAN KLINIK ILMU PENYAKIT JANTUNG
FAKULTAS KEDOKTERAN UNIVERSITAS SEBELAS MARET
RS. DR. MOEWARDI SURAKARTA
2018
Patient Status
 Identity
• Name : Mr. M
• Age : 54 yo
• Sex : Male
• Address : Kedungtungkul , Surakarta
• No MR : 0143xxxx
• Arrival : October, 7th 2018

Division of Cardiology
Chief complain

Chest Pain

Division of Cardiology
 Present Illness
A 54 years old male who prensented with chest pain was
admitted to our hospital. The onset of symptoms is six hours
before admitted to our hospital.

The pain got worse while doing activity and relieved when the
patient is resting. There was nausea, and cold sweats. The
patient was first admitted to Puskesmas Sibela to getting medical
attention then transferred to RSDM with diagnosis Suspect AMI
Extended anterior

The patient has history of Hypertension (uncontrolled) and a smoker

(three cigarrette per day) with no Diabetes or other heart disease

Division of Cardiology
 Physical examination
• General condition : moderate ill
• Consciousness : compos mentis
• BP : 160/90 mmHg
• HR/pulse : 61/61 x/min
• RR : 20 x/min
• Oxygen level : 100%

Divisi Cardiology

Eyes: CA-/-, SI -/-
Neck: JVP 5 +4 cmH20
Cor:
I : Ictus cordis not seen
P: Ictus cordis wider from
normal limit with border
enlargement (+),
caudolateral
A: 1st and 2nd heart sound
normal intensity, reguler,
murmur (-), gallop (-).

bowel sound (+) normal.

ballotement (-), epigastric pain
(-)
Vesicular (+/+) Ronkhi (-/-)

edema (-/-)
cold extremity (-/-)
edema (+/+)
cold extremity
(-/-)
Laboratory Examination

Division of Cardiology
 Pemeriksaan Hasil Satuan Nilai Rujukan
HEMATOLOGI RUTIN 08/10/2018 12:38 AM
Hemoglobin 14.0 g/dl 13.5 – 17.5
Hematokrit 45 % 33 – 45
Leukosit 11.3 ribu/ul 4.5 – 11.0
Trombosit 238 ribu/ul 150 – 450
Eritrosit 5.17 juta/ul 4.50 – 5.90
INDEX ERITROSIT
MCV 87.8 /um 80.0 – 96.0
MCH 27.1 Pg 28.0 – 33.0
MCHC 30.8 g/dl 33.0 – 36.0
RDW 11.9 % 11.6 – 14.6
MPV 8.3 Fl 7.2 – 11.1
PDW 17 % 25 – 65
Division of Cardiology
HITUNG JENIS
Eosinofil 1.40 % 0.00 – 4.00
Basofil 0.10 % 0.00 – 0.200
Netrofil 77.40 % 55.00 – 80.00
Limfosit 15.60 % 22.00 – 44.00
Monosit 5.50 % 0.00 – 7.00
KIMIA KLINIK
Gula Darah Sewaktu 128 mg/dl 60 – 140
SGOT 44 u/l < 35
SGPT 21 u/l < 45
Albumin 4.1 g/dl 3.5 – 5.2
Creatinin 1.9 mg/dl 0.9 – 1.3
Ureum 27 mg/dl <50
ELEKTROLIT
Natrium darah 139 mmol/L 136 – 145
Kalium darah 4.0 mmol/L 3.3 – 5.1
Calsium darah 109 mmol/L 98 – 106
Calsium Ion 1.21 mmol/L 1.17 – 1.29
SEROLOGI
HBsAg Non reactive Non reactive
HEMOSTASIS
PT 13.3 detik 10.0 – 15.0
Hematokrit 28.7 detik 20.00 – 40.00
INR 1.030 -
CARDIAC MARKER
CKMB Mass 21.9 ng/mL <4.3
Troponin – I 3.35 ng/mL <0.2
BNP 119 pg/mL <100
KIMIA KLINIK (8/10/2018) 9:36 a.m
HbA1c 5.2 % 4.8 – 5.9
Glukosa darah puasa 17 % 25 – 65
Glukosa 2 Jam PP 120 mg/dl 80 – 140
Asam Urat 7.6 mg/dl 2.4 – 6.1
Kolesterol total 151 mg/dl 50 – 200
Koleserol LDL 84 mg/dl 89 – 197
Kolesterol HDL 28 mg/dl 28 – 63
Trigliserida 213 mg/dl <150
SEROLOGI
Anti-HCV Nonreactive Nonreactive
ECG Examination

Division of Cardiology
Sinus takikardi, HR 150bpm
normoaxis, ST elevasi lead III, ST
dep V4-V6????? Division of Cardiology
Sinus takikardi, HR 150bpm
normoaxis, ST elevasi lead III, ST
dep V4-V6???????? Division of Cardiology
Sinus rhythm, with frequency
60 bpm, normoaxis, ????? Division of EKG
Cardiology
13/8/18
Chest X-ray Examination

Division of Cardiology
 1. Cardiac enlargement
with CTR 57%
2. Cardiac apex rounded

Conclusion (08/10/2018) :
1. Cardiomegaly with RVH

Division of Cardiology
 DIAGNOSIS
• Ax : STEMI Inferior (onset: 6h) with autolysis
• Fx : Killip 1
• Ex : CAD
• History : Hypertension Stage II
 DPH 0
• Therapy :
1. Total bed rest
2. O2 3 lpm NK (SpO2 < 90%)
3. DJ II 1700 kkal
4. RL 80 ml/h
5 Mintaspi 80 mg/24h
6. Clopidogrel 25mg/24h
7. Atorvastatin 40 mg
8. ISDN 5mg

• Plan :
- Lab
- Echocardiography
- EKG (chest pain)
- PCI
 DPH 1
• Therapy :
1. Total bed rest
2. O2 3 lpm NK (SpO2 < 90%)
3. DJ II 1700 kkal
4. RL 80 ml/h
5 Mintaspi 80 mg/24h
6. Clopidogrel 25mg/24h
7. Atorvastatin 40 mg
8. ISDN 5mg/8h
9. Inj. Enoxaparin 0,3 mg IV
10. Ramipril 5mg/h
11. Bisoprolol (delay)

• Plan :
- Lab
- Echocardiography
- EKG (chest pain)
- PCI
 DPH 2
• Therapy :
1. Total bed rest
2. O2 3 lpm NK (SpO2 < 90%)
3. DJ II 1700 kkal
4. RL 80 ml/h
5 Mintaspi 80 mg/24h
6. Clopidogrel 25mg/24h
7. Atorvastatin 40 mg
8. ISDN 5mg/8h
9. Inj. Enoxaparin 0,3 mg IV
10. Ramipril 5mg/h
11. Bisoprolol (delay)
12. Inj. Paracetamol 500mg/8h
13. Ketosteril 1tab/8h
14. NAC 200mg/h

• Plan : - EKG (chest pain)

- PCI
Myocardial Infarction

Division of Cardiology
 Pathogenesis
Most of the cases result from disruption of an
athersclerotic plaque with subsequent platelet
aggregation and formation of an intracoronary
thrombus

Division of Cardiology
Mechanism of Coronary Thrombus
Formation

Division of Cardiology
Consequences of Coronary
Thrombosis

Division of Cardiology
 Changes in Infarction
• Early Changes

Division of Cardiology
 Changes in Infarction
• Late Changes
Time Event
5-7 days Yellow softening from resorption of dead
tissue by macrophages
7+ days Ventricular remodeling

7 weeks Fibrosis and scarring complete

Division of Cardiology
 Changes in Infarction
• Functional Alterations
– Impaired contractility and compliance
– Ventricular remodeling

Division of Cardiology
 Diagnosis
Presenting symptoms
• The presence of substernal chest pain
• Discomfort provoked by exertion or emotional
stress
• Relieved by rest and/or nitroglycerin

ECG abnormalities

Cardiac serum markers

Division of Cardiology
 ECG Abnormalities
• Unstable Angina/NSTEMI

Division of Cardiology
 ECG abnormalities
• STEMI

Division of Cardiology
Cardiac Serum Markers

Division of Cardiology
 Treatment
General • Pain control
measures • Supplemental oxygen

• β blocker
Anti-ischemic • Nitrates
therapies • +/- calcium antagonist

Antithrombotic • Antiplatelet agents

therapies • Anticoagulants

Adjunctive • Statin
therapies • ACE inhibitor

Division of Cardiology
Complications

Division of Cardiology
Hypertension
DEFINITION
Hypertension is
defined as office
SBP values >_140
mmHg and/or
diastolic BP (DBP)
values >_90 mmHg.
This is based on
evidence from
multiple RCTs that
treatment of
patients with these
BP values is
beneficial. ESC, 2018
 PATHOGENESIS OF HYPERTENSION
Excess Reduced Endothelium
Genetic
sodium nephron Stress Obesity derived
alteration
intake number factors

Renal Decreased Sympathetic Renin- Cell

Hyper-
sodium filtration nervous angiotensin membrane
insulinemia
retention surface overactivity excess alteration

Increased
Venous
fluid
constriction
volume
Kaplan. Clinical Hypertension. 2006

Increased Functional Structural

contractability constriction hypertrophy
Increased
preload

BLOOD PRESSURE = CARDIAC OUTPUT x PERIPHERAL RESISTANCE

Hypertension = Increased Cardiac Output and/or Increased Peripheral Resistance

autoregulation
CLASSIFICATION
 FACTORS INflUENCING
CARDIOVASCULAR RISK IN PATIENTS
WITH HYPERTENSION
 DIAGNOSIS

MEDICAL
HISTORY
MEDICAL
HISTORY
MEDICAL
HISTORY
 PHYSICAL
EXAMINATION
 PHYSICAL
EXAMINATION
 HYPERTENSION URGENCIES AND
EMERGENCIE
Hypertension emergencies are
situations in which severe
hypertension (grade 3) is associated
with acute HMOD, which is often life
threatening and requires immediate
but careful intervention to lower BP,
usually with intravenous (i.v.)
therapy. Therateand magnitude of
an increasein BP may be at least as
important as the absolute level of BP
indetermining the magnitude of
organ injury
The term ‘hypertension urgency’ has
also been used to describe severe
hypertension in patientspresenting
to the emergency department in
whom there is no clinical evidence of
acute HMOD.405 Whilst these
patients require BP reduction, they
do not usually require admission to
hospital,and BP reduction is best
achieved with oral medication
according to the drug treatment
algorithm presented in Figure 4.
However, these patients will require
urgent out patient review to ensure
that their BP is coming under
control.
TREATMENT
THERAPEUTIC STRATEGIES IN HYPERTENSIVE There are strong
PATIENTS WITH CAD
epidemiological relationships
between CAD and
hypertension. The
INTERHEART study showed
that ~50% of the population-
attributable risk of a
myocardial infarction can be
accounted for by lipids, with
hypertension
Another accounting
registry-based for
study
of over 1 ~25%.
million patients
showed that ischaemic heart
disease (angina and
myocardial infarction)
accounted for most (43%) of
the CVD-free years of life lost
due to hypertension from the
age of 30 years
THANK YOU