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Case Presentation
Alyssa Amalia G 99162077

Khaniva Putu Y G 99162072
Nurul Fadilah G 99162083
Sekar Ayu Kinanti G 99171041
Kezia Enala G 99172098
dr. Tuko Srimulyo, SpJP, M.Kes, FIHA

KEPANITERAAN KLINIK ILMU PENYAKIT JANTUNG
FAKULTAS KEDOKTERAN UNIVERSITAS SEBELAS MARET
RS. DR. MOEWARDI SURAKARTA
2018
Patient Status
Division of Cardiology
Identity
• Name : Mr. H
• Age : 58 yo
• Sex : Male
• Address : Eromoko, Wonogiri
• No MR : 0142xxxx
• Arrival : August, 7th 2018
• Examination : August 13th 2018
Chief complain
Breathlessness
Present Illness
A 58 years old male who prensented with breathlessness was
admitted to our hospital. The onset of symptoms is 1 week
before admitted to our hospital.
The patient is more comfortable in half-sitting position, the

breathlessness did not relieved even when the patient is resting.
The patient also stated that he often awakened from his sleep
because of his breathlessness. There was no cough, no chest
pain, no palpitation and no problem with defecation or
mixturation.
The patient also complain about his stomach distended and
sweelling on his foot since 7 days before. There is no history of
hypertension, diabetes mellitus and smoker.
Physical examination
• General condition : moderate ill
• Consciousness : compos mentis
• BP : 110/80 mmHg
• HR/pulse : 104/104 x/menit
• RR : 24 x/menit
• Temperature : 37,3 oC
Divisi Cardiology
Cor:
Eyes: CA-/-, SI -/- I : Ictus cordis not seen
P: Ictus cordis wider from
normal limit (caudolateral)
border enlargement (+),
caudolateral
Neck: JVP 5 +4 cmH20 A: 1st and 2nd heart sound
normal intensity, reguler,
murmur (+), gallop (-).
bowel sound (+) normal.

ballotement (-), shifting
dullness (+), epigastric pain (-)
Vesicular (+/+) Ronkhi in
1/3 basal lung (+/+)
edema (-/-)
cold extremity (-/-)
edema (+/+)
cold extremity
(-/-)
Laboratory Examination
Pemeriksaan Hasil Satuan Nilai Rujukan
HEMATOLOGI RUTIN 07/08/2018
Hemoglobin 14.5 g/dl 13.5 – 17.5
Hematokrit 41 % 33 – 45
Leukosit 9.9 ribu/ul 4.5 – 11.0
Trombosit 173 ribu/ul 150 – 450
Eritrosit 4.79 juta/ul 4.50 – 5.90
INDEX ERITROSIT
MCV 86.4 /um 80.0 – 96.0
MCH 30.3 Pg 28.0 – 33.0
MCHC 35.0 g/dl 33.0 – 36.0
RDW 11.8 % 11.6 – 14.6
MPV 9.5 Fl 7.2 – 11.1
PDW 17 % 25 – 65
HITUNG JENIS
Eosinofil 0.80 % 0.00 – 4.00
Basofil 0.10 % 0.00 – 0.200
Netrofil 77.70 % 55.00 – 80.00
Limfosit 13.90 % 22.00 – 44.00
Monosit 7.50 % 0.00 – 7.00
KIMIA KLINIK
Gula Darah Sewaktu 108 mg/dl 60 – 140
SGOT 113 u/l < 35
SGPT 180 u/l < 45
CKMB 2.65 mg/ml <5.1
HS Troponin-1 25.0 mg/l 15-38
ELEKTROLIT ( 10/08/2018)
Natrium darah 126 mmol/L 136 – 145
Kalium darah 3.1 mmol/L 3.7 – 5.4
Calsium darah 0.95 mmol/L 1.17 – 1.29
SEROLOGI
HBsAg Non reactive Division ofNonCardiology
reactive
ECG Examination
Sinus rhythm, with frequency
110 bpm, LAD, LVH, OMI
anteroseptal Division of Cardiology
Sinus rhythm, with frequency 83
bpm, LAD, LVH, OMI anteroseptal Division of EKG
Cardiology
13/8/18
Chest X-ray Examination
1. Right cardium
border is 1/3
greater than
hemithorax
2. Left cardial
waist
dissapeared
3. Cardiac apex
grounded
Conclusion (07/08/2018) :
1. Cardiomegaly with pulmonary edem
2. Right pleural effusion
Diagnosis
• A(x) : OMI Anteroseptal
• F(x) : NYHA II ADHF
• E(x) : Coronary Artery Disease(CAD)
• Other :
– Ascites
– Increase of transaminase enzyme (OT/PT
113/100),
– Azotemia (Ur/Cr 39/1,4),
– Hyponatremia (127),
– Hypokalemia (95)
Therapy
Emergency
Therapy Plan:
unit:
•Inj Furosemid 60 mg • Half-sitting bedrest
ekstra IV • O2 3 lpm
•DC • Diet 1700 kkal
• IVFD RL 20 cc/h
• Inj Furosemid on SP dosage 5
mg/h
• Bisoprolol (delay)
• Aspilet 80 mg/24h
• Atorvastatin 40 mg/24h
• Ramipril 5 mg/24h
Plan
• Rontgen thorax
• Echocardiography
Myocardial Infarction
Pathogenesis
Most of the cases result from disruption of an
athersclerotic plaque with subsequent platelet
aggregation and formation of an intracoronary
thrombus
Mechanism of Coronary Thrombus
Formation
Consequences of Coronary
Thrombosis
Changes in Infarction
• Early Changes
• 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
• Functional Alterations
– Impaired contractility and compliance
– Ventricular remodeling
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

ECG Abnormalities
• Unstable Angina/NSTEMI
ECG abnormalities
• STEMI
Cardiac Serum Markers
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
Complications
Heart Failure
Heart Failure
• Heart failure is a clinical syndrome characterized
by typical symptoms (breathlessness, ankle
swelling and fatigue)
• Accompanied by signs (elevated jugular venous
pressure, pulmonary crackles and peripheral
oedema)
• Caused by a structural and/or functional cardiac
abnormality, resulting in a reduced cardiac output
and/ or elevated intracardiac pressures at rest or
during stress.
(ESC, 2016)
Heart failure is present when
The heart is unable to pump blood forward at a sufficient
rate to meet the metabolic demands of the body
(forward failure)
Is able to do so only if the cardiac filling pressures are

abnormally high (backward failure)
Both
Acute Heart Failure
Rapid onset or worsening of symptoms and or

signs of HF
A life threatening medical condition, requiring

urgent evaluation and treatment
• Key mediators of
cardiac output.
Determinants
• of the stroke volume
include contractility,
preload, and
afterload. Cardiac
output Heart rate
Stroke volume
Conditions that cause left-
sided heart failure through
impairment of ventricular
systolic or diastolic
function.
A Note that in chronic stable

stages the conditions in this
box may instead result in
heart failure with preserved
EF, due to compensatory
ventricular hypertrophy and
increased diastolic stiffness
(diastolic dysfunction).
Types of Heart Failure
• Systolic Dysfunction
• Coronary Artery Disease
• Hypertension
• Valvular Heart Disease
• Diastolic Dysfunction
• Hypertension
• Coronary artery disease
• Hypertrophic obstructive cardiomyopathy
(HCM)
• Restrictive cardiomyopathy
Classification of HF: Comparison Between
ACC/AHA HF Stage and NYHA Functional Class
ACC/AHA HF Stage1 NYHA Functional Class2
A At high risk for heart failure but without None

structural heart disease or symptoms
of heart failure (eg, patients with
hypertension or coronary artery disease)
I Asymptomatic
B Structural heart disease but without
symptoms of heart failure
II Symptomatic with moderate exertion

C Structural heart disease with prior or
current symptoms of heart failure
III Symptomatic with minimal exertion
D Refractory heart failure requiring IV Symptomatic at rest

specialized interventions
1Hunt SA et al. J Am Coll Cardiol. 2001;38:2101–2113. Division of Cardiology

2New York Heart Association/Little Brown and Company, 1964. Adapted from: Farrell MH et al. JAMA. 2002;287:890–897.
• Some factors that can
triggering acute heart
failure
Heart Failure as Complication of MI
• Acute cardiac ischemia results in impaired
ventricular contractility (systolic dysfunction)
and increased myocardial stiffness (diastolic
dysfunction), both of which may lead to
symptoms of heart failure.
• In addition, ventricular remodeling,
arrhythmias, and acute mechanical
complications of MI) may culminate in heart
failure.
Heart Failure as Complication of MI
• Can be directly caused by impaired contractility
resulting in both systolic and diastolic dysfunction
• More rarely results from papillary muscle infarction
or rupture causing moderate to severe mitral
regurgitation.
• Resuts from venticular septal rupture
Diagnostic of Acute Heart Failure
• Based on presenting symptoms and clinical findings
• History
• Physical examination
• ECG
• Chest X-ray
• Echocardiography
• Laboratory (BGA, etc)
ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2008
FLUID OVERLOAD > Acute Decompensated Heart
Failure (ADHF)/Pulmonary Edema
>Medical Emergency!
Monitoring
Non invasive:
 Vital Sign
 Oxygenation
 Urine output
 ECG
Invasive:
 Arterial line (haemodynamic unstable)
 Central venous lines
 Pulmonary artery catheter
 Coronary angiography
Goals of treatment
Immediate (ED/ICU/ICCU)
 Improved symptom
 Restore oxygenation and improve organ perfusion
 Limit cardiac/renal damage
 Minimize ICU length of stay
Intermediate (hospital)
 Stabilize patient & optimize treatment strategy
 Initiate appropriate pharmacology therapy
 Consider device therapy
 Minimize hospital length of stay
Long term and pre discharge management
 Plan follow up strategy
 Education
 Prevention
 Quality of life
Management
 Immediate symptomatic treatment
 Patient distressed or in pain >> analgesia, sedation
 Pulmonary congestion >> diuretic, vasodilator
 Arterial oxygen saturation < 95% >> increase FiO2,
consider CPAP, NIPPV, mechanical ventilation
 Heart rate and rhythm disorder >> pacing,
antiarrhythmics, electroversion
ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2008
Therapy
• It is important to identify the precipitant of heart failure and treat as the
HF episode is being treated.
• Diuretics: Lasix (furosemide)
– Helps eliminate excess fluid that the heart cannot accommodate (preload) and
improve stroke volume, thereby decreasing pulmonary and peripheral edema
• Morphine:
– Decreases preload by acting as a venodilator, and reduces sympathetic
activation and consequently demand on heart by procuring pain relief
• Nitrates:
– Decrease preload via venodilation, and improve oxygen delivery to the heart
• Oxygen:
– Oxygen +/- noninvasive ventilation – preserve ventilator drive and maintaining
blood oxygen saturation
• Positioning:
– Sit patient upright with legs dangling down to promote blood pooling in the
lower extremities and decrease preload
Therapeutic Algorithm HFrEF
Other Linked Diseases
Diabetes Mellitus (OCI)
• Mechanism of CHD occurrence in type 2 DM
very complex and associated with existence
atherosclerosis is influenced by various factors
among others, hypertension, hyperglycemia,
dyslipidemia, smoking, family history with
CHD, and obesity
• Yanti, et al at Dr. Kariadi Semarang in 2008 in his
research reported that risk factors which has been
shown to affect the incidence of CHD in patients with
type 2 diabetes is hypertension, levels triglycerides 150
mg / dl, HDL cholesterol levels <45 mg / dl, and fasting
blood glucose levels 126 mg / dl.1
• Source : Yanti, Suharyo H, Tony S. Faktor-Faktor Risiko

Kejadian Penyakit Jantung Koroner pada Penderita
Diabetes Melitus tipe 2 Studi Kasus di RSUP Dr. Kariadi
Semarang 2008
• Sorrentino MJ in Cholesterol reduction to
prevent CAD that the risk of CHD occurs in
men who 55 years old and in women aged 45
years applicable if the onset of menopause is
normal.
• Diabetes mellitus is associated with physical-
pathological changes in the system
cardiovascular. Among them may be
endothelial dysfunction and disorders blood
vessels that ultimately increase the risk of
coronary artery diseases (CAD). This condition
can lead to microangiopathy, fibrosis heart
muscle, and abnormalities of heart muscle
metabolism.
Pneumonia
• MI might be a complication of pneumonia in
the early phase of presentation
• A study by Cangemi et al (2014) suggests that
platelet activation is associated with
myocardial infarction in patients with
pneumonia
• Patients with pneumonia are found to have
Thromboxan-2 overproduction which can
enhance platelet activation
Pneumonia
• Platelet can also intact directly with LPS on the
surface of Gram-negative bacteria by a TLR4-
mediated mechanism, resulting in platelet
activation and aggregation, and eventually
thrombus formation
Source: Cangemi et al, 2014. Platelet Activation

Is Associated With Myocardial
Infarction In Patients With Pneumonia
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Case Presentation

Alyssa Amalia G 99162077

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

The patient is more comfortable in half-sitting position, the

bowel sound (+) normal.

7 weeks Fibrosis and scarring complete

Cardiac serum markers

Antithrombotic • Antiplatelet agents

Is able to do so only if the cardiac filling pressures are

Rapid onset or worsening of symptoms and or

A life threatening medical condition, requiring

A Note that in chronic stable

A At high risk for heart failure but without None

II Symptomatic with moderate exertion

D Refractory heart failure requiring IV Symptomatic at rest

1Hunt SA et al. J Am Coll Cardiol. 2001;38:2101–2113. Division of Cardiology

• Source : Yanti, Suharyo H, Tony S. Faktor-Faktor Risiko

Source: Cangemi et al, 2014. Platelet Activation

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