Skenario 5: Nyeri Dada disertai Berdebar

Seorang laki-laki usia 60 tahun datang ke UGD dengan keluhan nyeri dada dan berdebar 4 jam
sebelumnya. Penderita memiliki riwayat hipertensi lama dan merokok. Pada pemeriksaan fisik
didapatkan tekanan darah 140/90 mmHg, nadi 200 x/menit teratur, dan frekuensi nafas 24
x/menit. Pada pemeriksaan fisik tidak didapatkan ronki, akral dingin. Tidak didapatkan edema
tungkai. Pada pemeriksaan EKG didapatkan irama takikardia ventrikuler 200 x/menit.
Kata Kunci: Laki-laki 60 tahun, nyeri dada, berdebar, onset 4 jam, hipertensi lama, merokok,
nadi 200 x/menit, irama takikardia ventrikuler
Daftar Pustaka
http://www.uptodate.com/contents/differential-diagnosis-of-chest-pain-in-adults
NTRODUCTION
The differential diagnosis of patients presenting with chest pain is extensive, ranging from
benign musculoskeletal etiologies to life-threatening cardiac disease. Many of the diseases that
cause chest pain are reviewed in detail elsewhere. This topic will discuss the differential
diagnosis of chest pain in an approximate order of prevalence seen in primary care practice.
Within each subsection, diseases that may pose an immediate threat to life are emphasized,
including the following six entities: acute coronary syndrome, aortic dissection, effort rupture of
the esophagus, perforating peptic ulcer, pulmonary embolus, and tension pneumothorax. In the
primary care setting, reports of the etiology of chest pain are consistent, including
musculoskeletal (36 to 49 percent), cardiac (15 to 18 percent), gastrointestinal (8 to 19 percent),
pulmonary (5 to 10 percent), and psychiatric (8 to 11 percent) [1-4].
The office and emergency department evaluation of the patient with chest pain are discussed in
detail separately. (See "Diagnostic approach to chest pain in adults" and "Evaluation of the adult
with chest pain in the emergency department".)
CHEST WALL PAIN
Chest wall causes of pain are among the most common etiologies of chest pain seen by primary
care clinicians, accounting for 36 percent of episodes in one report (table 1) [1-4].
Musculoskeletal causes of chest pain are typically not life-threatening. However, it is important
to note that chest wall tenderness may present concomitantly with myocardial ischemia; the latter
should be considered first in any patient at risk by age, history, or associated symptoms [1].
Causes of true chest wall pain may be musculoskeletal or related to the skin and sensory nerves.
Musculoskeletal pain Demographic features, characteristics of the chest pain, and associated
symptoms may favor the diagnosis of musculoskeletal chest pain or suggest other causes of chest
discomfort (table 2). As an example, the patient may describe a history of repetitive or
unaccustomed activity involving the upper trunk or arms, consistent with a musculoskeletal pain
etiology. Certain characteristics of the chest pain or associated symptoms, such as dyspnea, may
suggest a non-musculoskeletal origin. (See "Clinical evaluation of musculoskeletal chest pain".)

Musculoskeletal chest pain is often insidious and persistent, lasting for hours to weeks. It is
frequently sharp and localized to a specific area (such as the xiphoid, lower rib tips, or
midsternum), but may be diffuse and poorly localized. The pain may be positional or exacerbated
by deep breathing, turning, or arm movement; positional or pleuritic components are also noted
in a variety of visceral processes, particularly those involving the pleura and pericardium
http://www.aafp.org/afp/2005/0215/p743.html
http://emedicine.medscape.com/article/1910735-overview
Practice Essentials
Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations ranging from
those for ST-segment elevation myocardial infarction (STEMI) to presentations found in non
ST-segment elevation myocardial infarction (NSTEMI) or in unstable angina. It is almost always
associated with rupture of an atherosclerotic plaque and partial or complete thrombosis of the
infarct-related artery.
Essential update: Study finds that STEMI mechanisms and stenting outcome are similar in
women and men
Despite their smaller coronary vessels and higher risk profile, women with STEMI appear to
respond just as well as men to primary PCI and stenting, according to the Optical Coherence
Tomography Assessment of Gender Diversity in Primary Angioplasty (OCTAVIA) study.
OCTAVIA, which was designed to examine gender differences at the time of primary PCI,
included 140 STEMI patients at 14 Italian centers, matched by age and risk factors, who received
an everolimus-eluting stent.[1]
On initial OCT, no differences by gender were found in the proportion of ruptured or eroded
plaques, thus suggesting that the pathophysiology of STEMI is nearly identical in men and
women. On repeat OCT at nine months, intended to assess stent healing, more than 90% of both
men and women had fully covered stent struts. Although OCTAVIA was not powered for clinical
end points, no significant differences in death, reinfarction, stroke, stent thrombosis, or target
vessel reintervention were evident at one year.[1]
Signs and symptoms
Atherosclerosis is the primary cause of ACS, with most cases occurring from the disruption of a
previously nonsevere lesion. Complaints reported by patients with ACS include the following:

Palpitations

Pain, which is usually described as pressure, squeezing, or a burning sensation across the
precordium and may radiate to the neck, shoulder, jaw, back, upper abdomen, or either
arm

Exertional dyspnea that resolves with pain or rest

Diaphoresis from sympathetic discharge

Nausea from vagal stimulation

Decreased exercise tolerance

Physical findings can range from normal to any of the following:

Hypotension: Indicates ventricular dysfunction due to myocardial ischemia, myocardial

infarction (MI), or acute valvular dysfunction

Hypertension: May precipitate angina or reflect elevated catecholamine levels due to

anxiety or to exogenous sympathomimetic stimulation

Diaphoresis

Pulmonary edema and other signs of left heart failure

Extracardiac vascular disease

Jugular venous distention

Cool, clammy skin and diaphoresis in patients with cardiogenic shock

A third heart sound (S3) and, frequently, a fourth heart sound (S4)

A systolic murmur related to dynamic obstruction of the left ventricular outflow tract

Rales on pulmonary examination (suggestive of left ventricular dysfunction or mitral

regurgitation)

Potential complications include the following:

Ischemia: Pulmonary edema

Myocardial infarction: Rupture of the papillary muscle, left ventricular free wall, and
ventricular septum

See Clinical Presentation for more detail.

Diagnosis
Guidelines for the management of non-ST-segment elevation ACS were released in 2011 by the
European Society of Cardiology (ESC).[2] The guidelines include the use of the CRUSADE risk

score (Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with
Early implementation of the ACC/AHA guidelines).
In the emergency setting, electrocardiography (ECG) is the most important diagnostic test for
angina. ECG changes that may be seen during anginal episodes include the following:

Transient ST-segment elevations

Dynamic T-wave changes: Inversions, normalizations, or hyperacute changes

ST depressions: These may be junctional, downsloping, or horizontal

Laboratory studies that may be helpful include the following:

Creatine kinase isoenzyme MB (CK-MB) levels

Cardiac troponin levels

Myoglobin levels

Complete blood count

Basic metabolic panel

Diagnostic imaging modalities that may be useful include the following:

Chest radiography

Echocardiography

Myocardial perfusion imaging

Cardiac angiography

Computed tomography, including CT coronary angiography and CT coronary artery

calcium scoring

See Workup for more detail.

Management
Initial therapy focuses on the following:

Stabilizing the patients condition

Relieving ischemic pain

Providing antithrombotic therapy

Pharmacologic anti-ischemic therapy includes the following:

Nitrates (for symptomatic relief)

Beta blockers (eg, metoprolol): These are indicated in all patients unless contraindicated

Pharmacologic antithrombotic therapy includes the following:

Aspirin

Clopidogrel

Prasugrel

Ticagrelor

Glycoprotein IIb/IIIa receptor antagonists (abciximab, eptifibatide, tirofiban)

Pharmacologic anticoagulant therapy includes the following:

Unfractionated heparin (UFH)

Low-molecular-weight heparin (LMWH; dalteparin, nadroparin, enoxaparin)

Factor Xa inhibitors (rivaroxaban, fondaparinux)

Additional therapeutic measures that may be indicated include the following:

Thrombolysis

Percutaneous coronary intervention (preferred treatment for ST-elevation MI)

Current guidelines for patients with moderate- or high-risk ACS include the following:

Early invasive approach

Concomitant antithrombotic therapy, including aspirin and clopidogrel, as well as UFH or

LMWH

See Treatment and Medication for more detail.

Image library

A 62-year-old woman with a history of chronic stable angina and

a "valve problem" presents with new chest pain. She is symptomatic on arrival, complaining of
shortness of breath and precordial chest tightness. Her initial vital signs are blood pressure =
140/90 mm Hg and heart rate = 98. Her electrocardiogram (ECG) is as shown. She is given
nitroglycerin sublingually, and her pressure decreases to 80/palpation. Right ventricular ischemia
should be considered in this patient.
Background
Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations ranging from
those for ST-segment elevation myocardial infarction (STEMI) to presentations found in non
ST-segment elevation myocardial infarction (NSTEMI) or in unstable angina. In terms of
pathology, ACS is almost always associated with rupture of an atherosclerotic plaque and partial
or complete thrombosis of the infarct-related artery. (See Etiology.)
In some instances, however, stable coronary artery disease (CAD) may result in ACS in the
absence of plaque rupture and thrombosis, when physiologic stress (eg, trauma, blood loss,
anemia, infection, tachyarrhythmia) increases demands on the heart. The diagnosis of acute
myocardial infarction in this setting requires a finding of the typical rise and fall of biochemical
markers of myocardial necrosis in addition to at least 1 of the following[3] (See Workup.):

Ischemic symptoms

Development of pathologic Q waves

Ischemic ST-segment changes on electrocardiogram (ECG) or in the setting of a coronary

intervention

The terms transmural and nontransmural (subendocardial) myocardial infarction are no longer
used because ECG findings in patients with this condition are not closely correlated with
pathologic changes in the myocardium. Therefore, a transmural infarct may occur in the absence
of Q waves on ECGs, and many Q-wave myocardial infarctions may be subendocardial, as noted
on pathologic examination. Because elevation of the ST segment during ACS is correlated with
coronary occlusion and because it affects the choice of therapy (urgent reperfusion therapy),
ACS-related myocardial infarction should be designated STEMI or NSTEMI. (See Workup.)
Attention to the underlying mechanisms of ischemia is important when managing ACS. A simple
predictor of demand is rate-pressure product, which can be lowered by beta blockers (eg,
metoprolol or atenolol) and pain/stress relievers (eg, morphine), while supply may be improved
by oxygen, adequate hematocrit, blood thinners (eg, heparin, IIb/IIIa agents such as abciximab,

eptifibatide, tirofiban, or thrombolytics), and/or vasodilators (eg, nitrates, amlodipine). (See

Medications.)
In 2010, the American Heart Association (AHA) published new guideline recommendations for
the diagnosis and treatment of ACS.[4]
Etiology
Acute coronary syndrome (ACS) is caused primarily by atherosclerosis. Most cases of ACS
occur from disruption of a previously nonsevere lesion (an atherosclerotic lesion that was
previously hemodynamically insignificant yet vulnerable to rupture). The vulnerable plaque is
typified by a large lipid pool, numerous inflammatory cells, and a thin, fibrous cap.
Elevated demand can produce ACS in the presence of a high-grade fixed coronary obstruction,
due to increased myocardial oxygen and nutrition requirements, such as those resulting from
exertion, emotional stress, or physiologic stress (eg, from dehydration, blood loss, hypotension,
infection, thyrotoxicosis, or surgery).
ACS without elevation in demand requires a new impairment in supply, typically due to
thrombosis and/or plaque hemorrhage.
The major trigger for coronary thrombosis is considered to be plaque rupture caused by the
dissolution of the fibrous cap, the dissolution itself being the result of the release of
metalloproteinases (collagenases) from activated inflammatory cells. This event is followed by
platelet activation and aggregation, activation of the coagulation pathway, and vasoconstriction.
This process culminates in coronary intraluminal thrombosis and variable degrees of vascular
occlusion. Distal embolization may occur. The severity and duration of coronary arterial
obstruction, the volume of myocardium affected, the level of demand on the heart, and the ability
of the rest of the heart to compensate are major determinants of a patient's clinical presentation
and outcome. (Anemia and hypoxemia can precipitate myocardial ischemia in the absence of
severe reduction in coronary artery blood flow.)
A syndrome consisting of chest pain, ischemic ST-segment and T-wave changes, elevated levels
of biomarkers of myocyte injury, and transient left ventricular apical ballooning (takotsubo
syndrome) has been shown to occur in the absence of clinical CAD, after emotional or physical
stress. The etiology of this syndrome is not well understood but is thought to relate to a surge of
catechol stress hormones and/or high sensitivity to those hormones.
Prognosis
Six-month mortality rates in the Global Registry of Acute Coronary Events (GRACE) were 13%
for patients with NSTEMI ACS and 8% for those with unstable angina.
An elevated level of troponin (a type of regulatory protein found in skeletal and cardiac muscle)
permits risk stratification of patients with ACS and identifies patients at high risk for adverse

cardiac events (ie, myocardial infarction, death) up to 6 months after the index event.[5, 6] (See
Workup.)
The PROVE IT-TIMI trial found that after ACS, a J-shaped or U-shaped curve association is
observed between BP and the risk of future cardiovascular events.[7]
LeLeiko et al determined that serum choline and free F(2)-isoprostane are also predictors of
cardiac events in ACS. The authors evaluated the prognostic value of vascular inflammation and
oxidative stress biomarkers in patients with ACS to determine their role in predicting 30-day
clinical outcomes. Serum F(2)-isoprostane had an optimal cutoff level of 124.5 pg/mL, and
serum choline had a cutoff level of 30.5 mol/L. Choline and F(2)-isoprostane had a positive
predictive value of 44% and 57% and a negative predictive value of 89% and 90%, respectively.
[8]

Testosterone deficiency is common in patients with coronary disease and has a significant
negative impact on mortality. Further study is needed to assess the effect of treatment on
survival.[9]
A study by Sanchis et al suggests renal dysfunction, dementia, peripheral artery disease, previous
heart failure, and previous myocardial infarction are the comorbid conditions that predict
mortality in NSTEMI ACS.[10] In patients with comorbid conditions, the highest risk period was
in the first weeks after NSTEMI ACS. In-hospital management of patients with comorbid
conditions merits further investigation.
Patients with end-stage renal disease often develop ACS, and little is known about the natural
history of ACS in patients receiving dialysis. Gurm et al examined the presentation,
management, and outcomes of patients with ACS who received dialysis before presentation for
an ACS. These patients were enrolled in the Global Registry of Acute Coronary Events
(GRACE) at 123 hospitals in 14 countries from 1999-2007.
NSTEMI ACS was the most common in patients receiving dialysis, occurring in 50% of patients
(290 of 579) versus 33% (17,955 of 54,610) of those not receiving dialysis The in-hospital
mortality rates were higher among patients receiving dialysis (12% vs 4.8%; p < 0.0001). Higher
6-month mortality rates (13% vs 4.2%; p < 0.0001), recurrent myocardial infarction incidence
(7.6% vs 2.9%; p < 0.0001), and unplanned rehospitalizations (31% vs 18%; p < 0.0001) were
found among those who survived to discharge. Outcomes in patients who received dialysis was
worse than was predicted by the calculated GRACE risk score for in-hospital mortality (7.8%
predicted vs 12% observed; p < 0.05). This suggests that the GRACE risk score underestimated
the risk of major events in these patients.[11]
In a study that assessed the impact of prehospital time on STEMI outcome, Chughatai et al
suggest that total time to treatment should be used as a core measure instead of door-toballoon time.[12] This is because on-scene time was the biggest fraction of "pre-hospital time.
The study compared groups with total time to treatment of more than 120 minutes compared
with 120 minutes or less and found mortalities were 4 compared with 0 and transfers to a tertiary
care facility were 3 compared with 1, respectively.

Patient Education
Patient education of risk factors is important, but more attention is needed regarding delays in
door-to-balloon time, and one major barrier to improving this delay is patient education
regarding his or her symptoms. Lack of recognition of symptoms may cause tremendous delays
in seeking medical attention.
Educate patients about the dangers of cigarette smoking, a major risk factor for coronary artery
disease (CAD). The risk of recurrent coronary events decreases 50% at 1 year after smoking
cessation. Provide all patients who smoke with guidance, education, and support to avoid
smoking. Smoking-cessation classes should be offered to help patients avoid smoking after a
myocardial infarction. Bupropion increases the likelihood of successful smoking cessation.
Diet plays an important role in the development of CAD. Therefore, prior to hospital discharge, a
patient who has had a myocardial infarction should be evaluated by a dietitian. Patients should be
informed about the benefits of a low-cholesterol, low-salt diet. In addition, educate patients about
AHA dietary guidelines regarding a low-fat, low-cholesterol diet.
A cardiac rehabilitation program after discharge may reinforce education and enhance
compliance.
The following mnemonic may useful in educating patients with CAD regarding treatments and
lifestyle changes necessitated by their condition:

A = Aspirin and antianginals

B = Beta blockers and blood pressure (BP)

C = Cholesterol and cigarettes

D = Diet and diabetes

E = Exercise and education

For patients being discharged home, emphasize the following:

Timely follow-up with primary care provider

Compliance with discharge medications, specifically aspirin and other medications used
to control symptoms

Need to return to the ED for any change in frequency or severity of symptoms