PEMICU 6 KGD

Denise Elycia
ACUTE CORONARY
SYNDROME
Chest pain
• Acute chest pain : recent onset of pain, pressure, or
tightness in the anterior thorax between the xiphoid,
suprasternal notch, and both midaxillary lines
• Unstable angina is a clinical diagnosis defined by chest
pain or an equivalent from inadequate myocardial
perfusion that is new, occuring with greater frequency,
less activity or at rest

Tintinalli’s Emergency Medicine 8th edition

• Classic chest pain (Classic cardiac chest pain) :
retrosternal left anterior chest crushing, squeesing,
tightness or pressure  exacerbated by exertion and
relieved by rest
• Non classic chest pain : chest pain lasting for seconds,
constant pains lasting for 12-24 hours or more without
waxing and waning intensity or pain worsened by specific
body movements or positions such as twisting and turning
of the thorax

Tintinalli’s Emergency Medicine 8th edition

Tintinalli’s Emergency Medicine 8th edition
Tintinalli’s Emergency Medicine 8th edition
• Diagnostic testing :
• Imaging  chest radiography or CT scan
• Cardiac troponins  cardiac muscle contraction
• ECG
• Within 10 minutes of ED arrival on patients with chest pain or other
symptoms concerning for ACS

Tintinalli’s Emergency Medicine 8th edition

Tintinalli’s Emergency Medicine 8th
edition
Tintinalli’s Emergency Medicine 8th
edition
 Acute Coronary Syndrome
• Risk factors:
• Age: 85% (>65 yrs)
• Gender: Men earlier, Women after menopause
• Genetic Factors and Family History: diabetes,
elevated cholesterol and high blood pressure.
• Race and Ethnicity: African-Americans (highest)
• Medical Conditions: Obesity & Metabolic Syndrome
• Lifestyle: Physical inactivity, smoking, alcohol, diet
• NSAID & COX-2 inhibitors (except aspirin)

http://umm.edu/health/medical/reports/articles/heart-attack-and-acute-coronary-syndrome
 Acute Coronary Syndrome
• Symptoms:
• Angina
• Palpitations
• Pain
• Exertional dyspnea that resolves with pain or rest
• Diaphoresis from sympathetic discharge
• Nausea from vagal stimulation
• Decreased exercise tolerance

http://umm.edu/health/medical/reports/articles/heart-attack-and-acute-coronary-syndrome
 Acute Coronary Syndrome
• Signs:
• Ongoing chest pain  lie quietly in bed and may
appear anxious, diaphoretic, and pale
• Hypotension
• Hypertension
• 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

http://umm.edu/health/medical/reports/articles/heart-attack-and-acute-coronary-syndrome
Lilly LS. Pathophysiology of Heart Disease, 5th ed. Philadelphia: Lippincott Williams &
Wilkins, 2011
Lilly LS. Pathophysiology of Heart Disease, 5th ed. Philadelphia: Lippincott
Williams & Wilkins, 2011
 2014 AHA/ACC Guideline for the Management of Patients
With Non–ST-Elevation Acute Coronary Syndromes

NSTEMI
Iskemi atau infark miokard akibat reduksi dari aliran darah
Definisi coroner tanpa elevasi segmen ST diikuti kenaikan biomarker
(troponin maupun CK-MB)

Ketidakseimbangan antara myocardial oxygen consumption

Etiologi
(MVO2) dan demand yg diakibatkan obstruksi arteri coroner

• Histori gejala:
• Nyeri dada seperti ditekan saat istirahat atau dengan
minimal 10 menit
Diagnosis • Sering dimulai dari retrosternal dan dapat menjalar ke
lengan kiri (sering) dan kanan, leher
• Disertai diaphoresis, dyspnea, nausea, abdominal pain,
atau syncope
 2014 AHA/ACC Guideline for the Management of Patients
With Non–ST-Elevation Acute Coronary Syndromes

NSTEMI
Lanjuta • Pemeriksaan fisik
n • Disfungsi ventricular  terdapat S4
diagnosi • Split paradoksikal bunyi jantung kedua
s • Dapat ditemukan murmur regurgitasi mitral akibat
disfungsi otot papilaris
• EKG
• Depresi segmen ST yg baru menunjukan iskemia akut
• New T-wave inversion
• 1-6% EKG normal
• Biomarker
• Tropnin T atau I positif dalam beberapa jam setelah onset
dan bertahan smpai 2 minggu
• CK-MB kurang spesifik karna ada d otot skeletl juga
(beberapa jam sampai 48 jam)
 2014 AHA/ACC Guideline for the Management of Patients
With Non–ST-Elevation Acute Coronary Syndromes

Tatalaksana Awal RS
Oksigen Bila saturasi O2 <90%, respiratory distress atau high
risk hypoxemia
Nitrogliserin Sublingual 0,4 mg, dapat diberikan 3 dosis interval 5
(NTG) menit
(mengurangi nyeri dada dan dilatasi PD ↓preload &
↑suplai  ↓kebutuhan O2 miokard
Analgesic Morfin  Mengurangi nyeri
therapy 1-5 mg IV, dapat diulang interval 5-30menit maks 20
mg
Aspirin Aspirin bukkal 160-325 mg di ruang emergency
Lanjutan: oral 75-162 mg
 2014 AHA/ACC Guideline for the Management of Patients
With Non–ST-Elevation Acute Coronary Syndromes

Tatalaksana Awal
Beta blocker IV Metoprolol 5 mg setiap 2-5 menit sampai 3 dosis
jika HR>60, sistol>100, PR interval <0,24 dan
ronki<10cm dr diafragma
Lanjutan : oral metoprolol 50 mg tiap 6 jam selama
48 jam dan dilanjutkan 100 mg tiap 12 jam
CCB Berikan bila:
• Beta blocker tidak berhasil
• Reccurent iskemi, KI beta blocker, resiko syok
kardiogenik, PR interval >0,24
Co:verapamil atau diltiazem
Cholesterol management
 2014 AHA/ACC Guideline for the Management of Patients
With Non–ST-Elevation Acute Coronary Syndromes

Tatalaksana
TAKIARITMIA
Tachycardia
• Tachycardia is a faster than normal heart rhythm (greater
than 100 beats per minute for an adult), can quickly
deteriorate to cardiac arrest if left untreated. When looking
at the ECG, can be classified as narrow complex (QRS
less than 0.12 secs) or wide complex (QRS exceeds 0.12
secs)
• A narrow complex rhythm, sinus tachycardia (ST) is not
considered an arrhythmia. Originating above the
ventricles of the heart, supraventricular tachycardia
(SVT) may have wide or narrow QRS complex. A wide
complex rhythm, VT can deteriorate to VF and cardiac
arrest so must be treated immediately.
 PAROXYSMAL SUPRAVENTRICULAR
TACHYCARDIA
• Results from sustained reentry occurring with the AV
node, with an ectopic atrial focus accounting for the
remaining 15% - 20%.
• QRS complex is of normal width, rapid, and regular.
• P waves are “buried” within the QRS complex in about 70% of
cases.
• Others: a P wave (so-called “retrograde” P wave) is found
immediately adjacent before, during, or after the QRS complex
without a measurable PR interval.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th

 Treatment
Clinical Significance • If applied early in the dysrhythmia
• >> females, with a peak = late course, vagal maneuvers are often
teenage and young adult effective
• Attention to technique is important to maximize
• The majority of pts (x) active success rate.
cardiovascular disease. • If there is no response to vagal
• Patients may be able to describe maneuvers, adenosine IV is
the abrupt onset of this reentrant recommended to convert to sinus
dysrhythmia and also note when it rhythm.
self-terminates. • It is the rare patient who requires β-
blocker or calcium channel blocker.
• Palpitations, lightheadedness,
• In patients with recalcitrant paroxysmal
and dyspnea are common
supraventricular tachycardia or who are
symptoms. unstable, use electrical cardioversion
to convert the dysrhythmia.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th

ACUTE HEART FAILURE
Acute Heart Failure
• AHF refers to rapid onset or worsening of symptoms and/or signs of
HF. It is a life-threatening medical condition requiring urgent
evaluation and treatment, typically leading to urgent hospital
admission.
• AHF may present as a first occurrence (de novo) or, more
frequently, as a consequence of acute decompensation of chronic
HF, and may be caused by primary cardiac dysfunction or
precipitated by extrinsic factors, often in patients with chronic HF.
• Acute myocardial dysfunction (ischaemic, inflammatory or toxic),
acute valve insufficiency or pericardial tamponade are among the
most frequent acute primary cardiac causes of AHF.
• Decompensation of chronic HF can occur without known precipitant
factors, but more often with one or more factors, such as infection,
uncontrolled hypertension, rhythm disturbances or non-
adherence with
drugs/diet 2016 ESC Guidelines for the diagnosis and management of Heart Failure
 Sign & symptoms
• Cardinal symptoms  fatigue
and shortness of breath
• In the early stages of HF,
dyspnea is observed only
during exertion; however, as
the disease progresses,
dyspnea occurs with less
strenuous activity, and it
ultimately may occur even at
rest
• Cheyne-stokes respiration 
caused by a diminished
sensitivity of the respiratory
center to arterial Pco2
• Acute pulmonary edema
• Gastrointestinal symptoms
• Orthopnea  dyspnea
occurring in the recumbent
position, is usually a later
manifestation of HF than is
exertional dyspnea
• Nocturnal cough
• Paroxysmal nocturnal
dyspnea (PND)  refers to
acute episodes of severe
shortness of breath and
coughing that generally occur
at night and awaken the
patient from sleep, usually 1–
3 h after the patient retires

Sumber: Harrison’s Cardiovascular Medicine, 2th ed.

 Physical Examination
• General appearance and vital signs • Pulmonary examination 
 patient appears to be in no pulmonary crackles (rales or
distress at rest except for feeling crepitations)
uncomfortable when lying flat for • Cardiac examination  If
more than a few minutes, systolic cardiomegaly is present, the
blood pressure may be normal or point of maximal impulse (PMI)
high in early HF, but it generally is usually is displaced below the ffth
reduced in advanced HF because of intercostal space and/or lateral to
severe LV dysfunction, the pulse the midclavicular line, and the
pressure may be diminished, impulse is palpable over two
reflecting a reduction in stroke interspaces.
volume, sinus tachycardia, cool • Abdomen and extremities
peripheral extremities and cyanosis
of the lips and nail bed • Cardiac cachexia
• Jugular veins  In the early stages
of HF, the venous pressure may be
normal at rest but may become
abnormally elevated with
sustained (∼1 min) pressure on the
abdomen (positive abdominojugular
reflux).

Sumber: Harrison’s Cardiovascular Medicine, 2th ed.

 Other examination
• Routine laboratory
testing
• Electrocardiogram
(ECG)
• CXR
• Assessment of LV
function
• Biomarkers
• Exercise testing

Sumber: Harrison’s Cardiovascular Medicine, 2th ed.

Sumber: Harrison’s Cardiovascular Medicine, 2th ed.
2016 ESC Guidelines for the diagnosis and management of
Heart Failure
Classification
2016 ESC Guidelines for the diagnosis and management of
Heart Failure
Initial management

acute heart failure.

of a patient with
2016 ESC Guidelines for the diagnosis and management of
Heart Failure
Management of
patients with

Heart Failure
2016 ESC Guidelines for the diagnosis and management of
acute heart failure
based on clinical
profile during an
early phase
 • i.v. = intravenous.
• aAlso a vasodilator.
• bNot recommended in acutely
worsened ischaemic heart
failure.
• cBolus not recommended in
hypotensive patients.

2016 ESC Guidelines for the diagnosis and management of Heart

2016 ESC Guidelines for the diagnosis and management of
Heart Failure
CARDIOPULMONARY
ARREST
 Cardiopulmonary Arrest
• Sudden loss of perfusing pulsatile blood flow 
cessation of cardiac mechanical activity
• Etiology: multitude of cardiovascular, metabolic,
infectious, neurologic, inflammatory, and
traumatic diseases
• 5 H's: Hypovolemia, Hypoxemia, H+ ion (acidosis),
Hypo-/Hyperkalemia, Hypothermia
• 5 T's: Tension pneumothorax, Tamponade, Toxins,
Thrombosis (pulmonary and cardiac)

http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/cardiovascular-emergencies/Default.htm
CAUSES OF CARDIAC ARREST

Rosen’s Emergency Medicine 7th Ed

 Cardiopulmonary Arrest
• Endpoint:
• Shockable:
• Pulseless ventricular tachycardia (VT)
• Ventricular fibrillation (VF)
• Pulseless electrical activity
• Asystole

http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/cardiovascular-emergencies/Default.htm
Cardiopulmonary Arrest

CHANGES 2005  2010 GUIDELINES:

• Airway (A) – Breathing (B) – Circulation (C) sequence to C-A-B
• Quality of CPR: rate and depth, complete chest recoil, minimizing
interruptions
• Importance of professional healthcare rescue teams in multiple tasks
during CPR

http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/cardiovascular-emergencies/Default.htm
Acute Cor Pulmonale
Etiology Cor pulmonale is a
state of cardiopulmonary
dysfunction that may result from
several different aetiologies and
pathophysiologic mechanisms
(table I):
• Pulmonary vasoconstriction
(secondary to alveolar hypoxia
or blood acidosis).
• Anatomic reduction of the
pulmonary vascular bed
(emphysema, pulmonary
emboli, etc.)
• Increased blood viscosity
(polycythaemia, sickle-cell
disease, etc.)
• Increased pulmonary blood flow

http://medind.nic.in/jac/t04/i2/jact04i2p128
 Symtomps
• Fainting spells during
activity
• Chest discomfort, usually
in the front of the chest
• Chest pain
• Swelling of the feet or
ankles
• Symptoms of lung
disorders, such as
wheezing or coughing
• Bluish lips and fingers
(cyanosis)
https://medlineplus.gov/ency/article/000129.htm http://medind.nic.in/jac/t04/i2/jact04i2p128
Evaluation
• Chest radiography
• Electrocardiography
• Two dimensional and Doppler
echocardiography (which can
provide an indirect
measurement of pulmonary
artery pressure when tricuspid
regurgitation is present)
• Pulmonary function tests
• Radionuclide ventriculography
• Magnetic resonance imaging
• Right heart catheterisation
• Lung biopsy
HT KRISIS
 Hypertension
• A hypertensive (high blood
pressure) crisis is when
blood pressure rises
quickly and severely
• Classification  urgency &
emergency hypertension

2013 ESH/ESC Guidelines for the

management
of arterial hypertension
Hypertensive crisis
• Hypertensive emergency  Acute elevation in BP (>/=
180/ 110mmHg) + active end-organ damage (ongoing
injury to the brain, heart, aorta, kidneys, and/or eyes)
• Hypertensive urgency  severe elevation in blood
pressure w/o acute end-organ dysfunction
Mechanism
• Sudden ↑ in SVR due to unregulated surge n circulating
vasocontrictors
• Spikes in BP  stress on vascular wall  endothelial
injury  ↑ vascular permeability, activation of platelets &
coagulation cascade, deposition of fibrin  2nd fibrinoid
necrosis of arteriolar end organ circulation  tissue
perfusion ↓  organ system dysfx
• Chronic HTN  shift to cerebral autoregulation  BP
elevation compensated  tolerate brain end organ
damage
ht Clinical manifestation
• Hypertensive encephalopathy 
neurologic complaints & mental status
changes (Drowsiness – coma)
• Intracranial hemorrhage  severe
headache (often sudden onset), focal
neurologic deficits, and/or altered
mental status
y • Acute pulmo edema  acute
e shortness of breath + Lower extremity
edema, jugular venous distention, and
an acces sory gallop (S3 or S4)
• Acute coronary syndrome  chest
pain + subtle signs of congestive heart
y failure
• Aortic dissection  severe chest
and/or back pain (tearing quality), BP
y b/w arms difference > 20 mmHg
• Acute renal failure  subtle SS,
nt hematuria, oliguria, or anuria, swelling
over the lower extremities + shortness
of breath
s,
• SS/:
• Severe chest pain
• Severe headache,
accompanied by
confusion and blurred
vision
• Nausea and vomiting
• Severe anxiety
• Shortness of breath
• Seizures
• unresponsiveness
GAMBAR EKG
Sinus rhythm
CPR FOR CARDIAC
ARREST AND TAKIARITMIA
Cardiac arrest
• Cardiac arrest is associated with one of the following rhythms:
• Asystole: cardiac standstill or flat line  absence of all evidence of electrical
activity on the ECG  no complexes visible on the monitor. Asystole will not
respond to shocks.
• Pulseless electrical activity (PEA): there are visible complexes on the
cardiac monitor but no pulses can be felt. Goal of treatment for PEA is to
identify and treat the underlying cause of the rhythm using the H's and T's.
PEA will not respond to shocks.
• Ventricular fibrillation (VF): chaotic electrical activity on the monitor, a victim
with VF will have no palpable pulses.
• Pulseless ventricular tachycardia (VT): Is usually seen as very wide QRS
complexes on the ECG. Victim will be pulseless. Without treatment, VT can
quickly deteriorate into VF; treatment is the same as for VF.

• Cardiac arrest: no pulse, unresponsive and not breathing. Prognosis

for survival is very poor. Therefore, it is critical to intervene BEFORE
cardiac arrest occurs.
• The goal of advanced life support is return of spontaneous circulation
(ROSC).
BLS • If the patient is not
responsive, the first
survey to use is the
BLS survey. The
ACLS survey
involves providing
advanced
treatments after the
BLS survey is
complete or when
the victim is awake
and responsive
• The final step in the BLS Survey is to begin CPR
1. Feel for the carotid pulse on the side of the neck behind the
trachea. Since a pulse may be difficult to find, attempt to feel
for the pulse for 5-10 seconds.
2. If you are not sure you feel a pulse, you should assume that
the pulse is not there. Start alternating 30 compressions and
2 breaths.
3. If the victim is not on his back, place him on his back on a
surface that will not compress as you do CPR.
4. Put the heel of your left hand on the bottom half of the
victim’s breastbone.
5. Rest the heel of your right hand on top of the left hand.
6. With your arms straight and shoulders directly over your
hands, begin compressions HARD and FAST. For an adult,
effective compressions will be at least 2 inches deep.
Effective compressions will be between 100 and 120 per
minute. Be sure that the chest fully expands between each
compression so that blood can flow back into the victim’s
heart. Do not lean on the chest between compressions.
7. After performing 30 hard and fast compressions, do a head
tilt and chin lift to open the victim’s airway. If you think the
victim may have a neck injury, use a jaw thrust to move the
jaw forward and open the airway.
8. If you have a barrier device, apply it to the victim’s nose
and/or mouth.
9. Give a slow deep breath over one second as you watch the
victim’s chest expand. Give a second breath.
10. Give another round of 30 compressions followed by 2
breaths over one second each.
11. If two or more rescuers are available, switch out every 2
minutes.
12. When a defibrillator arrives and is prepared, attach the
machine to the victim and defibrillate as soon as possible
and as directed.
13. CPR interruptions should be minimal
• When the BLS survey is complete, or if the patient is
conscious and responsive, the responder should conduct
the ACLS survey with a focus on the identification and
treatment of underlying cause(s) of the patient’s problem.
ACLS
Advanced life support includes:
• Determination of whether the cardiac rhythm is shockable
• Provision of vascular access for drug administration (see
Routes of Access for Medication Administration)
• Defibrillation
• Medication therapy
• Advanced airway management (although an ET tube is
preferred, efficient bag-mask ventilations can be just as
effective for short resuscitation efforts).
When to terminate resuscitation efforts
If the victim fails to respond to ACLS interventions, the team
leader must consider terminating treatment. Factors to consider
when making the decision to terminate resuscitation efforts
include:
• Failure to respond to ACLS interventions.
• Amount of time after collapse before CPR and defibrillation
began.
• Any other comorbid disease or conditions.
• Discovery of a “Do Not Resuscitate” order for the victim.
• Length of the resuscitation effort; increased time generally
results in poor outcomes.
• Policies of the healthcare facility.
• Low end-tidal carbon dioxide (ETCO2) after 20 minutes of CPR
in intubated victims (e.g., <10 mm Hg by quantitative waveform
capnography) along with other items listed above.
Post cardiac arrest care
Critical post-resuscitation treatments include:
• Therapeutic hypothermia: If the victim has ROSC but does not
respond to verbal stimulation, therapeutic hypothermia is
recommended. Lower the victim’s core temperature between
32°C and 36°C for at least 24 hours post resuscitation.
• Use quantitative waveform capnography to keep the PETCO2
at 35-40 mm Hg. This monitoring is the most accurate way to
optimize hemodynamics and ventilation.
• Transport the victim to a facility capable of surgical coronary
reperfusion using percutaneous coronary intervention (PCI).
• Control the glucose level to 144-180 mg/dL; do not attempt to
achieve a lower level since the risk of hypoglycemia outweighs
the benefits.
• Perform neurological testing before withdrawing treatment after
successful resuscitation
Tachycardia algorithm
1. Identify and treat the cause of the dysrhythmia.
2. Monitor cardiac rhythm, blood pressure and oxygenation.
3. Determine if the patient is stable or unstable. Unstable tachycardia = hypotension,
chest pain, symptoms of shock and possible decreased mentation.
4. For unstable tachycardia, perform immediate synchronized cardioversion:
a. If the QRS is narrow and regular, cardiovert with 50-100 Joules
b. If the QRS is narrow and irregular, cardiovert with 120-200 Joules
c. If the QRS is wide and regular, cardiovert with 100 Joules
d. If the QRS is wide and irregular, turn off the synchronization and defibrillate
immediately.
5. For stable tachycardia and a prolonged QRS complex (>0.12 seconds), go to Step 7.
6. For stable tachycardia with a normal or narrow QRS complex (≤0.12 seconds), consider
performing vagal maneuvers.
7. Establish an IV or IO to administer medications.
8. Consider giving adenosine 6 mg IV bolus; give a second double dose (12 mg) if needed.
9. If adenosine does not terminate the tachycardia, consider procainamide 20-50 mg IV
(maximum dose = 17 mg/kg IV). Start a maintenance infusion of procainamide at 1-4
mg/minutes. Instead of procainamide, you may consider giving amiodarone 150 mg IV
over 10 minutes with second dose for any recurrent VT. Start a maintenance infusion of
amiodarone at 1 mg/min IV.
Tachycardia
algorithm
• Klasifikasi CV emergency (cardiac arrest & non cardiac
arrest)
• Patfis sesuai kasus
• Tanda dan gejala cv emergency
• Prosedur diagnostik
• Gambaran ekg acs dan takiaritmia
• Tatalaksana cv emergency
• Algoritma basic and advanced cpr untuk cardiac arrest
dan takiaritmia
• Komplikasi dan prognosis