Pemicu KGD 1

MEIDY REGIANTO

ScenarioA 58-year-old man came to the Emergency Department with severe chest pain extending to his jaw and left arm. He suddenly felt the chest pain 3 hours ago while he was watching television, accompanied by excessive cold sweat, nausea, and vomiting. He also felt shortness of breath since an hour ago.He has a history of hypertension, diabetes mellitus and hypercholesterolemia in the past 3 years. He is not taking his medication regularly, has been smoking since the last 10 years and never exercises. Previosly, he had suffered an episode of mild chest pain but the symptom disappeared after resting. No history of stroke in the past.Physical examinationsd result : compos mentis (GCS 15), looks in pain, agitated, overweight and having mild-dyspneu. Blood pressure 170/90 mmHg, heart rate 120 beats per minute (regular with enough volume and firmness), afebrile and slight increases in JVP.

Inspection, palpation and percussion of the heart are in normal limits; S1 & S2 in heart auscultation are normal, no murmur is found. Inspection, palpation and percussion of the lungs are in normal limits but fine rales at the basis of the lung can be heard in auscultation. Abdomen examination is normal. His extremities are warm.ECG examination results : tachycardia sinus rhythm, QRS rate 130x/minute, QRS axis LAD, normal P-wave, P-R interval 0,12 sec, QRS duration 0,08 sec, Q-pathologic (-), ST-segment elevation in V1-V6 lead, inverted T-wave(-) and LVH (-).

What can you learn from this problem?

ACS

• UNSTABEL ANGINA• MI→STEMI and NSTEMI

ACS : Algorithm

ACS : Algorithm

ANGINA-CORONARY OCCLUSION

CORONARY OCCLUSION

CORONARY CIRCULATION

• Most tissues can increase O2 extraction with demand.

• Heart extracts near maximal amount of O2 at rest.

• Therefore can increase O2 demand by increasing the Coronary Blood Flow.

Various Coronary Arteries of Heart

Types Of Angina Pectoris

1. Stable Angina

2. Unstable Angina

3. Variant Angina (Prinzmetal’s Angina)

4. Anginal Equivalent Syndrome

5. Syndrome- X

6. Silent Ischemia

UNSTABLE ANGINA• This is characterized by Pain that occurs with less

excertion , cumulating pain at rest.• platelet-fibrin thrombus associated with a

ruptured atheromatous plaque without complete occulation of the vessels.

• The risk of infraction is subtanial, and the main aim of therapy is to reduce this.

Unstable angina

• is that characterized by rapidly worsening chest pain on minimal exertion or at rest.

• = ulcerated atheroma+ thrombus formation>>> reduction of coronary blood flow caused by thrombus>> angina at rest

Unstable angina

• Recent onset (less than 1 month).• Increase frequency and duration of episode.• Angina at rest not responding readily to

therapy.• If the pain more than 20 min.• MI

The Canadian Cardiovascular Society grading scale

• is used for classification of angina severity, as follows:

• Class I : Angina only during strenuous or prolonged physical activity

• Class II : Slight limitation, with angina only during vigorous physical activity

• Class III : Symptoms with everyday living activities, ie, moderate limitation

• Class IV : Inability to perform any activity without angina or angina at rest, ie, severe limitation

N.A.N 2009

The New York Heart Association classification

• is also used to quantify the functional limitation imposed by patients' symptoms, as follows:

• Class I : No limitation of physical activity (Ordinary physical

activity does not cause symptoms.) • Class II : Slight limitation of physical activity (Ordinary physical

activity does cause symptoms.) • Class III : Moderate limitation of activity (Patient is comfortable

at rest, but less than ordinary activities cause symptoms.) • Class IV : Unable to perform any physical activity without

discomfort, therefore severe limitation (Patient may be symptomatic even at rest.)

N.A.N 2009

Causes:

• Decrease in myocardial blood supply due to increased coronary resistance in large and small coronary arteries:

1. Significant coronary atherosclerotic lesion2. Coronary spasm (ie, Prinzmetal angina)

N.A.N 2009

Causes:

3. Abnormal constriction or deficient endothelial-dependent relaxation of resistant vessels associated with diffuse vascular disease (ie, microvascular angina)

4. Syndrome X 5. Systemic inflammatory or collagen vascular

disease, (scleroderma, systemic lupus erythematous, Kawasaki disease, polyarteritis nodosa, and Takayasu arteritis)

N.A.N 2009

Risk factors:

• Major risk factors for atherosclerosis: like family history of premature CAD, cigarette smoking,DM,hypercholesterolemia(Metabolic syndrome), or systemic HTN

• Other risk factors: These include LV hypertrophy, obesity,

N.A.N 2009

Precipitating factors:

• These include factors such as severe anemia, fever, tachyarrhythmias, catecholamines, emotional stress, and hyperthyroidism, which increase myocardial oxygen demand.

N.A.N 2009

Preventive factors:

• Factors associated with reduced risk of atherosclerosis are a high serum HDL cholesterol level, physical activity, estrogen, and moderate alcohol intake (1-2 drinks/d).

N.A.N 2009

Stable AnginaExercise Testing

• The goal of exercise testing is to induce a controlled, temporary ischemic state during clinical and ECG observation

N.A.N 2009

ECG

• ST segment depression with or without T wave inversion that reverse after ischemia disappears.

N.A.N 2009

ECG

• Elevation of ST segment in prinzmental’s angina.

N.A.N 2009

ECG

• The resting ECG may be normal between attacks however it may show old MI, heart block or LVH

N.A.N 2009

Exercise TestingContraindications

• MI—impending or acute• Unstable angina• Acute myocarditis/pericarditis• Acute systemic illness• Severe aortic stenosis• Congestive heart failure• Severe hypertension• Uncontrolled cardiac arrhythmias

N.A.N 2009

NON-ST ELEVATION MYOCARDIAL INFARCTION

a subtotally blockage in the coronary artery in the first few hours and disappear over time and there is

evidence myocardial infarction (elevated cardiac biomarker)

Pathophysiology

• ↓oxygen supply or ↑myocardial oxygen demand superimposed on a lesion (coronary arterial obstruction atherothrombotic coronary plaque)

4 pathophysiologic processes development of NSTEMI

1. plaque rupture or erosion NSTEMI (embolization of platelet aggregates or atherosclerotic debris)

2. dynamic obstruction (coronary spasm)3. progressive mechanical obstruction4. increased myocardial oxygen demand and/or

decreased supply (e.g., tachycardia, anemia)

Myocardial Infarction

RISK FACTOR:1. Smoking2. Hypertension3. hypercholesterolemia

thrombus coronary artery

Decrease coronary artery blood flow Arterosklerosis plaque

Ruptur plaque Thrombosit activationAgonis (kolagen, ADP, epinefrin dan serotonin)

Tromboxan A2

Aggregasi platelet

Myocardial Infarction

Coronary artery Occlusion

Risk Factors

• age > 65 years• three or more risk factors for CAD (carotid artery

disease), • documented CAD at catheterization, • development of UA/NSTEMI while on aspirin,• more than two episodes of angina within the

preceding 24 h• ST deviation 0.5 mm, and an elevated cardiac

marker

Clinical manifestation

• chest pain

• located in the substernal region or sometimes in the epigastrium, that radiates to the neck, left shoulder, and/or the left arm

• dyspnea and epigastric discomfort

Clinical manifestation

• Diaphoresis• cool skin• sinus tachycardia• a third and/or fourth heart sound• basilar rales (crackles) inflamation, fluid or

infection.• Hypotension resembling the findings of

large STEMI.

Diagnosis

• clinical history• ECG• Cardiac markers (recognize or exclude MI )• Stress testing (coronary imaging is an

emerging option).

Electrocardiogram

• ST-segment depression, transient ST-segment elevation, and/or T-wave inversion occur in 30 to 50% of patients

Cardiac Biomarkers

• elevated biomarkers of necrosis, such as CK-MB > 3 ng/ml and troponin >0.4 ng/ml

• High risk mortality if troponin incrase.

Prognosis

• NSTEMI exhibit a wide spectrum of early (30 days) risk of death, ranging from 1 to 10%, and of new or recurrent infarction of 3–5% or recurrent ACS (5-15%).

STEMI

1. Definition of AMI

• The actual definition includes the following, either one of these criteria satisfies the diagnosis for an acute, evolving, or recent MI :

1. Typical rise and gradual fall (troponin) or more rapid rise and fall (isoenzyme of creatine kinase with muscle and brain subunits [CK-MB]) of biochemical markers of myocardial necrosis with at least one of the following:

a. Ischemic symptoms;b. Development of pathologic Q waves on the ECG;c. ECG changes indicative of ischemia (T wave changes or ST segment elevation or depression); and/ord. Coronary artery intervention.

2. Pathologic findings of an AMI.

• AMI is further classified by findings on the ECG at presentation, as either ST elevation MI (STEMI) or non-ST elevation MI (NSTEMI).

• The differentiation between STEMI and NSTEMI has important implications in terms of management, therapeutic intervention, outcome, and prognosis for patients with AMI.

2. Etiology

• Atherosclerotic narrowing of coronary vessels• Vasospasm—although this is usually at rest

and considered unstable if new onset• Microvascular angina or abnormal relaxation

of vessels with diffuse vascular disease• Plaque disruption• Thrombosis

• Arteritis:– Lupus– Takayasu disease– Kawasaki disease– Rheumatoid arthritis

• Prolonged hypotension• Anemia– Hemoglobin <8 g/dL

• Hyperbarism or elevations in carboxyhemoglobin

• Coronary artery gas embolus• Structural abnormalities of coronary arteries:– Radiation fibrosis– Aneurysms– Ectasia

• Cocaine- or amphetamine-induced vasospasm

• Cardiac risk factors include:– Hypercholesterolemia– Diabetes mellitus– Hypertension– Smoking– Family history in a first-degree relative less than 55

years old– Men, age >55 years– Postmenopausal women

3.Pathofisiology

• The underlying pathophysiology of ACS is myocardial ischemia as a result of inadequate perfusion to meet myocardial oxygen demand.

• Myocardial oxygen consumption is determined by heart rate, afterload, contractility, and wall tension.

• Inadequate perfusion most commonly results from coronary arterial vessel stenosis as a result of atherosclerotic CAD.

a. Probable cause is the generation of a total coronary occlusion or functional collateral circulation:– Often indicates an complete ischemic event

b. Coronary plaque disruption:– Endothelial disruption exposes subendothelial

collagen and other platelet-adhering ligands, von Willebrand factor (vWF), and fibronectin.

• Release of tissue factors activates factor VII and extrinsic pathway

c. Thrombus generation:– Platelet adhesion via glycoprotein (GP) Ia/IIa to

collagen; GP Ib to vWF:• Platelet activation: release of ADP, thromboxane A2, and

serotonin alters the platelet GP IIb/IIIa receptor; also causes local vasoconstriction

• Platelet aggregation: GP IIb/IIIa receptor binds fibrinogen molecules, cross-links platelets forming local platelet plug

d. Platelet stabilization: thrombin converts fibrinogen to fibrin, provides fibrin mesh, stabilizes platelet aggregate

4. Signs and Symptoms

• Chest pain:– Most common presentation of myocardial

infarction (MI)– Substernal pressure– Heaviness– Squeezing– Burning sensation– Tightness

• Anginal equivalents (MI without chest pain):– Abdominal pain– Syncope– Diaphoresis– Nausea or vomiting– Weakness

• May localize or radiate to arms, shoulders, back, neck, or jaw

• Associated symptoms:– Dyspnea– Syncope– Fatigue– Diaphoresis– Nausea– Vomiting

• Symptoms are usually reproduced by exertion, eating, exposure to cold, or emotional stress

• Symptoms commonly last 30 minutes or more.• Symptoms may occur with rest or during exertion.• Often preceded by crescendo angina• May be improved or relieved with rest or nitroglycerin• Symptoms generally unchanged with position or

inspiration• Positive Levine sign or clenched fist over chest is

suggestive of angina.• Blood pressure (BP) is usually elevated during symptoms.

5. Diagnosis

• Essential Workup: – ECG– Cardiac markers– Chest radiograph

• Lab• Cardiac markers:– Troponins: specific indicators of myocardial infarction,

positive 3- 6 hours after MI, peaks at 9-10 days– Creatine kinase (CK): rises following infarction in 4-8 hours,

peaks at 18-24 hours, subsiding at 3-4 days; isoenzyme CK-MB more specific for cardiac origin

– Myoglobin: rises within 2-6 hours, returns to baseline within 24 hours, highly sensitive but very nonspecific

– LDH: rises within 24 hours, peaks at 3-6 days, baseline at 8-2 days

• CBC• Serum electrolytes including magnesium• ESR: nonspecific marker of inflammation, rises

within 3 days, elevated for several weeks• PT/PTT/INR for patients on warfarin

• Imaging• ECG:– ST-segment elevation indicates increased risk (ST segment

elevation may become evident. Morphologic variations of ST segment elevation can be seen from the J (or junction) point at the end of the QRS complex to the apex of the T wave)

– And Q waves letter• Chest radiograph:– To assess heart size, pulmonary edema/congestion or

identify other causes of chest pain

• Echocardiography:– To identify wall motion abnormalities and assess

left ventricular function• Radionuclide studies:– Thallium or sestamibi scanning: identifies viable

myocardium– Technetium 99: identifies recently infarcted

myocardium

6. Treatment

• Pre Hospital– IV access– Oxygen administration– Cardiac monitoring and treatment of arrhythmias– Aspirin, analgesia, anxiolytics

• Initial Stabilization– Oxygen administration– IV access– Cardiac monitoring and treatment of arrhythmias

• Anti-ischemic therapy to reduce myocardial demand and increase myocardial supply of oxygen:– Beta-blockers– Nitrates– Oxygen– Morphine sulfate– Calcium channel blockers (nondihydropyridines—e.g.,

diltiazem, verapamil) may be used in patients with ongoing ischemia and contraindications to beta-blockade.

• Antiplatelet therapy to decrease platelet aggregation:– Aspirin– Clopidogrel– GP IIb/IIIa inhibitors (eptifibatide, tirofiban):

• When catheterization and PCI is planned• Ongoing ischemia• Positive initial cardiac markers

• Antithrombotic therapy to prevent thrombus propagation:– Low molecular weight heparin (specifically enoxaparin)

preferred over unfractionated heparin• Anxiolytics to suppress sympathomimetic release

• Reperfusion:– Door to baloon inflation (PCI) , target : 90 minute– Door to nedle ( fibrinolisis) , target : 30 minute

7. Complication

• Bradydysrhythmia and atrioventricular (AV)• Tachydysrhythmias• Cardiogenic shock• Pericarditis• Hemorraghic Stroke

8. DD• Non ST-elevation myocardial infarction• Pulmonary embolus• Aortic dissection• Acute pericarditis• Pneumothorax• Pancreatitis• Pneumonia• Esophageal spasm/gastroesophageal reflux• Esophageal rupture• Musculoskeletal pain (diagnosis of exclusion)

Cardiac Arrest

Condition of blood circulation stops due to failure of the heart to contract effectively

Characterized by the absence of pulse and other signs of circulation

• Cardiac abnormalities can be caused by 4 rhythms :– Ventricular Fibrillation (VF)– Pulseless Ventricular Tachycardia (PVT)– Pulseless Electrical Activity (PEA)– Asystole

VF / PVT

• The wave ↑ different shapes and amplitude of waves

• ≠ look : QRS complex, ST segment, T wave

• Smooth fibrillation wave amplitude <0,2 mv often in the case of long-VF like asystole

Etiology VF/PVT

• Coronary heart disease, the accumulation of Ca ions, free radicals, cell metabolic disorders, autonomic modulation, etc

• Ischemic cell trigger• Other : electrolyte disturbances (hypo K and

Mg), drug toxicity (digitalis, phenotiazine, tricyclic and tetrasiklik, antidepressants)

• PVT VF

Clinical manifestations

• Heart only vibrate, unable to work as a pump Clinical death – biological death

• Patients are not aware of – no response

PEA / Asystole

• PEA there is a electrical picture on the monitor ECG, but no palpable pulse at A. carotid

• ECG : wide QRS complex with a low frequency (≤ 20 – 40x / min) idioventrikular rhythm

• Asystole the heart stops contracting• ECG : a straight line without ventricular activity

(≠ QRS complex)

ETIOLOGY FREQUENCY

Coronary Artery Disease Acute Coronary Syndrome Chronic Myocardial Scar

Approximately 80%

CardiomyopathieDilated Cardiomyopathies Hypertrophic Cardiomyopathies

Approximately 10% to 15%

Uncommon Causes Valvular/Congenital Heart Disease Myocarditis, Genetic Ion-Channel Abnormalities, etc.

< 5%

Contributing Causes Of Cardiac Arrest6H 5T

HypovolemiaHypoxiaHydrogen ion (acidosis)Hypokalemia/Hyperkalemia HypothermiaHypoglycemia

ToxinsTamponade, cardiacTension, pneumothoraxThrombosis (coronary or pulmonary)Trauma

symptomp

• the heart stops beating and blood is not supplied to the body

• The presentation is not subtle• immediate loss of consciousness occurs → not

aroused →fall over• No pulse will be able to be palpated and no signs of

breathing• pulses paradoxus, elevated jugular venous

pulsation, distant heart sounds, and electrical alternans on ECG

Heart attack warning sign

• Chest discomfort (center of the chest that lasts more than a few minutes, or that goes away and comes back. It can feel like uncomfortable pressure, squeezing, fullness or pain)

• Discomfort in other areas of the upper body (one or both arms, the back, neck, jaw or stomach)

• Shortness of breath• Other signs: cold sweat, nausea or lightheadedness

PATOFISIOLOGI

diagnosis

• Sudden cardiac arrest is an unexpected death in a person who had no known previous diagnosis of a fatal disease or condition. The person may or may not have heart disease.

DIFFERENTIAL DIAGNOSIS

• Acute insults (hypoxia, ischemia, acidosis, electrolyte imbalances, and toxic effects of certain drugs)

• DRUGS:– tricyclic antidepressants– neuroleptics– macrolide and quinolone antibiotics– antifungal agents– procainamide, quinidine, disopyramide (class IA

antiarrhythmics)– sotalol, dofetilide, and ibutilide (class III antiarrhythmics)

treatment

• Epinephrine – n a- and b-receptor agonist– increased peripheral vascular resistance via the

stimulation of a-receptors of the blood vessels. – redistribution of blood flow from visceral organs to the

heart and brain.• Atropine– asystole and slow PEA along with epinephrine and

vasopressin• Vasopresin, amiodarone, lidocaine

PROGNOSIS

related to the frequency of coronary artery disease.

In the adolescent population, increased awareness of hypertrophic cardiomyopathy and appropriate screening may decrease the frequency of sudden death.

Public education and widespread availability of AEDs will increase survival.

• BAD !!• Brain death and permanent death start to

occur in just 4 to 6 minutes after someone experiences cardiac arrest

• more than 95 percent of cardiac arrest victims die before reaching the hospital

Factors Associated With Improved Outcomes in Cardiac Arrest

Presenting rhythm of VT/VF Presenting rhythm of VT/VFEarly/bystander CPR Early/bystander CPREarly defibrillation Early defibrillationCPR prior to defibrillation in the circulatory phase of cardiac arrest Minimal interruptions to chest compressions In-hospital and out-of-hospital use of AEDs Amiodarone use in shock-resistant VT/VF Therapeutic hypothermia in comatose cardiac arrest victims

ECG

Emergency ECG

• Ventricular fibrillation• Pulseless Electrical Activity• Asystole

Ventricular fibrillation• reentrant pattern of excitation in the ventricles -> poorly synchronized and

inadequate myocardial contractions. • The heart consequently immediately loses its ability to function as a

pump. • As the initial reentrant pattern of excitation breaks up into multiple

smaller wavelets, the level of disorganization increases. • Sudden loss of cardiac output + subsequent tissue hypoperfusion ->

global tissue ischemia; brain and myocardium are most susceptible. • VF is the primary cause of sudden cardiac death (SCD).

• Ventricular fibrillation is shown in the rhythm strip below.

EpidemiologyFrequency• Ventricular fibrillation also is prevalent worldwide, with a reported

predominance in the northern hemisphere. Among some European populations, the annual incidence of cardiac arrests exceeds 6 cases per 10,000 people.

Race• Black males have the highest incidence of sudden cardiac death.Sex• Sudden cardiac death is more common among males than females,

although the rates become similar for patients older than 70 years. Age• Incidence initially peaks during the first 6 months of life, then rapidly

declines until a second peak in those aged 45-75 years.

History• Ventricular fibrillation (VF) often occurs without forewarning. • The following symptoms, while not necessarily specific for

sudden cardiac death or VF, may develop before any major cardiac event : – Chest pain and other angina equivalents– Dyspnea– Easy fatigue– Palpitations– Syncope– Immediately preceding acute cardiac arrest, possible increase in

heart rate, presence of premature ventricular contractions (PVCs), or period of VT

Physical

• No pulse or respiration.• Patients in cardiac arrest have absent or

abnormal (gasping) respirations. • Unconsciousness• Wide and chaotic QRS complexes on cardiac

monitor

Causes

Cardiac, structural heart disease Cardiac, no structural heart disease

• Myocardial ischemia or infarction due to coronary artery disease: Coronary atherosclerosis

• Cardiomyopathy: dilated, hypertrophic, or arrhythmogenic right ventricular cardiomyopathy or dysplasia.

• Aortic stenosis• Aortic dissection• Pericardial tamponade• Congenital heart disease• Myocarditis

• Catecholaminergic polymorphic ventricular tachycardia and right ventricular outflow tract tachycardia

• Mechanical (commotio cordis)[4] or electrical accidents

• Preexcitation (including Wolff-Parkinson-White syndrome)

• Heart block• Drug-induced QT prolongation with

torsades de pointes• Channelopathies: long QT syndrome,

short QT syndrome, or Brugada syndrome

Causes

Noncardiac respiratory Metabolic or toxic • Bronchospasm• Aspiration• Sleep apnea• Primary pulmonary

hypertension• Pulmonary embolism• Tension pneumothorax

• Electrolyte disturbances and acidosis

• Medications or drug ingestion• Environmental poisoning• Sepsis• Neurologic Seizure• Cerebrovascular accident -

Intracranial hemorrhage or ischemic stroke

• Drowning

Differential Diagnoses

• Hyperkalemia• Hypokalemia• Torsade de Pointes• Toxicity, Antidepressant• Toxicity, Cocaine• Toxicity, Digitalis• Ventricular Tachycardia

Laboratory Studies

• Serum electrolyte levels, including calcium and magnesium

• Cardiac enzymes to identify myocardial injury• Complete blood count (CBC) to detect

contributing anemia• Arterial blood gases (ABGs) to assess degree of

acidosis or hypoxemia• Toxicologic screens and levels as clinically

indicated

Imaging Studies

• Chest radiography may identify aspiration pneumonia, pulmonary edema, cardiomegaly, and injury (eg, secondary to cardiopulmonary resuscitation [CPR]).

Other Tests• Electrocardiography (ECG) to help identify

ischemic or proarrhythmic conditions

Pulseless Electrical Activity

• A clinical condition characterized by unresponsiveness and lack of palpable pulse in the presence of organized cardiac electrical activity.

Epidemiology

• The use of beta-blockers and calcium channel blockers may increase the frequency of PEA, presumably by interfering with cardiac contractility.

• Females are more likely to develop PEA than males. • The average patient age is 70 years. Older patients

are more likely to have PEA as an etiology of cardiac arrest.– Whether the patient outcome differs based on age is not

known; however, advanced age is likely associated with a worse outcome.

Etiology• severe prolonged hypoxia or acidosis or

extreme hypovolemia or flow-restricting pulmonary embolus.

• exacerbated by worsening acidosis, hypoxia, and increasing vagal tone

• inadequate mechanical activity, even though electrical activity is present

• Hypoxia : preload, afterload, or contractility often result in PEA.

Decreased preload

• decreased venous return to the left atrium), the left ventricle is unable to generate sufficient pressure to overcome its afterload.

• Cardiac tamponade may also cause decreased ventricular filling.

Increased afterload

• Afterload is inversely related to cardiac output.

• Severe increases in afterload pressure cause a decrease in cardiac output.

Decreased contractility

• Calcium influx and binding to troponin C is essential for cardiac contraction. – If calcium is not available (eg, calcium channel

blocker overdose) or – if calcium's affinity to troponin C is decreased (as

in hypoxia), contractility suffers.

Decreased contractility

• Depletion of intracellular adenosine triphosphate (ATP) reserves increase in adenosine diphosphate (ADP bind calcium, reducing energy reserves.

• Excess intracellular calcium can result in reperfusion injury severe damage to the intracellular structures, predominantly the mitochondria.

Additional etiologic factors• Hypovolemia• Hypoxia• Hydrogen ion (acidosis)• Hypokalemia/hyperkalemia• Hypoglycemia• Hypothermia• Toxins• Cardiac tamponade• Tension pneumothorax• Thrombosis (coronary or pulmonary)• Trauma

Differential Diagnoses• Accelerated Idioventricular Rhythm• Acidosis• Cardiac Tamponade• Drug overdose• Hypokalemia• Hypothermia• Hypovolemia• Hypoxemia• Myocardial Ischemia• Pulmonary Embolism• Syncope• Tension pneumothorax• Ventricular Fibrillation

Prevention

• The following measures may prevent some cases of in-hospital pulseless electrical activity:– Patients who have been on prolonged bed rest -

Should receive deep venous thrombosis (DVT) prophylaxis

– Patients who are on ventilators - Should be monitored carefully for auto-PEEP development

– Hypovolemia - Should be treated aggressively, especially in patients with active bleeding

Asystole

• Asystole is cardiac standstill.• No cardiac output & no ventricular

depolarization.• Eventually occurs in all dying patients.

Epidemiology

• Children• Women• higher in women than in men• more common in males until around age 75

years.

Pathophysiology

• Primary asystole occurs when the heart's electrical system intrinsically fails to generate a ventricular depolarization.

• Secondary asystole occurs when factors outside of the heart's electrical conduction system result in a failure to generate any electrical depolarization.

History

• Immediate diagnosis of asystole requires the recognition of a full cardiac arrest and a confirmed flat-line rhythm in 2 perpendicular leads.

• Lightheadedness or syncope may precede asystole when it follows a bradyasystolic rhythm.

Physical Examination

• If the rhythm is truly asystole and has been present for more than several seconds, the patient will be unconscious and unresponsive.

• A few agonal (final gasping) breaths may be noted, but detectable heart sounds and palpable peripheral pulses are absent.

Complications

• Complications from asystole include permanent neurologic impairment and complications from cardiopulmonary resuscitation (CPR) or invasive procedures (eg, liver laceration, fractured ribs, pneumothorax, hemothorax, air embolus, aspiration, gastric/esophageal rupture).

• Death often occurs.

Differential Diagnoses

• Hyperkalemia in Emergency Medicine• Hypothermia• Syncope• Ventricular Fibrillation

AMERICAN HEART ASSOCIATION

CHANGES IN THE 2010 GUIDELINES AFFECTING

ALL RESCUERS

AMERICAN HEART ASSOCIATION:2010 GUIDELINES

Health Care Provider* “PUSH HARD AND PUSH FAST”

At least 100 COMPRESSIONS / MINUTE*

Allow the chest to recoil -- equal compression and relaxation times

<10 seconds for pulse checks or rescue breaths

Compression Depth* Adults 2”

Child/Infant 1/3 depth of chest 1.5" infant 2" child

Avoid excessive ventilations

A-B-C changed to C-A-B* Critical element is chest compressions

Delay in A-B

Avoidance of A & B

Early defib

If alone--call and retrieve AED Exception asphyxial arrest

AMERICAN HEART ASSOCIATION:2010 GUIDELINES

• Cricoid pressure not recommended

• Advanced airway = 1 every 6-8 seconds• Adult: 1 every 5-6 Peds: 1 every 3

• With advanced airway- no pause

AMERICAN HEART ASSOCIATION:2010 GUIDELINES

Dispatcher Identification

• SCA = seizure & agonal gasps• Trained to ID – ask if breathing is normal• Only gasping???• Provide CPR instructions

AMERICAN HEART ASSOCIATION:2010 GUIDELINES

AHA ECC Adult Chain of Survival - New

Simplified Universal BLS algorithm

AMERICAN HEART ASSOCIATION:2010 GUIDELINES

CPR

CPR

• Combines external chest compressions with artificial ventilation

• Provides 30% (or less) of normal circulation• Only effective for short period of time

CPR – 1 Rescuer

• Assess responsiveness

• Summon EMS• Position the patient

CPR – 1 Rescuer

• Open the airway

CPR – 1 Rescuer

• Look, listen, and feel for breathing

CPR – 1 Rescuer

• If there is no breathing, give two breaths, each lasting 1 second

CPR – 1 Rescuer

• Check for a pulse (≤ 10 seconds)

CPR – 1 Rescuer

• If there is no pulse, find your landmarks, lower half of the sternum, between the nipples

CPR – 1 Rescuer

• Begin chest compressions

CPR – 1 Rescuer

• Perform 30 chest compressions

• Push hard• Push fast• Allow the chest to

recoil after each compression

CPR – 1 Rescuer

• Administer two ventilations then return to compressions

CPR – 2 Rescuer

1 2

3 4

CPR - Children

• Use heel of one hand

• Keep airway open with other hand

• 30 compressions:2 ventilations if alone (2 rescuers use 15:2)

CPR - Infant

• Give chest thrusts and puffs of air

• 30 compressions:2 ventilations if alone

• 15 compressions: 2 ventilations with 2 rescuers

AEDs

• Safe, accurate & lightweight• Easy to operate

What is public access defibrillation?

PAD

• AEDs in public places

• Training the public in CPR/AED

Special Considerations

• Children• Clothing• Body hair• Water• Transdermal

medication patches

• Implanted defibrillators or pacemakers

• Metal surfaces• Jewelry and glasses

AED

Assess • Check your patient

Universal Steps

Power↓

Patient↓

Analyze↓

Shock

Power

• Turn the power on

Patient

• Apply pads to patient

Analyze

• Stay clear while patient’s heart rhythm analyzed

Clear

• Head to toe and toe to head: everyone is clear!

Shock

• Defibrillate

Patient

• Standard is set of 1 shock

• Immediately restart CPR for 2 minutes then check pulse

conclusion

• We have discussed about UA, MI (NSTEMI&STEMI), cardiac arrest, emergency ECG, CPR.

• Related to the case, this patient : STEMI.

suggestion

• Adminisration defebrilation, PCI and lab examination (Myoglobin, Troponin and CK-MB)

REFERENCE

• Subagjo,agus,dkk. BCLS (Basic cardiac life support) ed.2011

• ACLS (advance cardiac life support) ed.2011• Rossen’s• Harrison princple ed.18th