Case 1

GROUP 13FACULTY OF MEDICINE TARUMANAGARA UNIVERSITY2013

Acute Coronary Syndrome

DefinitionAny condition brought on by sudden, reduced blood flow to the heart. ST-segment elevation myocardial infarction (STEMI) nonST-segment elevation myocardial infarction (NSTEMI) or in unstable angina

EpidemiologyACS is almost always associated with rupture of an atherosclerotic plaque and partial or complete thrombosis of the infarct-related artery. It's important to recognize the patient with unstable angina, because 5-17% suffer an MI within a week after admission & 3-15% die within a year.

EtiologyAcute 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).

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Risk FactorsOlder age (older than 45 for men and older than 55 for women)High blood pressureHigh blood cholesterolCigarette smokingLack of physical activityType 2 diabetesFamily history of chest pain, heart disease or stroke

Pathophysiology

Sign & SymptomsChest pain (angina) that feels like burning, pressure or tightness and lasts several minutes or longerPain elsewhere in the body, such as the left upper arm or jaw (referred pain)NauseaVomitingShortness of breath (dyspnea)Sudden, heavy sweating (diaphoresis)

OnsetProvocationQualityRadiationSeverityTimeAssessmentSigns and symptomsAllergiesMedicationsPast medical historyLast mealEvents leading up to the illiness

Criteria DiagnoseHistoryECG changesSerial changes in cardiac enzymes (detectors of myocardial damage)

HistoryPalpitationsPain, feels like pressure, squeezing, or a burning sensation across the precordium & may radiate to the neck, shoulder, jaw, back, upper abdomen or armExertional dyspnea that resolves with pain or restDiaphoresisNausea

Decreased exercise toleranceHypotensionHypertensionPulmonary edema & other signs of left heart failureJugular venous distentionCoold, clammy skinA third heart sound (S3) may be present & frequently, a fourth heart sound (S4) exists.

ECGChanges that may be seen during anginal episodes include the following:Transient ST-segment elevationsDynamic T-wave changes - Inversions, normalizations, or hyperacute changesST depressions - May be junctional, downsloping, or horizontal

Differential DiagnosisAortic StenosisAsthmaCardiomyopathyMyocardial InfarctionMyocarditisPericarditis and Cardiac Tamponade

ComplicationsPulmonary edemaRupture of the papillary muscle, left ventricular free wall, and ventricular septum

Myocardial Infarct

MYOCARDIAL INFARCTIONMyocardial necrosis due to blood flow to the heart muscle impaired

Non-ST elevation Myocardial InfarctionST elevation Myocardial Infarction

NON-ST ELEVATION MYOCARDIAL INFARCTIONa subtotally blockage in the coronary artery in the first few hours and disappear over time and there is evidence myocardial infarction (elevated cardiac biomarker)

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

4 pathophysiologic processes development of NSTEMI plaque rupture or erosion NSTEMI (embolization of platelet aggregates or atherosclerotic debris)dynamic obstruction (coronary spasm)progressive mechanical obstructionincreased myocardial oxygen demand and/or decreased supply (e.g., tachycardia, anemia)

Myocardial InfarctionRISK FACTOR:SmokingHypertensionhypercholesterolemiathrombus coronary arteryDecrease coronary artery blood flow Arterosklerosis plaqueRuptur plaqueThrombosit activationAgonis (kolagen, ADP, epinefrin dan serotonin)Tromboxan A2Aggregasi plateletMyocardial InfarctionCoronary artery Occlusion

Risk Factorsage > 65 yearsthree 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 hST deviation 0.5 mm, and an elevated cardiac marker

Clinical manifestationchest 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 manifestationDiaphoresiscool skinsinus tachycardiaa third and/or fourth heart soundbasilar rales (crackles) inflamation, fluid or infection.Hypotension resembling the findings of large STEMI.

Diagnosisclinical historyECGCardiac markers (recognize or exclude MI )Stress testing (coronary imaging is an emerging option).

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

Cardiac Biomarkerselevated biomarkers of necrosis, such as CK-MB > 3 ng/ml and troponin >0.4 ng/mlHigh risk mortality if troponin incrase.

PrognosisNSTEMI exhibit a wide spectrum of early (30 days) risk of death, ranging from 1 to 10%, and of new or recurrent infarction of 35% or recurrent ACS (5-15%).

ST ELEVATION MYOCARDIAL INFARCTIONa complete blockage in the coronary artery

ETIOLOGIcoronary artery occlusion caused by coronary embolicongenital abnormalitiescoronary spasmwide variety of systemicparticularly inflammatorydiseases

Pathophysiologycoronary artery thrombus (rapidly) at a site of vascular injury surface atherosclerotic plaque disrupted (rich lipid core and a thin fibrous cap ) thrombus forms coronary artery occlusion coronary blood flow.

thrombotic occlusion (atherosclerosis) or stenosis (slowly) coronary artery coronary blood flow.

Vascular injury cigarette smoking, hypertension, and lipid accumulation

Ruptur plaqueRuptur initial monolayer platelet formcollagen, ADP, epinephrine, serotoninplatelet activator tromboksan A2 (vasoconstrictor)resistance to fibrinolysischange in the glycoprotein IIb/IIIa receptor high affinity for soluble adhesive proteins (i.e., integrins) such as fibrinogen.platelet cross-linking and aggregation and fibrin strandscoagulation cascade activated prothrombin to thrombinAndfibrinogen to fibrin Factors VII and X are activated

myocardial damage caused by coronary occlusionsupplied by the affected vesselwhether or not the vessel becomes totally occludedthe duration of coronary occlusionthe quantity of blood supplied by collateral vessels to the affected tissuethe demand for oxygen of the myocardium whose blood supply has been suddenly limitedendogenous factors that can produce early spontaneous lysis of the occlusive thrombusthe adequacy of myocardial perfusion in the infarct zone when flow is restored in the occluded epicardial coronary artery

RISK FACTORSUnstable anginaHypercoagulabilitycollagen vascular diseasecocaine abuseintracardiac thrombi or masses that can produce coronary emboli.diabetes mellitus and age

Clinical manifestationPrecipitating factor present before STEMI (vigorous physical exercise, emotional stress, or a medical or surgical illness).Pain (deep, visceral, heavy, squeezing,rushing, stabbing or burning).commonly occurs at rest but when it begins during a period of exertion, it does not usually subside with cessation of activity

is usually more severe, and lasts longer

circadian variations are seen in the morning within a few hours of awakening

Typically, the pain involves the central portion of the chest, epigastrium and radiates to the arms, abdomen, back, lower jaw, and neck.

frequent location of the pain beneath the xiphoid and epigastrium

weakness, sweating, nausea, vomiting, anxiety, and a sense of impending doombreathlessness, which may progress to pulmonary edemasudden loss of consciousnessunexplained drop in arterial pressurePallor Coolness of the extremities

Physical examinationChest Pain (persisting for >30 min) anterior infarction sympathetic nervous system hyperactivity (tachycardia and/or hypertension), abnormal systolic pulsation inferior infarction show evidence of parasympathetic hyperactivity (bradycardia and/or hypotension).

ventricular dysfunction include fourth and third heart sounds

transient midsystolic or late systolic apical systolic murmur dysfunction of the mitral valve

pericardial friction rub is heard transmural STEMI

carotid pulse (volume) stroke volume

LABORATORYacute (first few hours7 days)healing (728 days)healed (> 29 days)

ECG, serum cardiac biomarkers, cardiac imaging, nonspecific indices of tissue necrosis and inflammation.

Electrocardiograminitial stage, total occlusion of an epicardial coronary artery ST-segment elevationDepresion Q wavesST-segment elevation will not develop Q waves the obstructing thrombus is not totally occlusivetransmural MI Q waves or loss of R waves and nontransmural MI only transient ST-segment and T-wave changes

Cardiac BiomarkersCardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI) troponin >0.4 ng/ml elevated for 710 days after STEMI.

CKMB > 3 ng/ml

Cardiac Imagingdetected accurately with high-resolution cardiac MRI

Initial Management

MANAGEMENT STRATEGIES

Management in the Emergency Department

Control of DiscomfortNitroglycerin three doses of 0.4 mg at about 5-min intervals myocardial oxygen demand (by lowering preload) and myocardial oxygen supply (vasoditasion). KI : low systolic arterial pressure (

Fibrinolysistissue plasminogen activator (tPA), streptokinase,tenecteplase (TNK),reteplase (rPA)

If contraindication fibrinolysis PCI (percutaneus coronary intervention)

Hospital Phase ManagementCoronary Care UnitThe cardiac ritm of each patient and hemodynamic monitor in selected patientsActivity Factor that increase the work of the heart increase the size of the infarct.Bed rest for the first 12 h.

Diet 30% total caloriesfat and cholesterol 300 mg/dhigh potassium, magnesium, and fiber,low in sodiumBowel managementBed rest Conspations dioctyl sodium sulfosuccinate (200 mg/d)

SedationDiazepam (5 mg),oxazepam (1530 mg), lorazepam (0.52 mg),

given 34 times daily

DDacute pericarditis (Radiation of discomfort to the trapezius )pulmonary embolismacute aortic dissection Costochondritisgastrointestinal disorders

ComplicationVentricular DysfunctionHemodynamic AssessmentHypovolemia

UNSTABLE ANGINA

UNSTABLE ANGINAit occurs at rest (or with minimal exertion), usually lasting >10 minutes.it is severe and of new onset (i.e., within the prior 46 weeks).it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than previously).

EtiologyAtherosclerotic narrowing of coronary vesselsVasospasm, although this is usually at rest and considered unstable if new onsetMicrovascular angina or abnormal relaxation of vessels with diffuse vascular diseasePlaque disruptionThrombosis

Arteritis:LupusTakayasu diseaseKawasaki diseaseRheumatoid arthritisAnemia:Hemoglobin

Cocaine- or amphetamine-induced vasospasmCardiac risk factors include:HypercholesterolemiaDiabetes mellitusHypertensionSmokingFamily history in a first-degree relative less than age 55Men: age >55 yearsPostmenopausal women

DiagnosisSigns and SymptomsUnstable angina is defined by either:New-onset symptomsSymptoms that occur at restA change in the patient's usual pattern of angina

Chest pain:Most common presentation of myocardial infarctionSubsternal pressureHeavinessSqueezingBurning sensationTightness

Occasional anginal equivalents:Abdominal painSyncopeDiaphoresisNausea or vomitingWeakness

May localize or radiate to arms, shoulders, back, neck, or jawMay be associated with dyspnea, syncope, fatigue, diaphoresis, nausea, or vomitingSymptoms are usually reproduced by exertion, eating, exposure to cold, or emotional stress.Symptoms commonly last 15 minutes or more.Usually improved or relieved with rest or nitroglycerinSymptoms generally unchanged with position or inspirationPositive Levine sign or clenched fist over chest is suggestive of anginaBlood pressure (BP) is usually elevated during symptoms.

Physical ExamPhysical exam is usually unrevealing.Occasional physical findings include:S3 or S4 due to left ventricular systolic or diastolic symptomsPapillary muscle dysfunction resulting in mitral regurgitationDiminished peripheral pulses

TestsECG:Will be normal approximately 50% of the timeST segment changes or T-wave inversions most often will be unchanged from previous tracings.Must be compared to prior tracings if availableNew ST segment changes or T-wave inversions are suspicious for unstable angina.Serial ECG tracings that remain unchanged may assist in differentiating stable from unstable angina.1-mm depression of the ST segment below the baseline, 80 msec from the J point, is characteristic of angina

LabCK-MB and troponin I or THematocritCoagulation profileCreatinine

ImagingChest radiograph:Usually normalMay show cardiomegalyCongestive heart failure is suggestive of unstable angina.May identify other etiologies of chest pain such as pneumoniaRest echocardiography may establish the diagnosis of acute coronary insufficiency (ACI):Has a sensitivity of 70% and specificity of 87% for ACI

Technetium Tc-99 sestamibi (rest):Has a sensitivity of 81% and specificity of 73% for ACI

Exercise stress testing may help establish the diagnosis of angina and provide prognostic information when the clinical presentation is equivocal:Exercise stress testing with ECG alone has a sensitivity of 68% and specificity of 77%.Exercise stress testing with echocardiography has a sensitivity of 85% and specificity of 77%.

Exercise stress testing with thallium-201 or technetium Tc-99m sestamibi has a sensitivity of 87% and specificity of 64%.1-mm depression of the ST segment below the baseline, 80 msec from the J point, in three consecutive beats and two consecutive leads is characteristic of cardiac ischemia.Early positive (within 3 minutes) stress tests are worrisome for unstable angina.

Differential DiagnosisAcute MIAnxietyAortic dissectionBiliary colicCostochondritisEsophageal refluxEsophageal spasmHerpes zosterPanic disorderPeptic ulcer diseasePneumoniaPsychogenicPulmonary embolusHiatal herniaMitral valve prolapseMI

TreatmentPre HospitalIV accessAspirinOxygenCardiac monitoringSublingual nitroglycerin for symptom relief

Initial StabilizationIV accessOxygenCardiac monitoringOxygen saturationContinuous BP monitoring and pulse oximetry

DrugsAspirinEnoxaparinGlycoprotein IIb/IIIa inhibitors:Eptifibatide (Integrilin):Tirofiban (Aggrastat):Abciximab (ReoPro):HeparinMetoprolol

MorphineNitroglycerinNitroglycerinNitropaste

CARDIAC ARREST

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Epidemiology50% of all cardiac deaths are sudden & unexpected, at least two-thirds of which are first cardiac events or occur among population subsets with previously known heart disease.

Unresponsiveness Pulselessness Shallow, gasping respirations may persist for a few minutes Occasionally preceded by chest pain, dyspnea, palpitation, seizure activity Immediately prior to arrest :Shock or hypotensionImpaired mentation

Signs & Symptoms

Laboratory tests :ElectrolytesBlood urea nitrogen/creatinineCreatinine kinase with isoenzymes, cardiac troponinArterial blood gas CBCTherapeutic drug levelsToxicological testing

Diagnostic Tests

ECG :Establish or rule out acute coronary syndromePericardial effusionWall motion abnormalityValvular dysfunctionCXR :Endotracheal tube positionCardiac silhouettePneumothorax

Sudden loss of consciousness with a palpable pulse:SyncopeSeizureAcute strokeHypoglycemiaAcute airway obstructionHead trauma & toxins

Differential Diagnose

ManagementThe initial response : basic life support & public access defibrillation (if available)Advanced life supportPost-resuscitation careLong-term management

Management (Pre-Hospital)Prompt initiation of standard CPR / active compression-decompression CPR (ACD-CPR) Confirm underlying rhythm Early defibrillation of ventricular tachycardia (VT) or ventricular fibrillation (VF):- Automated external defibrillator- EMT-D or layperson

Consider CPR before defibrillation, if arrest >5 minutes.Secure airway and provide adequate respirations:- Endotracheal intubation or Laryngeal mask airway Post-resuscitation care:- Identify cause of arrest- 12-lead ECG- Monitor vital signs

Transport to the closest facility:If return of spontaneous circulation, consider transport to center equipped for interventional cardiac care.Pediatric critical care center for childrenTermination of resuscitative efforts:Persistent, confirmed asystoleProlonged arrest

Initial Stabilization Initiate advanced cardiac life support (ACLS) Perform standard CPR as long as no pulse is palpable Consider ACD-CPR (stop CPR only briefly to check cardiac rhythm or intubate)

Secure the airwayObtain IV accessCardiac monitorTh/ based on the underlying rhythm according to ACLS protocols

Pulseless VT or VF Immediate defibrillation with up to three countershocks:200 J200 - 300 J360 JED Treatment

If defibrillation is unsuccessful:EpinephrineVasopressinIf refractory to defibrillation and epinephrine:AmiodaroneLidocaineProcainamideMagnesium for Torsades de Pointes

Asystole Dismal prognosis if this is the presenting rhythm Confirm in two or more leads Epinephrine Atropine Consider transcutaneous pacing for severe brady-asystolic rhythm.

PEA Epinephrine Atropine Treat for reversible cause :- Pneumothorax- Cardiac tamponade- Hypoxia- Pulmonary embolus- Hypovolemia (hemorrhage)

AmiodaroneAtropineEpinephrineLidocaineMedication (Drugs)MagnesiumProcainamideSodium bicarbonateVasopressin

Treat the underlying cause of the arrestVentilatory supportContinue antidysrhythmic therapyCorrect electrolyte abnormalities

Post Resuscitation

ECG Emergency

CARDIORESPIRATORY RESUSCITATION

DefinitionCPR is an organized, sequential response to cardiac arrest, includingRecognition of absent breathing and circulationBasic life support with chest compression and rescue breathingAdvanced cardiac life support (ACLS) with definitive airway and rhythm controlPostresuscitative carePrompt initiation of chest compression and early defibrillation (when indicates) are the key of success.

When to start CPRAnyone who initiate resuscitation knowledge and skills to initiate CPR when dealing with cases of cardiac arrest.

Incidence of cardiac arrest who witnessedIf we are witnessing the cardiac arrest, was should immediately started CPR. However, there are circumstances like this some underlying unnecessary CPR started:There is evidence of demand for familyCPR efforts will harm people who helpedPossible CPR can restore spontaneous circulation is very smallCardiac arrest happened on terminal illness who have been treated to the maximum

B. Incidence of cardiac arrest was not witnessedHelper ill cardiac know how long it's been going on. For something like this we do not need to start doing CPR if the state finds as follows:There is a sign that death does not change like rigor mortis / bruised corpseIt's getting no signs of decayPatients experiencing trauma that can not be saved, such as charred, decapitation

When to stop CPRThere are several compelling reasons for rescuers to stop CPR among other things:Helpers are doing basic and advanced life support optimal included: CPR, defibrillation in patients with VF / VT without a pulse, vasopressin / epinephrine IV, open the airway, ventilation and oxygenation using airway aid and all levels lanut rhythm after treatment performed.Helpers are considering whether there is a hypothermia patient. Helpers has established the presence / absence of hypothermia by measuring body temperature.

Helpers have considered whether patients exposed to toxic materials or an overdose that inhibits CNS.Helper was recorded through a monitor systolic settled for 10 minutes or more.The time interval pd cardiac resuscitation efforts were unsuccessful witnessed restore spontaneous circulation was 25-30 minutes.

General Technique of CPR continuedIf alone, alternate 30 chest compressions and 2 ventilations for any age patient In two-rescuer CPR for infant/child, alternate 15 compressions and 2 ventilationsChest-encircling method in infant Give each ventilation over 1 secondFollow local protocol regarding oxygen

Put hand(s) in correct position for chest compressions

Give 30 chest compressions at rate of 100 per minute Then give 2 ventilations

*****************Note: Plavix (clopidogrel bisulfate) is not indicated for all the conditions listed on this slide.Vascular disease is the common underlying disease process for MI, ischemia and vascular death.Acute coronary syndrome (ACS) is a classic example of the progression of vascular disease to an ischemic event.ACS (in common with ischemic stroke and critical leg ischemia) is typically caused by rupture or erosion of an atherosclerotic plaque followed by formation of a platelet-rich thrombus.Atherosclerosis is an ongoing process affecting mainly large and medium-sized arteries, which can begin in childhood and progress throughout a persons lifetime.Stable atherosclerotic plaques may encroach on the lumen of the artery and cause chronic ischemia, resulting in (stable) angina pectoris or intermittent claudication, depending on the vascular bed affected.Unstable atherosclerotic plaques may rupture, leading to the formation of a platelet-rich thrombus that partially or completely occludes the artery and causes acute ischemic symptoms.

*******************Treatment of acute coronary syndrome (ACS) should be directed by patient presentation.[1] The algorithm shown here shows the different treatment approaches (early invasive vs delayed invasive) that can be used in patients with unstable angina (UA) or nonST-segment elevation myocardial infarction (NSTEMI; also known as nonQ-wave MI).

Bowen WE, Mckay RG. Optimal treatment of acute coronary syndromesan evolving strategy. N Engl J Med. 2001;344:1939-1942. Editorial.Braunwald E, Antman EM, Beasley JW, et al. ACC/AHA guidelines for the management of patients with unstable angina and nonST-segment elevation myocardial infarction. Available at: www.acc.org. Accessed March 19, 2002.

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