Terminologi yang digunakan untuk menggambarkan spektrum klinis akibat terjadinya iskemia miokard akutAngina pektoris tidak stabil/APTS (unstable angina/UA)Infark miokard gelombang non-Q atau infark miokard tanpa elevasi segmen ST (Non-ST elevation myocardial infarction/ NSTEMI)Infark miokard gelombang Q atau infark miokard dengan elevasi segmen ST (ST elevation myocardial infarction/STEMI)

Sindroma Koroner Akut (SKA)UA/NSTEMISTEMI1,57 juta pasien dirawat dengan SKA1,24 juta pasien Setiap Tahun0,33 juta pasien Setiap Tahun

Activated Macrophages SMC Density SMC FunctionTiggers

CardiacPulmonaryHaematologicalVascularGastro-intestinalOrthopaedic/infectiousMyocarditisPulmonary embolismSickle cell crisisAortic dissectionOesophageal spasmCervical discopathyPericarditisPulmonary infarctionAnaemiaAortic aneurysmOesophagitisRib fractureCardiomyopathyPneumoniaPleuritisCerebrovascular diseasePeptic ulcerMuscle injury/inflammationValvular diseasePneumothoraxPancreatitisCostochondritisTako-TsubocardiomyopathyCholecystitisHerpes zosterCardiac trauma

Rest AnginaAngina yang timbul saat istirahatlamanya > 20 menitNew-onset AnginaAngina berat yang pertama kali timbulsetidaknya CCS IIICrescendo AnginaTelah diketahui angina, namun nyeri dirasakan makin sering, makin lama, dan timbul dengan aktivitas yang lebih ringan

Myoglobin

Penderita SKA memerlukan perawatan RS dan monitor koroner ICCURiwayat penyakit, Pem.Fisik, EKG ,Pem. Lab merupakan diagnostik yg penting.Tirah baring, Oksigen, Aspirin, Clopidogrel,Obat antikoagulan, Nitrat , Analgetik Opiat Trombolitik (STEMI).Sbg Pengobatan awal SKAStratifikasi resiko membantu pasien dgn resiko tinggi yg membutuhkan Gp IIb/IIIa inhibitor dan angiografi koroner.Pengobatan

*DRUGS for AMIMONACo greets all MI patients

M = MorphineO = OxygenN = NitrateA = AspirinCo= Clopidogrel

ACUTE PULMONARY EDEMA

Congestive Heart FailureorAcute Pulmonary Edema

INTRODUCTIONCongestive Heart Failure (CHF)??? :

A syndrome resulting from the inability of the heart to pump blood forward at a sufficient rate to meet the metabolic demands of the body (forward failure), or the ability to do so only if the cardiac filling pressures are abnormally high (backward failure), or both.

Results in retention of fluid congestion.

PULMONARY CIRCULATIONBlood flows from the right ventricle through the pulmonary arteryBlood reaches the capillaries surrounding alveoli where gas exchange occursOxygenated blood returns by pulmonary veins to the left ventricle where it is pumped into systemic circulation

ETIOLOGY AND PATHOPHYSIOLOGYSyndrome usually results from LV dysfunction and compensatory mechanisms

Cardiac performance is a function of 4 primary factors. What are they?

4 FACTORS DETERMINING CARDIAC PERFORMANCE

Preload Afterload ContractilityHeart Rate

Compensatory Mechanisms to Maintain Cardiac Output:The Frank-Starling mechanismMyocardial hypertrophyIncreased sympathetic toneAll result in increased myocardial O2 demand!Kidneys

CAUSES OF Congestive Heart FailureConditions that increase preload, e.g. aortic regurgitation, ventricular septal defects, fluid overloadConditions that increase afterload, e.g. aortic stenosis, systemic hypertension (vasoconstriction), Conditions that decrease myocardial contractility, e.g. MI, cardiomyopathies, pericarditis, tamponade

SIGNS &SYMPTOMS OF Congestive Heart Failure

Exertional dyspnea usually with Crackles - fatigue may be the first signIncreased respiratory rate and effortOrthopnea and/or PNDCyanosis and pallorTachycardiaJVDDependant edema

Framingham CriteriaMajor Criteria:PNDJVDRalesCardiomegalyAcute Pulmonary EdemaS3 GallopPositive hepatic Jugular reflex venous pressure > 16 cm H2O

Minor Criteria:Extremitas edemaNight cough Dyspnea on exertionHepatomegalyPleural effusion vital capacity by 1/3 of normalTachycardiaWeight loss 4.5 kg over 5 days managementFramingham Criteria

CATEGORIZING FAILURELeft or Right sided heart failureForward or Backward ventricular failureBackward failure is secondary to elevated systemic venous pressures.Forward ventricular failure is secondary to left ventricle failure and reduced flow into the aorta and systemic circulation

LV BACKWARD EFFECTSDecreased emptying of the left ventricleIncreased volume and end-diastolic pressure in the left ventricleIncreased volume (pressure) in the left atriumIncreased volume in pulmonary veins

Increased volume in pulmonary capillary bed = increased hydrostatic pressureTransudation of fluid from capillaries to alveoliRapid filling of alveolar spacesPulmonary edemaLV BACKWARD EFFECTS cont

LV FORWARD EFFECTSDecreased cardiac outputDecreased perfusion of tissues of body Decreased blood flow to kidneys and glandsIncreased reabsorption of sodium and water and vasoconstriction

Increased secretion of sodium and water-retaining hormones Increased extracellular fluid volumeIncreased total blood volume and increased systemic blood pressureLV FORWARD EFFECTS cont

RV BACKWARD EFFECTSDecreased emptying of the right ventricleIncreased volume and end-diastolic pressure in the right ventricleIncreased volume (pressure) in right atriumIncreased volume and pressure in the great veins

Increased volume in the systemic venous circulation

Increased volume in distensible organs (hepatomegaly, splenomegaly)

Increased pressures at capillary line

Peripheral, dependant edema and serous infusionRV BACKWARD EFFECTS cont

RV Forward EffectsDecreased volume from the RV to the lungsDecreased return to the left atrium and subsequent decreased cardiac outputAll the forward effects of left heart failure

Congestive Heart Failure Can Be Defined Based on:

How rapid the symptoms onset

Which ventricle is primarily involved

Overall cardiac output

CARDIOGENIC SHOCKThe most extreme form of pump failureOccurs when left ventricular function is so compromised that the heart cannot meet the metabolic needs of the bodyUsually caused by extensive myocardial infarction, often involving more than 40% of the left ventricle, or by diffuse ischemiaMAP drops below 70mmHg

New York Heart Associations functional classification of CHF

CLASS I

A patient who is not limited with normal physical activity by symptoms but has symptoms with exercise.

CLASS II

Ordinary physical activity results in fatigue, dyspnea, or other symptoms.

CLASS III

Characterized by a marked limitation in normal physical activity.

CLASS IV

Defined by symptoms at rest or with any physical activity.

Three Stages of Pulmonary EdemaStage 1 - Fluid transfer is increased into the lung interstitium; because lymphatic flow also increases, no net increase in interstitial volume occurs.Stage 2 - The capacity of the lymphatics to drain excess fluid is exceeded and liquid begins to accumulate in the interstitial spaces that surround the bronchioles and lung vasculature (which yields the roentgenographic pattern of interstitial pulmonary edema).

Three Stages of Pulmonary EdemaStage 3 - As fluid continues to build up, increased pressure causes it to track into the interstitial space around the alveoli.Fluid first builds up in the periphery of the alveolar capillary membranes and finally floods the alveoli . During stage 3 the x-ray picture of alveolar pulmonary edema is generated and gas exchange becomes impaired.

Acute Pulmonary EdemaMay be CARDIAC or NON-CARDIAC in origin.Results from conditions such as:Increased pulmonary capillary pressureIncreased pulmonary capillary permeabilityDecreased oncotic pressureLymphatic insufficiencymixed or unknown mechanisms

Etiology of Pulmonary EdemaIncreased fluid in lung interstitiumInterstitial edemaPulmonary hydrostatic pressure exceeds colloid osmotic pressureFluid tracks into interstitial spaces around alveoliFluid enters alveoli

Differential Diagnosis for APE:Cardiac causes of acute CHFCOPD exacerbationNon-cardiac pulmonary edema: Tansudate vs. Exudate fluid overloadinfectionARDSHigh altitudePulmonary EmbolismPneumonia

CLINICAL PRESENTATION:HistoryPhysical ExamEKG

This should provide enough information to establish a cardiac etiology, if one exists!

Symptoms Suspicious of Pulmonary CongestionAny complaint of dyspnea/ decreased exercise tolerance PND/ Orthopnea Feeling of suffocation or air-hunger Restlessness and anxietyCyanosis/DiaphoresisPallor

Symptoms Suspicious of Pulmonary CongestionCracklesWheezing (Cardiac Asthma)TachypneaCoughing (Dry cough may be med related)Retractions, accessory muscle useFrothy pink-tinged sputum

Physical Findings JVDEdema - ankle/pretibial vs sacralAscites - Positive Hepato-jugular reflex testBP and P are often markedly elevatedCardiac examS3 or intermittent S4 may be present?PMI may be shifted left

EKG Analysis:Search for evidence of infarction or ischemiaNon-specific findings may include:hypertrophychamber enlargementconduction disturbances

CHEST XRAY:Usually demonstrates increased heart sizeProgression of pulmonary congestion:first: Cephalizationsecond : Interstitial edemathird: Pulmonary (alveolar) edema

Treatment of APE:First and foremost is to increase oxygen saturationa reasonable approach is to base therapy on the Systolic Blood PressureDecrease the preload on the heartShift and then eliminate excess fluids

Prehospital Management:Patient sittingSupplemental O2 provided Cardiac monitoring/ Pulse oximetryInitiate necessary supportive therapyNitroglycerin for APE if patient matches protocolBe prepared to assist ventilationsPPV is an effective treatment

TREATMENT PHARMACOLOGYREDUCTION OF AFTERLOADSUBLINGUAL NITROGLYCERIN: 0.4 mg REPEAT 1-5 MINIV NITROGLYCERIN: 10-30 micg/min TITRATE TO 200 micg/minIV NITROPRUSSIDE: 2.5 micg/kg/min TITRATENESIRITIDE: ANTAGONIST TO RENIN- ANGIOTENSIN AXSIS, 2 micg/kg BOLUS, IV DRIP 0.01 micg/kg/min

VASODILATORS NOT RECOMMENED FOR HYPOTENSIVE PATIENTS, PATIENTS WITH CARDIOGENIC SHOCK

CONTRAINDICATIONS TO VASODIALATORSPRELOAD DEPENDENT STATESRIGHT VENTRICULAR INFARCTIONAORTIC STENOSISVOLUME DEPLETIONHYPERTROPHIC CARDIOMYOPATHYREDUCTION OF HEART RATE AND CONTRACTILITY WITH IV BETA BLOCKERS IS THERAPY OF CHOICE

TREATMENT PHARMACOLOGYFUROSEMIDE:NO PRIOR USE: 40 mg IVPPRIOR USE: DOUBLE LAST 24 HOUR USAGE: 80-180 mgNO RESPONSE IN 20-30 MIN RE-DOUBLE DOSEBUMETANIDE:1-3 MG DIURESIS BEGINS WITHIN 10 MINMONITORING OF ELECTROLYTES ESSENTIAL

TREATMENT PHARMACOLOGYACE INHIBITORSDECREASE MORTALITY AND HOSPITALIZATIONSALL HF PATIENTS SHOULD BE DISCHARGED WITH ACEI (DECREASES MORTALITY IN CLASS 4 HF BY 31%)

BETA BLOCKERSDECREASE MYOCARDIAL HYPERTROPHY, AFTERLOAD AND MYOCARDIAL OXYGEN DEMANDMETOPROLOL DECREASES 1 YEAR MORTALITY IN CLASS II-III BY 34%

Treatment ProcedurePatient in sitting position100% oxygen via NRB or BVM Cardiac monitor

Cardiac Arrest Arrhythmias

Cardiac ArrestMechanismsVentricular FibrillationPulseless Ventricular TachycardiaAsystolePulseless Electrical Activity (PEA)A condition; Not an ECG rhythm

Cardiac ArrestMost common rhythmsAdults: ventricular fibrillationChildren: Asystole, Bradycardic PEAPediatric V-fib suggests:Drug toxicityElectrolyte imbalanceCongenital heart disease

Cardiac ArrestABCs come first!Airway - unobstructed? manually openBreathing - no or inadequate ventilateCirculation - no pulse in 5 sec chest compressionsDo NOT wait on equipmentAssure effective BLS before going to ALSRise and fall of chestAir movement in lung fieldsPulse with compressions

Cardiac ArrestFirst ALS priority is defibrillationOnly cure for v-fib is defibThe quicker the betterProbability of resuscitation decreases 7-10% with each passing minute

Cardiac ArrestVascular accessAntecubital spaceArm, EJ, Foot (last resort)IO in peds < 6 y/o14 or 16 gaugeLR or NS30 sec - 60 sec of CPR to circulate drug

Cardiac ArrestIntubation as time allowsLess emphasis today as compared to pastEpi, atropine, lidocaine may be administered down tube2x IV doseIV is preferred

Analyze the Rhythm

Ventricular Fibrillation (VF)CharacteristicsChaotic, irregular, ventricular rhythmWide, variable, bizarre complexesFast rate of activityMultiple ventricular fociNo cardiac outputTerminal rhythm if not corrected quicklyMost common rhythm causing sudden cardiac death in adults

Ventricular Fibrillation (VF) TreatmentABCsWitnessed arrest: Precordial thumpLittle demonstrated value but worth a tryCPR until defibrillator availableQuick Look for VF or pulseless VTTreat pulseless VT as if it were VFDefibrillate200 J, 300 J, 360 JQuickly and in rapid successionIdentify cause if possible

Ventricular Fibrillation TreatmentIf still in VF/VT arrest, continue CPR for 1 minuteEstablish IV access and IntubateIf sufficient personnel, attempt both simultaneouslyIf not, quick attempt at IV access then attempt ETTVasopressor MedicationEpinephrine1 mg 1:10,000 IVPRepeat every 3-5 mins as long as arrest persistsVasopressin (alternative to Epinephrine)40 units IVP one time only

Ventricular Fibrillation TreatmentShock @ 360 J after each medication given as long as VF/VT arrest persistsAlternate epi-shock & antidysrhythmic-shock sequenceAntidysrhythmic Medicationamiodarone 300 mg IVP single doselidocaine 1-1.5 mg/kg IVP, q 5 min, max 3mg/kg totalprocainamide 100 mg IV, q 5 min, max 17 mg/kg totalmagnesium 10% 1-2 g IV if hypomagnesemic or prolonged QT

Ventricular Fibrillation TreatmentConsider NaHCO3 if prolongedOnly after effective ventilationsIn many EMS systems, consider terminating resuscitation efforts in consult with med control

Ventricular FibrillationThe ultimate unstable tachycardiaShock early-Shock oftenSequence is drug-shock-drug-shockSequence of drugs is epi-antiarrhythmic-epi-antiarrhythmic

AsystoleCharacteristicsThe ultimate unstable bradycardiaA terminal rhythmpoor prognosis for resuscitationbest hope if ID & treat causeNo significant positive or negative deflections

AsystolePossible CausesHypoxia: ventilatePreexisting metabolic acidosis: Bicarbonate 1 mEq/kgHyperkalemia: Bicarbonate 1 mEq/kg, Calcium 1 g IVHypokalemia: 10mEq KCl over 30 minutesHypothermia: rewarm body core

AsystolePossible CausesDrug overdoseTricyclics: BicarbonateDigitalis: Digibind (Digitalis antibodies)Beta-blockers: GlucagonCa-channel blockers: Calcium

Asystole & PEA Differentials (The 5Hs & 5Ts)HypovolemiaHypoxiaHydrogen ions (Acidosis)Hyper/hypo-kalemiaHypothermiaTablets (Drug OD)TamponadeTension PneumothoraxThrombosis, CoronaryThrombosis, Pulmonary

Asystole TreatmentPrimary ABCDConfirm Asystole in two leadsReasons to NOT continue?Secondary ABCDECG monitor/ET/IVDifferential Diagnosis (5Hs & 5Ts)TCP (if early)Epinephrine 1:10,000 1 mg IV q 3-5 min.Atropine 1 mg IV q 3-5 min, max 0.04 mg/kgConsider Termination

PEAPossibilitiesMassive pulmonary embolusMassive myocardial infarctionOverdose:Tricyclics - BicarbonateDigitalis - DigibindBeta-blockers - GlucagonCa-channel blockers - Calcium

PEAIdentify, correct underlying cause if possiblePossibilities:Hypovolemia: volumeHypoxia: ventilateTension pneumo: decompressTamponade: pericardiocentesisAcute MI: vasopressorHyperkalemia: Bicarbonate 1mEq/kgPreexisting metabolic acidosis: Bicarbonate 1mEq/kgHypothermia: rewarm core

PEA TreatmentABCDsETT/IV/ECG monitorDifferential DiagnosisFind the cause and treat if possibleEpinephrine 1:10,000 1 mg q 3-5 min. If bradycardic,Atropine 1 mg IV q 3-5 min, Max 0.04 mg/kgTCPIn many systems, consider termination of efforts

Managing Cardiac ArrestCheck pulse after any treatment or rhythm change

Post-resuscitation CareIf pulse present:Assess breathingPresent?Air moving adequately?Equal breath sounds?Possible flail chest?

Post-resuscitation CareIf pulse present:Protect airwayPosition to prevent aspirationConsider intubation100% Oxygen via BVM or NRBVascular access

Post-resuscitation CareAssess perfusionEvaluatePulsesSkin colorSkin temperatureCapillary refillBPKey is perfusion, not pressure

Post-resuscitation CareManagement of Decreased PerfusionFluid challengeCatecholamine infusionDopamine, orNorepinephrineTitrate to BP ~ 90 to 100 systolic

*Cardiac Arrest kuliah 2013

Cardiac Arrest kuliah 2013

Treat the patient, not the monitor . . . . . . . . .!!!

***1*Results from conditions such as:-Increased pulmonary capillary pressure-Increased pulmonary capillary permeability-Decreased oncotic pressure-Lymphatic insufficiency-mixed or unknown mechanisms

*4*5*6***3*7*8*10*12*15*14*18*19*Cephalization on Right- Due to pulmonary hypertension- Pulmonary veins become visible due to increased blood congestion- Decreases or clears after treatment

*20*21Stress DEPENDANT limbsIterate suction vs. PPV