dr. David D Ariwibowo, Sp.JPFakultas Kedokteran Universitas Tarumanagara2011

Review of Circulatory System

Cardiovascular EmergenciesAcute Coronary Syndrome.Cardiac ArrhythmiasCardiac TamponadeAcute Heart Failure Hypertensive Heart Failure (Hypertensive Emergency)Acute Pulmonary EdemaRight Ventricular FailureCardiogenic ShockCardiorespiratory ArrestAortic dissectionAcute Limb IschemicEtc.

Acute Coronary Syndrome3AMampu membuat diagnosis klinik berdasarkan pemeriksaan fisik dan pemeriksaan tambahan (misalnya : pemeriksaan laboratorium sederhana atau X-ray). Dokter dapat memutuskan dan memberi terapi pendahuluan, serta merujuk ke spesialis yang relevan (bukan kasus gawat darurat).3BMampu membuat diagnosis klinik berdasarkan pemeriksaan fisik dan pemeriksaan (misalnya : pemeriksaan laboratorium sederhana atau X-ray). Dokter dapat memutuskan dan memberi terapi pendahuluan, serta merujuk ke spesialis yang relevan (kasus gawat darurat).KompetensiSTANDAR KOMPETENSI DOKTER, KONSIL KEDOKTERAN INDONESIA 2008

Acute Coronary SyndromeUnstable Angina Pectoris (UAP)Acute Non ST-Elevation Myocardial infarction (NSTEMI)Acute ST-Elevation Myocardial infarction (STEMI)

PatophysiologyAtherosclerosis Timeline

DefinitionNSTEMISTEMI

EpidemiologyMurray CJ, Lopez AD. Lancet 1997; 349: 1269-1276 106

Chart1

0.9

1

1.1

2

2.2

2.4

2.9

4.3

4.4

6.3

Sheet1

lung cancerroad traffic accidentsmeaslestuberculosischronic obstructive lung Dxperinatal disordersdiarrhoeal diseaseslower respiratory infectionscerebrovascular accidentsischmic heart Dx

0.911.122.22.42.94.34.46.3

DiagnosisPresentationWorking DxECGCardiac BiomarkerFinal DxUANQMIQwMINo ST ElevationNSTEMIIschemic DiscomfortAcute Coronray SyndromeST ElevationUA

PresentationAngina klasik Rasa tidak nyaman / nyeri di daerah sternal > 20 menit.Menjalar ke lengan kiri, leher, rahang, punggung.Dapat bersifat tajam (ditusuk, terbakar) atau tumpul (seperti ditekan, diperas).Disertai keringat dingin, mual / muntah, kesulitan bernapas, berdebar-debar. Angina Equivalent Tidak ada nyeri / rasa tidak nyaman di dada yang khas.Gejala gagal jantung mendadak (sesak napas).Aritmia ventrikular (palpitasi, presinkop, sinkop)

PresentationFaktor Risiko :Usia : Tua > MudaGender : Laki-laki > PerempuanRiwayat Keluarga ( PJK ) HipertensiDiabetes MellitusPeningkatan Kadar Kolesterol Total dan LDLKadar Kolesterol HDL Rendah ObesitasKurang Aktivitas FisikDiet : Tinggi Lemak Jenuh dan KolesterolMerokok

Differential DxCardiacStable AnginaMVPAortic Stenosis Hypertrophic cardio myopathyPericarditisLungs Lung EmboliPnemoniaPneumothoraxPleuritisGastrointestinalReflux esofagusRuptur esofagusGall bladder diseasePeptic UlcerPancreatitisVascularAortic dissectionOthersMusculoskeletalHerpes zoster

ECGTo detect ischaemic changes or arrhythmias.Initial ECG has a low sensitivity for ACS.A normal ECG does not rule out ACS.ECG is the sole test required for emergency reperfusion selection (fibrinolytic or primary PCI).

ECGAffecting all ECG featuring ventricles

ECGT wave changesInverted TPada iskemia namun kurang spesifikPerubahan akhir pada STEMI, terjadi setelah ST elevasi kembali ke normal

Hyperacute TPerubahan awal pada STEMI

ECGST Segment changes With acute subendocardial ischemia the electrical forces (arrows) responsible for the ST segment are deviated toward the inner layer of the heart, causing ST depression in V5, which faces the outer surface of the heartWith acute transmural (epicardial) ischemia, electrical forces are deviated toward outer layer of the heart, causing ST elevation in the overlying lead.

ECGST depresionBermakna bila > 1 mm di bawah garis dasar PT di titik JTitik J adalah titik akhir kompleks QRS dan permulaan segmen STBentuk segmen ST : Horizontal Spesifik untuk iskemia.Down-sloping Paling spesifik. Up-sloping Tidak spesifik

ECGST elevationOccurs in the leads facing the infarction in the early stagesSlight ST elevation may be normal in V1 or V2

ECGQ waveQ wave duration of more than 0.04 seconds (1 mm)Q wave depth of more than 1/3 of ensuing R wave

ECGSequence of changes in evolving STEMI

ECG

ECGAnatomi Koroner & EKG 12 sandapanV1 & V2 menghadap septal area LV.V3 & V4 menghadap dinding anterior LVV5 & V6 + I & avL menghadap dinding lateral LVII, III & avF menghadap dinding inferior LV

aVRV1V4IIIIIILATERALINFERIORSEPTALANTERIORLATERALaVLaVFV2V3V5V6

012345678Cardiac troponin-no reperfusion Days After Onset of STEMIMultiples of the URLUpper reference limit125102050URL = 99th %tile of Reference Control Group100Cardiac troponin-reperfusion CKMB-no reperfusion CKMB-reperfusion Alpert et al. J Am Coll Cardiol 2000;36:959.Wu et al. Clin Chem 1999;45:1104.Cardiac Biomarkers in STEMILaboratorium

Diagnosis NomenclatureTiming at presentation :Acute (0-7 days)Recent (7-14 days)Old (>14 days)Infarct locationSeptal, anterior, anteroseptal, anterolateral, anterior extensiveInferior, inferolateral, lateralPosterior, right ventricular infarct

ExampleUAP Acute NSTEMIAcute Anterior STEMIRecent inferolateral MCIOld Inferior MCI

Anterior infarctionLeft coronary artery

Inferior infarctionRight coronary artery

Lateral infarctionLeft circumflexcoronary artery

ManagementSymptom RecognitionCall to Medical SystemEDCath LabPreHospitalDelay in Initiation of Reperfusion TherapyIncreasing Loss of MyocytesTreatment Delayed is Treatment Denied

Management

MONAMorphin 2- 5 q 5 min titrate to response and side effects.O2 Nasal cannula 4 L/mntNitrat: ISDN 5 mg SL 3 timesAspirin 160-320 mg

Options for Transport of Patients With STEMI and Initial Reperfusion TreatmentEMS TransportOnset of symptoms of STEMI9-1-1EMSDispatchEMS on-sceneEncourage 12-lead ECGs.Consider prehospital fibrinolytic if capable and EMS-to-needle within 30 min.GOALSPCIcapableNot PCIcapableHospital fibrinolysis: Door-to-Needle within 30 min.EMS Triage PlanInter-HospitalTransferGolden Hour = first 60 min.Total ischemic time: within 120 min.PatientEMSPrehospital fibrinolysisEMS-to-needlewithin 30 min.EMS transportEMS-to-balloon within 90 min.Patient self-transport Hospital door-to-balloon within 90 min.Dispatch1 min.5 min.8 min.

Select Reperfusion Treatment. If presentation is < 3 hours and there is no delay to an invasive strategy, there is no preference for either strategy.

Fibrinolysis generally preferred Early presentation ( 3 hours from symptom onset and delay to invasive strategy)Invasive strategy not an optionCath lab occupied or not available Vascular access difficultiesNo access to skilled PCI lab

Delay to invasive strategyProlonged transportDoor-to-balloon more than 90 minutes> 1 hour vs fibrinolysis (fibrin-specific agent) now

Select Reperfusion Treatment. Invasive strategy generally preferred Skilled PCI lab available with surgical backupDoor-to-balloon < 90 minutes

High Risk from STEMICardiogenic shock, Killip class 3

Contraindications to fibrinolysis, including increased risk of bleeding and ICH

Late presentation> 3 hours from symptom onset

Diagnosis of STEMI is in doubt

Percutaneous Coronary Intervention (PCI)

Percutaneous Coronary Intervention (PCI)

Percutaneous Coronary Intervention (PCI)

Percutaneous Coronary Intervention (PCI)

Coronary Artery Bypass Graft (CABG) Surgery

Acute Heart Failure3BMampu membuat diagnosis klinik berdasarkan pemeriksaan fisik dan pemeriksaan (misalnya : pemeriksaan laboratorium sederhana atau X-ray). Dokter dapat memutuskan dan memberi terapi pendahuluan, serta merujuk ke spesialis yang relevan (kasus gawat darurat).KompetensiSTANDAR KOMPETENSI DOKTER, KONSIL KEDOKTERAN INDONESIA 2008

DefinitionAHF Rapid onset or change in the signs & symptoms of HF.New or worsening of pre-existing chronic HF. The European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008

Causes & precipitating factors of AHFThe European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008These aetiologies & conditions often interact should be identified & incorporated into the treatment strategy.

Clinical presentationUsually characterized by pulmonary congestion cardiac output & tissue hypoperfusion may dominate the clinical presentationReflects a spectrum of conditions present in one of 6 clinical categories. Figure demonstrates the potential overlap between these conditionsThe European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008

Clinical presentationThe European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008

DiagnosisBased on the presenting symptoms & clinical findings.Confirmation by the history, physical examination, ECG, CXR, echocardiography, laboratory investigation, with blood gases & specific biomarkers. The European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008

Goals of treatment in AHFThe European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008

Immediate goals tissue oxygenation & haemodynamics permit further interventions by :Reduce fluid volume & filling pressures.Reduce systemic vascular resistance (SVR)Increase cardiac output (CO)

Therapeutic Goal ParametersClinicalHemodynamicSBP > 90 mmHgWarm extremitiesJVP < 8 cmNo orthopneaSBP> 90 mm Hg SVRI < 1200 dyne-s-cm-5 PCWP< 15 mm HgRAP < 8 mm Hg

Specific treatment strategy based on distinguishing the clinical conditionsThe European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008

Two Minutes Assessment of Haemodynamic ProfileThe Forrester classification is based on clinical signs & haemodynamic characteristics. Figure presents a modified from the Forrester classification.

Patient Treatment SelectionFonarow GC. Rev Cardiovasc Med. 2001;2(suppl 2):S7S12.

Initial treatment algorithmThe European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008

AHF treatment strategy according to systolic BPThe European Society of Cardiology, Guidelines on the diagnosis and treatment of acute heart failure, 2005

Loop diureticsIn the presence congestion & volume overload. Class I, level of evidence BThe European Society of Cardiology, Guidelines on the diagnosis and treatment of acute heart failure, 2005

VasodilatorsThe European Society of Cardiology, Guidelines on the diagnosis and treatment of acute heart failure, 2005

Inotropic agents The European Society of Cardiology, Guidelines on the diagnosis and treatment of acute heart failure, 2005

Cardiorespiratory Arrest3BMampu membuat diagnosis klinik berdasarkan pemeriksaan fisik dan pemeriksaan (misalnya : pemeriksaan laboratorium sederhana atau X-ray). Dokter dapat memutuskan dan memberi terapi pendahuluan, serta merujuk ke spesialis yang relevan (kasus gawat darurat).KompetensiSTANDAR KOMPETENSI DOKTER, KONSIL KEDOKTERAN INDONESIA 2008

Cardiorespiratory Arrest suatu keadaan dimana pasien: tidak sadartidak bernafastidak ada denyut nadi

Syarat dasar untuk hidupFungsiSirkulasiFungsiPernapasanHenti JantungHenti NapasTergangguTerganggu

Sebab tersering: serangan jantung

PrevalensiWHO (2004) 17,1 juta orang meninggal karena penyakit jantung. 2030 23,6 juta kematian karena penyakit jantung dan pembuluh darahEropa kasus henti jantung 700.000 / tahun.Indonesia (2007) Prevalensi Nasional PJK 7,2% 1. Prevalensi PJK di 16 Propinsi di Indonesia diatas angka Nasional

Bantuan hidup jantungKematian akibat penyakit jantung terutama disebabkan henti jantung mendadak, dengan irama terdokumentasi paling sering adalah ventrikel fibrilasi (VF).Pertolongan bantuan hidup dasar yang berhasil, dilakukan dalam 5 menit pertama dengan bantuan AEDBantuan hidup jantung merupakan gabungan pengamatan dan tindakan yang tidak terputus yang disebut Chain of Survival

Chain of Survival

Bantuan hidup dasarSerangkaian usaha awal untuk mengembalikan fungsi pernafasan dan atau sirkulasi pada seseorang yang mengalami henti nafas dan atau henti jantung.

LANGKAH-LANGKAHPastikan penolong dan korban dalam kondisi amanTempatkan korban di atas alas yang keras dalam posisi telentangLakukan langkah-langkah algoritme.

Cek ResponsCarilah tanda-tanda sirkulasi:BergerakBersuaraBernapasDengan cara menepuk dengan cukup kuat bahu/dada korban sambil memanggil korban

Minta tolong/panggil bantuanBila seorang diri, telepon dulu sarana kesehatan terdekat (RS, ambulans), ambil AED bila ada.Bila ada penolong lain, satu penolong memanggil bantuan dan ambil AED, yang lain langsung menolong korbanMeminta pertolongan harus jelas mengenai kejadian, jumlah korban, lokasi dll

Mulai Resusitasi Jantung Paru (RJP)Bila korban tidak memberi respons dan tidak bernapas/bernapas tidak normal segera lakukan RJP setelah memanggil bantuanRJP terdiri dari tindakan kompresi dada dan pemberian napas bantuanDilakukan berulang 30 kali kompresi dada diselingi 2 kali napas bantuan

A Change From A-B-C to C-A-BFor adults, children, and infants (excluding the newly born)The vast majority of cardiac arrests in adults & the highest survival rates witnessed arrest and an initial rhythm of VF or pulseless VT. The critical initial elements chest compressions and early defibrillation. In the A-B-C, chest compressions are often delayed while the responder opens the airway to give mouth-to-mouth breaths, retrieves a barrier device, or gathers and assembles ventilation equipment. In the C-A-B, chest compressions will be initiated sooner and the delay in ventilation should be minimal (ie, only the time required to deliver the first cycle of 30 chest compressions, or 18 seconds)

Kompresi DadaTekan cepat dan kuat(minimal 100x/menit) (minimal dalamnya 5 cm)

Napas bantuanBuka jalan napas dengan cara menengadahkan kepalaBeri 2 napas bantuanPertahankan posisi kepalaSatu kali napas 1 detikPastikan dada terangkat

30x302Ulangi kompresi dan pemberian napas bantuan dengan perbandingan 30 kali kompresi dan 2 kali napas bantuan

TERIMA KASIH

***Cardiac biomarkers in ST-elevation myocardial infarction (STEMI).Typical cardiac biomarkers that are used to evaluate patients withSTEMI include the MB isoenzyme of CK (CK-MB) and cardiac specific troponins. The horizontal line depicts the upper reference limit (URL)for the cardiac biomarker in the clinical chemistry laboratory. The URL is that value representing the 99th percentile of a reference control group without STEMI. The kinetics of release of CK-MB and cardiac troponin in patients who do not undergo reperfusion are shown in the solid green and red curves as multiples of the URL. Note that when patients with STEMI undergo reperfusion, as depicted in the dashed green and red curves, the cardiac biomarkers are detected sooner, rise to a higher peak value, but decline more rapidly, resulting in a smaller area under the curve and limitation of infarct size. Modified with permission from Alpert et al. J Am Coll Cardiol 2000;36:959 and Wu et al. Clin Chem 1999;45:1104.*Location of infarction and its relation to the ECG: anterior infarctionAs was discussed in the previous module, the different leads look at different aspects of the heart, and so infarctions can be located by noting the changes that occur in different leads. The precordial leads (V16) each lie over part of the ventricular myocardium and can therefore give detailed information about this local area. aVL, I, V5 and V6 all reflect the anterolateral part of the heart and will therefore often show similar appearances to each other. II, aVF and III record the inferior part of the heart, and so will also show similar appearances to each other. Using these we can define where the changes will be seen for infarctions in different locations. Anterior infarctions usually occur due to occlusion of the left anterior descending coronary artery resulting in infarction of the anterior wall of the left ventricle and the intraventricular septum. It may result in pump failure due to loss of myocardium, ventricular septal defect, aneurysm or rupture and arrhythmias. ST elevation in I, aVL, and V26, with ST depression in II, III and aVF are indicative of an anterior (front) infarction. Extensive anterior infarctions show changes in V16 , I, and aVL.*Location of infarction and its relation to the ECG: inferior infarctionST elevation in leads II, III and aVF, and often ST depression in I, aVL, and precordial leads are signs of an inferior (lower) infarction. Inferior infarctions may occur due to occlusion of the right circumflex coronary arteries resulting in infarction of the inferior surface of the left ventricle, although damage can be made to the right ventricle and interventricular septum. This type of infarction often results in bradycardia due to damage to the atrioventricular node. *Location of infarction and its relation to the ECG: lateral infarctionOcclusion of the left circumflex artery may cause lateral infarctions.Lateral infarctions are diagnosed by ST elevation in leads I and aVL.