Cardiovascular EmergenciesWidy – 405120022

Emergency Medicine

SHOCK

• Inadequate oxygen delivery to meet metabolic demands• Results in global tissue hypoperfusion & metabolic acidosis• Shock can occur with normal BP & hypotension can occur without

shock• Inadequate systemic oxygen delivery activates autonomic responses to

maintain systemic oxygen deliveryo Sympathetic nervous system- NE, epinephrine, dopamine, cortisol release

Causes vasoconstriction, HR increases, increase of cardiac contractility (cardiac output)

o Renin-angiotensin axis- Water & sodium conservation and vasoconstriction- Increase in blood volume & BP

• Cellular responses to decreased systemic oxygen delivery• Goal is to maintain cerebral & cardiac perfusion• Leads to systemic metabolic lactic acidosis that overcome’s the body

compensatory mechanism

• GLOBAL TISSUE HYPOXIA- Endothelial inflamation & disruption- Inability of oxygen delivery to meet deman- Results: Lactic acidosis

Cardiovascular insufficiencyIncreased metabolic demands

• MULTIORGAN DYSFUNCTION SYNDROME- Progression of psychologic effects as shock ensues

Cardiac depressionRespiratory distressRenal failureDIC

- Result in end organ failure

Empiric Criteria for Shock

4 of 6 criteria have to be meet

1. Ill appearance/altered mental status2. HR >1003. RR >22 (or PaCO2 < 32 mmHg)4. Urine output <0,5 ml/kg/hour5. Arterial hypotension > 20 minutes duration6. Lactate >4

SYOK KARDIOGENIK

• Gangguan yg disebabkan pe↓ curah jantung sistemik pada keadaan volume intravaskular yg cukup, dapat menyebabkan hipoksia jaringan

• TD sistolik < 90 mmHg selama >1 jam di mana:o Tak responsive dgn pemberian cairan sajao Sekunder thd disfungsi jantungo Berkaitan dengan tanda-tanda hipoperfusi atau cardiac index <2,2l/menit per

m2 & Pulmonary Capillary Wedge Pressure (PCWP) >18 mmHg• Termasuk dipertimbangkan dalam definisi:- Pasien dgn TD sistolik me↑ >90 mmHg setelah pemberian inotropik- Pasien meninggal dlm 1 jam hipotensi, tetapi memenuhi kriteria lain syok

kardiogenik• Etiologi: - Komplikasi mekanik AMI (ruptur septal ventrikel, ruptur atau disfungsi otot

papilaris, ruptur miokard)- Takiaritmia/bradiaritmia rekuren akibat disfungsi ventrikel kiri, dapat timbul

bersamaan dgn aritmia supraventrikular/ventrikular- Manifestasi tahap akhir disfungsi miokard progresif, termasuk akibat penyakit

jantung iskemia, kardiomiopati hipertrofik & restriktif

Patofisiologi

• Old: depresi kontraktilitas miokard yg mengakibatkan lingkaran setan (pe↓ curah jantung, TD↓, insufisiensi koroner) → pe↓ kontraktilitas & curah jantung

• New: tjd vasokonstriksi sistemik sbg kompensasi, dgn pe↑ resistensi vaskular sistemik yg tjd sbg respon pe↓ curah jantung

• Pasien pasca IM → tdpt aktivasi sitokin inflamasi yg mengakibatkan pe↑ kadar iNOS, NO, peroksinitrit → efek buruk multipel:- Inhibisi langsung kontraktilitas miokard- Supresi respirasi mitokondria pd miokard non-sistemik- Efek thd metabolisme glukosa- Efek proinflamasi- Pe↓responsivitas katekolamin- Memicu vasodilatasis sistemik

Keterangan:Disfungsi miokard sistole & diastole

↓Penurunan cardiac output & kongesti

pulmonal (jarang)↓

Terjadi hipoperfusi sistemik & koroner↓

Iskemia progresif

Meskipun bbrp mekanisme kompensasi di aktifkan utk support sirkulasi, mekanisme kompensasi tsb tidak bisa menyesuaikan & kondisi hemodinamik malah memburuk*Pengeluaran sitokin inflamasi setelah MI → menimbulkan ekspresi NO, kelebihan NO, inappropriate vasodilatationFurther = me↓ perfusi sistemik & koroner

* Disfungsi miokard yg progresif dpt menyebabkan kematian jika tidak di terapi

Clinical Findings

• Continued chest pain, dyspnea, pale, apprehensive, diaphoretic• Altered mental status : somnolence/confusion/agitation• Pulse typically weak & rapid (90–110 bpm) or severe bradycardia

(due to high-grade heart block)• Systolic BP is reduced (<90 mmHg), narrow pulse pressure (<30

mmHg)• Tachypnea, Cheyne-Stokes respirations, and jugular venous

distention may be present• S 1 is usually soft, and an S 3 gallop may be audible• Acute, severe MR and VSR usually are associated with characteristic

systolic murmurs• Rales are audible in most patients with LV failure causing CS• Oliguria (urine output <30 mL/h)

Laboratory Findings

• WBC count is typically elevated (left shift)• Blood urea nitrogen & creatinine rise progressively• Hepatic transaminases may be markedly elevated due to liver

hypoperfusion• Poor tissue perfusion → anion-gap acidosis & elevation of the lactic

acid level• Before support with supplemental O 2 , arterial blood gases usually

demonstrate hypoxemia and metabolic acidosis (may be compensated by respiratory alkalosis)

• Cardiac markers, creatine phosphokinase & MB fraction, and troponins I and T are markedly elevated

EKG

• CS due to acute MI with LV failure: Q waves and/or >2-mm ST elevation in multiple leads or left bundle branch block

• More than one-half of all infarcts associated with shock are anterior• Global ischemia due to severe left main stenosis usually is accompanied by

severe (e.g., >3 mm) ST depressions in multiple leads

• Pulmonary vascular congestion, pulmonary edema (often)• The heart size is usually normal (first MI), enlarged at previous MI

• Doppler mapping• Left-to-right shunt in patients with VSR, severity of MR• Proximal aortic dissection with aortic regurgitation or tamponade • Evidence for pulmonary embolism

CXR

Echocardiogram

Pulmonary Artery Catheterization

• Menggunakan kateter Swan-Ganz • Utk mengukur kardiak output atau filling pressure, dan optimalisasi

penggunaan cairan IV, agen inotropik, vasopresor pada syok yg persisten

• Blood samples for O 2 saturation measurement obtained from the right atrium, right ventricle, pulmonary artery to rule out a left-to-right shunt

• Mixed venous O2 saturations are low• Arteriovenous (AV) O2 differences are elevated, reflecting low

cardiac index and high fractional O2 extraction• The PCWP is elevated; sympathomimetic amines return these

measurements & systemic BP to normal• Systemic vascular resistance may be low, normal, or elevated• Equalization of right- and left-sided filling pressures (right atrial and

PCWP) suggests cardiac tamponade as the cause of CS

Left Heart Catheterization & Coronary Angiography

• Mengukur tekanan ventrikel kiri & menentukan anatomi koroner

• Kateter kardiak → jika ada rencana & memungkinkan utk dilakukan intervensi thd koronernya, atau jika diagnosis defenitif belum dapat ditegakkan dgn pemeriksaan yg lain

Treatment

• Vasopressor- Obat2an IV → me↑ TD & cardiac output → norepinefrin (1st line)

2-4 μg/min, titrasi- Dopamin → 2–5 μg/kg per min (naikkan dosis setiap 2-5 menit,

dosis maksimal 20–50 μg/kg per min)- Dobutamin

Treatment

• Aortic Counterpulsationo Intraaortic Balloon Pumping (IABP)o A sausage-shaped balloon is introduced percutaneously into the

aorta via the femoral artery; the balloon is automatically inflated during early diastole, augmenting coronary blood flow

o Stabilizing before and during cardiac catheterization and percutaneous coronary intervention (PCI) or before urgent surgery

o Contraindication: aortic regurgitation, aortic dissection

• Reperfusion-Revascularizationo PCI/CABG (Coronary Artery Bypass Graft) lebih menguntungkano Early revascularization dgn PCI/CABG → class I recomendation , utk:- Pasien < 75 thn dgn ST elevasi atau LBBB yg mengalami syok

kardiogenik 36 jam pasca MI- Pasien yg dapat direvaskularisasi dalam 18 jam onset syok

Treatment

Emergency• Goals: airway stability & improve myocardial pump function• Cardiac monitor, pulse oximetry• Supplemental oxygen, IV access• Pertimbangkan intubasi jika pasien mengalami hipoksia meski sudah diberi O2

suplemental/utk mengurangi kerja pernapasan

AMI• Aspirin, beta blocker, morphin, aspirin• No pulmonary edema → IV fluid• Pulmonary edema present:- Dopamine → increase heart rate & cardiac work- Dobutamine → may drop BP- Combination → may be more effective

RV infarct = fluids & dobutamine

Acute Mitral Regurgitation/VSD= pressors (dobutamine & nitroprusside)

SYOK HIPOVOLEMIK

• Pe↓ perfusi & oksigenasi jaringan disertai kolaps sirkulasi yg disebabkan oleh hilangnya volume intravaskular akut akibat berbagai keadaan bedah atau medis

• Gejala & tanda:- Baru mengalami trauma- Baru menjalani pembedahan- Mengalami ggn perdarahan- Hipotensi- Takikardia- Pe↓ status mental- Produksi urin sedikit- Tanda nyata trauma atau perdarahan- Gawat napas, pe↓ bunyi napas, perkusi redup → tanda cedera toraks- Distensi abdomen, nyeri tekan difus, peritonitis- Ekimosis pinggang (cedera pelvis)- AGD arteri → pe↓ defisit basa & pe↑ laktat (=asidosis laktat akibat

hipoperfusi)

Klasifikasi

• Hemoragik:- Perdarahan GIT- Trauma- Hemoptysis masive- AAA (abdominal aortic

aneurism) rupture- Kehamilan ektopik, perdarahan

post-partum

• Non-Hemoragik:- Muntah- Diare- Obstruksi usus, pankreatitis- Burns- Neglect, environmental

(dehidrasi)

Patofisiologi

Intravascular volume ↓↓

Venous return ↓↓

Ventricular filling ↓↓

Stroke volume ↓↓

Cardiac output ↓↓

Inadequate tissue perfusion

Klasifikasi

Treatment

• C-A-B• Supplemental oxygen, IV access• Pemantauan produksi urin• Cairan IV kristaloid (Normal Saline/RL >3l) & darah (PRBCs)• Control any bleeding• Konsultasi sesuai utk menentukan treatment selanjutnya• Harus dirawat

SYOK SEPTIK• 2 or more of SIRS criteria:

1.Temperature > 38 or < 36 C2.HR > 903.RR > 204.WBC >12.000 or < 4.000

• Plus the presumed existence of infection• BP can be normal• Plus refractory hypotension

After bolus of 20-40 ml/kg patient still has one of the following:- SBP < 90 mmHg- MAP < 65 mmHg- Decrease of 40 mmHg from baseline

• Clinical sign:- Hyperthermia/hypothermia- Tachycardia; wide pulse pressure, low BP (SBP < 90)- Mental status change- Beware of compensated shock: BP may be “normal”

SEPSIS

Treatment of Septic Shock

• 2 large bore IVs: normal saline IVF bolus- 1-2 l wide open (if no contraindication)

• Supplemental oxygen• EmpiricAB, based on suspected cause, ASAP!

• AB – survival correlates with how quickly the correct drug was given• Cover gram positive and negative bacteria- Zosyn 3.375 g IV & ceftriaxone 1 g IV, or- Imipenem 1 g IV• Add additional coverage as indicated- Pseudomonas – gentamicin/cefepime- MRSA – vancomycin- Intraabdominal or head/neck anaerobic infections -

clyndamycin/metronidazole- Asplenic – ceftriaxone for N.meningitidis, H.influenzae- Neutropenic – cefepime/imipenem

Treatment of Sepsis

SYOK NEUROGENIK

• Disfungsi otonom, disebabkan oleh cedera medula spinalis, yg menyebabkan hipotensi & bradikardia

• Gejala klinis:- Datang normal setelah mengalami trauma tumpul/trauma tembus medula

spinalis

• Patofisiologio Disebabkan cedera medula spinalis → ggn aliran keluar otonom simpatiso Sinyal tsb berasal dari kornu grisea lateralis medula spinalis antara T1 & L2o Konsekuensi pe↓ tonus adrenergik → ketidakmampuan me↑ kerja inotropik

jantung scr tepat & konstriksi buruk vaskularisasi perifer sbg respon thd stimulasi eksitasional

o Tonus vagal tidak mengalami perlawanan → hipotensi, bradikardio Vasodilatasi perifer → kulit hangat & kemerahano Hipotermia krn tidak adanya vasokonstriksi pengatur otonomik pada

redistribusi darah ke inti tubuho Lebih tinggi tingkat cedera → lebih berat syok neurogenik krn lebih banyak

massa tubuh yg terpotong dari regulasi simpatisnyao Syok neurogrnik tidak terjadi jika cedera dibawah T6

Patofisiologi

• Loss of sympathetic tone results in warm & dry skin• Shock usually last from 1-3

weeks• Any injury above T1 can

disrupt the entire sympathetic systemo Higher injuries = worse

paralysis

Pemeriksaan Fisik-Hipotensi-Bradikardia (90%)-Kulit hangat, kering

Treatment

• C-A-B!! Remember c-spine precautions !!

• Resusitasi cairan- Pertahankan MAP (Median Artery Pressure) utk 7 hari pertama- Pikirkan utk memperkecil kemungkinan cedera sekunder- Jika cairan kristaloid tidak cukup, gunakan vasopresor

• Cari penyebab lain hipotensi• Bradikadi → atropine, pacemaker • Kortikosteroid• Evaluasi neurologi & bedah saraf

ANAPHYLACTIC SHOCK

• Anaphylaxis – a severe systemic hypersensitivity reaction characterized by multisystem involvement → IgE mediated

• Anaphylactoid reaction - clinically indistinguishable from anaphylaxis, do not require a sensitizing exposure (not IgE mediated)

• Symptoms:- First – pruritus, flushing, urticaria appear- Next – throat fullness, anxiety, chest tightness, shortness of breath

& lighteadedness- Finally – altered mental status, respiratory distress, circulatory

collapsed• Mild, localized urticaria can progress to full anaphylaxis• Symtomps usually begin within 60 mins of exposure• Faster the onset of symptoms = more severe reaction• Biphasic phenomenon occurs in up tp 20% of patients

- Symptoms return 3-4 hrs after initial reaction has cleared• A “lump in my throat” and “hoarseness” heralds life-threatening

laryngeal edema

Patofisiologi Diagnosis

• Clinical diagnosis (airway compromise, hypotension, involevement of cutaneous, resporatory/GI systems

• Exposure to drug, food, or insect

• Labs have NO role

Treatment• CAB

- Angiodema & respiratory compromise require immediate intubation

• IV, cardiac monitor, pulse oximetry• IVFs, oxygen• Epinephrine- 0.3 mg IM of 1:1000 (epi-pen)- Repeat every 5-10 mins as

needed- Caution with patient taking B-

blockers (can cause severe HT due to unopposed alpha stimulation)

- For CV collapse, 1 mg IV of 1:10.000

- If refractory, start IV drip• Second line → corticosteroids, H1 &

H2 blockers

• Corticosteroids- Methylprednisolone 125 mg IV- Prednisone 60 mg PO

• Antihistamines- H1 blockers – Diphenhydramine

25-50 mg IV- H2 blockers – Ranitinide 50 mg

IV• Bronchodilators

- Albuterol nebulizer- Atrovent nebulizer- Mg sulfate 2 g IV over 20 mins

• Glucagon - For patient taking B-blockers &

with refractory hypotension- 1 mg IV 5 mins until

hypotension resolves

CORONARY HEART DISEASE

• Aterosklerosis = pengerasan dinding arteri sehingga dinding arteri menebal dan kaku akibat pengendapan lemak. Diameter arteri menyempit mengurangi aliran darah.

• Penyakit Jantung Koroner (PJK) = aterosklerosis pd A.koroner.• Sindrom Koroner Akut = kumpulan gejala klinis PJK akibat penurunan

mendadak aliran darah ke jantung shg iskemik miokard akut.o Penyebab : trombosis (ruptur plak aterosklerosis), spasme

A.koroner.o Unstable Angina Pectoris/UAPo NSTEMIo STEMI

• Angina Pectoris = gejala nyeri dada akibat iskemi miokardium krn defisiensi suplai & kebutuhan oksigen di jantung.o Karakteristik khas/atypical angina : rasa tindih benda berat,

diremas, ditekan, rasa penuh diretrosternal, menjalar ke leher, rahang bawah, lengan kiri, punggung, ulu hati.

o Nyeri tdk dapat dilokalisir (nyeri viseral).

Coronary Heart Disease• Infark Miokard = nekrosis akibat sumbatan mendadak A.koroner tersering

akibat trombus oklusif (plak yg ruptur).o Trombus : gumpalan darah krn respon sistem pembekuan darah pd injury

(luka/erosi/ruptur plak).o Sistem pembekuan darah : trombosit, protein pembekuan darah

(trombin, fibrin)o Trombus mengoklusi parsial atau total lumen A.koroner iskemi

miokard/infark miokard akut manifest salah satunya angina pektoris.• Patofisiologi

– Aterosklerosis proses perlahan & progresif dimulai usia anak-anak penebalan dinding dalam arteri dgn deposit lemak & kalsium penyempitan lumen arteri scr perlahan.

– Aterosklerosis pd A.koroner menyebabkan Penyakit Jantung Koroner • Angina pectoris stabil• Acute coronary syndrome (ACS)

– Plak ateroma ruptur memicu agregasi trombosit (white trombus) & pelepasan zat vasoaktif penyempitan & vasokonstriksi A.koroner gangguan aliran darah iskemi miokard (>20menit) infark miokard akut gangguan kontraktilitas miokard, aritmia, remodeling ventrikel.

Coronary Heart Disease

• Manifestasi klinis PJK1. Angina pectoralis stabil

– Nyeri dada konsisten & timbulnya dpt diprediksi– Timbul saat aktivitas fisik/stress emosional– Hilang saat istirahat/obat nitrat– Gejala muncul : stenosis A.koroner >70%

2. Acute Coronary Syndrome– Akibat ruptur plak dlm A.koroner shg membentuk trombus yg

dpt mengoklusi parsial (UAP & NSTEMI) atau mengoklusi total (STEMI atau Infark Miokard Akut).

– UAP & NSTEMI Angina saat istirahat durasi > 20 menit, terjadi dlm 1

minggu terakhir, no provocation. Angina new onset angina pertama kali dlm 2 bln terakhir,

timbul akibat aktifitas fisik ringan. Angina progresif (kurun wkt 2bln) cresendo pattern

(increase frequency, duration, intensity ischemic episode).

STEMI/IMA Chest discomfort more severe, lasts longer, radiate more widely (C7 –

T4 dermatomes : neck, shoulders, arms) result from release of mediators (adenosine or lactate) onto local nerve endings. MI persists and proceeds to necrosis provocative substances to accumulate and active afferent nerve for long period.

Systemic signs (subsequent catecholamine release) diaphoresis, tachycardia, cool & clammy skin (sympathetic signs)

Parasympathetic signs (vagal effects) nausea, vomiting, weakness. Ischemic affects large amount myocardium left ventricular contractile

reduce (systolic dysfunction) diastolic volume & LV pressure increase diastolic dysfunction left atrium & pulmonary veins congestion shallow breathing dysapnea.

Physical findings : S4 sound (atrial contraction into noncompliant left ventricle) S3 sound (volume overload in presence of failing LV systolic function) Systolic murmur (ischemic induced papillary muscle dysfunction

causes mitral valvular insufficiency). Low grade fever (myocardial necrosis activates inflammatory

cytokines)

• Life-threatening that can punctuate the course of patients with coronary artery disease at any time.• These syndromes form a continuum that ranges from unstable pattern of

angina pectoris acute myocardial infraction (condition of irreversible necrosis of heart muscle).

• Pathogenesis ACSo >90% of ACS result from disruption of atherosclerotic plaque with platelet

aggregration thrombus formation (interaction among the atherosclerosis plaque, coronary endothelium, circulating platelets, dynamic vasomotor of vessel wall, natural antitrombotic mechanisms).

o Pathogenesis coronary thrombosis1. PLAQUE RUPTURE

– Atherosclerosis plaque consist of lipid laden core surrounded by fibrous external cap.

– Chemical factors inflammatory cells release substances that compromise the fibrous cap then rupture plaque.

– Physical stresses sympathetic nervous system (BP, HR increase, force ventricular contraction).

ACUTE CORONARY SYNDROME

Acute Coronary Syndromes

– MI is most likely occur in the early morning hours relate to tendency physiologic stressors (systolic BP, blood viscosity, plasma ephineprine).

– Exposure tissue factor from atheroma triggers coagulation pathway activated platelets release the contents of their granules induce platelet aggregation.

– All of them contirbute to narrowing the vessel lumen.

2. Dysfunctional endothelium– Reduced amounts of vasodilators (N0 & prostacyclin are

released and inhibition of platelet aggregation) resulting loss of a key defense againt thrombosis.

oNonatherosclerosis causes ACS – Coronary embolism from infected cardiac valves– Acute vasculitis – Spontaneous coronary artery dissection– Intense transient coronary spasm– Cocaine abuse increase sympathetic by blocking presynaps reuptake

of norephineprine & enhancing release adrenal catecholamines.

Acute Coronary Syndromes (MI)

o Pathophysiology MI– MI (STEMI or NSTEMI) results when myocardial ischemia causes myocyte

necrosis.– Transmural infracts = entire thickness of myocardium and result from total,

prolonged occlusion of an epicardial coronary artery.– Subendocardial infarcts = innermost layers of myocardium.– Infraction represents of disastrous cascade of events : ischemia potentially

reversible to irreversible cell death extend adjacent tissue depend on : Mass of myocardium perfused by occluded vessel Magnitude & duration impaired coronary blood flow Oxygen demand of affected region Adequacy of collateral vessels Degree of tissue response the modifies the iscemic

process

– 2 stages : early changes at time of acute infraction & late changes during myocardial healing and remodeling.

Acute Coronary Syndromes (MI)

• Early changes Cellular changes

Occur 2 minutes following occlusive thrombosis 20 minutes be irreversible cell injury.

Oxygene levels fall in myocardium supplied by an abruptly occluded coronary vessel rapid shift from aerobic to anaerobic metabolism accumulation of lactic acid lowered pH (asidosis).

Elevation intracelullar Na and extracelullar K cellular edema & contributes transmembrane electrical potential predisposing myocardium arrhythmias.

• Late changes Clearing of necrotic myocardium by invade the macrophages to

inflamed myocardium shortly after neutrophil infiltration. Deposition of collagen to form scar tissue fibrosis is complete by 7

week after infraction.

Acute Coronary Syndromes (MI)

• Functional alterations Impaired contractility and compliance : destruction functional

myocardial cells impaired ventricular contraction (systolic dysfunction) cardiac output compromised. Ischemic/infraction impair diastolic relaxation diastolic dysfunction.

Stunned myocardium : prolonged systolic dysfunction after discrete episode of severe ischemia but has adequate restoration of adequate blood flow then gradually regains contractile force days to weeks later.

Ventricular remodelling : ventricular segment enlarges and wall thickness & dilatation of non-infarcted segment chamber dilatation serves compensatory role that increase cardiac output (Frank-starling mechanism) progressive enlargement lead to heart failure & predispose ventricular arrhythmias.

Acute Coronary Syndromes

• Diagnosis ACS Base of : presenting symptoms, acute ECG abnormalities, spesific serum markers of

myocardial necrosis.

Serum markers : Necrosis myocardial tissue causes disruption of sarcolemma

intacelullar macromolecules leak into cardiac interstitium then into bloodstream.

Cardiac troponins : begin to rise 3-4 hours onset discomfort, peak 18-36 hours, normal 10-14 days.

CK-MB : begin to rise 3-8 hours, peak 24 hours, normal 48-72 hours.

Feature Unstable angina NSTEMI STEMI

Typical symptoms Cresendo, rest or onset severe angina

Prolonged “crushing” chest pain, more severe & wider radiation than usual angina

Serum biomarkers No Yes Yes

ECG initial findings ST depression & T wave inversion

ST depression &T wave inversion

ST elevation &Q wave later

Algoritma Management Acute Coronary Syndromes• Anti-ischemic therapies : beta blocker, nitrates, CCB• General measures : pain control (morphine), supplement O2 if needed.• Antitrombotic agents : Aspirin, Clopidogrel, GP IIb/IIIa (high risk patient PCI)• Anticoagulant agents : LMWH, unfractionated IV heparin, fondaparinux, bivalirudin (high risk patient PCI)• Adjunctive therapies : statin, ACEi

STEMI NSTEMI

Emergent PCI available within 90 min

Fibrinolytic therapy

Primary PCI

Risk assessment (TIMI score)

Conservative strategy

Intensive strategy (PCI)

No Yes Low high

Acute Treatment Unstable Angina & NSTEMIAnti-ischemic medications

Beta-blocker decrease sympathetic drive to myocardium, reducing oxygen demand, contribute electrical stability.

• Exclude contraindication (bradycardia, broncospasm, decompensated HF, hypotension).

• Fisrt 24 hours to achieve target HR 60x/min Nitrates venodilation which lower myocardial oxygen demand by diminishing venous

return to the heart (reduce preload) improve coronary flow & prevent vasospasm.

• Nitroglycerin sublingual then continuous IV infusion. CCB decreasing HR & contractility and vasodilatation arteriol (reduce afterload).

Anti-thrombic therapy Antiplatelet drugs

• Aspirin inhibits platelet synthesis of thromboxane A2 that potent mediator platelet activation.

• Clopidogrel thyenopiridine derivate that blocks platelet activation of P2Y12 ADP receptor on platelet. Prasugrel another thyenopiridine that more efficiently & greater anriplatelet.

• GP IIb/IIIa antagonist abciximab, eptifibatide, tirofiban.

Acute Treatment Unstable Angina & NSTEMI Anticoagulant drugs

• Unfractionated heparin (UFH) binds antithrombin which greatly increase the potency of inactivation clot forming thrombin (inhibit coagulation factor Xa). – Measurements with aPTT

• Low molecular weight heparins (LMWHs)• Fondaparinux subcutaneously administered• Bivalirudin intravenously direct thrombin inhibitor

Thrombolysis in Myocardial Infraction (TIMI) risk score1. Age > 65 years old2. > 3 risk factors for coronary artery disease3. Coronary stenosis >50% by prior angiography4. ST segment deviations on ECG5. At least 2 anginal episodes in prior 24 hours6. Use aspirin in prior 7 days (aspirin’s resistence)7. Elevated serum troponin or CK-MB

Score >3 early intensive strategy.

Acute Treatment STEMI

• Completely occluded treatment that prompt reperfusion of jeopardized myocardium using either fibrinolytic drugs or percutaneous coronary mechanical revascularization.

• Anti-ischemic & anti-thrombic therapy• Fibrinolytic therapy

Accelerate lysis of occlusive intracoronary thrombus in STEMI. tPA (alteplase), rPA (reteplase), TNK-tPA (tenecteplase) streptokinase

that transforming inactive precusor plasminogen into the active protease plasmin that lysis clots.

Receive therapy 2 hours of onset symptoms of STEMI. After successful thrombolysis antithrombic regimens administered

(aspirin, clopidogrel, IV UFH for 48 hours)• Primary Precutaneous Coronary Intervention (PCI)

The procedure performed within 90 minutes of hospital presentation. For patients who : contraindication fibrinolytic therapy, cardiogenic

shock. Undergoing PCI : recieve IV GP IIb/IIIa antagonist. Coronary stents during PCI : oral clopidogrel for > 12months

• Condition of imbalance between myocardial oxygen supply and demand results in myocardial hypoxia and accumulation of waste metabolites.

• Pathophysiology of ischemiaFixed vessel narrowing Proximal vessels are subject to overt atherosclerosis that result stenosis

plaques. Distal vessels usually free of flow-limiting plaques and can adjust their vasomotor tone compensatory vasodilatation distal resistance.

If stenosis narrows lumen <60% maximal potential blood through artery isn’t significantly altered, the resistance vessels can dilate to provide adequate blood flow.

If stenosis narrows lumen >70% resting blood flow is normal, but maximal blood flow is reduced even with full dilatation of resistance vessels.

Dysfunctional endothelial cell

Myocardial oxygen supply•Coronary blood flow•Coronary perfusion pressure•Coronary vascular resistance•Local metabolites•Endothelial factors•Neural innervation

Myocardial oxygen demand•Wall stress•Heart rate•Contractility

ISCHEMIC HEART DISEASE

Ischemic Heart Disease

Ischemic syndromes• Stable angina

Pattern of predictable, transient chest discomfort during exertion or emotional stress.

During physical exertion (activation sympathetic nervous) increase HR, BP, contractility augment myocardial oxygen consumption oxigen supply inadequate chest discomfort of angina pectoris.

• Unstable angina Sudden incerase in the tempo & duration of ischemic episodes.

• Variant angina/Prinzmetal angina Episode of focal coronary artery spasm in the absence of overt

atherosclerotic lesions. Intense vasospasm reduces coronary oxygen supply and result

angina. The spasm may involve increased sympathetic activity.

• Silent ischemic Absence of perceptible(jelas) discomfort/pain. Most common among diabetic patients (impaired pain sensation

from peripheral neuropathy), elderly, women.

Ischemic Heart Disease

Clinical manifestation• Chest pain

Quality : pressure, tightness, heaviness, steading discomfort that lasts a few minutes (5-10 minutes), Levine sign (angina at sternum)

Location : diffuse, retrosternal area or left precordium, radiated to back, arm, neck, lower face, upper abdominal.

• Sympathetic and parasympathetic stimulation Tachycardia, diaphoresis Nausea, vomiting Dyaspnea, fatigue, weakness

Physical examination• Increase heart rate and blood pressure (sympathetic response)• S4 gallop during atrial contraction (late diastolic sound)• Carotid bruits

Ischemic Heart Disease

Diagnosis• ECG ST segment depression and T wave flattening or inversions.• Stress testing provocative exercise of pharmacologic stress test

(dobutamine, dipyridamole, adenosine).• Coronary angiography identifying coronary artery stenoses by

visualized radiographically following injection of radiopaque contrast material into artery.

Treatment acute episode angina Sublingual nitroglycerin : that effect in 1-2 minutes vascular smooth

muscle relaxation, venodilatation (preload decrease)Treatment prevent reccurent ischemic episode Organic nitrate (nitroglycerin, isosorbid dinitrate) oral or patch. B-blockers CCB Ranolazine (doesn’t affect the heart rate/blood pressure because it is

inhibit late phase of action potential inward sodium current in ventricular myocyte)

Ischemic Heart Disease

Treatment prevent acute cardiac events Antiplatelet therapy (aspirin, clopidogrel) Lipid regulating therapy (statin) ACEi

Revascularization Angina don’t respond adequately to antianginal drug therapy Unacceptable side effects of medications High risk coronary disease Percuatneous coronary intervention (PCI) under fluoroscopy

which balloon tipped catheter is inserted through peripheral artery (femoral, brachial, radial) – balloon at the end pf catheter inflated under high pressure to dilate the stenosis then removed – stent is left permanently for maintain arterial patency. (Stents are thrombogenic combination oral antiplatelet agents).

Coronary artery bypass graft (CABC) surgery.

HEART FAILURE

• Heart is unable to pump blood forward at a sufficient rate to meet the metabolic demands of the body (forward failure) or is able to do so only if the cardiac filling pressures are abnormally high (backward failure).

• Preload : ventricular wall tension at the end of diastole. It is stretch on the ventricular fibers just before contraction.

• Afterload : ventricular wall tension during contraction. Often approximated by systolic ventricular pressure.

• Contractility (inotropic rate) : heart muscle that accounts for changes in the strength of contraction, independent of preload and afterload.

• Stroke volume : volume of blood ejected from the ventricle during systole

• Cardiac output : volume of blood ejected from ventricle per minute• Compliance : pressure-volume relationship during filling.

Heart Failure

Pathophysiology Impaired contractility Increase afterload Impaired distolic filling HF with reduced ejection fraction

– Systoloic dysfunction because loss contractility result from destruction of myocytes, abnormal myocyte function, fibrosis.

– During dyastole, persistently elevated LV pressure is trasnmitted to the left atrium (throught mitral valve) pulmonary veins and capillaries result transudation of fluid into pulmonary interstitium pulmonary congestion.

HF with preserved ejection fraction– Left ventricle wall to become chronically stiffened

diastolic dysfunction vascular congestion because elevated diastolic pressure is transmitted retrogarde to pulmonary and systemic veins.

Heart Failure

Right-sided heart failure– The right ventricle is thin walled, highly compliant chamber

high compliance that is quite susceptible to failure in situations that present a sudden increase in afterload confronts the right ventricle because elevated pulmonary vascular pressures.

– Isolated right heart failure is less common. – RV overload owing to primary pulmonary disease cor

pulmonale.

Clinical manifestation• Symptoms

Dysapnea, orthopnea, paroxysmal nocturnal dysapnea (gradual reabsorption into circulation of lower extremity interstitial edema after lying down), fatigue (left-sided)

Peripheral edema, right upper quadrant discomfort (right-sided) Dulled mental status (reduced cerebral perfusion) Impaired urine output (decreased renal perfusion)

Heart Failure• Physical signs

Diaphoresis, tachycardia, pulmonary rales, S3 gallop, S4 gallop (left-sided)

Jugular venous distention, hepatomegaly, peripheral edema (right-sided)

Cachexia (wasted appearance because poor appetite and metabolic demand increased effort in breathing)

Pulsus alternans (strong and weak contractions detected in peripheral pulse)

• Diagnostic studies Chest radiography : cardiomegaly with cardiothoracic ratio >0,5 on PA

film.

• Treatment Diuretics Vasodilators Inotropic drugs : B-adrenergic agonist (dobutamine, dopamine), digitalis. Aldosteron antagonist therapy : spironolactone, eplerenon Additional therapy : anticoagulan, arrythmia (amiodarone)

Acute Heart Failure

• Serangan cepat (rapid onset) akibat fungsi jantung yg abnormal (disfungsi sistolik atau diastolik, keadaan irama jantung abnormal, ketidakseimbangan preload & afterload).

• Acute de novo (new onset) & dekompensasi akut dari gagal jantung kronik.

• Classification : Volume overload (wet & dry) Decreased cardiac output with reduced tissue perfusion (cold &

warm)

Wet & Warm Dry & Cold

Ortopnea Tekanan nadi sempit

Tekanan vena jugularis tinggi Ekstremitas dingin

Edema Mengantuk, lemas

Asites Suspek hipotensi

Refleks abdomino jugularis Suspek penurunan Na serum

Acute Heart Failure

• Treatment o Umum : atasi faktor presipitasi (diabetes, gagal ginjal, infeksi)o Oksigenasi : mempertahankan SO2 95-98% dilakukan dapat dgn 2

cara continous positive airway pressure (CPAP) atau Non-invasive positive pressure ventilator (NIPPV).

o Medikamentosa Morfin/analog morfin : bolus IV 3 mg segera setelah

pasang IV-line Antikoagulan : heparin atau LMWH (kec.sindrom koroner

akut, atrial fibrilation) Nitrat : meningatkan keutuhan oksigen utk miokard Sodium nitroprusid : predominan utk pasien gagal jantung

dgn peningkatan afterload (hipertensi, regurgutasi mitral) Diuretik : terutama gagal jantung dekompensasi dgn

retensi cairan Inotropik : fosfodiesterase inhibitor, levosimendan,

glikosida.

Gagal jantung dengan disfungsi sistemik

•Oksigen/CPAP•Furosemid + VasodilatorEvolusi klinis (leading to mechanism therapy)

TDS >100 mmHg

TDS 85-100 mmHg

TDS <100 mmHg

•Vasodilator(NGT, nitroprusid, BNP)

•Vasodilator•Inotropik (dobutamin, PDEI atau levoksimendan)

•Inotropik dan dopamin >5mg/kg/menit•Norepineprine

Tak ada respon : terapi mekanik dipertimbangkan, obat inotropik

Respons baik :Terapi oral furosemid, ACEi

HYPERTENSIVE EMERGENCY

• Krisis Hipertensi: Peningkatan kritis tekanan darah → TDD > 120 mmHg– Tidak harus demikian → derajat keparahan gambaran klinis tidak hanya

ditentukan angka absolut tekanan darah → dipengaruhi juga oleh besar dan laju kenaikan tekanan darah serta kondisi yang mendasari

• 2 jenis :– Hypertensive emergencies– Hypertensive urgencies

• Hypertensive Emergency: Krisis hipertensi + kerusakan organ akut / progresif yang mengancam nyawa :– ACS– Gagal ventrikel kiri akut dengan edema paru– Eklamsia– Diseksi aorta– Gagal ginjal akut– Ensefalopati hipertensif– Stroke iskemi / hemoragik

Hypertensive Urgency

• Krisis hipertensi tanpa kerusakan organ akut / progresif

• Tekanan darah harus diturunkan dalam 24 – 48 jam → cegah kerusakan organ akut dan baru

• JNC VII → hipertensi stage II batas atas + gejala (sakit kepala, pusing, ansietas berat, epistaksis, napas pendek)

Patofisiologi

– Kompleks dan belum diketahui seluruhnya– Diduga : ↑ resistensi vaskuler mendadak (dipicu oleh pelepasan

zat-zat vasodinamik seperti NE, angiotensin II) → dekompensasi dan kerusakan endotel → peningkatan tekanan darah; sekresi molekul proinflamasi dan adhesi

– Siklus tersebut berulang

• Manifestasi klinis:Asimtomatik s/d gejala spesifik yang menunjukkan kerusakan organ akut (misal: dispnea, nyeri dada, kelainan neurologis)

• Diagnosis:Anamnesis → riwayat penyakitStatus medisPenunjang → EKG, funduskopi, laboratorium

SICK SINUS SYNDROME

• Manifestation of sinus node dsyfunction• Patient may present with a wide range of bradyarrhythmias • Numerous arrythmias are associated with sick sinus syndrome, including

marked sinus bradycardia, sinus pause, sinus arrest, & SA Block (on occasion ventricular or atrial tachyarrhythmias)

• Tx indicated when pauses of more than 2-3 seconds occur or if the patient is symptomatic atropine or initiation of temporary cardiac pacing hospital admision, permanent pacemaker placement