Acute coronary syndrome, Schemes and Mind Maps of Cardiology

Download Acute coronary syndrome and more Schemes and Mind Maps Cardiology in PDF only on Docsity! Acute coronary syndromes CARD\ALOGY Acute coronary syndromes Acute coronary insufficiency, typically attributed to disruption or erosion of an atherosclerotic plaque, more or less vulnerable, with formation or embolisation of a thrombus (or plaque debris), materials that can narrow the coronary artery lumen, the coronary flow being intemittently or permanently compromised , Acute coronary syndromes Hey Stanley, I think you're having a heart attack. ACUTE CORONARY SYNDROMES 1. ACS without ST-segment elevation: • Unstable angina (negative myocardial necrosis markers) Non-ST segment elevation myocardial infarction – NSTEMI (positive myocardial necrosis markers ) 2.ST elevation ACS: • Acute with ST segment elevation myocardial infarction – STEMI (positive myocardial necrosis markers ) troponin rise/fall troponin normal | | Unstable Angina UNSTABLE ANGINA: BRAUNWALD CLASSIFICATION Roman numbers (I, II, III) = Severity of UA I = New onset angina (< 2 months), crescendo angina ,the absence of rest within the last 2 months II =Angina at rest, during the last 2 months, but not within the previous 48h III = Angina at rest within the last 48 h Roman letters (A, B, C) = Etiology / Clincal precipitating factors A = Precipitating factors (anemia, fever, thyroid disorders) B = Symptomatic stable angina only C = Postinfarction unstable angina (within the first 2weeks) Arabic numbers(1, 2) = Therapy before UA 1 = No treatment 2 = Usual angina therapy 3 = Maximal therapy II. Subjective symptoms. - Pain wich is similar to that of stable angina III. Physical examination. - Nonspecific – mitral regurgitation systolic murmur. NSTEMI ACS Paraclinical tests: 1. ECG • ISCHEMIA represents the expression of moderate hypoxia,that changes only the rapid repolarization phase ( T wave), depolarization normally occurs. - Subendocardial ischemia – flattened or more frequently, negative T-wave. - Subepicardial ischemia–symmetrically peaked, positive T-waves. Subendocardial T-wave vector A Electrode ECG The ST vector becomes directed towards the back in The T-wave vector may also be directed towards the subendocardial ischemia. The precis angle will vary back, which yields negative T-waves. depending on the location and size of the ischemic area, No ECG lead has an exploring electrode in front of the $T-vector, which is why no ST ele Subepicardial The Ty, Yectoy A, In the hyperacute phase of transmural ischemia (the first few minutes) the T-wave vector becomes amplified and it is directed from the endocardium to the epicardium in the ischemic area. This appears as hyperacute T-waves in leads with an exploring electrodes in front of the T-wave vector. Hyperacute T-waves only persist for a few minutes, whereafter ithe J-point (and entire ST-segment) will become elvated. ST Yecto, A Electrode The ST-vector in transmural ischemia will also be directed from the endocardium to the epicardium in the ischemic area. This causes ST-segment elevations in leads with exploring electrodes in front of the ST- vector. Leads with opposite angle of observation will instead who ST-segment depressions, which are simply mirror images of the ST-segment elevations. Such ST-segment depressions are referred to as “reciprocal ST-segment depressions” (not shown here). ST segment [PRSeement | gment |ST Elevation | ‘vatio: |ST Elevation | | ST Depression) | ST Depression) ssion 2. The Troponins Troponins are contractile proteins found in the cytoplasm of cardiac myocytes. • Cardiac troponin I (cTnI) and troponin T(cTnT) start to rise within 3-12 h after myocardial injury, and remain raised for 10-14 days • Serial measurement of cardiac troponins during the first 24-48 hours !!! 2.Other biomarkers • High-sensitivity C-reactive protein(hsCRP)!!! Marker of mortality, even with negative troponin level, but mostly when is associated with increased T troponin level!!! • Fibrinogen- reflects the activation of coagulation cascade . 3. Echocardiography •Left ventricular wall motion abnormalities areas. •LVEF •ACUTE REGURGITATION- in this case , mitral ! Unstable Angina-treatment •– immediate hospitalization– intensive therapy unit: BP, ECG, SpO2, biomarkers monitoring •– bed rest – calm “atmosphere” •– control of precipitating factors A. Medication - Goal : • T. against platelet activation/aggregat ion and thrombus formation • Antiaginal t. • Revascularization t. PARAL receptor Plasma clotting seade Thrombomane Ac anfarmationall activation of GPE Fibrinogen me Fiber specifications P2Y¥ 42 inhibitors Chemical clase Thienopyridine Thienopyridina Cydopenty!-triazolopyrimidine Stabilized ATP analogue Administration Oral Ord Oral Intravenous Dose 300-400 mg orally then 75 mga day 60 mg orally then 10 mga day 180 mg orally then 90 mg twice a day 30 pgikg bolus and 4 ygikg!min infusion Dosing in CKD + Stage 3 (GFR 30-59 mLimin!| 73m) No dose adjustment No dose adjustment No dose adjustment: No dose adjustment, + Sage 4 (eGR 15-29 mLiman!|.73m") No dose adjustment Nod justment No dose adjusement * Seage 5 GFR <15 mLimin!| 72m") Use only for selected indications (e.g stent thrombosis prevention) Not recommended Not recommended No doe adurement Binding reversibility irreversible Irreversible Reversible Reversible Activation Prodrug, with variable liver metabollem Prodrug, with predic lever metabolism Active drug, with addbtional active metabolite Active drug Onset of loading dose effect” 2-4 hours’ 30 min* 30 min* 2min Duration of effect 3-10 days 7-10 days 45 days |-2 hours Withdrawal before surgery 5 days’ 7 days 5 days™ | hour Plasma half-life of active P2Y,, inhibitor? 30-60 min. 30-60 mint 6-12 hours: 5-10 min Inhibition of adenosine reuptake No No Yes ‘Yes (Inactive’ metabole only} intestina | haemorrhage or peptic ulcer, and appropriate for patents with multiple odher ris fori infection, age ‘years, concurrent use of anticoagulants or steralds). a.Antiplatelet therapy 3.IIb/IIIa Inhibitors • Anti-aggregation effect ABCIXIMAB TIROFIBAN EPTIFIBATIDE • Continuous iv-infusion, but especially as bailout therapy, during PCI, in case of complications or massive intravascular thrombotic masses d. Treatment with ACE inhibitors (angiotensin converting enzyme inhibitors) or ARBs (AT II receptor blockers - sartans) • Increase survival and improve ventricular remodeling in patients with LV systolic dysfunction (EF <40%). •Zofenopril (SMILE 1-5) •Ramipril (RAMI, AIRE) •Trandolapril (TRACE) Losartan (OPTIMAAL) Valsartan (VALIANT) e. Hipolypemiant therapy • Mandatory. Not only for the hypocholesterolemic effect - actually prompt, but also for the "pleiotropic"effects. • Efficient statins based on trials: • Atorvastatin 80 mg/daily – TNT, PROVE-IT and MIRACL shows that the benefit of keeping the maximum dose has been extended to 5,5 years ! Revascularization The essential condition - promptness and quality “time is myocardium” ! •Transluminal angioplasty - PCI has an efficiency of 83 - 93%, with the decrease of ischemic episodes and the recovery of threatened territories. • Stenting following balloon expansion, when possible, primary! •Surgical revascularization Acute myocardial infarction with ST – segment elevation STEMI Diagnosis Initial diagnosis of MI: -chest pain/discomfort ; - ST segment elevation or LBBB (presumed) newly appeared on the ECG; - increased values of myocardial necrosis markers (CK-MB, troponins). The results of the biological markers should NOT be expected to start the reperfusion treatment !! Clinical examination: -allows the assessment of the extent of myocardial infarction: blood pressure level, rales or crakles in the lungs, peripheral vasoconstriction, acute pulmonary edema. – allows the diagnosis of a mechanical complication: systolic murmur of mitral regurgitation, pathological interventricular communication – the finding of signs of RV failure, in case of right ventricular infarction, complicating a inferior/posterior infarction. Clinical examination: • The characteristic symptom is pain.The most common localization of the pain is retrosternal, but it can also be located in the epigastric or interscapulovertebral region.Radiation of pain may occur in the left shoulder or upper limb, on the ulnar edge, in both arms, at the base of the neck. The character of the pain is constrictive, like a sensation of pressure, burning, its intensity being very high. The duration of pain is at least 20 minutes to several hours, characteristic is that does not subside to the administration of nitroglycerin. Other associated phenomena: anxiety, pallor, profuse sweating, hypotension, nausea, vomiting, dyspnea. Electrocardiogram A. ECG prior to MI B. nia from coronary artery occlusion results in ST depression (not shown) and peaked T-waves C. from ongoing ischemia results in marked ST elevation D/E. with appearance of pathologic Q-waves and T-wave inversion F. (months later) with persistent Q- waves, but normal ST segment and T- waves oN  Necrosis territory – anteroseptal: V1– V3 –extended anterior: V1– V6 , – apical: V4, V5 – lateral: D1, avL, V5– V6 – inferior: D2, D3, avF – posterior: V7– V9 – right ventricle: V3R– V5R. Acute anterior myocardial infarction with ST segment elevation Non-specific tests (but suggestive of the extend of infarction): • – hyperleukocytosis • – increase of ESR (erythrocyte sedimentation rate) • – hyperglycemia Differential diagnosis : • Aortic dissection Elements that make the aortic dissection diagnosis are intense and prolonged chest pain with dorsal or abdominal radiation, occurred in a patient known as hypertensive, quasi- abnormal electrocardiogram, the presence of a diastolic murmur of aortic insufficiency. • Acute pericarditis - characterized by increased pain on deep inspiration, non-specific electrical changes that do not correspond to a precise territory, especially ST-T elevations. • Pulmonary embolism - suggestive clinical context (venous thrombosis, prolonged immobilization, etc.). STEMI Theraphy I. Relieving pain, dyspnea and anxiety : • Intravenous opioids (4-8 mg morphine), with additional doses of 2 mg at 5 min intervals. • Oxygen (2-4 l / min), especially if the patient has dyspnea or heart failure. • Beta-blockers or intravenous nitrates, especially if the pain does not subside with opioids. • Anxiolytics Pharmacological therapy of reperfusion- fibrinolytic theraphy • Tenecteplase (TNK-tPA) bolus i.v.in 5 sec once - ex. 40 mg for 70-80 Kg body weight. • Reteplase (rPA) 10 U bolus twice at every 30 min. • Alteplase (tPA) 15 mg bolus then 50 mg in 30 min. , then 35 mg the next hour. • Streptokinases 1.5 mil in 1 hour. Co dications brinolytic therapy Contraindications to fibrinolytic therapy Previous intracranial haemorrhage or stroke of unknown origin at any time Ischaemic stroke In the preceding 6 months Central nervous system damage or neoplasms or atrioventricular malformation Recent major trauma/sumgery/head Injury (within the preceding 3 weeks) Gastrointestinal bleeding within the past month Known bleeding disorder (excluding menses) Aortic dissection Non-compressible punctures In the past 24h (e.g Iver biopsy, lumbar puncture) Transient Ischaemic attack In the preceding 6 months Oral anticoagulant therapy Pregnancy or within | week postpartum Refractory hypertension (systolic blood pressure > 180 mmHg and/or diastolic blood pressure >! 10 mmHg) Advanced Iver disease infective endocarditis Active peptic uloer Prolonged or traumatic resuscitation TEMI- Antithrombotic the Antiplatelets Aspirin oral or iv. (if unable to swallow) is recommended An ADP- receptor blocker is recommended in addition te aspirin. Options are: * Prasugrel in clopidegrel-naiwe patients, if no history of prior stroke!TIA, ape <75 years * Ticagretor. * Clopidogrel, preferably when pracugrel or ticagrelor are either not available or concraindicaed. GP Ibi lll inhibitors should be: considered for bailout therapy if there is angiographic evidence of massive thrombus, slow or no-reflow or a thrombotic complication. Roudne use of a GP [lb llla inhibiter ag an adjunee co primary PC] performed with undracienated heparin may be considered in Patients without cortraindecaticns Upstream use of a GP [bills inhibitor (vs.in-lab use) may be considered in high-risk patients undergoing transter for primary PCI. Options for GP lilb/lila inhibitors are: (with LoE for exch agent): * Abciximab * Eptifibatice (with double bolus) *Tirefiban (with a high balus dose) Long-term therapeutic measures (secondary prevention): • Lifestyle change measures:diet, smoking cessation, regular physical activity Therapeutic measures - cardioprotective medication DAPT: aspirin + P2Y12 inhibitor -Betablocker -ACE inhibitors/ARBs -Statin -unlimited time AMI-STEMI – COMPLICATIONS • Mechanical complications : • Free wall rupture is responsible for about 10% of STEMI secondary deaths, being more common in hypertensive, elderly patients at first heart attack. It is most frequently located at the level of the anterior wall, it occurs most frequently between days 1-4 after infarction. Clinically, there is a rapid installation of cardiogenic shock, with electromechanical dissociation secondary to cardiac tamponade. • Interventricular septal rupture occurs in 0.2% of patients with STEMI, and is also more common in elderly, hypertensive patients during the first week after onset. It is suggested by the appearance of a new holosystolic murmur of maximum intensity in the left intercostal space 4, the diagnosis being confirmed by echocardiography; • Ischemic mitral regurgitation can be caused by ischemia of a papillary muscle, less often by its rupture or by the installation of ventricular remodeling. • Ventricular aneurysm is a localized dilation area of the ventricular wall, which, at this level, is thin, dyskinetic. The diagnosis is echocardiographic considering that the persistence of ST segment elevation ("frozen" image) is suggestive for the presence of a ventricular aneurysm. AMI- STEMI- complications Hemodynamic complications: Left ventricular failure Cardiac pump dysfunction is one of the most common complications of myocardial infarction, the clinical signs vary depending on the severity, from the presence of dyspnea, sinus tachycardia and S3 heart sound (S3 gallop), to the installation of acute pulmonary edema. The degree of heart failure can be quantified according to the Killip classification: class 1:patients wihout clinical signs of heart failure (no rales or crackles in the lungs or S3 gallop); Class 2: mild heart failure with rales involving one half or less of the lung fields or S3 gallop.; class 3: pulmonary edema involving more than one half of the lungs field ; class 4: cardiogenic shock. Cardiogenic shock- found in 5-10% of cases of myocardial infarction, occurs when the process of necrosis affects more than 40% of myocardial mass, and is associated with increased mortality. Diagnostic: - hypotension (BP <80 mmHg); - deacresed cardiac output <1.8 l / min / m2; - pulmonary capillary pressure> 18 mmHg; - oliguria (<20 ml / hour) - cold, pale skin, confusion, drowsiness