Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Rules of treatment in selected emergency states: AMI, cerebral stroke, pulmonary oedema acute myocardial infarction AMI acute coronary syndromes (ACS) • acute myocardial infarction (AMI) • Unstable angina necrosis acute coronary syndrome test Cardiac biomarkers • Ecg • hFABP – heart fatty acid binding proteins • Mioglobin • Creatine kinase • Troponins • Enolase • Echocardiography • Lipids • CBC -complete blood count ECG • ST-segment elevation or presumed new LBBB is characterized by ST-segment elevation >1 mm (0.1 mV) in 2 or more contignous precordial leads or 2 or more adjacent limb leads and is classified as ST-elevation MI (STEMI). • Ischemic ST-segment depression ≥0.5 mm (0.05 mV) or dynamic Twave inversion with pain or discomfort is classified as high-risk UA/non–ST-elevation MI (NSTEMI). Nonpersistent or transient STsegment elevation ≥0.5 mm for <20 minutes is also included in this category. • Normal or nondiagnostic changes in ST segment or T waves are inconclusive and require further risk stratification. This classification includes patients with normal ECGs and those with ST-segment deviation of <0.5 mm (0.05 mV) or T-wave inversion of ≤0.2 mV. Serial cardiac studies (and functional testing) are appropriate. Cardiac biomarkers - creatine kinase (CK) • Elevation of the serum total CK is a sensitive enzymatic detector of AMI • False positive resalts in patients with: – – – – – – – – Muscle disease Alcohol intoxication DM Skeletal muscle trauma Vigorous exercise Convulsion Intramuscular injections Pulmonary embolism • Three isoenzymes of CK: CK-BB (brain and kidney), CKMM (skeletal muscle) and CK-MB (heart) • A ratio (relative index) of CK-MB/total CK > 6% is indicative of a myocardial rather then other source of the CK-MB elevation Cardiac biomarkers - troponin • Best diagnostic and prognostic marker of AMI • The troponin complex consist of three subunits that regulate the calcium mediated contractil process of strited muscle. – troponin I, T and C • Whereas CK-MB usually increases 10 to 20 fold above the upper limit of the reference range, troponin T and I typically increase more then 20 times above the reference range. Troponin T and I are more sensitive in diagnosis of minor myocardial damage • Troponin I and T –gold standard in diagnosis of AMI • < 4-6 h- small sensivity (10- 45%) • > 8 h- sensivity 95% • Measurment 2-time: 6- 12 h, 12- 24 h Cardiac biomarkers - the level of troponin increase in • • • • • • • • • • HF Aortic aneurysm Pulmonary embolism Toxic injure of heart muscle (chemiotherapy) miocarditis Injury of heart muscle Chronic renal failure Acute abdominal problem burns other: kardioversion, arrhythmias Cardiac biomarkers - mioglobin • Early marker of necrosis • Hight negative prognostic value . Reference range of mioglobin over 8 h after chest pain exclude MI. • reference range <70- 110 ng/ml, • AMI: 600- 1000 ng/ml Cardiac biomarkers - the level of mioglobin increase in • • • • • • • • Injury of heart muscle heatstroke, frostbite, burns hypothyreosis hypokaliemia, Convulsion, febrilis Sepsis Alcohol intoxication Medication - statines, fibrates (rabdomiolizis) Cardiac biomarkers • hFABP –heart fatty acid binding proteins • AST, ALT, LDH (lactic dehydrogenase) GGTP • CRP (C-reactive protein), fibrynogen, BNP, IL-6 (prognostic value) • GPBB (izoenzym glicogen fosforylaze – hight sensivity marker of cardiac ischemic in cardiosurgery) Cardiac biomarkers Marker Range of times to initial elevation (h) Mean time to peak elevation (h) Time to return to normal range hFABP Mioglobin Troponin T Troponin I CK-MB 1.5 1-4 3-12 3-12 3-12 5-10 6-7 24h-2d 24h 24 24h 24h 5-14d 5-10d 48-72h Initial diagnosis of AMI • History of cheat pain/discomfort • ST-elevations or (presumed) new LBBB on admissin ECG. –reapeated ECG recordings often needed • Elevated markers of myocardial necrosis (troponin, CK-MB) • 2D echocardiography and perfusion csintigraphy helpful to rule out AMI ACS – algorithm (1) ACS – algorithm (2) Relef of pain, breathlessness and anxiety • Opioids iv (4-8mg morphine) with additonal doses of 2mg at 5 min intervals • O2 (2-4l/min) if breathlessness or HF • Consider iv beta-blockers or nitrates if opioids fail to relieve pain • Transquilliser may helpful Out of hospital menagement • Recognition • Monitor, support ABCs. Be prepared to provide ALS • pharmacotherapy – – – – M O N A • ECG • Establish iv access Administer MONA – M – morphine iv if pain not relieved by nitroglycerine – O – oxygen at 4l/min – N – nitroglycerine sublingual, spray or iv – A – aspirine 300mg out-of-hospital fibrinolysis In summary, out-of-hospital administration of fibrinolytics to patients with STEMI with no contraindications is safe, feasible, and reasonable (Class IIa). • The ECC Guidelines 2005 recommended consideration of out-of-hospital fibrinolysis for patients with a transport time >1 hour. • But in a recent Swiss study, prehospital administration of fibrinolytics significantly decreased the time to drug administration even in an urban setting with relatively short transport intervals (<15 minutes). Fibrinolytic Therapy: Contraindications and Cautions for Fibrinolytic Use in STEMI From ACC/AHA 2004 Guideline Update Absolute Contraindications • Any prior intracranial hemorrhage • Known structural cerebral vascular lesion (eg, AVM) • Known malignant intracranial neoplasm (primary or metastatic) • Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours • Suspected aortic dissection • Active bleeding or bleeding diathesis (excluding menses) • Significant closed head trauma or facial trauma within 3 months Relative Contraindications • History of chronic, severe, poorly controlled hypertension • Severe uncontrolled hypertension on presentation (SBP >180 mm Hg or DBP>110 mm Hg) • History of prior ischemic stroke _3 months, dementia, or known intracranial pathology not covered in contraindications • Traumatic or prolonged (>10 minutes) CPR or major surgery (<3 weeks) • Recent (within 2 to 4 weeks) internal bleeding • Noncompressible vascular punctures • For streptokinase/anistreplase: prior exposure (>5 days ago) or prior allergic reaction to these agents • Pregnancy • Active peptic ulcer • Current use of anticoagulants: the higher the INR, the higher the risk of bleeding In hospital treatment STEMI • Reperfusion – pharmacologic – fibrinolytic therapy – mechanical – primary PCI (percutaneous coronary intervention) NSTEMI • fibrinolysis may be harmful • Pharmaclologic therapy: – – – – β-Adrenergic Receptor Blockers Calcium Channel Blockers Low-Molecular-Weight Heparin Clopidogrel and ASA PCI (percutaneous coronary intervention) • primary PCI • PCI combined with fibrinolysis • Rescue PCI cerebral stroke Stroke -Definition Stroke is defined as a sudden neurologic deficit due to central nervous ischaemia or haemorrhage. • We concentrate here on ischaemic stroke, which accounts for about 75% of all strokes. • Ischaemic stroke is caused by focal vessel occlusion leading to cessation of oxygen and glucose supply to the brain with subsequent breakdown of the metabolic processes in the affected territory. Signs and Symptoms Symptoms and signs vary with the brain territory involved. However, certain symptoms are frequently found. They include: • • • • • contralateral weakness and/or sensory loss aphasia, apraxia, dysarthria partial or complete hemianopsia disturbances of consciousness and confusion diplopia, vertigo, nystagmus, ataxia Facial Droop (have patient show teeth or smile): Normal—both sides of face move equally Abnormal—one side of face does not move as well as the other side One-sided motor weakness (right arm). Main goal in treatment • Stroke is a medical and occasionally also a surgical emergency. • Successful care of the acute stroke victim begins with the recognition both by the public and the health professional that stroke is an emergency, like acute myocardial infarction (MI) and trauma. Goals for Management of Patients With Suspected Stroke Algorithm (1). Goals for Management of Patients With Suspected Stroke Algorithm (2). Successful care of the acute stroke victim as an emergency depends on a 4-step chain: • (1) rapid recognition of and reaction to stroke warning signs, • (2) immediate use of emergency medical system (EMS) services, • (3) priority transport with notification of the receiving hospital (Patients with onset of stroke symptoms within less than 3 h should be given priority in evaluation/transportation by the EMS) and • (4) rapid and accurate diagnosis and treatment at the hospital. Emergent diagnostic tests in acute stroke 1 CT 2 ECG and chest X-ray 3 Clinical chemistry Complete blood count and platelet count, prothrombin time, INR, PTT Serum electrolytes, blood glucose CRP, sedimentation rate Arterial blood gas analysis, if hypoxia is suspected Hepatic and renal chemical analyses 4 Pulse oxymetry 5 Lumbar puncture (only if CT is negative, CT and subarachnoidal haemorrhage is clinically suspected) 6 Duplex and transcranial ultrasound 7 EEG1 8 MRI (magnetic resonance imaging) 1 and MRA1/CTA1(CT angiography) 9 Diffusion MR1 and perfusion MR1 10 ECG (transthoracic and transoesophageal)* • PTT = Partial thrombin time; CRP = C-reactive protein. 1 In selected cases. Emergent diagnostic tests in acute stroke 1 A head CT is the most important diagnostic tool in patients with suspected stroke to differentiate between ischaemia and haemorrhage. 2 Vascular imaging (ultrasound, CTA and MRA) in the acute condition gives additional information about the vessel patency in the brain and neck vessels and should supplement all imaging procedures already in the acute phase. 3 MRI/MRA can replace CT if performed appropriately and in particular T2-weighted imaging is necessary to identify even small haemorrhages. 4 Diffusion and perfusion MR may be of additional help for assessing the risk/benefit ratio for early revascularization therapy. 5 Early evaluation of physiological parameters, blood chemistry and haematology, and cardiac function (ECG, pulse oxymetry, chest Xray) is recommended in the management of acute stroke patients. Treatment 1. Continuous cardiac monitoring is recommended in the first 48 h of stroke onset particularly in patients with: 1. 2. 3. 4. 5. 6. previous known cardiac disease, history of arrhythmias, unstable blood pressure, clinical signs/symptoms of heart failure, abnormal baseline ECG and infarct involving the insular cortex. 2. Oxygenation monitoring with pulse oxymetry is recommended. 3. O2 administration is recommended in case of hypoxaemia (blood gas analysis or O2sat <92% at pulse oxymetry). 4. Intubation is recommended in case of potentially reversible respiratory insufficiency. 5. Routine blood pressure lowering is not recommended, except for extremely elevated values (>200–220 mm Hg systolic blood pressure or 120 mm Hg diastolic blood pressure for ischaemic stroke, >180/105 for haemorrhagic stroke) confirmed by repeated measurements. 6. Immediate antihypertensive therapy for more moderate hypertension is recommended in case of stroke and heart failure, aortic dissection, acute myocardial infarction, acute renal failure, thrombolysis or intravenous heparin, but should be applied cautiously. 7. Recommended target blood pressure in patients 1. with prior hypertension: 180/100–105 mm Hg, 2. without prior hypertension: 160–180/90–100 mm Hg and 3. under thrombolysis avoid systolic blood pressure above 180 mm Hg. Treatment 8. Recommended drugs for blood pressure treatment: intravenous labetalol or urapidil and intravenous sodium nitroprusside, nitroglycerin or oral captopril. Avoid nifedipine and any drastic blood pressure decrease. 9. Avoid and treat hypotension particularly in unstable patients by administering adequate amounts of fluids and, when required, volume expanders and/or catecholamines (epinephrine 0.1–2 mg/h plus dobutamine 5–50 mg/h). 10. Monitoring of serum glucose levels is recommended, particularly in known diabetic patients. - Treatment of serum glucose levels >110 mmol/l with insulin titration is recommended. 11. Glucose solutions are not recommended due to the detrimental effects of hyperglycaemia. Treatment 14. Immediate correction of hypoglycaemia is recommended by intravenous dextrose bolus or infusion of 10–20% glucose. 15. Treatment of body temperature >37.5° C • In case of fever, the search of a possible infection (site and aetiology) is recommended, in order to start tailored antibiotic treatment. 16. Antibiotic, antimycotic or antiviral prophylaxis is not recommended in immunocompetent patients. 17. Monitoring and correction of electrolyte and fluid disturbances are recommended. Characteristics of selected antihypertensive drugs that may be used in acute stroke (modified from Kaplan [1990] and Ringleb et al.1998) Suggested antihypertensive treatment in acute ischaemic stroke (modified from Brott et al. [1994] and Ringleb et al. [1998]; availability of substances may vary between countries) Specific Treatment Thrombolytic Therapy 1. Intravenous rtPA (0.9 mg/kg, maximum 90 mg), with 10% of the dose given as a bolus followed by an infusion lasting 60 min, is the recommended treatment within 3 h of onset of ischaemic stroke. 2. The benefit from the use of intravenous rtPA for acute ischaemic stroke beyond 3 h after onset of the symptoms is smaller, but present up to 4.5 h. 3. Intravenous rtPA is not recommended when the time of onset of stroke cannot be ascertained reliably; this includes persons whose strokes are recognised upon awakening. 4. Intravenous administration of streptokinase is dangerous and not indicated for the management of persons with ischaemic stroke. 5. Data on the efficacy and safety of any other intravenously administered thrombolytic drugs are not available to provide a recommendation. 6. Intra-arterial treatment of acute MCA occlusion in a 6-hour time window using pro-urokinase results in a significantly improved outcome. 7. Acute basilar occlusion may be treated with intra-arterial therapy in selected centres in an institutional protocol as experimental therapy or within a multicentre clinical trial. 8. Ancrod cannot presently be recommended for use in acute ischaemic stroke outside the setting of clinical trials. Specific Treatment • Aspirin (100–300 mg per day) may be given within 48 h after ischaemic stroke – – – • There is no recommendation for general use of heparin, lowmolecular weight heparin or heparinoids after ischaemic stroke – – • • • • given within 48 h after stroke reduces mortality and rate of recurrent stroke minimally, but statistically significantly If thrombolytic therapy is planned, no aspirin should be given. Aspirin is not allowed for 24 h after thrombolytic therapy. Full-dose heparin may be used when there are selected indications such as cardiac sources with high risk of re-embolism, arterial dissection, or high-grade arterial stenosis prior to surgery Low-dose subcutaneous heparin or low-molecular-weight heparins should only be considered for patients at high risk of DVT or pulmonary embolism. Infections after stroke should be treated with appropriate antibiotics. Aspiration pneumonia may not be prevented by nasogastric feeding Early mobilisation is helpful to prevent numerous complications after stroke including aspiration pneumonia, DVT and decubital ulcers. Administration of anticonvulsants to prevent recurrent seizures is strongly recommended. – Prophylactic administration of anticonvulsants to patients with recent stroke who have not had seizures is not recommended pulmonary oedema ACUTE HEART FAILURE Definition Acute heart failure is defined as rapid onset of symptoms and signs secondary to abnormal cardiac function. • It is often life threatening and requires urgent treatment. It may occur with or without previous cardiac disease. The cardiac dysfunction can be related to systolic or diastolic dysfunction, to abnormalities of cardiac rhythm or to preload and afterload mismatch heart failure - common causes of HF • Heart feilure is a result of acute pump dysfunction • • • • • • • • • IHD Valvular disfunctin Cardiomyopathy Acquired cardiomyopathy (toxic-alcohol, cocain; or metabolic – thyreotoxicosis) Myocarditis Constrictive pericarditis Cardiac tamponade Systemic hypertension Other – anemia, cardiac dysrhythmias ACUTE HEART FAILURE PRESENT WITH SEVERAL DISTINCT CLINICAL 1. Acute decompensated heart failure, de novo or decompensation of chronic heart failure 2. Hypertensive acute heart failure: 3. Pulmonary odema, as an acute heart failure accompanied by severe respiratory distress and usually O2 saturation < 90% on room air prior to treatment . 4. Cardiogenic shock: Cardiogenic shock is a continuum from low cardiac output syndrome to cardiogenic shock 5. High output failure 6. Right heart failure is characterised by low output syndrome with increased jugular venous pressure, increased liver size and hypotension heart failure - diagnosis • Echocardiography – gold standard • Chest X-ray • Natriuretic peptide (BNP) Brain natriuretic peptyde (BNP) • In normal state atrium is the main cardiac production site of BNP • Main stimuli for proBNP synthesis and secretion from cardiac myocytes are: myocyte stretch caused by volume overload, neurohormonal activation and hypoxia • Ventricular proBNP production is strongly upregulated in cardiac failure and locally in the area surrounding a myocardial infarction • biological effects of BNP: diuresis, vasodilatation, inhibition of renin and aldosterone production and of cardiac and vascular myocyte growth Synthesis of NTpBNP and BNP prepro- BNP (134 amino acids) Myocyte cardiac fibroblast signal peptyde (26 amino acids) pro- BNP (108 amino acids) blood NT-proBNP (76 amino acids) BNP (32 amino acids) biologically active Clinical significance of NTpBNP and BNP As a diagnostic tool: • marker of congestive heart failure, helpfull in assessment of acute dyspnea • Predictor of sudden cardiac death and cardiac events in heart failure • Predictor of development of heart failure and mortality after acute coronary syndrome • For monitoring of cardiotoxicity of antracyclins and of effects of therapy of heart failure • NTpBNP vs BNP: more stabile in serum in vivo and in vitro (storage), 3-6 times longer half-time of persistence in serum, more stabile concentration with lower sensivity to changes in the amount of systemic fluids • Both peptides have an excellent ability to distinguish heart failure from non-heart failure subject but NTpBNP is more sensitive and specific (Fonseca) Medical Treatment of AHF 1.Morphine 2. Anticoagulation 3. Vasodilators 4.ACE inhibitors 5. Diuretics 6.Beta-blocking agents 7. Inotropic agents Morphine • Indication – Early stages of AHF treatment, especially when associated with restlessness and dyspnea • Effects – Venodilation & mild arterial vasodilation – ↓ heart rate • Dosing – 3 mg boluses, which can be repeaded Anticoagulation • Indication Well established in ACS or AFib, with or without AHF Less evidence in AHF • Effects: few studies! Enoxaparine s.c. vs placebo in acutely ill pts* No clinical improvement Less DVT (deep vein thrombosis) No studies of LMWH vs unfractionated heparin • Administration Careful monitoring of coagulation system If Creatinine Clearance < 30 mL/min - Contraindicated or used with extreme care with anti-Factor Xa level monitoring IDN – isosorbide dinitrate Diuretics • Indication – Patients with AHF & ADHF with symptoms secondary to fluid retention • Effects Diuresis by water, NaCl & other ions excretion ↓ total body water & Na ↓ plasma & EC volume ↓ RV & LV filling pressures ↓ peripheral congestion & pulmonary edema Early vasodilation after i.v. administration – ↓ RV & LV filling pressures & PVR – Risk of reflex vasoconstriction after high doses May ↓ neurohumoral activation in the short-term (but not in the long-term) in severe ADHF Especially in ACS, administer low doses & give preference to nitrates Diuretics: Practical Use • Prefer i.v. loop diuretics (furosemide) – Therapy can be safely initiated before hospital admission • Start with individualized doses according to clinical conditions – Furosemide, 20-40 to 40-100 mg bolus with infusion at 5-40 mg/h – Prefer a bolus • Titrate according to clinical response – Diuresis / Relief of congestive symptoms • Thiazides & spironolactone can be used in combination • Dobutamine, dopamine and/or nitrates can be used in combination – Combinations are more effective and with fewer side effects than increasing diuretic dose New Diuretic Agents • Vasopressin V2 receptor antagonists • BNP • Adenosine Beta-blocking Agents: Indications • AHF considered a contraindication for beta-blockade – No study of beta-blocking therapy targeted at improving AHF – Patients with > basal pulmonary rales or hypotension excluded from BB trials in AMI • In AMI, beta-blockers ↓ infarct size, arrhythmias and pain ....Greater ↓ mortality & morbidity in pts with pulmonary congestion • Intravenous BBLs should be considered in pts with: – Ischemic chest pain resistant to opiates – Recurrent ischemia – Hypertension – Tachycardia – Tachyarrhythmias Beta-blocking Agents: Practical Use • Use cautiously in patients with overt AHF and > basal pulmonary rales – Consider i.v. metoprolol if • Ongoing ischemia • Tachycardia • Patients with AMI who stabilize after AHF – Start early beta-blocker • Patients with chronic HF – Start after AHF stabilization (usually > 4 days) Inotropic Agents: Indications • Peripheral hypoperfusion – Hypotension, ↓ renal function • With or without congestion or pulmonary oedema • Refractory to diuretics & vasodilators at optimal doses PDE – phosphodiesteraze inhibitors Practical Use of Dobutamine • Indication – Peripheral hypoperfusion (hypotension, renal function) with or without congestion or pulmonary eodema refractory to diuretics & vasodilators at optimal doses • Mode of administration – Initiated at 2-3 ug/kg/min without a loading dose – Progressive increase up to 20 ug/kg/min – Need of higher doses in patients on beta-blocker therapy – Possible combination with PDEi (amrinon, milrinon) PDE – phosphodiesteraze inhibitors Circulation 2005; 112: WWW.circullationaha.org