心血管系统急症课件_1

Emergency of Cardiovascular System Department of Emergency, Xuanwu Hospital of Capital Medical University nAcute coronary syndrome nArrhythmia nAcute heart failure nHypertensive emergency Part 1 Acute coronary syndrome A group of clinical syndrome caused by acute myocardial ischemia. Coronary atherosclerosis is the pathological basis of this kind of disease. It occurs because of acute myocardial hypoxia, and the imbalance of myocardial oxygen supply and demand. Most of the disease deteriorate from chronic stable angina Concept Introduction nACS is a dynamic evolutionary process. It can be divided into unstable angina, non ST-segment elevation myocardial infarction and ST segment elevation myocardial infarction according to the severity of acute myocardial hypoxia, the duration and the imbalance of oxygen supply nThe result of ongoing ischemia is myocardial infarction regardless of any kinds of myocardial ischemia. nThe pathogenesis of ACS is a dynamic process. So we will be able to save part of the ischemic myocardium, reduced infarct size, or even avoid the occurrence of myocardial infarction if early identification and rapid effective treatments are carried out. Type 1: Including unstable angina and non ST segment elevation myocardial infarction. The Lumen of blood vessel in Non-ST segment elevation myocardial infarction is incomplete occlusion because of the platelet thrombus, known as a white thrombus. Type 2: the ST segment elevation myocardial infarction. The thrombus is fibrin-based, also known as red thrombus, total occlusion of the lumen. Clinical Classification ACS depends on two kinds of factors: One:the formation of coronary atherosclerotic plaques. Second: including plaque rupture, platelet activation, leading to thrombosis, resulting in lumen obstruction. Generally, atherosclerotic plaques can cause vascular stenosis, but not completely blocked, and if there is thrombosis, it is easy to block the vessel lumen. Mechanism In addition, due to the impaired endothelial, prostacyclin and relaxing factor (EDRF) release reduced, and angiotensin (Ang ) generation increased, which lead to vasoconstriction, platelet aggregation and accelerate thrombosis. Diagnosis and differential diagnosis According to history and clinical manifestations, ECG changes and cardiac markers such as troponin T (TnT) and troponin I (TnI) Troponin is the main basis for the identification of unstable angina and non ST segment elevation myocardial infarction. They increased when acute myocardial infarction occur. The specificity of TnI is higher than TnT. Unstable angina: 1. Electrocardiographic ST segment elevation or depression 2. Not elevated cardiac markers Non-ST elevation myocardial infarction 1. Electrocardiographic ST segment depression 2. Elevated cardiac markers ST-segment elevation myocardial infarction 1. Electrocardiographic ST-segment elevation 2. Elevated cardiac markers Differential Diagnosis Treatment 1Pre-hospital treatment Including open venous access, oxygen inhalation, sublingual nitroglycerin, ECG, oxygen saturation monitoring. The 2000 International Guidelines recommend MONA recovery approach, M: (morphine) can effectively relieve pain and reduce oxygen demand and pre-load; O: (oxygen) to improve the anoxia; N: (nitroglycerin) can antagonize the vascular spasm, reducing the preload and after-load and oxygen demand; A: (aspirin) inhibits platelet aggregation induced by thrombin 2In-hospital treatment Including maintaining IV access, oxygen, oxygen saturation measuring, describing a 12-lead electrocardiogram, continuous ECG monitoring, troponin and cardiac enzymes monitoring and so on. Poor response to treatment-consultation. (1) ST-segment elevation myocardial infarction: thrombolysis or emergency intervention should be given immediately for the patients with no contraindications. Emergency thrombolysis is no longer restricted by age. The time for thrombolysis is prolonged form 6h to 12h. Commonly used thrombolytic drugs: urokinase (UK) 20 000 U / kg, 30min IV, streptokinase (SK) 1 500 000U/30 min IV, r-tPA 50 100mg/90min IV, rSK (recombinant streptokinase) 1 500 000 U/30 min IV. Indications for PTCA(percutaneous transcoronary angioplasty) : elderly, age 75 years of age, or with thrombolytic contraindications; intervention should first be considered if there is heart failure or cardiogenic shock. (2) Non-ST-segment elevation myocardial infarction or unstable angina treatment: Strengthening clinical observation, monitoring EKG and TnI, TnT dynamic changes, comprehensive treatment, including anticoagulation, nitroglycerin, -receptor blocker, calcium antagonists and so on. Part 2 Arrhythmia Classification n1 according to anatomical points: sinus arrhythmia, atrial arrhythmias, atrioventricular junction arrhythmia, ventricular arrhythmia n2 according to room rate of speed (clinical more practical): bradyarrhythmias and tachyarrhythmias Supraventricular arrhythmia Sinus tachycardia: in the emergency situation the key is to find the cause of sinus tachycardia (such as heart failure, infection, fever, hypoxia, etc.), rather than forcing to slower heart rate. Supraventricular tachycardia: the attack may be generally terminated through: Class c and antiarrhythmic drugs. Digitalis should not be used in Wolff-Parkinson-White syndrome accompanied by AF, cardioversion should be immediately carried out on the condition of angina pectoris, heart failure, syncope or shock and other serious symptoms. Atrial fibrillation or atrial flutter with rapid ventricular rate: Paroxysmal atrial fibrillation is best to be terminated. To slow the ventricular rate in majority of emergency cases. However, it should be terminated immediately if accompanied by pre-excitation, hypertrophic obstructive cardiomyopathy and other disorders which can cause hemodynamic disorder. Ventricular arrhythmia ventricular tachycardia: sporadic paroxysmal ventricular tachycardia can be observed which is not combined with organic heart disease. Sustained ventricular tachycardia, whether combined with other circumstances or not, should be given emergency treatment. ventricular fibrillation: must carry out CPR by the principle, and early defibrillation. Not all premature ventricular contractions are subject to emergency treatment, besides below: combined with myocardial ischemia, acute or severe heart failure, or certain special circumstances (such as hypokalemia, digitalis toxicity, QT prolonged syndrome, etc.), and the main measures is to deal with the predisposing factor and the primary disease . Principles of emergency treatment treatment of primary disease and incentives terminate arrhythmias: Arrhythmia itself can cause some very serious hemodynamic disorder, so the primary and immediate measures is to terminated arrhythmias improve the hemodynamic status: some arrhythmias is not easily to be terminated immediately, but the rapid ventricular rate can lead to hemodynamics diorders, slow down the heart rate can improve patients condition, such as rapid atrial fibrillation, atrial flutter. Treatment drugs n1 Bradycardia: atropine, adrenaline, isoprenaline, etc.; pacemaker n2 Tachycardia: four main categories: nClass : Sodium channel blockers a: as the representative of quinidine, procainamide b: lidocaine, mexiletine, represented c: propafenone, represented Class : adrenergic receptor blockers such as metoprolol, bisoprolol, represented Class : Kalium channel blockers such as amiodarone Class : Calcium channel blockers such as verapamil Other unclassified: adenosine, digoxin, etc. nNon-drug therapy : electrical cardioversion, pacemaker emergency drug in supraventricular arrhythmia treatment Atrial fibrillation / atrial flutter: Vagus nerve stimulation. Considering drug treatment: - with normal cardiac function: propafenone ( c), sotalol (), amiodarone (), digoxin. -impaired heart function: can only choose amiodarone and digoxin. - adenosine can be used to block atrioventricular nodal conduction, usually only for a clear diagnosis of atrial tachycardia Reentrant arrhythmias(Pre-excitation with atrial fibrillation / atrial flutter:): try to termination the attack. Drug treatment: First choice is c(propafenone) ) and Class (amiodarone ) Angina, heart failure, syncope or shock and other serious symptoms: cardioversion should be immediately carried out emergency drug in supraventricular arrhythmia treatment Hemodynamically stable wide-QRS tachycardia: First need to confirm the diagnosis: history, 12 lead ECG. VT: amiodarone, procainamide or sotalol can be applied, Supraventricular tachycardia and missions:adenosine is available When with a unclear diagnosis, procainamide and amiodarone can be used empirically, amiodarone can only be used when with a heart failure Sotalol, propafenone are used for supraventricular tachycardia only Ventricular fibrillation / pulseless ventricular tachycardia: 1. First: defibrillation 2. If can not maintain a stable perfusion rhythm : epinephrine, endotracheal intubation, etc. 3. Amiodarone is the first choice for arrhythmia Treatment process of ventricular fibrillation / pulseless ventricular tachycardia Defibrillation again Antiarrhythmic drugs: amiodarone Defibrillation again Adrenaline 1mgiv, repea every 3 5 minutes Secondary CPR (further evaluation and treatment) Continued VT / VF after defibrillation or recurrence Basic CPR and defibrillation Part 3 acute heart failure Introduction Acute heart failure is a clinical syndrome, which experienced a sharp decline of cardiac output, circulation or acute pulmonary congestion and tissue hypoperfusion when the heart is in a short term decrease of myocardial contractility and (or) a sudden increase in ventricular load. Classification: 1.Acute left heart failure 2.Acute right heart failure Acute left heart failure is clinically common with manifestations of acute pulmonary edema, and severe cardiogenic shock ,and cardiac arrest may occur. Acute right heart failure is less common, which is mainly caused by right ventricular infarction or massive pulmonary infarction. In this section we will focuse on acute left heart failure Etiology and pathogenesis: Any factors below can lead to sudden cardiac anatomy or function impairment, reduced cardiac output and sudden increase in pulmonary venous pressure which may cause acute left heart failure. 1Acute myocardial damage 2Acute pressure overload 3Acute volume overload 4Acute limited ventricular diastolic function Clinical manifestations 1Acute left heart failure mainly manifest as acute pulmonary edema. The abrupt increase in pulmonary capillary pressure, lead to plasma infiltration into alveolar and pulmonary interstitial, which will affect gas exchange. Patients present with sudden severe shortness of breath, rapid shallow breathing( up to 30 40/min), sat wheezing, frequent cough, spitting up a lot of white or pink foamy sputum. Patients often present with extreme irritability, sweating, looking pale, clammy skin, severe cases can be fuzzy due to cerebral hypoxia Auscultation: Covered with moist and dry rales in the bilateral lung fields Increase in heart rate The first heart sound around apex is low and blunt. Gallop can be heard during systolic and diastolic period. In early stage of lung interstitial edema, moist and dry rales can not be heard or with no foamy sputum. Auxiliary examination 1X-ray examination 2ECG 3Echocardiography 4Hemodynamic Monitoring 5Arterial blood gas analysis l It is not difficult to make a diagnosis based on typical symptoms and signs, combined with arterial blood gases, X-ray and previous history of heart disease lSometimes it is needed to be identified with bronchial asthma: Acute left heart failure - a lot of pink foamy sputum and apical diastolic gallop Asthma - long-term history of asthma, with obvious dry rales Diagnosis and differential diagnosisDiagnosis and differential diagnosis lAs the critical illness, acute left heart failure should be rapidly, positively given a comprehensive treatment based on etiological and incentives factor, and pathophysiologic changes. lPrimary goal - to reduce cardiac load, increase cardiac output, relief pulmonary congestion, improve and maintain adequate tissue oxygen supply TreatmentTreatment 1First aid measures (1) Position ： take sitting or semi- recumbent position, legs down, to increase lung capacity and vital capacity, to reduce preload (2) Oxygen inhalation and the elimination of alveolar exudation: High flow nasal cannula oxygen inhalation. In severe cases, continued respirator mask should be used to increase the alveolar pressure Role: 1. can enhance gas exchange 2. against the tissue fluid from penetrating into the alveolar. (3) Morphine：can reduce the patients restlessness and anxiety, reduce myocardial oxygen consumption, lower censitivity to carbon dioxide of respiratory center, expand peripheral venous and small arteries, reduce the heart preload and after load and limit pulmonary edema. (4)Quick diuresis: Furosemide can reduce cardiac preload by rapidly veins expanding and reducing the circulating blood volume , help to alleviate the pulmonary edema. 20 40mg intravenous injection commonly. If no effect in 30min, increase the dose may be effective. (5) Vasodilator: l Expansion of veins: reduce preload, decrease pulmonary capillary wedge pressure, reduce pulmonary congestion; lExpansion of peripheral arterial: reduce afterload and increase cardiac output, improve heart function, increasing organ perfusion. lSelection principle: Applications of vasodilators should be hemodynamic monitored. Commonly used drugs are sodium nitroprusside, nitroglycerin, phentolamine (6) Digitalis: lShould be chosen in acute left heart failure patients， especially with rapid supraventricular arrhythmia or left ventricular systolic dysfunction. lCommonly lanatoside C 0.4mg intravenously injection after dilution, repeat after 2 4h if necessary. Dopamine or dobutamine can be used intravenous in the condition of acute left ventricular failure with low blood pressure, they can be combined, and also be used alone. (7）Corticosteroids: lTo relieve bronchospasm, reduce capillary permeability, reduce exudation, stable the cell lysosomes and mitochondria, and promote urination l5 10mg of dexamethasone, 100 200mg of hydrocortisone, or 80 160mg of methylprednisolone intravenous injection or intravenous drip 2. Elimination of incentives: l Such as tachyarrhythmia, rapid infusion, infection, physical fatigue, agitation, dramatically blood pressure increasing, or acute myocardial infarction and so on l To find out them as soon as possible, and take the appropriate treatment to block the deterioration of the pathophysiology and improve the cardiac function Part 4 Hypertensive emergency Introduction nIt is also called as hypertensive crisis, or malignant hypertension-need to immediately lower blood pressure, protect the target organ nComplications nACS nHeart failure nAortic dissection nHypertensive encephalopathy nCerebral hemorrhage nRenal failure nEclampsia Pathophysiology A variety of incentives can cause acute and chronic effect of deterioration such as below: nSympathetic excitation nRAAS nSelf-regulation nChronic remodeling, apoptosis Pathophysiology n (1) increased activity of sympathetic adrenergic system - increasing release of catecholamines and other neurotransmitters nexcited receptors- increase heart rate, myocardial tension and contractility- increase myocardial oxygen consumption n excited receptors - vasoconstriction, leading to the rapid increase in blood pressure. Pathophysiology n(2)Nervous, humoral and endocrine mechanisms- further activation of the renin - angiotensin - aldosterone system (RAAS)- angiotensin II and aldosterone secretion- vasoconstriction and water-sodium retention- - high blood pressure Pathophysiology n（3）Abnormal independently regulating response to blood vessels of heart, brain, kidney-leading to organ perfusion decreased. n（4）Chronic hypertension - long-term damage of vascular system-remodeling and apoptosis, systemic atherosclerosis, -leading to the corresponding organ dysfunction, - decreasing ability of regulation when with a sudden high blood pressure which can increase target organ damage. Pathophysiology nChanges in target organs nheart：load、heart failure，Oxygen consumption，Coronary thrombosis nBrain ：Vascular rupture, spasm, thrombus nKidney ：Renal failure, proteinuria nVesses ： atherosclerosis Hypertensive encephalopathy nHeadache, vomiting or coma nPsychiatric symptoms nProgress in retinopathy nIdentification: bleeding, inflammation, cancer, poisoning (CT, laboratory) Stroke nHeadache, dizziness, vomiting nParalysis, numbness, blindness nPsychiatric symptoms, coma nIdentification: hemorrhagic disease, ischemia Acute pulmonary edema nShortness of breath, can not be supine, pink foam sputum nMoist and dry rales under the bilateral lung field nHeart rate , apical diastolic gallop nsymptoms of basic heart disease Acute coronary syndrome nUAP(unstable angina pectoris)，non-ST MI， ST MI，sudden death nChest pain 、ECG、myocardial enzyme change nMonitoring: ECG,