myocardial infarction in the elderly
Introduction
Introduction to myocardial infarction in the elderly Myocardial infarction is a pathological process in which a coronary artery is continuously ischemic and the myocardium is dominated by irreversible necrosis. The main cause of myocardial infarction in the elderly is coronary atherosclerosis. Common causes are excessive fatigue, high mental stress, cold stimulation, major surgery, high fat or full diet, smoking, carbon monoxide poisoning. The clinical symptoms of senile myocardial infarction are atypical. There are many other diseases (high blood pressure, diabetes, cerebrovascular disease, respiratory tract, gastrointestinal tract and urinary tract infections) before the onset of the disease, and the onset of day and night, most of the morning from 6 to 12 It may be related to changes in catecholamine levels in the body and to weather and climate change. basic knowledge The proportion of sickness: 0.406% Susceptible people: the elderly Mode of infection: non-infectious Complications: acute left heart failure in elderly patients, cardiogenic shock, heart failure
Cause
Causes of myocardial infarction in the elderly
1, the basic cause: coronary atherosclerosis, on the basis of the following trigger factors, can cause acute myocardial infarction (AMI):
(1) Acute platelet aggregation and thrombosis in the coronary arteries (90%).
(2) Hemorrhage in atherosclerotic plaque or under plaque, forming a local hematoma.
(3) Persistent coronary artery spasm.
Secondary triggering factors include:
1 sudden discharge of cardiac output: such as shock, blood loss, severe arrhythmia;
2 myocardial oxygen demand soared: such as heavy physical activity, blood pressure rose, emotional.
2, secondary causes: occasional coronary embolism, inflammation or congenital malformations.
Prevention
Elderly myocardial infarction prevention
1. Secondary prevention of senile myocardial infarction
Secondary prevention of senile myocardial infarction refers to long-term treatment after AMI. For more than 20 years, AMI has carried out thrombolytic therapy BPTCA on the basis of the original CCU monitoring and treatment, which has reduced the recent hospital mortality rate of AMI from 30% to 5%. Secondary prevention of AMI mainly refers to: 1 prevention and treatment of heart failure, re-embolic and sudden death, and elimination of risk factors; 2 risk factors for further development of arteriosclerosis, secondary prevention of myocardial infarction is to improve quality of life and prolong Life expectancy, reducing mortality, measures include drugs and non-drugs, non-drug prevention refers to changes in patients' lifestyles, such as smoking cessation, diet control to achieve weight loss and regulation of dyslipidemia, appropriate increase in physical activity, etc., drug prevention includes: antithrombotic Drugs, beta-blockers, lipid-modulating and anti-arrhythmic drugs, other ACEI inhibitors, vitamin C with antioxidant effects, etc., have also been reported in secondary prevention of myocardial infarction, since the 1990s A multi-center, double-blind randomized trial, if there is no corresponding contraindication for myocardial infarction, the "ABC" procedure A should be initiated as soon as possible (Aspr) i, ACEI), B (Beta Bloker), C (Cholesterol Lowering), these modern therapies, can significantly reduce the mortality rate and coronary heart disease events, improve clinical prognosis, the effect is definitely significant.
(1) Antiplatelet and anticoagulant therapy: Platelets play an important role in the formation of atherosclerosis, as well as coronary artery spasm, myocardial ischemia caused by thrombosis, myocardial infarction or sudden death, and become elderly myocardial infarction The drug of choice for long-term secondary prevention.
Aspirin mainly blocks TXA2 production by inhibiting cyclooxygenase in platelets. Various components in the blood such as ADP, serotonin, thrombin and collagen can increase TXA2 production by activating platelets, thus blocking TXA2 production. It plays an important role in inhibiting platelet aggregation and release. Studies have shown that low-dose aspirin can significantly inhibit the production of TXA2, but the inhibition of PGI2 production is small, so long-term secondary prevention of myocardial infarction in the elderly has chosen a small dose, ie 50 ~150mg/d.
American health studies showed that aspirin was given 325 mg every other day, and the incidence of myocardial infarction was the most obvious at 4 to 10 in the morning, with a decrease of 59.3%, and the other time was only decreased by 34.1%, which was consistent with the circadian rhythm of platelet aggregation, and platelet aggregation in the early morning. Sexual increase, acute myocardial infarction is higher during this time, aspirin inhibits platelet aggregation, so myocardial infarction is the most obvious reduction during this time.
Ticlopidine (Nefride) is another drug that inhibits platelet aggregation, its mechanism and characteristics:
1 inhibiting adhesion between fibrinogen and platelet receptor, inhibiting fibrinogen bridge formation between platelets;
2 activating adenylate cyclase to increase intraplatelet cAMP concentration, the latter inhibits calcium ion activation, thereby inhibiting platelet aggregation;
3 does not inhibit cyclooxygenase, and has no effect on platelet TXA2 and endothelial cell PGI2 production;
4 inhibition of platelet aggregation induced by most inducers, ticlopidine is applied in the same range as aspirin, the dose is 250mg, 2 times / d, after 1 to 2 weeks, changed to 250mg, once / d, ticlopidine in prevention It has a significant effect on infarction. It can be used as a contraindication to aspirin or a severe disease. It can replace aspirin. Aspirin combined with ticlopidine has a certain effect on preventing acute occlusion and chronic restenosis. Dipyridamole, sulfinpyrazone in myocardium The role of secondary prevention of infarction is unclear.
Long-term oral anticoagulants are beneficial for reducing mortality and reinfarction rates in elderly patients with myocardial infarction. Warfarin reduces blood hypercoagulability by inhibiting the synthesis of vitamin K-dependent coagulation factors (II, VII, IX, X). Farin is an effective anti-thrombotic alternative to aspirin in secondary prevention after senile myocardial infarction. It is often used for anterior or apical myocardial infarction, left ventricular dysfunction with or without wall thrombus, and patients with atrial fibrillation. .
The WARIS trial observed the effect of long-term oral warfarin therapy for myocardial infarction. After 3 years of follow-up, the mortality and non-fatal reinfarction rates in the anticoagulation group were reduced by 24% and 34%, respectively, and the incidence of fatal reinfarction was reduced. At 55%, the ASPECT trial showed that anticoagulant therapy reduced reinfarction by 53%, but there was no significant difference in the reduction of total mortality compared with the control group. The SPRS test observed the effect of anticoagulant therapy on elderly patients, with 878 candidates > Patients 60 years old who underwent anticoagulant therapy after myocardial infarction were randomly assigned to continue anticoagulant therapy group and placebo group. After 2 years, anticoagulant therapy group and control group mortality rate (7.6% vs 13.4%, P <0.017) and reinfarction rate (5.7% vs. 15.9%, P<0.0001) were significantly reduced.
A new generation of antiplatelet and anticoagulant preparations, platelet membrane GPIIb/IIIa receptor antagonists such as C7E3Fab, are platelet membrane glycoprotein receptor antagonists. After platelet activation, the conformational change of platelet membrane GPIIb/IIIa receptor becomes high affinity. The body is tightly bound to components such as fibrinogen, thereby causing platelets to aggregate together by fibrinogen, thereby achieving anti-platelet aggregation.
(2) -blockers: -blockers are currently recognized as effective drugs for secondary prevention after senile myocardial infarction, which can effectively reduce the incidence of non-fatal reinfarction and sudden death after myocardial infarction And total cardiac mortality.
A large number of clinical trials have shown that -blockers can reduce the mortality rate by 25% to 35% in the first year after acute myocardial infarction. Swedish studies have shown that patients with acute myocardial infarction should be given oral daily after intravenous injection of metoprolol 15 mg. 200mg, the 1-week mortality rate decreased by 36%. In a large-scale multi-center study, -blockers were started within 3 days of acute myocardial infarction, and the overall mortality and/or sudden death rate within 1 year after acute myocardial infarction. A 25% decline, some of which also showed that beta blockers can reduce the recurrence rate of acute myocardial infarction, and other studies have shown that within 12 hours of acute myocardial infarction chest pain, intravenous -blockers, after onset 1 The weekly mortality rate decreased by 15%. After 3 to 28 days after acute myocardial infarction, the -blocker without endogenous sympathomimetic activity was orally administered. The 1-year mortality rate after acute myocardial infarction decreased by 30%, one or more times. Surviving patients with acute myocardial infarction, especially with low left ventricular ejection fraction, persistent myocardial ischemia and asymptomatic frequent ventricular premature contraction, is a high-risk group of sudden death and recurrent infarction, studies have shown that acute myocardium After infarction Preventive treatment given - blockers can significantly improve the 2-year survival rate.
Principles for the application of -blockers:
1 Apply as early as possible, early intravenous administration, and then continue oral administration;
2 gradually increase gradually from the minimum dose until the patient reaches the maximum tolerance;
3 long-term maintenance, in the course of treatment should pay attention to monitoring heart rate, blood pressure changes and individualized dose differences, especially the elderly dose should be correspondingly reduced, indications include:
1 transient acute tachyarrhythmia and abnormal pump function in the acute phase of AMI (IVEF <40%);
2 combined with post-infarction angina pectoris, hypertension patients;
3 24h dynamic electrocardiogram monitoring before discharge found high-risk patients with complex ventricular arrhythmia, all older patients with AMI complications have better efficacy, contraindications: low blood pressure, bradycardia, severe congestive heart failure, AVB and Patients with obstructive pulmonary disease.
The mechanism of secondary prevention of -blockers in elderly patients with myocardial infarction includes anti-myocardial ischemia, reducing myocardial oxygen consumption, prolonging myocardial perfusion time, avoiding local myocardial catecholamine release during myocardial ischemia, preventing arrhythmia and antiplatelet Aggregation, partially increase vagal tone, slow heart rate, lower blood pressure and myocardial contractility, reduce the impact on coronary atherosclerotic plaque, thus reducing plaque damage, rupture, increase myocardial blood flow under the intima, improve ventricular wall local Abnormal segmental motion and left ventricular function.
(3) Angiotensin-converting enzyme inhibitors: Recent clinical trials have shown that administration of appropriate ACEI in elderly patients with myocardial infarction is safe for reducing the risk of death after myocardial infarction, reducing overall mortality, preventing further deterioration of heart failure and improving left ventricular function. And effective.
In the AMI ACEI treatment clinical trial, SAVE (using captopril), SOLVED (using enalapril) and AIRE (using ramipril) tests showed a 21% reduction in the risk of recurrent myocardial infarction in the treatment group, instability The risk of angina pectoris decreased by 15%, CUNESENSUS II (using enalapril), ISIS-4 (using captopril), CCS-1 (Chinese capsaicolic treatment after AMI) and other group trials showed that AMI In patients with ACEI, the risk of death in the first month after AMI decreased by 6.5%. In the above trial, the SAVE trial started 3 to 16 days after AMI (average 11 days), with no clinical cardiac function, but EF <40%. Patients were treated with captopril. After 42 months of follow-up, the total risk of death in the treatment group decreased by 19% (P=0.019). The AIRE trial was performed 3 to 5 days after AMI (mean 5 days) for those with clinical cardiac function. Treatment with ramipril was started, with an average follow-up of 5 months. The total death in the treatment group decreased by 27% (P=0.002). In the recent SMILE trial, AMI was not treated with thrombolysis, and there was no concurrent cardiac insufficiency or pulmonary edema. The patients were treated with zofenopril and found that the mortality of the patients at 6 weeks after the onset of AMI decreased significantly.
ACEI is used for secondary prevention of myocardial infarction and is mainly used in the following two cases:
1 After AMI with cardiac insufficiency (EF<4%) and no hypotension is a positive indication for ACEI treatment, both of which start ACEI treatment as soon as possible. The lower the EF value of AMI patients, the better the effect of ACEI treatment on prognosis improvement.
2 prevention or reduction of ventricular remodeling after AMI: ventricular remodeling after AMI is more common in large-area transmural myocardial infarction and no collateral blood donor, can make segmental expansion and thinning of early myocardial infarction (infarct expansion) Non-infarction segment thickening, causing left ventricular enlargement, and left ventricular enlargement affects cardiac function, leading to progressive decline in cardiac function, patients may have ventricular aneurysm, in accordance with one of the above two, ACEI can be applied.
A. Mechanism of action: The mechanism of action of ACEI includes inhibition of the renin-aldosterone system, dilation of blood vessels, regulation of endothelial function, inhibition of myocardial and vascular tissue growth, delaying coronary vascular wall thickening, improvement of subendocardial perfusion, and reduction of infarction Area extension and non-infarcted myocardial dilatation, improve ventricular remodeling, can prevent cardiac function deterioration in patients with myocardial infarction, this effect is most obvious in the early days of drug use, which is also an important mechanism for ACEI to improve the prognosis of myocardial infarction, in addition, The beneficial effects of ACEI on cardiac electrophysiology also reduce the mortality rate of myocardial infarction.
B. Usage and dosage: ACEI should be started from small doses in patients with acute myocardial infarction. It should be used after 2 days of onset. Premature application (24h) may result in hypotension due to unstable condition. Late application may lose the prevention of infarct extension. And the timing of reducing mortality, high-risk patients, such as anterior myocardial infarction, Q-wave myocardial infarction, combined with cardiac insufficiency, hypertension and elderly patients, preferably within 3 months after myocardial infarction, which has no ACEI contraindications and Those with no obvious side effects should be applied for a long time.
C. Antiarrhythmic drugs: The mortality rate in the first year after myocardial infarction is as high as 15%, and ventricular arrhythmia is one of the high risk factors for sudden death.
The first type of antiarrhythmic drugs can effectively reduce the incidence of ventricular premature contraction, but because of its arrhythmogenic effect, it can not effectively prevent the mortality after myocardial infarction, instead in the CAST test (cardiac arrhythmia suppression trial) An increased risk of death was observed.
The second type of antiarrhythmic drug beta blockers can reduce the mortality rate in the first year after AMI by 25% to 35%. The mechanism of action includes anti-myocardial ischemia, prevention of arrhythmia and anti-platelet aggregation, especially after AMI. Patients with cardiac insufficiency (LVEF <40%) are beneficial.
The third class of antiarrhythmic drugs may have a promising future in preventing post-AMI mortality. The amiodarone myocardial infarction arrhythmia test (CAMI-AT) published in 1997 showed that amiodarone (Dragon) can be reduced. The risk of ventricular fibrillation or arrhythmia death is 48.5%. In the same year, the European AMI test (EMLAT) after myocardial infarction was published. The results also showed that amiodarone reduced the risk of arrhythmia death by 35%. In 1998, one included the above 2 A trial of 13 clinical metastatic ATMA trials, summarized and analyzed the efficacy of amiodarone in high-risk patients with chronic heart failure and ventricular arrhythmia (sudden death) after myocardial infarction, the overall results: a. reduce arrhythmia The overall mortality rate was 29%; b. The total case fatality rate decreased by 13%, and the odds ratio was 0.87, indicating that the low-dose amiodarone has significant antiarrhythmic effects, and there is no obvious evidence of arrhythmia, which can be applied to chronic AMI. High-risk patients with heart failure or ventricular arrhythmia.
The fourth class of antiarrhythmic drugs, such as sustained-release verapamil, diltiazem, and sustained-release nifedipine, are beneficial for the prevention of ventricular arrhythmias after AMI only when the patient does not have heart failure.
Other oxygen radical scavengers such as antioxidants such as superoxide dismutase (SOD), catalase and vitamin C, E, -carotene, etc.; anti-leukocyte agents such as prostaglandins, non-sterols Anti-inflammatory drugs and lipid peroxidase inhibitors; and adenosine (adenosine) and other roles in the secondary prevention of senile myocardial infarction have also received attention, but there is still a lack of clinical large-scale trials.
2. Tertiary prevention of senile myocardial infarction
(1) Diagnosis and management of acute myocardial infarction complicated with arrhythmia: AMI arrhythmia may be caused by severe myocardial ischemia caused by complete coronary artery obstruction or myocardial ischemia-reperfusion injury due to infarction-related coronary recanalization. Prone to ventricular tachycardia and ventricular fibrillation, is the main cause of sudden death in early AMI, arrhythmia caused by myocardial ischemia is called ischemic arrhythmia; reperfusion caused by infarction-related coronary recanalization Arrhythmia.
1 sinus tachycardia: common causes include pain, anxiety, sympathetic excitation, fever, may also be related to drugs, pericarditis, insufficient blood volume, pump failure and other factors, continuous sinus tachycardia with S3 (S4) Malu is an early sign of left heart failure. The main treatment is to remove the cause. It is a sympathetic hyperthyroidism. You can try a small dose of -blocker. For patients with insufficient blood volume, the pump failure should be used for hemodynamic monitoring of floating catheter.
2 sinus bradycardia: the incidence rate is high within 1h after onset, especially in the inferior wall infarction. The sinus sinus is more related to the increase of reflex vagus nerve tension within 72h after onset. After 72h, it is more common in sinus node ischemia, simple sinus palsy, think There is less chance of ventricular fibrillation than sinus speed, generally no treatment, severe sinus palsy (<50 times / min) combined:
A. angina and/or ventricular arrhythmia;
B. Dizziness or fainting due to insufficient cardiac output;
C. Low blood pressure or poor peripheral circulation
D. Heart failure, only consider atropine 0.5mg intravenous injection, can be repeated application or change to intravenous drip, the drug can not be used for a long time, AMI patients with glaucoma and benign prostatic hyperplasia banned atropine, can be applied to anisodamine, Similar to atropine, the side effects are small, 10-20mg subcutaneous or intravenous injection, repeated injection if necessary, relieve vasospasm and improve microcirculation,
E. Sinus with pump failure and shock, dopamine 40 ~ 80mg into the Mg-GLK solution 500ml intravenous infusion, supplemented with vasodilator, cardiotonic and diuretic.
3 supraventricular premature beats: premature beats in atrial or border zone have little effect on hemodynamics, and their importance is to cause supraventricular tachycardia, atrial flutter or tremor, outdoor premature beat May be related to mental stress, sympathetic stimulation or certain drugs, but may also be related to atrial ischemic necrosis or left heart failure caused by pulmonary congestion, can not be treated temporarily, but should be closely monitored.
4 atrial flutter and atrial fibrillation: is an important arrhythmia in AMI, atrial fibrillation is rare in patients with AMI, accounting for 1% to 3% of the incidence of AMI, often transient, easy to change to atrial fibrillation or with the room Cochlear coexistence, its pathogenesis, predisposing factors and atrial fibrillation, the incidence of atrial fibrillation AMI 10% ~ 15%, of which 90% appeared in the first 4 days of AMI, most of them are paroxysmal, a few are persistent, the latter prompts There are multiple lesions, 90% stop within 24h, 75% to 80% of patients have left heart failure, and atrial fibrillation is associated with left atrial congestion; some patients are caused by atrial infarction; the arrhythmia increases with age, and may Associated with atrial muscle degeneration, with obvious hemodynamic disorders (such as hypotension, shock), should immediately DC cardioversion, especially atrial flutter is effective, 50 ~ 100J can be effective, the disease allows patients to use drugs Cardioversion, commonly used propafenone 35 ~ 70mg plus 10% glucose solution 20ml slow intravenous injection, combined with left ventricular dysfunction can be used gerberin C0.2 ~ 0.4mg plus 10% glucose solution 20ml slow intravenous injection, while applying vasodilation Medicines and diuretics to improve heart function.
5 supraventricular tachycardia: including paroxysmal atrial tachycardia and paroxysmal atrioventricular junction tachycardia, low incidence, often transient or recurrent episodes, most of the etiology and original Atrial bypass or atrioventricular node is related to double-path conduction. A few are related to atrial myocardium ischemia or atrial infarction. Rapid ventricular rate can aggravate myocardial ischemia and promote left heart failure. If not treated in time, it can often lead to blood flow. The kinetics deteriorate, but there is no adverse effect in other aspects. Those who have no cardiac insufficiency and hypotension can choose verapamil 5mg plus 10% glucose solution 20ml or propafenone (the same amount as before), or try ATP. 20mg plus atropine 0.5mg in 3s intravenously or with diltiazem slow intravenous injection, with cardiac insufficiency can be intravenous injection of geranin C to convert the heart rhythm, DC can be used in emergency situations.
6 non-paroxysmal junction tachycardia: the incidence rate within 24h of the onset is higher, in the case of acute inferior wall infarction, ventricular rate <80 times / min, in addition to the dying rhythm, the prognosis is good, no special treatment; In the acute anterior wall infarction, the ventricular rate is often >80 beats/min, mostly accompanied by left heart failure, the prognosis is poor, the treatment is poor, and the treatment is mainly to correct heart failure.
7-ventricular premature beats: almost all AMI patients have ventricular premature beats, there are 2 peaks, the first peak is the first 24 to 48 hours after the onset, related to acute myocardial ischemia and ECG instability or genus Reperfusion arrhythmia; the second peak is after 48 hours of onset, may be related to injury current, reentry mechanism or triggering activity around the infarction, often in patients with left heart failure, once found ventricular premature contraction, especially frequency Early hair chamber (>50 times / min), multi-source room early, paired or short-field bursts, RonT-type room early, often a precursor to ventricular fibrillation, should first use lidocaine 50 ~ 100mg plus 10% Glucose solution 20ml slowly intravenously, can be repeated after 10min, until the early control of the room or the total amount of up to 300ml, after the effective intravenous infusion of 1 ~ 2ml / min, maintained for more than 48h, then changed to oral drugs, such as mexiletine 200mg , 3 ~ 4 times / d, oral, prevent recurrence, lidocaine toxicity: toxic side effects such as drowsiness, dizziness, muscle twitching, loss of orientation, respiratory depression, and sinus slow, hypotension, etc., prevention of toxicity: A. administration according to the weight of the fat removed; B. Age (> 70 years), heart failure, shock, liver and kidney dysfunction and impaired nerve function should reduce the dosage as appropriate.
For patients who are not treated with lidocaine, the following drugs are available:
A. propafenone: the first dose of 35 ~ 70mg, after intravenous infusion, 10-15min can be repeated before the ineffective dose, until VPB disappears or the total amount reaches 350mg; or 210mg added 5% ~ 10% glucose solution 250ml in the static Drop, VPB disappeared to 150mg, 3 ~ 4 times / d, oral, for the elderly, cardiac insufficiency, conduction block, sick sinus syndrome, etc. with caution or disable,
B. Amiodarone: the first dose of 75mg, after intravenous infusion for 5 ~ 10min, 30min after 30min after ineffective, intravenous injection of 30 ~ 75mg, after the disappearance of VPB changed to 0.5 ~ 0.75mg / min intravenous infusion, the total <1200mg / d , continue medication for 2 to 3 days,
C.-blocker: Sotalol 20mg intravenously, can be repeated once every 10-15min after ineffective, after VPB disappears, changed to 20-80mg, oral, 2 times / d, can reduce its sudden death and then Infarction improves patient prognosis.
8 paroxysmal ventricular tachycardia: ventricular tachycardia often induces ventricular fibrillation, is a serious arrhythmia in elderly patients with AMI, short-term ventricular tachycardia for the treatment of ventricular premature contraction, lidocaine can also use propafenone , amiodarone, bromobenzylamine or procainamide slow intravenous injection, sustained ventricular tachycardia with hypotension, shock, A-Symbol or cardiac dysfunction, immediate DC cardioversion, and then with lidocaine 2mg /min intravenous drip maintenance, most people advocate that after the ventricular tachycardia, should continue to use antiarrhythmic drugs for 3 weeks to 3 months.
9 ventricular fibrillation: the incidence of ventricular fibrillation in elderly patients with AMI is 4% to 18%, almost common in Q-wave myocardial infarction, non-Q-wave myocardial infarction is rare, 90% of ventricular fibrillation occurs within 12 hours after infarction, can be divided into two Class: A. Primary ventricular fibrillation: There is no left heart failure and shock in patients. There is no atrial arrhythmia in ventricular fibrillation or arrhythmia in the first few seconds before ventricular fibrillation. It usually occurs within 4 hours of infarction and later with time. The incidence of metastasis decreased exponentially, rarely occurred after 12h, 95% success rate of recovery, rarely recurrence, good prognosis, B. secondary ventricular fibrillation: often secondary to heart failure or cardiogenic shock, 30% recovery Rate, easy to relapse, poor prognosis, patients with ventricular fibrillation should be subjected to DC shock cardioversion as soon as possible, the first 200J, 300J when ineffective, can be intravenously brominated with bromobenzylamine or amiodarone if there is no cardioversion condition, For patients with secondary ventricular fibrillation, the corresponding measures to correct heart failure and shock have been reported. It is reported that about 80% of patients with primary ventricular fibrillation can survive and discharge, while only 20% to 25% of secondary ventricular fibrillation survive.
10 Accelerated ventricular autonomy: more than 24 hours after infarction, patients with common inferior wall infarction may be related to sinus node ischemic injury and increased self-regulation outside the heart, mostly benign, hemodynamics No obvious effect, generally do not need special treatment, but a small number can also cause ventricular fibrillation, so those who last longer can use atropine 0.5 ~ 1mg intravenous injection, can also try lidocaine, generally do not use procainamide and quinidine.
Torsades ventricular tachycardia: senile AMI patients may have a torsade ventricular tachycardia or polymorphic ventricular tachycardia, which may be caused by triggering activity and early post-depolarization caused by slow channel Ca2+ influx. Very short (<0.28 s) ventricular premature contraction and pleomorphic (torsional) ventricular tachycardia, calcium channel blocker verapamil has a significant effect, and class Ib antiarrhythmic drugs are also often effective.
Atrioventricular block (AVB): AVB in acute inferior wall infarction occurred within 6 hours of onset, mostly associated with increased vagal tone; after 24 hours, most of them were caused by atrioventricular node ischemia, and sugar was applied while improving blood supply. Corticosteroids, magnesium sulfate may be effective, it has been reported that aminophylline 0.25 plus 10% glucose solution 20ml intravenous injection, the mechanism is that aminophylline can antagonize the adenosine produced by ischemia, AVB inferior wall infarction, more than once Or second degree I, even if the third degree AVB occurs, the ventricular rate is more than 45 times / min, QRS wave is supraventricular, temporary, low mortality, should be closely observed, not eager to apply artificial pacemaker Properly treated, it will return to normal within one week.
Acute anterior wall infarction block occurs mostly in the junction area, which is caused by necrosis of the indoor bundle branch system due to infarction. It is actually a complete or incomplete indoor three-branch block. Once complete AVB is formed, ventricular pacing The position of the point is low, the frequency is slow, the QRS is wide and deformed, and the A-Sigm sign is prone to occur. It is more common in a large range of anterior wall infarction, and the prognosis is poor. Almost all cases occur within the first 48 hours, and the latter occurs on the fourth day. Wall infarction combined with altitude or third-AVB, poor response to atropine and isoproterenol, temporary atrial pacemaker should be installed as soon as possible with or without A-Shr, and the block should still be installed permanently after 1 to 2 weeks. pacemaker.
Indoor conduction block, indoor conduction block refers to the conduction block below the branch of the Hissian bundle, divided into right bundle branch block, left bundle branch block, left bundle branch block (left front branch, left rear branch) And interval branch block), as well as indoor block, 3 indoor block and terminal indoor block, bundle branch block can be persistent or temporary, or intermittent or alternating.
A. Blood supply to the heart conduction system:
a. 90% of patients with atrioventricular node and His bundles were supplied by the distal branch of the right coronary artery at the atrioventricular node.
b. The first 1/3 of the right bundle branch is supplied by the atrioventricular nodal artery, and the second 2/3 is supplied by the left anterior descending coronary artery.
c. The left bundle branch is supplied by the left anterior descending coronary artery.
d. The left anterior branch is supplied by the left anterior descending coronary artery.
e. The left posterior branch is double-fed by the left anterior descending coronary artery and the posterior descending branch of the right coronary artery.
B. Elderly patients with acute myocardial infarction complicated with indoor bundle branch block often accompanied by severe left ventricular failure and/or cardiogenic shock, acute anterior wall infarction and acute inferior wall infarction can be combined with right bundle branch block, isolated right Bundle branch block with left anterior branch block rarely develops into complete atrioventricular block; right ventricular branch block with left anterior branch block (6% to 7.1%), 33% of which 43% can develop complete atrioventricular block; right bundle branch block with left posterior branch block is rare (0.2% to 2.6%), because the left posterior branch is thick and there are multiple blood vessels, only found in extensive infarction And in-depth interventricular septal involvement of indoor bundles, hospital mortality rate of up to 33% to 86%, incomplete or complete indoor three-branch block should be installed as soon as possible, even if the indoor conduction block disappears during the recovery period, but after infarction There is still the risk of sudden death within 3 weeks to 12 months. Sudden death may be secondary to an acute episode of internal three-branch block. Therefore, all patients with temporary indoor three-branch block should be treated with permanent pacing.
(2) Diagnosis and treatment of acute myocardial infarction with pump failure: pump failure includes acute left heart failure and cardiogenic shock, most patients with pump failure have a large infarct range (25% to 40%), and more than 40% of necrotic myocardium It is prone to cardiogenic shock, and its hemodynamic characteristics are: myocardial contractility is significantly reduced, wall compliance is poor (no infarction or contradictive expansion), resulting in a sharp decline in cardiac output, increased left ventricular end-diastolic pressure, Lead to pulmonary congestion and or pulmonary edema; on the other hand, the sharp decrease in myocardial contractility causes cardiac output, arterial blood pressure drop and insufficient perfusion of surrounding organs, which can lead to cardiogenic shock, the mechanism of which occurs:
1 cardiac dysfunction and ventricular remodeling after AMI in the elderly: mechanical complications of myocardial infarction (such as papillary muscle dysfunction or acute mitral regurgitation caused by rupture, ventricular septum or free wall rupture, pseudo ventricular aneurysm, etc.), Infarct extension, true ventricular aneurysm, and myocardial electromechanical separation can all contribute to or aggravate heart failure. Ventricular remodeling is the main mechanism of chronic cardiac insufficiency after myocardial infarction.
Left ventricular enlargement and cardiac insufficiency after myocardial infarction are one of the important factors affecting the prognosis of patients. The left ventricular end-diastolic volume (LVEDV) 90ml / m2 and LVEDV 111ml / m2 per 1000 patients 1 year of death For 45 and 175 patients, after myocardial infarction, in patients with equivalent left ventricular systolic function, the mortality rate of patients with left ventricular enlargement is higher, usually within the first few weeks after myocardial infarction, left ventricular dilatation and cardiac dysfunction It began to appear. If the treatment is not effective, the above process can be progressively aggravated. During the healing period of myocardial infarction, the necrotic myocardium is gradually replaced by scar tissue without contraction function. The latter is easy to be further elongated and thinned when inflated. In the presence of infarcted area, the incidence of cardiovascular events is significantly increased. In addition to early infarction, myocardial infarction may occur in addition to infarct expansion, followed by progressive enlargement of the left ventricle, the mechanism can not only be formed by myocardial scar tissue and infarcted myocardium Thinning is also related to the changes of myocardial morphology and geometric configuration in the infarct area during ventricular remodeling, and the detailed mechanism of ventricular remodeling after myocardial infarction It remains to be further clarified that current animal data suggest that there are three independent related factors: infarct size, infarct healing process and related myocardial structural changes and increased wall tension. In neurohumoral factors, myocardial local RAS system and catecholamine activity are enhanced. The role of ventricular remodeling is more certain. Clinical use of ACE inhibitors or beta blockers has been shown to be effective in reducing AMI mortality and reducing ventricular remodeling after myocardial infarction.
2 hibernating myocardium and stunned myocardium: another important cause of cardiac dysfunction caused by myocardial ischemia, the two are essentially different, hibernating myocardium is due to the continuous coronary artery stenosis caused by coronary blood flow reduction, resulting in myocardial and Left ventricular function continued to be damaged and the myocardium was suppressed due to transient (15-20 min) reperfusion after coronary occlusion. Although myocardial blood supply in the ischemic area was rapidly restored, myocardial systolic dysfunction still existed for a long time. Delayed myocardial mechanical dysfunction, acute left heart failure and cardiogenic shock are called pump exhaustion, and Killip classifies AMI cardiac pump function according to AMI symptoms and signs:
Grade I has no left heart failure.
Grade II mild to moderate left heart failure (third heart sounds galloping, lung sounds below the level of the two lungs disappeared).
Grade III acute pulmonary edema (pulmonary snoring exceeds two hilar levels).
Grade IV cardiogenic shock with or without acute pulmonary edema.
A. Mild to moderate left failure (Killip II):
Clinical features: chest tightness, shortness of breath, difficulty breathing, high lie position, third heart sound galloping, P2>A2, alternating pulse, normal or slightly lower arterial blood pressure, half of the lungs of the lungs <Xi lung field half, X-ray shows lung Congestion, PCWP is slightly elevated, the primary goal of drug selection is to reduce left ventricular filling pressure (LVFP) and increase cardiac output (CO).
Oral diuretic, reduce the pre-cardiac load; severely give furosemide 20mg / infusion, isosorbide for left ventricular preload increased, that is, LVFP increased significantly and CO2 and arterial blood pressure remained normal, at this time Yamanite is the drug of choice. 10 mg of isosorbide is added to 250 ml of 10% glucose. The instillation is started at a rate of 0.1 g/(kg·min). The growth rate is 5 g/min every 5 to 10 minutes until the hemodynamic index. To improve, add 20 mg of dobutamine to 250 ml of 10% glucose, and intravenously, from 2.0 g / (kg · min), gradually increase to 10 g / (kg · min), the latter can be obvious Increase CO2 and reduce LVFP, increase coronary artery perfusion pressure inferior wall AMI and disable diuretic and dilated vein-based vasodilator in right ventricular infarction, intravenous infusion of sodium nitroprusside (15 ~ 200g / min), infarction more than 24h, Heart failure can not be controlled at the same time with heart enlargement, you can add half-dose fast digitalis, commonly used venomous spines K0.125mg plus 10% glucose solution 20ml intravenously.
B. Acute pulmonary edema (Killip III):
Clinical features: cough, wheezing, cyanosis, sitting breathing, irritability, white or pink foam sputum, pale complexion, cold skin, lung wet voice and wheezing range > half lung field half, X line shows lung field Cloud-like shadows are centered on the hilum, PCWP is increased, cardiac output is low, peripheral vascular resistance is increased, and blood pressure is normal, increasing or decreasing.
Drug selection: morphine 10mg or pethidine 50mg intramuscular injection, but the elderly are used with caution, and those who are unconscious are disabled.
Vein vasodilator: nitroglycerin tablets 0.3mg / time, sublingually every 5 minutes, 6 times in a row; or nitroglycerin (10 ~ 100g / min) intravenous infusion.
Furosemide 40 ~ 60mg / intravenous injection, can quickly reduce the heart preload, reduce pulmonary edema but should avoid excessive diuresis, resulting in a significant reduction in blood volume, blood pressure and heart rate.
Normal or high blood pressure, intravenous infusion of sodium nitroprusside (15 ~ 200g / min), phentolamine (0.1 ~ 2mg / min).
Those with low blood pressure were intravenously infused with sodium nitroprusside (15-200 g/min) plus dopamine [4-10 g/(kg·min)].
Infarction for more than 24 hours, heart failure can not be controlled, with increased heart, can give half a rapid digitalis preparation.
C. Cardiogenic shock with or without acute pulmonary edema (Killip IV):
Clinical features: systolic blood pressure <10.7kPa, accompanied by insufficient perfusion of surrounding tissue, manifested as small pulse pressure, weak pulse, cold skin, sweating, apathy or irritability, urine output <30ml / h, heart index (CI) <2.2 L / (min · m2), may be associated with acute pulmonary edema (PCWP) > 25mmHg) or without acute pulmonary edema.
Drug selection:
Intravenous blood volume: no signs of pulmonary congestion or pulmonary congestion, but PCWP <18mmHg, should be appropriate intravenous rehydration, can be given low molecular dextran 50 ~ 100ml / 5min, while monitoring heart rate, breathing, blood pressure and lung snoring, if Heart rate, rapid breathing, and improved blood pressure, lung congestion, weight should be stopped, if the above situation, continue to replenish 50 ~ 100ml / 10min, when hemodynamic monitoring conditions, should make PCWP 18mmHg After the shock is improved, the glucose solution can be intravenously dripped during the maintenance phase.
Vasoactive drug application: low-dose and low-resistance patients, intravenous dopamine 4 ~ 10g / (kg · min), or dobutamine 5 ~ 15g / (kg · min), when the blood pressure is still very low, add hydroxylamine , but should not be used too much, blood pressure should be removed as soon as possible after withdrawal, low-ranking and high-resistance patients, sodium nitroprusside 15 ~ 100g / min and dopamine or dobutamine combined intravenous infusion (dose as before), blood pressure is still very When low, add intra-aortic balloon pump counterpulsation.
Others: Correct acidosis can give 5% sodium bicarbonate (should be based on blood gas analysis results); can also give dexamethasone 10 ~ 20mg / d or hydrocortisone 100 ~ 300mg / d intravenous infusion, the drug generally does not exceed 72h, After the condition is improved, it will be stopped 12 to 24 hours later.
(3) Infarct extension: Infarct extension refers to the expansion of myocardial infarction in the original infarct-related coronary blood supply site within 4 days after infarction (more than 24-72 hours), and new myocardial necrosis occurs. A new necrotic lesion was seen around the infarcted area that was healing, or a new necrotic lesion was present in the adjacent subepicardum.
1 Mechanism: The occurrence and development of infarct expansion mainly determines the severity of ischemic myocardium around the infarction, which is related to the degree of infarction-related coronary artery opening.
A. Early thrombolytic therapy in AMI: TIMI class III opener, the incidence of infarct expansion and reinfarction is small; TIMIII-level partial openers, due to infarction-related coronary wall residual thrombus and residual severe stenosis is caused by thrombosis The basis of the formation can cause the anterior blood flow of the infarct-related coronary artery to be occluded again.
B. AMI emergency PTCA: procoagulant factor can lead to local blood thrombosis after AS plaque secondary to PTCA, resulting in acute reocclusion.
C. There are multiple coronary artery lesions in patients with subendocardial myocardial infarction, accompanied by incomplete thrombosis (platelet thrombosis) occlusion, on the basis of any reduction of oxygen supply factors (coronary spasm, thrombosis, etc.) Infarction expansion can occur with increasing oxygen consumption factors (exercise, eating, anxiety, emotional agitation, etc.).
Establishment of collateral circulation in the infarcted area: if the infarct-related coronary artery is occluded or sub-occlusive, and another coronary artery that is unrelated to the infarct-related vessel is supplied to the infarct-related area via the collateral circulation, The myocardial ischemia around the original infarction is relieved. For example, the coronary artery that provides collateral blood flow is a multi-vessel disease. When the latter has severe stenosis, the infarct expansion can occur due to sudden decrease of blood flow through the collateral circulation.
2 clinical features:
A. Risk factors for infarct size expansion include: incomplete infarction, non-Q-wave infarction, hypotension or cardiogenic shock, cardiac insufficiency, prolonged chest pain, obesity, and women.
B. Post-infarction angina pectoris: angina pectoris recurring after complete relief of AMI pain, long-lasting pain, and repeated episodes, often complicated by arrhythmia, cardiac insufficiency or cardiogenic shock.
C. ECG characteristics: new infarct waves appear in the corresponding leads of the original infarct area, such as pathological Q wave or (and) ST-T changes, and the original infarct wave, such as pathological area necrotic myocardium, expands the defect range, with corresponding Local wall activity is reduced.
D. Myocardial contrast-enhanced ultrasonography (ECT): Ultrasound myocardial imaging: showing an enlarged range of filling defects in the infarcted necrotic myocardium with reduced local wall activity.
E. Myocardial zymogram: The second peak appeared in CK-MB.
F. Radionuclide (ECT): with UCG myocardial contrast.
3 prevention and treatment: prevention of infarction expansion is to prevent early re-infarction of AMI, A. AMI early thrombolytic therapy: as soon as possible, as soon as possible intravenous application of SK or UK 1.5 million to 2 million U, followed by adequate heparin anticoagulant therapy for 3 to 5 days And long-term application of antiplatelet drugs (aspirin or kelly), the best combination of thrombolytics, anticoagulants and antiplatelet drugs, is conducive to the full and continuous recanalization of infarcted blood vessels, B. successful rehydration of thrombolysis If there is recurrent myocardial ischemia or reinfarction within 4 weeks after thrombolysis, delay PTCA; C. thrombolytic therapy failure, with persistent chest pain and myocardial ischemia, should immediately make salvage PTCA, infarct vessels Open, D. If high-risk large-area infarction within 6 hours of AMI episode, thrombolysis contraindication, or AMI with cardiogenic shock or pump failure, emergency PTCA should be preferred, E. Anti-ischemic drug therapy: Body blockers, nitrates, ACE inhibitors and early administration of calcium antagonists, especially those who do not have Q-wave infarction, give Felizide (Ferxin), F. Give anti-platelet agglutination drug aspirin, G. Correct various susceptibility factors .
(4) Infarct expansion (IE): Inferior myocardial persistence disproportionate thinning and dilatation in the early infarct zone, endocardial and epicardial plane arc elongation, but not associated with necrotic myocardium The increase of the number of myocardium can be seen by microscopic examination. Microscopic examination shows that myocardial cells stretch and the cardiomyocytes slide and realign each other. The wall of the infarcted area swells as early as several hours to several days after the onset of large-area transmural Infarction area swells 24 hours after the onset of symptoms in patients with myocardial infarction, usually reaching the maximum 7 to 14 days after onset. In severe cases, the wall thickness is reduced to 1/2 to 1 of the normal wall after several days after onset. 3, in the repair period of myocardial infarction can still be progressively aggravated, due to the thinning of the segmental wall, resulting in increased left ventricular volume and wall stress, increased myocardial oxygen consumption and cardiac dysfunction, infarct wall dilation into the wall Tumor formation, adherent thrombus and perforation of the heart provide conditions for pump failure, arrhythmia, and increased complications of systemic embolism.
1 affect IE factors:
A. Transmural myocardial infarction IE occurs almost exclusively in transmural infarction. The degree of IE is inversely proportional to the thickness of the myocardium in the infarcted area. Non-transmural myocardial infarction rarely occurs.
B. Infarct size: In general, the greater the infarct size, the higher the incidence of wall swelling and the greater the degree.
C. Infarction site: The incidence of wall swelling of the anterior wall apex and anterior wall infarction is higher than other parts, which may be related to the heavier load in this part.
D. Intraventricular pressure: excessive load on the left ventricle before and after, causing excessive systolic or diastolic pressure in the chamber to form an important cause of wall swelling. Therefore, hypertension, sympathetic excitation, inappropriate application of positive inotropic drugs, capacity Excessive load is a disadvantage.
E. Drug effects: Glucocorticoids and non-steroidal anti-inflammatory drugs (indomethacin, ibuprofen) affect the healing of infarct scars, which can increase the incidence of wall swelling.
F. Early reperfusion: can save the subepicardial myocardium, thus preventing the wall from expanding.
Diagnosis of 2IE: Two-dimensional echocardiographic tomography can show the wall motion and wall thickness of each segment of the heart, and can dynamically observe the size of the infarct, wall thickness, and inner diameter of the heart chamber. And can be used to evaluate the effects of interventions, chest X-ray and radionuclide ventriculography also contribute to the diagnosis of wall expansion.
Prevention of 3IE:
A. Avoid the use of large amounts of hormones and non-steroidal anti-inflammatory drugs.
B. Reduce the load before and after the heart, according to the patient's condition: nitrates, captopril, intra-aortic balloon pump counterpulsation and other measures.
C. Minimize the use of positive inotropic drugs and boosting drugs.
D. Avoid getting out of bed early, exercise training and exercise tolerance test.
E. Proper use of negative inotropic drugs.
F. Early reperfusion such as early thrombolysis for percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass grafting (CABG), it is reported that reperfusion is restored within a few hours after onset to prevent IE.
Complication
Elderly patients with myocardial infarction complications Complications, elderly patients with acute left heart failure, cardiogenic shock, heart failure
Complications of acute myocardial infarction in the elderly increase with age. Common complications include severe arrhythmia, acute left heart failure, cardiogenic shock, ventricular aneurysm, and even heart rupture.
Symptom
Symptoms of myocardial infarction in the elderly Common symptoms Chest tightness Chest pain Breathing difficulty Arrhythmia Shock Irritability Uneasy heart cramps Dizziness and dizziness
1. Infarction aura
AMI 15% ~ 65% have pioneering symptoms, all over 40 years old, should be suspected and AMI in the following cases, timely treatment according to infarction, and dynamic observation of ECG and enzymology changes.
(1) The first episode of angina pectoris lasts for 15 to 30 minutes or longer, and the effect of nitroglycerin is poor.
(2) chest pain with nausea, vomiting, sweating, dizziness, palpitations.
(3) Sudden increase or sudden drop in blood pressure, or accompanied by arrhythmia or left ventricular dysfunction.
(4) It was originally a stable type of angina pectoris, and the number of recent pains, duration and pain were significantly aggravated.
(5) Pain with ST segment is obviously elevated or depressed, T wave coronal inverted or high tip.
2, symptoms
(1) Typical symptoms:
1 The typical pain is sternal crushing, suffocation, sudden death, duration can be up to 1 ~ 2h, or even more than 10 hours, nitroglycerin is not relieved.
2 systemic symptoms of fever more than 2 to 3 days after onset, usually around 38 ° C, rarely more than 39 ° C, lasting about 1 week.
3 frequent symptoms of gastrointestinal symptoms, frequent nausea, vomiting, upper abdominal pain; 1 week after remission, often loss of appetite, abdominal distension, individual hiccups.
4 severe cases may have complications such as arrhythmia, heart failure, cardiogenic shock.
(2) atypical symptoms: refers to clinical atypical pain, or painless and other systemic symptoms as the main manifestations, more common in the elderly or oral beta blockers.
1 The main manifestations of acute left heart failure are sudden chest tightness, difficulty breathing, and even sitting breathing, cardiogenic asthma attacks.
2 cerebral blood circulation disorders as the main manifestations such as dizziness, fainting, sudden loss of consciousness, even hemiplegia, convulsions.
3 The main manifestations of shock are older, sudden hypotension or shock, or sudden decrease in the original hypertension, but no other reasons should consider the possibility of AMI, manifested as slow response, dark complexion, head and neck Department and limbs sweating, skin cold and cold, no urine, mainly caused by myocardial infarction on the basis of myocardial infarction, resulting in decreased heart function.
4 or more abdominal pain is the main manifestation of upper abdominal pain, nausea, vomiting, esophageal burning, hiccups, etc., often misdiagnosed as esophagitis, gastritis, cholecystitis, pancreatitis.
5 with sore throat, toothache, numbness and acid in the left upper limb and back.
6 death: sudden death as the main manifestation of acute myocardial infarction is not uncommon, the direct cause of sudden death is ventricular fibrillation and cardiac arrest, the age of sudden death is more than 55 to 65 years old, with the incidence of sudden death, but the mortality rate increases obvious.
7 Others: 13.1% of patients with acute mental disorder after myocardial infarction, manifested as acute cerebral hypoxia such as agitation and irritability; limb arterial infarction accounted for 1.4%, manifested as intermittent claudication, limb ischemic gangrene; Extreme fatigue, dizziness and fatigue; some manifested as the only symptom of arrhythmia.
(3) completely asymptomatic: no symptoms, only electrocardiogram found suspicious myocardial infarction pattern, no myocardial enzymology changes, can be confirmed by ECG vector, more common in focal or old myocardial infarction.
3, signs
(1) Typical signs:
;4/5
AMI
A.
B.
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E.AMIS3S4
F.23
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2
50
Examine
12
1(CPK)
1312h1224h34
2CPK3CPK-BBCPK-MBCPK-MMCPK6
3CPK-MBCPK-MBCPK-MBCPK5%24hCPK-MBAMICPK-MBCPK-MBCPL-MB
2(AST/GOT)
1612h2448h36
2AST/GOTAST
3AST/ALT>1
3(LDH)
1810h2312
2LDH5LDH1,LDH2LDH3LDH4LDH5LDH2>LDH1>LDH3>LDH4>LDH5LDH1LDH1LDH2AMILDH1AMILDH
4-(HBDH) 1224h23714
5(MB) AMI23h612h24hAMI
6
1AMI(CA);;3(FAA)
271030100
3AMITI(CTnTCTnI)(28)CTnI(1224h)(510);CTnT(1296)h514CTnTCTnICK-MBAMI
7
112(1020)×109/L0.750.90/L
1/520×1010/L
2(ESR)23
8
1
10
A.RVAT0.045sQRS0.12sR
B.STST5mm2mm1015mm
CTTAMI
QRS-TQSTT;T
STT
2AMI
aVF 33QQ0.04saVFQ29%36%Q12%15%2aVFQ24%29%Q20%27%aVFQ0%8%aVFQRSW<+30°QRST-T
Rv1=0.04s75%Rv2=0.04s100%;V1R/S>160%V2R/S100%V1V2RV7V9QST-T
()V1V3rQSV4V6qV4V6qST-T
V4V5Q>3mmVT-T(Q)Rv4-5
Rv1-v3(Rv32Rv2-v3<2mmRv2V3(Rv2)1Rr12V1V3
(LAH)
A.aVFrSr<0.1mVr>raVF>rQSLAH
B.aVFrSrqrsrsrts()LAH
C.LAHaVR
D.QRS;LAH2040ms;LAH
JST-T
A.JSTTJSTT;JSTTUU
B.
C.JaVFV5V6
aVLV1V4
LBBBAMI
A.QRSST-T67%
B.STQRS>2mm>7mm54%(76%)
C.QaVFaVLV631%
D.Rv1Qv620%100%
E.CabreraV3V4S0.05s27%
F.ChapmanaVLV6R0.05sLBBBAMI
A.1943Dresslerqq(qRqRsqRRQRSQR)
B.LichtenbengV1QRQ0.04sQ/R=0.2024%87%aVFQ0.04sQ/R>0.1016%98%
C.SchamrothAMI
a.QRS
b.aVR
c.ST-S
3
A.;B.;C.;D.;E.ST-T;F.();G.;H.
QST-TSTT;TQQ
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9
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12h;
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B.
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A.
B.
C.
2Q
10
11T2T2;
12;
13
199mTc-
99mTc
5
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1
2
3
4
2
AMI12h4872h6714299mTc-
;;10%A.99mTc-;B.;C.;D.;E.;F.;G.;H.;I.3g
2201Ti
99mTc-MIBI
3
(short axis slices);;(;()1
(horizontal long axis slices)
(vertical long axis slices)()69mm
Diagnosis
1
2CTMRI
3S Q TSaVFQP
4STQ
5
6
