MindMap Gallery acute coronary syndrome (ACS)
ACS is a group of clinical syndromes based on the rupture or invasion of coronary atherosclerotic plaques, followed by complete or incomplete occlusive thrombosis.
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Dive into the world of the Chinese animated film Nezha 2: The Devil's Birth! This knowledge map, created with EdrawMind, provides a detailed analysis of main characters, symbolic elements, and their cultural significance, offering deep insights into the film's storytelling and design.
This is a mindmap about Nezha 2, exploring its political metaphors and cultural references. The diagram highlights the symbolism behind the Dragon Clan’s suppression, drawing parallels to modern geopolitical conflicts and propaganda manipulation. It also details Chinese historical and cultural elements embedded in the film, such as the Jade Void Palace, Ao Bing’s armor, Taiyi Zhenren’s magic weapon, and Nezha’s hairstyle.
This is a mindmap about the main characters of Nezha 2, detailing their backgrounds, conflicts, and symbolic meanings. It explores the personal struggles and transformations of Nezha, Ao Bing, Shen Gongbao, and Li Jing as they navigate themes of rebellion, duty, ambition, and sacrifice.
acute coronary syndrome (ACS)
concept
caused by acute myocardial ischemia Rupture of unstable atherosclerotic plaques, leading to acute intracoronary thrombosis
Unstable angina pectoris (UAP)
Non-ST segment elevation myocardial infarction (NSTEMI)
Non-ST segment elevation acute coronary syndrome (NSTE-ACS)
ST-segment elevation myocardial infarction (STEMI)
UAP/NSTEMI (NSTE-ACS)
The difference between the two: whether myocardial necrosis markers can be detected
Troponin (cTn) is the most sensitive and specific biomarker of myocardial injury in NSTE-ACS
Cause: Rupture of unstable atherosclerotic plaque, or platelet aggregation based on erosion, complicated by thrombosis, and worsening of ischemia
UAP with clear predisposing factors: secondary UAP
Increased myocardial oxygen consumption: hyperthyroidism, arrhythmia
Decreased coronary blood flow: hypotension
Decreased oxygen-carrying capacity of blood: anemia, hypoxemia
clinical manifestations
Symptoms: Retrosternal compressing pain
Radiating to the left upper arm, neck, or jaw (intermittent or persistent)
Signs: transient third or fourth heart sound, transient systolic murmur
Laboratory and other tests
electrocardiogram
ST segment depression or transient ST segment elevation, T wave flat or inverted
coronary angiography
Myocardial marker examination
other
echocardiogram
radionuclide inspection
Higher positive detection rate
Treatment points
Potentially serious illnesses that should keep patients under surveillance
General processing
Bed rest, 24-hour ECG monitoring
relieve pain
Nitrate preparations
Continuous intravenous infusion of nitroglycerin
beta receptor antagonist
Esmolol
calcium channel blockers
diltiazem
morphine
antithrombotic therapy
aspirin
cornerstone of antiplatelet therapy
P₂Y₁₂ receptor antagonists
clopidogrel, ticagrelor
anticoagulant drugs
heparin
low molecular weight heparin
coronary revascularization therapy
other
Use statins to stabilize plaques
STEMI
concept
Acute myocardial ischemic necrosis is a sudden reduction or interruption of coronary blood supply based on coronary artery disease, causing severe and lasting acute ischemia of the corresponding myocardium and leading to myocardial cell death.
Persistent severe retrosternal pain, fever, increased white blood cell count and serum myocardial cell necrosis markers, and progressive changes in electrocardiogram
Arrhythmias, shock, heart failure, and severe types of ACS can occur
Cause
Coronary atherosclerosis, vascular lumen stenosis, insufficient blood supply to the myocardium, and insufficient collateral circulation
Blood supply is sharply reduced or interrupted for more than 20-30 minutes
Pathogenesis
Plaque rupture, bleeding, intraluminal thrombosis, and complete occlusion of the vascular lumen
clinical manifestations
omen
Fatigue, chest discomfort, palpitations, shortness of breath, irritability, and angina a few days before the onset of the disease
Angina pectoris attacks are more frequent, more severe, and last longer, and nitroglycerin is less effective
symptom
pain
It is the earliest, usually occurs in the early morning, is more severe than angina pectoris, and feels like dying. It is not relieved by resting and taking nitroglycerin.
systemic symptoms
Pain appears 24-48 hours after onset, with fever, tachycardia, increased white blood cells, and increased erythrocyte sedimentation rate.
The body temperature rises to about 38°C, rarely exceeding 39, and lasts for about a week
gastrointestinal symptoms
Nausea, vomiting, epigastric distension and pain, flatulence, hiccups
Arrhythmia
Occurs within 1-2 days of onset
Ventricular arrhythmias are most common
R on T is often a precursor to ventricular fibrillation and is the main cause of death
hypotension and shock
heart failure
Mainly acute left heart failure
Killip rating
Grade I: No obvious heart failure
Grade II: Left heart failure, pulmonary rales <50% of lung fields
Grade III: Pulmonary rales >50% of the lung fields, acute pulmonary edema may occur
Grade IV: cardiogenic shock
physical signs
Heart dullness may be normal or slightly to moderately enlarged, and the fourth heart sound or third heart sound may be heard galloping.
complication
Papillary muscle dysfunction or rupture
ruptured heart
embolism
ventricular aneurysm
Mainly found in the left ventricle
post-myocardial infarction syndrome
Pericarditis, pleurisy or pneumonia. Fever, chest pain
Laboratory and other tests
Electrocardiogram
characteristic changes
The ST segment is arched and upward, often accompanied by mirror ST segment depression in the corresponding leads.
dynamic change
hyperacute phase changes
acute phase changes
subacute phase changes
Chronic phase changes
Echocardiogram
radionuclide inspection
laboratory tests
Diagnostic points
Clinical history of ischemic chest pain
Dynamic evolution of electrocardiogram
Dynamic changes in serum concentrations of myocardial necrosis markers
Treatment points
Early, rapid and complete opening of infarction-related arteries
General treatment
rest
Oxygen therapy care
monitor
relieve pain
morphine
Nitroglycerin
reperfusion myocardium
Recanalize occluded coronary arteries within 3-6 hours of onset of illness
antithrombotic therapy
Aspirin, P₂Y₁₂ receptor antagonist
Eliminate arrhythmia
ventricular premature, ventricular tachycardia
lidocaine
Ventricular fibrillation, sustained polymorphic ventricular tachycardia
Defibrillation, DC cardioversion
bradyarrhythmia
atropine
Second or third degree atrioventricular block
temporary pacemaker
Supraventricular tachyarrhythmias not controlled by medical therapy
synchronized direct current cardioversion
Control hypotension and shock
Treat heart failure
Mainly acute left heart failure
Mainly morphine (or pethidine) and diuretics
vasodilators
Digitalis should not be used within 24 hours
Other treatments
Beta antagonists, calcium channel blockers, angiotensin-digesting enzyme inhibitors
Nursing measures and basis
Pain: chest pain
rest
Diet care
Oxygen therapy care
Oxygen therapy for hypoxemia
painkillers
Morphine, pethidine, nitrates
Thrombolytic therapy
adverse reactions
Allergic reactions: Chills, fever, rash
Determine whether it is successful
Chest pain relieves or disappears
The elevated ST segment is reduced by 50%
reperfusion arrhythmia
Myocardial marker peaks advance
Decreased activity tolerance
Risk of constipation
potential complications
Arrhythmia, shock, acute left heart failure, sudden death
fear
health guidance
Disease knowledge guidance
ABCDE principles for secondary prevention of coronary heart disease