Features
Features:

Product Tour >

Edraw AI >

Paid Plans:

Individuals >

Business >

Eduaction >
Resources
Blog

History

How-tos & Tips

Discovery

Biography

Business Analysis

Examples

AI concept Map

Free AI Mind Map Generator

Onenote Mind Map

Bcg Matrix Examples

Nike Marketing Strategy

Unilever SWOT Analysis

Make Mind Maps in Google Docs

Guide

FAQs

What's New

Resource Center
Templates
All Templates

Brain Storming Templates

Strategy and Planning Templates

Project Management Templates

Product Management Templates

Human Resources Templates

Agile Workflow Templates

Marketing Templates

Education Templates

Fun and Games Templates

User Gallery
Download
Pricing
Enterprise

MindMap Gallery coronary atherosclerotic heart disease

coronary atherosclerotic heart disease

This is a mind map about coronary atherosclerotic heart disease, including mechanism and anatomy, Overview, angina pectoris, acute coronary syndrome, etc.

Edited at 2024-04-05 15:30:18

PlotWizard

Recent works View more works>>

coronary atherosclerotic heart disease

PlotWizard

Recent works View more works>>

Recommended to you
Outline

Coronary atherosclerosis

Mechanisms and Anatomy

mechanism

atherosclerosis

→Lipid penetration

Cholesterol, total cholesterol↑→LDL↑ (the particles are small and can directly penetrate the intima)

→Penetrate the intima

→phagocytosis by macrophages

→Foam cell formation

→Plasma components deposit in endothelium

Endothelial cell damage (such as smoking)

→Platelet aggregation

→Monocyte phagocytosis

→Foam formation

→Athheromatous plaque formation

→Fibrous cap formation (stabilizing plaque)

Stable type: fiber cap is not easy to break Unstable type:......................easy to break

Anatomy

①The blood supply to the heart comes from the coronary arteries

②Left coronary artery: supplies the left atrium, left ventricular anterior wall, lateral wall, and anterior 2/3 of the interventricular septum Right coronary artery: right atrium, right ventricle, posterior wall of left ventricle

③Coronary artery origin: aortic root

subtopic

Overview

Definition: Coronary atherosclerosis narrows or blocks the lumen of blood vessels, leading to heart disease caused by myocardial ischemia, hypoxia or necrosis, referred to as coronary heart disease.

Cause

Age and gender: ① People over 40 years old ② More men than women ③ The incidence rate increases in women after menopause (related to estrogen)

Dyslipidemia

The most important risk factors for abnormal lipid metabolism

↑: Total cholesterol TC, triglyceride TC, low-density lipoprotein LDL, Very low density lipoprotein VLDL, apolipoprotein B, apolipoprotein(a)

↓：High-density lipoprotein HLD, apolipoprotein A

hypertension

smoking

Smoking is not drinking

Diabetes and impaired glucose tolerance

Insulin deficiency → glycogen synthesis ↓ → fat synthesis ↑

Other risk factors: ① Obesity ② Family history ③ Type A personality ④ Oral contraceptive pills ⑤ Bad eating habits ⑥ Less physical activity ⑦ Stressful mental activity

Clinical classification

1970WHO

Silent type (silent coronary heart disease), angina pectoris, myocardial infarction, ischemic cardiomyopathy, sudden death

Classification in recent years

chronic ischemic syndrome

stable angina pectoris

Stable type: Rest and nitroglycerin can relieve Unstable type: ........................................cannot be alleviated

latent coronary heart disease

ischemic cardiomyopathy

acute coronary syndrome

unstable angina

Non-ST segment elevation myocardial infarction

ST segment elevation myocardial infarction

sudden death from coronary heart disease

Angina pectoris

mechanism

Demand↑

←Myocardial Oxygen Consumption↑

←HR↑

←cardioconstriction↑

Supply↓

←Coronary blood supply↑

← narrow

← Cramps

Pathogenesis

coronary artery sclerosis

→Athheromatous plaque formation

→lumen stenosis

→Myocardial ischemia and hypoxia

Tiredness, emotional excitement, full meal, cold stimulation

→心肌耗氧↑ 心脏负荷↑

→心肌需血量↑

→Metabolites ↑ (lactic acid, etc.)

→The cardiac autonomic nerves are stimulated (Sympathetic ganglia 1-5)

→Chest pain

clinical manifestations

Symptoms (episodes of chest pain)

Location: The middle and upper part of the sternum, which can involve the precordium, radiate to the left shoulder, the inner side of the left arm to the little finger, or to the submandibular, pharyngeal or mandibular area.

Properties: squeezing pain, accompanied by a sense of dying, not like acupuncture or knife-like pain

Triggers: emotional excitement, physical labor, heavy meals, cold, smoking, shock, tachycardia, etc.

Tachycardia: tachyarrhythmia: CO↓→coronary blood volume↓

Duration: mostly 3-5min

Relief methods: ① Rest ② Nitroglycerin sublingually

physical signs

Expression of anxiety, cold sweats, increased heart rate, and elevated blood pressure

Transient apical systolic murmur (caused by papillary muscle ischemia and dysfunction leading to mitral valve insufficiency)

Auxiliary inspection

laboratory tests

Electrocardiogram (most commonly used)

During attack, subendocardial ischemia → ST segment depression (≥0.1mV)

Coronary angiography (gold standard)

Diagnostic points

Angina Severity Grading

Level I: Not caused by general activities

Level II: restricted after meals, emotional excitement, 200m or above one floor

Level III: Angina pectoris may occur within 1km on level ground or going up a floor.

Level IV: slight activity or even rest until attack

Treatment points

During attack

rest

Rest immediately. Symptoms usually disappear after rest.

Drug therapy (nitrate preparations)

effect

Dilation of coronary arteries→↑coronary blood volume

Dilate peripheral blood vessels→cardiac load↓ →Myocardial oxygen consumption↓

drug

Nitroglycerin

① Sublingual administration: It takes effect in 1-2 minutes and disappears after 30 minutes. ②Reuse every 5 minutes ③Do not take it more than three times in a row. If it does not take effect, report it to your doctor.

Adverse reactions: flushing, head swelling, hypotension, (Be careful to prevent orthostatic hypotension when taking the first dose bucally)

Isosorbide Nitrate

Take sublingual administration for 2-5 minutes to take effect and last for 2-3 hours

remission period

medical treatement

Improve myocardial ischemia and reduce symptoms

B receptor antagonist

①Slow down the heart rate, weaken myocardial contractility, lower blood pressure. Reduce angina pectoris attacks. Long-term use reduces the risk of death and myocardial infarction in patients with angina pectoris

②Metoprolol, Bisoprolol

③Contraindications: bradycardia, atrioventricular block, asthma, copd

calcium channel blockers

①Dilate coronary arteries

②Nifedipine

Nitrate preparations

Isopear Camellia Nitrate

Prevent myocardial infarction and improve prognosis

cyclooxygenase inhibitor

Mechanism: Anti-platelet aggregation

drug

Irreversible COX inhibitor: aspirin

The cornerstone of antiplatelet

Reversible........................: Indoleacetic acid

Adverse reactions: gastrointestinal reactions (taken after meals)

P2Y12 receptor antagonist

Those with contraindications to stent implantation and aspirin

Drug: Clopidogrel

Adjust blood lipids

Statins: Simvastatin

Reduce TC and LDL Stabilize plaque and delay plaque progression,

ACEI/ARB

Patients with diabetes and heart failure

ACEI: Captopril

coronary revascularization therapy

Percutaneous coronary intervention PCI

coronary artery bypass graftingCABG

Nursing diagnosis

Pain: chest pain related to myocardial ischemia and hypoxia

rest

Rest in place immediately

subtopic

psychological care

pain observation

Medication care

Nitroglycerin

① Take it sublingually (the effect is better after chewing it), Keep some saliva under the tongue to facilitate drug absorption

②It can be reused after 3-5 minutes. Lie down after taking the medicine to prevent hypotension

③Intravenous drip: control the number of drops to prevent hypotension

④Adverse reactions: flushing, head swelling, dizziness, tachycardia

④Contraindications: hypotension, glaucoma

Glaucoma: intraocular pressure ↑ Nitroglycerin: blood dilation → intraocular pressure ↑↑↑

Activity intolerance is related to the imbalance of myocardial oxygen supply

Assess the level of activity restrictions

Develop activity plan

Patients in remission do not need bed rest

Observe and deal with adverse reactions during activities

Lack of knowledge: Lack of knowledge to correct risk factors, control predisposing factors, and prevent angina attacks

health guidance

Disease knowledge guidance

① Reasonable diet: consume a low-calorie, low-fat, low-cholesterol, and low-salt diet; Eat more fruits, vegetables, and crude fiber foods; to prevent constipation, eat small meals frequently

② Quit smoking and drinking

③Moderate exercise

④Psychological balance

Avoid trigger foods

①Avoid overwork, emotional agitation, heavy meals, and straining to defecate Cold stimulation, etc.

②Keep warm, do not take baths that are too cold or too hot, do not take baths when you are full or hungry, and the time should not be too long.

Disease monitoring

Regularly review electrocardiogram, blood pressure, blood sugar, blood lipids, and liver function

Medication guidance

Carry nitroglycerin with you. It will decompose easily when exposed to light and moisture. Keep it in a brown bottle. Replace the medicine every 6 months after opening

acute coronary syndrome

Pathological basis: unstable plaque rupture

Unstable angina pectoris UAP Non-ST segment elevation myocardial infarction

Clinical manifestations and characteristics

① Prolonged (>20min) resting angina

②New onset (1 month) angina pectoris, manifested as: spontaneous angina pectoris/exertional angina pectoris

③The symptoms of stable angina pectoris in the past have worsened in the past month, as long as CCS grade III (malignant angina pectoris)

④ Angina pectoris occurring within one month after myocardial infarction

Treatment points

General processing

relief the pain

Nitroglycerin, B-receptor antagonists, non-dihydropyridine calcium channel antagonists

antithrombotic therapy

① Once diagnosed: take clopidogrel and aspirin immediately at least 12 months

②Anticoagulation therapy: heparin

coronary revascularization therapy

Acute ST-segment elevation myocardial infarction STEMI

concept

Acute myocardial ischemic necrosis is a sharp reduction in coronary blood supply based on coronary artery disease. or interruption, resulting in severe and prolonged acute ischemia of the corresponding myocardium leading to myocardial cell death.

Severe types of ACS: arrhythmia, shock, heart failure

Cause and pathogenesis

Basic cause: coronary atherosclerosis; acute myocardial ischemia for more than 20-30 minutes

Causes of atheromatous plaque rupture, bleeding and thrombosis

1. Waking up at 6 o'clock in the morning means that the sympathetic nerves are excited at 12 o'clock, and the body's stress response is enhanced. Myocardial contractility, heart rate, and blood pressure increase, and coronary artery tension increases

2. After a heavy meal, especially a large amount of high-fat diet, blood lipids and blood viscosity will increase.

3. Heavy physical activity, excessive emotion, cold stimulation, and sharp increase in blood pressure Or when straining to defecate, the load on the left heart increases and myocardial oxygen consumption increases.

4. Shock, dehydration, bleeding, surgery or severe arrhythmia, A sharp decrease in cardiac output and coronary perfusion

clinical manifestations

aura

symptom

Chest pain (earliest and most prominent)

①The location and nature of the pain are similar to those of angina pectoris, but more severe

② Accompanied by a big man, irritable and restless, lasting for several hours or days

No relief with rest and nitroglycerin

systemic symptoms

Fever: up to 38° (absorbed heat), lasting for one week

gastrointestinal reactions

Nausea, vomiting, upper abdominal distension and pain

vagus nerve excitement

Arrhythmia

1. The onset of illness occurs within 1-2 days, and is most common within 24 hours.

2. Ventricular arrhythmias are the most common, especially premature ventricular arrhythmias

3. Ventricular fibrillation is the main cause of death before admission

4. Inferior wall myocardial infarction: atrioventricular block Anterior wall............: ventricular arrhythmias

Hypotension and shock

1. Cardiogenic shock: irritability, pale complexion, clammy skin, oliguria...

2. Cause: Extensive myocardial necrosis and sudden decrease in cardiac output

heart failure

Acute left heart failure is the most common

The contraction force of the heart is significant ↓↓↓/uncoordinated

Heart failure caused by acute myocardial infarction according to Killip classification

physical signs

Some patients may hear systolic murmurs or clicks in the precordial area: caused by dysfunction or rupture of the mitral valve papillary muscles.

complication

Papillary muscle dysfunction or rupture

Mitral valve papillary muscle ischemia and necrosis impede contractile function Causes mitral valve prolapse and insufficiency

ruptured heart

Seen within 1 week of onset, mostly due to ventricular free wall rupture

embolism

Left ventricular mural thrombus detachment

arterial embolism, venous embolism

ventricular aneurysm

Abnormal pulsation and continued elevation of the st segment

post-myocardial infarction syndrome

Appears in STEMI weeks to months

Manifestations: pericarditis (pericardial rub), fever and chest pain

Possibly an allergic reaction of the body to necrotic substances

Auxiliary inspection

electrocardiogram

characteristic changes

ST segment arched upward

R wave weakens

With or without: pathological Q wave

dynamic change

Hyperacute phase: T wave peaks

Acute stage: ST segment is significantly elevated, pathological Q wave and R wave are weakened

Subacute phase: T wave returns to baseline

Chronic phase: caused by T waves

Positioning diagnosis

V1-V3: Anteroseptal wall

V3-V6: limited to the front wall

V1-V6 wide front wall

anterior descending branch

V7-V8: Right back wall

left circumflex artery, right coronary artery

II, III, aVF: inferior wall

Right coronary artery, left circumflex artery

I. aVL: high side wall

Left anterior descending artery, left circumflex artery

laboratory tests

1. White blood cells and granulocytes↑

2. Serum myocardial necrosis markers

Troponin I (cTnI), troponin T (CTnT) (preferred): the most specific and sensitive indicators

Creatine kinase isoenzyme

Myoglobin: earliest appearance, low specificity

3. Creatine kinase, aspartate aminotransferase, lactate dehydrogenase: low specificity

Treatment points

General treatment

Absolute bed rest; oxygen therapy (4-10L/min); monitor ECG, blood pressure, and respiration, and put the defibrillator in a ready state

relief the pain

Morphine, pethidine

reperfusion myocardium

Emergency PCI

Acute ST-segment elevation myocardial infarction within 12 hours

Thrombolytic therapy

Overview

Start immediately (within 30 minutes after receiving the consultation)

PCI is preferred for those aged ≥75 years, and thrombolysis should be chosen with caution

Thrombolytic drugs: urokinase UK, streptokinase SK, recombinant tissue plasmin activator rt-PA

Absolute contraindications

①Severe trauma/surgery/head injury, gastrointestinal bleeding within 1 month

②Bleeding disorders of known cause

③Ischemic stroke occurring within 6 months

④Aortic dissection is clear, highly suspected or cannot be ruled out

⑤Receive non-compressive puncture (liver biopsy, lumbar puncture) within 24 hours

Relative contraindications

①Transient ischemic attack within 6 months

② Pregnancy or 1 week after delivery

③Severe uncontrolled hypertension

④Advanced liver disease, infective endocarditis, peptic ulcer

⑤Prolonged/Invasive Resuscitation

Criteria for successful thrombolysis

1. Chest pain relieves or disappears

2. The ST segment of the electrocardiogram drops by >50%.

Reperfusion arrhythmia (sinus bradycardia, sinus tachyarrhythmia) occurs within 3.2 hours Accelerated ventricular spontaneous heart rate, atrioventricular block, or sudden change or disappearance of conduction obstruction)

4. The peak value of cTnT is advanced to within 12 hours after onset.

Or directly indicate whether the coronary arteries are recanalized based on coronary angiography

antithrombotic therapy

Antiplatelet therapy: aspirin, clopidogrel

Anticoagulant therapy: heparin

Eliminate cardiac arrhythmias

Ventricular premature, ventricular tachycardia: lidocaine; recurrent attacks: amiodarone

Ventricular fibrillation/sustained multiple ventricular tachycardia: defibrillation

Bradyarrhythmia: Atropine

Second/third degree atrioventricular block: pacemaker

Supraventricular tachyarrhythmias: synchronized direct current cardioversion

Control hypotension and shock

Balloon counterpulsation

Treat heart failure

acute left heart failure

Morphine, diuretics...

Digitalis should not be used within 24 hours

Other treatments

B-receptor antagonists, calcium channel blockers, ACEI

polarizing solution therapy

Promote the entry of potassium ions into heart cells, ↓ the possibility of arrhythmia.

Nursing diagnosis

Pain: chest pain

Oxygen therapy, dietary care, drugs

rest

Absolute bed rest within 12 hours, restricted visits

Activities in bed within 24 hours

Day Three: Bedside Activities

Day 4: Increase activity

Days 5-7: Indoor walking

Early activity to prevent thrombosis

Inability to move

Monitoring during activities

Indications to avoid/stop exercise: Exercise is HR↑≥20 times per minute Diastolic blood pressure ≥110mmHg

Risk of constipation

Assess bowel movements

Instruct patients on defecation measures

①Eat more fiber-rich foods

② Give 20ml of honey and drink it with warm water every morning (for those without diabetes)

③Appropriate abdominal massage (clockwise)

④Laxatives (no diarrhea)

⑤Avoid straining to defecate

⑥Bed rail toilet

⑦Low-pressure saline enema

Potential complications: arrhythmia, shock, acute left heart failure, sudden death

fear

ABCDE principles for secondary prevention of coronary heart disease