Wondershare EdrawMind
MindMap Gallery Internal Medicine
- 27
- 1
Internal Medicine
Summary of internal medicine, the physiological functions of the kidney: ①Excretion of metabolites; ②Regulation of water, electrolytes, acid-base balance; ③Maintaining a stable internal environment and endocrine function.
Edited at 2023-12-21 17:35:33
- Aeon SWOT Analysis
Discover how Aeon can navigate the competitive online landscape with a strategic SWOT analysis. This comprehensive overview highlights Aeon’s strengths, such as its strong brand recognition, omnichannel capabilities, and customer loyalty programs, alongside its weaknesses, including digital maturity gaps and cost structure challenges. Opportunities for growth include enhancing e-commerce competitiveness and leveraging data-driven strategies, while threats from online-first players and market dynamics require attention. Explore how Aeon can strengthen its market position through innovation and customer-centric approaches in the ever-evolving retail environment.
- Aeon Market Segmentation, Targeting and Positioning Analysis
Discover how Aeon effectively tailors its offerings to meet the diverse needs of family-oriented consumers through a comprehensive Segmentation, Targeting, and Positioning (STP) analysis. Our approach begins with demographic segmentation, examining family life stages, household sizes, income levels, and parent age bands to identify distinct consumer groups. Geographic segmentation highlights store catchment types and community characteristics, while psychographic segmentation delves into family values and lifestyle orientations. Behavioral segmentation focuses on shopping missions, price sensitivity, and channel preferences. Finally, needs-based segmentation reveals core family needs related to value and budget considerations. Join us as we explore these insights to enhance family shopping experiences at Aeon.
- Nike Market Segmentation, Targeting and Positioning Analysis
Discover the dynamics of sneaker transactions with our Kream Sneaker Consumption Scene Analysis Template. This comprehensive framework aims to visualize the purchasing and consumption journeys of sneakers, identifying key demand drivers and obstacles. It covers user behavior within Kream and external influences, targeting various sneaker categories over specific timeframes and regions. The analysis defines user segments, including collectors, resellers, sneakerheads, casual trend followers, and gift purchasers, each with unique values and KPIs. It outlines the consumption journey from awareness to resale, highlighting critical touchpoints such as search, purchase, inspection, and sharing experiences. Key performance indicators are established to measure engagement and satisfaction throughout the process. Join us in exploring the intricate world of sneaker trading!
Internal Medicine
- Aeon SWOT Analysis
Discover how Aeon can navigate the competitive online landscape with a strategic SWOT analysis. This comprehensive overview highlights Aeon’s strengths, such as its strong brand recognition, omnichannel capabilities, and customer loyalty programs, alongside its weaknesses, including digital maturity gaps and cost structure challenges. Opportunities for growth include enhancing e-commerce competitiveness and leveraging data-driven strategies, while threats from online-first players and market dynamics require attention. Explore how Aeon can strengthen its market position through innovation and customer-centric approaches in the ever-evolving retail environment.
- Aeon Market Segmentation, Targeting and Positioning Analysis
Discover how Aeon effectively tailors its offerings to meet the diverse needs of family-oriented consumers through a comprehensive Segmentation, Targeting, and Positioning (STP) analysis. Our approach begins with demographic segmentation, examining family life stages, household sizes, income levels, and parent age bands to identify distinct consumer groups. Geographic segmentation highlights store catchment types and community characteristics, while psychographic segmentation delves into family values and lifestyle orientations. Behavioral segmentation focuses on shopping missions, price sensitivity, and channel preferences. Finally, needs-based segmentation reveals core family needs related to value and budget considerations. Join us as we explore these insights to enhance family shopping experiences at Aeon.
- Nike Market Segmentation, Targeting and Positioning Analysis
Discover the dynamics of sneaker transactions with our Kream Sneaker Consumption Scene Analysis Template. This comprehensive framework aims to visualize the purchasing and consumption journeys of sneakers, identifying key demand drivers and obstacles. It covers user behavior within Kream and external influences, targeting various sneaker categories over specific timeframes and regions. The analysis defines user segments, including collectors, resellers, sneakerheads, casual trend followers, and gift purchasers, each with unique values and KPIs. It outlines the consumption journey from awareness to resale, highlighting critical touchpoints such as search, purchase, inspection, and sharing experiences. Key performance indicators are established to measure engagement and satisfaction throughout the process. Join us in exploring the intricate world of sneaker trading!
- Recommended to you
- Outline
Internal Medicine
Summary
Physiological functions of the kidneys: ①Excretion of metabolites ②Regulation of water, electrolytes, and acid-base balance ③Maintaining a stable internal environment and endocrine function
Testing for kidney disease
Urine test: the main basis for diagnosing kidney disease
Proteinuria: The daily urine protein amount continues to be >150mg, or the urine protein/creatinine ratio is >200mg/g, which is called proteinuria.
Massive proteinuria: Daily urinary protein exceeds 3.5g/1.73m2 or 50mg/kg
Microalbuminuria: 30-300mg/24hr
Glomerular proteinuria: Mainly due to glomerular filtration membrane abnormalities, and rarely due to changes in glomerular capillary pressure
Selective proteinuria: The negative charge on the filtration membrane is reduced, and medium molecular weight proteins, mainly albumin, appear in the urine.
Non-selective proteinuria: Abnormally enlarged filtration membrane pores or severe damage to the glomerular capillary wall, proteins of various molecular weights containing macromolecular proteins appear in the urine
Renal tubular proteinuria: It is an impairment of the reabsorption of normally filtered protein by the proximal renal tubules, resulting in the excretion of small molecular proteins (such as β2 microglobulin) from the urine. It is seen in tubulointerstitial diseases caused by various causes (such as drugs). , heavy metal poisoning, etc.). The total amount of protein in the urine of such patients generally does not exceed 2g/d.
Overflow proteinuria: an abnormal increase in a certain protein in the blood, which is filtered by the glomerulus but not fully reabsorbed by the renal tubules.
hematuria
Gross hematuria: 1ml blood/1L urine
Microscopic hematuria: more than 3 red blood cells per high-power field in fresh centrifuged urine sediment
Cast urine
Leukocyturia, pyuria, and bacteriuria
Common syndromes of kidney disease
Nephrotic syndrome (three highs and one low)
① Massive proteinuria (>3.5g/d) ② Hypoalbuminemia (<30g/L) ③ Obvious edema and/or hyperlipidemia
.Nephritic syndrome
Syndrome characterized by hematuria, proteinuria, edema, and hypertension
Asymptomatic hematuria and/or proteinuria
acute kidney injury
Within 48 hours due to various reasons: serum Scr≧26.5 μmol/L or 50% higher than the basic value or urine output <0.5 ml/(kg·h), and lasts for more than 6 hours
chronic kidney disease
Kidney damage or GFR<60 ml/(min.1.73m2), lasting ≥3 months
Treatment: removal of inducements, general treatment, treatment targeting the cause and pathogenesis, prevention and treatment of complications, delaying the progression of kidney disease, and renal replacement therapy
acute kidney injuryacute kidney injury
concept
①Increase in SCr by ≥26.5umol/L within 48 hours
②Increase in SCr to ≥1.5 times baseline, which may occur within the prior 7 days
③Urine volume <0.5ml/kg/h for 6 hours
Pathophysiology
Pre-renal AKI (pre-renal)
Low perfusion states
Prolonged renal hypoperfusion will lead to Acute Tubular Necrosis
Hypovolaemia (low blood volume)
Cardiogenic causes
Distributive causes
Intrinsic renal AKI (renal)
Glomerular
Vascular
Interstitial
Selective renal ischaemia
Drugs affecting autoregulation
Post-renal AKI: Bilateral urinary outflow obstruction (bilateral urinary outflow obstruction)
Manifestations
Initiation:not apparent
Maintenance (oliguria stage)(oliguria)
Recovery (diuretic stage): (diuretic)
Treatment
Correct reversible causes
Pre-renal AKI: administer fluid balance; improve cardiac output treat sepsis
Post-renal AKI: relieve the obstruction
Intrinsic AKI: Glomerulonephritis/vasculitis: immunosupressive therapy
Acute interstitial nephritis: glucocorticoids
Correct and maintain normal electrolyte Hyperkalemia
Urgent hemodialysis
Be aware of patients who are at high risk for AKI
Avoid further renal injury
Closely monitor urinary output,creatinine,electroly (closely monitor urine output, creatinine, electrolytes)
chronic nephritis
chronic glomerulonephritis
It is a group of primary glomerular diseases with clinical manifestations of proteinuria, hematuria, hypertension and edema. Clinical characteristics: onset is insidious, the disease is protracted and slowly progresses, and eventually develops into chronic renal failure.
laboratory tests
Urine routine: varying degrees of proteinuria and/or hematuria
Routine blood test: early Hb normal or mildly abnormal
Renal function test: Ccr decreases, Cr increases in the late stage
B-mode ultrasound: Know kidney size
Kidney biopsy: guide treatment and estimate prognosis
Pathology: ① mesangial proliferative nephritis ② mesangial capillary nephritis ③ membranous nephropathy ④ focal segmental glomerulosclerosis ⑤ sclerosing glomerulonephritis
diagnosis
For patients with hematuria, proteinuria, edema, and hypertension, the diagnosis of chronic nephritis can be established after excluding secondary nephritis, hereditary nephritis, and other primary glomerular diseases.
secondary glomerulonephropathy
lupus nephritis
diabetic nephropathy
Hypertensive nephropathy
purpura nephritis
Hepatitis B associated nephritis
latent glomerulonephritis
acute glomerulonephritis
Alport syndrome: more common in adolescents; often has a positive family history; triad: renal damage (hematuria\mild to moderate proteinuria and progressive renal damage), neurological deafness and spherical crystals coexist
chronic pyelonephritis
treat
Purpose: To prevent or delay the progressive deterioration of renal function, improve or alleviate clinical symptoms, and prevent and treat serious complications
Actively control high blood pressure and reduce urinary protein (antihypertensive drugs: ACEI and ARB are preferred)
Limit protein and phosphorus intake in food
Glucocorticoids and cytotoxic drugs
Avoid factors that aggravate kidney damage
chronic renal failure
chronic kidney disease
Kidney structural or functional abnormalities caused by various reasons ≧3 months, including signs of kidney damage (albuminuria, abnormal urine sedimentation, renal tubule-related lesions, abnormal histological examination and abnormal imaging examination) or a history of kidney transplantation, With or without decrease in glomerular filtration rate, or unexplained decrease in GRF (<60ml/min) ≧3 months
Chronic renal failure (CRF)
The progressive development of chronic kidney disease causes irreversible loss of nephron and renal function, resulting in a clinical syndrome characterized by metabolite and toxin retention, water, electrolyte and acid-base balance disorders, and endocrine disorders.
clinical manifestations
Often asymptomatic in the early stage, fatigue, backache, increased nocturia, edema, hypertension, proteinuria, hematuria, uremia in the late stage, and multi-system damage.
Water and electrolyte acid-base disorders
metabolic acidosis
hyperkalemia
Hypokalemia
Water and sodium metabolism disorders
Calcium and phosphorus metabolism disorders
Cardiovascular system: Cardiovascular disease is the most common cause of death in patients with uremia
Hypertension, left ventricular hypertrophy, heart failure
Pericardial effusion, pericarditis
Coronary atherosclerosis
Various cardiac arrhythmias
respiratory system
Shortness of breath, shortness of breath, deep breathing, uremic pleurisy: pleural effusion, toxic lung: pulmonary edema
digestive system
Anorexia, nausea, vomiting, gastrointestinal bleeding
Blood system: ① Anemia ② Bleeding tendency ③ Thrombosis
neuropsychiatric system
Paresthesias: numbness, pain, burning, decreased or loss of sensation in limbs
Disorders of consciousness (uremic encephalopathy): confusion, delirium, coma, convulsions
Mental disorders: hallucinations, personality changes
Endocrine system: EPO, 1,25(OH)2VitD3, renin-angiotensin↑, secondary hyperparathyroidism, gonadal dysfunction, glucose metabolism disorder
Musculoskeletal system: muscle tremors, cramps, restless legs syndrome, abnormalities in bone mineral metabolism
treat
Treat underlying disease and aggravating factors
①Treat the primary disease ②Correct water and sodium retention or deficiency ③Control infection ④Relieve urinary tract obstruction ⑤Control heart failure ⑥Stop nephrotoxic drugs
Nutritional treatment: ① Low phosphorus diet, low sodium diet ② Low protein diet
Treatment of hyperkalemia
Stop using all potassium-containing foods and medications
① Intravenous infusion of 5% sodium bicarbonate ② Loop diuretic ③ Glucose-insulin solution: for every 4 to 6 g of glucose, add 1 U of insulin
④Calcium gluconate 10ml diluted and then intravenously pushed slowly ⑤Oral ion exchange resin ⑥Hemodialysis (serum potassium>6.5mmol/L)
Prevent and treat cardiovascular complications
Prevent and treat infection
Promote intestinal excretion of toxins
alternative treatment
Hemodialysis, peritoneal dialysis, kidney transplantation
Indications: ① Unrelievable uremia symptoms ② Hyperkalemia that is difficult to correct ③ Metabolic acidosis that is difficult to control
④ Heart failure, pulmonary edema ⑤ Uremic pericarditis ⑥ Uremic encephalopathy
General introduction to poisoning
Systemic diseases caused by toxic amounts of chemicals entering the human body causing damage to tissues and organs
Treatment principles
① Immediately terminate poison exposure ② Emergency resuscitation and symptomatic supportive treatment ③ Remove poisons that have been absorbed or not yet absorbed into the human body ④ Antidote drug treatment ⑤ Prevent complications
Organophosphorus insecticide poisoning
Poisoning mechanism (note): acetylcholinesterase organophosphorus insecticide → phosphorylated cholinesterase
clinical manifestations
acute cholinergic crisis
Muscarinic symptoms: smooth muscle spasm and increased secretion of eccrine glands
Nicotine-like symptoms
Excessive accumulation and stimulation of acetylcholine at the neuromuscular junction of striated muscles → striated muscle fibrillation, general muscle tonic spasm
Generalized tightness and pressure → muscle weakness, paralysis, respiratory muscle paralysis, respiratory failure
Acetylcholine stimulates sympathetic N postganglionic fibers → releases catecholamines → vasoconstriction, increased heart rate, blood pressure, and arrhythmia
central nervous system symptoms
After being stimulated by acetylcholine, dizziness, headache, fatigue, ataxia, restlessness, delirium, convulsions and coma may occur.
delayed polyneuropathy
① It usually occurs 2-3 weeks after the symptoms of acute poisoning disappear. ② Symptoms of sensory and motor polyneuropathy appear.
③ Mainly affects the distal limbs, resulting in paralysis of the lower limbs and muscle atrophy of the limbs. ④ It is related to the inhibition of nerve target esterase by pesticides and aging.
intermediate syndrome
1-4 days after severe OPI poisoning and patients who have insufficient dosage of ChE reenergizing drugs, the cholinergic crisis disappears after treatment, the consciousness is clear or has not recovered, and before the onset of delayed polyneuropathy, the neck flexors and limbs suddenly appear. End weakness and weakness of muscles innervated by cranial nerves may cause ptosis, eye abduction disorder and ventilator paralysis, causing ventilatory dyspnea or failure, which may lead to death.
It is related to the long-term inhibition of cholinesterase, affecting the postsynaptic function at the nerve-muscle junction.
Usually occurs 1-4 days after recovery from acute poisoning symptoms
Currently, there is paralysis of neck flexors, cranial nerve innervation muscles, proximal limb muscles and respiratory muscles.
It usually resolves in 4-18 days. In severe cases, death from respiratory failure may occur.
treat
① Immediately terminate poison exposure ② Emergency resuscitation and symptomatic supportive treatment ③ Remove poisons that have been absorbed or not yet absorbed into the human body
④Detoxification drug treatment ⑤Prevention of complications
Principles for antidote application: early, sufficient, combined, repeated
Antidote Type
Cholinesterase reenergizing drug: pralidoxime chloride
Cholinergic receptor blockers (anticholinergics)
Peripheral anticholinergics: representative drugs atropine and anisodamine
Centrally acting anticholinergics: representative drug scopolamine
Atropinization: After patients with organophosphorus insecticide poisoning reach a certain dose of atropine, they will clinically experience dilated pupils, dry mouth, dry skin, flushing of the face, disappearance of crackles in the lungs, and accelerated heart rate, that is, atropinization
bronchiectasis
Overview
It refers to the destruction of bronchial wall tissue caused by chronic inflammation of the bronchus and its surrounding lung tissue, resulting in irreversible expansion and deformation of the official cavity.
symptom
respiratory symptoms
Chronic cough, large amounts of purulent sputum
Recurrent hemoptysis, characteristic manifestations
recurrent lung infections
systemic symptoms
Symptoms of sexual infection poisoning, such as fever, night sweats, loss of appetite,
Weight loss, anemia, etc., which can affect children’s development
physical signs
Fixed and persistent localized crackles can be heard at the site
Cyanosis, clubbing of fingers (toes)
Auxiliary inspection
Chest X-ray
Increased, thickened, and disordered lung texture
Chest CT-HRCT is the gold standard for diagnosing bronchiectasis
According to the morphology of dilated bronchi
Columnar bronchiectasis: bronchial wall thickening and lumen widening
cystic dilation
hybrid expansion
Bronchoscopy
Pulmonary function test
Pathological examination
treat
General treatment
postural drainage
When hemoptysis, eat warm and cool food, keep stool smooth, and reduce activities
Prevent respiratory infections
medical treatement
control infection
Colonization with Gram-negative bacilli
Small amount of hemoptysis: oral hemostatic drugs or symptomatic treatment
Moderate hemoptysis: intravenous hemostatic drugs
Massive hemoptysis: If drug treatment is ineffective, surgical treatment should be considered
Surgical treatment
Treatment of complications of suffocation
Keep airways open and clear blood clots
COPD, cor pulmonale, respiratory failure
chronic bronchitis
Chronic non-specific inflammation of the mucosa and surrounding tissues of the trachea and bronchi
Etiology and pathogenesis
smoking
Physical and chemical factors: occupational dust, chemical substances, air pollution, etc. are related to its onset
Infect
Other factors (senior-related)
clinical manifestations
Slow onset, long course, recurring attacks, and worsening year by year
symptom
Cough (cough): Cough mainly in the morning, with paroxysmal cough or sputum production during sleep
Expectoration (phlegm): white sticky phlegm or foamy phlegm, mainly early in the morning
Wheezing (wheezing): Bronchospasm in some patients
Auxiliary inspection
Chest X-ray: The lung texture is increased, rough and reticular and cord-like, especially in the lower lungs.
Respiratory function: no change in the early stage, the maximum expiratory flow rate-volume curve is significantly reduced at 75% and 50% lung volume.
Blood tests: Increased white blood cell and neutrophil counts during bacterial infection
Sputum examination: pathogenic bacteria can be cultured. Gram-positive, Gram-negative bacteria and white blood cells can be seen in the smear
Differential diagnosis
Bronchial Asthma
eosinophilic bronchitis
bronchiectasis
Bronchial lung cancer
treat
acute exacerbation
Infection control: fluoroquinolones, cephalosporins, penicillins
Antitussive and expectorant: licorice mixture, dextromethorphan, ambroxol
Antiasthma: bronchodilators such as aminophylline, B2 receptor agonists
remission period
Quit smoking and avoid breathing harmful gases
Enhance physical fitness and prevent colds
chronic obstructive pulmonary disease COPD
COPD is a common preventable and treatable disease characterized by persistent respiratory symptoms and airflow limitation.
Pathophysiology
airflow restricted
Emphysema
diffusion disorder
Ventilation/blood flow imbalance
clinical manifestations
symptom
chronic cough
expectoration
Gradually worsening dyspnea: hallmark symptoms
physical signs
emphysema signs
laboratory tests
Respiratory function test
FEV1/FVC%＜70%, necessary condition for diagnosis
RV/TLC>40%
X-ray examination
Acute exacerbation of COPD (AECOPD): The patient's cough, sputum production, and dyspnea are worse than usual or the amount of sputum increases, or yellow sputum is coughed up, or the daily medication regimen needs to be changed.
treat
Treatment of stable COPD
Education and Management
Bronchodilators
β2 adrenoceptor agonists: albuterol, salmeterol, formoterol
Anticholinergic drugs: ipratropium bromide, tiotropium bromide
Theophylline: aminophylline, theophylline sustained-release or controlled-release tablets
Glucocorticoids Long-acting β2-receptor agonist (LABA)
Expectorants: Ambroxol hydrochloride, N-acetylcysteine
Long-term oxygen therapy (LTOT)
Treatment of acute exacerbations of COPD
Eliminate triggers
controlled low concentration oxygen therapy
Antimicrobial drug treatment
bronchodilator
Glucocorticoids
Mechanical Ventilation
Other measures: Maintain water, electrolyte and nutritional balance, prevent and treat complications
pulmonary heart disease
A disease in which lesions of the broncho-pulmonary tissue, thorax or pulmonary vessels cause increased pulmonary vascular resistance, resulting in pulmonary hypertension, and subsequent changes in right ventricular structure and/or function.
clinical manifestations
Lung and heart function compensation period
Symptoms: Cough, sputum, shortness of breath, palpitations, dyspnea, fatigue and decreased work endurance after exercise.
Signs: cyanosis, P2 hyperactivity, increased heart beat under the xiphoid process or systolic murmur in the tricuspid valve area, jugular vein filling and distension, or lowering of the diaphragm and downward shift of the liver border
Pulmonary and heart function decompensation stage - respiratory failure
respiratory failure
Symptoms: Dyspnea worsens, especially at night, often with headache, insomnia, loss of appetite, daytime drowsiness, and even symptoms of pulmonary encephalopathy such as apathy, delirium, etc.
Signs: obvious cyanosis, bulbar conjunctival congestion and edema, tendon firing disappeared or weakened, peripheral blood vessels dilated
right heart failure
Symptoms: Obvious shortness of breath, palpitations, lack of appetite, bloating, nausea
Signs: obvious cyanosis, jugular vein distention, increased heart rate, arrhythmia, systolic murmur heard under the xiphoid process, and even diastolic murmur, hepatomegaly with tenderness, positive hepatic jugular venous reflux sign, and lower limb edema. Severe cases may have abdominal effusion
treat
The principle is to actively control infection, clear the respiratory tract, improve respiratory function, correct hypoxia and CO2 retention, control respiratory failure and heart failure, and prevent and treat complications.
respiratory failure
Severe impairment of pulmonary ventilation and/or ventilatory function caused by various reasons prevents adequate gas exchange from being maintained at rest, resulting in hypoxemia with (or without) hypercapnia, which in turn causes a Series of pathophysiological states. Under sea level and breathing air conditions, arterial blood oxygen partial pressure (PaO2) <60mmHg, with or without carbon dioxide partial pressure (PaCO2) >50mmHg
Classification
Type I respiratory failure (hypoxic respiratory failure): PaO2<60mmHg, PaCO2 is normal or reduced
Type II respiratory failure (hypercapnic respiratory failure): PaO2<60mmHg, accompanied by PaCO2>50mmHg
lung cancer
pleural effusion
Etiology and pathogenesis
Increased hydrostatic pressure in pleural capillaries: transudate
Increased pleural permeability: exudate
Decreased colloid osmotic pressure in pleural capillaries: transudate
Parietal pleural lymphatic drainage disorder: exudate
Injurious pleural effusion: exudate
Iatrogenic pleural effusion: transudate or transudate
symptom
Difficulty breathing, chest pain
Auxiliary inspection
Chest X-ray
Chest CT and MRI
Ultrasound examination
Diagnostic pleural puncture and pleural fluid examination: critical
Histological examination
Diagnosis and differential diagnosis
Distinguish between transudate and transudate: Light standard
treat
Cause treatment
Aspiration of chest fluid: different diseases
Symptomatic and supportive treatment
Treatment of tuberculous pleurisy
Cause treatment: chemotherapy
Thoracic puncture and fluid extraction: Active, 2-3 times/week
Hormone: Severe toxicity symptoms, prolonged pleural effusion
Symptomatic support
Treatment of pneumonia-like pleural effusion and empyema
Treatment of the cause: Anti-infection
Drainage of pus
Symptomatic support: powerful nutritional supply
Surgery: Pleuralectomy
Treatment of malignant pleural effusion
Treat the cause; pump out pleural effusion; local treatment; symptomatic support
poor prognosis
pneumothorax
Definition: When air enters the pleural cavity and causes pneumothorax, it is called pneumothorax.
Cause classification
spontaneous pneumothorax
primary spontaneous pneumothorax
Spontaneous pneumothorax Seco
Traumatic pneumothorax
Iatrogenic pneumothorax:
Special type of pneumothorax
Clinical classification
closed pneumothorax
The pleural tear is small and closes on its own
No more air enters the pleural space
Pressure drops after pumping
open pneumothorax
Large and persistently open pleural tear
Air moves freely in and out of the pleural space
Intrapleural pressure fluctuates around 0cmH20
The pressure remains unchanged after pumping
tension pneumothorax
One-way valve
The intrapleural pressure continues to rise to form high pressure
After pumping, the pressure first decreases and then increases.
clinical manifestations
symptom
Sudden chest pain
With pale complexion, tachycardia, and cold sweats
Severe cases include difficulty breathing, such as tension pneumothorax
physical signs
affected chest
Reduced respiratory movements
The trachea is displaced to the healthy side and the voice tremor is weakened
drum sound upon percussion
Reduced or absent breath sounds
Videography
Chest X-ray: pneumothorax line, pneumothorax zone (no lung texture)
treat
Treatment principles:
· Evacuate air from the pleural cavity and promote recruitment of the affected lung
· Close the leak
·Eliminate the cause and reduce recurrence
Conservative treatment
Indications: first onset, no obvious symptoms, small closed pneumothorax (<20%)
·Oxygen
·Strict bed rest
exhaust therapy
thoracentesis
Closed chest drainage
chemical pleurodesis
Surgical treatment
Pulmonary embolism, pulmonary hypertension
pulmonary thromboembolism
Overview
Pulmonary embolism, PE: is a general term for a group of diseases or clinical syndromes caused by various emboli blocking the pulmonary artery or its branches, including: pulmonary thromboembolism (PTE), fat embolism syndrome, amniotic fluid embolism, air Embolism, cancer thrombus, etc.
Pulmonary thromboembolism (PTE): a disease caused by the obstruction of the pulmonary artery or its branches by thrombus from the venous system or right heart, with pulmonary circulation and respiratory dysfunction as its main clinical and pathophysiological characteristics.
Pulmonary infarction PI: refers to the necrosis of lung tissue caused by blockage or interruption of blood flow in the area dominated by pulmonary embolism.
Venous thrombosis (DVT): Blood components such as fibrin, platelets, and red blood cells form a clot (thrombus) in the deep vein lumen.
Venous Thromboembolism VTE: VTE = DVT PTE
clinical manifestations
Symptom 1 - non-specific, be sure to be vigilant
The triad of pulmonary embolism: chest pain, hemoptysis, and dyspnea is only seen in about 20% of patients.
physical signs
DVT Symptoms and Signs – DVT is a sign of PTE
Pain in the lower limbs; swelling of the lower limbs; increased skin temperature of the lower limbs
diagnosis
Auxiliary inspection
Contrast-enhanced CT of the pulmonary artery (CTPA)
Nuclide V/Q imaging
Magnetic ResonanceMRPA
Pulmonary angiography (PAA)
blood gas analysis
electrocardiogram
Chest X-ray
echocardiogram
Doppler vascular ultrasound
The preferred diagnostic tool for venous thrombosis
Confirmed
CTPA - the most important diagnostic method at present
Radionuclide lung ventilation/perfusion (VIQ) imaging
Magnetic resonance pulmonary angiography (MRPA)
Pulmonary angiography (PA): the “gold standard” for diagnosing PTE
Seek cause
Determine the presence of DVT: Deep venous compression ultrasound of the lower limbs
Looking for triggers for DVT and PTE: Unexplained PTE: Cancer Screening
Clinical classification of PTE - guiding treatment principles
acute pulmonary thromboembolism
High-risk PTE: shock or hypotension
Intermediate-risk PTE: hemodynamic stability, right ventricular dysfunction and/or myocardial injury
Low-risk PTE: hemodynamic stability, no right ventricular dysfunction and myocardial damage
chronic thromboembolic pulmonary hypertension
Differential diagnosis
coronary artery insufficiency
treat
supportive care
Rest in bed and have smooth bowel movements
Should be closely monitored
Oxygen therapy to correct hypoxemia
Correct right heart dysfunction
maintain blood pressure
anticoagulant therapy
Drugs: Unfractionated heparin, low molecular weight heparin, fondaparinux, warfarin,
Treatment timing: When PTE is clinically suspected, start treatment if there are no contraindications
Thrombolytic therapy
Indications
High-risk PTE
Some intermediate-high risk PTE
Thrombolysis time window: optimal within 48 hours, still effective within 14 days
Complications of thrombolysis: bleeding, allergy, rethrombosis
Drugs: urokinase (UK), streptokinase (SK), recombinant tissue plasminogen activator (rt-PA)
Surgery and Interventional Treatment
prognosis and prevention
Prognosis: related to underlying disease status, cause of embolism, and degree of embolism
Prevention: Caprini score, Padua score
General measures: early postoperative ambulation and ankle pump exercises
Mechanical prevention: gradient compression elastic stockings
Drug prophylaxis: anticoagulant drugs
pulmonary hypertension
Overview
Pulmonary hypertension (PH): a pathophysiological state in which pulmonary artery pressure is abnormally elevated due to known or unknown causes. Pulmonary hypertension often develops progressively, leading to right heart overload and right heart failure.
The hemodynamic standard is: mean pulmonary artery pressure mPAP ≥ 25 mmHg at sea level and resting state.
Classification
arterial pulmonary hypertension
Idiopathic pulmonary hypertension
hereditary arterial pulmonary hypertension
Pulmonary hypertension caused by drugs and poisons
Left heart disease associated pulmonary hypertension
Pulmonary disease and/or hypoxia-related pulmonary hypertension
Pulmonary artery obstruction due to CTEPH and other causes
Pulmonary hypertension caused by multiple unknown mechanisms
Classified by hemodynamics
Precapillary pulmonary hypertension: mPAP ≥ 25 mmHg and pulmonary capillary wedge pressure or left ventricular end-diastolic pressure ≤ 15 mmHg
Postcapillary pulmonary hypertension: mPAP≥25mmHg, PCWP or left ventricular end-diastolic pressure>15mmHg
clinical manifestations
Symptoms - the disease is insidious and usually asymptomatic in the early stages
Difficulty breathing
chest pain and fainting
Hemoptysis
tired, weak
Signs - non-specific
diagnosis
Auxiliary inspection
electrocardiogram
Chest X-ray
arterial blood gas analysis
Echocardiography: the most important non-invasive test for screening for pulmonary hypertension
Polysomnography
lung ventilation perfusion scan
Right heart catheterization, the gold standard
Acute Vascular Response Test: Evaluates pulmonary vascular responsiveness to short-acting vasodilators and identifies patients who may respond to treatment with oral calcium channel antagonists
Diagnostic criteria
Diagnostic criteria: Mean pulmonary artery pressure at rest at sea level measured by right heart catheterization ≥ 25 mmHg
treat
General treatment
Make appropriate adjustments to daily activities
Oxygen therapy
Prevent infection
Treatment of primary disease
medical treatement
calcium channel blockers
Prostacyclins
Endothelin-1 receptor antagonist ET-1: bosentan
Phosphodiesterase-5 inhibitors
Soluble guanylate cyclase (sGC) agonist
Nitric Oxide and L-Arginine
anticoagulant therapy
Combination medication
Interventions and surgeries
tuberculosis
clinical manifestations
symptom
Slow onset and long course of disease
Typical symptoms
Systemic symptoms: long-term fever, consumption symptoms
Local symptoms of the respiratory tract: cough, sputum, hemoptysis, chest pain: when the pleura is affected, shortness of breath: extensive lesions, large amounts of pleural effusion
physical signs
Caseous pneumonia: crackles are often heard, mostly located in the upper part of the lungs
Chronic fibrocavitary type: atelectasis
Tuberculous pleurisy: pleural effusion
Tuberculous rheumatism: skin erythema, nodules
Whole body: weight loss, anemia, etc.
Imaging examination and clinical classification
primary pulmonary tuberculosis
Primary syndrome: primary lesions in the lungs, lymphangitis, regional lymphadenitis (hilum)
Hematogenous disseminated (miliary) pulmonary tuberculosis
acute miliary tuberculosis
Spread a large amount at one time
Severe symptoms of poisoning: fever, fatigue, anorexia, etc.
X-ray: Diffuse miliary lesions (three uniform) (distribution, size, density)
subacute miliary tuberculosis
Spread in batches and in small quantities
Symptoms of poisoning are not obvious
X-ray: Diffuse miliary lesions (three uneven)
Secondary tuberculosis
Infiltrative pulmonary tuberculosis (the most common type of adult pulmonary tuberculosis)
blurry flakey shadows
Higher density patchy and nodular shadows
(Note: The density is uneven, which is the imaging identification point of pneumonia)
caseous pneumonia
cavitary tuberculosis
chronic fibrocavitary tuberculosis
More than 2 years
Result of recurring tuberculosis
tuberculosis balls
Diameter is generally less than 3cm
satellite lesions
tuberculous pleurisy
Tracheo-bronchial tuberculosis (new
Four major characteristics
Site of onset: Most common in the upper fields of both lungs, especially the posterior segment of the upper lobe tip and the dorsal segment of the lower lobe
Life time: long
Morphology: Polymorphism, uneven density
Prone to cavitation and spread
laboratory tests
Etiology (Mycobacterium tuberculosis) examination
The basis for diagnosis is also an important indicator for judging efficacy.
smear method
Cultivation method (gold standard)
Molecular Biology Methods: Rapid, Early Diagnosis
Submit for inspection
Phlegm (most common)
Positive: Confirmed (but note that non-tuberculous mycobacteria are excluded)
Negative: Tuberculosis cannot be ruled out!
fiber bronchoscopy
Tissue biopsy (one of the diagnostic methods)
Immunological examination
Tuberculin test (PPD skin test)
The average diameter of the induration at the injection site was measured after 72 hours.
Positive: Induration diameter >5mm
Gamma-interferon release test (T.spot-TB)
tuberculosis antibodies
tuberculosis antigen
diagnosis
Differential diagnosis
Symptom identification
Fever for more than 2 weeks: tuberculosis (common), typhoid fever, sepsis
Hemoptysis: bronchiectasis, lung cancer, and tuberculosis
x-ray identification
Primary type: hilar lymph node tuberculosis and central lung cancer
Blood-borne type: Alveolar cell carcinoma (lung adenocarcinoma)
Secondary types: pneumonia, obstructive pneumonia; tuberculosis and peripheral lung cancer
Tuberculous cavity: lung abscess, lung cancer
diagnosis method
Clinical symptoms and signs; imaging; etiology; immunology; pathology; diagnostic treatment
Diagnosis writing formula: type, site, smear/culture/molecular biology () initial/retreatment, drug resistance
Tuberculosis Overview
Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis
It can affect multiple organs throughout the body, with tuberculosis being the most common
Cause and pathogenesis
Routes of infection and human reactivity (immune and delayed allergic reactions)
Respiratory tract, digestive tract
Initial infection and reinfection
Koch phenomenon: the body's different responses to reinfection and primary infection with tuberculosis bacteria
pathology
Basic pathological changes
Exudation, hyperplasia, caseous necrosis
Outcome: Absorption, fibrosis, calcification, liquefaction, cavity
treat
The principle of "early, regular, full course, appropriate amount, and combination" medication
Anti-infection treatment (chemotherapy)
Chemotherapy principles
Early stage - best effect
Combination-prevent drug resistance and improve efficacy
Rules - Prevent drug resistance
The whole process--prevent recurrence and improve cure rate
Appropriate amount - best efficacy, least side effects
Commonly used drugs: isoniazid, rifampicin, pyrazinamide, streptomycin, ethambutol, para-aminosalicylic acid
Chemotherapy methods
Conventional chemotherapy and short-course chemotherapy (6 to 9 months)
Intermittent medication and two-stage medication to improve cooperation
Take it with a meal or in the air - to improve the efficacy
Supervise medication use-improve cooperation
Chemotherapy
First treatment (mostly sensitive tuberculosis)
The total treatment course is generally 6-9 months, individualized treatment
Retreatment (drug-resistant tuberculosis is common)
The total course of treatment is 1-2 years
drug-resistant tuberculosis
Mono-drug-resistant tuberculosis: tuberculosis that is resistant to only one of the drugs (especially rifampicin-resistant tuberculosis)
Multidrug-resistant tuberculosis: refers to tuberculosis that is resistant to both isoniazid and rifampicin but is sensitive to quinolones and aminoglycosides
Extensively drug-resistant tuberculosis: refers to tuberculosis that is simultaneously resistant to isoniazid, rifampicin, quinolones, and one of the other two drugs in group A drugs.
Assessment efficacy indicators
Phlegm bacteria: three consecutive times a month
x-ray or chest CT
Symptomatic treatment
Toxicity symptoms
General symptoms: Effective chemotherapy subsides within 1 to 2 weeks and does not need to be treated.
Corticosteroids: must be used on the basis of effective anti-tuberculosis
Hemoptysis
Small amount: Oral hemostatic drugs, such as Anluoxue and Yunnan Baiyao
medium large amount
Absolute bed rest: Lying on the affected side
Pituitaryin
Surgical treatment
Indications
Tuberculosis, diameter >3 cm, cannot exclude lung cancer
Unilateral lung damage with bronchiectasis, recurrent infection or hemoptysis
Multidrug-resistant tuberculosis, localized lesions, ineffective treatment
fiber thick wall cavity
Empyema treatment is ineffective
prevention
Bacillus Calmette-Guerin (BCG) - a non-virulent bovine tuberculosis vaccine. After vaccination, the human body acquires specific immunity to tuberculosis bacteria and can alleviate the disease.
Bronchial Asthma
definition
A heterogeneous disease characterized by chronic airway inflammation and airway hyperresponsiveness
Recurrent respiratory symptoms such as wheezing, shortness of breath, chest tightness, and coughing
Variable symptoms and variable expiratory airflow limitation are often triggered by infection, exposure to allergens, etc. Most patients can resolve themselves or after treatment.
Etiology and pathogenesis
Heterogeneous diseases caused by the interaction of genetic susceptibility genes and environmental factors
airway hyperresponsivenessAHR
The airway is highly sensitive to various irritating factors, such as allergens, physical and chemical factors, drugs, etc.
Excessive or premature contraction of the airway
Basic characteristics of asthma
pathology
Chronic inflammation of the airways—the essence of asthma
airway remodeling
clinical manifestations
symptom
typical
Episodes of expiratory dyspnea, chest tightness, or cough accompanied by wheezing
Changes in symptoms and severity over time are important features
Often attacks or gets worse at night and early in the morning
atypical asthma
Cough variant asthma (CVA)
Chest tightness variant asthma (CTVA)
physical signs
typical
Extensive and variable expiratory wheeze in both lungs, with prolonged expiratory sounds
Silent lungs, reduced breath sounds or disappearance, indicating a critical condition
There may be no abnormalities during the non-attack period
laboratory tests
Respiratory function testing—to identify variable expiratory airflow limitation
Ventilatory function test: obstructive ventilatory dysfunction during the attack, forced expiratory volume in 1 second (FEV1), rate in 1 second (FEV1/FVC) and peak expiratory flow (PEF) all decreased
bronchial provocation test
Measuring airway responsiveness
Positive standard: FEV1 decreases ≥20%
bronchodilation test
Testing airway reversibility
Positive standard: FEV1 increased by ≥12% compared with before medication, and the absolute value increased by ≥200ml
Determination of PEF and its mutation rate
PEF or day and night PEF fluctuation rate ≥ 20% within 24 hours
Non-invasive airway inflammation assay
Sputum examination: Eosinophils can be seen in the sputum smear
arterial blood gas analysis
When PaO2<60mmHg and PCO2≥45mmHg, it indicates a critical condition
Diagnostic criteria
History of respiratory symptoms and signs with typical variability
Determine variable expiratory airflow limitation (should have at least one positive lung function)
Staging and control level classification
Acute attack stage: mild, moderate, severe, critical
Non-acute attack phase (chronic ongoing phase): well controlled, partially controlled, uncontrolled
clinical remission period
Differential diagnosis
Wheezy dyspnea due to left heart failure
chronic obstructive pulmonary disease
Upper airway obstructive disease
Allergic bronchopulmonary aspergillosis (APBA)
treat
General treatment
Identify and reduce exposure to risk factors
medical treatement
Relief medications (bronchodilators)
Short-acting beta2-adrenoceptor agonist (SABA): albuterol
Short-acting inhaled anticholinergic drug (SAMA): ipratropium bromide
Short-acting theophylline
Controller drugs (anti-inflammatory drugs)
Inhaled corticosteroids (ICS): by far the most effective drugs for controlling asthma
Leukotriene receptor antagonist: montelukast
Long-acting beta2-agonist (LABA, not used alone)
anti-IgE antibody
Combination medications (such as ICS LABA)
Surgical Treatment: Bronchial Thermoplasty
Complications and their treatment: pneumothorax, pneumomediastinum, atelectasis, respiratory failure, cor pulmonale
Indications for referral
lung infection
Definition: Inflammation of frontal lung parenchyma caused by various causes
Classification
Anatomy or Imaging Credit
Lobular pneumonia
Lobar pneumonia
interstitial pneumonia
Disease environment classification
community acquired pneumonia
Refers to infectious pulmonary parenchymal inflammation suffered outside the hospital (community), including: existing upon admission and pneumonia occurring within 48 hours after admission.
Mainly G bacteria and atypical pathogens
nosocomial pneumonia
Pneumonia developed in the hospital without receiving invasive mechanical ventilation
Mainly G-bacteria
clinical manifestations
symptom
fever
Cough, expectoration
Chest pain: when the lesions spread to the pleura
Difficulty breathing (those with large lesions)
physical signs
Pulmonary rales
signs of pulmonary consolidation
pleural effusion sign
Auxiliary inspection
Blood routine
Pathological examination
chest imaging
diagnosis
Confirm the diagnosis of pneumonia (diagnosis basis)
New onset of cough and sputum, or worsening of existing symptoms and the appearance of purulent sputum
fever
Signs of pulmonary consolidation and/or crackles
WBC>10×109L or<4X109/L,N>80%
Chest X-ray: flaky, patchy infiltrative shadow or interstitial changes.
Diagnostic criteria: any one of ⑤ ①②③④ excluding other diseases
Severity assessment
Determine admission site and treatment strategy
The severity of pneumonia is determined by three main factors: the degree of local inflammation, the spread of lung inflammation, and the degree of systemic inflammatory response.
Criteria for diagnosing severe pneumonia (IDSA/ATS criteria)
Main criteria
Requires mechanical ventilation;
Septic shock requires vasoactive drug therapy;
secondary criteria
R≥30 times/min;
Oxygenation index PaO2/FiO2 is less than 250
multilobar infiltration
Disorders of consciousness or disorientation
Azotemia (BUN≥ 20mg/dL)
Leukopenia (WBC<4.0x109/L)
Thrombocytopenia (PLT<10.0x109/L)
Hypothermia T<36°C
Hypotension requires aggressive fluid resuscitation
Meeting 1 major criterion or >3 minor criteria requires admission to ICU.
●Requires respiratory support
●Cycle support
●Needs intensive monitoring and treatment
Differential diagnosis
Differentiating upper and lower respiratory tract infections
tuberculosis
lung cancer
pulmonary thromboembolism
treat
Anti-infective treatment
empiric treatment
Targeted treatment
Streptococcus pneumoniae pneumonia
Pathogen
G diplococci
rust-colored phlegm
Does not produce toxins
symptom
Systemic symptoms: sudden onset, high fever, chills, body muscle aches,
Respiratory symptoms: chest pain on the affected side, cough, rust-colored sputum, difficulty breathing
Typical symptoms: chills, high fever, chest pain, cough, rust-colored phlegm)
Pulmonary signs
Early stage: no obvious abnormality
Pulmonary consolidation stage: signs of pulmonary consolidation, turbid percussion, increased tactile fremitus, and bronchial breath sounds
Dissipation period: wet rales can be heard
Chest X-ray
Early stage: thickened lung texture or slightly blurred lung segments and lobes
Consolidation stage: The air bronchus sign can be seen in the consolidation shadow, and there may be a small amount of pleural effusion sign at the costophrenic angle.
Dissipation phase: inflammatory infiltration is gradually absorbed, pseudocavitation sign
Most of them completely disappear within 3 to 4 weeks of onset.
treat
antibiotic treatment
Drugs: Penicillin G is preferred; fluoroquinolones, cefotaxime or ceftriaxone are used for allergies
Course of treatment: Stop taking the medicine 3-5 days after the fever subsides
Supportive and symptomatic treatment
Treatment of complications
Staphylococcal pneumonia
Chest X-ray
Four major signs: lung infiltration, lung abscess, air cyst, empyema
The hematogenous dissemination type is multiple patches or masses of different sizes that shadow rapidly, and it is multiple air-containing cysts.
treat
Anti-infective
Large dose, sensitive medicine, long course of treatment
Enzyme-resistant penicillins, cephalosporins
Erythromycin
Methicillin-resistant strains: MRSA
Pulmonary mycosis
heart failure
It is a clinical syndrome in which changes in myocardial structure and function caused by various diseases lead to low ventricular pumping function, cardiac output cannot meet the body's metabolic needs, insufficient blood perfusion in organs and tissues, and symptoms and signs of pulmonary circulation or/and systemic circulation congestion. .
Pathophysiology
compensatory mechanism
Frank-Starling mechanism: Increase cardiac preload, increase return to the heart, increase ventricular end-diastolic volume, thereby increasing cardiac output and cardiac work
neurohumoral mechanisms
RAAS activation: RAAS activation promotes cardiac and vascular remodeling, aggravates myocardial damage and worsens cardiac function.
Atrial natriuretic peptide ANP, brain natriuretic peptide BNP: In heart failure, ventricular wall tension increases, and the secretion of BNP and ANP increases significantly. The degree of increase is positively correlated with the severity of heart failure, and can be used as an indicator to evaluate the progression of heart failure and judge prognosis.
Arginine vasopressin AVP: released by the pituitary gland, has antidiuretic and peripheral vasoconstrictive effects
ventricular remodeling
During the compensatory process of impaired cardiac function, expansion of cardiac chambers, and myocardial hypertrophy, corresponding changes occur in myocardial cells, extracellular matrix, collagen fiber network, etc., that is, ventricular remodeling.
diastolic dysfunction
chronic heart failure
clinical manifestations
left heart failure
Pulmonary circulation congestion
Difficulty breathing
exertional dyspnea
orthopnea
Paroxysmal nocturnal dyspnea
acute pulmonary edema
Cough, expectoration
Hemoptysis
Decreased cardiac output
Fatigue, tiredness, reduced exercise tolerance, dizziness, palpitation
physical signs
Pulmonary rales
cardiac signs
Regurgitation murmur in cardiomegaly and relative mitral regurgitation
Hyperactivity of the second heart sound in the pulmonic valve area and galloping rhythm of the third or fourth heart sound
right heart failure
Systemic circulation congestion is the main manifestation
symptom
Gastrointestinal symptoms: gastrointestinal and liver congestion causing abdominal distension, lack of appetite, nausea, and vomiting
exertional dyspnea
physical signs
Edema: symmetrical pitting edema in sagging areas of the body
Jugular venous sign: Positive hepatojugular reflux sign
Hepatomegaly
cardiac signs
Significant enlargement of the right ventricle resulting in a regurgitant murmur of tricuspid regurgitation
total heart failure
Staging and grading
installment
Stage A: Pre-heart failure stage: There are high-risk factors for heart failure, but there are currently no structural or functional abnormalities of the heart.
Stage B: Preclinical heart failure stage: The patient has no symptoms and signs of heart failure, but has structural changes in the heart.
Stage C: Clinical heart failure stage: The patient has structural changes in the heart and has past or current symptoms and signs of heart failure.
Stage D: Refractory end-stage heart failure stage: Although the patient has undergone strict and optimized medical treatment, he still has symptoms at rest and has cardiogenic cachexia.
Classification: New York Heart Association NYHA
Level 1: Patients with heart disease are not restricted in their daily activities, and general activities do not cause symptoms of heart failure such as fatigue and dyspnea.
Level 2: Patients with heart disease have mild limitations in physical activity, no conscious symptoms at rest, and symptoms of heart failure may occur during normal activities.
Level 3: Patients with heart disease have significant limitations in physical activity, and lower than normal activities can cause symptoms of heart failure.
Level 4: Heart disease patients cannot engage in any physical activity. Symptoms of heart failure exist even at rest and worsen after activity.
examine
natriuretic peptide
Troponin
Routine examinations: including blood routine, urine routine, liver and kidney function, blood sugar, blood lipids, electrolysis
echocardiogram
X-ray examination is the main basis for diagnosing left heart failure and pulmonary edema
Cardiac Magnetic Resonance CMR
coronary angiography CAG
Differential diagnosis
Bronchial Asthma
Pericardial effusion, constrictive pericarditis
Cirrhosis, abdominal effusion and lower limb edema
treat
General treatment
lifestyle management
patient education
weight management
Diet management
Rest and activities
Cause treatment
Hypertension, coronary heart disease, diabetes, metabolic syndrome
Anti-infective
medical treatement
diuretics
loop diuretics
Furosemide (furosemide) is a powerful diuretic that acts on the thick ascending branch of the medullary loop to excrete sodium and potassium.
Be aware of hypokalemia and monitor serum potassium
Thiazide diuretics
Represented by hydrochlorothiazide (hydrochlorothiazide), it acts on the proximal end of the renal distal convoluted tubule and the distal end of the ascending branch of the medullary loop, inhibiting sodium and potassium reabsorption.
It can inhibit the excretion of uric acid and cause hyperuricemia. Long-term use in large doses can affect sugar and lipid metabolism.
potassium sparing diuretics
Spironolactone (spironolactone), triamterene, and amiloride are often used in combination with the above two types of diuretics to enhance the diuretic effect and prevent hypokalemia.
AVP receptor antagonist (tolvaptan)
Does not increase uranium excretion and therefore can be used to treat heart failure associated with hypouranemia
RAAS inhibitors
Angiotensin-converting enzyme inhibitor ACEI
Inhibit RAAS; improve hemodynamics; improve ventricular remodeling
Side effects: hypotension, transient worsening of renal function, hyperkalemia, dry cough, and angioedema
Pregnant women and those allergic to ACEI should not use it
angiotensin receptor blocker ARB
ACEI is the first choice for treatment of heart failure patients. When ACEI causes dry cough and angioedema, those who cannot tolerate it can use ARB instead. Combined use is not recommended.
Angiotensin receptor neprilysin inhibitor ARNI
aldosterone receptor antagonist
Spironolactone, eplerenone
beta receptor antagonist
Including selective beta-receptor antagonists metoprolol and bisoprolol
With the non-selective adrenergic α, β1, β2 receptor antagonist carvedilol
positive inotropes
Digitalis drugs: Digoxin
Systolic heart failure associated with rapid atrial fibrillation/atrial flutter is the best indication for digitalis use.
non-pharmacological treatment
Cardiac Resynchronization Therapy (CRT)
Implantable cardioverter defibrillator (ICD)
Left ventricular assist LVAD
heart transplant
acute heart failure
Severity classification
Killip Rating
Level 1: No clinical symptoms and signs of heart failure
Level 2: There are clinical symptoms and signs of heart failure. Moist rales were present in less than 50% of the lung fields, and the third heart sound of the heart was galloping.
Grade 3: severe clinical symptoms and signs of heart failure, severe pulmonary edema, and moist rales in more than 50% of the lung fields.
Level 4: Cardiogenic shock
clinical manifestations
Sudden severe dyspnea, respiratory rate often reaches ~50 minutes, forced sitting, pale complexion, profuse sweating, irritability, frequent coughing, and coughing up pink frothy sputum
The main manifestations of cardiogenic shock are: persistent hypotension, systolic blood pressure falling below 90mmHg for more than 30 minutes, PCWP>18mmHg, CI less than 2.2, accompanied by tissue hypoperfusion, such as clammy skin, paleness and cyanosis, and significantly reduced urine output. Disorder of consciousness, metabolic acidosis
Pulmonary Edema
treat
General processing
Position: semi-recumbent or sitting upright, with legs hanging down to reduce venous return
oxygen
Preparation for treatment: opening of intravenous channel, indwelling urinary catheter, ECG monitoring and transcutaneous blood oxygen saturation monitoring
Attendance management
medical treatement
Sedation: Morphine 3-5 mg intravenously
Rapid diuresis: Furosemide 20~40mg is injected intravenously within 2 minutes and can be repeated once after 4 hours.
Amindaline: relieves bronchitis
Digitalis drugs: intravenous administration of triclosan
vasoactive drugs
vasodilators
nitroprusside
Nitrates
alpha receptor antagonist
Human recombinant brain natriuretic peptide rhBNP
inotropic drugs
beta receptor agonists
phosphodiesterase inhibitor
Zuo Ximendan
vasoconstrictor
non-pharmacological treatment
Mechanical Ventilation
Continuous renal replacement therapy CRRT
Mechanically assisted circulatory support device
Cause treatment
valvular heart disease
mitral stenosis
pathology
Rheumatic fever causes multiple parts of the mitral valve and adhesions fuse to cause mitral valve orifice stenosis.
Mitral valve orifice area
Normal adult: 4-6cm2
Mild stenosis: 1.5-2cm2
Moderate stenosis: 1.0-1.5cm
Severe stenosis: <1.0cm2
clinical manifestations
symptom
Dyspnea: most common, progressively worse
Hemoptysis: varying degrees
Cough: worse when lying down
Hoarseness: rare, compression of left recurrent laryngeal nerve
physical signs
Mitral valve appearance: double malar cyanosis
first heart sound
Hyperactive, open valve sound (soft valve leaves)
Decreased or absent valve sounds (valve leaflet calcification)
Apical murmur: mid-to-late diastolic, rumbling, localized, often accompanied by tremor
Hyperactive or split P2
Graham Steell's murmur: an early diastolic, wind-like murmur in the second intercostal space on the left sternal border, caused by pulmonary artery dilatation and relative pulmonary valve insufficiency.
Holosystolic blowing murmur in the tricuspid valve area, caused by relative tricuspid regurgitation
Laboratory and other tests
M-mode ultrasound: city wall-like changes, mitral valve anterior and posterior leaflets moving in the same direction
Differential diagnosis
Identification of diastolic rumble murmur in apical region
Increased transmitral blood flow: hyperthyroidism, anemia
Austin-Flint murmur: severe aortic regurgitation
Left atrial myxoma: tumor blockage, murmur changes with body position
complication
atrial fibrillation
Thromboembolism
acute pulmonary edema
right heart failure
infective endocarditis
lung infection
treat
General treatment
Prevent infection
Avoid strenuous physical activity and follow up regularly
Sodium restriction, diuretics, correction of anemia
Dealing with complications
Acute pulmonary edema: same treatment as acute left heart failure (diuresis, venous dilation, heart rate control)
Atrial fibrillation: rhythm control
Right heart failure: sodium restriction, diuresis
Massive hemoptysis: sedation, diuresis, lowering pulmonary venous pressure
Interventional treatment and surgical valve replacement—fundamental treatment measures
Mitral valve insufficiency
clinical manifestations
symptom
acute
Mild - exertional dyspnea
Severe - acute left heart failure, pulmonary edema, shock
Chronic
Mild asymptomatic
serious
Decreased cardiac output and fatigue
Long compensation period and short decompensation period
physical signs
acute
Apical beat: strong
Heart sounds: P2 hyperactivity, the fourth heart sound in the apical area is common
heart murmur
Reflux--low-key descending blow pattern during non-total systole
Severe reflux--S3 and diastolic rumble murmur
Chronic
Apical beat: left lower shift
heart sounds
S1: normal or weakened
S2: Split widening
S3: Severe reflux
Click sound: Mitral valve prolapse
Heart murmurs: apical, systolic, blowing murmurs
Leaflet contracture: holosystolic, high-pitched, consistent type
Mitral valve prolapse: after click, late systole
Coronary heart disease papillary muscle dysfunction: early, middle, late or full contraction
Rupture of chordae tendineae: seagulls or musical sounds
Severe reflux: short diastolic rumbling murmur
Laboratory and other tests
diagnosis
Acute: Cause Symptoms Murmur X-ray
Chronic: Typical murmur Left ventricular enlargement Ultrasound
Differential diagnosis
Systolic murmur at the left sternal border—confirmed by echocardiography
Mitral valve insufficiency
tricuspid valve insufficiency
ventricular septal defect
treat
acute
Treatment purposes: reduce pulmonary venous pressure; increase cardiac output; correct the cause of the disease
Surgical treatment is fundamental
Chronic
Medical treatment
Prevention of infections (endocarditis and rheumatic fever)
Managing complications: atrial fibrillation, anticoagulation, heart failure
Surgical treatment: The fundamental measure of treatment should be implemented before irreversible left ventricular dysfunction
Mitral valve repair (minor valve damage, no calcification of the valve leaflets)
Artificial valve replacement (valve calcification, severe subvalvular structural disease, infective endocarditis, combined with mitral stenosis)
aortic stenosis
Causes and pathology
rheumatic heart disease
congenital malformation
senile calcific degeneration
aortic valve area
Normal adult: ≥3cm2
Mild stenosis:>1.5cm2
Moderate stenosis: 1.0-1.5cm2
Severe stenosis: <1.0cm2 or average transvalvular pressure difference >50mmHg
clinical manifestations
symptom
triad
Dyspnea: appears later
Angina pectoris: induced by exercise, caused by myocardial ischemia
Syncope: caused by reduced left ventricular stroke volume, cerebral ischemia, and mostly occurs when standing upright and exercising
The mechanism of myocardial ischemia caused by severe aortic stenosis
Increased myocardial oxygen consumption
Relatively reduced myocardial capillary density
The intracardiac pressure increases during diastole, compressing the subendocardial coronary arteries.
Decreased diastolic coronary perfusion pressure
physical signs
Apical beat: localized, left lower shift
Heart sounds: S1 normal, S2 reversely split, audible and obvious S4
Murmur: aortic valve area, systolic, blowing, rough, increasing-decreasing type, often accompanied by tremor; calcification in the elderly has a musical sound
Others: thin and delayed pulse; systolic blood pressure and pulse pressure both decreased
Diagnosis and differential diagnosis
echocardiogram
Mitral regurgitation, tricuspid regurgitation, ventricular septum, left ventricular outflow tract obstruction disease
complication
Arrhythmias: atrial fibrillation, atrioventricular block, ventricular arrhythmias
sudden cardiac death
Heart failure: mainly left heart failure
infective endocarditis
systemic circulatory embolism
gastrointestinal bleeding
treat
Internal Medicine
Observe the progression of stenosis and choose the appropriate time for surgery
Prevent infection
Regular review
antiarrhythmic
anti-angina pectoris
Treat heart failure
surgical
Artificial valve replacement: main methods, long-term prognosis
Mild to moderate stenosis asymptomatic: no surgery
Severe stenosis without symptoms: If accompanied by heart enlargement or cardiac insufficiency, surgery may be required
Severe stenosis Symptomatic: Surgery
valve separation surgery under direct vision
percutaneous balloon angioplasty
aortic valve insufficiency
clinical manifestations
symptom
Acute: asymptomatic in mild cases, acute left heart failure and hypotension in severe cases
Chronic: no symptoms for many years
physical signs
Chronic
Blood vessel
Increased pulse pressure difference
peripheral vascular sign
Apical beat: shifted downward to the left, lifting-like beat
Heart sounds: weakened S1, weakened S2, common S3
Noise
Aortic valve area, diastolic, sighing, decremental murmur
Mild reflux: early diastole, high tone
Severe reflux: full diastole, rough
Valve leaflet prolapse: musical sound
Systolic ejection murmur at the base of the heart: rough, with tremor
Austin-Flint murmur: apical, mid- to late-diastolic, rumble-like murmur
acute
Blood vessels: No obvious peripheral vascular signs
Apical pulse: normal
Heart sounds: S1 decreases or disappears, P2 component increases, S3 is common
Heart murmur: shorter and lower-pitched in chronic cases
Diagnosis and differential diagnosis
Ultrasound confirmed
treat
Surgery should be performed before irreversible left ventricular dysfunction develops
Tricuspid and pulmonary valve disease
tricuspid stenosis
clinical manifestations
Signs: Systemic congestion signs (jugular venous distention, hepatomegaly, edema)
tricuspid valve insufficiency
Pulmonary stenosis (PS)
Pulmonary insufficiency (PI)
Graham Steell's murmur (secondary to pulmonary hypertension, left sternal border 2-4 intercostal space, early diastolic sigh-like decremental murmur)
polyvalvular disease
coronary heart disease
A disease caused by atherosclerosis in the coronary arteries that causes lumen stenosis or blockage, leading to myocardial ischemia, hypoxia, or necrosis. Clinically, it is referred to as coronary heart disease (CHD), also known as ischemic heart disease.
Risk factors: lipid metabolism disorders, hypertension, smoking, diabetes
Types
Asymptomatic coronary heart disease (occult type)
Angina pectoris
myocardial infarction
ischemic cardiomyopathy
sudden death
Angina pectoris
Based on the fixed severe stenosis of the coronary arteries, the increased myocardial load causes acute and temporary ischemia-hypoxia syndrome in the myocardium.
clinical manifestations
symptom
Location: retrosternal and precordial area, etc., can radiate to the shoulder and left arm, below the teeth, above the navel
Nature: pain, pressure, tightness, and suffocation
Accompanying symptoms: feeling of near-death
Triggers: overwork, excitement, cold, fullness, tachycardia, etc.
Duration: several minutes to more than ten minutes, usually less than half an hour.
Relief methods: rest, nitroglycerin
physical signs
Sympathetic nerve excitement: increased heart rate, increased blood pressure, pale complexion, sweating
Papillary muscle ischemia: transient apical systolic murmur
Cardiac insufficiency: transient third heart sound
Auxiliary inspection
Cardiac X-ray examination: no abnormality
Resting electrocardiogram: generally no abnormality
Electrocardiogram during attack: ST segment level or downward oblique depression (more than 0.1mV) appears in ischemia-related leads and/or T wave is significantly flat or inverted. ST segment elevation on electrocardiogram during variant angina pectoris attack
electrocardiogram stress test
Ambulatory ECG: continuous ECG recording for at least 24 hours
Radionuclides
echocardiogram
Coronary Angiography: The Gold Standard
diagnosis
risk factors
Typical clinical features of seizures
Auxiliary inspection
Types
exertional angina
stable angina
initial onset angina pectoris
Worsening angina
spontaneous angina
supine angina pectoris
variant angina
acute coronary insufficiency
Angina pectoris after death
mixed angina
CCS classification
Grade I: unrestricted activity, angina pectoris during extremely strenuous physical activity
Grade II: Mild limitation, angina pectoris during strenuous physical activity
Grade III: Obvious limitation, angina occurs during normal physical activity
Level IV: Angina can occur with slight activity or at rest.
Differential diagnosis
cardiac neurosis
Intercostal neuralgia and costochondritis
acute coronary syndrome
treat
attack period
Stop activity, inhale oxygen, sedate
Nitrates: Reduce preload
remission period
anti-ischemic drugs
Nitrates: 5 mononitrate preparations
Beta blockers: metoprolol, bisoprolol
Calcium channel blockers: diltiazem/diazepam
Metabolism: trimetazidine
sinoatrial node inhibitor
Statins lipid-lowering drugs
ACEI, ARB and sacubitril/valsartan
Antiplatelet (monoclonal antibody): aspirin, clopidogrel
Percutaneous coronary intervention PCI
Coronary Artery Bypass Grafting (CABG)
acute coronary syndrome (ACS)
A clinical syndrome of acute myocardial ischemia caused by the rupture or ulceration of unstable plaques in coronary atherosclerosis leading to local thrombosis in the blood vessels.
Pathological basis: role of platelets, thrombosis
Classification
Non-ST segment elevation acute coronary syndrome (UA unstable angina pectoris NSTEMI: myocardial infarction without ST segment elevation)
clinical manifestations
Typical ditto
Atypical: toothache, sore throat, upper abdominal pain, indigestion, chest pain like needles; easily ignored
Clinical features
Resting angina: attacks at rest, lasting more than 20 minutes
Initial angina pectoris: new onset within 1-2 months, CCS level 2 or Ⅲ
Worsened angina: worsening, CCS classification increased by 1 level
Physical examination
no obvious signs
Auxiliary inspection
Electrocardiogram: transient ST segment elevation (variant angina) or depression, or T wave flattening or inversion
Myocardial injury marker: cTn troponin
coronary angiography
treat
Antiplatelet therapy (dual antibodies): aspirin, clopidogrel
Anticoagulant therapy: low molecular weight heparin
Antimyocardial ischemia drugs: nitrates, beta blockers, calcium channel blockers
ACEI or ARB
Lipid-lowering treatment: statins
vascular reconstruction
Percutaneous coronary intervention PCI
Coronary Artery Bypass Grafting (CABG)
ST-segment elevation acute coronary syndrome (STEMI: ST-segment elevation myocardial infarction)
Myocardial infarctionMI
The coronary blood supply is sharply reduced or interrupted, and severe and long-lasting ischemia of the myocardium leads to ischemic necrosis of the myocardium. Arrhythmia, shock or heart failure can occur, which is a serious type of ACS.
Pathogenesis
Left main coronary artery occlusion: extensive left ventricular infarction
Left anterior descending coronary artery occlusion: left ventricular anterior wall, apex, inferolateral wall, anterior septal and premitral papillary muscle infarction
clinical manifestations
symptom
Aura: Before the onset, there may be fatigue, palpitations, chest discomfort, palpitations, shortness of breath, irritability, etc. during activities.
pain
appeared first
Compared with angina pectoris, it has the same location and nature, often has no obvious trigger, is more severe, and lasts longer (more than 30 minutes).
Resting and taking nitroglycerin tablets cannot provide relief.
Often accompanied by restlessness, sweating, fear, and a sense of impending death
Some pain radiates to the jaw, neck, and upper back
systemic symptoms
Fever (low grade fever), tachycardia, increased white blood cells and increased erythrocyte sedimentation rate
gastrointestinal symptoms
Nausea, vomiting, upper abdominal pain, hiccups
Arrhythmia
Ventricular arrhythmias are common, mostly in anterior wall myocardial infarction
Atrioventricular block and bundle branch block, more common in inferior wall myocardial infarction
hypotension and shock
heart failure
physical signs
heart
Heart rate increases, rarely slows down
S1 in the apical area is weakened, there may be S3 or S4, and galloping rhythm
Possible pericardial rub sound
There may be a rough systolic murmur in the apical area or a mid-late systolic click sound.
blood pressure
lower more
Auxiliary inspection
electrocardiogram
STEMI
Pathological Q waves, wide and deep
The ST segment is hunched upward and elevated
The T wave is high and sharp, then gradually becomes flat and inverted.
Regular: Acute
position
V1-V3--Anterior septal wall
V3-V5--limited to the front wall
V1-V5--wide front wall
Ⅰ. aVL--high side wall
Ⅱ, Ⅲ, AVF--lower wall
Myocardial injury marker: troponin
echocardiogram
Coronary angiography: the gold standard
diagnosis
Meet at least two of the following three criteria
Typical clinical manifestations, chest pain for more than 30 minutes
Characteristic electrocardiogram with dynamic changes
Dynamically changing myocardial injury markers
Differential diagnosis
acute pulmonary embolism
pneumothorax
aortic dissection
complication
Heart rupture: murmur
Papillary muscle dysfunction or rupture
ventricular aneurysm
ventricular septal perforation
post-myocardial infarction syndrome
treat
Restore myocardial blood perfusion as quickly as possible
Treat arrhythmias, heart failure, and various complications
General treatment
rest
ECG, blood pressure, respiratory monitoring
oxygen
Establish intravenous access
relieve pain
morphine
Nitrates
reperfusion therapy
percutaneous coronary intervention
Thrombolytic therapy
Thrombolytic therapy drugs
Best time: within 3 hours of onset of illness
Successful performance of thrombolysis
The elevated ST segment quickly decreased by >50% within 2 hours.
Chest pain is quickly relieved or disappears within 2 hours
Reperfusion arrhythmia occurs within 2 hours
The peak value of serum cardiac enzyme CK-MB is advanced to within 14 hours after onset.
antiarrhythmic
Ventricular arrhythmias: lidocaine, amiodarone
Bradyarrhythmias: atropine, temporary pacemaker
Anti-shock
Replenish blood volume
Anti-heart failure
Diuretics: Use with caution in right ventricular myocardial infarction
Try to avoid using digitalis within 24 hours after myocardial infarction
Vasodilators: Reduce the load on the heart
Antiplatelet and anticoagulation
Reduce fat
Rosuvastatin or atorvastatin
Postoperative prognosis
Aspirin, ACEI
Bβ blockers, blood pressure control
C cholesterol, smoking
D diet, diabetes
E education, exercise
infective endocarditis
Overview
Definition: Microbial infection of the lining of the heart, with the formation of vegetations
Neoplastic composition: platelets, cellulose, microorganisms, inflammatory cells
native valve endocarditis
Cause
acute
Most common: Staphylococcus aureus
Secondly: Pneumococcus, Neisseria gonorrhoeae
subacute
Most common: viridans streptococci
Second: D Streptococcus
Pathogenesis
Subacute, accounting for 2/3
hemodynamic factors
nonbacterial thrombotic endocarditis
transient bacteremia
bacterial infection sterile vegetations
acute
The pathogenesis is still unclear
Mainly affects normal heart valves
The amount of bacteria in the circulation is large and the bacteria are highly toxic
Aortic valve often affected
clinical manifestations
Symptoms: Fever, most common
Subacute patients have insidious onset
General malaise, fatigue, loss of appetite, and weight loss
Relaxing low-grade fever with chills and night sweats
Headaches, back pain, and muscle and joint pain are common
Acute cases are fulminant
High fever, chills, muscle and joint pain
septicemia
physical signs
heart murmur
Splenomegaly
Anemia: A common sign in subacute bacterial endocarditis (SBE)
Petechiae: skin, oral mucosa, palpebral conjunctiva
subungual bleeding
Roth spots: oval hemorrhagic spots on the retina
Janeway lesions: painless bleeding spots on palms and soles, seen in acute IE
Osler's nodules: painful nodular lesions, finger (toe) pads
complication
Heart: Heart failure (most common); Myocardial abscess; AMI; Myocarditis
Peripheral arterial embolism, infarction, metastatic abscess: brain, kidney, spleen
Laboratory and other tests
Urine: hematuria and proteinuria
Blood: anemia
Immunological examination: circulating immune complexes and rheumatoid factor (+)
Blood Culture: The Most Important Diagnostic Method
echocardiogram
Diagnosis and differential diagnosis
There are clinical manifestations and positive blood culture can make the diagnosis. The detection of vegetations by echocardiography is of great value in confirming the diagnosis.
treat
antimicrobial drug treatment
Medication principles
early, full, vein
The cause of the disease is unknown, medication based on experience
When isolating pathogens, select drugs based on drug susceptibility
empirical treatment
Acute: nafcillin plus ampicillin, or infusion of gentamicin
Subacute: According to the medication regimen for common pathogenic bacteria, penicillin is the main one or gentamicin is added.
Penicillin: 12-18 million U/d, intravenously divided into 4 times
Surgical treatment: artificial valve replacement
prognosis
Untreated acute patients almost always die within 4 weeks
The natural history of subacute patients is generally ≥6 months
Among the adverse prognostic factors, heart failure is the most serious
Causes of death--Heart failure, renal failure, embolism, ruptured bacterial aneurysm, and severe infection
prosthetic valve endocarditis
Early days
Within 60 days after valve replacement surgery
About 1/2 are staphylococci; followed by gram-negative bacilli and fungi
Often acute fulminant course
Late stage
60 days later
Streptococci are common, mainly viridans streptococci, followed by staphylococci and Staphylococcus epidermidis.
Subacute manifestations are common
High blood pressure
Hypertension: a cardiovascular syndrome characterized by persistent elevation of systemic arterial pressure.
Classification
Essential hypertension: 95% of causes unknown
Secondary hypertension: 5% have a clear and independent cause
essential hypertension
Definition: Clinic systolic blood pressure greater than 140mmHg and/or diastolic blood pressure greater than 90mmHg without the use of antihypertensive drugs
Cause
genetic factors
envirnmental factor
other factors
weight
Pathogenesis
Factors affecting blood pressure
The lateral pressure exerted on the walls of blood vessels when blood flows within them is called blood pressure
Blood pressure is mainly determined by cardiac output and systemic peripheral vascular resistance
neural mechanism
Sympathetic nervous system hyperactivity
Increased plasma catecholamine concentrations and enhanced contraction of resistance arterioles
kidney mechanism
Renal water and sodium retention, increased secretion of natriuretic hormones, and increased arteriolar resistance
Hormone mechanism
Renin-angiotensin-aldosterone system (RASS)
vascular mechanism
endothelial dysfunction
Insulin resistance
Normal glucose tolerance must be maintained at higher than normal levels of blood insulin release, indicating a reduced ability of body tissues to handle glucose with insulin.
Pathophysiology and pathology
heart
Left ventricular hypertrophy and dilation, hypertensive heart disease
brain
cerebral thrombosis
lacunar infarction
cerebral hemorrhage
kidney
chronic renal failure
fundus
retinal arteriolar spasm
retinal arteriosclerosis
Retinal exudation
retinal hemorrhage
Keith-Wagener fundus grading
Grade 1: Retinal artery narrowing
Grade 2: Retinal artery stenosis, arteriovenous cross-compression
Level 3: Fundus bleeding and cotton-like exudation
Grade 4: Hemorrhage or exudate with papilledema
Blood vessel
aortic dissection
clinical manifestations
There are no special clinical manifestations in the early stage. Later clinical manifestations are often related to the damage and insufficiency of the above-mentioned target organs.
symptom
dizziness, headache
Neck tightness, fatigue, palpitations, chest tightness
blurred vision
Nosebleeds
physical signs
High blood pressure
Hyperaortic second heart sound (A2)
Aortic valve area systolic murmur
laboratory tests
blood biochemistry
Three rules
24-hour ambulatory blood pressure monitoring ABPM: The instrument automatically measures blood pressure at intervals of 15 to 30 minutes in daily life, continuously for 24 hours or longer, and the circadian rhythm is "double peaks and one trough" (dipper type)
clinical indications
Diagnose patients with significant fluctuations in blood pressure
Diagnosing white coat hypertension
Detection of masked hypertension
Investigate the causes of stubborn and refractory hypertension
Assess blood pressure elevation and circadian rhythm
Assess treatment effectiveness
diagnosis
Standard: Generally, three blood pressure measurements on different days are required. If the systolic blood pressure is greater than 140mmHg and/or the diastolic blood pressure is greater than 90mmHg, hypertension can be diagnosed.
Risk factors used in risk stratification
Systolic and diastolic blood pressure levels (Grade 1-3)
Men >55 years old, women >65 years old
smoking
Total cholesterol >5.7mmol/L or LDL-C >3.3mmol/L
Impaired glucose tolerance and/or impaired fasting glucose
Family history of premature cardiovascular disease (age of onset <55 years old for men, <65 years old for women)
Abdominal obesity (BMI≥28 kg/m2)
Elevated blood homocysteine (≥10umol/L)
Target organ damage for risk stratification
left ventricular hypertrophy
atherosclerotic plaque
Decreased glomerular filtration rate
Microalbuminuria
Complications used for risk stratification
cerebrovascular disease
diabetic nephropathy
heart disease
vascular disease
treat
The ultimate goal of antihypertensive treatment: to reduce the incidence and mortality of cardiovascular and cerebrovascular diseases in patients with hypertension
Treatment principles
therapeutic lifestyle intervention
Antihypertensive drug treatment targets
Hypertension grade 2 and above
Hypertension combined with diabetes
Blood pressure control target value
It is generally recommended that the blood pressure control target value is at least <140/90mmHg
For patients with diabetes, chronic kidney disease, heart failure or coronary heart disease, the target blood pressure control value is <130/80mmHg
The target blood pressure reduction level for systolic hypertension in the elderly is systolic blood pressure ≤150/90mmHg
Collaborative control of multiple cardiovascular risk factors
Basic principles for the use of antihypertensive drugs
small dose
Prefer long-acting preparations
Combination medication
individualize
Basic antihypertensive medications
Angiotensin-converting enzyme inhibitor (ACEI), angiotensin II receptor blocker (ARB)----A
Representative drugs: perindopril, benazepril, valsartan, losartan
Indications: It has relatively good efficacy in patients with obesity, diabetes, and hypertensive patients with damaged heart and kidney target organs.
Contraindications: hyperkalemia, pregnancy, bilateral renal artery stenosis
β-receptor antagonist----B
Representative drugs: metoprolol, bisoprolol, propranolol, carvedolol
Contraindications: acute heart failure, bronchial asthma, sick sinus syndrome, atrioventricular block, peripheral vascular disease. Diabetic patients should use with caution
Adverse reactions: bradycardia
Calcium channel blockers (CCB)----C
Representative drugs: nifedipine, amlodipine, verapamil and diltiazem
Classification: dihydropyridines, non-dihydropyridines
Contraindications: Non-dihydropyridines are contraindicated in acute heart failure, sick sinus syndrome, and heart block.
Adverse reactions: increased heart rate
Diuretic (Diuretic)----D
Representative drugs: furosemide, hydrochlorothiazide, spironolactone
Contraindications: Thiazides are contraindicated in patients with gout; potassium-sparing diuretics should not be used in combination with ACEI, and patients with renal insufficiency are contraindicated.
Adverse reactions: hypokalemia
Other antihypertensive drugs
Alpha1 receptor antagonists: terazosin, doxazosin
Sympathetic inhibitors: reserpine, clonidine
Direct vasodilator: hydralazine
Commonly used combination medication regimens
ACEI/ARBCCB
ACEI/ARB Thiazide Diuretics
CCB (dihydropyridine) β-receptor antagonist
CCB (Dihydropyridine) Thiazide diuretic
Antihypertensive treatment of complications and comorbidities
combined with cerebrovascular disease
ARB, long-acting calcium antagonist, ACEI or diuretic can be used
Blood pressure target: 130/80mmHg
In the acute phase, antihypertensive treatment is only performed when blood pressure is extremely elevated (greater than 220/130mmHg), and the target should be no less than 160/100mmHg.
Combined with coronary heart disease
Beta blockers and long-acting calcium antagonists should be used for angina pectoris
People who have had myocardial infarction should use ACE inhibitors and beta-blockers to prevent ventricular remodeling.
combined with heart failure
Use ACEI and β-blockers asymptomatically
Treat symptoms with a combination of ACEI or ARB, diuretics, and beta-blockers
chronic renal failure
Combination of 3 or more antihypertensive drugs
ACEI or ARB are disabled in advanced stages
combined with diabetes
ARBs, ACEIs, long-acting calcium antagonists, and low-dose diuretics
Special types of high blood pressure
Hypertension in the elderly
isolated systolic hypertension
prone to orthostatic hypotension
high blood pressure in women
People who are pregnant or planning to become pregnant should avoid using ACE inhibitors or ARBs
hypertensive emergency
Definition: In patients with primary or secondary hypertension, under the action of certain inducements, the blood pressure suddenly and significantly increases (generally systolic blood pressure ≥180mmHg or diastolic blood pressure ≥120mmHg), accompanied by progressive heart, brain, and kidney disease. Symptoms of important target organ dysfunction such as
Including: hypertensive encephalopathy, intracranial hemorrhage (cerebral hemorrhage and subarachnoid hemorrhage), cerebral infarction, acute left heart failure, acute coronary syndrome, aortic dissection, acute renal failure, pheochromocytoma crisis, etc.
Processing principles
Lower blood pressure promptly
controlled blood pressure reduction
Reasonable selection of antihypertensive drugs
.Drugs to avoid: reserpine, diuretics, and strong diuretics
using drugs
sodium nitroprusside
Nitroglycerin
Nicardipine
Uradil
Hypertensive emergency
Blood pressure is significantly elevated without severe clinical symptoms and progressive target organ damage. May have headache, chest tightness, nose bleeding, irritability, etc.
Difference: whether there is recent acute progressive target organ damage
Treatment principle: lower blood pressure within 24-48 hours, use fast-acting oral antihypertensive drugs
resistant hypertension
Despite the use of a combination of more than three antihypertensive drugs at appropriate doses (including diuretics), the blood pressure still failed to reach the target level. Use four or more antihypertensive drugs to reach blood pressure target
secondary hypertension
Renal parenchymal hypertension
Treatment: Strictly control sodium intake, <3g/d; usually more than 3 antihypertensive drugs are needed to control blood pressure Below 130/80mmHg; combination therapy should include ACEI or ARB
Renovascular hypertension (renal artery stenosis)
Renal artery multi-slice CT or angiography can confirm the diagnosis
Disable ACEI or ARB
Pheochromocytoma
Typical attacks include paroxysmal increases in blood pressure accompanied by tachycardia, headache, sweating, and pale complexion.
At this time, blood and urine catecholamines and their metabolite VMA increased significantly.
Combined use of alpha and beta blockers to lower blood pressure
primary aldosteronism
Hypokalemia, decreased plasma renin activity, and increased blood and urinary aldosterone
Spironolactone and long-acting calcium antagonists
Cushing's syndrome
Central obesity, moon face, buffalo back, purple lines on skin, increased hair
Adrenal CT
aortic coarctation
The blood pressure of the upper limbs is increased but the blood pressure of the lower limbs is not high or actually decreased.
Aortography confirms diagnosis
Obstructive sleep apnea hypopnea syndrome (OSAHS)
Sleep apnea-hypopnea syndrome refers to repeated apnea or significant reduction in oral and nasal airflow due to the collapse of the pharyngeal muscles during sleep and obstruction of the airway.
Polysomnography: the “gold standard” for diagnosing OSAHS
Myocarditis, Cardiomyopathy
Viral MyocarditisAcute viral myocarditis
Myocarditis: refers to localized or diffuse inflammatory lesions of the myocardium, with diverse clinical manifestations ranging from mild to destructive changes.
clinical manifestations
Severe symptoms include acute left heart failure, Adams syndrome, cardiogenic shock, etc.
Auxiliary inspection
Myocardial enzyme spectrum: elevated CK-MB, cTnI, and cTnT
electrocardiogram
echocardiogram
Cardiac MRI
Nuclear heart function test
Coronary angiography, excluding myocardial infarction
Endomyocardial biopsy EMB, the “gold standard”
severe viral myocarditis
For example, the patient has an attack of Adams syndrome, congestive heart failure with or without myocardial infarction-like electrocardiographic changes, cardiogenic shock, acute renal failure, sustained ventricular tachycardia with hypotension, or myopericarditis, etc. One or more manifestations, including severe viral myocarditis, can be diagnosed.
Differential diagnosis
Avoid overdiagnosis of myocarditis
treat
Most viral myocarditis is self-limiting
rest
Symptomatic and supportive treatment
Device-assisted therapy
Antiviral treatment. No evidence of effectiveness
Immunosuppressants. No evidence-based medicine
prevention
Cardiomyopathycardiomyopathy
Classification
primary
Dilated Cardiomyopathy (DCM)
Hypertrophic Cardiomyopathy (HCM)
Specific
Dilated cardiomyopathy, DCM, dilated cardiomyopathy
A cardiomyopathy with unknown etiology, with reduced cardiac systolic function, heart failure, arrhythmia, and embolism as its basic clinical features. It can be progressive and the cause is unknown.
Pathophysiology
ventricular remodeling
Hemodynamic changes
symptom
Symptoms are basically equivalent to "heart failure", with difficulty breathing being the most prominent manifestation.
physical signs
Cardiomegaly
diastolic gallop
Jugular venous distention, hepatojugular reflux sign
Edema
Auxiliary inspection
Echocardiogram: "Big, small, thin, weak, thrombus"
Chest X-ray
electrocardiogram
diagnosis
Symptoms and signs of reduced cardiac systolic function
Typical changes on echocardiogram
Excluding other organic heart diseases
treat
Medication equals chronic heart failure
ACEI, ARB
ARNI (angiotensin receptor neprilysin inhibitor)
Beta-blockers
Aldosterone antagonists
Sodium-glucose cotransporter 2 inhibitor (SGLT-2i)
Non-drug (device) treatment
cardiac resynchronization therapy CRT
According to the principle of cardiac pacing, adjust the sequence of cardiac activation, improve the diastolic and systolic functions of the heart, improve the asynchrony of left and right ventricular contractions, reduce mitral valve regurgitation, and increase cardiac output, thereby achieving the purpose of treating heart failure.
Three-chamber pacing: right atrium, right ventricle, left ventricle
Indications
sinus rhythm
End left, LBBB (left bundle branch block)
Non-complete left, None LBBB: QRS ≥150
Other treatments
ICD
Hypertrophic cardiomyopathy, HCM hypertrophic cardiomyopathy
It is a group of autosomal dominant genetic abnormality diseases with different individual phenotypes. Typical features are "asymmetric myocardial hypertrophy, left ventricular outflow tract obstruction, and abnormal myocardial diastolic function."
pathology
Asymmetric septal hypertrophy (ASH)
Pathophysiology
left ventricular diastolic dysfunction
Left ventricular outflow tract obstruction, left ventricular outflow tract pressure gradient
SAM (Systolic anterior motion) phenomenon: forward movement of the anterior leaflet of the mitral valve during systole
venturi effect
Subendocardial ischemia and arrhythmias
clinical manifestations
symptom
Angina pectoris
Fainting or near fainting
sudden death
physical signs
Rough ejection systolic murmur in the 3rd to 4th intercostal space on the left sternal border, which may be accompanied by tremor
Weakened myocardial contractility, increased cardiac preload and afterload, weakened murmurs
Auxiliary inspection
echocardiogram
Asymmetric hypertrophy of the ventricular septum
The anterior leaflet of the mitral valve moves forward during systole (systolic anterior motion, SAM)
electrocardiogram
cardiac catheterization
There is a pressure difference between the left ventricular cavity and the outflow tract, greater than 30mmHg
Diagnosis and Differential Diagnosis
Echocardiography in typical cases can confirm the diagnosis
treat
medical treatement
Beta-blockers propranolol, metoprolol
Ca channel blockers verapamil, diltiazem
Antiarrhythmic drugs amiodarone
Avoid medications that worsen symptoms
non-pharmacological treatment
percutaneous septal myocardial ablation
hypertrophic septal resection
DDD pacemaker, ICD implantation if necessary
heart transplant
Prevent sudden death
Specific Cardiomyopathy
alcoholic cardiomyopathy
peripartum cardiomyopathy
Tachycardia cardiomyopathy
Takotsubo cardiomyopathy
A group of cardiomyopathies induced by stress and capable of spontaneous recovery
It often presents with chest pain and ST segment elevation on the electrocardiogram, which needs to be differentiated from myocardial infarction.
Octopus jar change
Arrhythmia
Definition: Abnormalities in cardiac rhythm, frequency, conduction velocity or activation sequence caused by abnormalities in the origin and/or conduction of cardiac impulses
The mechanism
Abnormal impulse formation (location, frequency, rhythm)
abnormal impulse conduction
reentry mechanism
There is a reentry loop
Unidirectional conduction block occurs in one of the channels
The other channel conducts slowly
Channels that were previously blocked are excited again
Classification
Abnormal impulse development
sinus arrhythmia
Sinus tachycardia, bradycardia, arrhythmia, asystole
Ectopic rhythm
Passive: escape beat or escape beat rhythm
Active: premature contractions and paroxysmal tachycardia; atrial flutter, fibrillation; ventricular flutter, fibrillation
abnormal impulse conduction
Physiological: interference and atrioventricular disconnection
Pathological: sinoatrial block, intraatrial block, atrioventricular block, intraventricular block
Abnormalities in the interventricular conduction pathway: preexcitation syndrome
symptom
Tachyarrhythmia (tachycardia)
Palpitations, amaurosis, syncope
Fatigue and decreased exercise tolerance
Symptoms related to heart failure
sudden stop
Bradyarrhythmias (bradycardia/conduction block)
Amaurosis, syncope
tired
physical signs
Tachyarrhythmia (tachycardia)
Fast heart rate, altered rhythm
In severe hemodynamic disorders, the pulse is weak or even non-pulse, and the blood pressure drops significantly or even cannot be measured.
Bradyarrhythmias (bradycardia/conduction block)
slow heart rate
Ⅲ degree AVB can hear the sound of cannons
May have split heart sounds
Auxiliary inspection
Confirming Arrhythmia Diagnosis: Electrocardiogram
Look for possible causes: Thyroid function
diagnosis method
History; physical examination; suggestive of arrhythmia
Electrocardiogram; dynamic electrocardiogram; preliminary diagnosis
Electrophysiological examination (esophagus/intracardiac) if necessary; further diagnosis
Electrolytes; thyroid function, etc.; determine whether there are related causes and incentives
Treatment principles
Causes, pathological treatments
Control heart rate and restore rhythm
Prevent recurrence
treatment method
medical treatement
Mechanism
reduce self-discipline
reduced afterdepolarization
Eliminate reentry
Antitachyarrhythmic drugs
Class I: Blocks Na channels; acts on atrium and ventricular myocardial working cells
Ⅰa: Quinidine: atrial fibrillation and atrial flutter
Ⅰb: lidocaine, slow heart rhythm: ventricular
Ⅰc: Smooth heart rhythm: All is OK
Class II: β-B, the only drug that improves patient endpoints
Class III: K channel blockers: broad spectrum, amiodarone
Category IV: CCB: slow-acting fiber, slows down sinus node frequency, atrioventricular conduction and triggers arrhythmia
Digitalis, ATP, MgSO4, KCl
Reasonable application
Treatment of underlying heart disease and correction of causes and triggers
Strictly control the indications for antiarrhythmic drugs
Pay attention to the side effects of antiarrhythmic drugs: effects on cardiac function, proarrhythmogenic effects and effects on other organs
non-pharmacological treatment
cardiac pacing
Cardioversion (surface, epicardial, ICD)
Radiofrequency Catheter Ablation (RFCA)
Surgery
sinus arrhythmia
sinus tachycardia
The impulse originates from the sinoatrial node and the frequency exceeds 100 times/min.
Clinical symptoms of palpitations and fatigue
Beta-blockers are preferred, but ivabradine is also an option
Less than three squares
sinus bradycardia
Sinus heart rate is less than 60 beats/min, often accompanied by sinus arrhythmia
Cardiac factors: sinus node disease, acute inferior wall myocardial infarction
Beta-blockers, calcium channel blockers, amiodarone, and arrhythmias
sinus arrest
Due to various reasons, the sinus node cannot produce impulses on time.
Amaurosis, syncope, A-S syndrome, and death may occur
In regular sinus P-P, there is a sudden long interval without P waves (often >2 seconds)
sinoatrial block
A delay or block in the conduction of impulses from the sinoatrial node to the atria
Sick Sinus Syndrome SSS
Sinus node hypofunction caused by lesions of the sinus node and its surrounding tissues, resulting in a variety of arrhythmia syndrome
ECG characteristics
Sustained and significant sinus bradycardia not caused by drugs, <50 beats/min
Sinus arrest and sinoatrial block
Simultaneous presence of sinoatrial block and atrioventricular block (binodal disease)
bradycardia-tachycardia syndrome: brady-tachycardia syndrome
diagnosis
Clinical symptoms combined with typical electrocardiographic findings
Atropine test
treat
Drug treatment: atropine, isopyrax, aminophylline
Pacemaker for severe or symptomatic patients
atrial arrhythmias
Premature atrial contractions/premature atrial contractions
ECG features
Early appearance of ectopic P′ waves
P′-R interval＞0.12s. The QRS wave shape is basically consistent with normal sinus shape
Incomplete compensation: Pairing interval The compensation interval is approximately less than 2 times the normal cardiac cycle
preterm contraction
Pairing interval (pairing interval): the time interval between the ectopic beat and its anterior sinus beat
Compensatory interval: the time interval between ectopic beat and posterior sinus beat, divided into complete compensation and incomplete compensation
treat
Often no treatment required
Beta blockers and calcium channel blockers
Catheter radiofrequency ablation in severe cases
atrial tachycardia
3 quick thrills in a row
Due to reentrant or increased self-discipline/triggering activities
Can be episodic or persistent
ECG features
Atrial rate 150 to 200 beats/min
If the wire between P’ is present, vagal stimulation does not terminate the tachycardia
treat
Treatment of etiological factors: discontinuation of digitalis and supplementation of potassium salts
control ventricular rate
Digitalis
beta blockers
calcium antagonist
Termination and relapse prevention
Class IA, IC and III antiarrhythmic drugs
Catheter Radiofrequency Ablation Treatment
atrial flutter
Mechanism: caused by large intra-atrial reentry
Thromboembolism may occur
ECG features
The P wave disappears and F waves of equal size appear with a frequency of 250 to 300 times/min. No equal wires between F waves
treat
acute attack
Control ventricular rate: digitalis, class II, IV drugs
Termination of seizures: overdrive suppression, electrical cardioversion, amiodarone, quinidine, and cardiac arrhythmia
Prevent attacks: quinidine, arrhythmide, amiodarone
Thromboembolism prevention: warfarin
RFCA (radiofrequency catheter ablation)
atrial fibrillation AF
The P wave disappears, and F waves of different sizes, shapes, and intervals appear.
Classification
First diagnosis of atrial fibrillation
Prophylactic antiarrhythmic drug therapy is not required unless symptoms are severe
Paroxysmal
Prevent recurrence, control ventricular rate and anticoagulate if necessary
Persistent
long term sustainability
permanent atrial fibrillation
The mechanism
Ectopic focal drive (focal): 90% is pulmonary veins and vestibule
Maintenance mechanism: atrial remodeling
complication
Thromboembolism - the biggest problem and threat
heart failure
Myocardial ischemia
Tachycardia cardiomyopathy
ECG features
The P wave disappears and is replaced by f waves of different sizes, shapes, and intervals, with a frequency of 350 to 600 times/min.
R-R intervals are definitely not equal
treat
Cause treatment
Control ventricular rate: Digitalis, Class II, Class IV (disabled for those with pre-excitation), Class III
Cardioversion: quinidine, arrhythmide, amiodarone, electrical cardioversion
Radiofrequency Catheter Ablation (RFCA)
Anticoagulant: warfarin
left atrial appendage occlusion
Anticoagulation index: CHADS2 score, if the score is greater than 2, anticoagulation is indicated
Atrioventricular junction zone related tachycardia
atrioventricular junctional premature contractions
ECG features
Premature appearance of normal QRS complex without associated sinus P wave
Retrograde P′ waves can be seen, the shape is different from that of sinus P, and the P′-R interval is <0.12 seconds.
Mostly complete compensation
Atrioventricular junctional escape beats and heart rhythm
nonparoxysmal atrioventricular junctional tachycardia
It is more common in digitalis poisoning. Electrical cardioversion is not recommended.
Paroxysmal supraventricular tachycardia PSVT
Classification
sinoatrial reentrant tachycardia
intraatrial reentrant tachycardia
Atrioventricular nodal reentrant tachycardia (AVNRT)
Atrioventricular reentrant tachycardia (AVRT)
ECG
Fast and neat narrow QRS complex, frequency 150~250 times/min
hidden P wave
mechanism
reentry conditions
Two or more pathways with inconsistent electrophysiological properties form a reentrant loop
Premature impulse causes unidirectional conduction block in one of the channels
The other channel conducts slowly enough that the previously blocked channel regains its excitability and is retrogradely excited to the proximal end of the reentry loop.
Excitement is once again transmitted along the previously transmitted channel
diagnosis
Typical symptoms of sudden and sudden palpitations
Typical electrocardiogram
treat
Terminate seizure
ATP, verapamil, -blockers, arrhythmias, digitalis
The Cure: Percutaneous Catheter Radiofrequency Ablation
Prevent recurrence: verapamil, beta-blockers, arrhythmia
ventricular arrhythmias
premature ventricular contractions
ECG features
A wide and deformed QRS appears early, the duration is >0.12s, and there is no P wave or related P wave before it.
Complete compensation: Pairing interval The compensation interval is approximately equal to 2 times the normal cardiac cycle
treat
No structural heart disease
Remove triggers
Drug therapy: β-blockers, Ib: lidocaine, slow heart rhythm, Ic: flat heart rhythm
catheter radiofrequency ablation
chronic organic heart disease
Treat underlying disease
Beta-blockers: Improve prognosis
ventricular tachycardia
Three consecutive premature ventricular contractions are called ventricular tachycardia
Ventricular tachycardia is a serious arrhythmia that often causes hemodynamic disturbance or death and requires active treatment.
ECG
The QRS wave is wide and deformed, often exceeding 0.12 seconds, and the ventricular rate is 100 to 250 beats/min.
Most P waves have nothing to do with QRS (ventricular-atrial dissociation)
Ventricular capture and ventricular fusion wave (an important basis for diagnosing ventricular tachycardia)
Torsades de pointes (TDP)
Every 3 to 10 QRS complexes continue to reverse the positive and negative directions of its main wave around the baseline.
treat
Terminate seizure
Hemodynamic instability: synchronized direct current cardioversion
Prevent recurrence
Amiodarone, beta-Blocker
RFCA (radiofrequency catheter ablation)
ICD
ventricular flutter and ventricular fibrillation
ECG
fatal arrhythmia
Emergency treatment: asynchronous electrical cardioversion, cardiopulmonary resuscitation
ICD implantation to treat ventricular tachycardia and ventricular fibrillation
atrioventricular block AVB
1st degree AVB: Atrioventricular conduction is delayed but can pass into the ventricles
PR interval is greater than 0.2 seconds, P-R interval is fixed
2nd degree AVB: Part of the atrium is excited and cannot be transmitted to the ventricle.
2 degrees type 1
P waves appear regularly, and the PR interval gradually lengthens until one QRS complex is missed after one P wave (Wenchen phenomenon)
2 degrees type 2
P waves appear regularly, and the PR interval is constant. Suddenly a P wave is followed by a QRS complex.
3rd degree AVB: All atrial excitement cannot be transmitted to the ventricles, also known as complete atrioventricular block
P-P intervals are equal, R-R intervals are equal
(P-R intervals are absolutely not equal) There is no fixed time relationship between P wave and QRS complex.
The atrial rate is faster than the ventricular rate (P-P interval < R-R interval)
There is a cannon sound
treat
Treatment of the cause or trigger
Drug treatment: atropine, isopropanol, aminophylline, glucocorticoids
intraventricular conduction block
right bundle branch block
Lead V1 shows rsR’ type or M waveform
left bundle branch block
More common in patients with organic heart disease
The q wave in leads I, AVL, V5, and V6 decreases or disappears, the main wave (R or S wave) widens, and the peak is rough or notched.
pericarditis
Refers to inflammatory lesions of the visceral and parietal layers of the pericardium
Pathology and pathophysiology
pericardial inflammation
Pericardial effusion (normal pericardium may have <50ml of ultrafiltrate)
Symptoms depend on "the amount of fluid and how quickly it develops."
symptom
chest pain
Difficulty breathing
Chronic pericardial effusion and related manifestations of right ventricular reflux disorder
Acute cardiac tamponade, dyspnea, profuse sweating, asphyxiation-like, shock-like changes
physical signs
pericardial friction rub
In acute cardiac tamponade, Beck's triad: hypotension, jugular venous distension, and distant heart sounds
laboratory tests
echocardiogram
X-ray examination
Myocardial enzyme spectrum
Detection of pericardial effusion
diagnosis
Pericarditis: pericardial friction rub
Pericardial effusion: confirmed by echocardiography
treat
Symptomatic treatment
Sedation and pain relief
Cause treatment
Antibacterial, antituberculosis, antirheumatic, treatment of primary tumors
constrictive pericarditis
The heart is surrounded by dense fibrotic pericardium, resulting in severe diastolic dysfunction
Pathology: pericardial thickening, adhesion, and calcification