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79-410: RVH may refer to: Right ventricular hypertrophy Royal Victoria Regional Health Centre Royal Victoria Hospital (disambiguation) Topics referred to by the same term [REDACTED] This disambiguation page lists articles associated with the title RVH . If an internal link led you here, you may wish to change the link to point directly to

158-780: A decline in the FEV1 . There is evidence of it causing some respiratory problems and its use in combination may have a cumulative toxic effect suggesting it as a risk factor for spontaneous pneumothorax, bullous emphysema , COPD and lung cancer. A noted difference between marijuana use and tobacco was that respiratory problems were resolved with stopping usage unlike the continued decline with stopping tobacco smoking. Respiratory symptoms reported with marijuana use included chronic cough, increased sputum production and wheezing but not shortness of breath. Also these symptoms were typically reported ten years ahead of their affecting tobacco smokers. Another study found that chronic marijuana smokers even with

237-527: A degree of airway hyperresponsiveness to irritants similar to those found in asthma. Low oxygen levels and eventually, high carbon dioxide levels in the blood , can occur from poor gas exchange due to decreased ventilation from airway obstruction, hyperinflation and a reduced desire to breathe. During exacerbations, airway inflammation is also increased, resulting in increased hyperinflation, reduced expiratory airflow and worsening of gas transfer. This can lead to low blood oxygen levels which if present for

316-462: A difficulty noted of determining the best treatment. The only genotype is the alpha-1 antitrypsin deficiency (AATD) genetic subtype and this has a specific treatment. The cause of the development of COPD is the exposure to harmful particles or gases, including tobacco smoke , that irritate the lung causing inflammation that interacts with a number of host factors. Such exposure needs to be significant or long-term. The greatest risk factor for

395-508: A genetic susceptibility, factors associated with poverty , aging and physical inactivity. Asthma and tuberculosis are also recognized as risk factors, as the comorbidity of COPD is reported to be 12 times higher in patients with asthma after adjusting for smoking history. In Europe airway hyperresponsiveness is rated as the second most important risk factor after smoking. A host factor of an airway branching variation , arising during development has been described. The respiratory tree

474-641: A greater exposure. These fuels are used as the main source of energy in 80% of homes in India , China and sub-Saharan Africa . Intense and prolonged exposure to workplace dusts , chemicals and fumes increases the risk of COPD in smokers, nonsmokers and never-smokers. Substances implicated in occupational exposure and listed in the UK, include organic and inorganic dusts such as cadmium , silica , dust from grains and flour and fumes from cadmium and welding that promote respiratory symptoms. Workplace exposure

553-552: A heterogeneous lung condition characterized by chronic respiratory symptoms ( dyspnea or shortness of breath , cough , sputum production and/or exacerbations) due to abnormalities of the airways ( bronchitis , bronchiolitis ) and/or alveoli ( emphysema ) that cause persistent, often progressive, airflow obstruction. The main symptoms of COPD include shortness of breath and a cough , which may or may not produce mucus . COPD progressively worsens , with everyday activities such as walking or dressing becoming difficult. While COPD

632-628: A high rate of morbidity and mortality and this rate is amplified when comorbid with COPD. Tuberculosis is a risk factor for the development of COPD, and is also a potential comorbidity. Most people with COPD die from comorbidities and not from respiratory problems. Anxiety and depression are often complications of COPD. Other complications include reduced quality of life and increased disability, cor pulmonale , frequent chest infections including pneumonia , secondary polycythemia , respiratory failure , pneumothorax , lung cancer, and cachexia (muscle wasting). Along with these complications, there

711-451: A history of exposure to risk factors for the disease. Spirometry is then used to confirm the diagnosis. Spirometry measures the amount of airflow obstruction present and is generally carried out after the use of a bronchodilator , a medication to open up the airways. Two main components are measured to make the diagnosis, the forced expiratory volume in one second (FEV1), which is the greatest volume of air that can be breathed out in

790-534: A marked decrease in the number of cold and flu infections during this time. Smoke from wildfires is proving an increasing risk in many parts of the world and government agencies have published protective advice on their websites. In the US the EPA advises that the use of dust masks do not give protection from the fine particles in wildfires and instead advise the use of well-fitting particulate masks . This same advice

869-593: A modified MRC scale that if used, needs to include other tests since it is simply a test of breathlessness experienced. Scores on CAT range from 0–40 with the higher the score, the more severe the disease. Spirometry may help to determine the severity of airflow limitation. This is typically based on the FEV1 expressed as a percentage of the predicted "normal" for the person's age, gender, height and weight. Guidelines published in 2011 by American and European medical societies recommend partly basing treatment recommendations on

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948-513: A possibility of certain inhaled corticosteroids for COPD providing a protective role against COVID-19. Differentiating COVID-19 symptoms from an exacerbation is difficult; mild prodromal symptoms may delay its recognition and where they include loss of taste or smell COVID-19 is to be suspected. Many definitions of COPD in the past included chronic bronchitis and emphysema but these have never been included in GOLD report definitions. Emphysema

1027-428: A prolonged period, can result in narrowing of the arteries in the lungs, while emphysema leads to the breakdown of capillaries in the lungs. Both of these conditions may result in pulmonary heart disease also classically known as cor pulmonale . The diagnosis of COPD should be considered in anyone over the age of 35 to 40 who has shortness of breath , a chronic cough, sputum production, or frequent winter colds and

1106-580: A reduced cardiac output . These include: People may rarely present with the symptoms of Ortner's syndrome , which include cough, haemoptysis and hoarseness. On physical examination, the most prominent features are due to the development of right-sided heart failure. These can include a raised jugular venous pressure , ascites , left parasternal heave and a tender, enlarged liver on palpation. On inspection, patients may be chronically ill, cyanotic , cachectic and occasionally jaundiced . On auscultation , an accentuated second pulmonary sound (S2),

1185-489: A significant and chronic inflammatory response to inhaled irritants which ultimately leads to bronchial and alveolar remodelling in the lung known as small airways disease . Thus, airway remodelling with narrowing of peripheral airway and emphysema are responsible for the alteration of lung function. Mucociliary clearance is particularly altered with a dysregulation of cilia and mucus production. Small airway disease sometimes called chronic bronchiolitis , appears to be

1264-427: A significant number of people. Chronic bronchitis does not always result in airflow limitation. However, in young adults with chronic bronchitis who smoke, the risk of developing COPD is high. Many definitions of COPD in the past included emphysema and chronic bronchitis, but these have never been included in GOLD report definitions. Emphysema and chronic bronchitis remain the predominant phenotypes of COPD but there

1343-408: A third heart sound termed a ‘right ventricular gallop’, as well as a systolic murmur over the tricuspid area accentuated by inspiration may be present. On occasion, the systolic murmur can be transmitted and auscultated over the liver. Less typically, diastolic murmur may also be heard as a result of pulmonary insufficiency. RVH usually occurs due to chronic lung disease or structural defects in

1422-402: A value above 5 mm considered to be hypertrophic. Right ventricular hypertrophy in itself is not the main issue, but what right ventricular hypertrophy represents is. Right ventricular hypertrophy is the intermediate stage between increased right ventricular pressure (in the early stages) and right ventricle failure (in the later stages). As such, management of right ventricular hypertrophy

1501-503: Is alpha-1 antitrypsin deficiency (AATD) and this is the only genotype (genetic subtype) with a specific treatment. This risk is particularly high if someone deficient in alpha-1 antitrypsin (AAT) also smokes. It is responsible for about 1–5% of cases and the condition is present in about three to four in 10,000 people. Mutations in MMP1 gene that encodes for interstitial collagenase are associated with COPD. The COPDGene study

1580-465: Is asthma-COPD overlap , which is a condition sharing clinical features of both asthma and COPD. Spirometry measures are inadequate for defining phenotypes and chest X-ray, CT and MRI scans have been mostly employed. Most cases of COPD are diagnosed at a late stage and the use of imaging methods would allow earlier detection and treatment. The identification and recognition of different phenotypes can guide appropriate treatment approaches. For example,

1659-476: Is tobacco smoking with an increased rate of developing COPD shown in smokers and ex-smokers. Of those who smoke, about 20% will get COPD, increasing to less than 50% in heavy smokers. In the United States and United Kingdom, of those with COPD, 80–95% are either current or previous smokers. Several studies indicate that women are more susceptible than men to the harmful effects of tobacco smoke. For

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1738-498: Is 4 per million people. RVH occurs in approximately 30% of these cases. PH is broadly split into five categories by the World Health Organization , based on the underlying cause. The incidence of RVH varies between the groups. Common causes of PH include chronic obstructive pulmonary disease (COPD), pulmonary embolism , and other restrictive lung diseases. RVH often occurs as a result of these disorders. RVH

1817-421: Is a chronic cough, which may or may not be productive of mucus as phlegm . Phlegm coughed up as sputum can be intermittent and may be swallowed or spat out depending on social or cultural factors and is therefore not always easy to evaluate. However, an accompanying productive cough is only seen in up to 30% of cases. Sometimes limited airflow may develop in the absence of a cough. Symptoms are usually worse in

1896-494: Is a filter for harmful substances and any variant has the potential to disrupt this. A variation has been found to be associated with the development of chronic bronchitis and another with the development of emphysema. A branch variant in the central airway is specifically associated with an increased susceptibility for the later development of COPD. A genetic association for the variants has been sometimes found with FGF10 . Alcohol abuse can lead to alcoholic lung disease and

1975-422: Is a sudden worsening of signs and symptoms that lasts for several days. The key symptom is increased breathlessness, other more pronounced symptoms are of excessive mucus, increased cough and wheeze. A commonly found sign is air trapping giving a difficulty in complete exhalation . The usual cause of an exacerbation is a viral infection , most often the common cold . The common cold is usually associated with

2054-440: Is about either preventing the development of right ventricular hypertrophy in the first place, or preventing the progression towards right ventricle failure. Right ventricular hypertrophy in itself has no (pharmacological) treatment. Since the main causes of right ventricular hypertrophy is tricuspid regurgitation or pulmonary hypertension (discussed above), management involves treatment of these conditions. Tricuspid regurgitation

2133-464: Is also associated with abdominal obesity , elevated fasting blood glucose, high systolic blood pressure , and fractional shortening of the left ventricular mid-wall. Other risk factors for RVH include smoking, sleep apnea , and strenuous activity. These increase the risk of heart and lung disease and hence RVH. Right ventricular hypertrophy can be both a physiological and pathophysiological process. It becomes pathophysiological (damaging) when there

2212-515: Is an air pollutant associated with an increased risk of hospitalization due to the exacerbations caused. Long-term exposure is indicated as an increased rate of mortality in COPD. Studies have shown that people who live in large cities have a higher rate of COPD compared to people who live in rural areas. Areas with poor outdoor air quality, including that from exhaust gas , generally have higher rates of COPD. Urban air pollution significantly effects

2291-578: Is an associated risk of developing pulmonary hypertension . The estimated prevalence of pulmonary hypertension complicating COPD was reported at 39% in a meta-analysis. Of the people with COPD listed for lung transplantation, 82% were documented as having pulmonary hypertension via right heart catheterization, noting a mean pulmonary arterial pressure greater than 20mm Hg. Despite pulmonary hypertension being relatively rare in people with COPD, mild elevations of pulmonary arterial pressure can lead to worse outcomes, including risk of death. Cognitive impairment

2370-410: Is an important risk factor for COPD. It is advised that everybody with COPD be screened for A1AD. Metabolic syndrome has been seen to affect up to fifty percent of those with COPD and significantly affects the outcomes. When comorbid with COPD there is more systemic inflammation. It is not known if it co-exists with COPD or develops as a consequence of the pathology. Metabolic syndrome on its own has

2449-544: Is an intermediate molecule in the signalling pathway and mice lacking PKC shown resistance to heart failure compared to mice overexpressing PKC which shown heart dysfunction. Targeting the renin–angiotensin (RAAS) system (using angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers) are a well-recognized clinical approach for reversing maladaptive cardiac hypertrophy independently of blood pressure. Catecholamines levels increase due to increased sympathetic nervous system activity. Catecholamines can act on

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2528-518: Is an ongoing longitudinal study into the epidemiology of COPD, identifying phenotypes and looking for their likely association with susceptible genes. Genome wide analyses in concert with the International COPD Genetics Consortium has identified more than 80 genome regions associated with COPD and further studies in these regions has been called for. Whole genome sequencing is an ongoing collaboration (2019) with

2607-502: Is believed to be the cause in 10–20% of cases and in the United States, it is believed to be related to around 30% of cases among never smokers and probably represents a greater risk in countries without sufficient regulations. The negative effects of dust exposure and cigarette smoke exposure appear to be cumulative. Genetics play a role in the development of COPD. It is more common among relatives of those with COPD who smoke than unrelated smokers. The most well known genetic risk factor

2686-428: Is common in those with COPD as it is for other lung conditions that affect airflow. Cognitive impairment is associated with the declining ability to cope with the basic activities of daily living . It is unclear if those with COPD are at greater risk of contracting COVID-19 , though if infected they are at risk of hospitalization and developing severe COVID-19. However, there are laboratory and clinical studies showing

2765-466: Is defined as enlarged airspaces ( alveoli ) whose walls have broken down resulting in permanent damage to the lung tissue . Chronic bronchitis is defined as a productive cough that is present for at least three months each year for two years. Both of these conditions can exist without airflow limitation when they are not classed as COPD. Emphysema is just one of the structural abnormalities that can limit airflow and can exist without airflow limitation in

2844-442: Is defined as enlarged airspaces ( alveoli ) whose walls break down resulting in permanent damage to the lung tissue and is just one of the structural abnormalities that can limit airflow. The condition can exist without airflow limitation but commonly it does. Chronic bronchitis is defined as a productive cough that is present for at least three months each year for two years but does not always result in airflow limitation although

2923-839: Is excessive hypertrophy. The pathophysiological process mainly occurs through aberrant signalling of the neuroendocrine hormones; angiotensin II , endothelin-1 and the catecholamines (e.g. noradrenaline ). Angiotensin-II and endothelin-1 are hormones that bind to the angiotensin (AT) and endothelin (ET) receptors. These are G-protein coupled receptors that act via internal signalling pathways. Through several intermediates, these pathways directly or indirectly increase reactive oxygen species (ROS) production causing accumulation in myocardial cells . This can subsequently induce necrotic cell death, fibrosis , and mitochondrial dysfunction. This has been demonstrated in animal studies. Protein Kinase C (PKC)

3002-454: Is incurable, it is preventable and treatable. The two most common types of COPD are emphysema and chronic bronchitis and have been the two classic COPD phenotypes . However, this basic dogma has been challenged as varying degrees of co-existing emphysema, chronic bronchitis, and potentially significant vascular diseases have all been acknowledged in those with COPD, giving rise to the classification of other phenotypes or subtypes. Emphysema

3081-409: Is more complex, with a diverse group of disorders of differing risk factors and clinical courses that has resulted in a number of subtypes or phenotypes of COPD being accepted and proposed. The two classic emphysematous and chronic bronchitic phenotypes are fundamentally different conditions with unique underlying mechanisms. Another subtype of COPD, categorized by some as a separate clinical entity,

3160-450: Is not sufficient for the diagnosis of COPD. Screening using spirometry in those without symptoms has uncertain effect and is generally not recommended; however, it is recommended for those without symptoms but with a known risk factor. A number of methods can be used to assess the affects and severity of COPD. The MRC breathlessness scale or the COPD assessment test (CAT) are simple questionnaires that may be used. GOLD refers to

3239-532: Is offered in Canada and Australia to the effects of their forest fires. The number of exacerbations is not seen to relate to any stage of the disease; those with two or more a year are classed as frequent exacerbators and these lead to a worsening in the disease progression. Frailty in ageing increases exacerbations and hospitalization. Acute exacerbations in COPD are often unexplained and thought to have many causes other than infections. A study has emphasized

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3318-575: Is often overlap between them and a number of other phenotypes have also been described. COPD and asthma may coexist and converge in some individuals. COPD is associated with low-grade systemic inflammation. The most common cause of COPD is tobacco smoking . Other risk factors include indoor and outdoor air pollution including dust , exposure to occupational irritants such as dust from grains , cadmium dust or fumes , and genetics , such as alpha-1 antitrypsin deficiency . In developing countries , common sources of household air pollution are

3397-509: Is required to work harder. Therefore, the main causes of RVH are pathologies of systems related to the right ventricle such as the pulmonary artery , the tricuspid valve or the airways. RVH can be benign and have little impact on day-to-day life or it can lead to conditions such as heart failure , which has a poor prognosis. Although presentations vary, individuals with right ventricular hypertrophy can experience symptoms that are associated with pulmonary hypertension , heart failure and/or

3476-481: Is seen in 76% of patients with advanced COPD and 50% of patients with restrictive lung disease. RVH also occurs in response to structural defects in the heart. One common cause is tricuspid insufficiency . This is a disorder where the tricuspid valve fails to close properly, allowing backward flow of blood. Other structural defects which lead to RVH include tetralogy of Fallot , ventricular septal defects , pulmonary valve stenosis , and atrial septal defects . RVH

3555-513: Is seen to be an independent risk factor for COPD. Mucociliary clearance is disrupted by chronic exposure to alcohol; macrophage activity is diminished and an inflammatory response promoted. The damage leads to a susceptibility for infection, including COVID-19 , more so when combined with smoking; smoking induces the upregulation of the expression of ACE2 , a receptor for the SARS-CoV-2 virus. The primary risk factor for COPD globally

3634-399: Is started, resulting in an increase in the total volume of air in the lungs at any given time, a process called air trapping which is closely followed by hyperinflation . Hyperinflation from exercise is linked to shortness of breath in COPD, as breathing in is less comfortable when the lungs are already partly filled. Hyperinflation may also worsen during an exacerbation. There may also be

3713-495: Is termed right ventricular failure. This right ventricular failure is the main complication of right ventricular hypertrophy. The mechanisms underlying the progression from hypertrophy to failure is not well understood, and the best management approach involves reducing/minimising the risk factors of progression. Lifestyle changes can often help to reduce the risk of this progression. Lifestyle changes include: eating less salty food as salt consumption leads to greater fluid retention by

3792-425: Is the frequent exacerbator. The frequent exacerbator has two or more exacerbations a year, has a poor prognosis and is described as a moderately stable phenotype. A pulmonary vascular COPD phenotype has been described due to cardiovascular dysfunction. A molecular phenotype of CFTR dysfunction is shared with cystic fibrosis . A combined phenotype of chronic bronchitis and bronchiectasis has been described with

3871-410: Is the second most commonly smoked substance, but evidence linking its use to COPD is very limited. Limited evidence shows that marijuana does not accelerate lung function decline. A low use of marijuana gives a bronchodilatory effect rather than the bronchoconstrictive effect from tobacco use, but it is often smoked in combination with tobacco or on its own by tobacco smokers. Higher use however has shown

3950-430: Is typically treated conservatively by aiming to treat the underlying cause and following up the patient regularly. Surgery is considered in more serious situations where the patient is severely symptomatic. Surgical options include either: replacement of the valve or repair of the valve (termed annuloplasty). When it comes to replacement, there is a choice between a bioprosthetic valve or a mechanical valve, depending upon

4029-544: Is well established but since the left ventricular activity is dominant on the ECG a large degree of RVH is often required for any detectable changes. Nonetheless, the ECG is used to assist with the diagnosis of RVH. A post mortem study on 51 adult male patients concluded that anatomical RVH may be diagnosed using one or more of the following ECG criteria: However, the American Heart Association recommended

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4108-573: The National Heart, Lung and Blood Institute (NHLBI) to identify rare genetic determinants. COPD is a progressive lung disease in which chronic, incompletely reversible poor airflow (airflow limitation) and an inability to breathe out fully ( air trapping ) exist. The poor airflow is the result of small airways disease and emphysema (the breakdown of lung tissue ). The relative contributions of these two factors vary between people. Air trapping precedes lung hyperinflation. COPD develops as

4187-519: The PDE4 inhibitor roflumilast is targeted at the chronic-bronchitic phenotype. Two inflammatory phenotypes show a phenotype stability: the neutrophilic inflammatory phenotype and the eosinophilic inflammatory phenotype. Mepolizumab , a monoclonal antibody , has been shown to have benefit in treating the eosinophilic inflammatory type rather than the use of oral corticosteroids, but further studies have been called for. Another recognized phenotype

4266-422: The connective tissue of the lungs by proteases (particularly elastase ) that are insufficiently inhibited by protease inhibitors . The destruction of the connective tissue of the lungs leads to emphysema, which then contributes to the poor airflow and finally, poor absorption and release of respiratory gases. General muscle wasting that often occurs in COPD may be partly due to inflammatory mediators released by

4345-439: The FEV1. The GOLD guidelines group people into four categories based on symptoms assessment, degree of airflow limitation and history of exacerbations. Weight loss, muscle loss and fatigue are seen in severe and very severe cases. Use of screening questionnaires, such as COPD diagnostic questionnaire (CDQ), alone or in combination with hand-held flow meters is appropriate for screening of COPD in primary care. A chest X-ray

4424-490: The United States in 2010 the economic cost was put at US$ 32.1 billion and projected to rise to US$ 49 billion in 2020. In the United Kingdom this cost is estimated at £3.8 billion annually. A cardinal symptom of COPD is the chronic and progressive shortness of breath which is most characteristic of the condition. Shortness of breath (breathlessness) is often the most distressing symptom responsible for

4503-405: The additional use of tobacco developed similar respiratory problems, but did not seem to develop airflow limitation and COPD. Exposure to particulates can bring about the development of COPD, or its exacerbations. Those with COPD are more susceptible to the harmful effects of particulate exposure that can cause acute exacerbations brought about by infections. Black carbon also known as soot ,

4582-731: The alpha-adrenergic receptors and beta-adrenergic receptors which are G-protein coupled receptors. This binding initiates the same intracellular signalling pathways as angiotensin and endothelin. There is also activation of cAMP and an increase in intracellular Ca2+ which leads to contractile dysfunction and fibrosis. Hormones are not the only cause of RVH. Hypertrophy can also be caused by mechanical forces, mTOR pathways, nitric oxide and immune cells . Immune cells can cause hypertrophy by inducing inflammation. The two main diagnostic tests used to confirm right ventricular hypertrophy are electrocardiography and echocardiography. The use of electrocardiogram (ECG) to measure cardiac chamber hypertrophy

4661-760: The associated anxiety and level of disability experienced. Symptoms of wheezing and chest tightness associated with breathlessness can be variable over the course of a day or between days and are not always present. Chest tightness often follows exertion. Many people with more advanced COPD breathe through pursed lips , which can improve shortness of breath. Shortness of breath is often responsible for reduced physical activity and low levels of physical activity are associated with worse outcomes. In severe and very severe cases there may be constant tiredness , weight loss, muscle loss and anorexia . People with COPD often have increased breathlessness and frequent colds before seeking treatment. The most often first symptom of COPD

4740-521: The body; smoking cessation; avoiding excessive alcohol consumption as alcohol reduces the force of heart contractions. Once right ventricular hypertrophy progresses to right ventricular failure, the treatment becomes that of heart failure. Briefly, this includes the use of: Chronic obstructive pulmonary disease Chronic obstructive pulmonary disease ( COPD ) is a type of progressive lung disease characterized by chronic respiratory symptoms and airflow limitation. GOLD 2024 defined COPD as

4819-449: The developing lung and its maturation, and contributes a potential risk factor for the later development of COPD. The overall effect in relation to smoking is believed to be small. Poorly ventilated fires used for cooking and heating, are often fueled by coal or biomass such as wood and dry dung , leading to indoor air pollution and are one of the most common causes of COPD in developing countries . Women are affected more as they have

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4898-503: The development of COPD is tobacco smoke. However, less than 50 percent of heavy smokers develop COPD, so other factors need to be considered, including exposure to indoor and outdoor pollutants, allergens, occupational exposure, and host factors. One of the known causes of COPD is the exposure to construction dust . The three main types of construction dust are silica dust , non-silica dust (e.g., dust from gypsum, cement, limestone, marble and dolomite) and wood dust . Host factors include

4977-424: The elderly. The National Institute for Health and Care Excellence criteria additionally require a FEV1 less than 80% of predicted. People with COPD also exhibit a decrease in diffusing capacity of the lung for carbon monoxide due to decreased surface area in the alveoli, as well as damage to the capillary bed. Testing the peak expiratory flow (the maximum speed of expiration), commonly used in asthma diagnosis,

5056-454: The first second of a breath and the forced vital capacity (FVC), which is the greatest volume of air that can be breathed out in a single large breath. Normally, 75–80% of the FVC comes out in the first second and a FEV1/FVC ratio less than 70% in someone with symptoms of COPD defines a person as having the disease. Based on these measurements, spirometry would lead to over-diagnosis of COPD in

5135-460: The global population). It typically occurs in males and females over the age of 35–40. In 2019 it caused 3.2 million deaths, 80% occurring in lower and middle income countries, up from 2.4 million deaths in 1990. In 2021, it was the fourth biggest cause of death, responsible for approximately 5% of total deaths. The number of deaths is projected to increase further because of continued exposure to risk factors and an aging population. In

5214-444: The heart. One of the most common causes of RVH is pulmonary hypertension (PH), defined as increased blood pressure in the vessels supplying blood to the lungs. PH leads to increased pulmonary artery pressure. The right ventricle tries to compensate for this increased pressure by changing its shape and size. Hypertrophy of individual myocytes results in an increase in right ventricular wall thickness. The worldwide incidence of PH

5293-407: The intended article. Retrieved from " https://en.wikipedia.org/w/index.php?title=RVH&oldid=933101035 " Category : Disambiguation pages Hidden categories: Short description is different from Wikidata All article disambiguation pages All disambiguation pages Right ventricular hypertrophy Since RVH is an enlargement of muscle it arises when the muscle

5372-407: The lungs into the blood. Narrowing of the airways occurs due to inflammation and subsequent scarring within them. This contributes to the inability to breathe out fully. The greatest reduction in air flow occurs when breathing out, as the pressure in the chest is compressing the airways at this time. This can result in more air from the previous breath remaining within the lungs when the next breath

5451-495: The morning. A chronic productive cough is the result of mucus hypersecretion and when it persists for more than three months each year for at least two years, it is defined as chronic bronchitis . Chronic bronchitis can occur before the restricted airflow diagnostic of COPD. Some people with COPD attribute the symptoms to the consequences of smoking. In severe COPD, vigorous coughing may lead to rib fractures or to a brief loss of consciousness . An acute exacerbation

5530-559: The possibility of a pulmonary embolism as sometimes being responsible in these cases. Signs can include pleuritic chest pain and heart failure without signs of infection. Such emboli could respond to anticoagulants . COPD often occurs along with a number of other conditions ( comorbidities ) due in part to shared risk factors. Common comorbidities include cardiovascular disease , skeletal muscle dysfunction, metabolic syndrome , osteoporosis , depression , anxiety , asthma and lung cancer . Alpha-1 antitrypsin deficiency (A1AD)

5609-588: The precursor for the development of emphysema. The inflammatory cells involved include neutrophils and macrophages , two types of white blood cells. Those who smoke additionally have cytotoxic T cell involvement and some people with COPD have eosinophil involvement similar to that in asthma. Part of this cell response is brought on by inflammatory mediators such as chemotactic factors . Other processes involved with lung damage include oxidative stress produced by high concentrations of free radicals in tobacco smoke and released by inflammatory cells and breakdown of

5688-402: The presence or not of collateral ventilation , evident in emphysema and lacking in chronic bronchitis. This terminology was no longer accepted as useful, as most people with COPD have a combination of both emphysema and airway disease. These are now recognized as the two major phenotypes of COPD — emphysematous phenotype and chronic bronchitic phenotype. It has since been recognized that COPD

5767-482: The release of excessive proteases in lungs, which then degrades elastin , the major component of alveoli. Smoke also impairs the action of cilia , inhibiting mucociliary clearance that clears the bronchi of mucus, cellular debris and unwanted fluid. Other types of tobacco smoke, such as from cigar, pipe , water-pipe and hookah use, also confer a risk. Water-pipe or hookah smoke appears to be as harmful or even more harmful than smoking cigarettes. Marijuana

5846-435: The risk of developing COPD is great. These older definitions grouped the two types as type A and type B . Type A were emphysema types known as pink puffers due to their pink complexion, fast breathing rate and pursed lips. Type B were chronic bronchitic types referred to as blue bloaters due to low oxygen levels causing a bluish color to the skin and lips and swollen ankles. These differences were suggested to be due to

5925-431: The same amount of cigarette smoking, women have a higher risk of COPD than men. In non-smokers, exposure to second-hand smoke (passive smoking) is the cause of 1.2 million deaths from the more than 8 million deaths worldwide each year due to tobacco smoke . Women who smoke during pregnancy , and during the early life of the child is a risk factor for the later development of COPD in their child. Inhaled smoke triggers

6004-478: The specific patient characteristics. Mechanical valve has greater durability, but requires anti-coagulation to reduce the risk of thrombosis. Treatment of pulmonary hypertension will depend on the specific cause of the pulmonary hypertension. On top of this, the following may also be considered: diuretic, oxygen and anti-coagulant therapy. After a prolonged period, the right ventricle fails to adapt sufficiently to pump against increased right ventricle pressure, which

6083-404: The use of additional diagnostic tests to diagnose RVH because no single criteria or set of criteria were considered sufficiently reliable. Echocardiography can be used to directly visualise right ventricular wall thickness. The preferred technique is the trans-oesophageal approach giving a view of 4 chambers. The normal thickness of a right ventricular free wall ranges from 2-5 millimetres, with

6162-896: The use of coal and biomass such as wood and dry dung as fuel for cooking and heating . The diagnosis is based on poor airflow as measured by spirometry . Most cases of COPD can be prevented by reducing exposure to risk factors such as smoking and indoor and outdoor pollutants. While treatment can slow worsening, there is no conclusive evidence that any medications can change the long-term decline in lung function. COPD treatments include smoking cessation , vaccinations , pulmonary rehabilitation , inhaled bronchodilators and corticosteroids . Some people may benefit from long-term oxygen therapy , lung volume reduction and lung transplantation . In those who have periods of acute worsening , increased use of medications, antibiotics , corticosteroids and hospitalization may be needed. As of 2015, COPD affected about 174.5 million people (2.4% of

6241-613: The winter months but can occur at any time. Other respiratory infections may be bacterial or in combination sometimes secondary to a viral infection. The most common bacterial infection is caused by Haemophilus influenzae . Other risks include exposure to tobacco smoke (active and passive ) and environmental pollutants  – both indoor and outdoor. During the COVID-19 pandemic , hospital admissions for COPD exacerbations sharply decreased which may be attributable to reduction of emissions and cleaner air. There has also been

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