Pulmonary heart disease

Rheumatic heart disease, pulmonary heart disease, pulmonary emphysema, anemia, nephritis, drugs that inhibit heartbeat and reduce blood pressure, poor nutrition or having a low calorie diet. 

Acute and chronic bronchitis, pneumonia, upper respiratory infection, pulmonary emphysema, pulmonary heart disease, heart failure, acute nephritis and renal failure, chronic nephritis, gastritis, hypothyroidism, hypoadrenalism, fibromyalgia, rheumatic arthritis and rheumatoid arthritis. 

Acute and chronic bronchitis, asthma, emphysema, pulmonary heart disease, heart failure. 

Rheumatic arthritis, rheumatoid arthritis, cervical or lumbar spondylosis, osteoarthritis, sciatica, Raynaud s disease, vasculitis, pulmonary heart disease, rheumatic heart disease, coronary heart disease, migraine, hemiplegia after cerebrovascular accident, paralysis, facial paralysis, facial spasm, skin diseases that are influenced by changes in the weather and are characterized by itchy, weeping, red or dry skin lesions. 

Primary pulmonary diseases (e.g. primary pulmonary hypertension, pulmonary fibrosis, chronic obstructive respiratory diseases) cause chronic hepatic congestion due to chronic pulmonary heart disease, possibly leading to insufficiency. Hypoxaemia as a result of acute or chronic respiratory insufficiency can impair metabolic liver functions considerably. In 40—70% of patients with cirrhosis, hypoxaemia can be found in about 50% of cases with advanced cirrhosis, a reduced diffusion capacity for CO is detectable. Furthermore, pulmonary tissue contains a high level of glutamine synthetase, so that ammonia detoxification is possible (ultimately by perivenous hepatocytes) before the blood reaches the systemic circulation. In existing pulmonary diseases, localized ammonia detoxification is impaired. 

Serious adverse effects of epinephrine potentially occur when it is given in an excessive dose, or too rapidly, for example, as an intravenous bolus or a rapid intravenous infusion. These include ventricular dysrhythmias, angina, myocardial infarction, pulmonary edema, sudden sharp increase in blood pressure, and cerebral hemorrhage. The risk of epinephrine adverse effects is also potentially increased in patients with hypertension or ischemic heart disease, and in those using (3-blockers (due to unopposed epinephrine action on vascular Ui-adrenergic receptors), monoamine oxidase inhibitors, tricyclic antidepressants, or cocaine. Even in these patients, there is no absolute contraindication for the use of epinephrine in the treatment of anaphylaxis [1,5,6]. 

Until recently, d-fenfiuramine was used to control appetite, in preference to d-amphetamine, because it has a lower affinity for the catecholamine transporter and so its uptake into noradrenergic and dopaminergic neurons is much less than that of amphetamine. This is thought to explain why, at anorectic doses, this compound lacks the psychotropic effects and dependence-liability that are real problems with if-amphetamine. Unfortunately, despite this therapeutic advantage, this compound has had to be withdrawn from the clinic because of worries that it might cause primary pulmonary hypertension, valvular heart disease and even long-term neuropathy. 

Common adverse reactions seen with phentermine use include heart palpitations, tachycardia, elevated blood pressure, stimulation, restlessness, dizziness, insomnia, euphoria, dysphoria, tremor, headache, dry mouth, constipation, and diarrhea. Phentermine should be avoided in patients with unstable cardiac status, hypertension, hyperthyroidism, agitated states, or glaucoma. In combination with fenfluramine or dexfenfluramine, pulmonary hypertension and valvular heart disease have been reported. The risk of developing either serious adverse effect cannot be ruled out with use of phentermine alone. Since phentermine is related to the amphetamines, the... 

The predominant mechanism of AF and atrial flutter is reentry, which is usually associated with organic heart disease that causes atrial distention (e.g., ischemia or infarction, hypertensive heart disease, valvular disorders). Additional associated disorders include acute pulmonary embolus and chronic lung disease, resulting in pulmonary hypertension and cor pulmonale and states of high adrenergic tone such as thyrotoxicosis, alcohol withdrawal, sepsis, or excessive physical exertion. 

Valvular heart disease with thrombogenic complications (e.g., pulmonary hypertension, atrial fibrillation, history of endocarditis)... 

Complex cyanotic congenital heart disease (e.g., single ventricle states) / Surgically constructed systemic pulmonary shunts or conduits... 

HIV infection1 12 13 CD4+T lymphocyte count Diabetes, heart disease, chronic pulmonary disease, chronic alcoholism Asplenia12 (Including elective splenectomy and terminal complement component deficiencies) Chronic liver disease Kidney failure, end-stage renal disease, receipt of hemodialysis... 

Cor pulmonare Heart disease developed as a result of pulmonary insufficiency latter part of the disease sequence of asbestosis reflecting the impaired transfer of oxygen and carbon dioxide through the blood vessels of the lung. 

Some studies of survivors of massive chlorine exposures have shown either persistent obstructive or restrictive deficits, but pre-exposure data on these patients were not available. Persistent respiratory symptoms, bronchial obstruction, and bronchial hyperresponsiveness were observed in 82%, 23%, and 41 % of chronically exposed pulp mill workers, respectively, 18-24 months after cessation of exposure." In most cases it is not known whether prolonged symptoms after chlorine exposure are due to aggravation of preexisting conditions such as tuberculosis, asthma, chronic obstructive pulmonary disease, or heart disease." "... 

Particulate matter air pollution is especially harmful to people with lung disease such as asthma and chronic obstructive pulmonary disease (COPD), which includes chronic bronchitis and emphysema, as well as people with heart disease. Exposure to particulate air pollution can trigger asthma attacks and cause wheezing, coughing, and respiratory irritation in individuals with sensitive airways. It was estimated in one major study that the excess risk of total mortality is 6.2% per each increase in 10pgPM2.s/m and 9.3% for cardiopulmonary mortality. ... 

In the overall US population, cardiovascular disease claims one life every 34 s, or more than the next five most frequent causes of death put together (cancer, chronic lower pulmonary disease, accidents, diabetes, and influenza and pneumonia). In 2002 cardiovascular disease accounted for 38% of all morbid events in the United States—1 of every 2.6 deaths (Figs. 1.1 and 1.2) [6]. It is estimated that approximately half a million people die of heart disease either before reaching the hospital or in the emergency department. 

Other reported side effects include vomiting, salivation, lacrimation, shivering, skin rash, and an interaction with thyroid preparations that may lead to hypertension and tachycardia. Ketamine also may raise intracranial pressure and elevate pulmonary vascular resistance, especially in children with trauma or congenital heart disease. Increases in intraocular pressure also may occur, and vigilance is required if ketamine is used in ocular surgery. 

Unlabeled Uses Cardiopulmonary bypass surgery hemodialysis pulmonary hypertension associated with acute respiratory distress syndrome, systemic lupus erythematosus, or congenital heart disease refractory CHF severe community-acquired pneumonia... 

Multivalvular heart disease, primary pulmonary hypertension and arrhythmias occur rarely... 

Primary pulmonary hypertension (PPH), psychotic episodes, and valvular heart disease rarely occur. 

Patients should be excluded from beta-blocker treatment if they have significant cardiorespiratory diseases (asthma and other pulmonary obstructive diseases, congestive heart failures, angina), insulin-dependent di-... 

There has been great interest in airborne particulate matter recently due to the results of a number of epidemiological studies showing a correlation between increased mortality and levels of airborne particles. Figure 2.14 shows one such correlation reported by Dockery et al. (1993). A clear relationship between mortality rates and the concentration of fine particles PM25, as well as with particle sulfate, is seen. Since sulfate is found primarily in fine particles, these observations are not independent. Schwartz et al. (1996) report a 1.5% increase in total daily mortality with an increase of 10 pg m-3 in PM25. Deaths due to chronic obstructive pulmonary disease increased by 3.3% and those to ischemic heart disease by 2.1%. 

Mitochondrial P oxidation of fatty acids is the principal source of energy for the heart. Consequently, inherited defects of fatty acid oxidation or of carnitine-assisted transport often appear as serious heart disease (inherited cardiomyopathy). These may involve heart failure, pulmonary edema, or sudden infant death. 

Reitz BA, Wallwork JL, Hunt SA, Pennock JL, et al. 1982. Heart-lunch transplantation Successful therapy for patients with pulmonary vascular disease. NEJM. 306 557-564. 

What the above amounts to is that the absolute excess risks per 10 000 woman-years attributable to the use of an estrogen plus a progestogen were seven more coronary heart disease events, eight more strokes, eight more pulmonary embolisms, and eight more invasive breast cancers, while the risk reductions per 10 000 woman-years were six fewer colorectal cancers and five fewer hip fractures. The absolute excess risk of events included in the global index was 19 per 10 000 woman-years. The overall harms in this study thus clearly exceeded the benefits. Allcause mortality was not affected. 

Reconsideration of contraindications has also been proposed in a prospective study in patients with serum creatinine concentrations of 130-220 pmol/1 and coronary heart disease (n — 226), congestive heart failure (n = 94) and chronic obstructive pulmonary disease (n = 91). Half of the patients continued to take metformin and the other half stopped (39). Bodyweight and HbAic increased over 4 years in those who stopped taking metformin. Lactic acid concentrations were similar in the two groups. Deaths were similar in the two groups (62 and 64 respectively). The incidences of myocardial infarction, all cardiovascular events, and cardiovascular mortality were the same. Changes in additional therapy were only significant for insulin (30% versus 45% respectively) and diet (25% versus 0% respectively). 

Bizzarre M, Gross I, Bizzarre M. Inhaled nitric oxide for the postoperative management of pulmonary hypertension in infants and children with congenital heart disease. Cochrane Database Syst Rev. 2005 CD005055. 

Although heart disease commonly affects the entire myocardium, congestive heart failure is sometimes divided into left and right heart failure (Fig. 24—2). In left heart failure, the left atrium and ventricle are unable to adequately handle the blood returning from the lungs. This causes pressure to build up in the pulmonary veins, and fluid accumulates in the lungs. Consequently, left heart failure is associated with pulmonary edema (see Fig. 24—2 A). 

As of 2002, it was not known whether sibutramine caused primary pulmonary hypertension. However, sibutramine was not recommended for people with conditions including heart disease, irregular heartbeat, or a history of stroke. 

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