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See patient information handout on pulmonary hypertension, written by the authors of this article.
Pulmonary hypertension is a complex problem characterized by nonspecific signs and symptoms and having multiple potential causes.
The symptoms of pulmonary fibrosis are likely to go unnoticed until the disease has advanced well beyond the stage of reversible lungs damage. At this point, additional symptoms are likely to emerge, such as chronic fatigue, significant and unexplained weight loss, and muscles and joints that ache or hurt. The human lung is quite intricate and understanding the causes of pulmonary fibrosis require an intricate understanding of the lungs.
There are various risk factors associated with pulmonary fibrosis including, age, gender, occupational hazards and other environmental concerns, previous radiation and chemotherapy, smoking, certain viruses, and genetic factors. For young and otherwise healthy patients, a lung transplant offers the only hope of real improvement. Some patients who combine treatment with prednisone and add 600 milligram doses three times daily of the enzyme N-acetylcysteine have experienced a greater relief of symptoms for a longer period of time.
Clinical trials can often open up new windows for patients, and there are usually several that are in need of willing participants.
Definition for submassive PE: Acute PE without systemic hypotension (systolic blood pressure ?90 mm Hg) but with either RV dysfunction or myocardial necrosis. Therapeutic anticoagulation with subcutaneous LMWH, intravenous or subcutaneous UFH with monitoring, unmonitored weight-based subcutaneous UFH, or subcutaneous fondaparinux should be given to patients with objectively confirmed PE and no contraindications to anticoagulation (Class I; Level of Evidence A).
Therapeutic anticoagulation during the diagnostic workup should be given to patients with intermediate or high clinical probability of PE and no contraindications to anticoagulation (Class I; Level of Evidence C). Thirteen placebo-controlled randomized trials of fibrinolysis for acute PE have been published, but only a subset evaluated massive PE specifically.
Data suggest that compared with heparin alone, heparin plus fibrinolysis yields a significant favorable change in right ventricular systolic pressure and pulmonary arterial pressure incident between the time of diagnosis and follow-up. The definition of respiratory insufficiency may include hypoxemia, defined as a pulse oximetry reading < 95% when the patient is breathing room air and clinical judgment that the patient appears to be in respiratory distress. Biomarker evidence of moderate to severe RV injury includes major elevation of troponin measurement or brain natriuretic peptides. Fibrinolysis is reasonable for patients with massive acute PE and acceptable risk of bleeding complications (Class IIa; Level of Evidence B).
Fibrinolysis may be considered for patients with submassive acute PE judged to have clinical evidence of adverse prognosis (new hemodynamic instability, worsening respiratory insufficiency, severe RV dysfunction, or major myocardial necrosis) and low risk of bleeding complications (Class IIb; Level of Evidence C).
Fibrinolysis is not recommended for undifferentiated cardiac arrest (Class III; Level of Evidence B). Depending on local expertise, either catheter embolectomy and fragmentation or surgical embolectomy is reasonable for patients with massive PE and contraindications to fibrinolysis (Class IIa; Level of Evidence C).
Catheter embolectomy and fragmentation or surgical embolectomy is reasonable for patients with massive PE who remain unstable after receiving fibrinolysis (Class IIa; Level of Evidence C).
For patients with massive PE who cannot receive fibrinolysis or who remain unstable after fibrinolysis, it is reasonable to consider transfer to an institution experienced in either catheter embolectomy or surgical embolectomy if these procedures are not available locally and safe transfer can be achieved (Class IIa; Level of Evidence C). Either catheter embolectomy or surgical embolectomy may be considered for patients with submassive acute PE judged to have clinical evidence of adverse prognosis (new hemodynamic instability, worsening respiratory failure, severe RV dysfunction, or major myocardial necrosis) (Class IIb; Level of Evidence C).
Catheter embolectomy and surgical thrombectomy are not recommended for patients with low-risk PE or submassive acute PE with minor RV dysfunction, minor myocardial necrosis, and no clinical worsening (Class III; Level of Evidence C). Also whilst we are on the topic of hyperoxia causing harm, you probably are aware that the Australian Heart FOundations 2011 addendum to their ACS guidelines has published a level C recommendation to avoid routine oxygen therapy in those with ACS, based on a Cochrane meta-analysis of 338 patients.
Thanks Minh – already planning to come to your talk since I saw your name on the program! I think the hyperoxia issue post arrest related to the CNS injury from arrest followed by reperfusion so I don’t think this extrapolates to PE. Slideshare uses cookies to improve functionality and performance, and to provide you with relevant advertising. Chronic obstructive pulmonary disease, left ventricular dysfunction and disorders associated with hypoxemia frequently result in pulmonary hypertension.
It may be defined as a pulmonary artery systolic pressure greater than 30 mm Hg or a pulmonary artery mean pressure greater than 20 mm Hg.The etiology of primary pulmonary hypertension is unknown.
This low pressure is due to the large cross-sectional area of the pulmonary circulation, which results in low resistance. These symptoms are often difficult to dissociate from those caused by a known underlying pulmonary or cardiac disorder.
Particular attention should be given to previous medical conditions, drug use (legal and illegal) and family history. Lung transplantation is an option in some patients younger than 65 years who have pulmonary hypertension that does not respond to medical management.
As a result of new treatments, patients without hemodynamic evidence of right ventricular dysfunction may survive for more than 10 years.The prognosis for patients with secondary pulmonary hypertension depends on the underlying disease, as well as right ventricular function. Multiple, thin, short, white lines which are perpendicular to the chest wall at the lung base are seen (white oval) representing fluid which has leaked into the interlobular septae as a result of congestive heart failure, one of the signs of CHF. Over time, the lungs become scarred and reduce the capacity for breath and oxygen consumption.
In most cases, patients believe that their shortness of breath and their dry cough are the results of a lingering cold or getting older. The air that travels into the lungs eventually ends up in the tiny air sacks called alveoli, where gases are exchanged in the process of human breathing. While there have been small children and infants who have developed the disease, most victims range in the middle to later adult years. A physician will systematically rule out other possibilities before identifying the problem as pulmonary fibrosis. Heart failure involving the right side, pulmonary hypertension (the increase of blood pressure inside the lungs) low blood oxygen levels, and respiratory failure. Many patients are initially treated with corticosteroids in order to help suppress the immune system.

Of course, with transplant lists being bogged with recipients and sparse with donors, finding a good match can be very difficult.
Not all patients respond to this sort of treatment, but those who do have a better quality of life for longer. At 24 hours, patients treated with heparin have no substantial improvement in pulmonary blood flow, whereas patients treated with adjunctive fibrinolysis manifest a 30% to 35% reduction in total perfusion defect. The implication is that even if adjunctive fibrinolytic therapy has extremely high efficacy, for example, a 30% relative reduction in mortality, the effect size on mortality due to submassive PE is probably < 1%. Alternatively, respiratory distress can be quantified by the numeric Borg score, which assesses the severity of dyspnea from 0 to 10 (0=no dyspnea and 10=sensation of choking to death).
These AHA guidelines are genuinely helpful in areas like this where a meta analysis and expert opinion can be combined to give something that’s practically useful. Does making everyone with acute PE oxygen saturations to 100% produce more harm based on your argument ? Routine oxygen therapy has been a mainstay of treatment of suspected cardiac chest pain for decades. If SpO2 is in the high 90’s I think there is a good argument for not giving supplemental oxygen.
Regardless of the etiology, unrelieved pulmonary hypertension can lead to right-sided heart failure. Secondary pulmonary hypertension can be a complication of many pulmonary, cardiac and extrathoracic conditions. Consequently, it is helpful to evaluate pulmonary vasoreactivity during catheterization, before a long-term therapy is selected.
For instance, patients with COPD and moderate airflow obstruction have a three-year mortality rate of 50 percent after the onset of right ventricular failure.26 Survival is similarly influenced in patients with interstitial lung disease and pulmonary hypertension.
Pulmonary fibrosis is considered the end stage of interstitial lung disease, which simply refers to a variety of lung diseases that lead to scarring of the lung tissue. Most patients do not realize the extent of their situation until after they are unable to breathe through the most mundane chores like eating and walking from one room to another.
However, when damaging particles or other elements are able to mar the thin interstitium tissue that is responsible for the lining and separating of the small air sacs, the sacs may not heal. Men are more susceptible to the disease than women, and people who have worked in environments laden with potentially harmful airborne debris run a very high risk of developing the disease. The only definitive test available for definite determination remains a biopsy of the tissue of the air sacs. Thus far, no treatment options have shown any real signs of slowing the progression of the disease nor helped to alleviate the symptoms.
Oxygen therapy and pulmonary rehabilitation can also help improve the patient’s quality of life. Those who participate offer a greater chance not only to themselves, but to others as well. Thus, secondary adverse outcomes such as persistent RV dysfunction, chronic thromboembolic pulmonary hypertension, and impaired quality of life represent appropriate surrogate goals of treatment. If you are still at Airmed perhaps turn up for my lecture on psychiatric retrievals on THursday morning and I can say hello then.
Could I ask your opinion on this recommendation by the AHF which I believe is in line with latest AHA and European guidelines as well? For those out there who have not seen Cliff deliver a lecture or teach in person I would recommend attending one of his courses .
In my life as an intensivist I’m very relaxed having ARDS or COPD patients with SpO2 of 88-92%. I think the UK (BTS) oxygen guidelines are in keeping with this but haven’t looked at them for a while. Cor pulmonale is enlargement of the right ventricle as a consequence of disorders of the respiratory system.
The condition has no racial predilection.1Secondary pulmonary hypertension is relatively common but is underdiagnosed. Executive summary from the World Symposium on Primary Pulmonary Hypertension 1998, Evian, France, September 6–10,1998, cosponsored by the World Health Organization. Commonly, suspicion is increased by the presence of increasing dyspnea on exertion in a patient with a known cause of pulmonary hypertension.In pulmonary hypertension, the electrocardiogram (ECG) may demonstrate signs of right ventricular hypertrophy, such as tall right precordial R waves, right axis deviation and right ventricular strain (Figure 1).
The most suitable drugs for testing acute response are potent, short-acting and titratable. Most physicians believe that pulmonary fibrosis is a progressive lung disease that begins with recurrent damage to the small air sacs in the lungs known as alveoli.
Even microscopic damage can accumulate over time and lead to significant scarring of these air sacs. Management of submassive PE crosses the zone of equipoise, requiring the clinician to use clinical judgment. The diagnosis should be suspected in patients with increasing dyspnea on exertion and a known cause of pulmonary hypertension. The higher the pulmonary artery pressure, the more sensitive is the ECG.12 The chest radiograph is inferior to the ECG in detecting pulmonary hypertension, but it may show evidence of underlying lung disease12 (Figure 2). In patients who show evidence of an acute hemodynamic response, long-term treatment with calcium channel blockers, administered orally in high dosages, can produce a sustained hemodynamic response and increase survival.18Epoprostenol (Flolan), or prostacyclin, is the single most important advance in the treatment of primary pulmonary hypertension. The immediate reduction in pulmonary artery pressure is associated with an improvement in right ventricular function.
Scarring, which is known as fibrosis, ultimately prevents the lungs from expanding and being able to take deep, full breaths, leading to inept oxygen saturation. This procedure entails the use of a very small and flexible tube which removes tissue samples about the size of a pin head. Two-dimensional echocardiography with Doppler flow studies is the most useful imaging modality in patients with suspected pulmonary hypertension. This potent, short-acting vasodilator and inhibitor of platelet aggregation is produced by vascular endothelium.

If pulmonary hypertension is present, further evaluation may include assessment of oxygenation, pulmonary function testing, high-resolution computed tomography of the chest, ventilation-perfusion lung scanning and cardiac catheterization. A careful examination often detects signs of pulmonary hypertension and right ventricular hypertrophy.The findings on lung examination are nonspecific but may point to the underlying cause of pulmonary hypertension.
Right axis deviation (short arrow), increased P-wave amplitude in lead II (black arrowhead), and incomplete right bundle branch block (white arrowhead) are highly specific but lack sensitivity for the detection of right ventricular hypertrophy.12FIGURE 1Electrocardiogram demonstrating the changes of right ventricular hypertrophy (long arrow) with strain in a patient with primary pulmonary hypertension.
In one study,19A  continuous intravenous infusion of epoprostenol improved exercise capacity, quality of life, hemodynamics and long-term survival in patients with class III or IV function (Table 2). Treatment with a continuous intravenous infusion of prostacyclin improves exercise capacity, quality of life, hemodynamics and long-term survival in patients with primary pulmonary hypertension.
Management of secondary pulmonary hypertension includes correction of the underlying cause and reversal of hypoxemia.
Lung transplantation remains an option for selected patients with pulmonary hypertension that does not respond to medical management.
Other anticoagulants are also being studied.Inotropic agents such as digoxin (Lanoxin) are currently under investigation. Echocardiography is the most useful imaging modality for detecting pulmonary hypertension13 and excluding underlying cardiac disease.
In one study,20 digoxin produced favorable acute hemodynamic effects in patients with right ventricular failure and primary pulmonary hypertension; however, the long-term consequences of this treatment are unknown.
Confirmation of pulmonary hypertension is based on identification of tricuspid regurgitation.
Shortterm parenterally administered inotropic drugs may also be of benefit.In patients with secondary pulmonary hypertension, management is directed at early recognition and treatment of the underlying disease (while it is still potentially reversible). Executive summary from the World Symposium on Primary Pulmonary Hypertension 1998, Evian, France, September 6–10, 1998, cosponsored by the World Health Organization. The addition of mean right atrial pressure to the peak tricuspid jet velocity gives an accurate noninvasive estimate of peak pulmonary pressure.
For instance, left ventricular dysfunction should be treated with afterloadreducing agents, digoxin and diuretics. Right ventricular dilatation and hypertrophy are late findings.All patients with documented pulmonary hypertension should undergo a comprehensive laboratory evaluation to clarify the etiology. Initial tests include complete blood count, prothrombin time, partial thromboplastin time, hepatic profile and autoimmune panel (if this panel is suggested based on the history or physical examination). Because the right heart is dependent on preload, care should be taken to avoid excessive diuresis and further reduction of cardiac output.Patients with persistent pulmonary hypertension despite aggressive management of the underlying disease should be referred for evaluation at a center that specializes in the management of this condition. HIV testing should be considered in all patients, especially those with a compatible history or risk factors.Arterial blood gas analysis should be performed to exclude hypoxia and acidosis as contributors to pulmonary hypertension. It is important to note that normal resting oxygenation does not exclude exertional or nocturnal oxygen desaturation. Approximately 20 percent of patients with COPD and normal awake arterial oxygen tensions have nocturnal nonapneic oxygen desaturation.14 Elevations of pulmonary artery pressure during transient oxygen desaturation are due to increases in pulmonary vascular resistance and cardiac output. Therefore, exercise and overnight oximetry should also be performed in all patients with pulmonary hypertension.Pulmonary function tests are necessary to establish airflow obstruction or restrictive pulmonary pathology. The most widely accepted theory suggests that certain persons may be predisposed to primary pulmonary hypertension.
Unless hypoxia is present, pulmonary hypertension cannot be attributed to these disorders until pulmonary function is severely reduced.
Computed tomographic (CT) scanning of the chest with high-resolution images is useful for excluding occult interstitial lung disease and mediastinal fibrosis when the pulmonary function tests and chest radiograph are nondiagnostic.If the cause of the pulmonary hypertension remains unexplained, chronic thromboembolism should be excluded before the diagnosis of primary pulmonary hypertension is accepted. Vascular-wall remodeling, vasoconstriction and thrombosis in situ all play a role.1Collagen vascular disease,4 portal hypertension,5 human immunodeficiency virus (HIV) infection6 and anorectic agents7 may produce a clinical picture similar to that of primary pulmonary hypertension.
Fortunately, ventilation-perfusion lung scanning is a reliable method for differentiating chronic thromboembolism from primary pulmonary hypertension.
The use of appetite-suppressant drugs for more than three months is associated with a greater than 30 times increased risk of developing pulmonary hypertension.8A  In the United States, the anorexic agents fenfluramine and dexfenfluramine were recalled in September 1997, only 18 months after they were released. The finding of one or more segmental or larger perfusion defects is a sensitive marker of embolic obstruction. This imaging technique has high specificity but undefined sensitivity for the diagnosis of pulmonary embolism.17Cardiac catheterization should be performed in patients with unexplained pulmonary hypertension, and remains the gold standard for its diagnosis and quantification. When pulmonary blood flow is markedly increased and pulmonary vascular capacity is reached, any further increase in blood flow causes a rise in pressure.Increased pulmonary pressure is also a potential consequence of any condition that impedes pulmonary venous drainage. The pulmonary hypertension that occurs in left ventricular dysfunction and mitral valve disease is the result of an increase in resistance to pulmonary venous drainage and backward transmission of the elevated left atrial pressure. More direct obstruction of pulmonary venous drainage occurs in association with unusual conditions such as mediastinal fibrosis and pulmonary veno-occlusive disease.Pulmonary hypertension frequently occurs in response to alveolar hypoxia.
A reduction in oxygen tension causes pulmonary vasoconstriction by a variety of actions on endothelium and smooth muscle.
Chronic mountain sickness and sleep apnea9 are common etiologies of pulmonary hypertension associated with hypoxemia.
Acidosis, which also causes pulmonary vasoconstriction, may compound the effects of hypoxia.10Hypoxia-induced vasoconstriction and capillary obliteration occur in interstitial lung disease and chronic obstructive pulmonary disease (COPD), which is the most common cause of pulmonary hypertension. During acute exacerbations of COPD, hypoxia and uncompensated hypercarbia can increase pulmonary blood pressure.Pulmonary hypertension may occur when blood flow through large pulmonary arteries is hindered. Acute pulmonary emboli induce only a mild to moderate elevation of pulmonary artery pressure.
Acutely, the right ventricle is unable to generate a systolic pressure greater than 50 mm Hg; a higher systolic value suggests a chronic process with right ventricular hypertrophy. Therefore, a massive pulmonary embolus may cause right ventricular failure but not severe pulmonary hypertension.

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