Dyspnea

Dyspnea is a discomfort felt the hard way by the patient during a regular physical activity, and under normal atmospheric pressure and temperature. It results from a mismatch between the required exercise and abilities of respiratory and / or cardiovascular system.

The patient of the results under different names: shortness of breath, tightness, lack of air sensation, poor tolerance to modest or minimal efforts. The perception of dyspnea at equal severity varies from one patient to another, and the non-perception of dyspnea, common in severe asthma, explains some delays in check and some unexpected deaths.

In clinical practice, two situations are opposed:

– Acute or subacute dyspnea, reflecting the emergence of a new phenomenon;

– Chronic dyspnea, possibly aggravated by exertion, but overall still like itself throughout the year.

Both types of dyspnea correspond to very different etiologies, although some associate, such as COPD (chronic lung disease) and manifestations of left ventricular failure.

SYMPTOMS:

Semiotics is based on various criteria:

– Acute or chronic respiratory discomfort;

– Modifi cations respiratory mode;

– Respiratory dysrhythmias;

– Main occurrence of circumstances;

– The associated signs.

Changes respiratory fashion:

Depending on the frequency, there are:

– Polypnoea (over 25 breaths / min);

– Bradypnea (less than 15 / min).

Depending on which part of the breathing cycle, there are:

– Dyspnoea inspiratory predominance: they cover the active time breathing, are accompanied by the involvement of accessory respiratory muscles (scalene, sterno-mastoid), a draw resulting in a trough digging supraclavicular and sussternal and higher intercostal spaces, sometimes a roaring or route disorders;

– Expiratory dyspnoea to dominance: they reflect the existence of a bronchospastic state, they are frequently associated with intrathoracic whistles, but sometimes auscultation only found a “lengthening of expiratory time” that reflects a difficulty the patient to exhale.

Dyspnoea fast pace (polypnées) usually involve both the inspiratory and expiratory time.

Inspiratory or expiratory dyspnea characteristics mainly based on clinical examination (inspection and auscultation).

Indeed, any dyspnea is felt by the patient as a hindrance to the penetration of air into the lungs, and it is usually unable to distinguish which part of the respiratory cycle.

Respiratory dysrhythmias:

There are special dyspnea based on a singular rhythm:

– Dyspnea Kussmaul is a slower pace in dyspnea with 4 stages: a deep breath followed by a respiratory pause and a deep breath and again an expiratory break. The anomalies thus concern a respiratory cycle. Related to metabolic acidosis, it was once observed in diabetic coma;

– Cheyne-Stokes dyspnea is expressed on a succession of cycles often anarchic respiratory dysrhythmia made of respiratory movements more and more and more and faster, often followed by an extended break.

Once observed in end stage renal disease, it is also the fact that a number of severe neurological diseases, and reflects disturbances in the bulbar respiratory centers.

Main circumstances of occurrence:

Several factors must be taken into consideration:

– The occurrence of dyspnea on exertion or at rest;

– The position of the patient:

– In the case of orthopnea (most common), dyspnea is aggravated by lying down, especially among the poor left heart,

– In the p latypnée, dyspnea is increased by sitting, and improves when lying down; it is observed in certain cardiac shunts (patent foramen ovale) or parenchyma, such as lung arteriovenous aneurysms or hépatopulmonaires syndromes. Long considered exceptional, the platypnea-orthodeoxia syndrome is confirmed by measuring the oxyhemoglobin saturation supine and sitting and inefficiency of oxygen therapy;

– The schedule: some dyspnea like asthma and manifestations of left ventricular failure readily occur at night;

– Triggers: the typical example is allergic asthma who majorises on the occasion of exposure to allergens to which the patient is sensitized.

Associated signs:

They are an essential argument to guide the diagnosis:

– Auscultatory lung abnormalities: Identify the vesicular murmur is normal or decreased, if there is bronchospasm, obstruction of bronchial rattles or only the presence of dry crackles to the database;

– Cardiovascular abnormalities: always look for symptoms suggestive of an underlying heart problem (tachycardia, changes in blood pressure, hepatomegaly with Hepatojugular reflux or leg edema);

– Other signs such as extrarespiratoires symptoms, confusion, agitation, cyanosis, consciousness disorders up to coma.

We exclude from this chapter the sleep apnea syndrome, where dyspnoea is only a secondary element of the clinical picture.

MEASUREMENT AND TESTING DYSPNEA:

Dyspnea scales:

Subjective sensation, the intensity of dyspnea should be evaluated. This quantification of dyspnea, essential for a chronic dyspnea respiratory or cardiac origin, led to the development of “dyspnea scales”

– The scale of Sadoul, best known Respiratory:

– Stage I: dyspnea for important efforts,

– Stage II: dyspnea brisk walking or gentle slopes,

– Stage III: dyspnea walking flat in normal pace,

– Stage IV: the slow march

– Stage V: dyspnea at the slightest effort (toilet, undressing, meals);

– The scale of NYHA (New York Heart

Association), used by cardiologists, and combining a measurement of the distance covered by the patient in 6 minutes;

– Other dyspnea scores that appeal directly to the patient:

– The Borg score: numbered 0 to 10, depending on the increasing severity of the discomfort perceived by the patient,

– Visual analog scale (VAS): single line of 10 cm long, one end marked “not at all out of breath” and the other “out of breath”; the patient lies on the line at a level it considers to match the level of dyspnea.

Despite its simplicity, the EVA has good reproducibility;

– The index of Mahler, more complex, reserved for the evaluation of dyspnea in certain therapeutic protocols.

Diagnostic tests:

Acute dyspnea is an emergency: clinical examination is preeminent, but diagnosis is difficult, especially in the elderly where the natural decline in lung function and cardiovascular system increases the frequency of mixed attacks.However, some diagnostic tests and targeted few are offered:

– First-line examinations: chest X-ray, blood gases, measuring peak expiratory flow in the bronchospastic and patient electrocardiogram; biologically face a suspected disease thromboembolism: D-dimer; if in doubt between cardiac dyspnea and dyspnea of pulmonary origin, dosage of Brain Natriuretic Peptide (BNP);

– 2nd line of tests for each case: emergency endoscopy, venous Doppler ultrasound of the lower limbs, ventilation scintigraphy perfusion, CT angiography or echocardiography.

Faced with chronic dyspnea, the practitioner has a time of reflection and may decide to play the range of respiratory and cardiovascular classic explorations.

FACE TO DIAGNOSIS OR ACUTE DYSPNEA SUBACUTE:

The diagnosis of dyspnea is based primarily on a full clinical examination of the patient’s inspection is a critical time.:

– The difficult slow pursed lips expiration is typical of an already severe obstructive pulmonary disease;

– The existence of a thoracic deformity (kyphoscoliosis, chest retraction) towards a dyspnea due to a restrictive component, etc.

However, to guide the diagnosis, it is convenient to distinguish two different groups based on auscultatory data:

– Dyspnoea with abnormal lung auscultation;

– Dyspnoea without abnormal lung sounds.

Dyspnea with abnormal lung auscultation:

Inspiratory dyspnea reflects an obstacle to the penetration of air into the airways.

Originally laryngeal tracheal or high, it combines an inspiratory bradypnea, raffle, wheezing, sometimes dysphonia when the vocal cords are involved in the pathological process.

The causes are:

– Edema of the glottis often integrated in the context of an anaphylactic shock (antibiotics, food allergy, stinging Hymenoptera).

He joins in a meaningful context with events of angioedema and generalized urticaria.

extreme emergency treatment: epinephrine (to be used intramuscularly to repeat as necessary) self-injectable form (Anapen®) dosed at 0.15 or 0.30 mg, respectively for the child and adult, to prescribe in at-risk patients who have at their disposal for acute accident;

– Edema hereditary angioneurotonique presents a similar picture, but occurs within a family context: the diagnosis is confirmed by the determination of inhibitor C1-esterase.

Treatment: IV injection of this factor (available to emergency services to the French Blood Establishment);

– Intrabronchial foreign body, especially in children, is characterized by a shrill with breathlessness, coughing, cyanosis: the penetration syndrome. Whatever the future development of symptoms, hospitalization and performing a bronchoscopy is necessary;

– In children, acute viral laryngitis. Treatment: Nebulizer topical corticosteroids and humidification of the inspired air;

– Acute epiglottitis in children is often related to infection with Haemophilus influenzae, the first line of treatment is the Augmentin®. Its frequency has fallen sharply since the routine infant vaccination against the haemophilus;

– Cancer of the larynx or trachea tumor can be revealed by this type of dyspnea, the inspiratory character is all the more marked that the lesion is close to the glottis.

In emergency, the treatment is symptomatic.

Excluding palliative phase, the patient must be transferred by ambulance urgently to the nearest hospital to be cared for in intensive care. We must put the patient in a half sitting position, administer oxygen (8-10 L / min to the mask, according to gravity), the infusion, give corticosteroids intravenously (eg Solumedrol® 80 to 160 mg IV according to gravity). In extreme cases, it may be necessary to perform an emergency tracheotomy.

Expiratory dyspnea with wheezing are characterized by an acute bronchospastic condition, very common. They fall under three main causes:

– An exacerbation of a chronic pulmonary disease (COPD), often the result of a bacterial or viral infection. It affects a smoker or former smoker patient who coughs and spits a long time, but dyspnea has recently increased. thoracic distension of the signs is sought, the existence of an expiry pursed lips reflecting the collapse bronchiolar and unconsciously encourages the patient to maintain a positive pressure of end-tidal, cyanosis or stigma hypercapnia excessive sweating, confusion, tremor, unexplained breakouts blood pressure.

The chest X-ray can rule out complications (pneumothorax, for example); blood gases assess the severity of the exacerbation: hypoxia, hypercapnia, the existence of a possible gas acidosis possible to direct support towards emergency structure.

In the absence of signs of severity requiring hospitalization, isolation and remoteness of the health facility, the patient can be treated at home. The treatment is then based on the introduction or increase of broncho dilators (beta 2 agonists roughly atropine) by metered dose inhalers (which can be coupled with a spacer), usually an antibiotic ( amoxicillin or amoxicillin-clavulanic acid orally 1 gr X 3, or fluoroquinolone Ofl ocetR 200 mg x 2 / day) in combination with inhaled or systemic corticosteroids (cf.asthme, especially since it is a component spatique) respiratory physiotherapy. If no improvement within 48 hours or the appearance of signs of severity, the patient should be admitted to emergency.

The treatment is then based on the administration of oxgène low rate (0.5 to 1 L / min usually) of beta-2 agonists of aerosols associated with atropine in air (eg Bricanyl® and Atrovent®) treating the cause (antibiotics with the same molecules as before but by intravenous route), often briefly corticosteroids (80 mg IV initially Solumedrol®), twice-daily chest physiotherapy active and preventive dose anticoagulation (eg Lovenox ® 0.4 mL SC once a day in the absence of renal failure). Tobacco should be in all cases of course stopped. In the most serious cases to the hospital, noninvasive ventilation may be an alternative to mechanical ventilation;

– An asthma attack, which often affects younger patients, allergic history.

It is essential, face an acute crisis, assess the severity level:

– A single acute attack is easily controlled by taking beta-2-agonists of short action used by inhalation (2 to 12 flashes using a spacer) associated with systemic corticosteroids (40 mg of Prednisone or Prednisolone)

– Facing a severe acute attack with tachypnea, tachycardia, cyanosis, agitation or consciousness disorders, hospitalization and transport by EMS is urgently needed: blood gases made on arrival at the emergency airlock possible depending on the level of hypoxia but especially the capnia (with normal or hypercapnia) to guide therapeutic management;

– A pseudo-cardiac asthma indicative of interstitial edema, which combines dyspnea, wheezing but crackles bases. A history of left ventricular failure (hypertension, ischemic heart disease), the existence of cardiomegaly and signs of interstitial edema on the chest radiograph assist in the diagnosis. This pathology electively affects the elderly, but is often associated with genuine COPD.

Treatment focuses bronchodilator (Salbutamol and Ipratropium), but especially diuretics and intravenous nitrates(Risordan) according to blood pressure tolerance.

From a distance, we introduce a basic treatment of left heart failure.

Dyspnea with the presence of crackles is a somewhat artificial context and include:

– The acute pulmonary edema (APO) cardiogenic diagnosis easy in its usual form. The treatment of cardiogenic OAP is treated in the section on heart failure.

It is based on furosemide and nasal oxygen therapy;

– Certain acute infectious pneumonitis where one finds, besides the infectious syndrome, crackles localized focus. The chest radiograph easily confirms the diagnosis and led to the introduction of antibiotics probabilistic (amoxicillin, optionally combined with a quinolone);

– Hypersensitivity pneumonitis (lung or lung farmer bird breeder), much less frequent, rarely of sudden onset. The acute form is most often reversible within hours. Treatment consists of corticosteroids and then identifying the allergen avoidance. It is usually symptomatic admnistration oxygen and corticosteroids (Cortancyl® 40 mg / d).

The patient must be given to the lung in order to perform the necessary tests. A vocational rehabilitation is often necessary;

– The s yndromes hemorrhagic alveolar representing another form of respiratory distress whose diagnosis is confirmed by bronchoalveolar lavage with a bloody uniform alveolar fluid, reflecting the distal bleeding, registering under a rapidly progressive glomerulonephritis , a Goodpasture’s syndrome or Wegener’s granulomatosis; these alveolar hemorrhages are a major emergency, but remain exceptional.

The treatment is hospital and specialist. The symptomatic treatment (oxygen therapy, transfusion eventually …) adds the causal therapy (corticosteroids, immunosuppressants …)

– Drug pneumonia (. Antibiotics, sulfa drugs, amiodarone, etc.) and frequent diagnostic diffi cult; more than 100 different drugs have been described, and only the systematic mention of this possibility in

the polymedicated allows patients to identify them. These iatrogenic pneumonia is a difficult trap to thwart, facing the constant renewal of the pharmacopoeia.

Dyspnea with auscultatory asymmetry:

These are the pleural pathologies which we oppose:

– Slowly progressive dyspnea of pleurisy;

– And the sudden and acute algic accident developer pneumothorax.

A careful clinical examination can easily ignore these diagnoses confirmed by chest radiograph.

Rapid paracentesis may relieve abundant pleurisy; she sometimes finds in a context traumatic hemothorax.

Acute pneumothorax requires hospitalization and sometimes extreme emergency drainage if compression.

Acute dyspnea without abnormal lung sounds:

These are non-respiratory dyspnea. They are dominated by cardiovascular etiologies, foremost among which include thromboembolic disease, heart rhythm disturbances and, to a lesser extent, pericardial effusion.

Pulmonary embolism with a higher risk of major diagnostic errors. Very frequently, it translates clinically by the onset of dyspnea varies in intensity, duration and accompanying signs fickle chest pain, rapid pulse, hypotension, malaise or anxiety.

The initial Pleuropulmonary examination and chest radiograph are usually normal. Blood gases objectify a shunt effect involving hypoxia and hypocapnia. The diagnosis is easy if there is a thrombophlebitis of the lower limbs, and the first review must be requested Doppler ultrasound of the lower limbs. In practice, two situations are opposed:

– Pulmonary embolism on previously healthy lung presents a typical picture: it makes the study of D-dimer, a ventilation perfusion scintigraphy. Associated with the identification of venous thrombosis by Doppler, these reviews often sufficient for diagnosis;

– Pulmonary embolism on pathological lung (pulmonary cancer, COPD, pneumoconiosis, etc.) has a degraded clinical translation; the symptoms are atypical, dyspnea existed, the study of D-dimer is insignificant because of an associated infectious condition; lung scintigraphy does not provide convincing information because of preexisting alterations in ventilation / perfusion relationships in the lungs. Priority should be given to new Doppler ultrasound of the lower limbs and, this time, the spiral CT has the advantage of providing useful information on pulmonary embolism itself and the associated causal affection. If in doubt, and if the patient’s condition allows, obviously pulmonary angiography remains the “gold standard” diagnosis of pulmonary embolism.

Treatment of pulmonary embolism: the patient must be hospitalized. In the presence of signs of seriousness, he will be hospitalized in intensive care if necessary after being taken by ambulance to the hospital. Treatment is based on the admnistration anticoagulants (anti Xa Innohep® 175 U / kg per day or Lovenox® 100 IU anti Xa / kg every twelve hours in the absence of renal impairment (creatinine clearance should be greater than 30 mL / min); Calciparine® otherwise subcutaneously at a dose of 500 IU / kg for 24 h divided in two or three injections per day with aPTT monitoring 4 to 6 hours after the first injection). Recall that platelets must be monitored twice weekly during treatment with LMWH. The measurement of anti-Xa activity with LMWH is only necessary in case of old age, overweight, accident anticoagulants, renal impairment (creatinine clearance greater than 30 mL / min). The relay by vitamin K (Previscan per os, 1 tab to adapt to INR 72 hours) should be as early as possible to avoid thrombocytopenia to heparin. It should be implemented six months if it is the first episode, if the trigger is reversible if it is a mutation of the factor V Leiden or prothrombin gene.

In other cases, it will be extended at least a year indefinitely see, especially if it is an antiphospholipid syndrome. The patient must stay in bed 48 hours after starting treatment and wear compression stockings.

Oxygen therapy is often necessary. In severe cases, intensive care, it may be necessary to perform thrombolysis, filling see inotropic if hypotension, rarely intubation. The use of surgical embolectomy is exceptional.

The IVC filter installation will be decided by the specialist (cons-indication to anticoagulant therapy, recurrent pulmonary embolism despite adequate treatment, following surgical embolectomy).

It should not be forgotten in all cases to practice etiological (think in particular, especially in the absence of obvious cause, a bleeding disorder in young patients and cancer in the elderly).

Preventive treatment mainly hospital patients. In an ambulatory patient at risk (thrombophilia, cancer, antiphospholipid syndrome …), it may be necessary to provide preventive treatment in high-risk situations (primarily air travel to medium or long haul: LMWH injection (Lovenox 0.4 ml SC once mostly), wearing stockings, hydration suffi cient, wandering, do not cross your legs.

The occurrence of cardiac arrhythmias (passage atrial fibrillation, flutter, tachysystole, ventricular tachycardia) is a common cause of acute dyspnea. Cardiac auscultation and ECG easily provide diagnosis: only the lifting of arrhythmia allows improved dyspnea symptom.

The lifting of arrhythmia based on antiarrhythmic admnistration on condition of effective anticoagulation especially if ACFA (atrial fibrillation) and often oxygen therapy.

In severe cases with disorders of poorly tolerated rate (tachycardia or ventricular fibrillation usually), the cardiologist or the emergency physician will resort to external electric shock.

Acute pericardial effusions (traumatic, neoplastic or purulent) are rare tamponade associated dyspnea type orthopnea, tachycardia with muffled heart sounds and distension of the jugular. The diagnosis is evoked if there cardiomegaly; it is confirmed by echocardiography to guide the puncture pericardium.

Hospitalization in intensive care or USIC is usually required if poorly tolerated effusion. Processing first rests in this case on the pericardial puncture in surgical or emergency, in addition to symptomatic measures (oxygen, filling) is then etiological.

FACE TO DIAGNOSTIC DYSPNEA CHRONIC:

The context is different: the patient consults for some old breathlessness, sometimes interspersed with paroxysms but without urgent action.

The balance sheet, including systematic cliché chest, pulmonary function tests (PFT) with blood gases, electrocardiogram and echocardiography if necessary, can identify many ailments integrating into the box:

– Chronic lung disease (chronic asthma, COPD and pulmonary diffuse infiltrative);

– A progressive heart failure;

– A primary or secondary pulmonary hypertension;

– Anomalies in transportation of quantitative oxygen (anemia) or qualitative (COHb and methemoglobinemia).

Chronic lung diseases:

When dyspnea is associated with bronchospasm, and obstructive ventilatory disorders, 2 etiologies must primarily be discussed: asthma and chronic obstructive pulmonary disease (COPD) Chronic asthma often follows a long history of acute paroxysmal. that fade with time.

Atopy, the identifi cation of one or more allergen (s), reversibility as beta-2-mimetics authenticate airway obstruction in asthma and COPD differs from that in 85% of cases concerns former smokers, chronic bronchitis long, in whom the onset of dyspnea heralding COPD. The EFR show an obstructive ventilatory disorders (TVO) and non-reversible air distension of stigma (increased residual volume and total lung capacity) that confirm the inspection data and radiology.

The prognosis of COPD depends in part on the reduction in FEV (forced expiratory volume in one second) and blood gas alterations. Some elderly asthmatics, the reversibility of TVO may disappear: it is asthma aged difficult to distinguish from COPD, especially if observed in a smoker or former smoker.

The treatment of chronic asthma based on allergen avoidance, inhaled corticosteroids and beta-2-agonists long-acting.

In COPD, the first requirement is smoking cessation, the infection prevention measures (influenza and pneumococcal vaccination) and anticholinergic bronchodilator and beta-2-agonists. In the 2 conditions, we may use fixed-dose combinations (beta-2-agonists and inhaled corticosteroids, long-acting), but their indication in COPD is strictly reserved for the most severe forms.

When dyspnea is associated with a restrictive ventilatory defect, it may be related to:

– Diffuse infiltrative pulmonary disease (formerly known as diffuse interstitial fibrosis).

It is characterized by progressive dyspnea, frequent cough, dry crackles predominant presence of the two bases. PFT show a pure ventilatory restriction with alteration of the diffusion of carbon monoxide and hypoxia. Their frequency increases with age, some are called idiopathic, others fit into the framework of systemic diseases (scleroderma, rheumatoid arthritis, etc.);

– Pneumoconiosis as asbestosis and pneumoconiosis due to inhalation of silica or coal dust. The job history and radiographic appearance is highly suggestive;

– Parietal involvement (spine, sternum, rib cage): severe kyphoscoliosis, old pleural sequelae or phrenic paralysis.

The treatment of these restrictive abuses is often difficult and specialist. It has in any case symptomatic hand (smoking cessation, influenza vaccination, chest physiotherapy, oxygen therapy if needed, bronchodilators if reversible obstructive share associated). To diffuse infiltrative lung diseases, it is based primarily on corticosteroids, immunosuppressants see for forms associated with connective or lung transplantation in some cases for idiopathic forms.

The factors triggering acute worsening (infection, pulmonary embolism …) should be sought and treated. For pneumoconiosis, again, the management remains symptomatic (long-term oxygen therapy, physiotherapy, treatment of complications). You must not forget the social care (compensation for occupational diseases, invalidity or reclassification). For parietal damage, symptomatic management is identical. It may be necessary to propose a surgical procedure on a serious kyphoscoliosis or a large amaigrisement in cases of morbid obesity.

Cardiovascular illnesses:

The cardiac dyspnea (cardiac consequences right chronic respiratory disease and left ventricular failure for whatever cause) is of great frequency.

His treatment will be a chapter.

Pulmonary arterial hypertension (PAH) primitive recently attracted attention, given the new treatment possibilities.

It results in rapidly progressive dyspnea occurred at any age; Pleuropulmonary clinical examination, chest X-ray are little changed. Echocardiography allows to quantify the level of PAH and the impact on the right cavities. It will lead to a thorough investigation to rule out underlying cause: pulmonary hypertension postembolic, connective drug causes the first of which were the anorectic now banned, but some severe liver disease and HIV infection.

The treatment of PAH is specialist.

In all cases, it is based, in the absence of indication-cons, on the effective anticoagulation in the long term, more or less associated with diuretics; in case of hypoxemia (Pa02 <60 mmHg), it will administer oxygen for long periods.

The results of cardiac catheterization and degree of dyspnea, it may be necessary to give calcium channel blockers (Tildiem® [diltiazem] For example, if the response to test NW during catheterization) or other vasodilators such inhibitors phosphodiesterase (Revatio® [sildénafi l)], antagonists of endothelin receptors (Tracleer [bosentan]) or prostacyclin analogues in the most severe cases (Flolan® [epoprostenol IV continuous pump] associated often to other treatments. the etiological treatment is necessary (stopping the anorectic anti retroviral treatment …). in the most severe cases, it may be necessary to provide a lung transplant.

Other causes:

Other chronic dyspnea causes are:

– The transport of oxygen anomalies.

Poisoning by carbon monoxide remains prevalent, the risk is permanent in the decrepit housing, favored by the use too frequently the oil fires inside the premises. Methemoglobinemia has become rarer; it is often iatrogenic: dapsone(dapsone) used in the treatment of leprosy or relapsing polychondritis was a large provider, but other drugs are involved, including the use of local anesthetics (benzocaine or lidocaine spray gel) during endoscopic procedures, dental surgery and more banal in the very young child with EMLA cream for cutaneous application (lidocaine and prilocaine Association). Treatment of poisoning carbon monoxide requires emergency hospitalization with emergency measure carboxyhemoglobin.

It is based on pure oxygen admnistration broadband and possibly passing hyperbaric depending on the gravity of the infringement and the CO levels. Possible complications will also be supported (eg, pulmonary edema, convulsions …).An investigation is needed to address in order to identify and eliminate the source of CO (often it is a defective heater);

– Some rare diseases such as hyperventilation syndrome. These patients often female, young (between 30 and 40) complain of a major dyspnea; all paraclinical investigations are negative, but the psychological context (anxiety with panic attacks), the “feeling unable to breathe deeply”, the presence of breaks, repeated sighs, the observed gas alkalosis possible to approach this diagnosis difficult. The treatment of hyperventilation syndrome is based on the admnistration anxiolytics (Euphytose®, 1-2 x 2-3 cps daily; 0.5 mg XanaxR 1-3 cps daily) view of inhibitors of serotonin reuptake (Deroxat® 1 per day) in case of panic disorder and proved a mild psychotherapeutic support that can be performed by the physician;

– Severe anemia sometimes unknown. The treatment of these anemia depend on their cause;

– Neuromuscular damage and in particular the vast chapter of myopathies.

CONCLUSION:

The exploration of dyspnea still requires rigorous physical examination backed some simple diagnostic tests. The attitude obviously differs depending on the acute or chronic dyspnea: quick intervention and immediate therapeutic decision in the first situation, wider call for paraclinique when dyspnea is long.

In all cases, the diagnosis remains difficult, given the great diversity encountered etiological. But our diagnostics will improve over time as evidenced by the recent introduction in the biomarkers of emergency services, especially the BNP (B Natriuretic Peptide). This peptide is secreted from cardiomyocytes during heart failure and in particular when there is a pressure increase of the cardiac cavities. Faced with acute dyspnea, this simple blood test helps distinguish acute dyspnea of cardiac or respiratory origin, and it has been shown recently used in a systematic way at the entrance to the emergency, this measure reduces the risk of diagnostic errors and also the time and therefore the overall cost of hospitalization.

Despite the contribution of modern biology, however it should be noted that the diagnosis of dyspnea remains primarily the job of the clinician.