Acute dyspnea

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I- Introduction:

  • AD is a common medical emergency, one of the main causes of emergency consultation
  • Multiple etiologies, some can be life-threatening
  • The dg is based on clinical examination and simple paraclinical examinations
  • Recognize major respiratory, cardiovascular or metabolic emergencies that require immediate dg and urgent treatment

II- Definitions:

  • Dyspnea is a painful subjective sensation, a gene during breathing, felt like shortness of breath, lack of air, choking
  • Acute – symptomatology< 2 weeks 2 =””></ 2 weeks>
  • Polypnea (tachypnea) – rapid breathing EN – 20/me, shallow
  • Orthopnea – Decubitus D that forces the patient to breathe while sitting

III- Pathophysiology:

  • Complex, imperfectly known
  • Perception in the muscles respi periph, inadequacy tension (CNS) and length
  • Disbalance between activation of central inhalecommand (activator signal) and ventilatory movement (inhibitory mechanisms)
  • Signals R chest wall, pulmonary, bronchial, YOU, central chemoR and periph
  • Integration into the brainstem, central cortex

IV- Diagnostic approach:

1- Interrogation:

  • Major importance
  • May be enough on its own to make the diagnosis
  • Age and sex
  • Pathological history
  • Clinical characteristics of dyspnea
  • Cardiovascular history:
Table I. – Clinical signs of severity in the presence of dyspnea.

HTA, coronary artery disease (angor, IDM, bypass)
Diffuse Atherosclerosis (stroke, Arteritis Ml)
Risk factors for MTE (ATCD, surgery, bed rest, neoplasia)

  • Pleuropulmonary history: Signs of COPD, occupational exposure (asbestos, silica, aerosols), medications, smoking (20 PA)
  • Immunodepression (HIV, hemopathy, chemo) swallowing disorders, context
  • Clinical features:
  • Intensity
  • Continuous, intermittent, rest, activity
  • Installation mode, spontaneous, brutal, progressive
  • Conditions of appearance: schedule, season, triggers
  • Rhythm, time (inspiratory, expiratory)
  • Change by position
  • Aggravation at night
  • Seniority
  • Accompanying signs

2- Physical review:

  • Simple gestures
  • Signs of gravity
  • Makes dg, the most likely cause

A- Pleuropulmonary review:

  • Inspection
  • Rhythm, chest deformity, abnormal movements
  • Chest dilation (COPD, asthma, emphysema)
  • Decrease in the expansion of a hemithorax
  • Neck inspection, over-sternal hollow, over-clavicular (drawing, mass, turgescence)
  • Inspiratory contraction of SCM muscle
  • Thoraco-abdominal swing, thoracic paradoxical movement
  • Flapping the wings of the nose
  • Cyanosis
  • Physical examination of the chest
  • Percussion: unilateral tympanism, dullness
  • Auscultation: asymmetry, decreased vesicular murmurs, crackling rails, sibilant rattles, stridor, pleural friction
Dyspnea: etiological orientation according to auscultation

B- Cardiovascular review:

  • Signs of heart failure: jugular turgescence, Hepatujug reflux, painful HPM, inf limb edema, PA measurement
  • Auscultation: galloping noise, breath, arrhythmia, pericardial friction

C- Clinical review:

  • The rest of the exam must be complete
  • Infectious syndrome, signs of anemia, neck and thyroid palpation, cervical lymph node areas

3- Additional reviews:

  • Useful, confirm the dgou assess the impact of the causal disease
  • 3 simple exams: Rxthorax- ECG -gasmetry
  • Other context functions, clinical examination, and simple exam results

A- Thorax X-ray:

  • Orients the etiological dg
  • Interpretation large radiological sd (Interstitial alveolar, bronchial, vascular, pleural,,,)
  • Chest distension (Asthma, IRSC)
  • Heart size

B- blood gas:

  • Two situations: hypoxemia with hypercapnia, hypoxemia without hypercapnia
  • Hypoxemia-hypocapnia – shunt effect
  • EP, asthma, OAP, bacterial lung disease
  • Hypercapnia

C- Electrocardiogram:

  • Heart causes
  • Myocardial ischemia, rhythm disorder, Hypertrophy, signs of EP (AD deviation, S1Q3, BBD…)

D- Echocardiography:

  • Non-invasive, heart cause
  • Valvulopathy, hypokinesis, hypertensive heart disease, pericardial effusion, signs of PE (acute pulmonary heart

E- Other reviews:

  • D-dimers
  • Inflammation markers (CRP, PCT)
  • Cardiac enzymes (Tropo, myoglobin, CPK, transaminases)
  • Type B (BNP) and NT-proBNP natriuretic peptide
  • Chest scanner
  • Pulmonary ultrasound

V- Etiological Diagnosis:

1- Acute asthma:

  • Dgfacile to history
  • Young, Nocturnal Wheezing Seizures, Stress or Spring, Personal or Family Allergy ATCD, Childhood Asthma, Bronchiolitis)
  • Sibilants, expiratory braking
  • RT (chest distension, triggering factor)
  • Signs of severity, threat syndrome
  • Severe acute asthma

Etiological treatment

  • Acute asthma:

2-mimetic aerosols: Salbutamol-terbutaline (Ventoline-Bricanyl)

Anticholinergics: Atrovent – Ipratropium Bromide Nebulization 5mg/0.5mg20min, 3 times/h then every 4h Corticosteroids: Solumedrol 2mg / kg, Hydrocortisone 15 mg/kg

2- Bronchopneumonia:

  • Table III. – Clinical manifestations of hypoxia and hypercapnia.

    TIME, fever, chills, tachypnea, tachycardia

  • Cough, purulent sputum, tho pain
  • Mateity, Crepe, tubal breath
  • Systeria opacity, pleurisy, bilateral images
  • Levies

Treatment:

Probabilistic early antibiotic therapy

  • fMactamine, clavAmoxicillin acid
  • C3G: Cefotaxim
  • Fuoroquinolones: Levofloxacin
  • Bacteriological samples

3- Acute DEcompensations of COPD:

  • Table VII. – Main causes of acute flare-ups of decompensation of chronic respiratory failure.

    Elderly subject, IRC

  • Decompensating factor
  • Polypnea, drawing, abdominothoracic breathing, sibilants
  • ICD signs, right gallop
  • Signs of hypoxemia – hypercapnia.
  • Chest radio, gasmetry

Treatment:

  • 2-mimetic aerosols
  • Anticholinergic
  • Mechanical ventilation
  • Trt of the cause

4- OAP:

  • Plasma liquid diffused in extravascular spaces of the lung
  • Pulmonary hair hyperpression edema (cardiogenic OAP)
  • Edema by alteration of the alveolo-capillary membrane (lesional edema)

OAP Lesional

  • Increased permeability coefficient by alteration of the alveolo-capillary membrane.
  • Pulmonary hair pressure is normal or low. The edema liquid has a very high protein content close to that of plasma.
  • Acute respiratory insufficiency with possible subsequent progression to interstitial fibrosis: acute respiratory distress syndrome.

Etiologies:

  • Infectious, flu, sepsis, septic shock…
  • Toxic, inhalation of toxic gases, ventilation of pure oxygen, inhalation of gastric fluid (Mendelsohn syndrome).

Evolution:

  • 3 phases:
  • Brutal start with pulmonary edema
  • 2nd phase with inflammatory lesions, edema, hyaline membrane constitution
  • 3rd is chronic pulmonary fibrosis.
  • The consequence – major gas exchange disorder, shunt-refractory hypoxemia by shunt effect
  • Zero ventilation and sustained infusion.

Cardiogenic OAP

  • Sudden or chronic elevation of pulmonary hair pressure.
  • Stress dyspnea, nocturnal orthopnea, dry cough, productive, frothy, salmon pink
  • Crackling rails, bases, “rising tide,” left gallop
  • RT: bilateral alveolar opacities in “butterfly wings”, cardiomegaly
  • ECG: causal heart disease

3 phases

  • Simple venous hypertension
  • Interstitial edema stadium
  • Alveolar pulmonary edema

Etiologies:

  • Left ventricular insufficiency
  • Mechanical obstacle without left ventricular insufficiency

Treatment:

  • Diuretics: Furosemide (Lasilix) / Bolus IV 40-80mg
  • Nitrous derivatives: Isosorbide di nitrate, glyceryl trinitrate (Risordan, Lenitral) 1-Bmg then infusion 3-10mg/h

PA monitoring:

  • Tonicardiaques: Dobutamine
  • Non-invasive ventilation
  • Treatment of the cause (IDM, rhythm disorder…)
Risk factor

5- Pulmonary embolism:

  • Difficult diagnosis
  • Favourable factors (DVT history, surgery, bed rest, cancer…)
  • Brutal start
  • Dyspnea, pain tho, hemoptysis
  • RT: pulmonary infarction, ECG (CPA)
  • Gasoline: hypoxemia-hypocapnia
  • D-dimers, echo – heartwriting, thoracic angioscanner, angiography, scan

Symptom/sign

Treatment:

  • Anticoagulation with curative dose: HBPM / Non-split heparin: massive forms
  • Thrombolysis: massive embolism, shock, acute pulmonary heart
  • Surgical embolectomy

6- Pneumothorax:

  • Traumatic or spontaneous post
  • Dyspnea – Inspiration chest pain
  • Tympanism
  • Emphysema under the skin
  • Radio
  • Exsufflation, drainage

7- Tuberculosis:

  • Contage
  • Alteration of the general condition
  • Signs of impregnation, night sweats
  • Adenopathies
  • Radio: effusion, cave, miliary, ADP
  • IDR – BK research
  • Tuberculosis treatment

8- Lung cancer:

  • Alteration of the general condition
  • Primary cancer
  • Radio – scanner
  • Surgery, chemotherapy

9- Metabolic:

  • Metabolic acidosis: diabetic ketoacidosis. Acute kidney failure…
  • Etiological treatment

10- Neuromuscular:

  • Acute PRN polyradiculonéuritis, myasthenia…
  • Specific treatment
  • Mechanical ventilation

11- Intra bronchial foreign body:

  • Young child
  • Context
  • Suffocation access, penetration syndrome
  • Radio – scanner
  • Bronchoscopy

12- Laryngé edema:

  • Quincke&rsquo;s edema
  • Anaphylactic shock
  • Traumatic
  • Adrenaline, corticosteroids

13- Other diagnoses:

  • Strangulation, submersion, drowning…
  • Intoxication

14- CO poisoning:

  • Carbon monoxide
  • Odorless, colourless, insipid gas
  • Frequent and serious
  • The cause of death from poisoning
  • Hemoglobin has a 230 times stronger affinity for CO than for oxygen

Pathophysiology:

  • Hypoxia, secondary to carboxyhemoglobin (HbCO) formation
  • Cell toxicity independent of hypoxemia immunological and inflammatory components

Initial signs: headache, nausea, vomiting, impaired consciousness, memory, dizziness, fatigue

Signs of gravity: deep coma, hypertonic calm, trismus, convulsions

Vegetative signs: hyperthermia, sweating and pink “cochineal” gingling of teguments

  • HTA, rhabdomyolysis and then acute kidney failure, respiratory distress
  • ECG: tachycardia, rhythm disorders, repoiarization disorders, myocardial infarction
  • Collective character and season
  • Biological diagnosis:
  • Oxycarbonemia (mi/100ml) – 0.2ml/100mii
  • CarboxyHb dosage – 5%
  • CPK, Troponine: myocischemia, muscular
  • Creatinine: IRA
  • Hyperleucocytosis
  • Normal gasmetry

CO support

  • The half-life of co is 320 minutes in ambient air, 90 minutes in FiO2 100%, and 23 minutes in a hyperbaric chamber with 3 atmospheres
  • FiO2 Oxygen Therapy 100%
  • Normobare with high concentration mask
  • 12 L / min 6 hours
  • Indications: no symptoms and HbCO< 15%></ 15%>
  • Hyperbaric oxygen therapy:
  • Indications:
  • Even brief loss of consciousness, consciousness disorder, convulsions, neurological sign, pregnancy, child, pre-existing cardio pulmonary pathology, modification of ECG
  • HbCO – 15% with symptoms
  • HbCO – 25% even without symptoms
  • Contraindications: pneumothorax not dreused major bronchospasm

WE- Treatment:

Symptomatic treatment:

  • Sitting
  • Oxygé notherapy (Sa02-90%)
  • Venous pathway
  • Airway freedom
  • Extracting the toxic atmosphere
  • Admission to resuscitation (signs of severity)

Ventilatory assistance:

  • Indications: refractory hypoxemia, respiratory exhaustion, consciousness disorders
  • Conventional mechanical ventilation: tracheal intubation after sedation
  • Non-invasive NIV ventilation: Facial mask, requires patient awareness and cooperation (OAP, COPD, pneumonia, immunosuppressed)

VII- Conclusion:

  • Acute dyspnea is a common reason for emergency consultation
  • Diagnosis is essentially based on clinical examination and simple paraclinical examinations
  • Early etiological diagnosis allows the start of appropriate treatment, a guarantee of better prognosis

Dr. FOUGHALI Course – Constantine Faculty