Lec.2 Acute severe breathlessness, Respiratory failure

Lec:2 Dr. Mohammed Alhamdany
Acute severe breathlessness
This is one of the most common and dramatic medical emergencies. The history and a rapid but careful examination will usually suggest a diagnosis which can
be confirmed by routine investigations, including chest X-ray, ECG and arterial blood gases.
The differential diagnosis include:
1-Pulmonary oedema: it associated with chest pain, palpitations, orthopnoea, and cardiac history.
On examination may show central cyanosis, ?JVP, sweating, cool extremities, basal crackles. On CXR show Cardiomegaly, oedema/pleural effusions.
2-Massive pulmonary embolus: by history the patient had associated Risk factors, chest pain, pleurisy, syncope, dizziness on examination there is central cyanosis, ?JVP, absence of signs in the lung, shock (tachycardia, hypotension)
The CXR often normal , on ABG there is ?PaO2 and ?PaCO2, the ECG show Sinus tachycardia, RBBB, S1Q3T3 pattern, invertedT(V1–V4).
3-asthma :history of asthma,with cough and, wheeze,and tachycardia, pulsus paradoxus, cyanosis (late), CXR show Hyperinflation only (unless complicated by pneumothorax) and there is ?PaO2 ?PaCO2 (?PaCO2 in extremis) and ECG show sinus tachycardia (bradycardia in extremis)
4-Acute exacerbation of COPD: history of smoking, cough and dyspnea. If in type II respiratory failure may be drowsy, on examination there is cyanosis, hyperinflation, signs of CO2 retention (flapping tremor, bounding pulses), on CXR there is bullae, or complicating pneumothorax , on ABG there is ?PaO2 and?PaCO2 in type II failure ad ?H+, ?HCO3 in chronic type II failure
5-Pneumonia: fever, rigors, pleurisy on examination there is fever, confusion, pleural rub, and sign of consolidation, cyanosis (if severe) on CXR there is pneumonic consolidation.
6-Metabolic acidosis: Evidence of diabetes mellitus or renal disease, aspirin or ethylene glycol overdose , Fetor (ketones), hyperventilation without heart or lung signs, dehydration, air hunger.
On the ABG there is normal PaO2 with normal or?PaCO2, ?H+
7-Psychogenic Previous episodes, digital or perioral dysaesthesia
No cyanosis, no heart or lung signs, carpopedal spasm ,Normal PaO2 normal, or?PaCO2, ?H+.


History
It is important to establish the rate of onset and severity of the breathlessness and whether associated cardiovascular symptoms (chest pain, palpitations, sweating and nausea) or respiratory symptoms (cough, wheeze, haemoptysis, stridor) are present. A previous history of repeated episodes of left ventricular failure, asthma or exacerbations of COPD is valuable. In the severely ill patient, it may be necessary to obtain the history from accompanying witnesses. In children, the possibility of inhalation of a foreign body or acute epiglottitis should always be considered.
Clinical assessment
The following should be assessed and documented:
• level of consciousness
• degree of central cyanosis
• evidence of anaphylaxis (urticaria or angioedema)
• patency of the upper airway
• ability to speak (in single words or sentences)
• cardiovascular status (heart rate and rhythm, blood pressure and degree of peripheral perfusion).
Pulmonary oedema is suggested by pink, frothy sputum and bi-basal crackles; asthma or COPD by wheeze and prolonged expiration; pneumothorax by a silent resonant hemithorax; and pulmonary embolus by severe breathlessness with normal breath sounds. The peak expiratory flow should be measured whenever possible. Leg swelling may suggest cardiac failure or, if asymmetrical, venous thrombosis. Arterial blood gases, a chest X-ray and an ECG should be obtained to confirm the clinical diagnosis, and high concentrations of oxygen given pending results. Urgent endotracheal intubation may become necessary if the conscious level declines or if severe respiratory acidosis is present.

Respiratory failure
The term ‘respiratory failure’ is used when pulmonary gas exchange fails to maintain normal arterial oxygen and carbon dioxide levels. Its classification into types I and II is defined by the absence or presence of hypercapnia (raised PaCO2).
Pathophysiology
When disease impairs ventilation of part of a lung (e.g. in asthma or pneumonia), perfusion of that region results in hypoxic and CO2-laden blood entering the pulmonary veins. Increased ventilation of neighbouring regions of normal lung can increase CO2 excretion, correcting arterial CO2 to normal, but cannot augment oxygen uptake because the haemoglobin flowing through these regions is already fully saturated. Admixture of blood from the underventilated and normal regions thus results in hypoxia with normocapnia, which is called ‘type I respiratory failure’. Diseases causing this include all those that impair ventilation locally with sparing of other regions.
Diseases that cause generalised, severe ventilation–perfusion mismatch, leaving insufficient normal lung to correct PaCO2, or a disease that reduces total ventilation. The latter includes not just diseases of the lung but also disorders affecting any part of the neuromuscular mechanism of ventilation.
Type I respiratory failure: it characterized by Hypoxia (PaO2 < 8.0 kPa (60 mmHg)) with normal or low PaCO2 (< 6.6 kPa (50 mmHg)), with normal PH and bicarbonate level.it either acute or chronic:
A-Acute: it cause by
1-Acute asthma
2-Pulmonary oedema
3-Pneumonia
4-Lobar collapse
5-Pneumothorax
6-Pulmonary embolus
7-ARDS
B-Chronic: it cause by
1-COPD(emphysema)
2-Lung fibrosis
3-Lymphangitis carcinomatosa
4-Right-to-left shunts
Type II respiratory failure: it characterized by Hypoxia (PaO2 < 8.0 kPa (60 mmHg)) raised PaCO2 (> 6.6 kPa (50 mmHg)) it either acute or chronic.
A-Acute: with decrease in the PH( respiratory acidosis), with normal bicarbonate level. It cause by:
1-Acute severe asthma
2-Acute exacerbation of COPD
3-Upper airway obstruction (e.g. foreign body inhalation)
4-Acute neuropathies/paralysis
5-Narcotic drugs
6-Primary alveolar hypoventilation
7-Flail chest injury
B-Chronic: with normal or decrease PH and raised bicarbonate level. It cause by:
1-COPD
2-Sleep apnoea
3-Kyphoscoliosis
4-Myopathies/muscular dystrophy
5-Ankylosing spondylitis


Management of acute respiratory failure
Prompt diagnosis and management of the underlying cause is crucial and as following:
1- For foreign body inhalation or laryngeal obstruction (angioedema, carcinoma or vocal cord paralysis), immediate intubation or emergency tracheostomy may be life-saving.
2- patient with the trachea deviated away from a silent and resonant hemithorax are likely to have tension pneumothorax, and air should be aspirated from the pleural space and a chest drain inserted as soon as possible.
3- Patients with generalised wheeze, scanty breath sounds bilaterally or a history of asthma or COPD should be treated with nebulised salbutamol with oxygen, repeated until bronchospasm is relieved. Failure to respond to initial treatment, declining conscious level and worsening respiratory acidosis (pH < 7.3), PaCO2 > 6.6 kPa (50 mmHg)) on blood gases are all indications that supported ventilation is required
4- A small percentage of patients with severe chronic COPD and type II respiratory failure develop abnormal tolerance to raised PaCO2 and may become dependent
on hypoxic drive to breathe. In these patients only, lower concentrations of oxygen (24–28% by Venturi mask) should be used to avoid precipitating worsening respiratory depression. In all cases, regular monitoring of arterial blood gases is important to assess progress.
5-Patients with acute type II respiratory failure who have reduced drive or conscious level may be suffering from sedative poisoning, CO2 narcosis or a primary failure of neurological drive (e.g. following intracerebral haemorrhage or head injury).
reversal of specific drugs with (for example) opiate antagonists is occasionally successful, but should not delay intubation and supported mechanical ventilation in appropriate cases.
6- type I respiratory failure, high concentrations of oxygen (40–60% by mask) will usually relieve hypoxia by increasing the alveolar PO2 in poorly ventilated lung units. Occasionally, however (e.g. severe pneumonia affecting several lobes), mechanical ventilation may be needed to relieve hypoxia. Patients who need high concentrations of oxygen for more than a few hours should receive humidified oxygen.

With best wishes