Respiratory II Flashcards
ADULT RESPIRATORY DISTRESS SYNDROME: What is it
This is a specific disease of the lung characterised by 1) hypoxaemia 2) alveolar inflammation 3) oedema pulmonary fibrosis develops later.
Typically the syndrome is recognised some hours or even days after the initial insult.
ARDS Histology
1) Early changes shows interstitial and alveolar oedema.
2) The alveoli contain cell debris, proteinaceous fluid, hyaline membrane and haemorrhage.
3) Chronic inflammation follows; organisation and fibrosis-damage now permanent.
ARDS Clinical
1) increased respiratory rate, cyanosis, and, on arterial blood gas analysis, hypercapnia.
2) Chest x-ray shows patchy white clouding.
3) The compliance of the lung is severely reduced, so that the work of breathing is beyond the patient’s capability. The patient soon requires ventilation, with high inspiratory pressures. The increased stiffness of the lungs is due to alveolar collapse and oedema.
Because the alveoli are filled with exudate and oedema, a large percentage of pulmonary blood flow goes through unventilated units, giving rise to severe inequality of ventilation and perfusion.
Treatment includes oxygen enrichment, often up to 100%, to correct hypoxaemia. PEEP often improves oxygen- ation by decreasing pulmonary oedema and recruiting underventilated alveoli.
A similar condition occurs in infants – infant respiratory distress syndrome. with profound hypoxaemia. Treatment is similar to that of adults, but the addition of synthetic surfactant to inspired oxygen helps correct the underlying defect, i.e. the inability of the premature fetal lung to produce sufficient surfactant.
Oxygen delivery: Face mask and nasal cannulae
Simple oxygen masks and nasal cannulae increase the patient’s inspired oxygen, but the increase depends upon the respiratory pattern, the rate and depth of breathing, and most importantly the patient’s peak inspiratory flow. If this significantly exceeds the rate of oxygen flowing into the mask, then there will be significant dilution with air. Simple oxygen masks and nasal cannulae are variable performance systems.
Oxygen delivery: Venturi masks
Oxygen masks utilising the Venturi principle provide accurate concentrations of oxygen of up to 60%, which will exceed the patient’s peak inspiratory flow. These devices rely on using a high flow, low pressure principle generated by passing oxygen through a narrow orifice into a special mask. Because fast moving gas has a low pressure, surrounding air enters the mask at a rate determined by the flow rate of oxygen and the size of special perforations in the mask.
Venturi masks are fixed performance systems. It is difficult to give spontaneously-breathing patients 100% oxygen without using an endotracheal tube and a special anaesthetic circuit. In practice this is probably no bad thing, because oxygen, like any other drug, has side effects.
Harmful effects of oxygen
• We have already seen how increasing the patient’s inspired oxygen concentration can result in depression of ventilation.
• Oxygen can also be directly toxic to the tissues.
Exposing alveoli to 100% oxygen for more than a few hours will result in normal subjects complaining of discomfort and difficulty in breathing. This is because, in the absence of nitrogen, alveoli tend to collapse as oxygen is rapidly removed.
- Further prolonged exposure to oxygen results in a progressive fall in arterial oxygen tensions, as the capillaries become increasingly permeable, leading to interstitial oedema,.
- After 48h, organisation and fibrosis occur in a similar fashion to ARDS. A vicious circle occurs, where ever-increasing oxygen enrichment is required to compensate for the deterioration in lung function caused by oxygen.
- The development of this syndrome requires exposure to high concentrations with time. It is much less likely to occur if inspired oxygen concentration is kept below 60%.
- In the newborn infant treated with high-inspired oxygen concentrations, a condition called retrolental fibroplasia may develop, with permanent blindness resulting.
Pneumothorax: Spontaneous
This most commonly occurs in young males 15–40 and is occasionally bilateral and recurrent.
Most pneumothoraces are spontaneous, because the pressure within the alveoli is always greater than intra- pleural pressure. The decreased negative pressure in the chest causes depression of the diaphragm and shift of the mediastinum away from the affected side. Increasing inspired oxygen, hastens reabsorption.
A primary spontaneous pneumothorax occurs in an otherwise healthy patient usually occurs in tall young men, in whom the negative pressure in the pleural space at the apex of the lung is greater than normal. Rupture of a small bulla in this area is the usual cause.
A small pneumothorax (less than 20% of the hemithorax) in a patient with healthy lungs requires no treatment. A large pneumothorax or one causing significant dyspnoea requires a chest drain with an underwater seal.
Secondary pneuomothorax
Secondary spontaneous pneumothorax usually occurs in patients over 30, and is almost always associated with pulmonary disease.
Causes include asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis, cancer and lung abscess.
Tension pneumothorax
This develops when the hole in the pleura remains unsealed, and a 1-way valve develops so that air can pass into the pleural space on inspiration but cannot escape during expiration.
- The pressure in the intrapleural space rises, so that the chest on the affected side becomes distended, the mediastinum is pushed away and the liver depressed. During inspiration the trachea moves away from the affected side.
- The patient rapidly deteriorates due to reduced venous return, and hypoxaemia caused by shunting through the compressed lung. Life-saving treatment is necessary and provided by rapid insertion of a hollow needle into the affected side of the chest.
- A tension pneumothorax may occur during IPPV of a patient with high pressures or with PEEP. Because of the positive pressure applied to the lungs the tension may develop with startling rapidity and catastrophic consequences if immediate treatment is not provided.
Pulmonary oedema: Pathology
Pulmonary oedema is the abnormal accumulation fluid in the tissues of the lung.
- The epithelium of the capillaries is very permeable to water, small molecules and ions. Large molecules such as proteins have a restricted capacity to diffuse across the cells. The alveolar epithelium is permeable to water, but not to small molecules or even ions.
- If excess fluid moves out of the circulation it will cause, first, interstitial oedema. This has little effect on primary function but can be seen on x-ray.
- If fluid continues to move into the lungs it will overwhelm the lymphatics, resulting in alveolar oedema. The alveoli become filled with fluid which increases surface tension forces, causing them to shrink.
- Ventilation of these units ceases, and, while they remain perfused, hypoxaemia results. If the passage of fluid continues it will fill the small and then large airways as frothy sputum, which may be tinged pink from red blood cells.
Pulmonary oedema: causes
1) Raised capillary hydrostatic pressure (commonest cause), usually seen after acute myocardial infarction, left ventricular failure, or transfusion overload. The left atrial pressure rises and there is an increase in pulmonary venous and pulmonary capillary pressures. If the pressure rise is slow and gradual, then remarkably high pressures may occur without alveolar oedema, although x-ray often reveals marked interstitial oedema. Sudden rises in capillary pressure will result in alveolar oedema.
2) The permeability of the capillaries may also rise, causing fluid to accumulate in the alveoli. This occurs from a variety of causes including endotoxic shock, exposure to irritant gases such as chlorine or nitric oxide, and as part of ARDS.
3) Lymphatic drainage of the lung becomes impaired/obstructed e.g. by tumour cells, then pulmonary oedema will result.
4) Pulmonary oedema can also occur during rapid ascent to high altitude. The aetiology is unclear, and pulmonary capillary wedge pressure is normal. Pulmonary artery pressure is raised, probably because of hypoxic vasoconstriction, and the condition is relieved by oxygen therapy or descent to a lower altitude.
5) Neurogenic pulmonary oedema may occur following insult to the central nervous system, usually severe head injury causing massive over- activity of the sympathetic nervous system.
Pulmonary oedema: Physiological
1) The compliance of the lung decreases as surface tension causes alveolar collapse.
2) Airway resistance increases, partly because of the smaller lung volume and partly because the larger airways may be partially blocked by oedema. Reflex bronchoconstric- tion also increases resistance.
3) Although interstitial oedema has little effect on pulmonary gas exchange, alveolar oedema has dramatic, and often fatal, effects. Those alveoli filled with fluid no longer take part in gas exchange, but instead collapse. They continue to be perfused, causing massive VA:VQ mismatch. Some lung units will have minimal ventilation and normal perfusion. These units are especially likely to collapse during oxygen therapy.
4) Pulmonary vascular resistance is increased because of hypoxic vasoconstriction and external pressure on the vessels due to interstitial oedema. There is often diversion of blood to the upper zones.
Pulmonary oedema: Clinical
1) Dyspnoea
2) Orthopnoea
3) Paroxysmal nocturnal dyspnea
4) Cough
5) Cyanosis
Breathing is rapid and shallow, driven by arterial hypoxaemia and an effort to minimise the increased work of breathing.
On auscultation fine inspiratory crepitations are heard at the lung bases.
A chest x-ray reveals an enlarged heart with prominent pulmonary vessels.
Interstitial oedema causes short, linear horizontal lines near the pleural surface in the lower zones – the Kerley B lines.
Pulmonary oedema: Treatment
1) High concentrations of oxygen
2) Vasodilators
3) Diuretics
4) Ultimately IPPV and PEEP.
5) The application of raised end expiratory pressure decreases oedema in the larger airways and decreases the shunt.
Pulmonary embolus
1) A large clot may completely obstruct the pulmonary outflow, resulting in death.
2) Smaller clots may block a single large artery or break up and block several small vessels.
3) The lower regions of the lung have the greatest blood flow and so are most often affected.
4) If the patient survives the initial insult, then there may either be distal infarction or haemorrhage into the affected segment.
The physiological effects of pulmonary emboli range from minimal to massive. The pulmonary artery resistance is only increased with large pulmonary emboli, since there is considerable reserve and capillary recruitment.
If pulmonary artery pressure rises significantly, then the right ventricle may fail. Occlusion of the pulmonary artery reduces in alveolar PCO2, causing bronchoconstriction in the small airways.
Physiological dead space and shunt are increased. Hypoxaemia occurs without a corresponding rise in PaCO2, because alveolar ventilation increases.
Pulmonary embolus: Clinical and treatment
Larger emboli produce: 1) Shock 2) Central chest pain 3) Sudden collapse 4) Sometimes distended neck veins. Rapid surgical intervention may be life-saving.
Small pulmonary emboli produce
1) Dyspnoea
2) Pleuritic pain.
3) There may be a raised temperature
4) Productive cough with bloodstained sputum.
5) There may be a tachycardia
6) Auscultation may reveal a pleural rub.
7) X-ray rarely reveals an abnormality, so that diagnosis depends on specialised techniques such as a ventilation-perfusion scan, which will reveal areas of normal ventilation but reduced perfusion.
The clinical sequelae depend on the size of the embolus. A saddle embolus at the bifurcation of the pulmonary arteries usually causes sudden death.
Occlusion of one of the main pulmonary arteries also frequently leads to death, although occasionally there is severe chest pain and shock and the patient may survive with appropriate treatment.
Occlusion of a lobar or segmental artery causes sudden onset of chest pain and leads to a wedge-shaped infarct of the periph- eral lung tissue.
Treatment is with antithrombolytics, anticoagulation and supplementary oxygen if required.
Pleural Effusion
Small effusions do not cause symptoms. Larger effusions may cause dyspnoea and pleuritic pain. There will be reduced movements on the affected side of the chest, decreased breath sounds, and dullness on percussion.
- The fluid that accumulates is either an exudate or a transudate. An exudate has a high protein content and is usually associated with infection or malignancy.
- A transudate is usually the result of capillary hypertension, for example, from left ventricular failure. The physiological effects are similar to those seen in a small simple pneumothorax.
- If the fluid in the pleural space is blood, from a haemorrhage, it is called a haemothorax. The physiological effects will be the same, but there may be associated haemorrhagic shock.
- Low blood pressure will result in decreased perfusion of alveoli, which will add to alveolar dead space and will lower arterial PO2.
