Acute respiratory failure

Respiratory failure means that respiratory system is not able to serve its function of oxygenation and carbon dioxide elimination. Clinically it is so when PaO2 is less than 60mmHg and PaCO2 is more than 50mmHg. It may be either acute or chronic.



Acute respiratory failure- Inability of respiratory system to maintain adequate level of blood gases oxygen and carbon dioxide, leading to life threatening derangement of these (PaO2 < 60mmHg, PaCO2 > 50mmHg) and pH of blood (7.3 or less)

In chronic respiratory failure there is time for metabolic compensation so pH is either normal or near normal

There are two types of respiratory failure

1. Hypoxemic respiratory failure- Primarily there is hypoxia (PaO2 < 60mmHg); most commonly it occurs in pulmonary conditions where PaO2 falls either due to ventilation and perfusion mismatch (V/Q) or intra pulmonary shunt.

2. Hypercapnic respiratory failure- PaCO2 is more than 50 mmHg. It occurs in condition associated with hypoventilation due to ventilation pump failure like neuromuscular diseases (polyneuropathies, acute GBS, myasthenia gravis, myopathies, hypnosedative overdose and respiratory center involvement).

In acute hypercapnic respiratory failure there is no time for metabolic compensation and pH is found 7.3 or lower however in chronic hypercapnic respiratory failure the pH is near normal (above 7.3) due to metabolic compensation

In chronic hypoxemic respiratory failure it is not that obvious on ABG analysis and the distinction between acute and chronic hypoxemic respiratory failure is suggested by presence of polycythaemia and cor pulmonale

Pathophysiology- Abnormality of any part of the respiratory system may lead to respiratory failure. It may be in respiratory center, peripheral nerves, chest wall, respiratory muscles, diaphragm, airways, alveoli or pulmonary vessels

The cause may be in respiratory system or it may be away from it, as in condition of shock, where hypo perfusion of lung tissue results in acute respiratory failure.

There are three main mechanisms of acute respiratory failure

1 Ventilation pump failure leading to alveolar hypoventilation

2 Ventilation perfusion mismatch (V/Q)

3 Shunt (intra pulmonary shunt)

Ventilation pump failure – The reason of ventilation pump failure may be one of these-
Respiratory drive is less. The respiratory center is depressed or diseased e.g. hypnosedative over dose, cerebrovascular accident involving brainstem.
Respiratory muscles are weak or chest wall structure or function is not adequate as in acute GBS, organophosphate poisoning, muscular dystrophy, Kyphoscoliosis, large flail chest segment.
Respiratory muscles are fatigued due to overload and can not work adequately- Often in patients of ARDS, pneumonia, severe asthma the workload on respiratory muscles is very high and respiratory muscles are not able to sustain the high workload after a certain time due to fatigue

Ventilation pump failure leads to low minute ventilation or alveolar hypoventilation

Alveolar ventilation (Va) and PaCO2 are inversely related to each other

When Va increases PaCO2 decreases, When Va decreases PaCO2 increases

So in ventilation pump failure alveolar hypoventilation occurs which leads to hypercapnia



In such situations the difference of partial pressure of O2 in alveoli( PAO2) and arterial O2 (PaO2) is normal and not abnormally increased. The hypoxaemia can readily be corrected by administering oxygen
Ventilation perfusion match V/Q

This is the most common mechanism responsible for hypoxaemia. Some areas of lung have insufficient ventilation for the amount of blood flow, where as others have excessive ventilation for the amount of regional blood flow.

Low V/Q areas of lung are those where ventilation is not adequate in proportion to blood flow so less oxygenated blood is reaching to arterial side contributing to hypoxemia


High V/Q ares of lung are those where blood flow is not adequate so ventilation is going waste contributing to more dead space. It contributes to wasted ventilation but gas exchange is not affected unless it is severe.

So in ventilation mismatch there is hypoxemia but more than ventilation pump failure and there is hypercapnia but less than ventilation pump failure

Intra pulmonary shunt – commonly known as shunt

In situations like ARDS pneumonia, pulmonary oedema, the alveoli are filled with fluid and there is no contact of inspired air with alveolar capillary blood flow so there is no oxygenation of the blood. This non oxygenated blood goes from venous side to arterial side like a shunt and contributes to hypoxemia. It is similar to an intra cardiac shunt where blood bypasses the lung. Here there are several intra pulmonary shunts leading to severe hypoxemia

Even very high concentration is not able to correct this hypoxemia as blood is not coming in contact of inspired air

Due to hypoxemia there is tachypnoea and an increase in minute ventilation so PaCO2 is either low or, less commonly normal

Respiratory pathophysiology	Blood gases	P (A-a) O2	Effect of increasing inspired oxygen	Common clinical situation
Ventilation pump failure	CO2      O2	Normal	Correct hypoxaemia	Neuromuscular diseases (usually non lung)
Ventilation perfusion mismatch	O2           CO2	Increased	Correct hypoxaemia	COPD Asthma
Shunt	O2    CO2	Further increased	Very difficult to correct hypoxemia	ARDS

Management of acute respiratory failure

Acute respiratory failure is an emergent situation, which can progress to life threatening situation rapidly. One must act fast and quick to recognize the dangerous situation and stabilize the patient

Initial assessment and stabilization – Adequate airway and breathing (oxygenation and ventilation) are ensured before further diagnostic workup. Cardiovascular stability must be assessed and established (adequate cardiac rhythm and secure I V access).

A quick clinical examination to assess respiratory rate, extra respiratory muscles effort, cyanosis, pattern of respiration (deep or shallow, calm or labored, quiet or rapid), chest wall configuration and its movement, rapid percussion and auscultation of each hemithorax, Pulse oximetry and ABG analysis give sufficient idea about initial evaluation of acute respiratory failure. A bedside X-ray chest should be done

The first priority is to establish adequate oxygenation and ventilation as hypoxia and hypercarbia may rapidly lead to dangerous cardiac arrhythmias and cardiovascular collapse. Many a times providing nasal oxygen is sufficient but if patient is not breathing immediate initial ventilation should be started with Bag and Mask (AMBU) connected with oxygen. Once adequate oxygenation had been achieved endotracheal intubation should be done and ventilation should be done with 100% oxygen. When adequate oxygenation and elimination of carbon dioxide had been achieved adjustment of FiO2 and other settings of ventilator to be done
Indications of putting patient on mechanical ventilator are-

1.Apnea or hypo apnea –it results into severe acute hypercapnic failure rapidly.

2. Severe hypoxemia – PaO2 is less than 60mmHg despite adequate oxygenation as happens in ARDS, severe pneumonia and sepsis

3. Very high workload of breathing expecting respiratory muscle fatigue- very high respiratory rate (40 or more than 40/mt), very high minute ventilation

4. Severe asthma – leading to hypoxemia and hypercapnea

5. Deteriorating trend of ABG which is not showing response to adequate supportive treatment

6. In case of shock, to divert blood from over working respiratory muscles to vital internal organs, the respiratory muscles are put at rest by applying ventilator

Treatment of acute respiratory failure comprises
Supportive treatment
Specific treatment of the underlying disorder
Mechanical ventilation

Supportive treatment and mechanical ventilation assist device are required to achieve and maintain the desired alveolar ventilation, adequate oxygenation and to stabilize and support the patient until the primary problem is corrected and to protect the patient from injuries and harms of the illness, medicines and mechanical ventilator. Acute respiratory failure is a dynamic condition where clinical situation changes frequently. Very close monitoring of vitals, ABG status, serum electrolytes, hourly urine output and clinical condition of patient is required.

The details can be read from any standard textbook of critical care medicine however few points are being mentioned
Endotraceal tube

Before intubation oxygenate the patient adequately using bag and mask ventilation connected with oxygen. There should be no hurry on this.

Naso tracheal intubation has the advantage of better fixation and patient comfort at later stage however lesser diameter can cause suction problem, difficulty in weaning and use of fibro optic bronchoscope if required

100% O2 should be administered before and after endotracheal suction. In most of the modern ventilator there is option for short period 100% oxygenation

Cuffed tube does not protect from aspiration of oropharyngeal secretions completely and frequent oral suction is required to prevent it.

Endotracheal tube should be properly secured and patient should be properly educated about the need and importance of the tube
Oxygen

Higher concentration of O2 in FiO2 more than 60% can cause harm and lung injury if given for more than few hours so FiO2 should not contain more than 60% of O2 for long. It is advisable to limit high concentration of oxygen(FiO2 >50%) not more than 72 hours if possible.
Broncodilators

B2 adrenergic agonists- are more effective in acute respiratory failure when given by inhalation route than oral or parenteral route. The onset of action is more rapid side effects are much less and effect last for sufficient time

Anticholinergics – Ipratropium bromide is quite effective in patients of COPD when given using nebulizer or inhaler. There are very few side effects even when used in large doses. It should always be used in combination of B2 adrenergic agonists. For nebulization an effective dose is 500 microgram every 6 to 8 hours

Theophylline- Use in acute respiratory failure had become less as safe and effective beta-adrenergic agonists and other agents are available. Aminophylline can be used in infusion cautiously if necessary. Avoid loading dose in patients who are already on theophyllin. In elderly, patients with hepatic, renal or cardiac failure, cor pulmonale use lower dose and infusion rate







Corticosteroids

In acute respiratory failure corticosterroids should be used intravenously as nebulized route is not effective enough in acute situation. After initial 3 to 5 days it can be changed to oral form.
Other supportive care includes

Sedatives and muscle relaxants – Muscle relaxants should be used by experienced persons only when necessary. Commonly patients on ventilator could be managed with combination of opiate analgesics to relieve pain and benzodiazapine do provide sedation and amnesia. Lorazepam, midzolam, diazepam, morphine are used for this
Antibiotics
Anticoagulation- Subcutaneous heparin or low molecular weight heparin, regular movement of feet and knee, pneumatic compression boot

Prophylaxis against gastric mucosal injury- by cytoprotective agents (sucralfate), antacid or H2 receptor antagonists
Nutritional support

By nasogastric or orogastric tube enteral feeding should be maintained in all intubated patients it should be started in 72 hr in malnourished and with in 7 days in well nourished patients. Peripheral nutrition may be given to support nutritional requirements


Ventilatory strategies

Variables to be set during mechanical ventilation (for volume cycled ventilation)



Mode How the breath should be initiated



Tidal Vol. Vol. of each ventilator breath

Resp. rate Ventilator breath rate in case of apnea or the number of patients

breaths supported by ventilator

FIO2 Concentration of oxygen in inspired air

Inspiratory flow How fast the inspiratory flow be delivered

PEEP end expiratory pressure ( pressure in alveoli at the end of expiration

In respect to atmospheric pressure



Peak pressure At what peak pressure the inspiratory flow should stop



I:E Ratio The ratio of inspiratory and expiratory time

Flow pattern Inspiratory flow is constant or descending or follow any other

Pattern














Ventilatory strategies



In deciding the ventilatory strategies one should keep in mind that hypoxemia is more dangerous than hypercapnia and hypercapnia is better tolerated. One should try to minimize barotrauma to lung tissue and adverse effect on cardiac output.

Tidal volume is kept on the lower side 6 to 8 ml/Kg of BW. It reduces the chances of injury to lung tissue and effect on cardiac output is also minimized.

Hyperventilation should be prevented to prevent dangerous alkalaemia in presence of elevated bicarbonates, which can lead to hypokalaemia

Prevent atelectasis and worsening of paO2 by applying PEEP of 3 to 5 cm of water



In COPD – expiration takes longer time, in positive pressure ventilation there are chances of developing hyperinflation leading to auto peep, which affect cardiac output adversely so hyperinflation should be prevented and enough time should be provided for expiration.

Keep long expiratory time I : E ratio 1 : 3

Shorten the inspiratory time-

By keeping high inspiratory flow rate – 1Litre/sec or more and low frequency of respiratory rate

Low tidal volume 6 ml/Kg of BW-

It will prevent hyperinflation and auto peep, adverse effect on cardiac output will be minimized but it will result in some rise (accumulation) of CO2. It should be allowed. (Permissive hypercapnia)

PEEP should be less than intrinsic PEEP

(PEEP< Intrinsic PEEP)


Ventilatory strategies in ARDS

In ARDS the problems are of severe hypoxaemia and stiff, less compliant lungs

To improve hypoxemia – use PEEP of 10cm of water

Fio2 <50%

To prevent volume trauma and adverse effect on Cardiac output-Tidal volume 6ml/Kg of BW, Low inspiratory flow, more time for inspiration, decelerating flow pattern, inspiratory platue pressure <30 cm of water

To meet the high ventilatory demand - High frequency of respiratory rate



Extra pulmonary causes which contribute to hypoxaemia - in case of worsening of PaO2 these factors should be considered and looked for
Cardiac output- adequate cardiac output should be ensured by BP, hourly urine output and hydration and if indicated should be corrected
Oxygen demand of tissues –if body activity or muscular activity is more, If the patient is restless or anxious or in pain or fighting with ventilator
Body temperature –if the body temperature is high.

If such is the situation attention should be given to these factors before changing the ventilator strategies




Complication of mechanical ventilation

Endotrcheal tube/ Tracheostomy tube related complications

Barotrauma -pneumothorax pneumomediastinum lung injury

Decreased cardiac output

Oxygen toxicity

Ventilator related pneumonia

Hypo/hyperventilation

Apnea due to disconnection

Mechanical/electrical failure

Accidental burns

Psychological dependence on ventilator





Weaning

Most patients are weaned off easily and safely

In patients with underlying disease of lung it has to be gradual

For successful weaning ventilatory capacity should be significantly more than ventilatory demand

F/Vt(L) < 100breath/L

VT->5ml/kg, Vc >10-15 ml/kg, f < 25, Negative inspiratory pressure >25cm of water, PaO2 >60 mmHg with FiO2<0.5

A successful trial of spontaneous breathing indicates possible weaning

T-tube, SIMV BiPAP, PSV all are same in outcome and it is a matter of personal preference that which method is chosen of


Noninvasive ventilation

The application of ventilatory support through a nasal or full face mask in place of ETT is increasingly being used for patients with acute or chronic respiratory failure

It should be considered inpatients with mild to moderate acute respiratory failure

The patient should be able to follow commands shoud be able to clear the secretions and swallow

It has been used successfully in COPD asthma, obesity hypoventilation syndrome, obstructive sleep apnea, decompensated CHF and mild to moderate pulmonary oedema non invasive ventilation is not used in patient who do not have their own respiratory drive or who are haemodynemically unstable or having large amount of secretions requiring frequent suction or suffering from facial injuries



Bibliography
Harrison’s principles of internal medicine16th edition 1583-1584,1588-1599
Current critical care diagnosis & Treatment Frederic S Bongard Darryl Y sue 2nd edition 268-303
Brochard L, Mancebo J, Wysocki M: Noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease. N Engl J Med 1995 Sep 28; 333(13): 817-22•