Acute respiratory failure

Sanjay joshi

(The following is a = simplified=20 version of acute respiratory failure and its management. This is to = create an=20 understanding of the subject. Several details are not covered here and = students=20 are advised to refer to standard textbooks)

Respiratory failure means that respiratory system = is not able=20 to serve its function of oxygenation and carbon dioxide elimination. = Clinically=20 it is so when PaO2 is less = than 60mmHg=20 and PaCO2 is=20 more than 50mmHg. It may be either acute or chronic.

Acute respiratory = failure-=20 Inability of respiratory system to maintain adequate level of blood = gases oxygen=20 and carbon dioxide, leading to life threatening derangement of these = (PaO2 < = 60mmHg,=20 PaCO2 = >=20 50mmHg) and pH of blood (7.3 or less)

In chronic respiratory = failure there=20 is time for metabolic compensation so pH is either normal or near normal =

There are two types of = respiratory=20 failure

1. Hypoxemic = respiratory=20 failure- Primarily there is hypoxia (PaO2 < = 60mmHg); most=20 commonly it occurs in pulmonary conditions where PaO2 falls = either due to=20 ventilation and perfusion mismatch (V/Q) or intra pulmonary shunt.

2. Hypercapnic = respiratory=20 failure- PaCO2 is more = than 50=20 mmHg. It occurs in condition associated with hypoventilation due to = ventilation=20 pump failure like neuromuscular diseases (polyneuropathies, acute GBS,=20 myasthenia gravis, myopathies, hypnosedative overdose and respiratory = center=20 involvement).

In acute hypercapnic = respiratory=20 failure there is no time for metabolic compensation and pH is found 7.3 = or lower=20 however in chronic hypercapnic respiratory failure the pH is near normal = (above=20 7.3) due to metabolic compensation

In chronic hypoxemic = respiratory=20 failure it is not that obvious on ABG analysis and the distinction = between acute=20 and chronic hypoxemic respiratory failure is suggested by presence of=20 polycythaemia and cor pulmonale

Pathophysiology- = Abnormality=20 of any part of the respiratory system may lead to respiratory failure. = It may be=20 in respiratory center, peripheral nerves, chest wall, respiratory = muscles,=20 diaphragm, airways, alveoli or pulmonary vessels

The cause may be in = respiratory=20 system or it may be away from it, as in condition of shock, where hypo = perfusion=20 of lung tissue results in acute respiratory failure.

There are three main = mechanisms of=20 acute respiratory failure

1 Ventilation pump = failure leading=20 to alveolar hypoventilation

2 Ventilation perfusion = mismatch=20 (V/Q)

3 Shunt (intra pulmonary = shunt)

Ventilation pump = failure =96=20 The reason of ventilation pump failure may be one of these-

Respiratory=20 drive is less. The respiratory center is depressed or diseased e.g.=20 hypnosedative over dose, cerebrovascular accident involving brainstem. =
Respiratory=20 muscles are weak or chest wall structure or function is not adequate = as in=20 acute GBS, organophosphate poisoning, muscular dystrophy, = Kyphoscoliosis,=20 large flail chest segment.=20
Respiratory=20 muscles are fatigued due to overload and can not work adequately- = Often in=20 patients of ARDS, pneumonia, severe asthma the workload on respiratory = muscles=20 is very high and respiratory muscles are not able to sustain the high = workload=20 after a certain time due to fatigue =20

Ventilation pump failure = leads to=20 low minute ventilation or alveolar hypoventilation

Alveolar ventilation = (Va) and=20 PaCO2 = are=20 inversely related to each other

When Va increases = PaCO2 = decreases, When Va=20 decreases PaCO2=20 increases

So in ventilation pump = failure=20 alveolar hypoventilation occurs which leads to hypercapnia

In such situations the = difference of=20 partial pressure of O2 in = alveoli( PAO2) and = arterial=20 O2 = (PaO2) is = normal and not=20 abnormally increased. The hypoxaemia can readily be corrected by = administering=20 oxygen

Ventilation perfusion match V/Q

This is the most common = mechanism=20 responsible for hypoxaemia. Some areas of lung have insufficient = ventilation for=20 the amount of blood flow, where as others have excessive ventilation for = the=20 amount of regional blood flow.

Low V/Q areas of lung are those = where=20 ventilation is not adequate in proportion to blood flow so less = oxygenated blood=20 is reaching to arterial side contributing to hypoxemia

High V/Q ares of lung = are those=20 where blood flow is not adequate so ventilation is going waste = contributing to=20 more dead space. It contributes to wasted ventilation but gas exchange = is not=20 affected unless it is severe.

So in ventilation = mismatch there is=20 hypoxemia but more than ventilation pump failure and there is = hypercapnia but=20 less than ventilation pump failure

Intra pulmonary = shunt =96=20 commonly known as shunt

In situations like ARDS = pneumonia,=20 pulmonary oedema, the alveoli are filled with fluid and there is no = contact of=20 inspired air with alveolar capillary blood flow so there is no = oxygenation of=20 the blood. This non oxygenated blood goes from venous side to arterial = side like=20 a shunt and contributes to hypoxemia. It is similar to an intra cardiac = shunt=20 where blood bypasses the lung. Here there are several intra pulmonary = shunts=20 leading to severe hypoxemia

Even very high = concentration is not=20 able to correct this hypoxemia as blood is not coming in contact of = inspired=20 air

Due to hypoxemia there = is tachypnoea=20 and an increase in minute ventilation so PaCO2 is either low or, less = commonly=20 normal

Respiratory=20 pathophysiology

Blood = gases

P (A-a) = O2

Effect of = increasing inspired=20 oxygen

Common clinical=20 situation

Ventilation pump=20 failure

=20 CO2 =20 O2

Normal

Correct hypoxaemia =

Neuromuscular = diseases=20 (usually non lung)

Ventilation = perfusion=20 mismatch

of=20 respiratory rate

Extra=20 pulmonary causes which contribute to hypoxaemia - = in case of=20 worsening of PaO2 these factors should be considered and looked for

Cardiac=20 output- = adequate=20 cardiac output should be ensured by BP, hourly urine output and = hydration and=20 if indicated should be corrected=20
Oxygen=20 demand of tissues = =96if body=20 activity or muscular activity is more, If the patient is restless or = anxious=20 or in pain or fighting with ventilator=20
Body=20 temperature = =96if the=20 body temperature is high.

If = such is=20 the situation attention should be given to these factors before changing = the=20 ventilator strategies

Complication of mechanical = ventilation

Endotrcheal tube/ Tracheostomy tube related = complications

Barotrauma -pneumothorax pneumomediastinum lung = injury

Decreased cardiac output

Oxygen toxicity

Ventilator related=20 pneumonia

Hypo/hyperventilation

Apnea due to=20 disconnection

Mechanical/electrical=20 failure

Accidental=20 burns

Psychological = dependence on=20 ventilator

Weaning

Most = patients are=20 weaned off easily and safely

In = patients with=20 underlying disease of lung it has to be gradual

For = successful=20 weaning ventilatory capacity should be significantly more than = ventilatory=20 demand

F/_Vt(L)=20 < 100breath/L

VT->5ml/kg,=20 Vc >10-15 ml/kg, f = < 25,=20 Negative inspiratory pressure >25cm of water, PaO2 >60 mmHg with=20 FiO2<0.5

A = successful trial of=20 spontaneous breathing indicates possible weaning

T-tube, = SIMV BiPAP,=20 PSV all are same in outcome and it is a matter of personal preference = that which=20 method is chosen of

Noninvasive=20 ventilation

The = application of=20 ventilatory support through a nasal or full face mask in place of ETT is = increasingly being used for patients with acute or chronic respiratory=20 failure

It should = be=20 considered inpatients with mild to moderate acute respiratory=20 failure

The = patient should be=20 able to follow commands shoud be able to clear the secretions and = swallow &n= bsp; =20

It has been used successfully in COPD asthma, = obesity=20 hypoventilation syndrome, obstructive sleep apnea, decompensated CHF and = mild to=20 moderate pulmonary oedema non invasive ventilation is not used in = patient who do=20 not have their own respiratory drive or who are haemodynemically = unstable or=20 having large amount of secretions requiring frequent suction or = suffering from=20 facial injuries

Bibliography

Harrison=92s = principles=20 of internal medicine16th edition 1583-1584,1588-1599=20
Current = critical care=20 diagnosis & Treatment =20 Frederic S Bongard Darryl Y sue 2^nd edition 268-303=20
Brochard L, Mancebo J, Wysocki M: = Noninvasive=20 ventilation for acute exacerbations of chronic obstructive pulmonary = disease.=20 N Engl J Med 1995 Sep 28; 333(13): 817-22=95 =