Respi

LO G O

Respiratory Failure Jiang

sheng-hua

O2 CO2

CO2 External respiration

circulation

Internal respiration

The act of respiration engages 3 processes:  (1) transfer of oxygen across the alveolus,  (2) transport of oxygen to the tissues,  (3) removal of carbon dioxide from blood into the alveolus and then into the environment.

 Respiration primarily occurs at the alveolar capillary units of the lungs, where exchange of oxygen and carbon dioxide between alveolar gas and blood takes place.  The quantity of oxygen combined with hemoglobin depends on the level of blood PaO2.

 This relationship, expressed as the oxygen hemoglobin dissociation curve, is not linear,  has a sigmoid-shaped curve with a steep slope between a PaO2 of 10 and 50 mm Hg and a flat portion above a PaO2 of 70 mm Hg.

 The carbon dioxide is transported in 3 main forms:  (1) in simple solution,  (2) as bicarbonate, and  (3) combined with protein of hemoglobin as a carbamino compound.

 in normal lungs, not all alveoli are ventilated and perfused perfectly  some units are underperfused while others are overperfused.  The optimally ventilated alveoli that are not perfused well are called high V/Q ： （ ventilation/perfusion ratio ） units (acting like dead space),  alveoli that are optimally perfused but not adequately ventilated are called low V/Q units (acting like a shunt).

Alveolar ventilation  the rate of carbon dioxide production by the tissues is constant and equals the rate of carbon dioxide elimination by the lung  Even normal lungs have some degree of V/Q mismatching and a small quantity of right-to-left shunt, alveolar PO2 is slightly higher than arterial PO2. However, an increase in alveolarto-arterial PO2 above 15-20 mm Hg indicates pulmonary disease as the cause of hypoxemia

What is respiratory failur  Respiratory failure develops when the rate of gas exchange between the atmosphere and blood is unable to match the body's metabolic demands.  It is diagnosed when the patient loses the ability to provide sufficient oxygen to the blood and develops hypoxemia or when the patient is unable to adequately ventilate and develops hypercarbia and hypoxemia.

 Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination.  In practice, respiratory failure is defined as a PaO2 value of less than 60 mm Hg while breathing air or a PaCO2 of more than 50 mm Hg. （ mmHg=millimeter hydrargyrum ）

2 ． Classification （ 1 ） According to PaCO2 ■ （ Type I ） respiratory failure （ Hypoxemic respiratory failure ） a PaO2 of less than 60 mm Hg with a normal or low PaCO2. Cause of ： Edema, Vascular disease, Chest Wall & Pleural disease. ■

（ TypeⅡ ） respiratory

failure （ Hypercapnic

respiratory failure ） a PaO2 low 60 mm Hg and PaCO2 of more than 50 mm

Hg.

Cause

Neuromuscular disease.

of ： Airway

obstruction,

 examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage  Common etiologies of type II include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (eg, asthma, chronic obstructive pulmonary disease [COPD]).

acutely or chronically  In acute respiratoryfailure, a sudden, catastrophic event leads to life-threatening respiratory insufficiency.  In chronic respiratory failure, gradual worsening of respiratory function leads to progressive impairment of gas exchange, the metabolic effects of which are partially compensated by adaptations in other systems

 chronic respiratory insufficiency  In patients with long-standing respiratory disease, resulting in a state in which patients do not have true respiratory failure but have little or no functional respiratory reserve.  acute on chronic respiratory failure a mild insult to the respiratory system

Distinctions between acute and chronic respiratory failure

 Acute hypercapnic respiratory failure develops over minutes to hours; therefore, pH is less than 7.3.  Chronic respiratory failure develops over several days or longer, allowing time for renal compensation and an increase in bicarbonate concentration. Therefore, the pH usually is only slightly decreased.

 The distinction between acute and chronic hypoxemic respiratory failure cannot readily be made on the basis of arterial blood gases.  The clinical markers of chronic hypoxemia, such as polycythemia or cor pulmonale, suggest a long-standing disorder

EPIDEMIOLOGY  Respiratory failure is a common diagnosis among patients in medical intensive care units (ICUs) and is associated with a poor prognosis.  The incidence of respiratory failure is 137 cases per100,000 population, or 360,000 cases per year in the United States,with 36% of these individuals failing to survive the hospitalization.

 Therapeutic advances in both mechanical ventilation and airwaymanagement have improved the prognosis for patients with respiratoryfailure over the past several decades.  ventilator support systems  Lung transplantation

PHYSIOLOGY  Normal respiration requires the integrated function of five separate components.  1. Nervous system.  2. Musculature (the pump).  3. Airways (a complex conduit system for bulk delivery of gases).  4. Alveolar units (an efficient, distensible, compact membrane system).  5. Vasculature (a network of conduits capable of transporting dissolved gases to and from the functioning organs throughout the body).

Brainstem Airway

Lung

Spinal cord root Nerve

Nerve

Pleura

Chest wall

Neuromuscular junction Respiratory muscle

Sites at which disease may cause ventilatory disturbance

 Respiratory failure due to diseases that cause dysfunction of the central control system can be thought of as controller dysfunction, or central apnea.  Hypoventilation can be caused by disease at any of the anatomical sites involved in ventilation. Brainstem injury or disease may result in impaired functioning of the respiratory centre, which may also be suppressed by depressant drugs

Brainstem Airway

Lung

Spinal cord root Nerve

Nerve

Pleura

Chest wall

Neuromuscular junction Respiratory muscle

Sites at which disease may cause ventilatory disturbance

Brainstem Airway

Lung Pleura

Chest wall

Spinal cord root Nerve

Nerve supplying respiratory muscles

Neuromuscular junction Respiratory muscle

Sites at which disease may cause ventilatory disturbance

Brainstem Airway

Lung

Spinal cord root Nerve

Nerve

Pleura

Chest wall

Neuromuscular junction Respiratory muscle

Sites at which disease may cause ventilatory disturbance

 Neuromuscular blockers or disease of the neuromuscular junction (eg myasthenia gravis) may impair transmission of nerve impulses to respiratory muscles Or the problem may be in the muscle itself.  Respiratory muscle fatigue, disuse atrophy and malnutrition are important causes of respiratory muscle failure in the ICU

Brainstem Airway

Lung

Spinal cord root Nerve

Nerve

Pleura

Chest wall

Neuromuscular junction Respiratory muscle

Sites at which disease may cause ventilatory disturbance

 Respiratory failure involving diseases that cause marked obstruction or dysfunction of the air passages can be thought of as airway system dysfunction  Alternatively the problem may be a problem of increased resistance to airflow. For example due to obstruction of the upper airway or bronchospasm

Brainstem Airway

Lung

Spinal cord root Nerve

Nerve

Pleura

Chest wall

Neuromuscular junction Respiratory muscle

Sites at which disease may cause ventilatory disturbance

 Respiratory failure due to diseases that cause ineffective function of the respiratory pump can be thought of as pump dysfunction. Under normal conditions, only elastic recoil is required for expiration, but during respiratory failure accessory muscles of expiration are required

Alveolar units

 Respiratory failure as a result of diseases that cause collapse, flooding, or injury to the alveolar networkcan be thought of as alveolar compartment dysfunction.

O2

CO2

Alveolar epithelium

Capillary endotheliocyte

 Respiratory failure as a result of disease involving the pulmonary vasculature can be thought of as pulmonary vascular dysfunction.

Pathophysiology  Failure of any one of these essential components or significant dysfunction of more than one essential component can lead to failure of the integrated system and produce clinical respiratory failure.  including the airways, alveoli, CNS, peripheral nervous system, respiratory muscles, and chest wall. Patients who have hypoperfusion secondary to cardiogenic, hypovolemic, or septic shock often present with respiratory failure.

 Hypoxemic respiratory failure: The pathophysiologic mechanisms that account for the hypoxemia observed in a wide variety of diseases are ventilation-perfusion (V/Q) mismatch and shunt.  These 2 mechanisms lead to widening of the alveolar-arterial oxygen difference, which normally is less than 15 mm Hg. With V/Q mismatch, the areas of low ventilation relative to perfusion (low V/Q units) contribute to hypoxemia.

肺泡通气与血流比例失调（ Ventilation-perfusion-mismatching ） （ 1 ） Type & cause of ventilation-perfusion-mismatching ■Decreased

ratio of V·A/ Q·（部分肺泡通气不足）

支气管哮喘、慢性支气管炎、阻塞性肺气肿、肺纤维化、肺水肿

·

·

VA/ Q 比值↓

气↓

部分病变严重的肺泡通

■Increased

· · VA/ Q （部分肺泡血流不足）

ratio of VA/ Q （部分肺泡血流不足）

肺动脉栓塞、肺内 DIC 、肺动脉炎、肺血管收缩 血流↓ ·

部分肺泡

· VA/Q↑ ＞ 60%

ventilation ）

死腔样通气（ Dead space like

功能死腔量（ Functional 呼衰 ， V ） space

dead

 A decrease in alveolar ventilation can result from a reduction in overall (minute) ventilation or an increase in the proportion of dead space ventilation. A reduction in minute ventilation is observed primarily in the setting of neuromuscular disorders and CNS depression.

Ventilatory capacity versus demand  Respiratory failure may result from either a reduction in ventilatory capacity or an increase in ventilatory demand (or both). Ventilatory capacity can be decreased by a disease process involving any of the functional components of the respiratory system and its controller. Ventilatory demand is augmented by an increase in minute ventilation and/or an increase in the work of breathing.

History  Does the patient have factors that increase the risk for respiratory failure? Factors may include young age; history of prematurity; immunodeficiency; and chronic pulmonary, cardiac, or neuromuscular disease (eg, cystic fibrosis, bronchopulmonary dysplasia, unrepaired congenital heart disease, or spinal muscular atrophy [SMA]).

 Does the patient have a cough, rhinorrhea, or other symptoms of an upper respiratory tract infection to define an etiology?  Does the patient have a fever or signs of sepsis? Several infections can lead to respiratory failure because of a systemic inflammatory response, pulmonary edema, or acute respiratory distress syndrome (ARDS) or because it can produce a power-load imbalance secondary to increased oxygen consumption

 How long have the symptoms been present? The natural course of a respiratory illness must be considered. Respiratory syncytial virus (RSV) infections frequently worsen over the initial 3-5 days before improvement occurs.

 Does the patient have any pain? Pain can suggest pleuritis or foreign-body aspiration.  Does the patient have a possible or known exposure to sedatives (eg, benzodiazepines, tricyclic antidepressants, narcotics) or has he or she recently undergone a procedure that used general anesthesia? This could suggest hypoventilation

 Does the patient have symptoms of neuromuscular weakness or paralysis? What is the distribution of weakness and duration of symptoms to narrow the differential diagnosis? Bulbar dysfunction suggests myasthenia gravis. Distal weakness that progresses upward suggests Guillain-Barré syndrome. Apnea associated with a traumatic injury suggests a cervical spinal cord injury.

 Does the patient have a history suggestive of a stroke or seizure?  Does the patient have a history of headaches? With chronic hypercapnia, headaches typically occur at nighttime or upon the patient's awakening in the morning.

Physical  During physical examination, clinicians should avoid interfering with the patient's mechanisms for compensation

General appearance Does the patient appear well or sick? Is the patient cyanotic?

Respiratory rate, quality, and effort  Bradypnea is most often observed in central control abnormalities. Slow and large tidal volume breaths also minimize turbulence and resistance in significant extrathoracic airway obstruction (eg, epiglottitis).

Respiratory rate, quality, and effort  The fast and shallow breathing of tachypnea is most efficient in intrathoracic airway obstruction. It decreases dynamic compliance of the lung.  Auscultation provides information about the symmetry and quality of air movement. Evaluate the patient for stridor, wheezing, crackles, and decreased breath sounds (eg, alveolar consolidation, pleural effusion).

Respiratory rate, quality, and effort  Grunting is an expiratory sound made by infants as they exhale against a closed glottis. It is an attempt to increase functional residual capacity and lung volume. This attempt is made in order to raise functional residual capacity above the critical closing volume and to avoid alveolar collapse. This is a concerning physical finding.

Respiratory rate, quality, and effort  Assess for accessory muscle use and nasal flaring. Suprasternal and intercostal retractions are present when highly negative pleural pressures are required to overcome airway obstruction or stiff lungs.

Chest wall findings:  Evaluate for paradoxical movement of the chest wall. In the presence of abnormalities of the pulmonary pump, paradoxical chest-wall movement occurs because of instability of the chest wall associated with absent intercostal muscle use. As the diaphragm contracts and pushes abdominal contents out, the chest wall retracts inward instead of expanding normally.

Cardiovascular findings  Tachycardia and hypertension may occur secondary to increased circulatory catecholamine levels.  A gallop is suggestive of myocardial dysfunction leading to respiratory failure.  Peripheral vasoconstriction may develop secondary to respiratory acidosis.

Neurologic findings  Patients may be lethargic, irritable, anxious, or unable to concentrate.  The inability to breathe comfortably creates anxiety, and superimposed hypoxemia and hypercapnia accentuates any restlessness and agitation. Increased agitation may indicate a general worsening of the patient's condition

Respiratory Failure Laboratory Testing

Arterial blood gas PaO2 PaCO2 PH Chest imaging Chest x-ray CT sacn Ultrasound pulmonary function tests

Laboratory Studies  This emphasizes the importance of measuring arterial blood gases in all patients who are seriously ill or in whom respiratory failure is suspected.  A complete blood count may indicate anemia, which can contribute to tissue hypoxia, whereas polycythemia may indicate chronic hypoxemic respiratory failure

 Measuring serum creatine kinase with fractionation and troponin I helps exclude recent myocardial infarction in a patient with respiratory failure.  An elevated creatine kinase with a normal troponin I may indicate myositis 肌炎 , which occasionally can cause respiratory failure.

 In chronic hypercapnic respiratory failure, serum thyroid-stimulating hormone should be measured to evaluate the possibility of hypothyroidism, a potentially reversible cause of respiratory failure.

Chest radiograph  Chest radiography is essential because it frequently reveals the cause of respiratory failure. However, distinguishing between cardiogenic and noncardiogenic pulmonary edema often is difficult.  Increased heart size, vascular redistribution, peribronchial cuffing, pleural effusions, septal lines, and perihilar bat-wing distribution of infiltrates suggest hydrostatic edema; the lack of these findings suggests ARDS.

Echocardiography  Echocardiography need not be performed routinely in all patients with respiratory failure. However, it is a useful test when a card  iac cause of acute respiratory failure is suspected.  The findings of left ventricular dilatation, regional or global wall motion abnormalities, or severe mitral regurgitation support the diagnosis of cardiogenic pulmonary edema.

 A normal heart size and normal systolic and diastolic function in a patient with pulmonary edema would suggest ARDS.  Echocardiography provides an estimate of right ventricular function and pulmonary artery pressure in patients with chronic hypercapnic respiratory failure.

pulmonary function tests  Patients with acute respiratory failure generally are unable to perform pulmonary function tests (PFTs). However, PFTs are useful in the evaluation of chronic respiratory failure.  Normal values of forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) suggest a disturbance in respiratory control.

 A decrease in FEV1 -to-FVC ratio indicates airflow obstruction, whereas a reduction in both the FEV1 and FVC and maintenance of the FEV1 -to-FVC ratio suggest restrictive lung disease.  Respiratory failure is uncommon in obstructive diseases when the FEV1 is greater than 1 L and in restrictive diseases when the FVC is more than 1 L.

Respiratory Failure Laboratory Testing Other tests Hemoglobin Electrolytes, blood urea nitrogen, creatinine Creatinine phosphokinase, aldolase Electromyography (EMG) Nerve conduction study

Respiratory muscle pressures MIP ( maximum inspiratory pressure) MEP ( maximum expiratory pressure)

Diagnosis  According to history, clinical manifestations, physical examination and blood gas analysis, we can diagnose respiratory failure. Especially arterial blood gas analysis may reveal hypoxemia and hypercapnia.

Diagnosis  According to history, clinical manifestations, physical examination and blood gas analysis, we can diagnose respiratory failure. Especially arterial blood gas analysis may reveal hypoxemia and hypercapnia.

Treatment  The principle of treatment includes  primary disease treatment  airway maintenance  correction of hypoxemia and hypercapnia  management of symptoms caused by hypoxemia and hypercapnia.

 Hypoxemia is the major immediate threat to organ function. Therefore, the first objective in the management of respiratory failure is to reverse and/or prevent tissue hypoxia. Hypercapnia unaccompanied by hypoxemia generally is well tolerated and probably is not a threat to organ function unless accompanied by severe acidosis.

(1)Airway maintenance and enhance the volume of ventilation  Assurance of an adequate airway is key in the patient with respiratory failure.

correctly use of bronchodilators  In severe cases intubation and mechanical ventilation may be used.

Bronchodilators  These agents are an important component of treatment in respiratory failure caused by obstructive lung disease. These agents act to decrease muscle tone in both small and large airways in the lungs. This category includes beta-adrenergics, methylxanthines, and anticholinergics.

 Terbutaline (Brethaire, Bricanyl) Acts directly on beta2-receptors to relax bronchial smooth muscle, relieving bronchospasm and reducing airway resistance  Albuterol (Proventil) Beta-agonist useful in the treatment of bronchospasm. Selectively stimulate beta2adrenergic receptors of the lungs. Bronchodilation results from relaxation of bronchial smooth muscle, which relieves bronchospasm and reduces airway resistance.

Theophylline (Theo-Dur, Slo-bid, Theo-24)  Has a number of physiological effects, including increases in collateral ventilation, respiratory muscle function, mucociliary clearance, and central respiratory drive.  Partially acts by inhibiting phosphodiesterase, elevating cellular cyclic AMP levels, or antagonizing adenosine receptors in the bronchi, resulting in relaxation of smooth muscle. However, clinical efficacy is controversial, especially in the acute setting.

Ipratropium bromide (Atrovent)  Anticholinergic medication that appears to inhibit vagally mediated reflexes by antagonizing action of acetylcholine, specifically with the muscarinic receptor on bronchial smooth muscle. Vagal tone can be significantly increased in COPD; therefore, this can have a profound effect. Dose can be combined with a beta-agonist because ipratropium may require 20 min to begin having an effect.

 To most of the chronic respiratory failure, correctly use of bronchodilators is very important. Table 2. Bronchodilators Route Dose salbutamol MDI and spacer 400-600µg q1-4h Aerosol solution 2.5-7.5mg q1-4h Ipratropium MDI and spacer 80-120µg q4-6h Aerosol solution Theophylline IV 5.6mg/kg 0.3-0.6mg/kg/hr oral

 Mechanical ventilation The aim of mechanical ventilation is to improve hypoxemia and to prevent hypercapnia. When do you select mechanical ventilation? This is a question we always meet in our clinical work. 1.progressive elevation in PaCO2>70-80mmHg 2.severe hypoxemia, after oxygen therapy, PaO2<40mmHg 3.respiratory rates>35 per minute or severe breathlessness 4.severe metabolic acidosis or pulmonary encephalopathy

 How to select artificial airway? face mask or nasal noninvasive intermittent positive pressure ventilation are delivered to augment alveolar ventilation and reducing the work of breathing. If hypoventilation can not be effectively reverses by noninvasive methods, intubation must be adopted. When artificial ventilation is required for more than 2 weeks, a tracheotomy is often required. Tracheotomy carries some risk of bleeding, pneumothorax, and local infection and incidence of aspiration.

(2)Antiinfectious therapy  Repeated bronchial and pulmonary infection is a major cause of chronic respiratory failure.  About 90% of COPD patients with respiratory failure is caused by acute bronchial or pulmonary infection.  Infection may also increase bronchial secretion and CO2 production.  So antiinfectious therapy is an important method to treat respiratory failure.

 Select effective antibiotics According to sputum culture, we can select sensitive antibiotics  Using combined antibiotics Because of multibacteria infection, it needs several kind of antibiotics. For example, we may combine second or third generation cephalosporin to aminoglycoside or fluoroguinolone.

(3)Oxygen therapy  The goal of oxygen therapy is to improve PaO2. It makes PaO2>60mmHg. In general, the lowest FiO2 achieving adequate oxygenation. sometimes, arterial oxygen saturation>90% should be used.

The methods of oxygen therapy: nasal prongs 1-3L/min to chronic respiratory failure venti mask 1-3L/min For type 1 respiratory failure, we can elevate the percentage of oxygen to maintain the PaO2. We can use higher inspirated fration of oxygen in type 1 respiratory failure oxygen therapy. But in type 2 respiratory failure we must select lower inspirated fration of oxygen .

Oxygen Therapy  Supplemental O2 therapy essential  titration based on SaO2, PaO2 levels and PaCO2  Goal is to prevent tissue hypoxia  Tissue hypoxia occurs (normal Hb & C.O.) - venous PaO2 < 20 mmHg or SaO2 < 40% - arterial PaO2 < 38 mmHg or SaO2 < 70%  Increase arterial PaO2 > 60 mmHg(SaO2 > 90%) or venous SaO2 > 60%  O2 dose either flow rate (L/min) or FiO2 (%)

Risks of Oxygen Therapy  O2 toxicity: - very high levels(>1000 mmHg) CNS toxicity and seizures lower levels (FiO2 > 60%) and longer exposure: - capillary damage, leak and pulmonary fibrosis - PaO2 >150 can cause retrolental fibroplasia - FiO2 35 to 40% can be safely tolerated indefinitely  CO2 narcosis: PaCO2 may increase severely to cause respiratory acidosis, somnolence and coma - PaCO2 increase secondary to combination of a) abolition of hypoxic drive to breathe b) increase in dead space

(4)Acid-base and electrolytes disturbance  There are many factors lead to acid-base and electrolytes disturbance.  These factors include severe pulmonary infection, hypoxemia or (and) hypercapnia. So airway maintenance, antibiotic therapy and use of bronchodilators are beneficial to treat it.

The acid-base disorder types in respiratory failure  Usually the disorders are compound types.  It is difficult to judge the type of disorder according to the clinical symptoms and signs. Arterial blood gas analysis is the major method to judge the type of disorder.

How to judge the acid-base disorder  PH  PaCO2  HCO3-

the acid-base index. the index of respiratory the metabolism

Treatment of acid-base disorders  looking for the etiology of the disorder is the most important .

Respiratory acidosis  It is most commonly encountered in clinical practice of respiratory diseases.(COPD)  It is essential to improve alveolar ventilation, while alkaline supplement is not necessary.  For example: PH:7.32;PCO276mmHg; PO276mmHg SO2%94% BE13.9 HCO3- 41mmol/L

Respiratory acidosis complicated with metabolic acidosis

 First of all, the cause of metabolic acidosis should be clarified and treated, such as severe hypoxia may lead to increase in lactic acid or it is due to renal dysfunction or diabetic ketoacidosis.  If the level of PH is less than 7.2, alkaline drugs should be treated.  5%NaHCO3(ml)=[normal HCO3-(mmol/L)-actual HCO3(mmol/L)] ×0.2×weight(Kg)

Respiratory acidosis complicated with metabolic acidosis  Arterial gas analysis: PH:7.20;PCO276mmHg; PO256mmHg SO2%86% BE-7; HCO3- 20mmol/L

(5)Use of respiratory stimulant  Nikethamide  Lobeline  Doxapram

(6)Corticosteroids  Methyprednisone is usually used to reduce the airway inflammation, and to improve FEV!. The treatment is recommended in all patients but it is not used for a longer time.

(7)Gastrointestinal bleeding treatment Because of hypoxemia, hypercapnia and by using corticosteroids, gastrointestinal bleeding always be happened. The treatment mathod include correct hypoxemia and hypercapnia, use of H2-blocker and some block bleeding drugs.

(8)Nutritional support therapy

Tracheal intubation–Indications  Hypoxemia which is not quickly reversed by supplemental oxygen  Airway obstruction  Impaired airway protection  Inadequate handling of secretions  Facilitation of mechanical ventilation

Trach eal in tubation

Mechanical ventilation–Indications  Apnea  Acute hypercapnia that is not quickly reversed by appropriate specific therapy  Severe hypoxemia  Progressive patient fatigue despite appropriate treatment

 Mechanical ventilation is used for 2 essential reasons:  (1) to increase PaO2  (2) to lower PaCO2.  (3) Mechanical ventilation also rests the respiratory muscles and is an appropriate therapy for respiratory muscle fatigue.

Ventilator management  The use of mechanical ventilation during the polio epidemics of the 1950s was the impetus that led to the development of the discipline of critical care medicine.  Prior to the mid 1950s, negative-pressure ventilation with the use of iron lungs was the predominant method of ventilatory support.

 Currently, virtually all mechanical ventilatory support for acute respiratory failure is provided by positive-pressure ventilation. Nevertheless, negative-pressure ventilation still is used occasionally in patients with chronic respiratory failure.  Over the years, mechanical ventilators have evolved from simple pressure-cycled machines to sophisticated microprocessorcontrolled systems. A brief review of mechanical ventilation is presented as follows

Mechanical ventilation–Modes  Assisted mechanical ventilation (AMV) or assist/control (A/C)  Synchronized intermittent mandatory ventilation (SIMV)  Pressure support ventilation (PSV)

Mechanical ventilation–Modes  Pressure control ventilation (PCV)  Continuous positive airway pressure (CPAP)  Positive end-expiratory pressure (PEEP)

Mechanical ventilation–Complications

 Atelectasis of the centrolateral lung and overdistention of the intubated lung  Barotrauma, manifested by subcutaneous emphysema, pneumomediastinum, subpleural air cysts, pneumothorax, or systemic gas embolism

Mechanical ventilation–Complications

   

Subtle parenchymal lung injury Acute respiratory alkalosis Hypotension Ventilator-associated pneumonia, mortality rate of this disorder is about 50– 60%

Bilateral airspace infiltrates on chest x-ray film secondary to acute respiratory distress syndrome that resulted in respiratory failure

Extensive left-lung pneumonia caused respiratory failure; the mechanism of hypoxia is intrapulmonary shunting

LO G O

www.themegallery.com