complications of ventilation

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Slide 1 :

COMPLICATIONS OF MECHANICAL VENTILATION

Slide 2 :

INTRODUCTION In patient on ventilator, all airway pressures are directly related to the tidal volume, airway resistance and peak inspiratory flow rate. And inversely related to compliance. The airway pressures and volumes have a direct impact on the intrathoracic pressure, blood flow and blood pressure. Mechanical ventilation also has many adverse effects on various systems of the body.

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CARDIOVASCULAR CONSIDERATIONS Positive pressure ventilation causes a higher mPaw(mean airway pressure)and also increased intrathoracic pressure. This increase in pressures results in a lower stroke volume and cardiac output. Also leads to decrease in O2 delivery.

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Positive pressure ventilation Increase in intrathoracic pressure Compression of pulmonary vessels Reduction in stroke volume Reduction of C.O. and pulmonary blood flow

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V/Q mismatch Hypoxemia Decrease in O2 content Decrease in O2 delivery

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BLOOD PRESSURE CHANGES During PPV, reverse pulsus paradoxus is observed in which the arterial blood pressure is slightly higher than that measured during spontaneous breathing. The mechanism appears to be a reduction in the left ventricular afterload. In patients with cardiopulonary disease, the BP may decrease during PPV. BP also decreases when PIP or PEEP is at a level that compromises cardiovascular function.

Slide 7 :

PULMONARY BLOOD FLOW Thoracic pump mechanism: - during inspiratory phase of PPV, the pulmonary vessels are compressed and blood flow from R to L ventricle is decreased. - during expiratory phase, the pulmonary vessels are not compressed and blood flow from R to L ventricle increases. - in hypotensive patients, an increase in tidal volume causes a decrease in pulmonary venous return to LV. - in hypertensive patients, use of large tidal volume increases venous return to LV.

Slide 8 :

HEMODYNAMIC CONSIDERATIONS Increase in intrathoracic pressure – due to compression of lungs against the chest wall. Decrease in pulmonary blood volume and increase in systemic blood volume. Decrease in CVP- due to decrease in venous return. Decrease in stroke volume of R ventricle – due to decreased venous return. Decrease in pulmonary artery pressure – due to decreased RV stroke volume and pulmonary blood flow. Decreased LV stroke volume – due to decreased RV stroke volume and pulmonary blood flow.

Slide 9 :

EFFECTS OF PEEP ON CIRCULATION Increase in pulmonary artery pressure – compression of pulmonary vessels. Increase in CVP – increase in PAP causes a higher RV pressure and hinders emptying blood return to RV leading to increase in pressure in systemic venous circulation. Decrease in aortic pressure – due to increased intrathoracic pressure and decrease in R and L ventricular stroke volumes. Decrease in cardiac output – due to decrease in R and L ventricular stroke volumes.

Slide 10 :

RENAL CONSIDERATIONS Kidneys are highly vascular structures receiving about 25% of the cardiac output. So they are highly vulnerable to decreases in blood flow which can occur during PPV. When renal perfusion decreases, urine output is decreased to correct the hypovolemic condition by retaining fluid. If hypoperfusion persists or worsens, renal failure may occur. Renal failure can cause poor elimination of drugs excreted through kidneys, causing elevated levels of these drugs in circulation. Monitor BUN, creatinine, Sr. electrolytes.

Slide 11 :

HEPATIC CONSIDERATIONS Hepatic perfusion accounts for 15% of the cardiac output. PPV alone does not decrease hepatic perfusion. But PEEP causes a decrease in hepatic perfusion and hepatic dysfunction. The decrease in hepatic blood flow is inversely related to the level of PEEP. Monitor PT, Sr. Bil, Sr. albumin. It may diminish the drug clearance from the liver.

Slide 12 :

ABDOMINAL CONSIDERATIONS PPV (esp. PEEP) can cause increase in intra- abdominal pressure(IAP). Increased IAP can lead to decreased cardiac output, decreased renal perfusion and pulmonary dysfunction like decreaser FRC and atelectasis. Splanchnic hypoperfusion may lead to stress related mucosal damage.

Slide 13 :

NEUROLOGIC CONSIDERATIONS PPV can cause headache, mental status changes, motor disturbances and ocular abnormalities. Hypercapnia can cause increased cerebral blood flow and raised ICP leading to headache, muscle tremors and ocular abnormalities. Hypoxemia can cause decreased mental and motor functions.

Slide 14 :

COMPLICATIONS RELATED TO PPV Barotrauma (pneumothorax, air leaks) Hypotension, decrease in cardiac output Arrhythmia Oxygen toxicity Bronchopleural fistula Bronchopulmonary dysplasia (in infants) Upper GI hemorrhage

Slide 15 :

RELATED TO EQUIPMENT (VENTILATOR AND ARTIFICIAL AIRWAY) Ventilator and alarm malfunction Ventilator circuit disconnection Accidental extubation Main bronchus intubation Postintubation stridor Endotracheal tube blockage Tissue damage Atelectasis

Slide 16 :

RELATED TO PATIENT CONDITION: Infection Physical and psychological trauma Multiple organ failure (may be pre-existing) RELATED TO MEDICAL PROFESSIONALS: Nosocomial pneumonia Inappropriate ventilator settings Misadventures

Slide 17 :

RELATED TO ENDOTRACHEAL INTUBATION During intubation: - trauma to teeth and soft tissue - esophageal intubation - vomiting and aspiration - hypoxia due to prolonged intubation attempts - arrhythmias - bradycardia due to vagal stimulation

Slide 18 :

While intubated: - obstruction by secretions - pneumonia and atelectasis - kinking of ET tube - aspiration - mucosal injury - laryngeal edema - displacement of ET tube - inadvertent extubation - sinusitis (nasal intubation)

Slide 19 :

Immediately after extubation: - aspiration - laryngospasm - hoarseness - laryngeal and subglottic edema Following extubation: - mucosal injuries - laryngeal stenosis - tracheal inflammation - vocal cord paralysis

Slide 20 :

Contd… Pharyngo-laryngeal Dysfunction: Post-extubation discomfort Hoarsness Slowing of the reflex swallowing mechanism and risk of aspiration Silent aspiration Laryngeal Injuries: Erosive ulcers of vocal cords (posterior commisure) Swelling and edema of the vocal cords Granulomas Tracheal Injuries Tracheal ulceration, edema and submucosal hemmorrhage Tracheal dilatation Tracheal stenosis:

Slide 21 :

Complications of assisted ventilation... Upper airway: -nasofacial cellulitis - subglottic edema - tracheal stenosis - palatal groove, abnormal dental development Lower airway: - bronchopulmonary dysplasia - extraneous air syndromes (air leaks) - pulmonary hemorrhage - pneumonia/ atelectasis

Slide 22 :

BAROTRAUMA (VOLUTRAUMA) Indicates lung tissue injury or rupture that results from alveolar overdistension. Generally, PIP > 50 cm H2O, Pplat >35, mPaw > 30 and PEEP > 10 may result in barotrauma. The risk of barotrauma also increases with the duration of PPV. Uneven distribution of ventilation may result in patients with significant airway obstruction and lung parenchymal changes. Preferential distribution to areas of low resistance and high compliance may result in overdistension and rupture. Lung injuries due to PPV include pulmonary interstitial emphysema, pneumomediastinum and pneumothorax.

Slide 23 :

EXTRANEOUS AIR SYNDROMES

Slide 24 :

HEMODYNAMIC COMPLICATIONS PPV can result in decreased cardiac output and arterial blood pressure. Patients with preexisting cardiovascular disease are more likely to suffer significant decreases in CO and BP. Increased pleural pressure due to PPV can lead to increased CVP and decreased venous return and in turn decreased cardiac output and hypotension. The increase in CVP depends on the airway pressure, lung compliance and chest wall compliance. Increased mPaw decreases venous return more than increase in PIP.

Slide 25 :

In patients with low lung compliance (stiff lungs), a given airway pressure will result in smaller increase in pleural pressure and hence smaller decrease in venous return and cardiac output. In patients with more compliant lungs, a given airway pressure may result in a more dramatic decrease in venous return and cardiac output. A low chest wall compliance will increase the pleural pressure more significantly for a given airway pressure.

Slide 26 :

VENTILATOR ASSOCIATED PNEUMONIA The incidence of VAP ranges from 10 to 65% The source of infection maybe the patient’s oropharynx, hands of care providers and equipments like ET tubes, NG tubes, suction catheters etc. Sputum C/S and gram staining via ET tube should be done as soon as infection is suspected and antibiotics started.

Slide 27 :

BRONCHOPULMONARY DYSPLASIA BPD occurs in immature lungs exposed to pressure induced trauma, at high O2 conc during periods of mechanical ventilation. RDS, pneumonia and MAS frequently precede the onset of BPD. Factors that initiate or enhance BPD include oxygen toxicity, barotrauma, infections, excessive fluids, L to R shunts across a PDA and nutritional insufficiencies. Prevention of BPD is better than treating it. Use of nasal CPAP when possible reduces the need for mechanical ventilation and hence reduces incidence of BPD.

Slide 28 :

MANAGEMENT OF BPD Diuretics: for treatment of abnormal microvasculature and pulmonary edema. Bronchodilators: for treatment of bronhospasm. Corticosteroids: prenatal use of steroids reduces the incidence of RDS and hence BPD. Sterioids are used postnatally to ameliorate or prevent BPD, by causing suppression of inflammatory mediators, improving lung function and facilitating early extubation. Nutrition: high calorie and low volume nutrition should be given.

Slide 29 :

COMPLICATIONS DUE TO PEEP During PEEP, pleural pressure becomes less negative, the pressure graadient between central venous drainage and right atrium decreases resulting in decreased venous return and CO. The effects of PEEP also depends on the compliance of the lungs, more pronounced in patients with normal or increased compliance. Decreased venous return from the head can result in raised ICP and headache. Decreased CO can lead to decreased renal perfusion . PEEP >10 cm H2O is associated with barotrauma.

Slide 30 :

COMPLICATIONS ASSO WITH CONTROL MODE Apnea and hypoxia if the patient becomes accidentally disconnected or when ventilator fails to operate- the patient’s ventilatory drive is blunted by sedation. Important alarms in this mode are the low exhaled volume alarm and the low inspiratory pressure alarm.

Slide 31 :

COMPLICATIONS ASSO WITH AC MODE Most important complication is alveolar hyperventilation resulting in hypocapnia and respiratory alkalosis. This can occur when the patient has high respiratory rate due to injury or disease . All the patient efforts are assisted in this mode leading to hyperventilation. In this condition the patient should be switched to SIMV mode.

Slide 32 :

COMPLICATIONS ASSO WITH SIMV MODE Rapid weaning leads to a increased work of breathing and ultimately to muscle fatigue and weaning failure. The ideal way to avoid this is to decrease the SIMV mandatory respiratory rate slowly and monitor the patient closely for signs of fatigue.

Slide 33 :

WEANING FAILURE Early signs of weaning failure include tachypnea, use of accessory muscles and paradoxical abdominal movements. Other indicators are dyspnea, chest pain, diaphoresis and delirium. Causes of weaning failure: - increase of air flow resistance - decrease of compliance - respiratory muscle fatigue.

Slide 34 :

MONITORING IN MECHANICAL VENTILATION Vital signs – HR, RR, BP, temp Pulse oximetry Chest movements should be monitored Chest should be auscultated frequently ABG ET CO2 monitoring

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