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Non-Pulmonary Complications of Mechanical Ventilation

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Presentation on theme: "Non-Pulmonary Complications of Mechanical Ventilation"— Presentation transcript:

1 Non-Pulmonary Complications of Mechanical Ventilation

2 Complications of Mechanical Ventilation
Complications related to Intubation Mechanical complications related to presence of ETT Pulmonary complications Cardiovascular complications Biomedical complications Neurological complications Other complications

3 Four major concepts Know the patient Know the ventilator
Put the ventilator between you and the patient Alive ill patients

4 Mechanicals Biophysical Inflammatory Cytokines Biochemical Medication
MV complications Mechanicals Biophysical Inflammatory Cytokines Biochemical Medication Modes Disease

5 MV are disease and pathopysiology realted

6 complications related to airways

7 Difficult Intubation Trauma Endobronchial intubation
Competence Confidence Vulnerability to complications Fixed Full stocmach Hypovolemia Hypotension Hypoxemia Hypercarbia Agitation Age and sex Unable to Open Mouth Trismus Small mouth Peri-oral scarring Fascial swealling Trauma Endobronchial intubation Esophageal intubation Severe hypoxia Severe hypotension Death Unable to insert laryngoscope Short neck Large chest Prominent upper incisors Small mandible Edema Difficult Intubation Unable to see glottis Fixed position of the head Small jaw Anterior larynx Obstructed by blood or vomit Environment No skilled help No specialized equipments Missing of defective equipment Poor positioning Unable to pass tube into trachea Fixed Unrecognizable glottis Too small glottis or sub-glottic diamete

8 Injuries to Face, Lips and Oro-pharynx
Trauma to the lips and cheeks from tube ties Peri-oral herpes Injuries to the tongue especially if entrapped between the endotracheal tube and the lower teeth Pressure ulcers to the palate and oropharynx

9 Skin Avulsion Tongue Injury Lip Injury Periorbital herpes

10 Maxillary Sinus and Middle Ear Effusion
Maxillary effusion 20% in patients intubated for > 7 days. 47% when the gastric tube is placed nasally 95% Secondarily infected maxillary effusion (45-71% of effusions) Middle ear effusion (29%) with 22% of them become infected Hearing impairment that may contributes to the confusion and delirium in elderly population

11 Laryngeal Injuries Some degree of glottic injury is seen in 94% of patients intubated for 4 days or longer Erosive ulcers of vocal cords (posterior commissures) Swelling and edema of the vocal cords Granulomas (7% in patients intubated for 4 days or more)

12 Vocal Cords Ulcers Granulomas Vocal Cord Hematoma Vocal Cord Edema

13 Pharyngo-laryngeal Dysfunction
Post-extubation discomfort (40% regardless of the duration) Hoarsness : edema, injury, disarticulate 52% in short-term intubation 70% in patients with prolonged intubation Slowing of the reflex swallowing mechanism and risk of aspiration 15.8% of patients who were intubated more than 4 days did not have a gag reflex Silent aspiration: Ventilator Associated Pneumonia 20% in young population 36% in older population

14 Tracheal Injuries Cuff pressure related tracheal mucosa ischemia
Cuff pressure tracheal damage: tracheal ulceration, edema and sub-mucosal hemorrhage Tracheal dilatation: tracheomalacia Tracheal stenosis: At the site of the cuff (50%) At the site of the tracheostomy (35%) Unclear (15%)

15 Granuloma and Ulceration
Tracheal Stenosis Glottic Stenosis Granuloma and Ulceration Tracheomalacia

16 Unplanned Extubation Self extubation (8%) and accidental extubation (1%) Longer ICU and hospital stay Increased ICU and hospital mortality

17 Cardiovascular complications of Mechanical Ventilation
Biomechanical effect Cardiovascular complications of Mechanical Ventilation

18 CVP CVP Pressure (mmHg) Pressure (mmHg) Exp Insp Exp Insp Right atrium
Extrathoracic veins Extrathoracic veins

19 Decreased Cardiac Output
Decreased Cardiac Output. Decreased Pressure Gradient for venous return and decrease RV preload PPV Decreased CO due to decreased RV filling Volume due to decreased venous return One of the first and most important physiological studies of the effects of PPV on cardiac function was by Cournand’s group, who in the late 1940s demonstrated a variable reduction in cardiac output in healthy volunteers receiving “mask” PPV.3 4 Cournand showed that right ventricular (RV) filling was inversely related to intrathoracic pressure, and as this became more positive so the RV preload fell, producing a detectable fall in cardiac output Let us consider the circulation to be a model with three compartments (fig 1): the thorax, the abdomen, and the periphery, where PRA is directly affected by intrathoracic pressure, abdominal pressure is affected by diaphragmatic descent, and the peripheral venous pressure is related to atmospheric pressure.5 PRA falls during inspiration and intraabdominal pressure increases with inspiratory diaphragmatic descent, whereas the peripheral venous pressure remains constant throughout the respiratory cycle. Systemic venous return, ordinarily the main determinant of cardiac output, depends on a pressure gradient between the extrathoracic veins (the driving pressure) and the PRA (back pressure). Spontaneous inspiration increases this gradient, and so accelerates venous return. Thus, RV preload and stroke volume all increase during spontaneous2 (or indeed negative pressure6–8) inspiration. Conversely, the increase in PRA during a Valsalva manoeuvre or positive pressure inspiration causes the venous return to decelerate; thus, RV preload and hence cardiac output can all fall as intrathoracic pressure is made more positive.9 10 PEEP prevents intrathoracic pressure from returning to atmospheric pressure during expiration, and at sufficient levels can diminish cardiac output throughout the respiratory cycle

20 Decreased Cardiac Output Decreased Right Atrial Distension
-2 mm Hg 6 mm Hg PPV Decreased CO due to decreased RV filling Volume due to decrease RA compliance 5 mm Hg 2 mm Hg 3 mm Hg 8 mm Hg As we Discussed previously about decrease venous return also the RA distension is also decrease being intrathoracic and getting Effect from PPV That also will decrease RV preload

21 Decreased BP PPV vs. Spontaneous Ventilation
120 5 3 -3 10

22 Decreased BP PPV VS. Spontaneous Ventilation
110 5 3 -3 8

23 Hypotension following MV
Other reasons are

24 PPV increase CO and BP Ventricular interdependence: decrease CO during spontaneous breathing due to : increase RV filling volume with shifting the intra ventricular septum causing mechanic impedance for LV decreasing its compliance causing decrease CO and BP PPV improve the dynamic shape of the septum providing better LV compliance, better preload and thus better Stroke Volume and BP. Increase in Trans mural pressure of the great arteries in the thorax. Transmural pressure represent how easy the blood vessels could distend in order to accommodate a room for the stroke volume, and thus decreasing afterload.

25 Cyclic BP effects is related to Volume status
Cyclic changes in Gas exchange and partial pressures Ventilation on sick individual

26 Effect of Changing Lung Volume on Pulmonary Vascular Resistance
Total pulmonary vascular resistance Pulmonary vascular Resistance Hypoxic vasoconstriction Intra-alveolar vaso-compression EFFECT OF CHANGES IN LUNG VOLUME ON RIGHT VENTRICULAR AFTERLOAD Pulmonary vascular resistance (PVR) is the main determinant of RV afterload and is directly affected by changes in lung volume.20 The total resistance of the pulmonary circulation depends on the balance in the vascular tone of its two components: the alveolar vessels, and the extra-alveolar or parenchymal vessels PVR can become raised at both extremes of lung volume (fig 2).21 When the lung is inflated above functional residual capacity (FRC), alveolar vessels become compressed as a result of alveolar distension. As lung volume falls from FRC towards residual volume two events can occur, and both can independently increase the PVR. First, the extra-alveolar vessels become increasingly tortuous and tend to collapse. Second, and perhaps more importantly, terminal airway collapse at low lung volumes can cause alveolar hypoxia and, at an oxygen tension of below 60 mm Hg, this results in hypoxic pulmonary vasoconstriction RV FRC TLC Lung Volume

27 Hemodynamic effects of mechanical Insuflation
Dec. LV ejection Inc. LV ejection The LV stroke volume is maximum at the end of the inspiratory period and minimum two to three heart beats later (ie during the expiratory period). The cyclic changes in LV stroke volume are mainly related to the expiratory decrease in LV preload due to the inspiratory decrease in RV filling and output End of inspiration Maximum of SBP, PP, Aortic velocity End of inspiration Minimum of SBP, PP, Aortic velocity .

28 Know the patient, Know the ventilator
Effect of Lung Volume No effect in Normal individual with PEEP less than 10 cmH2o Major effect in patients with Dynamic Hyperinflation such as asthmatic and COPD, and in pre-existing pulmonary hypertension Small changes in PVR can cause considerable hemodynamic compromise secondary to acute increase in PVR Avoid gas trapping in these patient If the healthy cardiopulmonary system is ventilated near “normal” FRC without excessive shifts in lung volume, it is unusual to see clinically important changes in RV afterload with a PEEP of less than 10 cm H2O. However, the situation can be very different in patients who have hyperinflated lungs secondary to asthma or obstructive pulmonary disease; and in children with pre-existing pulmonary hypertension. For the reasons described above, apparently small changes in lung volume can cause considerable haemodynamic compromise secondary to acute elevation of PVR in these patients, and particular care should be taken to avoid additional gas trapping, or large shifts in lung volume during mechanical ventilation Know the patient, Know the ventilator

29 Alveolar pressure and Gas exchange
Dead Space PaO2 Oxygen Transport AS Alveolar pressure increases the Oxygen trasport or oxygenation of the blood will decrease as the CO starts to fall The Dead sapce also tends to increase as the distending Al will compress the alveolar capillaries causing vented ares with limt or ;ow perfusion

30 Effects of PPV on hemodynamic
Pleural pressure Magnitude of Effect Venous Return V/Q Matching LV afterload Work of Breathing Fully Spontaneous Partial Ventilator support Fully Controlled

31 Intra arteriolar Vasodilatation
Bradycardia and intra-arteriolar vasodilatation Reflex Arrhythmias, Bradycardia Intra arteriolar Vasodilatation AUTONOMIC TONE The autonomic responses to changes in lung volume during tidal ventilation result in sinus arrhythmia, where spontaneous inspiration increases the heart rate by withdrawal of vagal stimulation, and the reverse happens during expiration. If the lungs are hyperinflated, or excessive tidal volumes are applied, then vagal overstimulation leads to a reduction in heart rate, and reflex arteriolar dilatation.13 Smaller infants in whom respiratory rate and resting sympathetic tone are high can be particularly sensitive to vagal overstimulation when PPV is initiated.

32 Effect of Preload on Cardiac Output
Normal cardiac function Congestive heart failure Cardiac Output Left Ventricular Preload

33 Biochemical effect of Mechanical Ventilation
Systemic inflammatory effect Biochemical effect of Mechanical Ventilation

34 Inflammatory Biochemical injury
Local and systemic Inflammation cascade

35 Micro vascular, Alveolar Fracture
Hotchkiss et all Critical care Med, 2002 Prot for Gas and Bacteria

36 Biochemical effect of MV
Pro- Inflammatory Cytokines during PPV

37 Neurological Functions during Mechanical Ventilation
Psychogenic effect Neurological Functions during Mechanical Ventilation

38 Acute Effects Vasoconstriction secondary to hypercapnia
Decreased intra-cerebral blood volume and intracranial pressure PEEP reduces cerebral perfusion pressure by decreasing venous return and increasing intracranial pressure 20-25% of is transmitted to the central venous pressure in a normal compliant lung >20% is transmitted in patients with decreased lung compliance

39 300 200 Non REM Sleep Time (minutes) Stage 4 Stage 3 100 Stage 2
REM 100 Age 40 Age 40 MV

40 Normal Sleep Pattern Stage 1 Stage 3 REM Stage 2 Stage 4 8 10 12 14 16
18 20 22 2 4 6 Stage 1 Stage 3 REM Stage 2 Stage 4

41 Hyponogram for a Patient on Mechanical Ventilation
8 10 12 14 16 18 20 22 2 4 6 Stage 1 Stage 3 REM Stage 2 Stage 4

42 Mechanisms by which mechanical Ventilation Disrupt Sleep
Noise disruption Ventilator alarm: inappropriate threshold Delayed alarm inactivation Humidifier alarms Disruption by nursing interventions Airway suction Nebulizer delivery Ventilation-related pharmacological disruption Benzodiazepines (↓REM, ↓deep NREM) Oipoids (↓REM, ↓deep NREM) Neuromuscular blocking drugs Ventilator mode Pressure support ventilation

43 Gastrointestinal Effects of Mechanical Ventilation
Systemic inflammatory and low perfusion effects Gastrointestinal Effects of Mechanical Ventilation

44 GI Effects of PPV Even without any evidence of ARDS

45 GI Effects of MV

46 Esophagus, Stomach and Small Intestine
Erosive esophagitis (30-50% of patients ventilated >48 hours) NG tube Poor lower esophageal sphincter tone and reflux Opiates and adrenergic agonists Duodenogastroesophageal reflux through the action of trypsin Upper gastrointestinal hemorrhage: Stress Decreased gastric mucosal protection secondary to a fall in splanchnic blood flow Decreased motility of stomach and small intestine

47 Liver and Gallbladder Reduction in portal venous flow secondary to the fall in cardiac output Increased hepatic arterial flow “ hepatic arterial buffer response” Normal total hepatic perfusion Hepatic engorgement Venous ischemia and elevation of serum transaminases and hyperbilirubinemia Reduction in drug clearance secondary to reduction of hepatic blood flow

48 Large Bowel Constipation Abdominal distension

49 Renal Functions during Mechanical Ventilation
Systemic inflammatory and ischemic effects Renal Functions during Mechanical Ventilation

50 Renal Effects of MV The usual renal response to reduction of cardiac output and mean arterial pressure Reduction in urine output secondary to a fall in the transmural pressure of the right atrium that results in reduction of the secretion of atrial naturitic peptide and the activation of renin-angiotensin-aldosterone system and pituitary vasopressin secretion

51 Acute Effects Vasoconstriction secondary to hypercapnia
Decreased intra-cerebral blood volume and intracranial pressure PEEP reduces cerebral perfusion pressure by decreasing venous return and increasing intracranial pressure 20-25% of is transmitted to the central venous pressure in a normal compliant lung >20% is transmitted in patients with decreased lung compliance

52 Asynchrony with Mechanical Ventilation
Patient, Mode, and Operator effects Asynchrony with Mechanical Ventilation

53 Asynchrony with the Ventiaitor
Fighting the ventilators Inconsistent tidal volume Increase work of breathing Barotraumas and thoracic air leak Insufficient gas exchange Disturbances in the cerebral blood flow

54 Ventilation complications Mode specific
Mode Specific Complications

55 Summery: MV complications
Procedure Mechanical Ventilation Mechanical Ventilation and Disease Mechanical Ventilation, Disease , and Operator


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