Mechanical Ventilation

Transcription

1 Mechanical Ventilation Effects of Mechanical Ventilation Cardiovascular Effects PPV Q T HR 1. intrathoracic pressure 2. card. tamponade effect 3. loss of +/- press chg in lungs w/spont breathing normal contractility vasoconstriction maintain BP 2 Blood Pressure Drop Drops if: normal compensatory mechanism lost Anesthesia, sedation Polyneuritis Anti-adrenergic drugs Catapres, Aldomet, Inderol, etc. hypovolemia 3 1

2 Cardiovascular Effects PPV Q T HR 1. intrathoracic pressure 2. card. tamponade effect 3. loss of +/- press chg in lungs w/spont breathing normal contractility vasoconstriction maintain BP 4 BP Fix Drop in BP Patient positioning IV fluids digitalis Dopamine Dobutamine Levophed epinephrine 5 Cardiac Output Drop will be greater:

3 To lessen drop in Q T Why Maintain BP? decreased Q T & BP 8 Assessment of Cardiovascular Effects Blood pressure normal = Cardiac output normal = 9 3

4 ICP and Cerebral Perfusion Amount of blood flow to the brain determined by: ** 4- ** 10 Cerebral Perfusion Pressure CPP = BP - ICP BP = systolic + (2 X diastolic 3 normal CPP = 11 Decreased CPP Decreased CPP cerebral blood flow cerebral hypoxemia cerebral edema 12 4

5 Causes of CPP BP uncommon in head injury seen more with spinal injuries and multiple trauma Q T CMV PEEP CPAP Hemorrhagic shock Heart failure 13 Vasodilation Causes of CPP ICP (pressure in CSF in subarachnoid space, ventricles) 14 Intracranial Pressure Skull is closed container Contains brain, blood, CSF Room for some expansion but not much Any increase in volume of 1 content without a decrease in volume of another 15 5

6 Intracranial Pressure Normally: if blood or brain volume, same volume of CSF is displaced so that ICP is maintained = 16 Intracranial Pressure ICP compresses brain tissue cerebral blood flow if sustained irreversible brain damage & death 17 Causes of ICP Closed head injury Tumors Craniotomy Cerebral hemorrhage CVA (ABI) Reyes Syndrome Meningitis Encephalitis Near-drowning or any severe anoxic episode CMV w/peep Cough Valsalva maneuver Trend position Elevated CVP Hypoventilation ( PaCO 2 ) Acidosis Profound hypoxia Vasodilating drugs 18 6

7 Prevent ICP Maintain BP if patient is at risk for increased ICP 19 Elevated ICP head near mid-line, no pillow, sedatives, muscle relaxants HOB low PEEP if possible hyperventilation ** ph cerebral vasoconstriction PaCO mmhg X hrs. 20 Elevated ICP hyperosmolar agents (osmotic diuretics) reduce brain water reduce total body water Mannitol loop diuretics furosemide (Lasix) acetazolamide (Diamox) 21 7

8 Elevated ICP barbiturate coma use of steroids is controversial removal of CSF in some cases hypothermia 22 Assessment of ICP Renal Effects Positive pressure ventilation has 3 renal effects

9 Renal Effects 1 decreased cardiac output renal blood flow glomerular rate 25 Renal Effects 2 redistribution of blood inside kidney 26 Renal Effects 3 release of Antidiuretic Hormone (ADH) 27 2 mechanisms: receptors in LA sense blood volume ADH receptors in carotid bodies, aortic arch sense chg in blood pressure, intrathoracic pressure ADH 9

10 Renal Effects ABGs also affect renal function: PaO 2 PaCO 2 28 Assessment of Renal Function I & O BUN 1-2- Normal = 4-29 Assessment of Renal Function Creatinine Metabolic waste-product Normal = < 2 mg/dl Increased in renal failure More sensitive than BUN 30 10

11 Assessment of Renal Function Osmolarity Particles in solution Renal failure retain H 2 O particles diluted osmolarity in blood, in urine 31 Specific gravity 1/ urine output Normal = Hepatic System Liver 1-2- Dysfunction caused by: Assessment of Hepatic System Bilirubin Produced by breakdown of RBC Hgb bilirubin + heme converted to H 2 O used to make soluble by liver new RBC broken down by bacteria in intestines 33 Normal = If increased 11

12 Assessment of Hepatic System Total serum protein Normal = Albumin = albumin total protein Skin color Mental status 34 Gastric, Splanchnic Effects 35 PPV resistance to blood flow may contribute to gastric mucosal edema GI bleeding altered GI function & bowel absorption properties malnutrition protein depletion altered healing metabolic acidosis diarrhea fluid depletion Assessment

13 Neurological Effects Neuro system affected by Hypoxia Decreased Q T Changes in acid-base status Build-up of metabolic waste products Decreased glucose levels 37 Neurological Effects PPV can ICP if: venous pressure Q T 38 Assessment Observe ventilatory pattern Airway reflexes Response to pain Purposeful movement Anxiety level, restlessness Level of consciousness (Glascow Coma Scale) 39 13

14 Glascow Coma Scale TEST RESPONSE RATING Eyes Open spontaneously Open to verbal command Open to pain No response Best motor response Obeys verbal command Localizes painful stimuli Flexion/withdrawal to pain Decorticate response to pain Decerebrate response to pain No response to pain Best verbal response Oriented and converses Disoriented and converses Inappropriate words Incomprehensible sounds No response Pulmonary Effects Ventilation Pulmonary Perfusion To the Blackboard! 41 Pulmonary Effects V/Q mismatch V D shunt 42 14

15 Pulmonary Effects - PVR airway pressure thinning & compression alveolar pressure of capillaries 43 However - If T E long enough & no PEEP or exp resistance, the drop in pulmonary perfusion is offset by normal flow during exp == no net effect on PVR 44 Remember! Severe hypoxia PVR by vasoconstriction causing pulmonary hypertension if PPV improves oxygenation reverses vasoconstriction 45 15

16 Using PEEP When FRC Alveoli open improving V/Q If too high: C L & PVR 46 Effect on Ventilatory Status Goal of eucapneic ventilation is not achieved if ventilator is mismanaged inducing abnormalities Hypoventilation Hyperventilation 47 Effect on Ventilatory Status 48 Hypoventilation PaO 2 PaCO 2 right shift oxyhgb curve ph cellular damage coma plasma K + cardiac dysfunction cerebral vasodilation ICP 16

17 Rx Hypoventilation Effect on Ventilatory Status Hyperventilation PaCO 2 left shift oxyhgb curve ph plasma K + cardiac arrhythmias cerebral vasoconstriction ICP if sustained tetany drive to breathe = alkalotic apnea 50 Rx Hyperventilation

18 Body Position Change position frequently to avoid atelectasis If unilateral lung disease - place patient how? 52 Hazards of O 2 Therapy O 2 -induced bradypnea Hypoxic drive (COPD) Problem if inadequate ventilation not provided 53 Hazards of O 2 Therapy Absorption atelectasis Esp. if F I O 2 > 0.70 Leads to shunt 54 18

19 Hazards of O 2 Therapy Oxygen toxicity Adults: F I O 2 > 0.60 > 6 hrs damage to pulmonary tissue Infants: PaO 2 > 80 mmhg ROP Best to use least F I O 2 necessary Use PEEP if F I O 2 > Barotrauma Normal lungs can withstand cmh 2 O Increased risk of barotrauma with: High MAP, high PIP, large V T with PEEP Monitor C L Pneumothorax, pneumomediastinum, pneumopericardium, pneumoperitoneum, subcutaneous emphysema Metabolic Acid-Base Imbalance Happens when PaCO 2 is near patient s normal but ph is not - ph 7.20 PaCO 2 40 mmhg HCO meq/l 57 19

20 Metabolic Acidosis May require administration of bicarb - meq req = base deficit x BW 4 Give 1/2, then repeat ABG Treat cause 58 Metabolic Alkalosis ph 7.58 PaCO 2 40 mmhg HCO meq/l Mechanical Failure Good monitoring Alarms on & functioning 60 20

21 Psychological Complications 61 Patients in ICU are very ill High noise level Patient-staff interaction 24 hrs of day Isolation from family Leads to Acute sleep deprivation Increasing confusion Lethargy Less responsiveness Psychological Complications Now add ventilator, lose control over: Breathing Mobility Privacy Speech Eating 62 Psychological Complications Plus, inadequate knowledge of Machines Tubes Monitors Alarms Decreased confidence in staff 63 21

22 64 To Help EXPLAIN Talk to Calendars, clocks Windows Quiet periods Coordinated care Communication boards Nutritional Complications Critical illness need nutrition If malnourished - Altered healing of wounds, infections Weakened respiratory muscles Decreased surfactant production Decreased albumin levels Overfeed VO 2, VCO 2 Feed emulsified fats 22