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Ventilation Perfusion Matching
• We have seen that proper gas exchange depends on both ventilation and perfusion
• How do we make sure that each lung unit is both ventilated and perfused?
Ventilation Perfusion Matching
• When a lung is not ventilated, the pAO2 falls
• Then, the vasculature constricts
• Then, the perfusion decreases
Ventilation Perfusion Matching
• When a lung is not perfused, the pACO2 falls
• This causes bronchoconstriction
• This leads to decreased ventilation.
Ventilation Perfusion Matching
• Thus, VQ matching is based on:
• Airways and the vessels sending air and blood away from mismatched areas.
Ventilation Perfusion Matching
• This is a great system to compensate for a focal problem (like pneumonia)
• It can be dangerous, however…
Ventilation Perfusion matching
• If there is a global problem with ventilation or perfusion, the whole lung tries to send air or blood elsewhere.
• This is a problem.
• ARDS
Pulmonary Function
• How do we adjust pulmonary function to compensate for changes in the periphery?
Pulmonary Function
• Ultimately, the job of the cardiopulmonary system is to deliver oxygen to the periphery
• As oxygen is used by the periphery, carbon dioxide is returned.
Pulmonary Function
• The cardiovascular system is responsible for delivering the oxygen to the periphery.
• The periphery is responsible for extracting oxygen from the blood
• The venous blood carries the resulting carbon dioxide back to the lung
• The pulmonary system, then, needs to compensate to excrete that carbon dioxide.
Pulmonary Function
• How do we increase the delivery of oxygen to the periphery?
• DO2 = CartO2 * CO
• CO = HR * SV
• CO = BP / SVR
Pulmonary Function
• Why doesn’t an increase in the CO cause a decrease in the oxygenation of the blood?
Pulmonary Function
• What kinds of Carbon Dioxide stresses do we need to deal with?
• Increased / Decreased production of CO2
• pH abnormalities affecting CO2 excretion
Pulmonary Function
• There are two types of protons carried in the blood
• “Volatile acids” that result from CO2 conversion to bicarbonate and protons
• “Non-volatile acids” that result from proton dissociation from other molecules (lactic acid, protein metabolism)
Pulmonary Function
• To increase the disposal of CO2 and remove volatile protons, we simply increase alveolar ventilation
• Minute Ventilation =
Respiratory Rate * Tidal Volume
Pulmonary Function
• Increased production of CO2 and volatile acid occurs primarily because of a change in metabolic substrates to fats
Pulmonary Function
• What about pH problems not related to carbon dioxide?
• They can occur by two mechanisms
• 1) the wrong number of protons
• 2) the wrong amount of buffer
Pulmonary Function
• The wrong number of protons can happen for a variety of reasons:
– Too many made (lactic acid, protein metabolism)
– Too many lost (vomiting stomach acid, renal losses)
– Not enough lost (renal failure)
Pulmonary Function
• The wrong amount of buffer can happen for two reasons:
– Too much buffer (ingestion of alkali, infusion of buffer)
– Too little buffer (loss of buffer with diarrhea, loss of buffer through kidney)
Pulmonary Function
• Since pH changes can affect cellular respiration and CO2 excretion, the lung must be able to compensate for pH changes.
• Ventilation changes cause pCO2 changes
• pCO2 changes cause pH changes
Pulmonary Function
• A high pH is called an alkalemia
• A low pH is called an acidemia
• A particular derangement that causes an increase in pH is called an alkalosis
• A particular derangement that causes a decrease in pH is called an acidosis.
Pulmonary Function
• If an acidosis or alkalosis is caused by changes in ventilation, it is called a Respiratory acidosis/alkalosis
• If is not caused by ventilation, then it is called a Metabolic acidosis/alkalosis
Pulmonary Function
• As we will see in acid-base physiology, the lung compensates for pH changes by changing ventilation and therefore changing pCO2
Mechanical Ventilation• ... is a therapy.
• What are the indications?
• What is the end point?
• How do we administer it?
• How do we assess it?
Indications for Mechanical Ventilation• Acute Respiratory Failure (66%)
– Acute Respiratory Distress Syndrome – Heart Failure (through pulmonary edema/hypertension)– Pneumonia– Sepsis– Complications of Surgery– Trauma
• Coma (15%)• Acute Exacerbation of Chronic Obstructive
Pulmonary Dz (13%)• Neuromuscular Disease (5%)
Esteban A, Anzueto A, Alia I, et al. How is mechanical ventilation employed in the intensive care unit? An international utilitzation review. American Journal of Respiratory Critical Care Medicine 2000; 161: 1450-1458
Discontinuing Mechanical Ventilation
• Death• Weaning
– Up to 25% of patients have respiratory distress severe enough to require reinstitution of ventilator.
• Extubation– 10 - 20 % of extubated patients who were
successfully weaned require reintubation.
Brochard L, Rauss A, Benito S, et al. Comparison of three methods of gradual withdrawing from ventilatory support during weaning from mechanical ventilation. American Journal of Respiratory Critical Care Medicine. 1994; 150: 896-903.
Esteban A, Frutos F, Tobin MJ, et al. A comparison of four methods of weaning patients from mechanical ventilation. New England Journal of Medicine. 1995; 332: 345-350.
CMV – Continuous Manditory Ventilation
• The Original Mechanical Vent– Understanding CMV is Vents 101
• Replaced the “medical student”
• Has since been replaced in most locations in the hospital by fancier settings
• Still used in the Operating Room
CMV• The Tidal Volume with the set FIO2 gets
blown into the patient at the set respiratory rate.
• This is Positive Pressure Ventilation!– (“regular” breathing is negative pressure
ventilation)
Airway Pressure
• If we measure the pressure in the tubing at the end of expiration, it will be barometric pressure. (To make it easier, we call it “zero”)
• Inhalation generates a negative pressure so that air will flow from “zero” to “negative”
• Machines generate a postitive pressure so that air will flow from “positive” to “zero”
CMV• CMV – RR / Vt / FIO2
– CMV 12 / 600 / 30%
• Minute Ventilation = Respiratory Rate * Tidal Volume– 12 / min * 600 cc = 7.2 L/min
• pAo2 = FIO2 * (760 – 47)– 30% * 713 = 213.9 mmHg O2
Assessment of Mechanical Ventilation
Arterial Blood Gas
pH / pCO2 / pO2 / Bicarb / BE / Sat%
7.40 / 40 / 90 / 24 / 0.0 / 99%
Pulse Ox
Driving Mechanical Ventilation
• Our Primary Concern is CO2
– Increase Ventilation by:• Increasing RR or Increasing Vt
– Decrease Ventilation by:• Decreasing RR or Decreasing Vt
• Our Secondary Concern is O2
– We will talk more about O2 in a moment
Driving CMV• Assess pCO2
– If pCO2 is high, we are hypoventilating
– Increase minute ventilation
– If pCO2 is low, we are hyperventilating
– Decrease minute ventilation
Driving CMV• Assess pO2
– If paO2 is normal or high, then the patient is oxygenating well.
– Turn down FIO2 to minimize oxygen toxicity and remove unnecessary other therapies.
Driving CMV• Assess pO2
– If paO2 is low, then the patient is oxygentating poorly.
– Turn up the FIO2 and institute other therapies to improve oxygenation.
CMV• Advantages
– Easy to set up: need a bellows, a motor, and a timer.
– Easy to adjust the settings
• Main Disadvantage– If the Patient is breathing spontaneously, the
patient will be fighting the ventilator.
Ventilators 201• CMV has its major limitation
• New, fancier machines were invented to try to coordinate a patient’s spontaneous breathing with ventilator support.
Assist – Control (AC)• If a patient is spontaneously breathing, the
patient will be assisted.
• If the patient fails to spontaneously breath, then the patient will be on Controlled Manditory Ventilation.
Assist - Control• How do we know if a patient is
spontaneously breathing?
• At end expiration, the pressure at the mouth is “zero.”
• If the patient tries to inhale, the pressure at the mouth is “negative.”
Assist - Control• What kind of assistance does a patient
need?
• The patient is spontaneously breathing so we are assisting his VENTILATION.– Respiratory Rate– Tidal Volume
Assist Control Settings• AC RR / Vt / FIO2
• Respiratory Rate– If the patient does not breath every 60 / RR seconds,
the patient gets a controlled ventilation.– If the patient initiates a negative pressure before 60 /
RR seconds, the patient gets a controlled ventilation.
Assist Control Settings
• Every Single Breath, whether assisted or controlled gets the full Tidal Volume.
Assist Control• Advantages
– allows spontaneous breathing– supports each tidal volume
• Disadvantages– gives a full tidal volume for each spontaneous breath– patient can overbreathe and hyperventilate
IMV - Intermittent Manditory Ventilation• The IMV setting is designed to assist the
patient in obtaining a minimum minute ventilation.
• If the patient tries to overbreathe, then the ventilator does not assist the patient.
IMV – Intermittent Manditory Ventilation• Originally, IMV was CMV
– The patient received CMV RR / Vt / FIO2
– The patient could attempt to spontaneously breathe against the resistance of the tubing (with or without success)
IMV – Intermittent Manditory Ventilation• Then, IMV was CMV with Pressure
Support
– The patient received CMV RR / Vt / FIO2
– If the patient attempted to spontaneously breathe, the patient would receive Pressure Support
Pressure Support
• Inspiratory Flow is proportional to the pressure gradient and inversely proportional to the resistance between the outside world and the lungs
• The ET tube and Vent Circuit generate a fixed resistance.
Pressure Support
• To overcome that increased resistance, the pressure gradient must increase.
• Either the patient must generate more negative pressures (very tiring) or the patient must be provided with more positive pressure from the ventilatory circuit.
Pressure Support
• This increased pressure from the ventilator circuit must be provided only during inspiration
• Thus, Pressure Support is triggered by spontaneous breath, and blows into the tubing at a fixed pressure until inspiration ends.– (Often when inspiratory flow drops)
SIMV – Synchronized Intermittent Manditory Ventilation
• IMV (CMV with PS) still had the disadvantage of not coordinating spontaneous breaths with mandatory breaths.
• Thus, SIMV was invented.
SIMV
• When the patient spontaneously breathes, there is pressure support.
• Intermittently, the ventilator “manditorily” ventilates to insure a minimum minute ventilation.
• These Intermittent Manditory Ventilations are synchronized to only occur on spontaneous breaths.
SIMV Synchronization
• Begin with a spontaneously triggered manditory ventilation
• The patient has 60 / RR seconds to spontaneously breath with PS
• At 60 / RR seconds, the next spontaneous breath receives a manditory full ventilation
• If there is no spontaneous breath, then a controlled manditory ventilation is delivered.
SIMV Assessment• Settings
– SIMV RR / Vt / FIO2 with PS– SIMV 8 / 700 / 30% with PS 12
• Assess– Settings / Arterial Blood Gas– Actual Respiratory Rate– Measured Minute Ventilation– Spontaneous Tidal Volume
SIMV Assessment
• Measured Minute Ventilation = IMV Minute Ventilation +
PS Minute Ventilation– IMV M.V. = RR * Vt
– PS M.V. = Total M.V – IMV M.V.– Average Spontaneous Tidal Vol = PS M.V /
(RRactual – RRset)
Oxygenation• How do we fix V-Q mismatch caused by
atelectasis?
• Recruit the unused alveoli to increase “V”
Oxygenation• How do we recruit alveoli?• PEEP
– Positive end expiratory pressure– Decreases the expiratory gradient– Causes air trapping– Trapped air tries to distribute evenly and leads to
opening of all airways.
Oxygenation• What about decreasing the expiratory time
relative to the inspiratory time?
• This leads to air trapping. Since it behaves like peep, we call it:
AUTO-PEEP
Oxygenation• All patients on a ventilator have some amount of
atelectasis
• When a patient is oxygenating poorly, we can try to improve VQ matching by fixing that atelectasis with PEEP or AUTO-PEEP
COPD• Clinical Diagnosis
– History– Physical
• Physiologic Diagnosis– Physiologic Testing
• Pathologic Diagnosis– Anatomic Changes– Pathologic (Histology) Changes
COPD
Asthma Emphysema
ChronicBronchitis
Clinical Diagnosis
Physiologic Diagnosis
PathologicDiagnosis
COPD
• Intrathoracic Obstruction:
• Inspiration– Transthoracic Pressure Gradient– Airways Pulled Open
• Expiration– Recoil or Transthoracic Gradient– Airways Pushed Closed
COPD
• Inspiration
• Relatively Normal Mechanics
• Expiration
• Abnormal Mechanics(Prolonged Expiratory Time)
COPD
• Early:– Enough Expiratory Reserve
• Middle:– Expiratory Reserve Depleted– Air Trapping– Shift of Hysteresis Curve
COPD
• Late:– Expiratory Reserve Depleted– Air Trapping causes Inefficiency– Inefficiency so severe Active Exhale
necessary just to allow inhalation
– Increase in Work of Breathing
COPD
• Very Late:– Air Trapping causes Inefficiency– Air Trapping changes Diaphragm
and Chest Dimensions
– Inefficiency so severe Active Exhalenecessary just to allow inhalation
– Dimensions Make Muscles functionSuboptimally Due to Angle and Length
COPD
• Why does pursed lip breathing work?
• Fixed airway obstructioncauses air trapping
• Air trapping causesAirways to stay open
COPD
Asthma Emphysema
ChronicBronchitis
Clinical Diagnosis
Physiologic Diagnosis
PathologicDiagnosis
Chronic Bronchitis
• Clinical Diagnosis
• History:– Cough that leads to Sputum– Almost Daily– At least 3 months of year– At least 2 years
Asthma
• Physiologic Diagnosis
• Obstructive Physiologyon Pulmonary Function Tests
• Gets better with Smooth MuscleRelaxant (beta-adrenergic agonist)
Emphysema
• Pathologic Diagnosis
• A Biopsy (or Autopsy)demonstrates destruction of alveoli and airway wallsleading to decreased elasticity
COPD
• USA:
• 14.2 Million People have COPD– 12.5 Million Chronic Bronchitis– 1.7 Million Emphysema
• Globally:
• 9-10% of people 40 and older
COPD
• The Truth:
• No one has just “one” disease.
• There are components of– Sputum Production and SOB– Physiologic reversible obstruction– Destruction of Lung Parenchyma
COPD• History:
• Generally starts 40-50 yrs• More frequently male• Chronic Cough, worse in morning• Sputum Clear or Carbonaceous• 20 cigarettes a day for 20 years• Shortness of breath, esp. on exertion
COPD
• History:
• Initially presents with either cough or acute illness (bronchitis/pneumonia)
• Over years, more frequent acute exacerbations / attacks
• By 60’s, usually breathless on minimal exertion
COPD• Physical Exam
• Not very good at mild/moderatestage of illness
• VERY sensitive for severe illness– Barrel Chest– Weight loss– Coughing– Pursed Lip Breathing
COPD
• Causes:
• Smoking
• Air Pollution
• Airway Hyper-responsiveness
• Alpha1-Anti-Trypsin Deficiency
Pathogenesis• Inflammation
• Case 1:– Stimulus leads to local inflammatory
mediators in airway– Smooth Muscle responds to cytokines by
increase in tone and reactivity– This leads to chronic secretion stasis– This leads to frequent acute attacks
Pathogenesis
• Inflammation
• Case 2:– Stimulus leads to local inflammatory
mediators in airway– Smooth Muscle responds by hypertrophy and
Connective tissue responds by Scar– This leads to chronic secretion stasis– This leads to frequent acute attacks
Pathogenesis
• Inflammation
• Case 3:– Inflammatory mediators lead to mucus gland
hypertrophy and increase in sputum– This leads to sputum trapping and stasis,
leading to more acute exacerbations
Pathogenesis
• Inflammation
• Case 4:– Inflammatory mediators lead to an imbalance
of proteinases (specifically MMP/TIMP imbalance)
– This leads to destruction of airway walls and pathophysiology of COPD
Pathogenesis
• In all cases:
• Chronic Inflammation withAcute Exacerbations
• Leads to some combination:– Secretions (Clinical)– Airway Reactivity (Physiologic)– Parenchymal Destruction (Pathologic)
Diagnosis
• Threshold of DiagnosisMUST be related to therapy
• Examples:– Smoking Cessation– Surgery
Diagnosis
• History
• Physical
• Chest XRay / CT scan
• Arterial Blood Gas
• Pulmonary Function Tests
• Autopsy
Therapy• Oxygen• Bronchodilators (Beta-Agonist)• Anticholinergic• Anti-inflammatory
– Topical Steriod– Oral/IV Steroid– Anti-Leukotrienes
• Mucolytic• Anti-Allergy• Antibiotics
NETT
• National Emphysema Treatment Trial
– 1996: Participating Centers announced– 1997: Screening for entry begins– July 2002: Recruitment Ends
NETT• After recruitment, patients:
– Underwent exercise testing, pulmonary function testing, and radiography.
– Met with a Pulmonologist, Cardiologist, and Thoracic Surgeon
– Completed a 6-10 week courseof lung mechanical physiotherapy
• Exercise Protocol and Classes
• Oxygen and Medication Adjustment
• Perioperative Teaching
– Randomized to Bilateral LVRSversus continuing physiotherapy
NETT
• Inclusion Criteria– Diagnosis of Emphysema– Met Radiologic and PFT criteria– Accepted by all Physicians– “Severe Impact on Function”
NETT
• Exclusion Criteria– Active smoker (within 4 months)– Unstable angina or cardiac arrhythmia– Heart attack within 6 months– Had certain thoracic or cardiac surgeries or
had another disease that was likely to interfere with participation in the trial or to reduce survival.
NETT
• Medical Arm– Continued Physiotherapy and
Oxygen/Medication managementby Center Pulmonologists
• Surgical Arm– Bilateral LVRS– Open (median sternotomy)
and Thoracoscopic both allowed
NETT
• 3777 people evaluated
• 1218 individuals selected
• 608 assigned surgery
• 610 assigned medical therapy only
• 95% received treatment as directed
• 99% surviving participants followup
NETT
• Interim Outcomes– May 2001 – – Homogenous Disease identified
as having less post operative benefit– Severe Emphysema with Homogenous
Disease noted to have increased risk of death– Interim results published in NEJM– Inclusion criteria adjusted
NETT
• Final Outcomes
– Overall Long-term Mortality identical between Surgical and Medical arms
• 3 month Mortality 7.9% in surgery arm• 3 month Mortality 1.3% in medical arm
NETT• Mostly upper-lobe emphysema:
– With low exercise capacity• More likely to live longer after LVRS• More likely to function better after LVRS than after
medical treatment
– With high exercise capacity • No difference in survival between the LVRS and
Medical participants• Surgical group more likely to function better than
medical group
NETT
• Mostly non upper-lobe emphysema:– With low exercise capacity
• Similar survival and exercise ability after LVRS as after medical treatment
• Had less shortness of breath.
– With high exercise capacity • Had poorer survival after LVRS than after medical
treatment• Both LVRS and Medical participants had similar
low chance of functioning better
NETT
• Identified and supported viaLevel One evidence
– Subset of Patients benefiting from surgery– Subset of Patients harmed by surgery
– Efficacy of Medical Therapy