Unique Characteristics of Pulmonary System
Central location
Large surface area
Greatest exposure to environment
100% of CO at lowest pressure
Anatomy
Apex - above clavical
Nipples 4-5 intercostal place
Sternal angle: Carina, pulmonary vessels, Aortic arch, T4 body
Safest spot for thoracentesis: inferior medial to point of scapula
Bloodflow
Deoxygenated blood returned from periphery via SVC & IVC, R atrium, Tricuspid Valve, R ventricle, Pulmonic Valve, Pulmonary Artery (deO2), progressive branching (in close association with bronchioles)
Pulmonary capillaries surround the alveoli where gas exchange occurs
Pulmonary system IS A HIGH FLOW, LOW PRESSURE SYSTEM (Transpulmonary gradient between pulm art & vein on only 7-8 mmHg VS ~ 90 mm Hg between arterial & CVP in systemic circulation
Pulmonary Veins (carrying O2 blood)Located more in loose connective tissue & interlobar spaces (unlike arteries which closely follow bronchioles). L atrium, mitral valve, L vent, Aortic Valve, systemic
Bronchial arteries (from aorta) and bronchial veins (azygous system) provide systemic perfusion making pulmonary infarction exceedingly rare
Sources of deoxygenated blood
Bronchial Veins - R->L Shunt
Coronary Venous Blood - L Atrium
Physiologic V/Q Mismatching
All above contribute to normal O2 sat = 97%
West Zones
Zone 1 - Palv > Part > Pv
Zone 2 - Part > Palv > Pv
Zone 3 - Part > Pv > Palv
Excess ventilation at apex, excess perfusion at bases --> physiologic V/Q mismatching
Airways
Upper Airway = Conducting Zone
Heating/cooling, humidification
Filtering - nasal, tracheobronchial
Transportation
Disorders of Upper Airways
Cystic fibrosis - Autosomal recessive chromosone 7 abnormal chloride anion transport thick mucous
Chronic Bronchitis - 2/2 smoking - chronic cough for 2 years - blue (cyanotic from hypoxia) bloaters (edema 2/2 hypoxia leading to pulmonary hypertension and congestive heart failure); contrasted with primarily emphysematous patients are pink (polycythemia prevents hypoxemia, bronchitis prevents extra oxygen from being absorbed); puffers (excess expiratory force required); COPD FEV1/FVC <75%
Katagener's Syndrome - autosomal recessive, immotile cilia syndrome, organs are often reversed (situs inversus)
VAP - ventilator associated pneumonia - bypasses all these defenses - colonization of lower airways within 72 hours seen in most intubated patients
Lower Airways = Respiratory Zone
Major role of lower airways is gas exchange
Bronchi --> broncheoles --> alveoli
Bronchi - have cartilage and can't collapse - not effected by bronchospasm
Bronchioles
don't have cartilage - effected by bronchospasm,
smooth muscle innervated by parasympathetics - cholinergic stimulation of muscarinic receptors causes bronchoconstriction, anti-cholinergic causes broncodilation
No direct sympathetic innervation but beta 2 receptors are present - beta 2 agonists cause bronchodilation
Circadian rhythm - AM bronchodilation / PM bronchoconstriction
Alveoli
3 Types of Alveolar Cells
Type 1 Pneumocytes - simple squamous, gas exchange, most common
Type 2 Pneumocytes - produce surfactant to overcome laplace law, can regenerate
Alveolar Macrophages - If overwhelmed=pneumonia
Laplace law - smaller a sphere's radius, the more pressure required to dilate it (blow a balloon)
change in pressure = gamma x 2 / R
Medullary Centers
Inspiratory neurons --> Dorsal respiratory Group --> ventral gray neurons of C3-5 --> diaphragmatic contraction --> inc thoracic volume
Inspiratory neurons --> Ventral respiratory group --> larynx and accessory respiratory muscles
Inspiratory neurons --> Ventral respiratory group --> Contraction of external intercostals, internal intercostals (chondral pattern) --> inc thoracic volume
Expiratory neurons in ventral respiratory group --> abdominal muscles, internal intercostal contraction --> decrease thoracic volume
Increased intrathoracic volume --> dec intraplaural pressure --> increased transpleural pressure --> lung/alveolar expansion --> dec alveolar pressure --> air flow into alveoli (ventilation) -> gas exchange
Stretch receptors of lung paranchema Harring-brewer reflex provides negative feedback, loss of autonomic function can lead to vent dependence
Pons helps with voluntary respiration
Central receptors in ventral lateral medula increases respiratory rate and tidal volume in response to acidosis
Peripheral chemoreceptors act similarly but also react to decreased PO2
Spirometry
TLC - total lung capacity ~ 6L
- IC - Inspiratory capacity ~ 3L
- FRC - Functional residual capacity ~3L
TLC:
- IRV - Inspiratory reserve volume ~ 2.5L
- TV - Tidal volume ~ 0.5L
- ERV - Expiratory reserve volume ~ 1.5L
- RV - Residual Volume ~1.5L
VC - Vital capacity ~ 4.5L = IRV + TV + ERV
Other issues in ventilation
Dead Space
- Anatomic - conducting zone
- Alveolar - unperfused alveoli
Static Compliance = TV/(Pplateau - PEEP)
Gas Exchange Alveolar space --> RBC
Alveolar space (100-300 microns)
Alveolocapillary membrane (0.15-5 microns)
- Surface lining (0.01 microns)
- Alveolar epithelium
- Basement membranes
- Capillary endothelium
Plasma
Erythrocyte (7.5 microns)
Arterial O2 Content
CaO2 = (1.34) (Hgb) (SaO2) + (0.003) (PaO2)
CaO2 = (1.34) (14) (.95) + (0.003) (150)
CaO2 = 17.8 + 0.45 = 18.25
Normal CaO2 = 16-22 mL O2/dL blood
O2 Sat not PaO2 is the crucial variable
O2 – Hgb Dissociation
Right shift - easier to unload O2 - like exercising muscle or high altitude (high dpg)
Left shift - harder to unload O2 - like opposite of exercising muscle or high altitude
O2 Extraction Ratio
VO2/DO2 = 180-280/640/1540 ~ 0.25 = ER
Bohr Effect
- Addition of H+ or CO2 to blood --> dec Hgb binding affinity --> offloading of O2 in periphery
Haldane Effect
- Addition of O2 to blood --> Hgb binding affinity --> offloading of CO2 in lungs
Principles of Mechanical Ventilation
Origins of mechanical ventilation
The era of ICU medicine began with positive pressure ventilation
Negative-pressure ventilators ("iron lungs")
- Non-invasive ventilation first used in Boston Children's Hospital in 1928
- Used extensively during polio outbreaks in 1940-150s
- Created negative pressure in abdomen as well as the chest, decreasing cardiac output
Positive pressure ventilators
- Invasive ventilation first used at Massachusetts General Hospital in 1955
- Now the modern standard of mechanical ventilation
Indications for intubation
Criteria
- Clinical Deterioration - some so systemically ill, need to control pulmonary system, but be wary of hypotension w/ removal of sympathetic stimulus
- Depressed mental status - can't protect airway
- Inability to clear secretions
- Tachypnea
- Hypoxia
- Hypercarbia
Typical Initial Vent Settings
- AC or PRVC w/ FiO2 = 50%, PEEP = 5cm H2O, RR = 12-15 breaths/min, VT = 6-8 mL/kg
- Settings are trended and impact clinical decision making (trend more important than number)
Conventional Positive Pressure Ventilation: Pressure ventilation vs. volume ventilation
Pressure-cycled modes (fixed pressure, variable volume)
- Pressure support ventilation (PSV)
- Pressure Control Ventilation (PVC)
- CPAP
- BiPAP
Volume-cycled modes (fixed volume, variable pressure)
- Control (historic)
- Assist (historic)
- Assist/control
- Intermittent mandatory ventilation (IMV) (historic)
- Synchronous intermittent mandatory ventilation (SIMV)
Pressure Support Ventilation (PSV)
Patient determines RR, VE, Inspiratory time - a purely spontaneous mode
Parameters
- Triggered by patients own breath
- Limited by pressure
- Affects inspiration only
Uses
- Complement volume-cycled modes (i.e., SIMV) - overcomes resistance created by ventilator tubing
- BiPAP (CPAP plus PS) - Spontaneous breathing trials prior to extubation: aka "CPAP", aka "PSV"
Pressure Control Ventilation (PCV)
Ventilator determines inspiratory time and delivers breaths to preset pressure
Parameters
- Triggered by time
- Limited by pressure
- Affects inspiration only
Uses
- Alternative mode in ARDS to ensure plateau pressures are kept down
- eg. PCV with Pip of 38, RR 14, FiO2 70%, PEEP 14
- Uncomfortable: usually used with neuromuscular blockade
- May also reverse I/E ratio
- Gradual wean Pip to mid/low twenties then usually switch back to AC/PRVC prior to weaning
CPAP and BiPAP
CPAP is essentially constant PEEP; BiPAP is CPAP plus PS
Can be applied both non-invasively and in intubated pratients
Parameters
- CPAP - PEEP set at 5-10 cm H2O
- BiPAP - CPAP with PS (5-10 cm H2O)
- Shown to reduce need for intubation and mortality in COPD patients
- Non-invasive BiPAP not a good option for unstable patients!
Indications
- Use in conjunction with bronchodilators, steroids, oral/parenteral steroids, antibiotics to prevent/delay intubation in COPD
- Weaning protocols
- Obstructive sleep apnea
Do not use non-invasive bipap in unstable patients - really only for OSA or COPD exacerbation
Assist/Control Mode
Ventilator delivers a fixed volume
Control mode
- Patient receives a set number of breaths and cannot breathe between ventilator breaths
- Similar to Pressure Control
- Disadvantages: uncomfortable, muscle atrophy --> seldom used
Assist mode
- Patient initiates all breaths, but ventilator cycles in at initiation to give a preset tidal volume
- patient controls rate but always receives a full machine breath
- Disadvantages: apnea, --> seldom used
Assist/Control mode
- Assist mode unless patient's respiratory rate falls below preset value: vent them switches to control mode
- Typical full support mode at MCW
Pressure Regulated Volume Control (PRVC) Mode
Full support mode of choice at MCE
Essentially = AC with addition of pressure limit
EG. PRVC Rate 14, TV 550, FiO2 50%, PEEP 5
Vent Pressures
Plateau Pressure (Pplat)
Represents the static end inspiratory recoil pressure of the respiratory system, lung, and chest wall (reflects static lung compliance)
Measured by occluding the ventilator 3-5sec at the end of inspiration (inspiratory hold)
To minimize ventilator induced lung injury keep < 30
Peak Pressure (Ppeak)
Ppeak = Pplat + Pres*
Goal < 40
*Pres reflects resistive element of the respiratory system (ET tube and airway)
Lung Protective Ventilation
Keep Pplat < 30
Keep Pip < 40
Lowering the tidal volume, however, failed to improve the outcome in 3 controlled trials. The discrepant findings can be explained by differences in trial design. Increased survival was demonstrable only when the patients undergoing conventional ventilation and plateau pressures > 32.
Pulmonary Pressures
The critical variable is not airway pressure itself but transpulmonary pressure. Patients with stiff chest walls such as those with intra-abdominal hypertension can have elevated Pplat without causing alveolar overdistention. Pressures should be adjusted in patients with abdominal compartment syndrome
Auto-PEEP (aka Intrinisic PEEP)
What is Auto-PEEP?
- Normally, at end expiration, the lung volume is equal to the FRC
- When PEEPi occurs, the lung volume at end expiration is greater than the FRC (ie. incomplete exhalation)
Causes of auto-PEEP (aka Intrinsic PEEP or PEEPi)
- Predisposing Vent. Characteristics: Excessive RR (max for most is 30), Excessive TV, Increased I/E ratio
- Predisposing patient characteristics: COPD, Asthma
Consequences of Auto PEEP
Increased Pip and Ppl --> barotrauma
Increased work of breathing
Decreased venous return --> hypotension
Hypercapnia
Diagnosis of Auto-PEEP
End expiratory hold maneuver
Treatment of Auto-PEEP
Decrease RR
Decrease TV
Increase Expiratory Time
IMV and SIMV
IMV introduced in 1971 to avoid auto PEEP in neonates with RDS
- Patient receives a set number of ventilator breaths
- Different from Control: patient can initiate own (spontaneous) breaths
- Different from assist: spontaneous breaths are not supported by machine with fixed TV --> "exercies respiratory muscles and avoid auto-PEEP"
- Ventilator always delivers breath, even if patient exhaling --> uncomfortable --> seldom used
SIMV
- Mandatory breaths are synchronized with the patient's inspiratory effort
- More comfortable than IMV
- Problem: both increase work of breathing
- Partially offset by using with pressure support (PS)
- Even with PS appears to prolong weaning process - not recommended for routine use by most authorities
- Current role: full support mode in tachypneic patient
Vent settings to improve oxygenation
FiO2
- Simplest maneuver to quickly increase PaO2
- Long-term toxicity in >60% - free radical damage
Inadequate oxygen despite high FiO2 usually due to pulmonary shunting:
- Collapse - Atelectasis
- Pus-filled alveoli - PNA
- Water/protein - ARDS
- Water - CHF
- Blood - Hemorrhage
PEEP
- Increases FRC - prevents progressive atelectasis and intrapulmonary shunting, prevents repetitive opening/closing injury
- Recruits collapsed alveoli and improves V/Q mismatching - Resolves intrapulmonary shunting and improves compliance
- Disadvantages - increases intrathoracic pressure and can decrease VR, barotrauma
I:E ratio (inverse ratio)
Settings to improve ventilation
Respiratory rate
- Max RR at 35 bpm - then autopeeping
- Efficiency of ventilation decreases with increasing RR - decreased time for alveolar emptying
TV
- risk of volutrauma as pressures must increase
I:E ratio
Other means to decrease PaCO2
- Reduce muscular activity/seizure
- Minimizing exogenous carbohydrate load
- Controlling hypermetabolic states
Permissive hypercapnea
- Can be preferable to dangerously high RR and TV as long as pH >7.15
Alternative Modes
I:E inverse ratio ventilation (IRV) - no statistical advantage over PEEP
Prone Positioning - no mortality benefit
ECHMO
Airway Pressure Release - occasionally helpful in ARDS
High-Frequency Oscillatory Ventilation (HFOV) - unclear mortality benefits
Trouble Shooting
Acute respiratory deterioration
Peak inspiratory pressure
--> decreased --> Air leak, hyperventilation
--> no change --> pulmonary embolus, extrathoracic process
--> increased --> plateau pressure
--> no change --> airway obstruction: aspiration, bronchospasm, secretions, tracheal tube, obstruction
--> increase --> decreased compliance: abdominal distention, asynchronous breathing, atelectasis, auto-PEEP, pneumothorax, pulmonary edema
Adjuncts to Ventilatory Support
Sedation
- intermittant dosing (better if tolerated) vs continuous infusion
- daily interuption
Ventilator associated pneumonia (VAP) prevention
- HOB up at >30 degrees
- BID oral cleansing and tooth brushing
- Dedicated suction lines, changed daily
- Avoidance of routine lavage with suctioning
- Flush NG with sterile water
Weaning
Admission --> treat acute respiratory failure --> suspect ready for weaning --> assess readiness to wean --> SBT --> extubation --> (reintubation -->) discharge
Determination of readiness to wean
Clinical parameters
- resolution/stabilization of disease process
- hemodynamically stable on minimal pressors
- awake
- cough and gag reflexes present
- not acidotic
- spontaneous respirations
- O2 sat > 90% on < 40% FiO2 and PEEP < 6
- Head off the bed test
Weaning parameters
- P/F: nrml >400, weaning >200
- Tidal volume: nrml 5-7 mL/kg, weaning 5 mL/kg
- RR: nrml 14-18 b/m, weaning <40 b/m
- VC: nrml 65-75 mL/kg, weaning 10 mL/kg
- Minute volume: 5-7 L/min, weaning <10 L/min
- NIF (Negative inspiratory force): nrml > -90 cm H2O, weaning >-25 cm H20
- RSBI (rapid shallow breathing index)(RR/TV): nrml <50, weaning < 100 (variably predictive) <80 --> 85% predictive of successful extubation - best indicator
-- No weaning parameter is completely accurate when used alone
30% of patients who successfully extubate never meet "readiness" criteria
50% of self-extubated patients are able to stay off vent
Ventilator Weaning Approaches
SIMV weaning
Pressure support ventilation (PSV) weaning
Spontaneous breathing trial
SBT
Settings:
- PEEP = 5, PS = 0-10, FiO2 < 40%
- Breathe independently for 30-120 minutes
- ABG obtained at end of SBT
Failed SBT criteria:
- RR >35 for >5 min
- SaO2 < 90% for >30 sec
- HR increase by >20 from baseline
- Systolic BP increase or decrease by more than 20 BPM
- Sustained increased work of breathing
- Diaphoresis/increased anxiety/increased work of breathing
- Worsened ABG
- SBTs do not guarantee that airway is stable or pt can clear secretions
Additional steps for extubation
Be around
Cuff leak test
Empty stomach
Discontinue or reduce sedatives