RC Respirology Flashcards
(1222 cards)
What is an abnormal pulsus paradoxus?
> /10 mmHg change of systolic BP between inspiration and expiration
DDX for abnormal pulsus
Tamponade
Asthma exacerbation
COPD exacerbation
Constrictive pericarditis
PE
Morbid obesity
Effects of hyperoxia on respiratory system
Hypercapnia, CO2 retention
Direct O2 toxicity from ROS - interstitial and alveolar edema due to leaky capillary endothelium, hyperoxic bronchitis
Absorption atelectasis
Instability of units with low V/Q ratios causing shunt
Retinopathy of prematurity (not respiratory)
Benefits of HFNC in patients with respiratory failure
Heated and humidified - reduces WOB, allows secretion clearance
Provides PEEP - decreases WOB, prevents atelectasis
Provides PEEP - prevents atelectrauma
High flows - washours out upper airway dead space, reliable FiO2 delivery due to minimal entrainment, decreases upper airway resistance
Who should have extubation to HFNC
Extubation of surgical patients
Extubation of non surgical patients at low/mod risk of extubation failure
Sources of physiological shunt
Bronchial arteries emptying into pulmonary veins
Thebesian veins emptying into left ventricle
Functional shunt: V/Q <1
Limitations/assumptions of the shunt equation
CcO2 = CAO2 = perfect diffusion between alveoli and capillaries
We assume PcO2 = PAO2 (from alveolar gas equation)
We assume that SaO2 = 1
Assumes all gas exchange occurs with ideal V/Q matching.
Differences between central and mixed venous gas
ScvO2 = central line, normal is 65-70% (>80% (high PaO2 or left to right shunt) vs <65% (impaired tissue oxygenation))
SvO2 = pulmonary artery, normal is 60-65%
basically ScvO2 should have higher O2 because it doesn’t get the low O2 blood from the IVC
DDX for high O2 Extraction Ratio
Sepsis, fever
Shock
Seizures
Hyperthyroidism
Hypoxemia
Anemia
DDX for low O2 Extraction Ratio
Hypothyroidism
Hypothermia
Sedation
Mitochondrial dysfunction in sepsis
Cyanide toxicity
Hyperbaric oxygen
Hyperoxia
Polycythemia
Impact of Positive Pressure Ventilation on the heart
Decreased preload to RV and LV
Increased afterload to RV, decreased afterload to LV
Overall, decreased SV and CO, decreased cardiac work
Impact of Positive Pressure Ventilation on dead space
Increased zone 1 respiration with high V/Q areas
Increases both alveolar and anatomic dead spaces
Lung volume is raised resulting in radial traciton on the airways increasing volume of anatomic dead space
Raised airway pressures divert blood flow away from ventialated regions causing high v/q ratio or even unperfused areas
Most common in uppermost regions of the lung.
Capillaries pressures fall below airway pressure and they collapse
Different Ventilator modes and settings
Assisted= mandatory patient triggered
Controlled= mandatory Time/volume triggered
Supported= spontaneous (patient triggered) flow terminated
PCV- you set inspiratory pressure. Volume will vary
VCV - you set TV peak flor and flow pattern. Pressure will vary
PSV - (Spontaneous Pressure Support Ventilation) al breaths supported (whatever TV the patient generates)
ASV - set EPAP, PS mirrors ventilation (higher at low flow periods)
SIMV (synchronized Intermittent Mandatory Ventilation- set RR with either Volume or PRessure target), patient can do what they want in between the set breaths
APRV - airway pressure release ventilation - Bilevel ventilation where you set PEEP and plateau. rescue therapy for ARDS, helps with recruitment to help with oxygenation, spontaneous breathing (increased WOB), risk of volutrauma, risk of DH
What are PIP, Pplat, driving pressures, delta P, airway resistance
PIP: (peak inspiratory Pressure) P to overcome resistance (airways, ETT) and lung elastic properties, target <35
Pplat: P to distend alveoli, reflects compliance, target <30 cmH2O
Driving pressure: Pplat - PEEP
Delta P: PIP-Pplat, reflects resistance: both elevated within 5 means reduced lung compliance or chestwall/diaphragm/pleural. Only Elevated PIP means increased airway resistance
Airway resistance: PIP-Pplat/Flow
Types of Respiratory Maneuvers on the ventilator
Inspiratory hold → Pplat
Expiratory hold → intrinsic PEEP
Only in volume control
DDx of reduced peak inspiratory pressure
Air leak
Hyperventilation
What do changes to the volume pressure curve represent on a ventilator?
Slope = static compliance
Width = dynamic compliance and airway resistance
Bird beaking = over distension = turn TV down
What are Static and dynamic compliance on a ventilator?
Static: chest wall and lung tissue compliance
Dynamic: chest wall, lung tissue compliance and airway resistance
what is the DDX for sudden increase in mechanical ventilation in critically ill patients
Increased dead space - collapsed lung, mucous plug, mainstem intubation/dislodged
Increased demand - sepsis, fever
Pain, anxiety
Decreased compliance
Benefits of PEEP
Improve oxygenation -improve atelectasis/VQ, moves peripheral edema into interstitium
Lessens required FIO2 and O2 toxicity
Improves lung compliance - think of equation Compliance = delta V/Delta P
Prevent atelectrauma
Decrease WOB
Decrease LV work/afterload
Mechanisms of hypotension with PEEP
Reduced preload to RV and LV
Increased RV afterload, RV failure
Reduced LV compliance
Consequences of autoPEEP
Barotrauma
Dynamic hyperinflation
Decreased lung compliance
Decreased tidal volumes and minute ventilation
Increased WOB
Cardiac - decreased preload, decreased CO, increased PVR
Neuro - increased ICP due to reduced central venous return
DDX of increased autoPEEP
Increased airway resistance e.g. bronchospasm, kinked tube, clogged tube
Increased tidal volume
Increased respiratory rate
Increased I:E time or ratio
Decreased expiratory time
Increased inspiratory time
Decreased inspiratory flow rate
Treatment of autoPEEP
Treat bronchospasm or reason for resistance
Decrease respiratory rate
Decrease tidal volume
Decrease I:E ratio
Increase expiratory time
Increase inspiratory flow rate
Increase or add PEEP **
Permissive hypercapnia ** (reduce demand)
Sedation and paralysis if dyssynchronous, treat anxiety/pain ** (reduce demand)