Respiratory Flashcards
Ficks law of diffusion states that gas moves across a sheet of tissue is proportional to _____&______ and inversely proportional to ______________.
area of the sheet and difference in gas partial pressure btw two sides ; tissue thickness
What are the conducting airways?
Trachea–> mainstem bronchi –> lobar bronchi –> segmental bronchi –> terminal bronchioles
Constitute anatomic dead space
Large proximal have ciliated columnar epithelium and increased cartilage compare to distally
Pressures through: RA, RV, LA, LV and systemic and pulmonary vascular networks
5 causes of hypoxemia, A-a difference and response to o2
- Hypoventilation - no A-a diff; responds to increased FiO2
- Diffusion impairment - increased A-a diff; responds to increased FiO2
- Shunt, increased A-a diff; minimal response to increased FiO2
- V/Q inequality - increased A-a doff; responds to increased FiO2
- low FiO2
Anchor points of O2 dissociation curve
Po2 100 = So2 97%, Normal arterial blood
Po2 40 = So2 75%, Normal venous blood
P50(50%sat) = 27, So2 = 50%
mechanisms of pulmonary hypertension
- Increased Pulmonary blood flow: L–> R shunt due to intra or extra cardiac defects (PDA, VSD, ASD)
- Increased Pulm vascular resistance: Pulm arterial vasoconstriction, PTE, pulm endothelial dysfunction, vascular remodeling, perivascular inflammation, vascular luminal obstruction, increased blood viscosity, arterial wall stiffening, pulm parnchymal destruction)
- INcreased pulmonary venous pressure: Left heart disease, compression or stenosis of large pulm veins
Phases of ARDS
- Acute Exudative Phase Neuts
- Days 1-7
- Diffuse alveolar damage with hyaline membrane formation & neutrophil influx
- DAmage to alveolar epithelial-cap endothelial barrier leads to alveolar flooding with fluid, protein, leuks, and RBCs → innate system activated → alveolar macs and recruitment of systemic macs and neuts→ widespread release inflam cytokines, ROS and eicosanoids
- Deleterious effects: alveolar epithelial cell damage, protein degradation, surfactant dysfunction, increased perm of endo-epi barrier of alveolus and development of local microthrombi - Fibroproliferative Phase
- Weeks following (Lasts 3 wks in humans – evidence fibrosis can begin as early as 48 hrs after onset of ARDS)
- Proliferation of Type II alveolar epithelial cells interstitial fibrosis and organization of exudate
- Fibrosis continues to progress and further derangement of architecture of the lung→ decreased lung compliance
Vet Criteria for ARDS
- Timing (<72 hrs resp distress)
- Origin of Edema (evidence pulm cap leak without increased Pulm cap pressure)
- Bilateral infiltrates on CXR
- Bilat Dependent density on CT
- Proteinacious fluid within conducting airways
- Increased EVLW - Evidence inefficient gass exchange
- Hypoxemia w/o PEEP or CPAP and known FiO2
( PaO2/FiO2 </=200; increased A-a gradient, or venous admixture)
- Increased dead space ventilation - Additional Criteria
- Evidence diffuse pulm inflamm: TTW/BAL with neutrophilia or biomarkers inflammation
- PET scan
Oxygenation Vs Ventilation
Oxygenation: movement of O2 from alveoli–> pulm caps. Dependent on gas exchange barrier
Ventilation: Fresh gas movement into the alveoli. Determines CO2 elimination
Oxygen induced hypercapnia (mechanisms)
- Depression of formerly hypoxic driven peripheral chemoreceptors causing worse hypoventation
- Releif of hypoxia driven pulmonary vasoconstriction in poorly ventilated lungs –> dec ability of areas to eliminateCO2 as perfusion increases without increased ventilation
- Significant correction of hypoxemia causes better saturation of Hgb so previous buffered protons (H+) on deoxyHgb are released and bucarb binds them, generating increased CO2 (Haldene effect)
Define hyperventilaation
PaCO2 <30-35 mmHg
Define Hypoventilation
PaCO2 >/= 45 mmHg
PvCO2>/=50 mmHg
Organ Interstitial fluid protein concentration
70-80% of plasma in myocardium, skeletal m., skin, lung, intestine, kidney, & liver
Cyanosis
- Blue color due to deoxygenated Hgb
- Seen at<O2 at 5 gm/dL
- Anemic patients would die before reaching this level of deoxygenated blood
ScvO2
Central venous O2 saturation
- Low (<70%) = inadequate O2 transport
- Hyperlactemia and HIGH ScvO2 = blind to local hypotension
- Assuming VO2 (oxygen consumption) is constant, SvO2 determined by CO, Hg concentration, and SaO2
- ScvO2 higher than SvO2 (mixed venous) in critically ill, they closely parallel each other in less severe disease
MC bacterial pneumonia organisms
Gram Neg: Pastuerella Sp & Enterobacteriaciae (E Coli)
Gram Positive: Staphylococcus Sp, Streptococcus Sp, Bordetella bronchiseptica
Mycoplasma (Maybe secondary)
Strep equi subsp zooepidemias –> hemorrhagic fatal pneumonia
PaO2 Normal
Sea Level 80-120 mmHg
- measure of ability of lungs to move O2 from atmosphere to blood
-Measured with silver anode/ patinum cathode system in an electrolyte solution separated from blood by semipermeable membrane
Preload Monitoring
RV preload measured by CVP
LV preload estimated by pulmonary artery occlusion pressure
Indication for PPV
- Severe Hypoxemia PaO2< 60 mmHg
SpO2<90 - Ventilatory Failure PaCO2 >60 mmHg
- Excessive Resp effort with impending fatigue or failure
- Severe hemodynamic compromise refractory to therapy
Parasites Airway Dz
- Aerostrongylus abstrusus (feline, Baermann or TTW)
- Capillaria aerophilia (K9 or Fe; TTW or Baer)
- Filaroides hirthi (K9; Zn Sulf, Baer or TTW)
- Crenosoma vulpis (K9; Baer or TTW)
- Paragonimus kellicotti (K9 or Fe; fecal sed or TTW)
- Toxocara canis migration (K9, fecal )
All respond to fenbendazole
Mechanisms venous admixture (causes and treatments)
- Low V/Q –> caused by edema, hemorrhage, pneumonia –> treat with O2
- Atelectasis –> caused by edema, hemorrhage, pneumonia–> responds to PPV not just O2
- Diffusion Defects –> caused by O2 toxicity, ARDS, or smoke inhalation –> opartially responds to o2
- R–> L shunts - caused by PDA, VSD, intrapulm AV anatomic shunts –> not responsive to O2 or PPV
Indications for O2
PaO2 <70 on room air
SaO2 <93% on room air
Increased respiratory effort/fatigue
Antibiotics that penetrate the lung tissue
Chloramphenicol
Doxycycline
Enroflox
TMS
Famethoxazole
Clindamycin
pCO2 gap
Venoarterial Co2 difference
Measures difference btw Pa-vCO2: can help identify under resuscitated patients
Values >6 mmHg suggest insufficient blood flow even with ScvO2 > 70%
J receptors
Juxtacap receptors in the lung
Bronchoconstriction due to noxious gasses, cold or inhaled dust
120 Rule
@ 21% O2 at sea level, PaCO2 + PaO2 = 120
_ If less than this, suggest presence of venous admixture
-Greater the discrepancy the worse the lung function
Minute ventilation
Total volume of gas exhaled per minute
= tidal volume x RR
FiO2 of different O2 administration techniques
Flow by @ 2-3 L/min - FiO2 25-40%
Face Masks @ 8-12 L/min - FiO2 50-60%
O2 Hood @ 0.5-1L/min - FiO2 30-40%
O2 Cage - FiO2 40-60%
Hypoxemia
PaO2 <80 mmHg (@ sea level)
SpO2 <95%
Inadequate O2 of ARTERIAL blood
Steps to hypoxemia treatment
- Airway Patency
- O2 Supplementation
- Hemodynamic stability to confirm/improve pulmonary perfusion
- Direct tx of hypoventilatory causes –> reverse opiates, sedatives or NMB agents
–> MV - O2 Supplementation
Nucleus tractus solitarius
- Part of dorsal group of medullary resp center
- Where visceral afferents from CN IX & X terminate
- primarily responsible for inspiration and basic rhythm of breathing
Oxygen toxicity phases
- Initiation: O2 derived free radicals (O2-, OH-, peroxide) cause direct damage to pulmonary epithelial cells as antioxidant stores become depleted (1st 24-72 hrs)
- Inflammatory: inflammatory recruitment and activation –> massive release of inflammatory mediators –> increased tissue permeability
- Destruction: local destruction
- Proliferation: Type II pneumocytes and monocytes, collagen deposition and interstitial fibrosis
Ventral group of medulla
Includes 4 nuclei:
- N. retroambiguus
-N. ambiguus
- N.retrofiacialis
- pre-botzinger complex
*Controls voluntary forced exhalation and acts to increase force of inspiration
Apneustic Center
Located in lower pons
Responsible for coordinating speed of inhalation and exhalation
Can be over-ridden by pneumotaxic center
Pneumotaxic center
Located in upper pons
Sends inhibitory impulses to inspiratory center –> terminates insp and therefore regulates insp volume and RR
Fine tuning of breathing
Suprapontine reflex
sneezing, coughing and swallowing
Airway management PPV
- ET cuff >/= 2.5 cmH2O can cause necrosis
- deflate and reposition every 4 hrs
Secure with nonporous material –> retie every 4 hrs
Change ET tube every 24-48 hours
Humidify: hot water humidifier vspassive heat moisture exchangers (can become obstructed)
Suction: open or closed system every 4 hours
Oral care PPV
Tongue: cover glycerine or saline soaked gauze –> not circumvent to avoid ranula formation
Suction subglottically for any secretions around E tube
Clean any gags or SpO2 devices in mouth
all q 4 hrs
Eye care PPV
lubricate eyes: moisture chaber like doggles; flush with saline and place lubricate every TWO hours
** Fluoroscene stain q 24 hrs
U/GI care PPV
Palpate/express urinary bladder every 4-6 hours
- if long term place ucath with closed system and indwelling care every 8 hours
Enteral nutrition controversial
- improved villous health and decreased GI bleeds
- may increase resp aspiration
Recumbency Care PPV
Diaphragm atrophy with in 18 hours MV –> short peroid of spontaneous help avoid this
Well padded area
Passive ROM every 4 hrs –> flex and extend every joint
Alter position every 4 hrs
Tilt table 30-45 degrees
MV Phase variables
Trigger: parameter that initiates inspiration
- typically P drop of 2 cmH2O or flow change of 2L/min
Cycle: parameter which inspiration is terminated (usually time)
- typically insp time 1sec
Limit: parameter breath cannot exceed
- typically pressure
Control: pressure, volume or flow - one is controlled, other two follow based off mechanics of lungs
Baseline: controlled during exhalation (Cm PEEP)
Common Causes patient ventilation asynchrony
- Patient Related: hypoxemia
hyperthermia
Drug Induced pant
Hypercapnia
Pneumothorax
Inadequate anesthetic Depth - Equipment Related
Disconnection or circuit leak
ET tube leak/obstruction/dislodg
Inapp trigger setting
Insuff tidal volume
I time too long
Criteria for spontaneous breathing trial
Improved primary Dz process
PaO2:FiO2 >150-200 with an FiO2 <0.5
PEEP</=5 cm H2O
Adequate respiratory drive
Hemodynamic stability
Absence major organ failure
Criteria failure spontaneous breathing trial
PaO2 <60 mmHg or SpO2<90
PaCo2 >55 mmHg or PvCO2 >60 or EtCO2 >50
TV <7 ml/kg
Tachycardic
Hypertensive
Hyperthermia or increased temp >1C
Anxiety
Clinical judgement
Inspired air partial pressures
Water vapor: 47 mmHg
O2: 150 mmhg
Nitrogen: 563 mmHg
Laryngeal and tracheal receptors
Laryngeal: cold, irritant, pressure, drive, C fibers
Tracheal/bronchi: slow adapting, rapid adapting, C fibers,. neuroepithelial bodies, A delta
volutrauma
overdistention and shearing injury
Barotrauma
high airway pressures possibly leading to alveolar rupture and pneumothorax
Biotrauma
lung injury secondary to release of inflammatory mediators during prolonged mechanical ventilation
Compare vent modes:
Continuous mandatory
Intermittent Mandatory
Continuous Spontaneous
CMV: Minimum RR set; all breaths are delivered as mandatory type.
- Includes controlled ventilation (no patient triggered breaths) and assist controlled (patients trigger RR)
- Includes VC+ as a form of assist controlled ventilation
IMV: set number mandatory breaths, but btw these spontaneous allowed; Vent tries to synchronize RR (SIMV); No control over mac RR or max minute ventilation
- includes ARPV and VC+
CSV: all breaths triggered and cycled by patient; RR, I time and VT determined by patient
- CPAP and Pressure support ventilation both forms of this (+ARPV)
ACVIM grades of pulmonary hypertension
Based of pressure in PA estimated of doppler echo
Mild PH 30-50 mmHg
Moderate PH 50-75 mmHG
Severe PH >75 mmHG
Classifications of PH secondary to (6 grades ACVIM)
- Pulm arterial hypertension
- Left Sided heart disease ( to meet this group must have documented LHD and unequivocal LA enlargement)
- Respiratory disease/hypoxia
- Pulmonary thrombotic or PTE
- Parasitic Disease (HW or angiostrongylus)
- Multifactoral or unclear mechanisms
Viral causes of infectious pneumonia
CAV - 2
Parainfluenza
Distemper
Resp coronavirus
Influenza (H3N8 & H3N2) → may result in hemorrhagic bronchopneumonia (80% mortality)
Pneumovirus
Herpesvirus
Lung protective ventilation & treatment goal
- Low tidal volume (4-6ml/kg)
- limited plateau pressure (<30 cm H2O)
** Low tidal volume may result in hypoventilation –> permissive hypercapnia
** PEEP beneficial in that it improved functional residual capacity, allows for reduction to less toxic FiO2 & decreases shunt fraction
** Human med goal PaO2 55-80 or SpO2 88-95
** Mod-severe ARDS improved survival with HIGH PEEP (low FiO2)
WHat is APRV
Airway Pressure release Ventilation
- time cycled, pressure controlled, IMV mode with extreme inverse I:E ratios
- Mandatory mode that allows unrestricted breathing during Phigh → may reduce asynchrony. Trigger for breathing is flow and pressure, time is constant btw high and low pressures
- Ventilation is determined by time spent at both pressures (Thigh & Tlow)
- Pressure and time chosen by clinician
Increased time for CO2 exhalation by decreasing Thigh may lead to excess time at Plow & Tlow → lung collapse and derecruitment - PIP and PEEP must be monitored closely
- Approximately 80-95% of resp cycle spent in Phigh, with transition to Plow set by ratio of end expiratory flow (EEF)/peak expiratory flow rate (PEFR)
- Benefits: lung protective (decreased alveolar shearing and microstrain), improved hemodynamics and decreased need for sedation and NM blockade
- Goal: increase alveolar surface area for gas exchange allowing improved V/Q matching
_ Increased mortality in peds patients, decreased in adults
Spontaneous breathing should contribute 10-30% total minute vent → avoid over sedation
Pressure regulated Volume controlled ventilation
ie VC+
- Used with assist controlled or SIMV
- Automatically adjusts breath to breath inspiratory pressure based on a set tidal volume & changing lung mechanics
- Vent alarms when pressure of 5 cm H2O below set pressure limit is required to deliver target tidal volume
** Disadvantage: airway pressure may increase with decrease compliance and set VT causing alveolar over distention
What is double triggering and what causes it?
Def: 2 delivered breaths separated vt an expiratory time less than half the mean expiratory time (occurs when Patient I effort continues throughout preset I time and remains present after –> trigger another breath that ends up having twice the desired tidal volume or preset size)
May be due to exceptionally high ventilatory demand of patient, too low of tidal volume, too short I time or a flow cycle threshold set too high
What is PV loop best for?
- Changes in compliance
- Changes in airways resistance
- Calculating UIP (PIP) and LIP (PEEP)
- Leaks
- Alveolar over distention
- Flow asynchrony
What is FV loop best for?
- Increased airway resistance
- flow asynchrony (saw tooth)
- Increased secretions
- Leak
What is flow scaler useful for?
- Inefective triggering
- Premature cycling
- AutoPEEP
- IN VC: flow asynchrony
- Ideal I time (and too long or too short)
Clinical effects of hyperoxia
- Lungs
- Peroxynitrite form in endo cells –> increased perm –> interstitial edema
-DAMPS released increases permeability further with inflamm cells
- Type I pneumocytes to type II –> decreased diffusion and pulm fibrosis
- Alvolar collapse (decreased surfactant, decreased nitrogen)
- Decreased mucocilliary clearance - Cardiovascular
- INcreased superoxide anion –> inhibition NO –> decreased vasocontriction
- Baroreceptos respond with decreasing HR and no change in SV –> decreased CO - CNS
- dcreased cerebral blood flow secondary to vasoconstricitve changes
- Increased cerebral excitotoxicity
