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%