Respiratory Flashcards
Ventilatory Responce Curve
What shifts it left?
What shifts it right?
Shift to left (ie. hyperventilation): surgical stimulus arterial hypoxemia metabolic acidemia increased ICP (if pt NOT anesthetized) INCREASED SLOPE
Shift to right:
opioids, barbituates
MAC <1 little parallel shift; MAC >1 same shift as opioids
DECREASED SLOPE
Effects of quitting smoking <48° 48-72° 2-4 weeks 4-6 weeks 8-12 weeks
12-24°: rightward shift of P50 of hgb —> improved oxygen delivery to tissues
48-72°: increased secretions and MORE reactive airway
2-4 weeks: decreased secretions and LESS reactive airway
4-6 weeks: immune system and metabolism normalize
8-12 weeks: improved mucociliary transport and small airway function
What does a rightward shift of oxygen-dissociation curve mean?
What causes rightward shift?
RIGHTward shift —> decreases hgb’s affinity for O and INCREASES O2 delivery to tissues
Causes:
- increased levels of 2,3 DPG (can happen with smoking cessation)
- increased H+ (acidosis)
- increased CO2
- increased temp
What does a leftward shift of oxy-hgb dissociation curve mean?
What causes leftward shift?
LEFTward shift INCREASES hgb’s affinity for O2 and REDUCES tissue delivery
Causes:
- decreased temperature
- carbon MONOXIDE
- hgb F
- methemoglobin
- hypophosphatemia (seen in critically ill)
Effects of obesity
Lung volumes: very marked decrease in ERV. With preserved residual volume, have reduction of FRC. TLC also reduced (modestly) —> inspiratory capacity INCREASED (IC = TLC-FRC)
Mechanics: compliance decreased, d/t tidal breathing occurring at smaller lung volumes
Airway function: both FEV1 and FVC are decreased proportionally, so ratio is preserved (acts like restrictive dz. )
Gas exchange: normal closing capacity + decreased FRC = airway closure within grange of tidal breathing —> decrease in PaO2
Modified Cormack-Lehane classification
Grade 1: full view of GLOTTIS
Grade 2a: partial view of glottis
Grade 2b: only posterior arytenoids and EPIglottis are visible
Grade 3: only EPIglottis visible
Grade 4: neither glottis nor epiglottis are visible
Effects of PEEP on Cardiac output in:
Normal pt?
CHF?
Right ventricular dysfunction?
PEEP increases intrathoracic pressure and right ventricular afterload
Hypo/normovolemic patient: acutely decreases venous return to heart —> cardiac output decreased
CHF: improved HDS. Pts are volume overloaded so decrease in preload—> decreased LVEDP. Also decreases transmural pressure across left ventricle (psi INside - psi OUTside) —> wall tension (afterload) of LV DECREASES, forward CO INCREASES, and LVEDP (surrogates : PCWP, PAOP, LAP) DECREASES
RIGHT VENTRICLE DYSFUNCTION: will cause acute right heart failure
Alveolar gas equation
PAO2 = FiO2(PB - PH2O) - (PCO2 / RQ)
PAO2 = alveolar O2 partial pressure PB = barometric pressure PH2O = vapor pressure of water RQ = respiratory quotient
Ex: PCO2 80 mm Hg on room air, what is PAO2?
PAO2 = .21(760-47) - (80/.8)
= 50 mm Hg
Causes of hypoventilation
Residual inhaled anesthetics, opioids, sedatives Residual neuromuscular blockade Abdominal binding Splinting from pain Respiratory acidosis Hypothermia Hypokalemia
In a healthy patient how does minute ventilation change in setting of increased PaCO2?
Increases linearly by ~2 L/min for every 1 mm HG increase in PaCO2
Arterial O2 content equation
CaO2
CaO2 = (Hgb * 1.36 * SaO2) + (0.003 * PaO2)
SaO2 = % of hgb saturated with O2 (nml: 93-100%)
Hgb nml range female 12-16; male 13-18
PaO2 = arterial O2 partial pressure (nml 80-100)
CaO2 directly reflects the total number of oxygen molecules in art blood; the oxygen bound to hgb + amount of O2 dissolved in arterial blood
Normal amount of undissolved O2 in blood (first part of equation) is 0.93-1
How to calculate the PERCENTAGE of dissolved O2
Use arterial O2 content equation. Take dissolved amount (second half of equation) / total amount of O2 (both half’s of equation)
Ex: healthy woman PaO2 100 mm Hg and hgb 12. Out of total O2 in her blood what % of that total is dissolved in blood?
Undissolved: (hgb * 1.36 * SaO2) = 12 * 1.36 * 95 = 15.5
Dissolved: (0.003 * PaO2) = 0.003 * 100 = 0.3
% dissolved = 0.3 / ( 15.5 + 0.3) = 0.019 * 100 = 1.9%
Signs of bronchospasm during GETA?
What other processes can cause a similar clinical picture?
Hypoxemia, wheezing, increased PAP, decreased exhaled Vt, and/or upsloping capnograph.
Obstructed or kinked ETT
Bronchial intubation
Pulm edema
Pneumothorax
What medicines can worsen/precipitate bronchospasm?
Des is a respiratory irritant (esp at high concentration) can actually increase airway resistance compared to sevo/iso
Thiopental may induce bronchospasm as a result of exaggerated histamine release
Central causes of Respiratory alkalosis?
Pulmonary causes of respiratory alkalosis?
Central: (increased respiratory drive)
Stroke, ASA overdose, anxiety, pain, progesterone
Pulmonary:
PE
Pna
Asthma
Metabolic effects of respiratory alkalosis
Hypocalcemia
Hypokalemia
Hypophosphatemia
Treatment of choice of methemoglobinemia in pts with G6PD deficiency?
Ascorbic acid
HCO3 compensation in ACUTE respiratory acidosis
pH decrease of 0.05
HCO3 increase of 1.0 mEq/L per ACUTE 10 mm Hg increase in PaCO2
HCO3 compensation in CHRONIC respiratory acidosis
Normal pH
HCO3 increase of 4-5 mEq/L per 10 mm Hg sustained increase in PaCO2
HCO3 compensation in ACUTE respiratory alkalosis
pH increase of 0.1
HCO3 decrease of 2 mEq/L per ACUTE mm Hg decrease in PaCO2
HCO3 compensation in CHRONIC respiratory alkalosis
pH (near) normal
HCO3 decreases 5-6 mEq/L per 10 mm Hg sustained decrease in PaCO2
Why does hyperventilation lead to parasthesias?
Hyperventilation leads to low CO2, draws hydrogen ions from albumin, Ca then binds with the Ca, leading to hypocalcemia
