• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/65

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

65 Cards in this Set

  • Front
  • Back

PH

= neg. log of H+. PH 5 = .00001 H+


Difference between PH 7 and PH 4 = 7-4 =3


10^3x more H+. (1000x)

Bronsted-Lowry definitions of acid/base?

Acid = proton donor


Base = proton acceptor

Henderson-Hasselbach equation?

PH=Pka + log (HCO3/0.03xPaCO2)


PH= 6.1 + log (24/0.03x40)


PH= 6.1 + log (24/1.2)


PH= 6.1 + log (20) = 7.4

4 buffer systems:

Bicarbonate, Hgb, IC Proteins, Phosphates


HCO3 = open system, 20x buffering capacity of closed/chemical systems

How is HCO3 reabsorbed?

by the kidneys, mechanism is Na+/H+ exchange (bicarb in tubule, joins with H+ (H2CO3), ca, H20 and CO2, pass tubule lumen into interstitium, reaction reverses, H+ go back to tubule, bicarb absorbed to bloodstream)

Most important noncarbonic buffer EC?

Hgb. Bicarb = 60% buffering, HHgb = 35%


plasma proteins = 5%


Histadine is the main buffer site of Hgb which represents a closed system

What is the major IC buffer?

IC proteins (slower process takes 2-4 hours)


Most important urinary buffer?

Phosphate system ( "P" most important in Pee)


H2PO4/HPO4

Ratio of HCO3 to CO2 (or metabolic to respiratory)?

20:1, 24/1.2 (think H/H equation)


PH = Metabolic/Respiratory


(Resp. faster response (minutes), Renal comp. most powerful but takes 12-48h, maximal in 5 days.)

Acidosis effects?

Cardiac/sm.muscle depression, less resp. to catecholamines, lower V. Fib threshold, Hyperkalemia, CNS depression, Cerebral vasodilation, augmentation of NDMR in resp. acidosis

Causes of Resp. Acidosis?

Hypoventilation OR increased CO2 production!


(MH, Sz, shivering, burns, thyroid storm)

Can Respiratory compensation fully correct a metabolic disturbance?

No, but metabolic compensation can fully correct a respiratory disturbance

Formula for HCO3 administration?

Only give if PH less than 7.2 or HCO3 less than 15


MEQ NaHCO3 = (kg wghtx0.3xBase deficit)/2


(1 amp of bicarb is 50mEq, so divide answer by 50 to get # of amps)


Anion Gap?

cations - anions


AG = Na+ - (Cl + HCO3), normal is 7-14


140-(104+24) = 12


High AG acidosis = greater than 30


MUDPILERS (Methanol,Uremia,DKA,Paraldehyde/Propofol, Iatrogenic/idiopathic,Lactic Acid, Ethylene Glycol/Ethanol, Rhabdo, Salicylates)

Normal AG acidosis causes?

GI losses of bicarb: Diarrhea, ileus, CaCl/MgCl, fistula drainage


Renal loss of bicarb: Renal tubular acidosis, ca inhibitors (Diamox)


Rapid ECF dilution with fluid lacking HCO3

Effects of Alkalosis?

Hypokalemia, Hypocalcemia (ionized), Left shift of OHDC, Vasoconstriction (SVR, Cerebral, CNS excitation/sz, coronary spasm), bronchoconstriction

Most common acid/base disorder in ICU?

Metabolic Alkalosis, from primary increase in plasma HCO3.


3 causes: chloride sensitive, chloride resistant, and massive blood transfusions (citrate metabolism)

Chloride Sensitive Met. Alkalosis?

Cl deficiency and ECF depletion of H+from:


1.GI losses (vomiting, GI drg., chloride diarrhea)


2. Renal (Diuretics, posthypercapnic, low Cl intake


3. Sweat (cystic fibrosis)


(ECF depletion causes Na+ resorption in kidneys, but not enough Cl to balance, so kidneys absorb more bicarb to maintain electroneutrality)


TX: IV Saline plus K+, H2 blockers

Chloride Resistant Met. Alkalosis?

INCREASED mineralocorticoid activity leads to H+ and K+ excretion, Na+ reabsorption. K+ depletion causes increased bicarb resorption in proximal and distal renal tubules


Cushings, hyperaldosteronism, Licorice injestion, Bartter's syndrome (JGA hypertrophy), severe hypokalemia


TX: IV hydrogen ions (HCL, ammonium chloride) or Diamox

Ways to figure out dissolved O2 and CO2 in blood?

Henry's law


O2: 0.003ml/dl/mmHg


CO2: 0.067ml/dl/mmHg OR 0.03mmol/L/mmHg at 37C (H/H equation)

P50 of OHDC?

P50 is the PaO2 at 50% saturation = 26.6mmHg or 27.


Sets the middle of the curve, increased P50 is a Right shift (takes more paO2 to hold 50% sat), decreased P50 is a left shift (O2 wants to stick to the Hgb, less PaO2 needed to achieve 50% sat)

Causes of Left and Right shift of OHDC?

Left: hypothermia, hypocarbia, alkalosis, decreased 2,3 DPG, CO, Methgb, Carboxyhemoglobinemia


Right: hyperthermia, hypercarbia, acidosis, increased 2,3 DPG, Pregnancy

Bohr Effect vs. Haldane effect?

B"o"hr = What O2 curve does in response to CO2 levels (lungs: low CO2, O2 curve shifts left to load. Periphery: high CO2, O2 curve shifts right to release)


Haldane = What CO2 curve does in response to O2 levels (lungs: high O2, CO2 curve shifts down and right (darn right) to release. Tissues: low O2, CO2 curve shifts up and left to load)

What three forms is CO2 transported in?

HCO3: 68%


Carbaminohemoglobin: 22%


Dissolved in plasma: 10%

Chloride (Hamburger) shift?

Chloride shifts from plasma to RBC and back to maintain electroneutrality. Chloride goes for the ride!


Tissues: CO2 to RBC, converted to bicarb. Bicarb diffuses to plasma. Cl shifts from plasma to RBC.


Lungs: Cl moves out of RBC. HCO3 reenters RBC and converts back to CO2. CO2 diffuses into alveoli.


CO2 change in apnea? PH change in CO2 change? K+ change in PH change?

CO2 increases 5-6mmHg in 1st minute of apnea and 3-4mmHg each min. thereafter (3456)


PCO2 change of 10mmHg = 0.08 change in PH


K+ conc. changes 0.6 mEq/L per 0.1 change in arterial PH (PH up K down, PH down K up)

Respiration (gas exchange) starts at the

Respiratory bronchioles.


Resp. bronchioles + alveolar ducts = transitional zone


Alveolar sacs = respiratory zone

Distance from mouth to cords? Mouth to carina? Length of ETT?

mouth to cords: 16-19cm


mouth to carina: 24-29cm


length of whole ETT: 29cm


mid trachea: 21-22cm

How does the bronchial tree get blood supply?

Trachea to pulmonary (Terminal?) bronchioles = bronchial circulation (2% of LV output)


Distal to terminal bronchioles (respiratory bronchioles, alveolar ducts/sacs) = total RV output

How much blood in the lungs at a given time?

450ml, 13% of CO. 70-100ml undergoing gas exchange.

What are the major respiratory centers and where are they located?

Dorsal resp. group: medulla, inspiration, pacemaker, phrenic n. to diaphragm, efferent to external intercostals


Ventral resp. group: medulla, expiration, not active during normal breathing (overdrive), efferent to internal intercostals


Pneumotaxic center: Pons, stops inspiration


Apneustic center: Pons, insp. gasps, apneuses

Central and peripheral chemoreceptor differences?

Central: sensitive to PCO2, NOT PO2! PaCO2 indirect stim., H+ direct stim./changes CSF PH


Peripheral: sensitive to both PCO2 and PO2, but response to PO2 is stronger (less than 60mmHg)


Response is faster than central chemoreceptors, more important for short term response.

Where are the peripheral chemoreceptors, which has a stronger influence, and what nerves carry their afferent signals?

Carotid Bodies: more influence than aortic. Hering's nerve (Glossopharyngeal IX) is its afferent pathway to DRG


Aortic Bodies: above and below aortic arch, less influence, Vagus X is its afferent pathway to DRG

What are the muscles of inspiration/expiration?

Inspiration: DESS: Diaphragm, External intercostals, Scalenes, Sternocleidomastoids


Inspiration is active.


Expiration: RIO-EO-I: (most important are of abdominal wall) Rectus abdominus, Internal Obliques, External Obliques, and Internal intercostals. Expiration is normally passive.

How do intrapleural and intrapulmonary pressures change with breathing?

Intrapulmonary (alveolar) pressure: Negative inspiration, positive expiration, ZERO at end inspiration/expiration


Intrapleural pressure: ALWAYS negative during normal breathing. Pressure varies from -5 to -10 cm H20, more negative on inspiration, less negative on expiration. Valsalva maneuver can make it positive.

Law of Laplace

T=PR for cylinder or T= (PR)/2 for sphere.


Describes why small spheres (alveoli) empty into larger ones. Surfactant (dipalmitoyl lecithin) reduces surface tension, which evens the pressure between small and large alveoli preventing collapse. surfactant from TYPE II alveolar cells.

Formula for partial pressure of inspired O2 and alveolar air equation?

PiO2 = (Pb-PH20)xFiO2 = (760-47)x.21 = 149.3


PAO2 = (Pb-PH20)xFiO2 - PaCO2/RQ


149.3 - 40/0.8 = 99.3mmHg


PAO2 shortcut rule of 6, take FiO2 x 6 (50% x 6 =300)

Formula for normal PaO2?

102-(age/3)


75y.o. = 102-(75/3) = 102-25 = 77mmHg

Formula for normal A-a gradient at .21% O2?

Age/4 + 4


70y.o.: 70/4 = 17.5+4 = 21.5mmHg


Normal A-a gradient 2-22, increases with age and FiO2

arterial oxygen content equation?

CaO2= 1.34xHgbxSaO2 + 0.003xPaO2


CaO2= 1.34x15x1.0 + 0.003x100mmHg


CaO2= 22.5 mlO2/dl


SHORT CUT = 1/2 HCT

Normal CvO2, DO2, VO2?

CvO2: 15 mlO2/dl


DO2: 1000 ml/min (CaO2 x CO)


VO2: 250 ml/min = (CaO2-CvO2)xCO

Resistance equals

change in pressure/flow


SVR=Map-Cvp/CO


R=P/Q

Lung volumes and their size?

Inspiratory Reserve Volume: 3000ml


Tidal Volume: 500ml


Expiratory reserve volume: 1100ml


Residual volume: 1200ml

Lung capacities and their size?

Vital capacity: IRV+TV+ERV: 4600ml


Inspiratory capacity: TV+IRV: 3500ml


Functional residual capacity: ERV+RV: 2300ml


Total lung capacity: all volumes: 5800ml


Closing capacity: closing volume + RV, usu. below FRC, but increases with age and by 66yo CC equals or exceeds FRC

Hypoxic pulmonary vasoconstriction results from

ALVEOLAR hypoxia, reduces shunt, and is disabled by: above 1 MAC volatiles, hypocarbia, vasodilators (ntg, nipride, CCB), and nitric oxide

General anesthesia decreases FRC by how much?

15-20%


also contributes to venous admixture by 5-10%


Supine position decreases FRC by 10%


So GA in supine position FRC decreased 30%

FEV1/FVC ratio levels of obstruction?

75% or greater: no obstruction/normal


60-70%: mild obstruction


50-60%: moderate obstruction


less than 50%: severe obstruction


Normal in restrictive disorders!


Lung volumes that increase in obstructive disorders?

RV, FRC, TLC (all the ones that we can't measure directly) VC, IRV, ERV decrease


restrictive: all decrease

Dead Space

Anatomic dead space: never changes (conducting airways)


Alveolar dead space: varies, alveoli without perfusion


Physiologic DS: Anatomic + Alveolar DS


Normal Anatomic DS: 2ml/kg or 150ml

A-a gradient due to?

Bronchial circulation and thebesian circulation that contribute to normal physiologic shunt and empty deoxygenated blood directly to pulm. arteries and LV.

Normal V/Q ratio?

Overall: 4L ventilation/ 5L CO = 0.8


Individual lung units: Varies.


increased V/Q ratio = DS, increased PO2, Decreased PCO2


Decreased V/Q ratio = Shunt, decreased PO2, increased PCO2

Where does the respiratory quotient come from?

CO2 out/ O2 in


VCO2/VO2


200ml/min / 250ml/min


Normal: 0.8

What are the West lung zones?

Describe relationship between alveolar, pulmonary arterial, and pulmonary venous pressures.


Zone I: PA>Pa>Pv (not normally present)


Zone II: Pa>PA>Pv (waterfall effect)


Zone III: Pa>Pv>PA (continuous capillary flow)


Want Swan in zone III


Where is ventilation and perfusion better?

The dependent lung, unless lateral position and paralyzed/anesthetized. In this case upper lung is better ventilated but not perfused (dead space) while the lower lung is poorly ventilated but perfused well (shunt) creating a V/Q mismatch

Main site of airway resistance?

Central airways (90%)

Greatest decrease in VO2 due to GA are by which two areas?

Cerebral and Cardiac oxygen consumption

Osmolality of ECF? ICF?

ECF: 290mosm/L


ICF: 310mosm/L

Plasma volume expansion equals:

PV/Vd


Colloids: 3/3= 1:1 (100%)


Isotonic Crystalloids: 3/14 = 1:5 (20%)


Hypotonic Cryst: 3/42 = 1:14 (7%)

First sign of Hypermagnesemia?

Loss of deep tendon reflex


Hyporeflexia

Cause of Hypophosphatemia?

Respiratory alkalosis, hyperparathyroid, hypercalcemia, alcoholism

How long do crystalloids last intravascularly?

20-30minutes

What cervical level is the larynx, hyoid, epiglottis, cords, thyroid, and cricoid cartilages?

larynx: C3-C6


hyoid: C3


epiglottis: C3 (C3-PO says "Hi" without epiglottis)


cords: C5


thyroid: C4-5


cricoid: C6

What are the muscles of the larynx and their function?

"Post LOTS of Crazy Things"


Posterior Cricoarytenoids (PCA) pulls cords apart, abducts the cords


Lateral Cricoarytenoids plus oblique and transverse arytenoids adduct cords (lots of stuff)


Cricothyroids (CCT = Cords can tug) tenses/elongates cords


Thyroarytenoids relax cords, shorten cords

What are the extrinsic muscles of the tongue?

"Mario's Pal Geno Has Style"


Palatoglossus, Genioglossus, Hyoglossus, Styloglossus


All intrinsic and extrinsic muscles of tongue are supplied by Hypoglossal (CN XII) except for palatoglossus supplied by CN X.


Taste of anterior 2/3 of tongue from Facial CN VII carried by lingual nerve. (taste and sensory posterior 1/3 = Glossopharyngeal CN IX)

Definition of Difficult Airway

situation where trained anesthesia professional experiences difficulty with mask ventilation, tracheal intubation or both