General anesthesia 3 cardiopulmonary function Flashcards
MAC50, what and how is it measured?
The end-tidal concentration, expressed as a percentage, of an inhalational anesthetic that prevents movement in response to a supramaximal noxious stimulus in 50% of the studied individuals
-50 volts at 50 cycles/sec for 10 msec
same anesthetic will have different effects on each brain system. how are movement in response to pain and autonomic reactions comparable at mac50?
more anesthetic required to stop autonomic reactions
anesthetics work on what receptors?
all
GABA, glycine (inhibitory receptors) increased
excitatory receptors decreased
Inhalation and injectable anesthetics CNS effects
Affect normal discharge of neurotransmitters and impact other
systems
resp center is where and works how?
- Located in the medulla oblongata and pons
- Information from peripheral and central chemoreceptors in response to blood levels of O2 and CO2 determines signals from RC to the respiratory muscles
cardiovascular center is where and works how?
- Located in the medulla
- Responds to information from arterial baroreceptors located in the carotid sinus and aortic arch
respiration vs ventilation
§ Respiration is the total process of delivering O2 to the cells and carrying away the byproduct of metabolism, CO2
* Gas exchange in the lungs (through ventilation) * Circulation of gases through the blood stream
* Transfer of gases at the cellular level
§ Ventilation is the process of moving gases through the respiratory tract
* CONTROLS O2 and CO2
anatomical deadspace
Volume of air in the mouth, pharynx, trachea and bronchi up to the terminal bronchioles.
alveolar dead space
Volume of air in the alveoli not participating of gas exchange
dead space related to panting/shallow breathing
§ Air flow may not reach areas of gas exchange
* Contributes to less removal of CO2 from the lung
* May affect oxygenation depending on FiO2
dead space vs shunt
Dead space- Ventilated but not perfused
* Hypoperfusion (V/Q > 1)
Shunt- Perfused but not ventilated
* Complete small airway closure
* Collapsed alveoli (atelectasis)
* Bronchoconstriction (V/Q < 1)
how does ventilation-CO2 relationship change when injectcatble anesthetic is adminitered?
the CNS is less responsive, so overall more CO2 will correspond to less ventilation, but the same linear relationship (ie. more CO2 -> more ventilation, at the same slope as sober) remains - shifts relationship to the right
how does ventilation change when you build up CO2
minute ventilation increased (RR xVt)
how does ventilation-CO2 relationship change when inhalant anesthetic is administered?
shift relationship to the right and make the relationship less linear
is you combine injectables and inhalants, CO2 response resembles
inhalants alone
arterial CO2 should be what level?
40
what is V/Q? how does gravity affect it?
volume over perfusion
-higher part of o lung has more air, less blood, so V/Q >1
-lower part has more blood, less air, so V/Q <1
what is hypoxemia? hypoxia?
hypoxemia: low oxygen in the blood
hypoxia: can have right amount of oxygen in the blood, but not in the tissue, eg. ischemia
causes of hypoxemia
altitude/ insipred O2 is low
hypoventilation
venous admixture
>shunting
>V/Q mismatch
>diffusion barrier eg. edema
how will arterial oxygen pressure scale with oxygen percentage in the air?
if air oxygen increases eg. 5x, arterial oxygen will increase more than 5x???
but conc remains similar
each hemoglobin binds how much oxygen? does binding get easier successively?
4
First oxygen is the hardest to bind. 2nd and 3rd are easier and the 4th is the easiest
hemoglobin has higher or lower affinity for oxygen in tissues? why?
lower,
high temp
high CO2
low pH
high DPG
(Bohr effect)
CO to different tissues
Heart 5% Brain 14%
Muscle 20%
Kidneys 22%
Liver 25%
Rest of the body 14%
CO is
CO = SV x HR
CO determined by
stroke volume
>preload
>afterload
>contractility
heart rate
>rhythm
what is preload
Ventricular volume at the end of diastole
* Volume present for the next contraction
* Depends on venous return
>Blood volume
>Vascular resistance on the venous side
what is afterload? how do drugs affect this?
Resistance to ventricular ejection
* Vascular resistance in the arterial system
- Vasoconstriction increases it
*α- agonists - Vasodilation decreases it
*α- antagonists
*β-2 agonists
what is contractility? what drugs increase it?
Ability of the myocardium to contract in the absence of any changes in preload or afterload
* Increases with inotropic drugs
* e.g., Dobutamine, Dopamine,
Norepinephrine, Epinephrine
*β-1 effects
