Stuff you should know Flashcards
Know how to monitor twitching in a stroke/paralyzed patient
After application of non-depolarising muscle relaxants (Atracurium, Mivacurium, Rocuronium, Vecuronium) a resistance of the paretic extremity against the relaxant used was shown in all cases. A possible explanation for this observation is the spreading out of abnormal acetylcholine receptors over the surface of denervated muscle cells which could lead to a false estimation of the depth of the neuromuscular blockade. Therefore, in the clinical practice, neuromuscular monitoring must always be carried out on the normal extremity of the patient.
know how positioning affects blood flow to brain and how to calculate appropriate BP if head goes above or below the heart
Cerebral autoregulation has been thought to maintain cerebral blood flow (CBF) constant between MAP of 50-150 mmHg
sitting: Hypotension risk
↓ Venous return – venous pooling in lower extremities
↓ MAP, CI, and cerebral perfusion pressure
Lithotomy: ↑ Venous return, CO, and ICP
Lithotomy: ↑ Venous return, CO, and ICP
trendelenburg : ↑ CO
↑ Venous return from blood in the lower extremities
↑ ICP and IOP (esp neuro or pts at risk, talk to surgeon to not do a too steep T)
REVERSE TRENDELENBURG: Hypotension risk
↓ Venous return – venous pooling in lower extremities- use SCDs!
Downward displacement of abdominal contents and diaphragm, easier to ventilate
↓ Perfusion to brain
If invasive arterial pressure monitoring is used then the arterial pressure transducer should be zeroed at the level of the Circle of Willis
Prone: ↓ Venous return through compression of the inferior vena cava
↓ CO
Position of patient’s arm, ↓ (or ↑) 8 mm Hg for every 10 cm above (or below) heart level
V/Q Matching
matching of ventilation and perfusion of the lungs is vital for ensuring continuous delivery of oxygen and removal of carbon dioxide from the body.
the ventilation rate is roughly 6L/min.
The different ratios for different areas are due to the relation of the area to the heart. Areas of lung below the heart have increased perfusion relative to ventilation due to gravity, reducing the V/Q ratio. As such the overall value in the average human lung is closer to 0.8.
When there is inadequate ventilation the V/Q reduces, and gas exchange within the affected alveoli is impaired. As a result, the capillary partial pressure of oxygen (pO2) falls and the partial pressure of carbon dioxide (pCO2) rises.
hypoxic vasoconstriction causes diversion of blood to better ventilated parts of the lung. However, in most physiological states the haemoglobin in these well ventilated alveolar capillaries will already be saturated. This means that red cells will be unable to bind additional oxygen to increase the pO2. As a result, the pO2 level of the blood remains low, which acts as a stimulus to cause hyperventilation, resulting in either normal or low CO2 levels.
Reduced ventilation-
Reduced ventilation can occur for a number of reasons. Here we will consider the more common causes. Reduced ventilation primarilly affects oxygen levels, as carbon dioxide is more soluble and continues to diffuse despite the impairment. Thus, the initial effect of reduced ventilation is type 1 respiratory failure (T1RF), with reduced pO2 and a normal/low pCO2.
All causes of T1RF may progress to type 2 respiratory failure with low pO2 and elevated pCO2 if they are sufficiently severe.
In pneumonia the alveoli are filled with exudate. This impairs the delivery of air to the alveoli and lengthens the diffusion pathway for the respiratory gases. This results in reduced ventilation and can cause hypoxia, and therefore T1RF.
Asthma and chronic obstructive pulmonary disease (COPD) can also result in a reduced ventilation. In asthma there is smooth muscle contraction which causes an increased resistance to alveolar airflow. In COPD, inflammatory changes induce structural airway damage. This leads to impaired gas exchange, which can worsen in an acute exacerbation.
The effect of reduced ventilation is hypoxia. However, as the rest of the lung can still remove CO2, hypercapnia does not occur. In cases of severely limited ventilation, hypercapnia may develop.
Reduced perfusion:
A pulmonary embolism can result in reduced perfusion of the lungs. Obstruction of some regions of pulmonary circulation limits blood flow to alveoli. As a result, blood is redirected to other areas of the lung. As the other areas receive an increased blood supply, the V/Q ratio will be <1. In this case, hypoxia still occurs because a vast majority of the lung is still working with a V/Q of <1.
Compounding MAC
(additive)
Concentration Effect:
The higher concentration of inhalation anesthetic (N2O) delivered to the alveolus, the faster the onset of action.
Second Gas Effect
The use of N2O during anesthetic induction will hasten the onset of a second gas (volatile). Rapid uptake of N2O into alveolus will cause it to shrink. The reduction in alveolar volume and augmented tracheal inflow on subsequent breath causes a relative increase in concentration of the second gas. This increases alveolar ventilation and augments FA.
ow do you speed up equilibrium of blood:gas (Fa/Fi ratio)?
Concentration Effect
Second Gas Effect
-Decreased CO
Inc alveolar Vm and Inc FGF(replaces anesthetic in blood so it is freed up)
Dec FRC
How does MAC affect autoregulation?
The cerebral vasculature continuously adjusts vessel diameter to maintain a constant cerebral blood flow between cerebral perfusion pressure of 50-150 mmHg. Volatile anesthetics disrupt autoregulation in a dose-dependent fashion. Cerebral blood flow becomes increasingly dependent on blood pressure as the concentration of the volatile agent is increased.
How do they affect EEG mapping; and motor mapping?
As a general rule, you should be concerned about nerve ischemia when amplitude decreases by > or = 50% or latency increases by > or = 10%
-Volatile anesthetics decrease amplitude and increase latency. The addition of N2O makes this worse.
-Other confounding factors that affect amplitude and/or latency include hypoxia, hypercarbia, and hypothermia.
-Hypoxia, hypercarbia, and hypothermia also disrupt amplitude and latency.
-Nerve ischemia also decreases amplitude and increases latency. So we don’t confuse the issue, we either omit or reduce our use of volatile agents in favor of an intravenous technique. Use TIVA w/o N2O if you don’t want to affect SSEPs and other mappings, if not… use 0.5% MAC and opiates or other methods but still no N2O.
