High Point Learning Flashcards

1
Q

How does methemoglobin affect reading of pulse ox?

A

reads right at 85%

if the oxygen saturation is over 85%, methemoglobinemia will cause the pulse oximeter to falsely underestimate the hemoglobin saturation. If the oxygen saturation is under 85%, it will cause it to falsely overestimate it.

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2
Q

Transducer placement below level of the heart and BP reading

A

Placement of the transducer below the level of the heart will overestimate the actual blood pressure and vice-versa.

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3
Q

How does NIBP location affect reading, and by how much in mm hg?

A

If the NIBP cuff is not level with the heart, then a correction must be made to compensate for the difference between arm and systemic pressure. For every 10 cm the cuff is above the level of the heart, you must add 7.5 mm Hg to estimate the systemic pressure accurately. Likewise, for every 10 cm the NIBP cuff is below the level of the heart, you must subtract 7.5 mm Hg to correctly estimate the systemic pressure.

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4
Q

What 3 issues with blood pressure cuff will result in an overestimation of BP

A

Placing a blood pressure cuff that is too loose, too small, or positioned below the level of the heart will result in a blood pressure that overestimates the actual blood pressure.

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5
Q

List interventions to lower ICP

A

Fluid restriction, diuretics, corticosteroids, CSF drainage, Propofol, MAP reduction, and hyperventilation. These actions lower intracranial hypertension and cerebral edema, which in turn lower the ICP

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6
Q

What is Cushing’s triad?

A

The Cushing reflex consists of bradycardia, hypertension, and respiratory irregularity. It is seen when ICP levels rise so significantly that brain stem herniation occurs.

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7
Q

What medication can be given to preserve cerebral blood flow?

A

Nicardipine

preserves cerebral blood flow.

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8
Q

Where do the preganglionic sympathetic nerve fibers arise

A

The preganglionic sympathetic nervous system fibers originate between the T-1 and L-2 nerve roots.

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9
Q

Where are the choroid plexus and which ones make the most CSF?

A

The choroid plexuses are located in the four ventricles. The ones located in the two lateral ventricles produce the greatest quantity of cerebrospinal fluid.

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10
Q

How long is a neurons supply off glycogen?

A

2 min

The neurons only contain about a 2-minute supply of glycogen.

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11
Q

What % of CO goes to the Brain? what is the brain % of body mass?

A

The brain only comprises about 2% of body mass but receives about 15% of the cardiac output.

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12
Q

What is the normal blood flow to the brain in ML/100g tissue/min

A

The normal blood flow to the brain is about 50-65 milliliters per 100 grams of brain tissue per minute. This amounts to about 750-900 milliliters/minute in the average adult.

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13
Q

How do volatiles affect EEG?

what occurs at 2 MAC on EGG?

A

All volatile anesthetics suppress the electroencephalogram (EEG) in a dose-dependent manner. When a volatile agent is administered, there is an initial increase in amplitude followed by a decrease in both amplitude and frequency. At about 2.0 MAC, the EEG may temporarily exhibit electrical silence. This is referred to as burst suppression.

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14
Q

What is the most serious side effect of chronic amiodarone administration ? what % get it and why?

A

The most serious side effect of chronic amiodarone administration is pulmonary toxicity resulting in alveolitis (pneumonitis). It occurs in 5-15% of patients treated with amiodarone. It is believed that amiodarone increases the production of free radicals that results in pulmonary toxicity. Because of this, it is recommended to avoid high inspired oxygen concentrations during general anesthesia for these patients as oxygen increases the production of free radicals.

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15
Q

How does nipride decrease BP and how does this affect the heart?

A

Nitroprusside causes dilation in both veins and arteries (an increase in vessel diameter). The result is a reduction of both preload and afterload which causes a reduction of cardiac filling pressures.

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16
Q

What is mexiletine and why is it given?

A

The antiarrhythmic mexiletine is an orally administered analogue of lidocaine. It is used for the chronic treatment of ventricular arrhythmias. Electrophysiological, it is most similar to lidocaine.

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17
Q

Why is amiodarone good for CHF patients?

A

Amiodarone reduces the risk of sudden cardiac death by 29% in patients with congestive heart failure. Therefore, it is the best alternative for patients who refuse or are not candidates for an AICD.

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18
Q

How doe ACEI work? what electrolytes may be affected?

A

ACE inhibitors result in decreased angiotensin II production. As a result, sodium and water retention are decreased and aldosterone levels are reduced. The reduction in serum aldosterone levels place the patient at increased risk for hyperkalemia.

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19
Q

What BB are given IV ? CCB IV? ACEI IV?

A

In the US, propranolol, metoprolol, and esmolol are available in intravenous form. Verapamil is a calcium channel blocker. Enalapril is an ACE inhibitor.

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20
Q

Which BB causes less bradycardia and why?

A

Because of its alpha-adrenergic blocking capability, labetalol produces less bradycardia than pure beta-adrenergic blockers, but has an increased incidence of orthostatic hypotension.

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21
Q

Describe BB and the pregnant mother

A

Beta-adrenergic blockers administered to a parturient cross the placenta and can produce bradycardia, hypoglycemia, and hypotension in the newborn. Beta-blockers are also likely to pass into breast milk.

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22
Q

What BB and what dose can be used to decrease amount of propofol on induction?

A

Esmolol administered as 1 mg/kg IV followed by a 250 mcg/kg/min infusion substantially reduces the dosage of propofol required to prevent patient movement upon skin incision. There is no known pharmacokinetic reaction between the two drugs that explains this phenomenon.

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23
Q

Discuss propranolol and affects on local anesthetics

A

Propranolol decreases the clearance of amide local anesthetics, but not ester anesthetics such as Chloroprocaine. The pulmonary uptake of fentanyl, however, is substantially decreased in patients taking propranolol. As a result, plasma concentrations shortly after injection can be 2-4 times higher than normal.

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24
Q

what are the effects of milrinone on the heart besides being inodilator?

A

Selective phosphodiesterase inhibitors such as amrinone and milrinone increase the cardiac output primarily by increasing cardiac contractility and decreasing systemic vascular resistance. They produce increased cardiac output, decreased LVEDP, decreased filling pressure, decreased venous return to the heart, decreased systemic vascular resistance, and decreased mean pulmonary artery pressures.

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25
Q

how does milrinone work in terms of receptors

A

The phosphodiesterase inhibitors such as amrinone and milrinone inhibit phosphodiesterase. This results in a decrease in the hydrolysis of cAMP (and subsequent elevated levels of cAMP within the myocardial and vascular smooth muscle cells).

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26
Q

discuss dopamine and immune system and its MOA?

A

Dopamine can negatively affect the immune system by its effects on hormones and lymphocyte function. It can depress the hypothalamic-pituitary system in a manner similar to that seen in chronic stress and critical illness. It also reduces prolactin levels, which is a regulator of T and B lymphocytes.
Dopamine is a fairly nonspecific agonist of alpha, beta, dopamine-1, and dopamine-2 receptors. The vasodilatory effects seen with low dose infusions are attributed to its effects on the dopamine-1 and dopamine-2 receptors.

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27
Q

Does Epinephrine have cerebral effects?

A

Epinephrine has few cerebral effects because it is not very lipid-soluble, making it difficult for the drug to cross the blood-brain barrier.

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28
Q

Name some vasodilating substances released by the body?

A

Under periods of high demand, vasodilating substances such as adenosine, potassium ions, carbon dioxide, hydrogen ions, and prostaglandins can dilate the coronary arteries and increase blood flow by three to four hundred percent.

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29
Q

Name some vasoconstrictive substances released by the body

A

Thromboxane, ATP, and endothelin are all endogenous agents with vasoconstrictive properties.

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30
Q

Name some side effects of sodium nipride?

A

Sodium nitroprusside preserves cardiac output well, but can result in reflex tachycardia, rebound hypertension, pulmonary shunting, and carries the risk of cyanide toxicity.

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31
Q

Name some meds to help decrease BP

A

Volatile anesthetics and opioids may be used to control blood pressure, as may beta-blockers, ACE inhibitors, nitroprusside, alpha-2 agonists such as clonidine, alpha-1 blockers such as droperidol, and calcium-channel blockers.

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32
Q

Which BP lowering med should be avoided with encephalopathy?

A

One caution is that nitroprusside may increase intracranial pressure and therefore must be used cautiously in the treatment of hypertensive crises associated with encephalopathy.

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33
Q

Name some reasons for an lower ETCO2?

A

Hypothermia, hypothyroidism, hyperventilation, hypoperfusion, and pulmonary embolism all result in a decreased ETCO2.

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34
Q

Name some factors that increase SVO2?

A

Factors that result in an increased SVO2 include cyanide toxicity, left-to-right shunts, sepsis, a wedged pulmonary artery catheter, and hypothermia.

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35
Q

Name some factors that decrease SVO2?

A

Factors that result in a decreased SVO2 include hyperthermia, shivering, hemorrhage, decreased cardiac output, and a decrease in the pulmonary transport of oxygen.

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36
Q

What happens to COPD pt’s PFTs?

A

A patient with COPD, the following would be seen in a PFT
FEV1/FVC ratio to Somewhat decreased
FEV 25-75 to Markedly decreased
FRC to Increased.

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37
Q

What factors increase CO2 production

A

Hyperthermia, sepsis, malignant hyperthermia, shivering, and hyperthyroidism are all factors that increase the metabolic rate and subsequently, the amount of carbon dioxide produced.

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38
Q

What are non metabolic causes of increased CO2?

A

Hypoventilation and rebreathing are non-metabolic causes of an increased ETCO2.

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39
Q

Name some factors that affect pulse oximeter readings?

A

The accuracy of an SpO2 monitor can be adversely affected by pathologic hemoglobin forms (carboxyhemoglobin, methemoglobin), intravenous dyes (methylene blue, indigo carmine), motion artifact, nail polish, ambient light, and even electrocautery.

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40
Q

What can lead to an overestimation of the oxygen saturation?

A

Anemia can result in an overestimation of the oxygen saturation.

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41
Q

What can cause erratic pulse ox readings?

A

Optical interference caused by ambient lights flickering at a frequency similar to the pulse oximeter LED can cause erratic readings.

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42
Q

What can result in underestimation of the oxygen saturation?

A

Nail polish and intravenous dyes can result in an underestimation of the oxygen saturation.

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43
Q

How will a decrease in arterial oxygen content or an increase in arterial oxygen extraction affect PvO2?

A

will reduce it

A decrease in arterial oxygen content or an increase in arterial oxygen extraction will reduce the PvO2.

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44
Q

What factors result in a increased SvO2?

A

Factors that result in an increased SVO2 include cyanide toxicity, left-to-right shunts, sepsis, a wedged pulmonary artery catheter, and hypothermia.

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45
Q

What factors result in a decreased SVO2?

A

Factors that result in a decreased SVO2 include hyperthermia, shivering, hemorrhage, decreased cardiac output, and a decrease in the pulmonary transport of oxygen.

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46
Q

How does anemia affect Sp)2 and SaO2 levels?

A

Severe anemia can result in overestimation of the SpO2, particularly at low oxygen saturations.
Non-hypoxic SaO2 values are typically normal in anemic patients, however.

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47
Q

What can result in underestimation of the SpO2.

A

Prominent venous pulsations and injection of certain dyes such as indigo carmine, lymphazurin, nitrobenzene, indocyamine green, methylene blue, and patent blue can result in underestimation of the SpO2.

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48
Q

Name some cardiac benefits of volatiles and how does this occur ?

A

Volatile anesthetics exhibit cardiac preconditioning effects. They appear to alter mitochondrial electron transport in myocardial cells. It is estimated that about 30-40% of the cardioprotective effects of volatile anesthetics occurs by reducing the overload of calcium within the cardiac cells and improving contractility.

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49
Q

Describe Sevo effects on preconditioning (how long in hours) & at what level do they occur ?

A

Sevoflurane has been shown to demonstrate late preconditioning for 24-48 hours after administration. The effects begin at 1 MAC with a dose of 1.5 MAC needed for maximum benefit.

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50
Q

CBF autoregulation when MAP is what?

A

Normally, cerebral blood flow is regulated through a range of mean arterial pressures from about 50 mmHg to 150 mmHg (some sources cite a narrower range of 60-140 mmHg).

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51
Q

Discuss Sevo and cerebral auto-regulation in comparison to ISO/DES

A

With sevoflurane, cerebral autoregulation is maintained up until about 1 MAC. Even at 1.5 MAC, autoregulation is maintained more effectively by sevoflurane than isoflurane or desflurane.

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52
Q

How do VA affect TV & RR?

A

Inhalation agents depress the respiratory system in a dose-dependent fashion. The tidal volume is primarily affected, followed by the respiratory rate. The tidal volume is decreased as the concentration of the agent increases. The respiratory rate increases, but this is typically insufficient to prevent increases in arterial CO2 due to hypoventilation.

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53
Q

When do you see Burst suppression with VAs?

A

Burst suppression on the EEG usually occurs between 1.5 and 2.0 MAC with desflurane and around 2.0 MAC with isoflurane and sevoflurane.

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54
Q

Sevo and epilepsy, is there any relation or not?

A

Sevoflurane can enhance seizure activity and needs to be used with caution in patients with a history of epilepsy.

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55
Q

Speed of induction with VQ deficit?

A

A ventilation-perfusion deficit slows the speed of induction. The effect is greatest in agents with a low blood: gas partition coefficient.

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56
Q

What is the blood gas partition coefficient of the VA & N2O?

A

The blood: gas partition coefficient of desflurane is 0.42, for nitrous oxide it is 0.47, for sevoflurane it is 0.6, and for isoflurane it is 1.4.

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57
Q

Why is N2O faster on the DEs with a higher blood/gas PC?

A

The effect may be more visible in nitrous oxide than in desflurane despite the difference in blood: gas partition coefficients because of the extremely high concentrations of nitrous oxide normally used compared to that of desflurane.

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58
Q

Name sevo effects on cerebral physiology?

A

In the normotensive patient with a normal CO2, sevoflurane has no significant effects on cerebral physiology.

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59
Q

What factors decrease MAC levels?

A

Increasing age, metabolic acidosis, hypoxia, hypothermia, hyponatremia, hypo-osmolality, pregnancy, acute ethanol intoxication, anemia, lidocaine administration, and decreased central neurotransmitter levels may decrease MAC levels.

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60
Q

How does blood/gas PC affect onset of gas?

A

The higher the blood: gas partition coefficient is, the more the onset will be slowed by an increase in cardiac output.

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61
Q

List the blood / gas pC of each gas !

A

The blood: gas partition coefficient of isoflurane is about 1.4, for sevoflurane it is about 0.7, for desflurane it is 0.42, and for nitrous oxide it is about 0.47.

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62
Q

discuss active scavenging disposal

A

Active scavenging disposal uses a dedicated evacuation system such as the wall suction and requires a vacuum capability of 30 liters per minute. The exhaust port of the system has to be an adequate distance from healthcare workers. A disadvantage of active disposal is that the wall suction may not be strong enough to serve anesthesia, the surgeon, and the scavenging system.

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63
Q

discuss a passive scavenging disposal and how it gets rid of the gases

A

Passive disposal routes for waste anesthetic gas utilize a through-the-wall conduit or the operating room ventilation system.

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64
Q

what is a thru the wall disposal system

A

In the through-the-wall disposal system , waste gas exits towards the outside through a duct in the floor, ceiling, wall, or window. This is achieved due to the preferential flow of gases into these disposal ducts because of the slightly positive pressure of the operative room created by OR ventilation.

65
Q

how can a thru the wall disposal system be affected

A

Positive pressure caused by winds can interfere with this disposal route.
Blockage of the exhaust port by birds, insects, and ice can also hinder proper functioning of the passive disposal route.

66
Q

Discuss OR ventilation of waste gases

A

The OR ventilation system can also be used for the passive disposal of waste gas. The system should be nonrecirculating (recirculating systems partially recirculate stale air), and it must also satisfy requirements set forth by the American Institute of Architects. To avoid inadvertent blockage of the hose connecting the scavenging interface to the ventilation outflow port, the hose should not be left on the floor.

67
Q

who mandates the use of active systems

A

Joint Commission accreditors in the United States mandate the use of active systems.

68
Q

how does cerebral oximetry work? does it check global or regional blood flow?

A

Cerebral oximetry is a monitor that uses near-infrared optical spectroscopy (NIRS) to non invasively measure the regional blood hemoglobin oxygenation saturation (rSO2). It is useful in patient populations at risk for stroke such as vascular or cardiac surgery patients, patients with a history of stroke, and neurosurgical patients. The technology used in cerebral oximetry is similar to that used in pulse oximetry.

69
Q

how is cerebral oximetry applied to patient?

A

To use the monitor, a noninvasive sensor is placed over the forehead, but away from the hair and scalp. The sensor can be placed on the right, left, or both frontal-temporal regions (preferable). The sensor emits low intensity light that penetrates the skin, skull, dura, and CSF into the blood located within the cerebral cortex. It is then reflected back to the skin sensor where the rSO2 is determined based upon the light intensity changes as it passes through the brain.

70
Q

what light wavelengths does cerebral oxygen emit

A

The light emitted is of two wave-lengths, 730 nm and 805 nm, emitted in alternating fashion through two light-emitting diodes. Cerebral oxygen saturation is related to three factors:

  1. The light intensity at the source
  2. The detector
  3. The length of the light path through the tissue according to the Beer law (The Beer law states that there is a logarithmic dependence between the transmission of light through a substance and the product of the absorption coefficient of the substance, and the distance the light travels through the material.)
71
Q

what is a normal cerebral oximeter value

A

An rSO2 value of 70% would be considered normal because this encompasses both venous, arterial, and capillary blood.

72
Q

what cerebral oximetry number would indicate a change

A

An index value of less than 50, or a change larger than 20%-30% would be indicative of neurological change.

73
Q

name a bunch of factors that can influence cerebral oximetry values

A

Factors that can result in rSO2 desaturation include: the administration of IV indigo carmine, cardiac arrest, hypothermia, blood steal syndromes, hypoxia, ischemia/embolic strokes, Trendelenburg position (leads to cerebral venous congestion), unilateral or bilateral cerebral atherosclerosis ,and the interference of hair, scalp, or hair follicles. A left-shifted curve can create false positives, and some patients have normal neurological function, yet have low baseline values.

74
Q

serotonin syndrome can occur due to what meds

A

Serotonin syndrome can occur due to ingestion of large quantities of medications such as SSRI’s, MAOI’s, cyclic and atypical antidepressants, cough medicines, drugs used to treat migraine headaches, weight reduction drugs, opiates, and illicit drugs such as ‘Ecstasy’.

75
Q

what are the symptoms of serotonin syndrome

A

Symptoms are related to autonomic hyper-reactivity and include hyperreflexia, delirium, clonus, agitation, and hyperthermia.

76
Q

how does skin temp correlate to core body temp

A

When exposed to a cold environment, there is a reduction in core and/or skin temperature. (A 1-degree reduction in skin temperature is equal to an approximate 0.2-degree reduction in core body temperature.)

77
Q

how does ESLD affect SVR, CI, and MvO2?

A

End stage liver disease is generally associated with a very low SVR, increased cardiac index, and increased mixed venous oxygen saturation.

78
Q

what is the primary inflammatory mediator implicated in disc herniation

A

Phospholipase A2, which is the rate-limiting enzyme in the conversion of arachidonic acid into prostaglandins and leukotrienes, is the primary inflammatory mediator implicated in disc herniation

79
Q

how do Corticosteroids injected into the epidural space work ?? on what fibers?

A

Corticosteroids injected into the epidural space inhibit cytokine release, inhibit phospholipase A2 activity, and exert a local anesthetic-like action on C fibers (but specifically, not A-beta fibers).

80
Q

where do visceral afferent fibers synapse spinal neurons ?

A

The central termination of visceral afferent fibers synapse spinal neurons in laminae I, II, V, and X and deliver visceral sensation information to supraspinal sites through the contralateral spinothalamic tract or the ipsilateral dorsal column.

81
Q

discuss the acid base issue of Pyloric stenosis

A

Pyloric stenosis results in fulminant, and often projectile, vomiting. Gastric acid (HCl) is lost during this process; this is the reason for the hypochloremia and alkalosis exhibited by the patient. The hypokalemia is due to potassium excretion in the kidney. The body trades K+ for Na+ in order to hold on to water and fight hypovolemia.

82
Q

how does adenoidal hyperplasia affect breathing

A

Adenoidal hyperplasia can result in nasopharyngeal obstruction resulting in obligate mouth breathing.

83
Q

what are adenoidal and tonsillar hyperplasia linked too

A

Both adenoidal and tonsillar hyperplasia are linked to sleep apnea with the potential for cor pulmonale and failure to thrive.

84
Q

how does baclofen work

A

Baclofen agonizes the GABA-B receptor to suppress neuronal transmission in the CNS.

85
Q

what are the The major risk factors contributing to apnea after anesthesia in preterm infants

A

The major risk factors contributing to apnea after anesthesia in preterm infants are the type of anesthetic, post-conceptual age, and the presence of anemia.

86
Q

how do certain eye drops affect the pupils

A

Decrease intraocular pressure to Mannitol.
Dilate the pupils to Phenylephrine drops
Constrict the pupils to Pilocarpine drops.

87
Q

how does obesity affect the kidneys

A

Obesity is characterized by an increased glomerular filtration rate, increased renal tubular resorption, and impaired sodium excretion which further worsens hypertension.

88
Q

what is triad of Hepatocellular syndrome

A

Hepatocellular syndrome (HPS) is characterized by the triad of hypoxemia, portal hypertension, and pulmonary vascular dilatations.

89
Q

how does pregnancy affect heart location, what about abnormal rhythms

A

As the patient gets closer to term, the diaphragm rises and shifts the heart upward and leftward. This makes the heart appear larger on chest Xray and produces a left axis shift on the ECG. In the third trimester, there is also an increased tendency for premature atrial contractions, supraventricular tachycardia, and ventricular dysrhythmias.

90
Q

Describes Cushing’s disease

A

The term ‘Cushing’s disease’ refers to Cushing’s syndrome that is cause by the over secretion of ACTH by a pituitary tumor.

91
Q

Symptoms of Cushing’s Disease

A

Symptoms of Cushing’s syndrome are sudden onset of weight gain, thickening of the facial fat giving a rounded shape to the face, facial telangiectasias, glucose intolerance, hypertension, decreased libido in men, oligomenorrhea, and spontaneous bruising.

92
Q

Cushing’s disease and electrolytes

A

Patients with Cushing’s disease have increased serum cortisol levels resulting in hypokalemia, hyperglycemia, and skeletal muscle relaxation which may require a decreased non-depolarizing muscle relaxant dose.

93
Q

Cushings and anesthesia

A

A low-dose infusion of etomidate may be helpful. Because patients undergoing bilateral adrenalectomy exhibit rapid decrease of serum cortisol levels, steroid replacement therapy should be initiated prior to or during surgery. Because of the tendency toward skeletal muscle weakness, it is recommended that patients with Cushing’s disease be mechanically ventilated whenever possible.

94
Q

pheochromotoma location

A

About 85% of pheochromocytomas are located in the medulla of one of the adrenal glands. They are also occasionally found in the spleen, broad ligament of the ovary, right atrium, or at the bifurcation of the aorta.

95
Q

Pheochromocytoma hypertension drug of choice

A

Nitroprusside is preferred for the treatment of hypertension (systolic pressures over 200 mmHg are common) during surgical excision of pheochromocytomas. Hypotension typically occurs following ligation of the vein draining the tumor. To prevent hypotension, the patient should undergo volume expansion until a pulmonary capillary wedge pressure of 16-18 mmHg is reached prior to ligation of the vein.

96
Q

pheochromocytoma and BP control high and low

A

Vasopressors should be utilized only after adequate volume expansion has been achieved.
Esmolol or labetalol are the agents of choice if it is primarily an epinephrine-secreting tumor. Esmolol offers the advantage of a short duration of action.
Pheochromocytomas typically release 85% norepinephrine and 15% epinephrine.

97
Q

which conditions cause hyperactive parathyroid gland

A

The parathyroid glands release parathyroid hormone which regulates calcium balance.
Any condition that results in even a slight decrease in calcium ion concentration in the extracellular fluid will stimulate the release of parathyroid hormone. The parathyroid glands become hyperactive and hypertrophied in conditions such as rickets, pregnancy, and lactation.

98
Q

what jobs does parathyroid gland do

A

The parathyroid decreases phosphate by increasing the renal excretion of phosphate.
Parathyroid hormone increases serum calcium levels by increasing bone resorption of calcium, limiting its renal excretion, and enhancing the gastrointestinal absorption of calcium by regulating vitamin D metabolism.

99
Q

parathyroid and 2 stages of bone resorption

A

Parathyroid hormone increases bone resorption of calcium and phosphate in two stages: the first stage begins within minutes and increases the resorption activity of osteoclasts. The second stage is much slower and may require several days or weeks as it stimulates the increased production of osteoclasts.

100
Q

parathyroid and phosphate and calcium

A

Parathyroid hormone can cause a rapid loss of phosphate ions in the urine by its effect on the proximal tubule. As more phosphate is excreted, calcium is retained. The increased calcium reabsorption takes place primarily in the collecting tubules and the late distal tubules.

101
Q

Cardiac signs and symptoms of hyperparathyroidism

A

Cardiac signs and symptoms of hyperparathyroidism: Hypertension, prolonged PR interval, and a shortened QT interval.

102
Q

Neuromuscular signs of hyperparathyroidism

A

Neuromuscular signs: Skeletal muscle weakness, bone demineralization, vertebral collapse, and pathologic fractures.

103
Q

renal signs of hyperparathyroidism

A

Renal signs: Skeletal muscle weakness, bone demineralization, vertebral collapse, and pathologic fractures.

104
Q

anestheisa and hyperparathyroidism

A

Your anesthetic with hyperparathyroidism should be aimed at dealing with underlying hypercalcemia. Because of this, hydration with normal saline and monitoring of urinary output is essential. Because hypercalcemia is associated with somnolence, the anesthetic requirement may be decreased. If personality changes due to chronic hypercalcemia are present, then ketamine may need to be avoided.

105
Q

hyperparathyroidism and ventilation

A

Acidosis increases the serum calcium level, so hypoventilation should be avoided.

106
Q

hyperparathyroidism and musclerelaxants

A

Baseline skeletal weakness may necessitate a decreased dose of nondepolarizing muscle relaxants; however, the increased calcium can antagonize muscle relaxants–in short, hyperparathyroidism is associated with an increased sensitivity to succinylcholine and a resistance to nondepolarizing muscle relaxants.

107
Q

parathyroidectomy and poisition, ETT & Fluids & Digoxin

A

As with thyroidectomy, there is a risk of damage to the recurrent laryngeal nerve during surgery, so a Nim(Registered) tube or similar device should be used to monitor nerve function during surgery. It is important to position patients with a risk of pathologic fractures carefully. Normal saline is preferred over Lactated Ringer’s solution for fluid management. The patient may be more sensitive to the effects of digoxin.

108
Q

Signs and symptoms of hypoparathyroidism:

A

Signs and symptoms of hypoparathyroidism: prolonged QT interval, muscle spasms, hypotension, and decreased responsiveness to beta agonists

109
Q

The treatment of hypoparathyroidism

A

The treatment of hypoparathyroidism is aimed at restoring low calcium levels to normal. An infusion of 10 mL of calcium gluconate 10% IV should be administered until signs of neuromuscular irritability resolve. Respiratory or metabolic alkalosis should be normalized.

110
Q

The treatment of hypoparathyroidism & diuretics

A

Thiazide diuretics may be helpful as they result in sodium depletion without the loss of potassium which tends to increase calcium levels.

111
Q

aortic stenosis pathophysiology

A

Patients with aortic valve stenosis have a fixed obstruction, whereas about 25% of patients with hypertrophic cardiomyopathy exhibit a dynamic obstruction which peaks in mid-to-late systole, can vary from beat to beat, and can worsen with enhanced ventricular contractility, decreased ventricular volume, and decreased left ventricular afterload. Many patients are asymptomatic, but those that do exhibit symptoms exhibit dyspnea on exertion, fatigue, syncope, or angina.

112
Q

The first manifestation of hypertrophic cardiomyopathy in patients younger than 30 years

A

is often sudden cardiac death, which is also the most common cause of death.

113
Q

HCOM and diastolic dysfunction effects

A

Patients with hypertrophic cardiomyopathy typically suffer from diastolic dysfunction which is exhibited by increased left ventricular end-diastolic pressures despite an often hyperdynamic left ventricular function. The diastolic stiffness is due to the increased muscle mass of the left ventricle which is typically concentrated in the upper septum just below the aortic valve.

114
Q

HCOM comorbidities of the heart & s/s

A

(hypertrophic cardiomyopathy) Patients often exhibit dynamic left ventricular outflow tract obstruction, mitral regurgitation, diastolic dysfunction, myocardial ischemia, and dysrhythmias. Many patients are asymptomatic, but those that do exhibit symptoms exhibit dyspnea on exertion, fatigue, syncope, or angina.

115
Q

what is a paradoxical embolism

A

Paradoxical embolus is the transfer of an embolus from the venous system to the arterial system and often to the brain via a patent foramen ovale or atrial septal defect.

116
Q

HCOM and anesthesia technique

A

Hypertrophic cardiomyopathy involves enlargement of the interventricular septum which results in left ventricular outflow obstruction. This obstruction is worsened by increased heart rate or increased myocardial contractility as well as decreases in preload or afterload. Anesthesia is usually maintained by controlled myocardial depression using volatile anesthetics.

117
Q

how does left side heart afailure affect right side of heart

A

As flow through the mitral valve opening into the left ventricle is decreased (thus decreasing the left ventricular volume), left atrial pressure increases, resulting in left atrial hypertrophy and distention. The increased pressure is transmitted into the pulmonary vasculature as the volume of pulmonary blood increases. This increased pulmonary vascular pressure represents an increase in right ventricular afterload and will cause right ventricular hypertrophy and failure. As pulmonary venous pressure increases above about 25 mmHg, fluid can leak into the pulmonary interstitial space resulting in a decrease in pulmonary compliance and increased work of breathing. If the change in pulmonary venous pressure occurs over a long period of time, an increase in pulmonary lymph flow can partially compensate for the fluid accumulation.

118
Q
name game with
Coarctation of the aorta 
Aortic stenosis  murmur
Patent ductus arteriosus treatment drug
Eisenmenger's syndrome - what is it
A

Coarctation of the aorta to Widened pulse pressure in the arms
Aortic stenosis to Systolic murmur over the 2nd right interspace
Patent ductus arteriosus to Can be treated with cyclooxygenase inhibitors
Eisenmenger’s syndrome to Reversal of a left-to-right shunt.

119
Q

ventricular dyssynchrony s/s

A

Kussmaul’s sign and pulsus paradoxus are both indicative of ventricular discordance (also known as ventricular dyssynchrony) that occurs due to the opposing response of the ventricles to filling during the respiratory cycle.

120
Q

pericarditis cause and pain relief

A

Pericarditis is often due to a viral illness but may often occur 1-3 days after a myocardial infarction.
Deep inspiration worsens the pain. It is often relieved by sitting forward.

121
Q

EKG changes with pericarditits

A

The ECG changes seen in acute pericarditis occur in four stages.
In stage I, there is diffuse ST segment elevation and depression of the PR segment.
In stage 2, the ST and PR changes normalize.
In stage 3, the T wave inverts, and in stage 4, the T waves normalize.
If no other associated pericardial disease is present, acute pericarditis does not alter cardiac function.

122
Q

CSf is made where?

CSF fluid pressure normal is ??

A

The choroid plexuses are located in the four ventricles.
The ones located in the two lateral ventricles produce the greatest quantity of cerebrospinal fluid.
When lying in a horizontal position, the normal cerebrospinal fluid pressure is about 130 mm of water or 10 mmHg.

123
Q

CO to brain

A

The brain only comprises about 2% of body mass but receives about 15% of the cardiac output.

124
Q

normal blood flow to the brain

A

The left and right carotid arteries and left and right vertebral arteries supply the blood to the brain. The normal blood flow to the brain is about 50-65 milliliters per 100 grams of brain tissue per minute. This amounts to about 750-900 milliliters/minute in the average adult.

125
Q

hydrogen ions effect on the brain

A

An increase in hydrogen ion concentration depresses neuronal activity. It also causes an increase in blood flow to the brain. By doing so, it will help ‘wash away’ the hydrogen ions, carbon-dioxide, and other acid precursors away from the brain which returns the hydrogen ion concentration back to normal

126
Q

Rexed laminae location

A

Rexed laminae I through laminae VI are located in the dorsal horn of the spinal column. Laminae VII, VIII, and IX comprise the ventral horn.

127
Q

normal CBF autoregulation limits

A

Normally, the body maintains a constant cerebral blood flow between mean arterial pressures of 60 and 140 mmHg. Chronic hypertension will shift both the upper and lower limits of the cerebral autoregulation curve to the right.

128
Q

Sodium and CSF

A

Secretion of cerebrospinal fluid by the choroid plexus is dependent upon the active transport of sodium through the epithelium of the choroid plexus. As the sodium is transported out, chloride is pulled outward as well because of its electrochemical attraction to sodium. The combination of sodium and chloride increases the osmotic pressure on the outside of the plexus which results in the osmosis of water through the plexus membrane. It is the fluid that forms the principal constituent of cerebrospinal fluid.

129
Q

The preganglionic sympathetic nervous system fibers originate where

A

between the T-1 and L-2 nerve roots.

130
Q

Central nervous system symptoms of hyponatremia at 120

A

confusion, restlessness, nausea, and vomiting begin to appear at about 120 mEq/L,

131
Q

CNS symptoms of hyponatremia at 115 and 100

A

with ECG changes occurring at 115 mEq/L, and ventricular tachycardia and fibrillation occurring below 100 mEq/L.

132
Q

The limbic and paralimbic regions are involved in what

A

The limbic and paralimbic regions (anterior cingulate cortex and insular cortex) are involved in the emotional and motivational aspect of pain sensation. The SI and SII somatosensory cortices are involved in determining the location and intensity of pain sensations.

133
Q

The major ascending spinal pathways involved in the transmission of nociceptive information

A

include the spinothalamic, spinohypothalamic, spinomedullar, and spinobulbar tracts.

134
Q

____ tract is most important for the transmission of pain, temperature, and itch sensations.

A

Of these, the spinothalamic tract is most important for the transmission of pain, temperature, and itch sensations.

135
Q

___ tract is important in integrating pain information with homeostasis and behavior mechanisms.

A

spinobulbar

136
Q

______tract is involved in the autonomic, neuroendocrine, and emotional aspects of pain.

A

spinohypothalamic

137
Q

The central termination of visceral afferent fibers synapse spinal neurons

A

in laminae I, II, V, and X and deliver visceral sensation information to supraspinal sites through the contralateral spinothalamic tract or the ipsilateral dorsal column.

138
Q

The majority of visceral afferent fibers are

A

A-delta and unmyelinated C fibers with a tiny portion of them being A-beta fibers in the mesentery. Group C fibers are unmyelinated, which would help you eliminate options in this question.

139
Q

Blockade of _______via a facet joint injection can relieve pain from sacroiliac joint syndrome.

A

of the medial branch of the dorsal rami of L5 and S1-S3

140
Q

The low-pressure system on an anesthesia machine

A

contains the flowmeters, hypoxia prevention devices, unidirectional valves, pressure relief devices, and the common gas outlet.

141
Q

The intermediate pressure system of an anesthesia machine contains

A

contains the pneumatic part of the master switch, pipeline inlet connections and pressure indicators, the gas power outlet, oxygen flush valve, oxygen pressure failure devices, and flow control valves.

142
Q

only machine safety device that evaluates the integrity of the low-pressure circuit in an ongoing fashion.

A

The oxygen analyzer

It is the only machine monitor that can detect problems downstream from the flow control valves.

143
Q

describe the pumping effect

A

The ‘pumping effect’, an intermittent back pressure caused by positive pressure ventilation or use of the oxygen flush valve results in elevated vaporizer output. It is more prominent with low flows, low vaporizer dial settings, low levels of anesthetic in the vaporizer chamber, high respiratory rates, and high peak inspiratory pressures.

144
Q

what temp and thyroid condition lower ETCO2

A

Both hypothermia and hypothyroidism will decrease the ETCO2 during anesthesia.

145
Q

Possible complications from overfilling a vaporizer

A

Possible complications from overfilling a vaporizer include liquid agent entering the fresh gas line and potentially delivering a lethal dose of agent to the patient or complete failure of the vaporizer. Some vaporizers have the filling port positioned so that overfilling cannot occur, but if the vaporizer is tipped overfilling is still a possibility.

146
Q

Thoracic neuraxial anesthesia will produce a

A

contracted gut with hyperperistalsis.

147
Q

thoracic neuraxial anesthesia effects on kidney, vital capacity and obese

A

Renal and hepatic blood flow decrease in parallel with the reduction in mean arterial pressure.
The vital capacity will decrease relative to the degree of abdominal and thoracic muscle paralysis from the anesthetic.
The decrease in vital capacity is more pronounced in obese patients.

148
Q

where do spinal and epidural exert their effect

A

Both spinal and epidural anesthetics exert their primary action on the nerve root.
Epidurally administered drugs reach their destination by coursing along the epidural space and then diffuse through the meninges and the dural cuff to reach the nerve root.

149
Q

If LMWH is planned postoperatively & waiting time

A

the epidural catheter should be removed at least 2 hours before the first dose

150
Q

An epidural catheter should be advanced about

A

5 cm into the epidural space. Advancing it further will increase the likelihood that a complication will result such as the catheter forming a knot, entering a vein, or puncturing the dura.

151
Q

what is differential block

A

Because different neurons have a different susceptibility to local anesthetics, specific sensations exhibit inhibition at different dermatome levels. This is referred to as differential block.

152
Q

spinal and pinprick vs temp

A

With regards to spinal anesthesia, light touch or cold sensation is inhibited at a higher dermatome level than pinprick sensation.

153
Q

what determines spinal block duration

A

The anesthetic drug used, and the total dose given determine the duration of action of the block

154
Q

The major ascending spinal pathways involved in the transmission of nociceptive information

A

include the spinothalamic, spinohypothalamic, spin medullar, and spinobulbar tracts.

155
Q

most important tract for the transmission of pain, temperature, and itch sensations.

A

spinothalamic tract

156
Q

this tract is important in integrating pain information with homeostasis and behavior mechanisms.

A

The spinobulbar

157
Q

this tract is involved in the autonomic, neuroendocrine, and emotional aspects of pain.

A

The spinohypothalamic

158
Q

obese and epidural

A

The obese patient should be in the sitting position when the epidural is placed to help in identifying landmarks. Because rostral spread of the anesthetic is more prevalent in obese patients and they are more prone to suffer respiratory symptoms as a result, you should have them sit up for a longer period of time after injection.