Anesthesia Qod

Anesthesia QOD

An 82-year-old female arrives to the OR for open reduction of a left intratrochanteric fracture. Significant past medical history includes hypertension, moderate aortic stenosis and dementia. The most appropriate anesthetic technique for this patient is:

opioid-based general anesthesia
spinal anesthesia
volatile-agent-based general anesthesia
epidural anesthesia

opioid-based general anesthesia

In patients with mild to moderate aortic stenosis, a primarily opioid-based technique results in minimal cardiac depression, less tachycardia and suppression of the sympathetic response to surgical stimulation. These are all desired effects as HTN and tachycardia may precipitate ischemia in these patients. Spinal or epidural anesthesia as well as a volatile-agent-based anesthesia can cause a fall in afterload with resulting severe hypotension.
pg. 474 Morgan, GE, Mikhail, MS, and Murray,

The loss of ventricular filling as a result of acute atrial fibrillation is approximately:

5%
10%
25%
50%

The loss of ventricular filling as a result of acute atrial fibrillation is approximately: 25%

The loss of ventricular filling as a result of acute atrial fibrillation is approximately: 25%. Passive flow accounts for about 75% of ventricular filling. The remaining 25% occurs as a result of atrial contraction, which is lost during atrial fibrillation.

♦ What percentage of cardiac output is delivered to the highly-perfused organs (heart, lungs, brain, kidneys, and liver)?Approximately 75% of resting cardiac output is delivered to the vessel-rich organs, although they constitute only 10% of total body mass. [Stocking, PPAP. At. 2006 pp5-6]
What determines blood flow through an organ or tissue? This is an application of what law?The two determinants of blood flow are pressure gradient (pressure dif-ference, AP) and resistance (R). Blood flow = (Pi-P2)/R. Blood flow to any tissue is directly proportional to the hydrostatic pressure gradient (P1-P2) and inversely proportional to vascular resistance (R). (Pi-P2) is usually (P arterial -Pvenous). This is an application
In general, blood flow to a tissue or organ is most directly related to what? Explain.Blood flow to a tissue or organ is generally direcdy related to tissue me-tabolism. Metabolites (local factors) dilate the vasculature, and blood flow to the tissue increases. [Guyton, TMP. 1 le. 2006 ppl96]
What are the two most important determi-nants of oxygen delivery to the tissues?Cardiac output and arterial blood 02 content. Arterial blood oxygen content is determined by the blood hemoglobin concentration and percent saturation. [Guyton, TMP, 1996, p516]
Describe the effect of hypercapnia on the cerebral vasculature and on the systemic vasculature.Hypercapnia causes dilatation of both the cerebral vasculature and the systemic vasculature. An increase in C02 concentration in the arterial blood perfusing the brain decreases cerebral vascular resistance and increases cerebral blood flow. Hypercapnia also relaxes systemic vascular smooth muscle causing decreased systemic vascular resistance (SVR). [Guyton, TMP, 1996, pp 200-201, 783; Miller, Anesthesia, 1994, pp 129-130
How does hypercarbia affect pulmonary vascular resistance?Pulmonary vascular resistance increases in response to hypercarbia. The pulmonary vasoconstrictor response to hypercarbia is opposite that observed in the systemic and cerebral vasculature. [Miller, Anesthesia, 1994
With hypercapnia is there hypertension or hypotension?Both hypertension and hypotension may occur with hypercapnia. Hypercapnia appears to cause direct depression of both cardiac muscle and vascular smooth muscle, but at the same time it causes reflex stimulation of the sympathoadrenal system. Thus, hypercapnia, like hypoxemia, may cause increased myocardial 02 demand (tachycardia, early hypertension) and decreased myocardial 02 supply (tachycardia, late hypotension). [Miller, Anesthesia, 5th ed. 2000, p613]
How does severe acidosis alter pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR)?Acidosis increases pulmonary vascular resistance (PVR) and decreases systemic vascular resistance (SVR). [Longnecker et al., PPA, 1998, p961; Barash, Clinical Anesthesia, 2001, p878]