Chapter 3 Clinical Cardiac and Pulmonary Physiology
Hemodynamics
Preload
14. How can “preload” be measured clinically?
15. When will central venous pressure (CVP) poorly reflect filling pressures in the left heart?
16. What is the Frank-Starling mechanism?
17. What are common causes of low preload?
18. What is systolic pressure variation and how might it be useful in analyzing hypotension?
Pulmonary gas exchange
Oxygen
38. How is blood oxygen measured?
39. What is the “P50”? What is a normal value?
40. What are common clinical factors that shift the oxyhemoglobin dissociation curve left and right?
41. What are the benefits of a rightward shift in the oxyhemoglobin dissociation curve?
42. What is the equation describing the effect of ventilation on oxygenation?
43. How does increased FIO2 improve oxygenation during hypercapnia?
44. Is it possible to deliver hypoxic gas mixtures with a modern anesthesia machine?
45. What does an A-a gradient mean with respect to a problem in oxygenation?
46. What is intrapulmonary shunt?
47. What is the shunt equation?
48. Is diffusion limitation a significant clinical cause of hypoxemia?
49. Which causes of hypoxemia are very responsive to supplemental oxygen and therefore easily treated with higher FIO2?
50. How does low mixed venous oxygen saturation affect arterial oxygenation?
Carbon dioxide
51. What are the three forms in which carbon dioxide is carried in the blood?
52. Why is hypercapnia a problem clinically?
53. What are the four physiologic causes of hypercapnia?
54. What are significant causes of increased CO2 production under anesthesia?
55. What are the various types of dead space?
56. What pathologic conditions may increase dead space?
57. What is a normal value for physiologic dead space?
58. What is the Bohr equation?
Control of breathing
Integration of the heart and lungs
Oxygen Extraction
89. Why is examining oxygen extraction clinically useful?
90. What is normal mixed venous oxygen saturation?
91. How would the arterial to venous oxygen content difference change with higher FIO2?
92. Why is the oxygen extraction ratio useful?
93. How can the body respond physiologically to anemia or increased metabolic demand (oxygen consumption)?
Answers*
Hemodynamics
Arterial Blood Pressure
1. Mean arterial pressure (MAP) is the average blood pressure. On modern monitors, MAP is calculated from integrating the arterial waveform over time. MAP can often be estimated by adding one third of the pulse pressure to the diastolic blood pressure. (50)
2. MAP is the product of cardiac output (CO) and SVR, or MAP = CO × SVR. This is similar to electricity where voltage = current × resistance. (If we were to be exactly correct, we would use the pressure drop across the systemic vascular system, or MAP – CVP.) (50)
3. Pulse pressure is the difference between systolic and diastolic blood pressure. (50)
4. Pulse pressure is produced from the stroke volume being pushed into the aorta. The compliance features of the aorta therefore have a very significant effect on pulse pressure so that a stiff aorta results in a higher pulse pressure, a common feature of aging. A lower diastolic pressure can reduce pulse pressure by moving to a more compliant part of the aortic compliance curve. A higher stroke volume generally increases pulse pressure. Lower SVR can decrease pulse pressure because part of the stroke volume “runs off” rapidly during ejection. Aortic insufficiency can increase pulse pressure as the diastolic pressure drops significantly during backward flow into the left ventricle. (50-51)
Systemic vascular resistance
5. Classic pathologic causes of low SVR include sepsis, anaphylactic and anaphylactoid reactions, and reperfusion of ischemic organs. Many anesthetic drugs and neuraxial anesthesia also lower SVR.
6. SVR = 80 × 
, where MAP is mean arterial pressure, SVR is systemic vascular resistant, CVP is central venous pressure, and CO is cardiac output. The factor “80” converts the SVR to the proper units. (51)
7. Most of the resistance in the vascular system is in the arterioles. Despite having smaller diameters, there are large numbers of capillaries in parallel, resulting in overall lower resistance at this level of the vascular tree. (51)
8. Resistance is inversely proportional to the fourth power of the radius of the vessel. (51)
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