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Terms in this set (282)

Ventricular systole: isovolumic contraction -> ejection. Ventricular diastole: isovolumic relaxation -> rapid ventricular filling -> diastasis -> atrial systole. A good way to think about the cycle is starting with the first heart sound which is the atrioventricular valves closing (beginning systole, C wave). This occurs when the ventricular pressure is larger than the atrial pressure. The time between when these valves close and when the aortic valve opens is called isovolumic contraction. The ventricular pressure and aortic pressure rise rapidly, once ventricular pressure is equal to the aortic pressure the aortic valve opens (ejection). Both the aortic and ventricular pressure continue to rise and then reach a peak. Eventually the aortic pressure is greater than the ventricular pressure, at which point the aortic valve closes (second heart sound, beginning diastole). The time between when the aortic valve closes and the atrioventricular valve opens is isovolumic relaxation (incisura wave), during this time atrial pressure increases slightly as it fills with blood (V wave). Once the atrial pressure is greater than the ventricular pressure the atrioventricular valves open, once this occurs the aortic pressure starts to increase and will not increase again until these valves close. This part is called rapid inflow as the ventricles fill with blood. After which diastasis occurs whereby the pressure in the atrium equals the pressure in the ventricular. Then atrial contraction / atrial systole occurs (A wave) which leads to an increase in the atrial pressure and ventricular pressure. Once the ventricular pressure is greater than the atrial pressure the atrioventricular valves close again (C wave). And the cycle continues.
Your next patient is a 58 year-old man who tells you that for the past few months, he has had an "aching pain" in his right leg when he walks up more than 1 flight of stairs. If he stops and rests, the pain goes away within 1-2 minutes. He also notes that when he takes long walks, his R leg feels very "heavy" by the end. He has had no swelling in his legs, chest pain or shortness of breath. The discomfort never occurs at rest. He has hypertension and hyperlipidemia. He does not have diabetes. He has smoked since he was 15 years old, at least 1 pack per day. Despite multiple attempts to quit, he has failed. On exam, he is obese and in NAD. His vital signs are: HR 82 bm, BP 138/82 mm Hg, RR 16/min, O2 100% on RA. His JVP is difficult to assess due to body habitus. He has soft bilateral carotid bruits. His heart exam reveals normal S1 and S2, regular rhythm, no murmurs but a prominent S4. His lungs are clear. He has diminished pulses in his R popliteal, posterior tibial and dorsalis pedis. You send him for an ankle brachial index test. It is 0.5 on the R and 0.8 on the L. You send him for pulse volume recordings (PVRs). They are abnormal. (See slide #7) You send him for a MR angiogram. (See slide #8) Questions 1. (CBCL-1, 10 minutes: Individual, 3 mins. Tables, 3 mins; Group, 4 mins) What is the pathophysiologic process causing his leg pain? Why does it only happen when he walks? How is this pathophysiology similar and different from your first patient's? 2. (large group, 5 minutes) Thinking about the underlying pathophysiology, what medical treatments or procedures might be helpful? (again, thinking broadly).
How is respiratory limiting exercise? 1/3 = prolonged. Hoover's sign = hyperinflation: Normally diaphragm dome shaped, so when contracts pull diaphragm down. But if hyperinflated when diaphragm contracts pulls inward, see chest change pull inward. Low FEV1/FVC ratio is low = obstructive disease (emphysema, COPD). Emphysema -> increased compliance and increased resistance -> dynamic hyperinflation (Hoover's sign & higher end expiratory volume / breath stacking). Exercise -> increase resp rate and increase tidal volume normally: RR x Vt = minute ventilation. If high resistance due to emphysema then not enough time to get air out = breath stacking -> larger tidal volume. Stimulate motor cortex -> sensory cortex -> dyspnea. External intercostal already stretch and so is diaphragm -> don't generate tension as well -> harder to breath. At exercising -> operating at less compliant part of respiratory curve -> more work. Lower O2 with exercise -> stimulate chemoreceptors -> dyspnea. Destruction alveoli from disease -> reduced surface area -> decreased diffusing capacity (PO2 decreased from 94 - 85): exercise -> increased CO -> increased blood velocity -> less gas exchange. Increased ventilation cannot help since hemoglobin-oxygen binding. Emphysema -> damages alveoli -> lower alveolar ventilation. Higher end expiratory volume suggests breast stacking. Normal person cardiac output limits exercise since can increase ventilation significantly since normal FEV1. Respiratory disease means limited. Low HR: 220 - age is max heart rate, since heart rate not at max now respiratory system limiting exercise, reduced FEV1.