SECTION III THE CARDIOVASCULAR SYSTEM Mitral Stenosis with Congestive Heart Failure A 54-year-old womn entered the hospital with severe shortness of breath. abdominal distension,and fatigue.She has a history of rheumatic fever and has had a heart murmur since childhood.In the past 3 years she has had progressive shor tness of breath and ankle edem that have required treatnent with digitalis and diuretics. Despite the therapy.the patient's symptoms hecame much worse,and hospital admission for evaluation and treatment was recommended.Physical examination revealed a dyspeeic,slightly cyanotic womn with ankle,pretibial,and sacral edema and distended neck veins.The heartheat was completely irregular,and the heart sounds varied in intensity.Heart rate at the apex,as determined by auscultation (listening).was 100 beats/nin.but as judged by the radial pulse,the beart rate was 70 beats/min.Arterial blood pressure was 100/65 mm Hg.There were loud rumbling diastolic murmurs heard best at the apex,an enlarged tender liver,aseites,and rales (crackling sounds)at both lung bases. 1.Why does the patient appear slightly cyanotic (blue)? 2.Why are neck veins distended,and is central venous pressure normal? 3.Why is the patient's blood volume increased? 4.Is velocity of peripheral blood flow increased,decreased,or normal? 5.What regulates capillary blood flow in this patient? 6.Venous pressure in the legs is elevated.Why don't the capillaries in the feet rupture？ 7.What effect does the elevated intravascular pressure have on the arterioles in the feet? 8.Does the endothelium play any role in the regulation of peripheral resistance in this patient? 9.hatd的rales at the lung bases mean'？
SECTION III THE CARDIOVASCULAR SYSTEM Mitral Stenosis with Congestive Heart Failure A 54-year-old woman entered the hospital with severe shortness of breath, abdominal distension, and fatigue. She has a history of rheumatic fever and has had a heart murmur since childhood. In the past 3 years she has had progressive shortness of breath and ankle edema that have required treatment with digitalis and diuretics. Despite the therapy, the patient's symptoms became much worse, and hospital admission for evaluation and treatment was recommended. Physical examination revealed a dyspneic, slightly cyanotic woman with ankle, pretibial, and sacral edema and distended neck veins. The heartbeat was completely irregular, and the heart sounds varied in intensity. Heart rate at the apex, as determined by auscultation (listening), was 100 beats/min, but as judged by the radial pulse, the heart rate was 70 beats/min. Arterial blood pressure was 100/65 mm Hg. There were loud rumbling diastolic murmurs heard best at the apex, an enlarged tender liver, ascites, and rales (crackling sounds) at both lung bases. 1. Why does the patient appear slightly cyanotic (blue)? 2. Why are neck veins distended, and is central venous pressure normal? 3. Why is the patient's blood volume increased? 4. Is velocity of peripheral blood flow increased, decreased, or normal? 5. What regulates capillary blood flow in this patient? 6. Venous pressure in the legs is elevated. Why don't the capillaries in the feet rupture? 7. What effect does the elevated intravascular pressure have on the arterioles in the feet? 8. Does the endothelium play any role in the regulation of peripheral resistance in this patient? 9. What do rales at the lung bases mean?
10.What caused the pulmonary edems in this patient? 11.Why does the patient have peripheral edema and ascites? 12.Is there iapairnent of water and/or sodiun noveneat between the vascular and the extravascular compartnents? 13.Is 0 and C0 exchange between blood and tissue mormal? 14.Are oncotic forces in the patient's blood norral? 15.If all capillaries are open,would this affect the formation of edema? 16.How would large molecules move between blood and tissue? 17.What role do the lymphatics play in this patient? 18.Why were the heart sounds irregular? 19.Why were the heart sounds of varying intensity,and shy was the heart rate at the apex by auscultation different fron that at the wrist by palpation? ANSVER 1.The patient appears slightly cyanotic hecause blood in the microvessels of the skin is not fully oxygenated:this is caused in part by greater extraction of oxygen hy the tissues secondary to a low blood flow (reduced cardiac output)and also to incomplete oxygenation of blood in the lungs because of edema and the consequent interference with oxygen diffusion from alveoli to capillaries. 2.The neck veins are distended because of an elevated central venous pressure. This venous pressure increase is in part caused by the fncreased resistance to flow through the heart at the mitral valve but more importantly to the large blood volume in the vascular system. 3.The blood volume is increased because of enhanced retention of sodiun and water by the kidneys.With a reduced cardiac output and a consequent reduction in renal blood flow and glorerular filtration rate (GFR)by renal arteriolar constriction,excretion of electrolytes and water is dimimished.The reduced GFR induces renin release:this leads to the formation of angiotensin,which enhances aldosterone release,and the latter increases the reabsorption of sodiun
10. What caused the pulmonary edema in this patient? 11. Why does the patient have peripheral edema and ascites? 12. Is there impairment of water and/or sodium movement between the vascular and the extravascular compartments? 13. Is O2 and CO2 exchange between blood and tissue normal? 14. Are oncotic forces in the patient's blood normal? 15. If all capillaries are open, would this affect the formation of edema? 16. How would large molecules move between blood and tissue? 17. What role do the lymphatics play in this patient? 18. Why were the heart sounds irregular? 19. Why were the heart sounds of varying intensity, and why was the heart rate at the apex by auscultation different from that at the wrist by palpation? ANSWER 1. The patient appears slightly cyanotic because blood in the microvessels of the skin is not fully oxygenated; this is caused in part by greater extraction of oxygen by the tissues secondary to a low blood flow (reduced cardiac output) and also to incomplete oxygenation of blood in the lungs because of edema and the consequent interference with oxygen diffusion from alveoli to capillaries. 2. The neck veins are distended because of an elevated central venous pressure. This venous pressure increase is in part caused by the increased resistance to flow through the heart at the mitral valve but more importantly to the large blood volume in the vascular system. 3. The blood volume is increased because of enhanced retention of sodium and water by the kidneys. With a reduced cardiac output and a consequent reduction in renal blood flow and glomerular filtration rate (GFR) by renal arteriolar constriction, excretion of electrolytes and water is diminished. The reduced GFR induces renin release; this leads to the formation of angiotensin, which enhances aldosterone release, and the latter increases the reabsorption of sodium
4.The velocity of peripheral blood flow is decreased in this patient because of the low cardiac output,the low blood pressure,and the compensatory arteriolar constriction. 5.Capillary blood flow is regulated primarily by the contractile state of the cognate arterioles.In this patient there is arteriolar constriction but also an increase in vemous pressure,so the pressure gradient across the capillary beds is reduced. 6.The vemous pressure in the legs is greatly elevated hecause of the hypervolemia.Despite the large transmural pressure across the capillary walls,the capillaries do not rupture hecause their small diameter allows them to withstand the high intravascular pressure.According to the Laplace equation.T pr,where Tis wall tension,p is transaural pressure,and r is vessel radius.Because r is so small in the capillaries,the wall tension will not be excessive even when P is elevated. 7.The increased intravascular pressure tends to stretch the arterioles, especially in the feet when the individual is erect.The arteriolar transmural pressure is elevated,and this elicits contraction of the arterfolar vascular smooth muscle by a myogenic mechanisn 8.The endothelium plays a role in the regulation of peripheral resistance (in this patient and in normal individuals)by releasing nitric oxide (a vascular snooth muscle relaxant)in respomse to a variety of physiologic stimuli. 9.The rales heard at the lung hases are attributable to fluid in the snall bronchi (and alveoli)and indicate some pulmonary edema.Fluid in the alveoli can interfere with gas exchange in the lung (especially with 0,)and the amount of oxygen taken up by the blood in the lungs. 10.The pulmonary edema is caused by the high pulmonary capillary pressure,which is attributable to the narrowed mitral valve.The left atrial pressure is high because of this valve lesion and because of the pressure generated by the hypertrophied left atrium in response to the obstruction.This high pressure is
4. The velocity of peripheral blood flow is decreased in this patient because of the low cardiac output, the low blood pressure, and the compensatory arteriolar constriction. 5. Capillary blood flow is regulated primarily by the contractile state of the cognate arterioles. In this patient there is arteriolar constriction but also an increase in venous pressure, so the pressure gradient across the capillary beds is reduced. 6. The venous pressure in the legs is greatly elevated because of the hypervolemia. Despite the large transmural pressure across the capillary walls, the capillaries do not rupture because their small diameter allows them to withstand the high intravascular pressure. According to the Laplace equation, T = pr, where T is wall tension, p is transmural pressure, and r is vessel radius. Because r is so small in the capillaries, the wall tension will not be excessive even when P is elevated. 7. The increased intravascular pressure tends to stretch the arterioles, especially in the feet when the individual is erect. The arteriolar transmural pressure is elevated, and this elicits contraction of the arteriolar vascular smooth muscle by a myogenic mechanism. 8. The endothelium plays a role in the regulation of peripheral resistance (in this patient and in normal individuals) by releasing nitric oxide (a vascular smooth muscle relaxant) in response to a variety of physiologic stimuli. 9. The rales heard at the lung bases are attributable to fluid in the small bronchi (and alveoli) and indicate some pulmonary edema. Fluid in the alveoli can interfere with gas exchange in the lung (especially with O2) and the amount of oxygen taken up by the blood in the lungs. 10. The pulmonary edema is caused by the high pulmonary capillary pressure, which is attributable to the narrowed mitral valve. The left atrial pressure is high because of this valve lesion and because of the pressure generated by the hypertrophied left atrium in response to the obstruction. This high pressure is
transmitted back to the pulmonary vasculature and can be assessed with a catheter threaded into a small pulmonary artery via a peripheral vein. 11.The patient has peripheral edema and ascites because the high hydrostatic pressure in the capillaries exceeds the oncotic pressure and results in capillary filtration into the tissues and abdoninal cavity.The dependent parts of the body (ankles during standing and sacral region during bed rest)have the highest hydrostatic pressure and bence the greatest amount of edema. 12.No.Water and sodiun readily diffuse across capillary neahranes in either direction,regardless of the presence of edema. 13.0 and CO exchange in the peripheral tissue is normal because of the high diffusibility of these gases.Bowever.in the lungs where the alveoli and small bronchi are filled with fluid,orygen diffusion will be impaired. 14.Plasma protein levels in this patient are probably normal:hence,the oncotic pressure is also probably normal.If there is some degree of liver failure caused by liver comgestion plus sone dilution by excessive water retention,the plasma albumin levels could be below normal. 15.If all the capillaries were open.the surface area for capillary filtration would be increased,and edema vould becone rore severe.When tissue pressure reaches levels that equal capillary hydrostatie pressure mimus plasma oncotfe pressure,the edema formation will cease. 16.The movenent of large nolecules between blood and tissue would be slowed by the edema,which increases the diffusion distance between capillaries and parenchymal cells.Some large molecules are transported by pinocytosis,and this process would also be slowed by transport across edematous tissue. 17.The lymphatic vessels carry tissue fluid and extravascular plasma proteins back to the blood stream and hence tend to correct the edema.However,obstruction of lymphaties or (as in the case of this patient)high venous pressure increases edema formation. 18.The heart sounds are irrepular because the patient has atrial fibrillation. In this condition (common in mitral stenosis with a hypertrophied and dilated left
transmitted back to the pulmonary vasculature and can be assessed with a catheter threaded into a small pulmonary artery via a peripheral vein. 11. The patient has peripheral edema and ascites because the high hydrostatic pressure in the capillaries exceeds the oncotic pressure and results in capillary filtration into the tissues and abdominal cavity. The dependent parts of the body (ankles during standing and sacral region during bed rest) have the highest hydrostatic pressure and hence the greatest amount of edema. 12. No. Water and sodium readily diffuse across capillary membranes in either direction, regardless of the presence of edema. 13. O2 and CO2 exchange in the peripheral tissue is normal because of the high diffusibility of these gases. However, in the lungs where the alveoli and small bronchi are filled with fluid, oxygen diffusion will be impaired. 14. Plasma protein levels in this patient are probably normal; hence, the oncotic pressure is also probably normal. If there is some degree of liver failure caused by liver congestion plus some dilution by excessive water retention, the plasma albumin levels could be below normal. 15. If all the capillaries were open, the surface area for capillary filtration would be increased, and edema would become more severe. When tissue pressure reaches levels that equal capillary hydrostatic pressure minus plasma oncotic pressure, the edema formation will cease. 16. The movement of large molecules between blood and tissue would be slowed by the edema, which increases the diffusion distance between capillaries and parenchymal cells. Some large molecules are transported by pinocytosis, and this process would also be slowed by transport across edematous tissue. 17. The lymphatic vessels carry tissue fluid and extravascular plasma proteins back to the blood stream and hence tend to correct the edema. However, obstruction of lymphatics or (as in the case of this patient) high venous pressure increases edema formation. 18. The heart sounds are irregular because the patient has atrial fibrillation. In this condition (common in mitral stenosis with a hypertrophied and dilated left
atriun)nany of the aberrant electrical inpulses arising in the atrium reach the ventricles when the ventricles are in a refractory state and hence do not elicit a ventricular contraction.Atrial impulses boahard the AV node and because of its long refractory period.the irpulses get through at irregular intervals. 19.Because many of the atrial impulses reach the ventricles during different tines in their cycle,inpulses that reach the ventricles when they are only partially filled,yet not refractory,vill elicit a weak comtraction.If the ventricles are only slightly filled when contraction occurs,the left ventricular contraction may not develop enough pressure to force open the aortic valve,and bence not eject any blood.When this occurs,sounds will be heard at the cardiac apex.but no pulse will be felt at the wrist
atrium) many of the aberrant electrical impulses arising in the atrium reach the ventricles when the ventricles are in a refractory state and hence do not elicit a ventricular contraction. Atrial impulses bombard the AV node and because of its long refractory period, the impulses get through at irregular intervals. 19. Because many of the atrial impulses reach the ventricles during different times in their cycle, impulses that reach the ventricles when they are only partially filled, yet not refractory, will elicit a weak contraction. If the ventricles are only slightly filled when contraction occurs, the left ventricular contraction may not develop enough pressure to force open the aortic valve, and hence not eject any blood. When this occurs, sounds will be heard at the cardiac apex, but no pulse will be felt at the wrist