A 63-year-old man comes to the office due to exertional dyspnea that has been progressively worsening over the last 3 weeks. He sleeps in a recliner with his head elevated because he gets short of breath when lying flat in bed. Medical history includes gout, dyslipidemia, and hypertension. Blood pressure is 154/89 mm Hg and pulse is 85/min. Physical examination shows distended jugular veins in the semi-recumbent position. An apical heave is present on cardiac examination. There is pitting edema in the bilateral lower extremities. Levels of which of the following substances will be higher in the pulmonary vein compared to the pulmonary artery in this patient?

Question

A 63-year-old man comes to the office due to exertional dyspnea that has been progressively worsening over the last 3 weeks.  He sleeps in a recliner with his head elevated because he gets short of breath when lying flat in bed.  Medical history includes gout, dyslipidemia, and hypertension.  Blood pressure is 154/89 mm Hg and pulse is 85/min.  Physical examination shows distended jugular veins in the semi-recumbent position.  An apical heave is present on cardiac examination.  There is pitting edema in the bilateral lower extremities.  Levels of which of the following substances will be higher in the pulmonary vein compared to the pulmonary artery in this patient?

Quizplus · Accepted Answer

11ec160b_3a84_4172_9249_9d49e39b6ddc_MD0001_00 This patient's exertional dyspnea, orthopnea (dyspnea when lying flat), jugular venous distension, cardiac heave, and peripheral edema are consistent with decompensated heart failure. The decreased cardiac output in heart failure reduces renal perfusion, which stimulates renin secretion by the juxtaglomerular cells of the kidney (Choice H) in a maladaptive effort to maintain effective blood volume and organ perfusion. Renin acts to convert angiotensinogen (produced by the liver) into angiotensin I in the systemic circulation (Choices B and E). Angiotensin I is then converted to angiotensin II, primarily within the small pulmonary vessels, by endothelial-bound angiotensin-converting enzyme. Because of the pulmonary location of angiotensin conversion, levels of angiotensin II are higher in the pulmonary vein (on the way out of the lungs) than in the pulmonary artery (on the way into the lungs). Angiotensin II is a potent vasoconstrictor of the systemic circulation and causes a rise in blood pressure (increased afterload) that worsens cardiac output. It also acts on the adrenal glands to stimulate aldosterone release, causing sodium retention and further worsening of volume overload (Choice A). (Choice D) The angiotensinases are a group of enzymes found in multiple tissues and are responsible for the breakdown of angiotensin II and other structurally similar enzymes. (Choice F) Arginine vasopressin (antidiuretic hormone) is released from the posterior pituitary in response to high serum osmolality or decreased arterial blood volume. Because reduced cardiac output causes the body to perceive hypovolemia, antidiuretic hormone secretion is typically increased in heart failure. (Choice G) Prostaglandins are produced in multiple cell types, including endothelial cells, mast cells, and macrophages. Prostaglandin E1 is a potent vasodilator that maintains patency of the ductus arteriosus and causes afferent arteriolar vasodilation in the kidneys. Educational objective: The reduced cardiac output in heart failure leads to decreased renal perfusion and consequent stimulation of the renin-angiotensin-aldosterone system in a maladaptive effort to maintain effective blood volume. Inactive angiotensin I is converted into active angiotensin II by endothelial-bound angiotensin-converting enzyme in the lungs.

A 63-Year-Old Man Comes to the Office Due to Exertional