Beachey: Respiratory Care Anatomy and Physiology, 2nd Edition

Answers to Concept Questions

Chapter 19: Control of Cardiac Output and Hemodynamic Measurements

19-1	Congestive failure engorges and stretches myocardial fibers, increasing the preload.

19-2	Drugs causing vasoconstriction increase resistance to ventricular output, increasing left ventricular afterload.

19-3	Calcium channel blockers impede Ca++ entry into the cell during myocardial contraction. Because Ca++ is necessary for the actin-myosin excitation-contraction reaction, Ca++ blockers diminish the force of contraction and thus the ejection fraction.

19-4	Pure right ventricular failure causes blood to back up into the right atrium, vena cavae, and systemic venous system. Signs include distended jugular veins and peripheral edema, especially lower leg and ankle edema. Left ventricular failure causes blood to back up into the left atrium, pulmonary veins, and pulmonary capillaries. Signs and symptoms include pulmonary edema and shortness of breath. Pulmonary capillary wedge pressure is elevated in left ventricular failure but is normal in pure right ventricular failure. Combined right- and left-sided heart failure produces dyspnea, as well as peripheral and pulmonary edema.

19-5	Pulmonary vascular resistance increases the difference between pulmonary artery end-diastolic pressure (PAEDP) and pulmonary capillary wedge pressure (PCWP) because the site of resistance lies between the two points at which these pressures are measured; PAEDP would rise, but PCWP would not be affected.

19-6	Decreased left ventricular contractility causes blood to back up into the pulmonary capillaries and ultimately the pulmonary artery. Thus mean pulmonary artery pressure rises.

19-7	Anything that obstructs the free flow of blood between the right ventricle and left atrium increases the mean pulmonary artery pressure–pulmonary capillary wedge pressure difference. Examples are pulmonary emboli, hypoxic pulmonary vasoconstriction, and loss of pulmonary capillary bed cross-sectional area (emphysema). All of these conditions increase pulmonary vascular resistance.

19-8	If blood volume and valvular function are normal, high pulmonary capillary wedge pressure implies that the left ventricle is not pumping blood effectively.

19-9	In left ventricular failure, compensatory vasoconstriction attempts to sustain the blood pressure in the face of a decreasing cardiac output. This aggravates the failure of an already weakened ventricle. Drugs that cause vasodilation reduce systemic vascular 
resistance, allowing the weak left ventricle to pump more blood with each stroke. The increased stroke volume and cardiac output tend to minimize the decrease in blood pressure that tends to occur when vasodilators are administered.

19-10	Drugs that cause vasodilation decrease the resistance against which the left ventricle must pump; thus although calcium channel–blocking drugs decrease the heart’s contractility, stroke volume and cardiac output do not necessarily decrease.