Beachey: Respiratory Care Anatomy and Physiology, 2nd Edition

Answers to Concept Questions

Chapter 16: Functional Anatomy of the Cardiovascular System

16-1	In a tension pneumothorax of the left lung, pressure builds up in the left pleural space crowding the lung and mediastinum—including the heart—toward the right side of the chest; thus the heart’s point of maximal impulse on the chest wall shifts to the right.

16-2	A leaking mitral valve would allow blood to flow backward (regurgitate) into the left atrium with each ventricular contraction, increasing mean left atrial pressure and ultimately pulmonary capillary pressure. High pulmonary capillary pressure could lead to pulmonary edema, which would interfere with pulmonary gas exchange.

16-3	Extremely high heart rates shorten ventricular diastolic time, leading to inadequate ventricular filling. Consequently, the ventricles eject smaller stroke volumes.

16-4	Because calcium ions are necessary for myocardial contraction, drugs that block their entry into the muscle fiber (calcium channel blockers) diminish the heart’s force of contraction, which in turn diminishes the heart’s oxygen demands.

16-5	Overdistension may stretch the myocardial muscle fibers so much that some actin-myosin cross-bridges disengage; as a result, the number of these bridges that can participate in muscle contraction decreases, diminishing the heart’s force of contraction.

16-6	An increased afterload (i.e., an increased resistance to stroke volume ejection) with no change in preload or contractility would result in a decreased stroke volume.

16-7	A drug that blocks parasympathetic activity would increase the heart rate because the inhibiting effect of parasympathetic stimulation would be removed.

16-8	Arterial wall rigidity would increase the difference between systolic and diastolic pressures (i.e., pulse pressure would be increased). The expansion of normally compliant arteries keeps systolic pressure from rising too high, and normal arterial recoil force keeps diastolic pressure from falling too low. Rigid arteries cannot expand normally to accommodate the stroke volume; hence systolic pressures would rise sharply. During diastole, diminished arterial wall recoil would allow diastolic pressure to decrease abruptly.

16-9	A decongestant drug constricts small arterioles feeding the mucosal capillary beds. This limits blood flow into the capillaries, diminishing their pressures and shrinking their sizes. Lowered capillary pressure allows capillaries to absorb edema fluid from the interstitial spaces, shrinking the mucosa.

16-10	Patient B has the greatest degree of peripheral vascular resistance, as shown by the higher diastolic pressure. High peripheral vascular resistance slows the arteriole runoff rate so much that diastolic pressure does not have enough time to fall to normal levels before the next ventricular contraction.

16-11	Positive pressure in the chest limits venous blood return to the heart, possibly preventing a poorly contracting heart from receiving more blood than it can pump effectively. A sudden withdrawal of mechanical ventilation removes the impediment to venous return, possibly overwhelming the heart with increased blood flow; thus discontinuing mechanical ventilation might precipitate acute congestive heart failure in patients with poor ventricular function.

16-12	Beta-receptor stimulators cause vasodilation, and alpha-receptor blockers prevent alpha-mediated vasoconstriction; thus both types of drugs might benefit the patient with high systemic vascular resistance.

16-13	Angiotensin-converting enzyme (ACE) inhibitors prevent the formation of angiotensin II, a vasoconstrictor. Thus ACE inhibitors are antihypertensive drugs used to control high blood pressure.