CORRECT ANSWERS
During the cardiac cycle, which structure directly delivers action potential to the ventricular
myocardium?
a. Sinoatrial (SA) node
b. Atrioventricular (AV) node
c. Purkinje fibres
d. Bundle branches - c. Purkinje fibres
Each cardiac action potential travels from the SA node to the AV node to the bundle of His (AV
bundle), through the bundle branches, and finally to the Purkinje fibres and the ventricular
myocardium, where the impulse is stopped.
The cardiac electrical impulse normally begins spontaneously in the sinoatrial (SA) node because it:
a. Has a superior location in the right atrium.
b. Is the only area of the heart capable of spontaneous depolarization.
c. Has rich sympathetic innervation via the vagus nerve.
d. Depolarizes more rapidly than other automatic cells of the heart - d. Depolarizes more rapidly than
other automatic cells of the heart
The electrical impulse normally begins in the SA node because its cells depolarize more rapidly than
other automatic cells.
What can shorten the conduction time of action potential through the atrioventricular (AV) node?
a. Parasympathetic nervous system
b. Catecholamines
c. Vagal stimulation
d. Sinoatrial node (SA) - b. Catecholamines
,Catecholamines speed the heart rate, shorten the conduction time through the AV node, and
increase the rhythmicity of the AV pacemaker fibers.
If the sinoatrial (SA) node fails, then at what rate (depolarizations per minute) can the
atrioventricular (AV) node depolarize?
a. 60 to 70
b. 40 to 60
c. 30 to 40
d. 10 to 20 - b. 40 to 60
If the SA node is damaged, then the AV node will become the heart's pacemaker at a rate of
approximately 40 to 60 spontaneous depolarizations per minute.
Within a physiologic range, what does an increase in left ventricular end-diastolic volume (preload)
result in?
a. Increase in force of contraction
b. Decrease in refractory time
c. Increase in afterload
d. Decrease in repolarization - a. Increase in force of contraction
This concept is expressed in the Frank-Starling law; the cardiac muscle, like other muscles, increases
its strength of contraction when it is stretched.
As stated in the Frank-Starling law, a direct relationship exists between the _____ of the blood in the
heart at the end of diastole and the _____ of contraction during the next systole.
a. Pressure; force
b. Volume; strength
c. Viscosity; force
d. Viscosity; strength - b. Volume; strength
,As stated in the Frank-Starling law, the volume of blood in the heart at the end of diastole (the length
of its muscle fibers) is directly related to the force (strength) of contraction during the next systole.
What physical sign is the result of turbulent blood flow through a vessel?
a. Increased blood pressure during periods of stress b. Bounding pulse felt on palpation
c. Cyanosis observed on excretion
d. Murmur heard on auscultation - d. Murmur heard on auscultation
Where flow is obstructed, the vessel turns or blood flows over rough surfaces. The flow becomes
turbulent with whorls or eddy currents that produce noise, causing a murmur to be heard on
auscultation, such as occurs during blood pressure measurement with a sphygomanometer.
What is the initiating event that leads to the development of atherosclerosis?
a. Release of the inflammatory cytokines
b. Macrophages adhere to vessel walls.
c. Injury to the endothelial cells that line the artery walls
d. Release of the platelet-deprived growth factor - c. Injury to the endothelial cells that line the
artery walls
Atherosclerosis begins with an injury to the endothelial cells that line the arterial walls. Possible
causes of endothelial injury include the common risk factors for atherosclerosis, such as smoking,
hypertension, diabetes, increased levels of low-density lipoprotein (LDL), decreased levels of high-
density lipoprotein (HDL), and autoimmunity.
What is the effect of oxidized low-density lipoproteins (LDLs) in atherosclerosis?
a. LDLs cause smooth muscle proliferation.
b. LDLs cause regression of atherosclerotic plaques. c. LDLs increase levels of inflammatory cytokines.
d. LDLs direct macrophages to the site in the endothelium. - a. LDLs cause smooth muscle
proliferation.
, Oxidized LDLs are toxic to endothelial cells, cause smooth muscle proliferation, and activate further
immune and inflammatory responses.
When endothelia cells are injured, what alteration contributes to atherosclerosis?
a. The release of toxic oxygen radicals that oxidize low-density lipoproteins (LDLs).
b. Cells are unable to make the normal amount of vasodilating cytokines.
c. Cells produce an increased amount of antithrombotic cytokines.
d. Cells develop a hypersensitivity to homocysteine and lipids. - b. Cells are unable to make the
normal amount of vasodilating cytokines.
Injured endothelial cells become inflamed and cannot make normal amounts of antithrombotic and
vasodilating cytokines.
What effect does atherosclerosis have on the development of an aneurysm?
a. Atherosclerosis causes ischemia of the intima.
b. It increases nitric oxide.
c. Atherosclerosis erodes the vessel wall.
d. It obstructs the vessel. - c. Atherosclerosis erodes the vessel wall
Atherosclerosis is a common cause of aneurysms because plaque formation erodes the vessel wall.
What is the usual source of pulmonary emboli?
a. Deep venous thrombosis
b. Endocarditis
c. Valvular disease
d. Left heart failure - a. Deep venous thrombosis
Pulmonary emboli originate in the venous circulation (mostly from the deep veins of the legs) or in
the right heart.