Cardiac output is defined as stroke volume times heart rate. Stroke volume (the volume of blood pumped out each heart beat) is influenced by preload (the volume of blood in the ventricles at the end of diastole) and afterload (the pressure that the heart must pump against to eject blood). Therefore, by definition, heart rate influences cardiac output, and so do preload and afterload, due to their influence on stroke volume. 

The pulmonary artery is the vessel that leaves the right ventricle and enters into the lung tissue to undergo oxygen exchange. The pulmonary artery is known to be the only artery in the body that does not carry oxygen-rich blood. 

An artery is defined as a vessel that leaves the heart and a vein is a vessel that returns to the heart. The pulmonary artery is the vessel carrying deoxygenated blood away from the heart. 

A "p-wave" in an ECG correlated to depolarization and contraction of the atria of the heart. The duration of the "p-wave" is associated with how low it takes an electrical signal to transfer across an atrium from the sinoatrial node to the atrioventricular node. Therefore, a prolonged "p-wave" can be commonly associated with an enlarged atrium because the electrical signal has further to travel across a dilated chamber.

Beta 1 receptors are the adrenergic receptor on the heart muscle that are responsive to epinephrine and norepinephrine released by the sympathetic nervous system.

Beta 2 adrenergic receptors are primarily located within the pulmonary tissue to cause bronchodilation during a sympathetic response.

Muscarinic cholinergic receptors are present on many tissue types, but are the receptors for acetylcholine rather than epinephrine or norepinephrine.

Alpha 1 adrenergic receptors are present on peripheral blood vessels and respond primarily to norepinephrine to cause vasoconstriction during a sympathetic response.

Alpha 2 adrenergic receptors are special receptors present on the preganglionic sympathetic neuron that help to depress a sympathetic response through negative feedback inhibition.

The tricuspid (atrioventricular) valve separates the right atrium from the right ventricle and prevents back-flow during systole (heart contraction). The path of blood in the heart goes as follows: right atrium, tricuspid valve, right ventricle, pulmonary valve, pulmonary artery, lungs, pulmonary vein, left atrium, mitral valve, left ventricle, aortic valve, aorta, systemic circulation.

Lead II is the limb lead that will show the best view of atrial depolarization. Remember, atrial depolarization starts at the sinoatrial node in the right atrium and spreads through the right and left atria. If you were to draw this on a heart, the net vector would be down (inferiorly) and to the left side of the heart. Also remember, lead II is the lead configuration that runs from the right arm to the left leg. aVR would show a good view of atrial depolarization (although it would be a negative deflection), but it is an augmented lead, not a limb lead. aVL is also an augmented lead.

The diameter of the vessels is the primary determinant of resistance. Our three factors affecting resistance of a vessel are length, viscosity, and diameter. Length of the vessel and viscosity of the blood are relatively constant, so that just leaves diameter. Hematocrit is percentage of blood as red blood cells and would represent viscosity.

Cardiac output is directly proportion to both heart rate and stroke volume. Decreasing ejection fraction decreases stroke volume, which would decrease cardiac output, not increase it.