Fundamentals of Cardiac Physiology Quiz

Cardiac output is calculated by multiplying the heart rate (HR) by the stroke volume (SV). This equation represents the amount of blood pumped by the heart per minute. The other options provided do not accurately represent the calculation of cardiac output.

Mean arterial pressure (MAP) is calculated by multiplying cardiac output (CO) by peripheral resistance (PR). This formula takes into account both the amount of blood pumped by the heart and the resistance to blood flow in the peripheral vasculature, providing a comprehensive measure of average pressure in the arteries.

In a healthy heart, cardiac output (CO) should be equal to venous return (VR), indicating an efficient circulation system. Other options do not correctly represent the key properties of a healthy heart.

The first heart sound is produced by the closing of the atrioventricular (A-V) valves, specifically the mitral and tricuspid valves. This event marks the beginning of the systole phase of the cardiac cycle.

The 2nd heart sound occurs during the closure of the aortic and pulmonic valves, not during their opening or any other event mentioned.

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Stroke volume is calculated by subtracting the end systolic volume (ESV) from the end diastolic volume (EDV). This difference represents the amount of blood ejected by the heart during each heartbeat.

End diastolic volume (EDV) is commonly estimated by measuring either end diastolic pressure (preload) or atrial pressure, as they are directly correlated with the volume of blood in the heart at the end of diastole.

Increasing the size of the heart allows it to hold more blood during diastole, leading to an increase in the volume of blood pumped out during systole, which in turn increases stroke volume.

A larger heart can lead to increased ventricular pressure due to the increased muscle mass and volume within the heart chambers.

Increasing the heart rate results in more calcium entering the heart muscle cells, allowing for stronger and more forceful contractions. This increase in calcium influx and release from the sarcoplasmic reticulum (SR) enhances the contractility of the heart, leading to more efficient pumping of blood.

Increasing catecholamine levels in the blood and increasing sympathetic ANS stimulation are known to increase the contractility of the heart by affecting the action of the heart muscles. Decreasing catecholamine levels or sympathetic ANS stimulation would have the opposite effect. Increasing parasympathetic ANS stimulation does not increase heart contractility, as the parasympathetic system generally has a calming effect on the heart.

Cholinergic stimulation leads to a decrease in contractility, which is the opposite effect of sympathetic stimulation that increases contractility. It is important to understand the differences in the effects of parasympathetic and sympathetic stimulation on the heart.

LaPlace's Law is the physical determinant of cardiac pressure development as it describes the relationship between the pressure in a vessel and the tension in its wall. Boyle's Law describes the relationship between the pressure and volume of a gas, Ohm's Law relates to the relationship between current, voltage, and resistance in electrical circuits, and Hooke's Law explains the relationship between the force applied to an elastic object and its corresponding deformation.

LaPlace's law refers to the relationship between the amount of muscle force required and the size of the heart in generating pressure in a ventricle. It does not pertain to the relaxation or contraction of the heart, heart rate regulation, or gas exchange in the lungs.

The heart muscle functions differently compared to skeletal muscle, therefore temporal summation and tetanus, which are mechanisms seen in skeletal muscle, do not apply to the heart. The heart uses other mechanisms to regulate force of contraction.

The heart muscle, unlike skeletal muscle, does not have motor units to recruit for increasing force of contraction. Instead, the heart relies on factors such as preload, afterload, and inotropic agents to modulate its strength of contraction.

The correct answer is sympathetic and parasympathetic as they are the main components of the autonomic nervous system that control the magnitude of force and velocity of contraction for heart muscle. The endocrine system primarily regulates hormones, the central nervous system controls basic body functions, and the renin-angiotensin-aldosterone system regulates blood pressure and fluid balance.

CICR is a process in muscle cells where the influx of calcium triggers the release of more calcium from the sarcoplasmic reticulum through ryanodine receptors. This cascade of events is crucial for muscle contraction as it amplifies the initial calcium signal.

While cardiomyocytes release calcium to initiate muscle contraction, it is not enough to saturate troponin. In contrast, skeletal muscle cells release enough calcium to fully saturate troponin, leading to muscle contraction.

The force of cardiac muscle contraction is primarily regulated by factors such as calcium levels, calcium handling by specific pumps, and changes in cross-bridge kinetics. Factors like oxygen levels, diet, and red blood cell count do not directly influence cardiac muscle contraction.

Ejection fraction is calculated by dividing the difference between End-Diastolic Volume (EDV) and End-Systolic Volume (ESV) by EDV, or by dividing Stroke Volume (SV) by EDV.

Increased venous return results in increased preload, which allows the heart to fill more efficiently and increase its stroke volume, leading to stronger and more forceful contractions.

When the afterload of the heart increases, it becomes harder for the heart to pump effectively, leading to a larger residual volume and changes in the end-diastolic and end-systolic volumes. The stroke volume remains the same, causing the heart to adapt by increasing in size while facing increased wall tension. This adaptation leads to a decrease in the reserve capacity of the heart.

Increased ANS catecholamines lead to various positive changes in heart function, such as improved emptying, decreased end-systolic volume, and increased reserve. These changes are crucial for maintaining proper cardiac performance under stress.

S2 splitting is primarily caused by changes in intrathoracic pressure and ventricular volumes during the cardiac cycle.

Purkinje fibers are specialized cardiac fibers with relatively large diameter and large rapid inward Na current, which allows for rapid conduction of electrical impulses through the heart.