Cardiac Physiology Quiz

The contraction phase of the atria, represented by the P wave on an electrocardiogram (ECG).

The first heart sound, a 'lub' sound, caused by the closure of the mitral and tricuspid valves during isovolumetric ventricular contraction.

The second heart sound, a 'dub' sound, caused by the closure of the aortic and pulmonary valves at the start of isovolumetric relaxation.

A heart sound heard during early diastolic filling, considered normal in children, but pathological in adults, often associated with dilated left ventricles (e.g., cardiomyopathy).

A heart sound heard during late diastole, caused by blood being pushed into a stiff ventricle, often seen in older adults with hypertension or hypertrophic hearts.

The percentage of blood ejected from the ventricle during systole, a measure of the heart's pumping efficiency.

Left Ventricular End Diastolic Volume, the volume of blood in the left ventricle at the end of diastole (before contraction).

Left Ventricular End Systolic Volume, the volume of blood remaining in the left ventricle after ejection during systole (after contraction).

Channels in cell membranes that allow potassium ions (K+) to flow out of the cell, leading to hyperpolarization (making the cell less excitable).

A decrease in heart rate, leading to bradycardia (slow heart rate).

Reduced conduction speed through the AV node, which slows down the transmission of electrical signals in the heart.

The amount of blood the heart pumps per minute. A normal cardiac output is about 5 liters per minute.

The volume of blood pumped out by the heart with each beat.

The driving force behind blood flow, calculated as the difference between Mean Arterial Pressure (MAP) and Central Venous Pressure (CVP).

The sympathetic nervous system increases blood pressure through vasoconstriction and increased heart rate, while the parasympathetic system decreases blood pressure by slowing the heart rate.

RAAS increases blood pressure by causing vasoconstriction and fluid retention through the release of angiotensin II and aldosterone.

Sympathetic activation increases blood pressure by promoting vasoconstriction, increasing heart rate and stroke volume, and boosting blood volume through the RAAS.

Parasympathetic activation decreases blood pressure by decreasing heart rate and stroke volume.

Prostaglandins (PGE, PGI2, PGF), nitric oxide (NO), and endothelium relaxation contribute to blood vessel dilation.

Angiotensin II, calcium ions, thromboxane, bacterial endotoxins, stress, bradykinin, trauma, substance P, acetylcholine, thrombin all contribute to blood vessel constriction.

A common type of fainting caused by a sudden drop in heart rate and blood pressure, often triggered by stress, pain, or prolonged standing.

The atrial contraction phase (P wave on ECG) helps ensure the ventricles are completely filled with blood before contraction.

The 'lub' sound, caused by the closure of the mitral and tricuspid valves during isovolumetric ventricular contraction.

The 'dub' sound, caused by the closure of the aortic and pulmonary valves at the start of isovolumetric relaxation.

A sound during early diastolic filling, normal in children but indicates a problem in adults, often associated with enlarged left ventricle.

A sound heard during late diastole, caused by blood being pushed into a stiff ventricle, often seen in older adults with hypertension.

LVEDV is the volume of blood in the left ventricle before contraction, while LVESV is the volume remaining after contraction. The difference helps determine the heart's efficiency.

Disrupted, irregular blood flow caused by high velocity, narrowed vessels, or plaque buildup.

Digoxin inhibits the Na+/K+ ATPase pump in heart cells, leading to increased intracellular sodium and calcium, which ultimately increases the force of contraction.

Increased force of contraction of the heart muscle, often achieved by medications like digoxin that increase intracellular calcium levels.

The amount of blood pumped by the heart per minute, calculated as the product of stroke volume (SV) and heart rate (HR).

The force driving blood flow, calculated by subtracting CVP from MAP.

Central Venous Pressure, reflecting the pressure in the venous system; usually close to 0 mmHg.

Increases blood pressure by: vasoconstriction (alpha-adrenergic receptors), ↑ heart rate and stroke volume (beta-adrenergic receptors), and increased blood volume (RAAS activation).

Decreases blood pressure by slowing down the heart rate and stroke volume (M2 receptors).

These are reflexes that adjust blood pressure in response to changes in blood pressure detected by receptors in the walls of blood vessels.

Prostaglandins (PGE/PGI2/PGF), Nitric Oxide (NO), and endothelial relaxation can dilate blood vessels.

Angiotensin II, calcium ions, thromboxane, bacterial endotoxins, stress, bradykinin, trauma, substance P, acetylcholine, and thrombin contribute to blood vessel constriction.

Fainting caused by a sudden drop in heart rate and blood pressure, often triggered by stress, pain, or prolonged standing.

The phase of the cardiac cycle where the ventricles are contracting, but the valves are still closed, so the volume inside the ventricles doesn't change.

The phase where the ventricles are relaxing, but the valves are still closed, so the volume doesn't change.

Central Venous Pressure. It represents the pressure in the venous system, typically around 0 mmHg.

The sympathetic nervous system increases blood pressure by constricting blood vessels (vasoconstriction) and increasing heart rate (tachycardia).

The parasympathetic nervous system decreases blood pressure by slowing the heart rate (bradycardia).

Vasoconstriction, narrowing of blood vessels, is caused by Angiotensin II, Calcium ions, Thromboxane, Bacterial endotoxins, Stress, Bradykinin, Trauma, Substance P, Acetylcholine, and Thrombin.

Vasodilation, widening of blood vessels, is caused by Prostaglandins (PGE/PGI2/PGF), Nitric Oxide (NO), and Endothelial relaxation.

Baroreflexes are automatic adjustments in blood pressure that respond to changes in blood pressure detected by receptors in the walls of blood vessels.

The number of heart beats per minute.

Channels in cell membranes allowing potassium ions (K+) to flow out, making the cells less excitable.

Making the cell less likely to fire an action potential.

Hypothyroidism causes a decrease in heart rate (bradycardia).

The electrical vector, representing the overall direction of electrical activity in the heart, moves slightly upward and to the left during ventricular depolarization, signifying the spread of the depolarization wave through the ventricular walls.

The small downward deflection (S wave) on the ECG is generated when the electrical activity moves away from the positive pole, toward the negative electrode, as the depolarization of the ventricles ends.

During ejection, blood is forcefully ejected from the left ventricle into the aorta. This phase begins when the aortic valve opens as left ventricular pressure surpasses the pressure in the aorta.

Stroke Volume is calculated by subtracting the End-Systolic Volume (ESV) from the End-Diastolic Volume (EDV). SV = EDV - ESV

The volume of blood in the ventricle just before it contracts (when the heart is full).

The volume of blood remaining in the ventricle after contraction (after the heart has pumped out blood).

The initial downward deflection (Q wave) indicates the depolarization of the interventricular septum, the wall separating the ventricles.

The sharp upward deflection (R wave) represents the depolarization wave moving towards the apex of the heart.

The return to baseline (S wave) indicates the final depolarization of the ventricles.

An electrocardiogram (ECG) measures the electrical activity of the heart, providing information about the heart's rhythm and electrical conduction.

The interventricular septum is the wall that separates the two ventricles, ensuring that blood flows correctly through the heart.

Depolarization is the electrical process that triggers muscle contraction in the heart.