Visceral Phys Exam II

Frank = LVEV increases systemic venous return

A heart rate of 60-100/minute represents normal sinus rhythm. This means that the electrical impulses in the heart are being generated and conducted properly, resulting in a regular heartbeat within the normal range. Sinus bradycardia refers to a heart rate below 60/minute, while sinus tachycardia refers to a heart rate above 100/minute. Therefore, the correct answer is normal sinus rhythm.

A weak myocardium would not result in a decrease if bradycardia is involved.

A decrease in venous return refers to a decrease in the amount of blood returning to the heart from the body's veins. This reduction in blood volume leads to a decrease in the amount of blood that the heart can pump out with each beat, known as stroke volume. Therefore, it is logical to conclude that a decrease in venous return will decrease subsequent stroke volume.

The normal axis of the heart refers to the average direction of the electrical activity as it travels through the heart during each heartbeat. This is measured in degrees. A normal axis falls between -30 degrees and +90 degrees. A measurement of 60 degrees falls within this range, indicating a normal axis.

The Frank-Starling Law of the heart states that the force of contraction of the heart increases as the volume of blood in the ventricles increases. This means that when systemic venous return increases, there is an increase in the volume of blood returning to the heart, leading to an increase in left ventricular ejection volume. Therefore, the given statement best correlates with the Frank-Starling Law.

During Phase 0 of the myocardial action potential, there is an increase in sodium ion influx. This phase is known as the depolarization phase, where the membrane potential rapidly rises due to the opening of voltage-gated sodium channels. This influx of sodium ions leads to the rapid depolarization of the cardiac cells, allowing for the initiation of the action potential and subsequent contraction of the heart muscle.

Angiotensinogen is synthesized in the liver and is converted to Angiotensin I by the enzyme Renin that is released from the granular cells in the afferent arterioles of the glomeruli.

Sodium helps maintain blood volume by regulating fluid balance in the body. It plays a crucial role in maintaining proper hydration levels and preventing dehydration. Sodium helps in retaining water in the bloodstream, which increases blood volume. This is important for maintaining adequate blood pressure and ensuring that blood can effectively transport oxygen and nutrients to the body's tissues and organs.

During the plateau phase of the myocardial action potential, there is a sustained influx of calcium ions into the cardiac cells. This influx of calcium ions prolongs the depolarization phase and maintains the cell in a depolarized state, allowing for the contraction of the cardiac muscle. The influx of calcium ions also triggers the release of additional calcium ions from the sarcoplasmic reticulum, leading to the contraction of the myocardium. Therefore, calcium plays a crucial role in the plateau phase of the myocardial action potential.

Arteriolar constriction refers to the narrowing of the arterioles, which are small blood vessels that regulate blood flow. This constriction is mediated by alpha-adrenergic receptors, which are found on the smooth muscle cells of the arterioles. When these receptors are activated by the neurotransmitter norepinephrine or epinephrine, they cause the smooth muscle cells to contract, leading to vasoconstriction. Muscarinic ACh receptors, nicotinic ACh receptors, and beta-adrenergic receptors do not play a direct role in arteriolar constriction.

Arteriolar constriction is not caused by Nicotinic, muscarinic, or beta-adrenergic receptors.

Renin is an enzyme released by the kidneys in response to low blood pressure or low blood volume. Its primary function is to convert angiotensinogen into angiotensin I. Unlike the other options listed, renin does not directly cause arteriolar constriction. Instead, it initiates a series of reactions that eventually lead to the production of angiotensin II, a potent vasoconstrictor. Therefore, renin indirectly contributes to arteriolar constriction, but it does not directly cause it.

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The speed of conduction in myocardial action potential is fastest in the Purkinje system.

A decrease in venous return will decrease subsequent stroke volume because venous return refers to the amount of blood returning to the heart from the periphery. If there is a decrease in venous return, it means that less blood is being returned to the heart, resulting in a decrease in the amount of blood available to be pumped out of the heart with each contraction (stroke volume). Therefore, a decrease in venous return will lead to a decrease in subsequent stroke volume.

The correct answer is "only a and b above are correct". Myocardial tissues function as syncitia due to their branched nature of the myocardial fiber and the presence of cell to cell communication pathways. The branched nature allows for coordinated contraction of the heart, while the cell to cell communication pathways allow for electrical impulses to spread rapidly throughout the tissue, ensuring synchronized contractions. The presence of a large number of mitochondria is important for providing energy to the myocardial cells, but it is not directly related to their function as syncitia.

The speed of conduction of the myocardial action potential is fastest in the Purkinje system. The Purkinje fibers are specialized cardiac muscle fibers that rapidly conduct electrical impulses throughout the ventricles, allowing for coordinated and efficient contraction of the heart. These fibers have a larger diameter and more gap junctions, which facilitate faster conduction compared to other parts of the conduction system such as the AV node or SA node. The Bundle of His and AV Node also contribute to conduction, but they are slower compared to the Purkinje system.

A weak myocardium can lead to a decrease in left ventricular ejection volume, which means that the heart is not able to pump as much blood out of the left ventricle with each contraction. This can result in a decrease in the overall amount of blood being pumped out of the heart and circulated throughout the body. Peripheral and pulmonary edema can also occur as a result of a weak myocardium. Edema is the accumulation of fluid in the tissues, and when the heart is not able to effectively pump blood, fluid can build up in the extremities (peripheral edema) and in the lungs (pulmonary edema).

Calcium ions play a crucial role in myocardial contractions. They bind to proteins in the muscle cells, causing the muscle fibers to contract. The major source of calcium ions for these contractions is the extracellular fluid. Calcium ions are present in higher concentrations in the extracellular fluid compared to other cellular compartments such as mitochondria, sarcoplasmic reticulum, or endoplasmic reticulum. Therefore, the extracellular fluid is the primary source of calcium ions for myocardial contractions.

Hyper-aldosteronism is a condition characterized by excessive production of aldosterone hormone by the adrenal glands. Aldosterone plays a crucial role in regulating sodium and potassium levels in the body. In hyper-aldosteronism, there is increased reabsorption of sodium and increased excretion of potassium in the kidneys, leading to hypokalemia (low potassium levels). Low blood volume can occur due to increased sodium reabsorption, and hypotension (low blood pressure) can result from the overall decrease in blood volume. Therefore, all of the above symptoms are commonly seen in a person with hyper-aldosteronism.

An increase in vagal tone refers to an increase in activity of the vagus nerve, which is responsible for regulating the parasympathetic nervous system. Activation of the parasympathetic nervous system typically leads to a decrease in heart rate and blood pressure. Therefore, an increase in vagal tone would not cause systemic blood pressure to rise, making it the exception among the given options.

Stimulation of mACh receptors in the SA node will not increase systemic blood pressure because mACh receptors are muscarinic receptors that bind to acetylcholine, which has an inhibitory effect on the heart. Activation of mACh receptors in the SA node leads to a decrease in heart rate, resulting in a decrease in cardiac output and therefore a decrease in systemic blood pressure.

Sympathetic stimulation is responsible for the "fight or flight" response, which causes vasoconstriction in most blood vessels, including the coronary arteries. This vasoconstriction reduces blood flow to the heart muscle, which can be detrimental in certain situations, such as during a heart attack. Therefore, sympathetic stimulation does not cause coronary vasodilation.

Arteriolar diameter in the cutaneous vascular bed is predominantly dependent upon sympathetic tone. This means that the constriction or dilation of the arterioles in the cutaneous vessels is mainly regulated by the sympathetic nervous system. The sympathetic tone can cause vasoconstriction, reducing blood flow to the skin, or vasodilation, increasing blood flow to the skin. This regulation helps in controlling body temperature and redistributing blood flow during various physiological conditions.

Phase 0 is influx of Na(sodium),
Phase 1 is Potassium
Phase 2 is plateau at, slow influx of Ca
Phase 3 is rapid repolarization, rapid efflux of K
Phase 4 is Na moves out, potassium in, Na/K pump

Atrial Natriuretic Peptide (ANP) is the correct answer because it is a hormone released by the atria of the heart in response to increased blood volume and pressure. ANP acts on the kidneys to increase the excretion of sodium (Na+) and water, thereby reducing blood volume and pressure. This hormone promotes the excretion of Na+ by inhibiting the reabsorption of sodium in the renal tubules, leading to increased urinary sodium excretion.

Sympathetic stimulation activates the sympathetic nervous system, which leads to various physiological responses. One of these responses is an increase in stroke volume, which refers to the amount of blood pumped out of the heart with each contraction. This increase in stroke volume subsequently leads to an increase in cardiac output, which is the total amount of blood pumped by the heart per minute. Additionally, sympathetic stimulation causes systemic vasodilation, which is the widening of blood vessels throughout the body. These responses help to increase blood flow and oxygen delivery to the tissues, making the statement true.

The tubulo-glomerular feedback mechanism is a process that helps to regulate urine formation. Renin is an enzyme that plays a crucial role in this mechanism. It is released by specialized cells in the kidneys in response to low blood pressure or low sodium levels. Renin acts on a protein called angiotensinogen to convert it into angiotensin I, which is then converted to angiotensin II by angiotensin converting enzyme. Angiotensin II causes vasoconstriction and stimulates the release of aldosterone, which promotes sodium reabsorption in the kidneys. This mechanism helps to maintain blood pressure and fluid balance in the body.

The slow depolarization in cells of the sino-atrial node is due to the influx of sodium ions. This is because the sino-atrial node is responsible for initiating the electrical signals that regulate the heartbeat. During the slow depolarization phase, the membrane potential gradually becomes more positive, leading to the generation of an action potential. This slow depolarization is primarily mediated by the influx of sodium ions through specific ion channels in the cell membrane.

Sympathetic stimulation typically results in vasoconstriction, which narrows the blood vessels and reduces blood flow. Since coronary vasodilation refers to the widening of the blood vessels in the coronary arteries, sympathetic stimulation would not cause this response. Therefore, sympathetic stimulation will not cause coronary vasodilation.

Angiotensin II is not normally involved in the Tubulo-Glomerular Feedback mechanism to regulate Glomerular Filtration Rate. The Tubulo-Glomerular Feedback mechanism involves the cells of the macula densa and granular cells of the afferent arteriole. The macula densa senses the sodium concentration in the distal tubule and sends signals to the granular cells. The granular cells then release renin, which leads to the production of angiotensin II. Angiotensin II constricts the efferent arteriole, increasing the glomerular filtration rate. Therefore, angiotensin II is not a part of the feedback mechanism itself, but rather a downstream mediator of the response.