Topic 6: Chpt 14 Flashcards

1
Q

What is broken heart syndrome, and how can it be fatal?

A

Broken heart syndrome, also known as stress cardiomyopathy, occurs when sudden, intense emotional stress triggers the release of stress hormones like adrenaline, which can overwhelm the heart. Although typically temporary, in severe cases, this syndrome can lead to heart muscle failure and potentially be fatal due to the acute stress on the cardiovascular system.

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2
Q

What are capillaries and who discovered them?

A

Capillaries are microscopic blood vessels where exchanges of gases, nutrients, and wastes occur between blood and tissues. They were first observed by Marcello Malpighi, an Italian anatomist, in the seventeenth century using a microscope,

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3
Q

How did William Harvey contribute to the understanding of the cardiovascular system?

A

William Harvey revolutionized cardiovascular physiology by demonstrating that blood circulates in a closed loop within the body, driven by the heart. He showed that the heart and veins had valves ensuring one-way blood flow, and that the liver was not the source of continuous blood production, debunking longstanding misconceptions about blood circulation and organ functions.

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4
Q

What is the significance of the discovery that blood recirculates in the body?

A

The discovery that blood recirculates, rather than being continuously consumed and produced, was pivotal. It corrected the fundamental misunderstandings about how blood traveled through the body and the roles of different organs in the circulatory process, laying the groundwork for modern cardiovascular physiology and medical practices.

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5
Q

What is the primary function of the cardiovascular system?

A

The primary function of the cardiovascular system is to transport nutrients, water, gases, and wastes to and from all parts of the body. It ensures that essential substances like oxygen and nutrients are delivered to cells and metabolic wastes are carried away for excretion.

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6
Q

How does the cardiovascular system contribute to cell-to-cell communication?

A

The cardiovascular system facilitates cell-to-cell communication by transporting hormones, which are secreted by endocrine glands and travel in the blood to their target cells. It also carries nutrients like glucose and fatty acids to cells, supporting metabolic activities.

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7
Q

What role does the cardiovascular system play in the body’s defense?

A

It transports white blood cells and antibodies throughout the body, helping to detect and eliminate foreign invaders.

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8
Q

How does the cardiovascular system manage heat distribution in the body?

A

The cardiovascular system manages heat distribution by carrying heat through the blood from the body core to the surface, where it can dissipate, helping to regulate body temperature. The cardiovascular system

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9
Q

What happens to the brain when blood flow is interrupted, and why?

A

Interruption of blood flow to the brain leads to loss of consciousness within 5-10 seconds and can cause permanent brain damage if oxygen delivery stops for 5-10 minutes. This is because brain neurons have high oxygen needs that cannot be met through anaerobic metabolism, making them extremely sensitive to hypoxia.

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10
Q

What are the major components of the cardiovascular system?

A

The cardiovascular system consists of the heart (the pump), blood vessels (tubes), and the blood itself (fluid). It includes arteries that carry blood away from the heart and veins that return blood to the heart.

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11
Q

How is blood flow directed in the cardiovascular system?

A

Blood flow in the cardiovascular system is directed by a system of valves in the heart and veins, ensuring one-way flow much like turnstiles at an amusement park prevent reverse movement.

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12
Q

What is the role of the heart in the cardiovascular system?

A

The heart functions as two independent pumps divided by a septum. The right side pumps deoxygenated blood to the lungs for oxygenation, while the left side pumps oxygenated blood to the rest of the body.

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13
Q

Describe the pathway of blood through the cardiovascular system starting from the right atrium.

A

Blood enters the right atrium, flows to the right ventricle, then to the lungs via the pulmonary arteries (pulmonary circulation). Oxygenated blood returns to the left atrium via pulmonary veins, moves to the left ventricle, and is pumped out through the aorta to the body (systemic circulation).

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14
Q

What is the significance of the color change in cardiovascular diagrams from blue to red?

A

In diagrams, blue indicates deoxygenated blood and red indicates oxygenated blood. This convention helps visualize the oxygenation process in the lungs and the delivery of oxygen-rich blood to the body.

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15
Q

What is the function of the coronary circulation?

A

The coronary circulation consists of coronary arteries and veins that supply blood to and drain blood from the heart muscle itself, ensuring it receives the necessary oxygen and nutrients for its functions.

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16
Q

Explain the hepatic portal system.

A

The hepatic portal system is a unique blood route in which the vein from the digestive tract flows directly to the liver instead of entering the general circulation. This allows the liver to process and detoxify nutrients and substances before they circulate throughout the body.

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17
Q

What is a portal system, and where can it be found in the body?

A

A portal system involves two capillary networks connected directly by a vein. Examples include the hepatic portal system between the digestive tract and liver, the renal portal system in the kidneys, and the hypothalamic-hypophyseal portal system linking the hypothalamus with the anterior pituitary.

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18
Q

What is the mechanistic explanation for blood flow in the cardiovascular system?

A

Mechanistically, blood flows because the heart creates a high-pressure area when it contracts, pushing blood into the blood vessels where the pressure is lower. Blood then flows down this pressure gradient, moving from areas of higher pressure to lower pressure.

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19
Q

How is blood pressure maintained throughout the cardiovascular system?

A

Blood pressure is highest in the aorta and systemic arteries as they receive blood from the left ventricle and decreases throughout the circuit, reaching its lowest just before blood re-enters the heart at the venae cavae. This gradient is due to friction between the blood and the vessel walls.

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20
Q

What physical laws govern the flow of blood in the cardiovascular system?

A

By laws that describe the interaction of pressure, volume, flow, and resistance. These principles are similar to those governing the flow of any liquid or gas and are crucial for understanding how blood moves through the body.

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21
Q

What is hydrostatic pressure in the context of the cardiovascular system?

A

Hydrostatic pressure is the force that a fluid in a static state exerts on the walls of its container. In the cardiovascular system, even though the blood is moving, the term hydrostatic pressure is used to describe the pressure exerted by the blood on the vessel walls, measured commonly in mm Hg.

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22
Q

How is pressure measured in the cardiovascular system, and what are the equivalents?

A

Pressure in the cardiovascular system is typically measured in millimeters of mercury (mm Hg). One mm Hg is equivalent to the pressure exerted by a 1-mm column of mercury. Other units include torr, which is equal to 1 mm Hg, and centimeters of water, where 1 cm H2O equals 0.74 mm Hg.

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23
Q

What happens to pressure in a system where fluid is moving, such as the cardiovascular system?

A

In a moving fluid system like the cardiovascular system, pressure decreases over distance due to energy loss from friction. The pressure has two components: a dynamic component related to the kinetic energy of moving fluid and a lateral component, which is the hydrostatic (or potential energy) pressure exerted on the walls of the vessels.

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24
Q

Why might textbooks use “hydraulic pressure” instead of “hydrostatic pressure” to describe blood pressure?

A

Some textbooks prefer “hydraulic pressure” over “hydrostatic pressure” for describing pressure in the cardiovascular system because hydraulics deals with fluids in motion, making it a more accurate term for systems like blood circulation where the fluid (blood) is continuously moving.

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25
Q

What happens when the walls of a fluid-filled container, like a balloon, contract?

A

When the walls of a fluid-filled container contract, the pressure within the container increases because the fluid (which is minimally compressible like water) transmits the pressure uniformly. This can cause the container to deform or even burst if the pressure is too high, similar to squeezing a water balloon.

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26
Q

How is the contraction of the heart’s ventricles analogous to squeezing a water balloon?

A

The contraction increases the pressure on the blood within, which is then forced out into the blood vessels, displacing blood with lower pressure. This process is termed the driving pressure and is essential for propelling blood through the cardiovascular system.

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27
Q

How do volume changes in the heart and blood vessels affect blood pressure?

A

Volume changes in the heart and blood vessels significantly influence blood pressure. When the heart expands during relaxation, the pressure decreases. Similarly, dilation of blood vessels leads to a drop in blood pressure, while constriction increases it, affecting overall circulatory system dynamics.

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28
Q

How is blood flow related to pressure gradients in the cardiovascular system?

A

Blood flow is directly proportional to the pressure gradient (∆P) across the vascular system, which is the difference in pressure between two points (P1 - P2). This means that higher pressure differences result in greater blood flow, irrespective of the absolute pressures involved.

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29
Q

What does it mean if there is no pressure gradient in a fluid system?

A

If there is no pressure gradient in a fluid system, meaning that the pressure at all points is equal, there will be no flow of fluid through the system. This illustrates the necessity of a pressure differential to drive fluid movement within tubes or blood vessels.

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30
Q

What is “resistance” in the context of the cardiovascular system?

A

In the cardiovascular system, resistance is the force that opposes the flow of blood through the vessels. It is determined by factors such as the viscosity of the blood, the length of the blood vessels, and most importantly, the radius of the vessels. An increase in resistance leads to a decrease in blood flow.

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31
Q

How does the resistance of a blood vessel affect blood flow?

A

Blood flow through a vessel is inversely proportional to the vessel’s resistance. This means that if resistance increases, blood flow decreases, and vice versa. This relationship is critical in regulating how blood circulates through the body.

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32
Q

What are the primary factors that influence blood vessel resistance according to Poiseuille’s law?

A

According to Poiseuille’s law, blood vessel resistance is influenced by three main factors: the length of the vessel (L), the viscosity of the blood (η), and the radius of the vessel (r). The most impactful of these is the radius, as resistance changes with the fourth power of the radius.

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33
Q

How does the radius of a blood vessel affect its resistance and consequently blood flow?

A

The resistance offered by a blood vessel changes inversely with the fourth power of its radius. A small decrease in the radius of a vessel significantly increases resistance, thereby reducing blood flow, while a small increase in the radius can drastically decrease resistance, enhancing flow.

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34
Q

What is the relationship between blood flow, pressure gradient, and resistance in the cardiovascular system?

A

Blood flow (Flow) in the cardiovascular system is directly proportional to the pressure gradient (∆P) and inversely proportional to resistance (R). Mathematically, this is expressed as Flow ∝ ∆P/R. This formula shows that flow increases with a higher pressure gradient or lower resistance, and decreases with a lower pressure gradient or higher resistance.

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35
Q

How do vasoconstriction and vasodilation affect blood flow?

A

Vasoconstriction, the narrowing of blood vessels, increases resistance and decreases blood flow through the vessel. Conversely, vasodilation, the widening of blood vessels, decreases resistance and increases blood flow. These mechanisms are vital for regulating blood flow and pressure within the cardiovascular system.

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36
Q

What is “flow rate” in cardiovascular physiology?

A

Flow rate, often referred to simply as “flow,” is the volume of blood that passes a given point in the cardiovascular system per unit of time. It is typically measured in liters per minute (L/min) or milliliters per minute (mL/min).

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37
Q

How does “velocity of flow” differ from “flow rate” in the cardiovascular system?

A

Velocity of flow, or simply velocity, is the speed at which blood moves past a given point and is measured by the distance a fixed volume of blood travels in a given period of time. In contrast, flow rate measures the volume of blood that flows past a point in a given period.

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38
Q

What is the relationship between flow rate, velocity, and cross-sectional area in a blood vessel?

A

The velocity of flow through a blood vessel is determined by the equation
𝑣 = 𝑄/𝐴, where 𝑣 is the velocity, 𝑄 is the flow rate, and 𝐴 is the cross-sectional area. Velocity is directly proportional to flow rate and inversely proportional to the cross-sectional area of the vessel.

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39
Q

How does the velocity of blood flow vary with the diameter of the blood vessel?

A

In a blood vessel, if the flow rate remains constant, the velocity of flow varies inversely with the diameter. This means that blood flows faster through narrower sections of a vessel and slower through wider sections.

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40
Q

What is the effect of vessel diameter on the velocity of flow, demonstrated by the behavior of a leaf in a stream?

A

In narrower sections of a stream, where the cross-sectional area is smaller, a leaf will move rapidly due to the higher velocity of the water. Conversely, in wider sections where the area is larger, the velocity decreases and the leaf moves more slowly.

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41
Q

What is Mean Arterial Pressure (MAP) and what factors influence it?

A

Mean Arterial Pressure (MAP) is the primary driving force for blood flow in the cardiovascular system. It is influenced by cardiac output (the volume of blood pumped by the heart per minute) and peripheral resistance (the resistance offered by blood vessels to blood flow).

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42
Q

Explain the relationship of MAP to cardiac output and peripheral resistance.

A

Mean arterial pressure is directly proportional to both cardiac output and peripheral resistance. An increase in either cardiac output or peripheral resistance will lead to an increase in MAP, thereby affecting blood flow throughout the cardiovascular system.

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43
Q

What is the significance of the heart’s structure as an inverted cone?

A

The heart is structured like an inverted cone with the apex pointing downward and the base facing upward. This orientation is crucial because it positions the heart optimally within the thoracic cavity, with the apex resting on the diaphragm and the base at the level of the sternum.

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44
Q

What is the function of the pericardium?

A

The pericardium is a tough membranous sac that encases the heart. It contains pericardial fluid, which lubricates the heart’s surface, reducing friction during heartbeats. Inflammation of this sac, known as pericarditis, can lead to decreased lubrication and a friction rub sound.

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45
Q

Describe the myocardium and its significance.

A

The myocardium is the heart muscle, primarily responsible for the pumping action of the heart. It is composed of cardiac muscle cells that contract to eject blood from the ventricles, and it is regulated by the heart’s electrical conduction system.

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46
Q

How is blood flow directed in the heart?

A

Blood enters the heart through the atria and flows into the ventricles through one-way valves. The right ventricle pumps blood to the lungs via the pulmonary trunk, while the left ventricle pumps it to the body via the aorta. Valves at the exits of the ventricles prevent backflow.

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47
Q

Explain the relationship between the heart’s anatomy and its contraction pattern.

A

The heart’s tubular embryonic development causes a twist, positioning arteries near the top of the ventricles. This arrangement necessitates that ventricles contract from bottom to top, efficiently pushing blood out. Four fibrous connective tissue rings around the valves not only provide structural support but also act as electrical insulators, ensuring coordinated contractions.

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48
Q

How does the heart’s electrical insulator system function?

A

The fibrous connective tissue around the heart valves serves as an electrical insulator, preventing the direct transmission of electrical signals between the atria and ventricles. This ensures that signals are channeled through the heart’s specialized conduction system, leading to efficient, coordinated contractions.

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49
Q

What is the primary function of the atrioventricular (AV) valves in the human heart?

A

The atrioventricular (AV) valves primarily prevent the backward flow of blood from the ventricles to the atria during ventricular contraction. Located at the opening between each atrium and its corresponding ventricle, these valves ensure unidirectional blood flow within the heart, critical for maintaining efficient cardiac output and pressure dynamics.

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50
Q

Describe the structural components of atrioventricular (AV) valves and their mechanism of operation.

A

AV valves consist of flaps of fibrous tissue connected at their base to a connective tissue ring. These flaps are tethered to papillary muscles by chordae tendineae, collagenous tendons. When ventricles contract, blood pushes against the flaps, closing the valve. Chordae tendineae prevent the valve from prolapsing (inverting into the atria), thus maintaining proper closure during the high-pressure phase of the cardiac cycle.

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51
Q

What are the differences between the tricuspid and mitral valves in terms of structure and naming?

A

The tricuspid valve, situated between the right atrium and ventricle, consists of three tissue flaps and is responsible for controlling blood flow on the heart’s right side. The mitral or bicuspid valve, located between the left atrium and ventricle, has two flaps and is named for its resemblance to a bishop’s miter (a type of ceremonial headwear). This structural distinction corresponds with the different physiological pressures and volumes handled by each side of the heart.

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52
Q

Explain the function and structural uniqueness of semilunar valves in the heart.

A

Semilunar valves, comprising the aortic and pulmonary valves, are located at the exits of the ventricles leading into the aorta and pulmonary artery, respectively. Each valve has three crescent-moon-shaped leaflets that fit together tightly when closed. These valves open to allow blood to exit the heart and snap shut to prevent backflow, operating without the need for chordae tendineae due to their unique shape and the support of arterial pressure.

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53
Q

How does valve prolapse affect heart function, and what are the primary causes?

A

Valve prolapse occurs when the valve flaps are pushed back into the atrium during ventricular contraction, usually due to malfunction or degradation of the chordae tendineae. This condition disrupts normal blood flow, potentially leading to regurgitation (reverse blood flow), which can decrease cardiac efficiency and increase the heart’s workload, leading to further complications if not managed effectively.

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54
Q

How are the atrioventricular and semilunar valves different in terms of their response to pressure changes during the cardiac cycle?

A

AV valves respond passively to changes in blood pressure: they open when atrial pressure exceeds ventricular pressure during diastole and close when ventricular pressure rises during systole. Semilunar valves also operate passively but are influenced by the pressure in the arteries they feed into; they open when ventricular pressure exceeds arterial pressure and close when it drops below arterial pressure, ensuring efficient ejection of blood from the heart and preventing backflow.

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55
Q

What is the coronary circulation and why is it significant?

A

The coronary circulation refers to the network of arteries and veins that provide blood supply directly to the heart muscle. It is crucial for delivering oxygen and nutrients to the heart itself, ensuring that the heart maintains the robust function required for its pumping action. The coronary arteries encircle the heart near its base, resembling a crown, which is reflected in the term “coronary.”

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56
Q

Describe the paths of the major coronary arteries.

A

The right coronary artery (RCA) originates from the aorta and encircles the right side of the heart, supplying the right atrium, most of the right ventricle, some of the left ventricle, and the posterior part of the interventricular septum. The left coronary artery (LCA) also starts at the aorta and branches into the circumflex artery and the anterior interventricular artery (LAD), supplying the left atrium, most of the left ventricle, interventricular septum, and parts of the right ventricle.

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57
Q

How does venous blood return from the coronary circulation to the heart?

A

Venous blood from the coronary circulation returns mainly through cardiac veins that drain into the coronary sinus located on the posterior aspect of the heart, which then empties directly into the right atrium. Additionally, smaller blood channels within the heart muscle and some veins from the anterior right ventricle also drain directly into the heart chambers.

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58
Q

Why is venous blood from the coronary circulation particularly low in oxygen content?

A

Cardiac muscle consumes an exceptionally high percentage of the oxygen delivered by the blood, estimated at 70–80%, which is more than double that used by other cells. This high consumption rate reflects the heart’s intense energy demands, particularly during periods of increased activity.

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59
Q

What are the consequences of reduced myocardial blood flow?

A

Reduced blood flow to the myocardium, often caused by blockage of a coronary artery or extremely low blood pressure, can lead to severe damage or death of heart muscle tissue. This underscores the critical nature of maintaining proper coronary circulation to support the heart’s continuous and demanding function.

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60
Q

What is the composition of the heart and the unique property of its muscle cells?

A

The heart is mostly made up of cardiac muscle cells, or myocardium. About 1% of these are specialized autorhythmic cells that generate action potentials spontaneously, allowing the heart to contract without external signals. This myogenic property enables the heart to beat even when disconnected from the body.

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61
Q

What are autorhythmic cells and their function in the heart?

A

Autorhythmic cells, also known as pacemaker cells, are specialized myocardial cells that set the heartbeat rate. They are smaller, contain few contractile fibers, and lack organized sarcomeres, contributing minimally to contractile force but crucially regulating the heart’s rhythm.

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62
Q

How does cardiac muscle differ structurally from skeletal muscle?

A

Cardiac muscle fibers are smaller than skeletal muscle fibers, generally containing a single nucleus. They form a complex network by branching and joining end-to-end at intercalated disks, which include desmosomes for physical connection and gap junctions for electrical connectivity, facilitating synchronized contraction.

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63
Q

How does cardiac muscle compare to skeletal and smooth muscle?

A

Unlike skeletal muscle, cardiac muscle has larger t-tubules, a smaller sarcoplasmic reticulum, and relies partially on extracellular calcium for contraction, similar to smooth muscle. It also resembles single-unit smooth muscle in how cells are electrically connected, allowing unified contraction.

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64
Q

What reflects the high energy demand of cardiac muscle cells?

A

Cardiac contractile fibers have mitochondria occupying about one-third of their cell volume, a reflection of the high energy requirements needed to sustain continuous heart contractions. This dense mitochondrial presence supports the intensive metabolic demands of cardiac tissue.

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65
Q

How does excitation-contraction coupling (EC coupling) initiate in cardiac muscle?

A

In cardiac muscle, EC coupling begins with an action potential originating spontaneously from the heart’s pacemaker cells. This action potential spreads to contractile cells via gap junctions, triggering the EC coupling process.

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66
Q

What role does calcium play in cardiac muscle contraction?

A

The action potential triggers voltage-gated L-type Ca²⁺ channels on the sarcolemma and t-tubules, allowing extracellular Ca²⁺ to enter the cell. This influx of Ca²⁺ then triggers ryanodine receptor (RyR) Ca²⁺ release channels on the sarcoplasmic reticulum, releasing stored Ca²⁺ into the cytosol, a process known as Ca²⁺-induced Ca²⁺ release (CICR).

67
Q

Describe the process of Ca²⁺-induced Ca²⁺ release in cardiac muscle.

A

When extracellular Ca²⁺ enters through L-type channels, it activates RyR channels on the sarcoplasmic reticulum, causing a release of stored Ca²⁺ into the cytosol, known as a Ca²⁺ “spark.” These sparks summate to create a full Ca²⁺ signal necessary for muscle contraction.

68
Q

How does calcium initiate contraction in cardiac muscle?

A

Calcium ions released into the cytosol bind to troponin, triggering crossbridge cycling between actin and myosin, similar to the sliding filament model seen in skeletal muscle. This interaction causes muscle contraction.

69
Q

How does relaxation occur in cardiac muscle?

A

Relaxation occurs when cytoplasmic Ca²⁺ levels decrease, allowing Ca²⁺ to unbind from troponin. Myosin releases actin, and the muscle fibers return to their relaxed state. Ca²⁺ is pumped back into the sarcoplasmic reticulum by Ca²⁺-ATPase and removed from the cell by the Na⁺/Ca²⁺ exchanger (NCX).

70
Q

What ion exchanges occur during cardiac muscle relaxation?

A

During relaxation, the Na⁺/Ca²⁺ exchanger (NCX) removes Ca²⁺ from the cell in exchange for Na⁺ entering down its electrochemical gradient. The Na⁺ that accumulates is then removed by the Na⁺/K⁺-ATPase, maintaining cellular ion balance and preparing the cell for the next contraction.

71
Q

What are graded contractions in cardiac muscle, and how do they differ from skeletal muscle contractions?

A

Graded contractions in cardiac muscle allow the muscle fiber to vary the force of contraction based on the amount of Ca²⁺ bound to troponin, unlike skeletal muscle where contraction is all-or-none. This mechanism allows cardiac muscle to adjust its force output according to varying demands.

72
Q

How does calcium influence the force of contraction in cardiac muscle?

A

In cardiac muscle, the force of contraction is proportional to the amount of Ca²⁺ that binds to troponin. Higher cytosolic Ca²⁺ concentrations result in more active crossbridges, increasing the contraction force. Additional extracellular Ca²⁺ entering the cell can trigger further release from the sarcoplasmic reticulum, amplifying the contraction.

73
Q

How does sarcomere length affect the force of contraction in cardiac muscle?

A

Sarcomere length at the onset of contraction influences the force generated by cardiac muscle. Stretching of cardiac fibers, due to increased blood volume in the heart’s chambers, enhances the sensitivity of troponin to Ca²⁺, allowing stronger contractions. This relationship is critical for the heart’s ability to adjust its pumping force in response to changes in blood volume.

74
Q

What is the physiological significance of stretch in cardiac muscle fibers?

A

Stretch in cardiac muscle fibers, corresponding to the volume of blood in the heart, enhances the contractile force by increasing Ca²⁺ sensitivity of the muscle. This mechanism, part of the Frank-Starling law of the heart, ensures that the heart pumps out an equivalent volume of blood as it receives, maintaining efficient circulation.

75
Q

What role does calcium (Ca²⁺) play in the action potentials of cardiac muscle?

A

In cardiac muscle, unlike in neurons and skeletal muscle, Ca²⁺ entry plays a crucial role in prolonging the action potential, contributing to the unique plateau phase. This extended action potential prevents tetanus and ensures the heart muscles relax between contractions.

76
Q

Describe the phases of the action potential in myocardial contractile cells.

A
  • Phase 0 (Depolarization): Rapid opening of voltage-gated Na⁺ channels, Na⁺ influx, cell depolarizes to +20 mV.
  • Phase 1 (Initial Repolarization): Na⁺ channels close, K⁺ exits the cell.
  • Phase 2 (Plateau): Ca²⁺ permeability increases and K⁺ permeability decreases, voltage-gated Ca²⁺ channels open, creating a plateau.
  • Phase 3 (Rapid Repolarization): Ca²⁺ channels close, “slow” K⁺ channels open, K⁺ exits rapidly, returning to resting potential.
  • Phase 4 (Resting Membrane Potential): Stable resting potential at about -90 mV.
77
Q

Compare the duration of action potentials in myocardial contractile cells to those in neurons and skeletal muscle.

A

Myocardial contractile cells have a much longer action potential duration (about 200 msec or more) compared to neurons and skeletal muscle fibers (1-5 msec). This longer duration is crucial for preventing tetanus in the heart, allowing time for the heart chambers to refill with blood.

78
Q

Why are long action potentials important in cardiac muscle?

A

Long action potentials in cardiac muscle ensure that the refractory period and contraction phase almost coincide, preventing the possibility of summation and tetanus. This allows the heart to relax fully between contractions, vital for effective blood pumping.

79
Q

How does the action potential duration in cardiac muscle prevent tetanus?

A

In cardiac muscle, the extended action potential and refractory period duration overlap with muscle contraction duration. This timing ensures that by the time a second action potential can occur, the muscle has almost fully relaxed, preventing any overlapping contractions (summation) and thus tetanus.

80
Q

What unique properties allow myocardial autorhythmic cells to generate spontaneous action potentials?

A

Myocardial autorhythmic cells possess an unstable membrane potential called pacemaker potential, which continuously drifts from -60 mV toward the threshold, triggering spontaneous action potentials without input from the nervous system.

81
Q

What is a pacemaker potential and how is it maintained in myocardial autorhythmic cells?

A

A pacemaker potential is an unstable membrane potential that slowly depolarizes until it reaches the threshold to fire an action potential. This is maintained by the unique ion flow through If channels, which are permeable to both K⁺ and Na⁺, allowing a net influx of positive ions and gradual depolarization.

82
Q

Describe the role of If channels in the pacemaker potential of autorhythmic cells.

A

If channels, also known as funny current channels or HCN channels, open at negative potentials around -60 mV. They allow Na⁺ to flow into the cell more than K⁺ flows out, causing a net positive charge influx and gradual depolarization toward threshold.

83
Q

How does calcium influence the action potentials of myocardial autorhythmic cells?

A

As the membrane potential of autorhythmic cells becomes more positive, If channels close and voltage-gated Ca²⁺ channels open, accelerating depolarization. This calcium influx drives the cell to threshold, initiating the steep depolarization phase of the action potential.

84
Q

What causes the repolarization phase in myocardial autorhythmic cells?

A

Repolarization occurs when Ca²⁺ channels close and slow K⁺ channels open, allowing K⁺ to leave the cell. This efflux of K⁺ restores the negative membrane potential, similar to the repolarization process in other excitable cells.

85
Q

How can the heart rate be influenced by changes in the pacemaker cells?

A

The heart rate is determined by the rate of depolarization in pacemaker cells. Modifying the permeability of these cells to various ions can alter the duration of the pacemaker potential and thereby adjust the heart rate.

86
Q

How do autorhythmic cells trigger the heart’s pumping action?

A

Autorhythmic cells generate spontaneous action potentials that spread through myocardial cells via gap junctions, ensuring synchronized contraction necessary for effective heart pumping.

87
Q

Describe how electrical signals coordinate contractions in the heart.

A

Electrical signals initiate at the sinoatrial (SA) node and spread through internodal pathways to the atrioventricular (AV) node, then to the ventricles via the AV bundle and Purkinje fibers, coordinating sequential contraction of atria and ventricles.

88
Q

What are the components of the heart’s specialized conducting system?

A

The heart’s conducting system includes the SA node, AV node, AV bundle (bundle of His), bundle branches, and Purkinje fibers, which rapidly transmit electrical signals throughout the heart.

89
Q

What is the function of the SA node in the heart?

A

The SA node acts as the primary pacemaker of the heart, initiating depolarization that triggers heartbeats, located in the right atrium.

90
Q

How do electrical signals travel through the heart, and what are the speeds involved?

A

Signals start at the SA node, slow at the AV node (to allow complete atrial contraction), then speed through the AV bundle and Purkinje fibers up to 4 m/sec for coordinated ventricular contraction.

91
Q

Why is the AV node crucial for coordinating heart contractions?

A

The AV node serves as the only electrical connection between the atria and ventricles, providing a delay to ensure atria contract fully before ventricles, optimizing efficient blood pumping from the apex to the base.

92
Q

What mechanical function does the AV node delay serve during heart contractions?

A

The delay allows ventricles time to fill completely with blood from the atria before they begin to contract, ensuring effective upward pumping of blood towards the major arteries.

93
Q

Why must the electrical signals travel to the apex of the heart before ventricular contraction begins?

A

Directing signals to the apex ensures that contraction starts at the bottom, pushing blood upwards towards the exits at the base, similar to squeezing from the bottom of a toothpaste tube.

94
Q

What establishes the hierarchy among the heart’s pacemakers?

A

The SA node usually sets the heart’s pace due to its faster rhythm compared to other pacemaker cells like the AV node or Purkinje fibers. If the SA node fails, the next fastest pacemaker takes over.

95
Q

What is the role and typical firing rate of the SA node?

A

The SA node acts as the primary pacemaker of the heart, setting the rhythm at about 70 beats per minute, guiding the overall heart rate.

96
Q

What happens if the SA node fails?

A

If the SA node fails, the AV node often takes over as the pacemaker at a slower rate of 50 beats per minute. If the AV node also fails, Purkinje fibers may set the pace at 25-40 beats per minute.

97
Q

How can multiple pacemakers affect heart function?

A

In cases like complete heart block, different parts of the heart may follow different pacemakers, leading to desynchronized contractions and a potentially inefficient heartbeat.

98
Q

Describe the condition and consequences of complete heart block.

A

Complete heart block occurs when signals from the SA node can’t reach the ventricles, causing atria and ventricles to beat at different rates. This often results in a significantly slower and potentially inadequate ventricular rhythm.

99
Q

Why might a mechanical pacemaker be necessary?

A

Mechanical pacemakers are used to maintain a sufficient heart rate when the heart’s natural pacemakers are unable to maintain a rate adequate to support effective blood circulation, especially in cases of severe arrhythmias or heart block.

100
Q

How does electrical signal propagation change in complete heart block?

A

In complete heart block, electrical signals from the atria do not reach the ventricles, which then rely on slower ventricular pacemakers, leading to a lower heart rate.

101
Q

What is an ECG and how does it record heart activity?

A

An ECG (electrocardiogram) records the summed electrical activity of the heart using surface electrodes. It captures the composite of all action potentials from the heart’s cells, providing a non-invasive look at cardiac function.

102
Q

Who is considered the father of modern ECG and what contributions did he make?

A

Walter Einthoven is known as the father of modern ECG. He named the parts of the ECG, refined the technique in the early 20th century, and created “Einthoven’s triangle” to conceptualize electrode placement.

103
Q

Describe Einthoven’s triangle and its relevance to ECG recording.

A

Einthoven’s triangle is a hypothetical triangle formed around the heart with electrodes on both arms and the left leg. It helps in understanding the leads in ECG recording, with each side of the triangle representing a pair of electrodes.

104
Q

What defines a lead in an ECG and how does it affect the ECG wave?

A

In an ECG, a lead refers to the use of two electrodes, one acting as positive and the other as negative. The direction of electrical waves relative to these electrodes determines whether the ECG wave points up or down.

105
Q

What are the major waves in an ECG and what do they represent?

A

The P wave represents atrial depolarization, the QRS complex signifies ventricular depolarization, and the T wave indicates ventricular repolarization. Atrial repolarization is hidden within the QRS complex.

106
Q

How can the direction of an ECG wave vary and why?

A

The direction of ECG waves, such as the P and T waves, depends on the direction of current flow relative to the lead axis. This is why similar physiological events (depolarization vs. repolarization) can appear as upward or downward deflections in different leads.

107
Q

Compare the amplitude of ventricular action potentials to that of ECG signals.

A

A ventricular action potential involves a voltage change around 110 mV, whereas the amplitude of an ECG signal is much smaller, about 1 mV by the time it reaches the body’s surface.

108
Q

Why can’t you determine the type of cardiac event (depolarization or repolarization) solely from the ECG wave direction?

A

The shape of ECG waves relative to the baseline does not inherently indicate depolarization or repolarization. Their appearance is influenced by the direction of current flow relative to the electrode setup.

109
Q

What initiates a cardiac cycle in an ECG?

A

The cardiac cycle in an ECG starts with atrial depolarization and includes a series of electrical events that trigger mechanical heart actions like contraction and relaxation.

110
Q

How is atrial depolarization represented in an ECG, and what follows it?

A

Atrial depolarization is marked by the P wave on an ECG. Atrial contraction begins during the latter part of the P wave and continues into the P-R segment.

111
Q

What occurs during the P-R segment of an ECG?

A

During the P-R segment, the electrical signal slows as it passes through the AV node, allowing time for the atria to complete their contraction before ventricular contraction begins.

112
Q

When do ventricular depolarization and contraction occur in the cardiac cycle?

A

Ventricular depolarization begins just after the Q wave, and contraction continues through the T wave, as indicated by the QRS complex.

113
Q

What does the T wave represent in an ECG, and what follows it?

A

The T wave represents ventricular repolarization. It is followed by ventricular relaxation during the T-P segment, when the heart is electrically quiet.

114
Q

Why are multiple leads used when recording an ECG?

A

Multiple leads provide different electrical ‘views’ of the heart, much like viewing a car from different angles. This helps in assessing different regions of the heart for comprehensive diagnostic information

115
Q

What is the significance of a 12-lead ECG in clinical settings?

A

A 12-lead ECG is standard for thorough cardiac assessment as it uses various combinations of electrodes to provide detailed insights into the heart’s electrical activity and health.

116
Q

What are the primary benefits of using an ECG in medical diagnostics?

A

ECGs are crucial diagnostic tools because they are quick, painless, and noninvasive, providing essential data on the heart’s electrical function without breaking the skin

117
Q

How is heart rate determined using an ECG?

A

Heart rate on an ECG is typically measured from the start of one P wave to the start of the next, or from one R wave peak to the next. A normal resting rate is 60-100 bpm, with variations for athletes and conditions like tachycardia or bradycardia

118
Q

How is heart rhythm evaluated on an ECG?

A

Heart rhythm is assessed by checking if the heartbeats occur at regular intervals. Irregular rhythms, or arrhythmias, may indicate issues ranging from benign extra beats to serious conditions like atrial fibrillation.

119
Q

What does the presence and form of waves on an ECG indicate?

A

Analyzing an ECG involves ensuring all normal waves (P, QRS, T) are present in recognizable forms. Any abnormalities might indicate underlying heart issues.

120
Q

What does the relationship between QRS complexes and P waves reveal in an ECG?

A

Each P wave should be followed by a QRS complex. A constant P-R interval suggests normal signal conduction. Variability or absence of QRS post-P wave might indicate AV node conduction problems, like heart block.

121
Q

What are some pathologies that can be identified through subtle changes in an ECG?

A

Changes in wave shape, timing, or duration on an ECG can point to issues like conduction velocity changes, heart enlargement, or tissue damage from ischemia.

122
Q

What are cardiac arrhythmias and how are they identified on an ECG?

A

Arrhythmias are electrical issues in heart rhythm or conduction visible on ECGs, ranging from benign dropped beats to severe premature ventricular contractions (PVCs).

123
Q

What is Long QT Syndrome (LQTS) and how is it related to ECG?

A

LQTS is an alteration in the QT interval due to genetic defects in ion channels or membrane proteins like ankyrin-B. It can also be induced by medications that affect K+ channels, such as the now-banned antihistamine Seldane.

124
Q

Why is monitoring the QT interval important in clinical settings?

A

Monitoring the QT interval is crucial for detecting potential life-threatening conditions like LQTS, which can lead to arrhythmias and sudden cardiac events.

125
Q

What are the five phases of the cardiac cycle?

A

1) Heart at rest: atrial and ventricular diastole, 2) Completion of ventricular filling: atrial systole, 3) Early ventricular contraction and first heart sound, 4) The heart pumps: ventricular ejection, 5) Ventricular relaxation and second heart sound.

126
Q

What happens during the heart at rest phase?

A

Both atria and ventricles are relaxed. Atria fill with blood from the veins, and ventricles fill with blood from the atria via open AV valves, driven by gravity and atrial pressure.

127
Q

What occurs during atrial systole?

A

Atrial contraction pushes the remaining 20% of blood into the ventricles, increasing ventricular volume to the end-diastolic volume (EDV). A small amount of blood may also flow back into the veins, observed as a jugular pulse

128
Q

Describe the early phase of ventricular contraction and its associated heart sound.

A

As ventricles contract, blood pressure closes the AV valves, creating the ‘lub’ sound (S1). This phase is isovolumic as ventricular volume remains constant due to closed AV and semilunar valves.

129
Q

What is ventricular ejection?

A

Ventricles continue contracting, generating enough pressure to open the semilunar valves, allowing blood to be ejected into the arteries. This phase determines the stroke volume and the arterial pressure.

130
Q

What happens during ventricular relaxation?

A

Ventricles repolarize and relax, decreasing internal pressure. When ventricular pressure drops below arterial pressure, semilunar valves close, creating the ‘dup’ sound (S2). This phase is also isovolumic until AV valves reopen.

131
Q

How does the cardiac cycle continue after ventricular relaxation?

A

As ventricular pressure falls below atrial pressure, AV valves reopen, allowing blood accumulated in the atria to rush into the ventricles, marking the start of a new cardiac cycle.

132
Q

Why is it significant that blood remains in the ventricles at the end of each contraction?

A

The end-systolic volume (ESV) provides a safety margin that allows the heart to increase its output during more forceful contractions. This ensures that even under stress, the heart can efficiently supply additional blood to the body

133
Q

How is stroke volume (SV) calculated?

A

Stroke volume is the amount of blood pumped by one ventricle during a contraction, calculated as EDV minus ESV (End-Diastolic Volume - End-Systolic Volume).

134
Q

What is ejection fraction and how is it calculated?

A

Ejection fraction is the percentage of the end-diastolic volume (EDV) that is ejected with each ventricular contraction. It is calculated as (stroke volume / EDV) * 100%.

135
Q

How does stroke volume vary with the heart’s contraction force?

A

Stroke volume increases with the force of ventricular contractions. For example, during exercise, both stroke volume and ejection fraction increase, enabling more blood to be pumped to meet the body’s increased oxygen demand.

136
Q

How does stroke volume relate to cardiac output (CO)?

A

Stroke volume is a key component in determining cardiac output, which is calculated by multiplying heart rate by stroke volume. This measure indicates the volume of blood pumped by one ventricle in a given period.

137
Q

How can the effectiveness of the heart as a pump be assessed?

A

Cardiac output provides a measure of the heart’s effectiveness as a pump by indicating the total volume of blood pumped by one ventricle per minute. This is crucial for assessing overall blood flow through the body.

138
Q

What initiates heart rate in humans?

A

Heart rate is initiated by autorhythmic cells in the SA node and is modulated by both neural and hormonal input.

139
Q

How does parasympathetic activity affect heart rate?

A

Parasympathetic activity, through the neurotransmitter acetylcholine, slows heart rate by increasing K+ permeability (hyperpolarizing the cell) and decreasing Ca2+ permeability. This delays the pacemaker potential’s depolarization, increasing the time taken to reach threshold and slowing down the heart rate.

140
Q

What effect does sympathetic stimulation have on heart rate?

A

Sympathetic stimulation increases heart rate by enhancing cation flow through I f and Ca2+ channels in pacemaker cells, speeding up the depolarization rate, and causing faster action potential firing. Catecholamines like norepinephrine and epinephrine activate β1 adrenergic receptors, increasing heart rate.

141
Q

How do neurotransmitters influence the ion channels in pacemaker cells?

A

Acetylcholine increases potassium permeability and decreases calcium permeability, slowing heart rate. Norepinephrine and epinephrine increase the permeability of sodium and calcium, speeding up heart rate. They act through a cAMP second messenger system that affects the ion channel properties.

142
Q

Describe the role of tonic control in regulating heart rate.

A

Tonic control is typically dominated by parasympathetic activity, which slows the intrinsic rate of SA node depolarization (90-100 bpm) to achieve the resting heart rate (70 bpm). Sympathetic activity is required to increase the heart rate above the intrinsic rate.

143
Q

How do autonomic branches alter conduction through the AV node?

A

Acetylcholine decreases the conduction speed, increasing AV node delay and slowing heart rate. Catecholamines increase the conduction speed, reducing AV node delay and speeding up heart rate.

144
Q

What is stroke volume in cardiac physiology?

A

Stroke volume is the amount of blood pumped by one ventricle during a contraction, measured in milliliters per beat. It is calculated as the difference between end-diastolic volume (EDV) and end-systolic volume (ESV).

145
Q

What factors determine the force of ventricular contraction?

A

The force of ventricular contraction is influenced by the length of the muscle fibers at the beginning of contraction (determined by EDV) and the contractility of the heart, which is the intrinsic ability of cardiac muscle fibers to contract and is influenced by Ca2+ interaction with contractile filaments.

146
Q

How does the length of cardiac muscle fibers affect stroke volume?

A

According to the length-tension relationship, the longer the cardiac muscle fiber and sarcomere at the onset of contraction, the greater the tension and stroke volume. Increased ventricular wall stretch from additional blood volume leads to a more forceful contraction.

147
Q

Describe the Frank-Starling law of the heart.

A

The Frank-Starling law states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end-diastolic volume), thereby increasing the fiber length of cardiac muscle prior to contraction. This means the heart will automatically pump out more blood if more blood flows in.

148
Q

What are the primary factors that affect venous return to the heart?

A

Venous return is influenced by (1) the skeletal muscle pump, which uses muscle contractions to push blood towards the heart, (2) the respiratory pump, which utilizes pressure changes during breathing to enhance blood flow to the heart, and (3) sympathetic innervation of veins, which induces venous constriction and increases blood return.

149
Q

How do the skeletal and respiratory pumps enhance venous return?

A

The skeletal muscle pump compresses veins during muscle contractions, aiding blood flow to the heart, especially during activity. The respiratory pump lowers thoracic pressure and raises abdominal pressure during inhalation, promoting blood flow from the abdomen to the thorax.

150
Q

How does sympathetic activity affect venous return?

A

Sympathetic activation causes veins to constrict, decreasing their volume and pushing more blood towards the heart, thus increasing EDV and the subsequent force of contraction. This redistribution supports more forceful cardiac output during sympathetic stimulation.

151
Q

What are inotropic agents?

A

Inotropic agents are chemicals that affect the contractility of cardiac muscle. Positive inotropic agents increase the force of contraction, while negative inotropic agents decrease it.

152
Q

Which chemicals are known to have positive inotropic effects?

A

Catecholamines like epinephrine and norepinephrine, along with drugs such as digitalis, enhance cardiac contractility and are considered positive inotropic agents.

153
Q

How do catecholamines enhance cardiac contractility?

A

Catecholamines bind to β1 adrenergic receptors, increasing cyclic AMP, which phosphorylates voltage-gated Ca2+ channels. This increases their opening and the amount of Ca2+ entering the cell, leading to stronger contractions.

154
Q

What role does phospholamban play in cardiac muscle?

A

Phospholamban regulates the Ca2+ ATPase in the sarcoplasmic reticulum. When phosphorylated by catecholamines, it enhances Ca2+ uptake into the sarcoplasmic reticulum, increasing Ca2+ available for muscle contraction.

155
Q

How do cardiac glycosides increase cardiac contractility?

A

Cardiac glycosides, such as digitoxin, inhibit the Na+ K+ ATPase, leading to increased Na+ in the cell. This reduces the efficiency of the Na+ Ca2+ exchanger, causing an increase in cytosolic Ca2+, which enhances the force of contraction.

156
Q

What are the negative effects of using cardiac glycosides?

A

While effective in increasing cardiac contractility, cardiac glycosides are highly toxic and can depress Na+ K+ ATPase activity across all cells, not just cardiac cells, potentially leading to severe side effects.

157
Q

How does the length-tension relationship affect cardiac contractility?

A

Similar to skeletal muscle, cardiac muscle exhibits a length-tension relationship where increased sarcomere length (due to increased ventricular filling) enhances sensitivity to Ca2+, thereby increasing contractility.

158
Q

What is afterload in the context of cardiac function?

A

Afterload refers to the resistance the heart must overcome to eject blood during ventricular contraction. It includes the resistance provided by arterial blood pressure and the arterial system’s compliance

159
Q

Can you provide an analogy to explain afterload?

A

Imagine a waiter pushing a tray through a swinging door: the tray represents the load of blood in the ventricles (EDV), and the door represents the arterial resistance (afterload). If the door has additional resistance (like furniture stacked against it), more force is required, similar to increased afterload in the heart.

160
Q

What conditions can lead to an increase in afterload?

A

Elevated arterial blood pressure and reduced compliance of the aorta are common conditions that increase afterload, requiring the heart to exert more force during ventricular contraction.

161
Q

What are the consequences of chronically increased afterload?

A

Chronic high afterload can lead to myocardial hypertrophy, where the heart’s ventricular walls thicken, increasing the heart muscle’s need for oxygen and ATP, potentially leading to heart disease.

162
Q

How is afterload clinically assessed?

A

Clinicians often use arterial blood pressure as an indirect measure of afterload. Echocardiography can also assess ventricular function and detect changes such as ventricular wall thickening due to increased afterload.

163
Q

How is echocardiography used in assessing heart function?

A

Echocardiography uses ultrasound waves to visualize heart structures. It can show heart chamber enlargement, valve malfunctions, and abnormal heart wall movements, and measure ejection fraction.