Trivia: Cardiac Pharmacology Exam! Quiz

The correct answer is SA node - atrium - AV node - purkinje fibres - ventricle. This is the correct sequence of conduction through the heart. The SA node, or sinoatrial node, located in the right atrium, initiates the electrical signal. The signal then travels through the atria, causing them to contract. Next, the signal reaches the AV node, or atrioventricular node, located between the atria and ventricles. The AV node delays the signal slightly, allowing the atria to fully contract before the ventricles receive the signal. From the AV node, the signal travels through the bundle of His and then into the purkinje fibers, which spread the signal throughout the ventricles. Finally, the ventricles contract, pumping blood out of the heart.

Sodium channels remain depolarized for only a few milliseconds. This means that the sodium channels open and allow sodium ions to enter the cell for a very short period of time before closing again. This depolarization is necessary for the generation of action potentials, which are the electrical signals that allow nerve cells to communicate with each other. If the sodium channels remained depolarized for longer periods of time, it could disrupt the proper functioning of the nervous system.

The correct answer is "spontaneous, intrinsic rhythm generated by the SA node cells". The SA node, also known as the sinoatrial node, is located in the right atrium of the heart and is often referred to as the natural pacemaker of the heart. It generates electrical impulses that regulate the heart's rhythm and initiate each heartbeat. These impulses cause the atria to contract and then travel to the AV node, which conducts the electrical signals to the ventricles, causing them to contract as well. Therefore, the SA node is responsible for setting the pace of the heart's contractions.

The presence of calcium channels in the SA and AV nodes, rather than sodium channels, means that the action potential and time for repolarization are prolonged. This is because calcium channels have a slower conduction compared to sodium channels. This prolonged action potential and repolarization time can have an impact on the heart rate and rhythm, potentially leading to tachycardias or arrhythmias.

The SA node is the natural pacemaker of the heart, responsible for initiating the electrical signals that regulate the heart's rhythm. However, if the SA node becomes damaged or dysfunctional, other cardiac tissues, such as the AV node, can take on the role of a pacemaker. This allows the heart to continue generating electrical signals and maintaining a regular rhythm, even if the SA node is not functioning properly. This serves as a safety mechanism to prevent the heart from stopping or experiencing severe arrhythmias if the SA node fails.

L-type channels are the main voltage-dependent calcium channels in the heart. They play a crucial role in the working myocardium and specialized conducting regions of the heart. These channels are responsible for the influx of calcium ions into cardiac cells during the action potential, which triggers muscle contraction and regulates the electrical signals that coordinate the heart's pumping action. By increasing the transmission rate of electrical signals, L-type channels contribute to the proper functioning of the heart and the regulation of cardiac contraction.

Ectopic pacemakers are abnormal pacemaker cells that can generate electrical impulses in the heart. When these pacemakers fire inappropriately, meaning they fire at a faster rate than the normal pacemaker cells, it can lead to tachyarrhythmias. Tachyarrhythmias are abnormal heart rhythms characterized by a fast heart rate. Therefore, the problem with ectopic pacemakers is that if they're inappropriately firing, they can cause tachyarrhythmias.

Stage 0 in B represents the rapid depolarization of the cell membrane, which is caused by the rapid influx of sodium ions. During this stage, the cell membrane potential rapidly shifts from negative to positive as sodium ions enter the cell, leading to the initiation of an action potential.

In ventricular muscle, delayed after-depolarization refers to a depolarization that occurs after the completion of an action potential. This abnormal depolarization can trigger additional action potentials, leading to ventricular tachycardia (VT). Abnormally raised Ca2+ levels can cause an influx of ions, disrupting the normal electrical activity of the heart and triggering abnormal action potentials. This can result in VT. Therefore, the main cause of delayed after-depolarization in ventricular muscle is abnormally raised Ca2+.

After the rapid depolarization phase, the cell starts to undergo partial repolarization. This occurs as the sodium channels begin to close, allowing the cell to partially repolarize. The closure of sodium channels and partial repolarization are closely linked, as the sodium channels closing is what allows the cell to start repolarizing. Therefore, all of the given options are correct explanations for what follows rapid depolarization.

Various factors can disrupt the order of sinus rhythm. Anatomic heart disease refers to structural abnormalities in the heart that can interfere with the normal electrical conduction system. Myocardial infarction, commonly known as a heart attack, can damage the heart muscle and disrupt the normal rhythm. Drugs, including certain medications or substances like alcohol and caffeine, can have an impact on the electrical activity of the heart. Circulating hormones, such as thyroid hormones or adrenaline, can also influence the heart's rhythm. Age can also be a contributing factor as the electrical system of the heart may become less efficient with age.

During the repolarization phase of an action potential, the closure of calcium channels stops the influx of calcium ions into the cell. This is followed by the re-opening of potassium channels, allowing potassium ions to flow out of the cell. The efflux of potassium ions leads to the restoration of the cell's negative membrane potential, which is necessary for repolarization. Therefore, the closure of calcium channels and the re-opening of potassium channels and efflux of ions are the triggers for repolarization.

The rapid depolarization of the myocardium occurs at a membrane potential voltage of around -60mV. This means that when the membrane potential reaches -60mV, there is a sudden and significant change in the electrical charge across the myocardial cells, leading to depolarization. This depolarization is an important step in the generation of an action potential and the subsequent contraction of the myocardium.

Re-entry occurs when the impulse conducted to the ventricles does not die out in the surrounding refractory tissue after contraction. Instead, it re-excites the myocardium, triggering a premature impulse and sudden contraction. This phenomenon can lead to abnormal heart rhythms, such as atrial fibrillation or ventricular tachycardia.

The correct answer is plateau. A plateau is a phase in an action potential where the membrane potential remains depolarized for an extended period of time. This is caused by the influx of calcium ions into the cell and the opening of calcium channels. Additionally, the blockage of potassium channels prevents the efflux of potassium ions, contributing to the maintenance of the plateau phase.

Number III in section B above is the opening of potassium channels. This is caused by the closure of calcium channels during the process of rapid repolarization.

The correct answer is voltage dependent plasma membrane and intracellular. Calcium channels play a crucial role in regulating the electrical activity of the heart. Voltage dependent plasma membrane channels are responsible for the influx of calcium ions during the depolarization phase of the action potential, which triggers muscle contraction. Intracellular calcium channels, such as those located on the sarcoplasmic reticulum, are involved in the release of stored calcium ions, which further contribute to muscle contraction.

Dysrhythmias can be caused by several phenomena. Re-entry refers to the abnormal electrical pathway in the heart that causes the electrical signals to circulate repeatedly, leading to irregular heartbeats. Delayed after-depolarisation occurs when an extra electrical impulse is generated after the normal heartbeat, causing arrhythmias. Ectopic pacemaker activity refers to the abnormal firing of electrical signals from a location other than the sinoatrial node, disrupting the normal heart rhythm. Heart block occurs when the electrical signals are delayed or blocked as they travel through the heart's electrical system, resulting in irregular heartbeats.

The plateau in cardiac action potentials is caused by the opening of calcium channels, which are triggered by the depolarization of sodium ions. The slow influx of calcium ions into the cell helps to maintain the plateau phase. Additionally, the depolarization is maintained by the blocking of outward potassium conduction. This combination of calcium influx and blocked potassium conduction helps to prolong the depolarization phase and maintain cardiac contraction.

Stage I, represented in B, is partial repolarization. This stage occurs due to the closure of sodium channels. During an action potential, sodium channels open, allowing sodium ions to enter the cell and depolarize it. Once the cell reaches its peak depolarization, the sodium channels begin to close, causing a decrease in the influx of sodium ions. This closure of sodium channels leads to partial repolarization, where the cell starts to return to its resting membrane potential.

Heart block is a condition where there is a disruption in the electrical signals that regulate the heartbeat. In this case, the correct answer states that fibrous or ischaemic damage to the conducting system, usually the AV node, triggers heart block. This means that the damage to the AV node, which is responsible for transmitting the electrical signals from the atria to the ventricles, leads to a disruption in the coordination of the atria and ventricles. As a consequence, the atria and ventricles start firing independently of each other, with the ventricles being supplied by ectopic pacemakers.

Delayed after-depolarisation is mediated by high levels of extracellular calcium. This causes an influx of ions into the cell, leading to transiently increased normal after-depolarisation waves, which can be seen as peaked T waves. This can be caused by cardiac glycosides, NA or phosphodiesterase inhibitors that increase intracellular calcium. The increased normal after-depolarisation waves trigger a repetitive discharge and contraction that is independent of pacemaker stimulus. It is important to note that this phenomenon can occur in the non-pacemaker cells of the heart.

The difference between conduction in SA and AV nodes, compared to normal muscle and nerve conduction, is that there are no fast sodium channels present in SA and AV nodes, only slow calcium channels. Additionally, there are no sodium channels at all in SA and AV nodes, only calcium channels. The conduction in SA and AV nodes occurs via slow calcium channels.

IV in section B indicates pacemaker depolarization, which is the initiation of the electrical impulse in the sinoatrial (SA) node. This depolarization is caused by a slow influx of sodium ions into the SA node, leading to a gradual increase in sodium levels in the SA node. This process is crucial for the generation of the electrical signals that regulate the heart's rhythm and contraction.

Troponin, to which Ca2+ binds and triggers a conformational change, intrinsically influences myocardial contractility and pulse pressure. This is because troponin plays a crucial role in regulating muscle contraction in the heart. When Ca2+ binds to troponin, it causes a conformational change that allows actin and myosin fibers to interact, leading to muscle contraction. The strength of this interaction determines the force of contraction, which directly affects myocardial contractility. Additionally, changes in myocardial contractility can also influence pulse pressure, which is the difference between systolic and diastolic blood pressure.