WEEK 3: The rhythm of the heart Flashcards
What is cardiac cycle?
Cardiac cycle
Sequence of event in a single heartbeat.
Each cycle includes electrical and mechanical activation (systole) and recovery (diastole).
*Contractions are preceded by electrical activity.
The timing and synchronization of cardiac contraction are controlled by noncontractile cells of the pacemaking and conduction system.
State components of the conducting system of the heart.
Sinoatrial node
AV node
Bundle of His
Right and Left bundle
Purkinje Fibres
Discuss the SA node.
What controls the SA node?
-Normal origin for electrical discharge (pacemaker)
-Has an intrinsic rate of 60 - 100 beats/minute.
Controlled by
*Vagal activity: slows the heart rate
*Sympathetic activity: accelerates.
When the sinus rate becomes unduly slow, a lower center may assume the role of pacemaker.
Where can the Rythm arise from?
This escape rhythm may arise from the
-AV node (nodal rhythm)
-Ventricles (idioventricular rhythm)
Discuss the Atrioventricular (AV) Node.
Back-up pacemaker with an intrinsic rate of 40 - 60 beats/minute.
Slows electrical conduction to synchronize the atrial contribution to ventricular pumping.
The only structure capable of conducting impulses from the atria to the ventricles.
Describe the intraventricular conduction pathways.
Common bundle (bundle of His)»_space;> Right (RBB) & left bundle branch (LBB)
*LBB fans out into fascicles that proceed along the left septal surface and toward the two papillary muscles of the mitral valve.
*RBB remains compact until it reaches the right distal septal surface
Discuss Purkinje cells.
Purkinje cells:
-Act as both pacemakers and rapid conductors of electrical impulses.
-Form networks that extend just beneath the surface of the right and left ventricular endocardium.
Define Cardiac action Potential.
Is the entire sequence of changes in the cell membrane potential, from the beginning of depolarization to the end of repolarization.
Results from a series of opening and closing of voltage gated Na +, K +, Ca 2+ channels.
Divided in phases 0 to 4.
Describe the process of cardiac action potential.
Phase 0 - Rapid Depolarization: This phase marks the rapid depolarization of the cell membrane. It is initiated by the opening of voltage-gated sodium channels, allowing an influx of sodium ions into the cell. This rapid influx of positive charge rapidly depolarizes the membrane potential, leading to the initiation of the action potential.
Phase 1 - Early Repolarization: Following the rapid depolarization, there is a brief period of early repolarization. During this phase, voltage-gated sodium channels begin to inactivate, and transient outward potassium channels open, allowing potassium ions to flow out of the cell. This results in a small decrease in membrane potential.
Phase 2 - Plateau: The plateau phase is characterized by a prolonged period of membrane depolarization. It is primarily mediated by the balance between inward movement of calcium ions through L-type calcium channels and outward movement of potassium ions. The influx of calcium ions prolongs the action potential and contributes to the sustained contraction of the cardiac muscle fibers.
Phase 3 - Rapid Repolarization: Following the plateau phase, there is a rapid repolarization of the membrane potential. This is primarily mediated by the opening of voltage-gated potassium channels, allowing an efflux of potassium ions out of the cell. As potassium ions leave the cell, the membrane potential returns to its resting state, preparing the cell for the next action potential.
Phase 4 - Resting Membrane Potential: This phase represents the resting state of the cell, where the membrane potential is relatively stable. The resting membrane potential is maintained by the balance of ion concentrations across the cell membrane, primarily through the activity of sodium-potassium pumps and other ion channels.
- Upstroke-voltage-gated Na+ channels open.
- Inactivation of voltage-gated Na+ channels. Voltage gated K+ channels begin to open.
- Plateau-Ca2+ influx through voltage-gated Ca2+ channels, balances K+ efflux.
- Repolarization - due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels.
5.
What is the function of plateau phase in the heart functioning?
Sustained Contraction: During the plateau phase, the prolonged depolarization of the cell membrane allows for sustained contraction of the cardiac muscle fibers. This is particularly important for the ventricular muscle cells, as it ensures that the ventricles remain contracted for a sufficient duration to eject blood effectively into the systemic circulation (in the case of the left ventricle) or the pulmonary circulation (in the case of the right ventricle).
Prevention of Tetany: The plateau phase helps prevent tetany (sustained contraction) of the cardiac muscle cells. By prolonging the action potential and maintaining depolarization, the plateau phase ensures that the heart muscle fibers do not contract continuously but instead undergo a regulated contraction and relaxation cycle. This prevents the heart from becoming locked in a state of contraction, which would impair its ability to pump blood effectively.
Synchronization of Contraction: The plateau phase synchronizes the contraction of adjacent cardiac muscle cells within the heart chambers. This coordinated contraction is essential for generating the force needed to propel blood through the circulatory system efficiently. The plateau phase helps ensure that the contraction of different regions of the heart occurs in a coordinated manner, contributing to the overall effectiveness of cardiac function.
Discuss Pacemaker action potential.
Occurs in the SA> AV nodes> bundle of His/Purkinje fibers.
Lacks stable membrane potential during phase 4.
Have a slow depolarization towards a threshold.
Action potential is generated once the threshold is reached.
Describe the events in pacemaker action potential generation.
Phase 4 - Pacemaker Potential (Diastolic Depolarization):
Unlike typical cardiac muscle cells, pacemaker cells do not have a stable resting membrane potential. Instead, they exhibit a slow, spontaneous depolarization during diastole, known as the pacemaker potential.
During phase 4, the membrane potential gradually becomes less negative, starting from around -60 mV.
The slow depolarization during phase 4 is primarily due to a combination of two main currents: the funny current (If) and the T-type calcium current (ICaT).
Threshold Potential and Action Potential Initiation:
As the membrane potential reaches a critical threshold level (typically around -40 to -50 mV), voltage-gated calcium channels (L-type calcium channels, ICaL) begin to open more rapidly, leading to a rapid influx of calcium ions.
This rapid influx of calcium ions triggers the upstroke of the action potential, initiating phase 0.
Phase 0 - Rapid Depolarization:
During phase 0, the rapid influx of calcium ions through voltage-gated calcium channels causes a rapid depolarization of the membrane potential.
This rapid depolarization leads to the action potential reaching its peak voltage.
Phase 3 - Repolarization:
After reaching its peak voltage, voltage-gated potassium channels (IK) begin to open, allowing potassium ions (K+) to exit the cell.
This efflux of potassium ions leads to repolarization of the membrane potential, returning it to its resting state.
Repolarization in pacemaker cells is relatively slow compared to cardiac muscle cells, contributing to the gradual decline of the action potential.
Phase 4 - Pacemaker Potential Re-initiation:
Following repolarization, the membrane potential gradually begins to depolarize again, initiating a new cycle of action potential generation.
The cycle repeats continuously, with the SA node setting the rhythm for the heart’s electrical activity.
Compare cardiac action potential and pacemaker action potential.
Location:
Cardiac action potential: Occurs in working myocardial cells found throughout the heart’s atria and ventricles.
Pacemaker action potential: Occurs specifically in the specialized pacemaker cells located in the sinoatrial (SA) node of the heart.
Initiation:
Cardiac action potential: Typically initiated by an external stimulus, such as an electrical impulse from neighboring cells or the conduction system.
Pacemaker action potential: Spontaneously generated by pacemaker cells due to their intrinsic ability to undergo slow, spontaneous depolarization during diastole.
Resting Membrane Potential:
Cardiac action potential: Resting membrane potential is relatively stable and typically around -90 millivolts (mV) in cardiac muscle cells.
Pacemaker action potential: Resting membrane potential gradually becomes less negative during diastole due to the slow depolarization of the pacemaker potential, starting from around -60 mV.
Depolarization:
Cardiac action potential: Initiated by a rapid influx of sodium ions (Na+) during phase 0, leading to rapid depolarization.
Pacemaker action potential: Initiated by a combination of the “funny” current (If) and T-type calcium current (ICaT) during the pacemaker potential, leading to gradual depolarization.
Threshold Potential:
Cardiac action potential: Typically around -70 millivolts (mV) in cardiac muscle cells, at which voltage-gated sodium channels open, initiating phase 0.
Pacemaker action potential: Typically around -40 to -50 millivolts (mV) in pacemaker cells, at which voltage-gated calcium channels open, triggering the upstroke of the action potential.
Repolarization:
Cardiac action potential: Repolarization is mainly mediated by the efflux of potassium ions (K+) during phase 3.
Pacemaker action potential: Repolarization occurs gradually as voltage-gated potassium channels open, allowing potassium ions to exit the cell, contributing to the decline of the action potential.
Repetition:
Cardiac action potential: Individual action potentials are triggered by external stimuli and occur in response to specific events, such as contraction or electrical conduction.
Pacemaker action potential: Generated continuously by pacemaker cells, setting the rhythm for the heart’s electrical activity and initiating action potentials rhythmically.
Discuss ANS Pacemaker action potential control.
Sympathetic Nervous System (SNS):
*Norepinephrine binds to beta-1 adrenergic receptors on pacemaker cells, activating them.
Activation of beta-1 adrenergic receptors leads to an increase in the inward “funny” current (If) and calcium current (ICaT), enhancing the rate of pacemaker potential depolarization.
*There is also decreased repolarization.
Parasympathetic Nervous System (PNS):
-Acetylcholine binds to muscarinic (M2) receptors on pacemaker cells, leading to their activation.
Activation of M2 receptors increases the outward potassium current (IK), hyperpolarizing the membrane potential and slowing down the rate of pacemaker potential depolarization.
-This results in a slower rise in membrane potential, delaying the reaching of threshold for action potential initiation.
What is an ECG (Electrocardiogram)?
An ECG is the recording (gram) of the electrical activity (electro) generated by the cells of the heart (cardio) that reaches the body surface.
Both cardiac depolarization and repolarization can be recorded from the skin surface by ECG
Action Potential and Electrocardiogram explained.
- Action Potential:
The action potential represents the sequence of electrical changes that occur within cardiac muscle cells (cardiomyocytes) during each heartbeat.
The action potential of cardiac muscle cells consists of several phases, including depolarization, plateau, and repolarization.
These electrical changes result from the movement of ions across the cell membrane through various ion channels, including sodium, potassium, and calcium channels.
- Electrocardiogram (ECG):
The ECG is a graphical representation of the electrical activity of the heart recorded from electrodes placed on the skin’s surface.
The ECG waveform consists of several deflections, including the P wave, QRS complex, and T wave.
Each deflection on the ECG corresponds to specific electrical events in the heart’s action potential.
Discuss the Correlation between Action Potential and ECG.
Correlation between Action Potential and ECG:
The P wave on the ECG corresponds to atrial depolarization, which occurs as the action potential spreads through the atria, leading to atrial contraction.
The QRS complex represents ventricular depolarization, which occurs as the action potential spreads through the ventricles, leading to ventricular contraction.
The T wave corresponds to ventricular repolarization, which occurs as the action potential returns to baseline following ventricular contraction.
Discuss the QRS complex.
Q wave:
-The initial negative deflection in QRS.
-It represents the initial depolarization of the interventricular septum as the electrical impulse spreads from the bundle branches through the Purkinje fibers.
-A small, narrow Q wave is considered normal.
An abnormally deep or wide Q wave may indicate myocardial infarction or other cardiac pathology affecting the septum.
R wave:
-The first positive deflection is termed
-It represents the depolarization of the main mass of the ventricles, as the electrical impulse spreads through the ventricular myocardium.
-The R wave is typically the tallest wave in the QRS complex and is used to measure the R wave amplitude.
S wave:
-A negative deflection after an R wave.
-It represents the completion of ventricular depolarization, particularly in the regions farthest from the positive electrode.
-The S wave may be small or absent in leads where the electrical vector of ventricular depolarization is directed away from the electrode.
Subsequent positive or negative waves are R’ and S’, respectively.
R’ and S’ Waves:
-R’ and S’ waves refer to subsequent positive or negative deflections, respectively, that occur after the main R and S waves in the QRS complex.
-These additional waves may appear in certain conditions such as bundle branch blocks or ventricular hypertrophy, where the normal pattern of ventricular depolarization is altered.
