Lecture 25: Cardiovascular System III Flashcards

Cardiac electrophysiology
Terms Definitions
Action Potential of a Cardiac Muscle Cell
The action potential of single cardiac muscle cells vary in shape, depending on the cell.
Difference in action potential between cardiac and nerve or skeletal muscle
Duration: a cardiac potential lasts as long as 250 milliseconds, whereas a keletal muscle or nerve action potential lasts only a few millisecondsShape: a cardiac muscle potential has a very pronounced plateu, which is not present is not present in a skeletal muscle or nerve action potential
Phases of the cardiac Action Potential: Phase 0
is the same as nerve or skeletal muscle. It is caused by the rapid opening of the usual voltage-gated sodium channels.
Phases of the cardiac Action Potential:Phase 1
also similar to nerve and skeletal muscle, and is due to the closing of the voltage-gated sodium channels
Phases of the cardiac Action Potential: Phase 2
the plateau - this is the phase that makes cardiac muscle different. The sarcolemma of cardiac muscle, unlike nerve and skeletal muscle plasma membranes, has a very lage population of slow, voltage-gated calcium channels. These calcium channels open at the beginning of Phase 2 and remain open throughout the plateau part of the action potential. During this period, calcium ions flow into the cellthere is also a reduction potassium permiability, unlike cardiac action potential
Exicitation-contraction coupling
the calcium that enter the myocardial cells during the plateu phase causes an increase in intracellular calcium concentration. Additionally, it is believed to induce therelease of calcium from sarcoplasmic reticulum, causing a further increase in the calcium concentration of the sarcoplasm.Note that these events take time, and therefore the electrical changes always precede the mechanical response.
Catecholamines (epinephrine and norepinephrine)
which are released at sympathetic nerve terminals or from the adrenal during sympathetic activation, increase the inward calcium current. This is how sympatheric stimulation enhances cardiac contraction enhances cardiac contractility.
the action of catecholamines on the heart is blocked by a group of drugs called beta-blockers. They derive their name from the fact that they bind to., effect of sympathetic stimulation on the heart, which includes acceleration of heart rate and increased contractility of the cardiac muscle cells. This decreases the strain on the heart during stress, and diminishes the frequency and severity of anginal attacks
Phases of the cardiac Action Potential: Phase 3
is due to the closing of the slow calcium channels, and is accompanied by an increase of potassium permeability back to normal
Phases of the cardiac Action Potential: Phase 4
represents the resting potential
Effective refractory period
During most of the plateau phase (2), the arrival of a second depolarizing impulse has no effect - this period is called the effective refractory period. Because it lasts for quite a long time, cardiac muscle cannot display tetanus when stimulated at high frequency as is observed in skeletal muscle
Pacemaker Cells
The heart beats in response to a continuos train of electrical signals (action potentials) generated by rhythmic depolarization of a special region in the posterior wall of the right atrium below the opening of the superior vena cava. This region is often called the pacemaker, and its anatomical name is the sinoatrial node (or S-A node)
S-A node
are specialized cardiac muscle fibers containing very few contractile elements. They are capable of entirely spontaneous, rhythmic deporalization and repolarization. They are continuous with the muscle fibers of the atrium, and therefore any action potentials that begin in the S-A node spread immediately into the myocardium of the atria, causing the two atria to contraction almost simultaneously. As we shall see in the next section, this wave of deporization ultimately spreads via special pathways into the ventricles and into ventricular myocardium.
Pacemaker depolarization
pacemaker cell are rather different from other cells. They are always leaky to sodium ions, and this tends to depolarize them. Further, unlike nerve and skeletal muscle fibers, their action are not generated by voltage-gated sodium channels, but by voltage-gated calcium channels.
The rhythmic and spontaneous depolarization that is seen in pacemaker cells depends on a very complex interplay between channels for sodium, calcium and potassium. These channels can be affected both by drugs by neurotransmitters of the autonomic nervous system. Parasympatheric and sympathetic stimulation alter the rate of firing of the pacemaker cells by action on the potassium channels.
Parasympathetic: Pacemaker
stimulation releases acetylcholine, which binds to muscarine receptors on the pacemaker cells and causes an increase in potassium permeability, lengthening the time it takes for an action potential to be generated. Therefore, the rhythmic activity of the sinoatrial node is slowed, and this reduces the heart rate. This action is blocked by atropine.
Sympathetic: Pacemaker
stimulation releases norepinephrine, which binds to Beta-adrenergic receptors on the pacemaker cells and increases the rate of closure of voltage-gated potassium channels. This increases the heart rate.
The Cardiac Pacemaker and Conduction System
Contraction of the myocardium is normally triggered by rhythmic depolarization of the pacemaker cells in the sinoatrial node. The wave of depolarization initiated by these cells spreads to the ventricles via specialized myocardial cells that make up the conduction system of the heart. The sequence of events is as follows
heart Conduction event 1
The cells in the sinoatrial node depolarize
heart Conduction events 2
A wave of depolarization spreads over the surface of the atria, causing them to contract.
heart Conduction event event 3
The wave of depolarization arrives at the atrioventrial node (A-V node).Because the atria and ventricles are electrically insulated from each other by the fibrous 4-ringed “skeleton of the heat,’’ the wave of electrical depolarization can only reach the ventricles by passing through the A-V node.
When the wave of depolarization hits the A-V node
it suddenly slow down, causing a dealy in conduction of the electrical pulse through the node. This delay (about .13 sec) gives the atria time to contract before the ventricles start to contract. It is caused by the fact that the fibers to the A-V node are very thin, and therefore conduct electrical changes very slowly (just like in nerve, where conduction rate decreases as the diameter of the nerve fiber decreases). Also, there are very few gap junctions between the conducting cells.
heart Conduction events: events 4
When the electrical impulse emerges from the A-V node it speeds up again it entersthe A-V bundle (also known as the bundle His). The A-V bundle the divides then divides into left and right bundle branches, which serve the left and right ventricles, respictevley.
heart Conduction events 5
the Purkinge fibers then carry the cardiac impulse at a speed of 2-4 meters per second into inner, endocardial layer of myocardium
heart Conduction event 6
From the endocardial surface, excitation spreads outwards at the slower rate of the .3-.5 meters per second through the thickness of the myocardium towards epicardial surface.Depolarizing impulses arrive via the Purkinje fibers then carry the ventricles, so permitting these parts to contract synchronously.
Three standard limb leads
are designated I, II, III. They are attached to the two wrists and the left leg (a “ground” lead is usually attached to the right lef)
P wave
Depolarization of the atria, indicates S-A node function. The onset of the Pwave precedes the onset atrial contraction
P-R interval
Indicative of the time it takes for the impulse through the A-V node into the ventricles (atrioventricular conduction time).
QRS complex
Depolarization of the ventricles - the QRS duration indicates the time in which ventricular depolarization occurs. The onset of the QRS wave precedes the onset of ventricular contraction.
T wave
Repolarization of the ventricles, at which time they are ready to be stimulated again.
S-T segment
The part of the electrocardiogram between the S-wave of the QRS complex and the T-wave. Its elevation or depression with respect to the baseline can be important in diagnosing a myocardial infarction
One complete cardiac cycle
Cardiac arrhythmia (also known as a dysrhymia)
is an abnormal cardiac rate or rhythm.
Causes of Arrythmias and conduction problems
lack of oxygen, drug effects, electrolyte imbalance, and myocardial or conduction system damage to myocardial ischemia.
Arrythmias and conduction problems may arise from factors operating in the following areas.
- Sinus node = sinoatrial (S-A) -Atria-A-V nodal (junctional)-A-V block and bundle branch block-Venreicles
Sinus Node: Sinus tachycardia
is an elevation in heart rate observed at rest. It is caused by an increased rate of depolarization and repolarization of the sinus node. the rhythm is often normal, but the rate is usually greater than 100 beats per minute. Sinus tachycardia may sometimes be a normal, physiological condition due to elevated body temerature or sympathetic stimulation. At other times, sinus tachycardia may be brought on by drugs or certain toxic conditions.
Sinus Node: Sinus bradycardia
is a slow heart rate at rest coused by a decreased rate of depolarization and repolarization of the sinus node. The heart rate is below 60 beats per minute, and may be quite normal in a trained athlete. In that event, the slow heart rate is probably caused by an increase in the frequency of nerve impulses in the parasympathetic vagus nerve.
Atrial flutter
example of atrial arrhythmia. Atrial flutter can be caused by waves of depolarization around the bands of atrial muscle fibers. In atrial flutter, the atria may beat as fast as 250-300 beats per minute. not all these impulses may in passing through the A-V node, so the ventricular rate may be fairly regular and moderate (e.g. 75 beats per minute). Atrial flutter can progress to atrial fibrilation.
A-V nodal arrhythmias (junctional arrhythmias)
occur when various parts of the A-V node take over the pacemaker duties of the S-A node, possibly because of the damage to the S-A node. Generally, the rate of the A-V node is lower than the rate of the S-A node, so the ventricles may beat at the rate of 40-60 beats per minuteThe P wave may be lost in the QRS complex and appear to be absent, or it may be inverted because the depolarization moves in a direction opposite to normal.
A-V block and bundle branch block
the atrial rate is normal but there is a problem with conduction of the wave of depolarization from the atria to the ventricles or through one of the bundle branches
First degree A-V block
Each P-wave is followed by a QRS but the P-R interval is prolonged (normally it is .2 seconds or less)
Second degree A-V block
This is an intermittent block. Some QRS are dropped, so that every P wave is followed by a QRS. For example, every second atrial beat may fail to get through to the ventricles -- therefore, the atrial rate will be twice the ventricular rate, and this particular example of a second degree block is called a 2:1 block.
Third degree A-V block
This is a complete heart block. The atria and ventricles beat independently of each other, so there is no relationship between the P-wave and QRS. The QRS rate always has a lower frequency than a P-wave rate. For example, the Purkinje cells of the ventricles may take over as pacemkers and cause the between 20 and 30 times per minute (the atria, of course, will beat at their normal rate). This abnomarly slow ventricular rate and causes and inadequate cardiac output, and calls for immediate action by the cardiologist.
Arrhythmias of ventricles
are always serious. The ventricles are the chmbers that pump blood into the aorta, and if the heart is to function efficiently as a blood pump, the contraction of the ventricles must be properly coordinated.
Premature ventricular contraction (PVC)
example of ventricular arrhythmia. this occurs before it is expected in a normal series of ECG’s. Premature ventricular contraction often generate wide and bizarre QRS complexes that do not have a preceding P wave
Ectopic focus
A premature ventricular contraction is caused by what is called an ectopic focus in one of the ventricles. An ectopic focus is a small region of the ventricular myocardium that decides to depolarize all on its own, possibly because of inflatommatory disease, lack of blood or drugs. The depolarization from such an ectopic focus may then travel throughout the myocardium of the ventricles, causing the ventricles to contract.
Danger of PVC
In itself, premature ventricular contraction is not life-threatening. However, it has the potential to be dangerous if it occurs during the ventricular repolarizing phase. This vulnerable phase corresponds to the point in the ECG when the T wave is being generatedThe danger arises because at this time some of the cells are repolarized and therefore excitable, while others are still refractory.
Ventricular tachycardia
If an ectopic focus generates a depolarizing stimulus during the T-wave, it can set up circular waves of depolarization that pass repeatedly around the ventricular walls. This can cause ventricular tachycardia, whre the ventricles can beat 250-350 contractions per minute. Under these conditions, the pumping effeciency of the heart is very poor because the ventricles do not have time to fill and empty properly.
Ventricular fibrillation
Ventricular tachycardia can lead to the lethal condition know as ventricular fibrillation. The electrical record in ventricular fibrillation is rapid and chaotic. Parts of the myocardium contract at random, and without any coordination. Consequently, the heart no longer pumps blood, and death will follow unless action is taken.
The only effective treatment for a fibrillation episode is to use a defibrillator to administer a direct-current shock to the thoracic region over the heart. THis defibrilating shock stimulates and depolarizes all parts of the ventricle simultaneously, and causes the whole myocardium to become refractory at the same time. All activity stops, then after 3-5 seconds the heart may begin to beat normally again, either with the S-A node or another pacemaker
Cardiopulmonary resuscitation (CPR)
Revival after a fibrillation episode may be facilitated by first aministering cardiopulmonary resucitation or CPR. The purpose is to force oxygynated blood into the aorta and more importantly into coronary circulation. A defibrillating shock may then be successful, because some oxygenated blood is available for use by the reactivated myocardium.
A myocardial infarction
is a heat attack. It is caused by part of the myocardium receiving insufficient blood, possibly because of blockage or thrombosis of a coronary artery. The result is injury or death of cardiac muscle cells.
Myocardial infarction: S-T segment
the ST segment can be important diagnostically. Normally, this part of the ECGT is close to the baseline (that is, it is “isoelectric”). However, it may be elevated or depressed following a myocardial infarction. If the ST segment becomes elevated or depressed during a stess test, this indicates that the person may be at risk for a myocardial infarction
Myocardial infarction:T-wave
the T-wave may be inverted after a myocardial infarction.
Myocardial infarction: Q-wave
The Q-wave may increase in size following a myocardial infarction
Cocaine and the Heart
Death from cocaine abuse is usually caused by lethal cardiac events, including myocardial infarction, ventricular fibrillation and other rhythm disorders. Partly this is caused by direct action on the heart (cocaine is a local anesthetic that blocks sodium channels) and also to the fact that cocaine can potentiate the effects of sympathetic stimulation by inhibiting the reuptake of norepinephrine at axon terminals in the heat (similar to its action on dopamine in the limbic system). An increase in the levels of norepinephrine in the heart can cause premature depolarization events, such as premature ventricular contraction, leading to fibrillation and death.
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