109 Physiology of the Heart

Electrical Events

Cardiac contraction is initiated in the excitable cells of the sinoatrial (SA) node by both spontaneous depolarization and sympathetic activity.

Learning Objectives

Describe the electrical events of the heart

Key Takeaways

Key Points

  • The sinoatrial (SA) and atrioventricular (AV) nodes make up the intrinsic conduction system of the heart by setting the rate at which the heart beats.
  • The SA node generates action potentials spontaneously.
  • The SA node fires at a normal rate of 60–100 beats per minute (bpm), and causes depolarization in atrial muscle tissue and subsequent atrial contraction.
  • The AV node slows the impulses from the SA node, firing at a normal rate of 40-60 bpm, and causes depolarization of the ventricular muscle tissue and ventricular contraction.
  • Sympathetic nervous stimulation increases the heart rate, while parasympathetic nervous stimulation decreases the heart rate.

Key Terms

  • pacemaker: A structure that sets the rate at which the heart beats. Under normal conditions, the SA node serves this function for the heart.
  • atrioventricular (AV) node: The bundle of conducting tissue that receives impulses from the SA node and delays them before stimulating depolarization in the muscles of the ventricles.

The heart’s activity is dependent on the electrical impulses from the sinoatrial (SA) node and atrioventricular (AV) node, which form the intrinsic conduction system of the heart. The SA and AV nodes act as a pacemaker for the heart, determining the rate at which it beats, even without signals from the larger nervous system of the human body. The SA and AV nodes initiate the electrical impulses that cause contraction within the atria and ventricles of the heart.

Sinoatrial Node

The SA node is a bundle of nerve cells located on the outer layer of the right atria. These cells are specialized to undergo spontaneous depolarization and generation of action potentials without stimulation from the rest of the nervous system. The SA node nerve impulses travel through the atria and cause direct muscle cell depolarization and contraction of the atria. The SA node stimulates the right atria directly and stimulates the left atria through the Bachmann’s bundle. The SA node impulses also travel to the AV node, which stimulates ventricular contraction.

The SA node generates its own action potentials, but may be influenced by the autonomic nervous system. Without autonomic nervous stimulation, the SA node will set the heart rate itself, acting as the primary pacemaker for the heart. The SA node fires to set a heart rate in a range of 60–100 beats per minute (bpm), a normal range that varies from person to person.

Atrioventricular Node

The AV node is a bundle of conducting tissue (not formally classified as nerve tissue) located at the junction between the atria and ventricles of the heart.  The AV node receives action potentials from the SA node, and transmits them through the bundle of His, left and right bundle branches, and Purkinje fibers, which cause depolarization of ventricular muscle cells leading to ventricular contraction. The AV node slightly slows the neural impulse from the SA node, which causes a delay between depolarization of the atria and the ventricles.

The normal firing rate in the AV node is lower than that of the SA node because it slows the rate of neural impulses. Without autonomic nervous stimulation, it sets the rate of ventricular contraction at 40–60 bpm. Certain types of autonomic nervous stimulation alter the rate of firing in the AV node. Sympathetic nervous stimulation still increases heart rate, while parasympathetic nervous stimulation decreases heart rate by acting on the AV node.

This diagram of the cardiac conduction system indicates the SA node, AV node, left posterior bundle, right bundle, Purkinje fibers, His bundle, and Bachmann's bundle.

The Cardiac Conduction System: The system of nerves that work together to set the heart rate and stimulate muscle cell depolarization within the heart.

Electrocardiogram and Correlation of ECG Waves with Systole

An electrocardiogram, or ECG, is a recording of the heart’s electrical activity as a graph over a period of time.

Learning Objectives

Describe electrocardiograms and their correlation with systole

Key Takeaways

Key Points

  • An ECG is used to measure the rate and regularity of heartbeats as well as the size and position of the chambers, the presence of damage to the heart, and the effects of drugs or devices used to regulate the heart, such as a pacemaker.
  • The ECG device detects and amplifies the tiny electrical changes on the skin that are caused when the heart muscle depolarizes during each heartbeat, and then translates the electrical pulses of the heart into a graphic representation.
  • A typical ECG tracing of the cardiac cycle (heartbeat) consists of a P wave (atrial depolarization ), a QRS complex (ventricular depolarization), and a T wave (ventricular repolarization). An additional wave, the U wave ( Purkinje repolarization), is often visible, but not always.
  • The ST complex is usually elevated during a myocardial infarction.
  • Atrial fibrillation occurs when the P wave is missing and represents irregular, rapid, and inefficient atrial contraction, but is generally not fatal on its own.
  • Ventricular fibrillation occurs when all normal waves of an ECG are missing, represents rapid and irregular heartbeats, and will quickly cause sudden cardiac death.

Key Terms

  • fibrillation: A condition in which parts of the ECG do not appear normally, representing irregular, rapid, disorganized, and inefficient contractions of the atria or ventricles.
  • ST segment: The line between the QRS complex and the T wave, representing the time when the ventricles are depolarized before repolarization begins.

An electrocardiogram (ECG or EKG) is a recording of the heart’s electrical activity as a graph over a period of time, as detected by electrodes attached to the outer surface of the skin and recorded by a device external to the body. The graph can show the heart’s rate and rhythm. It can also detect enlargement of the heart, decreased blood flow, or the presence of current or past heart attacks. ECGs are the primary clinical tool to measure electrical and mechanical performance of the heart.

The ECG works by detecting and amplifying tiny electrical changes on the skin that occur during heart muscle depolarization. The output for the ECG forms a graph that shows several different waves, each corresponding to a different electrical and mechanical event within the heart. Changes in these waves are used to identify problems with the different phases of heart activity.

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ECG: Illustration of a patient undergoing a 12-lead ECG.

The P Wave

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Normal Systole ECG: The U wave is not visible in all ECGs.

The first wave on an ECG is the P wave, indicating atrial depolarization in which the atria contract (atrial systole ). The P wave is the first wave on the ECG because the  action potential for the heart is generated in the sinoatrial (SA) node, located on the atria, which sends action potentials directly through Bachmann’s bundle to depolarize the atrial muscle cells.

Increased or decreased P waves can indicate problems with the potassium ion concentration in the body that will alter nerve activity. A missing P wave indicates atrial fibrillation, a cardiac arrhythmia in which the heart beats irregularly, preventing efficient ventricular diastole. This is generally not fatal on its own.

The QRS Complex

The QRS complex refers to the combination of the Q, R, and S waves, and indicates ventricular depolarization and contraction (ventricular systole). The Q and S waves are downward waves while the R wave, an upward wave, is the most prominent feature of an ECG. The QRS complex represents action potentials moving from the AV node, through the bundle of His and left and right branches and Purkinje fibers into the ventricular muscle tissue. Abnormalities in the QRS complex may indicate cardiac hypertrophy or myocardial infarctions.

The T Wave and ST Segment

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Animation of a Normal ECG Wave: The red lines represent the movement of the electrical signal through the heart.

The T Wave indicates ventricular repolarization, in which the ventricles relax following depolarization and contraction. The ST segment refers to the gap (flat or slightly upcurved line) between the S wave and the T wave, and represents the time between ventricular depolarization and repolarization. An elevated ST segment is the classic indicator for myocardial infarctions, though missing or downward sloping sloping ST segments may indicate myocardial ischemia.

Following the T wave is the U wave, which represents repolarization of the Purkinje fibers. It is not always visible on an ECG because it is a very small wave in comparison to the others.

Ventricular Fibrillation

When ECG output shows no identifiable P waves, QRS complexes, or T waves, it imdicates ventricular fibrillation, a severe arrhythmia. During ventricular fibrillation, the heart beats extremely fast and irregularly and can no longer pump blood, acting as a mass of quivering, disorganized muscle movements. Ventricular fibrillation will cause sudden cardiac death within minutes unless electrical resuscitation (with an AED) is performed immediately. It generally occurs with myocardial infarcations and heart failure, and is thought to be caused by action potentials that re-enter the AV nodes from the muscle tissue and induce rapid, irregular, weak contractions of the heart that fail to pump blood.

Heart Sounds

The two major heart sounds are “lub” (from the closure of AV valves) and “dub: (from the closure of aortic and pulmonary valves).

Learning Objectives

Describe the sounds the heart makes

Key Takeaways

Key Points

  • The heart tone “lub,” or S1, is caused by the closure of the mitral and tricuspid atrioventricular (AV) valves at the beginning of ventricular systole.
  • The heart tone “dub,” or S2 ( a combination of A2 and P2), is caused by the closure of the aortic valve and pulmonary valve at the end of ventricular systole.
  • The splitting of the second heart tone, S2, into two distinct components, A2 and P2, can sometimes be heard in younger people during inspiration. During expiration, the interval between the two components shortens and the tones become merged.
  • Murmurs are a “whoosh” or “slosh” sound that indicate backflow through the valves.
  • S3 and S4 are a “ta” sound that indicates ventricles that are either too weak or too stiff to effectively pump blood.

Key Terms

  • dub: The second heart tone, or S2 (A2 and P2), caused by the closure of the aortic valve and pulmonary valve at the end of ventricular systole.
  • lub: The first heart tone, or S1,  caused by the closure of the atrioventricular valves (mitral and tricuspid) at the beginning of ventricular contraction or systole.
  • Heart murmurs: A sound made by backflow of blood through either set of valve that cannot close or open properly.

The closing of the heart valves produces a sound. This sound may be described as either a “lub” or a “dub” sound. Heart sounds are a useful indicator for evaluating the health of the valves and the heart as a whole.

S1

The first heart sound, called S1, makes a “lub” sound caused by the closure of the mitral and tricuspid valves as ventricular systole begins. There is a very slight split between the closure of the mitral and tricuspid valves, but it is not long enough to create multiple sounds.

S2

The second heart sound, called S2, makes a “dub” sound caused by the closure of the semilunar (aortic and pulmonary) valves following ventricular systole. S2 is split because aortic valve closure occurs before pulmonary valve closure. During inspiration (breathing in) there is slightly increased blood return to the right side of the heart, which causes the pulmonary valve to stay open slightly longer than the aortic valve. Due to this, the naming convention is to divide the second sound into two second sounds, A2 (aortic), and P2 (pulmonary). The time between A2 and P2 is variable depending on the respiratory rate, but the split is generally only prominent in children during inspiration. In adults and during expiration, the split is usually not long enough to suggest two sounds.

Abnormal Heart Sounds

Abnormal heart sounds may indicate problems with the health of the valves. Heart murmurs sound like a “whoosh” or “slosh” and indicate regurgitation or backflow of blood through the valves because they cannot close properly. Heart murmurs are common and generally not serious, but some may be more severe and/or caused by severe underlying problems within the heart. Murmurs may also be caused by valve stenosis (improper opening) and cardiac shunts, a severe condition in which a defect in the septum allows blood to flow between both sides of the heart.

Third and fourth heart sounds, S3 and S4, differ from S1 and S2 because they are caused by abnormal contraction and relaxation of the heart instead of the closure of valves and are more often indicative of more severe problems than are heart murmurs. S3 represents a flabby or weak ventricle that fills with more blood than it is able to pump, while S4 represents a stiff ventricle, such as those found in cardiac hypertrophy. S3 makes a “ta” sound after the “lub-dub” while S4 makes a “ta” sound before the “lub-dub.”

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Opening and Closing of Heart Valves: The closing of the heart valves generates the “lub, dub” sounds that can be heard though a stethoscope.

Cardiac Cycle

The cardiac cycle describes the heart’s phases of contraction and relaxation that drive blood flow throughout the body.

Learning Objectives

Describe the cardiac cycle and its three phases

Key Takeaways

Key Points

  • Every single beat of the heart involves three major stages: cardiac diastole, when chambers are relaxed and filling passively; atrial systole when the atria contract leading to ventricular filling; and ventricular systole when blood is ejected into both the pulmonary artery and aorta.
  • Pulse is a way of measuring heartbeat, based on the arterial distensions or pulses that occur as blood is pushed through the arteries.
  • Resting heart rate typically ranges from 60 to 100 bpm (beats per minute). Athletes often have significantly lower than average heart rates while the sedentary and obese typically have elevated heart rates.
  • Systolic blood pressure is the pressure during heart contraction, while diastolic blood pressure is the pressure during heart relaxation.
  • The normal range for blood pressure is between 90/60 mmHg and 120/80 mmHg.

Key Terms

  • cardiac cycle: The term used to describe the relaxation and contraction that occur as a heart works to pump blood through the body.
  • cardiac output: The volume of blood pumped by the heart each minute, calculated as heart rate (HR) X (times) stroke volume (SV).
  • pulse: Pressure waves generated by the heart in systole move the arterial walls, creating a palpable pressure wave felt by touch.

The cardiac cycle is the term used to describe the relaxation and contraction that occur as the heart works to pump blood through the body. Heart rate is a term used to describe the frequency of the cardiac cycle. It is considered one of the four vital signs and is a regulated variable. Usually heart rate is calculated as the number of contractions (heartbeats) of the heart in one minute and expressed as “beats per minute” (bpm). When resting, the adult human heart beats at about 70 bpm (males) and 75 bpm (females), but this varies among individuals. The reference range is normally between 60 bpm (lower is termed bradycardia) and 100 bpm (higher is termed tachycardia). Resting heart rates can be significantly lower in athletes and significantly higher in the obese. The body can increase the heart rate in response to a wide variety of conditions in order to increase the cardiac output, the blood ejected by the heart, which improves oxygen supply to the tissues.

Pulse

Pressure waves generated by the heart in systole, or ventricular contraction, move the highly elastic arterial walls. Forward movement of blood occurs when the arterial wall boundaries are pliable and compliant. These properties allow the arterial wall to distend when pressure increases, resulting in a pulse that can be detected by touch. Exercise, environmental stress, or psychological stress can cause the heart rate to increase above the resting rate. The pulse is the most straightforward way of measuring the heart rate, but it can be a crude and inaccurate measurement when cardiac output is low. In these cases (as happens in some arrhythmias), there is little pressure change and no corresponding change in pulse, and the heart rate may be considerably higher than the measured pulse.

Cardiac Cycle

Every single heartbeat includes three major stages: atrial systole, ventricular systole, and complete cardiac diastole.

  • Atrial systole is the contraction of the atria that causes ventricular filling.
  • Ventricular systole is the contraction of the ventricles in which blood is ejected into the pulmonary artery or aorta, depending on side.
  • Complete cardiac diastole occurs after systole. The blood chambers of the heart relax and fill with blood once more, continuing the cycle.

Systolic and Diastolic Blood Pressure

Throughout the cardiac cycle, the arterial blood pressure increases during the phases of active ventricular contraction and decreases during ventricular filling and atrial systole. Thus, there are two types of measurable blood pressure: systolic during contraction and diastolic during relaxation. Systolic blood pressure is always higher than diastolic blood pressure, generally presented as a ratio in which systolic blood pressure is over diastolic blood pressure. For example, 115/75 mmHg would indicated a systolic blood pressure of 115 mmHg and a diastolic blood pressure or 75 mmHG. The normal range for blood pressure is between 90/60 mmHg and 120/80 mmHg. Pressures higher than that range may indicate hypertension, while lower pressures may indicate hypotension. Blood pressure is a regulated variable that is directly related to blood volume, based on cardiac output during the cardiac cycle.

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The Cardiac Cycle: Changes in contractility lead to pressure differences in the heart’s chambers that drive the movement of blood.

Cardiac Output

Cardiac output (Q or CO) is the volume of blood pumped by the heart, in particular by the left or right ventricle, in one minute.

Learning Objectives

Describe cardiac output and its function in the cardiovascular system

Key Takeaways

Key Points

  • Cardiac output, a measure of how much blood the heart pumps over the course of a minute, is calculated by multiplying heart rate by stroke volume.
  • The heart rate is increased by sympathetic nervous stimulation and decreased by parasympathetic nervous stimulation.
  • Stroke volume is end diastolic volume (venous return) minus end systolic volume, the amount of blood left over in the heart after systole.
  • The ejection fraction is stroke volume divided by end diastolic volume.
  • Mean arterial blood pressure is cardiac output multiplied by total peripheral resistance. A twofold change in vascular size will cause a 16-fold change in resistance in the opposite direction.
  • Starling’s mechanism states that changes in venous return (preload) to the heart will change cardiac output, which will also change mean arterial blood pressure in the same direction. This means that blood volume and blood pressure are directly related to one another.

Key Terms

  • mean arterial blood pressure: A measure of blood pressure based on cardiac output and vascular resistance.
  • cardiac output: The volume of blood pumped by the heart, in particular by the left or right ventricle, in the time interval of one minute.

Cardiac output (CO) is a measure of the heart’s performance. While there are many clinical techniques to measure CO, it is best described as a physiological and mathematical relationship between different variables. When one of the variables change, CO as a whole will change as a result. This can also be used to predict other regulated variables, such as blood pressure and blood volume. The mathematical description of CO is that [latex]\text{CO}=\text{Heart Rate (HR)}\times\text{Stroke Volume (SV)}[/latex]. Changes in HR, SV, or their components, will change CO.

Heart Rate

The heart rate is determined by spontaneous action potential generation in the sinoatrial (SA) node and conduction in the atrioventricular (AV) node. It refers to the number of heartbeats over the course of a minute. Sympathetic nervous system activation will stimulate the SA and AV nodes to increase the heart rate, which will increase cardiac output. Parasympathetic nervous system activation will conversely act on the SA and AV nodes to decrease the heart rate, which will decrease cardiac output. For the SA node, the rate of depolarization is altered, while the AV node’s rate of conduction is altered by autonomic nerve stimulation.

Stroke Volume

Stroke volume refers to the amount of blood ejected from the heart during a single beat. It is a measure of the contractility of the heart based on end diastolic volume (EDV), mathematically described as [latex]\text{SV}=\text{EDV}-\text{ESV (end systolic volume}[/latex]. EDV is the volume of blood in the ventricles at the end of diastole, while ESV is the volume of blood left inside the ventricles at the end of systole, making SV the difference between EDV and ESV. Contractility of the heart refers to the variability in how much blood the heart ejects based on changes in stroke volume rather than than changes in heart rate.

Additionally, another indicator known as the ejection fraction (EF) is used to evaluate stroke volume and contractility. It is described as [latex]\text{EF}=\left(\frac{\text{SV}}{\text{EDV}}\right)\times{100}\%[/latex] and is a measure of the proportion of blood ejected during systole compared to the amount of blood that was present in the heart. A higher EF suggests more efficient heart activity.

Mean Arterial Pressure

Cardiac output is an indicator of mean arterial blood pressure (MAP), the average measure of blood pressure within the body. It is described as [latex]\text{MAP}=\text{CO}\times\text{TPR (total peripheral resistance)}[/latex]. TPR is a measure of resistance in the blood vessels, which acts as the force by which blood must overcome to flow through the arteries determined by the diameter of the blood vessels. The exact relationship is such that a twofold increase in blood vessel diameter (doubling the diameter) would decrease resistance by 16-fold, and the opposite is true as well. When CO increases, MAP will increase, but if CO decreases, MAP will decrease.

Starling’s Law of the Heart

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Frank Starling’s Law: This chart indicates stroke volume compared to ventricular preload, with labels for preload dependent zone, responsive patient SVV > 10%, and nonresponsive patient SVV < 10 %.

CO can also predict blood pressure based on blood volume. Starling’s law of the heart states that the SV of the heart increases in response to an increase in EDV when all other factors remain constant. Essentially, this means that higher venous blood return to the heart (also called the preload) will increase SV, which will in turn increase CO. This is because sarcomeres are stretched further when EDV increases, allowing the heart to eject more blood and keep the same ESV if no other factors change.

The main implication of this law is that increases in blood volume or blood return to the heart will increase cardiac output, which will lead to an increase in MAP. The opposite scenario is true as well. For example, a dehydrated person will have a low blood volume and lower venous return to the heart, which will decrease cardiac output and blood pressure. Those that stand up quickly after lying down may feel light-headed because their venous return to the heart is momentarily impaired by gravity, temporarily decreasing blood pressure and supply to the brain. The adjustment for blood pressure is a quick process, while blood volume is slowly altered. Blood volume itself is another regulated variable, regulated slowly through complex processes in the renal system that alter blood pressure based on the Starling mechanism.

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