Term Paper on the Human Heart | Cardiovascular System | Biology

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Term Paper on the Human Heart

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Term Paper # 1. Introduction to the Human Heart:

The human heart is a hollow, muscular organ about the size of a fist. It is responsible for pumping blood through the blood vessels by repeated and rhythmic contractions. The term “cardiac” means “related to the heart” and comes from the Greek word kardia, for “heart”. Human heart is a four-chambered, double pump and is located in the thoracic cavity between the lungs (Fig. 6.1).

Heart Chambers:

The human heart has four chambers, two atria and two ventricles.

The atria are smaller with thin walls, while the ventricles are larger and much stronger.

Atrium:

There are two atria on either side of the human heart. On the right side is the atrium that contains blood which is poor in oxygen. The left atrium contains blood which has been oxygenated and is ready to be sent to the body. The right atrium receives deoxygenated blood from the superior vena cava and inferior vena cava. The left atrium receives oxygenated blood from the left and right pulmonary veins.

Ventricles:

The ventricle is a heart chamber which collects blood from an atrium and pumps it out of the heart. There are two ventricles- the right ventricle pumps blood into the pulmonary circulation for the lungs, and the left ventricle pumps blood into the systemic circulation for the rest of the body. Ventricles have thicker walls than the atria, and thus can create the higher blood pressure. Comparing the left and right ventricle, the left ventricle has thicker walls because it needs to pump blood to the whole body.

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Term Paper # 2. Layers of the Human Heart:

i. Endocardium:

Smooth endothelial lining of the heart and entire cardiovascular system. This helps to reduce friction of blood flow and prevent clotting.

ii. Myocardium:

The myocardium is the muscular tissue of the heart. The myocardium is composed of specialized cardiac muscle cells with an ability not possessed by muscle tissue elsewhere in the body. Cardiac muscle, like other muscles, can contract, but it can also conduct electricity, like nerves. The blood to the myocardium is supplied by the coronary arteries.

iii. Pericardium:

Surrounding the heart is a sac known as the peri­cardium, which consists of two membranes. The outer layer being the fibrous parietal pericardium and the inner layer being the serous visceral pericardium. It is the serous visceral pericardium that secretes the pericardial fluid into the pericardial cavity (the space between the two pericardial layers). The pericardial fluid reduces friction within the pericardium by lubricating the epicardial surface allowing the membranes to glide over each other with each heart-beat.

iv. Septum:

The interventricular septum is the thick wall separating the lower chambers (the ventricles) of the heart from one another. The greater portion of it is thick and muscular and constitutes the muscular ventricular septum. Its upper and posterior part, which separates the aortic vestibule from the lower part of the right atrium and upper part of the right ventricle, is thin and fibrous, and is termed the membranous ventricular septum. The interatrial septum separates right and left atrium.

v. Valves:

The two atrioventricular (AV) valves are one-way valves that ensure that blood flows from the atria to the ventricles, and not the other way. The right AV valve is also called the tricuspid valve because it has three flaps. It is located between the right atrium and the right ventricle.

The tricuspid valve allows blood to flow from the right atrium into the right ventricle. The left AY valve is also called the bicuspid valve because it has two flaps. It is also known as the mitral valve due to the resemblance to a bishop’s mitre (liturgical headdress). This valve prevents blood in the left ventricle from flowing into the left atrium.

The two semilunar (SL) valves are present in the arteries leaving the heart; they prevent blood from flowing back into the ventricles. They have flaps that resemble half-moons. The pulmonary semilunar valve lies between the right ventricle and the pulmonary trunk. The aortic semilunar valve is located between the ventricle and the aorta.

The sound heard in a heartbeat is due to the closure of the heart valves.

vi. Subvalvular Apparatus:

The chordae tendinae are attached to papillary muscles that cause tension to better hold the valve. Together, the papillary muscles and the chordae tendinae are known as the subvalvular apparatus. The function of the subvalvular apparatus is to keep the valves from prolapsing into the atria when they close. The subvalvular apparatus have no effect on the opening and closing of the valves. This is caused entirely by the pressure gradient across the valve.

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Term Paper # 3. Human Heart Rate:

It is the number of heart beats per minute. The resting heart rate is about 72/minute (60-80/minute).

Intrinsic Heart Rate:

Heart rate is normally determined by the pacemaker activity of the sinoatrial node (SA node) located in the posterior wall of the right atrium. The SA node exhibits automaticity that is determined by spontaneous changes in Ca⁺⁺, Na⁺, and K⁺ conductances. This intrinsic automaticity, if left unmodified by neurohumoral factors, exhibits a spontaneous firing rate of 100-115 beats/min. This intrinsic firing rate decreases with age.

Tachycardia:

Increase in heart rate >100/min.

Physiological:

1. Newborn 120-150/min

2. Comparatively high in females, and in pregnancy

3. Emotional excitement

4. Exercise

5. Diurnal variation ― High in evening.

Pathological:

1. Fever (for 1 degree rise, there is increase of 10-14 beats/min)

2. Thyrotoxicosis

3. Atrial flutter and fibrillation

4. Circulatory shock

Bradycardia:

Decrease in heart rate <60/min

Physiological:

1. Athletes

2. Sleep

Pathological:

1. Myxedema

2. Heart block

3. General weakness and debility

Regulation of Heart Rate:

There are two different factors involved in heart rate management:

1. Intrinsic

2. Extrinsic.

1. Intrinsic:

Intrinsic regulation of heart rate is the result of the unique nature of cardiac tissue. It is self-regulating and maintains its own rhythm without direction.

2. Extrinsic:

Extrinsic controls are those that come from both hormonal responses as well as the commands from the nervous system ― The central nervous system and the autonomic nervous system. Extrinsic regulation can cause the heart rate to change rapidly because of chemicals that circulate in the blood or by direct action of nerves that go to the heart.

Medullary Centers Controlling Heart Rate:

The vasomotor center is located bilaterally in the reticular formation of the medulla oblongata and contains the following areas:

Vasoconstrictor Area (Cardioaccelerator Area):

It is located in the upper anterolateral region of the medulla. The fibers from here pass down the spinal cord to connect with the cells of origin of the sympa­thetic nerves which innervate both blood vessels and heart.

Vasodilator Area (Cardioinhibitory Area):

It is more medially placed close to the dorsal motor nucleus of vagus and the nucleus ambiguous which send impulses via the vagus nerves.

Sensory Area:

It is located in the upper posterolateral region of the medulla in the nucleus tractus solitarius. This area receives afferents from the baroreceptors and other receptors mainly via the vagus and glossopharyngeal nerves which in turn conveys impulses to the vasomotor areas.

Methods for Controlling Heart Rate:

i. Hormonal Control:

The sympathetic components increase heart rate by releasing the neural hormone catecholamines ― epinephrine and norepinephrine.

The parasympathetic components decrease heart rate. These neurons release the neurohormone acetylcholine, which inhibits heart rate.

ii. Nervous Control:

Higher brain (hypothalamus) ― Stimulates the center in response to exercise, emotions, “fight or flight”, and temperature.

iii. Reflex Control:

Sinoaortic Baroreceptor Reflex:

Baroreceptors present are:

i. Carotid sinus which is a dilatation at the commence­ment of the internal carotid artery

ii. The arch of aorta.

They are branched and coiled myelinated nerve endings which respond to changes in blood pressure. Even though both rapid and sustained change stimulates baroreceptors, the effects are greater for the former. The impulses from the carotid sinus are carried by the carotid sinus nerve, a branch of glossopharyngeal nerve and from the aortic arch by the vagus. The impulses are sent up to the nucleus tractus solitarius and then to the vasomotor centers. The nerves are together called as sinoaortic nerves and are referred to as buffer nerves, since they buffer blood pressure changes.

Normally there is low frequency impulse discharge in these nerves, which are responsible for vagal tone. When blood pressure rises, the rate of discharge is increased, and when BP decreases, the discharge rate is slowed down.

When the arterial BP rises, there is a reflex slowing of the heart rate. The increased BP stimulates the baroreceptors, which stimulates NTS, from where impulses pass onto the cardioinhibitory region, then via vagus to decrease the heart rate. When BP falls, opposite effects occur.

Marey’s Law:

Marey’s Law states that the heart rate is inversely proportional to blood pressure. This is due to sinoaortic baroreceptor reflex. There are two exceptions, they are exercise and sleep.

Reflexes from Sinoaortic Chemoreceptors:

Chemoreceptors are present in the carotid and aortic bodies. These are stimulated by hypoxia, hypercapnea and H⁺. Chemoreceptor stimulation increases heart rate, but is of minor importance.

Bainbridge Reflex:

The venous engorgement of the right side of the heart (atria and great veins) causes tachycardia, and is brought about by stimulation of stretch receptors. The vagus is the afferent pathway and the efferents are both vagus and sympathetic nerves. A part of this reflex may be mechanical, resulting from stretching of SA node when right atrium is distended (to prevent accumulation of blood in the atria and the great veins).

Bezold-Jarish Reflex (Coronary Chemoreflex):

Injection of substances like phenyl diguanidine, serotonin, veratridine into the left ventricle via coro­nary artery supplying the left ventricle in experi­mental animals causes reflex slowing of the heart, hypotension, apnea followed by rapid shallow breathing. This is called as Bezold-Jarish reflex. The receptors are unmyelinated C fiber endings.

Pulmonary Chemoreflex:

Injection of substances like phenyl diguanidine, serotonin, veratridine into the pulmonary vascular bed produces bradycardia, hypotension, apnea followed by rapid shallow breathing. This is called as pulmonary chemoreflex. The receptors are unmyeli­nated C fiber endings located close to the pulmonary capillaries, the juxtacapillary J receptors of Paintal.

Respiratory Sinus Arrhythmia (RSA):

It is a naturally occurring variation in heart rate that occurs during a breathing cycle. Heart rate increases during inspiration and decreases during expiration.

It may be:

i. Reflexly produced by afferent impulses from stretch receptors in the lungs. When the lungs inflate during inspiration, the impulse discharge along the vagus increases and on deflation, the impulse discharge decreases.

ii. Irradiation of impulses from the respiratory center to the cardio inhibitory areas.

Oculocardiac Reflex:

Pressure on the eyeball causes reflex slowing of the heart, by increasing the vagal tone. The afferent impulses pass via the trigeminal nerve. Most painful stimuli also increase heart rate.

Cerebral ischemia due to raised intracranial pressure causes bradycardia by indirect effect due to rise of BP.

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Term Paper # 4. Innervation of the Human Heart:

Heart is innervated by fibers from autonomic nervous system which contain both afferent and efferent fibers.

Vagus Nerves (Parasympathetic):

The preganglionic fibers arise in the dorsal nucleus of vagus in the medulla. They descend in the trunk of vagus nerve, and end in the ganglia in the SA node and AV nodes, the right chiefly in the SA node and left in the AV node. Short postganglionic fibers from here are distributed to the cells in the SA node, AV node and bundle, some to the atrial muscle, but very few to the ventricle. Vagus nerves are cardioinhibitory.

Sympathetic Nerves:

Preganglionic fibers arise from the lateral horns of the upper 4 or 5 thoracic segments of the spinal cord, relay in the cervical sympathetic (stellate) ganglia, reach the heart and innervate the SA and AV nodes, bundle of His and branches and atrial and ventricular muscles. Vagal and sympathetic fibers mingle in the superficial and deep cardiac plexus. Sympathetic fibers cause acceleration and augmentation of the heart.

Atrial and ventricular muscles have much sympa­thetic innervations but vagal innervation is sparse, especially to the ventricular muscle.

Afferent Nerves from the Heart Travel Via:

i. The vagal nerves into the medulla to the cardio­inhibitory region of the vasomotor area. They mediate most of the cardiac reflexes.

ii. Along sympathetic nerves enter the spinal cord via posterior nerve root and ascend up the spinal cord to reach the brain. They mostly convey pain impulses from the heart.

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Term Paper # 5. Actions of the Nerves on Human Heart:

I. Actions of Vagus:

Cardioinhibitory

Weak Stimulation Causes:

i. Decrease in the rate of impulse formation in the SA node

ii. Diminishes the rate of conduction in the AV node, bundle and its branches

iii. Diminishes the force of atrial contraction

iv. There is no direct action on the ventricles. The ventricular slowing is the effect of ―

a. Decreased impulse formation in the SA node.

Strong Stimulation Causes:

i. Stoppage of impulse formation in the SA node

ii. Stoppage of impulse transmission through the AV junction.

With strong stimulation, initially both atria and ventricles stop beating completely, but after a varying interval, the ventricles begin to beat on their own, but at a much smaller rate (20-40/min). This phenomenon is called vagal escape. It is the ventricles that escape from the effect of vagus.

Right vagal stimulation predominantly reduces impulse formation in the SA node, whereas the left vagal stimulation predominantly reduces AV conduction.

Mode of Action of Vagus Nerve:

Vagus acts by release of Acetylcholine at its post­ganglionic terminals. The acetylcholine increases K⁺ permeability and K⁺ efflux resulting in hyper- polarization of the membrane and the tissue becomes less excitable.

Vagal Tone:

Impulses from cardioinhibitory region of the medulla are continually passing down the vagus nerves to the heart and keep the heart rate slower. This is called vagal tone. Vagal tone is minimal in the newborn and is well-developed in athletes.

II. Actions of Sympathetic Nerves:

Acceleration and augmentation:

i. Increases the rate of impulse formation in the SA node (positive chronotropism)

ii. Increases the conductivity (positive dromotropism)

iii. Increases the force of contraction (positive inotropism).

Mode of Action of Sympathetic:

It acts by releasing noradrenaline at the postganglionic terminals. Noradrenaline increases heart rate by acting on SA nodal cells causing reduction in K⁺ efflux, followed by opening of transient Ca⁺⁺ channels. Adrenaline also has a similar action.

Sympathetic Tone:

It is due to impulses from the medulla and hypotha­lamus.

Homometric Regulation:

Nervous control of force of contraction without change in muscle fiber length is called as homometric regulation.

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Term Paper # 6. Arterial Pulse and Venous Pulse:

Arterial Pulse:

It is the regular, recurrent expansion and contrac­tion of an artery, produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. The pulse is easily detected on superficial arteries, such as the radial and carotid arteries, and corresponds to each beat of the heart.

Arterial Pulse Tracing:

The arterial pulse wave can be measured by a sphygmograph. The resulting tracing shows ascending and descending limbs.

The ascending limb is steep and is called anacrotic limb or the percussion wave. It is due to expansion of the artery resulting from rapid ejection phase of ventricular systole.

The descending limb is called the catacrotic limb. Here, the dicrotic notch and dicrotic wave is present. Sometimes, a small tidal wave is present soon after the percussion wave.

i. Dicrotic Notch:

When the pressure in the ventricle falls below that in aorta at the end of systole, the aorta recoils now, causing the blood column to sweep back toward the heart resulting in dicrotic notch.

ii. Dicrotic Wave:

The reverse flow of blood closes the aortic valve and the blood column rebounds from the closed aortic valve resulting in dicrotic wave.

Abnormal Pulses:

a. Water-Hammer: Large amplitude, rapidly rising

i. Hypertrophic cardiomyopathy

ii. Aortic regurgitation

iii. Mitral regurgitation (severe)

iv. Patent ductus arteriosus

b. Pulses parvus et tardus (small amplitude, slow rising)

i. Aortic stenosis

ii. Diminished cardiac output

c. Pulsus alternans (alternating strong and weak pulse)

i. Left ventricular systolic dysfunction

d. Pulsus paradoxus (diminished pulse on inspiration)

i. Cardiac tamponade

ii. Congestive heart failure (severe)

iii. Chronic obstructive pulmonary disease (severe)

iv. Asthma

v. Constrictive pericarditis

e. Pulsus bisferiens (double-peak pulse)

i. Aortic regurgitation

ii. Hypertrophic cardiomyopathy.

Venous Pulse:

Description:

The jugular venous pressure (JVP) provides an indirect measure of central venous pressure. The internal jugular vein connects to the right atrium without any intervening valves—thus acting as a column for the blood in the right atrium. The JVP consists of certain waveforms and abnormalities of these can help diagnose certain conditions.

Waveforms of the JVP:

a: Presystolic; produced by right atrial contraction.

c: Bulging of tricuspid valve into the right atrium during ventricular systole (isovolumic phase).

v: Occurs in late systole; increased blood in right atrium from venous return.

Descents:

x: Combination of atrial relaxation, downward move­ment of the tricuspid valve and ventricular systole.

y: Tricuspid valve opens and blood flows into the right ventricle.

Causes of a Raised JVP:

i. Heart failure

ii. Constrictive pericarditis (JVP increases on inspira­tion called Kussmaul’s sign)

iii. Cardiac tamponade

iv. Fluid overload, e.g. renal disease

vi. Superior vena cava obstruction (no pulsation).

Abnormalities of the JVP:

Abnormalities of the a-Wave:

i. Disappears in atrial fibrillation

ii. Large a-waves occur in any cause of right ventricular hypertrophy (pulmonary hypertension and pulmo­nary stenosis) and tricuspid stenosis

iii. Extra-large a waves (called cannon waves) in complete heart block and ventricular tachycardia.

Prominent v Waves:

Tricuspid regurgitation is called cv or v waves and occur at the same time as systole (combination of v wave and loss of x descent); there may be ear lobe movement.

Slow y Descent:

i. Tricuspid stenosis

ii. Right atrial myxoma

Steep y Descent:

i. Right ventricular failure

ii. Constrictive pericarditis

iii. Tricuspid regurgitation

(The last two conditions have a rapid rise and fall of the JVP called Friedreich’s sign).

Central Venous Pressure:

Central venous pressure (CVP) describes the pressure of blood in the thoracic vena cava, near the right atrium of the heart. CVP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood into the arterial system.

It is a good approximation of right atrial pressure, which is a major determinant of right ventricular end- diastolic volume.

Measurement:

CVP can be measured by connecting the patient’s central venous catheter to a special infusion set which is connected to a small diameter water column. If the water column is calibrated properly the height of the column indicates the CVP.

Normal values are 2-8 mm Hg.

Factors Affecting CVP:

a. Factors that increase CVP:

1. Hypervolemia

2. Forced exhalation

3. Tension pneumothorax

4. Heart failure

5. Pleural effusion

6. Decreased cardiac output

7. Cardiac tamponade

b. Factors that decrease CVP:

1. Hypovolemia

2. Deep inhalation

3. Distributive shock

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