Cardiovascular system: Physiology of Human Heart

Conducting system of the heart

The physiology of human heart possesses the property of auto rhythmicity, which means it generates its own electrical impulses and beats independently of nervous or hormonal control, i.e. it is not reliant on external mechanisms to initiate each heartbeat.

However, it is supplied with both sympathetic and parasympathetic nerve fibres, which increase and decrease respectively the intrinsic heart rate. In addition, the heart responds to a number of circulating hormones, including adrenaline (epinephrine) and thyroxine.
Small groups of specialised neuromuscular cells in the myocardium initiate and conduct impulses, causing coordinated and synchronised contraction of the heart muscle.

Sinoatrial node (SA node)

This small mass of specialised cells lies in the wall of the right atrium near the opening of the superior vena cava. The sinoatrial cells generate these regular impulses because they are electrically unstable. This instability leads them to discharge (depolarise) regularly, usually between 60 and 80 times a minute. This depolarisation is followed by recovery (repolarisation), but almost immediately their instability leads them to discharge again, setting the heart rate. Because the SA node discharges faster than any other part of the heart, it normally sets the heart rate and is called the pacemaker of the heart. Firing of the SA node triggers atrial contraction.

Atrioventricular node (AV node)

• This small mass of neuromuscular tissue is situated in the wall of the atrial septum near the atrioventricular valves.
• Normally, the AV node merely transmits the electrical signals from the atria into the ventricles.
• There is a delay here; the electrical signal takes 0.1 of a second to pass through into the ventricles. This allows the atria to finish contracting before the ventricles start.
  The AV node also has a secondary pacemaker function and takes over this role if there is a problem with the SA node itself, or with the transmission of impulses from the atria. Its intrinsic firing rate, however, is slower than that set by the SA node (40–60 beats per minute).

Atrioventricular bundle (AV bundle or bundle of His)

• This mass of specialised fibres originates from the AV node. The AV bundle crosses the fibrous ring that separates atria and ventricles then, at the upper end of the ventricular septum, it divides into right and left bundle branches.
• Within the ventricular myocardium the branches break up into fine fibres, called the Purkinje fibres.
• The AV bundle, bundle branches and Purkinje fibres transmit electrical impulses from the AV node to the apex of the myocardium where the wave of ventricular contraction begins, then sweeps upwards and outwards, pumping blood into the pulmonary artery and the aorta.

Cardiac cycle

At rest, the healthy adult heart is likely to beat at a rate of 60–80 beats per minute (b.p.m.). During each heartbeat, or cardiac cycle, the heart contracts (systole) and then relaxes (diastole).

Stages of the cardiac cycle

Taking 74 b.p.m. as an example, each cycle lasts about 0.8
of a second and consists of:

• atrial systole – contraction of the atria
• ventricular systole – contraction of the ventricles
• complete cardiac diastole – relaxation of the atria and
  ventricles.

Events of Cardiac Cycle

• The chambers of the heart contract and relax in a coordinated fashion. The contraction phase is referred to as ‘systole’ and the relaxation phase, when the heart fills up again, as ‘diastole’.
• The RA and LA synchronise during atrial systole and diastole, while the RV and LV synchronise during ventricular systole and diastole. One complete cycle of these events is referred to as the cardiac cycle.
• During the cardiac cycle, the pressure in the cardiac chambers increases or falls, affecting valve opening or closure, thereby regulating blood flow between the chambers.
• Pressures in the left side of the heart are around five times higher than in the right side, but the same volume of blood is pumped per cardiac beat.
• The cardiac cycle can be broken down into a sequence of events based on the principle that any blood flow through the chambers depends on pressure changes, as blood will always flow from a high-pressure to a low-pressure area.
• First the pulmonary and aortic valves close, then the atrioventricular valves open and the cycle begins again. This sequence of opening and closing valves ensures that the blood flows in only one direction.

Atrial systole and ventricular filling

At this part of the cardiac cycle, the pressure in the heart is low and the blood from the circulation passively fills the atria on both sides. This culminates in the opening of the atrioventricular valves and blood moving into the ventricles.

Around 70% of ventricular filling occurs during this phase. After depolarisation of the atria (P wave on an electrocardiogram [ECG]), the atria contract compressing blood in the atrial chambers and push residual blood out into the ventricles.

This signifies the last part of the ventricular resting phase (diastole) and the blood within the ventricles is referred to as the end diastolic volume (EDV). The atria then relax and then the electrical impulse is transmitted to the ventricles, which undergo depolarisation (QRS wave on an ECG).

Ventricular systole

At this point, the atria are relaxed, and the ventricles begin to contract. This contraction of the ventricles leads to an increase in ventricular pressures within the cavity.

As the pressure rises, it exceeds the pressure within the arteries, forcing the opening of the aortic and pulmonary valves as blood is ejected from ventricles and into these large vessels.

Complete cardiac diastole

At this point, the ventricles relax and any blood remaining in the chamber is called end systolic volume (ESV). The ventricular pressure precipitously drops and as this occurs, blood within the aorta and pulmonary trunk momentarily backflow and the aortic and pulmonary valves close.

This backflow causes a brief rise in the pressure in the aorta giving a characteristic change in the pressure of the cardiac cycle called the dicrotic notch. While the ventricles have been in systole, the atria are in diastole and fill again ready for the next cardiac cycle.

Electrical changes in the heart

• The body tissues and fluids conduct electricity well, so the electrical activity in the heart can be recorded on the skin surface using electrodes positioned on the limbs and/or the chest.
• This recording, called an electrocardiogram (ECG) shows the spread of the electrical signal generated by the SA node as it travels through the atria, the AV node and the ventricles.
• The normal ECG tracing shows five waves which, by convention, have been named P, Q, R, S and T.
• The P wave arises when the impulse from the SA node sweeps over the atria (atrial depolarisation).
• The QRS complex represents the very rapid spread of the impulse from the AV node through the AV bundle and the Purkinje fibres and the electrical activity of the ventricular muscle (ventricular depolarisation).
• Note the delay between the completion of the P wave and the onset of the QRS complex.
• This represents the conduction of the impulse through the AV node, which is much slower than conduction elsewhere in the heart and allows atrial contraction to finish completely before ventricular contraction starts.
• The T wave represents the relaxation of the ventricular muscle (ventricular repolarisation). Atrial repolarisation occurs during ventricular contraction and so is not seen because of the larger QRS complex.
• The ECG described above originates from the SA node and is called sinus rhythm. The rate of sinus rhythm is 60–100 b.p.m. A faster heart rate is called tachycardia and a slower heart rate, bradycardia.

Cardiac output and stroke volume

Cardiac output (CO) is the amount of blood pumped out by the heart in one minute. CO can be calculated using a simple equation: the stroke volume (SV) – the volume of blood pumped by the ventricles with each heartbeat – multiplied by the heart rate.

First, one needs to calculate the SV – the difference between the EDV (the volume of blood left in the ventricles during diastole) and the ESV (the volume of blood remaining in the ventricles after it has contracted).

If the EDV is 120ml and the ESV is 50ml, the SV will be:

• 120ml (EDV) – 50ml (ESV) = 70 ml/beat (SV)

Once the SV has been determined, the CO can be calculated. If the SV is 70mls and the heart rate is 70bpm, the CO will be:

• 70ml (SV) x 70bpm (heart rate) = 4,900ml/min (CO)

The CO can vary; for example, it will increase in response to metabolic demands such as exercise or pregnancy. In pathological states such as heart failure, the CO may not be sufficient to support simple activities of daily living or to increase in response to demands such as mild-to-moderate exercise.

Arterial blood pressure.

This affects the stroke volume as it creates resistance to blood being pumped from the ventricles into the great arteries. This resistance (sometimes called afterload) is determined by the distensibility, or elasticity, of the large arteries and the peripheral resistance of arterioles. Increasing afterload increases the workload of the ventricles, because it increases the
pressure against which they have to pump. This may actually reduce stroke volume if systemic blood pressure becomes significantly higher than normal.
Blood volume. This is normally kept constant by the kidneys. Should blood volume fall, e.g. through sudden haemorrhage, this can cause stroke volume, cardiac output and venous return to fall. However, the body’s compensatory mechanisms will tend to return these values towards normal, unless the blood loss is too sudden or severe for compensation.

Venous return

Venous return is the major determinant of cardiac output and, normally, the heart pumps out all blood returned to it. The force of contraction of the left ventricle ejecting blood into the aorta is not sufficient to push the blood through the arterial and venous circulation and back to the heart. Other factors are involved.

The position of the body.

Gravity assists venous return from the head and neck when standing or sitting and offers less resistance to venous return from the lower parts of the body when lying flat.

Muscular contraction.

Backflow of blood in veins of the limbs, especially when standing, is prevented by valves. The contraction of skeletal muscles surrounding
the deep veins compress them, pushing blood towards the heart. In the lower limbs, this is called the skeletal muscle pump.

The respiratory pump.

During inspiration, the expansion of the chest creates a negative pressure within the thorax, assisting flow of blood towards the heart. In addition,
when the diaphragm descends during inspiration, the increased intra-abdominal pressure pushes blood towards the heart.

Regulation of heart rate

The regulation of heart rate is a critical component of cardiovascular physiology, influencing overall heart function and health. Heart rate (HR) is defined as the number of times the heart beats within a minute.

Heart rate is controlled by two main mechanisms:

• Autonomic nervous system activity
• Hormone activity.
  Resting heart rate is also affected by factors such as age, gender, temperature and physical fitness

Autonomic nervous system activity

• When activated by a stimulus, such as exercise or stress, the sympathetic nerve fibres release noradrenaline at their cardiac endings as a neurotransmitter. This leads to the excitation of the sinoatrial node and an increase in its production of acti on potentials and thus an increase in heart rate.
• Alternatively, when the parasympathetic nervous system is stimulated this results in the release of acetylcholine at the parasympathetic cardiac nerve endings which has the effect of reducing the rate of action potential generation in the sinoatrial node and thus reducing heart rate.
• Both the sympathetic and parasympathetic nervous systems are active at all times, but the parasympathetic nervous system normally has the dominant influence. This can be seen if the vagus nerve (cranial nerve X) is cut, for instance in heart transplant patients. In these situations, the sinoatrial node will normally produce action potentials at a rate of 100 a minute and therefore the heart rate increases to 100 beats per minute.
• The removal of the influence of the parasympathetic nervous system (by the disconnection of the vagus nerve) removes the heart rate, reducing effect of this system.

Baroreceptors and the cardiovascular centre

Baroreceptors are specialised mechanical receptors located in the carotid sinus and the aortic arch. They are sensitive to the amount of stretch in these blood vessels and have direct outflow via the autonomic nervous system to the cardiovascular centre in the medulla oblongata.

The cardiovascular centre of the medulla oblongata is the main centre for the control of autonomic nervous activity that affects the heart. The cardiovascular centre is made up of two sub – centres:

• The cardioinhibitory centre directly controls parasympathetic outflow to the heart (especially the sinoatrial node), thus increased outflow from this centre has the effect of reducing heart rate
• The vasomotor centre is further divided into the pressor area and the depressor area. The pressor area has a relatively constant outflow of acti on potentials to the heart via the sympathetic nervous system. This has a direct effect on both heart rate and the force of ventricular
  contraction (and therefore stroke volume) as well as effects on the vasculature which subsequently will affect heart function by changing preload and afterload. Outflow from the pressor area is moderated by nerves transmitting impulses from the depressor area which have a directly inhibiting effect on the transmission of impulses from the pressor area. Thus it can be thought that the nerve impulses of the depressor area act like a ‘ collar ’ or tap; the greater the number of impulses from the depressor area the tighter the collar or tap is made,
  reducing the number of impulses from the pressor area to the heart and thus the effect on heart rate and force of contraction.

Hormone activity

• Two hormones are normally associated with the control of heart rate
• Adrenaline – from the adrenal medulla. Adrenaline has the same effect as noradrenaline released by the sympathetic nervous system
• Thyroxine – from the thyroid gland. Released in large quantities thyroxine has the effect of increasing the heart rate.

Regulation of Blood Pressure

Blood pressure is the force or pressure that the blood exerts on the walls of blood vessels. Systemic arterial blood pressure maintains the essential flow of blood into and out of the organs of the body. Keeping blood pressure
within normal limits is very important. If it becomes too high, blood vessels can be damaged, causing clots or bleeding from sites of blood vessel rupture. If it falls too low, then blood flow through tissue beds may be inadequate.

This is particularly dangerous for essential organs such as the heart, brain or kidneys. The systemic arterial blood pressure, usually called simply arterial blood pressure, is the result of the discharge of blood from the left ventricle into the already full aorta.

Blood pressure varies according to the time of day, the posture, gender and age of the individual. Blood pressure falls at rest and during sleep. It increases with age and is usually higher in women than in men.

Systolic and diastolic pressures.

When the left ventricle contracts and pushes blood into the aorta, the pressure produced within the arterial system is called the systolic blood pressure.

In adults it is about 120 mmHg or 16 kPa.

In complete cardiac diastole when the heart is resting following the ejection of blood, the pressure within the arteries is much lower and is called diastolic blood pressure.

In an adult this is about 80 mmHg or 11 kPa.

The difference between systolic and diastolic blood pressures is the pulse pressure.
Arterial blood pressure (BP) is measured with a sphygmomanometer
and is usually expressed with the systolic pressure written above the diastolic pressure:

Elasticity of arterial walls.

There is a considerable amount of elastic tissue in the arterial walls, especially in large arteries. Therefore, when the left ventricle ejects
blood into the already full aorta, the aorta expands to accommodate it and then recoils because of the elastic tissue in the wall. This pushes the blood forwards, into the systemic circulation. This distension and recoil occur throughout the arterial system. During cardiac diastole the elastic recoil of the arteries maintains the diastolic pressure.

REFERENCES

1. Ross and Wilson Anatomy& Physiology in Health and Illness, 12th Edition,2014 Elsevier Ltd. ISBN 978-0-7020-5325-2
2. Marieb EN, Hoehn KN (2015) Human Anatomy and Physiology (10th edn). London: Pearson.
3. Fundamentals of anatomy and physiology for student nurses / edited by Ian Peate and Muralitharan Nair. Blackwell Publishing, ISBN 978-1-4443-3443-2.
4. Oberman R, Shumway KR, Bhardwaj A. Physiology, Cardiac. [Updated 2023 Jul 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK526089/

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