Basics about Cardiovascular System : Structure and Function

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Cardiovascular diseases (CVD) are conditions that affect the structures or functions of your heart. It is the leading cause of mortality in India. According to global Burden of Disease study age standarized estimates, nearly a quarter of all the death in India are attributed to CVD. The age standarized CVD death rate of 272 per 1,00,000 population in India is higher than global average of 235 per 1,00,000 population. 

CVD affects patients in many aspects of performance areas (activities of daily living, work, lesiure), performance components (muscles strength, endurance, psychological stress, breathlessness, early fatigue during work, cognitive disturbance), performance context (social participation, disability status, development). 

Fig : Diagnosing, medical treatment and  rehabilitation of Cardiovascular Diseases is essential

An understanding of the normal function of the cardiopulmonary system, the pathology of cardiovascular disease, common risk factors, clinical terminology, medical interventions, precautions, and standard treatment techniques will guide the Physiotherapist and Occupational therapist in providing effective care and promoting recovery of function in clients with compromised cardiovascular systems. Every living cell of the body has three major requirements for life: (1) a constant supply of nutrients and oxygen, (2) continual removal of carbon dioxide and other waste products, and (3) a relatively constant temperature. The cardiovascular and pulmonary systems play key roles in meeting these requirements. But in this post we will gain knowledge about various CVD in adult patients and its impact on their daily living.

Basic concepts about heart anatomy Andrew how it works : Therapists should have a sound knowledge about these concepts when dealing with cardiac patients and when making decisions about rehabilitation plan for them. 

Various parts of cardiovascular system to focus on are heart chambers (left-right atria and ventricles), heart musculature (endocardium, myocardium, epicardium, pericardium), input valves (bicuspid and tricuspid valves) and output valves (pulmonary and aortic valves), pulmonary artery and vein, aorta, superior and inferior vena cava coronary arteries supplying heart muscles and specialized electrical conduction system (Sinoatrial node, Atrioventricular node, Bundle of His and its Left and right branches, Purkinje fibers) and peripheral blood vessels (arteries and veins)

Fig : Anatomy of heart : Inner structure of heart

Fig : Anatomy of heart : Outer structure of heart

Various functions of cardiovascular system to focus on are :

1) Cardiac output (CO), Heart rate (HR) and stroke volume (SV): HR and SV determines cardiac output, which is the amount of blood ejected by the heart each minute. (CO = HR × SV)

• HR, or the number of beats per minute, can be monitored by feeling the patient’s pulse at the radial, brachial, or carotid sites. Normally humans have their heart rate between 70 to 90 beats per minute. Athletes have a lower basal heart rate while stress, exercises and anxiety in normal persons often raises the heart rate.
• Stroke volume : is the volume of blood pumped out of the left ventricle of the heart during each systolic cardiac contraction. Average (normal) stroke volume of a person is 70 ml. SV is increased mainly by an increase in end diastolic volume (the Frank-Starling mechanism) and by an increase in contractility due to sympathetic nerve stimulation or to epinephrine. Afterload can also play a significant role in certain situations.
• Normal CO is 5 to 6 liters per minute. It can increase upto 30 liters per minute during exercise or stress conditions. CO is influenced by strength of contraction of each ventricles, rate of contraction, amount of venous return available to the ventricles (Preload).
• Preload : 'Preload' is the hemodynamic load or stretch on the myocardial wall at the end of the diastole (end diastolic volume) just before the contraction begins. For ventricles, there are several possible measures of preload : 1) end diastolic pressure, 2) end diastolic volume, 3) wall stress at end diastole, 4) end diastolic sarcommere length (but this is not possible)
• Afterload : 'Afterload' is the hydrolic/ mechanical load imposed on the ventricles during ejection. Under normal physiological conditions, this is determined by the arterial system. The load is usually imposed on the heart by the arterial system (aorta and peripheral arteries), but under pathological conditions when the mitral valve is incompetent ( i.e. leaky) or the aortic valve is stenotic ( i.e. constricted) 'afterload' is determined by the factors other than the properties of the arterial system. Indices of afterload include, aortic pressure, ejection wall stress, total peripheral resistance (TPR) and arterial impedance.

• Venous Return : Quantity of blood flowing from peripheral veins back into the right atrium each minute. Venous return is important in maintaining normal circulation. Efficient amount of CO, in the subsequent cardiac cycle, is controlled or maintained by amount of venous return. The pressure in the veins is the driving force for filling the heart, called as venous pressure. Various factors which determines the venous pressure and venous return are : 1) action of skeletal muscle pump, 2) pressure change within the thoracic cavity during inspiration and expiration, 3) sympathetic activity will reduce venous compliance and improve blood flow, 4) the greater blood volume in the veins, the greater the flow, 5) efficient working of the heart to maintain CO and peripheral blood flow.
• Cardiac Index (CI) : it is cardiac output per minute per square meter of body surface area (BSA). Normal cardiac index is 2.5 to 4.2 liter/minute/square meter of body surface area for adults. CO is frequently explained in terms of CI. This is a more accurate measure of cardiac function than CO. It is calculated as follows : Cardiac index (CI) = CO ÷ BSA. It indicates whether the heart is supplying body with adequate oxygen and nutrients.
• Cardiac Reserve (CR) : it is the difference between cardiac work performance (cardiac output) at rest or basal conditions and that performed at maximal exercise conditions. (CR = maximum CO during exercise - CO during rest). CR refers to the heart's ability to adjust to the demands placed upon it.  Mechanism of cardiac reserve includes 1) short term mechanisms is rapid in onset with moment to moment body needs : HR reserve, SV reserve, 2) long term mechanisms occurs in cases of prolonged excess work done by heart during increased afterload : cardiac muscle hypertrophy, dilatation of cardiac chambers.
• Cardiac Output is affected in patients with myocardial infarction, heart failure, dilated cardiomyopathy, Rheumatic heart disease.

Fig : Cardiac Output is determined by heart rate and stroke volume ejected per minute

Fig : Determinants of cardiac output

Fig : Determinant of cardiac output

Fig : Why understanding Cardiac index is necessary with respect to Cardiac output.

2) Properties of Cardiac cell i.e. Cardiac tropism :

Properties of cardiac cell or muscle fibers :

• Automaticity : Heart has the capability to contract even in the absence of neural control.
• Conductivity : the ability to conduct excitation through cardiac tissue. Impulses produced in th SA node is conducted by the specialized conducting pathway.
• Excitability : ability of the cardiac muscle to respond to different stimuli.
• Rhythmicity : ability to initiate heart beat (electrical impulse) continuously and regularly without external stimulation. 
• Contractility : Cardiac muscle contracts in response to stimulus.
• Distensibility : it occurs due to compliance of heart muscles.
• Refractoriness : the refractory period of cardiac muscles allows complete emptying of the ventricles prior to next contraction. Refractoriness of each phase of action potential is governed by the number of sodium channels ready to activate. The effective refractory period (ERP) is the amount of time in which the cell cannot respond to a new conducted stimulus. This period is how the heart stays in rhythm and prevent arrhythmias. The atrial ERP is much shorter than ventricular ERP. Problems with the atrial ERP will lead to atrial arrhythmias, such as atrial flutter and atrial fibrillation. If ERP of ventricles is affected then it leads to ventricular fibrillation. The ERP is shortened due to tachycardia and low potassium levels in body.
• Functional syncytium : cardiac muscle cells are mechanically, chemically and electrically connected to one another, thus the entire tissue resembles a single, enormous muscle cell. When one cardiac cell undergoes an action potential, the electrical impulses spreads to all other cell that are joined by gap junctions so they become excited and contract as a single functional syncytium. Heart is composed of  two syncytium namely the atrial syncytium and the ventricular syncytium. Thus this two separate syncytium allows the atria to contract a short time ahead of ventricular contraction.

Cardiotropy based on cardiac muscles properties:

• Chronotropic (Heart rate)
• Inotropic (Contractility)
• Dromotropic (Conduction velocity)
• Bathmotropic (Excitability)
• Lusitropic (Relaxation)

Cardiac electrical conductivity is affected in cases namely, atrial fibrillation, atrial arrhythmias, ventricular fibrillation, conduction block (first degree, second degree, third degree) etc.

Fig : Electrical conduction System of heart

3) Cardiac Cycle and myocardial contractility : 

Cardiac cycle is maintained by continuous activity (24×7) of a specialized electrical conduction system that causes the heart to contract and relax. 

• The sequence of changes in the pressure and flow in the cardiac chambers and blood vessels in between two subsequent contractions is known as cardiac cycle. The cardiac cycle occurs in two phases: input (diastole) and output (systole).
• Normal duration of the cardiac cycle is 0.8 sec. It consists of Ventricular systole: 0.3 sec, Ventricular diastole: 0.5 sec, Atrial systole: 0.1 sec and Atrial diastole: 0.7 sec.

Fig : Cardiac cycle phases

Myocardial contractility : Each cell within the electrical conduction system of the heart can respond to, conduct, resist for a brief period, and generate an electrical impulse. 

• During the input phase, blood flows through the atria and into the ventricles. The atria contract and push more blood into the ventricles. Once the pressure inside the ventricles is equal to the pressure in the atria, the input valves (tricuspid in the right ventricle and mitral [or bicuspid] in the left ventricle) close. The ventricles then contract, which results in rapidly increasing ventricular pressure. 
• When the pressure inside the ventricles exceeds the pressure in the blood vessels beyond (aorta and systemic BP), the output valves (pulmonary in the right and aortic in the left) open, and the ventricles continue to contract and squeeze blood under greater and greater pressure into the pulmonary and body circulation. 
• When pressure in the emptying ventricles falls below the pressure in the blood vessels beyond (aorta and systemic BP), the output valves to close. Then atria starts to refill again from superior and inferior vena cava and the input phase begins

Rules controlling Contractility :

1) All or None Law :

• The cardiac muscles contracts either maximally or not at all (under constant conditions)
• The Atria contract as one unit and the ventricles contract as one unit.
• This ia significant for efficient pumping of the blood

2) Staircase or Treppe Phenomenon :

• Rapidly repeated stimulation of the cardiac muscles produce gradual increase in the strength of contraction.
• The earlier contractions produce better conditions (heat, less viscosity between muscle fibers, more calcium) for the following contractions.

3) Frank-Starling Law : 

• Within limits, the greater the initial length of the cardiac muscle fibre (stretch), the greater the force of contraction.
• The initial length is determined by the volume of blood filling ventricles at end of diastole (End diastolic volume).
• Cardiac performance (its ability to generate pressure or to pump blood) increases as preload is increased.

4) Ejection fraction (EF) : it refers to how well person's left or right ventricles pumps blood with each heart beat. Most times, EF refers to the amount of blood being pumped out of the left ventricle each time it contracts. The left ventricle is the heart's main pumping chamber. An EF that is below normal can be a sign of heart failure. 

• Patient's EF is expressed as a percentage. It is calculated using following formula : EF = (Stroke volume ÷ End diastolic volume) × 100
• Average (normal) stroke volume of a person is 70 ml. EF > 60% (mainly left ventricular EF) suggest normal heart functioning. Normal end diastolic volume is 120 ml of blood and normal end systolic volume is 50 ml of blood.
• EF is often used as a clinical index to evaluate the inotropic status of heart.
• Low EF (less than 60%) is suggestive of sign of  cardiac dysfunction such as 1) damage to heart muscles due to myocardial infarction, 2) Cardiac muscle diseases (cardiomyopathy), 3) Cardiac valve dysfunction, 4) High blood pressure that has not been under control for a long time.
• In heart failure, specifically in dilated cardiomyopathy, EF can be very small as SV decreases and end diastolic volume increases. In severe heart failure, EF can be 20% or less. It is important to note that, in certain cases EF may be normal but still the ventricles will be in failure. For example, in diastolic dysfunction caused by ventricular hypertrophy in which, the filling is impaired because of low ventricular compliance (i.e. 'stiff' heart) and SV is therefore reduced. For this reason, low EF is generally associated with systolic dysfunction rather than diastolic dysfunction.

Fig : Ejection fraction of heart

5) Blood pressure (BP) : BP is the pressure that the blood exerts against the walls of any vessel as the heart beats. It is highest in the left ventricle during systole and decreases in the arterial system with distance from the heart. BP reading consists of two parameters namely, systolic BP and Diastolic BP.

• The systolic BP is the measure of highest pressure force within arteries, when your heart contracts and pushes out the blood in peripheral body circulation. Normal systolic BP is 120 mm of Hg.
• The diastolic BP is the measure of lower pressure within the arteries, during brief 'resting' period between heartbeats (heart ventricle muscle relaxes). Normal diastolic BP is 80 mm of Hg.
• Pulse pressure : it is the difference between systolic and diastolic pressure. The normal range of pulse pressure is between 40 to 60 mm Hg. Pulse pressure tends to increase after the age of 50 because the arteries (aorta and other large arteries) and blood vessels stiffness gradually progresses with age. The greater your pulse pressure, the stiffer and more damaged the blood vessels becomes. High pulse pressure (greater than 60 mm Hg) is considered a risk factor for cardiovascular disease (especially for older adults) namely HTN,  heart attack, stroke. Low pulse pressure can indicate decreased cardiac output, in cases of heart failure.
• Blood pressure is the force that moves the blood through our circulatory system. Blood pressure  gradient is essential and responsible for the flow of blood within vasculature. Thus, it helps to delivers essential nutrients, transport oxygen and carbon dioxide, delivers white blood cells and antibodies for immunity, hormones such as insulin etc.

• High blood pressure / hypertension increases the work of heart to pump the blood into the body circulation i.e. afterload/resistance is increased. Blood pressure rises when the arteries are blocked and the blood can no longer flow freely. This is particularly pronounced during strenuous situations, as the heart must work even harder to supply the body with enough oxygen and nutrients. High BP damages the interior linings of blood vessels and thus making them more rigid (less elastic). The damaged lining increases the risk of fat deposition (atherosclerosis or plaque formation), thereby impending blood flow. Continuous strain on the heart may lead to hypertrophy of ventricular muscles (mostly left ventricle). For maintaining the blood output for peripheral circulation, the blood supply to the heart muscles through coronary arteries must also be sufficient enough to provide energy, oxygen and nutrients for continuous working. If coronary artery blood supply is compromised, insufficient oxygen supply takes place, and part of the heart muscles may die due to ischemia thus leading to myocardial infarction.

Fig : Blood Pressure category 

6) Cardiac muscles nerve innervation and its function :

• Without neuronal influences, SA node will drive at rate of its spontaneous activity.
• Normally heart rate (chronotropic effect) is influenced by sympathetic and parasympathetic activity.
• Autonomic innervation of SA node is main controller of HR. Sympathetic and parasympathetic nerve fibers modify rate of spontaneous depolarization.
• Heart rate is increased by stimulation of sympathetic nerve to the heart (norepinephrine) and epinephrine. Heart rate is decreased by stimulation of parasympathetic nerve to the heart (acetylcholine)
• Sympathetic stimulation of heart increases heart rate (positive chronotropy), inotropy and conduction velocity (positive dromotropy and dilatation of coronary arteries, whereas parasympathetic stimulation on heart has opposite effect.
• Parasympathetic nerve stimulation results in reduction in rate and force of contraction of heart and constriction of coronary arteries.

Coordinated work between cardiovascular system and respiratory system: 

• Cardiac and Respiratory disorders includes Myocardial infarction, Rheumatic heart disease, heart failure, Cardiac arrhythmia, Chronic obstructive pulmonary disease, Pneumonia, Interstitial lung disease etc.
• Proper functioning of heart and lungs is essential for adequate blood and oxygen supply respectively in the body. Continuous circulation of blood throughout the body is necessary for sufficient oxygen supply, removal of carbon dioxide, gases exchange in lungs and capillaries, adequate ATP production for energy, regulating body temperature and support the immune system.

• Cardiac impairments might lead to decrease in functioning of cardiac musculature or  decrease in cardiac output and ejection fraction or insufficient cardiac contractility. This leads to insufficient amount of blood availability for oxygenation and carbon dioxide removal within lungs. To compensate for the impaired function, the unaffected cardiac musculature has to put more efforts in order to fullfill the patient's work demands to complete a task i.e. work of heart is increased compared to premorbid state of person's heart.
• Respiratory impairments might lead to decreased lung capacity or decreased tidal volume, impaired gases exchange.
• All the above pathological changes affects occupational performance as patients feel early fatigability, breathlessness, syncope, cough, decrease in quality and quantity of work, difficult and slowness in occupational functioning.

Thankyou for reading!!!

Dr. Pallavi Khadse-Kolhe, Dr. Ashwini Sangar, Dr. Sheetal Tatar-Dhande.