Cardiovascular System

 Chapter 4

CARDIOVASCULAR SYSTEM 

Introduction to Cardiovascular System 

The heart is muscular organ about the size of a closed fist located in the chest between the lungs behind the sternum and above the diaphragm. It is surrounded by the pericardium. On its superior end, the base of the heart is attached to the aorta, pulmonary arteries and veins, and the vena cava. The inferior tip of the heart, known as the apex, rests just superior to the diaphragm. The base of the heart is located along the body’s midline with the apex pointing toward the left side. Because the heart points to the left, about 2/3 of the heart’s mass is found on the left side of the body and the other 1/3 is on the right.

Heart is the pump which is responsible for maintaining adequate circulation of oxygenated blood around the vascular network of the body. It takes in deoxygenated blood through the veins and delivers it to the lungs for oxygenation before pumping it into the various arteries.

 Anatomy of the Heart 

• Pericardium: The heart is placed within a fluid filled cavity called as pericardial cavity. The walls and lining of the pericardial cavity are made up of a special membrane known as the pericardium. Pericardium is a type of serous membrane that produces serous fluid to lubricate the heart and prevent friction between the ever-beating heart and its surrounding organs. Besides lubrication, the pericardium serves to hold the heart in position and maintain a hollow space for the heart to expand when it is full. The pericardium has two layers, a visceral layer that covers the outside of the heart and a parietal layer that forms a sac around the outside of the pericardial cavity.
• Epicardium: The epicardium is the outermost layer of the heart wall. It is also referred to as visceral pericardium, which is inner layer of pericardium. The epicardium is a thin layer of serous membrane that helps to lubricate and protect the outside of the heart.

• Myocardium: Myocardium is the thick middle layer of heart wall and consists of numerous layers of cardiac muscle fibers that wrap around the heart. Contraction of myocardium pumps blood out of the heart into the aorta and pulmonary trunk arteries. 

• Endocardium: Endocardium is the simple squamous endothelium layer that lines inside the heart. The endocardium is very smooth and is responsible for keeping blood from sticking to the inside of the heart and forming potentially deadly blood clots. 

• Heart Chambers: The heart contains four chambers: the right atrium, left atrium, right ventricle and left ventricle. The atria are smaller than the ventricles and have thinner, less muscular walls than the ventricles. The atria act as receiving chambers for blood, so they are connected to the veins that carry blood to the heart. The ventricles are the larger, stronger pumping chambers that send blood out of the heart. The ventricles are connected to the arteries that carry blood away from the heart.

• Heart Valves: The heart functions by pumping blood both to the lungs and to the systems of the body. To prevent blood from flowing backwards or “regurgitating” back into the heart, a system of one-way valves are present in the heart. The heart valves can be divided into two types: atrioventricular and semilunar valves. 

• Atrioventricular Valves (AV): The AV valves are located in the middle of the heart between the atria and ventricles and only allow blood to flow from the atria into the ventricles. The AV valve on the right side of the heart is called the tricuspid valve because it is made of three cusps (flaps) that separate to allow blood to pass through and flow backward. The AV valve on the left side of the heart is called the mitral valve or the bicuspid valve because it has two cusps. The AV valves are attached on the ventricular side to tough strings called chordae tendineae.

• Semilunar Valves: The semilunar valves, so named for the crescent moon shape of their cusps, are located between the ventricles and the arteries that carry blood away from the heart. The semilunar valve on the right side of the heart is the pulmonary valve, so named because it prevents the backflow of blood from the pulmonary trunk into the right ventricle.

Conduction System of the Heart 

• The heart is able to set its own rhythm and also to conduct the signals necessary to maintain and co-ordinate this rhythm throughout its structures. About 1% of the cardiac muscle cells in the heart are responsible for forming the conduction system that sets the pace for the rest of the cardiac muscle cells.

• The conduction system starts with the pacemaker of the heart and a small bundle of cells known as the sinoatrial (SA) node. The SA node is located in the wall of the right atrium, inferior to the superior vena cava. The SA node is responsible for setting the pace of the heart as a whole and directly signals the atria to contract. The signal from the SA node is picked up by another mass of conductive tissue known as the atrioventricular (AV) node.

• The AV node is located in the right atrium in the inferior portion of the interatrial septum. The AV node picks up the signal sent by the SA node and transmits it to the bundle of His. The AV bundle is a strand of conductive tissue that runs through the interatrial septum and into the interventricular septum. 

• The AV bundle splits into left and right branches in the interventricular septum and continues running through the septum until they reach the apex of the heart. From the left and right bundle branches are many. Purkinje fibers that carry the signal to the walls of the ventricles, stimulate the cardiac muscle cells to contract in a coordinated manner to efficiently pump blood out of the heart.

 Physiology of the Heart 

At any given time, the chambers of the heart may be found in one of two states:

• Systole: During systole, cardiac muscle tissue is contracting to push blood out of the chamber.

• Diastole: During diastole, the cardiac muscle cells relax to allow the chamber to fill with blood. Blood pressure increases in the major arteries during ventricular systole and decreases during ventricular diastole. This leads to the two values associated with blood pressure, (i) systolic blood pressure is the higher value and (ii) diastolic blood pressure is the lower value. For example, a blood pressure of 120/80 describes the systolic pressure (120) and the diastolic pressure (80).

The Cardiac Cycle 

The cardiac cycle includes all of the events that take place during one heartbeat. There are three phases to the cardiac cycle:trial systole, ventricular systole and relaxation.

• Atrial systole: During the atrial systole phase of the cardiac cycle, the atria contract and push blood into the ventricles. To facilitate this filling, the AV valves stay open and the semilunar valves stay closed to keep arterial blood from re-entering the heart. The atria are much smaller than the ventricles, so they only fill about 25% of the ventricles during this phase. The ventricles remain in diastole during this phase.

• Ventricular systole: During ventricular systole, the ventricles contract to push blood into the aorta and pulmonary trunk. The pressure of the ventricles forces the semilunar valves to open and the AV valves to close. This arrangement of valves allows for blood flow from the ventricles into the arteries. The cardiac muscles of the atria repolarize and enter the state of diastole during this phase.

• Relaxation phase: During the relaxation phase, all four chambers of the heart are in diastole as blood pours into the heart from the veins. The ventricles fill to about 75% capacity during this phase and will be completely filled only after the atria enter systole. The cardiac muscle cells of the ventricles repolarize during this phase to prepare for the next round of depolarization and contraction. During this phase, the AV valves open to allow blood to flow freely into the ventricles while the semilunar valves close to prevent the regurgitation of blood from the great arteries into the ventricles. 

Blood Flow Through the Heart 

• Deoxygenated blood returning from the body first enters the heart from the superior and inferior vena cava. The blood enters the right atrium and is pumped through the tricuspid valve into the right ventricle. From the right ventricle, the blood is pumped through the pulmonary semilunar valve into the pulmonary arteries.

• The pulmonary artery carries blood to the lungs where it releases carbon dioxide and absorbs oxygen. The blood in the lungs returns to the heart through the pulmonary veins. From the pulmonary veins, blood enters the heart again in the left atrium. The left atrium contracts to pump blood through the bicuspid (mitral) valve into the left ventricle. 

The Electrocardiogram 

• The electrocardiogram (also known as an EKG or ECG) is a non-invasive device that measures and monitors the electrical activity of the heart through the skin. The ECG produces a distinctive waveform in response to the electrical changes taking place within the heart.

• The first part of the wave, called the P wave, is a small increase in voltage of about 0.1 mV that corresponds to the depolarization of the atria during atrial systole. The next part of the EKG wave is the QRS complex which features a small drop in voltage (Q) a large voltage peak (R) and another small drop in voltage (S). The QRS complex corresponds to the depolarization of the ventricles during ventricular systole. The atria also repolarize during the QRS complex but have almost no effect on the EKG because they are so much smaller than the ventricles. 

• The final part of the EKG wave is the T wave, a small peak that follows the QRS complex. The T wave represents the ventricular repolarization during the relaxation phase of the cardiac cycle. Variations in the waveform and distance between the waves of the EKG can be used clinically to diagnose the effects of heart attacks, congenital heart problems, and electrolyte imbalances 

Heart Sounds  

• The sounds of a normal heartbeat are known as “lubb” and “dupp” and are caused by blood pushing on the valves of the heart. The “lubb” sound comes first in the heartbeat and is the longer of the two heart sounds. The “lubb” sound is produced by the closing of the AV valves at the beginning of ventricular systole. During a normal heartbeat, these sounds repeat in a regular pattern of lubb-dupp-pause.

• Any additional sounds such as liquid rushing or gurgling indicate a structure problem in the heart. The most likely causes of these extraneous sounds are defects in the atrial or ventricular septum or leakage in the valves.

Cardiac Output  

Cardiac output (CO) is the volume of blood being pumped by the heart in one minute. The equation used to find cardiac output is:

• CO = Stroke Volume × Heart Rate: Stroke volume is the amount of blood pumped into the aorta during each ventricular systole, usually measured in millilitres. Heart rate is the number of heart beats per minute. The average heart can push around 5 to 5.5 litres per minute at rest. 

• Arteries: The blood vessels which carry blood from the heart to various body organs are called arteries. All arteries carry oxygenated blood, except pulmonary artery, which carries deoxygenated blood.

• Veins: The vessels which carry blood from various body organs to the heart are known as veins. All veins carry deoxygenated blood except pulmonary vein, which carries oxygenated blood.

• Capillaries: Capillaries are the most common, smallest and thinnest of the blood vessels in the body. They can be found running throughout almost every tissue of the body and border the edges of the body’s vascular tissues. Capillaries connect to arterioles on one end and venules on the other. Capillaries carry blood very close to the cells of the tissues of the body in order to exchange gases, nutrients, and waste products.

Functions of Cardiovascular System 

The cardiovascular system has three major functions: transportation, protection and regulation of the body’s homeostasis.

• Transportation: The cardiovascular system transports blood to almost all of the body’s tissues. The blood delivers essential nutrients and oxygen and removes wastes and carbon dioxide to be processed or removed from the body. Hormones are transported throughout the body via the blood’s liquid plasma.

• Regulation: The cardiovascular system is instrumental in the body’s ability to maintain homeostatic control of several internal conditions. Blood vessels help maintain a stable body temperature by controlling the blood flow to the surface of the skin. Blood vessels near the skin’s surface open during times of overheating to allow hot blood to dump its heat into the body’s surroundings. In the case of hypothermia, these blood vessels constrict to keep blood flowing only to vital organs in the body’s core. Blood also helps to balance the body’s pH due to the presence of bicarbonate ions, which act as a buffer solution. Finally, the albumins in blood plasma help to balance the osmotic concentration of the body’s cells by maintaining an isotonic environment.

• The Circulatory Pump: The heart is a four-chambered “double pump”, where each side (left and right) operates as a separate pump. The left and right sides of the heart are separated by a muscular wall of tissue known as the septum of the heart. The right side of the heart receives deoxygenated blood from the systemic veins and pumps it to the lungs for oxygenation. The left side of the heart receives oxygenated blood from the lungs and pumps it through the systemic arteries to the tissues of the body. Each heartbeat results in the simultaneous pumping of both sides of the heart, making the heart a very efficient pump.

• Regulation of Blood Pressure: Several functions of the cardiovascular system can control blood pressure. Certain hormones along with autonomic nerve signals from the brain affect the rate and strength of heart contractions. Greater contractile force and heart rate lead to an increase in blood

Hypertension 

• Hypertension is a chronic medical condition that arises when the blood pressure is abnormally high (greater than 140 mm of Hg systolic and 90 mm of Hg diastolic). Hypertension occurs when the body’s smaller blood vessels (the arterioles) narrow, causing the blood to exert excessive pressure against the vessel walls and forcing the heart to work harder to maintain the pressure. Although the heart and blood vessels can tolerate increased blood pressure for months and even years, eventually the heart may enlarge (a condition called hypertrophy) and be weakened to the point of failure.

• Blood pressure is actually a measure of two pressures, the systolic and the diastolic. The systolic pressure is the force that blood exerts on the artery walls as the heart contracts to pump the blood to the peripheral organs and tissues. The diastolic pressure is residual pressure exerted on the arteries as the heart relaxes between beats. A diagnosis of hypertension is made when blood pressure reaches or exceeds 140/90 mmHg (read as “140 over 90 millimetres of mercury”

Types of Hypertensions  

There are two major types of hypertensions and four less frequently found types:

• Primary (Essential) Hypertension: About 95% of people with high blood pressure have essential hypertension or primary hypertension. This condition has no identifiable medical cause. Elevated blood pressure usually begins to appear between age 30 and 50 but can begin at older ages. Usually, people with essential hypertension have no symptoms, but may experience frequent headaches, tiredness, dizziness, or nose bleeds. Although the cause is unknown, but contributing factors for essential hypertension may be, obesity, smoking, alcohol, diet and inherited.

• Secondary Hypertension: About 5%-10% of people with high blood pressure have secondary hypertension. This condition has definite cause; the most common cause of secondary hypertension is an abnormality in the arteries supplying blood to the kidneys. Other causes include airway obstruction during sleep, diseases and tumors of the adrenal glands, hormone abnormalities, thyroid disease, and too much salt or alcohol in the diet. Drugs can cause secondary hypertension, including OTC medications such as ibuprofen and pseudoephedrine.

• Isolated Systolic Hypertension: In this case, the systolic blood pressure (the top number) is consistently above 160 mm Hg, and the diastolic below 90 mmHg. This may occur in older people, and results from the age-related stiffening of the arteries. The loss of elasticity in arteries, like the aorta, is mostly due to arteriosclerosis. The Western lifestyle and diet is believed to be the root cause.

• Malignant hypertension: Malignant hypertension is the most threatening form of high blood pressure. It is marked by an unusually sudden rise in blood pressure to dangerous levels. Diastolic pressure often reaches 130 mm Hg or higher. However, malignant hypertension may also occur at lower, less alarming levels, if the rise is particularly sudden. Unlike other kinds of high blood pressure, malignant hypertension is usually accompanied by dramatic symptoms such as severe headache, shortness of breath, chest pain nausea and vomiting, blurred vision, or even blindness, seizures and loss of consciousness.

• Resistant Hypertension: If blood pressure cannot be reduced to below 140/90 mmHg, despite a triple-drug regimen of antihypertensive medications called as resistant hypertension. Resistant hypertension may occur in 20 to 30 % of high blood pressure cases. It may have a genetic component and is more common in people who are older, obese, and female or have an underlying illness, such as diabetes or kidney diseas.

• Hypertension during Pregnancy: High blood pressure occurs in 6 % to 8 % of pregnancies, and in most of these cases, it is diagnosed during a first pregnancy. Pregnancy can cause high blood pressure due to hormonal changes or from a serious complication of pregnancy known as preeclampsia, a condition that causes tightening of arteries throughout the mother’s body and placenta, as well as unpredictable blood clotting.  

Epidemiology 

• As per the World Health Statistics 2012, of the estimated 57 million global deaths in 2008, 36 million (63%) were due to noncommunicable diseases (NCDs). The largest proportion of NCD deaths is caused by cardiovascular diseases (48%). In terms of attributable deaths, raised blood pressure is one of the leading behavioral and physiological risk factors to which 13% of global deaths are attributed. Hypertension is reported to be the fourth contributor to premature death in developed countries and the seventh in developing countries. Recent reports indicate that nearly 1 billion adults (more than a quarter of the world’s population) had hypertension in 2000, and this is predicted to increase to 1.56 billion by 2025. Earlier reports also suggest that the prevalence of hypertension is rapidly increasing in developing countries and is one of the leading causes of death and disability.

• Children: Most childhood hypertension, particularly in preadolescents, is secondary to an underlying disorder. Apart from obesity, kidney disease is the most common (60–70%) cause of hypertension in children. Adolescents usually have primary (essential) hypertension, which accounts for 85–95% of cases.

Etiology 

The exact causes of high blood pressure are not known, but several factors and conditions may play a role in its development, including:

1.   Smoking 
2.   Being overweight or obese 
3.   Lack of physical activity 
4.  Too much salt in the diet 
5.  Too much alcohol consumption

• Many people with kidney disorders have secondary hypertension. The kidneys regulate the balance of salt and water in the body if the kidneys cannot rid the body of excess salt and water, blood pressure goes up. 

• Kidney infections, a narrowing of the arteries that carry blood to the kidneys, called renal artery stenosis and other kidney disorders can disturb the salt and water balance.

• Cushing’s syndrome and tumors of the pituitary and adrenal glands often increase levels of the adrenal gland hormones like cortisol, adrenaline and aldosterone, which can cause hypertension. 

Pathophysiology  

• Hypertension causes three major circulatory abnormalities: increased arteriolar resistance, increased large artery stiffness, and early or premature reflection of arterial pulse waves. Increased resistance and vessel stiffness in younger hypertensive patients result from structural changes, including thinning and fracturing of elastin, increased collagen deposition, and increased wall thickness. These changes manifest primarily as a greater rise in systolic pressure greater than diastolic pressure.

• In elderly, an increased arterial stiffness is the greater factor and may contribute to isolated systolic hypertension, in which systolic pressure is elevated but diastolic pressure is normal or low. Patients with isolated systolic hypertension are at substantially increased risk for stroke, coronary heart disease, and congestive heart failure. Pulse wave reflection referes to the backward rebound of some of the cardiac output as it encounters the resistance of the arteries. When arteries are normally complaint, this reflected flow occurs during diastole and assists with filling of the coronary arteries. In hypertension, however, reflection occurs prematurely, during systole, contributing to vascular overload in the aortic arch and in the coronary carotid and renal arteries. 

• Secondary hypertension accounts for approximately 5-10% of all cases of hypertension, with the remaining being primary hypertension. Secondary hypertension has an identifiable cause whereas primary hypertension has no known cause (i.e., idiopathic).

Stress: Emotional stress leads to activation of the sympathetic nervous system, which causes increased release of norepinephrine from sympathetic nerves in the heart and blood vessels, leading to increased cardiac output and increased systemic vascular resistance. Furthermore, the adrenal medulla secretes more catecholamines (epinephrine and norepinephrine). Activation of the sympathetic nervous system increases circulating angiotensin.

Sleep Apnea: Sleep apnea is a disorder in which people repeatedly stop breathing for short periods of time (10-30 seconds) during their sleep. This condition is often associated with obesity, although it can have other causes such as airway obstruction or disorders of the central nervous system. These individuals have a higher incidence of hypertension. The mechanism of hypertension may be related to sympathetic activation and hormonal changes associated with repeated periods of apnea-induced hypoxia and hypercapnea, and from stress associated with the loss of sleep. 

Pheochromocytoma: Catecholamine secreting tumors in the adrenal medulla can lead to very high levels of circulating catecholamines (both epinephrine and norepinephrine). This leads to α-adrenoceptor mediated systemic vasoconstriction and β-adrenoceptor mediated cardiac stimulation, both of which contribute to significant elevations in arterial pressure. Despite the elevation in arterial pressure, tachycardia occurs because of the direct effects of the catecholamines on the heart and vasculature.

Preeclampsia: This is a condition that sometimes develops during the third trimester of pregnancy that causes hypertension, sometimes with fluid retention and proteinuria due to increased blood volume and tachycardia. The former increases cardiac output by the Frank Starling mechanism. 

Arch of the aorta: Obstruction of the aorta at this point reduces distal arterial pressures and elevates arterial pressures in the head and arms. The reduced systemic arterial pressure activates the renin angiotensin-aldosterone system, which leads to an increase in blood volume. These further increases arterial pressures in the upper body and may largely offset the reduction in lower body arterial pressures

Symptoms 

High blood pressure usually causes no symptoms and high blood pressure often is labelled “the silent killer”. People who have high blood pressure typically do not know it until their blood pressure is measured. Sometimes people with markedly elevated blood pressure may develop: 

1. Headache 
2. Dizziness 
3. Blurred vision 
4.  Nausea and vomiting, and 
5.  Chest pain and shortness of breath. 

People often do not seek medical care until they have symptoms arising from the organ damage caused by chronic (ongoing, long-term) high blood pressure. The following types of organ damage are commonly seen in chronic high blood pressure: 

1.   Heart attack. 
2.   Heart failure. 
3.   Stroke or transient ischemic attack (TIA). 
4.   Kidney failure. 
5.   Eye damage with progressive vision loss. 
6.   Peripheral arterial disease-causing leg pain with walking (claudication). 
7.   Outpouchings of the aorta, called Aneurysms.

It is of extreme importance to realize that high blood pressure can be unrecognized for years, causing no symptoms but causing progressive damage to the heart, other organs, and blood vessels. 

Diagnosis  

• High blood pressure is diagnosed based on the results of a blood pressure test. The test yields two numbers: systolic and diastolic. Blood pressure values are often written as systolic pressure/diastolic pressure; for example, 120/80. The unit of measurement for blood pressure is millimetres of mercury (mmHg).

• Isolated systolic hypertension: It refers to high blood pressure in which only the systolic number is high. It occurs in about two-thirds of people over ages 60 who have high blood pressure. This condition should be taken as seriously as high blood pressure in which both values are elevated, because it can cause just as much harm if left untreated.

Treatment 

• There is no cure for primary hypertension, but blood pressure can almost always be lowered with the correct treatment. The goal of treatment is to lower blood pressure to levels that will prevent heart disease and other complications of hypertension.

• In secondary hypertension, the disease that is responsible for the hypertension is treated in addition to the hypertension itself. Successful treatment of the underlying disorder may cure the secondary hypertension. 

Prevention  

Having high blood pressure can be prevented by eating healthily, maintaining a healthy weight, taking regular exercise, drinking alcohol in moderation and not smoking, reducing salt intake, managing stress.

Congestive Heart Failure  

• Congestive Cardiac failure is a condition associated with heart disorders leading to impairment of the heart to supply sufficient blood to meet the body requirements. Cardiac Failure may be associated with the failure of the right or left ventricle or both. Cardiac failure causes the blood to move through the heart and body at a slower rate, leading to increased pressure in the heart. As a result, the heart is unable to pump enough oxygen and nutrients to meet the body's requirements. The heart chambers thus respond by stretching in order to hold more blood to pump through the body or by becoming stiffer and more thickened. Such mechanism helps to keep the blood moving for a short while, but the heart muscle walls tend to weaken with time and then are unable to pump with enough strength.

• The direct result of the reduced contractility of the cardiac muscles especially those of the ventricles, cause a decrease in the cardiac output and increase in the blood volume of the heart. This causes the kidneys to often respond by causing the body to retain fluid (water) and sodium, as the systemic blood pressure and the renal blood flow both are reduced. This results into building up of fluid in the arms, legs, ankles, feet, lungs or other organs causing oedema which makes the body congested, hence the name Congestive cardiac failure.

• The term congestive heart failure is used for the chronic form of heart failure in which the patient has evidence of congestion of peripheral circulation and of lungs; CHF is the end result of various forms of serious heart diseases.

Etiology 

There are many causes of congestive heart failure including:

• Coronary artery disease leading to heart attacks and heart muscle weakness. 
• Primary heart muscle weakness from viral infections or toxins such as prolonged alcohol exposure.
• Heart valve disease causing heart muscle weakness due to too much leaking of blood or heart muscle stiffness from a blocked valve, and  
• Hypertension.

Rarer causes of heart failure include:

• Viral myocarditis (an infection of the heart muscle). 
• Infiltrations of the muscle such as amyloidosis.
• HIV cardiomyopathy (caused by Human Immunodeficiency Virus).  
• Connective tissue diseases such as Systemic lupus erythematosus.  
• Abuse of drugs such as alcohol. 
• Pharmaceutical drugs such as chemotherapeutic agents. 
• Arrhythmias.

Pathogenesis  

Heart failure may be caused by one of the following factors either singly or in combination.

• Intrinsic Pump Failure: The most common and most important cause of heart failure is weakening of the ventricular muscle due to disease so that the heart fails to act as an efficient pump. The various diseases which may culminate in pump failure by these mechanisms are as under:

1. Ischaemic heart disease
2. Myocarditis
3. Cardiomyopathies 
4. Metabolic disorders like beriberi, 
5. Disorders of the rhythm e.g. atrial fibrillation and flutter

• Increased workload on the heart: Increased mechanical load on the heart results in increased myocardial demand resulting in myocardial failure. Increased load on the heart may be in the form of pressure load or volume load.

Types of Heart Failure

• Congestive heart failure (CHF) is generally classified as systolic or diastolic heart failure and becomes progressively more common with increasing age. In addition, patients with risk factors for heart disease are more likely to develop congestive heart failure.

•  Systolic heart failure: This condition occurs when the pumping action of the heart is reduced or weakened. A common clinical measurement is ejection fraction (EF). The ejection fraction is a calculation of how much blood is ejected out of the left ventricle (stroke volume) divided by the maximum volume remaining in the left ventricle at the end of diastole, or when the heart is relaxed after filling with blood. A normal ejection fraction is greater than 55%. Systolic heart failure is diagnosed when the ejection fraction has significantly decreased below the threshold of 55%.

• Diastolic heart failure: This condition occurs when the heart can contract normally but is stiff, or less compliant, when it is relaxing and filling with blood. The heart is unable to fill with blood properly, which produces backup into the lungs and heart failure symptoms. Diastolic heart failure is more common in patients older than 75 years of age, especially in patients with high blood pressure, and it is also more common in women.

•  Acute heart failure: It is sudden and rapid development of failure following massive myocardial infarction, valve rupture, myocarditis etc. The sudden reduction in cardiac output, hypotension without edema is prominent features.

• Chronic heart failure: It develops slowly with gradual reduction in cardiac output. It is commonly seen in slowly progressive valvular heart disease, systemic arterial hypertension, chronic obstructive pulmonary diseases etc. Blood pressure is well maintained but is associated with peripheral edema.

Clinical Manifestations  

• The most common manifestation of left ventricular failure is dyspnoea, or a sense of breathlessness. This is caused predominantly by decreased lung compliance resulting from pulmonary edema and congestion, and by increased activity of autonomic stretch receptors within the lung. Dyspnea is most noticeable during periods of physical activity. It is also prominent when the person is lying down (Orthopnea), because of the increased amount of venous blood returned to the thorax from the lower extremities and because the diaphragm is elevated in this position.

• Paroxysmal nocturnal dyspnea is an especially dramatic form of dyspnea that awakens the patients with sudden severe shortness of breath, accompanied by coughing, a chocking sensation, and wheezing. Other manifestations of left ventricular failure include muscle fatigue, an enlarged heart, tachycardia, a third heat sound and fine edematous pulmonary alveoli. With progressive ventricular dilation, the papillary muscles are displaced laterally, causing mitral regurgitation and a high-pitched systolic murmur. Chronic dilation of the left atrium may also occur, and it is often associated with the development of atrial fibrillation manifested by an irregular heartbeat.

• Fluid Retention and Swelling:  Puffy swelling (edema) in the legs, the feet, and the ankles may occur, particularly at the end of the day or after prolonged sitting. Often, the swelling is more noticeable in the ankles or on the lower leg in the front where the bone, the tibia, is close to the skin Pitting edema can occur when pressing down on the skin in the puffy areas. The indentation where the finger pressed may be visible for a few minutes. Pitting edema is not synonymous with heart failure; it can have other causes, including liver and kidney failure. Nonpitting edema is generally not caused by heart failure.

Treatment  

Treatment of Congestive Cardiac Failure is focused on improving the symptoms and preventing the progression of the disease. The major and often neglected form of treatment is lifestyle improvement, which includes: 

• Regulation of the salt and fluid intake: As the entire body suffers from congestion due to fluid accumulation and also that sodium leads to increased fluid accumulation in the body tissues, it is often recommended to restrict the sodium and fluid intake during the cardiac failure.

• Exercise: It is recommended to do any activity which one can sustain for more than just a few minutes while your heart, lungs and muscles work overtime. Such an exercise is known as aerobic exercise. Regular exercise, according to the patient's tolerance level, appears to provide significant benefits and should be used only when the patient is compensated and stable.

Pharmacological Treatment

Pharmacological treatment involves the use of following category of medications:

• Caridac glycosides: The digitalis glycosides are used due to its positive inotropic effect and negative chronotropic effect e.g., Digoxin, digitoxin etc. 

• ACE inhibitors: These agents act by inhibiting the Angiotensin converting enzyme which is responsible for conversion of Angiotensin I (inactive) to Angiotensin II (active). ACE Inhibitors improve symptoms, decrease mortality and reduce ventricular hypertrophy. E.g: Candesartan. 

• Diuretics: These removes excess extracellular fluid in patients with systolic or diastolic heart failure.   

 Ischaemic Heart Disease

  Ischaemic heart disease (IHD) is defined as 'acute or chronic form of a cardiac disability arising from imbalance between the myocardial supply and demand of oxygenated blood'. The alternate term coronary artery disease (CAD) is used synonymously with IHD. Depending on the rate and severity of coronary artery narrowing and the myocardial response, one of four syndromes may develop.

1. Angina pectoris (Chest pain)
2. Acute myocardial infarction 
3. Chronic ischemic heart disease with congestive heart failure
4. Sudden cardiac death

• Etiology: The most common cause of ischemic heart disease is a reduction in coronary arterial blood supply due to atherosclerosis of the coronary arteries. Factors that contribute to the development of ischemic heart disease are similar to those responsible for atherosclerosis in general, and include Hypertension, diabetes mellitus, smoking, high cholesterol, high levels of low-density lipoprotein, and genetic factors and non-atherosclerotic causes are vasospasm, coronary artery stenosis, inflammation of coronary arteries, thrombotic disease, trauma, aneurysms and compression. 

• Pathogenesis: Symptomatic ischemic heart disease is typically associated with a critical stenosis, defined as a 75% or greater reduction in the lumen of one or more coronary arteries by atherosclerotic plaque. With this level of fixed obstruction, the augmented coronary blood follow that may occur as a result of compensatory coronary vasodilation is insufficient to meet even moderate increase.

• Calcium: Channel Blockers: Calcium antagonist inhibits the passage of calcium ions through voltage-dependent L-type calcium channels in cell membranes in the heart and vascular smooth muscle as well as some other excitable tissues. e.g., Amlodipine Nifedipine.

Angina Pectoris 

• Angina pectoris is a clinical syndrome of ischemic heart disease  (IHD) resulting from transient myocardial ischaemia if the heart muscle does not get as much blood as it needs. This usually happens because one or more of the heart's arteries is narrowed or blocked. It is characterized by paroxysmal pain in the substernal or precordial region of the chest which is aggravated by an increase in the demand of the heart and relived by a decrease in the work of here. Often, the pain radiates to the left arm, neck jaw or right arm.

• It can also be referred to as exertional angina. It is associated with sever narrowing of the coronary artery due to build-up of plaque (plaque is excess cholesterol and other debris that has built up inside a coronary artery). With exertion, like walking up a hill or climbing stairs, the heart works harder and needs more oxygen. If it cannot get enough oxygen, a person develops symptoms of Angina, the condition improves with rest. During the attacks, there is depression of ST segment in the ECG due to poor perfusion of the subendocardial region of the left ventricle.

• Unstable angina occurs when the narrowing of the coronary artery due to build-up of plaque becomes so severe that not enough blood gets through to keep the heart functioning normally, even at rest. In most patients, it is induced by acute plaque change with superimposed partial thrombosis, distal embolization of the thrombus, and/or vasospasm. The morphologic changes in the heart are essentially those of coronary atherosclerosis and its associated lesions. In unstable angina, lack of oxygen to the heart leads to necrosis of heart tissue. Thus, increasing the chances of myocardial infarction, requires emergency treatment. Distinction between unstable angina and acute myocardial infarction is made by ST segment changes on ECG.

• Rare type of angina caused basically due to spasm of coronary arteries. Variant angina may occur during resting or active state, presence or absence of clogged arteries from atherosclerosis. Spasms lead to decreased blood flow to the heart and hence increase the risk of heart attack. ECG shows ST segment elevation due to transmural ischaemia. These patients respond well to vasodilators like nitroglycerin. 

Myocardial Infarction (Heart Attack) 

• Myocardial Infarction is a condition resulting from decreased blood and oxygen supply to the heart, causing cell death. The major cause is sudden blockage of coronary arteries. Coronary arteries are blood vessels that supply the heart muscle with blood and oxygen. Blockage of a coronary artery deprives the heart muscle of blood and oxygen, causing injury to the heart muscle causing chest pain and chest pressure sensation. If blood flow is not restored to the heart muscle within 20 to 40 minutes, irreversible death of the heart muscle will begin to occur. Muscle continues to die for six to eight hours at which time the heart attack usually is "complete." The dead heart muscle is eventually replaced by scar tissue.

• Myocardial infarction (MI) is the irreversible death (necrosis) of heart muscle which usually results from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in an epicardial coronary artery, resulting in an acute reduction of blood supply to a portion of the myocardium. Acute MI is the single most common cause of death in industrialized nations. Among fatal cases, nearly half of the patients die before reaching the hospita.

• Major risk factors include previous cardiovascular disease (such as angina, a previous heart attack or stroke), older age (especially men over 40 and women over 50), tobacco smoking, high blood levels of certain lipids (triglycerides, low-density lipoprotein or "bad cholesterol") and low levels of high density lipoprotein (HDL, "good cholesterol"), diabetes, high blood pressure, obesity, chronic renal failure, heart failure, excessive alcohol consumption, the abuse of certain drugs (such as cocaine and methamphetamine), and chronic high stress level.

• Rupture of an atherosclerotic plaque exposes the subendothelial collagen to platelets which undergo aggregation, activation and release reaction. These events contribute to the build-up of the platelet mass that may give rise to emboli or initiate thrombosis.

• lowly developing coronary ischaemia from stenosis coronary atherosclerosis of high grade may not cause acute MI but continue to produce episodes of angina pectoris. But acute complications in coronary atherosclerotic plaques in the form of superimposed coronary thrombosis due to plaque rupture and plaque hemorrhages is frequently encountered in cases of acute.

Arteriosclerosis

• Arteriosclerosis can occur when arteries grow thick and stiff and restrict blood flow to organs and tissues in the body. This gradual process, also known as hardening of the arteries, weakens arteries and can develop in various organs, most commonly the heart.

• Arteries circulate blood throughout the body, but when plaque, fat, cholesterol and other cellular waste deposite on artery walls, arteriosclerosis can develop.

• Arteriosclerosis can develop into atherosclerosis. This condition can cause heart disease, strokes, circulation problems in the arms and legs, aneurysms that can cause life-threatening internal bleeding and chronic renal failure.

• The lesions of arteriosclerosis begin as the intima (innermost layer of blood vessel wall) of the arterial wall start to fill up with the deposition of cellular wastes. As this start to mature, they can take different forms of arteriosclerosis. All are linked through common features such as the stiffening of arterial vessels, thickening of arterial walls and degenerative nature of the disease. 

Arteriosclerosis subtypes: Pathologically, there are two subtypes of arteriosclerosis:

• Transplant arteriopathy is intimal enlargement without atherosclerotic changes seen in the walls. Transplant arteriopathy affects large and small muscular arteries and veins as well. It commonly causes inflammation in the 1 or more of the 3 layers in the blood vessel walls.

• Usually, the intima is affected more than the media or adventitia, but all three layers may be affected. After inflammation there is fibrosis and finally calcification and thrombosis may occur. 

Blood test: Blood tests check the levels of certain fats, cholesterol, sugar and protein in the blood that could indicate heart conditions.

• CT scan: X-rays and computers are used to create images of the aorta, heart and blood vessels. This provides a more detailed picture than an ultrasound. 

• Electrocardiogram (EKG): This test measures the electrical activity of the heart and can help to determine if parts of the heart are enlarged, overworked or damaged. 

• Stress testing: Used along with an EKG, the test can show changes to the heart’s rate, rhythm or electrical activity as well as blood pressure. 

• Ultrasound: An ultrasound device can measure blood pressure on various points of arm or leg, which will help to determine any blockages and how quickly blood flows through arteries.