VALVULAR DISEASES OF HEART
 Dr. Bindu.K  BHMS, MD(Hom)

CARDIOVASCULAR SYSTEM
The Heart And Circulation
The adult human heart weighs 250 - 350gms. 60 % of the weight of the heart is constituted by the left ventricle . The left ventricle is 1- 1.5 cm in thickness , the right ventricle is about 0.5cm in thick .Heart uses 8-10 ml of Oxygen per minute . The heart occupies in middle mediastinum and has four chambers ; right atrium ,left atrium and right and left ventricles. Right and left atria are separated by a interatrial septum ; right and left ventricles by a interventricular septum . The blood from right atrium enters in to the right ventricle through right atrioventricular orifice which is approximately 2.5cm in diameter. The blood leaves from right ventricle through pulmonary orifice which is approximately 2cm in diameter . Blood from left atrium goes in to left ventricle through left ventricle through left atrioventricular orifice which is approximately 3cm in diameter [5 cm2 in area ]. The blood leaves from left ventricle through aortic orifice which is approximately 2.5 cm in diameter . All the orifices are guarded by a valve.

Right atrioventricular valve - Tricuspid valve.
Left atrioventricular valve - Mitral valve .
Pulmonary and Aortic valve - Semilunar valves.

Surface anatomy of Heart
The superior border of the heart is formed by the upper margins of the atria and is mainly hidden by the ascending aorta and the pulmonary trunk. The border extends from the upper part of the left second intercostal space [ 1 -2 cm from the margins of the sternum ] to the lower part of the same space on the right . close to the margin of the sternum . A line joining these points also marks the line of the pulmonary arteries which lie along this border of the heart .
The right border of the heart extends from the right end of the superior border to a point on the right sixth costal cartilage
1 - 2 cm from the margin of the sternum . The convex border is formed by the right atrium .
The inferior border extends from the lower extremity of the right border to the apex of the heart . This lies in the fifth left intercostal space immediately medial to a vertical line dropped through the midpoint of the clavicle . This lies in the fifth left intercostal space immediately medial to a vertical line dropped through the midpoint of the clavicle. This border formed mainly by the right ventricle , lies at a lower level in the erect than in the recumbent posture and in inspiration than in expiration It is normally slightly concave , but any condition leading to hypertrophy of the right ventricle ,eg; increased pulmonary arterial pressure , makes it convex, giving the heart a globular shape. The left border is marked by a convex line joining the left ends of the superior and inferior borders . It is formed by the left ventricle except for a small part formed by the left auricle superiorly . The pulmonary orifice lies posterior to sternal end of the third left costal cartilage . The aortic orifice is posterior to the left margin of the sternum at the third intercostal space . Mitral orifice is posterior to the left half of the sternum at the level of the fourth costal cartilage .tricuspid orifice is posterior to the middle of the sternum at the level of the fourth intercostal space .

ARTERIES SUPPLYING THE HEART
The heart is supplied by two coronary arteries
i. Right coronary artery and
ii. Left coronary artery
They are greatly enlarged vasavasorum which arise from two of the three sinuses(dilatations) at the root of the aorta.
The right coronary artery arises from the right aortic sinus. It passes forwards between the auricle of the right atrium and the upper part of the infundibulum and turns inferiorly in the coronary sulcus to the inferior border of the heart. Here it gives off the marginal branch and then turns to the left in the posterior part of coronary sulcus where it gives off its largest posterior interventricular, branch along the posterior interventricular sulcus towards the apex. The right coronary continues in the coronary sulcus supplying a variable amount of the left ventricle and atrium. On the sternocostal surface the right coronary artery supplies the right atrium and a larger part of the right ventricle. It ends without anastomosing the left atrium coronary artery (end artery) .While in the posterior part of the coronary sulcus, it supplies the remainder of the right atrium, all of the diaphragmatic part of the right ventricle and a variable amount of the left atrium and ventricle . The posterior interventricular branch also supplies the posteroinferior part of the interventricular septum [ including AVnode and bundle] and has small anastomoses with the anterior interventricular branch of the left coronary artery in the septum .
The left coronary artery arises from the left aortic sinus . It runs to the left between the pulmonary trunk and the left auricle . Emerging from between them ,it divides into anterior interventricular and circumflex branches. The anterior interventricular branch descends in the anterior interventricular sulcus to the apex. It supplies both ventricles and anterosuperior part of the interventricular septum and reaches the diaphragmatic surface. The circumflex branch curves posteroinferiorly with the great cardiac vein in the left part of the coronary sulcus. It ends to the left of the posterior interventricular sulcus and gives branches to the left atrium and ventricle including a left marginal branch.
The coronary arteries are the only arterial supply to the heart. The two arteries anastomose so inadequately that blockage [coronary thrombosis] of any but smallest branches of one artery usually leads to the death of the muscle which it supplies .The damaged muscle is replaced by fibrous tissue if the individual survives the blockage. If the node or other parts of the conducting system of the heart are affectd by the blockage, the ventricles may continue to contract at their own slow rate, independent of the atrial contractions [ Heart block].

VEINS OF THE HEART
Are the great cardiac vein, Middle cardiac vein, Small cardiac vein, Posterior vein of the left atrium, Right marginal vein, Anterior cardiac veins and the Venae cordis minimae. All veins except the last two drain in to the Coronary Sinus which opens in to the right atrium
A, The Coronary sinus:- This is the largest vein of the heart. It is situated in the left posterior coronary sulcus. It is about 3cm long.It ends by opening in to the posterior wall of the right atrium. It receives the following tributaries .
1,The great cardiac vein accompanies [first] the anterior interventricular artery and then the left coronary artery to enter the left end of the coronary sulcus.
2,The middle cardiac vein accompanies the posterior interventricular artery and joins the right end of the coronary sulcus.
3,The small cardiac vein accompanies the right coronary artery in the posterior coronary sulcus and joins the right end of the coronary sinus. The right marginal vein may drain into the small cardiac vein.
4,The posterior vein of the left ventricle runs on the diaphragmatic surface of the left ventricle and ends in the middle of the coronary sinus.
5,The oblique vein of the left atrium [of Marshall] is a small vein running on the posterior surface of the left atrium. It terminates in the left end of the coronary sinus.It develops from the left common cardinal vein[duct of cuvier] which may sometimes form a large left superior vena cava.
6,The right marginal vein accompanies the marginal branch of the right coronary artery. It may either drain into the small cardiac or may open directly into the right atrium.
B, The anterior cardiac veins are 3-4 small veins which run parallel to one another on the anterior wall of the right ventricle,and usually open directly into the right atrium through its anterior wall.]
C, The venae cordis minimae [Thebesian veins or smallest cardiac veins] :-Are numerous small veins present in all four chambers of the heart which open directly into the cavity. These are more numerous on the right side of the heart than on the left. This may be one reason why left sided infarcts are more common.

Cardiac Cycle
A series of events must take place in a regular systematic manner for the heart to function as an effective pump to drive the blood through the circulatory system . This train of events is repeated in the proper sequence over and over again and because it is cyclical in nature , it is known as the cardiac cycle . As the human heart beats about 72 times per minute on an average ,the duration of cycle is 60 or 72 of a second and the cycle is repeated every 0.8 of a second.

Events in the cardiac cycle
The main events of the cardiac cycle are the auricular systole and diastole, followed by ventricular contraction and relaxation. Since auricular relaxation occurs during ventricular systole, there are only three events in time sequence

Auricular systole
The auricular systole is usually taken as the arbitrary initial point in the cardiac cycle. Auricular contraction must naturally cause an elevation in the auricular pressure which is reflected by the positve 'a' segment of the 'acv' curve it also pushes in some blood to the ventricles. Nevertheless, the ventricles are filled by a passive filling process and auricular contraction does not contribute to any significant increase in the pressure inside the ventricles. The ' p' wave of the electrocardiogram results from auricular activity.

Ventricular systole
The auricular systole is followed immediately by the ventricular systole. This, inturn , can be subdivided into the isometric contraction ,maximum ejection and reduced ejection phases. The ventricular contraction begins immediately after the QRS complex in the ECG.

Isometric contraction phase
At the beginning of the ventricular contraction phase, the AV valves are open. As the pressure in the ventricles rises , the AV valves are forcibly closed The aortic and pulmonary valves are closed already and thus the ventricle is converted into a closed cavity contracting on itself. Since there is no change in the length of the muscle fibres, this is called the isometric contraction. During this period the pressure inside the ventricle registers a steep rise. As the intra ventricular pressure rises , it ultimately exceeds the aortic pressure, and pushes(open) the aortic valve. Blood rushes into the aorta and next phase begins.

Ejection phases
With the opening of the aortic orifice , the ventricle and the aorta become one cavity and there is maximal rush of blood into the aorta , signifying the maximal ejection phase . Ventricular repolarisation starts almost at the end of this phase and the T wave is seen in the ECG. After the transfer of major quantity of blood into the aorta, the ventricular musculature registers weak isotonic contractions. This is the reduced ejection phase during which auricular filling starts and the T wave is completed.

Ventricular relaxation
It can also be divided into the 3 phases of isometric relaxation, rapid filling or diastasis corresponsding to the 3 phases of ventricular contraction.

Isometric relaxation phase
When the ventricular ejection is complete, the intraventricular pressure falls and consequently, the aortic valve closes after a short protodiastolic interval. Since the A-V valves continue to remain closed, the ventricle is again converted into closed cavity which is relaxing on itself now. Since it undergoes no volume changes, this phase is called isometric relaxation phase. Isometric relaxation brings about a sudden fall in the pressure, as a result of which the A-V valves open bringing an end to this phase.

Ventricular filling
Once the A-V valve opens blood naturally rushes into the ventricles from the auricles where it is now at a high pressure. This period of rapid filling is followed by a variable interval of slow filling or diastasis. This phase of diastasis ends the cycle and is followed by the atrial systole of the next cycle.

HEART SOUNDS
First heart sound (S1):- At the onset of ventricular systole the mitral and tricuspid valves close consecutively to give the first heart sound, M1T1. High frequency sound
Second heart sound (S2):- The closure of the aortic and pulmonary valves gives rise to the two components of the second heart sound; A2P2. normally P2 follows A2 and the splitting is widest during inspiration and narrowest in expiration (physiological spitting) High frequency sound.
Third and fourth heart sounds (S3 & S4):- Caused by abnormal filling patterns in the ventricles. S3 occurs in early diastole at the time of maximum ventricular filling.s4 occurs when the bolus of blood is delivered in to the ventricle from atrial contrition.

Cardiac out put
The heart is designed as pump and the most important external manifestation of the efficiency of any pump is its out put.

Definitions
Stroke volume is the out put of each ventricle per beat and is about 70 - 80 ml.

The minute volume which is popularly known as Cardiac Output , is the total amount of blood ejected by each ventricle per minute and is the product of heart rate and stroke volume . In a healthy individual it is about
5 - 6 L [ 70 x72 ml ] .

Cardiac Index is the term denoting the output of each ventricle per minute per square metre of body surface area . Normal cardiac index is
3.4 L /m 2/ mt [ range 2.8 -4.2 ].

Cardiac Output is governed by several factors such as effective venous return , heart rate , distensibility of the ventricles to receive blood in diastole [ie Compliance ] , contractile force , obstruction to atrial or ventricular outflow and blood flow .

PHYSIOLOGICAL VARIATIONS
A Muscular exercise :-cardiac output may shoot up to 20 to 30 litres
B Stress :- release of adrenaline also exhibit considerable augemenation of cardiac output.
C Pregnancy :-cardiac output increased to meet the needs of growing foetus.
D Temperature :-cardiac output has a direct relationship with rise in temperature.
E Lack of oxygen and cabondioxide excess :-cardiac output increased.
F Digestion :- cardiac output rises to about 30 to 40 times of the
normal during the process of digestion.
G Posture :- cardiac output is altered by posture being higher in the recumbent position.
H Sleep :- it reduces the cardiac output slightly

PATHOLOGICAL VARIATIONS

 
CYANOSIS
Is bluish , greyish, slate - like or dark purple colouration of the skin and mucous membranes caused by the presence of excessive amounts of reduced haemoglobin in arterial blood .

For cyanosis to become visible the amount of reduced hemoglobin should exceed 5gm%. In severely anaemic patients since this level of reduced haemoglobin can not be reached , cyanosis may not develop even when there is hypoxaemia . The opposite is true of polycythemia in which cyanosis may be present under ordinary conditions .

Cyanosis may be due to central causes or peripheral causes. Mixing of arterial and venous blood at the level of the heart or great vessels and defective oxygenation in the lungs and give rise to central cyanosis . In central cyanosis the central parts of the body such as the tongue as well as the peripheral such as the nail beds, tips of fingers and toes and the tip of the nose are cyanosed. The extremities are warm. Central cyanosis is seen characteristically in congenital cyanotic heart disease, chronic bronchitis, emphysema and other pulmonary diseases impairing gas exchange in the alveoli. Inhalation of pure oxygen does not correct the cyanosis in case of congenital heart disease. In the case of pulmonary disease, unless the lesion is far advanced inhalation of oxygen helps to correct the cyanosis partially. Central cyanosis is associated with the development of secondary polycythemia.

Peripheral cyanosis denotes the condition where the extremities (tip of fingers and the nail beds and tip of the nose ) are cyanosed ;while the central parts like the tongue are not. The extremities are cold to feel. Warming the part may relieve cyanosis.

Peripheral cyanosis is caused by excessive extraction of oxygen of oxygen by the tissues from the capillaries and this is due to impaired circulating state either due to reduction in cardiac output or vasospasm.

CLUBBING OF FINGERS
In normal subjects the level of proximal margins of the nail is slightly lower than the nail is slightly than the nail fold when examined from the side. In several conditions the tissues in the nail bed and finger pulp hypertrophy give rise to convexity of the the nail and drumstick appearance of the finger tips.This is called clubbing. Since the process develops gradually ,clubbing is graded as below :-

First degree :- The nail bed becomes more fluctuant than normal .
Second degree :-Obliteration of the angle between the nail and nail bed .
Third degree :- [parrot beak appearance] Bulbous appearance of the nail and finger tip .
Fourth degree :- Finger tip appears as in third degree and in addition , painful thickening of the ends of long bones of the limbs - Hypertrophic pulmonary osteoarthropathy .
Though in a few persons clubbing may be present as a familial trait , in the vast majority its presence indicates disease .

Common Causes
1, Cardiovascular system :- cyanotic congenital heart disease , Infective endocarditis .
2, Respiratory system :- Bronchiectasis , Lung abscess , Bronchogenic carcinoma , Empyaema , Pulmonary intrestitial disease
Less Common Causes
Carcinoma liver , Amoebic liver abscess ,Cirrhosis of liver , Crohn's disease , Ulcerative colitis , Grave's disease [primary exophthalmic goitre]
In many cases the toes and fingers are affected together and both sides are symmetrically involved . Unilateral clubbing of the upperlimbs may develop in aneurism of the ipsilateral subclavian artery . Clubbing recedes when the underlying lesion is cured .
At times persons whose occupations lead to regular minor trauma to the fingertips develop clubbing . eg:- carpenters and masons .

MURMURS
May be organic or functional . Organic murmurs are caused by anatomical abnormalities of valves or arteries , whereas functional murmurs
are caused by purely haemodynamic factors .
When a murmur is detected , ascertain the following points by auscultation .
1 , what is its timing ?
Systolic , diastolic or continuous .
2 , when does it start and what is its duration ?
Murmur commencing with first sound and continuing throughout systole upto second is termed pansystolic murmur.
Murmur that starts a little while after the first heart sound , increases in midsystole and dies out before the second sound - is called midsystolic murmur or ejection murmur ,because the timing and intensity of the murmur closely follow the timing and dynamics of ventricular ejection.
If the murmur occupies the latter half of systole it is called a late -systolic murmur .
Diastolic murmur that starts along with the second heart sound is called early diastolic murmur. It may extend through variable periods in to diastole . Such murmurs are heard in Aortic regurgitation & pulmonary regurgitation .

Murmurs that start in mid-diastole ie a while after the onset of diastole are called mid-diastolic murmurs . These may extend for variable periods during diastole . If they exist till late diastole they are termed as presystolic. If during this period, there is accentuation of murmur, it is called presystolic accentuation.this is seen in mitral stenosis with normal sinus rhythm.

3, what is its quality?
Murmurs may be high pitched and blowing in type or low pitched and rough.blowing murmurs are characteristic of abnormal blood flow from high pressure areas to low pressure areas with high velocity and force

eg:-1)Mitral regugitation and tricuspid regurgitation in which blood flows from ventricles in to atria during systole.
2)Blood from, the aorta or pulmonary artery leaking into the ventricles in diastole in incompetence of the corresponding valves.

In ventricular septal defect the high pitched pansystolic murmur is produced by blood flowing from the left ventricle to the right ventricle across the defect , under high pressure . The smaller the orifice , greater is the intensity and pitch of the murmur. Murmurs tend to be low pitched and rough if they are produced by blood flow across roughened surfaces or if the pressure gradient is small. In aortic and pulmonary stenosis the systolic murmur tends to be low pitched and rough since the valve surfaces are roughened .

4. What is its intensity ?
Murmurs can be graded depending upon their intensity .
Grade 1 : Faint murmur heard by an experienced observer in a quiet room after prolonged auscultation.
Grade 2 : Faint, but definite murmurs heard from the beginning of auscultation.
Grade 3 : moderately loud.
Grade 4 : louder murmur associated with thrill.
Grade 5 : loud murmur with thrill, can be heared even with the rim of the stethoscope.
Grade 6 : loud murmur with thrill, which can be heard even when the stethoscope is not in contact with the chest wall.
The severity of lesion and intensity of murmur do not correlate at all times.

5. what is the direction of conduction ?
Murmur may be conducted along specific directions. If the murmur is heard with the same or even increasing intensity as one proceeds away from the site of production it is said to be conducted in that direction.
Mid diastolic murmurs occurring in mitral stenosis and tricuspid stenosis are not conducted. Pansystolic murmur of mitral regurgitation is conducted laterally to the axilla and even as far behind as the scapular angle or back. Tricuspid systolic murmur may also be conducted to the angle of scapula or back.The ejection systolic murmur of aortic stenosis is conducted up along the carotids. At times it may be conducted to all other areas as well. Early diastolic murmur of aortic incompetence is conducted down to the epigastrium along the left and right borders of sternum .

Pulmonary systolic murmur may be conducted upto the left clavicle. Pulmonary diastolic murmur may be heard over a short distance only to the left of the sternum in the third and fourth intercostal spaces .

Conduction of the systolic murmur of mitral valve prolapse depends upon the valve leaflet maximally affected and the direction of the regurgitant stream .It may be conducted towards the axilla in prolapse of the anterior leaflet and medially in prolapse of the posterior mitral leaflet.

6. What is the change in the murmur with change of position of the patient?
Murmurs arising from the mitral valve are heard better in left lateral position .Murmurs arising from the tricuspid valve are heard best in the supine position with lower limbs elevated . Aortic and pulmonary murmurs are best heard with the patient sitting up and leaning forward . The murmur of mitral valve diminishes during squatting and becomes more prominent on standing .
7 .What is the effect of the phases of respiration on the intensity of the murmur?
Murmurs arising from the left sided valves become more audible on expiration while those on the right are better heard during inspiration

8. what is the effect of isometric exercise on the intensity of the murmur?
Make the patient tightens the fist strongly or clench his teeth. The systolic murmur of the hypertrophic cardiomyopathy and mitral valve prolapse decreases with the exercise.

DISEASES OF THE HEART VALVES
A diseased valve may be narrowed (stenosed) or it may fail to cause adequately and thus permit regurgitation of blood. The term 'incompetence' may be used synonymously with regurtitation or reflux but the latter preferable.

PRINCIPAL CAUSES OF VALVE DISEASE

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