Here is an essay on ‘Cardiac Diagnosis’ for class 8, 9, 10, 11 and 12. Find paragraphs, long and short essays on ‘Cardiac Diagnosis’ especially written for school and medical students.
Essay on Cardiac Diagnosis
The most important part of the clinical examination is history taking. This is a very special art which cannot be learnt by reading books only, but this has to be mastered in the hospital wards and from seniors and expert clinicians during periods of clinical clerkship and horsemanship.
Even sophisticated instruments may fail to give a correct cardiac diagnosis if history, clinical findings are not properly evaluated. History not only pertains to the patient’s symptoms but his age sex, country, climate environment, occupation, perinatal situations, milestones of growth in childhood’ addictions and family background are all very important.
Student must always try to take good history before he proceeds to make physical examination. But while attending any life-saving emergency, history may have to be taken in several stages while emergency treatment is in progress.
During examination of a cardiac diagnosis case, firstly note the skin colour and observe the respiratory movements, (dyspnoea, orthopnoea, irregular respiration). Also make a note whether there is anaemia, dehydration, cyanosis, puffiness of face or abnormal pulsations is neck. Arterial pulse can be felt but venous pulse cannot be felt but easily seen especially by using a back rest.
Examine the extremities, if skin is warm and moist (peripheral vasodilatation), severe thyrotoxicosis, anaemia and high fever might be the causes.
Skin may be cold and pale in peripheral vasoconstriction. When cardiac diagnosis is less this phenomemon is observed as in primary cardiac diseases.
The importance of good inspection cannot be over emphasised. The body configuration is an important clue to many diseases. In Marfan’s syndrome the patient is tall, slim, with long extremities. His arm span is longer than head and torso (head to pubis). It is associated with congenital heart disease.
A patient with hypertension may have trunkal obesity with slim limbs, denoting Cushing’s syndrome. Extreme obesity may be a case of Pickwickian syndrome.
Squatting and cyanosis are classical features of Fallot’s tetralogy. Muscular dystrophies may be associated with heart disease.
Facial characteristics of Mongol, Down’s syndrome, Morquio’s syndrome and Hurler’s syndrome are well-known.
Clubbing:
It is due to thickening and expansion of the terminal phalanges. In early stage the skin at the root of nail appears shiny and angle between the nail and skin fold may get obliterated and some spongy sensation is felt at the root of nail. It occurs in cyanotic congenital heart disease, SBE, bronchogenic carcinoma, bronchiectasis, lung abscess, cirrhosis of liver, chronic diarrhoea, e.g. ulcerative colitis and malabsorption syndrome. It may also be congenital and be present in childhood.
Skin and mucous membranes become blue if arterial oxygen saturation is below 85%. Cyanosis may be central or peripheral.
Pulse:
Arterial pulse is a wave due to pressure changes affecting its wall due to flow of blood.
Therefore it has two components, i.e.:
(1) Pressure-effects with each systole of heart
(2) Volume and velocity of blood flow.
During clinical examination of arterial pulse both radials, carotids; femorals, popliteals, posterior tibialis and dorsalis pedis should be palpated. Femoral pulse is weak and delayed in coarctation of aorta. Peripheral vessels of the leg are obliterated in Buerger’s disease.
Examination of Radial Pulse:
Feel both the radial pulses and note if there is any difference. Sometimes there is anomalous course of one radial artery, hence it is not felt. An emboli on the other hand may cause obliteration of a radial artery. Similarly, aortic aneurysm, a large mediastinal growth, cervical rib, pulseless disease (Takayasu’s syndrome), scalenus anticus syndrome may cause inequality of pulses or obliteration of one radial pulse.
The qualities to be assessed during examination of pulse are as follows:
(1) Rate:
Usually pulse rate varies with age. Generally, the range lies between 60 and 90 per minute at rest.
There are wide variations between the individuals. If above 90 per minute, it is called tachycardia. If below 60 per minute, it is called bradycardia. Neither tachycardia nor bradycardia is essentially a sign of heart disease. When pulse is irregular, compare it with heart rate and note the difference. Infants and children have high pulse rate than adults. Pulse rate in newborn is about 140 and up to one year 120 pm. It slows down by third year to 100 pm and in school age to about 90 pm. In old people it is around 80 pm.
(2) Rhythm:
Normal pulse has a regular rhythm. In disease it may become irregular. Irregularity might be irregularly irregular. Pulse rate might quicken during inspiration and slow during expiration. There might be an extra beat (ectopic) or a beat might be missed (dropped beat). For details refer to chapter on arrhythmias.
(3) Character or Quality:
Difference between systolic and diastolic pressures, is called pulse pressure which determines amplitude or volume. When stroke-volume is large and there is diminished peripheral resistance, collapsing pulse occurs. This is best appreciated by holding up the patient’s hand. The examiner’s hand will feel a slap of radial pulse (rapid rise and rapid fall). It is also known as Corrigan’s pulse. Special types of pulse should be recognised at bedside for clinical diagnosis.
(4) Volume:
The volume is related to cardiac output. It corresponds to amplitude of the movement of arterial wall. A low volume or so-called hypokinetic or weak pulse, e.g. mitral stenosis, aortic stenosis, acute myocardial infarction, shock CCF, cardiac tamponade, constrictive pericarditis, toxic myocarditis and coarctation of aorta.
A large volume pulse is due to high output state or hyperkinetic pulse e.g. fever, anaemia, thyrotoxicosis, cor pulmonale, high blood pressure, cirrhosis of liver, arterio-venous fistula, beriberi and Paget’s disease. This may occur to some degree during physical exercise and pregnancy.
(5) Tension:
It gives a rough idea of diastolic pressure. When tension is low the artery is easily compressible without much resistance. If diastolic pressure is high the arterial pulse remains more or less palpable during systole and diastole.
Nature of Arterial Wall:
‘Wear and tear’ phenomenon occurs in aging arteries. In younger people arterial wall is so elastic that it cannot be distinguished from the adjacent structures. In older age artery gets hardened and even calcified and can be felt like a hard rope. Loss of elasticity may lengthen the arteries to be tortuous. Tortuosity is easily observed on brachials and sometimes in the neck. Condition of the retinal vessels can also be visually assessed by ophthalmoscopic examination of fundus oculi. Every medical student who aspires to be a good physician should master the technique of ophthalmoscopy.
Arterial Blood Pressure:
Method of recording arterial blood pressure (B.P.) has been discussed in detail in the chapter on systemic hypertension.
Special Types of Pulse:
1. Water Hammer or Collapsing Pulse:
It is also called Corrigan’s pulse after the name of Dominic Corrigan. It is found in aortic incompetence, P.D.A., aortopulmonary window, rupture of sinus of Valsalva into ventricle, as well as in all high output states.
2. Anacrotic Pulse:
A slow sustained rise of the pulse is felt in severe aortic stenosis. The anacrotic notch may also be felt well in carotids. A slow rise and slow fall also may occur in aortic stenosis which is called pulsus parvus tardus.
3. Dicrotic Pulse:
As if there is double beat during diastole, the second wave is smaller.
4. Pulsus Bisferiens:
The first peak of the pulse (percussion wave) is followed by a second peak (tidal wave). This is felt in aortic incompetence with stenosis and in hypertrophic subaortic stenosis.
5. Pulsus Alternans:
An alternate strong and weak pulse usually present in LVF or toxic myocarditis. It has a bad prognosis but in a healthy person, sometimes it may occur in association with paroxysmal tachycardia, the latter having no adverse prognosis.
6. Pulsus Bigeminus (Coupling of Pulse):
Pulse beats occurring in couples with a pause. This may be noted in digitalis toxicity, ischaemic heart disease, rheumatic heart disease etc. A.V. block with ventricular escape or block in atrial flutter (2: 1, 3: 1 or 4: 1) may mimic this.
Pulsus Paradoxus:
The pulse volume to be lower during inspiration as found in massive pericardial effusion and chronic constrictive pericarditis.
Jugular Venous Pulse (J.V.P.):
Examine the patient is semi recumbent position usually at an angle of 45°. Sometimes it can be seen at 30° or may be necessary to elevate the patient above 60°. The idea is to see the upper level of venous pulse. The light should be enough and neck should be relaxed by turning the head slightly to the right side and by placing a pillow under the neck.
Expose the whole area above the clavicle by removing the clothes. In this position, venous pulsation (internal jugular vein) may be visible just above the clavicle. Sternal angle is taken as reference point because it is always 6 cm. above mid-point of right atrium in lying, sitting or standing position.
Vertical height of jugular venous pulse is normally 0-2 cms. above the sternal angle. A venous pressure of +4 cm or more is taken as abnormal. If pulsation is not seen, gentle manual pressure over the right subcostal area makes it visible (hepatojugular reflux), JVP is raised in right ventricular failure and obstruction to superior vena cava. In non-cardiac diagnosis cases, though jugular veins are engorged, they are not pulsatile.
Level of JVP rises during expiration and falls with inspiration when intrathoracic pressure decreases. Persistently elevated JVP is always pathological.
Mean JVP is raised in the following conditions:
1. R.V. failure
2. High output states
3. Superior vena cava obstruction (distended veins do not pulsate as in raised venous pressure).
4. Constrictive pericarditis
5. Tricuspid stenosis
6. Right atrial myxoma
7. Emphysema, pleural effusion and pneumothorax (due to loss of negative pressure in/the thorax).
The normal JVP has three positive (a, c, and v) and two negative waves (x and y). These waves denote intracardiac pressure events and helps in bed-side diagnosis. Along with ECG tracings and heart-sound recording (phonocardiography), many cardiac diagnosis disorders can be diagnosed.
The first heart sound (S1) is synchronized with the end of a wave i.e. where also c wave begins a wave is due to right atrial systole and c wave is due to the beginning of ventricular systole. During v-wave right atrium gets filled by blood from venous side.
The period c and v is period of ventricular systole. Y descent occurs in diastole. When there is resistance to flow, waves are exaggerated.
Cannon Waves:
High venous pressure waves synchronous with carotid pulse are produced by auricular contractions against closed tricuspid valve. It therefore means auricular contraction coinciding with ventricular systole.
Abnormal “a” Waves:
Large ‘a’ Waves:
1. Pulmonary stenosis (or atresia)
2. Pulmonary hypertension
3. Tricuspid stenosis (or atresia).
Absent ‘a’ Waves:
Auricular fibrillation.
Abnormal “v” Waves:
Large “v” Wave:
Tricuspid incompetence (due to reflux of blood in right atrium during ventricular systole).
Accentuated ‘x’ Descent:
1. Constrictive pericarditis
2. Cardiac tamponade
Slow ‘Y’ Descent:
When there is obstruction of flow in the right atrium, e.g. tricuspid stenosis or myxoma in the auricle.
Palpation:
Apex-Beat:
First find out the position of the apex beat furtherest to left and downwards. When the finger feels the impulse it is the apex beat (cardiac impulse). Start palpating from axillary side towards sternum by finger-tips. Describe position of the apex beat from left sternal line and note whether it is inside or outside the midclavicular or midaxillary line and in which intercostal space it is located. Do not forget to note the position of trachea. Shifting of trachea denotes mediastinal shift.
Precordium should be carefully palpated to find out:
1. Cardiac enlargement
2. L.V.H.
3. R.V.H.
4. Thrills
5. Palpable heart sounds
6. Palpable friction rub.
In L.V. hypertrophy, the apex beat moves downwards and outwards and is sustained and thrusting.
In R.V. hypertrophy, the apex beat moves outwards but not downwards and sustained heave is felt near left border of sternum. This is called left parasternal heave.
Heart Sounds:
Tapping apex beat due to loud Si is felt in mitral stenosis. Pulmonary valve closure (P2) may be felt in third left interspace.
Thrill:
Press the hand over the chest and you may feel a vibrating sensation. This is called thrill. The thrills may be systolic, diastolic or systolo-diastolic (continuous) thrills at apex are better felt if the – patient lies flat and half-turn on his left side. Basal thrills are best felt if the patient leans forwards and holds the breath in expiration.
Percussion:
Radiology is a better guide than percussion to assess cardiac border, still it must be practised as it is quite useful. Its main importance lies in patients with pericardial effusion. Here the area of dullness is absolute and increases both sideways and upwards. Cardiac dullness may be found to the right of sternum in dextrocardia or to left of sternum in lung collapse or fibrosis (left). In the latter case, a band of resonance can be percussed on left of sternum.
Auscultation:
It is essential to have a good stethoscope which has diaphragm and bell, with well-fitting earpiece, with elastic tube not too long. Modern electronic stethoscopes are not for general practice and have special advantages over the classical ones, provided the user knows how to auscultate.
A rigid diaphragm should be used. St. George’s style stethoscope is locally available. In a busy street-side room, auscultation is never satisfactory. A quiet room, a relaxed patient and well-trained ears are the triads of good auscultation.
There are two major sounds ‘lub’ and ‘dup’. These are called first and second sounds.
Between the second and first there are minor sounds and clicks not always present in normal heart and are quite important, e.g. third and fourth heart sounds, ejection clicks and opening snaps (O. S.). Besides these, there are murmurs which should be recognised clinically and all these require repeated and properly guided bed-side work under a ‘Guru’. Presence of a murmur does not always indicate heart disease. Wrong interpretation leads to unnecessary waste of time and money and also cardiac diagnosis neurosis.
First Heart Sound:
It is longest of all four heart sounds and is heard at the apex, caused by closure of the mitral and tricuspid valves. Echocardiography recorded with phonocardiography will be helpful. As contraction of left and right ventricles is not always synchronous, splitting of first sounds may occur and gives the clue. Mitral valve closure is best heard at the apex of L.V. (mitral area) while tricuspid has a softer note, heard best at the lower left sternal area (tripuspid area).
Wide splitting (not changing with respiration) suggests right bundle branch block (RBB) due to delayed contraction of right ventricle. First sound may be weak (valves not closing properly), in mitral regurgitation, myocarditis, ischaemic heart disease and due to calcified mitral valves. It is loud in tachycardia and ASD but loudest in mitral stenosis. Variations of intensity of first sound may occur in complete AV dissociation, e.g. heart block.
Second Heart Sound:
It is caused by closure of aortic (A2) and put monary valves (P2); the two components are almost synchronous in expiration but are heard separately as two distinct sounds in full inspiration, due to increased blood flow into right ventricle and decreased in left ventricle at this point of time. When P2 is louder than A2, pulmonary hypertension is suspected as in atrial septal defect (A.S.D.).
Delayed P2 suggests RBBB. In ASD there is wide and fixed splitting of A2 and P2. In advanced right heart failure also P2 is delayed as well as loud (due to pulmonary hypertension). In complete HB also there will be wide splitting of first and second sounds. Shortened L.V. systole will also produce wide splitting of second heart sound (A2 before P2) and will be heard in mitral incompetence and VSD.
Prolonged L.V. systole as in LBB and aortic stenosis will result in P2 occurring before A2 in expiration (L.V. contracting late). However, sounds will come closer or splitting disappears in inspiration (called reversed splitting).
Similar phenomena may also occur in severe hypertension.
Diastolic Sounds:
There are several sounds (besides murmurs) which should be recognised in diastolic phase. These are to be carefully mastered at bed-side during clinical clerkship as they have great diagnostic significance.
Third Heart Sound:
It is a sound produced at the beginning of the left ventricular filling and is often heard normally in young age group. In older patients it usually signifies abnormal ventricular flow as may occur in mitral incompetence or ischaemic heart disease (I.H.D.), due to altered left ventricular compliance. It is best heard by the bell of the stethoscope.
Systolic Click:
An early systolic click occurs at the point of Opening of the semilunar valves i.e. just at the onset of ejection often present in hypertensive heart disease or stenosis of semilunar valves (aortic or pulmonary). A mid systolic click may be heard in prolapse of the mitral valve.
Fourth Heart Sound:
It is a low frequency sound produced due to atrial systole and is always abnormal, and is best heard by the bell of the stethoscope. Normally atrial systolic sound is not audible. It is heard in left ventricular hypertrophy (LVH), I.H.D. or cardiomyopathy (CMP) and is related to hypertrophied or diseased left ventricle.
Opening Snap (O.S.):
It follows P2 (i.e. A2, P2 and US) and is heard in mitral stenosis unless the mitral valve is calcified. It is more high-pitched than 2nd sound and well heard in the left border of sternal area nearer to apex beat by the diaphragm of the stethoscope.
Gallop Rhythm:
When additional sounds, e.g. S3 (third heart sound) or S4 (fourth heart sounds) are heard it is called gallop rhythm. It may be triple gallop or quadruple gallop.
Sites of Auscultation:
Sites of auscultation —
A — Aortic area
A 2nd right costal cartilage
P — pulmonary area
2nd Intercostal space just left to sternum
T = Tricuspid area — Lower end of sternum
M = Just medial to apex beat – mitral area
Cardiac murmurs are continuous vibrations which vary in length, intensity, pitch and quality.
They may be classified as systolic and diastolic, systolic murmurs are heard between S1 and S2, while diastolic murmurs are heard between S2 and S1
Diastolic murmurs indicate organic heart disease while systolic may or may not. Diastolic murmurs are fainter and little more difficult to recognise.
Murmurs have to be graded according to their intensity, i.e. Grades 1 to 6 as follows:
Grade 1 – Very faint (audible only in quiet room)
Grade 2 – Faint murmurs
Grade 3 – Moderately loud
Grade 4 – loud
Grade 5 – Very loud
Grade 6 – loudest possible.
Murmurs are conducted towards the direction of blood flow, causing the sound.
Murmurs produced in the left side of heart are better heard during expiration while in right side -of heart are better heard during inspiration.
Thus a murmur is described as per timing (systolic or diastolic), intensity (Grade), conduction and relation with phases of respiration.
Systolic murmurs are further divided into:
(a) Mid-systolic or ejection
(b) Pansystolic
(c) Flow.
Diastolic murmus are further divided into:
(a) Early diastolic murmur
(b) Mid-diastolic murmur
(c) Pre-systolic or late diastolic murmur.
Pericardial Friction Rubs:
When pericardium gets inflammed, movements of the parietal and visceral layers during each heart beat produce harsh creaking noise, the pericardial rub. When fluid separates two layers of pericardium (pericardial effusion) friction sound disappears, and rub may still be audible in a small area of precordium unless the effusion is large. When diaphragm of the stethoscope is pressed on precordium both layers of pericardium come still nearer, and the friction sound is intensified.
Approach to Cardiac Diagnosis Auscultation:
You should ausculate your own heart daily and as many normal individuals as possible.
(1) Auscultate over 4 classical areas.
(2) Beginners should make a habit of drawing auscultatory events.
(3) When you listen by stethoscope, ask yourself the following questions:
(a) Do I hear normal heart sounds S1 and S2?
(b) Are there other sounds S3, S4, Os, and EC?
(c) Are there any murmurs?
(d) Is there a friction rub?
(e) Are there sounds which are non-cardiac?
(4) Get your finding confirmed by your teachers.
Cardiac auscultation is rewarding after long experience at the end of which one recognises the music of heart disease. Auscultation is better recognised rather than listened to.
Lung Bases:
Listen over posterior part of lower lobes. If crepitations are present, they indicate pulmonary congestion, pneumonitis or bronchiectasis. If any doubt, ask the patient to cough twice and then listen again.
Inspection of the Chest:
Following observations should be made:
(1) One side more prominent than the other – Scoliosis or congenital heart disease large pleural effusion
(2) Prominent or depressed sternum – Pigeon breast or funnel-shaped chest
(3) Visible pulsation at the apex beat – Thin chest wall or cardiac enlargement
(4) Pulsations in left 2nd and 3rd I.C. space – Dilated pulmonary artery
(5) Pulsation at the root of neck – Dilated aorta
(6) Collateral vessels on the scapulae behind – Aortic coarctation
(7) Epigastric pulsations – R V enlargement, hepatic congestion, aneurysmal abdominal aorta or thin nervous subject
(8) Pectus excavatum – May cause shifting of apex beat to left.
Hepatomegaly:
Central venous pressure is further reflected by palpation of liver firmly. The transmission of venous pulse may be felt and seen in presence of passive liver congestion as in congestive heart failure and hepatomegaly. In tricuspid stenosis, liver may pulsate with each heart beat and if varicose veins are present pulsation may be transmitted to them also.
Oedema:
When in subcutaneous tissues excess fluid is present, it is called oedema. Firm pressure with a finger or thumb for at least five seconds produces a depression in swollen area, (pitting oedema) which takes some minutes to disappear when pressure is released (vide supra).
Oedema is usually elicited over ankles, tibia and sacrum.
Legs should be observed for:
(a) Oedema;
(b) Varicose-veins and ulcers;
(c) If one leg is more oedematous than the other, if superficial veins are distended or if calf muscle is tender, suspect deep venous thrombosis of leg.