Pulse is the expansion and elongation of the arterial wall imparted by the column of blood and is passively produced by the pressure changes during ventricular systole and diastole. Commonly we examine the pulse in the radial artery in hand, which is one of the most accessible peripheral artery. Moreover, as soon as the hand (radial artery) of a patient is touched, it builds the doctor-patient relationship. Pulse, blood pressure, respiration, temperature and level of consciousness are regarded as ‘vital signs’ in clinical medicine.
Points to note in the examination of pulse :
1. Rate.
2. Rhythm.
3. Volume.
4. Condition of the arterial wall.
5. Comparison between two radial pulses
6. Radio-femoral delay.
7. Any special character.
8. Palpation of other peripheral arteries
N.B.: Pulse should always be described under these eight points. “Tension’ Is the indirect estimation of blood pressure. Estimation of tension by palpation is totally unreliable and thus, it is not included within the points under examination of pulse. Tension (i.e., blood pressure) should be accurately measured by a sphygmomanometer.
How to examine the pulse?
The radial pulse at the right wrist of the patient (present lateral to the flexor carpi radialis tendon) is generally examined with the pulp of three fingers (index, middle and ring finger). The patient’s forearm will be semipronated and the wrist slightly flexed.
The rate and rhythm are better palpated in the radial artery. To note the volume and character of the arterial pulse, one should examine the carotid artery (It is the nearest pulse to the aorta). Brachial pulse is felt to record blood pressure.
How to count the rate?
Always count the beats for 15 seconds and multiply by four to get the pulse rate but it is worthwhile to remember that in a patient with arrhythmia, one must count the beats for at least one minute.
What are the variations in pulse rate?
Definition of rate — Number of beats per minute. Normally it ranges between 60 to 100 beats per minute (average of 72 beats per minute in an adult). Usually, it remains 140 beats per minute at birth. SA node is the natural pacemaker of the heart (i.e., the normal cardiac rhythm is ‘sinus rhythm’).
(A) Tachycardia — Pulse rate is above 100 per minute. Normally it is found in children.
a) Sinus tachycardia — Pulse rate is above 100 per minute where the impulse is originating from the SA node. The heart rate In sinus tachycardia varies between 100-160 per minute. The common causes are,
(i) Exercise, emotion, excitement, intense pain, anxiety, and in children
(ii) heart failure.
(iii) Thyrotoxicosis.
(Iv) Severe anaemia.
(v) Pyrexia.
(vi) Shock (e.g, acute myocardial infarction).
(vii) Myocarditis.
(viii) Acute haemorrhage.
ix) Pregnancy.
(x) Hypoxia.
(xi) Drugs like salbutamol, nifedipine or atropine.
b) Relative tachycardia — Read the section on Abnormal temperature’.
c) Paroxysmal tachycardia — Pulse rate is above 160 beats per minute. It is divided into two types:
1) Supraventricular (PSVT) [i.e., atrial (PAT) or nodal (PNT)).
2) Ventricular (VT).
Common causes of paroxysmal tachycardia are rheumatic carditis, ischaemic heart disease (IHD), thyrotoxicosis, hypertensive heart disease, cardiomyopathy, WPW syndrome.
(B) Bradycardia—Pulse rate is below 60 per minute. It is commonly found in,
(i) Athletes, yoga, meditation or during deep sleep.
(ii) Myxoedema.
(iii) Obstructive jaundice.
(iv) Increased intracranial tension.
(v) Drugs like propranolol or digitalis.
(vi) Hypothermia.(vii) 2° heart block, complete heart block (CHB)
(viii) Sick sinus syndrome (sino-atrial disease).
(ix) Vasovagal attacks.
(x) Severe hypoxia.
* Athletes, yoga and meditation develop a high vagal tone but during sleep the sympathetic activity is reduced.
N.B.: Regular athletic training and myxoedema are the commonest causes of bradycardia.
a) Sinus bradycardia—Pulse rate is below 60 per minute where the impulse is originating from the SA node. The common causes are All the causes mentioned above in ‘bradycardia’ except complete heart block (in CHB, idioventricular rhythm occurs at the rate of 36 per minute).
N.B.: Idioventricular rhythm—when the cardiac impulse arises from the ventricle at the rate of 36 per minute, the pulse rate at ventricular rhythm will be 36 (30-40) per minute, and is known as idioventricular rhythm; nodal rhythm—when the SA node fails, often the AV node originates impulse at the rate of 40 – 60 per minute resulting in a pulse rate of 40-60 per minute.
b) Relative bradycardia — Read the section on ‘Abnormal temperature.
Bradycardia associated with convulsions :
1. Complete heart block (Stokes-Adams syndrome).
2. Increased intracranial tension due to meningoencephalitis, brain tumour, and CVA.
3. Prior to the development of coma in myxoedema.
Disproportionately rapid pulse in shock :
1. Acute myocardial infarction.
2. Septic shock.
3. Myocarditis.
4. Tachyarrhythmias.
What is pulse deficit?
Definition—it is the difference between the heart rate and the pulse rate. It is commonly found in atrial fibrillation and multiple ectopic beats. The method of detection of pulse deficit are :
1. First count the heart rate for one minute and then the pulse rate for the next one minute (examination in two different cardiac cycles) — commonly practised method, or
2. One examiner counts the heart rate and the other examiner counts the pulse rate at the same time (using a single cardiac cycle) for one minute (best method), or
3. One may put his stethoscope at the apex and simultaneously count the dropped beats in the pulse (using single cardiac cycle) for one minute.
* Pulse deficit is obtained in atrial fibrillation (> 10/min) and multiple ectopics (< 10/min).
What is an ectopic beat?
In ectopic rhythm, the impulse arises from sites other than the SA node and may arise from the atrial wall, AV node or ventricular wall. The ectopic beat is small, occurs prematurely and followed by a compensatory pause. The compensatory pause results in a ‘missed-or ‘dropped’ beat in pulse.
Pulse felt at the wrist: Small pause followed by small beat, big pause followed by big beat.
Causes: Overindulgence of tea, coffee, cigarettes, alcohol; anxiety, dyspepsia; rheumatic, ischaemic, hypertensive, thyrotoxic and cardiomyopathic heart diseases; digitalis overdose.
Synonym of ectopic beat: Premature beat, extrasystoles.
* Ectopic beats occur as occasional or repeated irregularities superimposed on a regular pulse rhythm.
How can you modify ectopics (supraventricular) in a patient?
Ectopics can be abolished by vagotonic procedures, and vagolytic procedures increase ectopics. When ectopic pacemaker is situated in the atrium (producing paroxysmal atrial tachycardia), vagotonic produces often terminate the attack. Vagotonic procedures have no effect on ventricular tachycardia.
Vagotonic procedures: Mechanical measures like carotid sinus massage (the patient lies flat with extended neck. Exclude occlusive carotid disease, i.e., there should not be any carotid bruit. Now put your left thumb first on the right side of the neck at the level of the upper border of thyroid cartilage and massage for 3-5 seconds at a time; next try on the left side with right thumb), self-induced gagging or vomiting, pressure over the eyeballs, Valsalva manoeuvre, coughing as well as breath-holding, head lowering between the knees, stretching the arms and body; drug like digitalis.
Vagolytic procedures: Exercise; drugs like atropine and amyl nitrite.
Irregularities in the rhythm :
Rhythm is the spacing of successive beats (pulse wave) in time. Normal pulse is regular in rhythm and is known as sinus rhythm, because it is generated by the SA node. Irregularities are of two types :
1. Regularly irregular — i.e., irregularity comes at regular interval and is seen in extrasystoles, 2° heart block, sinus arrhythmia, pulsus bigeminus etc.
2. Irregularly irregular or completely irregular — i.e., irregularity between two pulse beats in every aspect (rate, rhythm, volume etc, i.e., totally chaotic). It is commonly seen in atrial fibrillation, multiple extrasystoles, atrial flutter with varying degrees of heart block etc.
What is sinus arrhythmia?
Definition — It is the increase in pulse rate with inspiration and decrease in pulse rate with expiration. It is a physiological phenomenon commonly observed in children and athletes.
Mechanism — The increased amount of blood which comes in the left ventricle in expiration increases the stroke volume. This event immediately stimulates the baroreceptors (i.e., vagal stimulation) leading to a slowing of the heart rate.
* Sinus arrhythmia may be absent in CCF and autonomic neuropathy
Differentiation between multiple ectopics and atrial fibrillation (AF) :
Both the conditions present as an irregularly irregular pulse. So, they have to be differentiated :
1. First count the pulse rate. If it is > 100 per minute, it is AF but if the pulse rate is < 100 per minute, it may be multiple ectopics or digitalised AF (treated case of AF).
2. The ectopic beat is a small one and occurs prematurely. So one may get the typical phenomenon of : small pause followed by small beat, big pause (compensatory pause) followed by big beat. If this typical cadence is felt, it is ectopic and not a case of atrial fibrillation (totally chaotic).
3. Now count the pulse deficit. If it is > 10, it is AF. If the pulse deficit is < 10. again it may be multiple ectopics or digitalised AF. To differentiate between the last two, following measures are adopted.
4. The patient is allowed to do mild exercise (if the condition permits). He will sit and touch the toes with his lingers, and will lie down again. This is done for 5-6 times successively. It is known that the heart of AF becomes more irregular after exercise. If after exercise the pulse deficit goes above 10, it is a case of digitalised AF and if the pulse deficit remains same (below 10) or diminished, the diagnosis of multiple ectopics becomes obvious.
5. Next the patient is examined for :
a) JVP—a-wave is absent in AF; a-wave is present in multiple ectopics.
b) Sj—Varying intensity of St in AF; no change in multiple ectopics.
c) Auscultation of the apex—If MS is the aetiology of AF, presystolic component of the murmur will disappear; no change of murmur in multiple ectopics.
6. ECG—‘P’ waves will be replaced by ‘f waves in AF; ectopics are easily diagnosed by ECG.
7. Fluoroscopy—Definite contraction of atria is absent in AF. Atria contracts normally in ectopics.
Irregular rhythm with normal heart rate :
1. Multiple extrasystoles.
2. Digitalised AF.
3. Sinus arrhythmia.
What is the volume of the pulse?
It is the amplitude of the pulse wave or the excursion felt at the wrist, and usually reflects the width of pulse pressure (systolic BP minus diastolic BP), which depends on two factors :
(i) Stroke volume, and
(ii) Compliance of the arteries.
The carotid, brachial or femoral arteries are more useful for assessing pulse volume and character than the radial pulse. Normal pulse pressure is 30-60 mm of Hg (i.e., normal pulse volume).
What are the changes in the pulse volume?
(A) High volume pulse (i.e., pulse pressure > 60 mm of Hg) :
1. Hyperkinetic circulatory states like.
(i) After exercise.
(ii) Severe anaemia.
(iii) Pyrexia.
(iv) Pregnancy.
(v) Aortic incompetence
(vi) Thyrotoxicosis.
(vii) Arteriovenous communications like patent ductus arteriosus (PDA), Paget’s disease etc.
(viii) Chronic cor pulmonale.
(ix) Hepato-cellular failure.
(x) Beri-beri.
2. Atherosclerosis (the arteries are rigid, i.e., less compliant; so there is wide pulse pressure as the systolic BP is high). ,
3. Complete heart block or bradycardia due to any cause.
* In aortic incompetence: systolic BP T and diastolic BP 4-; atherosclerosis: systolic BP T and diastolic BP normal; hyperkinetic circulation: systolic BP t and diastolic BP near normal.
(B) Low volume pulse (pulsus parvus; pulse pressure < 30 mm of Hg) :
1. Shock due to any cause e.g., acute myocardial infarction, massive haemorrhage, hypovolaemia or septicaemic shock (as a result of poor vascular tone).
2. Severe aortic stenosis.
3. Tight mitral stenosis.
4. Pericardial effusion.
5. Constrictive pericarditis.
6. Congestive cardiac failure.
What is a thready pulse?
This a low volume pulse with a rapid pulse rate. This type of pulse is seen in peripheral circulatory failure, e.g., cardiogenic shock, haemorrhage or dehydration.
* ‘jerky pulse’ is felt in idiopathic hypertrophic subaortic stenosis (IHSS).
How to assess the condition of the arterial wall?
Normally the arterial wall is impalpable and may be palpable in old age due to arteriosclerosis. The artery becomes tortuous, thickened and feels like a cord in arteriosclerosis which is known as “Monckeberg’s medial sclerosis” (calcification of the medial coat of large arteries). This is an age-related change; remember, atherosclerosis occurs in intima and often associated with occlusive arterial disease.
In the presence of thickened and tortuous artery, one may observe locomotor brachialis. Condition of the arterial wall is assessed by :
a) Compress the brachial artery above the elbow by ball of the left thumb (i.e., making a bloodless column) and now roll the radial artery over radius by index and middle fingers of the right hand,
Or
b) First place the index and middle fingers of both the left and right hand over the radial artery side by side and exsanguinate the artery by moving the two middle fingers in opposite direction.
The radial artery is now rolled over the radius by two index fingers.
Causes of absent radial pulse :
1. Anatomical abnormality.
2. Severe atherosclerosis.
3. Takayasu’s disease.
4. Embolism in the radial artery.
5. [Death].
* Raynaud’s disease doesn’t affect the peripheral pulse because it is a disease of arterioles.
Inequality between two radial pulses (radio-radial delay) :
Simultaneously palpate both the radial arteries by both of your hands, using your left hand for patient’s right hand and vice-versa for the other hand. Causes of inequality or radio-radial delay are :
1. Normal anatomical variations.
2. Thoracic inlet syndrome e.g., cervical rib.
3. Aneurysm of the arch of aorta.
4. Pre-subclavian coarctation.
5. Supravalvular aortic stenosis (congenital).
6. Pulseless disease (Takayasu’s disease).
7. Peripheral embolism or atheromatous plaque.
8. Atherosclerosis of aorta.
9. Pressure over axillary artery by lymph nodes.
10. Iatrogenic—Blalock-Taussig shunt operation in Tetralogy of Fallot.
Causes of radio-femoral delay :
For detection of radio-femoral delay, standing on the right side of the patient, one should palpate the radial artery with the left hand and femoral artery with the right hand simultaneously. Normally there is no radio-femoral delay (in health, radial and femoral pulsations are felt equally and synchronously) but it should be remembered that the pulsation of arteria dorsalis pedis comes 0.02 to 0.03 seconds later than the radial artery. In radio-femoral delay, the femoral pulse is of small volume and occurs after the radial pulse. Causes of radio-femoral delay are:
1. Coarctation of aorta (important bedside diagnostic clue in a young hypertensive).
2. Atherosclerosis of aorta.
3. Thrombosis or embolism of aorta.
4. Aortoarteritis.
Basic bedside features of coarctation of aorta :
1. A male patient with headache, claudication, palpitation, anginal pain or cold extremities.
2. The upper extremity and thorax may be more developed in comparison to lower extremities.
3. Palpation of pulses may reveal radio-femoral dealy (symmetrical reduction and delay of femoral pulses in comparison to radial pulses). All the pulses like radial, carotid, brachial, femoral, popliteal and arteria dorsalis pedis should be examined in details.
4. Prominent suprasternal and carotid pulsation.
5. Collateral pulsation are present (seen as well as felt) in axilla, trunk and infrascapular area (Suzman’s sign). Suzman’s sign (dilated, tortuous and pulsatile arteries) is best elicited when the patient stands and bends forward with arms hanging down at sides.
6. Systemic hypertension (upper extremity high BP with low or normal BP in lower extremity).
7. Bruit over the collaterals. ‘Cork-screw’ appearance of retinal arteries (fundoscopy).
8. Left ventricular type of cardiac enlargement (heaving apical impulse); a systolic murmur may be heard over the anterior chest and back. The continuous murmur may be present over collaterals.
9. Clinical associations: Bicuspid aortic ralve, PDA. VSD, berry aneurysm, polycystic kidneys, Turner’s syndrome.
10. [Rib notching from 3rd to 8th rib in chest X-ray — known as Dock’s sign].
11. [Barium swallow of oesophagus shows double indentations due to pre- and post-coarctation dilatation—‘3 sign’ or ‘reverse E sign’.]
* Post-subclavian type is the commonest variety of coarctation of aorta.
Examination of other peripheral pulses :
1. Ulnar artery : At the wrist on medial side where it crosses the distal end of radius.
2. Brachial artery : Palpated by the thumb (left thumb for left arm and vice-versa for right arm) at or just above the elbow (just medial to the tendon of biceps muscle).
3. Subclavian artery : Ask the patient to shrug his shoulders. The artery is felt from behind by pressing the index finger downwards, from above the middle of the clavicle.
4. Carotid artery : Palpated with the thumb (left thumb for right carotid and vice-versa), medial to sternomastoid and at or just below the level of thyroid cartilage. Pressure over the carotid sinus may sometime induce syncope and this is why carotid artery should always be palpated one by one with the patient lying in bed. Dancing carotids in AI, slow upstroke in AS and jerky carotids are characteristic of HOCM.
‘ 5. Femoral artery : Lies midway between anterior superior iliac spine and pubic tubercle, at the level of the groin or inguinal ligament.
6. Popliteal artery : The patient lies supine with semiflexed knee. The fingertips of both hands are pressed in the middle of the popliteal fossa while both thumbs rest on tibial tuberosity. It may be palpated in prone position with knee partly flexed.
7. Posterior tibial artery : Lies approximately in the midway between the medial malleolus and heel; better palpated after inversion of the foot as it causes relaxation of the flexor retinaculum.
8. Arteria dorsalis pedis : Palpated lateral to the extensor hallucis longus tendon on the proximal part of dorsum of the foot; it may be absent in about 10% people. Before palpation, make the extensor hallucis longus tendon prominent by asking the patient to extend his great toe against resistance.
Describe the normal arterial pulse (adult) :
The rate is 72 per minute. The beats are regular in rhythm, and normal as well as equal in volume.
There is no inequality between the two upper limbs, and the upper and the lower limbs. The condition ofthe arterial wall is normal (neither thickened nor tortuous) and the pulses are of normal character (catacrotic pulse). All the peripheral pulses are symmetrically palpable.
The character of the pulse is described in the section on ‘Water-hammer pulse’.
Throbbing carotids in aortic incompetence is known as ‘Corrigan’s pulse’.
Examination of the pulse is one of the most ancient and time-honoured practices of the medical profession. Try to comment on pulse deficit while describing the pulse of atrial fibrillation.
Pulse becomes faster (rapid) after a meal, after smoking, during menstruation and in the evening.