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Showing posts with label vitals monitoring. Show all posts
Showing posts with label vitals monitoring. Show all posts

What are the causes of radiofemoral delay

Normally the radial and femoral pulses are palpated simultaneously.If there an appreciable delay in the femoral pulse compared to radial pulse it is called as radiofemoral delay.
Radiofemoral delay is seen in following conditions
1. Coarctation of aorta
2. Aortoarteritis
3. Atheroslerosis of aorta
4. Thrombosis or embolism of aorta.    
1. Coarctation of aorta
Coarctation of the aorta may lead to hypertension in the circulatory system serving the head and upper limbs.It is an important bedside diagnostic clue in a young hypertensive patients
Narrowing or constriction of the aortic lumen may occur anywhere along its length but it is most common distal to the origin of the left subclavian artery near the insertion of the ligamentum arteriosum. Coarctation is seen in approximately 7% of patients with congenital heart disease,this  is more common in males than females, and is particularly frequent in patients with gonadal dysgenesis for example Turner syndrome. 
Clinical manifestations of coarctaion of aorta is dependent on the following factors
  • The site and extent of obstruction 
  • Presence of associated cardiac anomalies
The most common congenital heart disease associated with coarctation is a bicuspid aortic valve. Circle of Willis aneurysms is seen in up to 10%, and pose a high risk of sudden rupture and death.
2. Aortoarteritis.
Aortitis, a term referring to inflammatory disease of the aorta, it may be caused by
  • Large vessel vasculitides such as Takayasu’s arteritis and giant cell arteritis,
  • Rheumatic and HLA-B27–associated spondyloarthropathies
  • Behçet’s syndrome
  • Antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitides
  • Cogan’s syndrome
  • Infections such as syphilis, tuberculosis, and Salmonella
Clinical presentation of aortitis
Aortitis may result in th following features
  • Aneurysmal dilation and aortic regurgitation
  • Occlusion of the aorta and its branch vessels
  • Acute aortic syndromes.
Prototype of aortoarteritis is takayasu arteritis its signs and symptoms are given below
There are two phases for this disease.Initial inflammatory phase followed by secondary pulseless phase.
Initial "inflammatory phase"
Initial "inflammatory phase" characterized by systemic illness with signs and symptoms of malaise, fever, night sweats, weight loss, joint pain, fatigue, and fainting is seen in some patients. 
Fainting episodes are due to subclavian steal syndrome or carotid sinus hypersensitivity. Nonspecific markers of inflammation such as anemia and marked elevation of the ESR or C-reactive protein is seen. 
Secondary pulseless phase
The "pulseless phase" is characterized by vascular insufficiency due to intimal narrowing of the vessels presenting as
  • Arm or leg claudication
  • Renal artery stenosis causing hypertension, 
  • Neurological features due to decreased blood flow to the brain.These symptoms vary depending on the degree and  the nature of the blood vessel obstruction; it can range from lightheadedness to seizures in severe cases
  • One rare,but important feature of the Takayasu's arteritis is eye involvement in form of visual field defects, vision loss, or retinal haemorrhage
Some individuals with Takayasu's arteritis may present with only late vascular changes, without a preceding inflammatory phase
In the advanced stage, weakness of the arterial walls may give rise to localized aneurysms. And there is risk of rupture and vascular bleeding so requires frequent monitoring. 
3. Atherosclerosis of aorta.
Atherosclerosis may affect the either the thoracic and abdominal aorta. 
Occlusive aortic disease caused by atherosclerosis usually it is a confined to the distal part of abdominal aorta below the origin of renal arteries.Frequently the disease extends to the iliac arteries Claudication pain involves the buttocks, thighs, and calves muscle and may be associated with impotence in males (Leriche syndrome)
The severity of the clinical presentation  depends on the adequacy of collaterals.If there is sufficient collateral blood flow, even a complete occlusion of the abdominal aorta can occur without the development of ischemic symptoms.
The physical findings include the following
  • Absence of femoral and other distal pulses bilaterally 
  • An audible bruit over the abdomen (usually at or below the umbilicus) and the common femoral arteries. 
  • Atrophic skin, loss of hair, and coolness of the lower extremities 
  • In advanced cases of ischemia, rubor on dependency and pallor on elevation may be observed.
The diagnosis of atherosclerosis of aorta is usually established by physical examination and noninvasive testing which include
  • Leg pressure measurements,
  • Doppler velocity analysis
  • Pulse volume recordings
  • Duplex ultrasonography. 
  • The extend of lesion may be defined by MRI, CT, or conventional aortography, specifically performed for the purpose of  revascularization. 
Catheter-based endovascular or operative treatment is indicated in patients with lifestyle-limiting or debilitating symptoms of claudication and in patients with critical limb ischemia.
4. Thrombosis or embolism of aorta.
Acute occlusion in the distal abdominal aorta is a medical emergency as it threatens the viability of the lower extremities; This is usually from an occlusive or saddle embolus that almost always originates from the heart. Rarely, acute occlusion of aorta may be seen as a  result of in situ thrombosis in a preexisting severely narrowed segment of the aorta.
The clinical picture is one of acute ischemia of the lower extremities. 
  • Severe rest pain
  • Coolness, and pallor of the lower extremities and the absence of distal pulses bilaterally are the usual manifestations.
Diagnosis is by MRI, CT, or aortography.
Emergency thrombectomy or revascularization is the treatment.

What is the mechanism of radiofemoral delay?

What is radiofemoral delay?
Simultaneous palpation of two pulses can be diagnostic in radiofemoral delay. Normally the femoral and the radial pulses occur simultaneously.When the femoral pulse lags behind the radial (radio-femoral delay), occlusion of the aorta either due to coarctation or atherosclerosis is diagnosed. Reduced amplitude and delayed timing of the pulses in the lower body compared to the pulses in the upper body are classic features of aortic coarctation. All hypertensive patients should be examined for radiofemoral delay. Unilateral absence of a pulse can aid in the diagnosis of a dissected aortic aneurysm.
Where to palpate for femoral and radial pulse ?
Radial pulse is located on the lateral of the wrist (radial artery). This  can also be found in the anatomical snuff box.
Femoral pulse is located in the inner thigh, at the mid-inguinal point, halfway between the pubic symphysis and anterior superior iliac spine (femoral artery).
Diminished or absent femoral pulses indicating proximal occlusion is often seen in peripheral vascular disease.
What is the mechanism of radiofemoral delay?
Similar to aortic stenosis, coarctation of aorta cause a decrease in the rate of ejection of blood because of narrowing of vessel  and the Venturi effect sucking the vessel  walls inwards, it will create a reduction in the flow and amplitude of the pulse distal to the occlusion.
In addition, the following factors are essential in the mechanism of a pulse that is seen in any type of coarctation
The coarctation creates a pulse wave reflection sitewhich is much closer to the heart. This means the pulse wave is reflected earlier and faster, resulting in a higher blood pressure proximal to the stricture.
There are fewer cushioning properties (i.e. less compliance of the arterial segment involved
proximal to the coarctation), this will further increase blood pressure at or just prior to the stricture.
The flow and pressure pulsations are damped in the long and dilated collateral vessels that form to
provide flow distal to the coarctation.
The differential effects of the anatomical variations in coarctation of aorta 
  • The differential effects of the anatomical variations in coarctation of aorta may be diagnosable at the bedside if you carefully compare the brachial pulses between the two arms.
  • If both the brachial pulses and the carotids are strong with delayed or diminished femoral pulses, it indicate that the coarctation is distal to the left subclavian artery
  • When the left brachial arterial pulse is weak or diminished compared to the right, it indicate that the coarctation is proximal to the left subclavian artery.
  • If the right subclavian has an anomalous origin from the aorta distal to the coarctation, then the right brachial pulse will be diminished or poor.
What is Sign value
There is limited evidence as to the value of the sign and this can be difficult to elicit. The presence of the systolic murmur that is heard under the left clavicle or under the left scapula caused by turbulent blood flow across the coarctation is said to be more common.

Examination of pulse

How to examine the Pulse ?

What are the variations in pulse rate?

Bradycardia and its causes

Relative bradycardia and relative tachycardia

What is pulse deficit?

What is pulse volume and what are its alterations?

High volume pulse and its causes

What are the causes of low volume pulse?

What is water-hammer pulse ?

What is Hyperkinetic Pulse?

High volume jerky pulse (Spike and Dome Pulse)

What is anacrotic pulse?

What is Dicrotic pulse

What is catacrotic pulse?

What is pulsus alternans ?

Pulses bigeminus

Pulses paradoxus or Kussmaul's pulse

What is pulsus bisferiens ?

Describe the pulse in complete heart block (CHB)

How to assess the condition of the arterial wall?

What is the cause of radioradial and radiofemoral delay?

What are the basic bedside features of coarctation of aorta ?

Different cardiac rhythms

Temperature recording and fever

Significance of hydration of patient

To assess the hydration of the patient you should examine for 
  • Dryness of oral mucosa and tongue.
  • Sunken eyes.
  • Skin turgor - pinch the patients skin, on releasing normal skin returns within 2 seconds exception to this is old age and infancy
  • Postural fall of BP > 10 mmHg/postural dizziness
  • Oliguria
  • Invisible jugular venous column in lying posture
In dehyadration there is loss of ECF volume, ICF volume and IVF volume 
Extracellular fluid (ECF ) loss produce the following clinical features
  • Dryness of oral mucosa and tongue
  • Sunken eyes
  • Reduced  skin turgor
Intravascular fluid (IVF) loss produce the following features
  • Postural fall of BP > 10 mm Hg/postural dizziness
  • OliguriaTachycardia
  • Prerenal azotemia
  • Increased PCV
Intracellular fluid ICF volume loss produce 
  • Altered sensorium
  • Encephalopathy
  • Seizure
  • Features of shock
What are the clinical signs of dehydration?
  • Face is drawn.
  • Shrunken eyes.
  • Pinched up nose.
  • Parched lips.
  • Hollowness of temporal fossa.
  • Depressed anterior fonlanelle in infants.
  • Tongue is dry and coated,
  • Skin is dry and wrinkled : subcutaneous tissue feels lax.
  • The sign of ridge- If the skin is pinched up by index finger and thumb, and then released,instead of it springing back with normal elasticity, a ridge is formed which subsides slowly this is seen in severe dehydration 
  • The eyeballs are soft due to lowering of intraocular tension.
  • There is hypotension with weak pulse.
  • Urine is scanty, dark, concentrated  with specific gravity.


Pulses paradoxus or Kussmaul's pulse

Pulses paradoxus is defined as an exaggerated narrowing of the pulse volume due to fall of systolic BP during inspiration, as evidenced by inspiratory fall of systolic BP > 10 mm Hg during quiet breathing.
The difference in pressure between expiration and inspiration is < 10 mm Hg normally In pulses paradoxus, it is >10 mm Hg.
In normal individuals also, inspiratory filling of left ventricle is less, stroke volume is less, pulse volume is less, but may not be clinically detectable.
In pulses paradoxus the pulse volume decreases with inspiration and volume increases with expiration (it not truly the opposite of sinus arrhythmia which denotes the changes in pulse rate only). The paradox in this situation is that the heartsounds may still be heard on auscultation over the cardiac apex at a time when no pulse is palpable at the radial artery. 
It is commonly seen in.
  • Acute severe asthma.
  • Cardiac tamponade (rapidly developing pericardial effusion).
  • Chronic constrictive pericarditis..
  • Restrictive cardiomyopathy.
The probable mechanisms of pulses paradoxus is 
  • Intrapericardial pressure rises more during inspiratiory phase due to the traction on the pericardium which in turn decreases cardiac output by causing obstruction in venous return seen in cardiac tamponade.
  • Anti-Bernhelm effect is seen in inspiration, more blood comes in the right ventricle which will pushe the interventricular septum to the left side hence diminish the left ventricular cavity and resulting in low cardiac output.
  • Pulsus paradoxus is the exaggeration of normal physiological phenomenon, ie. an exaggerated inspiratory fall in systolic BP of more than 10 mm of Hg during quiet breathing.
What are the mechanism of pulses paradoxus?
  • In pericardial diseases like constrictive pericarditis, cardiac chambers are held in rigid pericardium, inspiratory increased filling of RV is taking place at the expense of the LV volume. Thus LV volume is decreased left ventricular filling is decreased, stroke volume is decreased  pulse volume is decreased. Ventricles cannot,increase its size during diastole due to thickened pericardium or due to increase in intrapericardial pressure as in pericardial effusion.
  • During inspiration, there is a fall in negativity of pressure in all the structures inside the chest. The fall in pressure is more in pulmonary vein than in left atria which is kept inside the rigid pericardium, thus the pressure gradient between pulmonary vein and left atrium is increased left atrial  filling is reduced LV filling is reduced and stroke volume and pulse volume is reduced.
  • During inspiration as there is stretch of pericardium by the downward movement of diaphragm, this will further reduce  the volume of the cardiac chambers including left ventricle impeding the filling further resulting in further reduction of stroke volume and pulse volume
How will you demonstrate Pulses paradoxus?
This can be demontrated accurately by using sphygmomanometer demonstrating systolic pressure fall > 10n Hg during inspiration. Patient should be in quiet breathing, by raising the pressure You should now occlude the arterial pulse, then slowly release the pressure initially one will hear the korotkoff sound
Expiration - Korotkoff sounds 
11111 11111 11111
Inspiration - Korotkoff sounds 
11111 11111 11111 11111 11111
Difference in systolic pressure in expiration  and inspiration > 10 mm Hg
Reverse pulses paradoxus 
Inspiratory rise in pulse volume and arterial pressure.
Causes are:
  • HOCM
  • Isorhythmic AV dissociation
  • Intermittent positive pressure ventilatior


What is water-hammer pulse ?


Bounding pulse is commonly seen in hyperkinetic circulatory states, here the pulse volume is high due to highpulse pressure with increased blood flow.
What is water-hammer pulse (or high volume collapsing pulse)?
This pulse is characterised by :
  • High pulse volume 
  • Sharp rise.
  • Ill-sustained
  • Sharp fall.
High volume pulse gives the water-hammer character when the pulse pressure is at least more than  60 mm of Hg. A collapsing pulse usually occurs when there is rapid run-off of blood from the aorta or the arterial system. Carotid artery is used for detecting collapsing nature of pulse
The striking features of collapsing pulse are: 
  • Abrupt upstroke, ill sustained peak and  abrupt downstroke and collapsing feel under the palpating hand
  • Thrust produced by the abrupt upstroke of the collapsing  pulse will resemble the thrust produced by the tilting of the water hammer toy and the abrupt downstroke of the pulse produces collapsing feel.
How will you demonstrate the water-hammer pulse ?
  • First you should palpate the wrist in such a way that your webs fall on the radial artery and rest of the palm lies over the ulnar artery of the patient Now you should e xamine the volume of the pulse for few seconds. 
  • Elevate the whole upper limb suddenly above the  patients shoulder ( you may give a support in the elbow to prevent its flexion) mean while trv to recognise any changes in the volume of the pulse. In water-hammer pulse, the  pulse volume increases from the basal level (i.e. volume at the beginning of the examination) after elevation of patients upper limb.
  • For examination of the pulse in this manner  one should stand within the ‘angle’ formed between the patients body and the said upper extremity. The right sided pulse should be examined by the right hand with the examiner standing on the right side of patient , and vice-versa for the left. You can observe the increase in pulse volume sharp rise and the sharp fall.
Why the name water-hammer pulse is given?


This pulse is so termed after a toy called water-hammer’. This is a peculiar toy with a glass cylinder that is half filled with water and half with vacuum (two ends being closed). If the toy is suddenly placed upside down, the column of water will strike the other end of the cylinder with a blowing sound. This is why this pulse is termed  waterhammer pulse where the pulse strikes the fingers like the thud of a hammer.
What is most important the cause of water-hammer pulse?
It is aortic regurgitation
Why this type of pulse is seen in Aortic regurgitation?
Waterhammer pulse is seen in AR due to the following reasons
High systolic pressure occur due to
  • In AR, as the left ventricular stroke volume is high systolic pressure is also high and it is responsible for sharp rise' in the pulse.
The collapsing nature is due to low diastolic pressure which is seen due to 
  • Diastolic leak back into the left ventricle from aorta.
  • There is rapid run-off to the periphery as a result of decreased systemic vascular resistance, the barorcceptors in the aortic arch is stimulated by increased cardiac output and result is reflex vasodilatation of the peripheral vessels into which the blood flows rapidly.
Why do you elevate the arm for eliciting the collapsing pulse?
  • Due to the effect of gravity, there is fall of blood column with resulting in vasodilatation and thus, it helps to reduce the diastolic pressure more. Hence  the pulse pressure widens,
  • It may be so that while we elevate the limb the artery palpated becomes more in line with that of aorta after elevation of the arm.So it allows direct systolic ejection and diastolic backward flow resulting in collapsing pulse.
What are the other parts to be examined in water hammer pulse?
  • You should count the rate (bradycardia in complete heart block: tachycardia in thyrotoxicosis).
  • See the condition of the vessel wall (for atherosclerosis).
  • See the facies for exophthalmos or examine for tremor to rule out thyrotoxicosis).
  • You should record the surface temperature (pyrexia).
  • Examine for anaemia (severe anaemia).
  • Examine for jaundice to rule out cirrhosis with hepato-cellular failure.
  • Examine the chest for emphysema (chronic cor pulmonale).
  • Always auscultate the aortic and neoaortic area for an earlv diastolic murmur of AR.
  • Search for peripheral signs of AR such as , for capillary pulsation, digital pulsation, carotid dance, pistol shot sound which are associated features of water-hammer pulse.





What is pulsus bisferiens ?

Pulsus bisferiens is a high volume double-beating pulse which has single pulse wave with two peaks in systole
.It is best palpated In large arteries like brachial and carotid arteries.
The first lift is due to P wave (percussion wave) and the second lift is due to T or tidal wave.
It is said that if the P>T. then AI>AS  
and if the T>P. usually AS>AI.
AS-Aortic stenosis
AR-Aortic regugitation
So this will help us to determine the dominant lesion in valve
Pulsus bisferiens is commonly found in.
  • Combined AS and Al (commonest).
  • Isolated Al.
  • IHSS.
What is the pathophysiology of Pulses bisferiens?

This is due to the 'ventury effect' within the left ventricle
Another view explains that the dip in the pulse is felt due to energy dissipation in the productlon of a loud systolic murmur of AS. .
Pulses bisferiens is better felt over the proximal vessels like Carotid and brachial artery.
How to elicit the bisferiens pulse?
  • With your fingers, try to press and occlude the brachial artery. On slowly releasing the pressure, you may feel the double peaking of the pulse.
  • The first component of the pulse is due to large volume of blood ejected in systole and the second component is produced due to elastic recoil in the arteries This is the best reasoning
Three different causes of double-beating pulse are 
  • Bisferiens pulse. 
  • Anacrotic pulse 
  • Dicrotic pulse.


Pulses bigeminus

It is a pulse wave with a normal beat followed by a premature beat and a compensatory pause, occurring in rapid succession, resulting in alternation of the strength of the pulse Since the second beat is an ectopic, there is a pause after it. 
Pulses bigeminus is commonly found in Digitalis toxicity and 3 : 2 heart block
In pulsus trigeminus, three beats and a pause recur in a regular fashion.
Differential diagnosis of pulsus bigeminus is pulses alternans.
In pulsus alternans the compensatory pause is absent,
But in pulsus bigeminus, compensatory pause is present. Pulsus bigeminus is a sign of digitalis toxicity.

What is pulsus alternans ?

Pulsus alternans is characterised by high and low volume of pulse which is due to alternate high and low stroke
In pulses alternans the alternate pulse waves are weak that is of low volume. In contrast to the ectopics, the rhythm remains regular. In a patient with severe left ventricular failure, pulsus alternans is said to be present.This is better demonstrated in radial arteries in LVF. This is seen due to the some ventricular muscle fibres are healthy and others are degenerated and so, produces normal and weak beat respectively. 
You should always search for gallop rhythm and basal crepitations when pulsus alternans is felt.
What is the mechanism of pulses alternanas ?
This is a reflex mediated process, initiated by an extra systole in LVF, that is sensed by the sensitive baroreceptors of the Carotid sinus. Left ventricular contraction following an extrasystole is strong as there is more diastolic filling during compensatory pause,  which increase the stroke volume hence the pulse volume is increased. This is sensed by the baroreceptors of the Carotid sinus and in turn send inhibitory impulse to atria via Carotid vagoatrial reflex resulting in weak contraction of atria, ventricular filling is reduced and stroke volume and pulse volume is reduced , which is again sensed by the baroreceptor which send the facilitator impulses via Carotid sympathetic atrial reflex resulting in increased atrial contraction and ventricular filling is increased  and also stroke volume is increased hence pulse volume is increased. This reflex activity occuring alternatively producing high and low pulse volume.
How will you demonstrate the Pulses alternans ?
It can be can be felt by palpating fingers but definite demonstration is by sphygmomanometer. Occlude the pulse by raising the pressure, then you should slowly reduce the pressure. Initially the Korotkoff sounds due to the passage of the high volume pulse is heard, further reduction will allow the passage of the weak beat also.
This will produce sudden doubling of the Korotkoff sounds called  as  Gallavardin sign.

High volume jerky pulse (Spike and Dome Pulse)

It is seen in HOCM It is the only obstructive cardiac lesion producing high volume pulse due to the dynamic obstruction of LV outflow tract. Jerky pulse resembles Bisferiens pulse.
Mechanism of jerky pulse
  • In the Initial phase there is  no obstruction – stroke volume is high
  • During the maximal ejection phase there is obstruction to ejection of stroke volume resulting in  reduced stroke volume.
  • In the late phase there is relaxation so the obstruction is relieved and stroke volume again increase


What is Hyperkinetic Pulse?

It is a  high amplitude pulse with a rapid rise (large volumeand wide pulse pressure).
Causes of hyperkinetic pulse are
  • High output states—Anaemia, pyrexia, beriberi
  • Mitral regurgitation
  • Ventricular septal defect.


What is Dicrotic pulse

It is double peaked pulse with one peak in systole and one peak in diastole due to very low stroke volume with decreased peripheral vascular resistance. 
  • This is also a low volume pulse.
  • Double peak is due to the palpability of dictrotic wave.
  • Dicrotic pulse is typically found due to hypotonia of the vessel wall in toxic fever will lead to the appearance of dicrotic wave.
Causes of dicrotic pulse are
1.Second week of typhoid fever (possibly due to the presence of circulating vasculotoxins).
2.Endotoxic shock.
3.Hypovolaemic shock.
4.Left ventricular failure
5.Dilated cardiomyopathy
6.Cardiac tamponade.

What is anacrotic pulse?

Anacrotic pulse is a low volume pulse with slow upstroke, sustained peak and a slow downstroke, also a palpable notch in the ascending limb of pulse.
Cause  of anacrotic pulse
Aortic stenosis - here the percussion wave is delayed beyond the tidal wave. The typical pulse in aortic stenosis is known as pulsus parvus et tardus'
Parvus means low volume 
Tardus means slow or late. 
You  may also feel carotid shudder in the presence of anacrotic pulse

What is catacrotic pulse?

The normal arterial pulse is known as catacrotic pulse. 
  • It has a percussion wave (P wave which is the rapid upstroke in pulse)
  • Tidal wave (T wave). 
  • Dicrotic notch and dicrotic wave. 
In the peripheral arterial pulses, dicrotic notch and wave are not clearly discernible. 
The typical description of pulse is given below
  • The normal arterial pulse is 72 per minute  
  • Regular in rhythm 
  • Normal and equal in volume without any unequality between the two upperlimb or between the upper limb and lower limb
  • The arterial wall is normal not thickened or tortous 
  • Normal in character called as catacrotic pulse.
  • All the peripheral pulses are symmetrically palpable 
What is the normal character of pulse?
Normal character of the pulse is smooth upstroke, peak and a smooth down stroke.
What are the different characters of pulse?
1.Anacrotic pulse
2.Dicrotic pulse.
3.Waterhammer pulse.
4.Pulsus paradoxus.
5.Pulsus bisfcriens.
6.Pulsus alternans.
7.Pulsus bigemlnus.
The wavy pattern of pulse is not felt normaly since it is obliterated by the normal vascular tone.

What is pulse deficit?

Definition of pulse deficit- it is the difference between the heart rate and the pulse rate. It is commonly found in atrial fibrillation and multiple ectopic beats.
Following are the method of detection of pulse deficit ;
1.First you should count the heart rate for one minute and then the pulse rate for next one minute (examination in two different cardiac cycles) .This is the  commonly practised method.
2.One examiner counts the heart rare and the other examiner counts the pulse rate at the sametime (using single cardiac cycle) for one minute.
3.Examiner may put his stethoscope at the apex and simultaneously count the dropped beats in the pulse (using single cardiac cycle) for one minute.
What is an ectopic beat?
In ectopic rhythm, the impulse originate from sites other than the SA node, and this may arise from the atrial wall, AV node or ventricular wall.
The ectopic beat is 
  • Small 
  • It ocurs prematurely
  • It is followed by a compensatory pause.
Palpate the pulse at the wrist , small pause followed by small beat, big raise is followed by big beat.
Causes of ectopic beat are the following
  • Overindulgence of tea,coffee, cigarettes, alcohol, anxiety. 
  • Dyspepsia
  • Digitalis overdosage
  • Rheumatic fever
  • Ischaemic
  • Hypertensive
  • Thyrotoxic and cardiomyopalhic heart diseases 
What are the synonym of ectopic beat: 
Ectopic beat is also known as premature beat, extrasystoles.
How can you modify ectopics in a patient?
Ectopics can be abolished by vagotonic procedures, and increased by vagolytic procedures
If the ectopic pace-maker is situated in the atrium ,resulting in paroxysmal atrial tachycardia vagotonic procedures can terminate it. Vagotonic procedures have no effect on ventricular tachycardia.
What are the Vagotonic procedures? 
Mechanical measures like carotid sinus massage (put your right thumb on the right side at the level of the upper border of thyroid cartilage in the neck and then on the left side  massage for 3-5 seconds at a time). Before the procedure always examine for both carotid pulse and auscultate for carotid bruit.
The other procedures are self-induced gagging or vomiting, pressure over the eyeballs.
Valsalva manoeuvre, stretching the arms and body.
Drug like digitalis.
Coughing as well as breath holding, head lowering between the knees.
What are the Vagolytic procedures : Exercise
Drugs like atropine and amyl nitrite.
How will you differentiate  between multiple ectopics and atrial fibrillation ?
Both these conditions present as irregularly irregular pulse. Sothey have to be differentiated from one another
1.First count the pulse rate. If this is > 100 per minute, it is AF but if the pulse rale is < 100 per
minute. It can be multiple ectopics or digitalised AF (treated case of Af).
2.The ectopic beat is a small one and occurs prematurely. So you 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, this is definitely ectopic and it is not a case of atrial fibrillation.
3.Calculate the pulse deficit. If it is > 10, it is AF. It the pulse deficit is < 10. But this can be again multiple ectopics or digitalised AF. To diiferentiate between these two following measures are adopted.
The patient is allowed to do mild exercise (if the condition permits). He will sit and touch the toes
with his fingers, and will lie down again. This is done for 5-6 times successively. The heart of AF becomes more irregular after exercise. If the pulse deficit is more than 10 after exercise ,it is a case of digitalised AF and if the pulse deficit remains same (below 10) or diminished after exercise , the diagnosis of multiple ectopics becomes obvious.
The patient is examined for
a) JVP-a-wave is absent in AF : a-wave is present in multiple ectopics.
b) S1-Varying intensity of S1 is heard  in AF: no change in multiple ectopics.
c) Auscultation of the apex-If MS is the cause of AF, presystolie component of the diastolic murmur will disappear but no change of murmur is heard  in multiple ectopics.
d)ECG-P' waves will be replaced by T waves in AF; ectopics are easily diagnosed by ECG.
What are the causes of irregular rhythm with normal heart rate :
1) Multiple extrasystoles.
2) Digitalised AF.
3) Sinus arrhythmia.

What is the cause of radioradial and radiofemoral delay?

Normal situation radial and femoral pulsations are felt equally and synchronously.The inequality between two radial pulses is known as Radio radial delay.The delay between the radial pulse and femoral pulse is called as Radiofemoral delay.

Radio radial delay
To detect the radioradial delay you should simultaneously palpate both the radial arteries by both your hands, using  your left hand for  patients right radial artery and vice versa

Following are the  causes of radio-radial delay 
What is radiofemoral delay and what are its causes?
To detect the  radio-femoral delay, you should palpate the radial and femoral artery simultaneously Normally there is no radio-femoral delay .
Delay of the femoral compared with the right radial pulse is found in coarctation of the aorta
Causes of radio-femoral delay are the following
  • Coarctation ol aorta (It is an important bedside diagnostic clue in a young hypertensive).
  • Atherosclerosis of aorta.
  • Thrombosis or embolism of aorta.
  • Aortoarteritis.

Time at which pulse wave arrives after cardiac systole in artery
Carotid =30 Milliseconds
Brachial =60 Milliseconds
Femoral =75 Milliseconds
Radial  =80 Milliseconds

What are the basic bedside features of coarctation of aorta ?

Coarctation of aorta is characterised by the following features
  • Usually seen in male patient and they presents with headache, claudication, palpitation, anginal pain or cold extremities.
  • The upper extremity and thorax may be more developed compared to lower extremities.
  • Radiofemoral delay is present .
  • All the peripheral pulses shoud be examined carefully
  • Prominent suprasternal and carotid pulsations are present
  • Collateral pulsation may be seen and felt over the axilla .trunk and infrascapular areas.This is clled as Suzmans sign and is best elicited with patient bending forwad with arms hanging by the side of the body
  • Systemic hypertension.
  • Bruit over the collaterals.
  • Left ventricular type of cardiac enlargement and heaving apex is seen.
  • A systolic murmur may be heard over the  anterior chest and back.Continuous murmur is heard over the collaterals
Clinical association of coarctation are 
  • Bicuspid aortic valve
  • Turners syndrome 
  • Berry aneurysm 
  • Polycystic kidney

How to assess the condition of the arterial wall?

Normally the arterial wall is impalpable and it may be palpable in old age due to atherosclerotic changes. The artery becomes tortuous and it feels like a cord in atherosclerosis this is also known as Monckeberg's medial sclerosis ( which is characterised by the calcification of the media of large arteries),If there is  thickened and tortuous artery are present, one may observe locomotor brachialis. 
This is assessed by :
1.First place your index and middle fingers of both the left and right hand over the radial artery side by side and then 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, or
2.You can also compress the brachial artery above the elbow by ball of your left thumb (that is making a bloodless column) and now roll the radial artery over radius by index and middle fingers of the right hand.
Condition of the vessel wall  can be  assessed by the palpation of the radial artery
  • Normal vessel wall is  - soft
  • Thickened vessel feel as firm to hard and cord like 
Thickness of the vessel is increased due to
  • Atherosclerosis
  • Monckeberg's medial calcific sclerosis
What are the causes of absent radial pulse :
  • Anatomical abnormality.
  • Severe atherosclerosis.
  • Takayasu's disease.
  • Embolism in the radial artery.