pulse

1. PULSE
K. JAI SHANKAR MD,DM
CONSULTANT CARDIOLOGIST
INSTITUTE OF CARDIOVASCULAR DISEASES
MADRAS MEDICAL MISSION

2. PULSE
DEFINITION:
 Pulse is the palpability over peripheral arteries, a
pulse wave which is a transmitted wave from the root
of aorta along the vessel wall traveling 10 times
faster than blood.
 Blood travels at speed of - .5 mt/sec.
 Pulse travels at speed of - 5 mt/sec.

3. PULSE WAVE
 The arterial pulse reflects the performance of LV
 “Mirror of the heart”
 It is propagated by incompressible blood both forwards and laterally.
The lateral movement distends the arterial wall and is felt as pulse.

4. PULSE - HISTORY
HIPPOCRATES – 4TH CENTURY BC
Thought that arteries are air ducts
GALEN
Arteries contain blood & not air.
HEROPHILUS
Recognized that arterial pulses & cardiac pulses
were synchronous.

5. PULSE - HISTORY
Nei Ching Su Weri – The yellow emperors book of medicine.
The oldest book of medicine still existing. It quotes that
chief means of diagnosis than was pulse.
 It was palpated for hours in a dozen sites
 It was noted whether strong or weak
regular or irregular
 At that time as watches were not invented pulse was timed
by the physicians respiratory excursions.

6. Determinents of Arterial pulse
Left Ventricle: Stroke volume
LV contractility
Velocity of LV ejection
Aortic Valve : Normal
Stenosis
Regurgitation
Both stenosis and regurgitation
Arterial system: Compliance or distensibility
Peripheral vascular resistance
Aortic run off

7. BLOOD FLOW
LV pressure when it rises above aortic pressure
becomes driving force for movement of blood into
aorta
Driving force is dependent on
1) Contractility
2) Size & shape of LV
3) Heart rate.
This driving force is opposed by several forces that impede the
flow
1) Resistance2) Inertia3) Compliance

9. SYSTOLIC UPSTROKE TIME
Onset of pulse wave to its peak
Normal range = 90-160 ms
Brachial artery = 120 ms
 Acceleration time in Echo

11. PULSE WAVE COMPONENTS
 Percussion wave is impulse generated by LV ejection
 Tidal wave is percussion wave reflected from upper
part of the body
 Dicrotic wave is reflected from lower part of the body
often recorded but not palpable
 Anacrotic notch occurs towards the end of rapid
ejection phase just before max pressure is reached
 Incisura Occurs in Isovolumic relaxation phase prior to
aortic valve closure.
 Upstroke comes with S1
 Peak is reached well before S2

13. CENTRAL PULSE
 The central pulse begins with AV opening and onset of LV
ejection
 The rapid rising portion of the arterial pressure curve is termed
anacrotic limb (Greek – upbeat)
 An anacrotic notch is frequently recorded on the ascending limb
towards the end of rapid ejection phase.
 Peak Aortic flow velocity occurs slightly earlier than the peak
pressure.
 The Pulse shows 2 systolic waves “Percussion wave” and “Tidal
wave”

14. CENTRAL PULSE
 The descending limb of the carotid arterial pulse
is less steep than the ascending limb
 The descending limb is interrupted by a incisura a
sharp downward deflection in end systole related
to isovolumic relaxation phase
 The subsequent small positive “dicrotic wave” is
attributed to
1) Elastic recoil of aorta and AV
2) Reflected waves from most distal arteries.

15. ALTERATIONS IN CENTRAL
PULSE PERIPHERALLY
 Upstroke becomes steeper
 Systolic peak becomes higher
 Anacrotic notch disappears
 Systolic upstroke time becomes shorter (120msec)

16. CENTRAL PULSE PERIPHERAL PULSE

17. ALTERATIONS IN CENTRAL
PULSE PERIPHERALLY
 Systolic ejection time becomes more (320msec)
 The dicrotic notch occurs much later
 Systolic pressure increases
 Diastolic pressure & mean pressure decreases

18. CAUSES FOR CHANGE IN CENTRAL PULSE CONTOUR
WHEN TRANSMITTED PERIPHERALLY
1)Distortion & damping of pulse wave components
2) Different rates of transmission of various components
3) Differences in distensibility & caliber of arteries
4) Changes in the vessel wall due to age & or disease

19. CHANGES IN PULSE WITH AGING
1) Increase in the height of tidal wave
2) Increase in the height of the incisura
3) Systolic upstroke time is longer
4) Amplitude & duration of dicrotic wave decreases
Normally PW is taller than TW and TW is not palpable.
In old age, diabetes & arteriosclerosis TW is taller and
this is clinically appreciated as the pulse reaching a
peak in late systole.

20. PERIPHERAL ACCESSIBLE ARTERIES
1) Head & Neck 1) Superficial Temporal
2) Carotids
3) Subclavian
2) Upper Limb 4) Axillary
5) Brachial
6) Radial
3) Abdomen 7) Abdominal aorta
4) Lower Limb 8) Femoral
9) Popliteal
10) Posterior Tibial
11) Dorsalis Pedal

21. Localization of arteries
 The CCA terminates at C4 level at upper border of thyroid
cartilage
 The ECA is palpated medial to the sternocleidomastoid
above upper border of the thyroid cartilage
 The ICA is palpated placing a hand in the mouth and
palpating the tonsillar fauces.
 The subclavian artery is felt in the posterior triangle. With
the shoulder depressed, pressure is exerted down back and
medially in the angle between sternocleidomastoid and
clavicle.

22. Localization of arteries
 Brachial-Palpation of the right brachial pulse is accomplished
with the thumb of the examiners right hand as the patients arm
lies supinated at his or her side
 Axillary- compression against the humerus.

23. RADIAL
For radial pulse palpation the pts hand should be
supinated & comfortably supported. The
examiners thumb or tip of a single finger
preferably the index is applied to the pulse.
In infants palpation of radial pulse has inherent
limitations
1) Radial artery is very small
2) Padding of subcutaneous fat is more.

24. EVALUATION OF ARTERIAL PULSE
1) Rate& rhythm
2) Volume &tension
3) Character
4) Vessel wall
5) Peripheral pulses
Grade the palpability
Brachio or radio- femoral and brachio-brachial delay
Bruit
Palpation of abdominal artery
Ocular fundi
Allen’s test

25. GRADING OF PULSES
GRADE
0 -absent pulse
+ - feeble
++ - palpable but diminished compared to other side
+++ - normal
++++ - high volume or bounding pulse

26. ABNORMAL PULSES
1) Pulsus Parvus
2) Pulsus Tardus
3) Hypokinetic Pulse
4) Hyperkinetic Pulse
( Bounding)
5) Brisk or Jerky Pulse
6) Water Hammer Pulse
7) Collapsing Pulse
8) Corrigans Pulse
9) Anacrotic Pulse
10) Bisferrians Pulse
11) Dicrotic Pulse
12) Pulsus Paradoxsus
13) Pulsus Alternans
14) Pulsus Bigeminny

27. PULSUS PARVUS
A slow rising pulse
Low volume pulse
Best appreciated in carotids
Seen in severe AS and severe heart failure.

28. PULSUS TARDUS( Anacrotic pulse)
Late peaking
Peak is delayed and nearer to S2
Best appreciated by simultaneous auscultation of the
heart and palpation of carotid pulse
Seen in all forms of fixed obstruction to the LVOT

29. ANACROTIC PULSE
Pulsus parvus et tardus with accentuation of the
anacrotic notch and a small volume pulse.
Characterized by-
1)Slow upstroke
2)Delayed peak
3)Small volume

30. CHARACTERISTICS OF ANACROTIC PULSE
1)Pulsus parvus
2)Pulsus tardus
3)Small volume
4)Prominent anacrotic notch which appears earlier
5)Dicrotic notch disappears
It is well felt in the carotids
Earlier the anacrotic notch severe the stenosis → correlates with a
gradient of 70 mmHg

31. Normal arterial pulse with AS
 Mild AS
 Associated AR
 HOCM
 Supravalvular AS, CoA
 In children and elderly

32. HYPOKINETIC PULSE
Small or diminished pulse
1) Low CO
2) LV Dysfunction
3) CCF
4) Hypotension
5) LVOT Obstruction
In Hypokinetic pulse
Normal upstroke indicates decreased SV
Slow uprise indicates LVOT obstruction

33. HYPERKINETIC PULSE
1) Anxiety
2) Anaemia
3) Thyrotoxicosis
4) Exercise
5) Hot humid environment
6) Alcohol intake
7) Cigarette smoking
8) SHT with Atherosclerosis
9) Isolated Systolic HT

34. HYPERKINETIC PULSE
Hyperkinetic pulse has a larger than normal amplitude
and results from
1) Increased LV ejection velocity
2) Increased Stroke volume
3) Increased arterial pressure.

35. Mechanisms of high pulse volume
Atherosclerotic nondistensible
arterial system
Elderly
Increased SV
Emotional excitability, anxiety
Increased SV
Low diastolic pressure
High cardiac output status
Low diastolic pressure
Increased SB
Conditions with aortic runoff
Nondistensible arterial system
Systemic hypertension

36. The arterial pulse in MR
Significance
Characteristic pulse
Severe MR with good LV function
Normal volume with collapsing
pulse
MR in association with HOCM
Bisferiens pulse
MR in association with HOCM
Brockenbrough sign
Functional MR with AS
Slow rising pulse
Secondary MR with
cardiomyopathy or Myocariditis
Pulsus alternans
Rheumatic MR
Irregularly irregular pulse of AF
C-TGA with left AV valve
regurgitation
Slow but regular pulse
Infective endocarditis with
systemic embolism
Asymmetry of pulses

37. JERKY PULSE
Jerky pulse is a pulse with a brisk or sharp upstroke
that literally taps against the palpating fingers. The
pulse volume is not increased
Rapid upstroke / Normal downstroke / Normal
volume
Seen typically in HCM

38. COLLAPSING OR WATER HAMMER PULSE
Thomas Watson(1844) coined the term after victorian toy.
The collapsing pulse is due to :
i) Diastolic run off into the LV
ii) Reflex vasodilatation mediated by carotid baroreceptors
secondary to large stroke volume
iii) Rapid run off from the periphery due to decreased systemic
vascular resistance.
Best appreciated at the radial pulse with the palmer side of the examiner’s hand
and with the patient’s arm suddenly elevated above the shoulder.
This may be related to the artery becoming more in the line with the central
aorta, allowing direct systolic ejection and diastolic backward flow.

39. COLLAPSING PULSE
With aortic run off:
AR, PDA, AP window, RSOV into
right side and AV fistula.
Cyanotic CHD :
 Truncus arteriosus with truncal
run off in to PA or truncal
insufficiency,
 Pulmonary atresia with AP
collaterals,
 TOF with AP
collaterals/associated PDA/
associated AR / after BT shunt.
Hyperkinetic states
Pregnancy, Anemia,
thyrotoxicosis, Beriberi, Fever,
Paget’s disease of Bone
Normal Volume
Collapsing Pulse
1) MR 2) VSD

40. PERIPHERAL SIGNS OF AR
HEAD & NECK
1) De Mussets sign Head bobbing
2) Light House Sign Alt flushing & blanching of face
3) Landolfis sign Alteration in pupillary size with cardiac cycle
3) Quinckies sign Capillary pulsation over lips
4) Mullers sign Uvula pulsation
5) Carotid shudder Thrill over carotid during upstroke
6) Corrigans Pulse Visible carotid pulse of AR
7) Julians sign Pulsation of retinal vessels.
8) Minervini’s sign Strong lingual pulsations. Tongue
depressor moves up and down when
tongue is depressed.
9) Logue’s sign Pulsation of sternoclavicular junction when AR is
associated with aortic dissection.

41. PERIPHERAL SIGNS OF AR
LIMBS
10) Bisferiens Pulse Double peaked Pulse
11) Locomotor Brachi Dancing Brachialis
12) Hills sign LL SBP > 20 mm than UL
Mild 20-40 mmhg
Moderate 40-60 mmhg
severe >60mmhg
13) Pistol shot Femoralis Systolic sounds over FA
14) Traubes sign Systolic & Diastolic sounds
15) Durozies murmur. Distal occlusion diastolic murmur
Proximal occlusion systolic murmur
16) Palfrey’s sign Pistol shot sound over radial artery

42. PERIPHERAL SIGNS OF AR
ABDOMEN
17) Rosenbachs sign - Liver Pulsation
18) Gerhardts sign - Splenic Pulsation
19) Dennison’s sign - Presence of
pulsations in cervix

43. Bisferiens pulse
Normally percussion wave is felt but not the tidal
wave. In all the conditions where percussion wave is
prominent, tidal wave also becomes prominent.
Mechanism:
In combined AS and AR, the stenotic component
permits a jet, & lateral to the jet there is a fall in
pressure( Bernoulli Phenomenon), this results in a
dip or inward movement in the pulse with secondary
outward movement in a pulse or tidal wave.

44. Bisferiens pulse

45. Bisferiens pulse
Normally both waves are prominent in patients with severe AR.
In HOCM, the initial part of left ventricular ejection is rapid, resulting in
rapid upstroke.
As obstruction to the outflow starts later in the systole, due to SAM, a
sudden interruption to left ventricular ejection occurs resulting in a
dip in the pressure pulse followed by the slow rising pulse wave, which
is characteristic of HOCM ( spike and dome pattern).
The percussion wave is more prominent than tidal wave in HOCM.
Seen in Severe AR,AS with AR,HOCM,hyperkinetic circulatory
state,after exercise

46. DICROTIC PULSE
Dicrotic pulse has an accentuated dicrotic wave and hence is a twice beating pulse, one in
systole and one in diastole.
Requirements :
1) Hypotension
2) Reduced Peripheral Vascular Resistance
When the reflection wave travels rapidly and meets the original wave well in advance, it is
lost in it.
In rigid and nondistensible arterial system, as in SHT, dicrotic pulse in never present.
It is differentiated from the bisferiens pulse by the simultaneous auscultation of the heart
sounds.

47. DICROTIC PULSE
It is more noticeable in the beat following a PVC.
It is better appreciated during inspiration or
inhalation of amyl nitrite.
IABP-augmented wave due to diastolic flow
occlusion in descending aorta
Rarely present when BP > 130 mmHg and in
patients beyond 50 years of age.

48. DICROTIC PULSE
1) Healthy young adults
2) Fever
3) Hypovolemic shock
4) CCF
5) Cardiac tamponade
6) Sepsis
7) Post AVR
8) IABP

49. TWICE BEATING PULSE
Anacrotic, Bisferiens ,Dicrotic
Differentiation:
The double peaking occurs
A) On the upstroke in Anacrotic; late peaking
B) On the peak in Bisferiens- Both in Systole;
rapid rising
C) On the downstroke in Dicrotic ; normal rising
One in Systole & One in Diastole

50. PULSUS PARADOXUS
Paradox about the pulse is absence of pulse during
inspiration but presence of heart sounds & was
coined by Adolph Kussmaul in 1873.
Suspected if the pulse varies with inspiration in all
accessible arteries.
MISNOMER- the term paradoxus is that normally
there is a fall in BP during inspiration (4-
6mm/hg) which in PP is exaggerated (>10mm/hg)

51. PULSUS PARADOXUS
LV filling is reduced during inspiration because exaggerated
RV filling causes
1) Leftward shift of IVS reducing LV volume & diastolic compliance
2) Elevated intrapericardial pressure which is transmitted to the LA but
not the extraparenchymal pulmonary veins and hence a decreased
pulmonary vein – LA pressure gradient
3)Inspiratory pooling of blood in the pulmonary bed produces decline in
LA and LV filling.
[Underfilled LV may be operating in the steep ascending limb of Starling
curve so that any inspiratory reduction of LV filling results in marked
depression of the LV stroke volume and the systolic pressure].

52. Pulsus paradoxus

53. MEASUREMENT
 To detect pulsus paradoxus inflate the cuff rapidly
above the systolic pressure and then slowly deflate it.
 The difference of the systolic pressure at which
sounds are first heard only during expiration and
later during both expiration and inspiration is a
measure of the magnitude of PP.

54. PULSUS PARADOXUS - CAUSES
 Physiological - 1) Obesity
2) Pregnancy
 RS - 3) Bronchial Asthma
4) Emphysema
5) COPD
6) Large Bilateral Pleural effusion

55. PULSUS PARADOXUS - CAUSES
 CVS 7) Cardiac Tamponade
8) Constrictive Pericarditis (1/3rd)
9) Hypovolemic shock
10) Pulmonary embolism
11) RV Infarct
12) Cardiomyopathy
13) SVC Obstruction
14) Post Thoracotomy

56. DETERMINANTS OF PP
1) Venous return
2) LV afterload
3) Diastolic ventricular interdependence
4) Lung volume
5) Circulatory reflexes
The principal determinant is underfilling of LV during
inspiration in relation to RV

57. PULSUS PARADOXUS
CARDIAC CAUSE
 Inspiratory increase in venous pressure
(Kussmauls sign)
RESPIRATORY CAUSE
 Expiratory increase in venous pressure.

58. CARDIAC TAMPONADE WITHOUT PP
1) LVH
2) RVH
3) PHT
4) ASD,VSD
5) AR
6) Regional Tamponade
Mechanism for absence of PP is lack of competitive
ventricular filling during inspiration.

59. REVERSED PP
In Reversed Pulsus Paradoxus there is an increase in systemic
pressure with inspiration
1) HOCM : Mechanism unknown.
2) Isorhythmic AV dissociation : Atrial activity precedes QRS
during inspiration and marches into QRS during expiration. The
atrial activity during inspiration increases the stroke volume and
its lack during expiration decreases the stroke volume and
systolic pressure.
3) IPPV : Intrathoracic pressure is higher during inspiration and
lower during expiration.

60. PULSUS ALTERNANS
Beats occur at regular intervals but in which there is a
regular attenuation of the systolic height of the pressure
pulse.
It was first described by Traube in 1872.
Pulsus Alternans is a peripheral manifestation of LV failure
1) Alteration in the height of the pressure pulse
2) Alteration in the rate of rise.
It is the latter that is appreciated during palpation.

61. PULSUS ALTERNANS
 PA is better felt in distal vessels than proximal- rate of rise
& peak pressure developed are accentuated during
peripheral transmission of the arterial pulse pressure.
 Light pressure is applied to palpate Pulsus alternans.
 Mild degree of PA is detected by sphygmomanometer.
Inflate the BP cuff rapidly above SBP and then deflate
slowly until Korotkoffs sounds are audible. At this point
beats are heard at one half of the heart rate. When the cuff
is deflated further the rate doubles.

62. PULSUS ALTERNANS - MECHANISM
 It is due to alteration of the contractile state of at
least part of the myocardium, caused by failure of
electromechanical coupling in some cells during
weaker contraction.
 Alternate more and less number of contractile
elements participate in each contraction.
 Correlates with alteration in intensity f Korotkoff
sounds.

63. Types of Pulsus Alternans:
Total: When the weak beat is not percieved at all or when involving both
sides of the heart.
Partial: When invloving only RV ( as in PE) or LV (as in AS).
Concordant alternans: Simultaneous alternans of right and left
ventricles.
Discordant alternans: Alternating alternans of right and left
ventricles.

64. HOW TO LOOK FOR PA
1) Regular HR
2) Felt in peripheral arteries
3) Light pressure should be applied
4) Breath should be held in mid expiration
5) Can be brought out or exaggerated by decreasing venous return by
a) Sitting
b) Standing
c) Head up tilting
6) It is usually associated with S3.

65. PVC, rapid atrial pacing, IVC occlusion, myocardial
ischemia and intracoronary injection of contrast
during coronary arteriography are known to
induce alternans.
By infusion of nitroglycerine, Valsalva maneuver
and in the presence of aortic regurgitation or
systemic hypertension, pulsus alternans can be
exaggerated.

66. PULSUS ALTERNANS - CAUSES
1. LV Failure of any cause
2. Myocarditis,DCM
3. Acute pulmonary embolism
4. Severe AS with failure
5. Severe PS with failure
6. Severe AR with failure specially after aortic valve replacement.
7. Briefly during or after supraventricular tachycardia
8. Severe systemic hypertension.
9. Transient right ventricular outflow occlusion during balloon
dilatation of pulmonary stenosis.

67. DIFFERENTIATING PA FROM BIGEMINY
1) Pulsus Alternans is associated with LVS3
2) In PA the interval between the weak & strong
beats are equal
3) In Pulsus Bigeminy the weaker beats arise
prematurely and the stronger beats occur after a
pause resulting in ventricular cycles that are
alternatively short and long.

70. TIME TAKEN BY AORTIC PULSE WAVE TO REACH
1) Carotids - 30 ms.
2) Brachials - 60 ms.
3) Femoral - 75 ms.
4) Radial - 80 ms.

71. RADIOFEMORAL DELAY
It is not the delayed arrival of the femoral pulse wave
but instead a slow rate of rise to a delayed peak.
CAUSES :
Coarctation of Aorta.
Occlusive disease of the bifurcation of the aorta,
common iliac or external iliac arteries.
RIGHT RFD- Supravalvular AS

72. CoA WITH ABSENT RFD
 CoA + BAV with AS or AR
 CoA with MR
 CoA with Supravalvular AS
 Pseudo Coarctation.

73. PULSE DEFICIT
 Difference between apex beat and radial pulse > 10
beats/mt occurs in AF
 With VPC if they are too weak to open the aortic
valve.

74. Irregular pulse
 Irregularly irregular-AF
 Regularly irregular- frequent VPC
 Sinus arrhythmia-phasic variation in heart rate
a)Respiratory
b) Nonrespiratory-digitoxicity

75. Causes of rapid irregular pulse
Atrial fibrillation
Atrial flutter with varying block
Atrial tachycardia with varying block
Multifocal ventricular tachycardia
AF with WPW syndrome
Frequent multifocal atrial and ventricular ectopy

76. Causes of Rapid Regular pulse
Sinus tachycardia
Supraventricular tachycardia
Paroxysmal atrial tachycardia
Junctional tachycardia
Atrial tachycardia with fixed block
Atrial flutter with fixed block
Ventricular tachycardia

77. Causes of Bradycardia
Sinus bradycardia
Complete heart block
High grade heart block
Bigeminal rhythm with impalpable premature beat
Pulsus alternans with impalpable weak beat

78. FREQUENT VPC Vs AF
VPC – 2 beats in quick succession followed by a long
pause. (Normal beat followed by premature beat)
APC – 2 beats in quick succession followed by a short
pause.
AF - Irregular in rate ,rhythm & force
Long pause that is not preceded by 2
beats in quick succession.

79. UNEQUAL UPPER & LOWER LIMB PULSE
 Coarctation of Aorta
 Aortoarteritis
 Dissection of Aorta
 Atherosclerosis
 Trauma

80. UNEQUAL CAROTIDS
 Aortoarteritis
 Dissecting aneurysm of Aorta
 Atherosclerosis
 Thromboembolic occlusion
 Supravalvular AS

81. UNEQUAL RADIALS
 Aortoarteritis
 Dissecting aneurysm of Aorta
 Thromboembolic obstruction
 Previous catheterization
 Cervical rib
 Scalenus Anticus syndrome
 Anomalous Rt Subclavian artery
 Aberrant course of Radial artery
 Arteritis.

82. ABSENT FEMORALS
 Dissecting aneurysm
 Coarctation of aorta
 Pseudoxanthoma elasticum
 Hypoplastic External Iliac artery.

83. Points to remember
1)If the arterial pulse is regular in a patient with established atrial fibrillation on digitalis
therapy, digitoxicity with AV nodal rhythm should be considered.
2)Presence of dicrotic wave always suggests a grave prognosis.
3) Severe MR with good LV function results in normal volume collapsing pulse. This is due
to rapid ejection by the LV with the advantage of lesser afterload and more preload. With
the onset of LV dysfunction, pulse loses its collapsing character
4)Electrical alternans has no relationship to pulsus alternans