and digoxin
Heart block
Raised intracranial tension
(Cushing’s reflex)
Physiological:
Infants, children, emotion, exertion, anxiety and pregnancy
Pathological:
Tachyarrhythmias
High output states: Severe anemia, thyrotoxicosis, beri-beri, Paget’s disease of the bone,
cirrhosis of liver, AV fistula
Cardiac failure
Cardiogenic shock
Drugs (e.g. atropine, nifedipine, salbutamol, terbutaline, nicotine, and caffeine)
Relationship between pulse to temperature
For every degree F rise in temperature, the pulse rate increases by 10
Relative tachycardia Relative bradycardia
Acute rheumatic carditis
Diphtheric myocarditis
Tuberculosis
Yellow fever (Faget’s sign)
Dengue fever
First week of enteric fever
Pyogenic meningitis/intracerebral abscess
Brucellosis
Legionella
Psittacosis
Typhus
Q fever
Leptospirosis
Noninfectious:
Patients on β-blockers
Lymphomas
Factitious fever
Drug fever
Rhythm
Rhythm is assessed by palpating the radial pulse. The normal rhythm is regular.
Causes of irregular rhythm
Regularly irregular
Atrial tachyarrhythmias with fixed AV blocks, sinus arrhythmia, partial/second degree atrioventricular (AV) blocks
Ventricular bigeminy and trigeminy
Irregularly irregular
Ventricular ectopics/ventricular premature complexes (VPCs)
Atrial fibrillation (AF)
Atrial tachyarrhythmia with varying AV blocks
Regular with occasional irregularity
Extrasystoles
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Arrhythmias with Regular Rhythm
Atrial flutter
Ventricular tachycardia
First degree heart block
Second degree heart block
Pulse deficit (Apex-pulse deficit) (Fig. 2B.2) is the difference between the heart rate (counted by
auscultation) and pulse rate when counted simultaneously for one full minute by two individuals.
Causes
Pulse deficit of more than 10/minute occurs in atrial fibrillation (AF) and less than 10/minute may be
found with ventricular premature beats or slow/controlled AF.
Differences Between Atrial Fibrillation and Ventricular Premature complexes (VPCs)
Atrial fibrillation VPCs
Apex pulse deficit Usually >10 Usually <10
JVP ‘a’ wave Absent Normal
S1 Variable intensity Normal
Effect of exercise/hand grip Irregularity persists Pulse becomes regular
Fig. 2B.2: Demonstration of apex pulse deficit.
Volume of the Pulse
Volume of the pulse is a measure of the pulse pressure. The pulse pressure is the difference between
systolic and diastolic blood pressure.
Normal pulse pressure is 30–60 mm Hg
<30 mm Hg (low volume) Hypokinetic pulse >60 mm Hg (high volume) Hyperkinetic pulse
Congestive cardiac failure
Hypovolemia
Shock
Mitral stenosis
Aortic stenosis (pulsus minimus)
Constrictive pericarditis
Physiological:
Fever, pregnancy, alcoholism, and exercise
Pathological:
High output states: Anemia, beriberi, hypercarbia
Cirrhosis liver (hypoproteinemia) thyrotoxicosis,
Arterio-venous fistula (AV) fistula
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Paget’s disease of the bone
Cardiac causes (pulsus magnus):
Aortic regurgitation
Severe mitral regurgitation
Complete heart block
Patent ductus arteriosus (PDA)
Rupture of sinus of Valsalva and aortopulmonary window
Varying volume: Seen in atrial fibrillation
Anisosphygmia: Varying volume of pulses in bilateral brachial/radial vessels. Seen in Takayasu’s arteritis
Coanda effect: In supravalvular aortic stenosis, pulse volume is better in the right upper limb compared to left due to the
selective jet of the blood directed to the right subclavian vessel.
Note: Pulsus alternans, pulsus bigeminus, and pulsus paradoxus are also abnormalities in volume (described under the section of
character of pulse).
Grading of Pulse
The examination of the arterial pulses is tabulated using a scale as follows:
Grade Description
0 Complete absence of pulsation
1 Small or feeble/reduced pulsation
2 Palpable but diminished as compared to other side
3 Normal pulsation
4 Large or high volume/bounding pulsation
Character of Pulse
Best assessed in the carotids.
Exceptions:
Collapsing pulse which is appreciated better at radial artery
Pulsus bisferiens best appreciated in brachial artery.
Trisection Method
Varying degrees of pressure are applied with the finger pads of the thumb or first two fingers to assess
upstroke, systolic peak and diastolic slope of the pulse.
Components of pulse wave (Figs. 2B.3A and B):
Individual components of pulse waveform
Wave Description
Percussion wave It is due to arrival of the impulse generated by LV ejection
Tidal wave It is due to the reflected waves from the upper part of the body
Dicrotic wave It is due to the reflected waves from the lower part of the body
Dicrotic notch or incisura This corresponds to S2
(closure of aortic and pulmonary valves)
Speed of Pulse Wave and Time Taken to Reach the Peripheral Arteries
Speed of pulse wave 5 m/sec
Speed of blood flow 0.5 m/sec
Time taken for transmission of pulse to
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Carotid 30 ms
Brachial 60 ms
Femoral 75 ms
Radial 80 ms
Normally radial pulse is felt 5–10 msec later than femoral pulse.
Fig. 2B.3A: Arterial pulse tracing. Fig. 2B.3B: Waveform showing different components of pulse
wave.
Characters of pulse (Fig. 2B.4)
Character Description Condition seen
Catacrotic pulse It is the normal character of the pulse
Pulsus parvus et
tardus
A low amplitude pulse (parvus) with a slow rising
and late peak (tardus)
Severe aortic stenosis (AS)
Pulsus anacroticus Single peak low volume Severe aortic stenosis
Spike and Dome pulse Seen in HOCM
Water hammer pulse
or collapsing pulse or Watsons pulse or
pulsus celer
High (large) volume pulse
Sharp rise (systolic pressure is high)
Ill-sustained, sharp fall (diastolic pressure is low)
Pulse pressure is at least 60 mm Hg
Aortic regurgitation, patent ductus arteriosus
(PDA), aortopulmonary window, rupture of sinus
of valsalva, arteriovenous fistula, severe mitral
regurgitation
Twin beating pulse
Pulsus bisferiens Two peaks in systole Severe aortic regurgitation (AR)
Moderate AR +AS
Hypertrophic obstructive cardiomyopathy
(HOCM)
Pulsus dicroticus One peak in systole, other peak in diastole. Seen
when pulse rate and diastolic pressure is low
Typhoid fever
Severe left ventricular failure (LVF)
Dehydration
Dilated cardiomyopathy endotoxic shock
Alternating volume pulses
Pulsus alternans Alternating high volume and low volume pulse Left ventricular failure
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Regular rhythm
Korotkoff sounds double on lowering cuff
pressures
Pulsus bigeminus Pulse wave with normal beat followed by a
premature beat and a compensatory pause,
occurring in rapid succession, resulting in alteration
of the strength of pulse
Digoxin toxicity
Pulsus paradoxus
Pulsus paradoxus Systolic blood pressure falls more than 10 mm Hg
during inspiration (exaggeration of normal
phenomenon)
Constrictive pericarditis
Acute severe asthma/chronic obstructive
pulmonary disease (COPD)
Cardiac tamponade, tension pneumothorax,
and massive pulmonary embolism
Others—anaphylactic shock, and obesity
Reverse pulsus paradoxus (inspiratory rise in pulse volume and pressure): seen in intermittent positive-pressure ventilation in
the presence of left ventricular failure, hypertrophic obstructive cardiomyopathy (HOCM) and isorhythmic AV dissociation
Absent pulsus paradoxus in constrictive pericarditis: If associated with large atrial septal defect/ventricular septal
defect/aortic regurgitation (ASD/VSD/AR)/pericardial adhesions
Method of Eliciting Pulsus Paradoxus (Fig. 2B.5)
Pulsus paradoxus refers to an exaggerated fall in a patient’s blood pressure during inspiration by
greater than 10 mm Hg
Patient is placed in a semirecumbent position; respirations should be normal. Do not instruct them to
change their breathing pattern as the depth of respiration influences the magnitude of pulsus
paradoxus and will be amplified in patients with pulmonary disease
The blood pressure cuff is inflated to at least 20 mm Hg above the systolic pressure and slowly
deflated until the first Korotkoff sounds are heard
Initially sounds will be heard only during expiration. Note the level
As the cuff is further deflated, the first korotkoff sound will be heard during both inspiration and
expiration. Note this level.
If difference between the two is more than 10 mm Hg, then it is pulsus paradoxus
Fig. 2B.4: Image showing different pulse waveforms.
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Fig. 2B.5: Pulsus paradoxus.
This is not a true paradox as it is an exaggeration of normal phenomenon of fall of BP during
inspiration.
Then, What is the Paradox?
The paradox is that, in patients in patients with constrictive pericarditis, during inspiration the blood
pressure might drop significantly enough that the peripheral pulses will be absent; however, the heart
sounds will still be heard.
Other Paradoxes in Medicine
French paradox: The observation that the French suffer a relatively low incidence of coronary
heart disease, despite having a diet relatively rich in saturated fats.
“Thrombotic paradox” of hypertension (or) “Birmingham paradox”: Hypertension is a
prothrombotic state, hence paradoxially thrombotic strokes are more common than hemorrhagic.
Venous paradox—Kussmaul sign is a paradoxical rise in jugular venous pressure (JVP) on
inspiration, or a failure in the appropriate fall of the JVP with inspiration.
Ulnar paradox: Higher the lesion minimal is the deficit.
Paradoxical respiration: It causes the chest to contract while inhaling and to expand during
exhaling, the opposite of how it should move. The causes of paradoxical breathing include chest
trauma and diaphragmatic paralysis. Neurological problems that can paralyze the diaphragm.
Kinesia paradoxa: Seen in parkinsonism, patients who generally cannot move but under certain
circumstances exhibit a sudden, brief period of mobility (walking or even running).
Method of Elicitation of Pulsus Alternans (Fig. 2B.6)
Pulsus alternans refers to alternating high and low volume pulses.
Patient is placed in a semirecumbent position.
The blood pressure cuff is inflated to at least 20 mm Hg above the systolic pressure and slowly
deflated until the first Korotkoff sounds are heard.
Initially, the Korotkoff’s sounds due to the high volume pulses will be heard.
On lowering the blood pressure, Korotkoff sounds will be heard due to both high volume and low
volume pulses.
This will produce doubling of Korotkoff’s sounds.
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