The Clinical Pulse: A Comprehensive Review for the Modern Internist

Dr Neeraj Manikath , claude.ai

Abstract

The pulse examination remains a cornerstone of cardiovascular assessment despite technological advances in modern medicine. This comprehensive review explores the physiological basis, examination techniques, pathological variations, and clinical significance of pulse assessment in internal medicine. We examine traditional pulse characteristics alongside contemporary evidence-based applications, providing practical pearls for postgraduate medical education. Understanding pulse pathophysiology enhances diagnostic accuracy and clinical reasoning in diverse cardiovascular and systemic conditions.

Introduction

The pulse has been central to medical diagnosis for millennia, dating back to ancient Egyptian, Chinese, and Greek medicine. In the modern era of echocardiography and advanced hemodynamic monitoring, the humble pulse examination retains remarkable clinical utility. The pulse provides immediate, non-invasive information about cardiac output, vascular compliance, and systemic perfusion—making it an indispensable skill for internists.

This review synthesizes classical pulse semiology with contemporary evidence, offering practical insights for postgraduate training in internal medicine.

Physiological Basis of the Arterial Pulse

Pulse Generation and Propagation

The arterial pulse represents the pressure wave generated by left ventricular ejection traveling through the arterial tree. This wave propagates at 5-15 m/s, significantly faster than the actual blood flow velocity (0.5-1 m/s)—a distinction often confused in clinical teaching.

The pulse waveform comprises:

Anacrotic limb: Rapid upstroke during ventricular systole
Peak systolic pressure: Maximum arterial pressure
Dicrotic notch: Corresponds to aortic valve closure
Dicrotic limb: Decline during diastole

Pearl: The pulse felt peripherally is NOT the blood itself moving, but a pressure wave—analogous to a wave traveling through water.

Determinants of Pulse Character

The pulse character reflects the complex interplay of:

Stroke volume: Volume ejected per beat
Ejection velocity: Speed of ventricular contraction
Arterial compliance: Vessel wall elasticity
Peripheral resistance: Arteriolar tone
Blood viscosity: Rheological properties

These factors explain why pulse abnormalities may indicate either cardiac or vascular pathology.

Systematic Pulse Examination

Sites of Examination

While multiple pulse sites exist, the radial artery remains the standard for routine examination due to its accessibility and superficial location. However, comprehensive vascular assessment requires evaluation of:

Carotid: Best for waveform analysis, closest to central aortic pulse
Brachial: Useful for blood pressure measurement
Radial: Standard site for rate and rhythm
Femoral: Assessment of aortoiliac disease
Popliteal: Often overlooked, important for peripheral vascular disease
Dorsalis pedis and posterior tibial: Distal perfusion assessment

Hack: Always palpate the carotid pulse when assessing murmurs—it provides the best temporal correlation with cardiac events and helps distinguish systolic from diastolic murmurs.

Technique: The Seven S's of Pulse Examination

Site: Document which artery
Side: Compare symmetry bilaterally
Synchronicity: Radio-radial, radio-femoral delay
Speed: Rate (beats per minute)
Strength: Volume and amplitude
Shape: Character and waveform
Special features: Irregularity, paradox, alternans

Pearl: Palpate the pulse with your fingertips (more sensitive mechanoreceptors), not your thumb (contains its own pulse, may cause confusion).

Rate Assessment

Normal resting heart rate: 60-100 bpm in adults

Clinical Classifications:

Bradycardia: <60 bpm
- Physiological: Athletes, sleep
- Pathological: Hypothyroidism, increased intracranial pressure, sick sinus syndrome, complete heart block, drugs (beta-blockers, calcium channel blockers, digoxin)
Tachycardia: >100 bpm
- Physiological: Exercise, emotion, fever, pregnancy
- Pathological: Anemia, hyperthyroidism, heart failure, sepsis, arrhythmias

Oyster: Faget's sign—relative bradycardia despite high fever—classically described in typhoid fever, but also seen in brucellosis, yellow fever, and occasionally legionnaires' disease. This paradoxical finding warrants consideration of atypical infections.

Rhythm Assessment

Assess rhythm over 30-60 seconds by palpation:

Regular: Sinus rhythm, controlled atrial fibrillation with rapid ventricular response
Regularly irregular: Second-degree AV block (Mobitz I or II), bigeminy, trigeminy
Irregularly irregular: Atrial fibrillation (most common), multifocal atrial tachycardia, frequent premature beats

Hack: If the pulse is irregularly irregular, it's atrial fibrillation until proven otherwise—this simple rule has >90% positive predictive value in patients over 65 years.

Pearl: In suspected atrial fibrillation, always check for pulse deficit (difference between apical rate and radial rate). A pulse deficit indicates hemodynamically compromised beats that fail to generate peripheral pulses, suggesting poor ventricular filling or very rapid rates.

Pathological Pulse Characteristics

Volume and Amplitude Variations

Large Volume (Bounding) Pulses

Characterized by rapid upstroke, high amplitude, and rapid descent.

Causes:

Aortic regurgitation (classically described with multiple eponyms)
High cardiac output states: Hyperthyroidism, severe anemia, arteriovenous fistula, Paget's disease, beriberi
Patent ductus arteriosus
Complete heart block (large stroke volume)
Fever, anxiety

Classical Eponyms in Aortic Regurgitation:

Corrigan's pulse: Water-hammer pulse (rapid upstroke and collapse)
De Musset's sign: Head nodding with each heartbeat
Quincke's sign: Visible capillary pulsations in nail beds
Müller's sign: Systolic pulsations of uvula
Duroziez's sign: Systolic and diastolic murmurs over femoral artery with compression
Traube's sign: Pistol-shot femorals (sharp systolic sounds)

Pearl: While these signs are taught extensively, their presence indicates severe, chronic aortic regurgitation—by the time multiple peripheral signs appear, the diagnosis should be clinically obvious. Their absence does NOT exclude significant aortic regurgitation.

Small Volume (Weak) Pulses

Decreased amplitude with normal or slow upstroke.

Causes:

Heart failure with reduced ejection fraction
Hypovolemia/shock
Severe mitral stenosis
Cardiac tamponade
Constrictive pericarditis
Severe aortic stenosis (when combined with slow upstroke)

Character Variations

Slow-Rising (Plateau/Pulsus Parvus et Tardus)

Delayed upstroke, sustained peak, diminished amplitude.

Classic for: Severe aortic stenosis

The slow upstroke reflects delayed and reduced left ventricular ejection through the stenotic valve.

Clinical Significance: Best appreciated at the carotid artery. If easily palpable at the carotid with normal character, severe aortic stenosis is unlikely.

Oyster: In elderly patients with calcific aortic stenosis and stiff, atherosclerotic vessels, the vessel rigidity may paradoxically normalize the pulse character, masking the slow-rising nature—this can lead to underestimation of stenosis severity. Always correlate with other findings (narrow pulse pressure, late-peaking systolic murmur, diminished A2).

Collapsing (Waterhammer/Corrigan's)

Rapid, forceful upstroke followed by sudden collapse.

Pathophysiology: Rapid runoff of blood from arterial system due to:

Aortic regurgitation (most common)
Patent ductus arteriosus
Arteriovenous fistula
Severe peripheral vasodilatation

Examination technique: Elevate the patient's arm above heart level while palpating the radial pulse—the pulse will feel like a sudden tap against your fingers (traditionally likened to the old water-hammer toy).

Pearl: The collapsing pulse requires both adequate stroke volume AND rapid diastolic runoff. In acute severe aortic regurgitation, tachycardia and decreased stroke volume may prevent the classical collapsing character, potentially delaying diagnosis.

Bisferiens Pulse

Double-peaked systolic pulse with two positive waves during systole.

Causes:

Mixed aortic valve disease (regurgitation + stenosis)
Hypertrophic cardiomyopathy
Isolated severe aortic regurgitation (less common)

Pathophysiology: First peak represents initial ventricular ejection; second peak (tidal wave) results from reflected waves from periphery or rapid ejection in HOCM.

Clinical note: Difficult to appreciate; best felt at carotid artery in young patients with compliant vessels.

Dicrotic Pulse

Exaggerated dicrotic notch creating a palpable double impulse (one in systole, one in early diastole).

Causes: Low cardiac output states with high peripheral resistance

Severe heart failure
Cardiac tamponade
Hypovolemic shock

Pearl: Unlike bisferiens (two systolic peaks), dicrotic pulse has one systolic and one early diastolic peak. This is rare and indicates severe hemodynamic compromise.

Pulsus Alternans

Regular rhythm with alternating strong and weak beats.

Pathophysiology: Alternating strong and weak ventricular contractions despite regular electrical activation.

Clinical Significance: Indicates severe left ventricular systolic dysfunction. May precede overt heart failure.

Mechanism: Likely related to alternating calcium availability for excitation-contraction coupling in failing myocardium.

Hack: If you cannot palpate alternans clearly, inflate the blood pressure cuff slowly while listening with a stethoscope—you'll hear alternating loud and soft Korotkoff sounds, with pressure difference sometimes exceeding 20 mmHg between strong and weak beats.

Oyster: Electrical alternans (alternating QRS amplitude on ECG) plus pulsus alternans strongly suggests large pericardial effusion with tamponade physiology—consider urgent echocardiography.

Pulsus Paradoxus

Exaggerated decrease (>10 mmHg) in systolic blood pressure during inspiration.

Normal Physiology: Systolic BP normally drops up to 10 mmHg with inspiration due to:

Increased venous return to right heart
Pooling in expanded pulmonary vessels
Decreased left ventricular filling

Pathological Causes (>10 mmHg drop):

Cardiac tamponade (classic finding)
Constrictive pericarditis
Severe obstructive airway disease (COPD, asthma exacerbation)
Massive pulmonary embolism
Right ventricular infarction

Measurement Technique:

Patient breathing normally (not deep breaths)
Inflate cuff above systolic pressure
Deflate slowly (2 mmHg/second)
Note pressure where first Korotkoff sounds heard intermittently (only during expiration)
Continue deflating until sounds heard throughout respiratory cycle
Difference between these two pressures = paradox magnitude

Pearl: The term "paradoxus" is a misnomer—it's an exaggeration of normal physiology, not a reversal. Named by Kussmaul, who noted the pulse could disappear during inspiration despite heart sounds remaining audible.

Critical Clinical Hack: In tamponade, look for the triad:

Pulsus paradoxus >10 mmHg
Jugular venous pressure >10 cm H₂O
Muffled heart sounds (Beck's triad when hypotension added)

Oyster: Absence of pulsus paradoxus does NOT exclude tamponade in:

Atrial septal defect
Severe aortic regurgitation
Regional tamponade (post-cardiac surgery)
Severe left ventricular dysfunction

Pulsus Bigeminus

Irregular rhythm with coupling of beats (normal beat followed by premature beat, then pause).

Cause: Ventricular or atrial premature contractions occurring after every normal beat.

Clinical Distinction: Unlike pulsus alternans (same electrical rhythm, varying mechanical force), bigeminus has different electrical activation for each beat pair.

Radio-Femoral Delay

Normally, radial and femoral pulses are synchronous.

Clinical Significance: Palpable delay indicates:

Coarctation of aorta (most important diagnosis)
Severe aortoiliac atherosclerosis (less common in young patients)
Dissection involving descending aorta

Examination Technique: Simultaneously palpate right radial and right femoral pulses. The femoral pulse should be felt simultaneously or slightly before the radial pulse. A palpable delay is abnormal.

Oyster: In coarctation, also check for:

Upper limb hypertension with lower limb hypotension
Weak or absent femoral pulses
Continuous murmur over back (collateral vessels)
Rib notching on chest X-ray (chronic collaterals)

Clinical Pearl: Always check femoral pulses in any young patient (<40 years) with hypertension—this simple examination can reveal a surgically correctable cause.

Special Clinical Scenarios

Pulse in Arrhythmias

Atrial Fibrillation

The irregularly irregular pulse of AF results from:

Random atrial electrical activity
Variable AV nodal conduction
Varying ventricular filling time affecting stroke volume

Rate assessment: Count for full minute (irregularity makes shorter periods inaccurate).

Pearl: Very irregular pulse with rates >180 bpm suggests AF with rapid ventricular response or multifocal atrial tachycardia. Regular tachycardia >180 bpm suggests supraventricular tachycardia or atrial flutter.

Ventricular Ectopy

Occasional PVCs: Irregular pulse with occasional early, weak beats followed by pause
Bigeminy: Regularly irregular (normal-PVC-pause-normal-PVC-pause)
Trigeminy: Regularly irregular (normal-normal-PVC-pause pattern)

Compensatory pause: After PVC, the pause before next normal beat is prolonged, creating characteristic pattern.

Pulse in Shock States

Pulse characteristics help classify shock:

Hypovolemic/Cardiogenic Shock:

Weak, thready pulse
Narrow pulse pressure
Cool extremities
Delayed capillary refill

Distributive Shock (septic, anaphylactic):

Bounding pulse (early sepsis)
Wide pulse pressure
Warm extremities (early sepsis)
Normal or increased pulse pressure initially

Obstructive Shock (tamponade, PE, tension pneumothorax):

Weak pulse
Pulsus paradoxus (tamponade)
Elevated JVP
Clear lungs

Hack: In undifferentiated shock, pulse character plus skin temperature provides rapid clue:

Weak pulse + cool skin = pump or volume problem
Bounding pulse + warm skin = distributive (sepsis until proven otherwise)

Clinical Pearls and Teaching Points

Pearl 1: The "Rule of Thumb" for Radial Pulse

If you can easily feel the radial pulse, systolic BP is likely >80 mmHg. If you need the femoral or carotid to feel pulse, systolic BP may be <80 mmHg. While not precise, this provides rapid bedside estimate in emergencies.

Pearl 2: Pulse Pressure (PP) as Hemodynamic Window

PP = Systolic BP - Diastolic BP (normal: 40-60 mmHg)

Narrow PP (<25% of systolic):

Hypovolemia
Heart failure
Cardiac tamponade
Severe aortic stenosis

Wide PP (>60 mmHg):

Aortic regurgitation
Hyperthyroidism
Arteriovenous fistula
Atherosclerosis (reduced arterial compliance)
Isolated systolic hypertension (elderly)

Hack: In elderly patients, PP >60 mmHg is a stronger predictor of cardiovascular events than systolic or diastolic BP alone.

Pearl 3: The Carotid—The "Truth-Teller"

The carotid pulse is closest to the aorta and least affected by peripheral factors. When in doubt about pulse character:

Slow-rising in AS? Check carotid
Collapsing in AR? Check carotid
Timing murmurs? Palpate carotid while auscultating

Safety note: Never compress both carotids simultaneously. Avoid vigorous or prolonged carotid massage, especially in elderly patients with bruits (atherosclerotic disease).

Pearl 4: Hill's Sign in Aortic Regurgitation

Popliteal systolic BP exceeding brachial systolic BP by >20 mmHg suggests severe, chronic aortic regurgitation. While traditional teaching emphasized this, modern evidence suggests it lacks sensitivity and specificity—echocardiography remains gold standard.

Pearl 5: Pulse in Cardiac Tamponade

Beyond pulsus paradoxus, look for:

Tachycardia (compensatory)
Low-volume pulse
Absent y descent in JVP
Electrical alternans on ECG

Oyster: "Low-pressure tamponade" occurs in hypovolemia—patients lack elevated JVP despite tamponade physiology. Volume resuscitation may be needed before definitive pericardiocentesis, but must be done cautiously.

Pearl 6: The Diagnosis of Coarctation at the Bedside

Simple examination sequence in suspected coarctation:

Measure BP in both arms (may be equal in coarctation)
Measure BP in leg (should be 10-20 mmHg higher than arms normally)
Palpate radio-femoral delay
Examine back for continuous murmur

This takes 3 minutes and can diagnose a surgically correctable cause of secondary hypertension.

Pearl 7: Pulse in Hypertrophic Cardiomyopathy

The rapid upstroke (brisk) pulse in HOCM differs from the slow-rising pulse of AS, despite both causing LVOT obstruction. This is because:

HOCM: Dynamic obstruction occurring mid-to-late systole (rapid initial ejection)
AS: Fixed obstruction from the start (slow initial ejection)

Maneuvers: Valsalva or standing increases HOCM murmur and pulse abnormality (decreased preload worsens obstruction). Squatting or leg raise decreases HOCM findings.

Contemporary Evidence and Diagnostic Accuracy

Despite technological advances, recent studies confirm pulse examination utility:

Atrial Fibrillation Detection: Pulse palpation has 92-96% sensitivity for AF detection in primary care, with irregularly irregular pattern being highly specific.
Peripheral Arterial Disease: Absent dorsalis pedis or posterior tibial pulse has 50-70% sensitivity but >95% specificity for significant PAD (ABI <0.9).
Pulse Pressure in Risk Stratification: Multiple large studies (Framingham, SHEP, Syst-Eur) show pulse pressure is an independent predictor of cardiovascular events, particularly in elderly patients.
Pulsus Paradoxus in Tamponade: Meta-analyses show >10 mmHg paradox has 82% sensitivity for tamponade, but absence doesn't exclude diagnosis (60% specificity).

Integration with Modern Investigations

The pulse examination guides further investigation:

Irregular Pulse → ECG (AF, frequent ectopy) Radio-femoral Delay → CT angiography/MRI (coarctation) Slow-rising Pulse → Echocardiography (AS severity) Collapsing Pulse → Echocardiography (AR quantification) Pulsus Paradoxus → Echocardiography (tamponade, constrictive physiology) Asymmetric Pulses → Duplex ultrasound/CTA (atherosclerotic disease)

Teaching Strategies for Postgraduate Education

Bedside Teaching Approaches

Comparative Palpation: Have trainees compare pulses in normal volunteers versus patients with pathology on the same ward round
Blind Palpation Exercise: Trainees palpate pulse without knowing diagnosis, then predict underlying pathology before echocardiography review
Video Documentation: Record high-quality videos of examination technique and abnormal findings for case-based learning
Simulation: Use pulse simulators to teach rhythm recognition and character assessment before bedside application

Common Trainee Errors

Using thumb instead of fingers: Contains own pulse
Inadequate palpation time: <30 seconds insufficient for rhythm assessment
Neglecting bilateral comparison: Misses asymmetry
Forgetting radio-femoral assessment: Misses coarctation
Poor carotid technique: Failure to use carotid for character assessment
Confusing rate with rhythm: Focus on one parameter at a time

Future Directions

Wearable Technology

Smartwatches and fitness trackers now detect AF with reasonable accuracy (>95% sensitivity in some studies). However, clinical pulse examination provides contextual information technology cannot replicate—volume, character, synchronicity, and integration with overall cardiovascular assessment.

Point-of-Care Ultrasound

Integration of handheld ultrasound with pulse examination enhances diagnostic accuracy, particularly for:

Real-time visualization of pulse waveform abnormalities
Confirmation of cardiac findings (AS, AR, tamponade)
Assessment of volume status

The future internist combines traditional pulse examination with modern technology for comprehensive cardiovascular assessment.

Conclusion

The pulse examination remains a sophisticated, nuanced, and clinically powerful tool in internal medicine. While technological investigations provide precise quantification, the pulse offers immediate, integrative information about cardiovascular physiology and pathology. Mastery of pulse examination distinguishes the accomplished internist, providing diagnostic insights at the bedside that guide investigation and management.

For postgraduate trainees, systematic practice, correlation with imaging findings, and repeated bedside examination remain the path to expertise. The pulse, humble yet revealing, continues to speak volumes to those trained to listen.

Key References

McGee S. Evidence-Based Physical Diagnosis. 5th ed. Philadelphia: Elsevier; 2022.
Constant J. Bedside Cardiology. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2012.
Mangione S. Physical Diagnosis Secrets. 3rd ed. Philadelphia: Elsevier; 2023.
Cook DJ, Simel DL. The Rational Clinical Examination: Evidence-Based Clinical Diagnosis. JAMA. 2019.
Franklin SS, Khan SA, Wong ND, et al. Is pulse pressure useful in predicting risk for coronary heart disease? The Framingham Heart Study. Circulation. 1999;100(4):354-360.
Lowenstein J. The Clinical Examination. BMJ. 2006;333(7562):233-236.
Roy CL, Minor MA, Brookhart MA, Choudhry NK. Does this patient with a pericardial effusion have cardiac tamponade? JAMA. 2007;297(16):1810-1818.
Simel DL, Rennie D, Keitz SA. The Rational Clinical Examination: Evidence-Based Clinical Diagnosis. New York: McGraw-Hill; 2009.
Goldberger AL, Goldberger ZD, Shvilkin A. Clinical Electrocardiography: A Simplified Approach. 9th ed. Philadelphia: Elsevier; 2018.
Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease. Circulation. 2021;143(5):e72-e227.
Fuster V, Harrington RA, Narula J, Eapen ZJ. Hurst's The Heart. 14th ed. New York: McGraw-Hill; 2017.
Mant J, Hobbs FD, Fletcher K, et al. Warfarin versus aspirin for stroke prevention in an elderly community population with atrial fibrillation (the Birmingham Atrial Fibrillation Treatment of the Aged Study, BAFTA): a randomised controlled trial. Lancet. 2007;370(9586):493-503.
Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J. 2015;36(42):2921-2964.
Aboyans V, Ricco JB, Bartelink MEL, et al. 2017 ESC Guidelines on the Diagnosis and Treatment of Peripheral Arterial Diseases. Eur Heart J. 2018;39(9):763-816.
Pereira J, Candiani T, Escaned J, Jiménez-Quevedo P. The Pulse Examination as a Tool for Cardiovascular Diagnosis in the Modern Era. Rev Esp Cardiol (Engl Ed). 2020;73(3):248-255.

Summary: Top 10 Clinical Hacks for Pulse Examination

Irregularly irregular pulse = AF until proven otherwise (>90% PPV in patients >65)
Palpate carotid while auscultating = best way to time murmurs and assess character
Radio-femoral delay check in young hypertensives = may find surgically correctable coarctation
Pulse pressure >60 mmHg in elderly = stronger cardiovascular risk predictor than BP alone
Pulsus alternans + electrical alternans = think large pericardial effusion/tamponade
Palpable radial pulse = systolic BP likely >80 mmHg (rough bedside estimate)
Weak pulse + cool skin = cardiogenic/hypovolemic shock; bounding + warm = distributive/septic
Count irregular rhythms for 60 seconds = shorter periods inaccurate in AF
Slow BP cuff deflation = easiest way to detect pulsus alternans (alternating Korotkoff sounds)
Always compare pulses bilaterally = asymmetry suggests vascular disease or dissection

This review article synthesizes classical teaching with contemporary evidence to enhance postgraduate medical education in cardiovascular examination. The pulse remains an elegant window into hemodynamics when examined systematically and interpreted thoughtfully.