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Collapsing pulse
Collapsing pulse
Collapsing pulse
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Collapsing pulse
Other namesCorrigan's pulse
Differential diagnosisaortic regurgitation

Watson's water hammer pulse, also known as Corrigan's pulse or collapsing pulse, is the medical sign (seen in aortic regurgitation) which describes a pulse that is bounding and forceful,[1] rapidly increasing and subsequently collapsing,[2] as if it were the sound of a water hammer that was causing the pulse.

Diagnosis

[edit]

To feel a water hammer pulse: with the patient reclining, the examiner raises the patient's arm vertically upwards. The examiner grasps the muscular part of the patient's forearm. A water hammer pulse is felt as a tapping impulse that is transmitted through the bulk of the muscles. This happens because the blood that is pumped to the arm during systole is emptied very quickly due to the gravity effect on the raised arm. This results in the artery emptying back into the heart during diastole, increasing preload, and therefore increasing cardiac output, (as per the Frank–Starling mechanism) so that systolic blood pressure increases and a stronger pulse pressure can be palpated. [3]

Causes

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Water hammer pulse is commonly found when a patient has aortic regurgitation. It can also be seen in other conditions which are associated with a hyperdynamic circulation. A more comprehensive list of causes follows:[4]

Eponym

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"Watson's water hammer pulse" and "Corrigan's pulse" refer to similar observations. However, the former usually refers to measurement of a pulse on a limb, while the latter refers to measurement of the pulse of the carotid artery.[1]

  • "Corrigan's pulse" is named for Sir Dominic Corrigan, the Irish physician, who characterized it in 1832.[5][6]
  • "Watson's water hammer pulse" is named for Thomas Watson, who characterized it in 1844.[1]

See also

[edit]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Collapsing pulse

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from Grokipedia
A collapsing pulse, also known as Corrigan's pulse or water hammer pulse, is a clinical observed during that describes a bounding and forceful arterial featuring a rapid upstroke followed by a quick diastolic collapse. This waveform results from a widened , where systolic pressure is markedly elevated and diastolic pressure is significantly reduced, often palpated at the radial or . The collapsing pulse is most prominently associated with , a where the fails to close properly, allowing blood to flow backward into the left ventricle during , thereby exaggerating the pulse's amplitude and rapidity. It can also arise in other hyperdynamic circulatory conditions, including , thyrotoxicosis, severe , fever, , or arteriovenous fistulas, which increase or decrease peripheral vascular resistance. Physiologically, it may occur transiently during exercise or emotional stress due to heightened . To elicit the collapsing pulse, the examiner elevates the patient's arm above the level of the heart while palpating the with the palm; the pulse feels like a sharp tapping or hammering sensation due to rapid runoff of blood into the dilated arterial system during . Historically, the sign was first described in 1832–1833 by Irish physician Dominic John Corrigan, who noted the visible arterial pulsations in the neck, and later analogized to the "water hammer" toy by Thomas Watson in 1844, emphasizing the sudden cessation of flow. Its detection remains a key bedside finding in cardiovascular assessment, aiding in the diagnosis of underlying hemodynamic abnormalities, though is often required for confirmation.

Definition and Characteristics

Definition

A collapsing pulse is a peripheral characterized by a rapid upstroke, known as the percussion wave, followed by a quick collapse, due to exaggerated , resulting in a bounding and forceful quality. This physical sign manifests as a palpable arterial distension that abruptly recedes, often giving a sensation of a sharp tap followed by sudden emptying. It is also known by several alternative names, including water hammer pulse, Corrigan's pulse, and hyperkinetic pulse. The collapsing pulse is observed in conditions featuring high and rapid diastolic runoff, leading to visible or palpable arterial expansion and subsequent collapse. A classic example is its association with .

Physical Characteristics

The collapsing pulse, also known as the water hammer pulse, presents with a bounding and forceful amplitude characterized by a rapid upstroke followed by an abrupt descent, creating a tactile sensation akin to a "tap" or "hammer" against the examining finger. This distinct waveform is most readily palpated at the radial, brachial, or femoral arteries, where the pulse feels like a sudden impulse traveling through the or limb. Visually, the pulse manifests as prominent pulsations in the carotid arteries of the neck, with abrupt distention and collapse, or in the nail beds through alternate blanching and flushing indicative of pulsations (Quincke's sign). These observable features highlight the exaggerated arterial excursion in affected individuals. The phenomenon is associated with a widened , often exceeding 60 mmHg, typically featuring systolic pressures above 140 mmHg and diastolic pressures below 60 mmHg, reflecting the hemodynamic extremes. The intensity varies by severity: subtle in mild presentations, requiring attentive , but dramatically visible and forceful in severe cases. Such characteristics may also appear in high-output states like .

Pathophysiology

Hemodynamic Mechanism

The collapsing pulse arises from a primary hemodynamic mechanism involving increased , which leads to rapid systolic filling of the peripheral arteries, followed by accelerated diastolic emptying due to retrograde flow through incompetent valves or shunts, thereby creating an exaggerated between and . This dynamic is classically associated with , where the left ventricle ejects a larger volume of blood into the arterial system to compensate for volume loss. Pulse pressure, defined as the difference between systolic and diastolic (systolic BP - diastolic BP), widens significantly in this condition due to elevated systolic ejection from the augmented and impaired diastolic pressure maintenance from rapid runoff. The arterial exhibits a prominent upstroke, or anacrotic phase, characterized by a steep ascent reflecting the forceful and rapid ejection into compliant arteries, contrasting with the more gradual rise in normal waveforms. This is followed by a pronounced , or catacrotic phase, with a sharp descent as arterial pressure plummets during . The role of arterial compliance is critical, as reduced diastolic pressure results from excessive runoff into low-resistance beds, such as from the back to the left ventricle, which diminishes the that normally sustains diastolic pressure and amplifies the collapsing sensation. In the arterial pressure tracing, this manifests as a steep ascent and rapid descent, often with a diminished or absent dicrotic notch—representing closure—compared to the normal waveform's distinct notch and slower downslope, highlighting the loss of diastolic buffering.

Physiological Basis

The collapsing pulse arises from the body's adaptive responses to conditions that widen , involving compensatory mechanisms that maintain despite rapid diastolic runoff. activation in response to low diastolic triggers a reflex , mediated by increased sympathetic outflow, to sustain overall and counteract the hemodynamic widening of . Additionally, in high-output states, peripheral promotes increased venous return and , further enhancing the pulse's rapid descent as blood empties quickly into dilated vessels. Systemic factors such as amplify these effects without necessitating primary valvular pathology. In , reduced blood viscosity lowers systemic , facilitating greater and a more pronounced collapsing quality to the pulse. Similarly, thyrotoxicosis elevates metabolic demand, inducing widespread and sympathetic activation that boost , thereby exaggerating the pulse's bounding rise and fall through enhanced runoff during . These influences collectively reduce total peripheral resistance, allowing for the characteristic quick collapse as diastolic pressure drops precipitously. Vascular factors play a key role in modulating the pulse's expression, with peripheral directly contributing to the low total peripheral resistance that accelerates diastolic emptying. Large artery compliance, rather than , permits unimpeded transmission of the high and rapid recoil, intensifying the collapsing sensation; conversely, increased could dampen this by limiting vessel distensibility. Over time, chronic exposure to elevated prompts adaptive left , including eccentric , as the myocardium thickens to handle the persistent volume load while preserving ejection efficiency.

Etiology

Valvular Causes

The primary valvular cause of collapsing pulse is , a condition in which the leaflets fail to coapt fully during , permitting retrograde blood flow from the into the left ventricle. This regurgitant flow creates a rapid diastolic "runoff" that lowers aortic pressure abruptly, producing the hallmark bounding upstroke and sudden collapse of the peripheral pulse. AR accounts for the vast majority of collapsing pulse cases among valvular etiologies, with chronic forms being particularly prevalent in clinical presentations of this sign. Aortic regurgitation manifests in acute and chronic forms, each with distinct underlying mechanisms tied to valvular pathology. Acute AR typically arises from sudden structural disruption, such as damaging valve leaflets or compromising valvular support, leading to immediate and severe retrograde flow. In contrast, chronic AR develops progressively from congenital or acquired defects, including (a common congenital anomaly affecting up to 1-2% of the population and predisposing to early degeneration), (which causes leaflet thickening and fusion, especially in developing regions), and connective tissue disorders like . In , genetic mutations in fibrillin-1 lead to aortic root dilation, stretching the valve annulus and preventing proper leaflet closure. Leaking aortic valve prostheses can also cause AR and contribute to collapsing pulse. Other valvular conditions contributing to collapsing pulse include mixed and regurgitation, often seen in degenerative or bicuspid valves where partial obstruction coexists with leakage, exacerbating and pulse dynamics. Rarely, severe may indirectly promote a collapsing pulse through significant left ventricular and , though this is far less common than AR. The clinical impact of these valvular causes correlates with regurgitation severity, quantified by regurgitant volume per beat via : mild AR involves less than 30 mL/beat, while severe cases exceed 60 mL/beat, intensifying the pulse's and collapse due to greater diastolic runoff. This wide in severe AR amplifies the collapsing pulse's detectability during .

Non-Valvular Causes

Non-valvular causes of collapsing pulse arise primarily from hyperdynamic circulatory states or abnormal vascular communications that lead to increased and reduced peripheral vascular resistance, mimicking the hemodynamic effects of valvular incompetence without involving structural defects. These conditions result in a rapid upstroke and quick diastolic collapse of the pulse due to enhanced or diastolic runoff into low-pressure systems. High-output states represent a major category, where systemic and elevated produce the characteristic bounding and collapsing pulse. Severe decreases blood viscosity and oxygen-carrying capacity, prompting compensatory and increased that manifests as a collapsing pulse. Thyrotoxicosis, characterized by elevated free T4 levels and suppressed TSH, induces widespread and , leading to high and a prominent water hammer pulse. Similarly, beriberi from impairs myocardial energy metabolism, causing peripheral and high-output heart failure with a collapsing pulse. , through extensive arteriovenous shunting in affected skeletal tissue, elevates overall and can produce this pulse finding. Liver and cor pulmonale can also lead to and collapsing pulse. Shunt-related etiologies involve abnormal connections that allow diastolic runoff from the to lower-pressure compartments, accelerating the pulse collapse. (PDA) creates a persistent left-to-right shunt, resulting in wide and a collapsing peripheral due to runoff into the . Arteriovenous fistulas, such as those formed for access, divert arterial blood directly to veins, lowering diastolic and eliciting a bounding, collapsing . Ruptured sinus of Valsalva aneurysm typically presents with acute hemodynamic instability and a water hammer from the sudden aorto-right heart shunt. Rare conditions like aortopulmonary window similarly cause runoff into the , producing high-volume collapsing s. Other transient or physiologic factors can induce a collapsing pulse through temporary . represents a physiologic high-output state with reduced systemic and increased , often yielding a bounding that collapses rapidly. Fever and anxiety elevate via sympathetic activation and , transiently mimicking the finding. These non-valvular causes differ from valvular etiologies by lacking primary aortic incompetence, instead relying on peripheral resistance drops or extracardiac shunts to generate the pulse abnormality; they account for a minority of cases compared to valvular disease.

Clinical Diagnosis

Examination Techniques

The detection of a collapsing pulse, also known as a water hammer pulse, primarily relies on palpation during the physical examination to identify its characteristic rapid upstroke and abrupt diastolic collapse. The patient is typically positioned supine with a slight recline to facilitate access to peripheral arteries, though a seated or standing position may be used to accentuate the finding during maneuvers. Palpation begins at the , where the examiner wraps the fingers around the patient's to feel the . The wrist elevation test involves lifting the patient's arm above the head while maintaining ; this enhances the gravitational runoff of blood, allowing the examiner to sense a tapping impulse in the due to the rapid diastolic emptying. The water hammer test further emphasizes this by elevating the arm while observing for visible collapse of the artery, often with the palm placed over the to appreciate both radial and ulnar pulsations. For the , similar arm elevation is performed during in the antecubital fossa to assess involvement. The is palpated in the for lower limb , particularly to detect bounding or , though it is less commonly emphasized than upper extremity sites. Bilateral of pulses is essential to identify any , which may indicate underlying hemodynamic differences. The severity of the collapsing pulse is graded subjectively on a scale from 1+ (subtle, barely perceptible collapse) to 4+ (dramatic, visible pulsation with forceful rebound), based on the and of the , akin to general peripheral grading systems. Patient positioning can enhance detection; for instance, transitioning from to sitting may increase the prominence of the due to orthostatic effects on vascular tone. This sign is often associated with a wide , reflecting the underlying . In cases of severe , the collapsing pulse has poor as a peripheral sign, but is useful when combined with other findings. Pitfalls include reduced palpability in patients with , where excess tissue may obscure arterial impulses and complicate detection.

Associated Signs

Several peripheral signs often accompany the collapsing pulse, particularly in the context of severe , reflecting the underlying and wide . Corrigan's sign manifests as a visible, forceful pulsation in the followed by rapid collapse, resembling the jerk of a water hammer. Quincke's sign involves observable capillary pulsations in the nail beds, elicited by gentle pressure on the nail tip, resulting in alternating blanching and flushing synchronized with the heartbeat. De Musset's sign appears as a subtle bobbing motion of the head with each , due to exaggerated arterial pulsations transmitted to the vessels. Hill's sign is characterized by an exaggerated systolic gradient between the upper and lower extremities, typically with popliteal pressure exceeding brachial pressure by more than 20 mmHg, and greater differences indicating more severe disease. Duroziez's sign consists of a to-and-fro murmur over the : a systolic component distal to compression and a diastolic component proximal, heard when light pressure is applied with a . Traube's sign refers to sharp, pistol-shot sounds auscultated over the during and , attributable to rapid arterial distension and collapse. These signs frequently cluster together in severe , aiding in syndromic diagnosis of the hyperdynamic state, whereas they are uncommon in mild cases.

Historical Aspects

Eponym Origin

The collapsing pulse, also known as Corrigan's pulse, is eponymously named after Sir Dominic John Corrigan (1802–1880), an influential Irish physician and medical reformer. In 1832, Corrigan first described the sign as "visible and extensive pulsations of the arterial trunks of the head, neck, and superior extremities" in patients with aortic valve insufficiency. This description appeared in Corrigan's seminal paper, "On Permanent Patency of the Mouth of the , or Inadequacy of the Aortic Valves," published in the Edinburgh Medical and Surgical Journal (volume 37, pages 225–245). The work highlighted the in the context of aortic diseases, including cases linked to , a prevalent cause of valvular in the . Initially termed "Corrigan's ," the sign's evolved in the mid-19th century to "collapsing " to emphasize its rapid upstroke and diastolic collapse. It also became known as the "water hammer ," an drawn by Sir Watson in 1844 to the forceful expulsion and sharp sound of air or water from Victorian hydraulic hammers. In contemporary , the eponym "" persists in textbooks and clinical literature as a classic sign of . The World Health Organization's classification lacks a dedicated code for the but associates it with related valvular conditions, such as nonrheumatic aortic insufficiency (I35.1).

Historical Descriptions

Early descriptions of the collapsing can be traced to ancient medical texts, where physicians noted variations in character associated with febrile illnesses. (129–c. 200 CE), a prominent Greco-Roman physician, extensively documented qualities in his treatises, including descriptions of a "full" or bounding observed during fevers, which he attributed to imbalances in bodily humors such as excess blood or heat. These observations laid foundational groundwork for later diagnostics, though they lacked specific linkage to valvular . In the , more precise accounts emerged connecting bounding or collapsing pulses to aortic conditions. French physician Raymond Vieussens (1641–1716) provided one of the earliest detailed reports in 1715, describing a forceful, rapidly collapsing radial in a with suspected aortic , which he corroborated through findings of an enlarged left ventricle and aortic abnormalities. Vieussens' work highlighted the pulse's rapid upstroke and descent, distinguishing it from other arterial waveforms, though the full hemodynamic implications remained unexplored at the time. The marked a pivotal era for understanding the collapsing pulse, particularly through Irish physician Dominic Corrigan's 1832 publication, where he systematically linked the sign to incompetence via post-mortem examinations of affected patients. Corrigan's observations emphasized the pulse's exaggerated visible pulsations in the neck and extremities, correlating them with valvular defects that allowed retrograde blood flow. This period's clinical context was dominated by infectious etiologies; , through aortitis leading to root dilation, and , causing valvular inflammation, were prevalent causes of in , contributing to the sign's relative commonality among patients. Advancements in the early enabled quantitative assessment of the collapsing pulse. The widespread adoption of sphygmomanometry, refined by Nikolai Korotkoff's auscultatory method in 1905 and gaining clinical prominence by the 1920s, allowed measurement of elevated pulse pressures—often exceeding 60 mmHg in severe cases—providing objective confirmation of the wide systolic-diastolic disparity underlying the sign. Post-World War II developments in , pioneered by Inge and Carl Hellmuth Hertz in 1953, further transformed recognition by visualizing incompetence and regurgitant flow directly, diminishing reliance on physical pulse examination for . In contemporary , the collapsing pulse has become less frequently observed due to effective interventions against its primary historical causes. Antibiotic treatments for since the mid-20th century, along with rheumatic fever prophylaxis using penicillin from the , have drastically reduced infectious valvular damage. Additionally, surgeries, first successfully performed in 1960 by Dwight Harken using caged-ball prostheses, have offered curative options for severe regurgitation, further contributing to the sign's rarity in clinical practice today.

References

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  21. https://emedicine.medscape.com/article/150490-clinical
  22. https://www.healio.com/cardiology/learn-the-heart/cardiology-review/topic-reviews/duroziezs-sign
  23. https://pubmed.ncbi.nlm.nih.gov/7013091/
  24. https://www.healio.com/cardiology/learn-the-heart/cardiology-review/topic-reviews/traube-sign
  25. https://litfl.com/aortic-regurgitation-eponymythology/
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  28. https://www.icd10data.com/ICD10CM/Codes/I00-I99/I30-I5A/I35-/I35.1
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