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Pulse pressure
Pulse pressure variation (PPV) in different arteries and veins

Pulse pressure is the difference between systolic and diastolic blood pressure.[1] It is measured in millimeters of mercury (mmHg). It represents the force that the heart generates each time it contracts. Healthy pulse pressure is around 40 mmHg.[1][2] A pulse pressure that is consistently 60 mmHg or greater is likely to be associated with disease, and a pulse pressure of 50 mmHg or more increases the risk of cardiovascular disease.[1][3] Pulse pressure is considered low if it is less than 25% of the systolic. (For example, if the systolic pressure is 120 mmHg, then the pulse pressure would be considered low if it were less than 30 mmHg, since 30 is 25% of 120.)[2] A very low pulse pressure can be a symptom of disorders such as congestive heart failure.[3]

Calculation

[edit]

Pulse pressure is calculated as the difference between the systolic blood pressure and the diastolic blood pressure.[3][4]

The systemic pulse pressure is approximately proportional to stroke volume, or the amount of blood ejected from the left ventricle during systole (pump action) and inversely proportional to the compliance (similar to elasticity) of the aorta.[5]

e.g. normal 120 mmHg – 80 mmHg = 40 mmHg[3]
low: 100 mmHg − 80 mmHg = 20 mmHg
high: 160 mmHg − 80 mmHg = 80 mmHg
  • Pulmonary pulse pressure is normally much lower than systemic blood pressure due to the higher compliance of the pulmonary system compared to the arterial circulation.[6] It is measured by right heart catheterization or may be estimated by transthoracic echocardiography. Normal pulmonary artery pressure is 8 mmHg–20 mmHg at rest.[7]
e.g. normal 15mmHg – 8mmHg = 7mmHg
high 25mmHg – 10mmHg = 15mmHg

Values and variation

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Low (narrow) pulse pressure

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A pulse pressure is considered abnormally low if it is less than 25% of the systolic value.[2] If the pulse pressure is extremely low, i.e. 25 mmHg or less, it may indicate low stroke volume, as in congestive heart failure.[3]

The most common cause of a low (narrow) pulse pressure is a drop in left ventricular stroke volume. In trauma, a low or narrow pulse pressure suggests significant blood loss.[8]

A narrow pulse pressure is also caused by aortic stenosis.[3] This is due to the decreased stroke volume in aortic stenosis.[9] Other conditions that can cause a narrow pulse pressure include blood loss (due to decreased blood volume), and cardiac tamponade (due to decreased filling time). In the majority of these conditions, systolic pressure decreases, while diastolic pressure remains normal, leading to a narrow pulse pressure.[9]

In the Postural Orthostatic Tachycardia Syndrome it is postulated that declining venous return reduces stroke volume and frequently results in low pulse pressure. In extreme cases, patients experience a drop in pulse pressure to 0 mm Hg upon standing, rendering them practically pulseless while upright. This condition leads to significant morbidity, as many affected individuals struggle to remain standing.[10]

High (wide) pulse pressure

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Consistently high

[edit]

A pulse pressure of 50 mmHg or more can increase the risk of heart disease, heart rhythm disorders, stroke and other cardiovascular diseases and events. Higher pulse pressures are also thought to play a role in eye and kidney damage from diseases such as diabetes.[3] There are currently no drugs approved to lower pulse pressure, but some antihypertensive drugs have been shown to modestly lower pulse pressure, while other drugs used for hypertension can actually have the counterproductive side effect of increasing resting pulse pressure.[11]

The aorta has the highest compliance in the arterial system due in part to a relatively greater proportion of elastin fibers versus smooth muscle and collagen. This serves to dampen the pulsatile ejection fraction of the left ventricle, thereby reducing the initial systolic pulse pressure, but slightly raising the subsequent diastolic phase. If the aorta becomes rigid, stiff and inextensible because of disorders, such as arteriosclerosis, atherosclerosis or elastin defects (in connective tissue diseases), the pulse pressure would be higher due to less compliance of the aorta.[12]

In hypertensive patients, a high pulse pressure can often be an indicator of conduit artery stiffness (stiffness of the major arteries).[13] When the arterial walls are stiffer (less compliant), the heart has to beat harder to overcome the resistance from the stiff arteries, resulting in an increased pulse pressure.[14]

Other conditions that can lead to a high pulse pressure include aortic regurgitation,[15] aortic sclerosis, severe iron-deficiency anemia (due to decreased blood viscosity), arteriosclerosis (due to loss of arterial compliance), and hyperthyroidism[15] (due to increased systolic pressure), or arteriovenous malformation, among others.[9] In aortic regurgitation, the aortic valve insufficiency results in the backward flow of blood (regurgitation) that is ejected during systole, and its return to the left ventricle during diastole. This increases the systolic blood pressure, and decreases the diastolic blood pressure, leading to a widened pulse pressure.[9][3]

A high pulse pressure combined with bradycardia and an irregular breathing pattern is associated with increased intracranial pressure, a condition called Cushing's triad seen in people after head trauma with increased intracranial pressure.[16]

Common causes of widening pulse pressure include:[3]

From exercise

[edit]

For most individuals, during aerobic exercise, the systolic pressure progressively increases while the diastolic pressure remains about the same, thereby widening the pulse pressure. These pressure changes facilitate an increase in stroke volume and cardiac output at a lower mean arterial pressure, enabling greater aerobic capacity and physical performance. The diastolic drop reflects a reduced systemic vascular resistance of the muscle arterioles in response to the exercise.[18]

Clinical significance

[edit]

Pulse pressure has implications for both cardiovascular disease as well as many non-cardiovascular diseases. Even in people without other risk factors for cardiovascular disease, a consistently wide pulse pressure remains a significant independent predictor of all-cause, cardiovascular, and, in particular, coronary mortality.[19] There is a positive correlation between high pulse pressure and markers of inflammation, such as c-reactive protein.[20]

Cardiovascular disease and pulse pressure

[edit]

Awareness of the effects of pulse pressure on morbidity and mortality is lacking relative to the awareness of the effects of elevated systolic and diastolic blood pressure. However, pulse pressure has consistently been found to be a stronger independent predictor of cardiovascular events, especially in older populations, than has systolic, diastolic, or mean arterial pressure.[3][13] This increased risk has been observed in both men and women and even when no other cardiovascular risk factors are present. The increased risk also exists even in cases in which high pulse pressure is caused by diastolic pressure decreasing over time while systolic remains steady or even slightly decreases.[21][19]

A meta-analysis in 2000 showed that a 10 mmHg increase in pulse pressure was associated with a 20% increased risk of cardiovascular mortality, and a 13% increase in risk for all coronary end points. The study authors also noted that, while risks of cardiovascular end points do increase with higher systolic pressures, at any given systolic blood pressure the risk of major cardiovascular end points increases, rather than decreases, with lower diastolic levels.[22] This suggests that interventions that lower diastolic pressure without also lowering systolic pressure (and thus lowering pulse pressure) could actually be counterproductive.[9]

People who simultaneously have a resting diastolic pressure of less than 60 mmHg and a pulse pressure of greater than 60 mmHg have double the risk of subclinical myocardial ischaemia and a risk of stroke that is 5.85 times greater than normal.[23] For such patients, it may be dangerous to target a peripheral systolic pressure below 120 mmHg due to the fact that this could cause the diastolic blood pressure in the cerebral cortex in the brain to become so low that perfusion (blood flow) is insufficient, leading to white matter lesions. Nearly all coronary perfusion and more than half of cerebral perfusion occurs during diastole, thus a diastolic pressure that is too low can cause harm to both the heart and the brain.[24]

Increased pulse pressure is also a risk factor for the development of atrial fibrillation.[25]

Effects of medications on pulse pressure

[edit]

There are no drugs currently approved to lower pulse pressure. Although some anti-hypertensive drugs currently on the market may have the effect of modestly lowering pulse pressure, others may actually have the counterproductive effect of increasing pulse pressure. Among classes of drugs currently on the market, a 2020 review stated that thiazide diuretics and long‐acting nitrates are the two most effective at lowering pulse pressure.[15]

It has been hypothesized that vasopeptidase inhibitors and nitric oxide donors may be useful at lowering pulse pressure in patients with elevated pulse pressure by increasing the distensibility of the large arteries.[22][13] There is evidence that glyceryl trinitrate, a nitric oxide donor, may be effective at lowering both pulse pressure and overall blood pressure in patients with acute and sub-acute stroke.[26]

A 2001 randomized, placebo-controlled trial of 1,292 males, compared the effects of hydrochlorothiazide (a thiazide diuretic), atenolol (a beta-blocker), captopril (an ACE inhibitor), clonidine (a central α2-agonist), diltiazem (a calcium channel blocker), and prazosin (an α1-blocker) on pulse pressure and found that, after one year of treatment, hydrochlorothiazide was the most effective at lowering pulse pressure, with an average decrease of 8.6 mmHg. Captopril and atenolol were equal as least effective, with an average decrease of 4.1 mmHg. Clonidine (decrease of 6.3 mmHg), diltiazem (decrease of 5.5 mmHg), and prazosin (decrease of 5.0 mmHg) were intermediate.[11]

Pulse pressure and sepsis

[edit]

Diastolic blood pressure falls during the early stages of sepsis, causing a widening of pulse pressure. If sepsis becomes severe and hemodynamic compromise advances, the systolic pressure also decreases, causing a narrowing of pulse pressure.[27] A pulse pressure of over 70 mmHg in patients with sepsis is correlated with an increased chance of survival. A widened pulse pressure is also correlated with an increased chance that someone with sepsis will benefit from and respond to IV fluids.[28]

See also

[edit]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Pulse pressure

View on Grokipedia
from Grokipedia
Pulse pressure is the difference between systolic blood pressure and diastolic blood pressure, typically around 40 mm Hg in healthy adults, such as in a reading of 120/80 mm Hg. It arises from the physiological interaction between the heart's —the amount of blood ejected per beat—and the compliance of the arterial system, which refers to the arteries' ability to expand and recoil to accommodate blood flow. This relationship can be approximated by the formula pulse pressure ≈ / arterial compliance, where reduced compliance (stiffer arteries) or increased widens the pressure. Factors like aging, , , , and high cholesterol decrease arterial compliance, thereby elevating pulse pressure, while wave reflections from peripheral arteries can further augment systolic pressure and widen it. Clinically, pulse pressure serves as an important indicator of cardiovascular , with a widened value greater than 60 mm Hg signaling and independently predicting risks for heart disease, , heart attack, and overall mortality—an increase of 10 mm Hg is associated with about a 20% higher cardiovascular risk. Conversely, a narrowed pulse pressure, defined as less than 25% of systolic pressure (e.g., below 25 mm Hg in severe cases), often reflects conditions like , significant blood loss, or , indicating reduced . In specific populations, such as those with or with preserved , elevated pulse pressure correlates with adverse outcomes like hospitalization for and is influenced by factors including and left . Monitoring pulse pressure can guide interventions, such as lifestyle modifications or medications like ACE inhibitors that improve arterial compliance, potentially reducing cardiovascular events.

Fundamentals

Definition

Pulse pressure is defined as the difference between systolic , which represents the peak arterial pressure occurring during cardiac contraction (), and diastolic , the minimum arterial pressure during cardiac relaxation (). This difference quantifies the pulsatile nature of arterial blood flow, distinguishing it from the steady-state component of circulation. Physiologically, pulse pressure reflects the interaction between the volume of blood ejected by the left ventricle () and the compliance of the arterial system, which determines how much the arteries can expand and recoil to accommodate the ejected . It embodies the pulsatile component of flow, driven by ventricular ejection and modulated by arterial elasticity, which helps maintain continuous to organs despite intermittent . Reduced arterial compliance, often due to aging or , amplifies this pulsatile stress on the vascular wall. The concept of pulse pressure emerged in the late with the invention of the by Scipione Riva-Rocci in 1896, which first allowed accurate measurement of systolic and diastolic pressures, enabling clinicians like Thomas Lewis to explore arterial waveforms in the early . It is expressed in millimeters of mercury (mmHg), with a typical value around 40 mmHg in healthy adults. Pulse pressure serves as a complementary hemodynamic parameter to (MAP), which averages pressure over the to indicate overall perfusion adequacy.

Calculation and Measurement

Pulse pressure is calculated by subtracting the diastolic blood pressure (DBP) from the systolic (SBP), expressed as: PP=SBP−DBP\text{PP} = \text{SBP} - \text{DBP} where values are typically measured in millimeters of mercury (mmHg). To derive pulse pressure, SBP and DBP are first obtained through established techniques. In non-invasive methods, the auscultatory approach uses a with a : the is inflated above the expected SBP to occlude arterial flow, then gradually deflated while listening for —the first sound marks SBP, and the disappearance of sounds indicates DBP. The oscillometric method, common in automated devices, detects oscillations in pressure during deflation; algorithms estimate SBP and DBP from the peak oscillation amplitude and surrounding patterns, respectively. Invasive measurement involves arterial catheterization, where a connected to an intra-arterial directly records the arterial ; SBP is the peak pressure, and DBP is the trough, allowing precise pulse pressure computation from continuous tracings. This method is reserved for critical care settings due to its invasiveness but offers higher fidelity than non-invasive techniques. Accuracy in obtaining SBP and DBP—and thus pulse pressure—depends on factors such as appropriate size and positioning. The bladder width should be at least 40% of the circumference (measured midway between the and ) to avoid overestimation of SBP by up to 20 mmHg with undersized cuffs or underestimation with oversized ones. The 's must be supported at heart level, as unsupported positioning can elevate readings by 10-40 mmHg. For example, in a patient with an SBP of 120 mmHg and DBP of 80 mmHg measured via , the pulse pressure is 40 mmHg. Limitations include errors from irregular heart rhythms, such as , which can cause oscillometric devices to underestimate SBP or overestimate DBP due to variable pulse amplitudes, reducing reliability in up to 20-30% of readings; or invasive methods are preferred in these cases. Improper technique, like rapid cuff deflation (>2-3 mmHg/second), may also lead to inaccurate Korotkoff sound detection.

Physiological Variations

Normal Values

In healthy adults, pulse pressure typically ranges from 40 to 60 mmHg, with a mean value around 43 mmHg. This value is derived from the difference between systolic and diastolic readings. Slight variations exist by and ; pulse pressure tends to be higher in males than in females in younger age groups but higher in females after age 50, and higher in non-Hispanic Black individuals than in in U.S. populations. Age-related norms show pulse pressure increasing from approximately 40 mmHg in young adults to over 50 mmHg in the elderly, primarily due to progressive arterial stiffening that reduces vascular compliance. Large-scale studies, such as the , have documented these average trends, revealing a steady rise in pulse pressure across age groups in community-based cohorts. There is no single universally defined "ideal" pulse pressure specifically for a 50-year-old woman, as guidelines focus primarily on overall blood pressure rather than pulse pressure alone. In a study of healthy adults, women aged 50-59 had a mean pulse pressure of 45 mmHg, with an optimal range of approximately 35-55 mmHg (mean ±1 SD) associated with favorable cardiovascular health metrics. Daily fluctuations are minor, influenced by the , with pulse pressure generally higher in the morning upon waking and lower during nighttime rest. A pulse pressure below 40 mmHg or above 60 mmHg in healthy individuals warrants further clinical evaluation to assess underlying physiological factors.

Narrow Pulse Pressure

Narrow pulse pressure, typically less than 25 mmHg or below 25% of systolic , physiologically arises from reduced , such as in conditions with low , including or , where the heart ejects less blood per beat.

Wide Pulse Pressure

Wide pulse pressure, often exceeding 60 mmHg, results physiologically from increased stroke volume (e.g., in hyperdynamic states like exercise or anemia) or decreased arterial compliance due to stiffening from aging, atherosclerosis, or other vascular changes, leading to greater pressure transmission from the heart to the periphery.

Clinical Relevance

Cardiovascular Disease Associations

Wide pulse pressure (PP) serves as an independent predictor of adverse cardiovascular outcomes, often providing stronger prognostic value than systolic blood pressure (SBP) alone in certain populations, particularly older adults and those with diabetes. Meta-analyses of cohort studies have shown that elevated PP is associated with heightened risks of myocardial infarction, stroke, and heart failure, with hazard ratios indicating a 15-25% increase in events per 10 mmHg elevation after adjusting for traditional risk factors. For instance, in a pooled analysis of 65,382 patients with atherosclerotic cardiovascular disease from five cardiovascular outcome trials, each 10 mmHg increase in PP was associated with an 11% higher risk of death, myocardial infarction, or stroke (HR 1.11, 95% CI 1.08-1.14). This predictive superiority stems from PP's reflection of arterial stiffness, which captures cumulative vascular aging beyond isolated SBP measurements. The pathophysiological mechanisms linking wide PP to cardiovascular disease involve excessive pulsatile stress on the vascular system, leading to endothelial dysfunction, left ventricular hypertrophy (LVH), and end-organ damage. Increased PP amplifies shear stress and pressure waves transmitted to distal arterioles, impairing endothelial production and promoting and . This contributes to LVH by imposing a chronic volume and pressure overload on the left ventricle, as evidenced in echocardiographic studies where PP >60 mmHg was independently associated with concentric remodeling and diastolic dysfunction. Furthermore, sustained wide PP accelerates end-organ damage, including renal microvascular injury and cerebral small vessel disease, through microvascular and , with longitudinal data showing a dose-dependent relationship to and white matter hyperintensities. In specific conditions like isolated systolic hypertension (ISH), wide PP exceeding 60 mmHg is a hallmark feature and amplifies cardiovascular risk. ISH, characterized by SBP ≥140 mmHg and DBP <90 mmHg, reflects reduced arterial compliance and is linked to a 2-3-fold increase in stroke and heart failure incidence compared to normotension, with PP serving as a key mediator. Similarly, in coronary artery disease (CAD), PP holds prognostic significance; longitudinal studies of post-revascularization patients demonstrate that baseline PP >65 mmHg predicts recurrent ischemia and all-cause mortality (HR 1.32 per 10 mmHg increment), independent of severity or profiles. Evidence from large-scale longitudinal cohorts underscores these associations, including the Risk in Communities (ARIC) study, which reported increased cardiovascular mortality associated with higher pulse pressure. Wide PP also extends to (PAD), where it correlates with accelerated and limb complications.

Role in Sepsis and Shock

In , pulse pressure often widens, typically exceeding 50 mmHg, as a result of profound and a marked reduction in systemic driven by the systemic inflammatory response. This hemodynamic profile characterizes , where high fails to compensate for the drop in diastolic pressure, serving as an early indicator of . Clinicians recognize this widening as a key feature distinguishing from other forms, with low diastolic pressures and warm extremities reflecting the . In contrast, pulse pressure narrows in hypovolemic and cardiogenic shocks due to reduced from volume depletion or impaired cardiac contractility, respectively, leading to a proportional decrease in both systolic and diastolic pressures. Monitoring trends in pulse pressure helps differentiate these states and guide therapy, particularly in assessing fluid responsiveness during . For instance, a narrow pulse pressure in these shock types signals the need for volume expansion, unlike the wide pulse pressure in where vasopressors may be prioritized alongside fluids. Pulse pressure variation (PPV), the cyclic change in pulse pressure during , serves as a dynamic for predicting response to volume resuscitation in critically ill patients with shock. A PPV threshold greater than 13% indicates likely fluid responsiveness, helping avoid unnecessary fluid administration that could exacerbate in . The Surviving Sepsis Campaign guidelines recommend incorporating PPV, alongside other dynamic measures, for fluid management in settings when invasive monitoring is available.

Effects of Medications and Interventions

Various pharmacological agents influence pulse pressure (PP) through differential effects on systolic blood pressure (SBP) and diastolic blood pressure (DBP). Vasodilators, such as ACE inhibitors and , typically widen PP by preferentially lowering DBP more than SBP, thereby reducing peripheral resistance while maintaining or slightly reducing . For instance, administration in normotensive models markedly increased PP due to a less pronounced reduction in central aortic SBP compared to DBP, with PP elevation linked to altered aortic elasticity and wave reflection dynamics. Similarly, ACE inhibitors like exhibit modest PP widening during chronic use, as they reduce DBP to a greater extent than SBP in hypertensive patients, though less effectively than diuretics. In contrast, beta-blockers narrow PP primarily by decreasing SBP through reductions in and , with minimal impact on DBP. Atenolol, a selective beta-blocker, reduced PP by 4.1 mm Hg after one year of treatment in a randomized trial of hypertensive men, reflecting its negative inotropic and effects that limit . This narrowing is more pronounced in vasodilating beta-blockers like , which combine beta-blockade with nitric oxide-mediated to further attenuate central SBP amplification. Angiotensin receptor blockers (ARBs) effectively reduce wide PP in isolated systolic hypertension (ISH) over time by blocking angiotensin II-mediated , leading to balanced reductions in SBP and DBP. A of 46 randomized controlled trials involving 13,451 participants showed ARBs at maximum doses reduced PP by 3.4 mm Hg compared to , with eprosartan specifically lowering PP from 68 mm Hg to 59 mm Hg in ISH patients after 12 weeks. This effect is attributed to improved arterial compliance and reduced wave reflections, making ARBs a preferred option for elderly patients with ISH. Statins modestly narrow PP through plaque stabilization and improvements in endothelial function, independent of lipid-lowering effects. In a cross-sectional analysis of 16,507 individuals from the CARTaGENE cohort, statin use in primary prevention was associated with a 1.3 mm Hg reduction in central PP, mediated partly by lower cholesterol levels and enhanced vascular compliance. Recent evidence supports this via mechanisms like reduced and arterial remodeling, though a specific 2024 on plaque stabilization highlights consistent but small PP benefits in high-risk cohorts. Sodium-glucose cotransporter 2 (SGLT2) inhibitors, such as empagliflozin, reduce PP in patients by lowering central SBP and improving vascular stiffness. In a sub-analysis of a randomized trial in patients (many with heart failure comorbidities), empagliflozin decreased central PP by 2.8 mm Hg over 12 weeks, correlated with reductions in ambulatory SBP and inflammatory markers like hsCRP. This effect stems from natriuresis-induced volume reduction and direct vascular benefits, contributing to decreased cardiac . Procedural interventions like surgical (SAVR) normalize PP in by restoring and alleviating outflow obstruction. Preoperatively, severe often presents with narrowed PP due to diminished ; post-SAVR, PP widens toward normal values (typically 40-60 mm Hg) as left ventricular ejection improves, with studies showing acute increases in amplitude and normalization within months. Changes in PP serve as a surrogate marker for treatment efficacy in trials, reflecting improvements in and cardiovascular risk beyond . In the Veterans Affairs Single-Drug Therapy trial, PP reductions varied by agent class, with greater decreases (e.g., 8.6 mm Hg for hydrochlorothiazide) predicting better long-term vascular outcomes and serving as an endpoint in assessing drug-specific hemodynamic benefits. Similarly, the LIFE study used baseline and on-treatment PP to evaluate prognostic value, confirming its role in monitoring therapeutic responses in ISH cohorts.

References

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