Blood pressure (BP) has most commonly been measured manually using aneroid or mercury sphygmomanometers although electronic oscillometric BP measurement is increasingly used in many office settings [
One particular error in manual BP measurement, the failure to detect the presence of an auscultatory gap, results in a falsely low estimate of systolic BP [
The mechanism for an auscultatory gap is uncertain but may in part relate to increased stiffness of the arterial wall [
We designed a study to determine the prevalence and clinical correlates of auscultatory gaps in patients with SSc seen at the University of Utah SSc center.
The study was accepted by the Institutional Review Board at the University of Utah (IRB number 00038705). Inclusion criteria included adult patients (≥18 years) with a diagnosis of SSc as accepted by the American College of Rheumatology [
First, the same clinic medical assistant performed a single manual auscultatory measurement using a calibrated aneroid manometer and a high-quality Littmann, Cardiology III stethoscope with short tubing. Without palpating the radial artery, the cuff was inflated to 160–180 mmHg and then deflated at a rate of 2-3 mmHg/second. The systolic BP was noted as the first of two discrete, tapping Korotkoff sounds and the diastolic BP as the disappearance of the Korotkoff sounds.
After a period of five minutes, the BP measurement was repeated by the medical assistant using the Omron HEM-907 device, a validated electronic oscillometric device, which automatically performs three sequential BP measurements at one-minute intervals and averages them. Following another five-minute interval, a single manual BP measurement was performed by the author (T.M. Frech) using the same aneroid manometer and stethoscope as the medical assistant; TF was blinded to the results of the two prior BP measurement approaches. TF palpated the radial artery, inflated the cuff 30 mmHg beyond the disappearance of the radial pulse, and then deflated the cuff at a rate of 2 mmHg/second. The systolic BP was again noted as the first of two discrete, tapping Korotkoff sounds. The presence and magnitude of any auscultatory gap were noted and recorded.
In order to assess for interobserver agreement, another author (J. Penord) assessed ten of the SSc patients. JP was blinded to the results of TF. TF and JP also assessed twelve consecutive patients presenting to the Internal Medicine clinic to assess a comparison of auscultatory gap prevalence.
The presence of the following clinical risk factors for vascular stiffness for SSc patients was noted: age, BMI, presence of proteinuria (trace or greater on urine dipstick), estimated glomerular filtration rate (MDRD formula), tobacco use, and diabetes mellitus. Additionally, risk factors for SRC and evidence of organ damage were documented, including the presence of RNA polymerase III antibodies, prednisone use, pulmonary arterial hypertension (PAH), and interstitial lung disease (ILD). Medications that can affect BP, including current use of nonsteroidal antiinflammatory drugs (NSAIDs), anti-hypertensive agents, and immunosuppressive medications were also recorded.
Nonparametric analysis using the Kruskal-Wallis test was used to look for statistical relationships between categorical data such as the presence of an auscultatory gap and possible arterial stiffness variables: age, diabetes mellitus, tobacco use, and BP medication use. Additionally, potential markers for more severe SSc vasculopathy-immunosuppressant use, nonsteroidal anti-inflammatory (NSAID) use, RNA polymerase III antibody, pulmonary arterial hypertension (PAH), and interstitial lung disease (ILD), were examined for a statistical relationship with the presence of an auscultatory gap. Correction using the Bonferroni method was used to adjust the
Analyses of variance (ANOVA) were used to examine the relationship of modified Rodnan skin score (mRSS) as a continuous variable with the same arterial stiffness variables. These analyses were performed using R [
Intraobserver agreement was used to calculate the number of patients needed for assessment of prevalence in the Internal Medicine Clinic and SSc clinic.
In our SSc study population, 92% of subjects were female, 87% were white, and 13% were Hispanic. The age range was 27 to 80 years. The mRSS ranged from 4 to 28, with 85% of patients being in the limited cutaneous SSc subset. There was evidence of end-organ damage due to SSc (PAH and/or ILD) in 65% of patients. In this study 89% of patients were taking one or more antihypertensive agents, most commonly a calcium channel blocker used to treat their Raynaud’s phenomenon. An auscultatory gap was heard in 16 patients for a prevalence of 32% in this study population. The mean auscultatory gap in these 16 patients was 6.1 mmHg and ranged from 4 mmHg to 12 mmHg. In two patients the recognition of this gap reclassified them into the hypertensive range (SBP ≥ 140 mmHg). One of these two patients subsequently required hospitalization for scleroderma renal crisis. In two other patients, the auscultatory gap reclassified the patients into the upper portion of the prehypertensive range (systolic BP of 130–139 mmHg). Thus, four patients would have required medication adjustment based on the more accurate recognition of their true BP.
As presented in Table
Auscultatory gap association with possible arterial stiffness and vasculopathy variables in SSc.
Arterial stiffness variable | Kruskal-Wallis chi-squared | |
---|---|---|
Diagnosis type | 8.37 | 0.01* |
Age | 26.43 | 0.43 |
Tobacco use | 0.12 | 0.73 |
Diabetes mellitus | 0.06 | 0.81 |
BP medication | 16.32 | 0.43 |
NSAID use | 0.06 | 0.81 |
Immunosuppression | 3.00 | 0.56 |
RNA polymerase III | 7.31 | 0.01* |
PAH | 3.43 | 0.33 |
ILD | 4.29 | 0.12 |
SSc: systemic sclerosis; BP: blood pressure; NSAID: nonsteroidal anti-inflammatory use; PAH: pulmonary arterial hypertension; ILD: interstitial lung disease;
When ANOVA was used to evaluate the relationship of arterial stiffness variables to skin thickness (mRSS), we found age (
When the presence of an auscultatory gap was assessed in 10 of the SSc patients by a second physician, the inter-observer agreement was 0.8. The gap was 4–6 mmHg in the patients in which there was discordance between investigators. Additionally, when the presence of an auscultatory gap was assessed in twelve internal medicine patients, it was found 10–25% of the time. The clinical correlates of auscultatory gap in the Internal Medicine patients were not recorded and are a limitation of this study. The interobserver agreement was 0.83. The gap was 4 mmHg in the patients in which there was discordance between investigators.
We measured systolic BP by palpation of the radial pulse and then by auscultation at the brachial artery and detected an auscultatory gap in 16 out of 50 consecutively examined SSc patients (32%) in our clinic. In four of the sixteen patients, the magnitude of the auscultatory gap would have resulted in a clinically important underestimate of systolic BP had it remained undetected. Detection of the auscultatory gap reclassified two patients as hypertensive with systolic BPs of 144 mmHg and 148 mmHg, and two other patients were reclassified into the upper portion of the prehypertensive range with systolic BPs of 132 mmHg and 136 mmHg (Table
Manual blood pressure in SSc patients with auscultatory gap.
Patient | Manual BP without radial pulse occlusion (MA) | Manual BP after pause (TF) | Manual BP with radial pulse palpation (TF) | Auscultatory Gap |
---|---|---|---|---|
1 | 120/62 | 118/68 | 126/62 | 8 |
2 | 130/68 | 132/72 | 144/74 | 12** |
3 | 110/60 | 112/60 | 118/62 | 6 |
4 | 104/64 | 102/68 | 110/70 | 8 |
5 | 136/64 | 138/60 | 148/62 | 10** |
6 | 114/60 | 110/54 | 116/62 | 6 |
7 | 128/80 | 128/78 | 136/76 | 8* |
8 | 126/68 | 122/68 | 132/70 | 10* |
9 | 110/70 | 104/70 | 112/64 | 8 |
10 | 110/60 | 108/64 | 114/72 | 6 |
SSc: systemic sclerosis; BP; blood pressure; MA: medical assistant; TF: Tracy Frech; *change to prehypertensive; **change to hypertensive.
The presence of an auscultatory gap in our SSc patients was statistically associated with the presence of RNA polymerase III antibody, a known marker for increased risk of SRC. It has previously been postulated that the auscultatory gap is a marker of increased vascular stiffness [
Skin thickening as measured by the mRSS was correlated to other possible factors that may contribute to arterial stiffness in this SSc population including age, ILD, presence of an RNA polymerase III antibody, and diagnosis type. This suggests that severity of vasculopathy and fibrosis may be a second important reason to detect an auscultatory gap in this patient population. Additionally, if an auscultatory gap is found, a more extensive look for internal organ disease may be warranted.
Our study has some limitations. It is a small study population, and some of the arterial stiffness and SSc vasculopathy variables studied did not have adequate power to exclude their association. For example, only three tobacco users and eight patients with diabetes mellitus were included in the study. Additionally, the use of BP medication at low doses for Raynaud’s phenomenon rather than for BP control challenges our use of BP medication as an arterial stiffness variable. Our study population is primarily Caucasian; thus our data may not be able to be generalized to other races and ethnicities.
Nonetheless, our study provides important information on measurement of BP in SSc. An auscultatory gap appears to be common occurring in up to 32% of SSc patients, and failure to detect it may result in clinically important underestimation of systolic BP and missed opportunities to intervene early in hypertensive patients. Future studies should validate whether the auscultatory gap in SSc patients can predict associated internal organ involvement.
The authors declare they have no conflict of Interests.