BEDSIDE MEDICINE
Year : 2015 | Volume
: 1 | Issue : 2 | Page : 128--129
Adolf Kussmaul and Kussmaul's sign
Navreet Singh1, Devinder Singh Chadha2, Prashant Bharadwaj3, Naveen Agarwal1,
1 Department of Cardiology, Command Hospital, Chandimandir, Panchkula, Haryana, India
2 Department of Cardiology, Military Hospital, Pune, Maharashtra, India
3 Department of Cardiology, Army Hospital, New Delhi, India
Correspondence Address:
Navreet Singh
Command Hospital, Chandimandir - 134 107, Panchkula, Haryana
India
Abstract
Kussmaul's has provided us with three important signs: Pulses paradoxus, Kussmaul's sign and Kussmaul Breathing. This article discusses Kussmaul's sign, its discovery, first description, pathophyiology and exceptions.
How to cite this article:
Singh N, Chadha DS, Bharadwaj P, Agarwal N. Adolf Kussmaul and Kussmaul's sign.J Pract Cardiovasc Sci 2015;1:128-129
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How to cite this URL:
Singh N, Chadha DS, Bharadwaj P, Agarwal N. Adolf Kussmaul and Kussmaul's sign. J Pract Cardiovasc Sci [serial online] 2015 [cited 2023 May 28 ];1:128-129
Available from: https://www.j-pcs.org/text.asp?2015/1/2/128/166317 |
Full Text
Definition
A paradoxical increase or loss of the normal physiological pattern of decreasing jugular venous pressure (JVP) with inspiration is commonly referred to as Kussmaul's sign.
Clinical Relevance
This clinical sign indicates the presence of significant pericardial constriction.[1]
History
Adolf Kussmaul was born on February 22, 1822, in Wurzburg, Germany [Figure 1]. The oldest of seven children, both his grandfather and father being physicians, he was exposed to medicine from a young age. He excelled in his studies at the University of Heidelberg and was appointed as a Professor of Medicine in 1845 at the young age of 23 years. He had diverse clinical interests and included almost all the aspects of medicine.{Figure 1}
In his 1873 paper, entitled “Ueber Schwielge Mediastinopericarditis und den Paradoxen Puls” (“Concerning Callous Mediastinopericarditis and the Paradoxical Pulse”), he described the phenomenon, originally discovered by Greisinger in 1854, in which “the jugular veins became considerably swollen and by each inspiration, a slight increase of its contents could be noted.”
He is also credited with the vivid description of abnormal labored breathing of diabetic ketoacidosis, commonly known as Kussmaul's breathing. Kussmaul died of coronary atherosclerosis at the age of 80 years on May 28, 1902.
Adolf Kussmaul's careful observations and clinical pathological correlations have provided us with a legacy of three important physical signs: Pulsus paradoxus, Kussmaul's sign, and Kussmaul breathing. All of these are still used in the diagnostic assessment of patients despite the expansion of technology to confirm the diagnoses of pericardial tamponade, constrictive pericarditis, and metabolic acidosis.[2],[3]
Physiology and Pathophysiology
The jugular venous pulse is observed with the patient in sitting or semi-reclining position. A beam of light is then shone obliquely at the right internal jugular vein between the two heads of the sternocleidomastoid muscle and the upper level is determined. The pre- and post-inspiratory rise of the upper level of the JVP is observed to ascertain the presence or absence of Kussmaul's sign.
In healthy individuals, pressure within the pleural, pericardial, and mediastinal cavity is nearly equal, due to the compliant of pleura and pericardium. In a disease-free state, inspiration creates negative intra-pleural (intra-thoracic) pressure, while the contraction of the diaphragm creates an increase in the intra-abdominal pressure. This pressure difference increases the rate of the venous return to the right side of the heart. The right atrium, right ventricle (RV) and the pulmonary vasculature being low pressure, and compliant chambers redistribute the increased return during inspiration without an appreciable rise in the right atrial pressure. In patients with constrictive pericarditis, on the other hand, the pericardium is noncompliant and result in the failed redistribution of increased systemic venous return. Consequently, the pressure in the right atrium rises much more than the fall in pleural pressure causing inspiratory distension of the neck veins.[4]
This paradoxical rise in the right atrial pressure is not unique to pericardial constriction but is seen in many pathologies with impaired right ventricular filling. These are observed in the following states:
Mechanical inelasticity and “encasing” by constrictive pericarditisPlasticity or hypoelasticity of the myocardium by fibrosis and infiltrative (restrictive) cardiomyopathyImpaired right ventricular filling and function due to the right-sided myocardial infarction, massive pulmonary embolism, right-sided heart failure, and tricuspid stenosis.
Failure of cardiac chambers to accommodate increased venous return, especially on the right side and elevated atrial pressure is the prerequisites for Kussmaul's sign to be demonstrable.
However, in left heart failure leading to congestive features, the physiological compliance is still maintained and thus the Kussmaul's sign is negative.
Why No Kussmaul Sign in Cardiac Tamponade?
The presence of Kussmaul's sign in patients with constrictive pericarditis and/or restrictive cardiomyopathy and not cardiac tamponade can be accounted for the physiological differences in filling patterns. In constrictive pericarditis or restrictive cardiomyopathy, the restriction to diastolic filling of the RV is prevented by the fixed, less compliant constricting pericardium or myocardium, respectively. That is, there is a loss of the effective “elastance” of the thin-walled RV at higher filling volumes. Furthermore, the inspiratory thoraco-abdominal pressure gradient is not transmitted to the cardiac chambers because of the inelastic pericardium. This results in the paradoxical increase in the JVP with inspiration. In cardiac tamponade, there is “coupled constraint” on both the left ventricle (LV) and RV because the increase in intra thoracic pressure is transmitted equally through the pericardium to both the ventricles compressing the entire heart during inspiration. Due to the greater ventricular interdependence, increased inspiratory filling of the RV results in a proportional reduction in filling of the LV causing pulsus paradoxus and not Kussmaul's sign.[5]
Thus, compared to the “coupled constraint” in cardiac tamponade, there is an “uncoupled restraint” in constrictive pericarditis wherein the restrain on the thin-walled right ventricular is more than the LV.
Cardiac conditions with positive Kussmaul's sign
Constrictive pericarditisRestrictive cardiomyopathyRight ventricular myocardial infarctionMassive pulmonary embolismSevere pulmonary hypertensionRight heart failureRight-sided cardiac tumorsSuperior vena caval obstruction.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References
| 1 | Meyer TE, Sareli P, Marcus RH, Pocock W, Berk MR, McGregor M. Mechanism underlying Kussmaul's sign in chronic constrictive pericarditis. Am J Cardiol 1989;64:1069-72. |
| 2 | Takata M, Beloucif S, Shimada M, Robotham JL. Superior and inferior vena caval flows during respiration: Pathogenesis of Kussmaul's sign. Am J Physiol 1992;262(3 Pt 2):H763-70. |
| 3 | Johnson SK, Naidu RK, Ostopowicz RC, Kumar DR, Bhupathi S, Mazza JJ, et al. Adolf Kussmaul: Distinguished clinician and medical pioneer. Clin Med Res 2009;7:107-12. |
| 4 | Bilchick KC, Wise RA. Paradoxical physical findings described by Kussmaul: Pulsus paradoxus and Kussmaul's sign. Lancet 2002;359:1940-2. |
| 5 | Mansoor AM, Karlapudi SP. Images in clinical medicine. Kussmaul's sign. N Engl J Med 2015;372:e3. |
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