Pulsus alternans is a cardiovascular phenomenon characterized by alternating strong and weak pulse pressures during a sinus rhythm. This alternation is evident predominantly in the arterial waveform because the amplitude of the systolic beat differs with every other beat. No changes are apparent on electrocardiograms or in diastolic filling time. (1,2)
Pulsus alternans may indicate severe ventricular failure? Pulsus alternans occurs in aortic and mitral valve stenosis, hypertrophic and congestive cardiomyopathy, effusive pericarditis, and instances in which general anesthesia is used. (1, 4-10) Its occurrence always warrants further evaluation to determine the cause.
The
mechanism of pulsus alternans is not entirely clear, but it has long been a subject of great interest. Pulsus alternans is attributed to an alteration in the stroke volume with every other cardiac cycle and is typically seen in patients with advanced myocardial disease. see
NEJM Pathophysiology of Pulsus Alternans
The theories about the cause of pulsus alternans can be narrowed down to 2 basic physiological actions. These physiological activities provide the basis for the clinical findings, such as the distinct pattern of the arterial waveform.
The first action is an alteration in end-diastolic pressure that affects the efficiency of the Frank-Starling mechanism. (12) The Frank-Starling mechanism accounts for the ability of the heart to increase its output in response to alterations in venous return. When an increased amount of blood enters the ventricle during diastole (ie, when preload increases), the heart is stretched to accommodate the increased volume. Filling of the ventricle is similar to the stretching of a rubber band. The farther the rubber band is stretched, the greater recoil it has. Similarly, the ventricle pumps with a greater force in response to an increased preload. (13)] Thus, an increase in end-diastolic pressure causes an increase in the force of the contraction. This mechanism prevents an increase in the venous pressure during an increase in circulating blood volume. The Frank-Starling mechanism does have its limitations. The ventricle eventually reaches a point at which an increase in preload no longer leads to an increase in contractility (Figure 3).
In a study of 5 children with myocardial disease who had pulsus alternans, Harris et al (12) found that 3 factors influenced the production of pulsus alternans in regard to left ventricular end-diastolic volume. (1) The diastolic interval preceding the small beats was shorter than the interval preceding the large beats, even when the R-R interval was kept constant by pacing the heart. (2) The left ventricular residual volume was larger after a small beat than after a large beat. This increased volume led to a larger end-diastolic volume preceding the large beat. And as Lee and Sutton (14) reported, a smaller end-diastolic volume preceded the small beat because of the increased emptying with the previous large beat. (3) The left ventricle did not recover after a large beat. The lack of recovery led to a decrease in diastolic compliance, thus inhibiting ventricular filling for the preceding small beat.
The second physiological action that may be the cause of pulsus alternans is the alteration in cellular handling of calcium. (15) Calcium acts directly on the cardiac muscle as a catalyst that leads to a contraction. As the action potential is conducted through the heart, it passes through the T tubules and enters the sarcoplasm. The entry into the sarcoplasm causes a release of calcium from the sarcoplasmic reticulum. Calcium also enters into the myofibrils by way of the T tubules. These tubules act as conduits that connect the myofibrils to the extracellular fluid. The calcium traveling into the myofibrils causes a contraction via the sliding of the actin and myosin filaments. At the end of the contraction, the calcium goes back into the sarcoplasmic reticulum and exits via the T tubules. (13)
Calsequestrin is a protein i n the inner membrane surface of the sarcoplasmic reticulum that binds and stores calcium. Schmidt et al (15) found that mice that overexpressed calsequestrin had pulsus alternans during high heart rates. Schmidt et al concluded that the mice had a delay between the uptake and release of calcium from the sarcoplasmic reticulum and that this alteration in calcium cycling and use led to pulsus alternans.
Clinical Features of Pulsus Alternans
Pulsus alternans can be detected via palpation of the artery, use of a sphygmomanometer, and examination of arterial and plethysmographic waveforms. (8, 12, 16) Pulsus alternans is difficult to assess by palpation when the difference between large and small systolic beats is less than 20 mm Hg. (12) The difference in the beats is best detected by palpating the femoral pulses rather than the brachial, radial, or carotid pulses.
For detection with a sphygmomanometer, the cuff is inflated to a pressure greater than peak systolic pressure. The cuff is then slowly deflated while the operator listens for the first audible systolic beats. At this point, only the strong pulses are heard. The cuff is then deflated until all of the systolic beats can be heard. Subtracting the pressure noted at the point when the first beats were heard from the pressure noted at the point where all the beats were heard can be used to quantify the severity of pulsus alternans. (16)
The tracings of I.B. reflect the ability to detect pulsus alternans with the plethysmographic waveform. Monitoring the plethysmographic waveform can be an alternative diagnostic tool if no indwelling arterial catheter is in place. The only other documented use of plethysmographic waveforms to detect pulsus alternans was published by Saghaei and Mortazavian. (8) Pulsus alternans was determined by examination of the plethysmographic waveform in patients undergoing surgery of the lower extremities. Saghaei and Mortazavian concluded that plethysmographic waveforms could be used to diagnose pulsus alternans, although the sensitivity and specificity of this method have not been determined.
Considerations
In most cases, pulsus alternans is an ominous sign that suggests severe cardiac failure. Critical care nurses must be aware of pulsus alternans and its implications. Patients with this abnormality require further assessment of cardiovascular function. Indications of heart failure may include increased adrenergic activity, congestive hepatomegaly, edema, ascites, pulmonary crackles, and fever.
During severe heart failure, sympathetic and renin-angiotensin activities increase as a compensatory mechanism in response to a decreased cardiac output. These increases lead to an initial increase in circulating catecholamines and an increase in angiotensin II, which is a potent vasoconstrictor. (11) The peripheral vasoconstriction leads to pallor, diaphoresis, and cyanosis of the nail beds. (16)
As heart failure progresses, venous engorgement occurs because of the heart's inability to eject a large blood volume. The liver often becomes engorged before overt edema develops. The edge of the liver may be palpable below the costal margin, and eliciting the hepatojugular reflux can be used to assess the amount of engorgement. This assessment can be performed by manually pressing in the right upper quadrant of the abdomen for 1 minute. The jugular veins will become engorged as the edematous liver is emptied. (16)
The venous engorgement associated with heart failure also can cause generalized edema, ascites, and pulmonary crackles. As the systemic venous pressure increases, extracellular fluid is transduced into the surrounding tissue, including the alveoli, leading to the edema and crackles. (16) Peripheral vasoconstriction may also lead to fever. The vasoconstriction causes an increase in temperature by decreasing the amount of surface area available for conductive loss of heat. (16)
Pulsus alternans can also occur m patients who are not in heart failure. Thus, it is not always an ominous sign. (17) Schaefer et al (18) found that pulsus alternans could be induced in patients undergoing cardiac catheterization. Atrial pacing techniques such as premature atrial contraction and rapid atrial pacing were used to induce pulsus alternans. All of the patients had cardiac disease that required cardiac catheterization, but they did not have pulsus alternans at rest.
Conclusion
Pulsus alternans may be a sign of severe ventricular failure. This cardiovascular phenomenon can be caused by alterations in both the Frank-Starling mechanism and intracellular calcium cycling. Pulsus alternans is manifested in various disease states, including mitral and aortic valve disease and hypertrophic and congestive cardiomyopathy. The patient described in the case study had pulsus alternans and congestive cardiomyopathy associated with a pheochromocytoma. Any patient with pulsus alternans should be assessed for signs and symptoms of severe ventricular failure. Such assessment may decrease the prevalence of undiagnosed heart failure.
References
(1.) Laskey WK, Sutton M, Untereker WJ, Martin JL, Hirshfeld JW Jr, Reichek N. Mechanisms of pulsus alternans in aortic valve stenosis. Am J Cardiol. 1983;52:809-812.
(2.) Brown RC. Pulsus alternans as a complication of anesthesia. Anesthesiology. 1974;40:509-510.
(3.) Cheng TO. The significance of right-sided pulsus alternans. Catheter Cardiovasc Interv. 1999;47:340.
(4.) Kern MJ. Mitral stenosis and pulsus alternans. Cathet Cardiovasc Diagn. 1998;43:313-317.
(5.) Cannon RO III, Schenke WH, Bonow RO, Leon MB, Rosing DR. Left ventricular pulsus alternans in patients with hypertrophic cardiomyopathy and severe obstruction to left ventricular outflow. Circulation. 1986;73:276-285.
(6.) Lee YC, Sutton FJ. Pulsus alternans in patients with congestive cardiomyopathy. Circulation. 1982;65:1533-1534.
(7.) Schweitzer P. Pulsus alternans in effusive pericarditis [letter]. Chest. l975;67:506.
(8.) Saghaei M, Mortazavian M. Pulsus alternans during general anesthesia with halothane: effects of permissive hypercapnia. Anesthesiology. 2000;93:91-94.
(9.) Kotsanas G, Holroyd SM, Young R, Gibbs CL. Mechanisms contributing to pulsus alternans in pressure-overloaded cardiac hypertrophy. Am J Physiol. 1996;271(6 pt 2): H2490-H2500.
(10.) Freeman AB, Steinbrook RA. Recurrence of pulsus alternans after fentanyl injection in a patient with aortic stenosis and congestive heart failure. Can Anaesth Soc J. 1985;32:654-657.
(11.) Rubin E, Farber JL. Pathology 2nd ed. Philadelphia, Pa: JB Lippincott Co; 1994:1140.
(12.) Harris LC, Nghiem QX, Schreiber MH, Wallace JM. Severe pulsus alternans associated with primary myocardial disease in children. Observations on clinical features, hemodynamic findings. Mechanisms and prognosis. Circulation. 1966;34:948-961.
(13.) Guyton AC, Hall JE. Textbook of Medical Physiology. 10th ed. Philadelphia, Pa: WE Saunders Co; 2000:98-99, 103-104.
(14.) Lee YC, Sutton FJ. Pulsus alternans: echocardiographic evidence of reduced venous return and alternating end-diastolic fiber length as causative factors. Chest. 1981;80:756-759.
(15.) Schmidt AG, Kadambi VJ, Ball N, et al. Cardiac-specific overexpression of calse-questrin results in left ventricular hypertrophy, depressed force-frequency relation and pulsus alternans in vivo. J Mol Cell Cardiol. 2000;32:1735-1744.
(16.) Givertz MM, Colucci W, Braunwald E. Clinical aspects of heart failure: high-output heart failure; pulmonary edema. In: Braunwald E, Zipes DP, Libby P, eds. Heart Disease. A Textbook of Cardiovascular Medicine. 6th ed. Philadelphia, Pa: WB Saunders Co; 2001:534-561.
(17.) McCloy RB, Nakano J. Pulsus alternans. J Okla State Med Assoc. 1966;59:174-175.
(18.) Schaefer S, Malloy CR, Schmitz JM, Dehmer GJ. Clinical and hemodynamic characteristics of patients with inducible pulsus alternans. Am Heart J. 1988;115:1251-1257. Source: Pulsus alternans a case study - Pediatric Care by Mark Weber
Whereas
Pulsus bigeminus consists of groups of two beats close together, is an alternating strong and weak pulse caused by an arrhythmia such as ventricular bigeminy. The weaker pulse (during the ventricular premature contraction) typically follows a shorter time interval than the stronger pulse.
How to distinguish from Pulsus bigeminus? I guess
Pulsus alternans occurs in Sinus rhythm where as Pulsus bigeminus in PVC not in sinus rhythm.
We talked so many things about Pulsus Alternans and bigeminus lets talk little bit about the Pulse:
A
pulse is the rhythmic expansion of an artery that can be digitally palpated (or visualized) during physical examination. Physiologically, the pulse pressure is the difference between systemic systolic and diastolic pressures.
Pulse deficits are absent pulses despite auscultation of a heart beat and are thus detected during simultaneous auscultation and pulse palpation. These occur as a result of ectopic ventricular contractions (arrhythmias) that occur so prematurely (rapidly) that the ventricles are unable to fill sufficiently to result in ejection of blood.
Bounding pulses (an increase in pulse pressure) can be noted in patients with aortic insufficiency or patent ductus arteriosus.
Weak pulses (a reduction in pulse pressure) can be noted in patients with heart failure or subaortic stenosis. Dogs with severe subaortic stenosis may demonstrate a pulse pressure that slowly increases during ventricular systole and reaches a peak pressure late in systole called
pulsus parvus et tardus .
Pulsus paradoxus is a decrease in pulse pressure during inspiration and an increase in pulse pressure during expiration. This is a normal occurrence but, it is usually too subtle to observe on physical examination. Patients with pericardial effusion and cardiac tamponade, however, demonstrate an exaggeration of this finding.
Vibrating pulse is a sharp, jerky pulse associated with lesions of the heart muscle, congestive heart failure, cardiac muscle hypertrophy and resistance to ventricular filling.
Linear Mode
