Description, Causes and Risk Factors:
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. 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. Its occurrence always warrants further evaluation to determine the cause.
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. 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 (i.e., 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. 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 second physiological action that may be the cause of pulsus alternans is the alteration in cellular handling of calcium. 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.
It also has been suggested that a change in ventricular contractility is the primary mechanism, causing changes in end-diastolic volume and pressure. In the experimental animal model, acute myocardial ischemia is associated with regional pulsus alternans, leading to the hypothesis that alternating potentiation and attenuation or deletion of contraction accounts for the pulse abnormality. Thus pulsus alternans may result primarily from an alternating contractile state of the ventricle. The magnitude of the alteration of pressure and stroke volume during pulsus alternans, indices of pump function, reflects the interaction of an alternating contractile state with changes in preload and afterload.
In most cases, pulsus alternans is an ominous sign that suggests severe cardiac failure.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.As the systemic venous pressure increases, extracellular fluid is transduced into the surrounding tissue, including the alveoli, leading to the edema and crackles.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.
Pulsus alternans can be detected via palpation of the artery, use of a sphygmomanometer, and examination of arterial and plethysmographic waveforms.Pulsus alternans is difficult to assess by palpation when the difference between large and small systolic beats is less than 20 mmHg.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.
Monitoring the plethysmographic waveform can be an alternative diagnostic tool if no indwelling arterial catheter is in place. Pulsus alternans was determined by examination of the plethysmographic waveform in patients undergoing surgery of the lower extremities.Plethysmographic waveforms could be used to diagnose pulsus alternans, although the sensitivity and specificity of this method have not been determined.
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.
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. Treating high blood pressure usually reduces pulse pressure as well. If the patient suffers from elevated pulse pressure, treatment may include medications that address this factor, such as an angiotensin-converting enzyme inhibitor (ACE inhibitor). An anticoagulant is the most effective treatment to reduce the risk of stroke. Myocardial infarction (cardiac failure) should be treated using standard measures (e.g., consider thrombolytic administration or PTCA). Long QT syndrome may be treated with removal of offending drugs or correction of metabolic abnormalities.
Most diseases that cause true pulses alternans do not require surgical treatment. Pulmonary embolectomy may be required for unresolved large pulmonary emboli. Left-sided cervicothoracic sympathetic ganglionectomy may be required for patients with congenital long QT syndrome who continue to have episodes of syncope despite drug therapy. Recurrent pericardial effusions may benefit from pericardiectomy.
NOTE: The above information is for educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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