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The authors report the occurrence of pulsus alternans, a condition characterised by the alternance of pulses of higher and lower amplitude, in two dogs and one cat under general anaesthesia. The presence of an underlying cardiac disease was confirmed in the cat but not in either dog, which - based on history and clinical findings - had presumably normal cardiovascular function before the anaesthetic. Possible mechanisms, including negative inotropy and haemodynamic and Frank-Starling effects, as well as the role of general anaesthesia as the potential triggering factor, are discussed in this report. Ephedrine resulted in the successful treatment of pulsus alternans, as demonstrated by the return of normal pulse and synchronisation of heart and pulse rates in the cat and in one dog. In the other dog, pulse pattern and frequency returned to normal once the guidewire for central line placement was withdrawn.

Graphical abstract, Highlights • PA and SAR are both related to heart failure. • The authors describe “phantom systole,” a remarkable finding of FE. • PVCs play a key role in worsening systolic heart failure.

Pulsus alternans is a rare condition characterized by alternation between strong and weak pulses during regular heart rhythm. Although pulsus alternans occurs mostly in severe heart failure, it can also be seen in other conditions that alternate ventricular contraction such as rapid tachycardia and extrasystole. Here, we report the case of a patient with peripartum cardiomyopathy who developed worsening pulsus alternans after a premature ventricular contraction.

Timing of events, as well as the pattern of occurrences, are important details to pay attention to. Occasionally, a discrepancy can be found between electrical and mechanical activity of the heart, and echocardiography can be a tool to identify such inconsistency. Moreover, there can be a discrepancy between the mechanical activation of the heart, and the efficiency of the heart (i.e., the production of cardiac output), and echocardiography can play a central role in diagnosing such a situation. Combining information from ECG tracing, 2D and tissue Doppler assessment of contractility, and spectral tracing across the LVOT can provide evaluation of the electrical activation of the heart, mechanical activation of the heart, and the ultimate “success” of these activation efforts in producing cardiac output.

The heterozygous phospholamban (PLN) p.Arg14del (R14del) mutation is found in patients with dilated or arrhythmogenic cardiomyopathy. The PLN R14del mutation triggers cardiac contractile dysfunction and arrhythmogenesis by affecting intracellular Ca2+ dynamics. Little is known about the physiological processes preceding PLN R14del induced cardiomyopathy, which is characterized by sub-epicardial accumulation of fibrofatty tissue, and a specific drug treatment is currently lacking. Here, we addressed these issues using a knock-in PLN R14del zebrafish model. Hearts from adult zebrafish with the R14del mutation display age-related remodeling with sub-epicardial inflammation and fibrosis. Echocardiography revealed contractile pulsus alternans before overt structural changes occurred, which correlated at the cellular level with action potential duration (APD) alternans. These functional alterations are preceded by diminished Ca2+ transient amplitudes in embryonic hearts. We found that istaroxime treatment ameliorates the in vivo Ca2+ dysregulation, rescues the cellular APD alternans, while it improves cardiac relaxation. Thus, we present novel insight into the pathophysiology of PLN R14del cardiomyopathy and identify istaroxime as a potential novel drug for its treatment.

Omecamtiv mecarbil (OM) is a promising novel drug for improving cardiac contractility. We tested the therapeutic range of OM and identified previously unrecognized side effects. The Ca2+ sensitivity of isometric force production (pCa50) and force at low Ca2+ levels increased with OM concentration in human permeabilized cardiomyocytes. OM (1 µM) slowed the kinetics of contractions and relaxations and evoked an oscillation between normal and reduced intracellular Ca2+ transients, action potential lengths and contractions in isolated canine cardiomyocytes. Echocardiographic studies and left ventricular pressure–volume analyses demonstrated concentration-dependent improvements in cardiac systolic function at OM concentrations of 600–1200 µg/kg in rats. Administration of OM at a concentration of 1200 µg/kg was associated with hypotension, while doses of 600–1200 µg/kg were associated with the following aspects of diastolic dysfunction: decreases in E/A ratio and the maximal rate of diastolic pressure decrement (dP/dtmin) and increases in isovolumic relaxation time, left atrial diameter, the isovolumic relaxation constant Tau, left ventricular end-diastolic pressure and the slope of the end-diastolic pressure–volume relationship. Moreover, OM 1200 µg/kg frequently evoked transient electromechanical alternans in the rat in vivo in which normal systoles were followed by smaller contractions (and T-wave amplitudes) without major differences on the QRS complexes. Besides improving systolic function, OM evoked diastolic dysfunction and pulsus alternans. The narrow therapeutic window for OM may necessitate the monitoring of additional clinical safety parameters in clinical application. Supplementary Information The online version contains supplementary material available at 10.1007/s00395-021-00866-8.

This chapter summarizes some of the emerging concepts concerning the anatomy and function of intrathoracic afferent, efferent, and local circuit neurons involved in cardiac regulation as well as some of the possible interactions that may occur between them. Intrathoracic vascular mechanoreceptors appear to be length-sensitive receptors and are located on the vena cavae, pulmonary arteries, pulmonary veins, all along the thoracic aorta, and on the major arteries arising from the aorta. Cardiovascular-related activity of intrathoracic local circuit neurons sometimes also occurs during every other beat when pulsus alternans is present. Some intrathoracic efferent sympathetic neurons are activated via reflexes following distortion of mechanoreceptors in limited regions of the heart or great thoracic vessels. Physiological evidence has implicated intrathoracic local circuit neurons in cardiac regulation. Although a number of authors have described the presence of neurons on mammalian hearts, including the human heart, little is known about their function.

Resumo Contexto As cardiopatias podem causar alterações no formato das ondas da ultrassonografia vascular (UV) em vasos periféricos. Essas alterações, tipicamente bilaterais e sistêmicas, são pouco conhecidas e estudadas. Objetivo Avaliar as ondas periféricas da UV de pacientes idosos para identificar alterações decorrentes de cardiopatias. Métodos Foram estudados 183 pacientes idosos submetidos a UV periférica no ano de 2014. Resultados Foram avaliados 102 mulheres (55,7%) e 81 homens (44,3%) com idade entre 60 e 91 anos (média de 70,4±7,2 anos). Encontraram-se alterações pela UV em 84 pacientes (45,9%). Foram identificadas 138 alterações de oito dos 13 tipos descritos na literatura: arritmia, onda bisferiens de pico sistólico, baixa velocidade de pico sistólico, pulsatilidade em veias femorais, bradicardia, taquicardia, onda de pulso parvus tardus e onda de pulso alternans. Houve baixa concordância entre a presença e a não presença de alterações na UV e na avaliação cardiológica. Na análise específica das alterações, os exames tiveram uma concordância variável, que foi boa para o achado de taquicardia, moderada para arritmia e baixa para bradicardia. Não houve concordância entre a UV e os exames cardiológicos para as demais alterações. Conclusões É possível identificar determinadas alterações cardíacas em idosos por meio da análise do formato das ondas periféricas da UV. É importante reconhecer e relatar a presença dessas alterações, pela possibilidade de alertar para um diagnóstico ainda não identificado nesses pacientes. Entretanto, mais estudos são necessários para que seja definida a importância das alterações no formato das ondas Doppler periféricas no reconhecimento de cardiopatias. Abstract Background Heart diseases can cause changes to vascular ultrasonography (VUS) waveforms in peripheral vessels. These changes are typically bilateral and systemic, they have been little studied, and little is known about them. Objective To assess peripheral VUS waveforms in elderly patients in order to identify changes caused by heart diseases. Methods During 2014, a total of 183 elderly patients were examined with peripheral VUS and the results were analyzed. Results The sample comprised 102 women (55.7%) and 81 men (44.3%) with ages ranging from 60 to 91 years (mean of 70.4±7.2 years). Abnormalities were identified in VUS waveforms in 84 patients (45.9%). A total of 138 abnormalities were identified and classified into eight of the 13 categories described in the literature, as follows: arrhythmia, systolic pulsus bisferiens, low peak systolic velocity, pulsatile flow in femoral veins, bradycardia, tachycardia, pulsus tardus et parvus and pulsus alternans. There was low agreement between presence/absence of VUS abnormalities and cardiological assessments. Analysis of specific abnormalities revealed variable levels of agreement between VUS and cardiological assessments, ranging from good for tachycardia, moderate for arrhythmia, to low for bradycardia. There was no agreement between VUS and cardiological examinations for the remaining categories of abnormalities. Conclusions Certain cardiac abnormalities can be identified in elderly patients by analysis of peripheral VUS waveforms. It is important to recognize and report the presence of these abnormalities because there is a possibility that they may serve to signal hitherto unidentified diagnoses in these patients. However, further studies are needed to determine the importance of changes to peripheral Doppler waveforms to recognition of heart diseases.

Pulsus alternans is a type of arrhythmia that shows alternate contraction forces of ventricular muscles and is a sign of cardiac complications. In this study, we investigate the parameter dependence of pulsus alternans generation using a mathematical crustacean cardiac cell model with automaticity. Specifically, we modified the parameter values in the model so that they resemble realistic waveforms of the membrane potential and then analyzed the modified model. We also conducted physiological experiment and observed pulsus alternans as irregular heartbeats. We reproduced the generation of pulsus alternans in the modified mathematical model. Numerical results showed that the conductance of the transient calcium current and the calcium-dependent potassium current for the small cell (pacemaker of crustacean heart) is the key to generating such pulsus alternans.

In ventricular myocytes, membrane depolarization during the action potential (AP) causes synchronous activation of multiple L-type CaV1.2 channels (LTCCs), which trigger the release of calcium (Ca2+) from the sarcoplasmic reticulum (SR). This results in an increase in intracellular Ca2+ (Cai) that initiates contraction. During pulsus alternans, cardiac contraction is unstable, going from weak to strong in successive beats despite a constant heart rate. These cardiac alternans can be caused by the instability of membrane potential (Vm) due to steep AP duration (APD) restitution (Vm-driven alternans), instability of Cai cycling (Ca2+-driven alternans), or both, and may be modulated by functional coupling between clustered CaV1.2 (e.g. cooperative gating). Here, mathematical analysis and computational models were used to determine how changes in the strength of cooperative gating between LTCCs may impact membrane voltage and intracellular Ca2+ dynamics in the heart. We found that increasing the degree of coupling between LTCCs increases the amplitude of Ca2+ currents (ICaL) and prolongs AP duration (APD). Increased AP duration is known to promote cardiac alternans, a potentially arrhythmogenic substrate. In addition, our analysis shows that increasing the strength of cooperative activation of LTCCs makes the coupling of Ca2+ on the membrane voltage (Cai→Vm coupling) more positive and destabilizes the Vm-Cai dynamics for Vm-driven alternans and Cai-driven alternans, but not for quasiperiodic oscillation. These results suggest that cooperative gating of LTCCs may have a major impact on cardiac excitation-contraction coupling, not only by prolonging APD, but also by altering Cai→Vm coupling and potentially promoting cardiac arrhythmias., Author summary Recent experimental studies have suggested that clusters of L-type CaV1.2 channels (LTCCs) can open and close in unison (i.e., cooperative or coupled gating) and that this gating modality may regulate excitation-contraction coupling in the heart. However, whether amplification of Ca2+ influx by cooperative gating of LTCCs promotes alternans is unknown. In this study, we developed a novel computational model of cooperative gating of LTCCs from experimental data. We incorporate the model into a physiologically detailed action potential (AP) model and investigated how changes in coupling strength of LTCCs may impact dynamics of AP and Ca2+ alternans. Our data suggest that increasing coupling strength of LTCCs prolongs AP duration and leads to Ca2+ overload. In addition, our theoretical and computational approaches elucidate that increasing coupling strength of LTCCs promotes positive Cai→Vm coupling, which could lead to Vm-driven and Ca2+-driven alternans.

A previously healthy 21-month-old presented with new-onset dilated cardiomyopathy. Evaluation noted pulsus alternans, with beat-to-beat alternations in aortic pulse wave amplitude, both clinically and on diagnostic studies. Pulsus alternans is an infrequent, complex pathophysiologic sign often associated with severe heart failure. The mechanisms are incompletely understood, but theorised aetiologies include beat-to-beat changes in left ventricular loading conditions, variations in myocardial oxygen supply/demand, and alternations in myocardial contractility. Recognition of pulsus alternans is important as it provides significant clinical information, may suggest suboptimal medical management, and may be the first warning sign of severe cardiac dysfunction.

A 15-year-old, previously healthy teenager who had fatigue, shortness of breath, vomiting, chest discomfort, lower extremity oedema and inability to lay flat for 3 weeks prior to her initial presentation. She was warm, well perfused with alternating strong and weak central as well as peripheral pulses and laterally displaced cardiac impulse. Her monitoring showed visual evidence of ‘pulsus alternans’—alternating low and high amplitude waveforms on the arterial waveform and plethysmography (figure 1). Her echocardiography showed severely …

Background Mechanical alternans (MA) and electrical alternans (EA) are predictors of cardiac events. Experimental studies have suggested that refractoriness of calcium cycling underlies these cardiac alternans. However, refractoriness of left ventricular contraction has not been examined in patients with cardiac alternans. Methods In 51 patients with miscellaneous heart diseases, incremental right atrial pacing was performed to induce MA and EA. MA was quantified by alternans amplitude (AA: the difference between left ventricular dP/dt of a strong beat and that of a weak beat), and AA at 100/min (AA100) and maximal AA (AAmax) were measured. EA was defined as alternation of T wave morphology in 12-lead electrocardiogram. Relative refractoriness of left ventricular contraction was examined by drawing the mechanical restitution curve under a basal coupling interval (BCL) of 600 ms (100/min) and was assessed by the slope at BCL (Δmechanical restitution). Postextrasystolic potentiation (PESP) was also examined and the slope of PESP curve (ΔPESP) was assessed as a property to alternate strong and weak beats. Results MA and EA were induced in 19 patients and in none at 100/min or less, and at any heart rate in 32 and in 10, respectively. AA100 and AAmax correlated positively with Δmechanical restitution and negatively with ΔPESP. Patients with EA had a significantly larger Δmechanical restitution and a significantly larger absolute value of ΔPESP than those without. Conclusions In patients with MA and EA, the left ventricular contractile force during tachycardia is under relative refractoriness and prone to cause large fluctuation of contractile force.

In patients with severe left ventricular (LV) dysfunction, visible pulsus alternans coincides with visible T-wave alternans (TWA), but a similar relationship has not been described for nonvisible microscopic systolic pressure alternans (MSPA) and microvolt TWA (MTWA).The purpose of this study was to determine the prevalence of MSPA and its relationship to MTWA in patients with cardiomyopathy.Using the spectral method, MSPA was measured from finger pressure during incremental atrial pacing and then validated against MSPA measured from the LV pressure in 12 patients. In 23 other patients with cardiomyopathy (LV ejection fraction40%), noninvasive MSPA and MTWA were measured simultaneously during incremental atrial pacing.MSPA (1 mm Hg) was detected in 80% of patients with cardiomyopathy and in 43% of controls. The presence of finger MSPA showed 100% positive concordance with LV MSPA; however, finger MSPA was 20% larger due to peripheral augmentation. Finger MSPA was highly concordant (96% positive concordance and 90% negative concordance) with MTWA. The magnitudes of MSPA and MTWA showed a linear correlation (R = 0.66, P.001), and the k value, a measure of signal-to-noise ratio, was significantly larger for MSPA compared to MTWA (108 ± 88 vs 24 ± 48, P.001). Premature beats resulted in concordant and coincident changes in MSPA and MTWA. During follow-up (454 ± 274 days), 2 (8.6%) patients experienced ventricular tachycardia, and both manifested MSPA and MTWA during pacing at 600 ms.MSPA can be detected noninvasively in patients with cardiomyopathy and is coupled to MTWA, suggesting a common mechanism. The high signal-to-noise ratio of MSPA may provide a novel robust metric of sudden cardiac death risk in these patients.

We wish to report an important clinical observation that combined several forms of imaging followed by pharmacological intervention that saved a patient froma potentially unnecessary surgical intervention. This was in a 65-year-old lady with previous Ultracor single tilting disc mitral valve replacement in 1996, systemic hypertension, chronic atrial fibrillation and epilepsy; who complained of worsening breathlessness. Clinically, she had physical signs of right heart failure. Trans-thoracic echocardiogram (TTE) showed mild left ventricular systolic impairment, dilated left atrium, significantly dilated right ventricle, moderate right ventricular systolic impairment, moderate rise of the systolic pulmonary artery pressure (55 mmHg), and a well-seated mechanical mitral valve prosthesis with no para-valvular leak. However, the Ultracor single-tilting-disc mechanical MV prosthesis was not opening on alternate cardiac cycles, Fig. 1. We did not agree with those who suspected a catastrophic malfunctioning of mechanical MV prosthesis and proposed a re-do operation. We noted that the function of the MV prosthesis was normal on alternate beats. We postulated that the intermittentmalfunction indicated a dynamic intermittent problem most likely related to the impact of the high right sided pressure on the diastolic pressure of the left ventricle which is preventing themechanicalMVprosthesis fromopeningeveryother beat. This is similar, though intermittent, to tamponade. We called that tamponade alternans of the MV prosthesis. We went on to confirm our hypothesis and performed fluoroscopy and an invasive simultaneous left and right heart catheter study [1]. Fluoroscopy confirmed the intermittent opening of the Ultracor singletilting-disc mechanical MV prosthesis every other beat (Fig. 2). The invasive studies showed severe pulsus alternans. The beats with the lower cardiac output were preceded by equalisation of right and left ventricular diastolic pressures (Fig. 2). The beats with the higher left ventricular output were preceded by a left ventricular end diastolic pressure higher than the right ventricular end diastolic pressure. The pulmonary artery pressure was 50/23 mm Hg with a mean of 38 mm Hg. The pulmonary capillary wedge pressure was high at 34/28 mm Hg. We had thus confirmed our hypothesis that the pulmonary hypertension is pushing the inter-ventricular septum paradoxically to the left (Fig. 2), and raising the left ventricular diastolic pressure to a level higher than the left atrial pressure as shown by changes in the diastolic left ventricular pressure curves (Fig. 2). This is preventing the opening of themitral valve. However, by the following cardiac cycle, the

No abstract available. Article truncated at 150 words. A 52 year old man with a known past medical history of morbid obesity (BMI, 54.6 kg/m2), heart failure with preserved ejection fraction, hypertension, untreated obstructive sleep apnea, and obesity hypoventilation syndrome presented with increasing dyspnea over several months accompanied by orthopnea and weight gain that the patient had treated at home with a borrowed oxygen concentrator. On arrival to the Emergency Department, the patient was in moderate respiratory distress and hypoxic to SpO2 70% on room air. Physical examination was pertinent for pitting edema to the level of the chest. Assessment of jugular venous pressure and heart and lung auscultation were limited by body habitus, but chest radiography suggested pulmonary edema. The patient refused aggressive medical care beyond supplemental oxygen and diuretic therapy. Initial transthoracic echocardiography was limited due to poor acoustic windows but suggested a newly depressed left ventricular ejection fraction (LVEF) of

Objective: The photoplethysmographic wave is displayed by most pulse oximeters. It may be used as anon-invasive alternative to invasive arterial blood pressure trace analysis for continuous haemodynamic monitoring in selected situations. Patients and setting: Four cardiac patients treated in atertiary neonatal-paediatric intensive care unit. Measurements: Simultaneous monitoring of the photoplethysmographic wave, ECG, and invasive blood pressure. Results and conclusions: Photoplethysmography allows for monitoring pulse rate in patients with (possible) heart rate/pulse rate dissociation (pacemaker dependency, pulsatile ventricular assist device); monitoring sudden changes in heart beat volume, which are unrelated to respiration (pulseless electrical activity, pulsus alternans); and monitoring respiratory-dependent fluctuations of the plethysmographic wave (heart failure, hypovolaemia, asthma, upper airway obstruction, pericardial effusion). Deterioration, slowly evolving over time, may be detected by this method

Objectives: To report the clinical findings associated with pulsus alternans in English cocker spaniels with dilated cardiomyopathy and to review the phenomenon of mechanical alternans, usually found in patients with severe left ventricular systolic dysfunction. Methods: The case records of 10 English cocker spaniels with dilated cardiomyopathy and pulsus alternans were reviewed. All dogs had been referred in moderate to severe congestive heart failure. Pulsus alternans was clinically recognised by palpation of a regular alternation of femoral pulse amplitude and confirmed by echocardiography in all cases. Pulsus alternans was an intermittent finding in all 10 dogs. Results: Phonocardiographic recordings were obtained in three dogs to document variation in the intensity of the heart sounds, with one case exhibiting absence of the second heart sound in alternate beats. M-mode echocardiography performed in all dogs showed alternation of the pattern of mitral valve diastolic motion. Doppler echocardiography showed marked alternation in stroke volume in the aortic outflow in all cases. It also showed alternation in mitral regurgitation and in the velocity of early ventricular filling. Clinical Significance: Pulsus alternans may be more prevalent in English cocker spaniels than in other breeds, and because of its intermittent nature, its incidence may be higher than that previously reported. It has diagnostic relevance as it usually indicates severe myocardial depression. Echocardiography allows non-invasive detection of mechanical alternans and provides further insights into its pathophysiology and clinical significance.

echanical pulsus alternans is sometimes seen inpatients with severe heart failure. This case reportdescribes a patient with medically refractory acute heartfailure due to severe left ventricular (LV) systolic dys-function withpulsusalternans,whereshort-termadaptiveservo-ventilation (ASV)therapyimmediatelyamelioratedthe mechanical pulsus alternans.A 52 year-old male was admitted to the hospitaldue to progressive exertional dyspnoea. Auscultationof the chest revealed fine crackles over both lungs.An S3 gallop rhythm and a grade 2/6 of pansystolicmurmur were audible at the apex. His blood pres-sure was 110/70mmHg and heart rate was 120bpm.Chest X ray showed cardiomegaly with bilateral pul-monary congestion. The electrocardiogram showed sinustachycardia with normal QRS duration. Blood exami-nation on admission revealed remarkable elevation inthe serum level of brain natriuretic peptide (BNP) of1740 pg/dl (

[Ca2+]i is used as a signal in many tissues. In this review we discuss the mechanisms that regulate [Ca2+]i and, importantly, what determines their stability. Brief mention is made of the effects of feedback gain and delays on stability. The control of cytoplasmic Ca concentration is shown to be generally stable as Ca pumping is essentially an instantaneous function of [Ca2+]i. In contrast, regulation of the Ca content of intracellular stores may be less stable. One example of this is instability in the control of sarcoplasmic reticulum (SR) Ca content in cardiac muscle. An increase of SR Ca content increases the systolic Ca transient amplitude. This in turn decreases Ca influx into the cell and increases efflux, thereby restoring SR Ca to control levels. This feedback system has an inherent delay and is potentially unstable if the gain is increased beyond a certain level. This instability produces Ca transients of alternating amplitude and may contribute to the clinical syndrome of pulsus alternans.

Introduction: Progressive heart failure and ventricular fibrillation are major causes of death in patients with chronic heart failure. Mechanical alternans (pulsus alternans) has been observed in patients with severe congestive heart failure. Visible T wave alternans occasionally is a precursor of ventricular fibrillation. We investigated the occurrence of both cardiac alternans in 94 patients with chronic heart failure. Methods and Results: Mean left ventricular ejection fraction (LVEF) of the study population was 35 ± 10%. Mechanical alternans was detected in left ventricular pressure during diagnostic cardiac catheterization. Only sustained mechanical alternans was included in the study. Visible T wave alternans, not microvolt alternans, was noted on standard surface ECG. Cardiac alternans was examined at rest, during physiologic tachycardia, and during stepwise dobutamine loading (2–4–8 μg/kg/min). Prevalences of mechanical and electrical alternans were 19.1% and 4.4% at rest, 45.5% and 8.0% during physiologic tachycardia, and 62.1% and 9.5% under dobutamine loading. Overall, 70 patients (74.5%) showed mechanical alternans and 10 patients (10.6%) showed T wave alternans. T wave alternans always appeared with large mechanical alternans. Among patients with mechanical alternans, cases with T wave alternans showed lower LVEF than those without (27.5 ± 4.4 and 35.1 ± 10.2, P < 0.002). Conclusion: Visible T wave alternans was detectable in patients with chronic heart failure, especially under tachycardia or catecholamine exposure. Investigating mechanical and mechanoelectrical alternans may bring new insights into the management of patients with chronic heart failure. (J Cardiovasc Electrophysiol, Vol. 15, pp. 295-299, March 2004)

We have previously found that the postextrasystolic (PES) potentiation (PESP) of the left ventricular (LV) contractility (Emax) decays typically in transient alternans even in the normally ejecting canine heart. This contradicted the general expectation that arterial pressure (AP) and LV pressure (LVP) usually decay exponentially during PESP. We hypothesized this contradiction to be due to the different cardiodynamic behaviors of AP and LVP from LV Emax during PESP. We tested this hypothesis by measuring AP, LVP, LV volume, Emax, effective arterial elastance (Ea) as an index of afterload, and pulse pressure (PP) during PESP in eight anesthetized open-chest dogs by using the conductance catheter system. We changed Ea by changing the total peripheral resistance (TPR) with methoxamine hydrochloride (iv) and repeated the measurements. Although the Emax alternans patterns during PESP were comparable between the normal and high afterloads, LVP and PP were slightly potentiated and alternated under the normal afterload, whereas LVP and PP were obviously potentiated and alternated under the high afterload. We also simulated the effects of Ea/Emax on the transient alternans of AP and LVP on a computer. Despite the same alternans pattern of Emax, a higher Ea/Emax, which is typical in heart failure, caused a larger PP alternans, whereas a lower Ea/Emax, which is typical in normal hearts, almost eliminated it. These results suggest that a transient alternans of LV contractility during PESP could be overlooked when AP and LVP are monitored in in situ normal hearts.

ANALYSIS OF THE arterial pressure waveform is useful to the clinician in that alterations in the waveform morphology may indicate changes in cardiovascular parameters, such as stroke volume, systemic vascular resistance, or preload. Distinct arterial waveform morphologies, such as pulsus alternans and pulsus paradoxus, may indicate specific conditions and are helpful in directing therapy. The dicrotic pulse is a unique arterial pressure waveform associated with specific physiologic conditions. Recognition and understanding of factors associated with dicrotic pulse formation should aid the clinician in patient management. As opposed to anacrotic and biferious pulses, in which 2 pulsations occur during systole, a dicrotic pulse is characterized by 2 palpable pulsations with 1 upstroke in systole and 1 upstroke in diastole. Meadows et al1 defined a fully dicrotic pulse when the dicrotic wave (peak of the dicrotic wave pressure dicrotic notch pressure) is 30% of the pulse pressure and when the pressure difference between the dicrotic notch and the diastolic pressure is 10% of pulse pressure. A dicrotic pulse historically has been associated with typhoid fever and more recently described with a variety of low cardiac output states.1,2 After mitral or aortic valve replacement, a dicrotic pulse has been correlated with left ventricular dysfunction and is an indicator of a poor postoperative prognosis.3 This case report describes the occurrence of a dicrotic pulse in a patient with cardiac tamponade that resolved after surgical drainage of pericardial fluid.