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Cannon A waves are large-amplitude waves seen in the jugular veins during a physical exam. They are caused by simultaneous contraction of atria and ventricle leading to exaggerated right atrial pressure. Usually, Cannon A waves are irregular and intermittent. They are seen in patients with cardiac conduction defects or certain cardiac dysrhythmias. Cannon A waves can also be seen on the EKG.[1][2][3][2]

Cannon A waves are related to rhythm disturbances causing changes in the normal cardiac blood flow causing a large pressure vein in the jugular vein. Different dysrhythmias may cause cannon A waves. Heart block may lead to cannon A waves, in particular, third-degree (complete) heart block. It may be seen with ventricular tachycardia (VT) as a result of the underlying atrioventricular (AV) dissociation. Another cause is Pacemaker syndrome without proper synchronization of atria and ventricles. [4]

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Cannon A waves need to be distinguished from giant A waves that occur in right heart structural changes such as tricuspid valvulopathies, right ventricular hypertrophy, and pulmonary hypertension. To the observer of the jugular, venous-pressure giant A waves and Cannon A waves may appear similar. From physical exams alone it might be difficult to differentiate between them.

Jugular vein pulsation (JVP) provides clinically meaningful information about the central venous pressure (CVP). JVP is an important and reproducible tool to diagnose various cardiac conditions which can cause a change in CVP. Canon A wave can be easily missed without close attention during bedside examination especially due to declining physical exam skills in contemporary clinical practice. Recent literature does not describe the frequency of cannon A waves in rhythm disturbances.

The normal function of the heart is to create forward blood flow. During each cardiac cycle, blood is pushed from the atria to the ventricles passing through the atrioventricular valves. Central venous pressure is measured in the right atrium. The bedside clinician can directly assess the jugular venous pulse by observing the patients neck. When obtaining a central or jugular venous pressure curve, its course can be described as 3 positive and 2 negative deflections. [5][6]The 3 positive deflections are:

A proper heart function requires a synchronized action of the myocardium. When the cardiac rhythm is disturbed, the heart cannot provide proper blood flow. Cannon A waves are an example of this. Electrical disturbances cause mechanical problems causing atrial contraction to occur when the tricuspid valve is closed. The reflection of the pressure wave travels up the venous system and can be examined in the jugular vein as exaggerated A wave pulsation.

Patients may complain of pulsations in the neck and abdomen as the pulse wave travels back into the venous system. Other symptoms such as a headache, cough, and jaw pain can occur. Ask the patient for polyuria since increased atrial stress leads to higher BNP levels which in return will cause polyuria. Since Cannon A waves are associated with higher right atrial pressures. Erlebacher et al. describe that this may result in baroreceptor mediated systemic hypotension.

The inspection of jugular venous pulsation should be in conjunction with auscultation of the heart. Remember the relation of the venous pressure curve to the heart sounds. The A wave is followed closely by the S1 heart sound as the atrial contraction is followed by the closure of the atrioventricular valves.

According to Ranjith et al., it is helpful to differentiate between regular and irregular Cannon waves since regular Cannon A waves might be caused by junctional rhythm or supraventricular tachycardia. Whereas, atrioventricular dissociation, ectopic atrial beats can result in irregular A waves.

Patients complaining of symptoms that can be related to cannon A waves or direct physical exam positive for Cannon A waves should undergo further testing. To identify the cause of Cannon A waves and to distinguish from giant A waves an ECG and echocardiography should be performed. The ECG is helpful to look for rhythm disturbances. If P waves fall within QT interval should prompt examining for Cannon A waves. For assessing the structural changes, an ultrasound examination of the heart should be performed with attention to the right heart looking for hypertrophy, tricuspid pathology, and pulmonary hypertension.[7][1][8]

The venous pressure curve can be altered in different ways and Cannon A waves may be mistaken. For example, giant C and V waves can occur in tricuspid regurgitation. This is called Lancisi's sign. Jugular vein distension can result from a pulmonary embolism as part of Beck's Triad. Elevated JVP without venous pulsations should raise the suspicion of superior vena cava obstruction. This illustrates the importance of venous pressure as a window to the right heart.

Clinicians (nurse practitioners, physicians, physician assistants) may notice a pulsating sensation in the neck. One cause for this might be a phenomenon called Cannon A wave. It is an exaggerated pulse wave. In normal healthy people, when the atria contract blood is pushed into the ventricles. When the cardiac action is not well synchronized as might be the case in cardiac rhythm abnormalities, blood pushes against the closed tricuspid valve and create a large reverse pulsation into the venous system. This pressure wave might be felt in the neck, jaw, and abdomen. A feeling of pulsation should prompt further investigation. When Cannon A waves are found, further investigations may be needed to identify the reason why the heart rhythm is not well synchronized. Cardiology consultation may be necessary.

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Purpose: A decrease of electrocardiographic T-wave voltage with increasing training loads has been reported in elite endurance athletes and ascribed to training-related adaptation in sympathetic activity to the ventricles. A switch from vagal to sympathetic predominance in sino-atrial node regulation on going from low to peak training load has been reported in world-class rowers. In this study on world-class endurance athletes, we tested the hypothesis that training-induced variations in T-wave amplitude at higher training loads are paralleled by changes in HR spectral profile.

Methods: We studied eight male rowers of the Italian national team in the season culminating with the Rowing World Championship. Athletes were evaluated at 50 and 100% of training load, approximately 20 d before the World Championship, and during the World Championship, when the intensity was markedly reduced. We assessed T-wave maximum amplitude in chest lead V6 and cardiac autonomic regulation by power spectral analysis of R-R interval variability.

Results: The increase in training load from 50 to 100% was accompanied by a significant decrease in high frequency and a significant increase in low-frequency R-R variability (in normalized units) with a concomitant significant decrease in T-wave amplitude (microV). Reduction in training load during the World Championship resulted in a return of spectral profile to the level observed at 50% training load and in a partial recovery of T-wave amplitude. HR did not change significantly.

Left ventricular myocardial stiffness could offer superior quantification of cardiac systolic and diastolic function when compared to the current diagnostic tools. Shear wave elastography in combination with acoustic radiation force has been widely proposed to noninvasively assess tissue stiffness. Interestingly, shear waves can also result from intrinsic cardiac mechanical events (e.g., closure of valves) without the need for external excitation. However, it remains unknown whether these natural shear waves always occur, how reproducible they can be detected and what the normal range of shear wave propagation speed is. The present study, therefore, aimed at establishing the feasibility of detecting shear waves created after mitral valve closure (MVC) and aortic valve closure (AVC), the variability of the measurements, and at reporting the normal values of propagation velocity. Hereto, a group of 30 healthy volunteers was scanned with high-frame rate imaging (>1000 Hz) using an experimental ultrasound system transmitting a diverging wave sequence. Tissue Doppler velocity and acceleration were used to create septal color M-modes, on which the shear waves were tracked and their velocities measured. Overall, the methodology was capable of detecting the transient vibrations that spread throughout the intraventricular septum in response to the closure of the cardiac valves in 92% of the recordings. Reference velocities of 3.20.6 m/s at MVC and 3.50.6 m/s at AVC were obtained. Moreover, in order to show the diagnostic potential of this approach, two patients (one with cardiac amyloidosis and one undergoing a dobutamine stress echocardiography) were scanned with the same protocol and showed markedly higher propagation speeds: the former presented velocities of 6.6 and 5.6 m/s; the latter revealed normal propagation velocities at baseline, and largely increased during the dobutamine infusion (>15 m/s). Both cases showed values consistent with the expected changes in stiffness and cardiac loading conditions.

In most leads, the T wave is positive. This is due to the repolarization of the membrane. During ventricle contraction (QRS complex), the heart depolarizes. Repolarization of the ventricle happens in the opposite direction of depolarization and is negative current, signifying the relaxation of the cardiac muscle of the ventricles. But this negative flow causes a positive T wave; although the cell becomes more negatively charged, the net effect is in the positive direction, and the ECG reports this as a positive spike.[2] However, a negative T wave is normal in lead aVR. Lead V1 generally have a negative T wave. In addition, it is not uncommon to have a negative T wave in lead III, aVL, or aVF. A periodic beat-to-beat variation in the amplitude or shape of the T wave may be termed T wave alternans. ff782bc1db