AV junctional escape beats were mentioned previously in the section on sinus arrest. An AV junctional escape beat is simply a beat comes after a pause because the normal sinus pacemaker fails to function. The AV junctional escape beat, therefore, is a “safety beat.” Following this escape beat, the normal sinus pacemaker may resume function. However, if this does not occur, a slow AV junctional escape rhythm may continue. An AV junctional escape rhythm is simply a consecutive run of AV junctional beats. The heart rate is usually slow, between 30 and 60 beats/min.
AV junctional escape rhythms can be seen in a number of clinical setting – digitalis toxicity, toxic reactions to betablockers or calcium-channel blockers, acute myocardial infarction, hypoxemia, hyperkalemia,
AV Junctional tachycardias
The AV junction can also be the site of ectopic stimuli producing premature AV junctional contractions (PJCs) and junctional tachycardia.
PJCs are simply premature beats formed in the AV junction. They resemble premature atrial contractions (PACs), except that the P waves, when seen, will be retrograde with a PJC. If no P wave is seen before the premature beat, then there is no way of telling if it is a PAC (with P wave lost in the preceding T wave) or a PJC (with the P wave buried in the QRS complex). The distinction is purely academic. PACs and PJCs have the same clinical significance, and treatment is the same.
An AV junctional tachycardia, analogous to PAT, is simply a run of three or more consecutive PJCs. AV junctional tachycardia and PAT can be considered clinically as a single entity. They have the same clinical significance and treatment.
Atrial flutter and Atrial Fibrillation
Atrial flutter and atrial fibrillation are two distinct but related arrhythmias. Like PAT, atrial flutter and atrial fibrillation are ectopic atrial rhythms. With all three arrhythmias, the atria are not stimulated from the sinus node but from an ectopic site. In PAT the atria are stimulated at a rate generally between 140 and 250 beats/min. In atrial fullter, the atrial rate is even faster, generally between 250 and 350 beats/min. Finally, with atrial fibrillation, the atrial depolarization rate is between 400 and 600 beats/min. You can consider these three ectopic atrial tachyarrhythmias on a continuum from PAT to atrial flutter to atrial fibrillation, with the atrial rate becoming progressively more rapid in each case.
Atrial flutter shows the following;
Characteristic sawtooth flutter waves occur instead of P waves.
The ventricular rate may vary. For example, QRS complexes may occur with every fourth flutter wave. This is called 4:1 flutter. With 2:1 flutter, there is one QRS complex for every two flutter waves, and the ventricular rate is half the atrial rate. A 1:1 atrial flutter with a ventricular rate about 300 beats/min is rare.
Atrial flutter rarely, if ever, occurs in normal hearts and is most often seen in patients with valvular heart disease, ischemic heart disease, lung disease, cardiomyopathy, pulmonary emboli, and after cardiac surgery.
Rapid irregular undulations of the baseline (fibrillatory wave) occur instead of P waves.
A ventricular rate that is usually grossly irregular is seen. When the patient is given digitalis, the ventricular rate will slow.
In some cases, atrial fibrillation occurs chronically. In other cases, it is paroxysmal. Atrial fibrillation occasionally occurs in normal people. Common cause of atrial fibrillation are coronary artery disease, hypertensive heart disease, and rheumatic valvular heart disease. Atrial fibrillation may also occur with hyperthyroidism, cardiomyopathy, cardiac surgery, pulmonary emboli, chronic pericarditis, and other conditions.
4 Ventricular Arrhythmias
PREMATURE VENTRICULAR CONTRACTIONS (PVCs)
Premature ventricular contractions (PVCs) are premature beat arises in either the right or the left rntricle. Therefore, the ventricles will not be stimulated simultaneously, and the stimulus will spread through the ventricles in an aberrant direction. Thus the QRS complex will be wide with PVCs just as it is with a bundle branch block pattern.
PVCs have two major characteristics:
They are premature and occur before the next normal beat is expected.
They are aberrant in appearance. The QRS complex is abnormally wide (usually 0.12 sec or more). The T wave and the QRS complex usually point in opposite directions.
A fully compensatory pause.
There are several features of PVCs that are of clinical importance.
PVCs may occur with varying frequency. Two in a row are called a couplet. Three in a row are ventricular tachycardia. When a PVCs occurs regularly after each normal beat. This is called ventricular bigeminy. When the rhythm is two normal beats followed by a PVC, this is ventricular trigeminy.
The term coupling interval is refers to the interval between the PVC and the preceding normal beat. There are two types of coupling interval. one is fixed coupling interval. Another is variably coupling interval.
A PVC is often followed by a fully compensatory pause before the next beat. A full compensatory pause indicates that the interval between the normal QRS complexes immediataly before and immediately after the PVC is exactly twice the basic RR interval. A full compensatory pause is more characteristic of PVCs than of PACs. Sometimes a PVC will fall almost exactly between two normal beats, and in such cases the PVC is said to be interpolated.
Uniform PVCs have the same shape in a single lead. Multiform PVCs have different shapes in the same lead.
When a PVC occurs simultaneously with the apex of the T wave of the preceding beat, this is called an R on T phenomenon. It may be the forerunner of ventricular tachycardia or ventricular fibrillation.
PVCs are among the most commonly seen arrhythmias. They may occur both in normal people and also in those with serious organic heart disease. They may be a stable and benign finding. Or they may be precursors of cardiac arrest and sudden death from ventricular fibrillation.
PVCs may cause by anxiety or excessive caffeine. Certain drugs, such as epinephrine, isoproterenol, and aminophylline. PVCs are very common in cardiac disease, such as valvular heart disease, hypertensiove heart disease, ischemic heart disease with or without myocardial infarction, hypoxemia, congestive heart failure, digitalis toxicity or toxicity due to other drugs, hypokalemia, hypomagnesemia and so on.
Ventricular tachycardia is a run of three or more PVCs. Ventricular tachycardia may occur as a single isolated burst, may recur paroxysmally, or may persist for a long run. The heart rate is generally between 100 and 200 beats/min. Very rapid ventricular tachycardia with a sine-wave appearance is sometimes referred to as ventricular flutter and usually leads to ventricular fibrillation.
Sustained ventricular tachycardia is a life-threatening arrhythmia for tow major reasons. First, most patients are not able to maintain an adequate blood presure with this rapid a heart rate and quickly become hypotensive. Second, sustained ventricular tachycardia may degenerate into ventricular fibrillation, producing cardiac arrest.
The etiologic factors of ventricular tachycardia are the same as those discussed earlier with PVCs. The same list of reversible cause of PVCs also applies in evaluating patients with ventricular tachycardia.
In ventricular fibrillation, the ventricles do not beat in any coordinated fashion but instead fibrillate or twitch asynchronously and ineffectively. There is no cardiac output, and the patient becomes unconscious immediately. Ventricular fibrillation is one of the three major ECG patterns seen with cardiac arrest. The other two are asystole and electromechanical dissociation.
The ECG in ventricular fibrillation shows characteristic fibrillatory waves with an irregular pattern that may be either coarse or fine.
Ventricular fibrillation may occur in patients with heart disease of any type. It may be preceded by warning arrhythmias, such as PVCs or ventricular tachycardia, or it may occur spontaneously. Ventricular fibrillation may also occur in normal hearts, owing to the toxic effects of drugs such as epinephrine, during anesthesia, with lightning stroke, and so on.
ACCELERATED IDIOVENTRICULAR RHYTHM (AIVR)
AIVR is a ventricular arrhythmia that resembles a slow ventricular tachycardia with a rate between 50 and 100 to 110 beats/min. The ECG with AIVR shows wide QRS complexes without P waves. It is commonly seen with myocardial infarction and is usually self-limited.
TORSADES DE POINTES: A SPECIAL FORM OF VENTRICULAR TACHYCARDI
Torsades de pointes is the name of a recently described form of ventricular tachycardia in which the QRS complexes appears to rotate cyclically, pointing downward for several beats and then twisting and pointing upward in same lead.
This arrhythmia classically occurs in the setting of delayed ventricular repolarization, evidenced by prolongation of the QT interval or the presence of prominent U wave. Reported causes include
Drug toxicity, particularly that due to quinidine and related antiarrhythmic agents
Electrolyte imbalance, including hypokalemia, hypomagnesemia, and hypocalcemia, which prolong repolarization
Miscellaneous factors such as complete heart block, hereditary QT prolongation syndrome, liquid protein diets, and myocardial ischemia
5 AV Heart Block
Heart block is the general term for atrio-ventricular (AV) conduction disturbances. Normally, the AV junction acts like an apparent bridge between the atria and the ventricles. The PR interval is between 0.12 and 0.2 second. Heart block occurs when there is impaired condition through the AV junction, either transiently or permanently. The mildest form of heart block is called first-degree heart block. The second-degree heart block is an intermediate grade of AV conduction disturbance. The most extreme form of heart block is called third-degree or complete heart block. Here the AV junction does not conduct any stimuli between the atria and ventricles.
First-degree AV block- the RP interval is uniformly prolonged beyond 0.2 second.
Second-degree AV block- there are two subtypes:
Wenckebach (mobitz type 1) AV block – increasing prolongation of the PR interval occurs until a P wave is blocked and not followed by a QRS complex. This produces a distinctive clustering of QRS complexes separated by a pause resulting from the dropped beat. The QRS clustering is known as group beating.
Mobitz type II AV block – a series of P waves occurs without QRS complexes, followed by a P wave and a QRS complex; for example, with 3:1 block, every third P wave is conducted and followed by a QRS complex. The conduced P waves have the same PR interval.
Third-degree (complete) AV block – this shows the following:
The atria and ventricle beat independently because stimuli cannot pass through the AV junction.
The atrial rate is faster than the ventricular rate.
The PR interval constantly changes.
Chapter 2 Ultrasonic Examination
All diagnostic ultrasound applications are based on the detection and display of acoustic energy reflected from interfaces within the body. These interactions provide the information needed to generate high-resolution, gray-scale images of the body as well as display information related to blood flow. The unique imaging attributes of ultrasound have made it an important and versatile medical imaging tool.
In the past 50 years, along with the development of acoustic theory, computer technology, the diagnostic ultrasound, which developed from the earliest A-mode and M-mode one-dimensional ultrasound imaging, B-mode two-dimensional imaging to the dynamic real-time three-dimensional imaging, from grey-scale ultrasound to color Doppler flow imaging, has experienced unprecedented advancement.
Since diagnostic ultrasound now is used not only to observe appearance, but also detect human organ function and blood flow, it plays an important role in clinical diagnosis and treatment. Ultrasonic diagnostics has now become a mature subject and an important branch in the medical imaging.
Physics of Ultrasound
In nature, acoustic frequencies span a range from less than 1 Hz to more than 100,000 Hz(100 kHz). Human hearing is limited to the lower part of this range, extending from 20 to 20,000 Hz. Ultrasound differs from audible sound only in its frequency, and is more than 20,000 Hz.
Sound frequencies used for diagnostic applications typically range from 2.5 to 10 MHz.
In tissue and fluids, ultrasound propagation is along the direction of particle movement(longitudinal waves). The propagation velocity of sound, c, is related to frequency and wavelength by the following simple equation:
The velocity at which the wave moves through tissue varies greatly and is affected by the physical properties of the tissue. Propagation velocity is largely determined by the resistance of the medium to compression. This, in turn, is influenced by the density of the medium and its stiffness or elasticity. Propagation velocity is increased by increasing stiffness and reduced by increasing density. In the body, propagation velocity may be regarded as constant for a given tissue and is not affected by the frequency or wavelength of the sound. In the body, the propagation velocity of sound is assumed to be 1540 m/sec. This value is the average of measurements obtained from normal tissue. Although this is a value representation of most soft tissues, some tissues, such as aerated lung and fat, have propagation velocities significantly less than 1540 m/sec, and others, such as bone, have greater velocities.
Acoustic impedance, Z, is determined by product of the density, ρ, of the medium propagating the sound and the propagation velocity, c, of sound in that medium(Z=ρc). At the junction of tissues or materials with different acoustic impedance, acoustic interfaces are present.
When ultrasound strikes an acoustic interface, the direction of propagation will change, which produces reflection, refraction and scatter.
Figure 1 Incidence, reflection and refraction
Absorption and Attenuation
Contributing to the attenuation of sound are the transfer of energy to tissue resulting in heating (absorption), and the removal of energy by reflection and scattering. Attenuation depends on the insonating frequency as well as the nature of the attenuating medium. High frequencies are attenuated more rapidly than lower frequencies, and transducer frequency is a major determinant of the useful depth from which information can be obtained with ultrasound. Attenuation determines the efficiency with which ultrasound penetrates a specific tissue and varies considerably in normal tissues.
When high-frequency sound impinges on a stationary interface, the reflected ultrasound has essentially the same frequency or wavelength as the transmitted sound. If, however, the reflecting interface is moving with respect to the sound beam emitted from the transducer, there is a change in the frequency of the sound scattered by the moving object. This change in frequency is directly proportional to the velocity of the reflecting interface relative to the transducer and is a result of the Doppler effect. The relationship of the returning ultrasound frequency to the velocity of the reflector is described by the Doppler equation:
ΔF is the Doppler frequency shift; FR is the frequency of sound reflected from the moving target; FT is the frequency of sound emitted from the transducer; v is the velocity of the target toward the transducer; and c is the velocity of sound in the medium; θ is the angle between the axis of flow and the incident ultrasound beam.
A transducer is any device that converts one form of energy to another. In the case of ultrasound, the transducer converts electric energy to mechanical energy and vice versa. In diagnostic ultrasound systems, the transducer servers two functions. It converts the electric energy provided by the transmitter to the acoustic pulses directed into the patient. The transducer also serves as the receiver of reflected echoes, converting weak pressure changes into electric signals for processing. Ultrasound transducers use piezoelectricity. Piezoelectric materials have the unique ability to respond to the action of an electric field by changing shape. They also have the property of generating electric potentials when compressed. Changing the polarity of a voltage applied to the transducer changes the thickness of the transducer, which expands and contracts as the polarity changes. This results in the generation of mechanical pressure waves that can be transmitted into the body. The piezoelectric effect also results in the generation of small potential across the transducer when the transducer is struck by returning echoes. Positive pressures cause a small polarity to develop across the transducer; negative pressure during the rarefaction portion of the acoustic wave produces the opposite polarity across the transducer. These tiny polarity changes and the voltages associated with them are the source or all of the information processed to generate an ultrasound image or Doppler display.
Figure 2 Piezoelectric effect
(1)Positive pressure (2) negative pressure
Mode and properties of ultrasonography
A-mode devices displayed the voltage produced across the transducer by the backscattered echo as a vertical deflection on the face of an oscilloscope. The horizontal sweep of the oscilloscope was calibrated to indicate the distance from the transducer to the reflecting surface. In this form of display, the strength or amplitude of the reflected sound is indicated by the height of the vertical deflection displayed on the oscilloscope. With A-mode ultrasound, only the position and strength of a reflecting structure are recorded. At present, it is used for diagnosis of intracranial diseases.
M-mode ultrasound, displays echo amplitude and shows the position of moving reflectors. M-mode imaging uses the brightness of the display to indicate the intensity of the reflected signal. The time base of the display can be adjusted to allow for varying degrees of temporal resolution, as dictated by clinical application. M-mode ultrasound is interpreted by assessing motion patterns of specific reflectors and determining anatomic relationships from characteristics patterns of motion. Today, the major application of M-mode display is in the evaluation of the rapid motion of cardiac valves and of cardiac chamber and vessel walls, which is called M-mode echocardiography.
The mainstay of imaging with ultrasound is provided by real-time, gray-scale, B-mode display in which variations in display intensity or brightness are used to indicate reflected signals of differing amplitude. To generate a two-dimensional (2-D) image, multiple ultrasound pulses are sent down a series of successive scan lines, building a 2-D representation of echoes arising from the object being scanned. When an ultrasound image is displayed on a black background, signals of greatest intensity appear as white; absence of signal is shown as black; and signals of intermediate intensity appear as shades of gray.
Real-time ultrasound produces the impression of motion by generating a series of individual 2-D images at rates from 24 to 30 frames per second. Real-time, 2-D, B-mode ultrasound is now the major method for ultrasound imaging throughout the body and is the most common form of B-mode display.
In contrast to A-mode, M-mode, and B-mode gray-scale ultrasonography, which display the information from tissue interfaces, Doppler ultrasound instruments according to the Doppler effect are optimized to display flow information regarding the direction and velocity of blood. More commonly, the Doppler shift data are displayed in graphic form as a time-varying plot of the frequency spectrum of the returning signal.
The most common form of Doppler ultrasound to be used for radiology applications is color Doppler flow imaging. In color flow imaging systems, flow information determined from Doppler measurements is displayed as a feature of the image itself. Signal phase provides information about the presence and direction of motion, and changes in echo signal frequency relate to the velocity of the target. Backscattered signals from red blood cells are displayed in color as a function of their motion toward or away from the transducer, and the degree of the saturation of the color is used to indicate the relative velocity of the moving red cells.
CW: chest wall; ARVW: anterior right ventricular wall; RVOT: right ventricular outflow tract; RV: right ventricle; PA: pulmonary artery; PV: pulmonary valve; RA: right atrium; LA: left atrium; LAW: left anterior wall; LVOT: left ventricular outflow tract; LV: left ventricle; IVS: interventricular septum; AO: aorta; AOV: aortic valve; AMVL: anterior mitral valve leaflet; PMVL: posterior mitral valve leaflet; ATVL: anterior tricuspid valve leaflet; Ch: chorda tendineae; PPM: posterior papillary muscle; En: endocardium; EP: epicardium; L: lung; APS: atriopulmonic sulcus
Cross sectional echocardiography
Long-axis view: transecting the heart parallel to the long axis of the heart. We can see right ventricle, left ventricle, left atrium, interventricular septum, aorta, aorta valve and mitral valve in this view.
Short-axis view at the level of the base of the heart: transecting the heart perpendicular to the long axis of the heart. Aorta, aorta valve, left atrium, right atrium, tricuspid valve, right ventricle, right ventricular outflow tract, pulmonary valve, left coronary artery can be seen in this view.
Short-axis view at the level of mitral valve: left ventricle, right ventricle, interventricular septum and mitral orifice can be seen in this view.
Subcostal four-chamber view: with the transducer in the subcostal position. Left and right atrium, left and right ventricle, interatrial septum and interventricular septum is visualized in this view.
four-chamber and five-chamber view over the cardiac apex: left and right atrium, left and right ventricle, interatrial septum, interventricular septum, mitral valve, tricuspid valve, aortic root and left ventricular outflow tract.
① Clinical manifestation
Classic mitral stenosis accounts for 40% of rheumatic heart diseases. The main pathological change is the orifice stenosis caused by the thickness and adhesion of the valve leaflets.
2-D ultrasound provides a spatial image of the valve and allows direct mearsurement of the valve orifice.
M-mode: Great Wall-like picture
Anterior and posterior leaflets of the mitral valve move in the same direction
Color Doppler flow imaging: turbulent flow at the mitral orifice during diastole
P ulsed Doppler: the peak velocities are increased
Figure 4 M-mode ECG of mitral stenosis
Increased thickness of MV; no A wave; decreased EF; Great Wall-like picture (arrow); anterior and posterior move in the same direction
Atrial septal defect
① Clinical manifestation
Atrial septal defect is the most common disease in the congenitive cardiomyopathy. It is classified into the ostium secundum type and the primum type defect according to the involved region of the atrial septum.
2-D ultrasound: direct sign is the presence of an atrial septal defect; indirect sign is the enlargement of right atrium and ventricle, and the widened pulmonary artery.
M-mode: dialated right ventricle and abnormal septal motion
Pulsed-Doppler: diastolic turbulent flow with upward spectrum
C olor Doppler flow imaging: red-encoded blood passing from the left atrium to the right atrium through the defect.
Figure 5 B-mode echocardiography of atrial septal defect
The defect of atrial septum and enlarged RA and RV is shown in the four-chamber view
USG of normal liver
Size: the upper border of the liver lies at the level of the fifth intercostal space at the midclavicular line. The lower border extends to or slightly below the costal margin.
The longitudinal diameter of the liver in the midclavicular line <13cm
The mean anteroposterior diameter of the left lobe at the left costal border <5cm
Echotexture: homogeneous, contains fine-level echoes, and is either minimally hyperechoic or isoechoic compared to the normal renal cortex. The liver is hypoechoic or isoechoic compared to the spleen.
Portal vein: an echogenic wall
travels along to the liver long axis, like “工” in the left lobe of liver.
Hepatic vein: right, middle and left hepatic veins which all drain into the inferior vena cava
right hepatic vein runs in the intersegments of the the right lobe, divides of anterior and posterior segments of the right lobe
middle hepatic vein courses in the main lobe fissure, separating right and left lobe
left hepatic vein runs in the intersegments of the left lobe, divides of medial and lateral segments of the left lobe