The student, through understanding normal cardiac function, diagnoses and appreciates the consequences of common cardiac abnormalities:
Detects common cardiac arrhythmias from the electrocardiogram, identifies their physiological bases, and describes their physiological consequences.
Lists 4 common cardiac valve abnormalities for the left side of the heart and describes the alterations in intracardiac and arterial pressures, flow patterns, and heart sounds that accompany them.
Identifies the consequences of similar valve abnormalities for the right side of the heart.
Recall that effective, efficient ventricular pumping action depends on proper cardiac function in 5 basic aspects. This chapter focuses on the abnormalities in 3 of these aspects: (1) abnormal cardiac excitation and rhythmicity, (2) valvular stenosis (inadequate valve opening), and (3) valvular insufficiency (incomplete valve closure). Discussion of abnormalities in myocardial force production and cardiac filling is presented in Chapter 11. The material presented here is an introduction to the more common cardiac electrical and cardiac valve dysfunctions, with an emphasis on the primary physiological consequences of these abnormal situations.
ELECTRICAL ABNORMALITIES AND ARRHYTHMIAS
Many cardiac excitation problems can be diagnosed from the information in a single lead of an electrocardiogram. The lead II electrocardiogram traces at the top of Figures 5–1 and 5–2 are identified as normal sinus rhythms based on the following characteristics: (1) the frequency of QRS complexes is approximately 1/s, indicating a normal beating rate; (2) the shape of the QRS complex is normal for lead II and its duration is less than 120 ms, indicating rapid depolarization of the ventricles via normal conduction pathways; (3) each QRS complex is preceded by a P wave of proper configuration, indicating sinoatrial (SA) nodal origin of the excitation; (4) the PR interval is less than 200 ms, indicating proper conduction delay of the impulse propagation through the atrioventricular (AV) node; (5) the QT interval is less than half of the R-to-R interval, indicating normal ventricular repolarization; and (6) there are no extra P waves, indicating that no AV nodal conduction block is present. The subsequent electrocardiographic tracings in Figures 5–1 and 5–2 represent irregularities commonly found in clinical practice. Examination of each of these traces with the above characteristics in mind will aid in the differential diagnosis.
The physiological consequences of abnormal excitation and conduction in the heart depend on whether the electrical abnormality evokes a tachycardia, which will limit the time for cardiac filling between beats; evokes a bradycardia, which is inadequate to support sufficient cardiac output; or decreases the coordination of myocyte contraction, which will reduce stroke volume.
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