Page 213 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

Cardiac Arrhythmias propagation velocities, and shorter durations.
This leads to re-excitation of myocardial areas
Arrhythmias are pathological changes in car- that have already been stimulated (re-entry cy-
diac impulse generation or conduction that can cles). Ventricular fibrillation can be caused by
be visualized by ECG. Disturbances of impulse electrical accidents and can usually be cor-
generation change the sinus rhythm. Sinus rected by timely electrical defibrillation.
tachycardia (! A2): The sinus rhythm rises to
100 min –1 or higher e.g., due to physical exer- Extrasystoles (ES). The spread of impulses arising
from an supraventricular (atrial or nodal) ectopic
tion, anxiety, fever (rise of about 10 beats/min focus to the ventricles can disturb their sinus rhythm,
for each 1 !C) or hyperthyroidism. Sinus brady- leading to a supraventricular arrhythmia. When atrial
–1
cardia: The heart rate falls below 60 min (e.g., extrasystoles occur, the P wave on the ECG is dis-
due to hypothyroidism). In both cases the torted while the QRS complex remains normal.
rhythm is regular whereas in sinus arrhythmias Nodal extrasystoles lead to retrograde stimulation
Cardiovascular System pendent (heart rate increases during inspira- shortly thereafter (! B1 right). Since the SA node
of the atria, which is why the P wave is negative and is
the rate varies. In adolescents, sinus arrhyth-
either masked by the QRS complex or appears
mias can be physiological and respiration-de-
often is discharged by a supraventricular extrasys-
tion and decreases during expiration).
tole, the interval between the R wave of the extrasys-
Ectopic pacemakers. Foci in the atrium, AV
tole (R ES) and the next normal R wave increases by
the amount of time needed for the stimulus to travel
node or ventricles can initiate abnormal ec-
topic (heterotopic) impulses, even when nor-
from the focus to the SA node. This is called the post-
" RR and (RR ES + R ESR) # 2 RR (! B1).
node is taking place (! A). The rapid discharge
Ventricular (or infranodal) ES (! B2, B3) distorts
8 mal (nomotopic) stimulus generation by the SA extrasystole pause. The RR intervals are as follows: R ESR
of impulses from an atrial focus can induce
the QRS complex of the ES. If the sinus rate is slow
atrial tachycardia (serrated baseline instead of enough, the ES will cause a ventricular contraction
normal P waves), which triggers a ventricular between two normal heart beats; this is called an in-
–1
response rate of up to 200 min . Fortunately, terpolated (or interposed) ES (! B2). If the sinus rate
only every second or third stimulus is trans- is high, the next sinus stimulus reaches the ventricles
mitted to the ventricles because part of the im- while they are still refractory from the ectopic excita-
pulses arrive at the Purkinje fibers (longest tion. Ventricular contraction is therefore blocked
until the next sinus stimulus arrives, resulting in a
APs) during their refractory period. Thus, compensatory pause, where RR ES + R ESR = 2 RR.
Purkinje fibers act as impulse frequency filters.
Elevated atrial contraction rates of up to Disturbances of impulse conduction: AV block.
350 min –1 are defined as atrial flutter, and all First-degree AV block: prolonged but otherwise
higher rates are defined as atrial fibrillation normal impulse conduction in the AV node (PQ
(up to 500 min ). Ventricular stimulation is interval " 0.2 sec); second-degree AV block:
–1
then totally irregular (absolute arrhythmia). only every second (2:1 block) or third (3:1
Ventricular tachycardia is a rapid train of im- block) impulse is conducted. Third-degree AV
pulses originating from a ventricular (ectopic) block: no impulses are conducted; sudden car-
focus, starting with an extrasystole (ES) (! B3; diac arrest may occur (Adam–Stokes attack or
second ES). The heart therefore fails to fill ade- syncope). Ventricular atopic pacemakers then
quately, and the stroke volume decreases. This take over (ventricular bradycardia with nor-
can lead to ventricular fibrillation (extremely mal atrial excitation rate), resulting in partial
frequent and uncoordinated contractions; or total disjunction of QRS complexes and
! B4). Because of failure of the ventricle to P waves (! B5). The heart rate drops to 40 to
transport blood, ventricular fibrillation can be 55 min –1 when the AV node acts as the pace-
fatal. maker (! B5), and to a mere 25 to 40 min –1
Ventricular fibrillation mainly occurs when when tertiary (ventricular) pacemakers take
an ectopic focus fires during the relative re- over. Artificial pacemakers are then used.
fractory period of the previous AP (called the Bundle branch block: disturbance of conduction in
“vulnerable phase” synchronous with T wave
200 on the ECG; ! p. 193 A). The APs triggered a branch of the bundle of His. Severe QRS changes
occur because the affected side of the myocardium is
during this period have smaller slopes, lower activated by the healthy side via abnormal pathways.
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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