Atropine -- paradoxical bradycardia
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        Worsening of AVB with the administration of atropine has been
described even in patients with Wenckebach (1,2) block.  Garry's
observation that low doses (< 0.5 mg in adults or < 0.1 mg in children) may
cause a paradoxical slowing of heart rate through a central
parasympathomimetic effect is correct (3) but, I do not think, explains
why Type II second degree block is more likely than type I block to
experience paradoxic slowing at higher dosages (i.e., nodal vs infranodal
block).   One (old) study (4) suggested that atropine may may different
effects on sinus node automaticity as opposed AV nodal conduction.  If
this conclusion has beeen borne out by more recent literature I would
wonder whether using low dose (< 0.5 mg) atropine would both slow the
sinus rate (avoiding the problem of increasing refractoriness at the AVN
that occurs with increased sinus rates in some cases of Type II block) and
enhance AV conduction.  Just speculation.

        Although many references described worsening conduction in cases
of Wenckebach with atropine I have been unable to find any original
references to the oft-quoted admonition against using it for infranodal
blocks (Type II).  You might look at ref 5 (which I don't have handy) which
used atropine to  establish the site of block in cases of 2:1 AVB where
the surface ECG is often not helpful in predicting it's origin.

H. Louzon MD

(1)
Castellanos A  Garcia HG  Rozanski JJ  Zaman L  Pefkaros K  Myerburg RJ
Atropine-induced multilevel block in acute inferior myocardial
  infarction. A possible indication for prophylactic pacing.
Pacing Clin Electrophysiol (1981 Sep) 4(5):528-37
The degree of A-V block increased after intravenous administration of
  atropine in 10 nondigitalized patients with acute inferior myocardial
  infarction who had narrow QRS complexes during periods of 1:1 A-V
  conduction. Short episodes of 3:1, 4:1 and 5:1 A-V block were seen to
  emerge: (a) in 6 patients, directly from Wenckebach periods; (b) in 3
  patients, from alternating Wenckebach periods; and (c) in 1 patient,
  from a 3:2 Wenckebach period which led to a short-lived alternating
  Wenckebach period. Apparently, the predominance of the chronotropic
  effects on the sinus node over the dromotropic effects on the A-V
  node led to a tachycardia-dependent (more ischemic than vagal)
  process, exposing or producing multi- (two, three or four) level
  block involving the A-V node (and perhaps the His bundle).
  Subsequently, therapeutic pacing was instituted in 9/10 patients
  because they developed spontaneous symptomatic advanced A-V block.
  Therefore, it is possible that the early effects of atropine
  identified a narrowly-defined subset of patients in whom prophylactic
  pacing may be indicated. However, more studies are necessary to
  corroborate these assumptions.

(2)
Lewin RF, Kusniec J, Sclarovsky S, Strasberg B, Arditti A, Pinchas A,
Agmon J
Alternating Wenckebach periods in acute inferior myocardial infarction:
clinical, electrocardiographic, and therapeutic characterization.
Pacing Clin Electrophysiol 1986 Jul;9(4):468-75
We report on twelve patients with alternating Wenckebach periods (AWP)
occurring during an acute inferior myocardial infarction (AIMI). There were
nine males and three females, with a mean age of 61 years (range, 43 to 75).
AWP appeared during the first 48 hours of the AIMI in 10 patients and on the
fourth day of hospitalization in two patients. AWP occurred spontaneously in
nine patients and following the administration of atropine in the remaining
three patients. Mean systolic blood pressure significantly decreased during
AWP as compared to the period preceding or following the bradyarrhythmia (93
+/- 42 mmHg vs 123 +/- 37 mmHg, p less than 0.02). Killip functional class
was significantly higher during AWP as compared to the period preceding or
following the bradyarrhythmia (2.1 +/- 1.2 vs 1.5 +/- 0.8, p less than
0.02). Pacemaker therapy was initiated prophylactically in two patients,
because of syncope in six, because of hemodynamic deterioration in two, and
for syncope and hemodynamic deterioration in two. Three patients died in
cardiogenic shock despite pacemaker therapy. No evidence of right
ventricular infarction was seen in the patients. Atropine administration
during AWP significantly increased the sinus rate and significantly
decreased the ventricular rates and the systolic blood pressure. In
addition, three patients developed long bouts of paroxysmal AV block.
Isoproterenol administration improved AV conduction in one patient, caused
no change in two patients and induced non-sustained ventricular tachycardia
in three patients. In conclusion, AWP occurring during AIMI is a symptomatic
bradyarrhythmia associated with hemodynamic deterioration.(ABSTRACT
TRUNCATED AT 250 WORDS)

(3)
Epstein AE, Hirschowitz BI, Kirklin JK, Kirk KA, Kay GN, Plumb VJ
Evidence for a central site of action to explain the negative chronotropic
effect of atropine: studies on the human transplanted heart.
J Am Coll Cardiol 1990 Jun;15(7):1610-7
The chronotropic response to atropine is biphasic; low doses cause slowing
of the sinus rate and high doses cause acceleration. Although it is accepted
that atropine functions as a competitive antagonist at high doses, the
mechanism of the negative chronotropic response at low doses is
controversial. Specifically, it is unclear whether the effect is mediated
centrally or peripherally. Since at the time of cardiac replacement all
central nervous system connections to the heart are severed, the
transplanted heart is a unique model for separating these effects. Graded
doses of atropine sulfate (0.5, 1.0, 2.0, 4.0, 8.0 and 40.0 micrograms/kg
body weight) were administered to 12 human heart transplant recipients to
test the hypothesis that the bradycardiac effect of low dose atropine is
centrally mediated. The baseline sinus cycle lengths of the decentralized
donor and innervated native sinus nodes were 694 +/- 20 and 733 +/- 27 ms,
respectively. At the 0.5 and 1.0 microgram/kg doses, the cycle lengths of
the native sinus node increased by 29.1 +/- 13.5 and 23.1 +/- 14.2 ms,
respectively. At the 2.0 micrograms/kg dose the sinus cycle length again
shortened to control. At the maximal dose of atropine the sinus cycle length
shortened by 138.3 +/- 29.7 ms compared with control. In contrast, the
decentralized donor sinus node exhibited a flat dose response to atropine.
High dose atropine (40 micrograms/kg) caused no change in the donor heart's
atrial effective refractory period, corrected sinus node recovery time, or
sinoatrial conduction time measured by either the Strauss or the Narula
method.(ABSTRACT TRUNCATED AT 250 WORDS)

(4)
Das G, Talmers FN, Weissler AM
New observations on the effects of atropine on the sinoatrial and
atrioventricular nodes in man.
Am J Cardiol 1975 Sep;36(3):281-5
Previous observations of slowing of the heart rate after administration of
atropine in doses smaller than 0.4 mg and recent reports of development of
rhythm disorders in patients with acute myocardial infarction given atropine
prompted us to evaluate systematically the effects of various doses of
atropine (0.1 to 0.8 mg) on the response of the sinoatrial (S-A) and
atrioventricular (A-V) nodes in healthy volunteers. The response of the S-A
node to atropine was characteristically bimodal, slowing at smaller doses
and accelerating at larger doses. In contrast, the A-V node showed
acceleration of conduction in response to all doses of atropine used. A
hypothesis based on current understanding of the electrophysiologic
parameters governing impulse formation and impulse conduction is advanced to
explain the apparent paradox in the S-A and A-V nodal responses to small
doses of atropine. The results suggest the need for caution and continuous
rhythm monitoring when giving atropine to patients with acute myocardial
infarction.

(5)
Mangiardi LM  Bonamini R  Conte M  Gaita F  Orzan F  Presbitero P
  Brusca A
Bedside evaluation of atrioventricular block with narrow QRS
  complexes: usefulness of carotid sinus massage and atropine
  administration.
Am J Cardiol (1982 Apr 1) 49(5):1136-45
Second-degree intra-His bundle block is frequently of type I
  (Wenckebach periods) or 2:1. In this situation, the surface
  electrocardiogram does not permit distinction between intranodal
  (atrioventricular [A-V] and subnodal (intra-His) block. This study
  examined the value of bedside carotid sinus massage and atropine
  administration in diagnosing the site of block from the standard
  electrocardiogram in subjects with chronic A-V block and narrow QRS
  complexes. Fifteen patients had intra-His bundle block and 10 had
  intranodal block. The combination of two tests correctly located the
  site of block in 22 subjects, and was noncontributory in 3. Thirteen
  of the 15 intra-His bundle blocks and 9 of the 10 intranodal blocks
  were properly identified; in three cases the results were
  nondiagnostic, but no wrong diagnoses were made. The noninvasive
  bedside method of carotid sinus massage and the use of atropine
  permit both the localization and the determination of the type of
  block in the majority of cases of second degree A-V block and narrow
  QRS complexes. In a proper clinical context they can obviate the need
  for invasive electrophysiologic studies.