Discussion
This case interested us due to the combination of bradycardia and a
hypertensive emergency that was refractory to medical treatments. BP
markedly improved following treatment of CHB with permanent pacemaker
implantation. A summary of BP readings during the clinical course are
shown in figure 3. It was interesting to note that the lowest diastolic
BP before pacing was 51 mmHg and immediately rose after initiation of
pacing to 80 mmHg. Pulse pressure before pacing was between 100-140 mmHg
and after pacing fell to around 50 mmHg. We suspected this was a direct
effect of increasing HR, shortening the diastolic period and limiting
the fall in arterial pressure before the next cardiac cycle. We
confirmed before pacing that the large pulse pressure did not have an
alternative cause such as aortic regurgitation.
Systolic BP also decreased by 20 mmHg following device implantation
without the need to restart the GTN infusion and even once the effects
of sedation had worn off. A combination of factors may have played a
part however the contrast was striking. Whilst it proved impossible to
wean off GTN prior to pacing, it was no longer required at all
afterwards. The reduction in diastolic filling time could have reduced
ventricular preload and stroke volume (SV) to some extent, but it is
difficult to say how much this contributed to the reduction of systolic
BP.
BP is a function of cardiac output (CO) calculated by the formula CO =
HR x SV. A lower HR should therefore reduce CO, but this is mitigated by
a rise in SV due to increased diastolic filling time and ventricular
preload. Historically, it has been described that as HR slows, pulse
pressure widens i.e. diastolic BP drops and systolic BP
increases.[2,3] The haemodynamic effects of artificial pacing in CHB
have also been described, suggesting that increasing HR lowers
SV.[4] Conversely, SV has been shown to increase on induction of CHB
in the animal model.[5]
RV pacing may directly affect SV by induction of dyssynchronous
myocardial contraction. Prior to pacing in this case, the escape rhythm
was junctional in nature, hence LV activation will have been via the
normal His-Purkinje system. Change in the pattern of regional myocardial
strain by pacing has been demonstrated in dogs by MRI imaging. SV was
significantly reduced by RV apical pacing due to dyssynchronous LV
myocardial contraction.[6] Another study looking at lengthening AV
delay during pacing showed an immediate increase in both SV and BP.
However, BP quickly declined after a few seconds whilst SV was
maintained, suggesting compensatory peripheral vasodilatation.[7]
Artificial pacing algorithms to shorten AV delay have been proposed as a
treatment for hypertension, however this has so far remained restricted
to clinical studies.[8,9]
BP is also dependent on systemic vascular resistance (SVR) under
autonomic control via baroreceptors. Cardiogenic shock induces a
sympathetic response to compensate with peripheral vasoconstriction and
increases SVR acutely.[10] Chronically raised SVR may have played a
role in this case with evidence of longstanding hypertension,
echocardiography revealing moderate concentric LV hypertrophy and there
was heavy proteinuria. SVR is also known to increase with advanced age
associated with atherosclerosis.[11,12] Higher SVR may have
exaggerated the BP response to increased SV.
We noted only one previous case report of bradycardia and malignant
hypertension. A case of a 65-year-old man presenting with left upper
limb weakness, bilateral foot paraesthesia and headache with a BP of
240/90 and an ECG showing CHB at 39 bpm. Brain imaging was normal, and
symptoms resolved after BP control with intravenous GTN. After permanent
pacing BP improved to 140/80. The authors attributed better BP control
to reduced diastolic filling time and SV.[13]
In hindsight, pacemaker implantation was unduly delayed due to a
combination of inter-speciality logistics and lab availability. Greater
efforts to enable earlier pacemaker implantation may have led to sooner
control of BP and shorter hospital stay, and this is a learning point.
We could also make mention of alternative pacing sites such as RV
outflow tract, RV septum or His bundle pacing which may have preserved
more physiological ventricular contraction, and although the
haemodynamic effects have been studied with relation to intracardiac
function, the effect in this context on systemic BP needs further
study.[14]