Pacemaker syndrome pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2] Raviteja Guddeti, M.B.B.S. [3] Tayebah Chaudhry[4]

Overview

The loss of physiologic timing of atrial and ventricular contractions, or sometimes called AV dyssynchrony, leads to different mechanisms of symptoms production. This altered ventricular contraction will decrease cardiac output, and in turn, will lead to systemic hypotensive reflex response with varying symptoms.

Pathophysiology

Pacemaker Syndrome Mechanisms:

AV dyssynchrony leads to various symptoms with different mechanisms of symptom production.

  • Loss of AV synchrony
  • Valvular incompetence
  • Asynchronous ventricular contractions
  • Ventriculoatrial conduction
  • Echo beats
  • Arrhythmias

Loss of Atrial Contraction

Inappropriate pacing in patients with decreased ventricular compliance, which may be caused by diseases such as:

All of the above causes result in loss of atrial contraction and significantly reduces cardiac output because in such cases the atria are required to provide 50% of cardiac output, which is normally only 15% - 25%.[1][2]

Cannon A Waves

Increased Atrial Pressure

Increased Production of Natriuretic Peptides

VA Conduction

  • A major cause of AV dyssynchrony is VA conduction.
  • VA conduction, sometimes referred to as retrograde conduction, leads to delayed, nonphysiologic timing of atrial contraction in relation to ventricular contraction.
  • Nevertheless, many conditions other than VA conduction promote AV dyssynchrony.[4][1][3]
  • Ventricular paced rhythms cause a reduction in cardiac output by causing a nonphysiologic depolarization of the ventricles.
  • Depolarization patterns and contraction are altered when pacemaker leads are placed in the apex of the right ventricle.
  • This will further decrease blood pressure and cause a secondary increase in ANP and BNP.[5][6]
  • In patients with heart failure it has been shown that institution of biventricular pacing mode has been associated with a better cardiac output.

References

  1. 1.0 1.1 1.2 Petersen HH, Videbaek J (1992). "[The pacemaker syndrome]". Ugeskr. Laeg. (in Danish). 154 (38): 2547–51. PMID 1413181. Unknown parameter |month= ignored (help)
  2. Gross JN, Keltz TN, Cooper JA, Breitbart S, Furman S (1992). "Profound "pacemaker syndrome" in hypertrophic cardiomyopathy". Am. J. Cardiol. 70 (18): 1507–11. doi:10.1016/0002-9149(92)90313-N. PMID 1442632. Unknown parameter |month= ignored (help)[dead link]
  3. 3.0 3.1 Schüller H, Brandt J (1991). "The pacemaker syndrome: old and new causes". Clin Cardiol. 14 (4): 336–40. doi:10.1002/clc.4960140410. PMID 2032410. Unknown parameter |month= ignored (help)
  4. 4.0 4.1 Ellenbogen KA, Gilligan DM, Wood MA, Morillo C, Barold SS (1997). "The pacemaker syndrome—a matter of definition". Am. J. Cardiol. 79 (9): 1226–9. doi:10.1016/S0002-9149(97)00085-4. PMID 9164889. Unknown parameter |month= ignored (help)
  5. 5.0 5.1 Theodorakis GN, Panou F, Markianos M, Fragakis N, Livanis EG, Kremastinos DT (1997). "Left atrial function and atrial natriuretic factor/cyclic guanosine monophosphate changes in DDD and VVI pacing modes". Am. J. Cardiol. 79 (3): 366–70. doi:10.1016/S0002-9149(97)89285-5. PMID 9036762. Unknown parameter |month= ignored (help)
  6. 6.0 6.1 Theodorakis GN, Kremastinos DT, Markianos M, Livanis E, Karavolias G, Toutouzas PK (1992). "Total sympathetic activity and atrial natriuretic factor levels in VVI and DDD pacing with different atrioventricular delays during daily activity and exercise". Eur. Heart J. 13 (11): 1477–81. PMID 1334465. Unknown parameter |month= ignored (help)
  7. Mollazadeh R, Mohimi L, Zeighami M, Fazelifar A, Haghjoo M (2012). "Hemodynamic effect of atrioventricular and interventricular dyssynchrony in patients with biventricular pacing: Implications for the pacemaker syndrome". J Cardiovasc Dis Res. 3 (3): 200–3. doi:10.4103/0975-3583.98892. PMC 3425026. PMID 22923937. Unknown parameter |month= ignored (help)

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