Pacemaker syndrome pathophysiology: Difference between revisions
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Sara Usman (talk | contribs) →Pathophysiology: <ref name="pmid3910239">{{cite journal| author=Ausubel K, Boal BH, Furman S| title=Pacemaker syndrome: definition and evaluation. | journal=Cardiol Clin | year= 1985 | volume= 3 | issue= 4 | pages= 587-94 | pmid=3910239 | doi= | pmc= |
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==Pathophysiology== | ==Pathophysiology== | ||
'''<u>Pacemaker Syndrome Mechanisms:</u>''' | |||
* Loss of AV synchrony | |||
* Valvular incompetence | |||
* Asynchronous ventricular contractions | |||
* Ventriculoatrial conduction | |||
* Echo beats | |||
* Arrhythmias | |||
===Loss of Atrial Contraction=== | ===Loss of Atrial Contraction=== | ||
Inappropriate pacing in patients with decreased [[ventricle (heart)|ventricular]] compliance, which may be caused by diseases such as [[hypertensive heart disease|hypertensive cardiomyopathy]], [[hypertrophic cardiomyopathy]], [[restrictive cardiomyopathy]], and [[aging]], can result in loss of [[atrium (heart)|atrial]] contraction and significantly reduces [[cardiac output]]. Because in such cases the atrias are required to provide 50% of [[cardiac output]], which normally provides only 15% - 25% of [[cardiac output]].<ref name="pmid1413181">{{cite journal |author=Petersen HH, Videbaek J |title=[The pacemaker syndrome] |language=Danish |journal=Ugeskr. Laeg. |volume=154 |issue=38 |pages=2547–51 |year=1992 |month=September |pmid=1413181 |doi= |url=}}</ref><ref name="pmid1442632">{{cite journal |author=Gross JN, Keltz TN, Cooper JA, Breitbart S, Furman S |title=Profound "pacemaker syndrome" in hypertrophic cardiomyopathy |journal=Am. J. Cardiol. |volume=70 |issue=18 |pages=1507–11 |year=1992 |month=December |pmid=1442632 |doi= 10.1016/0002-9149(92)90313-N|url=http://linkinghub.elsevier.com/retrieve/pii/0002-9149(92)90313-N |format=}} {{dead link|date=May 2010}}</ref> | Inappropriate pacing in patients with decreased [[ventricle (heart)|ventricular]] compliance, which may be caused by diseases such as [[hypertensive heart disease|hypertensive cardiomyopathy]], [[hypertrophic cardiomyopathy]], [[restrictive cardiomyopathy]], and [[aging]], can result in loss of [[atrium (heart)|atrial]] contraction and significantly reduces [[cardiac output]]. Because in such cases the atrias are required to provide 50% of [[cardiac output]], which normally provides only 15% - 25% of [[cardiac output]].<ref name="pmid1413181">{{cite journal |author=Petersen HH, Videbaek J |title=[The pacemaker syndrome] |language=Danish |journal=Ugeskr. Laeg. |volume=154 |issue=38 |pages=2547–51 |year=1992 |month=September |pmid=1413181 |doi= |url=}}</ref><ref name="pmid1442632">{{cite journal |author=Gross JN, Keltz TN, Cooper JA, Breitbart S, Furman S |title=Profound "pacemaker syndrome" in hypertrophic cardiomyopathy |journal=Am. J. Cardiol. |volume=70 |issue=18 |pages=1507–11 |year=1992 |month=December |pmid=1442632 |doi= 10.1016/0002-9149(92)90313-N|url=http://linkinghub.elsevier.com/retrieve/pii/0002-9149(92)90313-N |format=}} {{dead link|date=May 2010}}</ref> | ||
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{{main|Atrial natriuretic peptide}} | {{main|Atrial natriuretic peptide}} | ||
{{main|Brain natriuretic peptide}} | {{main|Brain natriuretic peptide}} | ||
Patients with [[artificial pacemaker|pacemaker]] [[syndrome]] exhibit increased plasma levels of [[atrial natriuretic peptide|ANP]]. That's due to increase in [[left atrium|left atrial]] pressure and [[left ventricle|left ventricular]] filling pressure, which is due to decreased [[cardiac output]] caused by dyssynchrony in [[atrium (heart)|atrial]] and [[ventricle (heart)|ventricular]] contraction in ventricle paced rhythms. [[atrial natriuretic peptide|ANP]] and [[brain natriuretic peptide|BNP]] are potent [[artery|arterial]] and [[vein|venous]] [[vasodilation|vasodilators]] that can override [[common carotid artery|carotid]] and [[aorta|aortic]] [[baroreflex|baroreceptor reflex]]es attempting to compensate for decreased [[blood pressure]]. Usually patients with [[cannon A waves|cannon a waves]] have higher plasma levels of [[atrial natriuretic peptide|ANP]] than those without [[cannon A waves|cannon a waves]].<ref name="pmid9164889"/><ref name="pmid9036762">{{cite journal |author=Theodorakis GN, Panou F, Markianos M, Fragakis N, Livanis EG, Kremastinos DT |title=Left atrial function and atrial natriuretic factor/cyclic guanosine monophosphate changes in DDD and VVI pacing modes |journal=Am. J. Cardiol. |volume=79 |issue=3 |pages=366–70 |year=1997|month=February |pmid=9036762 |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914997892855 |doi=10.1016/S0002-9149(97)89285-5}}</ref><ref name="pmid1334465">{{cite journal |author=Theodorakis GN, Kremastinos DT, Markianos M, Livanis E, Karavolias G, Toutouzas PK |title=Total sympathetic activity and atrial natriuretic factor levels in VVI and DDD pacing with different atrioventricular delays during daily activity and exercise |journal=Eur. Heart J.|volume=13 |issue=11 |pages=1477–81 |year=1992 |month=November |pmid=1334465 |doi= |url=http://eurheartj.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=1334465}}</ref><ref name="pmid22923937">{{cite journal |author=Mollazadeh R, Mohimi L, Zeighami M, Fazelifar A, Haghjoo M |title=Hemodynamic effect of atrioventricular and interventricular dyssynchrony in patients with biventricular pacing: Implications for the pacemaker syndrome |journal=J Cardiovasc Dis Res |volume=3 |issue=3 |pages=200–3 |year=2012 |month=July |pmid=22923937 |pmc=3425026 |doi=10.4103/0975-3583.98892 |url=}}</ref> | Patients with [[artificial pacemaker|pacemaker]] [[syndrome]] exhibit increased plasma levels of [[atrial natriuretic peptide|ANP]]. That's due to increase in [[left atrium|left atrial]] pressure and [[left ventricle|left ventricular]] filling pressure, which is due to decreased [[cardiac output]] caused by dyssynchrony in [[atrium (heart)|atrial]] and [[ventricle (heart)|ventricular]] contraction in ventricle paced rhythms. [[atrial natriuretic peptide|ANP]] and [[brain natriuretic peptide|BNP]] are potent [[artery|arterial]] and [[vein|venous]] [[vasodilation|vasodilators]] that can override [[common carotid artery|carotid]] and [[aorta|aortic]] [[baroreflex|baroreceptor reflex]]es attempting to compensate for decreased [[blood pressure]]. Usually patients with [[cannon A waves|cannon a waves]] have higher plasma levels of [[atrial natriuretic peptide|ANP]] than those without [[cannon A waves|cannon a waves]].<ref name="pmid9164889" /><ref name="pmid9036762">{{cite journal |author=Theodorakis GN, Panou F, Markianos M, Fragakis N, Livanis EG, Kremastinos DT |title=Left atrial function and atrial natriuretic factor/cyclic guanosine monophosphate changes in DDD and VVI pacing modes |journal=Am. J. Cardiol. |volume=79 |issue=3 |pages=366–70 |year=1997|month=February |pmid=9036762 |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914997892855 |doi=10.1016/S0002-9149(97)89285-5}}</ref><ref name="pmid1334465">{{cite journal |author=Theodorakis GN, Kremastinos DT, Markianos M, Livanis E, Karavolias G, Toutouzas PK |title=Total sympathetic activity and atrial natriuretic factor levels in VVI and DDD pacing with different atrioventricular delays during daily activity and exercise |journal=Eur. Heart J.|volume=13 |issue=11 |pages=1477–81 |year=1992 |month=November |pmid=1334465 |doi= |url=http://eurheartj.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=1334465}}</ref><ref name="pmid22923937">{{cite journal |author=Mollazadeh R, Mohimi L, Zeighami M, Fazelifar A, Haghjoo M |title=Hemodynamic effect of atrioventricular and interventricular dyssynchrony in patients with biventricular pacing: Implications for the pacemaker syndrome |journal=J Cardiovasc Dis Res |volume=3 |issue=3 |pages=200–3 |year=2012 |month=July |pmid=22923937 |pmc=3425026 |doi=10.4103/0975-3583.98892 |url=}}</ref> | ||
===VA Conduction=== | ===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 [[atrium (heart)|atrial]] contraction in relation to [[ventricle (heart)|ventricular]] [[muscle contraction|contraction]]. Nevertheless, many conditions other than VA conduction promote AV dyssynchrony.<ref name="pmid9164889"/><ref name="pmid1413181" /><ref name="pmid2032410"/> 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. | A major cause of AV dyssynchrony is VA conduction. VA conduction, sometimes referred to as retrograde conduction, leads to delayed, nonphysiologic timing of [[atrium (heart)|atrial]] contraction in relation to [[ventricle (heart)|ventricular]] [[muscle contraction|contraction]]. Nevertheless, many conditions other than VA conduction promote AV dyssynchrony.<ref name="pmid9164889" /><ref name="pmid1413181" /><ref name="pmid2032410" /> 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 secondary increase in [[atrial natriuretic peptide|ANP]] and [[brain natriuretic peptide|BNP]].<ref name="pmid9036762"/><ref name="pmid1334465"/> In patients with heart failure it has been shown that institution of biventricular pacing mode has been associated with a better cardiac output. | This will further decrease [[blood pressure]], and secondary increase in [[atrial natriuretic peptide|ANP]] and [[brain natriuretic peptide|BNP]].<ref name="pmid9036762" /><ref name="pmid1334465" /> In patients with heart failure it has been shown that institution of biventricular pacing mode has been associated with a better cardiac output. | ||
==References== | ==References== | ||
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{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} | ||
<ref name="pmid3910239">{{cite journal| author=Ausubel K, Boal BH, Furman S| title=Pacemaker syndrome: definition and evaluation. | journal=Cardiol Clin | year= 1985 | volume= 3 | issue= 4 | pages= 587-94 | pmid=3910239 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3910239 }}</ref> | |||
[[Category:Electrophysiology]] | [[Category:Electrophysiology]] | ||
[[Category:Cardiology]] | [[Category:Cardiology]] | ||
[[Category:Disease]] | [[Category:Disease]] | ||
[[Category:Needs overview]] | [[Category:Needs overview]] | ||
Revision as of 01:06, 10 April 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2]
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.[1]
Pathophysiology
Pacemaker Syndrome Mechanisms:
- 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 hypertensive cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, and aging, can result in loss of atrial contraction and significantly reduces cardiac output. Because in such cases the atrias are required to provide 50% of cardiac output, which normally provides only 15% - 25% of cardiac output.[2][3]
Cannon A Waves
Atrial contraction against a closed tricuspid valve can cause pulsation in the neck and abdomen, headache, cough, and jaw pain.[2][4]
Increased Atrial Pressure
Ventricular pacing is associated with dyssynchrony between the atria and ventricles causing an elevated right and left atrial pressures, as well as elevated pulmonary venous and pulmonary arterial pressures, which can in turn lead to symptomatic pulmonary and hepatic congestion.
Increased Production of Natriuretic Peptides
Patients with pacemaker syndrome exhibit increased plasma levels of ANP. That's due to increase in left atrial pressure and left ventricular filling pressure, which is due to decreased cardiac output caused by dyssynchrony in atrial and ventricular contraction in ventricle paced rhythms. ANP and BNP are potent arterial and venous vasodilators that can override carotid and aortic baroreceptor reflexes attempting to compensate for decreased blood pressure. Usually patients with cannon a waves have higher plasma levels of ANP than those without cannon a waves.[1][5][6][7]
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.[1][2][4] 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 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
- ↑ 1.0 1.1 1.2 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) - ↑ 2.0 2.1 2.2 Petersen HH, Videbaek J (1992). "[The pacemaker syndrome]". Ugeskr. Laeg. (in Danish). 154 (38): 2547–51. PMID 1413181. Unknown parameter
|month=ignored (help) - ↑ 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] - ↑ 4.0 4.1 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) - ↑ 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) - ↑ 6.0 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) - ↑ 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)
- ↑ Ausubel K, Boal BH, Furman S (1985). "Pacemaker syndrome: definition and evaluation". Cardiol Clin. 3 (4): 587–94. PMID 3910239.
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