Pacemaker syndrome pathophysiology: Difference between revisions
No edit summary |
|||
| Line 3: | Line 3: | ||
{{CMG}}; {{AE}} {{RT}} | {{CMG}}; {{AE}} {{RT}} | ||
== | ==Overview== | ||
The loss of [[physiology|physiologic]] timing of [[atrium (heart)|atrial]] and [[ventricle (heart)|ventricular]] contractions, or sometimes called AV dyssynchrony, leads to different mechanisms of [[symptom]]s production. This altered ventricular contraction will decrease [[cardiac output]], and in turn will lead to systemic hypotensive reflex response with varying symptoms.<ref name="pmid9164889">{{cite journal |author=Ellenbogen KA, Gilligan DM, Wood MA, Morillo C, Barold SS |title=The pacemaker syndrome—a matter of definition |journal=Am. J. Cardiol. |volume=79 |issue=9 |pages=1226–9 |year=1997 |month=May |pmid=9164889|doi= 10.1016/S0002-9149(97)00085-4|url=http://linkinghub.elsevier.com/retrieve/pii/S0002914997000854}}</ref> | The loss of [[physiology|physiologic]] timing of [[atrium (heart)|atrial]] and [[ventricle (heart)|ventricular]] contractions, or sometimes called AV dyssynchrony, leads to different mechanisms of [[symptom]]s production. This altered ventricular contraction will decrease [[cardiac output]], and in turn will lead to systemic hypotensive reflex response with varying symptoms.<ref name="pmid9164889">{{cite journal |author=Ellenbogen KA, Gilligan DM, Wood MA, Morillo C, Barold SS |title=The pacemaker syndrome—a matter of definition |journal=Am. J. Cardiol. |volume=79 |issue=9 |pages=1226–9 |year=1997 |month=May |pmid=9164889|doi= 10.1016/S0002-9149(97)00085-4|url=http://linkinghub.elsevier.com/retrieve/pii/S0002914997000854}}</ref> | ||
==Pathophysiology== | |||
===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> | ||
Revision as of 00:26, 11 February 2013
|
Pacemaker syndrome Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Pacemaker syndrome pathophysiology On the Web |
|
American Roentgen Ray Society Images of Pacemaker syndrome pathophysiology |
|
Risk calculators and risk factors for Pacemaker syndrome pathophysiology |
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
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]
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)
- Pages with citations using unsupported parameters
- CS1 maint: Multiple names: authors list
- CS1 maint: Unrecognized language
- All articles with dead external links
- Articles with dead external links from May 2010
- Articles with invalid date parameter in template
- Electrophysiology
- Cardiology
- Disease
- Needs overview