Pacemaker syndrome pathophysiology: Difference between revisions
Created page with "__NOTOC__ {{Pacemaker syndrome}} {{CMG}}; {{AE}} {{RT}} ==Pathophysiology== The loss of physiologic timing of atrial and [[ventricle (heart)..." |
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==Pathophysiology== | ==Pathophysiology== | ||
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}} | 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}} | ||
===Loss of Atrial Contraction=== | ===Loss of Atrial Contraction=== | ||
Revision as of 01:19, 9 February 2013
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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]
Pathophysiology
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.Closing </ref> missing for <ref> tag[1]
Cannon A Waves
Atrial contraction against a closed tricuspid valve can cause pulsation in the neck and abdomen, headache, cough, and jaw pain.[2][3]
Increased Atrial Pressure
Ventricular pacing is associated with elevated right and left atrial pressures, as well as elevatedpulmonary venous and pulmonary arterial pressures, which can lead to symptomatic pulmonary andhepatic congestion.[4]
Increased Production of Natriuretic Peptides
Patients with pacemaker syndrome exhibit increased plasma levels of ANP. That's due to increase inleft atrial pressure and left ventricular filling pressure, which is due to decreased cardiac output caused by dyssynchrony in atrial and ventricular contraction. ANP and BNP are potent arterial and venous vasodilators that can override carotid andaortic 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.[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 ofatrial contraction in relation to ventricular contraction. Nevertheless, many conditions other than VA conduction promote AV dyssynchrony.[5][8][9][2][3]
This will further decrease blood pressure, and secondary increase in ANP and BNP.[6][7]
References
- ↑ 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] - ↑ 2.0 2.1 Invalid
<ref>tag; no text was provided for refs namedpmid1413181 - ↑ 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) - ↑ Invalid
<ref>tag; no text was provided for refs namedpmid7511223 - ↑ 5.0 5.1 Invalid
<ref>tag; no text was provided for refs namedpmid9164889 - ↑ 6.0 6.1 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) - ↑ 7.0 7.1 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) - ↑ Invalid
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