Postinfarction conduction abnormalities: Difference between revisions

Jump to navigation Jump to search
No edit summary
 
(28 intermediate revisions by 2 users not shown)
Line 1: Line 1:
__NOTOC__
__NOTOC__
{{SI}}
{{ST elevation myocardial infarction}}
{{CMG}} {{AE}} {{RT}}
{{CMG}}; {{AE}} {{RT}}


==Overview==
==Overview==
Ischemia of the conduction system results in conduction abnormalities in the heart. Atrioventricular blocks are common in inferior infarcts and intraventricular blocks are common in anterior wall infarcts.
[[Ischemia]] of the conduction system results in conduction abnormalities of the heart. [[Atrioventricular blocks]] are common in inferior infarcts and intraventricular blocks are common in anterior wall infarcts.


==Classification==
==Classification==
Conduction abnormalities post-infarction can be classified as atrioventricular blocks and intraventricular blocks.
Conduction abnormalities post-infarction can be classified as atrioventricular blocks and intraventricular blocks.
* Atriventricular blocks:
** [[Second degree block]]s (Mobitz type I and II)
** [[Third degree AV block]]
* Intraventricular block:
** [[Bundle branch block]]s
** [[Bifascicular block]]s
These blocks can be temporary or persistent.
==Pathophysiology==
===Atrioventricular blocks===
* High grade [[AV block]]s (second and third degree blocks) occur in up to 20% of patients with [[inferior MI]].
* AV blocks are common in inferior infarcts than in anterior infarcts by three fold. The frequency is even more when the right ventricle is involved in the inferior infarcts than when not involved.
* In majority of inferior infarcts the blocks are transient.
* Presence of Av blocks in anterior infarcts indicates a larger infarction and there is a significant increase in short term mortality compared to patients without AV block.
* Mechanisms on AV block include:
** In inferior MI:
*** Increased [[parasympathetic]] tone
*** Ischemic stunning of [[AV node]]
*** Increased local [[potassium]] due to [[infarction]]
*** Increased local release of [[adenosine]]
===Intraventricular blocks===
* [[Bundle branch block]]s and [[fascicular block]]s are markers for larger infarctions.
* Up to 22% of patients with new bundle branch block will progress to high grade AV block.
* New bifascicular block with or without [[PR prolongation]] has the highest likelihood of developing [[complete heart block]].
* In approximately 25% of patients the conduction abnormalities are temporary.
* Mechanism of intraventricular blocks involves extensive necrosis of infra-His conduction system.
Patients with transient blocks have similar mortality compared to patients without blocks.  Mortality rates for patients with [[bundle branch blocks]] (BBB) are significantly increased and patients who develop BBB in hospital have higher mortality rates than those who present with BBB.
==Treatment==
===Pacemaker recommendations in patients with post-infarction conduction abnormalities===
* Transcutaneous:
** New [[bundle branch block]] (BBB)
** [[RBBB]] or [[LBBB]] with [[first degree AV block]]
* Transvenous:
** [[Mobitz Type II Block|Mobitz type II block]]
** Alternating BBB
** [[Bifascicular block]] with [[first degree AV block]]
* Permanent:
** Persistent [[second degree AV block]] with bilateral [[bundle branch block]]
** [[Complete heart block]]
** Transient second degree or [[third degree heart block|third degree block]] with bundle branch block
** Symptomatic second or third degree AV block
==References==
{{Reflist|2}}
[[Category:Disease]]
[[Category:Cardiology]]
[[Category:Ischemic heart diseases]]
[[Category:Intensive care medicine]]
[[Category:Emergency medicine]]
[[Category:Up-To-Date]]
[[Category:Up-To-Date cardiology]]
[[Category:Mature chapter]]
{{WH}}
{{WS}}

Latest revision as of 14:15, 31 January 2013

Acute Coronary Syndrome Main Page

ST Elevation Myocardial Infarction Microchapters

Home

Patient Information

Overview

Pathophysiology

Pathophysiology of Vessel Occlusion
Pathophysiology of Reperfusion
Gross Pathology
Histopathology

Causes

Differentiating ST elevation myocardial infarction from other Diseases

Epidemiology and Demographics

Risk Factors

Triggers

Natural History and Complications

Risk Stratification and Prognosis

Pregnancy

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

EKG Examples

Chest X Ray

Cardiac MRI

Echocardiography

Coronary Angiography

Treatment

Pre-Hospital Care

Initial Care

Oxygen
Nitrates
Analgesics
Aspirin
Beta Blockers
Antithrombins
The coronary care unit
The step down unit
STEMI and Out-of-Hospital Cardiac Arrest
Pharmacologic Reperfusion
Reperfusion Therapy (Overview of Fibrinolysis and Primary PCI)
Fibrinolysis
Reperfusion at a Non–PCI-Capable Hospital:Recommendations
Mechanical Reperfusion
The importance of reducing Door-to-Balloon times
Primary PCI
Adjunctive and Rescue PCI
Rescue PCI
Facilitated PCI
Adjunctive PCI
CABG
Management of Patients Who Were Not Reperfused
Assessing Success of Reperfusion
Antithrombin Therapy
Antithrombin therapy
Unfractionated heparin
Low Molecular Weight Heparinoid Therapy
Direct Thrombin Inhibitor Therapy
Factor Xa Inhibition
DVT prophylaxis
Long term anticoagulation
Antiplatelet Agents
Aspirin
Thienopyridine Therapy
Glycoprotein IIbIIIa Inhibition
Other Initial Therapy
Inhibition of the Renin-Angiotensin-Aldosterone System
Magnesium Therapy
Glucose Control
Calcium Channel Blocker Therapy
Lipid Management

Pre-Discharge Care

Recommendations for Perioperative Management–Timing of Elective Noncardiac Surgery in Patients Treated With PCI and DAPT

Post Hospitalization Plan of Care

Long-Term Medical Therapy and Secondary Prevention

Overview
Inhibition of the Renin-Angiotensin-Aldosterone System
Cardiac Rehabilitation
Pacemaker Implantation
Long Term Anticoagulation
Implantable Cardioverter Defibrillator
ICD implantation within 40 days of myocardial infarction
ICD within 90 days of revascularization

Case Studies

Case #1

Case #2

Case #3

Case #4

Case #5

Postinfarction conduction abnormalities On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Postinfarction conduction abnormalities

CDC on Postinfarction conduction abnormalities

Postinfarction conduction abnormalities in the news

Blogs on Postinfarction conduction abnormalities

Directions to Hospitals Treating ST elevation myocardial infarction

Risk calculators and risk factors for Postinfarction conduction abnormalities

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

Overview

Ischemia of the conduction system results in conduction abnormalities of the heart. Atrioventricular blocks are common in inferior infarcts and intraventricular blocks are common in anterior wall infarcts.

Classification

Conduction abnormalities post-infarction can be classified as atrioventricular blocks and intraventricular blocks.

These blocks can be temporary or persistent.

Pathophysiology

Atrioventricular blocks

  • High grade AV blocks (second and third degree blocks) occur in up to 20% of patients with inferior MI.
  • AV blocks are common in inferior infarcts than in anterior infarcts by three fold. The frequency is even more when the right ventricle is involved in the inferior infarcts than when not involved.
  • In majority of inferior infarcts the blocks are transient.
  • Presence of Av blocks in anterior infarcts indicates a larger infarction and there is a significant increase in short term mortality compared to patients without AV block.
  • Mechanisms on AV block include:

Intraventricular blocks

  • Bundle branch blocks and fascicular blocks are markers for larger infarctions.
  • Up to 22% of patients with new bundle branch block will progress to high grade AV block.
  • New bifascicular block with or without PR prolongation has the highest likelihood of developing complete heart block.
  • In approximately 25% of patients the conduction abnormalities are temporary.
  • Mechanism of intraventricular blocks involves extensive necrosis of infra-His conduction system.

Patients with transient blocks have similar mortality compared to patients without blocks. Mortality rates for patients with bundle branch blocks (BBB) are significantly increased and patients who develop BBB in hospital have higher mortality rates than those who present with BBB.

Treatment

Pacemaker recommendations in patients with post-infarction conduction abnormalities

References

Template:WH Template:WS