Long PR interval: Difference between revisions
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{{SK}} Long PR, prolonged PR, prolonged PR interval, PR prolongation, PR interval lengthened | {{SK}} Long PR, long P-R, prolonged PR, prolonged P-R, prolonged PR interval, prolonged P-R interval, PR prolongation, P-R prolongation, PR interval lengthened, P-R interval lengthened | ||
==Overview== | ==Overview== | ||
Long PR interval is prolongation of the time required by impulse generated at the normal atrial pacemaker (SA node) to conduct via the normal conduction pathway and activate the ventricle. Normally the conduction time is 0.12 to 0.21 seconds (normal PR interval). A PR interval above 0.21 seconds is called as long PR interval. PR interval is usually longer when the conduction of atrial impulse through AV node is slowed either as a consequence of withdrawal of sympathetic tone or due to an increase in vagal inputs. It is also important to emphasize that long PR intervals can exist in subjects who are otherwise normal.<ref name=" | Long [[PR interval]] is prolongation of the time required by impulse generated at the normal atrial pacemaker ([[SA node]]) to conduct via the [[Electrical conduction system of the heart|normal conduction pathway]] and activate the [[ventricle]]. Normally the conduction time is 0.12 to 0.21 seconds (normal PR interval). A PR interval above 0.21 seconds is called as long PR interval. PR interval is usually longer when the conduction of [[atrial]] impulse through [[AV node]] is slowed either as a consequence of withdrawal of [[Sympathetic nervous system|sympathetic tone]] or due to an increase in [[vagal]] inputs. It is also important to emphasize that long PR intervals can exist in subjects who are otherwise normal.<ref name="pmid13190611">{{cite journal | author = PACKARD JM, GRAETTINGER JS, GRAYBIEL A | title = Analysis of the electrocardiograms obtained from 1000 young healthy aviators; ten year follow-up | journal = [[Circulation]] | volume = 10 | issue = 3 | pages = 384–400 | year = 1954 | month = September | pmid = 13190611 | doi = | url = http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=13190611 | issn = }}</ref> In [[atrioventricular dissociation]] where both atria and ventricle beat independently without conducting each others impulse either antegradely or retrogradely, PR interval may vary from beat to beat. In some beats, the PR interval may be long. | ||
==Pathophysiology== | ==Pathophysiology== | ||
===First Degree AV Block=== | ===First Degree AV Block=== | ||
First degree AV block may be due to conduction delay in the AV node, His-Purkinje system (made up by the bundle of His and the Purkinje fibers), or a combination of the two. The majority of cases are due to a | [[First degree AV block]] may be due to conduction delay in the AV node, [[His-Purkinje system]] (made up by the [[bundle of His]] and the [[Purkinje fibers]]), or a combination of the two. The majority of cases are due to a dysfunction of the AV node; however, when first degree heart block coexists with a [[bundle-branch block]], the cause is more likely to be a conduction delay in the His-Purkinje system. Although there are no missed beats in first degree AV block with all impulses from atria being transmitted to ventricle and thus resulting in a regular ventricular beat rhythm, the conduction delay involving AV node alone typically causes a long PR interval. If the conduction delay also involves the His-Purkinje system, the long PR interval will be associated with [[wide QRS complex]]. | ||
===Mobitz Type I Second Degree AV Block=== | ===Mobitz Type I Second Degree AV Block=== | ||
The classic site of block in Mobitz type I second degree block is the AV node (70%-75%). In the remaining 25%-30% of the cases the site is infra-nodal (His bundle, bundle branches or fascicles). Mobitz type I is composed of two variations, classic and atypical, based on periodicity. Classic variety usually occurs within the AV node. There is a gradually increasing PR interval and eventually a dropped beat. It is also accompanied by a gradually decreasing R-R interval. The PR interval is usually shortest in the initial beat and gradually increases ending in a dropped beat and the cycle repeats. This classic Wenckebach phenomenon occurs usually with ratios of 3:2, 4:3 or 5:4. This results in grouped beating. In Atypical variant of Wenckebach pattern the conduction ratios usually exceed 6:5 or 7:6 and the last few beats of the cycle, before a dropped beat, show a relatively constant PR interval (maximum variation of 0.02 sec among them). The beats after the dropped beat again show gradually prolonging PR intervals.<ref name="pmid737095">{{cite journal |author=El-Sherif N, Aranda J, Befeler B, Lazzara R |title=Atypical Wenckebach periodicity simulating Mobitz II AV block |journal=Br Heart J |volume=40 |issue=12 |pages=1376–83 |year=1978 |month=December |pmid=737095 |pmc=483582 |doi= |url=}}</ref> | The classic site of block in [[Second degree AV block pathophysiology#Mobitz Type I|Mobitz type I second degree block]] is the AV node (70%-75%). In the remaining 25%-30% of the cases the site is infra-nodal (His bundle, bundle branches or fascicles). Mobitz type I is composed of two variations, classic and atypical, based on periodicity. Classic variety usually occurs within the AV node. There is a gradually increasing PR interval and eventually a dropped beat. It is also accompanied by a gradually decreasing R-R interval. The PR interval is usually shortest in the initial beat and gradually increases the ending in a dropped beat and the cycle repeats. This classic [[Wenckebach phenomenon]] occurs usually with ratios of 3:2, 4:3 or 5:4. This results in grouped beating. In Atypical variant of Wenckebach pattern the conduction ratios usually exceed 6:5 or 7:6 and the last few beats of the cycle, before a dropped beat, show a relatively constant PR interval (maximum variation of 0.02 sec among them). The beats after the dropped beat again show gradually prolonging PR intervals.<ref name="pmid737095">{{cite journal |author=El-Sherif N, Aranda J, Befeler B, Lazzara R |title=Atypical Wenckebach periodicity simulating Mobitz II AV block |journal=Br Heart J |volume=40 |issue=12 |pages=1376–83 |year=1978 |month=December |pmid=737095 |pmc=483582 |doi= |url=}}</ref> | ||
===Atrial Premature Beats=== | ===Atrial Premature Beats=== | ||
In atrial premature beats, also known as [[atrial premature contractions]] or [[premature atrial contractions]], with increasing prematurity, the partial penetration of the premature beat (concealed) prolongs the refractory period of the AV node and causes prolongation of the PR interval of the next sinus beat. The PR interval progressively increases until the effective refractory period of AV node is reached, when the atrial premature beats get blocked within the node and | In [[atrial premature beats]], also known as [[atrial premature contractions]] or [[premature atrial contractions]], with increasing prematurity, the partial penetration of the premature beat (concealed) prolongs the [[refractory period]] of the AV node and causes prolongation of the PR interval of the next sinus beat. The PR interval progressively increases until the effective refractory period of AV node is reached, when the atrial premature beats get blocked within the node and non-conducted.<ref name="pmid4102931">{{cite journal | author = Damato AN, Lau SH | title = Concealed and supernormal atrioventricular conduction | journal = [[Circulation]] | volume = 43 | issue = 6 | pages = 967–70 | year = 1971 | month = June | pmid = 4102931 | doi = | url = http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=4102931 | issn = }}</ref> | ||
===Pseudo-Long PR Interval in Atrioventricular Dissociation=== | ===Pseudo-Long PR Interval in Atrioventricular Dissociation=== | ||
In [[Atrioventricular dissociation]], the atrial impulse does not conduct to the ventricle, but the atrium and the ventricle may separately beat at similar or different rates and the PR interval may vary from beat to beat. In some beats, the PR interval may be long. Although this may appear to be a sinus rhythm with a long PR interval, there is no true impulse conduction between the atrium and ventricle, and hence the name "pseudo long PR interval". | In [[Atrioventricular dissociation]], the atrial impulse does not conduct to the ventricle, but the atrium and the ventricle may separately beat at similar or different rates and the PR interval may vary from beat to beat. In some beats, the PR interval may be long. Although this may appear to be a [[sinus rhythm]] with a long PR interval, there is no true impulse conduction between the atrium and ventricle, and hence the name "pseudo long PR interval".<ref name="pmid11993309">{{cite journal | author = Levy MN, Edflstein J | title = The mechanism of synchronization in isorhythmic A-V dissociation. II. Clinical studies | journal = [[Circulation]] | volume = 42 | issue = 4 | pages = 689–99 | year = 1970 | month = October | pmid = 11993309 | doi = | url = http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=11993309 | issn = }}</ref><ref name="pmid13473052">{{cite journal | author = MILLER R, SHARRETT RH | title = Interference dissociation | journal = [[Circulation]] | volume = 16 | issue = 5 | pages = 803–29 | year = 1957 | month = November | pmid = 13473052 | doi = | url = http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=13473052 | issn = }}</ref> | ||
===Trifascicular | ===Trifascicular Block=== | ||
On ECG, trifascicular block may manifest with a long PR interval. Trifascicular block involves conduction delay in the right bundle branch plus delay in the main left bundle branch or in both the left anterior and the left posterior fascicles. The diagnosis of trifascicular block requires an electrocardiographic pattern of bifascicular block plus evidence of prolonged conduction below the AV node. This below the AV node conduction delay is most specifically observed as a prolongation of the His-ventricular (HV) time in intracardiac recordings. PR interval includes conduction time in both AV node as well as in the intraventricular conduction system. Prolonged intraventricular conduction may be insufficient to extend the PR interval beyond normal limits, thus a prolonged PR interval can reflect delay in the AV node rather than in all three intraventricular fascicles. So the finding of a long PR interval in the presence of an electrocardiographic pattern consistent with bifascicular block is not diagnostic of trifascicular block, whereas the presence of a normal PR interval does not exclude this finding either. Thus long PR interval is only a concomitant finding in trifascicular block. | On ECG, [[trifascicular block]] may manifest with a long PR interval. Trifascicular block involves conduction delay in the right bundle branch plus delay in the main left bundle branch or in both the left anterior and the left posterior fascicles. The diagnosis of trifascicular block requires an electrocardiographic pattern of [[bifascicular block]] plus evidence of prolonged conduction below the AV node. This below the AV node conduction delay is most specifically observed as a prolongation of the His-ventricular (HV) time in intracardiac recordings. PR interval includes conduction time in both AV node as well as in the intraventricular conduction system. Prolonged intraventricular conduction may be insufficient to extend the PR interval beyond normal limits, thus a prolonged PR interval can reflect delay in the AV node rather than in all three intraventricular fascicles. So the finding of a long PR interval in the presence of an electrocardiographic pattern consistent with bifascicular block is not diagnostic of trifascicular block, whereas the presence of a normal PR interval does not exclude this finding either. Thus long PR interval is only a concomitant finding in trifascicular block. | ||
==Causes== | ==Causes== | ||
===Life Threatening Causes=== | ===Life Threatening Causes=== | ||
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. | Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. | ||
*[[Heart transplantation|Acute cardiac allograft rejection]] | |||
*[[Acute myocardial infarction]] | |||
*[[Bacterial endocarditis]] | |||
*[[Complete heart block]] | |||
*[[Diabetic ketoacidosis]] | |||
*[[Digitalis toxicity]] | |||
*[[Hypokalemia]] | |||
*[[Myocardial rupture]] | |||
*[[Organophosphate poisoning]] | |||
*[[Pulmonary embolism]] | |||
*[[hypothermia|Severe hypothermia]] | |||
===Common Causes=== | ===Common Causes=== | ||
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*[[Acid-base disturbances]] | |||
*[[Acute coronary syndrome]] | |||
*[[Acute rheumatic fever]] | |||
*[[Antiarrhythmic agents]] | |||
*[[Aortic stenosis]] | |||
*[[Bacterial endocarditis]] | |||
*[[Beta blockers]] | |||
*[[Calcium channel blockers]] | |||
*[[Cardiomyopathy]] | |||
*[[Chronic renal failure]] | |||
*[[Congestive heart failure]] | |||
*[[COPD]] | |||
*[[Coronary heart disease]] | |||
*[[Digitalis toxicity]] | |||
*[[Vasovagal syncope#Cardioinhibitory Response|Enhanced vagal tone]] | |||
*[[Hyperkalemia]] | |||
*[[Hypertensive heart disease]] | |||
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*[[Hyperthyroidism]] | |||
*[[Hypokalemia]] | |||
*[[Hypomagnesemia]] | |||
*[[Iatrogenic]] after surgical correction of [[VSD]], [[tetralogy of Fallot]], and [[endocardial cushion defect]] | |||
*[[Ischemic heart disease]] | |||
*[[Lev's disease]] | |||
*[[Mitral valve sclerosis]] | |||
*[[Myocardial infarction]] | |||
*[[Myocarditis]] | |||
*[[Obstructive sleep apnea]] | |||
*[[Pneumonia]] | |||
*[[Sick sinus syndrome]] | |||
*[[Sinus arrest]] | |||
*[[Sinus bradycardia]] | |||
*[[Sympathomimetic agents]] | |||
*[[Systemic lupus erythematosus]] | |||
*[[Valvular heart disease]] | |||
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===Causes Based on Pathophysiologic Origin=== | |||
====First Degree AV Block and Mobitz Type I Second Degree AV Block==== | |||
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*[[Acute myocardial infarction]] | |||
*[[Acute rheumatic fever]] | |||
*[[Amyloidosis]] | |||
*[[Ankylosing spondylitis]] | |||
*[[ASD]] | |||
*[[Bacterial endocarditis]] | |||
*[[Beta blockers]] | |||
*[[Calcific aortic stenosis]] | |||
*[[Calcium channel blockers]] | |||
*[[Cardiac glycosides]] | |||
*[[Cardiac tumors]] | |||
*[[Chagas disease]] | |||
*[[Cholinesterase inhibitors]] | |||
*[[Clonidine]] | |||
*[[Dermatomyositis]] | |||
*[[Digitalis]] | |||
*[[Dilated cardiomyopathy]] | |||
*[[Diltiazem]] | |||
*[[Diphtheria]] | |||
*[[Disopyramide]] | |||
*[[Dolasetron]] | |||
*[[Donepezil]] | |||
*[[Ebstein's anomaly]] | |||
*[[Emery-Dreifuss muscular dystrophy]] | |||
*[[Vasovagal syncope#Cardioinhibitory Response|Enhanced vagal tone]] | |||
*[[Eslicarbazepine acetate]] | |||
*[[Fabry disease]] | |||
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*[[Fesoterodine]] | |||
*[[Fingolimod]] | |||
*[[Glycogenosis type 2b]] | |||
*[[HCM]] | |||
*[[Neuromuscular disease|Hereditary neuromuscular disease]] | |||
*[[Hodgkin lymphoma]] | |||
*[[Hyperkalemia]] | |||
*[[Carotid sinus hypersensitivity|Hypersensitive carotid sinus syndrome]] | |||
*[[Hyperthyroidism]] | |||
*[[Hypokalaemia]] | |||
*[[Hypothermia]] | |||
*[[Ibutilide]] | |||
*[[Ischemic heart disease]] | |||
*[[Kearns-Sayre syndrome]] | |||
*[[Labetalol]] | |||
*[[Lacosamide]] | |||
*[[Lanatoside C]] | |||
*[[Lenegre's disease]] | |||
*[[Lev's disease]] | |||
*[[Lyme disease]] | |||
*[[Multiple myeloma]] | |||
*[[Muscular dystrophy]] | |||
*[[Myocardial bridging]] | |||
*[[Myocarditis]] | |||
*[[Myotonic dystrophy]] | |||
*[[Myxedema]] | |||
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*[[Neonatal lupus erythematosus]] | |||
*[[Paliperidone]] | |||
*[[aortic valve replacement|Post aortic valve replacement ]] | |||
*[[catheter ablation|Post catheter ablation for arrhythmias]] | |||
*[[Ventricular septal defect surgery|Post closure of a ventricular septal defect]] | |||
*[[mitral valve replacement|Post mitral valve replacement]] | |||
*[[Procainamide]] | |||
*[[Propoxyphene]] | |||
*[[Propranolol]] | |||
*[[Protozoa|Protozoal infection]] | |||
*[[Quinidine]] | |||
*[[Quinine]] | |||
*[[Rheumatic fever|Rheumatic mitral valve disease]] | |||
*[[Sarcoidosis]] | |||
*[[SLE]] | |||
*[[Systemic sclerosis]] | |||
*[[Terodiline]] | |||
*[[Tetralogy of Fallot]] | |||
*[[periodic paralysis|Thyrotoxic periodic paralysis]] | |||
*[[Tolterodine]] | |||
*[[Transposition of the great vessels]] | |||
*[[vagus nerve|Vagal maneuvers]] | |||
*[[Valsalva maneuver]] | |||
*[[Valvular heart disease]] | |||
*[[Verapamil]] | |||
*[[VSD]] | |||
{{col-end}} | |||
=== | ====Atrial Premature Beats==== | ||
{| | {{col-begin|width=80%}} | ||
| | {{col-break|width=33%}} | ||
*[[5-fluorouracil]] | |||
*[[Heart transplantation|Acute cardiac allograft rejection]] | |||
| | *[[Alpha interferon]] | ||
*[[Aminophylline]] | |||
*[[Amiodarone]] | |||
*[[Amlodipine]] | |||
*[[Bulimia nervosa]] | |||
*[[Calcium channel blocker]] | |||
*[[Cannabis]] | |||
*[[Cardiac transplantation]] | |||
*[[Cardioversion]] | |||
*[[Chronic renal failure]] | |||
*[[Cocaine]] | |||
*[[Congenital heart disease]] | |||
*[[Congestive heart failure]] | |||
*[[COPD]] | |||
*[[Coronary heart disease]] | |||
*[[Cushing's syndrome]] | |||
*[[Diabetic ketoacidosis]] | |||
*[[Dilated cardiomyopathy]] | |||
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*[[Diltiazem]] | |||
*[[Digoxin]] | |||
| | *[[Dobutamine]] | ||
*[[Ephedrine]] | |||
*[[Holiday heart syndrome]] | |||
*[[Hypercapnia]] | |||
*[[Hypertensive heart disease]] | |||
*[[Hypertrophic cardiomyopathy]] | |||
*[[Hypokalemia]] | |||
*[[Hypomagnesemia]] | |||
*[[Hypoxia]] | |||
*[[Idiopathic]] | |||
*[[Ischemic heart disease]] | |||
*[[Isoproterenol]] | |||
*[[Metabolic syndrome]] | |||
*[[Mitral regurgitation]] | |||
*[[Mitral stenosis]] | |||
*[[Mitral valve prolapse]] | |||
*[[Myocardial infarction]] | |||
*[[Myocarditis]] | |||
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*[[Obstructive sleep apnea]] | |||
*[[Artificial pacemaker|Pacemaker malfunction]] | |||
*[[Phenylephrine]] | |||
*[[Pneumonia]] | |||
*[[Pulmonary embolism]] | |||
*[[Pulmonary hypertension]] | |||
*[[Respiratory acidosis]] | |||
*[[Salbutamol]] | |||
*[[Subarachnoid hemorrhage]] | |||
*[[hyperthyroidism|Subclinical hyperthyroidism]] | |||
*[[Sympathomimetic agents]] | |||
*[[Tacrolimus]] | |||
*[[Takotsubo cardiomyopathy]] | |||
*[[Theophylline]] | |||
*[[Thiazides]] | |||
*[[Thyrotoxicosis]] | |||
*[[Transjugular intrahepatic portosystemic shunts]] | |||
*[[Valvular heart disease]] | |||
*[[Verapamil]] | |||
{{col-end}} | |||
| | |||
| | |||
| | |||
=== | ====Atrioventricular Dissociation==== | ||
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{{col-break|width=33%}} | {{col-break|width=33%}} | ||
*[[ | *[[Acetylcholine]] | ||
*[[ | *[[Aconitine]] | ||
*[[ | *[[Acute coronary syndrome]] | ||
*[[ | *[[Acute renal failure]] | ||
*[[Stroke|Acute stroke]] | |||
*[[Addisonian crisis]] | |||
*[[Alimemazine]] | |||
*[[All-trans retinoic acid]] | |||
*[[Almokalant]] | |||
*[[Amiodarone]] | |||
*[[Amitriptyline]] | |||
*[[Amphetamines]] | |||
*[[Amyloidosis]] | |||
*[[Andersen cardiodysrhythmic periodic paralysis]] | |||
*[[Ankylosing spondylitis]] | |||
*[[Anorexia nervosa]] | |||
*[[Anthracyclines]] | |||
*[[Antiarrhythmic drugs]] | |||
*[[Aortic stenosis]] | |||
*[[Arrhythmogenic right ventricular dysplasia]] | |||
*[[Arsenic trioxide]] | |||
*[[Asenapine]] | |||
*[[Aspergillosis]] | |||
*[[Astemizole]] | |||
*[[Atrial septal defect]] | |||
*[[Azimilide]] | |||
*[[Azithromycin]] | |||
*[[Bacterial endocarditis]] | |||
*[[Barbiturate]] | |||
*[[Becker muscular dystrophy]] | |||
*[[Bepridil]] | |||
*[[Berberine]] | |||
*[[Beta blockers]] | |||
*[[Bretylium]] | |||
*[[Brugada syndrome]] | |||
*[[Budipine]] | |||
*[[Bupivacaine]] | |||
*[[Calcium channel blockers]] | |||
*[[carbamate|Carbamate poisoning]] | |||
*[[Carbamazepine]] | |||
*[[Cardiac catheterization]] | |||
*[[Cardiac glycosides]] | |||
*[[cardiac tumor#heart in lymphomas|Cardiac lymphoma]] | |||
*[[Cardiac resynchronization therapy]] | |||
*[[Cardiac transplantation]] | |||
*[[Carotid sinus hypersensitivity|Cardioinhibitory syncope]] | |||
*[[Cardiomyopathy]] | |||
*[[Cardioversion]] | |||
*[[Catecholaminergic polymorphic ventricular tachycardia]] | |||
*[[Chagas disease]] | |||
*[[Chloroquine]] | |||
*[[Cholinesterase inhibitor]] | |||
*[[Churg-Strauss syndrome]] | |||
*[[Cibenzoline]] | |||
*[[Cimetidine]] | |||
*[[Cisapride]] | |||
*[[Citalopram]] | |||
*[[Claritin]] | |||
*[[Clomipramine]] | |||
*[[Clonidine]] | |||
*[[Clozapine]] | |||
*[[Cocaine]] | |||
*[[Complete heart block]] | |||
*[[Congenital heart disease]] | |||
*[[Congestive heart failure]] | |||
*[[COPD]] | |||
*[[Coronary artery bypass grafting]] | |||
*[[reperfusion injury|Coronary reperfusion therapy]] | |||
*[[Crizotinib]] | |||
*[[Cushing's syndrome]] | |||
*[[Daunorubicin]] | |||
*[[Defibrillation]] | |||
*[[Desipramine]] | |||
*[[Diabetic ketoacidosis]] | |||
*[[Digitalis toxicity]] | |||
*[[Dilated cardiomyopathy]] | |||
*[[Diltiazem]] | |||
*[[Diphenhydramine]] | |||
*[[Diphtheria]] | |||
*[[Disopyramide]] | |||
*[[Dofetilide]] | |||
*[[Dolasetron]] | |||
*[[Donepezil]] | |||
*[[Doxepin]] | |||
*[[Doxorubicin]] | |||
*[[Dronedarone]] | |||
*[[Droperidol]] | |||
*[[Ebstein's anomaly]] | |||
*[[Edrophonium]] | |||
*[[Emery-Dreifuss muscular dystrophy]] | |||
*[[Endocardial cushion defect]] | |||
*[[Vasovagal syncope#Cardioinhibitory Response|Enhanced vagal tone]] | |||
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*[[ | *[[Epirubicin]] | ||
*[[ | *[[Erb's dystrophy]] | ||
*[[ | *[[Eribulin mesylate]] | ||
*[[ | *[[Erythromycin]] | ||
*[[Fabry disease]] | |||
*[[Fluconazole]] | |||
*[[Flumazenil]] | |||
*[[Fontan procedure]] | |||
*[[Giant cell myocarditis]] | |||
*[[Granisetron]] | |||
*[[Grayanotoxin]] | |||
*[[Grepafloxacin]] | |||
*[[Guanethidine]] | |||
*[[Halofantrine]] | |||
*[[Haloperidol]] | |||
*[[Halothane]] | |||
*[[Hashimoto's thyroiditis]] | |||
*[[Heart surgery]] | |||
*[[Heat stroke]] | |||
*[[Hemochromatosis]] | |||
*[[Hodgkin disease]] | |||
*[[Hypereosinophilic syndrome]] | |||
*[[Hyperkalemia]] | |||
*[[Hypermagnesemia]] | |||
*[[Hypertensive heart disease]] | |||
*[[Hyperthyroidism]] | |||
*[[Hypertrophic cardiomyopathy]] | |||
*[[Hypocalcemia]] | |||
*[[Hypoglycemia]] | |||
*[[Hypokalemia]] | |||
*[[Hypomagnesemia]] | |||
*[[Hypothermia]] | |||
*[[Hypothyroidism]] | |||
*[[Hypoxia]] | |||
*[[Ibutilide]] | |||
*[[Idarubicin]] | |||
*[[Idiopathic]] | |||
*[[Imipramine]] | |||
*[[Indapamide]] | |||
*[[Ischemic heart disease]] | |||
*[[Isoprenaline]] | |||
*[[Isoproterenol infusion]] | |||
*[[Jervell and Lange-Nielsen syndrome]] | |||
*[[Junctional escape rhythm]] | |||
*[[Junctional tachycardia]] | |||
*[[Kearns-Sayre syndrome]] | |||
*[[Ketanserin]] | |||
*[[Ketoconazole]] | |||
*[[Lenegre’s disease]] | |||
*[[Leptospirosis]] | |||
*[[Lev's disease]] | |||
*[[Lidoflazine]] | |||
*[[Limb-girdle muscular dystrophy|Limb-girdle muscular dystrophy type 1B (LGMD1B)]] | |||
*[[Lithium]] | |||
*[[Long QT syndrome]] | |||
*[[Lubeluzole]] | |||
*[[Lyme disease]] | |||
*[[Mepivacaine]] | |||
*[[Mesalamine]] | |||
*[[Metabolic acidosis]] | |||
*[[Methadone]] | |||
*[[Methadyl acetate]] | |||
*[[Methamphetamine]] | |||
*[[Methyldopa]] | |||
*[[Methylprednisolone]] | |||
*[[Midodrine]] | |||
*[[Mitochondrial myopathy]] | |||
*[[Mitral valve prolapse]] | |||
*[[Mizolastine]] | |||
*[[Moxifloxacin]] | |||
*[[Multiple myeloma]] | |||
*[[Muscular dystrophy]] | |||
*[[Myocardial bridging]] | |||
*[[Myocardial contusion]] | |||
*[[Myocardial infarction]] | |||
*[[Myocardial rupture]] | |||
*[[Myocarditis]] | |||
*[[Myotonic dystrophy]] | |||
*[[Myxedema]] | |||
*[[Nail-patella syndrome]] | |||
*[[Naratriptan]] | |||
*[[Nelfinavir]] | |||
*[[Neonatal lupus erythematosus]] | |||
*[[Neostigmine]] | |||
*[[Nicardipine]] | |||
*[[Nicorandil]] | |||
*[[Nilotinib]] | |||
*[[NSTEMI]] | |||
*[[Obstructive sleep apnea]] | |||
*[[Ondansetron]] | |||
*[[organophosphate|Organophosphate poisoning]] | |||
*[[Parathion poisoning]] | |||
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*[[ | *[[Pasireotide]] | ||
*[[ | *[[Pazopanib]] | ||
*[[ | *[[Pentamidine]] | ||
*[[Pericarditis]] | |||
*[[Phenothiazine]] | |||
*[[Phenytoin]] | |||
*[[Pheochromocytoma]] | |||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vendhan Ramanujam M.B.B.S [2]
Synonyms and keywords: Long PR, long P-R, prolonged PR, prolonged P-R, prolonged PR interval, prolonged P-R interval, PR prolongation, P-R prolongation, PR interval lengthened, P-R interval lengthened
Overview
Long PR interval is prolongation of the time required by impulse generated at the normal atrial pacemaker (SA node) to conduct via the normal conduction pathway and activate the ventricle. Normally the conduction time is 0.12 to 0.21 seconds (normal PR interval). A PR interval above 0.21 seconds is called as long PR interval. PR interval is usually longer when the conduction of atrial impulse through AV node is slowed either as a consequence of withdrawal of sympathetic tone or due to an increase in vagal inputs. It is also important to emphasize that long PR intervals can exist in subjects who are otherwise normal.[1] In atrioventricular dissociation where both atria and ventricle beat independently without conducting each others impulse either antegradely or retrogradely, PR interval may vary from beat to beat. In some beats, the PR interval may be long.
Pathophysiology
First Degree AV Block
First degree AV block may be due to conduction delay in the AV node, His-Purkinje system (made up by the bundle of His and the Purkinje fibers), or a combination of the two. The majority of cases are due to a dysfunction of the AV node; however, when first degree heart block coexists with a bundle-branch block, the cause is more likely to be a conduction delay in the His-Purkinje system. Although there are no missed beats in first degree AV block with all impulses from atria being transmitted to ventricle and thus resulting in a regular ventricular beat rhythm, the conduction delay involving AV node alone typically causes a long PR interval. If the conduction delay also involves the His-Purkinje system, the long PR interval will be associated with wide QRS complex.
Mobitz Type I Second Degree AV Block
The classic site of block in Mobitz type I second degree block is the AV node (70%-75%). In the remaining 25%-30% of the cases the site is infra-nodal (His bundle, bundle branches or fascicles). Mobitz type I is composed of two variations, classic and atypical, based on periodicity. Classic variety usually occurs within the AV node. There is a gradually increasing PR interval and eventually a dropped beat. It is also accompanied by a gradually decreasing R-R interval. The PR interval is usually shortest in the initial beat and gradually increases the ending in a dropped beat and the cycle repeats. This classic Wenckebach phenomenon occurs usually with ratios of 3:2, 4:3 or 5:4. This results in grouped beating. In Atypical variant of Wenckebach pattern the conduction ratios usually exceed 6:5 or 7:6 and the last few beats of the cycle, before a dropped beat, show a relatively constant PR interval (maximum variation of 0.02 sec among them). The beats after the dropped beat again show gradually prolonging PR intervals.[2]
Atrial Premature Beats
In atrial premature beats, also known as atrial premature contractions or premature atrial contractions, with increasing prematurity, the partial penetration of the premature beat (concealed) prolongs the refractory period of the AV node and causes prolongation of the PR interval of the next sinus beat. The PR interval progressively increases until the effective refractory period of AV node is reached, when the atrial premature beats get blocked within the node and non-conducted.[3]
Pseudo-Long PR Interval in Atrioventricular Dissociation
In Atrioventricular dissociation, the atrial impulse does not conduct to the ventricle, but the atrium and the ventricle may separately beat at similar or different rates and the PR interval may vary from beat to beat. In some beats, the PR interval may be long. Although this may appear to be a sinus rhythm with a long PR interval, there is no true impulse conduction between the atrium and ventricle, and hence the name "pseudo long PR interval".[4][5]
Trifascicular Block
On ECG, trifascicular block may manifest with a long PR interval. Trifascicular block involves conduction delay in the right bundle branch plus delay in the main left bundle branch or in both the left anterior and the left posterior fascicles. The diagnosis of trifascicular block requires an electrocardiographic pattern of bifascicular block plus evidence of prolonged conduction below the AV node. This below the AV node conduction delay is most specifically observed as a prolongation of the His-ventricular (HV) time in intracardiac recordings. PR interval includes conduction time in both AV node as well as in the intraventricular conduction system. Prolonged intraventricular conduction may be insufficient to extend the PR interval beyond normal limits, thus a prolonged PR interval can reflect delay in the AV node rather than in all three intraventricular fascicles. So the finding of a long PR interval in the presence of an electrocardiographic pattern consistent with bifascicular block is not diagnostic of trifascicular block, whereas the presence of a normal PR interval does not exclude this finding either. Thus long PR interval is only a concomitant finding in trifascicular block.
Causes
Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
- Acute cardiac allograft rejection
- Acute myocardial infarction
- Bacterial endocarditis
- Complete heart block
- Diabetic ketoacidosis
- Digitalis toxicity
- Hypokalemia
- Myocardial rupture
- Organophosphate poisoning
- Pulmonary embolism
- Severe hypothermia
Common Causes
Causes Based on Pathophysiologic Origin
First Degree AV Block and Mobitz Type I Second Degree AV Block
Atrial Premature Beats
Atrioventricular Dissociation
References
- ↑ PACKARD JM, GRAETTINGER JS, GRAYBIEL A (1954). "Analysis of the electrocardiograms obtained from 1000 young healthy aviators; ten year follow-up". Circulation. 10 (3): 384–400. PMID 13190611. Unknown parameter
|month=
ignored (help) - ↑ El-Sherif N, Aranda J, Befeler B, Lazzara R (1978). "Atypical Wenckebach periodicity simulating Mobitz II AV block". Br Heart J. 40 (12): 1376–83. PMC 483582. PMID 737095. Unknown parameter
|month=
ignored (help) - ↑ Damato AN, Lau SH (1971). "Concealed and supernormal atrioventricular conduction". Circulation. 43 (6): 967–70. PMID 4102931. Unknown parameter
|month=
ignored (help) - ↑ Levy MN, Edflstein J (1970). "The mechanism of synchronization in isorhythmic A-V dissociation. II. Clinical studies". Circulation. 42 (4): 689–99. PMID 11993309. Unknown parameter
|month=
ignored (help) - ↑ MILLER R, SHARRETT RH (1957). "Interference dissociation". Circulation. 16 (5): 803–29. PMID 13473052. Unknown parameter
|month=
ignored (help)