Bradyarrhythmia Flashcards
Bradyarrhythmia: Sinoatrial (SA) Node Dysfunction
Normal Conduction
**SA node : **
-SA original pacemaker
- Blood supply R side of heart
**AV Node “ **
Activates when node SA supressed
Bradyarrhymia
- Failure of impulses **initiaton **or impulse conduction At level of SA lnode
- Depressed Atuomaticity
Subsidiary Pacemakers
Discharge at slower rate
Risk of tissue HyPOPERFUSION
Most common causes of Pathologic Bradycardia
> SA node dysfunction andAV Conduction block
What is SA Node
> **Fusoform cells in sulcus terminalis on epicardial surface **
Richly innervated by SNS and PNS and Ganglia
Arises for RCA 55 to 60% and LCx 40 to 45%
Extrinsic SA Node dysfunction
> Often Reversible and should be corrected prior to pacer insertio
Drugs and ANS Influences
Hypothyroidism
OSA
Hypothermia
Hypoxemia
ICP
ETT suction
Intrinsic SA node dysfuntion
> Degenerative - Fibrous Replacement of SA node
**> Acute vs Chronic CAD **
Inflammatory Processes (Pericartitis, Myocarditis, Rheumatic Heart disease)**Connective Tissue Disorder **( SLE, RA, MCTD- mixed connective tissio disorder)I**nfiltrative Disoder ** Amiloidosis**Latrogenic Causes ** Direct Injury to SA node** Sick Sinus Syndrome (SSS): **
Increase in Fibrous tissue
Increased onset with
C AD, DM, HTN, Valvular disease,cardiomyopathies
Risk Factors for SA Node Dysfunction
> SVT 33 to 50%
Atrial Fibrillation or Atrial Flutter W RVR
25% develop concurrent AV conduction diseases
> **A-Fib Incidence : **
- Advance age
- HTN, DM,
- LV dilation, Valvular Heart Disease
- Ventricular Pacing
-
- > **Tachycardia- Bradycardia **
- SSS varient
- Risk for Thromboembolism : need antigoagulation
- Left Ventricular Dysfuction
- Atrial Enlargement
- Hx of CVA or Valvular disease
Bradyarrhythmia :
Signs and Symptoms
> **Asymptomatic At times **
** Identify on EKG: **
- Sinus Bradycardia, Sinus Arrest, Exit Block
- Alternating A-Fib and Bradycardia (slow and fast HR)
S/S Tachycrdia /Bradycardia
Palpitations
Angina Pertoris
HF
—————-
Hypotenison
Pre-Syncope
Fatingue-and Weakness
Sick Sinus Syndrom (SSS)
> Fast and slow Rate
Prolonge Pauses»_space;» Syncope
HR symptoms
Pathologic and Physiologic Sinus Bradycardia
****SA node driven **
HR <60 bpm
Chronic Incompetence > Inability to Increase HR appropriately
If it does physiologic **
If it does nOt - Pathologic SA node
Sinus Pauses
> ** Failure of SA node to discharge**
Producing a pause
Sinus Exit Block
> ** Intermttent Failure **of conduction
Produces sinus exit block
SA Node Dysfunction :
> Diagnosis
> Clinical or EKG diagsosis (Most common Find EKG )Long Term Recording and Symptoms Correlation
- Holter or event monitor
- Implantable ECG (loop 12 month)
> ** Chrontitropic Incopetence: **Exercise Testing
> Autonomic NST:
- **Aministration of Propranolol 0.2 mg /kg & Atropine 0.04 mg/kg **
- Low Intrisic Heart Rate»_space;» SA disease
SA Node Dysfunctin
Treatment Plan
> Main Aim: Alleviation of Symptoms
Exclusion of Exrinsic Causes
Pharmacologic considerations > Consider Discontinue (BBB, CCB, Arrhymic Medications class I and II )
> ** Permanent Pacemaker **
- Only Reliable Therapy
- Dual Chamber Pacemakers > Fever Syncopal Episodes
Bradyarrhythmia
**AV NOde Dysnfunction > **
< Overview >
> Atrioventricular (AV) Node **
- Blood Suppl from LAD (left anterior descending artery )
- AV node Highly Innervated of **
Postganglionic Sympathetic and Parasympathetic Nerves
**Conduction Block **: Variety of Reasons
> **AV block Classification: **
- 1st to 3rd degree
- Location of the block
Fuctional VS Structural Etiology
_ **Functional/Extrinsic
- Reversible
- Autonomic
- Metablolic
- Endocrine
- Drug
Fuctional VS Structural Etiology
> Structioral > Fibrosis
- Common Cause of AV block - permanent
**> Aging : **
**- Sclerosis Left cardiac Stent **
- Begins in 4th decade of life
- Accelerated by athelorsclerisis
> **Coronary Artery Disease **
- Acute Myocardial Infarction
- Transient AV block: 1st, 2nd, 3rd seen AMI
- 2nd degree in High grade AV block: Inferior (lower ) AMI vs superior
>
Fuctional VS Structural Etiology
> Structioral > Aging
**- Sclerosis Left cardiac Stent **
- Begins in 4th decade of life
- Accelerated by athelorsclerisis
> **Coronary Artery Disease **
- Acute Myocardial Infarction
Transient AV block: 1st, 2nd, 3rd seen AMI
2nd degree in High grade AV block: Inferior AMI vs superior
>
Fuctional VS Structural Etiology
> Structioral >
> Coronary Artery Disease
- Acute Myocardial Infarction
Transient AV block: 1st, 2nd, 3rd seen AMI
2nd degree in High grade AV block: Inferior AMI vs superior
>
Fuctional VS Structural Etiology
> Structioral>
> Hereditary Muation >
Cadiac NA + channel Gene **SCNSA **
Ventricular Arrthymia
Impaired Cardiac Conduction
Fuctional VS Structural Etiology
> Structioral>
Autoimmune and infiltration Diseases
Lupus
RA
MCTD
Schelordemra
Amyloid
Sarcoid
Hemochromatosis > AV conduction
Fuctional VS Structural Etiology
> Structioral>
> Infectious Disease >
Lyme disease
Chagal disease
Syphilis
AV Node Dysfunction :
Clinical Manifestations and DX
> Bradycaria :
- most common Findings
- secondary to Compromized AV node conduction
- Fatique syncope, death
- EKG: DX
1St degree aV block
> PR intervals > 200 ms
** Wide QRS: **
- Delay distal condution system
** > Narrow WRS **
- Delay in AV node proper or Bundle of His
2nd degree
> Intermittent failure of elecrical impulses
Subcalss**ifed Mobitx 1 or Mobitz 2
Mobitx 1 — Winckebox **
- prolog proglangatio of PR then drop QRS complex
> Mobitz 2 **
- Sudden drop in QRS complex
-
3 rd degree AV block
complete block
* TX aV block*
Medicatiio Reconciliation
**Correct Electrolytes **
**Temporary pacing **
Aropine, Isoproteronol
