no slide · pdf filerhythm: see next slide. 3 87-year-old woman: ... •medications:...

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Bradyarrhythmia

Ass. Prof. Tomon Thongsri, MD

Buddhachinaraj Phitsanuloke Hospital

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Case Scenario

An 87-year-old woman reports feeling weak

and short of breath for 2 hours while

walking short distances. She feels exhausted

moving from the car to the ED stretcher.

On physical exam she is pale and sweaty;

HR = 35 /min; BP = 90/60 mm Hg;

RR = 24 /min.

Rhythm: see next slide.

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87-Year-Old Woman: Symptomatic Bradycardia

Identify A, B, and C

Which one is most likely

to be her rhythm? A

B

C

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Rhythms to Learn

Sinus bradycardia

Sick sinus syndrome

AV blocks

• 1st degree

• 2nd degree type I

• 2nd degree type II

• 3rd degree

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Cardiac Conduction System

Primary pacemaker

• Sinus node

• 60-100 /min

Escape pacemakers

• AV node (junction)

• 40-60 /min

• Ventricular

• 20-30 /min

Role of cardiac role

1. จุดก ำเนิดไฟฟ้ำท่ีปล่อยเร็วกวำ่ยอ่มชนะและกดจุดท่ีปล่อยชำ้กวำ่ 2. จุดต่ำงๆ บนเสน้ทำงน ำกระแสไฟฟ้ำสำมำรถปล่อยกระแสฟ้ำได ้3. จุดก ำเนิดไฟฟ้ำยิง่อยูต่ ่ำยิง่ปล่อยชำ้ 4. จุดก ำเนิดไฟฟ้ำยิง่อยูต่ ่ำ QRS ยิง่กวำ้ง

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Cardiac Conduction System

Primary pacemaker

• Sinus node

• 60-100 /min

Escape pacemakers

• AV node (junction)

• 40-60 /min

• Ventricular

• 20-30 /min

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Case Scenario






HR = 35 /min; BP = 90/60 mm Hg;

RR = 24 /min.


What is the rhythm?

87-Year-Old Woman: Symptomatic Bradycardia

What is the rate?

• Approximately 35 beats per minute

What is the rhythm?

• Is it regular : yes

• Is there a p wave before every QRS and vice versa? : yes

• P wave come from sinus node? : yes

P wave of sinus : + in I, II, III, aVF, regular

P from sinus node

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P wave of sinus : + in I, II, III, aVF, regular

Sinus Bradycardia

Sinus Bradycardia

Sinus rhythm with a resting heart rate of 60

beats/minute or less

actually become symptomatic until

HR < 50 beats/minute

History:

• most often asymptomatic

• Symptom:

– Syncope

– Dizziness

– Lightheadedness

– Chest pain

– Shortness of breath

Sinus Bradycardia

Physical examination:

• Cardiac auscultation and palpation of peripheral pulses reveal : slow, regular heart rate.

• The physical examination : nonspecific

– Decreased level of consciousness

– Cyanosis

– Peripheral edema

– Pulmonary vascular congestion

– Dyspnea

– Poor perfusion

– Syncope

Sinus Bradycardia

– Physiologic causes : increased vagal tone

eq. bradycardia in athletes

vomitting

Causes: Sinus Bradycardia

Pathologic Causes: • most common : sick sinus syndrome.

• Medications:

– digitalis glycosides, beta-blockers

– calcium channel-blocking agents

• Medications: antiarrhythmic drug class I and amiodarone.

• toxins :

– lithium, paclitaxel, toluene, dimethyl sulfoxide (DMSO)

– topical ophthalmic acetylcholine

fentanyl, alfentanil, sufentanil, reserpine

– clonidine.

Sinus Bradycardia

Pathologic Causes (cont.):

• Inferior wall MI

• Electrolyte imbalance: hyperkalemia

• hypothermia, hypoglycemia, hypothyroidism

• sleep apnea

• Increase intracranial pressure

• Less commonly:

– diphtheria

– rheumatic fever

– viral myocarditis.

Sinus Bradycardia

Sick Sinus Syndrome

• Involves a dysfunction in the ability of the sinus node to generate or transmit an action potential to the atria

• signs and symptoms :

– cerebral hypoperfusion, in association with

sinus bradycardia,

sinus arrest,

sinoatrial (SA) block,

carotid hypersensitivity

or alternating episodes of bradycardia and tachycardia

Sinus arrest

Sino-atrial block

Sick Sinus Syndrome

• Involves a dysfunction in the ability of the sinus node to generate or transmit an action potential to the atria

• signs and symptoms :

– cerebral hypoperfusion, in association with

sinus bradycardia,

sinus arrest,

sinoatrial (SA) block,

carotid hypersensitivity

or alternating episodes of bradycardia and tachycardia

Sick sinus syndrome

• Most commonly occurs in elderly patients with

concomitant cardiovascular disease and follows an

unpredictable course.

• The majority of cases remain idiopathic.

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Case Scenario 2






HR = 35 bpm; BP = 90/60 mm Hg;

RR = 18 rpm.


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What Is This Rhythm?

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First degree AV Block

• Definition:

– Prolongation of the PR interval > 200 msec ( 5 ช่องเลก็) • Pathophysiology:

– Every atrial impulse is transmitted to the ventricles, resulting in a regular ventricular rate.

– Can arise from delays in the conduction system in the AV node itself (most common), the His-Purkinje system, or a combination of both.

• Mortality/Morbidity: – In and of itself, first-degree AV block is a benign condition, with no

associated increase in morbidity or mortality.

• Treatment – Define causes : drug overdose, acute MI, myocarditis, degenerative

– No treatment indicated if asymptomatic.

First degree AV Block

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P P P P P P P P

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Second Degree AV Block Type I

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P P P P P P

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Second Degree AV Block Type II

Second degree AV block

• Refers to a disorder of the cardiac conduction system in which some atrial impulses are not conducted to the ventricles.

• Electrocardiographically, some P waves are not followed by a QRS complex

Mobitz I • Characterized by a progressive prolongation of the PR interval, which

results in a progressive shortening of the R-R interval. Ultimately, the atrial impulse fails to conduct, a QRS complex is not generated, and there is no ventricular contraction.

Mobitz II • Characterized by an unexpected nonconducted atrial impulse. Thus, the

PR and R-R intervals between conducted beats are constant.

Pathophysiology: • Mobitz type I block

– Caused by conduction delay in the AV node in 72% of patients and by conduction delay in the His-Purkinje system in the remaining 28%.

• Mobitz type II block – Conduction delay occurs infranodally. The QRS complex is likely to be wide,

except in patients where the delay is localized to the bundle of His.

Mortality/Morbidity: • Mobitz type I second-degree AV block localized to the AV node

– Not associated with any increased risk of morbidity or death, in the absence of organic heart disease.

– No risk of progression to a type II second-degree block or complete heart block exists.

– When a Mobitz type I block occurs during an acute myocardial infarction, mortality is increased.

• Mobitz type II block – risk of progressing to complete heart block

– increased risk of mortality.


Causes:

• Mobitz I block – high vagal tone: athletes or young children.

– structural heart disease : tetralogy of Fallot

– valvular surgery (especially mitral valve).

– myocardial infarction (especially inferior wall)

– drug induced : beta-blockers, calcium channel blockers, amiodarone, digoxin, and possibly pentamidine)

• Mobitz II block – most commonly : AMI (anterior or inferior wall)

– Drug-induced

– degenerative


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P P P P P P P

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Third Degree AV Block Type III

Third degree AV Block

• Disorder of the cardiac conduction system where there is no conduction through the AV node.

• Complete disassociation of the atrial and ventricular activity exists.

• Ventricular escape mechanism can occur anywhere from the AV node to the bundle-branch Purkinje system.

• QRS complexes being conducted at their own rate and totally independent of the P waves.


Mortality/Morbidity:

• Frequently hemodynamically unstable

• The patient may experience syncope, cardiovascular collapse, or death.

History:

• Complete heart block has a wide range of clinical presentations; most patients are symptomatic.

• Patients occasionally are asymptomatic or have only minimal symptoms related to hypoperfusion.

• symptoms include the following:

– syncope

– Fatigue

– Dizziness

– Impaired exercise tolerance

– Chest pain


Physical: • Notable for bradycardia, which can be quite severe.

• Signs of congestive heart failure as a result of decreased cardiac output may be present and include the following:

– Tachypnea or respiratory distress

– Rales

– Jugular venous distention

• Patients may have signs of hypoperfusion, including the following: – Altered mental status

– Hypotension

– Lethargy

• In patients with concomitant myocardial ischemia or infarction, corresponding signs may be evident on examination:

– Signs of anxiety such as agitation or unease

– Diaphoresis

– Pale or pasty complexion

– Tachypnea


Causes:

• congenital vs acquired

Congenital

• Block at the level of the AV node

• asymptomatic at rest but symptoms on exert

because the fixed heart rate

• In the absence of major structural abnormalities, congenital heart block is often associated with maternal antibodies to SS-A (Ro) and SS-B (La).

Complete AV Block

Acquired • Drug induced : beta-adrenergic, and calcium channel

blocking agents.

• Drugs or toxins – Class Ia : quinidine, procainamide, disopyramide

– Class Ic : flecainide, encainide, propafenone

– Class II : beta-blockers

– Class III : amiodarone, sotalol, dofetilide, ibutilide

– Class IV : calcium channel blockers

– Digoxin or other cardiac glycosides

Complete AV Block

Acquired

• degenerative • Infection:

– Lyme carditis

– acute rheumatic fever

• Metabolic disturbances : severe hyperkalemia • Ischemia

– MI - Anterior wall MI can be associated with an infra-nodal AV block.

– < 10% of cases of acute inferior MI and often resolves within hours to a few days.

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Differentiation of Second- and Third-degree AV Blocks

More P’s than QRSs

PR fixed?

no

QRSs that look alike regular?

no

yes

yes

yes

2nd-degree AV block Fixed

Mobitz II

3rd-degree AV block

2nd-degree AV block Variable Mobitz I

Wenckebach

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Case Scenario






HR = 35 bpm; BP = 90/60 mm Hg;

RR = 18 rpm.


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Junctional bradycardia

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Case Scenario






HR = 35 bpm; BP = 90/60 mm Hg;

RR = 18 rpm.


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EKG Changes

EKG Changes Widening of QRS Complex

EKG Changes Ventricular Tach/Torsades

Treatment

1 Stabilize myocardial membrane

• 10%calcium gluconate 10 ml IV push

2 Drive extracellular potassium into the cells

• 2 Agonists (albuterol) 5 ml nebulizer

• 50% glucose 50ml + RI 10 u IV push

• 7.5% NaHCO3 1 amp IV push

3 Removal of Potassium from the body

• Loop diuretic, kayexalate, hemodialysis

BREAK TIME

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