gemc- cardiovascular board review session 1- resident training

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Document Title: Cardiovascular Board Review for www.EMedHome.com

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Cardiovascular

Board Review for

www.EMedHome.com

Joe Lex, MD, FACEP, MAAEM

Professor of Emergency Medicine

Department of Emergency Medicine

Temple University School of Medicine

Philadelphia, PA USA 3

http://www.emedhome.com/

This Review Will Cover…

1. Cardiopulmonary Arrest / SIDS

2. Congenital Abnormalities

3. Disorders of Circulation

Arterial

Venous

4. Disturbances of Rhythm

Ventricular

Supraventricular 4


5. Diseases of the Myocardium

Cardiac Failure

Cardiomyopathy

CHF

Coronary Syndromes

Myocardial Infarction

Myocarditis

Ventricular Aneurysm 5


6. Disease of the Pericardium

Pericardial tamponade

Pericarditis

7. Endocarditis

8. Hypertension

9. Tumors

10.Valvular disorders

6

Today – Part One 1. Cardiopulmonary Arrest / SIDS

2. Congenital Abnormalities

3. Disorders of Circulation

Arterial

Venous

4. Disturbances of Rhythm

Ventricular

Supraventricular 7

3.1 Cardiopulmonary

Arrest

8

Cardiopulmonary Arrest

Abrupt cessation of pump function

in heart

No palpable pulse

Unconscious and not breathing

May be expected outcome to

serious illness

May be possible to reverse

9

Cardiopulmonary Arrest

Shockable

Ventricular tachycardia

Ventricular fibrillation

Non shockable

Asystole

Pulseless electrical activity (PEA)

10

Primary Causes

Coronary heart disease

Present in 60-70%

Autopsy: 30% had recent MI

Cardiomyopathy

Cardiac rhythm disturbances

Hypertensive heart disease

Congestive heart failure

11

When Does It Occur?

Most likely to occur in first few

hours after awakening from sleep

More likely to occur in winter rather

than summer

12

Other Causes: Noncardiac

Trauma

Non-trauma bleeding

Gastrointestinal

Aortic rupture

Intracranial hemorrhage

Overdose

Pulmonary embolism

13

Recognizing Arrest

International Liaison Committee

on Resuscitation (ILCOR)

Diagnose cardiac arrest in all

casualties who are unconscious

and not breathing normally

Carotid artery palpation no longer

gold standard

14

Various Guidelines

Resuscitation Guidelines

BLS: Basic Life Support

ALS: Advanced Cardiac Life

Support

PALS: Pediatric Advanced Life

Support

NRP: Neonatal Resuscitation

Program 15

Cardiopulmonary Resuscitation

Start as soon as possible, interrupt

as little as possible

benefit chest compressions

Proper CPR survival

Tracheal intubation: no survival

Assisted ventilation may

outcome

Prehospital intubation survival 16

Automated External Defibrillator

AED: they’re automated, not

automatic

Diagnoses shockable rhythm

Tells operator to shock

ILCOR recommends universal sign

to identify location

17

ACLS Drugs

Medications included in guidelines

Not shown to survival to hospital

discharge from out of hospital

cardiac arrest (OHCA)

Includes epinephrine, atropine,

amiodarone

18

ACLS Drugs

Vasopressin: does not improve or

worse outcomes

Possible benefit in those with

asystole especially if used early

Epinephrine: appears to improve

short term outcomes such as return

of spontaneous circulation (ROSC)

19

ACLS Drugs in ET Tube

Lidocaine: rarely used

Epinephrine

Atropine: no longer recommended

for PEA

Naloxone

20

Chain of Survival

21

1. Early recognition and call for help - To prevent cardiac arrest

2. Early CPR - To buy time

3. Early Defribilation - To restart the heart

4. Post resuscitation care - To restore quality of life

Chain of Survival

Early recognition

Each minute untreated arrest

survival ~10%

Early CPR

Blood and oxygen to vital organs

Early defibrillation

Only known effective therapy

Early advanced care 22

Survival from Cardiac Arrest

Initial emergency care by

ambulance ROSC ~15%

Defibrillation in <5 min ~30%

23

Therapeutic Hypothermia

Cooling after cardiac arrest with

return of spontaneous circulation

(ROSC) but without return of

consciousness improves outcomes

Target temperature of 32–34 °C

(90–93 °F)

Death rates in hypothermia group

35%

24

3.1.1 Sudden Infant

Death Syndrome

25

SIDS

Sudden Infant Death Syndrome

aka SUDI: sudden unexpected

death in infancy

aka cot death or crib death

Not predicted by medical history

Unexplained after thorough

forensic autopsy and detailed death

scene investigation 26

SIDS

Cause: unknown, many theories

Prenatal associations:

Maternal age: teenage mothers at

greatest risk

Delayed / poor prenatal care

Maternal smoking

27

SIDS

Postnatal associations:

Low birth weight

Exposure to tobacco smoke

Prone sleeping position

No breastfeeding

Room temperature too high or low

Excesses of bedding, clothing, soft

sleep surfaces, stuffed animals 28

Differential Diagnosis

Infant botulism

Long QT syndrome (<2%)

Helicobacter pylori infections

Shaken baby syndrome / other

nonaccidental trauma

Overlying

29

Caring for Survivors

Family-centered / team-oriented

Provide personal, compassionate,

individualized support to families

Respect social, religious, cultural

diversity

Notify primary care physician

Identify / report child maltreatment

30

3.2 Congenital

Abnormalities of the

Cardiovascular System

31

Congenital Heart

Disease (CHD)

32

Noncyanotic Defects

Ventricular septal defect 20 – 25%

Atrial septal defect 5 – 10%

Patent ductus arteriosus 5 – 10%

Coarctation of aorta 8%

Pulmonic Stenosis 5 – 8%

Aortic Stenosis 5% 33

Cyanotic: Terrible T’s

Tetralogy of Fallot 10%

Transposition of Great

Arteries 5%

Tricuspid Atresia 1 – 2%

Total anomalous

pulmonary venous return 1%

Truncus Arteriosus <1% 34

Typical Presentations

Cyanosis

Shock

Heart Failure

35

Present with Cyanosis

Tetralogy of Fallot (to 12 weeks)

Transposition of the great arteries

Tricuspid atresia

TAPVR

Truncus arteriosus

Pulmonary atresia

Hypoplastic right or left heart

All others birth to 2 weeks 36

Present with Shock

Coarctation of aorta

Aortic stenosis from 1st week on

37

Present with Heart Failure

Ventricular septal defects

Patent ductus arteriosus from 4

weeks on

38

Some Clues

Central cyanosis with minimal

respiratory distress (“comfortably

blue”): suggests CHD rather than

pure pulmonary problem

39

Cornelia Csuk (Wikipedia)

http://en.wikipedia.org/wiki/Double_inlet_left_ventriclemediaviewer/File:HLHS.jpg

Some Clues

Worsening cyanosis with crying

suggests cardiac rather than purely

pulmonary etiology

40

Clue: Give 100% Oxygen

Purely pulmonary: PaO2 should rise

to 250 mm Hg

Cyanotic CHD associated with

blood flow: PaO2 may occasionally

reach as high as 150 mm Hg

Cyanotic CHD associated with

blood flow: PaO2 will not rise

>100 mm Hg

41

Clue: Chest X-Ray

Boot-shaped heart: tetralogy of

Fallot

Egg-on-a-string silhouette:

transposition of the great vessels

Snowman-shaped or figure-of-eight

heart: total anomalous pulmonary

venous return (TAPVR)

42

Clue: Chest X-Ray

Boot-shaped heart: tetralogy of

Fallot

43 Source Undetermined

Tet Spell: Cyanosis When Crying

44

Tet Spell: Cyanosis When Crying

45 Melimama (Wikimedia Commons)

http://commons.wikimedia.org/wiki/File:Crying_newborn.jpg

Narrowing of pulmonary valve 46

Source Undetermined

Ventricular septal defect 47

Source Undetermined

Aorta displaced over VSD 48

Source Undetermined

Treatment for Tet

Place in knee-to-chest position

SVR R to L shunt across VSD

Supplemental O2 (limited value)

Morphine: 0.1–0.2 mg/kg IV or IM

Fentanyl as alternative

Sodium bicarbonate: 1 mEq/kg IV

ketamine / propranolol /

phenylephrine 49

Clue: Chest X-Ray

Egg-on-a-string silhouette:

transposition of the great vessels


Clue: Chest X-Ray

Snowman or figure-of-8 heart: total

anomalous pulmonary venous

return (TAPVR)


Patent Ductus Ateriosus

More severe / complex lesions may

not be clinically apparent until

ductus arteriosus begins to close

First several weeks of life

Defects with obstructive lesions of

the pulmonary or systemic

circulations will be unmasked

Present with cyanosis, shock, both

53

Patent Ductus Ateriosus

Preserves blood flow from aorta to

the pulmonary circulation

Or

Preserves blood flow from main

pulmonary artery to systemic

circulation

54

Patent Ductus Arteriosus

55

National Institutes of Health (Wikipedia)

http://en.wikipedia.org/wiki/File:Patent_ductus_arteriosus.jpg

CHDs Requiring Patent Ductus

To preserve blood flow from aorta to

the pulmonary circulation:

Tetralogy of Fallot

Tricuspid atresia

Pulmonary atresia

Hypoplastic right heart syndrome

Transposition of the great vessels

56

CHDs Requiring Patent Ductus

To preserve blood flow from main

pulmonary artery to systemic

circulation:

Severe coarctation of aorta

Severe aortic stenosis

Hypoplastic left heart syndrome

57

Patent Ductus Arteriosus

Prostaglandin E2 is responsible for

keeping ductus patent

NSAIDs can help close a PDA

If beneficial to prevent closure,

administer prostaglandin analog:

alprostadil, misoprostol

History: prostglandins first isolated

from seminal fluid of prostate

58

Prostaglandin E1 Therapy

PGE1 infusion: start at 0.05 to 0.1

µg/kg/min

Apnea common: intubate first

Controlled ventilation will also

help work of breathing

Other adverse reactions: fever,

seizures, bradycardia, hypotension,

flushing, platelet aggregation

59

3.3.1 Arterial


3.3.1.1 Arterial

Aneurysm

61

Arcadian (Wikimedia Commons)

http://upload.wikimedia.org/wikipedia/commons/3/32/Illu_artery.jpg

Aneurysms

Dilation of arterial wall to >1.5 times

its normal diameter

Larger aneurysm more likely to

rupture

Once stress on vessel wall

exceeds tensile strength, it

ruptures

62

Aneurysms

True aneurysm: involves all three

layers of arterial wall

Atherosclerotic, syphilitic,

congenital, ventricular

False aneurysm / pseudo-

aneurysm: collection of blood

leaking out of artery, but confined

next to vessel by surrounding tissue

63

Abdominal Aortic Aneurysm



Disease of aging

Occurrence expected to as

population of elderly grows

Rare before age 50 years

Average age at diagnosis: 65 to 70

Men >> women

Most common and most important

complication rupture 65


Normal diameter: 2 cm

AAA: 3 cm

<4 cm: rupture uncommon

>5cm: high risk for rupture

When unruptured, symptoms

vague and nonspecific

Symptomatic usually large and

palpable 66

Signs & Symptoms

Abdominal bruit: ~5 – 10%

Most have normal femoral pulses

Rupture often first manifestation

CLASSIC TRIAD: pain, BP,

pulsatile abdominal mass

BP inconsistent, often late finding

Contained retroperitoneal bleed

67

Signs & Symptoms

Syncope (10%)

Flank / back / abdominal pain

Common misdiagnosis: kidney stone

GI bleed from aortoduodenal fistula

Extremity ischemia from thrombus

embolization

Shock

Sudden death 68

Aorto-Enteric Fistula

AAA erodes into GI tract

Usually 3rd or 4th portion duodenum

AKA Aorto-duodenal fistula

Hematemesis, melenemesis, melena,

or (if rapid transport) hematochezia

History aortic graft placement

greatly clinical suspicion

69

Other Findings

Periumbilical ecchymosis Cullen

Flank ecchymosis Grey Turner

70 Source Undetermined Source Undetermined

Diagnosis: Radiograph

May be picked up incidentally on

plain x-ray eggshell calcification

Not sensitive or specific

71

Source Undetermined Source Undetermined

Diagnosis: Ultrasound

Virtually 100% sensitive

Measurement of aortic diameter

accurate and reproducible

Relatively inexpensive

Requires no contrast agents or

radiation exposure

Performed at bedside

CANNOT determine rupture 72


73

Source Undetermined

Diagnosis: CT

Virtually 100% accurate

Less subject to technical problems

and interpretation errors

IV contrast desirable, not essential

Better than US at retroperitoneal

bleeds

75

Diagnosis: CT

76

Source Undetermined

Ruptured = Unstable

Large bore IV access x 2

Type & Cross 6 Units PRBC

Volume controversial: permissive

hypotension vs aggressive

resuscitation

Get to operating room as soon as

possible

50% mortality 77

Post-Op Complications

Graft infection: local vs general

Most common: inguinal portion of

aortofemoral graft

Aortoenteric fistula: discussed

above

Pseudoaneurysm

Endoleak: blood flow outside graft

lumen but within aneurysm sac 78

3.3.1.2 Aortic

Dissection


Definition

Tear of aorta intimal lining with

expanding blood collection

forces layers apart false lumen

Death due to blood supply to

other organs, cardiac failure

Rupture uncommon

Aneurysm dissection RARE

80

Epidemiology

Men > women

Incidence with age

Hypertension in most patients

History cardiac surgery in ~18%

Bicuspid aortic valve in ~14%

Atherosclerosis rarely involved at

dissection site

May have positive family history 81

Epidemiology

82

CardioNetworks (Wikimedia Commons)

http://commons.wikimedia.org/wiki/File:Aortic_valve_pathology_(CardioNetworks_ECHOpedia).svg

Epidemiology

Uncommon <40 years

Other: stimulant use, exertion,

trauma

High-speed deceleration injury

usually causes traumatic aortic

rupture different disease

83

Epidemiology

Exception: congenital heart

disease, giant-cell arteritis, Ehlers-

Danlos or Marfan’s syndrome,

>40% Marfan’s aortic dissection

Women with Marfan’s at risk during

pregnancy

84

Marfan’s Syndrome

Noted in 5–9%

of people with

aortic dissection

85

BQmUB2010144 (Wikimedia Commons)

http://commons.wikimedia.org/wiki/File:Aracnodactilia.jpg

Classification

Anatomic classification important

for diagnosis and therapy

Stanford classification

Type A ascending: ~60%

More lethal

Type B descending: ~40%

Acute if <2 weeks duration

About 2/3 are acute 86

Symptoms

Pain in >90% of patients

Painless implies chronic

Usually excruciating

Occurs abruptly

Most severe at onset

Typically described as “sharp”

more than “tearing” or “ripping”

87

Symptoms: pain

Anterior chest: think ascending

aorta

Neck and jaw: think aortic arch

Interscapular: think descending

thoracic aorta

Lumbar / abdomen: think below

diaphragm

88

Symptoms

Pain migration consistent with

propagation

Occurs in <20%

Onset often accompanied by

visceral pain symptoms: nausea,

vomiting, diaphoresis, severe

apprehension, lightheadedness

89

Blood Pressure

Variable at presentation

Proximal: ~35% BP, ~25% BP

Distal: ~70% BP, ~5% BP

Severe BP grave prognosis

Associated with severe aortic

insufficiency, pericardial tamponade,

rupture

90

Blood Pressure

Pseudohypotension: false BP

Involvement of brachiocephalic

artery supplying right arm

Involvement of left subclavian

artery supplying left arm

91

92

Rob Swatski (Flickr)

https://www.flickr.com/photos/rswatski/5909402617/sizes/z/

93

brachiocephalic

artery supplies

right arm

Rob Swatski (Flickr)


left subclavian

artery supplies

left arm

94 Rob Swatski (Flickr)


Aortic Insufficiency

Occurs in half to two-thirds of

ascending aortic dissections

Aortic insufficiency murmur audible

in one-third of proximal dissections

May be inaudible if BP

95

Aortic Insufficiency

96

Myocardial Infarction

1–2% of dissections

Involves coronary arteries

RCA > LCA

Inadvertently treat with lysis

>70% mortality

97

Diagnosis

Difficult, often missed

D-dimer <500 mcg/mL MAY be

able to rule out (not definitive)

Wide mediastinum on chest x-ray:

moderate sensitivity, low specificity

Up to 20% normal chest x-ray

Calcium sign suggestive

98

Wide Mediastinum


Calcium Sign


Computerized Tomography

Noninvasive

Requires peripheral vein injection

of iodinated contrast

Sensitivity 96 – 100%

Specificity 96 – 100%

Poorly identifies site of intimal tear

101


102

Source Undetermined


103

Source Undetermined

MRI

Current gold standard

Sensitivity = 98%, specificity = 98%

Locates intimal tear, secondary

tears, involved branch vessels

Non-invasive test, no iodinated

contrast material

Disadvantage: not always

available, time consuming 104

MRI


Transesophageal Echo (TEE)

Sensitivity ~98%, specificity ~97%

Relatively non-invasive: patient

swallows echocardiography probe

Especially good to evaluate aortic

insufficiency, coronary artery

involvement

106

Transesophageal Echo (TEE)


Aortogram

No longer “gold standard”

108

Source Undetermined

Management

Stanford type A (ascending aortic):

surgical management

Stanford type B (uncomplicated

distal aortic): medical management

109 J. Heuser (Wikipedia)

http://fr.wikipedia.org/wiki/Dissection_aortiquemediaviewer/Fichier:Aortic_dissection_class.jpg

Management

Presenting as hypertensive

emergency strict blood pressure

control

Target mean arterial pressure

(MAP) of 60 to 75 mmHg

Also: shear-force dP/dt (force of

blood ejection from left ventricle)

110

Management

1st line treatment: beta-blocker

Rapidly acting, titratable parenteral

agent preferred

Esmolol, propranolol, labetalol

Do NOT use vasodilators alone

cause reflex tachycardia

May be used as supplement to

control BP 111

Risk of Death

25% in first 24 hours

50% in first 48 hours

75% in first week

90% in first month

112

3.3.1.3 Arterial

Thromboembolism

113

Source Undetermined

Peripheral Arterial Disease

Defined as ankle-brachial index

(ABI) of <0.9

Prevalent in ~15% over age 70

Risk factors: diabetes, tobacco use

Acute occlusion irreversible

changes in peripheral nerves and

skeletal muscle tissue in 4 – 6 hrs

114


ABI = SBP arm / SBP leg

Normal >0.9; <0.4 critical

Cuff inflated proximal to artery in

question

90% sensitive, 98% specific for

hemodynamically significant leg

artery stenosis (i.e. >50% occlusion

in major leg arteries)

115


“Six Ps": pain, pallor, poikilothermia

(coldness), pulselessness,

paresthesias, and paralysis

Pain earliest symptom, may with

limb elevation

Mottling, splotchiness, cool

temperature also common

distal pulse unreliable finding

116


Claudication cramplike pain,

ache, tiredness brought on by

exercise and relieved by rest

Reproducible, resolves within 2

to 5 minutes of rest

Acute limb ischemia pain not well

localized, not relieved by rest or

gravity

117


Claudication

cramplike pain,

ache, tiredness

brought on by

exercise and

relieved by rest

118

NHLBI (Wikipedia)

http://en.wikipedia.org/wiki/Peripheral_vascular_diseasemediaviewer/File:Peripheral_Arterial_Disease.gif


Most common cause acute arterial

occlusion: thromboembolic disease

Differential diagnosis: vasculitis,

Raynaud disease, thromboangiitis

obliterans, blunt or penetrating

trauma, or low-flow shock states

(sepsis)

119

Acute Arterial Occlusion

Stabilize

Fluid resuscitation, pain control

Dependent positioning can

perfusion pressure

ECG, echocardiography to

assess for conditions associated

with embolism

120


Give aspirin

Unfractionated heparin: 80 U/kg

bolus, 18 U/kg//hr

Definitive treatment in consultation

with vascular surgeon and

interventional radiologist

Preferred: catheter-directed

embolectomy

121


Reperfusion injury after

revascularization can cause

myoglobinemia, renal failure,

hyperkalemia, and metabolic

acidosis

122

Source Undetermined

Chronic Arterial Occlusion

If no immediate limb threat and no

co-morbidities: discharge on

aspirin (75 milligrams daily)

Close vascular surgical follow-up


3.3.2.1 Venous

Thromboembolism

Covered in another

section, but… 124

Phlegmasia cerulea dolens

Literally: painful blue edema

Uncommon severe form of DVT

Extensive thrombotic occlusion of

major and collateral extremity veins

Sudden severe pain, swelling,

cyanosis, edema

High risk of massive pulmonary

embolism, even when treated 125

Phlegmasia cerulea dolens


3.4 Disturbances of

Cardiac Rhythm

127

Sinus Rhythm

Rate: 60 – 100 beats / minute

Rhythm: regular with 1:1

relationship of P to QRS

PR interval: 0.12 – 0.20 seconds

QRS complex: 0.06 – 0.10 seconds

P waves upright in Leads I, II, AVF

128

3.4.1 Cardiac

Dysrhythmias

129

Premature Atrial Contraction

Extra beat

Originates outside sinus node from

ectopic atrial pacemaker

Usually interspersed throughout

underlying rhythm

Underlying rhythm is usually sinus

130


Ectopic P wave

Upright in Lead II

Appears earlier than next expected

sinus beat

Has different configuration than

normal P wave

May or may not be conducted

through AV node 131


QRS complex usually normal

May be widened due to aberrant

conduction

QRS generally followed by

noncompensatory pause

SA node reset returning sinus

beat occurs ahead of schedule

132


133

Source Undetermined


Most frequent cause of EKG pause

Can be normal variant

Can be caused by drugs or

underlying disease

Can precipitate supraventricular

tachycardia, atrial fibrillation, atrial

flutter

134


135

Source Undetermined


Asymptomatic: no treatment

indicated

Frequent or symptomatic: correct

underlying cause

136

Sinus Tachycardia

Rate: >100 beats / minute (usually

<160 beats / minute)






137

Sinus Tachycardia

Newborn: 110 – 150 bpm

2 years: 85 – 125 bpm

4 years: 75 – 115 bpm

6 years+: 60 – 100 bpm

138

Sinus Tachycardia

P-wave hidden in T-wave

139

Source Undetermined

Sinus Tachycardia


“Camel hump” appearance

140

Source Undetermined

Sinus Tachycardia


“Camel hump” appearance

141

Source Undetermined Arpingstone (Wikimedia Commons)

http://commons.wikimedia.org/wiki/File:Bactrian.camel.sideon.arp.jpg

http://commons.wikimedia.org/wiki/File:Bactrian.camel.sideon.arp.jpg

Sinus Tachycardia

Common causes

Drugs

Fever

Hyperthyroid

Pulmonary

embolism

Hypovolemia

Anemia

Hypoxia

Pain

Anxiety:

diagnosis of

exclusion 142

Sinus Tachycardia

Treatment: fix underlying cause

Acute myocardial infarction: may

be useful to treat “inappropriate”

tachycardia with beta-blocker to

slow heart rate

Cocaine toxicity: may be helpful to

treat with benzodiazepine

143

Sinus Bradycardia

Rate: <60 beats / minute






144

Sinus Bradycardia

145

Source Undetermined

Sinus Bradycardia

Common causes

Acute inferior wall

MI

Vasovagal event

(e.g. vomiting)

vagal tone (e.g.

athlete)

Vagal stimulation

(e.g. pain)

Hypothermia

Hypothyroidism

Brainstem

herniation

Myocarditis

Sick sinus

syndrome

146

Sinus Bradycardia

Common causes,

pharmacologic

Beta-blocker

Calcium-channel

blocker

Digoxin

Amiodarone

Opiate

Central alpha-2

agonist (clonidine,

dexmedetomidine)

GABA-ergic agent

(barbiturate,

benzodiazepine,

baclofen, GHB)

Organophosphate

poisoning

147

Sinus Bradycardia

Treat if symptomatic

Shock

Hypotension

Short of breath

Chest pain

mentation


PVCs in acute myocardial infarction 148

Sinus Bradycardia

Atropine 0.5-1mg q5 minutes prn

Total: 0.03 – 0.04 mg/kg

Acute myocardial infarction: may

worsen ischemia, precipitate

dysrhythmia

Mobitz II and 3°AV Block with

wide complex: atrial rate AV

block ventricular rate, BP

149

Sinus Bradycardia

Atropine ineffective in patient with

heart transplant

Atropine dose <0.5mg can be

parasympathomimetic

Produce further in heart rate

150

Sinus Bradycardia

Transcutaneous pacing (TCP)

Treatment of choice if no response

to atropine or severe symptoms

May need analgesic / sedative

Transvenous pacing

Persistent symptomatic

bradycardia

More about pacing in Part 3 151

Sinus Bradycardia

Dopamine 5-20 mcg/kg/min

No response to atropine and / or

TCP not readily available

Epinephrine 2-10 mcg/min

Particularly useful if significant

hypotension

152

Sinus Bradycardia

Isoproterenol 2-10 mcg/min

Only in low doses as last resort

Significant negative effects

myocardial oxygen consumption

Peripheral vasodilatation

Serious dysrhythmias

153

3.4.1.1 Ventricular

Dysrhythmias

154

Premature Ventricular Contractions

Abnormal QRS complexes and T

waves occurring in another

underlying rhythm



Six characteristics:

1. Occur earlier than expected

normal QRS (premature)

2. Wider than normal QRS, usually

≥0.12 sec

3. Bizarre QRS morphology

156


4. No preceding P wave: retrograde

conduction occasionally causes

inverted P wave after QRS

5. ST and T deflection opposite that

of QRS: generally followed by

compensatory pause

6. SA node not reset, so next P

wave occurs at usual time

157


Bigeminy: every other beat PVC

Trigeminy: every 3rd beat PVC

Quadrigeminy: every 4th beat

Couplet: 2 consecutive PVCs

Triplet: 3 consecutive PVCs

158


Common Causes

Hypokalemia

Hypomagnesemia

Cardiomyopathy

Hyperthyroidism

Myocardial

Infarction

Hypoxia

CHF

Mechanical:

catheter in RV

Myocardial

contusion

159


Common causes: Drugs

Alcohol / tobacco / caffeine

Cocaine

Digitalis or quinidine toxicity

Most common dysrhythmia seen

with digitalis toxicity

Methylxanthines: theophyline

160


Treatment

No symptoms no treatment

May be normal variant

Correct underlying cause

Pull back central line

Deflate Swann balloon to avoid

floating in to outflow track 161


Escape PVCs associated with

bradycardia

Treat with atropine: lidocaine may

suppress existing functioning

rhythm

162


Associated with acute MI or ischemia

treatment controversial

CONSIDER: frequent (> 30/hr),

multiform / multifocal or associated

with runs of ventricular tachycardia

Occur in couplets

R-on-T phenomenon during

ventricular depolarization

163


Associated with acute MI or ischemia

Treat underlying ischemia /

infarction: oxygen, nitroglycerine,

morphine, ASA, fibrinolytic therapy

If these measures fail, most experts

say watchful waiting, but a few

advocate treatment

164


Pharmacologic agent: lidocaine

1 – 1.5mg/kg bolus, then 2 – 4

mg/min drip. May repeat boluses

0.5 – 0.75mg/kg every 5 – 10

minutes as needed to maximum

total 3mg/kg

165


Pharmacologic agent if lidocaine

ineffective: procainamide

15 – 18 mg / kg IV until…

…favorable response noted

…QRS widens 50% >original width

…hypotension develops

…total 17mg / kg administered

166


Pharmacologic agent: magnesium

sulfate

Decreases frequency of PVCs

1 – 2 grams slow IV push over 1 –

2 minutes followed by infusion of 1

– 2 gms/hr

167

Ventricular Tachycardia

168

Source Undetermined


Three or more consecutive PVCs

occurring at a rate >100 / minute

Non-sustained: 3 ventricular beats

for maximum 30 seconds

Sustained: lasts >30 seconds (less

if treated by electrocardioversion

within 30 seconds)

169


Monomorphic VT: all ventricular

beats have same configuration

Polymorphic VT: ventricular beats

have a changing configuration and

heart rate is 100-333 bpm

Biphasic VT: ventricular

tachycardia with a QRS complex

that alternates from beat to beat

170

Monomorphic VTach

171

Source Undetermined

Polymorphic VTach

172

Source Undetermined

Bidirectional VTach

173

Source Undetermined


P waves: usually absent

If present: retrograde or not related to

QRS (AV- dissociation)

QRS complexes: wide (≥ 0.12 sec)

and may be bizarre

174


± Fusion beat: cross between

bizarre QRS and normal QRS

Pathognomonic for ventricular

tachycardia



± Capture beat: atrial impulse

penetrates AV node from above to

stimulate (“capture”) ventricles

QRS looks normal: ventricular

conduction via normal pathway

Rare

Pathognomonic for ventricular

tachycardia

176


Deflection of ST segment and T

wave is generally opposite that of

QRS complex

Rate: >100 bpm, usually 150 – 200

Rhythm: generally regular, but

beat-to-beat variation may occur

178


QRS axis: generally constant

Monomorphic: QRS complexes

look the same

Polymorphic: QRS complexes have

varying morphology

Current therapeutic modalities

based on this classifications

179

Wide Complex Tachycardia


V-Tach vs. Aberrant SVT

1. Ventricular tachycardia vs.

2. SVT with aberrant conduction due

to bundle branch block vs.

3. SVT with aberrant conduction due

to WPW

Assume ventricular tachycardia

Unstable synchronized

cardioversion 181


PROBABLY V-TACH

Age >35 PPV 85%

Structural heart disease

Ischemic heart disease

Previous MI


Cardiomyopathy

FHx sudden cardiac death 182


MAYBE ABERRANCY

Prior ECG bundle branch block

with identical morphology

Prior ECG evidence of WPW

Patient has history of similar

successfully terminated with

adenosine or vagal maneuvers

183


Stable procainamide or

amiodarone

Both convert SVT or V-Tach

Procainamide contraindicated with

cyclic anti-depressant overdose

Adenosine may initially slow either

rhythm, but it may recur

184


Stable procainamide or

amiodarone

Drug therapy fails synchronized

cardioversion

185


EKG suggests V-Tach

Absence typical RBBB / LBBB

morphology

Extreme axis deviation: QRS

positive in aVR, negative in I + aVF

Very broad complexes: >160ms

AV dissociation: P and QRS

complexes at different rates 186


EKG suggests V-Tach

Fusion beats: sinus and ventricular

beat coincide to produce hybrid

complex

Capture beats: sinoatrial node

transiently ‘captures’ ventricles in

midst of AV dissociation to produce

a QRS complex of normal duration

187


± Fusion beat: cross between

bizarre QRS and normal QRS

Pathognomonic for VT






Pathognomonic for VT

189

Source Undetermined


EKG suggests V-Tach

Positive or negative concordance

throughout chest leads

Leads V1-6 show entirely positive

(R) or entirely negative (QS)

complexes, with no RS complexes

seen

190


EKG suggests V-Tach

RSR’ complexes with taller left

rabbit ear

Most specific finding in favor of VT

In RBBB, right rabbit ear is taller

193



Verapamil accelerates heart rate,

drops blood pressure and does not

convert rhythm

Adenosine can convert

catecholamine-induced VT to sinus

(very rare)

CANNOT use adenosine to

distinguish VT from SVT

aberrancy 194

Torsades de Pointes

AKA Polymorphic ventricular

tachycardia (PVT)

195

Source Undetermined

Torsades de Pointes

“Twisting of the points”

QRS complexes “twist” around the

isoelectric line

Must be evidence of both PVT

and QT prolongation

Rate: usually 200-240

196

Torsades de Pointes

Causes: drugs

Class IV antidysrhythmics:

quinidine, procainamide

Class I-C: propafenone, flecainide

Tricyclic antidepresssants

Droperidol / haloperidol

Phenothiazines

197

Torsades de Pointes

Drug combinations: e.g.

terfenadine + ketoconazole or

erythromycin

Other causes: hypomagnesemia,

hypokalemia


Torsades de Pointes

During short runs, “twisting” may

not be apparent

Bigeminy in patient with known

prolonged QT may herald imminent

TdP

TdP with heart rate >220 beats /

minute more likely to degenerate

into ventricular fibrillation

199

Ventricular Flutter

200

Source Undetermined

Ventricular Flutter

Extreme ventricular tachycardia

Loss of organized electrical activity

Rapid, profound hemodynamic

compromise

Usually short lived due to

progression to ventricular fibrillation

Treat as ventricular fibrillation

201

Ventricular Flutter

Continuous sine wave

No identifiable P waves, QRS

complexes, or T waves

Rate usually > 200 beats / min

ECG looks identical when viewed

upside down!

202

203

Source Undetermined

Ventricular Fibrillation

204

Source Undetermined


Most common: fine or coarse

zigzag pattern without discernible P

waves, QRS complexes or T waves

Sometimes looks like ventricular

tachycardia

Patient without pulse, unresponsive:

treatment same

205


Most important shockable

cardiac arrest rhythm

Ventricles attempt to contract at

rates of up to 500 / minute

Ventricles unable to contract in

synchronised manner immediate

loss of cardiac output

206


Heart no longer effective pump

Invariably fatal without ACLS

Prolonged ventricular fibrillation:

coarse VF fine VF asystole

Due to progressive depletion of

myocardial energy stores

207


Treatment: DEFIBRILLATE

IMMEDIATELY

3 successive “stacked” shocks,

checking only the monitor between

shocks

Start with 200J

If persistent, defibrillate again with

200-300J and then 360J

208


If defibrillation unsuccessful, start

ACLS

Look for reversible causes (H’s &

T’s)

209

Reversible Causes

5 H’s

Hypovolemia (most common)

Hypoxemia

Hydrogen ions (acidosis)

Hyperkalemia / Hypokalemia

Hypothermia

5 T’s

Tablets (drugs)

Tamponade (cardiac)

Tension pneumothorax

Thrombosis, coronary

Thrombosis, pulmonary

210


Persists despite treatment of

reversible cause give anti-

fibrillatory drug

Amiodarone or procainamide

Lidocaine as last resort

Continue shocks every 30 – 60

seconds while meds being drawn

Defibrillate with 360J after each drug

dose 211

Pulseless Electrical Activity

212

Source Undetermined


Electrical activity other than V-Tach

or V-Fib without pulse

Electromechanical dissociation

(EMD)

Idioventricular rhythms

Ventricular escape rhythms

Bradyasystolic rhythms

THIS IS CARDIAC ARREST 213


Often occur in association with 5

H’s and 5 T’s

214


Causes: same as ventricular

fibrillation and pulseless ventricular

tachycardia

Treatment: ACLS

CPR, intubation, start an IV

Search for and treat underlying cause

215


Hypoxia: ventilate 100% oxygen

Hypovolemia: administer fluid bolus

Hypothermia: check core body

temperature, warm prn

Hydrogen ions: bicarbonate for

suspected severe acidosis

Hyperkalemia: seek EKG changes

216


Epinephrine 1 mg every 3–5 min

Atropine NO LONGER

RECOMMENDED (2010 ACLS)

Sodium bicarbonate not

recommended EXCEPT preexisting

metabolic acidosis, hyperkalemia,

tricyclic antidepressant overdose

217


Tablets: history, toxidrome

Tamponade: distended neck veins,

EMBU

Tension pneumothorax: breath

sounds, ease of manual ventilation

Thrombosis, heart: assess EKG

Thrombosis, lungs: EMBU for right

heart strain 218

Asystole / Flatline

CPR

Epinephrine

5 H’s and 5 T’s

Atropine and defibrillation NO

LONG RECOMMENDED

219

Source Undetermined

3.4.1.2

Supraventricular

220

Supraventricular Tachycardia

Any tachydysrhythmia arising from

above the level of Bundle of His

Often used synonymously with AV

nodal re-entry tachycardia (AVNRT)

Paroxysmal SVT (pSVT): abrupt

onset / offset, characteristically

seen with re-entrant tachycardias

involving AV node such as AVNRT

221


Atrial rate: 120-200 beats / minute

Rhythm: regular

P waves: abnormal, may be hidden

in preceding T wave

If P waves visible: 1:1 P to QRS ratio

QRS: usually narrow, may be wide

due to aberrant conduction

Extra beats: none 222


Can be classified based on site of

origin (SA or AV node) or regularity

(regular or irregular)

Classification based on QRS width

not helpful

Influenced by pre-existing bundle

branch block, rate-related aberrant

conduction, accessory pathways

223


224

Source Undetermined


225

Source Undetermined


Treatment

Vagal maneuvers: may respond

Adenosine: mainstay of treatment

Calcium-channel blocker, beta-

blocker, amiodarone: 2nd line

MAY be effective: procainamide,

amiodarone, sotalol

227


Treatment

Vagal maneuvers: may respond

228


NO LONGER RECOMMENDED

Vasopressors: norepinephrine,

methoxamine, phenylephrine

Cholinergic drugs: edrophonium

DC synchronized cardioversion:

rarely required

Catheter ablation: for recurrent

episodes not amenable to medicine

229

Multifocal Atrial Tachycardia

Form of supraventricular

tachycardia

Irregular rhythm sometimes

mistaken for atrial fibrillation

Originates from many different

atrial sites

Characterized by P waves of

varying shape

230


P waves: 3 morphologies in 1 lead

Atrial rate: 100 – 180 beats/minute

Rhythm: irregularly irregular

PP, PR, and RR intervals vary

QRS complex: normal configuration

Nonconducted (blocked) P waves

frequently present, particularly

when the atrial rate is rapid 231


232

Source Undetermined


Causes

Most common: decompensated COPD


Sepsis

Theophylline toxicity

Right atrial dilatation (cor pulmonale)

Hypoxia / hypercarbia 234


Treatment

Correct underlying disease process

Unsuccessful, patient symptomatic:

Calcium channel blocker: slows

ventricular rate, atrial ectopy

Magnesium: atrial ectopy

Metoprolol: slows ventricular rate

Digoxin / cardioversion usually

ineffective 235

AV Node + His Bundle =

AV Junction

236

Madhero88 (Wikipedia)

http://en.wikipedia.org/wiki/Bundle_of_Hismediaviewer/File:ConductionsystemoftheheartwithouttheHeart-en.svg

Junctional Premature Contractions

Far less common than PACs/PVCs

From ectopic focus in AV node or

bundle of His ABOVE bifurcation

P wave: different shape / deflection

Usually inverted in II, III, and AVF

Can occur before, during or after

QRS complex

237


When P wave precedes QRS: PR

interval is shorter than normal

QRS complex premature

QRS complex normal shape

Unless aberrant conduction

Usually compensatory pause: SA

node NOT reset so next P wave

occurs at its usual time

238


239

Source Undetermined

Source Undetermined


Causes: digitalis toxicity, coronary

artery disease, congestive heart

failure, acute myocardial infarction

(especially inferior wall)

Treat underlying cause

If precipitate lethal dysrhythmias:

intravenous procainamide

240

Junctional Escape

Sinus intrinsic rate: ~75 beats /

minute

Junctional intrinsic rate: 40 – 60

beats/minute

If sinus too slow, junctional may

take over as “back-up” rhythm

Hence “junctional escape”

241

Junctional Escape

242

Source Undetermined

Junctional Tachycardia

Ectopic pacemaker in AV junction

overtakes sinus node

Rate >100 beats / minute

junctional tachycardia


Accelerated Junctional Rhythm

Ectopic AV junction pacemaker too

fast for junctional escape, but too

slow for junctional tachycardia


Atrial Fibrillation

Uncoordinated atrial activation and

random ventricular depolarization

Rhythm: irregularly irregular

Most common sustained

dysrhythmia;

2% of the general population

5% of people > 60 years old

P waves absent no PR interval

245

Atrial Fibrillation

Atria discharge electrical impulses

to ventricles

No single impulse depolarizes atria

completely

Atria don’t pump

Occasional impulse gets through to

AV node

246

Atrial Fibrillation

May see small irregular deflections

in the baseline (“f waves”)

Atrial rate: 400 – 700 beats/minute

QRS complexes: normal, unless

aberrant conduction

Ventricular response rate: variable,

generally 160 – 180 beats/minute

247

Atrial Fibrillation

248

Source Undetermined

Atrial Fibrillation


Atrial Fibrillation

If rate >200 beats/minute + wide

QRS complex: think Wolf-

Parkinson-White syndrome with

antegrade conduction through

accessory pathway

If regular, slow ventricular rate:

think digitalis toxicity

No extra beats

250

Atrial Fibrillation: Causes

Ischemic heart

disease

Hypertension

Valvular heart

disease (esp. mitral)

Acute infection

Electrolyte

disturbance

(hypokalemia,

hypomagnesemia)

Thyrotoxicosis

Drugs (e.g.

sympathomimetics)

Pulmonary embolus

Pericardial disease

Acid-base

disturbance

Pre-excitation

syndromes

Cardiomyopathies:

dilated, hypertrophic

Pheochromocytoma 251

Atrial Fibrillation: Type

1st detected episode vs. recurrent

Paroxysmal (<7 days): terminated

spontaneously

Persistent (>7 days): sustained or

terminated therapeutically

Permanent (>1 year):

cardioversion failed or not

attempted

252

Atrial Fibrillation: Treatment

Treatment depends on:

Cardiovascular stability

Duration of dysrhythmia

Underlying cause / condition

Presence / absence of accessory

pathway

253


1. Treat underlying condition

2. Determine risk for stroke

High risk for cardiogenic

thromboembolism: cardiac

surgery, AMI, hyperthyroidism,

myocarditis, acute pulmonary

disease

254


Other risks for stroke:

Cardiac: congestive heart failure,

coronary artery disease, elevated

systolic blood pressure

Non-Cardiac: prior stroke or TIA,

hypertension, advanced age,

diabetes

255


Control rhythm: restore and

maintain sinus rhythm

Control rate: allow atrial fibrillation

to continue, control ventricular rate

256


Unstable: immediate synchronized

cardioversion

Sedate if possible

Start with 100J

Last resort if digitalis toxic: start with

10J

Heparinize if >48 hrs or hypertrophic

cardiomyopathy

257


Stable, onset <48hrs: pharmacologic

Control ventricular rate first

Goal <100 beats/minute

Calcium channel blocker: diltiazem

Beta blocker: esmolol, metoprolol

If EF < 40%

Digoxin, diltiazem, amiodarone: will

not further depress cardiac function

258


Stable, onset <48hrs: pharmacologic

Patient takes digoxin: add MgSO4

(2.5gm IV x 20mins, then 2.5gm

infused over 2 hrs)

May slow heart rate even more and /

or convert to sinus rhythm

WPW: amiodarone

Avoid beta blocker, calcium channel

blocker 259


Stable: onset / duration > 48hrs

(higher risk systemic embolization)

No immediate cardioversion if

possible

Cardioversion anticipated in 24 hrs

Consider heparin

Consider cardiology consult for TEE

to exclude atrial clot

260

Atrial Flutter

Rapid atrial rhythm: 250-300/min

Slower ventricular response 2o to

nodal delay

Always occurs with AV block

Not all impulses conducted

Variable conduction 2:1, 3:1, 4:1, etc.

P waves: sawtooth pattern

Called “F” or flutter waves

261

Atrial Flutter

Best seen: inferior leads, V1, V2

PR interval (when present) always

normal

Not every P wave followed by QRS

complex

QRS complexes normal

configuration

262

Atrial Flutter

Ventricular rate: most common

~150 beats / minute

Depends on degree of block

May be variable

Suspect atrial flutter with 2:1 block

in patients with regular ventricular

rate of 130 – 150 beats / minute

263

Atrial Flutter

Causes: similar to atrial fibrillation

Often associated with post-cardiac

surgery and peri-infarction periods

Usually transitional rhythm between

sinus rhythm and atrial fibrillation

Treatment determined by stability,

duration, accessory pathway

264

Atrial Flutter – 3:1 block

265

Source Undetermined

Atrial Flutter

Treatment: unstable

Sedate (if possible)

Synchronized cardioversion: start

with 50J

Treatment: stable

Vagal maneuvers and adenosine

may be useful to slow rate for

diagnostic confirmation 266

Atrial Flutter

Rate control first

Diltiazem (first choice), verapamil,

esmolol, metoprolol

Digoxin no longer first line

Magnesium may be useful adjuvant

267

Atrial Flutter

Rhythm control second

Procainamide

Synchronized cardioversion

Accessory pathway present

Avoid calcium channel blocker,

beta blocker, digoxin, adenosine

Synchronized cardioversion

Procainamide if stable 268

269

Source Undetermined

Pre-Excitation Syndromes

270


Pre-excitation: early activation of

ventricles due to impulses

bypassing AV node via accessory

pathway

AV node would normally slow this

down

271


WPW: accessory pathway referred

to as Bundle of Kent, or

atrioventricular bypass tract

Accessory pathway can conduct

impulses

anterograde (towards ventricle)

retrograde (away from ventricle)

in both directions 272


Majority of pathways allow

conduction in both directions

Retrograde-only: ~15% of cases

Anterograde-only: very rare

273

Orthodromic (left) Conduction

274

Orthodromic Circular

Tachycardia in a patient with

an accessory pathway

Tom Lück (Wikipedia)

http://en.wikipedia.org/wiki/Wolff%E2%80%93Parkinson%E2%80%93White_syndromemediaviewer/File:WPW.jpeg

Orthodromic (left) Conduction

275

Tom Lück (Wikipedia)

Source Undetermined



Antedromic (right) Conduction

276

Drj (Ecgpedia)

http://nl.ecgpedia.org/wiki/Bestand:OCT_ACT.svg

Antedromic (right) Conduction

277

Drj (Ecgpedia)

http://nl.ecgpedia.org/wiki/Bestand:OCT_ACT.svg

WPW in Sinus Rhythm

PR: <120ms

Delta wave: slurring slow rise of

initial portion of QRS

QRS: prolonged >110ms

ST segment and T wave discordant

changes – i.e. in the opposite

direction to the major component of

the QRS complex

278


Pseudo-infarction pattern in up to

70% of patients

Due to negatively deflected delta

waves in inferior / anterior leads

(“pseudo-Q waves”), or as a

prominent R wave in V1-3

(mimicking posterior infarction).

279


Suspect accessory pathway if

ventricular rate > 200/min

Synchronized cardioversion may

be 1st line, regardless of stability

Procainamide prolongs refractory

period of accessory pathway

May be therapy of choice in

hemodynamically stable patient

280


CONTRAINDICATED: calcium

channel blockers, beta blockers,

digoxin, adenosine

All block AV nodal conduction

All can conduction down

accessory pathway, producing in

ventricular response ventricular

fibrillation

281


Lown-Ganong-Levine Syndrome

Accessory pathway (James fibers)

connects atria directly to proximal

His bundle, completely bypassing

AV node

Very short PR interval

Narrow QRS complexes

No evidence of delta waves

282


283

Source Undetermined

3.4.2 Conduction

Disorders

284

Bundle Branch Blocks

Conduction abnormality, not rhythm

disturbance

Ventricles depolarize in sequence

rather than simultaneously

Produces wide QRS complex

285

Bundle Branch Blocks

Incomplete BBB QRS ranges

from 0.09 – 0.11 seconds

Complete BBB QRS ≥0.012 sec

ST segment has slope opposite

that of terminal half of QRS

complex

286

Right BBB

288

Source Undetermined

Source Undetermined

Right BBB

Unifasciular

Right ventricle activation delayed

Left ventricle activated normally

early part of QRS complex

unchanged

Depolarization spreads across

septum from left ventricle

289

Right BBB

Delayed right ventricular activation

produces secondary R wave (R’) in

right precordial leads (V1-3) and

wide, slurred S wave in lateral leads

V-6 V-1

290


Right BBB

Also causes 2o repolarization

abnormalities: right precordial leads

show ST depression and T wave

inversion

Isolated RBBB: cardiac axis

unchanged

Left ventricular activation proceeds

normally via left bundle branch

291

Right BBB Criteria

Long QRS >120 ms

RSR’ pattern in V1-3

Wide, slurred S wave in lateral

leads (I, aVL, V5-6)

ST depression, T wave inversion in

right precordial leads (V1-3)

292

Right BBB Criteria

ST depression, T wave inversion in

right precordial leads (V1-3)

293

Source Undetermined

Left BBB

Septum is usually activated left

right, producing small Q waves in

lateral leads

LBBB: septal depolarization

reversed (right left)

Impulse spreads first to RV

through right bundle branch and

then to LV through septum

295

Left BBB

This sequence extends QRS

duration to >120 ms

Eliminates normal septal Q waves

in lateral leads

Depolarization direction produces

tall R waves in lateral leads (I, V5-

6) and deep S waves in right

precordial leads (V1-3)

296

Left BBB

Depolarization from right to left

produces tall R waves in lateral

leads (I, V5-6) and deep S waves in

right precordial leads (V1-3) usually

leads to left axis deviation

V6

V1

297


Left BBB Criteria

QRS 120 ms

Dominant S wave in V1

Broad monophasic R wave in

lateral leads (I, aVL, V5-V6)

No Q waves in lateral leads (I, V5-

V6; small Q waves allowed in aVL)

Prolonged R wave peak time >60

ms in left precordial leads (V5-6) 298

Left BBB

R waves in lateral leads may be:

‘M’ shaped or notched

299

Source Undetermined

Left BBB

R waves in lateral leads may be:

Monophasic rather than biphasic

300

Source Undetermined

Incomplete Left BBB

Typical LBBB morphology with

QRS duration <120ms

301

Source Undetermined

Heart Blocks

302

Atrioventricular Block

Impaired conduction between atria

and ventricles

Normal: SA node sets pace

impulses travel to ventricles

AV block: message does not reach

ventricles or impaired along way

303

1st Degree AV Block

PR interval >200ms (five small

squares)

“Marked” 1o block: PR > 300ms


1st Degree AV Block

May be normal variant

vagal tone

Athletic training

Inferior MI

Mitral valve surgery

Myocarditis (e.g. Lyme disease)

Hypokalaemia

305

1st Degree AV Block

AV nodal-blocking drugs: beta-

blockers, calcium channel blockers,

digoxin, amiodarone

306

Source Undetermined

1st Degree AV Block

Does not cause hemodynamic

disturbance

No specific treatment required

307

2nd Degree, Mobitz I

AKA Wenckebach

Progressive prolongation of PR

interval culminating in non-

conducted P wave

PR interval is longest immediately

before dropped beat

PR interval is shortest immediately

after dropped beat

308


P-P interval relatively constant

Greatest increase in P-R interval

typically between 1st and 2nd beats

of cycle

309

Source Undetermined


R-R interval progressively shortens

with each beat of cycle

Wenckebach pattern tends to

repeat in P:QRS groups with ratios

of 3:2, 4:3 or 5:4

310

Source Undetermined


Usually reversible conduction block

at level of AV node

Malfunctioning AV node cells tend

to progressively fatigue until they

fail to conduct impulse

His-Purkinje cells tend to fail

suddenly and unexpectedly (i.e.

producing Mobitz II block)

311


Drugs: beta & calcium channel

blockers, digoxin, amiodarone

vagal tone (e.g. athletes)

Inferior wall MI

Myocarditis

After cardiac surgery: mitral valve

repair, Tetralogy of Fallot repair

312


Usually benign rhythm

Minimal hemodynamic disturbance

Low risk of progression to 3o block

Asymptomatic: no treatment

Symptomatic: atropine usually

works

Permanent pacing: rarely required

313

2nd Degree, Mobitz II

314

Source Undetermined

Source Undetermined

Mobitz II: Description

Intermittent non-conducted P

waves without progressive

prolongation of PR interval

PR interval in conducted beats

remains constant

P waves at constant rate

315

Mobitz II: Description

RR interval surrounding dropped

beat(s): exact multiple of preceding

RR interval

2x preceding RR interval for

single dropped beat

3x preceding RR interval for two

dropped beats

316

Mobitz II: Mechanism

Usually due to conduction failure at

His-Purkinje system (i.e. below AV

node)

317

Madhero88 (Wikipedia)

http://en.wikipedia.org/wiki/Bundle_of_Hismediaviewer/File:ConductionsystemoftheheartwithouttheHeart-en.svg


More likely then Mobitz I to be due

to structural damage to conducting

system

Typically have pre-existing LBBB or

bifascicular block

Produced by intermittent failure of

remaining fascicle

“bilateral bundle-branch block”

318


In ~75%: conduction block distal to

Bundle of His broad QRS

complexes

319

Source Undetermined


In ~25%: conduction block within

His Bundle itself narrow QRS

complexes

320

Source Undetermined


Recall Mobitz I AV node fatigue

Mobitz II is “all or nothing”

His-Purkinje cells suddenly fail to

conduct supraventricular impulse

May be fixed relationship between

P waves and QRS complexes…

…but may be no pattern to

conduction blockade 321

Mobitz II: Causes 1

Anterior MI: septal infarct with

necrosis of bundle branches

Idiopathic fibrosis of conducting

system

Cardiac surgery close to septum,

like mitral valve repair

Inflammatory conditions: rheumatic

fever, myocarditis, Lyme disease

322

Mobitz II: Causes 2

Autoimmune: lupus, systemic

sclerosis

Infiltrative myocardial disease:

amyloidosis, hemochromatosis,

sarcoidosis

Hyperkalemia

Drugs: beta- & calcium channel

blockers, digoxin, amiodarone

323

Mobitz II: Significance

Much more likely than Mobitz I to

be associated with hemodynamic

compromise, severe bradycardia,

progression to 3rd degree block

Hemodynamic instability can be

sudden and unexpected

syncope (Stokes-Adams attacks) or

sudden cardiac death

324

Mobitz II: Significance

Risk of asystole: ~35% per year

Mandates admission for cardiac

monitoring, backup temporary

pacing, ultimately insertion of

permanent pacemaker

325

Source Undetermined

3rd Degree / Complete Block

326

Source Undetermined

Source Undetermined


No atrial impulses conducted

Atria and ventricles beat

independently of one another

327

Source Undetermined





328

Source Undetermined





329

Source Undetermined


P waves: normal

PR interval: variable P waves

not related to QRS complexes

PP interval: regular

RR interval: regular

Perfusing rhythm maintained

by junctional or ventricular escape

rhythm 330


Block can occur at level of AV

node, bundle of His or bundle

branches

QRS complexes: narrow or wide

depending on location of block

Above His bundle narrow

At or below His bundle wide

331


End point of either Mobitz I or II

Progressive fatigue of AV nodal

cells 2o to increased vagal tone in

acute phase of inferior MI

Sudden complete conduction

failure throughout His-Purkinje

system 2o to septal infarction in

acute anterior MI

332


High risk of ventricular standstill

and sudden cardiac death

Urgent admission for cardiac

monitoring, backup temporary

pacing, and (usually) insertion of

permanent pacemaker

333

AND FINALLY…

334

Sinus Node Dysfunction

335


AKA “sick sinus syndrome”

Abnormality of cardiac impulse

formation AND intra-atrial and AV

nodal conduction

Wide variety / combinations of

bradyarrhythmias and

tachyarrhythmias

Most common in elderly

336


Presenting symptoms may include:

Dizziness

Palpitations

Dyspnea

Fatigue

Lethargy

Syncope

337


Causes: intrinsic

Idiopathic degenerative fibrosis

Ischemia

Cardiomyopathies

Infiltrative diseases: sarcoidosis,

haemochromatosis

Congenital abnormalities

338


Causes: extrinsic

Drugs: digoxin, beta- & calcium

channel blockers

Autonomic dysfunction

Hypothyroidism

Electrolyte abnormalities:

hyperkalemia

339


Diagnosis: documentation of

bradyarrhythmia or tachyarrhythmia

in associated with these symptoms

340

Source Undetermined

Source Undetermined


Treatment: stable

Refer to cardiologist for demand

pacemaker and antidysrhythmic therapy

Treatment: unstable

Bradydysrhythmia rate stimulation

Atropine, isoproternol, pacemaker

Tachydysrhythma rate control

Digoxin, beta- or calcium channel blocker

341

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