gemc- cardiovascular board review session 3- resident training

Project: Ghana Emergency Medicine Collaborative

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

Part 3

Author(s): Joe Lex, MD (Temple University School of Medicine)

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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

Part Three

6. Disease of the Pericardium

Pericardial tamponade

Pericarditis

7. Endocarditis

8. Hypertension

9. Tumors

10.Valvular disorders

AND… 4

Part Three

PLUS: 3 bonus sets

1. Cardiac Transplant Patient

2. Pacemakers and AICDs

3. EKG Morphology

3.6 Diseases of the

Pericardium

3.6.1 Pericardial

Tamponade

Cardiac Tamponade

Fluid accumulates in space

between heart and surrounding sac

Diastolic filling impaired

cardiac output & jugular venous

pressure

cardiac output & left

ventricular stroke volume

arterial pressure

Cardiac Tamponade

pressure on R atrium CVP

systemic arterial pressure

despite central venous pressure

pressure on heart septum

bends into left ventricle stroke

volume obstructive shock

Cardiac Tamponade

Rapid fluid accumulation: trauma,

myocardial rupture, proximal aortic

dissection

Gradual fluid accumulation: cancer,

uremia, pericarditis, cardiac surgery

Occurs in ~10% of cancer patients

Fluid exudate, blood, pus, gas

Heart compensates by rate

Signs & Symptoms

Symptoms usually nonspecific

Chest pain, cough, dyspnea

Classic Beck’s triad: hypotension,

distended neck veins, muffled heart

sounds

Large in systolic blood pressure

and pulse wave amplitude during

inspiration

Diagnostic Studies

Chest x-ray: cardiomegaly only if

large fluid accumulation (250 mL)

ECG: voltage or electrical

alternans

Echocardiography: effusion +

paradoxical systolic wall motion =

diagnosis

Diagnostic Studies

Chest x-ray: cardiomegaly only if

large fluid accumulation (250 mL)

Source Undetermined

Diagnostic Studies

ECG: voltage or electrical

alternans

Source Undetermined

Diagnostic Studies

Echocardiography: effusion +

paradoxical systolic wall motion =

diagnosis

15 Source Undetermined

Management

IV fluid: right ventricle filling

pressure to overcome pericardial

constriction

Pericardiocentesis: treatment of

choice

Withdraw enough fluid to stabilize

If recurs, repeat or place drainage

catheter in pericardial space

Management

Warning: intubate with caution!!

Positive-pressure breathing

intrathoracic pressure preload

precipitous blood pressure

Management

Pericardiocentesis: carries risk

Cardiac dysrhythmias

Hemorrhage from injured

coronary vessel

Aspiration of as little as 50 to

100 mL can temporarily alleviate

pathologic process

Management

Blind subxiphoid approach 16-

or 18-gauge needle inserted at 30

to 45o angle to skin near left

xiphocostal angle, aiming toward

left shoulder

Management

Blind subxiphoid approach

20 Ribs: Mikael Häggström (Wikimedia Commons)

Xiphoid process

Syringe, Clker.com

Management

Ultrasound guided use

transducer to find largest

concentration of fluid and / or to

actively guide placement of needle

Drickey (Wikimedia Commons)

Management

Ultrasound guided

5th rib

6th rib

5th rib

6th rib

Xiphoid process

Right 5th

Intercostal

space Left 5th

Intercostal

Mikael Häggström (Wikimedia Commons)

3.6.2 Pericarditis

Constrictive Pericarditis

Late consequence of viral

pericarditis

Tuberculosis leading cause in

some countries

incidence as result of improved

survival of patients with chronic

renal disease

Symptoms and signs

indistinguishable from CHF

Dyspnea, fatigue, weight gain

Hepatomegaly, marked pitting

lower extremity edema, ascites

Characteristic auscultatory finding

pericardial knock early diastole

Friction rub may also be audible

Virtually identical to restrictive

cardiomyopathy (RCM): venous

pressure and small heart size

Echocardiogram may show

infiltrative myocardial disease in

patients with RCM

Therapy of choice: pericardiectomy

Pericarditis

Many causes, 80% idiopathic

15 – 35 mL plasma ultrafiltrate

normally in pericardial space

Accumulation when venous or

lymphatic drainage obstructed

Signs & Symptoms

History of fever, myalgia common

Chest pain, usually retrosternal

Sharp, pleuritic, varies with

respiration

Typically relieved by sitting

forward

Worsened by lying down, deep

inspiration, swallowing 30

Signs & Symptoms

Typically relieved by sitting forward

Signs & Symptoms

No single test is diagnostic

ECG: most reliable diagnostic tool

Evolves through stages over time

Stages of Pericarditis

Stage 1: first two weeks

Widespread ST elevation and PR

depression with reciprocal changes

in aVR

Stage 2: 1 to 3 weeks

Normalization of ST changes;

generalized T wave flattening

Stages of Pericarditis

Stage 3: 3 weeks and beyond

Flattened T waves become

inverted

Stage 4: several weeks

ECG returns to normal

Stage 1: Acute Pericarditis

Widespread concave ST and PR

throughout precordial (V2-6) and limb

leads (I, II, aVL, aVF)

Reciprocal ST and PR in aVR 35

Source Undetermined

Stage 1: Acute Pericarditis

Widespread concave ST and PR

throughout precordial (V2-6) and limb

leads (I, II, aVL, aVF)

Reciprocal ST and PR in aVR, V1 36

Source Undetermined

STEMI vs Acute Pericarditis

Is there ST depression in a lead

other than AVR or V1? This is a

Is there convex up or horizontal ST

elevation? This is a STEMI

Is there ST elevation greater in III

than II? This is a STEMI

STEMI vs Acute Pericarditis

PR depression in multiple leads

suggests pericarditis, especially if

there is a friction rub

Ventricular dysrhythmias rare in

pericardial disease

Could theoretically be

concomitant myocarditis

Management

Symptomatic

Treatment of choice: nonsteroidal

anti-inflammatory drug (NSAID)

Ibuprofen in anti-inflammatory

doses (2400 mg/day in adults)

Management

Oral prednisone for chronic

pericarditis and for acute

pericarditis in patients who cannot

tolerate NSAIDs

Methylprednisolone and colchicine

effective for recurrent pericarditis

3.7 Infective

Endocarditis

Current term infective endocarditis

Older classifications of acute,

subacute, and chronic: obsolete

Bacteria remain most common

etiology

Other causes: viruses, fungi, and

rickettsiae

Endocarditis

Inflammation of endocardium

Usually also involves heart valves,

native or prosthetic

May involve interventricular

septum, chordae tendineae, mural

endocardium, or intracardiac

devices (pacer wires, etc)

Endocarditis

Most patients have predisposing

valvular abnormality

Most common in elderly: calcific or

degenerative aortic and mitral valve

In developing countries: rheumatic

heart disease

Endocarditis

High-pressure gradient congenital

cardiac lesions

Ventricular septal defects

Pulmonary stenosis

Tetralogy of Fallot

Prior endocarditis is major risk

factor for recurrence

Injection Drug Users

Injection drug use: 150 – 200 /

100,000 person-years

Classic: right-sided endocarditis

Any valve can be affected

Prosthetic Valves

Prosthetic valve: unique and

potentially devastating complication

Incidence in prosthetic valve

recipients: 0.5 to 4% / year

Early or late after surgery

Timing of infection reflects

different epidemiology and

microbiology

5 Year Mortality Rates

Native valve endocarditis ~20%

Prosthetic valve ~60%

Right-sided endocarditis in injection

drug use ~10%

IE Lesions

Classic lesion: vegetation

Originates as sterile thrombus

Microorganisms adhere and colonize

May form at site of mechanical

damage: inflammation, abnormal

turbulence, degenerative changes

Injection drug users: contaminants

like talc

Causative Agents (%)

Staphylococcus aureus 32

Viridans group streptococci 18

Enterococci 11

Coagulase-negative

staphylococci 11

Streptococcus bovis 7

Other streptococci 5

Culture negative 8

Clinical Features

Symptoms nonspecific and diverse

Most common: intermittent fever

(85%) and malaise (80%)

Many have no cardiac murmur

indistinguishable from febrile viral

illness

“Classic triad” fever, anemia, heart

murmur RARE

Clinical Features

<35% of IV drug users with

endocarditis present with murmur

Substantial minority have vasculitic

lesions

Petechiae

Splinter hemorrhages

Osler's nodes

Janeway lesions

Petechiae

Splinter Hemorrhages

Osler's Nodes (raised)

PAINFUL nodules

Janeway Lesions (flat)

PAINLESS macules

Clinical Features

~30% have splenomegaly

Retinal hemorrhage: characteristic

pale center surrounded by red halo

Roth's spots

Roth’s Spots

Source Undetermined

Laboratory Findings

Nonspecific, like other infectious

conditions,

Leukocytosis in ~50%

Microscopic hematuria in ~50%

ESR / CRP nonspecific

Most have mild anemia

Other Diagnostic Findings

Chest x-ray: may show signs of

heart failure

ECG: may show conduction

abnormalities if abscess has formed

in myocardium

Blood Cultures

3 blood cultures from 3 separate

venipuncture sites

1st & last drawn at least 1h apart

~90 – 95% are positive unless

antibiotics administered

If septic, may obtain more rapidly

Continuous bacteremia: don’t wait

for chills / rigors

Echocardiography

Transthoracic echocardiography

(TTE) highly specific for vegetations

May be nondiagnostic in up to 20%

Sensitivity of TTE <60%

Transesophageal echocardiogram

(TEE): far superior to TTE

Negative predictive value of normal

TEE without prosthetic valves

Management: Native Valve

Penicillin G 5 million units IV q 4 hr +

nafcillin 2 g IV q 4 hr

Vancomycin 15 mg/kg IV q 12 hr

Gentamicin 1 mg/kg IV q 8 hr

Native Valve + Injection

Prosthetic Valve

Gentamicin 1 mg/kg IV q 8 hr

Prophylaxis: Rare in the ED

Virtually all procedures routinely

performed in ED do NOT require

prophylactic antibiotics, including:

Laceration repair

Endotracheal intubation

Central venous catheter placement

Vaginal deliveries

Foley catheter placement in absence

of infection

3.8 Hypertension

Pathophysiology

Pathophysiology of hypertensive

emergencies poorly understood

Appears to be critical arterial

pressure that overwhelms target

organ ability to compensate for

arterial pressure limits blood flow

End result: hypoperfusion of end-

organs ischemia and dysfunction

Associations with BP

Disease Threshold

Percentage of

Patients with

Subarachnoid hemorrhage >140 mmHg SBP 100.0

Ischemic stroke >140 mmHg SBP 76.5

Hemorrhage stroke >140 mmHg SBP 75.0

Type B aortic dissection >150 mmHg SBP 70.1

Type A aortic dissection >150 mmHg SBP 35.7

Acute heart failure >140 mmHg SBP >50.0

NSTEMI-ACS >140 mmHg SBP >50.0

Encephalopathy

Altered mental status

Headache

Vomiting

Seizures

Visual disturbances

Papilledema, retinal hemorrhages

or exudates

Hematuria 69

Treatment: “Emergencies”

2008 Cochrane review: no

evidence antihypertensive drugs

mortality or morbidity in patients

with hypertensive emergencies

Insufficient trial evidence to

recommend one agent over

another, again using morbidity and

mortality as outcome measure

Aortic Dissection

Therapeutic goal: systolic BP

ranging from <140 to <110 mm Hg

Treatment of pain with morphine is

important part of the management

Aortic Dissection

Labetalol GOALS

SBP 100–120 mm

Hg (expert review

and guidelines)

shear forces by

BP and HR

HR <60 beats/min

Esmolol

Nicardipine*

Nitroprusside*

* After beta-blockade 72

Pulmonary Edema

Nitroglycerin

BP by 20%–30%

Promote diuresis

after vasodilation

Symptom relief

Enalaprilat

Nicardipine

Nitroprusside

Acute Myocardial Infarction

Nitroglycerin

No more than 20%–

30% SBP >160

ischemia

-Blocker:

metoprolol,

labetalol

Acute Renal failure

Labetalol

BP by no more

than 20%

Nicardipine

Fenoldopam

Dialysis

Eclampsia / HELLP

Labetalol

<160 / 100

Hydralazine too

unpredictable, no

longer recommended

Nifedipine /

nicardipine

Encephalopathy

Labetalol

MAP 15 – 20%

Too aggressive

ischemic infarct

Nicardipine

Fenoldopam

Subarachnoid Hemorrhage

Labetalol SBP <160 mm Hg or

MAP <130 mm Hg to

prevent rebleeding

SBP >120 to

preserve cerebral

perfusion

Nicardipine

Esmolol

Acute Ischemic Stroke

Labetalol If fibrinolytic therapy

planned, treat if

>185/110 mm Hg

Lowering BP may

significantly worsen

ischemia and deficit

Nicardipine

Nitroglycerin

Asymptomatic Hypertension

Traditionally associated with HTN:

headache, visual changes, chest

pain, dyspnea, dizziness

Reality: poor correlation

Pain / anxiety traditionally blamed

Not supported by data

Common in patients with epistaxis

Not related to severity of HTN

Asymptomatic Hypertension

No evidence ever that acute

treatment of asymptomatic severe

hypertension prevents or reduces

patient morbidity or mortality

Special Cases

Clonidine rebound: give 0.2 mg po

Cocaine: unopposed -blocker

Drug of choice: benzodiazepine

Pheochromocytoma: -blockade /

phentolamine

3.9 Tumors

Atrial Myxoma

Most common, most important

Can cause ball valve type

obstruction

~75% in left atrium

Right atrial myxomas associated

with tricuspid stenosis and atrial

fibrillation

More common in women 84

Symptoms

Usually with body position change

Platypnea: difficulty breathing

upright, relief when supine

Dyspnea on exertion

Paroxysmal nocturnal dyspnea

Dizziness / fainting / palpitations

Often mimic mitral stenosis

Diagnosis

Right atrial myxomas rarely

produce symptoms until they have

grown to be at least 13 cm wide

“Tumor plop” related to movement

of tumor, abnormal heart sounds, or

murmur

Sound may change when patient

changes position

Echo / CT / MRI 86

Ultrasound

Source Undetermined

CT Scan

3.10 Valvular Disorders

Anatomy

Tricuspid, pulmonic, aortic: 3 cusps

Mitral: 2 cusps

Cusp: double layer of endocardium

attached to fibrous skeleton of heart

Cusp margins attached to papillary

muscles of ventricles via chordae

tendineae

Anatomy

Gray's Anatomy (Wikipedia)

ER Docs Need to Know

Mitral stenosis

Mitral regurgitation

Mitral valve prolapse

Aortic stenosis

Aortic insufficiency / regurgitation

Prosthetic valve failure

#1 symptom: SHORT OF BREATH

Mitral Stenosis

Most common cause: rheumatic

heart disease

Symptoms usually delayed 10-30y

Most common complication: atrial

fibrillation

CLASSIC symptom: hemoptysis

(rare)

Late: heart failure 94

Mitral Stenosis

Diuresis for vascular congestion

Anticoagulation for atrial fibrillation

Median survival without

intervention: 7 years

ED management: identify and treat

precipitants, refer for definitive

intervention

Mitral Regurgitation: Acute

True emergency: SURGICAL, not

medical

Idiopathic chordae rupture

Papillary muscle dysfunction /

rupture 2 – 7 days postinfarction

Low left atrial compliance left

atrial pressure acute pulmonary

congestion

Presentation: fulminant pulmonary

Harsh, midsystolic murmur that

radiates to base,but NOT axilla

Treat pulmonary edema with

nitrates and diuretics

Emergency echocardiography

Cardiac catheterization

Hypotension: counterpulsation

intra-aortic balloon pump may

bridge to surgery

Mitral Regurgitation: Chronic

Presentation ~chronic systolic heart

failure

Symptoms decompensated CHF

Murmur: holosystolic

ECG left atrial and ventricular

hypertrophy

Atrial fibrillation common

CXR: left atrial enlargement 99

Mitral Valve Prolapse

Generally benign

Infrequently associated with MR,

endocarditis, arrhythmias

True prevalence <1% in both men

and women

Old data: 5% women > men

Mitral Valve Prolapse

Associated with chest pain,

palpitations, dyspnea,

lightheadedness, fatigue, etc.

Current data: no cause-and-effect

Cardioselective -blockers may

As of 2007: AHA no longer says

prophylactic antibiotics

Aortic Stenosis

Calcific degeneration in elderly with

coronary artery disease

Severe or critical AS: very preload

dependent with little reserve

Precipitous decompensation with

minimal stressors: ischemia, atrial

fibrillation, dehydration, anemia,

Aortic Stenosis

Classic symptoms: angina,

exertional syncope, CHF

Classic murmur: crescendo-

decrescendo systolic heard best at

base (right 2nd intercostal space)

and radiates into carotids

Carotid pulses delayed (tardus)

and diminished in intensity (parvus).

Aortic Stenosis

Natural history: slow progression

without symptoms for years

Symptoms reduce survival unless

valve replaced

Medical management: limited role

Aortic Stenosis: Acute

Judicious fluid resuscitation

Transfuse blood prn

Restore sinus rhythm

AVOID vasodilators, diuretics,

inotropic agents

If no response intra-aortic

balloon pump may bridge to surgery

Aortic Insufficiency: Acute

left ventricular compliance

left ventricular pressure acute

pulmonary congestion

May present with suggestions of

aortic dissection or aneurysm

May present in severe respiratory

distress or frank cardiogenic shock

May be very subtle

Aortic Insufficiency: Acute

Surgical emergency requiring

immediate valve replacement

Medical stabilization: cautious use

of vasodilators and diuretics

INTRA-AORTIC BALLOON

COUNTERPULSATION IS

CONTRAINDICATED

Aortic Insufficiency: Chronic

Widened pulse pressure

Rapid rise and fall carotid pulse

(water-hammer or Corrigan’s pulse)

Spontaneous nailbed pulsations

(Quincke’s sign)

High-pitched, blowing, diastolic

murmur at left sternal border

Artificial Valves

Source Undetermined

Prosthetic Valves

Mechanical: entirely synthetic

Biologic: porcine or human

Bioprosthetic: bovine pericardium

Complications: structural failure,

hemolysis, endocarditis, thrombosis

systemic embolization

Prosthetic Valves: Failure

1o structural failure: extremely rare

Presentation: acute severe

regurgitation and shock

emergent replacement

Biologic valves: structural failure

less dramatic but more common

Symptoms usually insidious,

mimic native valve disease

Prosthetic Valves: Clots

Prosthetic valve thrombosis ~2%

per year, both with biologic and

appropriately anticoagulated

mechanical valves

Symptoms of variable duration,

generally subacute, mimic CHF

Suggested by or absent valve

click, new regurgitant murmur, loud

stenotic murmur 112

Prosthetic Valves: Clots

Systemic embolization ~1% / year

Mitral rate 2x aortic

Biologic valve mechanical valve if

appropriately anticoagulated

Target INR 3.0 - 3.5 for mitral

valve, 2.5 – 3.0 for aortic

Prosthetic Valves: Hemolysis

From shear forces

Usually mild, subclinical

Severe in up to 15%

Features subtle: dyspnea, fatigue,

jaundice, dark urine

Iron replacement effective in

majority

Prosthetic Valves: IE

Highest during initial months

Mechanical & bioprosthetic similar

Within 60d of surgery: perioperative

pathogen morbidity / mortality

After 60d: transient bacteremia

more benign

Prosthetic Valves: IE

Most common symptom: fever

Normal echocardiogram does not

rule out endocarditis

ED diagnosis presumptive

Definitive diagnosis requires

blood cultures or biopsy

Patient with prosthetic valve + fever

without other source: assume IE 116

Bonus 1: Transplant

Heart Transplant

>3000 / year in USA

5-year survival rates for adults and

children: 72 and 80%

Recipient heart removed, replaced

by donor heart: orthotopic

More than 1/3 will visit ER in first 3

60% will be admitted 118

Heart Transplant

Most common complaints

Fever (37%)

Shortness of breath (13%)

Nausea, vomiting, diarrhea: (10%),

Chest pain (9%)

Most common ED admit diagnoses

Sepsis (18%)

Rejection (11%)

Pneumonia (8%)

Heart Transplant

Chest pain rarely related to cardiac

ischemia

Denervated heart incapable of

producing angina

Acute rejection in 75 to 85% of

patients within first 3 months

Severe rejection QRS, new

S3, new CHF or atrial dysrhythmia

Heart Transplant

Any heart transplant patient

presenting with CHF, fever

(>38° C), shortness of

breath, hypoxia, hypotension,

poorly controlled

hypertension, or new

dysrhythmia ADMIT

Heart Transplant

Source Undetermined

Heart Transplant

Source Undetermined

Heart Transplant

Heart rate can with exercise or

stress through endogenous

catecholamines

Up to 70% maximum for age

Exogenous pressor drugs work well

Slightly enhanced response to

norepinephrine and isoproterenol

Atropine no: vagal denervation 124

Heart Transplant

Infection: one-fourth of deaths

after transplant

Most vulnerable period: first 3 mo,

immunosuppression maximal

1st month: nosocomial

N/V/D think CMV

New headache: think brain abscess

Heart Transplant

Risk of endocarditis antibiotic

prophylaxis for invasive procedures

likely to cause bacteremia

Abscess drainage, urethral

catheterization

NOT for endotracheal intubation

Bonus 2:

Pacemakers

Steven Fruitsmaak (Wikipedia)

External Pacemaker

128 STERNUM APEX FRONT Mikael Häggström (Wikimedia Commons)

Transvenous Pacemaker

Gregory Marcus, MD (Wikipedia)

Emergent Pacemaker 1

Acute myocardial infarction with:

Asystole

Symptomatic bradycardia

Sinus bradycardia with

hypotension

Mobitz Type I 2o AV block with

hypotension not responsive to

atropine 130

Acute myocardial infarction with:

Bilateral bundle branch block (BBB)

New or indeterminate age

bifascicular block with 1o AV block

Mobitz type II 2o AV block

Bradycardia not associated with

acute myocardial infarction:

Asystole

Second-degree or third-degree AV

block with hemodynamic

compromise or syncope at rest

Ventricular tachyarrhythmias

secondary to bradycardia

Prophylactic (standby kit at bedside)

Stable bradycardias

1 of following in setting of acute MI

Symptomatic sinus node dysfunction

Mobitz II

Complete heart block

Newly acquired or age-indeterminate

LBBB, RBBB, alternating BBB or

bifasicular block 133

Pacemaker: Temporary

Preferred access: right internal

jugular vein (most direct route)

Ideal location of catheter tip: lodged

in trabeculae of right ventricle apex

Fluoroscopic or ECG guidance

preferred to blind placement

More time consuming

Not always possible

Pacemaker: Temporary

Pacing results in abnormal QRS

morphology

Catheter tip properly placed in right

ventricle RV stimulated first, with

delayed stimulation of left ventricle

Produces left bundle branch block

pattern on EKG

Implanted Pacemaker

Source Undetermined

Pacemaker Components

Pulse generator

Power source / battery

Control circuitry

Transmitter / receiver

Reed switch: magnet activated

Single or multiple

Unipolar or bipolar 137

Pacemaker Classification

By nature of pacing mode

Series of up to 5 letters

Follows code developed by North

American Society of Pacing and

Electrophysiology (NASPE) and

British Pacing and

Electrophysiology Group (BPEG)

Last revised in 2002 – some

textbooks use earlier classification 138

chambers

sensed

response

to sensing

modulation

multisite

pacing

0 = none 0 = none 0 = none 0 = none

A = atrium T = trigger R = rate

modulation

atrium

V = ventricle I = inhibit V =

ventricle

D = dual, both` D = dual D = dual,

NASPE / BPEG Code (2002)

I: chambers

II: chambers

sensed

III: response

to sensing

0 = none 0 = none

A = atrium T = trigger

V = ventricle I = inhibit

D = dual, both` D = dual

What You Need To Know

Note that response is PACEMAKER

response, not heart response. 140

DDD – Most Common Mode

Senses and paces both atrium and

ventricles

If no native atrial activity for set

time atrial pacing

If no native ventricle activity for set

time following atrial activity

ventricle pacing

AAI – aka Atrial Demand

Atrial pacing and sensing

If native atrial activity sensed

pacing inhibited

If no native activity sensed for pre-

determined time atrial pacing

initiated

Used in sinus node dysfunction

with intact AV conduction

Ventricle pacing and sensing

Similar to AAI, but involves

ventricles instead of atrium

Used in patients with chronic atrial

impairment e.g. atrial fibrillation or

flutter

Magnet Mode

Applying magnet usually initiates

asynchronous pacing mode: AOO,

VOO, or DOO

Asynchronous modes deliver

constant rate paced stimuli

regardless of native rate of rhythm

Magnet Mode

In asynchronous ventricle pacing

there is a risk of pacemaker-

induced ventricular tachycardia

Differs from magnet application to

an Implantable Cardioversion

Defibrillator (ICD) results in

defibrillator deactivation

Paced EKG

Appearance depends on pacing

mode used, placement of pacing

leads, device pacing thresholds,

and presence of native electrical

activity

Paced EKG

Pacing spikes

Vertical spikes of short duration:

usually 2 ms

Hard to see in all leads

Bipolar leads much smaller

pacing spike than unipolar leads.

Epicardial leads smaller pacing

spikes than endocardial 148

Paced EKG

Atrial Pacing

Pacing spike precedes p wave

P wave morphology depends on

lead placement, may look normal

Paced EKG

Ventricular Pacing

Pacing spike before QRS complex

Right ventricle pacing lead

placement QRS morphology

similar to LBBB

Left epicardial pacing lead

placement QRS morphology

similar to RBBB

Paced EKG

Ventricular Pacing

ST segments and T waves should

be discordant with the QRS

complex

Major terminal portion of QRS

complex is located on opposite side

of baseline from ST segment and T

Paced EKG

Dual Chamber Pacing

Dependent on areas begin paced

May exhibit features of atrial

pacing, ventricular pacing or both

Pacing spikes may precede only P

wave, only QRS complex, or both

Paced EKG

Atrial pacer spikes

Source Undetermined

Paced EKG

Atrial and Ventricular pacer spikes

Source Determined

Paced EKG

Atrial and ventricular pacing spikes

visible before each QRS complex

Source Undetermined

Paced EKG

100% atrial capture: small P waves

follow each atrial pacing spike

Source Undetermined

Paced EKG

100% ventricular capture: QRS

complex follows each ventricular

pacing spike 157

Source Undetermined

Paced EKG

QRS complexes broad with LBBB

morphology ventricular pacing

electrode is in right ventricle 158

Source Undetermined

Abnormal Pacing

Atrial non-capture: atrial pacing

spikes are not followed by P waves

Source Undetermined

Atrial undersensing: atrial pacing

spikes occur regardless of P waves

Pacemaker is not “seeing”

intrinsic activity

Abnormal Pacing

Source Undetermined

Abnormal Pacing

Ventricular non-capture: ventricular

pacing spikes not followed by QRS

complexes

Source Undetermined

Abnormal Pacing

Ventricular undersensing:

ventricular pacing spikes occur

regardless of QRS complexes

Pacer not “seeing” intrinsic activity

Failure to Capture

Pacer does not generate spike

when it should 164

Source Undetermined

Failure to Capture

Causes

Insufficient pacer energy

Low pacemaker battery

Dislodged, loose, fibrotic, or

fractured electrode

Electrolyte abnormalities: acidosis,

hypoxemia, hypokalemia

Poor cardiac output 165

Failure to Capture

Solutions

View rhythm in different leads

Change electrodes

Check connections

Increase pacer output (↑mA)

Change battery, cables, pacer

Reverse polarity

Failure to Sense

Causes

Pacemaker not sensitive enough to

patient’s intrinsic electrical activity

Insufficient myocardial voltage

Dislodged, loose, fibrotic, or

fractured electrode

Electrolyte abnormalities

Low battery 167

Failure to Sense

Pacer does not recognize normal

beat, generates unnecessary spike

Source Undetermined

Failure to Sense

Danger: potential for paced

ventricular beat to land on T wave

Source Undetermined

Failure to Sense

Solution

Change electrodes

Check connections

Increase pacemaker’s sensitivity

Change cables, battery, pacemaker

Reverse polarity

Check electrolytes

Oversensing

Pacing does not occur when

intrinsic rhythm is inadequate

Oversensing

Causes

Pacemaker inhibited due to

sensing of P waves & QRS

complexes that do not exist

Pacemaker too sensitive

Possible wire fracture, loose

contact

Pacemaker failure 172

Oversensing

Solution

Change electrodes

Check connections

Decrease pacemaker sensitivity

Change cables, battery, pacemaker

Check electrolytes

Competition

Pacemaker & patient’s intrinsic rate

are similar

Unrelated pacer spikes to P wave,

QRS complex fusion beats

Source Undetermined

Competition

Causes

Asynchronous pacing

Failure to sense

Mechanical failure: wires, bridging

cables, pacemaker

Loose connections

Competition

Solution

Assess underlying rhythm

Slowly turn pacer rate down

Troubleshoot as for failure to sense

Increase pacemaker sensitivity

Increase pacemaker rate

Gejordan (Wikipedia)

Automatic Implantable Cardioverter

– Defibrillator

Indications: patients at high risk for

fatal dysrhythmia (V-Tach, V-Fib)

and sudden cardiac death (SCD)

Survivor of Sudden Cardiac Death

Brugada Syndrome

risk of SCD from 30-45% per

year to < 2% per year

Components include:

Lead system: both sensing and

shocking electrodes

Logic circuitry: analyze sensed signal

A pulse generator: to generate shock

Capacitor: to deliver shock

Longevity varies with generation of

AICD and frequency of use

Third generation devices can

deliver ~200 shocks, have projected

life-span of 7-8 years

AICD Issues in ED

Ineffectiveness

Lead fracture: +/- seen on x-ray

Failure of another component, such

as battery

Failure from strong electromagnetic

fields and interference from

appliances and security / anti-theft

devices

AICD Issues in ED

Frequent / recurrent AICD discharge

May be reported or result from

…more frequent episodes of

ventricular fibrillation / tachycardia

…sensing malfunction / false sensing

(e.g. sensing and shocking SVT or

muscular contractions)

…ghost shocks: patient reports

shocks but none have occurred 182

AICD Issues in ED

Frequent / recurrent AICD discharge

Evaluation should include

Continuous cardiac monitoring

EKG and CXR

Cardiac markers and drug levels

Potassium, magnesium, and

calcium levels

Telemetry interrogation of AICD 183

AICD Issues in ED

Inactivation: placing magnet over

AICD generator will inactivate it and

prevent further shocks

AICD & CPR

Perform CPR in usual manner

Provider may perceive AICD shock:

not uncomfortable or dangerous

Perform external transthoracic

defibrillation in usual manner

Keep paddles away from AICD

generator

AICD & Magnets

2nd generation AICD: place donut-

shaped magnet over upper right

quadrant of pulse generator for 30

seconds inactivates anti-

tachycardic pacing and shock

therapy components of AICD

Reapply magnet for 30 seconds to

reactivate

AICD & Magnets

3rd generation AICD: place

magnet over pulse generator

inactivates anti-tachycardic pacing

therapy and shocks for as long as

magnet remains in place over AICD

Remove magnet reactivate

device

AICD and Infection

Erythema / induration / drainage at

generator site hospitalize for IV

antibiotics

Early infection usually caused by

staphylococcal species

Source Undetermined

Bonus 3: EKG

Basics

Basic Principles

Recordings obtained at paper

speed of 25mm/sec

Vertical axis measures distance

Each small box = 1mm x 1mm

Horizontal axis measures time

Each small box = 0.04 sec/mm

Monitor Lead Placement

White – right arm

Black – left arm

Red – left leg

“White is right

smoke above fire”

Mikael Häggström (Wikimedia Commons

Precordial Lead Placement

V1 – right parasternal 4th ICS

V2 – left parasternal 4th ICS

V3 – midway between V2 and V4

V4 – 5th ICS L midclavicular line

V5 – 5th ICS L anterior axillary line

V6 – 5th ICS L midaxillary line

Source Undetermined

Right-Sided Leads

V1R – left parasternal 4th ICS

V2R – right parasternal 4th ICS

V3R – midway between V2R and V4R

V4R – 5th ICS R midclavicular line

V5R – 5th ICS R anterior axillary line

V6R – 5th ICS R midaxillary line

Right-Sided Leads

V1R V2R

V4R V5R

Mikael Häggström (Wikimedia Commons)

Posterior Leads

V7 – Posterior Axillary Line

V8 – Scapular Tip

V9 – Paraspinous 196

Scapula

V7 V8 V9

Anatomically Contiguous

Source Undetermined

Wave Morphology

P Wave

Atrial depolarization

Upright in Leads I, II, AVF, V4-V6

Inverted in AVR

Normal: <0.10 seconds wide,

<3mm tall

Normal P-R interval: 0.12 seconds

P Wave

QRS Complex

Ventricular depolarization

Normal QRS: 0.06 – 0.10 seconds

Normal Q wave: <0.04 seconds

wide and <3mm deep

Abnormal if >3mm deep or >1/3 of

QRS complex

Normal R wave: ≤7.5mm high

QRS Complex

QT Interval

From beginning of Q to end of T

Varies with heart rate and gender

Normal: 0.33 – 0.42 seconds at

normal HR or <½ preceding R-R

interval

QT Interval

T Wave

Ventricular repolarization

Upright in Leads I, II, V3-V6,

inverted in AVR

Normal: ≤ 5mm high in limb leads

and ≤ 10mm in V leads

T Wave

U Waves

Ventricular afterpotential

Any deflection after T wave

Usually low voltage

Same polarity as T wave

Most easily seen in lead V3

Can be normal

U Waves

Prominent U waves may indicate…

Hypokalemia (< 3meq/L)

Hypercalcemia

Drugs: digitalis, phenothiazines,

quinidine, epinephrine, inotropic

agents, amiodarone

U Waves

Inverted U waves may indicate…

Acute coronary ischemia

Ventricular strain / dilation

Hypertension

Intracranial or subarachnoid

hemorrhage

Abnormal

Morphologies

Abnormal Morphologies

Hypothermia

Hypokalemia

Hyperkalemia

Hypocalcemia

Hypercalcemia

Hypomagnesemia

Digitalis effect

Digitalis toxicity 211

HYPOTHERMIA

Hypokalemia

Hyperkalemia

Hypocalcemia

Hypercalcemia

Hypomagnesemia

Digitalis effect

Hypothermia

Core temperature < 35°C (95°F)

J Wave or Osborn Wave: broad

upright deflection at end of an

upright QRS complex

Conduction delays: PR, QRS, QT

intervals are all prolonged

Hypothermia

Source Undetermined

Hypothermia

Dysrhythmias: most common

sinus bradycardia, atrial fibrillation

with slow ventricular response

Risk increases as core temperature

falls 30°C (86°F)

At core temperatures <25°C

(77°F), spontaneous ventricular

fibrillation and asystole may occur

Hypothermia

Treatment: most dysrhythmias

require no therapy, revert

spontaneously with rewarming

Source Undetermined

Potassium Abnormalities

Evan-Amos (Wikipedia)

Hypothermia

HYPOKALEMIA

Hyperkalemia

Hypocalcemia

Hypercalcemia

Hypomagnesemia

Digitalis effect

Hypokalemia

Potassium level <3.5 mEq/L

Moderate hypokalemia <3.0 mEq/L

Severe hypokalemia <2.5 mEq/L

EKG changes appear when K+ falls

below about 2.7 mEq/L

Hypokalemia

Early: flattened T waves

Late: inverted T waves

Progressively more prominent U

waves: best seen in V3

Hypokalemia

Source Undetermined

Hypokalemia

Depressed ST segment

Prominent P wave

Prolonged PR interval

Apparent long QT interval due to

fusion of T and U waves long

QU interval

Hypokalemia

Source Undetermined

Hypokalemia

Predisposes to digitalis toxicity and

associated dysrhythmias

supraventricular and ventricular

ectopics

Supraventricular tachyarrhythmias:

atrial fibrillation, atrial flutter, atrial

tachycardia

Hypokalemia

potential for life-threatening

ventricular arrhythmias: ventricular

tachycardia, ventricular fibrillation,

Torsades de Pointes

Hypokalemia Hypokalemia

Hypothermia

Hypokalemia

HYPERKALEMIA

Hypocalcemia

Hypercalcemia

Hypomagnesemia

Digitalis effect

Hyperkalemia

Worsening hyperkalaemia

suppression of impulse generation

by SA node

conduction by AV node / His-

Purkinje system

bradycardia / conduction blocks

ultimate cardiac arrest

Hyperkalemia

Early: tall “hyperacute” T waves

Prolonged PR interval

Flattened or absent P wave

Wide QRS complex

Eventually blends with T wave to

assume “sine wave” appearance

Heart blocks

QT interval normal or shortened 229

Hyperkalemia

Potassium level >5.5 mEq/L

Moderate hyperK+: >6.0 mEq/L

Severe hyperK+: >7.0 mE/L

230 Acdx (Wikipedia)

Hyperkalemia

Potassium > 5.5 mEq/L

repolarization abnormalities:

peaked T waves

Hyperkalemia

Potassium > 6.5 mEq/L

progressive paralysis of atria

P wave widens and flattens

PR segment lengthens

P waves disappear

Hyperkalemia

Source Undetermined

Hyperkalemia

Potassium >7.0 mEq/L

bradycardia and conduction

abnormalities

Prolonged QRS interval with

bizarre QRS morphology

High-grade AV block with slow

junctional and ventricular escape

rhythms

Hyperkalemia

Any kind of conduction block:

bundle branch blocks, fascicular

blocks

Sinus bradycardia or slow atrial

fibrillation

Sine wave appearance: pre-

terminal

Hyperkalemia

Source Undetermined

Hyperkalemia

Calcium

MigGroningen (Wikimedia Commons)

Hypothermia

Hypokalemia

Hyperkalemia

HYPOCALCEMIA

Hypercalcemia

Hypomagnesemia

Digitalis effect

Hypocalcemia

Normal calcium: 9 – 10.5 mg/dL

(2.2 – 2.6 mmol/L

Normal ionized calcium: 4.5 – 5.6

mg/dL (1.1 – 1.4 mmol/L)

Mild-moderate: 7.6 – 9.0 mg/dL

(1.9 – 2.2 mmol/L

Severe: <7.6 mg/dL (1.9 mmol/L)

Hypocalcemia

QTC prolongation: primarily by

prolonging ST segment

T wave usually unchanged

Dysrhythmias uncommon, but atrial

fibrillation reported

Torsades de pointes less common

than with low potassium or

magnesium

Hypocalcemia

QT interval: time from start of Q

wave to end of T wave

Time for ventricular depolarization

and repolarization

Corrected QT interval = QTC

Estimates QT interval at heart rate

= 60 bpm

Bazett’s formula: QTC = QT / √ RR 243

Hypocalcemia

If heart rate = 60, then QT = QTC

QTC prolonged if > 440ms in men

or > 460ms in women

QTC > 500 ms associated with

risk torsades de pointes

QTc abnormally short if < 350ms

Normal QT <half preceding RR

QT Interval

Source Undetermined

Hypocalcemia

Hypothermia

Hypokalemia

Hyperkalemia

Hypocalcemia

HYPERCALCEMIA

Hypomagnesemia

Digitalis effect

Hypercalcemia

Most reliable ECG change:

shortening of QT interval

Nearly always seen when calcium

concentration exceeds 12mg/dL

(3.0 mmol/L)

Calcium

Source Undetermined

Hypothermia

Hypokalemia

Hyperkalemia

Hypocalcemia

Hypercalcemia

HYPOMAGNESEMIA

Digitalis effect

Hypomagnesemia

Normal magnesium = 1.5 – 2.5

mg/dL (0.8 – 1.0 mmol/L)

Hypomagnesemia = <1.5 mg/dL

Usually associated with other

electrolyte abnormalities

hypokalemia, hypocalcemia

Predisposes to digitalis toxicity and

its associated dysrhythmias

Hypomagnesemia

Prolonged PR and QTC intervals

Widened QRS

ST segment abnormalities

Flattened or inverted T waves,

especially in precordial leads

Ventricular dysrhythmias: PVCs,

ventricular tachycardia, ventricular

fibrillation, torsades de pointes 252

Hypomagnesemia

Digitalis

254 Jcart1534 (Wikimedia Commons)

Enrico Blasutto (Wikipedia)

Hypothermia

Hypokalemia

Hyperkalemia

Hypocalcemia

Hypercalcemia

Hypomagnesemia

Digitalis toxicity

DIGITALIS EFFECT

Digitalis Effect

Sagging ST segment with upward

concavity: resembles hockey stick

(or Salvador Dali’s mustache)

Source Undetermined Roger Higgins (Wikipedia)

Digitalis Effect

Short QT interval

Flattened or inverted T wave

Modestly prolonged PR interval

Most prominent in lateral leads

Occur in most patients who are

adequately digitalized; NOT an

indication of digitalis toxicity

Digitalis Effect

Hypothermia

Hypokalemia

Hyperkalemia

Hypocalcemia

Hypercalcemia

Hypomagnesemia

Digitalis effect

DIGITALIS TOXICITY 259

Digitalis Toxicity

Poisons Na+-K+-ATPase pump

intracellular entry of Na+ and

Ca++ / egress of K+ excitability

ectopy / tachydysrhythmias

vagal tone and automaticity

conduction in AV node

bradydysrhythmias / AV blocks

Digitalis Toxicity

Predisposing factors

potassium / magnesium,

calcium / potassium

Hypoxia

Metabolic Alkalosis

Underlying diseases

Drugs: quinidine, erythromycin,

amiodarone, captopril, ibuprofen 261

Digitalis Toxicity

Most common EKG finding: PVCs,

often bigeminal and multiform

Pathognomonic EKG finding:

paroxysmal atrial tachycardia with

AV block

Digitalis Toxicity

Paroxysmal atrial

tachycardia with block

Source Undetermined

Digitalis Toxicity

Regularized Atrial Fibrillation

Digitalis Toxicity

Can also see

Atrial fibrillation with slow

ventricular response

Sinus arrest

Junctional tachycardia (common)

Ventricular tachycardia

Digitalis Toxicity

Can also see

Bidirectional ventricular tachycardia

(highly suggestive but rare)

Ventricular fibrillation

Sinus bradycardia

SA and AV nodal blocks

Digitalis Toxicity

For presentation and treatment:

see Toxicology Section

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diagnostic

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large fluid

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