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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
Page 4
Part Three
6. Disease of the Pericardium
Pericardial tamponade
Pericarditis
7. Endocarditis
8. Hypertension
9. Tumors
10.Valvular disorders
AND… 4
Page 5
Part Three
PLUS: 3 bonus sets
1. Cardiac Transplant Patient
2. Pacemakers and AICDs
3. EKG Morphology
5
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3.6 Diseases of the
Pericardium
6
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3.6.1 Pericardial
Tamponade
7
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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
8
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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
9
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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
10
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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
11
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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
12
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Diagnostic Studies
Chest x-ray: cardiomegaly only if
large fluid accumulation (250 mL)
13
Source Undetermined
Page 14
Diagnostic Studies
ECG: voltage or electrical
alternans
14
Source Undetermined
Page 15
Diagnostic Studies
Echocardiography: effusion +
paradoxical systolic wall motion =
diagnosis
15 Source Undetermined
Page 16
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
16
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Management
Warning: intubate with caution!!
Positive-pressure breathing
intrathoracic pressure preload
precipitous blood pressure
17
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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
18
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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
19
Page 20
Management
Blind subxiphoid approach
20 Ribs: Mikael Häggström (Wikimedia Commons)
Xiphoid process
Syringe, Clker.com
45
°
Page 21
Management
Ultrasound guided use
transducer to find largest
concentration of fluid and / or to
actively guide placement of needle
21
Drickey (Wikimedia Commons)
Page 22
Management
Ultrasound guided
22
5th rib
6th rib
5th rib
6th rib
Xiphoid process
Right 5th
Intercostal
space Left 5th
Intercostal
space
Mikael Häggström (Wikimedia Commons)
Page 23
3.6.2 Pericarditis
23
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Constrictive Pericarditis
24
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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
25
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Constrictive Pericarditis
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
26
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Constrictive Pericarditis
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
27
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Pericarditis
Many causes, 80% idiopathic
15 – 35 mL plasma ultrafiltrate
normally in pericardial space
Accumulation when venous or
lymphatic drainage obstructed
29
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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
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Signs & Symptoms
Typically relieved by sitting forward
31
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Signs & Symptoms
No single test is diagnostic
ECG: most reliable diagnostic tool
Evolves through stages over time
32
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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
33
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Stages of Pericarditis
Stage 3: 3 weeks and beyond
Flattened T waves become
inverted
Stage 4: several weeks
ECG returns to normal
34
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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
Page 36
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
Page 37
STEMI vs Acute Pericarditis
Is there ST depression in a lead
other than AVR or V1? This is a
STEMI
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
37
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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
38
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Management
Symptomatic
Treatment of choice: nonsteroidal
anti-inflammatory drug (NSAID)
Ibuprofen in anti-inflammatory
doses (2400 mg/day in adults)
39
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Management
Oral prednisone for chronic
pericarditis and for acute
pericarditis in patients who cannot
tolerate NSAIDs
Methylprednisolone and colchicine
effective for recurrent pericarditis
40
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3.7 Infective
Endocarditis
41
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Endocarditis
Current term infective endocarditis
Older classifications of acute,
subacute, and chronic: obsolete
Bacteria remain most common
etiology
Other causes: viruses, fungi, and
rickettsiae
42
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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)
43
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Endocarditis
Most patients have predisposing
valvular abnormality
Most common in elderly: calcific or
degenerative aortic and mitral valve
In developing countries: rheumatic
heart disease
44
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Endocarditis
High-pressure gradient congenital
cardiac lesions
Ventricular septal defects
Pulmonary stenosis
Tetralogy of Fallot
Prior endocarditis is major risk
factor for recurrence
45
Page 46
Injection Drug Users
Injection drug use: 150 – 200 /
100,000 person-years
Classic: right-sided endocarditis
Any valve can be affected
46
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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
47
Page 48
5 Year Mortality Rates
Native valve endocarditis ~20%
Prosthetic valve ~60%
Right-sided endocarditis in injection
drug use ~10%
48
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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
49
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Causative Agents (%)
Staphylococcus aureus 32
Viridans group streptococci 18
Enterococci 11
Coagulase-negative
staphylococci 11
Streptococcus bovis 7
Other streptococci 5
Culture negative 8
50
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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
51
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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
52
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Petechiae
53 Source Undetermined
Page 54
Splinter Hemorrhages
54 Source Undetermined
Page 55
Osler's Nodes (raised)
PAINFUL nodules
55 Source Undetermined
Page 56
Janeway Lesions (flat)
PAINLESS macules
56 Source Undetermined
Page 57
Clinical Features
~30% have splenomegaly
Retinal hemorrhage: characteristic
pale center surrounded by red halo
Roth's spots
57
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Roth’s Spots
58
Source Undetermined
Page 59
Laboratory Findings
Nonspecific, like other infectious
conditions,
Leukocytosis in ~50%
Microscopic hematuria in ~50%
ESR / CRP nonspecific
Most have mild anemia
59
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Other Diagnostic Findings
Chest x-ray: may show signs of
heart failure
ECG: may show conduction
abnormalities if abscess has formed
in myocardium
60
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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
61
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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
~100%
62
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Management: Native Valve
Penicillin G 5 million units IV q 4 hr +
nafcillin 2 g IV q 4 hr
Or
Vancomycin 15 mg/kg IV q 12 hr
Plus
Gentamicin 1 mg/kg IV q 8 hr
63
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Native Valve + Injection
Vancomycin 15 mg/kg IV q 12 hr
Prosthetic Valve
Vancomycin 15 mg/kg IV q 12 hr
Plus
Gentamicin 1 mg/kg IV q 8 hr
64
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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
65
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3.8 Hypertension
66
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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
67
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Associations with BP
Disease Threshold
Value
Percentage of
Patients with
BP
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
68
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Encephalopathy
Altered mental status
Headache
Vomiting
Seizures
Visual disturbances
Papilledema, retinal hemorrhages
or exudates
Hematuria 69
Page 70
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
70
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Aortic Dissection
Therapeutic goal: systolic BP
ranging from <140 to <110 mm Hg
Treatment of pain with morphine is
important part of the management
71
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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
Page 73
Pulmonary Edema
Nitroglycerin
BP by 20%–30%
Promote diuresis
after vasodilation
Symptom relief
Enalaprilat
Nicardipine
Nitroprusside
73
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Acute Myocardial Infarction
Nitroglycerin
No more than 20%–
30% SBP >160
mm Hg
ischemia
-Blocker:
metoprolol,
labetalol
74
Page 75
Acute Renal failure
Labetalol
BP by no more
than 20%
Nicardipine
Fenoldopam
Dialysis
75
Page 76
Eclampsia / HELLP
Labetalol
<160 / 100
Hydralazine too
unpredictable, no
longer recommended
Nifedipine /
nicardipine
76
Page 77
Encephalopathy
Labetalol
MAP 15 – 20%
Too aggressive
ischemic infarct
Nicardipine
Fenoldopam
77
Page 78
Subarachnoid Hemorrhage
Labetalol SBP <160 mm Hg or
MAP <130 mm Hg to
prevent rebleeding
SBP >120 to
preserve cerebral
perfusion
Nicardipine
Esmolol
78
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Acute Ischemic Stroke
Labetalol If fibrinolytic therapy
planned, treat if
>185/110 mm Hg
Lowering BP may
significantly worsen
ischemia and deficit
Nicardipine
Nitroglycerin
79
Page 80
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
80
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Asymptomatic Hypertension
No evidence ever that acute
treatment of asymptomatic severe
hypertension prevents or reduces
patient morbidity or mortality
81
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Special Cases
Clonidine rebound: give 0.2 mg po
Cocaine: unopposed -blocker
storm
Drug of choice: benzodiazepine
Pheochromocytoma: -blockade /
phentolamine
82
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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
Page 85
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
85
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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
Page 87
Ultrasound
87
Source Undetermined
Page 88
MRI
88
Source Undetermined
Page 89
CT Scan
89 Source Undetermined
Page 90
3.10 Valvular Disorders
90
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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
91
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Anatomy
92
Gray's Anatomy (Wikipedia)
Page 93
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
93
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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
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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
95
Page 96
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
96
Page 97
Mitral Regurgitation: Acute
Presentation: fulminant pulmonary
edema
Harsh, midsystolic murmur that
radiates to base,but NOT axilla
97 Source Undetermined
Page 98
Mitral Regurgitation: Acute
Treat pulmonary edema with
nitrates and diuretics
Emergency echocardiography
Cardiac catheterization
Hypotension: counterpulsation
intra-aortic balloon pump may
bridge to surgery
98
Page 99
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
Page 100
Mitral Valve Prolapse
Generally benign
Infrequently associated with MR,
endocarditis, arrhythmias
True prevalence <1% in both men
and women
Old data: 5% women > men
100
Page 101
Mitral Valve Prolapse
Associated with chest pain,
palpitations, dyspnea,
lightheadedness, fatigue, etc.
Current data: no cause-and-effect
Cardioselective -blockers may
help
As of 2007: AHA no longer says
prophylactic antibiotics
101
Page 102
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,
etc.
102
Page 103
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).
103
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Aortic Stenosis
Natural history: slow progression
without symptoms for years
Symptoms reduce survival unless
valve replaced
Medical management: limited role
104
Page 105
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
105
Page 106
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
106
Page 107
Aortic Insufficiency: Acute
Surgical emergency requiring
immediate valve replacement
Medical stabilization: cautious use
of vasodilators and diuretics
INTRA-AORTIC BALLOON
COUNTERPULSATION IS
CONTRAINDICATED
107
Page 108
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
108
Page 109
Artificial Valves
109
Source Undetermined
Page 110
Prosthetic Valves
Mechanical: entirely synthetic
Biologic: porcine or human
Bioprosthetic: bovine pericardium
Complications: structural failure,
hemolysis, endocarditis, thrombosis
systemic embolization
110
Page 111
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
111
Page 112
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
Page 113
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
113
Page 114
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
114
Page 115
Prosthetic Valves: IE
Highest during initial months
Mechanical & bioprosthetic similar
Within 60d of surgery: perioperative
pathogen morbidity / mortality
After 60d: transient bacteremia
more benign
115
Page 116
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
Page 117
Bonus 1: Transplant
117
Page 118
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
years
60% will be admitted 118
Page 119
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%)
119
Page 120
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
120
Page 121
Heart Transplant
Any heart transplant patient
presenting with CHF, fever
(>38° C), shortness of
breath, hypoxia, hypotension,
poorly controlled
hypertension, or new
dysrhythmia ADMIT
121
Page 122
Heart Transplant
122
Source Undetermined
Page 123
Heart Transplant
123
Source Undetermined
Page 124
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
Page 125
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
125
Page 126
Heart Transplant
Risk of endocarditis antibiotic
prophylaxis for invasive procedures
likely to cause bacteremia
Abscess drainage, urethral
catheterization
NOT for endotracheal intubation
126
Page 127
Bonus 2:
Pacemakers
127
Steven Fruitsmaak (Wikipedia)
Page 128
External Pacemaker
128 STERNUM APEX FRONT Mikael Häggström (Wikimedia Commons)
Page 129
Transvenous Pacemaker
129
Gregory Marcus, MD (Wikipedia)
Page 130
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
Page 131
Emergent Pacemaker 2
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
131
Page 132
Emergent Pacemaker 3
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
132
Page 133
Emergent Pacemaker 4
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
Page 134
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
134
Page 135
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
135
Page 136
Implanted Pacemaker
136
Source Undetermined
Page 137
Pacemaker Components
Pulse generator
Power source / battery
Control circuitry
Transmitter / receiver
Reed switch: magnet activated
Leads
Single or multiple
Unipolar or bipolar 137
Page 138
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
Page 139
I:
chambers
paced
II:
chambers
sensed
III:
response
to sensing
IV:
rate
modulation
V:
multisite
pacing
0 = none 0 = none 0 = none 0 = none
A = atrium T = trigger R = rate
modulation
A =
atrium
V = ventricle I = inhibit V =
ventricle
D = dual, both` D = dual D = dual,
both
NASPE / BPEG Code (2002)
139
Page 140
I: chambers
paced
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
Page 141
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
141
Page 142
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
142
Page 143
VVI
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
143
Page 145
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
145
Page 146
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
146
Page 147
Paced EKG
Appearance depends on pacing
mode used, placement of pacing
leads, device pacing thresholds,
and presence of native electrical
activity
147
Page 148
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
Page 149
Paced EKG
Atrial Pacing
Pacing spike precedes p wave
P wave morphology depends on
lead placement, may look normal
149
Page 150
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
150
Page 151
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
wave
151
Page 152
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
152
Page 153
Paced EKG
Atrial pacer spikes
153
Source Undetermined
Page 154
Paced EKG
Atrial and Ventricular pacer spikes
154
Source Determined
Page 155
Paced EKG
Atrial and ventricular pacing spikes
visible before each QRS complex
155
Source Undetermined
Page 156
Paced EKG
100% atrial capture: small P waves
follow each atrial pacing spike
156
Source Undetermined
Page 157
Paced EKG
100% ventricular capture: QRS
complex follows each ventricular
pacing spike 157
Source Undetermined
Page 158
Paced EKG
QRS complexes broad with LBBB
morphology ventricular pacing
electrode is in right ventricle 158
Source Undetermined
Page 159
Abnormal Pacing
159
Page 160
Abnormal Pacing
Atrial non-capture: atrial pacing
spikes are not followed by P waves
160
Source Undetermined
Page 161
Atrial undersensing: atrial pacing
spikes occur regardless of P waves
Pacemaker is not “seeing”
intrinsic activity
Abnormal Pacing
161
Source Undetermined
Page 162
Abnormal Pacing
Ventricular non-capture: ventricular
pacing spikes not followed by QRS
complexes
162
Source Undetermined
Page 163
Abnormal Pacing
Ventricular undersensing:
ventricular pacing spikes occur
regardless of QRS complexes
Pacer not “seeing” intrinsic activity
163 Source Undetermined
Page 164
Failure to Capture
Pacer does not generate spike
when it should 164
Source Undetermined
Page 165
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
Page 166
Failure to Capture
Solutions
View rhythm in different leads
Change electrodes
Check connections
Increase pacer output (↑mA)
Change battery, cables, pacer
Reverse polarity
166
Page 167
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
Page 168
Failure to Sense
Pacer does not recognize normal
beat, generates unnecessary spike
168
Source Undetermined
Page 169
Failure to Sense
Danger: potential for paced
ventricular beat to land on T wave
169
Source Undetermined
Page 170
Failure to Sense
Solution
Change electrodes
Check connections
Increase pacemaker’s sensitivity
Change cables, battery, pacemaker
Reverse polarity
Check electrolytes
170
Page 171
Oversensing
Pacing does not occur when
intrinsic rhythm is inadequate
171 Source Undetermined
Page 172
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
Page 173
Oversensing
Solution
Change electrodes
Check connections
Decrease pacemaker sensitivity
Change cables, battery, pacemaker
Check electrolytes
173
Page 174
Competition
Pacemaker & patient’s intrinsic rate
are similar
Unrelated pacer spikes to P wave,
QRS complex fusion beats
174
Source Undetermined
Page 175
Competition
Causes
Asynchronous pacing
Failure to sense
Mechanical failure: wires, bridging
cables, pacemaker
Loose connections
175
Page 176
Competition
Solution
Assess underlying rhythm
Slowly turn pacer rate down
Troubleshoot as for failure to sense
Increase pacemaker sensitivity
Increase pacemaker rate
176
Page 177
AICDs
177
Gejordan (Wikipedia)
Page 178
AICDs
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
178
Page 179
AICDs
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
179
Page 180
AICDs
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
180
Page 181
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
181
Page 182
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
Page 183
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
Page 184
AICD Issues in ED
Inactivation: placing magnet over
AICD generator will inactivate it and
prevent further shocks
184
Page 185
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
185
Page 186
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
186
Page 187
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
187
Page 188
AICD and Infection
Erythema / induration / drainage at
generator site hospitalize for IV
antibiotics
Early infection usually caused by
staphylococcal species
188
Source Undetermined
Page 189
Bonus 3: EKG
Basics
189
Page 190
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
190
Page 191
Monitor Lead Placement
White – right arm
Black – left arm
Red – left leg
“White is right
smoke above fire”
191
Mikael Häggström (Wikimedia Commons
Page 192
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
192
Page 193
V1 V2
V4
V3
V5 V6
193
Source Undetermined
Page 194
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
194
Page 195
Right-Sided Leads
195
V1R V2R
V3R
V4R V5R
V6R
Mikael Häggström (Wikimedia Commons)
Page 196
Posterior Leads
V7 – Posterior Axillary Line
V8 – Scapular Tip
V9 – Paraspinous 196
Scapula
V7 V8 V9
Page 197
Anatomically Contiguous
197
Source Undetermined
Page 198
Wave Morphology
198
Page 199
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
199
Page 200
P Wave
200 Source Undetermined
Page 201
QRS Complex
Ventricular depolarization
Normal QRS: 0.06 – 0.10 seconds
wide
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
201
Page 202
QRS Complex
202 Source Undetermined
Page 203
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
203
Page 204
QT Interval
204 Source Undetermined
Page 205
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
205
Page 206
T Wave
206 Source Undetermined
Page 207
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
207
Page 208
U Waves
Prominent U waves may indicate…
Hypokalemia (< 3meq/L)
Hypercalcemia
Drugs: digitalis, phenothiazines,
quinidine, epinephrine, inotropic
agents, amiodarone
208
Page 209
U Waves
Inverted U waves may indicate…
Acute coronary ischemia
Ventricular strain / dilation
Hypertension
Intracranial or subarachnoid
hemorrhage
209
Page 210
Abnormal
Morphologies
210
Page 211
Abnormal Morphologies
Hypothermia
Hypokalemia
Hyperkalemia
Hypocalcemia
Hypercalcemia
Hypomagnesemia
Digitalis effect
Digitalis toxicity 211
Page 212
Abnormal Morphologies
HYPOTHERMIA
Hypokalemia
Hyperkalemia
Hypocalcemia
Hypercalcemia
Hypomagnesemia
Digitalis effect
Digitalis toxicity 212
Page 213
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
213
Page 214
Hypothermia
214
Source Undetermined
Page 215
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
215
Page 216
Hypothermia
Treatment: most dysrhythmias
require no therapy, revert
spontaneously with rewarming
216
Source Undetermined
Page 217
Potassium Abnormalities
217
Evan-Amos (Wikipedia)
Page 218
Abnormal Morphologies
Hypothermia
HYPOKALEMIA
Hyperkalemia
Hypocalcemia
Hypercalcemia
Hypomagnesemia
Digitalis effect
Digitalis toxicity 218
Page 219
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
219
Page 220
Hypokalemia
Early: flattened T waves
Late: inverted T waves
Progressively more prominent U
waves: best seen in V3
220
Page 221
Hypokalemia
221
Source Undetermined
Page 222
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
222
Page 223
Hypokalemia
223
Source Undetermined
Page 224
Hypokalemia
Predisposes to digitalis toxicity and
associated dysrhythmias
supraventricular and ventricular
ectopics
Supraventricular tachyarrhythmias:
atrial fibrillation, atrial flutter, atrial
tachycardia
224
Page 225
Hypokalemia
potential for life-threatening
ventricular arrhythmias: ventricular
tachycardia, ventricular fibrillation,
Torsades de Pointes
225
Page 226
Hypokalemia Hypokalemia
226 Source Undetermined
Page 227
Abnormal Morphologies
Hypothermia
Hypokalemia
HYPERKALEMIA
Hypocalcemia
Hypercalcemia
Hypomagnesemia
Digitalis effect
Digitalis toxicity 227
Page 228
Hyperkalemia
Worsening hyperkalaemia
suppression of impulse generation
by SA node
conduction by AV node / His-
Purkinje system
bradycardia / conduction blocks
ultimate cardiac arrest
228
Page 229
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
Page 230
Hyperkalemia
Potassium level >5.5 mEq/L
Moderate hyperK+: >6.0 mEq/L
Severe hyperK+: >7.0 mE/L
230 Acdx (Wikipedia)
Page 231
Hyperkalemia
Potassium > 5.5 mEq/L
repolarization abnormalities:
peaked T waves
231 Source Undetermined
Page 232
Hyperkalemia
Potassium > 6.5 mEq/L
progressive paralysis of atria
P wave widens and flattens
PR segment lengthens
P waves disappear
232 Source Undetermined
Page 233
Hyperkalemia
233
Source Undetermined
Page 234
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
234
Page 235
Hyperkalemia
235 Source Undetermined
Page 236
Hyperkalemia
Any kind of conduction block:
bundle branch blocks, fascicular
blocks
Sinus bradycardia or slow atrial
fibrillation
Sine wave appearance: pre-
terminal
236
Page 237
Hyperkalemia
237
Source Undetermined
Page 238
Hyperkalemia
238 Source Undetermined
Page 239
Calcium
239
MigGroningen (Wikimedia Commons)
Page 240
Abnormal Morphologies
Hypothermia
Hypokalemia
Hyperkalemia
HYPOCALCEMIA
Hypercalcemia
Hypomagnesemia
Digitalis effect
Digitalis toxicity 240
Page 241
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)
241
Page 242
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
242
Page 243
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
Page 244
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
244
Page 245
QT Interval
245
Source Undetermined
Page 246
Hypocalcemia
246 Source Undetermined
Page 247
Abnormal Morphologies
Hypothermia
Hypokalemia
Hyperkalemia
Hypocalcemia
HYPERCALCEMIA
Hypomagnesemia
Digitalis effect
Digitalis toxicity 247
Page 248
Hypercalcemia
Most reliable ECG change:
shortening of QT interval
Nearly always seen when calcium
concentration exceeds 12mg/dL
(3.0 mmol/L)
248
Page 249
Calcium
249
Source Undetermined
Page 250
Abnormal Morphologies
Hypothermia
Hypokalemia
Hyperkalemia
Hypocalcemia
Hypercalcemia
HYPOMAGNESEMIA
Digitalis effect
Digitalis toxicity 250
Page 251
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
251
Page 252
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
Page 253
Hypomagnesemia
253 Source Undetermined
Page 254
Digitalis
254 Jcart1534 (Wikimedia Commons)
Enrico Blasutto (Wikipedia)
Page 255
Abnormal Morphologies
Hypothermia
Hypokalemia
Hyperkalemia
Hypocalcemia
Hypercalcemia
Hypomagnesemia
Digitalis toxicity
DIGITALIS EFFECT
255
Page 256
Digitalis Effect
Sagging ST segment with upward
concavity: resembles hockey stick
(or Salvador Dali’s mustache)
256
Source Undetermined Roger Higgins (Wikipedia)
Page 257
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
257
Page 258
Digitalis Effect
258 Source Undetermined
Page 259
Abnormal Morphologies
Hypothermia
Hypokalemia
Hyperkalemia
Hypocalcemia
Hypercalcemia
Hypomagnesemia
Digitalis effect
DIGITALIS TOXICITY 259
Page 260
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
260
Page 261
Digitalis Toxicity
Predisposing factors
potassium / magnesium,
calcium / potassium
Hypoxia
Metabolic Alkalosis
Underlying diseases
Drugs: quinidine, erythromycin,
amiodarone, captopril, ibuprofen 261
Page 262
Digitalis Toxicity
Most common EKG finding: PVCs,
often bigeminal and multiform
Pathognomonic EKG finding:
paroxysmal atrial tachycardia with
AV block
262
Page 263
Digitalis Toxicity
Paroxysmal atrial
tachycardia with block
263
Source Undetermined
Page 264
Digitalis Toxicity
Regularized Atrial Fibrillation
264 Source Undetermined
Page 265
Digitalis Toxicity
Can also see
Atrial fibrillation with slow
ventricular response
Sinus arrest
Junctional tachycardia (common)
Ventricular tachycardia
265
Page 266
Digitalis Toxicity
Can also see
Bidirectional ventricular tachycardia
(highly suggestive but rare)
Ventricular fibrillation
Sinus bradycardia
SA and AV nodal blocks
266
Page 267
Digitalis Toxicity
For presentation and treatment:
see Toxicology Section
267