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A few words first...
? Review, review, review
? Handout more comprehensive
? I'l focus on key points
? Special attention to red underlined text
? Special attention to "most common cause of..."
? Special attention to triads, quadrads
? Know ACLS 2010
? Always consider deadly causes first

Acute Coronary Syndrome
? Spectrum of disease due to myocardial
?Unstable angina to acute MI
? Ischemic heart disease is the most common
cause of death in the US
? 2 mil ion MI and unstable angina patients
each year

Causes of ACS
? Usual y due to atherosclerosis
?Fixed lesion, critical stenosis
?Plaque disruption, platelet
aggregation, thrombus formation
? Results in oxygen supply/demand imbalance
leading to cardiac muscle damage

Non-Atherosclerotic Causes of ACS
? Trauma
? Connective tissue diseases (vasculitis)
? Metabolic diseases (thickening of vessels)
? Congenital anomalies
? Thrombus (DIC, TTP)
? Emboli (bacterial, non-bacterial)
? Thoracic aortic dissection
? Drugs (cocaine)
? Infectious diseases

Cocaine-Associated Chest Pain
Acad Emerg Med 2000
? How often is chest pain associated with cocaine use
reflective of an AMI?
? Only 6% had an AMI (consistent with other studies)
? Acute use of cocaine markedly increases the risk of
acute MI
? Chronic use of cocaine causes premature
atherosclerosis (recent literature -- controversial)

ACS: Unstable angina Non-STEMI STEMI
? Unstable angina
?New onset
Increasing severity
?High risk of MI or death
?Duration >20 minutes, hypotension, CHF,
dynamic ST changes
Prinzmetal's angina (variant angina):
Coronary artery spasm, occurs at rest,
ST elevation (not depression), may not have CAD

Acute Myocardial Infarction (AMI)
? Classification of AMI
?STEMI/Q wave: transmural infarction involving
ful thickness of myocardium
?Non-STEMI/Non-Q wave: subendocardial
infarction involving partial wal thickness. Has
lower initial mortality and morbidity, but long
term prognosis is similar

AMI EKG Changes
? 4% of AMIs have normal EKG
? Hyperacute T waves (early)
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)

AMI EKG Changes
? ST segment changes
?1mm of elevation in two anatomical y contiguous leads
?Elevation usual y corresponds to areas of involvement
? Exception: AMI with LBBB
?Depression over areas opposite injury (reciprocal
changes). Predictor of larger MI, increased mortality
? T wave inversion: within 4 hours is good Px sign
? Significant Q waves: 1 square wide, 1/3 of height of R

The EKG in AMI (1)
? The EKG can guide therapy in AMI by helping:
?Identify who needs emergent reperfusion
?Identify the infarct-related artery
?Predict the amount of myocardium at risk
?Reflect reperfusion
?Identify new dysrhythmias / conduction issues

The EKG in AMI (2)
? EKG indications for emergent reperfusion
? STE > 1 mm in 2 contiguous leads (incl. posterior)
? New left bundle branch block
? Old left bundle branch block with Sgarbossa criteria
? ST-segment elevation measuring 1 mm concordant with the QRS
in any lead.
? ST-segment depression measuring 1 mm in any of the V1
through V3 leads.
? Discordant ST-segment elevation measuring 5 mm (lower utility)

Normal LBBB
Rule of appropriate discordance
(true for pacemakers also)
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)

The EKG in AMI (2)
Concern in leads aVL, V5-6
? EKG indications for emergent reperfusion
From ECGs for the Emergency Physician Vol 2 (Mattu, Brady; Blackwel 2008)

The EKG in AMI (2)
Concern in lead V3
? EKG indications for emergent reperfusion
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)

The EKG in AMI (2)
Concern in leads V1-2
From ECGs for the Emergency Physician Vol 2 (Mattu, Brady; Blackwel 2008)

The EKG in AMI (2)
? Predictors of reperfusion
?Normalization of ischemia-related ST elevation
? Failure to normalize may indicate the need for
"rescue PCI"
?Early T wave inversions can be highly specific markers of
?An accelerated idioventricular rhythm (60-120) is also
highly specific for reperfusion / benign, don't suppress it

EKG Anatomy (1)
Anterior wall
Left main
Left anterior
descending artery
Lateral wall
Septal wall
I, aVL, V5-V6


EKG Anatomy (2)
(from left coronary
Posterior wall
Right coronary
Lateral wall
Inferior wall
Leads II, III, aVF
descending artery

EKG Anatomy (3)
I lateral
V1 septal V4 anterior
II inferior aVL lateral
V2 septal
V5 lateral
III inferior aVF inferior V3 anterior V6 lateral
? RV infarct: inferior injury pattern + ST elevation V4R
? True posterior infarct: R>S waves V1 and V2, upright Ts, ST
depression in V1-2

The EKG in AMI (1)
? Inferior MI (ST elevation II, III, aVF)
?80% right coronary, 20% circumflex
? Right ventricular MI (ST elev. V1 and II, III, aVF)
?Always right coronary artery
? Anterior MI (ST elevation in V1, V2, V3)
?Left anterior descending coronary artery (LAD)

The EKG in AMI (3)
? Bradycardias or conduction defects associated early with
inferior AMIs tend to resolve spontaneously and are
atropine-sensitive (tend to reflect self-resolving edema)
? Conductions abnormalities associated with anterior AMIs
carry a worse prognosis because they reflect necrosis of
the conduction tissue (early pacing if any new or partial
BBB develops)

The EKG in AMI (4)
? Tachycardias
?Causes = reperfusion, altered autonomic tone or
hemodynamic instability
?New atrial fib = increased vagal tone, increase left atrial
pressure, atrial infarction or pericarditis (is a marker of a
worse prognosis no matter the cause)
?Sustained V. tach over 150 = very large infarction
?Ventricular fibril ation - early = ischemia / late (3 weeks) =
progressive pump failure
?Ventricular fibril ation in early AMI indicates lack of
reperfusion = PCI
?PVCs don't predict sustained ventricular dysrhythmias /
don't routinely suppress

Cardiac Markers (1)
? Myoglobin
?1-2 hours (rises)
?4-6 hours (peaks)
?24 hrs (normalizes)
? Troponin
?3-6 hours (rises)
?12-24 hours (peaks)
?7 days (normalizes)
?3-4 hours (rises)
?12-24 hours (peaks)
?1-2 days (normalizes)

Cardiac Markers (2)
? Myoglobin
?Advantage: early detection
?Disadvantage: poor specificity, especial y in
trauma, renal failure, hemolytic syndromes
? Troponin: more specific for AMI than CK-MB
?High values predict complications and mortality
?Elevation without infarction (skeletal disease,
muscle exertion, cocaine, renal failure)
?Comparing MB to total CK improves specificity
?30-40% false negatives in UA = NSTEMI

Therapy of AMI (1)
? Oxygen
? Nitrates (sublingual, topical, IV)
?Contraindicated if sildanefil (Viagra) etc. within 24
hours or if hypotensive
?Caution/avoid in RV MI
? ASA (162-325 mg)
?ASA alone reduces mortality 23%
?Combined with thrombolytics, ASA reduces
mortality 42%
? Morphine for persistent pain

Therapy of AMI (2)
? Heparin (Unfractionated or LMWH)
?60 u/kg IVP, fol owed by 12u/kg/hr IVPB
?30 mg IVP, fol owed by 1 mg/kg SQ q 12 hrs
? Beta blocker (metoprolol) early IV discouraged
?Give within 24 hours oral y but no rush
?Contraindications (asthma, CHF, bradycardia,
hypotension; caution in RV MI)
? Platelet inhibitors
?GP Ilb/IIIa receptor antags IV
?Clopidogrel: 300-600 mg oral load or
?Prasugrel 60 mg oral load at cath; avoid if
history of TIA or stroke

Therapy of AMI (3)
? Thrombolysis vs. percutaneous coronary
?Outcomes have shown consistent benefit with
PCI over thrombolytics
?Guidelines recommend PCI if bal oon inflation
can be performed within 90 minutes
? Window of benefit extended if chest pain > 6 hours
or if cardiogenic shock

Thrombolytic Therapy Indications
? Chest pain greater than 30 minutes but less than
12 hours, not relieved by nitroglycerin
? Acute change in EKG with any of the fol owing
?At least 1 mm ST elevation in two contiguous
?New LBBB or Sgarbossa criteria
? PCI delayed greater than 90 minutes
A RBBB should not obscure the diagnosis
of an acute MI

Contraindications to Thrombolytic Therapy
? (PCI immediately available) ? History of GI bleed
? Active bleeding from any
? Prolonged CPR
? Surgical or invasive procedure
within 3 weeks
? CVA within 6 months or
? Severe bleeding diathesis or
hemorrhagic CVA at any
time in the past
? Uncontrol ed hypertension
(diastolic >120 after treatment)
Intracranial or intraspinal
? Significant trauma within 4
surgery or trauma within 2
? Pregnancy or <10 days post-
? Intracranial or intraspinal
neoplasm, aneurysm or AV ? Active cavitary lung disease
? Known al ergy to agent
? Suspected aortic dissection

No Thrombolytics

Complications of Thrombolytic Therapy
? Bleeding (send blood for type and screen)
? Serious bleeding in 5%
? Intracranial hemorrhage: approximately 0.5%.
Higher risk with uncontrol ed BP, age > 65, low
body weight
Evidence of Reperfusion
? Chest pain resolved
? ST elevation resolved
? Reperfusion dysrhythmias

Early Complications of AMI (1)
? Blood supply to pacemaker and conduction tissue
?Sinus node (right coronary, 60% / circumflex,40%)
?AV node (right coronary, 90% / circumflex, 10%)
?Septal conduction (left anterior descending)
? Good prognosis
?Bradycardia (without hypotension)
?2? Mobitz type 1 AV block (Wenckebach)
?3? AV block with inferior MI (resolves)
? Narrow QRS complexes
?Early non-sustained V tach

Early Complications of AMI (2)
? Poor prognosis
?2? Mobitz II (progress to 3?)
?3? AV block from anterior MI
?Persistent sinus tach, SVT, A-fib
?New BBB, bifascicular block (RBBB
(RBBB + hemiblock)
?Left posterior hemiblock (large infarct size)
?Increased risk of pump failure, mortality
High-grade blocks (i.e. Mobitz II, 3? AV block)
seen in anterior MI due to structural loss of
conduction tissue need pacemaker

Early Complications of AMI (3)
? Cardiogenic shock: usual y >40% of LV muscle
?High mortality
?Treatment: fluids, inotropes, IABP (intra-aortic
bal oon pump) to increase coronary blood flow
? Papil ary muscle dysfunction
? Acute mitral regurgitation (usual y due to
ischemic dysfunction of papil ary muscles)
? Recurrent chest pain
? Ischemia vs reinfarction (may require PTCA or

Early Complications of AMI (4)
? Right ventricular infarction
?Associated with inferior MI
?Do right sided chest leads (especial y V4R)
looking for ST elevation
Triad of hypotension, JVD and clear lungs
?RV loses function, acts as conduit only (not
?Heart becomes very preload-dependent
?Use NTG and MS with caution (can drop BP
?Treat as any other MI but use fluids liberal y to
augment preload

Late Complications of AMI (1)
? Recurrent chest pain
? Embolism (from mural thrombus)
? Pericarditis
?Post-MI (seen 1-7 days after transmural infarct)
?Treatment: NSAIDs
? Dysrhythmias
Dressler's Syndrome: pericarditis 2-8 weeks post-MI
(probably a continuum with earlier pericarditis)
Fever, leukocytosis, friction rub, pericardial and
pleural effusions. Treatment: NSAIDs & steroids

Late Complications of AMI (2)
? Myocardial rupture
?LV free wal : often results in acute tamponade,
hypotension and death within two weeks
? Papil ary muscle rupture
?Results in acute MR and acute onset CHF
? Septal wal rupture
?Results in acute VSD with acute onset CHF
?Anterior or inferior MI
?Treatment: afterload reduction, aortic bal oon,
All seen 1-7 days post-MI and treated surgical y

Heart Failure
? Heart failure is the heart's inability to maintain
sufficient perfusion for adequate organ function
? Congestive heart failure is the inability to clear
venous return
? Stroke volume of heart depends on
? Frank-Starling curve shows the relationship
between these


Etiology of Heart Failure
? Primary myocardial diseases (low output failure)
?Hypertension (most common cause)
?Coronary artery disease, MI
?Valvular heart disease
?Cardiomyopathy (i.e. ischemic)

Etiology of Heart Failure
? Increased workload on heart (high output failure)
?A-V fistula
?Paget's disease of the bone

Classification of Heart Failure
? Left-sided or right-sided systolic dysfunction
?Impaired contractility low ejection fraction,
low cardiac output (e.g. MI, dilated
cardiomyopathy) high renin and angiotensin
levels, high afterload

Classification of Heart Failure
? Diastolic dysfunction
?Impaired relaxation of heart in diastole leads to
decreased LV fil ing and pulmonary congestion
?May eventual y lead to systolic dysfunction
?Causes: ischemia, hypertrophy, amyloidosis

Presentation of Heart Failure (1)
? Left sided failure
?S3 gal op
Pulmonary edema
?Kerley B lines (Interstitial edema / lymphatic
?Alveolar edema

Congestive Heart Failure
Interstitial edema

Congestive Heart Failure
Alveolar edema

Presentation of Heart Failure (2)
? Causes of acute right sided failure (rare)
?Pulmonary embolism
?RV infarction
? Signs and symptoms
?Peripheral edema
? Right upper quadrant pain (liver engorgement)
?Pulsatile, enlarged liver
? The most common cause of right sided failure
is left sided failure
? Longstanding heart failure is usual y due to
dysfunction of both ventricles

Treatment of Acute Heart Failure (1)
? Refractory heart failure (5 year mortality is 50%)
? Antidysrhythmics do not lower fatal arrhythmias
?AICDs commonly used now chronical y
? ACE inhibitors prolong survival
? Treat underlying cause (remember ischemia!)
? Symptomatic treatment with O2, CPAP, BiPAP
? Afterload reduction with
?IV nitroglycerin
?ACE inhibitors

Treatment of Acute Heart Failure (2)
? Preload reduction with
?Diuretics (after afterload reduction)
?Nesiritide (??)
?Morphine (??)
?Phlebotomy (decrease circulatory volume, best
with renal failure)
? Inotropes

Valvular Heart Disease

Infective Endocarditis (1)
? Risk factors for infective endocarditis (IE)
?Rheumatic or congenital heart disease
?Prosthetic valves
?Acquired valvular disorders (e.g. AS)
?Mitral valve prolapse (smal risk)
?Cardiac pacemakers
?Prior history of endocarditis
? Median age is increasing
?More prosthetic heart valve survivors

Infective Endocarditis (2)
? Valvular involvement (MATP)
?Mitral > aortic > tricuspid (IVDA) > pulmonic
? Native valve endocarditis: age > 50, M > F
?Predisposing factors: rheumatic heart disease
(<20%), calcifications (50%, usual y elderly, aortic
valve) congenital heart disease (15%),
?Most have normal valves (75%)
?Tricuspid valve most common (50%)
?Staph. aureus is the most common pathogen
? Prosthetic valves
?Staph. aureus

Infective Endocarditis (3)
? Pathogenesis of IE
?GU, GI, major dental procedures, IVDA
? Abnormal turbulent flow
? Platelet aggregation and fibrin deposition (sterile
? Bacteria colonize sterile vegetations

Infective Endocarditis (4)

? Acute IE
?Younger, normal valves in half
?Virulent strains
?Higher morbidity and mortality
?Staph. aureus
? Subacute IE
?Older, abnormal valves
?Anemia of chronic disease
?Strep. viridans (50-60%)

Infective Endocarditis (5)

? Left sided IE
?S. viridans, S. aureus
?Gram negatives (IVDA or contaminated catheters)
?Cause of death is heart failure
?Emboli: CNS and systemic infarction
? Right sided IE
?IVDA, indwel ing catheters
?S. aureus, S. pneumoniae, gram negatives
?Emboli: pulmonary infarction & infection
?Less heart failure, mortality rate lower

Infective Endocarditis (6)

? Prosthetic valve IE
?Most common during first two months post-op
? S. epidermidis, S. aureus
?Late causes similar to native valve endocarditis
? S. viridans, Serratia, Pseudomonas

Infective Endocarditis (7)
? Etiology
?Streptococci (various species) are the most
common cause with native heart valves
?Staph aureus most common in IV drug users
(IVDA), prosthetic valves (also Staph
epidermidis), catheter-related sepsis
?Gram negatives & fungi (IVDA)
? Findings of IE
?Fever, chil s, "flu-like" il ness, back pain
?Heart murmur
?Valvular incompetence (the most common
cause of acute AR)

Infective Endocarditis (8)
? Embolic and vasculitic components
?Osler nodes: tender nodules on the tips of the
fingers and toes (Osler = Ow!)
?Janeway lesions: nontender, hemorrhagic
plaques on the palms and soles
?Roth spots: retinal hemorrhages with central
?Petechiae and splinter hemorrhages

Septic Emboli

Janeway Lesion

Osler Nodes

Splinter Hemorrhages

Roth Spots

Infective Endocarditis (9)
? Laboratory
?Two blood cultures: > 90% sensitivity if
?Anemia and elevated ESR
? Diagnosis: ultrasound (TEE) for vegetations
? Treatment: penicil ins, vancomycin,

Infective Endocarditis (9)
? Surgical indications
?Refractory CHF
?Valve ring abscess
?Multiple major emboli
?Medical failure
?Mycotic aneurysm

Infective Endocarditis (10)
? Prophylaxis
? High-risk cardiac conditions
?Prosthetic cardiac valve
?History of infective endocarditis
?Congenital heart disease (CHD)
?Cardiac transplantation recipients with cardiac valvular

Infective Endocarditis (11)
? Major dental and invasive respiratory only
? GU/GI: No prophylaxis

Rheumatic Heart Disease (1)
? Diagnosis of rheumatic fever: Jones criteria
?2 major criteria or
?1 major and 2 minor
?Plus evidence of preceding Strep infection
(scarlet fever, positive group A strep throat
culture, elevated ASO titer)
Degenerative valvular disease is the most common
cause of valvular disease overal

Rheumatic Heart Disease (2)
? Jones major criteria (CASES)
Sydenham's chorea
Erythema marginatum
Subcutaneous nodules
? Jones minor criteria
?Previous history of RF or RHD
?Elevated ESR
?Prolonged PR interval

Aortic Stenosis (1)
? Etiology
?Usual y congenital bicuspid valve, or acquired
through RHD
? Pathophysiology
?Smal valve orifice LV outflow obstruction
fixed output unable to meet higher demands
Often presents with exertional dyspnea,
chest pain and syncope
(exertional syncope = think aortic stenosis)

Aortic Stenosis (2)
? Physical exam
?Carotid pulse is weak, with a slow rate of rise
?Systolic murmur radiating into neck
?Hypotension is a late finding
?LVH with strain pattern

Aortic Stenosis (3)
? Natural history
?LVH leads to heart failure
?Sudden death from dysrhythmias and acute LV
? Medical management
?Avoid strenuous exertion
?Treat CHF
?Avoid nitrates and vasodilators (may drop BP
?Endocarditis prophylaxis (s/p replacement)
? Surgical management
?Valve replacement

Aortic Regurgitation (1)
? Etiology
?Acute: endocarditis, dissection
?Chronic: RHD; also seen with Marfan's
? Pathophysiology of AR
?Incompetent valve run-off into LV volume
overload LV dilation CHF (usual y no
symptoms until CHF develops)
Acute MI + acute AR: rule out dissection

Aortic Regurgitation (2)
? Physical exam
?Diastolic decrescendo murmur at left lower
sternal border
?"Water hammer" (bounding) pulse
?Duroziez's murmur (to-and-fro femoral murmur)
?Quincke's sign (pulsatile blushing of nail beds)
?Austin-Flint murmur (diastolic murmur 2? to AR
with regurgitant jet hitting mitral valve)
? CXR: LV and LA enlargement

Aortic Regurgitation (3)
? Natural history
?Symptoms late in disease course
?Prognosis much worse after symptoms develop
? Complications include
?Infective endocarditis
? Medical management
?Afterload reduction
?Inotropes (digoxin)
?Endocarditis prophylaxis (s/p replacement)

Mitral Stenosis (1)
? Pathophysiology
?Smal valve orifice LV inlet obstruction
LAE increased LA pressure pulmonary
edema increased right sided pressures and
RV failure loss of atrial kick with A-fib may
cause acute decompensation
RHD is the most common cause of mitral

Mitral Stenosis (2)
? Symptoms
?DOE (or dyspnea in pregnancy, anemia,
?Orthopnea, PND, hemoptysis
? Physical exam
?Diastolic rumble in mitral area
?Loud S1, opening snap
? EKG: LAE, A-fib
Suspect MS if murmur and pulmonary
edema are present in pregnancy

Mitral Stenosis (3)
? Natural history
?Gradual onset of CHF
? Complications include
?Systemic emboli
? Medical management
?Treat A-fib with rate control and anticoagulation
?Endocarditis prophylaxis (s/p replacement)
? Surgical management
?Valve replacement

Mitral Regurgitation (1)
? Etiology of acute MR
?Chordae tendineae rupture (trauma, IE, MI)
?Papil ary muscle dysfunction (ischemia, MI)
? Etiology of chronic MR
?Dilated cardiomyopathy
?Mitral annulus calcification

Mitral Regurgitation (2)
? Pathophysiology of acute MR
?Sudden mitral valve incompetence sudden
increase LA pressure pulmonary edema
RV pressure overload and right sided failure
? Pathophysiology of chronic MR
?Gradual valve incompetence gradual LA
pressure increase LAE compensation
gradual CHF late right sided failure

Mitral Regurgitation (3)
? Symptoms
?Acute: dyspnea, CHF, right-sided failure
?Chronic: CHF (compensated)
? Physical exam
?Acute: loud holosystolic murmur (may have no
murmur if chordae rupture, resulting in wide-
open valve)
?Palpable LV heave and thril
?CXR: cardiomegaly, CHF

Mitral Regurgitation (4)
? Acute complications
?Acute pulmonary edema
?Cardiogenic shock
? Chronic complications

Mitral Regurgitation (5)
? Medical management of acute MR
?Afterload reduction
?IABP to temporize until surgery
? Medical management of chronic MR
?Symptomatic treatment of CHF
?Treatment of A-fib
?Endocarditis prophylaxis (s/p replacement)
? Surgical management
?Valve repair or replacement

Mitral Valve Prolapse (1)
? Idiopathic myxomatous degeneration of
leaflets (leaflets become too thick to appose
wel )
? Symptoms
?Chest pain (atypical)
? Mostly young women

Mitral Valve Prolapse (2)
? Physical exam
?Mid-systolic click, late systolic murmur
?Nonspecific ST-T wave changes
?Ectopy and PSVT common
?Not helpful
? Echocardiogram
?Regurgitation uncommon (requires prolapse of
both leaflets)

Mitral Valve Prolapse (3)
? Natural history
?Very common. The vast majority never have a
?Increased incidence of arrhythmias
?Thromboembolic disease
?Endocarditis rarely
? Management
?No longer requires endocarditis prophylaxis
unless ful -blown regurgitation develops
?Anticoagulation if embolic disease is present
?Beta blockers helpful for chest pain

? Group of diseases directly altering cardiac
structure, impairing myocardial function
? Three types
?Dilated cardiomyopathy
?Hypertrophic cardiomyopathy
?Restrictive cardiomyopathy

Dilated Cardiomyopathy (1)
? Dilated cardiomyopathy
?Idiopathic (most common)
?Viral (myocarditis)
?End-stage CAD

Dilated Cardiomyopathy (2)
? Pathophysiology
?Decreased contractility
dilatation of al chambers
decreased output
? Clinical presentation
CHF (biventricular failure)
?Sudden death
?Globular heart

Dilated Cardiomyopathy (3)
? Treatment
?Largely supportive
?Afterload reduction

Hypertrophic Cardiomyopathy (1)
? Often familial autosomal dominant
? Asymmetric thickening of septum causing two
?Noncompliant ventricle with decreased diastolic
?Dynamic obstruction of LV outflow (with mitral
valve leaflets blocking outflow tract)

Hypertrophic Cardiomyopathy (1)
? Clinical manifestations
?Exertional syncope
?Sudden death
?Cardiac ischemia

Hypertrophic Cardiomyopathy (2)
? Physical exam
?Harsh, mid-systolic murmur at LLSB
?Murmur louder with decreased preload
(hypovolemia, standing, Valsalva, amyl nitrite,
beta agonists)
?Murmur decreased with increased afterload
(squatting, Trendelenburg, hand grip, volume
expansion, alpha agonists)

Hypertrophic Cardiomyopathy (3)

Hypertrophic Cardiomyopathy (4)
? EKG: hypertrophy in septal leads
? CXR: nondiagnostic
? Treatment of hypertrophic cardiomyopathy
?Avoid exertion
(worsens obstruction and leads to arrhythmias)
?Negative inotropes (beta blockers, calcium
channel blockers) to decrease obstruction
?Never use digoxin or positive inotropes
(increased obstruction)
?Surgical myomectomy

Pericarditis (1)
? Etiology
?Viral (most common)
?Acute MI (Dressler's syndrome)
?Connective tissue disease

Pericarditis (2)
? Clinical manifestations
?Chest pain (may radiate to trapezius)
?Chest pain increases with inspiration and
swal owing
?Relief on sitting up, bending forward (and may
hear the rub better in this position)
?Fever, malaise

Pericarditis (3)
? Physical exam
? Rub (increased by leaning forward)
? Tachycardia, pulsus paradoxus (an
exaggerated BP response to breathing ? BP
goes down on inspiration and up on expiration)

Pericarditis (3)
? EKG: four stages
? Stage 1: Diffuse ST elevation (does not
correspond to coronary artery distribution) &
PR segment depression
? Stage 2: ST-segments and PR return to
? Stage 3: T wave inversions
? Stage 4: Normalization of EKG

Acute Pericarditis
ST elevation diffusely
PR segment depression

Acute Pericarditis

Pericarditis (4)
? CXR: usual y normal
? Echocardiogram: pericardial effusion
? Complications
?Dysrhythmias (atrial)
?Large pericardial effusions, tamponade
?Residual pericardial constriction
? Treatment
?Treat underlying cause if possible
?ASA, NSAIDs, colchicine; steroids controversial

Pericardial Tamponade
? Causes
?Trauma, uremia, anticoagulation, neoplasm
? Clinical signs
?Hypotension, JVD, muffled heart sounds, pulsus
?Electrical alternans (beat to beat alteration in the
amplitude of the QRS complex), low voltage
? ECHO findings
?RV diastolic col apse (specific for tamponade)

Pericardial Effusion
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003) 105

Pericardial Effusion

Myocarditis (1)
? Inflammation of the myocardium
?Often associated with pericarditis
? Etiology
?Infectious (usual y viral, especial y coxsackie B
?Connective tissue disease

Myocarditis (2)
? Clinical manifestations
?"Flu-like" il ness
?Fever, sinus tach (out of proportion to exam)
?Symptoms of CHF
?Sudden death
? EKG: nonspecific changes, conduction blocks
? CXR: possibly enlarged heart
? Lab: elevated biomarkers

Myocarditis (3)
? Natural history
?Most recover
?May have sudden death
?May have dilated cardiomyopathy
? Treatment
?Supportive care

Hypertension (1)
? Definition (JNC VII)
?Normal: Systolic lower than 120, diastolic lower
than 80
?Prehypertension: Systolic 120-139, diastolic
?Stage 1: Systolic 140-159, diastolic 90-99
?Stage 2: Systolic equal to or more than 160,
diastolic equal to or more than 100
?Cardiovascular risk: BP > 120/80

Hypertension (2)
Definition / Classification
? Hypertensive urgency (DBP > 110)
?No signs or symptoms of organ damage
?Acute intervention may be harmful
?Behavior modification, initiation of therapy
?Close fol ow up, e.g. in several days

Hypertension (3)
Definition / Classification
? Hypertensive emergency
?Malignant hypertension
?End-organ and CNS signs
?Immediate BP reduction

Hypertensive Emergencies (1)
? Severe elevation of BP with associated end-
organ damage
No specific BP level
? End-organs include
?Heart (ACS, CHF, dissection)
?Brain (encephalopathy, hemorrhage)
?Eyes (hemorrhages, exudates)
?Kidneys (failure, preeclampsia)

Hypertensive Emergencies (2)
? Types
?Stroke syndromes
?Malignant hypertension (eyes)
?Acute pulmonary edema
?Acute coronary syndromes
?Aortic dissection
?Acute renal failure
?Preeclampsia, eclampsia
?Catecholamine crises

Hypertensive Emergencies (2)
? Pediatric hypertension emergencies
?Blood pressure > 95th percentile
?Common causes: renovascular, nephritis,

Hypertensive Emergencies (3)
? Malignant hypertension
?Hypertension with end-organ damage and
papil edema
?Not defined by absolute blood pressure reading
?Goal is to reduce mean arterial pressure by
30% in 30 minutes
MAP = DBP + (SBP ? DBP) / 3
Treatment is nitroprusside and/or labetalol

Hypertensive Emergencies (4)
? CNS: encephalopathy, hemorrhagic CVA
? Ischemic stroke
?Hypertension usual y resolves within hours
?Transient and cerebroprotective
?Treatment: observe, labetalol, nicardipine
? Pregnancy-induced hypertension, eclampsia
?Magnesium sulfate for seizures

Hypertensive Emergencies (5)
? Cardiac: angina, CHF
?IV nitroglycerin
? Aortic dissection
?Need to decrease rate of rise of BP (dP/dT) to
decrease shear forces on aorta
?Beta blockers (esmolol, labetalol, propranolol),
then nitroprusside

Hypertensive Emergencies (6)
? Catecholamine surge (pheochromocytoma,
MAOI crisis, cocaine overdose)
?Alpha plus beta blocker is best
?Do not use beta blocker alone
(avoid unopposed alpha effect)
?Labetalol plus phentolamine

Hypertensive Emergency Medications (1)
? Sodium nitroprusside
?Mode of action: arterial and venous dilatation
?Onset of action: 1-2 minutes
?Half life: 3-4 minutes
?Metabolized to thiocyanate (cyanide)
?Ideal medication for hypertensive emergencies
(rapid onset, potent, short half life)
?Can cause reflex tachycardia, therefore use
with beta blocker

Hypertensive Emergency Medications (2)
? Labetalol
?Alpha and beta blocker (primarily beta)
?Onset of action: 5-10 minutes
?Half life: 5.5 hours
?No reflex tachycardia
?Low doses may lead to paradoxical
hypertension due to predominant beta effect
(unopposed alpha)
Contraindicated in bronchospasm, CHF,

Hypertensive Emergency Medications (3)
? Nitroglycerin
?Arteriolar and venous dilatation
?Onset: immediate
?Half life: 4 minutes
?Ideal for cardiac emergencies such as CHF, MI
?Side effects: headache and tachycardia

Hypertensive Emergency Medications (4)
? Hydralazine
?Direct arteriolar vasodilator
?Onset: 10 min (IV)
?Half life: 2-4 hours
?Indicated in pregnancy-related hypertension,
pediatric nephritis
Side effects include
reflex tachycardia (limits use in CAD, dissection)
Chronic use associated with "lupus-like" syndrome

Syncope (1)
? Defn. = Sudden, brief LOC and postural tone with
spontaneous recovery due to a decrease in
cerebral blood flow
? Causes:
?Neural y mediated (reflex-mediated HR or
vascular tone changes):
?Vasovagal (18%), situational (5%), carotid sinus (1%)
?Psychiatric causes (2%)
?Panic attacks, anxiety, somatization
?Orthostatic hypotension (8%)

Syncope (2)
?Medications (3%)
?Neurologic disease (10%)
?Cardiovascular causes:
?Organic heart disease (4%), arrhythmia (14%)
?Vascular ? subclavian steal (syncope associated with
arm exercise)
?Unknown (34%)
?Tilt table tests suggest that most of these are neural y

Aortic Dissection (1)
? Dissection of intima from media
? Depends on the rate of rise in blood pressure
? Bimodal age distribution
? Young with predisposing factors
? Col agen vascular disorders such as Marfan's
? Pregnancy (especial y third trimester)
? Chest trauma, iatrogenic (cardiac catheterization)
? Bicuspid aortic valve
? Aortic coarctation
? Elderly males with chronic hypertension
? Atherosclerotic risk factors (smoking,
hypertension, cholesterol, diabetes)

Aortic Dissection (2)
? Clinical presentation
?Tearing chest pain with radiation to back
?Migrating, dynamic pain pattern
?Sudden onset of severe pain
?Aortic insufficiency
?Pulse deficits
?Syncope, acute paralysis
? Physical exam
?Hypertension, normal BP or hypotension
?Asymmetric pulses, asymmetric BP
?Acute aortic regurgitation

Aortic Dissection (3)
? Stanford classification
?Type A: any dissection which involves
ascending aorta (surgical treatment)
?Type B: descending aorta only (primarily
medical management)

Stanford Type A

Stanford Type B


Aortic Dissection (4)
?May show acute MI if dissection is proximal and
involves coronary ostia
?Up to 8% with Type A wil have ST elevations
?Widened mediastinum in majority
?Intimal calcium separation
?Left pleural effusion

Aortic Dissection (5)
?Very sensitive and specific
?Usual y impractical due to inability to monitor
patient and time constraints
? CT with contrast
?Helpful if negative (high sensitivity) but does not
provide details needed for OR
?Does not show valve competence
?Shows thrombosed false lumen
?Requires dye load
? TEE (transesophageal echo)
?Very sensitive and specific ? best test if
?Done in ED (safer for patient)

Dissecting Aneurysm

Aortic Dissection

Aortic Dissection (6)
? Aortography
?Higher risk, logistical y difficult and expensive
?Provides anatomy necessary for OR, including
coronary involvement
?False negatives possible (thrombosed false
? Treatment
?Beta blockers, then nitroprusside for both types
?Stanford A usual y requires surgery also
?Stanford B usual y doesn't require surgery
All types need control of blood pressure
and decreased contractility (decrease dP/dT)

Abdominal Aortic Aneurysm (1)
? Pathophysiology
?Increase in diameter >50% over normal artery
?Due to medial degeneration (usual y
?Majority are infrarenal
? Risk factors
?Elderly male with atherosclerosis, hypertension
?Connective tissue disease

Abdominal Aortic Aneurysm (2)
? Clinical Presentation
?Asymptomatic until bleed or rupture
?Abdominal, flank or back pain
?Most common misdiagnosis: renal colic
? More unusual presentations
?Erosion into duodenum aortoenteric fistula
with massive GI bleed
?Partial bowel obstruction
?Erosion into IVC aortocaval fistula with
embolization distal y

Abdominal Aortic Aneurysm (3)
? Physical exam
?Pulsatile mass is found in <50%
?Abdominal or femoral bruits
?Decreased femoral pulses
? Diagnosis
?Plain films: rule out calcified aneurysm
?Abdominal cross table lateral
?Lateral L-spine

Abdominal Aortic Aneurysm

Abdominal Aortic Aneurysm (4)
? Ultrasound
?Excel ent bedside screening tool
?Very sensitive
?Unable to determine leakage (unless free fluid)
?May help to differentiate kidney stone
(hydronephrosis, dilated ureter) from aneurysm

Abdominal Aortic Aneurysm (4)
? Ultrasound

Abdominal Aortic Aneurysm (4)
? CT scan
?Useful in stable patients
?Able to visualize leakage into retroperitoneal
?Risky because patient is out of department

Abdominal Aortic Aneurysm (5)
? Management
?Hypotensive or unstable
?Priority is resuscitation and OR (multiple
large-bore IVs, type and cross 10 units)
?Leaking: Emergent operation
?Asymptomatic: elective repair if >5 cm
Any back or abdominal pain in a patient known
to have an aneurysm must be presumed to be
leaking or ruptured AAA until proven otherwise

Abdominal Aortic Aneurysm (6)
Blood clot
Normal Aorta < 3 cm
AAA > 3 cm

Acute Limb Ischemia (1)
? Emboli
?Usual y cardiac
?Mural thrombus from MI
? Arterial source
?Atherosclerotic disease
? Paradoxical embolus
?From venous emboli through septal defect

Acute Limb Ischemia (2)
? Embolus
?Sudden onset
?No previous arterial insufficiency
? Thrombus
?Etiology: atherosclerosis (most common)
?Low-flow states
?Develops slowly
?Past history of claudication
?Chronic arterial insufficiency

Acute Limb Ischemia (3)
? Signs of acute ischemia (6 P's)
?Pal or
Consider aortic
in al these cases
?Pulselessness (late finding)
?Poikilothermia (polar, cold)
? Treatment of acute limb ischemia
?Embolectomy, thrombolytics
?Bypass for atherosclerotic disease

Deep Venous Thrombosis (1)
? Pathogenesis (Virchow's triad)
?Endothelial damage
? Risk factors
?Estrogen use

Deep Venous Thrombosis (2)
? Presentation
?Pain and swel ing (unilateral)
?Low-grade fever
?Physical exam (e.g.Homans' sign) is insensitive

Deep Venous Thrombosis (2)
? Diagnosis
?Duplex ultrasonography: very sensitive and
specific for proximal thrombi
?Venography: "gold standard" but invasive and
has phlebitis as complication
?D-dimer (if negative, rules out DVT in low risk
?CT venography

Deep Venous Thrombosis (3)
? Treatment
?Heparin therapy initial y
?Then oral warfarin for 3-6 months
?LWMH al ows early outpatient treatment
?Caval filter when there is a contraindication to,
or failure of, long-term anticoagulation
?Recurrent DVT

Deep Venous Thrombosis (4)
? Phlegmasia cerulea dolens and phlegmasia
alba dolens
?Uncommon, severe presentation of DVT
?Massive iliofemoral DVT
?Acute, severe, massive swel ing
?Cyanotic, congested extremity (cerulea)
?Pale (alba) if arterial spasm causes "milk leg"
?Increased compartment pressure, ischemia
?May require surgery for compartment syndrome

Deep Venous Thrombosis (5)
Phlegmasia cerulea dolens
Phlegmasia alba dolens


EKG - AMI (1)
? Acute Q wave MI (transmural)
?ST elevation
?Q waves
?T wave inversion
? Non-Q wave MI (subendocardial)
?ST depression with ischemia
?T wave inversion
? Left ventricle divided into 4 regions
?Anterior (precordial V leads)
?Posterior (suggested from V1-V3 or post. leads)
?Lateral (I, aVL, V5-V6)
?Inferior (II, III, aVF)

Lateral Ischemia
Classic findings:
- ST depression / T wave in I, AVL, V5, V6

EKG - AMI (2)
? Anterior
?LAD occlusion
?ST elevation in any of V1-V4
?Reciprocal changes inferiorly

Anterior MI
Classic findings:
-ST elevation and poor R wave progression in V1-V4
-Reciprocal changes inferiorly

Med-Chal enger ? EM

EKG - AMI (3)
? Anteroseptal
?Septal branches of LAD
?ST elevations V1-V2
? Anterolateral
?LAD or left circumflex
?ST elevations V5, V6, I and AVL
?Reciprocal changes inferiorly
? Inferior MI
All potentially
?RCA occlusion
include pathologic
Q waves
?ST elevations II, III, AVF
?Reciprocal changes anteriorly

Septal MI
Classic findings:
- ST elevation V1-V2
- Q waves V1-V2

Med-Chal enger ? EM

Anterolateral MI
Classic findings:

- ST elevation V1 - V6 +/- I and AVL

- Reciprocal changes inferiorly
Med-Chal enger ? EM

Inferior (and posterior?) MI
Classic findings:
- ST elevation in II, III, AVF
- Reciprocal ST changes I and AVL

Med-Chal enger ? EM

EKG - AMI (4)
? Lateral MI
?Circumflex occlusion
?ST elevations I, AVL, V5, V6
?Reciprocal changes inferiorly
? Posterior MI
?Usual y accompanies inferior MI due to RCA
? 4% wil be isolated posterior MI
?Large R waves with ST depressions in V1, V2
? R:S > 1
?Mirror image of septal MI

Inferior-Posterior MI
Classic findings:
- ST elevation II, III, AVF
- Large R waves with ST depression in V1 ? V3
- Mirror image of septal MI
Med-Chal enger ? EM

Isolated posterior MI
Classic findings:
- Large R waves with ST depression in V1, V2
- Mirror image of septal MI

EKG - ST Elevation
? Differential diagnosis of ST segment elevation
?Acute MI
?Prinzmetal's angina (vasospasm)
?Ventricular wal aneurysm
?Benign early repolarization
?Bundle branch block

ST Segment Elevation
Predictors of MI
? Factors that increase the specificity
?ST elevation (horizontal or convex upwards)
?Fol ows coronary anatomy
?Reciprocal ST depression
?Changes over time (minutes to hours)
?May see hyperacute T waves (early)
?Q waves usual y only after hours to days

Hyperacute T-Waves
Early sign of Ischemia

Anterolateral MI: Horizontal ST segments
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)

Inferior MI: Convex upward ST segments
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)

Causes of ST Segment Elevation:
Prinzmetal's angina/spasm
? Convex or concave upwards morphology
? Transient over minutes
? More common in women
? Difficult to distinguish from true STEMI

Causes of ST Segment Elevation:
Ventricular Aneurysm
? Convex or concave upwards morphology
? Persistent ST elevation
? Q waves usual y present
? Usual y in anterior leads
? Easily seen on echo
? No reciprocal depression
? Look for old ECGs -- no change
? No serial changes


Causes of ST Segment Elevation:
"Early Repolarization"
? Concave upwards morphology
? In many leads, maximal in mid-precordial
leads with "fishhook" J-point
? Doesn't change over time
? No reciprocal depression
? Men > women, young > old


From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)

EKG - Hyperkalemia
? Hyperkalemia
?Flat P waves
?Peaked T waves
?Wide QRS
?Prolonged QT (due to hypoCa) and PR
?Bradycardias and AV blocks
?Eventual sine wave and Vfib

EKG ? Hypokalemia
? Hypokalemia
?U waves
?Prolonged QT
?ST segment depression

Hypokalemia / Hyperkalemia

EKG - Hypercalcemia / Hypocalcemia
? Hypercalcemia
? Shortened QT interval
? ST segment depression
? Hypocalcemia
? Prolonged QT interval

EKG - Electrolyte-Induced QT
? Electrolyte abnormalities that prolong QT
? Hypokalemia
? Hypocalcemia
? Hypomagnesemia
? Hyperphosphatemia
? Prolonged QT leads to ventricular
tachydysrhythmias (torsade de pointes, Vfib)

EKG - Torsade De Pointes
? Torsade de Pointes
?Polymorphic Vtach ("twisting of the points")
?Associated with prolonged QT interval
? Causes
?Quinidine, procainamide
No Procainamide
?Electrolyte abnormalities
or amiodarone
?Low Mg+, low K+, low Ca++

EKG - Torsade De Pointes
? Treatment
?Magnesium (wil shorten QT interval)
?Overdrive pacing
?Cardioversion/defibril ation
?Magnesium infusion for prophylaxis after

Torsade de Pointes
Classic findings:
- Polymorphic V. Tach - "a twisting of the points"
- Associated with increased QT interval

EKG - Hypothermia
? Hypothermia (< 30o C)
?Prolonged intervals
?Sinus bradycardia
?Muscle tremor artifact
?Slow A-fib
?Osborne J waves
?Vfib, asystole

Classic findings:
- Prolonged intervals
- Sinus bradycardia
- +/- muscle tremor artifact
- Slow a. fib
- Osborne (J) wave
- V. fib / asystole

EKG - Digoxin
? Causes increased automaticity with conduction
block (PAT with block)
? Therapeutic levels may cause
?T wave depression
?ST downsloping (Salvador Dali moustache)
?QT shortened
? Toxic levels
?PVCs (most common dysrhythmia)
?Sinus and AV node blocks
?AV dissociation
?SVT (especial y with blocks)
?Sinus bradycardia

Digitalis Effects
Classic findings:
- T wave depression
- ST down sloping (Salvador Dali moustache)
- QT shortened

EKG ? Cyclic Antidepressants
? Sinus tachycardia (most common)
? Prolonged QT
? Right axis deviation
? QRS width > 100 ms
? Conduction blocks

EKG ? Cyclic Antidepressants
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)

EKG - Supraventricular Tachycardia
? Supraventricular tachycardia
?Usual y re-entrant mechanism
?Regular, narrow complex tachycardia
?Rate 150-200
?Absent or retrograde P waves
?Treatment: adenosine, calcium channel
blockers (diltiazem, verapamil)
?Don't use calcium channel blockers if a long
acting beta blocker was recently administered

Supraventricular Tachycardia
Classic findings:
- Regular, narrow complex tachycardia
- Rate 150-200
- Absent P waves or retrograde

EKG - Atrial Fib / Flutter (1)
? Etiologies
?Digoxin toxicity
?Chronic obstructive pulmonary disease
?PE, hypoxia
?Electrolyte abnormalities

EKG - Atrial Fib / Flutter (2)
? Atrial flutter
?Regular, narrow complex with atrial rate 250-350
?Ventricular rate usual y blocked (2:1, 3:1, 4:1)
?Sawtooth baseline (flutter waves)
? Atrial fibril ation
?Irregularly irregular rhythm with undulating
baseline (associated with thyrotoxicosis, CAD,
CHF, PE, LAE, alcohol)

EKG - Atrial Fib / Flutter (3)
? Treatment: rate control (chemical, electrical)
?Stable: diltiazem, beta blockers, amiodarone,
?Atrial flutter: synchronized cardioversion
(start at 50 J)
?A-fib: synchronized cardioversion
(start at 200 J)
?Anticoagulation for long term A-fib

Atrial Flutter
Classic findings:
- Regular, narrow complex with atrial
rate = 250-350
- Ventricular rate usually blocked -
2:1, 3:1, 4:1
- Sawtooth baseline (flutter waves)

Atrial Fibrillation
Classic findings:
- Irregularly, irregular rhythm

EKG - Multifocal Atrial Tachycardia
? Multifocal atrial tachycardia
?Irregularly irregular narrow complexes, rate
?At least 3 different P wave morphologies
?Variable PR intervals
?Associated with
?Theophylline toxicity
?Treat underlying condition
?MgSO may be helpful; no shocks!

Multifocal Atrial Tachycardia
Classic findings:
- Irregularly irregular with narrow complex, rate >100
- At least 3 different P wave morphologies, Variable PR 238

EKG - Wolff-Parkinson-White Syndrome (1)
? Bypass tract joining atria to ventricles with no
conduction delay (short PR interval)
? A-fib with 1:1 conduction of atrial rate death
? Delta wave when conduction is through bypass
tract during NSR
?Delta wave is not reliably seen in

EKG - Wolff-Parkinson-White Syndrome (1)
? Avoid digoxin and calcium channel blockers
(verapamil, diltiazem) during A-fib
?These drugs block the AV node but not the
bypass tract. All impulses then go through the
bypass tract (not slowed down at AV node)
?Procainamide or electrical cardioversion is safe
?Adenosine and other AV nodal blockers are
contraindicated during A-fib

EKG - Wolff-Parkinson-White
Syndrome (2)
? Treatment is based on QRS width
?Narrow-complex tachycardia
?Treat like SVT
?Wide-complex tachycardia, no history of WPW
?Treat like Vtach
?A-fib with known history of WPW
?Procainamide, cardioversion
?Do not use digoxin, verapamil, diltiazem,
adenosine, ?amiodarone (AVN blocker)

Wolff-Parkinson-White Syndrome
Classic findings:
- Wide complex seen with delta wave when
conduction through bypass tract

Wolff-Parkinson-White Syndrome
SVT classic findings:
- Regular tachycardia
- Treat as any other regular NCTs or WCTs


Wolff-Parkinson-White Syndrome
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)
A-fib classic findings:
- Irregularly irregular tachycardia
- QRS morphologies change
- Treat with procainamide or electricity


EKG - Ventricular Tachycardia (1)
? Ventricular tachycardia
?Regular, wide-complex, rate >120
(usual y >150)
?Associated with
?Underlying heart disease (CAD, cardiomyopathy,
?Electrolyte disturbances
?Toxic ingestions
?If stable: procainamide > amiodarone > lidocaine,
?If unstable: sync cardioversion

Ventricular Tachycardia
Classic findings:
- Regular wide complex with rate > 120

(usually >150)

EKG - Ventricular Fibrillation
? Ventricular fibril ation
?Primary: no preceding hemodynamic
?Secondary: prolonged LV dysfunction, shock
?Structural heart disease, ischemia
?Total y disorganized, non-perfusing rhythm
?Associated with CAD, MI, toxic ingestions,
electrolyte disturbances
?Treatment: defibril ation (ACLS protocols)

Ventricular Fibrillation
Classic findings:
- Totally disorganized, non-perfusing rhythm

EKG - Premature Ventricular
Contractions (1)
? Premature ventricular contractions (PVCs)
?Premature, wide complex, no preceding P wave
(compensatory pause)
?Unifocal or multifocal
? Associated with
?Normal heart, alkalosis, CHF, MI, hypokalemia,
hypoxia, cardiomyopathy, drugs, digoxin toxicity
? PVCs in acute MI
?Indicate electrical instability
?Prophylactic treatment not proven to decrease

EKG - Premature Ventricular
Contractions (2)
? Treatment
?Treat underlying cause (e.g. electrolytes,
ischemia, hypoxia)
?Consider magnesium, beta blockers
?Treat sustained VT (> 30 seconds or if
hemodynamic instability develops)

EKG - Premature Ventricular
Contractions (2)
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)

EKG - Accelerated
Idioventricular Tachycardia
? Accelerated idioventricular rhythm ("slow
?Wide complex regular rhythm with rate 40-120
?Runs may last few minutes
?Associated with acute MI and reperfusion
?Treatment: observe!
? Is self-terminating, NOT destabilizing
?If hypotensive, consider atrial pacing

Accelerated Idioventricular Rhythm
Classic findings:
- Wide complex rhythm with rate = 40-120

Accelerated Idioventricular Rhythm
(rate < 120)
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)

EKG - Junctional Rhythm
? Regular escape beats, rate 40-60, no P waves,
usual y narrow-complex
? Abnormal automaticity (accelerated junctional
rhythm): rate 60-100, retrograde P waves
? Associated with
?Digoxin toxicity
? Treatment
?Usual y none
?Underlying condition
?Atropine only if needed to speed rate

Junctional Rhythm
Classic findings:
- Regular usually narrow complex with rate = 40-100
- No P wave or retrograde P wave


EKG - First Degree Heart Block
? First degree AV block
?PR interval > 200 ms
? No treatment necessary, but look for
underlying cause
? Causes: increased vagal tone, cardiac drugs,
myocarditis, endocarditis, AMI (inferior),
hypothermia, hyperkalemia, age-related
degeneration (common in elderly)

First Degree AV Block
Classic findings:
- PR interval > 200 ms

EKG - Second Degree Heart Block
? Mobitz I (Wenckebach)
?Progressively longer PR and shorter RR until a beat is
dropped, then starts over
?Causes: same as 1st degree block, common with inferior
MI, often transient; treatment if hemodynamic instability
?Atropine or transcutaneous pacemaker usual y sufficient
? Mobitz II
?Constant PR interval and dropped beats
?Associated with anterior MI and destruction of conduction
?Usual y associated with bundle branch block
?May progress to complete heart block
?Temporary pacer often needed in the setting of AMI

Second Degree AV Block Type I
(Mobitz I, Wenkebach)
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)

Second Degree AV Block Type II
(Mobitz II)
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)

EKG - Third Degree Heart Block
? Third degree AV block (complete heart block)
?AV dissociation: no relation between P and
QRS ? PR interval changes randomly
?Junctional (narrow QRS's) or ventricular (wide
QRS's) escape beats
?Associated with anterior MI and destruction of
conduction tissue
?Narrow complex: may be temporary due to
vagal tone
?Wide complex: usual y requires transvenous

Third Degree AV Block
Classic findings:
- AV dissociation no relation between P and QRS

- PR interval changes randomly

AV Dissociation
? Atria and ventricles beat independently
? Atrial rate > ventricular rate
?Sinus dysfunction, bradycardia and block (3o
block is a form of AV dissociation) leads to
ventricular escape rhythms
? Causes
?Ischemia (inferior MI)
?Myocarditis (acute rheumatic fever)
?Drug toxicity (digoxin)
?Vagal reflex
? Fusion beats are common

Premature Ventricular
Contractions (PVCs)
Classic findings:
- Premature, wide complex with no preceding P wave
- Unifocal or multifocal

Brugada Syndrome
? Syncope or sudden death in young patients
with a structural y normal heart resulting from
venticular fibril ation
? Most common cause of sudden death in young
males without heart disease
? Familial autosomal dominant
? Particularly common in SE Asian males
? Pseudo-RBBB pattern
? ST elevations in V1 and V2
? Implantable defibril ator is treatment

Brugada Syndrome
? Precipitants of Dysrhythmias
? Beta blockers
? Sodium channel blockers (TCAs, Type I
antiarrhythmics, cocaine)
? Ethanol
? Fever, hot ambient temperature
? Electrolyte abnormalities (high K and Cal, low K)
? Increased alpha adrenergic tone
? Pacing
? Vagal maneuvers
? Combinations of glucose and insulin

Brugada Syndrome

Brugada Syndrome
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)

Ventricular Tachycardia vs. SVT
? VTach findings
?AV dissociation ("cannon" A waves in neck,
variable intensity S1, variable pulse amplitude
?Fusion beats
?QRS >14 ms
?Elderly patients
?History of CAD or MI
? SVT findings
?QRS in same direction as normal QRS

Ventricular Tachycardia vs. SVT
? VTach findings
?AV dissociation ("cannon" A waves in neck,
variable intensity S1, variable pulse amplitude
?Fusion beats
?QRS >14 ms
?Elderly patients
?History of CAD or MI
? SVT findings
?QRS in same direction as normal QRS

Ventricular Tachycardia vs. SVT
? VTach findings
?AV dissociation ("cannon" A waves in neck,
variable intensity S1, variable pulse amplitude
?Fusion beats
Always assume a regular
?QRS >14 ms
WCT on the boards is Vtach
?Elderly patients
?History of CAD or MI
? SVT findings
?QRS in same direction as normal QRS


Which of the following factors is
consistent with Prinzmetal
's (variant)

A. It is associated with ST depression rather
than elevation
B. It usual y comes on during exertion rather
than rest
C. Most patients have some mild evidence of
coronary artery disease on angiography
D. Never results in myocardial infarction
E. Patients undergoing cardiac cath are rarely
diagnosed with variant angina
CA 1

Which of the following statements
is true regarding aortic regurgitation?

A. Results in a decrescendo systolic murmur at
the left sternal border
B. Is responsible for producing a "water hammer"
pulse and Austin-Flint murmur
C. Endocarditis prophylaxis and afterload
reduction are general y not indicated
D. Is never associated with Marfan's syndrome
E. ECG reveals RVH
CA 2

A patient had a myocardial infarction three
weeks prior and today he presents
with chest discomfort (made worse on
swallowing), fever, and pleural effusion.
The preferred treatment for the most likely
diagnosis is:

A. Angiography
C. Nitrates
D. Antibiotics
E. Thrombolytics
CA 3

A patient presents with a regular pulse at
a rate of ~ 220/min. The patient
's BP is
135/80. A
"delta wave" is noted on one of
the patient
's old ECGs. Which of the
following is the most appropriate for this

A. Digoxin
B. Verapamil
C. Procainamide
D. Adenosine
E. All of the above
CA 4

A patient presents with an irregularly irregular
rhythm with a rapid ventricular response (120/
min), which later increases to 220/min. He
has a known history of WPW. The BP is
100/60. Which of the following is the most
appropriate treatment?

A. Amiodarone
B. Diltiazem
C. Procainamide
D. Synchronized cardioversion (zap!)
E. Adenosine
CA 5

Classic ECG finding of hypothermia

A. Delta wave
B. Prolonged intervals
C. J wave
D. Osgood wave
E. Asystole
CA 6

In non-embolic limb ischemia,
which of the following is the last
sign to develop?

A. Pain
B. Pulselessness
C. Pal or
D. Paresthesias
E. Coolness
CA 7

A patient presents with a blood pressure
of 260/150, dyspnea and chest pain.
Which of the following agents is most
likely to be successful for reducing this
's blood pressure?
A. Diltiazem
B. Nitroprusside
C. Clonidine
D. Nifedipine
E. Nitroglycerin
CA 8

Which of the following statements
is true regarding endocarditis?
A. The pulmonic valve is the most commonly
B. A murmur is auscultated in less than 5% of
C. Optimal antibiotic therapy consists of first or
second generation cephalosporins
D. TEE is considered the "gold standard" for
detecting valvular vegetations
E. Roth spots are noted on the palms and soles
CA 9

Which of the following are causes of
myocardial infarction?

A. Aortic dissection
B. Atherosclerosis
C. Cocaine
D. Emboli
E. All of the above
CA 10

Which of the following is consistent with
unstable angina?

A. Positive cardiac markers
B. Consistent chest pain relieved by rest and
C. Chest pain with acute ST-segment elevations
D. Chest pain at rest
E. Unchanged frequency and severity
CA 11

65 y/o diabetic patient presents to the ED
with new onset C.P. Troponin I and CPK
MB are normal, ECG = SR without ischemic
changes. Which plan is the most

A. Discharge the patient as his enzymes and
ECG are normal
B. Repeat a second set of enzymes and
discharge if normal
C. Admit the patient to rule out ACS
D. Administer thrombolytics
E. Perform a CT to rule out PE
CA 12

A 72 y/o male patient presents with an MI
ECG = 3rd degree AV block and ST
elevation in leads 2, 3 and AVF. The
patient experiences a brief non-sustained
run of V-tach. Which of the following is
A. These are reperfusion dysrhythmias
B. This patient needs a transvenous pacemaker
placed immediately
C. 3rd degree AV block is associated with poor
prognosis in anterior wal MIs
D. Thrombolytics wil not be effective in this case
E. The patient should be treated with intravenous
CA 13

Which is an absolute contraindication for
thrombolytic administration?
A. CVA within 6 months
B. Squamous cel carcinoma
C. Menstruation
D. Spinal surgery 6 months ago
E. Coumadin
CA 14

A 45 y/o patient presents with C.P. The ECG
= SR with ST elevations in leads 2, 3 and
AVF. BP = 90/60. PE: Lungs clear +JVD.
What is the most appropriate next step,
based on the most likely diagnosis?

A. Oxygen, IV nitroglycerin
B. ASA PO and IV NS bolus 500cc
C. Sublingual nitroglycerin x3 and morphine 2 mg
D. Oxygen, IV nitroglycerin and IV dopamine
E. Cal for Intra-aortic bal oon pump placement
CA 15

Which of the following is not one of
Jones major criteria?

A. Subcutaneous nodules
B. Sydenham's chorea
C. Arthritis
D. Carditis
E. Erythema migrans
CA 16

Exertional syncope, dysrhythmias, cardiac
ischemia and sudden death are all
associated with which of the following?
A. Pericarditis
B. Restrictive cardiomyopathy
C. Hypertrophic cardiomyopathy
D. Dilated cardiomyopathy
E. Amyloidosis
CA 17

A 56 y/o patient's BP = 190/115. The
patient has no complaints, excluding mild
frontal headache. PE: Normal. Which
option is appropriate?
A. Reassurance and defined fol ow-up
B. Nifedipine 10 mg PO
C. Clonidine 0.1 mg PO
D. Labetalol 20 mg IVP
E. Fol ow-up as needed (prn)
CA 18

A 64 y/o patient presents with C.P. & SOB.
PE: JVD; rales; Dyspnea; Grade 5/6
holosystolic murmur radiating into the
axilla. ECG: Acute anterior wall MI. CXR:
Pulmonary edema. What is this patient's
A. Dressler's syndrome
B. Aortic dissection
C. Atrial septal defect
D. Chordae tendonae rupture
E. Pericardial effusion
CA 19

A 74 y/o male patient presents with an
acute onset of mid-abdominal pain that
radiates to the right flank. PMHx: CAD
BP 80/40. What is the most appropriate
next step for the most likely diagnosis?
A. Order a CT of the abdomen with triple contrast
B. Order a selective mesenteric angiogram
C. Consult surgery for emergent exploratory
D. Order an abdominal ultrasound
E. Order a renal protocol CT
CA 20

Cardiology Answer Key
1. C
11. D
2. B
12. C
3. B
13. C
4. E
14. A
5. D
15. B
6. C
16. E
7. B
17. C
8. B
18. A
9. D
19. D
10. E
20. C

















The ECG of this 71-year-old man shows:
? Normal sinus rhythm, rate 70
? Left anterior fascicular block
? Anterior infarct, probably acute with increased ST segment elevation since earlier this date
? Reciprocal inferior ST segment depression
ECG: Acute Pericarditis: findings of acute pericarditis:
? ST segment elevations in all limb leads except aVR
? ST segment elevations in all precordial leads except V1
? PR segment depression in multiple leads
NOTE: As is typical for pericarditis, the ST segments are concave upward and the T waves have not inverted prior to
return of the ST segments to near baseline. PR segment depression is characteristic and helps differentiate acute
pericarditis from ischemia or infarction and early repolarization. In stage three, the T-waves invert, followed by
normalization in stage four.
The ECG of this 64-year-old woman shows:
? Atrial flutter with 4:1 conduction, A-rate 272
? Diffuse ST-T abnormalities
? Poor R wave progression in leads VI
The serum calcium must be less than 8 mg/100 mL for recognizable EKG changes to occur. Characteristic
changes include:
? The QT interval is consistently prolonged.
? The PR interval may also be prolonged.
? Terminal negativity of the T waves in the precordial leads may occur.
Sinus rhythm with borderline 10 AVB and Left bundle branch block:
? ST segment elevation in leads V1-v3
? Acute anterior wall myocardial infarction

? Signs of acute injury in the context of LBBB include ST elevation of > 1 mm in leads with a positive QRS deflection, ST
segment elevation > 5 mm in leads with negative QRS deflections and ST depression > 1 mm in leads V1-V3.
None of the standard EKG leads overlie the posterior aspect of the heart, so Q waves and ST elevations are not seen
with posterior infarction. Posterior infarction is indicated by reciprocal large R waves and ST depressions in the
anteroseptal leads, with non-inverted T-waves. It is usually accompanied by inferior infarction, as demonstrated in this
ECG findings in this patient with hyperkalemia include:
? Absent P waves: "sinoventricular rhythm" of hyperkalemia
? Prominent narrow based T waves, suggestive of hyperkalemia
? Widening of the QRS is a late finding of hyperkalemia
NOTE: that marked hyperkalemia can depress or suppress activation of the atrial myocardium, resulting in loss of P
waves, while conduction through the atrial internodal tracts is preserved (sinoventricular rhythm).
The ECG of this hypothermic woman shows:
? Bradycardia with an idioventricular or junctional escape rhythm
? Prominent J waves in the anterior leads
This 80-year-old woman was found lying down in her backyard. Her rectal temperature was 80 degrees F. The ECG
shows an idioventricular or junctional (more likely) escape rhythm at a rate of less than 45 beats per minute. The QRS
axis is normal. There are diffuse ST abnormalities. The positive deflection at the end of the QRS complex, most notable
in the anterior leads, is known as the Osborn or J wave that is characteristic, but not pathognomonic, of hypothermia.
The ECG of this 96-year-old woman shows:
? Absent P waves and narrow QRS complexes
? Consider atrial fibrillation
? Regular rate and rhythm with bradycardia, ventricular rate 36
? Junctional escape rhythm
? Non-specific ST-T abnormalities
The ECG of this 84-year-old man shows:
? Normal sinus rhythm, rate 65
? Left bundle branch block
? Left axis deviation

The ECG of this 85-year-old woman shows:
? Multifocal atrial tachycardia
? Ventricular premature complexes
? Left axis deviation
? Late transition
? Diffuse non-specific T wave abnormalities
? This rhythm may be drug related
? Rare aberrant complexes
? No change from 10/3/94
This patient with a pulmonary embolus has a typical "S1, Q3, T3" pattern of acute right ventricular strain and right axis
deviation. An S wave develops in aVL or V1 and a Q wave in aVF and L3. The overall pattern usually resembles RBBB or
RBBB plus LPFB. In some cases, the T wave becomes negative in the inferior leads, resulting in the classic "S1, Q3, T3"
pattern. ECG findings include:
? S wave in L1with
? Q waves in aVF and L3, suggesting
? Acute right ventricular strain
This 72-year-old woman's ECG shows:
? Normal sinus rhythm, rate 78
? Right axis deviation
? Right bundle branch block
? Inferior T wave abnormality
The ECG in this 96-year-old man with tachy-brady syndrome and syncope shows:
? Sinus bradycardia, rate 47
? A four beat run of supraventricular tachycardia
? Left axis deviation
? Possible inferior infarct
? Old anterior infarct
This 75-year-old woman's ECG shows findings of:
? Sinus rhythm, rate 62
? Multiple atrial premature complexes
? Left ventricular hypertrophy by voltage criteria
? QT interval prolongation

? Diffuse ST-T abnormalities, consistent with
? Ischemia and/or subendocardial infarction
The ECG of this 45-year-old woman shows:
? Supraventricular tachycardia, rate 189
? Right axis deviation
? Diffuse ST-T abnormalities
There appear to be P wave deflections on the initial part of the ST segment. These are particularly evident in Leads II, III
and V3. These suggest a supraventricular tachycardia of the short RP interval category, most likely typical AV nodal
reentrant tachycardia (AVNRT) or orthodromic AV reentrant tachycardia (AVRT).
The ECG of this 59-year-old man shows:
? Regular P waves at a rate of approximately 125/minute
? Complete (third degree) AV block
? Ventricular or junctional escape, rate 29
? Superior QRS axis
These EKGs are from a patient with WPW type A in NSR and in tachycardia with antegrade conduction down the
accessory pathway and subsequent slurred QRSs, rapid ventricular response, and hypotension.
NOTE: In most cases of WPW, antegrade conduction follows the normal pathway during tachycardia with retrograde
conduction up the accessory path. In those cases, the rate and QRS morphology are the same as for SVT without WPW,
and the delta waves are detectable only during NSR.
The ECG shows:
? Sinus rhythm with 10 AVB
? T-wave inversions in I and AVL, indicative of lateral wall ischemia
The third and succeeding QRSs on this rhythm strip are wide with retrogradely conducted P waves, suggesting
a ventricular origin or a junctional origin with Intraventricular conduction delay. The rate is more rapid (>40 bpm) than is
usual for ventricular escape. Findings summary:
? Wide QRS complexes
? Intermittent retrograde conduction of P waves
? Accelerated idioventricular rhythm or junctional rhythm with intraventricular conduction delay.

Retrograde P waves immediately follow the trailing edge of the last four QRS complexes. The first two QRS complexes are
narrower than the others and are preceded by P waves.
This patient has:
? Tachycardia with narrow QRS complexes
? Strongly consider atrial flutter with a 2:1 conduction ratio.
The heart rate is fast and regular at 150. An abnormal P wave precedes each QRS, but may be difficult to see, due to the
rapid rate.
This rhythm strip shows findings of:
? Regular rhythm with wide QRS complexes
? Dual pacemaker spikes preceding each QRS complex (AV sequential pacemaker)
NOTE: one spike followed by an abnormal P wave (atrial capture) followed by a second spike producing a wide QRS
(ventricular capture). Pacing the atrium and ventricle sequentially improves cardiac output.
Findings on this ECG rhythm strip include:
? Normal sinus rhythm, with
? Brief run of ventricular tachycardia
This rhythm strip shows findings of:
? Regular P waves
? Complete (third degree) AV block with prolonged ventricular asystole
? Ventricular or junctional escape rhythm
? Artificial pacemaker with failure to discharge and failure to capture, earlier in the rhythm strip.
NOTE: The missing pacemaker spikes and secondary asystole. Discharge or output failure can be due to oversensing by
the pacemaker, a weak battery, a cracked or broken wire, electrode displacement, or fibrosis about the electrode.
Findings on this rhythm strip include:
? Sinus rhythm
? Frequent PVCs in a bigeminy pattern
? Every other complex is a PVC. This is called ventricular bigeminy.

Findings on this ECG rhythm strip include:
? Classic "J" wave of hypothermia
? Baseline artifact
This ECG rhythm strip shows:
? Mobitz I second degree AV block (Wenckebach)
NOTE: the gradually lengthening PR interval prior to each dropped beat.
Simultaneous leads from a patient with hypokalemia showing the torsade de pointes type of
ventricular tachycardia (VT). The last three sinus beats, at the beginning of the strip, show an underlying sinus
tachycardia of about 140 beats per minute. The run of VT with a gradually rotating axis begins with a bidirectional VT.
(adapted from D.M. Krickler and P.V.L. Curry, Br. Heart J. 38:117, 1976)
This ECG rhythm strip shows:
? Coarse ventricular fibrillation
? The rhythm is extremely rapid and irregular.
Sinus Rhythm with Brugada Syndrome:
? Pseudo RBBB pattern
? ST elevations in V1 and V2

This post was last modified on 24 July 2021