Download MBBS Cardiology Lecture Notes

Cardiology
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A few words first...
? Review, review, review
? Handout more comprehensive

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? 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

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? Always consider deadly causes first
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Acute Coronary Syndrome
(ACS)
? Spectrum of disease due to myocardial

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ischemia
?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

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each year
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Causes of ACS
? Usual y due to atherosclerosis
?Fixed lesion, critical stenosis

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?Plaque disruption, platelet
aggregation, thrombus formation
? Results in oxygen supply/demand imbalance
leading to cardiac muscle damage
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Non-Atherosclerotic Causes of ACS
? Trauma
? Connective tissue diseases (vasculitis)
? Metabolic diseases (thickening of vessels)
? Congenital anomalies

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? Thrombus (DIC, TTP)
? Emboli (bacterial, non-bacterial)
? Thoracic aortic dissection
? Drugs (cocaine)
? Infectious diseases

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Cocaine-Associated Chest Pain
Acad Emerg Med 2000
? How often is chest pain associated with cocaine use
reflective of an AMI?

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? 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)

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ACS
ACS: Unstable angina Non-STEMI STEMI
? Unstable angina
?Resting

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?New onset
?
Increasing severity
?High risk of MI or death
?Duration >20 minutes, hypotension, CHF,

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dynamic ST changes
Prinzmetal's angina (variant angina):
Coronary artery spasm, occurs at rest,
ST elevation (not depression), may not have CAD
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Acute Myocardial Infarction (AMI)
? Classification of AMI
?STEMI/Q wave: transmural infarction involving
ful thickness of myocardium
?Non-STEMI/Non-Q wave: subendocardial

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infarction involving partial wal thickness. Has
lower initial mortality and morbidity, but long
term prognosis is similar
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AMI EKG Changes

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

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AMI EKG Changes

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? 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

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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
wave
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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

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?Reflect reperfusion
?Identify new dysrhythmias / conduction issues
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The EKG in AMI (2)
? EKG indications for emergent reperfusion

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? 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.

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? ST-segment depression measuring 1 mm in any of the V1
through V3 leads.
? Discordant ST-segment elevation measuring 5 mm (lower utility)
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Normal LBBB
Rule of appropriate discordance
(true for pacemakers also)
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From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)

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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)

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The EKG in AMI (2)
Concern in lead V3
? EKG indications for emergent reperfusion

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From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)
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The EKG in AMI (2)
Concern in leads V1-2

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From ECGs for the Emergency Physician Vol 2 (Mattu, Brady; Blackwel 2008)
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The EKG in AMI (2)
? Predictors of reperfusion
?Normalization of ischemia-related ST elevation

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? Failure to normalize may indicate the need for
"rescue PCI"
?Early T wave inversions can be highly specific markers of
reperfusion
?An accelerated idioventricular rhythm (60-120) is also

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highly specific for reperfusion / benign, don't suppress it
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EKG Anatomy (1)
Anterior wall
V3-V4

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Left main
coronary
artery
Right
coronary

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Circumflex
artery
artery
Left anterior
descending artery

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Lateral wall
Septal wall
I, aVL, V5-V6
V1-V2

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EKG Anatomy (2)
Circumflex
artery
(from left coronary

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artery)
Posterior wall
Right coronary
Lateral wall
artery

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Inferior wall
Posterior
Leads II, III, aVF
descending artery
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EKG Anatomy (3)
I lateral
aVR
V1 septal V4 anterior
II inferior aVL lateral

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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

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depression in V1-2
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The EKG in AMI (1)
? Inferior MI (ST elevation II, III, aVF)
?80% right coronary, 20% circumflex

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? 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)
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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

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carry a worse prognosis because they reflect necrosis of
the conduction tissue (early pacing if any new or partial
BBB develops)
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The EKG in AMI (4)

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? 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

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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

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reperfusion = PCI
?PVCs don't predict sustained ventricular dysrhythmias /
don't routinely suppress
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Cardiac Markers (1)

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? Myoglobin
?1-2 hours (rises)
?4-6 hours (peaks)
?24 hrs (normalizes)
? Troponin

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?3-6 hours (rises)
?12-24 hours (peaks)
?7 days (normalizes)
? CK-MB
?3-4 hours (rises)

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?12-24 hours (peaks)
?1-2 days (normalizes)
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Cardiac Markers (2)
? Myoglobin

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?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

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? CK-MB
?Elevation without infarction (skeletal disease,
muscle exertion, cocaine, renal failure)
?Comparing MB to total CK improves specificity
?30-40% false negatives in UA = NSTEMI

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Therapy of AMI (1)
? Oxygen
? Nitrates (sublingual, topical, IV)
?Contraindicated if sildanefil (Viagra) etc. within 24

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hours or if hypotensive
?Caution/avoid in RV MI
?Vasodilatation
? ASA (162-325 mg)
?ASA alone reduces mortality 23%

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?Combined with thrombolytics, ASA reduces
mortality 42%
? Morphine for persistent pain
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Therapy of AMI (2)

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? 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

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?Contraindications (asthma, CHF, bradycardia,
hypotension; caution in RV MI)
? Platelet inhibitors
?GP Ilb/IIIa receptor antags IV
?Clopidogrel: 300-600 mg oral load or

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?Prasugrel 60 mg oral load at cath; avoid if
history of TIA or stroke
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Therapy of AMI (3)
? Thrombolysis vs. percutaneous coronary

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intervention
?Outcomes have shown consistent benefit with
PCI over thrombolytics
?Guidelines recommend PCI if bal oon inflation
can be performed within 90 minutes

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? Window of benefit extended if chest pain > 6 hours
or if cardiogenic shock
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Thrombolytic Therapy Indications
? Chest pain greater than 30 minutes but less than

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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
leads
?New LBBB or Sgarbossa criteria

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? PCI delayed greater than 90 minutes
A RBBB should not obscure the diagnosis
of an acute MI
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Contraindications to Thrombolytic Therapy

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Absolute
Relative
? (PCI immediately available) ? History of GI bleed
? Active bleeding from any
? Prolonged CPR

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site
? Surgical or invasive procedure
within 3 weeks
? CVA within 6 months or
? Severe bleeding diathesis or

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hemorrhagic CVA at any
thrombocytopenia
time in the past
? Uncontrol ed hypertension
?

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(diastolic >120 after treatment)
Intracranial or intraspinal
? Significant trauma within 4
surgery or trauma within 2
weeks

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months
? Pregnancy or <10 days post-
? Intracranial or intraspinal
partum
neoplasm, aneurysm or AV ? Active cavitary lung disease

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malformation
? Known al ergy to agent
? Suspected aortic dissection
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No Thrombolytics

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Complications of Thrombolytic Therapy
? Bleeding (send blood for type and screen)
? Serious bleeding in 5%
? Intracranial hemorrhage: approximately 0.5%.

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Higher risk with uncontrol ed BP, age > 65, low
body weight
Evidence of Reperfusion
? Chest pain resolved
? ST elevation resolved

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? Reperfusion dysrhythmias
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Early Complications of AMI (1)
? Blood supply to pacemaker and conduction tissue
?Sinus node (right coronary, 60% / circumflex,40%)

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?AV node (right coronary, 90% / circumflex, 10%)
?Septal conduction (left anterior descending)
? Good prognosis
?Bradycardia (without hypotension)
?2? Mobitz type 1 AV block (Wenckebach)

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?3? AV block with inferior MI (resolves)
? Narrow QRS complexes
?PVCs, PACs
?Early non-sustained V tach
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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

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?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)

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seen in anterior MI due to structural loss of
conduction tissue need pacemaker
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Early Complications of AMI (3)
? Cardiogenic shock: usual y >40% of LV muscle

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necrosed
?High mortality
?Treatment: fluids, inotropes, IABP (intra-aortic
bal oon pump) to increase coronary blood flow
? Papil ary muscle dysfunction

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? Acute mitral regurgitation (usual y due to
ischemic dysfunction of papil ary muscles)
? Recurrent chest pain
? Ischemia vs reinfarction (may require PTCA or
CABG)

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Early Complications of AMI (4)
? Right ventricular infarction
?Associated with inferior MI
?Do right sided chest leads (especial y V4R)

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looking for ST elevation
Triad of hypotension, JVD and clear lungs
?RV loses function, acts as conduit only (not
pump)
?Heart becomes very preload-dependent

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?Use NTG and MS with caution (can drop BP
precipitously)
?Treat as any other MI but use fluids liberal y to
augment preload
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Late Complications of AMI (1)
? Recurrent chest pain
? Embolism (from mural thrombus)
? Pericarditis
?Post-MI (seen 1-7 days after transmural infarct)

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?Treatment: NSAIDs
? Dysrhythmias
Dressler's Syndrome: pericarditis 2-8 weeks post-MI
(probably a continuum with earlier pericarditis)
Fever, leukocytosis, friction rub, pericardial and

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pleural effusions. Treatment: NSAIDs & steroids
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Late Complications of AMI (2)
? Myocardial rupture
?LV free wal : often results in acute tamponade,

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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

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?Anterior or inferior MI
?Treatment: afterload reduction, aortic bal oon,
surgery
All seen 1-7 days post-MI and treated surgical y
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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

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? Stroke volume of heart depends on
?Preload
?Afterload
?Contractility
? Frank-Starling curve shows the relationship

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between these
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Etiology of Heart Failure
? Primary myocardial diseases (low output failure)

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?Hypertension (most common cause)
?Coronary artery disease, MI
?Valvular heart disease
?Cardiomyopathy (i.e. ischemic)
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Etiology of Heart Failure
? Increased workload on heart (high output failure)
?Thyrotoxicosis
?Anemia
?A-V fistula

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?Beriberi
?Paget's disease of the bone
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Classification of Heart Failure
? Left-sided or right-sided systolic dysfunction

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?Impaired contractility low ejection fraction,
low cardiac output (e.g. MI, dilated
cardiomyopathy) high renin and angiotensin
levels, high afterload
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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

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?Causes: ischemia, hypertrophy, amyloidosis
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Presentation of Heart Failure (1)
? Left sided failure
?Dyspnea

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?Orthopnea
?Tachycardia
?S3 gal op
Pulmonary edema
?Redistribution

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?Kerley B lines (Interstitial edema / lymphatic
engorgement)
?Alveolar edema
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Congestive Heart Failure

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Interstitial edema
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Congestive Heart Failure
Alveolar edema
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Presentation of Heart Failure (2)
? Causes of acute right sided failure (rare)
?Pulmonary embolism
?RV infarction
? Signs and symptoms

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?Peripheral edema
? Right upper quadrant pain (liver engorgement)
?JVD
?Pulsatile, enlarged liver
? The most common cause of right sided failure

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is left sided failure
? Longstanding heart failure is usual y due to
dysfunction of both ventricles
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Treatment of Acute Heart Failure (1)

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? 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!)

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? Symptomatic treatment with O2, CPAP, BiPAP
? Afterload reduction with
?IV nitroglycerin
?ACE inhibitors
?Nitroprusside

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Treatment of Acute Heart Failure (2)
? Preload reduction with
?Nitrates
?Diuretics (after afterload reduction)

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?Nesiritide (?)
?Morphine (?)
?Phlebotomy (decrease circulatory volume, best
with renal failure)
? Inotropes

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?Dopamine
?Dobutamine
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Valvular Heart Disease

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Infective Endocarditis (1)

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? Risk factors for infective endocarditis (IE)
?Rheumatic or congenital heart disease
?Prosthetic valves
?IVDA
?Acquired valvular disorders (e.g. AS)

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?Mitral valve prolapse (smal risk)
?Cardiac pacemakers
?Prior history of endocarditis
? Median age is increasing
?More prosthetic heart valve survivors

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Infective Endocarditis (2)
? Valvular involvement (MATP)
?Mitral > aortic > tricuspid (IVDA) > pulmonic
? Native valve endocarditis: age > 50, M > F

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?Predisposing factors: rheumatic heart disease
(<20%), calcifications (50%, usual y elderly, aortic
valve) congenital heart disease (15%),
? IVDA
?Most have normal valves (75%)

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?Tricuspid valve most common (50%)
?Staph. aureus is the most common pathogen
? Prosthetic valves
?Staph. aureus
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Infective Endocarditis (3)
? Pathogenesis of IE
?GU, GI, major dental procedures, IVDA
? Abnormal turbulent flow
? Platelet aggregation and fibrin deposition (sterile

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vegetations)
? Bacteria colonize sterile vegetations
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Infective Endocarditis (4)
Types

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? Acute IE
?Younger, normal valves in half
?Virulent strains
?Higher morbidity and mortality

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?Staph. aureus
? Subacute IE
?Older, abnormal valves
?Anemia of chronic disease
?Strep. viridans (50-60%)

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Infective Endocarditis (5)
Types

? Left sided IE

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?S. viridans, S. aureus
?Gram negatives (IVDA or contaminated catheters)
?Cause of death is heart failure
?Emboli: CNS and systemic infarction
? Right sided IE

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?IVDA, indwel ing catheters
?S. aureus, S. pneumoniae, gram negatives
?Emboli: pulmonary infarction & infection
?Less heart failure, mortality rate lower
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Infective Endocarditis (6)
Types

? Prosthetic valve IE
?Most common during first two months post-op

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? S. epidermidis, S. aureus
?Late causes similar to native valve endocarditis
? S. viridans, Serratia, Pseudomonas
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Infective Endocarditis (7)

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? 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

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epidermidis), catheter-related sepsis
?Gram negatives & fungi (IVDA)
? Findings of IE
?Fever, chil s, "flu-like" il ness, back pain
?Heart murmur

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?Valvular incompetence (the most common
cause of acute AR)
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Infective Endocarditis (8)
? Embolic and vasculitic components

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?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

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clearing
?Petechiae and splinter hemorrhages
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Septic Emboli

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Janeway Lesion
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Osler Nodes
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Splinter Hemorrhages
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Roth Spots

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Infective Endocarditis (9)
? Laboratory
?Two blood cultures: > 90% sensitivity if
bacteremic

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?Anemia and elevated ESR
? Diagnosis: ultrasound (TEE) for vegetations
? Treatment: penicil ins, vancomycin,
aminoglycosides
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Infective Endocarditis (9)
? Surgical indications
?Refractory CHF
?Valve ring abscess
?Multiple major emboli

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?Medical failure
?Mycotic aneurysm
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Infective Endocarditis (10)
? Prophylaxis

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

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

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Rheumatic Heart Disease (1)
? Diagnosis of rheumatic fever: Jones criteria
?2 major criteria or
?1 major and 2 minor

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?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

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Rheumatic Heart Disease (2)
? Jones major criteria (CASES)
Carditis
Arthritis

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Sydenham's chorea
Erythema marginatum
Subcutaneous nodules
? Jones minor criteria
?Previous history of RF or RHD

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?Arthralgia
?Elevated ESR
?Prolonged PR interval
?Fever
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Aortic Stenosis (1)
? Etiology
?Usual y congenital bicuspid valve, or acquired
through RHD
? Pathophysiology

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?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)

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

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?Hypotension is a late finding
? EKG
?LVH with strain pattern
?LBBB
? CXR

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?LVH
?LAE
72

---

Aortic Stenosis (3)
? Natural history

--- Content provided by‍ FirstRanker.com ---

?LVH leads to heart failure
?Sudden death from dysrhythmias and acute LV
failure
? Medical management
?Avoid strenuous exertion

--- Content provided by​ FirstRanker.com ---

?Treat CHF
?Avoid nitrates and vasodilators (may drop BP
precipitously)
?Endocarditis prophylaxis (s/p replacement)
? Surgical management

--- Content provided by‌ FirstRanker.com ---

?Valve replacement
73

---

Aortic Regurgitation (1)
? Etiology
?Acute: endocarditis, dissection

--- Content provided by FirstRanker.com ---

?Chronic: RHD; also seen with Marfan's
syndrome
? Pathophysiology of AR
?Incompetent valve run-off into LV volume
overload LV dilation CHF (usual y no

--- Content provided by⁠ FirstRanker.com ---

symptoms until CHF develops)
Acute MI + acute AR: rule out dissection
74

---

Aortic Regurgitation (2)
? Physical exam

--- Content provided by‌ FirstRanker.com ---

?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)

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?Austin-Flint murmur (diastolic murmur 2? to AR
with regurgitant jet hitting mitral valve)
? EKG: LVH, LAE
? CXR: LV and LA enlargement
75

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---

Aortic Regurgitation (3)
? Natural history
?Symptoms late in disease course
?Prognosis much worse after symptoms develop
? Complications include

--- Content provided by​ FirstRanker.com ---

?CHF
?Dysrhythmias
?Infective endocarditis
? Medical management
?Afterload reduction

--- Content provided by⁠ FirstRanker.com ---

?Inotropes (digoxin)
?Endocarditis prophylaxis (s/p replacement)
76

---

Mitral Stenosis (1)
? Pathophysiology

--- Content provided by​ FirstRanker.com ---

?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

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RHD is the most common cause of mitral
stenosis
77

---

Mitral Stenosis (2)
? Symptoms

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?DOE (or dyspnea in pregnancy, anemia,
infection)
?Orthopnea, PND, hemoptysis
? Physical exam
?Diastolic rumble in mitral area

--- Content provided by‍ FirstRanker.com ---

?Loud S1, opening snap
? EKG: LAE, A-fib
? CXR: LAE, CHF
Suspect MS if murmur and pulmonary
edema are present in pregnancy

--- Content provided by‌ FirstRanker.com ---

78

---

Mitral Stenosis (3)
? Natural history
?Gradual onset of CHF
? Complications include

--- Content provided by⁠ FirstRanker.com ---

?Systemic emboli
?CHF
?A-fib
?Endocarditis
? Medical management

--- Content provided by​ FirstRanker.com ---

?Treat A-fib with rate control and anticoagulation
?Endocarditis prophylaxis (s/p replacement)
? Surgical management
?Commissurotomy
?Valve replacement

--- Content provided by FirstRanker.com ---

79

---

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

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? Etiology of chronic MR
?MVP
?Dilated cardiomyopathy
?RHD
?Mitral annulus calcification

--- Content provided by​ FirstRanker.com ---

80

---

Mitral Regurgitation (2)
? Pathophysiology of acute MR
?Sudden mitral valve incompetence sudden
increase LA pressure pulmonary edema

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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

--- Content provided by‍ FirstRanker.com ---

81

---

Mitral Regurgitation (3)
? Symptoms
?Acute: dyspnea, CHF, right-sided failure
?Chronic: CHF (compensated)

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? Physical exam
?Acute: loud holosystolic murmur (may have no
murmur if chordae rupture, resulting in wide-
open valve)
?Palpable LV heave and thril

--- Content provided by‍ FirstRanker.com ---

?EKG: LAE, LVH
?CXR: cardiomegaly, CHF
82

---

Mitral Regurgitation (4)
? Acute complications

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?Acute pulmonary edema
?Cardiogenic shock
? Chronic complications
?CHF
?A-fib

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83

---

Mitral Regurgitation (5)
? Medical management of acute MR
?Afterload reduction
?IABP to temporize until surgery

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? Medical management of chronic MR
?Symptomatic treatment of CHF
?Treatment of A-fib
?Endocarditis prophylaxis (s/p replacement)
? Surgical management

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?Valve repair or replacement
84

---

Mitral Valve Prolapse (1)
? Idiopathic myxomatous degeneration of
leaflets (leaflets become too thick to appose

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wel )
? Symptoms
?Chest pain (atypical)
?Dyspnea
?Anxiety

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?Palpitations
? Mostly young women
85

---

Mitral Valve Prolapse (2)
? Physical exam

--- Content provided by FirstRanker.com ---

?Mid-systolic click, late systolic murmur
? EKG
?Nonspecific ST-T wave changes
?Ectopy and PSVT common
? CXR

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?Not helpful
? Echocardiogram
?Diagnostic
?Regurgitation uncommon (requires prolapse of
both leaflets)

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86

---

Mitral Valve Prolapse (3)
? Natural history
?Very common. The vast majority never have a
problem

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?Increased incidence of arrhythmias
?Thromboembolic disease
?Endocarditis rarely
? Management
?No longer requires endocarditis prophylaxis

--- Content provided by FirstRanker.com ---

unless ful -blown regurgitation develops
?Anticoagulation if embolic disease is present
?Beta blockers helpful for chest pain
87

---

Cardiomyopathy

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

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?Restrictive cardiomyopathy
88

---

Dilated Cardiomyopathy (1)
? Dilated cardiomyopathy
?Idiopathic (most common)

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?Alcohol
?Peripartum
?Viral (myocarditis)
?End-stage CAD
?Sarcoidosis

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?Amyloidosis
?Hypothyroidism
89

---

Dilated Cardiomyopathy (2)
? Pathophysiology

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? EKG
?Decreased contractility
?LVH
dilatation of al chambers
?

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decreased output
LAE
? Clinical presentation
?Conduction
?

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defects
CHF (biventricular failure)
?
?
Emboli

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A-fib
?Dysrhythmias
?Sudden death
? CXR
?Globular heart

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?CHF
90

---

Dilated Cardiomyopathy (3)
? Treatment
?Largely supportive

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?Diuretics
?Afterload reduction
?Anticoagulation
?Antidysrhythmics
?Transplantation

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91

---

Hypertrophic Cardiomyopathy (1)
? Often familial autosomal dominant
? Asymmetric thickening of septum causing two
problems

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?Noncompliant ventricle with decreased diastolic
filling
?Dynamic obstruction of LV outflow (with mitral
valve leaflets blocking outflow tract)
92

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---

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

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?Dysrhythmias
93

---

Hypertrophic Cardiomyopathy (2)
? Physical exam
?Harsh, mid-systolic murmur at LLSB

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?Murmur louder with decreased preload
(hypovolemia, standing, Valsalva, amyl nitrite,
beta agonists)
?Murmur decreased with increased afterload
(squatting, Trendelenburg, hand grip, volume

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expansion, alpha agonists)
94

---

Hypertrophic Cardiomyopathy (3)
95

---

Hypertrophic Cardiomyopathy (4)

--- Content provided by FirstRanker.com ---

? EKG: hypertrophy in septal leads
? CXR: nondiagnostic
? Treatment of hypertrophic cardiomyopathy
?Avoid exertion
(worsens obstruction and leads to arrhythmias)

--- Content provided by​ FirstRanker.com ---

?Negative inotropes (beta blockers, calcium
channel blockers) to decrease obstruction
?Never use digoxin or positive inotropes
(increased obstruction)
?Surgical myomectomy

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96

---

Pericarditis (1)
? Etiology
?Infectious
?Viral (most common)

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?Bacterial
?TB
?Fungal
?Acute MI (Dressler's syndrome)
?Connective tissue disease

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?Neoplasm
?Uremia
?Radiation
97

---

Pericarditis (2)

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? Clinical manifestations
?Chest pain (may radiate to trapezius)
?Chest pain increases with inspiration and
swal owing
?Dysphagia

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?Relief on sitting up, bending forward (and may
hear the rub better in this position)
?Fever, malaise
98

---

Pericarditis (3)

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? 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)

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99

---

Pericarditis (3)
? EKG: four stages
? Stage 1: Diffuse ST elevation (does not
correspond to coronary artery distribution) &

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PR segment depression
? Stage 2: ST-segments and PR return to
baseline
? Stage 3: T wave inversions
? Stage 4: Normalization of EKG

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100

---

Acute Pericarditis
ST elevation diffusely
PR segment depression
125

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---

Acute Pericarditis
126

---

Pericarditis (4)
? CXR: usual y normal
? Echocardiogram: pericardial effusion

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? Complications
?Dysrhythmias (atrial)
?Large pericardial effusions, tamponade
?Residual pericardial constriction
? Treatment

--- Content provided by‌ FirstRanker.com ---

?Treat underlying cause if possible
?ASA, NSAIDs, colchicine; steroids controversial
103

---

Pericardial Tamponade
? Causes

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?Trauma, uremia, anticoagulation, neoplasm
? Clinical signs
?Hypotension, JVD, muffled heart sounds, pulsus
paradoxus
? EKG

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?Electrical alternans (beat to beat alteration in the
amplitude of the QRS complex), low voltage
? ECHO findings
?Effusion
?RV diastolic col apse (specific for tamponade)

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104

---

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

---

Pericardial Effusion

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Apex
RV
RA
LV

---

Myocarditis (1)

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? Inflammation of the myocardium
?Often associated with pericarditis
? Etiology
?Idiopathic
?Infectious (usual y viral, especial y coxsackie B

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virus)
?Chemotherapy
?Connective tissue disease
107

---

Myocarditis (2)

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? Clinical manifestations
?"Flu-like" il ness
?Fever, sinus tach (out of proportion to exam)
?Symptoms of CHF
?Dysrhythmias

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?Emboli
?Sudden death
? EKG: nonspecific changes, conduction blocks
? CXR: possibly enlarged heart
? Lab: elevated biomarkers

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108

---

Myocarditis (3)
? Natural history
?Most recover
?May have sudden death

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?May have dilated cardiomyopathy
? Treatment
?Supportive care
109

---

Hypertension (1)

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? Definition (JNC VII)
?Normal: Systolic lower than 120, diastolic lower
than 80
?Prehypertension: Systolic 120-139, diastolic
80-89

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?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
110

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---

Hypertension (2)
Definition / Classification
? Hypertensive urgency (DBP > 110)
?No signs or symptoms of organ damage
?Acute intervention may be harmful

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?Behavior modification, initiation of therapy
?Close fol ow up, e.g. in several days
111

---

Hypertension (3)
Definition / Classification

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? Hypertensive emergency
?Malignant hypertension
?End-organ and CNS signs
?Immediate BP reduction
112

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---

Hypertensive Emergencies (1)
? Severe elevation of BP with associated end-
organ damage
No specific BP level
? End-organs include

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?Heart (ACS, CHF, dissection)
?Brain (encephalopathy, hemorrhage)
?Eyes (hemorrhages, exudates)
?Kidneys (failure, preeclampsia)
113

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---

Hypertensive Emergencies (2)
? Types
?Encephalopathy
?Stroke syndromes
?Malignant hypertension (eyes)

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?Acute pulmonary edema
?Acute coronary syndromes
?Aortic dissection
?Acute renal failure
?Preeclampsia, eclampsia

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?Catecholamine crises
114

---

Hypertensive Emergencies (2)
? Pediatric hypertension emergencies
?Blood pressure > 95th percentile

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?Common causes: renovascular, nephritis,
pheochromocytoma
115

---

Hypertensive Emergencies (3)
? Malignant hypertension

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?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

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MAP = DBP + (SBP ? DBP) / 3
Treatment is nitroprusside and/or labetalol
116

---

Hypertensive Emergencies (4)
? CNS: encephalopathy, hemorrhagic CVA

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?Nitroprusside
?Labetalol
? Ischemic stroke
?Hypertension usual y resolves within hours
?Transient and cerebroprotective

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?Treatment: observe, labetalol, nicardipine
? Pregnancy-induced hypertension, eclampsia
?Hydralazine
?Labetalol
?Magnesium sulfate for seizures

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117

---

Hypertensive Emergencies (5)
? Cardiac: angina, CHF
?IV nitroglycerin
?Nitroprusside

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? 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

--- Content provided by​ FirstRanker.com ---

118

---

Hypertensive Emergencies (6)
? Catecholamine surge (pheochromocytoma,
MAOI crisis, cocaine overdose)
?Alpha plus beta blocker is best

--- Content provided by‌ FirstRanker.com ---

?Do not use beta blocker alone
(avoid unopposed alpha effect)
?Labetalol plus phentolamine
119

---

Hypertensive Emergency Medications (1)

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? Sodium nitroprusside
?Mode of action: arterial and venous dilatation
?Onset of action: 1-2 minutes
?Half life: 3-4 minutes
?Metabolized to thiocyanate (cyanide)

--- Content provided by FirstRanker.com ---

?Ideal medication for hypertensive emergencies
(rapid onset, potent, short half life)
?Can cause reflex tachycardia, therefore use
with beta blocker
120

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---

Hypertensive Emergency Medications (2)
? Labetalol
?Alpha and beta blocker (primarily beta)
?Onset of action: 5-10 minutes
?Half life: 5.5 hours

--- Content provided by FirstRanker.com ---

?No reflex tachycardia
?Low doses may lead to paradoxical
hypertension due to predominant beta effect
(unopposed alpha)
Contraindicated in bronchospasm, CHF,

--- Content provided by​ FirstRanker.com ---

AV-blocks
121

---

Hypertensive Emergency Medications (3)
? Nitroglycerin
?Arteriolar and venous dilatation

--- Content provided by‍ FirstRanker.com ---

?Onset: immediate
?Half life: 4 minutes
?Ideal for cardiac emergencies such as CHF, MI
?Side effects: headache and tachycardia
122

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---

Hypertensive Emergency Medications (4)
? Hydralazine
?Direct arteriolar vasodilator
?Onset: 10 min (IV)
?Half life: 2-4 hours

--- Content provided by‍ FirstRanker.com ---

?Indicated in pregnancy-related hypertension,
pediatric nephritis
Side effects include
reflex tachycardia (limits use in CAD, dissection)
Chronic use associated with "lupus-like" syndrome

--- Content provided by FirstRanker.com ---

123

---

Syncope (1)
? Defn. = Sudden, brief LOC and postural tone with
spontaneous recovery due to a decrease in
cerebral blood flow

--- Content provided by​ FirstRanker.com ---

? Causes:
?Neural y mediated (reflex-mediated HR or
vascular tone changes):
?Vasovagal (18%), situational (5%), carotid sinus (1%)
?Psychiatric causes (2%)

--- Content provided by⁠ FirstRanker.com ---

?Panic attacks, anxiety, somatization
?Orthostatic hypotension (8%)
124

---

Syncope (2)
?Medications (3%)

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?Neurologic disease (10%)
?Cardiovascular causes:
?Organic heart disease (4%), arrhythmia (14%)
?Vascular ? subclavian steal (syncope associated with
arm exercise)

--- Content provided by​ FirstRanker.com ---

?Unknown (34%)
?Tilt table tests suggest that most of these are neural y
mediated
125

---

Aortic Dissection (1)

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? 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

--- Content provided by FirstRanker.com ---

? Pregnancy (especial y third trimester)
? Chest trauma, iatrogenic (cardiac catheterization)
? Bicuspid aortic valve
? Aortic coarctation
? Elderly males with chronic hypertension

--- Content provided by⁠ FirstRanker.com ---

? Atherosclerotic risk factors (smoking,
hypertension, cholesterol, diabetes)
126

---

Aortic Dissection (2)
? Clinical presentation

--- Content provided by‍ FirstRanker.com ---

?Tearing chest pain with radiation to back
?Migrating, dynamic pain pattern
?Sudden onset of severe pain
?Aortic insufficiency
?Pulse deficits

--- Content provided by⁠ FirstRanker.com ---

?Syncope, acute paralysis
? Physical exam
?Hypertension, normal BP or hypotension
?Asymmetric pulses, asymmetric BP
?Acute aortic regurgitation

--- Content provided by‌ FirstRanker.com ---

?Tamponade
127

---

Aortic Dissection (3)
? Stanford classification
?Type A: any dissection which involves

--- Content provided by FirstRanker.com ---

ascending aorta (surgical treatment)
?Type B: descending aorta only (primarily
medical management)
128

---

Stanford Type A

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129

---

Stanford Type B
130

---

131

---

Aortic Dissection (4)

--- Content provided by‌ FirstRanker.com ---

? EKG
?May show acute MI if dissection is proximal and
involves coronary ostia
?Up to 8% with Type A wil have ST elevations
? CXR

--- Content provided by‌ FirstRanker.com ---

?Widened mediastinum in majority
?Intimal calcium separation
?Left pleural effusion
132

---

Aortic Dissection (5)

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? MRI
?Very sensitive and specific
?Usual y impractical due to inability to monitor
patient and time constraints
? CT with contrast

--- Content provided by‌ FirstRanker.com ---

?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

--- Content provided by‌ FirstRanker.com ---

? TEE (transesophageal echo)
?Very sensitive and specific ? best test if
available
?Done in ED (safer for patient)
133

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---

Dissecting Aneurysm
158

---

Aortic Dissection
159

---

Aortic Dissection (6)

--- Content provided by‍ FirstRanker.com ---

? Aortography
?Higher risk, logistical y difficult and expensive
?Provides anatomy necessary for OR, including
coronary involvement
?False negatives possible (thrombosed false

--- Content provided by FirstRanker.com ---

lumen)
? Treatment
?Beta blockers, then nitroprusside for both types
?Stanford A usual y requires surgery also
?Stanford B usual y doesn't require surgery

--- Content provided by​ FirstRanker.com ---

All types need control of blood pressure
and decreased contractility (decrease dP/dT)
136

---

Abdominal Aortic Aneurysm (1)
? Pathophysiology

--- Content provided by‌ FirstRanker.com ---

?Increase in diameter >50% over normal artery
?Due to medial degeneration (usual y
atherosclerosis)
?Majority are infrarenal
? Risk factors

--- Content provided by​ FirstRanker.com ---

?Elderly male with atherosclerosis, hypertension
?Connective tissue disease
137

---

Abdominal Aortic Aneurysm (2)
? Clinical Presentation

--- Content provided by‌ FirstRanker.com ---

?Asymptomatic until bleed or rupture
?Abdominal, flank or back pain
?Most common misdiagnosis: renal colic
?Syncope
? More unusual presentations

--- Content provided by‌ FirstRanker.com ---

?Erosion into duodenum aortoenteric fistula
with massive GI bleed
?Partial bowel obstruction
?Erosion into IVC aortocaval fistula with
embolization distal y

--- Content provided by​ FirstRanker.com ---

138

---

Abdominal Aortic Aneurysm (3)
? Physical exam
?Pulsatile mass is found in <50%
?Abdominal or femoral bruits

--- Content provided by FirstRanker.com ---

?Decreased femoral pulses
? Diagnosis
?Plain films: rule out calcified aneurysm
?Abdominal cross table lateral
?Lateral L-spine

--- Content provided by​ FirstRanker.com ---

139

---

Abdominal Aortic Aneurysm
164

---

Abdominal Aortic Aneurysm (4)
? Ultrasound

--- Content provided by⁠ FirstRanker.com ---

?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

--- Content provided by‌ FirstRanker.com ---

141

---

Abdominal Aortic Aneurysm (4)
? Ultrasound
142

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---

Abdominal Aortic Aneurysm (4)
? CT scan
?Useful in stable patients
?Able to visualize leakage into retroperitoneal
space

--- Content provided by FirstRanker.com ---

?Risky because patient is out of department
143

---

Abdominal Aortic Aneurysm (5)
? Management
?Hypotensive or unstable

--- Content provided by‌ FirstRanker.com ---

?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

--- Content provided by FirstRanker.com ---

to have an aneurysm must be presumed to be
leaking or ruptured AAA until proven otherwise
144

---

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Abdominal Aortic Aneurysm (6)
Blood clot
Aorta
IVC
Vertebra

--- Content provided by​ FirstRanker.com ---

Normal Aorta < 3 cm
AAA > 3 cm

---

---

---

Acute Limb Ischemia (1)
? Emboli
?Usual y cardiac

--- Content provided by FirstRanker.com ---

?Mural thrombus from MI
?A-fib
?Endocarditis
? Arterial source
?Aneurysm

--- Content provided by‌ FirstRanker.com ---

?Dissection
?Atherosclerotic disease
? Paradoxical embolus
?From venous emboli through septal defect
148

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---

Acute Limb Ischemia (2)
? Embolus
?Sudden onset
?No previous arterial insufficiency

--- Content provided by​ FirstRanker.com ---

? Thrombus
?Etiology: atherosclerosis (most common)
?Low-flow states
?Develops slowly
?Past history of claudication

--- Content provided by​ FirstRanker.com ---

?Chronic arterial insufficiency
149

---

Acute Limb Ischemia (3)
? Signs of acute ischemia (6 P's)
?Pain

--- Content provided by​ FirstRanker.com ---

?Pal or
Consider aortic
?Paresthesias
dissection
?

--- Content provided by‌ FirstRanker.com ---

in al these cases
Paralysis
?Pulselessness (late finding)
?Poikilothermia (polar, cold)
? Treatment of acute limb ischemia

--- Content provided by​ FirstRanker.com ---

?Heparin
?Embolectomy, thrombolytics
?Bypass for atherosclerotic disease
150

---

Deep Venous Thrombosis (1)

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? Pathogenesis (Virchow's triad)
?Stasis
?Hypercoagulability
?Endothelial damage
? Risk factors

--- Content provided by FirstRanker.com ---

?Immobilization
?Pregnancy
?Estrogen use
?Neoplasm
?Trauma

--- Content provided by‌ FirstRanker.com ---

151

---

Deep Venous Thrombosis (2)
? Presentation
?Pain and swel ing (unilateral)
?Erythema

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?Low-grade fever
?Physical exam (e.g.Homans' sign) is insensitive
152

---

Deep Venous Thrombosis (2)
? Diagnosis

--- Content provided by⁠ FirstRanker.com ---

?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

--- Content provided by⁠ FirstRanker.com ---

patients)
?CT venography
153

---

Deep Venous Thrombosis (3)
? Treatment

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?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

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?Recurrent DVT
?Emboli
154

---

Deep Venous Thrombosis (4)
? Phlegmasia cerulea dolens and phlegmasia

--- Content provided by‌ FirstRanker.com ---

alba dolens
?Uncommon, severe presentation of DVT
?Massive iliofemoral DVT
?Acute, severe, massive swel ing
?Cyanotic, congested extremity (cerulea)

--- Content provided by‌ FirstRanker.com ---

?Pale (alba) if arterial spasm causes "milk leg"
?Increased compartment pressure, ischemia
?May require surgery for compartment syndrome
155

---

Deep Venous Thrombosis (5)

--- Content provided by‌ FirstRanker.com ---

Phlegmasia cerulea dolens
Phlegmasia alba dolens
156

---

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EKGs
157

---

EKG - AMI (1)
? Acute Q wave MI (transmural)
?ST elevation

--- Content provided by⁠ FirstRanker.com ---

?Q waves
?T wave inversion
? Non-Q wave MI (subendocardial)
?ST depression with ischemia
?T wave inversion

--- Content provided by‌ FirstRanker.com ---

? 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)

--- Content provided by FirstRanker.com ---

158

---

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

--- Content provided by⁠ FirstRanker.com ---

---

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

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?Reciprocal changes inferiorly
160

---

Anterior MI
Classic findings:

--- Content provided by‍ FirstRanker.com ---

-ST elevation and poor R wave progression in V1-V4
-Reciprocal changes inferiorly
Med-Chal enger ? EM

---

EKG - AMI (3)
? Anteroseptal

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?Septal branches of LAD
?ST elevations V1-V2
? Anterolateral
?LAD or left circumflex
?ST elevations V5, V6, I and AVL

--- Content provided by⁠ FirstRanker.com ---

?Reciprocal changes inferiorly
? Inferior MI
All potentially
?RCA occlusion
include pathologic

--- Content provided by FirstRanker.com ---

Q waves
?ST elevations II, III, AVF
?Reciprocal changes anteriorly
162

---

Septal MI

--- Content provided by‌ FirstRanker.com ---

Classic findings:
- ST elevation V1-V2
- Q waves V1-V2
Med-Chal enger ? EM

---

Anterolateral MI

--- Content provided by​ FirstRanker.com ---

Classic findings:

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

- Reciprocal changes inferiorly

--- Content provided by FirstRanker.com ---

Med-Chal enger ? EM

---

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

--- Content provided by⁠ FirstRanker.com ---

Med-Chal enger ? EM

---

EKG - AMI (4)
? Lateral MI
?Circumflex occlusion
?ST elevations I, AVL, V5, V6

--- Content provided by‍ FirstRanker.com ---

?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

--- Content provided by FirstRanker.com ---

? R:S > 1
?Mirror image of septal MI
166

---

Inferior-Posterior MI
Classic findings:

--- Content provided by​ FirstRanker.com ---

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

---

--- Content provided by​ FirstRanker.com ---

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

---

EKG - ST Elevation

--- Content provided by‍ FirstRanker.com ---

? Differential diagnosis of ST segment elevation
?Acute MI
?Prinzmetal's angina (vasospasm)
?Pericarditis
?Ventricular wal aneurysm

--- Content provided by‌ FirstRanker.com ---

?Benign early repolarization
?Bundle branch block
169

---

ST Segment Elevation
Predictors of MI

--- Content provided by‌ FirstRanker.com ---

? Factors that increase the specificity
?ST elevation (horizontal or convex upwards)
?Fol ows coronary anatomy
?Reciprocal ST depression
?Changes over time (minutes to hours)

--- Content provided by‌ FirstRanker.com ---

?May see hyperacute T waves (early)
?Q waves usual y only after hours to days
170

---

Hyperacute T-Waves

--- Content provided by​ FirstRanker.com ---

Early sign of Ischemia

---

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

--- Content provided by‍ FirstRanker.com ---

---

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

---

Causes of ST Segment Elevation:

--- Content provided by⁠ FirstRanker.com ---

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

--- Content provided by⁠ FirstRanker.com ---

174

---

Causes of ST Segment Elevation:
Ventricular Aneurysm
? Convex or concave upwards morphology
? Persistent ST elevation

--- Content provided by‍ FirstRanker.com ---

? Q waves usual y present
? Usual y in anterior leads
? Easily seen on echo
? No reciprocal depression
? Look for old ECGs -- no change

--- Content provided by‍ FirstRanker.com ---

? No serial changes
175

---

VENTRICULAR ANEURYSM

---

Causes of ST Segment Elevation:

--- Content provided by FirstRanker.com ---

"Early Repolarization"
? Concave upwards morphology
? In many leads, maximal in mid-precordial
leads with "fishhook" J-point
? Doesn't change over time

--- Content provided by‍ FirstRanker.com ---

? No reciprocal depression
? Men > women, young > old
177

---

EARLY R
Be

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EPOLARIZATION
J-point

---

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

---

EKG - Hyperkalemia

--- Content provided by‍ FirstRanker.com ---

? Hyperkalemia
?Flat P waves
?Peaked T waves
?Wide QRS
?Prolonged QT (due to hypoCa) and PR

--- Content provided by‌ FirstRanker.com ---

?Bradycardias and AV blocks
?Eventual sine wave and Vfib
180

---

EKG ? Hypokalemia
? Hypokalemia

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?PVCs
?U waves
?Prolonged QT
?ST segment depression
181

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---

Hypokalemia / Hyperkalemia

---

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

--- Content provided by‌ FirstRanker.com ---

? Hypocalcemia
? Prolonged QT interval

---

EKG - Electrolyte-Induced QT
Prolongation
? Electrolyte abnormalities that prolong QT

--- Content provided by​ FirstRanker.com ---

interval
? Hypokalemia
? Hypocalcemia
? Hypomagnesemia
? Hyperphosphatemia

--- Content provided by‌ FirstRanker.com ---

? Prolonged QT leads to ventricular
tachydysrhythmias (torsade de pointes, Vfib)
184

---

EKG - Torsade De Pointes
? Torsade de Pointes

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?Polymorphic Vtach ("twisting of the points")
?Associated with prolonged QT interval
? Causes
?Quinidine, procainamide
?TCAs

--- Content provided by‍ FirstRanker.com ---

?Phenothiazines
No Procainamide
?Electrolyte abnormalities
or amiodarone
?Low Mg+, low K+, low Ca++

--- Content provided by⁠ FirstRanker.com ---

185

---

EKG - Torsade De Pointes
? Treatment
?Magnesium (wil shorten QT interval)
?Overdrive pacing

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?Isoproterenol
?Cardioversion/defibril ation
?Magnesium infusion for prophylaxis after
conversion
186

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---

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

---

EKG - Hypothermia

--- Content provided by‍ FirstRanker.com ---

? Hypothermia (< 30o C)
?Prolonged intervals
?Sinus bradycardia
?Muscle tremor artifact
?Slow A-fib

--- Content provided by⁠ FirstRanker.com ---

?Osborne J waves
?Vfib, asystole
188

---

Hypothermia
Classic findings:

--- Content provided by‌ FirstRanker.com ---

- Prolonged intervals
- Sinus bradycardia
- +/- muscle tremor artifact
- Slow a. fib
- Osborne (J) wave

--- Content provided by‌ FirstRanker.com ---

- V. fib / asystole

---

EKG - Digoxin
? Causes increased automaticity with conduction
block (PAT with block)

--- Content provided by​ FirstRanker.com ---

? Therapeutic levels may cause
?T wave depression
?ST downsloping (Salvador Dali moustache)
?QT shortened
? Toxic levels

--- Content provided by​ FirstRanker.com ---

?PVCs (most common dysrhythmia)
?Sinus and AV node blocks
?AV dissociation
?SVT (especial y with blocks)
?Sinus bradycardia

--- Content provided by‍ FirstRanker.com ---

190

---

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

--- Content provided by‌ FirstRanker.com ---

- QT shortened

---

EKG ? Cyclic Antidepressants
? Sinus tachycardia (most common)
? Prolonged QT
? Right axis deviation

--- Content provided by​ FirstRanker.com ---

? QRS width > 100 ms
? Conduction blocks
192

---

EKG ? Cyclic Antidepressants

--- Content provided by‍ FirstRanker.com ---

From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)
193

---

EKG - Supraventricular Tachycardia
? Supraventricular tachycardia
?Usual y re-entrant mechanism

--- Content provided by‌ FirstRanker.com ---

?Regular, narrow complex tachycardia
?Rate 150-200
?Absent or retrograde P waves
?Treatment: adenosine, calcium channel
blockers (diltiazem, verapamil)

--- Content provided by FirstRanker.com ---

?Don't use calcium channel blockers if a long
acting beta blocker was recently administered
194

---

Supraventricular Tachycardia
Classic findings:

--- Content provided by⁠ FirstRanker.com ---

- Regular, narrow complex tachycardia
- Rate 150-200
- Absent P waves or retrograde

---

EKG - Atrial Fib / Flutter (1)
? Etiologies

--- Content provided by FirstRanker.com ---

?AMI, HTN, RHD
?Thyrotoxicosis
?Digoxin toxicity
?Chronic obstructive pulmonary disease
?Pericarditis

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?PE, hypoxia
?WPW
?Electrolyte abnormalities
196

---

EKG - Atrial Fib / Flutter (2)

--- Content provided by​ FirstRanker.com ---

? 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

--- Content provided by‌ FirstRanker.com ---

?Irregularly irregular rhythm with undulating
baseline (associated with thyrotoxicosis, CAD,
CHF, PE, LAE, alcohol)
197

---

EKG - Atrial Fib / Flutter (3)

--- Content provided by‌ FirstRanker.com ---

? Treatment: rate control (chemical, electrical)
?Stable: diltiazem, beta blockers, amiodarone,
digoxin
?Unstable
?Atrial flutter: synchronized cardioversion

--- Content provided by FirstRanker.com ---

(start at 50 J)
?A-fib: synchronized cardioversion
(start at 200 J)
?Anticoagulation for long term A-fib
198

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---

Atrial Flutter
Classic findings:
- Regular, narrow complex with atrial
rate = 250-350
- Ventricular rate usually blocked -

--- Content provided by FirstRanker.com ---

2:1, 3:1, 4:1
- Sawtooth baseline (flutter waves)
235

---

Atrial Fibrillation
Classic findings:

--- Content provided by⁠ FirstRanker.com ---

- Irregularly, irregular rhythm
236

---

EKG - Multifocal Atrial Tachycardia
? Multifocal atrial tachycardia
?Irregularly irregular narrow complexes, rate

--- Content provided by‌ FirstRanker.com ---

>100
?At least 3 different P wave morphologies
?Variable PR intervals
?Associated with
?Hypoxia

--- Content provided by‌ FirstRanker.com ---

?COPD
?Theophylline toxicity
?Treat underlying condition
?MgSO may be helpful; no shocks!
4

--- Content provided by⁠ FirstRanker.com ---

201

---

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

--- Content provided by​ FirstRanker.com ---

---

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

--- Content provided by‌ FirstRanker.com ---

tract during NSR
?Delta wave is not reliably seen in
tachyarrhythmias
203

---

EKG - Wolff-Parkinson-White Syndrome (1)

--- Content provided by​ FirstRanker.com ---

? 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)

--- Content provided by‍ FirstRanker.com ---

?Procainamide or electrical cardioversion is safe
?Adenosine and other AV nodal blockers are
contraindicated during A-fib
204

---

EKG - Wolff-Parkinson-White

--- Content provided by‍ FirstRanker.com ---

Syndrome (2)
? Treatment is based on QRS width
?Narrow-complex tachycardia
?Treat like SVT
?Wide-complex tachycardia, no history of WPW

--- Content provided by‍ FirstRanker.com ---

?Treat like Vtach
?A-fib with known history of WPW
?Procainamide, cardioversion
?Do not use digoxin, verapamil, diltiazem,
adenosine, ?amiodarone (AVN blocker)

--- Content provided by​ FirstRanker.com ---

205

---

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

--- Content provided by‍ FirstRanker.com ---

242

---

Wolff-Parkinson-White Syndrome
SVT classic findings:
- Regular tachycardia

--- Content provided by‌ FirstRanker.com ---

- Treat as any other regular NCTs or WCTs
243

---

Wolff-Parkinson-White Syndrome
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)

--- Content provided by⁠ FirstRanker.com ---

A-fib classic findings:
- Irregularly irregular tachycardia
- QRS morphologies change
- Treat with procainamide or electricity
244

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---

EKG - Ventricular Tachycardia (1)
? Ventricular tachycardia
?Regular, wide-complex, rate >120
(usual y >150)
?Associated with

--- Content provided by‌ FirstRanker.com ---

?Underlying heart disease (CAD, cardiomyopathy,
MVP)
?Hypokalemia
?Electrolyte disturbances
?Toxic ingestions

--- Content provided by​ FirstRanker.com ---

?If stable: procainamide > amiodarone > lidocaine,
?If unstable: sync cardioversion
209

---

Ventricular Tachycardia

--- Content provided by‌ FirstRanker.com ---

Classic findings:
- Regular wide complex with rate > 120

(usually >150)
246

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EKG - Ventricular Fibrillation
? Ventricular fibril ation
?Primary: no preceding hemodynamic
compromise
?Secondary: prolonged LV dysfunction, shock

--- Content provided by​ FirstRanker.com ---

?Structural heart disease, ischemia
?Total y disorganized, non-perfusing rhythm
?Associated with CAD, MI, toxic ingestions,
electrolyte disturbances
?Treatment: defibril ation (ACLS protocols)

--- Content provided by​ FirstRanker.com ---

211

---

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

--- Content provided by⁠ FirstRanker.com ---

248

---

EKG - Premature Ventricular
Contractions (1)
? Premature ventricular contractions (PVCs)
?Premature, wide complex, no preceding P wave

--- Content provided by​ FirstRanker.com ---

(compensatory pause)
?Unifocal or multifocal
? Associated with
?Normal heart, alkalosis, CHF, MI, hypokalemia,
hypoxia, cardiomyopathy, drugs, digoxin toxicity

--- Content provided by FirstRanker.com ---

? PVCs in acute MI
?Indicate electrical instability
?Prophylactic treatment not proven to decrease
mortality
213

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---

EKG - Premature Ventricular
Contractions (2)
? Treatment
?Treat underlying cause (e.g. electrolytes,
ischemia, hypoxia)

--- Content provided by‍ FirstRanker.com ---

?Consider magnesium, beta blockers
?Treat sustained VT (> 30 seconds or if
hemodynamic instability develops)
214

---

--- Content provided by‌ FirstRanker.com ---

EKG - Premature Ventricular
Contractions (2)
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)
215

---

EKG - Accelerated

--- Content provided by FirstRanker.com ---

Idioventricular Tachycardia
? Accelerated idioventricular rhythm ("slow
Vtach")
?Wide complex regular rhythm with rate 40-120
?Runs may last few minutes

--- Content provided by​ FirstRanker.com ---

?Associated with acute MI and reperfusion
?Treatment: observe!
? Is self-terminating, NOT destabilizing
?If hypotensive, consider atrial pacing
216

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---

Accelerated Idioventricular Rhythm
Classic findings:
- Wide complex rhythm with rate = 40-120
253

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---

Accelerated Idioventricular Rhythm
(rate < 120)
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)
254

--- Content provided by‍ FirstRanker.com ---

---

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

--- Content provided by⁠ FirstRanker.com ---

? Associated with
?CHF, AMI
?Myocarditis
?Hypokalemia
?Digoxin toxicity

--- Content provided by‌ FirstRanker.com ---

? Treatment
?Usual y none
?Underlying condition
?Atropine only if needed to speed rate
219

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---

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

--- Content provided by‍ FirstRanker.com ---

256

---

EKG - First Degree Heart Block
? First degree AV block
?PR interval > 200 ms
? No treatment necessary, but look for

--- Content provided by FirstRanker.com ---

underlying cause
? Causes: increased vagal tone, cardiac drugs,
myocarditis, endocarditis, AMI (inferior),
hypothermia, hyperkalemia, age-related
degeneration (common in elderly)

--- Content provided by‍ FirstRanker.com ---

221

---

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

--- Content provided by​ FirstRanker.com ---

258

---

EKG - Second Degree Heart Block
? Mobitz I (Wenckebach)
?Progressively longer PR and shorter RR until a beat is
dropped, then starts over

--- Content provided by​ FirstRanker.com ---

?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

--- Content provided by FirstRanker.com ---

?Associated with anterior MI and destruction of conduction
tissue
?Usual y associated with bundle branch block
?May progress to complete heart block
?Temporary pacer often needed in the setting of AMI

--- Content provided by⁠ FirstRanker.com ---

223

---

Second Degree AV Block Type I
(Mobitz I, Wenkebach)
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)
224

--- Content provided by FirstRanker.com ---

---

Second Degree AV Block Type II
(Mobitz II)
225
From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)

---

EKG - Third Degree Heart Block

--- Content provided by⁠ FirstRanker.com ---

? 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

--- Content provided by FirstRanker.com ---

?Associated with anterior MI and destruction of
conduction tissue
?Narrow complex: may be temporary due to
vagal tone
?Wide complex: usual y requires transvenous

--- Content provided by⁠ FirstRanker.com ---

pacer
226

---

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

--- Content provided by​ FirstRanker.com ---

- PR interval changes randomly
263

---

AV Dissociation
? Atria and ventricles beat independently

--- Content provided by​ FirstRanker.com ---

? Atrial rate > ventricular rate
?Sinus dysfunction, bradycardia and block (3o
block is a form of AV dissociation) leads to
ventricular escape rhythms
? Causes

--- Content provided by​ FirstRanker.com ---

?Ischemia (inferior MI)
?Myocarditis (acute rheumatic fever)
?Drug toxicity (digoxin)
?Vagal reflex
? Fusion beats are common

--- Content provided by⁠ FirstRanker.com ---

228

---

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

--- Content provided by‌ FirstRanker.com ---

- Unifocal or multifocal
265

---

Brugada Syndrome
? Syncope or sudden death in young patients
with a structural y normal heart resulting from

--- Content provided by⁠ FirstRanker.com ---

venticular fibril ation
? Most common cause of sudden death in young
males without heart disease
? Familial autosomal dominant
? Particularly common in SE Asian males

--- Content provided by FirstRanker.com ---

? Pseudo-RBBB pattern
? ST elevations in V1 and V2
? Implantable defibril ator is treatment
266

---

Brugada Syndrome

--- Content provided by FirstRanker.com ---

? Precipitants of Dysrhythmias
? Beta blockers
? Sodium channel blockers (TCAs, Type I
antiarrhythmics, cocaine)
? Ethanol

--- Content provided by FirstRanker.com ---

? Fever, hot ambient temperature
? Electrolyte abnormalities (high K and Cal, low K)
? Increased alpha adrenergic tone
? Pacing
? Vagal maneuvers

--- Content provided by FirstRanker.com ---

? Combinations of glucose and insulin
267

---

Brugada Syndrome
268

---

Brugada Syndrome

--- Content provided by‍ FirstRanker.com ---

From ECGs for the Emergency Physician Vol 1 (Mattu, Brady; Blackwel 2003)
269

---

Ventricular Tachycardia vs. SVT
? VTach findings
?AV dissociation ("cannon" A waves in neck,

--- Content provided by​ FirstRanker.com ---

variable intensity S1, variable pulse amplitude
beat-to-beat)
?Fusion beats
?QRS >14 ms
?Elderly patients

--- Content provided by​ FirstRanker.com ---

?History of CAD or MI
?Concordance
? SVT findings
?QRS in same direction as normal QRS
234

--- Content provided by FirstRanker.com ---

---

Ventricular Tachycardia vs. SVT
? VTach findings
?AV dissociation ("cannon" A waves in neck,
variable intensity S1, variable pulse amplitude
beat-to-beat)

--- Content provided by​ FirstRanker.com ---

?Fusion beats
?QRS >14 ms
?Elderly patients
?History of CAD or MI
?Concordance

--- Content provided by FirstRanker.com ---

? SVT findings
?QRS in same direction as normal QRS
235

---

Ventricular Tachycardia vs. SVT
? VTach findings

--- Content provided by FirstRanker.com ---

?AV dissociation ("cannon" A waves in neck,
variable intensity S1, variable pulse amplitude
beat-to-beat)
?Fusion beats
Always assume a regular

--- Content provided by‍ FirstRanker.com ---

?QRS >14 ms
WCT on the boards is Vtach
?Elderly patients
?History of CAD or MI
?Concordance

--- Content provided by‍ FirstRanker.com ---

? SVT findings
?QRS in same direction as normal QRS
236

---

CARDIOLOGY QUESTIONS
237

--- Content provided by FirstRanker.com ---

---

Which of the following factors is
consistent with Prinzmetal's (variant)
angina?
A. It is associated with ST depression rather
than elevation

--- Content provided by​ FirstRanker.com ---

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

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E. Patients undergoing cardiac cath are rarely
diagnosed with variant angina
CA 1

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Which of the following statements
is true regarding aortic regurgitation?

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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

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reduction are general y not indicated
D. Is never associated with Marfan's syndrome
E. ECG reveals RVH
CA 2

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A patient had a myocardial infarction three

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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:

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A. Angiography
B. NSAIDs
C. Nitrates
D. Antibiotics
E. Thrombolytics

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CA 3

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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

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following is the most appropriate for this
situation?
A. Digoxin
B. Verapamil
C. Procainamide

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D. Adenosine
E. All of the above
CA 4

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A patient presents with an irregularly irregular
rhythm with a rapid ventricular response (120/

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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

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

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Classic ECG finding of hypothermia
is:
A. Delta wave
B. Prolonged intervals
C. J wave

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D. Osgood wave
E. Asystole
CA 6

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In non-embolic limb ischemia,
which of the following is the last

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sign to develop?
A. Pain
B. Pulselessness
C. Pal or
D. Paresthesias

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E. Coolness
CA 7

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A patient presents with a blood pressure
of 260/150, dyspnea and chest pain.
Which of the following agents is most

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likely to be successful for reducing this
patient's blood pressure?
A. Diltiazem
B. Nitroprusside
C. Clonidine

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D. Nifedipine
E. Nitroglycerin
CA 8

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Which of the following statements
is true regarding endocarditis?

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A. The pulmonic valve is the most commonly
infected
B. A murmur is auscultated in less than 5% of
cases
C. Optimal antibiotic therapy consists of first or

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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

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Which of the following are causes of
myocardial infarction?
A. Aortic dissection
B. Atherosclerosis
C. Cocaine

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D. Emboli
E. All of the above
CA 10

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Which of the following is consistent with
unstable angina?

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A. Positive cardiac markers
B. Consistent chest pain relieved by rest and
nitroglycerin
C. Chest pain with acute ST-segment elevations
D. Chest pain at rest

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E. Unchanged frequency and severity
CA 11

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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

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changes. Which plan is the most
appropriate?
A. Discharge the patient as his enzymes and
ECG are normal
B. Repeat a second set of enzymes and

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discharge if normal
C. Admit the patient to rule out ACS
D. Administer thrombolytics
E. Perform a CT to rule out PE
CA 12

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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

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true?
A. These are reperfusion dysrhythmias
B. This patient needs a transvenous pacemaker
placed immediately
C. 3rd degree AV block is associated with poor

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prognosis in anterior wal MIs
D. Thrombolytics wil not be effective in this case
E. The patient should be treated with intravenous
lidocaine
CA 13

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Which is an absolute contraindication for
thrombolytic administration?
A. CVA within 6 months
B. Squamous cel carcinoma
C. Menstruation

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D. Spinal surgery 6 months ago
E. Coumadin
CA 14

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A 45 y/o patient presents with C.P. The ECG
= SR with ST elevations in leads 2, 3 and

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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

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C. Sublingual nitroglycerin x3 and morphine 2 mg
IV
D. Oxygen, IV nitroglycerin and IV dopamine
E. Cal for Intra-aortic bal oon pump placement
CA 15

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Which of the following is not one of
Jones major criteria?
A. Subcutaneous nodules
B. Sydenham's chorea

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C. Arthritis
D. Carditis
E. Erythema migrans
CA 16

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Exertional syncope, dysrhythmias, cardiac

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ischemia and sudden death are all
associated with which of the following?
A. Pericarditis
B. Restrictive cardiomyopathy
C. Hypertrophic cardiomyopathy

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D. Dilated cardiomyopathy
E. Amyloidosis
CA 17

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A 56 y/o patient's BP = 190/115. The
patient has no complaints, excluding mild

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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

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D. Labetalol 20 mg IVP
E. Fol ow-up as needed (prn)
CA 18

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A 64 y/o patient presents with C.P. & SOB.
PE: JVD; rales; Dyspnea; Grade 5/6

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holosystolic murmur radiating into the
axilla. ECG: Acute anterior wall MI. CXR:
Pulmonary edema. What is this patient's
complication?
A. Dressler's syndrome

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B. Aortic dissection
C. Atrial septal defect
D. Chordae tendonae rupture
E. Pericardial effusion
CA 19

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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?

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A. Order a CT of the abdomen with triple contrast
B. Order a selective mesenteric angiogram
C. Consult surgery for emergent exploratory
laparotomy
D. Order an abdominal ultrasound

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E. Order a renal protocol CT
CA 20

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Cardiology Answer Key
1. C
11. D

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2. B
12. C
3. B
13. C
4. E

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14. A
5. D
15. B
6. C
16. E

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7. B
17. C
8. B
18. A
9. D

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19. D
10. E
20. C

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2

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3
4

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5
6

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7
8

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9
10

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11
12

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13
14

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15

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16

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18

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19
20

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21
22

---

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23
24

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25
26

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28

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29
30

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ECG REVIEW ? ECG ANSWER KEY

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SLIDE #1
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

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? Reciprocal inferior ST segment depression
SLIDE #2
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

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? 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.

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SLIDE #3
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

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SLIDE #4
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.

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? Terminal negativity of the T waves in the precordial leads may occur.
SLIDE #5
Sinus rhythm with borderline 10 AVB and Left bundle branch block:
? ST segment elevation in leads V1-v3
? Acute anterior wall myocardial infarction

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? 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.
SLIDE #6
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

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anteroseptal leads, with non-inverted T-waves. It is usually accompanied by inferior infarction, as demonstrated in this
EKG.
SLIDE #7
ECG findings in this patient with hyperkalemia include:
? Absent P waves: "sinoventricular rhythm" of hyperkalemia

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? 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).
SLIDE #8

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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

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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.
SLIDE #9
The ECG of this 96-year-old woman shows:
? Absent P waves and narrow QRS complexes

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? Consider atrial fibrillation
? Regular rate and rhythm with bradycardia, ventricular rate 36
? Junctional escape rhythm
? Non-specific ST-T abnormalities
SLIDE #10

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The ECG of this 84-year-old man shows:
? Normal sinus rhythm, rate 65
? Left bundle branch block
? Left axis deviation

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SLIDE #11
The ECG of this 85-year-old woman shows:
? Multifocal atrial tachycardia
? Ventricular premature complexes
? Left axis deviation

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? Late transition
? Diffuse non-specific T wave abnormalities
? This rhythm may be drug related
? Rare aberrant complexes
? No change from 10/3/94

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SLIDE #12
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:

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? S wave in L1with
? Q waves in aVF and L3, suggesting
? Acute right ventricular strain
SLIDE #13
This 72-year-old woman's ECG shows:

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? Normal sinus rhythm, rate 78
? Right axis deviation
? Right bundle branch block
? Inferior T wave abnormality
SLIDE #14

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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

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? Old anterior infarct
SLIDE #15
This 75-year-old woman's ECG shows findings of:
? Sinus rhythm, rate 62
? Multiple atrial premature complexes

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? Left ventricular hypertrophy by voltage criteria
? QT interval prolongation

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? Diffuse ST-T abnormalities, consistent with
? Ischemia and/or subendocardial infarction
SLIDE #16

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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

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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).
SLIDE #17
The ECG of this 59-year-old man shows:
? Regular P waves at a rate of approximately 125/minute

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? Complete (third degree) AV block
? Ventricular or junctional escape, rate 29
? Superior QRS axis
SLIDE #18
These EKGs are from a patient with WPW type A in NSR and in tachycardia with antegrade conduction down the

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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.
SLIDE #19

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The ECG shows:
? Sinus rhythm with 10 AVB
? T-wave inversions in I and AVL, indicative of lateral wall ischemia
SLIDE #20
The third and succeeding QRSs on this rhythm strip are wide with retrogradely conducted P waves, suggesting

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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.

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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.
SLIDE #21
This patient has:
? Tachycardia with narrow QRS complexes

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? 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.
SLIDE #22
This rhythm strip shows findings of:

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? 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.
SLIDE #23

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Findings on this ECG rhythm strip include:
? Normal sinus rhythm, with
? Brief run of ventricular tachycardia
SLIDE #24
This rhythm strip shows findings of:

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? 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

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the pacemaker, a weak battery, a cracked or broken wire, electrode displacement, or fibrosis about the electrode.
SLIDE #25
Findings on this rhythm strip include:
? Sinus rhythm
? Frequent PVCs in a bigeminy pattern

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? Every other complex is a PVC. This is called ventricular bigeminy.

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SLIDE #26
Findings on this ECG rhythm strip include:
? Classic "J" wave of hypothermia
? Baseline artifact

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SLIDE #27
This ECG rhythm strip shows:
? Mobitz I second degree AV block (Wenckebach)
NOTE: the gradually lengthening PR interval prior to each dropped beat.
SLIDE #28

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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)
SLIDE #29

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This ECG rhythm strip shows:
? Coarse ventricular fibrillation
? The rhythm is extremely rapid and irregular.
SLIDE #30
Sinus Rhythm with Brugada Syndrome:

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? Pseudo RBBB pattern
? ST elevations in V1 and V2
? TX: AICD

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