Left Anterior Fascicular Block

Cardiology Revision Notes - Left Anterior Fascicular Block

Characteristics

Normal activation of the left ventricle proceeds down the left bundle branch, which consist of two fascicles the left anterior fascicle and left posterior fascicle. Left Anterior Fascicular Block (LAFB), which is also known as Left Anterior Hemiblock (LAHB), occurs when a cardiac impulse spreads first through the left posterior fascicle, causing a delay in activation of the anterior and lateral walls of the left ventricle which are normally activated via the left anterior fascicle.

Although there is a delay or block in activation of the left anterior fascicle there is still preservation of initial left to right septal activation as well as preservation of the inferior activation of the left ventricule (preservation of septal Q waves in I and aVL and small initial R wave in leads II, III, and aVF). The delayed and unopposed activation of the remainder of the left ventricle now results in a shift in the QRS axis leftward and superiorly, causing marked left axis deviation. This delayed activation also results in a widening of the QRS complex, although not to the extent of a complete LBBB

 

Criteria for LAFB

• Left axis deviation (usually between -45° and -90°), some consider -30° to meet criteria
• QRS interval < 0.12 seconds
• qR complex in the lateral limb leads (I and aVL)
• rS pattern in the inferior leads (II, III, and aVF)
• Delayed intrinsicoid deflection in lead aVL (> 0.045 s)

 

Exceptions

It is important not to call LAFB in the setting of a prior inferior wall myocardial infarction which may also demonstrate left axis deviation due to the initial forces (Q wave in a Qr complex) in leads II, III, and aVF. As opposed to LAHB, the left axis shift is due to terminal forces (i.e., the S wave in an rS complex) being directed superiorly,

 

Effects of LAFB on Diagnosing infarctions and Left Ventricular Hypertrophy

LAHB may be a cause of poor R wave progression across the precordium causing a pseudoinfarction pattern mimicking an anteroseptal infarction. It also makes the electrocardiographic diagnosis of LVH more complicated, because both may cause a large R wave in lead aVL. Therefore to call LVH on an EKG in the setting of an LAHB you should see the presence of a “strain” pattern when you are relying on limb lead criteria to diagnose LVH.

 

Clinical Signficance

• It can be seen in approximately 4% of cases of acute myocardial infarction
  • It is the most common type of intraventricular conduction defect seen in acute anterior myocardial infarction, and the left anterior descending artery is usually the culprit vessel.
  • It can be seen with acute inferior wall myocardial infarction.
• It also associated with hypertensive heart disease, aortic valvular disease, cardiomyopathies, and degenerative fibrotic disease of the cardiac skeleton.

 

References

1. Mirvis DM, Goldberger AL. Electrocardiography. In: Braunwald E, Zipes DP, Libby P, eds. Heart disease: a textbook of cardiovascular medicine, 6th edn. Philadelphia: WB Saunders; 2001:82–125.
2. Surawicz B, Knilans TK. Chou’s electrocardiography in clinical practice: adult and pediatric, 5th edn. Philadelphia: W.B. Saunders; 2001.

ASD Primum Defect

Cardiology Notes - ASD Primum Defect

EKG

Characteristics

Patients with Atrial Septal Defects may have Atrial Fibrillation, Atrial Tachycardia, or Atrial Flutter, but these arrythmias are not usually seen until patients grow older. Features also seen on the EKG include Right Atrial Enlargement, PR prolongation and advanced AV block. When you suspect a patient has an ASD based on the findings of an incomplete Right Bundle Branch Block with a rSr' or rSR' the next thing you should do is examine the frontal plane QRS. The frontal plane QRS is the most helpful clue to help you differentiate Secundum ASD from Primum ASD. In Primum defects left axis deviation is seen in most patients with an axis of > -30 degrees and very few patients have right axis deviation. In contrast Secundum defects have an axis between 0 degrees and 180 degrees with most cases to the right of 100 degrees.

In the EKG above, you can see an example of the rSR' pattern in V1 with a R' greater than S with T wave inversion which is commonly seen in volume overload Right Ventricular Hypertrophy.

 

References

Pryor R, Woodwork MB, Blount SG: Electrocardiographic Changes in Atrial Septal Defects:Ostium Secundum versus Ostium Primum defect. Am Heart J 58:689, 1959. 

Acute Pericarditis - 2

Acute Pericarditis - Cardiology Revision Notes

 

Major clinical manifestations:

• Chest pain
• Pericardial friction rub
• Widespread ST Elevation or PR depression
• Pericardial effusion
• 2 out of 4 necessary to make diagnosis
• Myopericarditis: depressed LV function, elevated biomarkers

 

 

 

 

 

 

 

Biomarkers

• Troponin elevated in 32-49% of patients with acute idiopathic pericarditis
• Features associated with + Tn:
• Younger age
• Male
• Pericardial effusion
• Recent infection
• ST segment elevations

 Evolution of EKG changes

1. Acute phase: ST elevations and PR depression
2. Normalization of ST and PR segments
3. Diffuse T wave inversions
4. T wave inversions may persist or normalize

 EKG Changes

• ST elevation begins at J-point
• Rarely greater than 5 mm
• Usually remains concave
• ST depression absent
• ST elevation and T wave inversion don’t occur together
• PR depression due to atrial current of injury
• No hyperacute T waves or Q waves

 Diagnostic Workup

• ECG
• CXR
• PPD
• ANA if appropriate
• HIV
• Blood cultures if febrile

 Echo

• All patients with suspected pericardial disease
• ACC/AHA/ASE Class I recommendation
• Finding of an effusion is helpful in making the diagnosis
• Absence of effusion does not rule out dx
• Helpful in diagnosis of purulent pericarditis, myocarditis or ruling out MI

 Hospital Admission

• Subacute symptoms
• High fever (>38ºC) and leukocytosis
• Evidence suggesting tamponade
• Large pericardial effusion (> 20 mm)
• Immunosuppressed state
• Coumadin
• Acute trauma
• Failure to respond to NSAIDs in 7 days

 Treatment

• ASA or NSAIDS
• ESC recommends ibuprofen
• Ibuprofen: 400-800mg Q6-8 hrs
• Aspirin: 800mg Q6-8 hrs
• May need to treat as long as 3-4 weeks

 Colchicine

• COPE trial
• Open-label randomized trial:
• 120 pts with 1st episode acute pericarditis
• ASA or ASA plus Colchicine for 3-4 weeks
• Colchicine dosing: 2mg x 1, then 0.5mg BID
• Colchicine group:
• Significantly lower recurrence rate (10.7% v 32.3%) and rate of persistent sx at 72 hrs (11.7% v 36.7%)

 Steroids

• Should only be considered if sx refractory to NSAIDS or colchicine
• Associated with recurrence of symptoms
• 2004 ESC guidelines:
• Acute pericarditis due to connective tissue disease
• Autoreactive (immune-mediated) pericarditis
• Uremic pericarditis

 References

1.  Imazio M, Bobbio M, Cecchi E, Demarie D, Demichelis B, Pomari F, Moratti M, Gaschino G, Giammaria M, Ghisio A, Belli R, Trinchero R. Colchicine in addition to conventional therapy for acute pericarditis: results of the COPE trial. Circulation. 2005; 112: 2012–2016

Aortic Regurgitation

Aortic Regurgitation - Cardiology Notes

Assessment of Severity

• Color flow of AI
  • Severe if >60% of LVOT area
• Measure Pressure Half Time
  • <250 severe
  • >400 mild
• Measure Flow in descending Aorta
• Measure size of Aorta including annulus, ascending aorta, and arch
• Measure size of Vena contracta
  • >6mm is severe
• Measure Pisa
  • ERO > 0.4 is severe
• Measure for Diastolic Flow Reversal in aorta
• Look for Increased LV Size

Classification of Severity

Indicator	Mild	Moderate	Severe
Angiographic Grade	1+	2+	3+
Vena Contracta Width (mm)	<0.3	0.3 to 0.60	>.6
Regurgitant Orifice Area	<0.2	0.2 to 0.39	>.4

 

Indications for Surgery

• LVED dimensions > 7.5 cm and LVES dimensions >5.5 cm (The 55 rule)
• EF < 50%
• FC III or IV
• FC II angina

 

Quantification of Aortic Insufficiency by Aortography

The pigtail catheter is placed a few centimeters above the aortic root. Grading the amount of regurgitation is based on the amount of opacification of the ventricle 2 complete cardiac cycles after injection compared to that of the aortic root.

1+  Brief and incomplete ventricualar opacification. Clears rapidly.

2+  Moderate opacification of the ventricle that clears in less that 2 cycles. 

Never greater than aortic root opacification. 

2+ AI Marfan Syndrome

3+  Opacification of the ventricle equal to aortic root opacification within 2 cycles. 

Delayed clearing of ventricle over several cycles.

3+ AI

4+  Opacification of the ventricle almost immediately that is greater than 

that of the aortic root with delayed clearing of the ventricle.

4+ AI

Aortic Stenosis - 2

Aortic Stenosis - CardioNotes 2

Introduction

Aortic Stenosis is the most common cause of left ventricular outflow tract obstruction. It is most often is due to calcification of a congenitally bicuspid or normal trileaflet valve. Calcific changes are felt to be caused by an active disease process characterized by lipid accumulation, inflammation, and calcification

 

Signs and Symptoms

The presence of symptoms with aortic stenosis usually indicate that the AS is severe The most common symptoms include angina, syncope, and heart failure. Aortic stenosis often is first diagnosed by the finding of a murmur on exam. However, while a soft murmur with a preserved S2 reliably excludes severe stenosis and a severe grade 4 murmur with diminished carotid upstrokes confirms severe obstruction, between these extremes physical examination is not accurate for evaluation of disease severity.

Causes

• Bicuspid Aortic Valve, Unicuspid, and quadricuspid Aortic Valves
• Calcified
• Look for Supravalvular Stenosis, Subaortic Membrane, and HOCM

 

Echocardiographic Assessment

1. Obtain maximal aortic jet velocity 4V²
2. Calculate mean gradient by measuring VTI or 2.4V²
3. Obtain LVOT gradient and velocity 1 cm proximal to the aortic valve with pulse wave Doppler
4. Calculate Aortic Valve Area=d² x 0.785 x LVOT VTI (pulse wave)/ AV VTI (Cw)
5. Calculate dimensionless index (0.25 is severe)
6. Aortic velocity is the most reproducible and is the strongest predictor of clinical outcome. Aortic velocity allows classification of stenosis as mild (2.6 to 3.0 m/s), moderate (3 to 4 m/s), or severe (>4 m/s). Leaflet thickening and calcification with adequate leaflet motion and a velocity <2.5 m/s is called aortic sclerosis.

 

Classification of Severity

Classification of Severity

Indicator	Mild	Moderate	Severe
Jet Velocity	Less than 3	3 -4	>4
Mean Gradient (mm Hg)	<25	25-40	>40

 

Indications for Surgery

• Symptoms are needed in most patients with AS which includes angina, syncope, or heart failure.
• In the absence of symptoms the following are indications
  • Need for High Risk Operation
  • Severe CAD with concominant CABG
  • Left Ventricular Dysfunction

Severe Aortic Stenosis by Flouroscopy

 

Management

 

References

1. J Am Coll Cardiol 2006; 47:2141–51