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 

Appropriateness of Exercise Stress Test in an Asymptomatic Individual

 

Class IIa

• Evaluation of asymptomatic persons with diabetes mellitus who plan to start vigorous exercise

 

Class IIb

• Evaluation of persons with multiple risk factors as a guide to risk-reduction therapy.
• Evaluation of asymptomatic men older than 45 years and women older than 55 years:
  • Who plan to start vigorous exercise (especially if sedentary) or
  • Who are involved in occupations in which impairment might impact public safety or
  • Who are at high risk for CAD due to other diseases (e.g., peripheral vascular disease and chronic renal failure)

 

Class III

• Routine screening of asymptomatic men or women.

 

References

Cardiac Radionuclide Imaging: ACC/AHA/ASNC 2003 Guideline Update for the Clinical Use of Cardiac Radionuclide Imaging

Atrial Fibrillation - 2

Atrial Fibrillation - CardioNotes 2

EKG Characteristics

Atrial Fibrillation is a supraventricular tachyarrhythmia characterized by uncoordinated atrial activation with consequent deterioration of atrial mechanical function. On the electrocardiogram (ECG), it is described by the replacement of consistent P waves by rapid oscillations or fibrillatory waves that vary in size, shape, and timing, associated with an irregular, frequently rapid ventricular response when atrioventricular (AV) conduction is intact

 

Introduction

Atrial fibrillation is the most common sustained arrhythmia seen in clinical practice with an estimated 2 million patients with atrial fibrillation in the United States. The prevalence and incidence of atrial fibrillation increase with advancing age. The mainstay of therapy includes pharmacologic rate control, antiarrhythmic therapy, cardioversion, and anti-thromboembolic management. Non-pharmacologic therapies, include ablation with a Pulmonary Vein Isolation, Surgical PVI or Maze Procedure.

 

Prevalence of Atrial Fibrillation

• 0.4% general population
• 0.2% in population 25-34 yrs old
• 2-5% in population >60 yrs old
• 10% in population > 80 yrs old
• 8-14% in hospitalized patients

 

Incidence of Atrial Fibrillation

• 0.1%/year (>160,000 new U.S. cases/yr)
• 20-40% after cardiac surgery

 

Causes of Atrial Fibrillation

• Hypertension
• Ischemic heart disease
• Advancing age
• Rheumatic Heart Disease (especially mitral valve disease)
• Nonrheumatic valvular disease
• Cardiomyopathies
• Congestive Heart Failure
• Congenital heart disease
• Sick sinus syndrome
• Wolff-Parkinson-White Syndrome
• Pericarditis
• Pulmonary Embolism
• Thyrotoxicosis
• Chronic lung disease
• Neoplastic disease
• Postoperative
• Diabetes Mellitus
• Normal hearts affected by high adrenergic states, alcohol, stress, drugs (especially sympathomimetics), excessive caffeine, Hypoxia, Hypokalemia, Hypoglycemia, or systemic infection.

 

References

• Bellet S. Clinical Disorders of the Heart Beat. 3rd ed. Philadelphia: Lea & Febiger, 1971.
• ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the North American Society of Pacing and Electrophysiology 

Endocarditis

Infective endocarditis is defined as an infection of the endocardial surface of the heart, which may include one or more heart valves, the mural endocardium, or a septal defect. Endocarditis can be broken down into the following categories:

• Native valve (acute and subacute) endocarditis
• Prosthetic valve (early and late) endocarditis
• Endocarditis related to intravenous drug use

Native valve endocarditis (acute and subacute)

Native valve acute endocarditis usually has an aggressive course. Virulent organisms, such as Staphylococcus aureus and group B streptococci, are typically the causative agents of this type of endocarditis. Underlying structural valve disease may not be present.

Subacute endocarditis usually has a more indolent course than the acute form. Alpha-hemolytic streptococci or enterococci, usually in the setting of underlying structural valve disease, typically are the causative agents of this type of endocarditis.

Prosthetic valve endocarditis (early and late)

Early prosthetic valve endocarditis occurs within 60 days of valve implantation. Traditionally coagulase-negative staphylococci, gram-negative bacilli, and Candida species have been the common infecting organisms. Recent data suggest Staphylococcus aureus may now be the most common infecting organism in both early and late prosthetic valve endocarditis.¹

Late prosthetic valve endocarditis occurs 60 days or more after valve implantation. Staphylococci, alpha-hemolytic streptococci, and enterococci are the common causative organisms.

Endocarditis related to intravenous drug use

Endocarditis in intravenous drug abusers commonly involves the tricuspid valve. S aureus is the most common causative organism.

Pathophysiology 

Infective endocarditis generally occurs as a consequence of nonbacterial thrombotic endocarditis, which results from turbulence or trauma to the endothelial surface of the heart. Transient bacteremia then leads to seeding of lesions with adherent bacteria, and infective endocarditis develops.

Pathologic effects due to infection can include local tissue destruction and embolic phenomena. In addition, secondary autoimmune effects, such as immune complex glomerulonephritis and vasculitis, can occur.

Frequency

United States

Incidence is 1.4-4.2 cases per 100,000 people per year.

International

Incidence of disease appears to be similar throughout the developed world.

Mortality/Morbidity

• Increased mortality rates are associated with increased age,² infection involving the aortic valve, development of congestive heart failure, central nervous system (CNS) complications, and underlying disease such as diabetes mellitus. Mortality rates also vary with the infecting organism and seem particularly higher when Staphylococcus aureus is the infecting organism.^1,3
• Mortality rates in native valve disease range from 16-27%. Mortality rates in patients with prosthetic valve infections are higher. More than 50% of these infections occur within 2 months after surgery.

Sex

The male-to-female ratio is approximately 2:1.

Age

Although endocarditis can occur at any age, the mean age of patients has gradually risen over the past 50 years. Currently, more than 50% of patients are older than 50 years.⁴

Mendiratta et al found that, in their retrospective study of hospital discharges from 1993-2003 of patients aged 65 years and older with a primary or secondary diagnosis of infective endocarditis, hospitalizations for infective endocarditis increased 26%, from 3.19 per 10,000 elderly patients in 1993 to 3.95 per 10,000 in 2003.⁵

Clinical

History

• Present illness history is highly variable. Symptoms commonly are vague, emphasizing constitutional complaints, or complaints may focus on primary cardiac effects or secondary embolic phenomena.
• Primary cardiac disease may present with signs of congestive heart failure due to valvular insufficiency. Secondary phenomena could include focal neurologic complaints due to an embolic stroke or back pain associated with vertebral osteomyelitis.
• Fever and chills are the most common symptoms.
• Anorexia, weight loss, malaise, headache, myalgias, night sweats, shortness of breath, cough, or joint pains are common complaints.
• As many as 20% of cases present with focal neurologic complaints and stroke syndromes.
• Dyspnea, cough, and chest pain are common complaints of intravenous drug users. This is likely related to the predominance of tricuspid valve endocarditis in this group and secondary embolic showering of the pulmonary vasculature.

Physical

• Fever, possibly low-grade and intermittent, is present in 90% of patients.
• Heart murmurs are heard in approximately 85% of patients. Change in the characteristics of a previously noted murmur occurs in 10% of these patients and increases the likelihood of secondary congestive heart failure.
• One or more classic signs of infective endocarditis are found in as many as 50% of patients. They include the following:
  • Petechiae - Common but nonspecific finding;
  • Splinter hemorrhages - Dark red linear lesions in the nailbeds
  • Osler nodes - Tender subcutaneous nodules usually found on the distal pads of the digits
  • Janeway lesions - Nontender maculae on the palms and soles
  • Roth spots - Retinal hemorrhages with small, clear centers; rare and observed in only 5% of patients.
• Signs of neurologic disease occur in as many as 40% of patients. Embolic stroke with focal neurologic deficits is the most common etiology. Other etiologies include intracerebral hemorrhage and multiple microabscesses.⁶
• Signs of systemic septic emboli are due to left heart disease and are more commonly associated with mitral valve vegetations. Multiple embolic pulmonary infections or infarctions are due to right heart disease.
• Signs of congestive heart failure, such as distended neck veins, frequently are due to acute left-sided valvular insufficiency.
• Splenomegaly
• Other signs
  • Stiff neck
  • Delirium
  • Paralysis, hemiparesis, aphasia
  • Conjunctival hemorrhage
  • Pallor
  • Gallops
  • Rales
  • Cardiac arrhythmia
  • Pericardial rub
  • Pleural friction rub

Causes

• Native valve endocarditis
  • Rheumatic valvular disease (30% of native valve endocarditis [NVE]) - Primarily involves the mitral valve followed by the aortic valve
  • Congenital heart disease (15% of NVE) - Underlying etiologies include a patent ductus arteriosus, ventricular septal defect, tetralogy of Fallot, or any native or surgical high-flow lesion.
  • Mitral valve prolapse with an associated murmur (20% of NVE)
  • Degenerative heart disease - Including calcific aortic stenosis due to a bicuspid valve, Marfan syndrome, or syphilitic disease
  • Approximately 70% of cases are caused by Streptococcus species including Streptococcus viridans, Streptococcus bovis, and enterococci. Staphylococcus species cause 25% of cases and generally demonstrate a more aggressive acute course.
• Prosthetic valve endocarditis
  • Early disease, which presents shortly after surgery, has a different bacteriology and prognosis than late disease, which presents in a subacute fashion similar to native valve endocarditis.
  • Infection associated with aortic valve prostheses is particularly associated with local abscess and fistula formation, and valvular dehiscence. This may lead to shock, heart failure, heart block, shunting of blood to the right atrium, pericardial tamponade, and peripheral emboli to the central nervous system and elsewhere.
  • Infection that occurs early after surgery may be caused by a variety of pathogens, including S aureus and S epidermidis. These nosocomially acquired organisms are often methicillin-resistant (MRSA). Late disease is most commonly caused by streptococci.
• Endocarditis associated with intravenous drug use
  • This condition most commonly involves the tricuspid valve, followed by the aortic valve.
  • Two thirds of patients have no previous history of heart disease and no murmur on admission. A murmur may not be heard in patients with tricuspid disease because of the relatively small pressure gradient across this valve. Pulmonary manifestations may be prominent in patients with tricuspid infection: one third have pleuritic chest pain, and three quarters demonstrate chest radiographic abnormalities.
  • Diagnosis of endocarditis in intravenous drug users can be difficult and requires a high index of suspicion.
  • S aureus is the most common (<50% of cases) etiologic organism. Other causative organisms include streptococci, fungi, and gram-negative rods (eg, pseudomonads, Serratia species).⁸ Methicillin-resistant S aureus (MRSA) accounts for an increasing portion of S aureus infections and has been associated with previous hospitalizations, long-term addiction, and nonprescribed antibiotic use.
• Healthcare-associated endocarditis
  • Endocarditis may be associated with new therapeutic modalities involving intravascular devices such as central or peripheral intravenous catheters, rhythm control devices such as pacemakers and defibrillators, hemodialysis shunts and catheters, and chemotherapeutic and hyperalimentation lines.⁴
  • These patients tend to have significant comorbidities, more advanced age, and predominant infection with Staphylococcus aureus.
  • The mortality rate is high in this group.
• Fungal endocarditis⁹
  • Fungal endocarditis is found in intravenous drug users and intensive care unit patients who receive broad-spectrum antibiotics.
  • Blood cultures are often negative, and diagnosis frequently is made after microscopic examination of large emboli.
• Diagnosis: Definitive diagnosis of infective endocarditis is generally made using the Duke criteria. Major criteria include (1) multiple positive blood cultures for the infecting organism and (2) echocardiographic evidence of endocardial involvement or a new regurgitant murmur on physical examination. 

Cardiology: Exercise Tolerance Test (ETT)

Exercise tolerance test(aka Exercise ECG testing)

Used to:

-       Confirm the diagnosis of angina

-       Give an indication of the severity of CAD – thus allowing you to asses risk. This can be done either in a patient with CAD, or in somebody with CAD who has had a previous MI.

It is possible to have a normal resting ECG, even if there is considerable narrowing of the coronary arteries.

The test has:

-       Specificity of 80%

-       Sensitivity of 70%

…for CAD

The Bruce protocol was established in the 1960’s, and this says that:

-       1) – the patient should at an incline of 10% at 1.7mph. This is gradually increased – both the incline and the speed. The gradient is increased by 2& each time, and the speed by roughly 0.8mph.

-       You continue to increase these until the patient reaches their target heart rate. The target rate is:

o   Men – 220 – age

o   Women – 210 – age

-       The target heart rate is approximately 85% of the maximum heart rate – the whole aim of the test is to reach this target heart rate! – note that the changes in the ECG can appear during the resting period after exercise, eve if they didn’t appear in the ECG during the original exercise!

-       Beta-blockers should be stopped the day before the test – as these can prevent the target heart rate being reached

-       Digoxin should be stopped a week before the test – as this can alter the ST segment, and make interpretation for the test difficult.

-       The Bruce protocol technically states that patients should exercise for 21 minutes, however they rarely exercise for this long. Normally the test is stopped once the target heart rate is reached.

Measurements during the test

-       The patent is hooked up to a 12 lead ECG – a reading is taken before the test, and also recorded throughout the duration of the test

-       Blood pressure should be taken at the beginning of the test, and at the beginning of each new stage of the test

o   Systolic BP often rises – it is not unusual for it to go above 220mmHg

o   Diastolic BP often falls slightly  

-       A normal test does not necessarily rule out CAD – however, if you have CAD and have a negative test, then your prognosis is still good

-       20% of those with a positive test result actually don’t have CAD. These kinds of results are much more common in young people, thus it is controversial to test young, asymptomatic patients.

o   Also note that a disproportionately small amount of women are tested – and as well as this, women are more likely to have atypical symptoms of CAD.

Those who have a strongly positive test (which is ST depression within 6 minutes) and those most suitable for coronary angiography.

The test is probably most useful as a prognostic tool – and not as useful as a diagnostic tool. If you already know the diagnosis, then a positive test at a low workload is a poor prognostic sign.

Complications

-       Death or MI occurs in 0.01% of patients. You should select patients carefully to minimise this risk

-       VT or VF can occur in 1 in 0.02%

Contraindications

-       Acute MI in the last 4-6 days

-       Unstable angina – with pain at rest in the last 48 hours

-       Uncontrolled heart failure

-       Systemic infection , myocarditis, pericarditis

-       DVT

-       Uncontrolled hypertension (sys >220, dias >120)

-       Severe aortic stenosis – this can cause sudden death!

-       Arrhythmia

-       Aneurysm

-       Recent aortic surgery

Findings

-       ST depression – should be >1mm. The deeper the depression, and the lower the HR at which is occrs generally indicate the severity of the disease

-       T wave elevation – where this occurs to >1mm and there are no Q waves (in that particular lead) then this can be a bad prognostic sign

Reasons to stop the test

-       ST depression >3mm

-       Target heart rate reached

-       ST elevation of >1mm in a lead with no Q waves

-       VT

-       New atrial fibrillation

-       Development of new BBB

-       Cardiac arrest

-       The most common reason the test is stopped is fatigue and breathlessness as the patient is unaccustomed to exercise!

REMEMBER!:

-       ST depression – Ischaemia

-       ST elevation - Infarction

Notes by Tom Leach

Cardiology: Echocardiogram

Echocardiogram Notes

This is basically an ultrasound of the heart. It gives a reasonably accurate picture of the valves and chambers of the heart, and also gives an idea of the velocity of blood flow in certain areas (thus helping you to determine if there is backflow/ reduced flow in valve defects).

Structures visualised

-          Valves

-          All 4 chambers

-          Wall thickness

-          Amount of muscle contraction

-          Pericardium

-          Intracardiac masses

-          Ascending aorta

Types of echo

Transthoracic

-          The patient lies of their left hand side with their arm behind their head. The transducer is placed at various intercostal spaces to the left of the sternum, and at the anterior axillary line.

-          This is the preferred test for valve defects

Transoesophageal (TOE –Trans-Oesophageal Echocardiogram)

-          Usually performed under sedation (midazolam), and with facilities for resuscitation

-          It provides high resolution due to the probes proximity to the heart.

-          Provides good views of the posterior part of the heart – i.e. the left atrium, and descending aorta.

-          This is the investigation of choice for infective endocarditis, prosthetic valve management, and searching for causes of thromboembolism.

-          This is an invasive procedure!

Stress echocardiogram

-          You would normally do this is conjunction with a normal transthoracic echo and compare images. You can either stress the heart with exercise, or you can give an infusion of dobutamine.

-          It is basically used to evaluate CHD.

-          The presence of reversible systolic regional wall motion abnormalities are characteristic of CHD

-          This is basically an alternative to ETT (exercise tolerance testing) – but is not used as often

Uses of echo

-          Find valve dysfunction

-          Asses prosthetic valve function

-          Assessment of left ventricular function – can be used to estimate left ventricular ejection fraction

-          Atrial fibrillation

-          Congenital heart disease

-          Cardiomyopathy

-          IE

-          After embolic stroke – to try and find a possible cause; e.g. patent foramen ovale.

-          Pericardial disease

Other stuff

These things are generally not looked for on ECHO, unless you especially specify them to look!:

-          Right ventricular function

-          Diastolic function

-          Possible cause of stroke

Notes by Tom Leach

Cardiology: Cardiac Catheterization

Cardiac catheterization Notes

This is not necessarily the same as coronary angiography, although the two terms are sometimes used interchangeably.

Cardiac catheterisation is the process by which you gain catheter access to the veins or arteries of the heart. Thus, in the procedures of coronary angiography, and angioplasty, you perform cardiac catheterisation as part of the procedure.

Reasons for catheterisation

-          Injection of dye in angiography

-          Measurement of intracardiac pressures and oxygen saturations

-          Passage of electrophysiological instruments

-          Passage of angioplasty and valvuloplasty balloons

During catheterisation, the patient is usually awake throughout, and the catheter is guided by fluoroscopy.

Left heart catheterisation

This is performed via an arterial route. The catheter is usually inserted into the femoral artery (again, brachial artery is sometimes used), and then passed up the artery, and into the aorta. Eventually it reaches the aortic arch, and can be passed directly into the left ventricle.

-          The radial artery is gaining favour as a preferred site – as some studies report fewere complications. it is also useful when there is femoral artery stenosis, or obesity obscures natural landmarks used to identify the femoral artery.

Uses

Assessment of:

-           left ventricular function

-          Severity of mitral and aortic valve disease

-          Outflow tract obstruction

-          Extent of coronary artery disease

-          Allows biopsies to be taken – e.g. in cardiomyopathies

-          Allows electrophysical provocation studies – e.g. for VT

-          Allow placement of stents (PCI)

-          Allows balloon valvotomy

Right sided catheterisation

-          This is performed via the venous route. The catheter is inserted via the femoral, internal jugular, subclavian or forearm veins.

Uses

Allows:

-          Measurement of cardiac output

-          Measurement of left ventricular filling pressure

-          Measurement of pulmonary artery wedge pressure (PWP) – this is the pressure in the pulmonary artery distal to an occlusion of the artery. This is useful because it provides an estimation of the left atrial pressure. It is useful in determining the cause of acute pulmonary oedema. This is likely to be present if there is a PWP >20mmHg. Normal physiological pressure is 6-12mmHg.

-          Direct thrombolysis of the pulmonary artery for massive pulmonary embolism

-          Insertion of electrodes for cardiac pacemaker devices

Measurement of the PWP can involve the insertion of a Swan-Ganz catheter (pulmonary artery catheter). This catheter is purely diagnostic and is used to monitor left and right ventricular function. This catheter is usually inserted via the internal jugular or subclavian vein.

Indications for Swan-Ganz:

-          Shock (cardiogenic vs non-cardiogenic)

-          Respiratory distresses

-          Complicated MI

-          Monitoring effects of drugs (e.g. ionotropes)

-          Assesing fluid requirements

-          Thrombolysis for PE

The procedure

-          Not normally painful. Patient may feel a warm flushing sensation when the dye is used

-          Patients may be given some sedation if they feel anxious – normally this is diazepam (did you know this is Valium?!)

-          Patients with renal impairment (creatinine of over 200) will require 1L of IV saline at least 1 hour before the treatment to reduce the risk of x-ray contrast nephropathy

Contraindications

There are no absolute contraindications. However, you still have to consider the relative risks for each patient. If they have a large number of relative risks you might want to reconsider giving the catheter. These include:

-          Severe hypertension

-          Shock

-          Severe anaemia

-          Acute renal failure

-          Severe congestive cardiac failure

-          Allergy to contrast

-          Active infection or PUO

Also remember that catheterisation is part of other procedures (e.g. PCI) and thus not always just done on its own.

Complications

-          Haemorrhage from entry site

-          False aneurysm – this would need to be confirmed by ultrasound

-          Dye reaction

-          Infection

-          Angina and MI

-          Arrhythmias

-          Pericardial tamponade

-          Stroke

Notes by Tom Leach