There are four type of SVT from reentry .
1-atrioventricular nodal reentrant tachycardia (AVNRT)
2- Atrioventricular reciprocating ( or reentrant ) tachycardia ( AVRT)
3- sinoatrial reentrant tachycardica ( SART)
4- intra-atrial tachycardia ( IART) .
Atrioventricular nodal reentrant tachycardia
The most common SVT , young and healthy without structural heart , twice more in women than men .
AVNRT is type of reentrant SVT with two separate pathways , these two pathways have different EP properties and are both location within or around AV node.
- Slow pathway
- Fast pathway
ECG findings
Narrow QRS tachycardia with regular R-R interval
And no visible Pwave
In 2,3,avf the P wave are inerted but not visible in ECG because the atria and ventricle is activated simultaneously this is in 66% OF CASES .
Its not perfectly synchronous , if the retrograde P wave occurs immediately after the QRS complex . The Pseudo-Q , pseudo-S , and pseudo-r’ wave should resolve on conversion of the tachycardia to normal sinus rhythm .
In current pediatric and adult cardiology practices, an attempt is made at understanding the pathophysiologic diagnosis ( the what and how) of the arrhythmia. This allows the cardiologist to evaluate mechanisms and components of the arrhythmia in order to evaluate vulnerable parameters and target the arrhythmia on a subcellular level. Ultimately this intervention leads to, for the most part, making the ECG and the patient appear more “normal”!
A simple example of this would be the diagnosis and treatment of AV node reentry tachycardia.
The diagnosis of this arrhythmia can be made on a surface electrocardiogram. However, when a Pediatric Cardiologist evaluates this more closely, the AV node reentry circuit that is responsible for this tachycardia is secondary to an anatomic fast and slow pathway within the AV node. The AV node slow conduction pathway provides a retrograde circuit making this much like other types of reentry tachycardia. The vulnerable perimeter in this case would be the AV nodal action potential. On a subcellular level, the L-type calcium channel is prominent within the AV node. Therefore, interventions could be aimed at interfering with this channel either directly with a calcium channel blocker or indirectly with a beta-blocker. In either case, the clinical outcome would be the same and that is returning the patient to sinus rhythm.
Vaughn-Williams Classification
The Vaughn-Williams classification of antiarrhythmic therapy takes into account some of this approach. It is a somewhat confusing mechanism of memorizing antiarrhythmics and we will spend little time discussing the classification system itself. It is based on the cellular properties of the normal his-Purkinje cells. Classification of drugs is dependent upon the ion currents responsible for depolarization and repolarization as well as the beta-adrenergic receptors. Its advantages are that it is a physiologically based system and highlights the beneficial and deleterious effects of the specific drugs. Unfortunately, its disadvantages are that all cells are not normal. Therefore in addition to this, all cells in the heart are not his-purkinje in origin and therefore have different dysrhythmia profiles.
The Vaughn-Williams classification as I stated before divides antiarrhythmics based on certain ion channels they affect. Class I antiarrhythmics are sodium channel blockers and have direct membrane action upon the sodium channel. Class II antiarrhythmics are the beta-blockers and affect the heart by sympatholysis (beta blocking). Class III antiarrhythmics prolong repolarization by affecting the potassium channels and Class IV antiarrhythmics are calcium channel blockers. In addition to these classes other antiarrhythmics would include purinergic agonists and the digitalis glycosides, which do not fall in any of the above classifications...
SCD must be defined carefully
Sudden cardiac death is defined as unexpected death, occurring within 1 hour from the onset of symptoms, that is not directly attributable to other factors.
It is the leading cause of mortality in industrialized nations, accounting for 12% of all natural deaths and 50% of all deaths attributable to cardiovascular disease
The immediate cause leading to the final common pathway of total hemodynamic collapse is most frequently ventricular tachycardia (VT) and ventricular fibrillation (VF); asystole, pulseless electrical activity, aortic rupture, and cardiac tamponade account for the remainder
-The proximate events leading to these fatal ventricular arrhythmias result from a wide spectrum of underlying disease states, mediated by physiologic and environmental triggers.
What is VF ?
VF is the primary cause of sudden cardiac death (SCD). Ventricular fibrillation (VF) is the most commonly identified arrhythmia in cardiac arrest patients.
I is a rapidly fatal rhythm and if resuscitation is not begun within 5 to 7 minutes , death is virtually certain .
The heart consequently immediately loses its ability to function as a pump.
As the initial reentrant pattern of excitation breaks up into multiple smaller wavelets, the level of disorganization increases.
Sudden loss of cardiac output with subsequent tissue hypoperfusion creates global tissue ischemia; brain and myocardium are most susceptible.
If the fibrillatory waves are large the arrhythmia is described as course ventricular fibrillation.
Fibrillation waves which are greater than 3mm in height
Course VF indicates a more recent onset and is more likely to be reversed by defibrillation alone
If the fibrillatory waves are small the arrhythmia is described as fine ventricular
Fibrillation waves which are smaller than 3mm in height.
Fine VF indicates the arrhythmia has been present longer and may, before require drug therapy first, then defibrillationre the arrhythmia can be reversed. Fine reversed.
Fine ventricular fibrillation can progress to asystole if left untreated.
What is VT( ventricular tachycardia )
An arrhythmia originating in an ectopic focus in the bundle, Purkinje network, or ventricular myocardium
Series of wide QRS complexes firing at a rapid rate (minimum of three or more consecutive premature ventricular contractions)
Impulses originating from ventricular tissue do not produce P
What is Asystole ?
Asystole is the absence of electrical activity in the myocardium. “Flat line” possible causes : - Power off - Lead not attached - Lead selection -Fine VF (Rare) -asystole
How do you Confirm the Rhythm in Asystole ?
Confirm rhythm in two leads
Always check your leads are attached
Should you Defibrillate Asystole ?
Be sure to check in two leads that the rhythm is not “Fine” VF. - In this case you would follow the V-Fib algorithm
No evidence that defibrillation is beneficial
1- assess the lung expansion
2- assess the pleura
3- look for infiltrate
4- look at the mediastinum
5-Assess the abdomen
Techniques
Volume of PE and whether it’s mobile or loculated.
Sensitive method for detecting small quantity of PF(50-100ml).
Nondependent hemithorax to confirm a pneumothorax in a patient who could not be examined erect .
if the layering fluid is 1 cm thick, indicates an effusion of greater than 200 mL that is amenable to thoracentesis
The patient should be in full inspiration .
Shows better intrapulmonary abnormalities
The diaphragm fount at about the level of the 8th -10th posterior ribs or 5th -6th anterior rib on good inspiration
On a good PA film , the thoracic spine disk spaces should be barely visible through the heart but bony details of the spine are not usually be seen through the heart .
On the lateral view , proper penetration and inspiration is seen through the spine appears to darken as you move caudally . This is due to more air in lung in the lower lobes and less chest wall .
The patient must be flat against the cassette , if there is rotation of the patient , the mediastinum may look very unusual .
Clavicular heads whether they are in equal distance from the spinous process of the thoracic vertebral bodies .
Recognizing a technically adequate Chest x ray
Factors to evaluate :
1- Penetration
2- Inspiration
3- Rotation
4- Angulation
You should be able to just see the thoracic spine through the Heart .
About 10 posterior ribs visible is an excellent inspiration
In many Hospitalized patient 9 posterior ribs is an adequate Inspiration .
Posterior ribs are those that are most apparent on the chest x ray .they rum more or less horizontally.
Anterior ribs will be visible but are harder to see . They run more or less at a 45 degree angle downward to ward the feet ,
AP Versus PA the effect of magnification
In al PA film the heart is closer to the film and thus less magnified .
- the standard chest X-ray is a PA film .
In a AP film , the heart is farther from the films and is more magnified .
- Portable chest X-ray are almost always done AP.
When can CPR be withheld? Virtually all hospitals have policies which describe circumstances under which CPR can be withheld. Two general situations arise which justify withholding CPR: when CPR is judged to be of no medical benefit (also known as "medical futility"and when the patient with intact decision making capacity (or when lacking such capacity, someone designated to make decisions for them) clearly indicates that he / she does not want CPR, should the need arise.
When is CPR "futile"? CPR is “Futile” when it offers the patient no clinical benefit. When CPR offers no benefit, you as a physician are ethically justified in withholding resuscitation. Clearly it is important to define what it means to "be of benefit." The distinction between merely providing measurable effects (e.g. normalizing the serum potassium) and providing benefits is helpful in this deliberation.
When is CPR not of benefit? One approach to defining benefit examines the probability of an intervention leading to a desirable outcome. CPR has been prospectively evaluated in a wide variety of clinical situations. Knowledge of the probability of success with CPR could be used to determine its futility. For instance, CPR has been shown to be have a 0% probability of success in the following clinical circumstances: Septic shock Acute stroke Metastatic cancer Severe pneumonia
Function is to regulate the temp of the testicles through the cremaster muscle and the dartos fascia in the scrotum.
Ideal temp is about 34.4, > 36.7 may damage sperm count.
Acute scrotal pain
Causes;
Acutely painful scrotum is torsion of testis until proven otherwise.
Strangulated inguino-scrotal hernia is tender, painful, irreducible groin lump.
Torsion of the hydatid of Morgagni
Acute epididymitis
Haematocoele - trauma or scrotal surgery
Fournier’s gangrene-necrotising fasciitis
Appendicitis - referred pain (same visceral afferent nerve supply as testis - T10)
Chronic scrotal pain
Causes;
Inflammation
Chronic bacterial epididymitis
Recurrent incomplete testicular torsion
Chronic scrotal discomfort-in absence of infection. Often hx of scrotal surgery or trauma.
TB
Testicular torsion in newborn infant
Twist of the whole spermatic cord due to unfixed nature of newly descended testis.
Almost all of such torsions present late with overt testicular necrosis
Pain and tenderness are not prominent.
scrotum usually red and swollen and contains hard testicular mass
surgery to excise damaged organ and to fix other testis.
Testicular torsion in older boys and adults
Many cases yearly of ‘epididymitis‘ treated with antibiotics.
Slight left sided bias, incidence higher in winter months
Major predisposing factor is undescended testis
Symptoms include severe testicular pain which may radiate to the groin +/- nausea and vomiting.
Examination - gentle. high riding or horizontal testis. No specific path gnomonic clinical signs to differentiate from epididymitis.
Treatment - successful testicular salvage highly dependent on time b/w start of symptom and surgery. Detorsion and fixation of viable testis. contra lateral testis fixed at same time.
The main symptoms are progressive dysmenorhea, premenstrual syndrome, changes in basal body temperature during menstruation and dyspareunia.
MITHS AND FALACIES TO BE BURIED:
"The disease is most frequently seen above the age of 30, though not a few cases are encountered in the late twenties” (Novak & Novak.Text book of Gynecology.Page 557. Fifth Edition 1956.
Adolescents with severe dysmenrrhea are given prescriptions of analgesics or contraceptive pills and are reassured with concepts such as “when you get married pains will stop”or their mothers say “how can a gynecologist see her if she is a virgin”
Numerous papers on Adolescence, pelvic pain and laparoscopies (Reese, Vercellini, grupo Emory, Kontoradvis, Chatman, Creatsas, Laufer & others), report a prevalence of endometriosis ranging from 32 to 73%. Reports of normal internal genitaliae range from 20 to 60%. Therefore....
We believe that invasive procedures should not be used in adolescents with severe dysmenorrhea if their basal body temperature, the so called “Benjamin sign”, has not been investigated.
The premenstrual syndrome was present in 53%.
Cycle alterations only in 35%. (most of them oligomenorrheas)
These 2 items appear to be irrelevant but if one adds them to the others, they turn to be relatively important.
We also obtained important data from their sexual activity.
Dysmenorrhea is to be considered the most important symptom and the most frequent reason for consulting.
Cramps progressing in intensity throughout the years, not responding to conventional therapy, with diarrhea, N & V, changes in character, premenstrual tension, dyspareunia etc. were present in most of our adolescents in different degrees of intensity but at a very high level.
• 4-8% of 50-79 year old patients have ICA stenosis >50%
• ICA stenosis causes mostly (90%) embolic strokes, rarely failure of perfusion
Carotid Artery Stenosis
• Asymptomatic
• Symptomatic
Natural History
Short term (2-3 years)1-3% incidence of unheralded ipsilateral CVA
• Approximate event rate of <1%/year for <50% stenosis
• Approximate event rate of 1%/year for >50% stenosis
Asymptomatic Carotid Atherosclerosis Study
Limitations of ACAS
Absolute stroke risk reduction of 1.2%/year
– Eg pt with 3%/year stroke risk now with 1.8%/year stroke risk
– Risk of cardioembolic, lacunar CVA NOT reduced
• Perioperative complication rate 2.3%; death 0.1%
– Good risks; 25 pts screened for every 1 enrolled
– Other studies show 4.6-5.1% incidence of perioperative
stroke/death in aysmptomatic ICA with CEA
– If 5% event rate applied, results of ACAS are nullified
• CEA not beneficial for women with ICA 60-99%!
• No incremental benefit for increasing stenoses
– 60-69% stenosis had HIGHER benefit than 80-89%!
Asymptomatic Carotid Surgery Trial
Largest prospective study to date, most recent
(May 2004)
• 3120 patients, 5 year followup; 10 year period
• ICA >60% stenosis (ultrasound)
• Immediate CEA vs. Deferred CEA (+ ‘usual
therapy)
• 5 year stroke risk – 6.4% CEA; 11.8% medical
– Men and women, all age groups, all stenosis subsets
– 3% perioperative event rate
Screening Methods
Carotid duplex US
– 85% sensitivity/specificity for 70-99% vs <70%
• Digital Subtraction Angiography
– Clinical periprocedure CVA rate of 1%
– Gold standard
• MRA (Elliptic Centric Contrast Enhanced MRA)
– 95% sensitivity/ 90% specificity for 70-99% vs <70%
• Spiral CTA
– 74-100% sensitivity/ 83-100% specificity for 70-99%
vs <70%
Understand Tricuspid and Pulmonic valvestenosis and regurgitation
Diagnosis
Treatment options
Specific conditions
Ebstein anomaly
Carcinoid Syndrome
Right AtrialWaveform
a wave - RA contraction
elevated in RV failure
c wave - tricuspid closure
v wave - passive filling of RA during
ventricular systole = T wave on ECG
elevated in tricuspid regurgitation
x descent - atrial diastole
y descent - atrial emptying
Tricuspid Stenosis
Etiology
Almost always rheumatic
Other causes are rare
Congenital tricuspid atresia
Right atrial tumors
Carcinoid syndrome
More often tricuspid regurgitation
Endomyocardial fibrosis
Vegetations
Pacemaker lead
Extracardiac tumors
Rheumatic Tricuspid Stenosis
rheumatic heart disease
But clinically significant in only 5%
Isolated TS is rare
Almost always mitral valve involvement
Also aortic valve involvement common
Pathologic Findings
Rheumatic Tricuspid Stenosis
Similar to mitral stenosis
Fusion and shortening of chordae tendineae
Fusion of leaflet edges
Calcification is rare
Right atrial dilatation, wall thickening
Heart rate is slow, causing hemodynamic compromise
Sick sinus syndrome
Sinus bradycardia or atrial fibrillation with slow heart rate
response (generally <40 bpm)
Heart block
3rd degree
2nd degree type 2 (Mobitz)
Malignant Tachyarrhythmia caused by bradycardia
Torsades de Pointes
Clinical settings for temporary pacemaker
Syncope
Myocardial infarction
Especially inferior
Shock due to bradycardia
Myocarditis
Lyme disease
Pacemaker Nomenclature
CommonModes
VVI – Single chamber (ventricle)
DDD – Dual chamber
AAI (uncommon) – Single chamber (atrium)
1st Letter is chamber PACED
2nd Letter is chamber SENSED
3rd Letter is response
I = Inhibit
T = Triggered (Unusual)
D = Dual (Inhibit or Pace)
4th Letter – R = Rate responsive (permanent pacers)
Sites of insertion for a temporary pacemaker
Right internal jugular
Left subclavian vein
Right subclavian vein
Either femoral vein (Fluoroscopy required)
Left IJ is possible but very difficult
Seldinger technique for percutaneous vascular access
General steps
•Trendelenberg position or leg elevation can
facilitate access to IJ and subclavian veins
•Sterile Field
•Anesthetize skin with lidocaine
•Access vein with Cook needle
•Insert guidewire
•Remove needle
•Consider making a skin nick with scalpel
•Insert 6-8F introducer sheath with dilator over
guidewire
•Remove dilator and guidewire
•Flush sheath using side port
•Advance temporary pacemaker to right
ventricle
and chest pains x 2 weeks
• DOE over past month, worsening x 2 weeks
• Palpitations last a few minutes follow by
diaphoresis, lightheadedness, and chest pain
• Chest pain is substernal chest pressure, radiates
to left arm, 8/10 intensity; exertional in nature
and relieved with rest or leaning forward
Thyroid hormone
T4 prohormone converted to T3 active
• Animal studies demonstrate
– Direct positive inotropic effect
• Increases sodium-calcium-ATPase which increases calcium
influx
– Increase in LV cavity without change in EDP
• Increases rate of depolarization
• Decreases refractory period
Hyperthyroidism
Symptoms
– Palpitations
– Dyspnea
• Signs
– Tachycardia
– Systolic hypertension
– Hyperactive precordium
– Loud S1, accentuated P2, S3
– Occasional systolic click, midsystolic murmur
– Means-Lerman scratch – systolic scratch near LUSB
Hyperthyroidism and Atrial Fibrillation
Previously thought that hyperthyroid patients
have 5-15% incidence of atrial fibrillation
– Studies involved older patients with known structural
heart disease
• 1996 study demonstrates only 1% of new onset
atrial fibrillation is caused by overt
hyperthyroidism
• Treatment involves restoration of euthyroid state
Hyperthyroid Angina & CHF
Previously thought only to occur in presence of
coronary disease
– CHF occurs experimentally in animals by administering T4
– CHF has developed in children with thyrotoxicosis and no
coronary disease
– Angina has been reported in a patient with normal
coronaries, thought to be thyroid mediated coronary arterial
vasospasm
– Abnormal exercise LV function not reversed with b blockade,
but is reversed by treating hyperthyroidism
– Thyroid mediated cardiomyopathy may not be reversible
• Early mortality of 1%/hour for proximal
dissection
• Two theories of formation
– Breach of intimal layer of aorta allows blood to
encroach on a diseased medial layer, creating a false
lumen and intimal flap.
– Rupture of vasa vasorum in medial layer causes local
hematoma causing dissection; no flap is formed. 13%
of autopsy cases cannot identify flap.
Etiology
Medial degeneration
– Chief cause of atraumatic dissections
– Marfan syndrome
• 5-9% of all aortic dissections
• Dissections occur at a young age
• Thoracic aortic aneurysms
• Proximal aortic dissections
– Ehlor’s-Danlos syndrome
– Familial aortic aneurysm
• Mutation of fibrillin-1 gene with loss of elastic fibers
– Nonclassic degeneration associate with age,
hypertension
Peak incidence age 60’s to 70’s
• M:F 2:1
• 72-80% with preexisting hypertension
• Bicuspid aortic valve found in 7-14% of all aortic
dissections
• Associated with Noonan, Turner syndromes
• Vasculitis, especially giant cell
• Reports describe association with cocaine in
young men
Pregnancy and Aortic Dissection
Of aortic dissections in women <40, half
are during pregnancy
• Generally in the third trimester
• Some in postpartum
• Marfan syndrome poses special risk
• Uncertain causality; not fully explained by
increases in BP, CO, blood volume
• Possible reporting bias
Symptoms
Common Manifestations
• Severe “tearing” pain, usually sudden onset
• Migratory pain described in 17% of cases
• Location
– Ascending aorta
• Anterior pain involves ascending aorta in 90% of cases
• Neck, throat, jaw, face
– Descending aorta
• Interscapular pain involves descending aorta in 90% of cases
• Back, abdomen, lower extremity pain
Uncommon Manifestations
• Syncope (9%)
• Congestive heart failure (7%)
– Due to acute aortic regurgitation
• CVA (5%)
• Peripheral neuropathy
• Paraplegia
• Sudden death
• Tamponade (hemopericardium due to rupture)
Dissection Extension
Proximal dissection involves coronary
artery in 1-2% of cases
– Most commonly flap involves right coronary
ostium, causing inferior infarct
– Chest xray may not be sufficient to rule out
dissection
• Distal dissection can extend
– 5-8% of cases involve renal artery
– 3-5% involve mesenteric ischemia/infarction
