BOOKS

About ECG:
1. The ECG in acute MI_Smith
2. Challenging ECGs_Marriott
3. .....too many.......

PPM:
1.Cardiac Pacemakers Step by Step: An Illustrated Guide

EP:
1. Handbook of Cardiac Electrophysiology: A Practical Guide to Invasive EP Studies and Catheter Ablation

ECHO:
1. Textbook of Clinical Echocardiography_Otto
2. Essential Echocardiography: A Practical Handbook with DVD

Hemodynamics:
1. Textbook of Clinical Hemodynamics_Ragosta

Cardiac CATH:
1. The Cardiac Catheterization Handbook_Kern

Bible:
#### 1. Braunwald’s Heart Disease_!!!!!! Absolute bile!
2.Hurst's the Heart, 12th Edition

[CATH]acute coronary thrombus aspiration cathter

1. Fetch

Device Common Name: Embolectomy Catheter
Device Trade Name: FETCH (TM) Aspiration Catheter
http://www.medrad.com/en-us/info/products/Pages/FetchAspirationCatheter.aspx
The FETCH Aspiration Catheter is a rapid exchange catheter approved for the removal of fresh, soft emboli and thrombi from vessels in the arterial system and coronary vasculature

The Fetch Aspiration Catheter provides the outstanding handling characteristics of an AngioJet catheter with the smallest crossing profile of any manual aspiration device. The Fetch is designed for enhanced trackability and performance for small, discrete thrombus volume cases.


2. Thrombuster


3. QXT

[ECG] Parasystole

http://en.wikipedia.org/wiki/Parasystole

Parasystole
From Wikipedia, the free encyclopedia
Parasystole
Classification and external resources
MeSH D017574
Parasystole is a kind of arrhythmia caused by the presence and function of a secondary pacemaker in the heart, which works in parallel with the SA node. Parasystolic pacemakers are protected from depolarization by the SA node by some kind of entrance block. This block can be complete or incomplete.
Parasystolic pacemakers can exist in both the atrium or the ventricle. Atrial parasystolia are characterized by narrow QRS complexes
Two forms of ventricular parasystole have been described in the literature, fixed parasystole and modulated parasystole. Fixed ventricular parasystole occurs when an ectopic pacemaker is protected by entrance block, and thus its activity is completely independent from the sinus pacemaker activity. Hence, the ectopic pacemaker is expected to fire at a fixed rate. Therefore, on ECG, the coupling intervals of the manifest ectopic beats will wander through the basic cycle of the sinus rhythm. Accordingly, the traditional electrocardiographic criteria used to recognize the fixed form of parasystole are: i) the presence of variable coupling intervals of the manifest ectopic beats; ii) inter-ectopic intervals that are simple multiples of a common denominator; iii) fusion beats.
According to the modulated parasystole hypothesis, Rigid constancy of a pacemaker might be expected if the entrance block were complete, but if there is an escape route available for the emergence of ectopic activity, then clearly there must be an effective ionic communication, not complete insulation, between the two tissues. If there is an electrical communication between the two, then the depolarization of the surrounding ventricle may influence the ectopic pacemaker. That influence will be electrotonic; depolarization of the surrounding field will induce a partial depolarization of the pacemaker cells. Therefore, appropriate diagnosis of modulated parasystole relies upon the construction of a “phase response curve” as theoretical evidence of modulation of the ectopic pacemaker cycle length by the electrotonic activity generated by the sinus discharges across the area of protection. In this case, the timing of the arrival of the electronic stimulus will serve to delay or advance the subsequent pacemaker activation. In this case, the coupling intervals between the manifest ectopic and sinus discharges will be either fixed or variable, depending on the cycle length relations between the two pacemakers.


http://www.wikidoc.org/index.php/Ventricular_Parasystole

http://library.med.utah.edu/kw/ecg/ecg_outline/Lesson5/ventricular.html

Ventricular Parasystole

Non-fixed coupled PVCs where the inter-ectopic intervals (i.e., timing between PVCs) are some multiple (i.e., 1x, 2x, 3x, . . . etc.) of the basic rate of the parasystolic focus

PVCs have uniform morphology unless fusion beats occur

Usually entrance block is present around the ectopic focus, which means that the primary rhythm (e.g., sinus rhythm) is unable to enter the ectopic site and reset its timing.

May also see exit block; i.e., the output from the ectopic site may occasionally be blocked (i.e., no PVC when one is expected).

Fusion beats are common when ectopic site fires while ventricles are already being activated from primary pacemaker

[ECG] Proarrhythmia

http://en.wikipedia.org/wiki/Proarrhythmia

促心律不整性(proarrhythmia)

Proarrhythmia is a new or more frequent occurrence of pre-existing arrhythmias, paradoxically precipitated by antiarrhythmic therapy, which means it is a side effect associated with the administration of some existing antiarrhythmic drugs, as well as drugs for other indications. In other words, it is a tendency of antiarrhythmic drugs to facilitate emergence of new arrhythmias.

[ECG] VPCs, VPBs, PVBs

Treatment of ventricular premature beats
http://www.uptodate.com/online/content/topic.do?topicKey=carrhyth/38779&view=print
General principles —
Two issues need to be addressed in the patient found to have VPBs. The first relates to the possible presence of underlying structural heart disease, which has prognostic significance and may require specific therapy which, in some cases, may also reduce VPBs.
The two major examples are beta blockers, which improve survival in patients with a prior myocardial infarction or heart failure, and antihypertensive therapy to induce regression of LVH in patients with hypertension [23].
The second issue relates to whether the VPBs produce symptoms. As noted in the preceding discussions, there is no clear evidence that VPBs alone are an independent risk factor for mortality or that VPB suppression with antiarrhythmic drugs improves overall survival in patients who have not had a major arrhythmic event. Thus, the only indication for the use of antiarrhythmic drugs for VPB suppression is in symptomatic patients. In addition to symptoms related to ectopy, frequent VPBs can result in deterioration of left ventricular function in patients with left ventricular dysfunction [21].
Limited role for antiarrhythmic drugs — In addition to the lack of benefit from VPB suppression in asymptomatic patients, some antiarrhythmic drugs (eg, flecainide, encainide, and d-sotalol) are associated with increased mortality due to proarrhythmia, primarily when given to patients with a prior MI. Proarrhythmia is less of a concern in patients without organic heart disease [35].
When an antiarrhythmic drug is given to suppress symptomatic VPBs, the drugs of choice are a beta blocker and amiodarone, both of which are effective and have no or little potential for proarrhythmia(促心律不整性), respectively. Sotalol is an alternative agent [36]. Furthermore, among patients with a prior MI or heart failure, a beta blocker should be part of standard therapy because of a clear survival benefit. This benefit may be associated with a reduction in VPBs.
Beta blockers are the first-line drugs for suppression of symptomatic VPBs. The lowest dose of beta blockers that relieves symptoms should be used in order to minimize side effects with the exception of patients with a prior MI or heart failure in whom the dose is titrated to that recommended for treatment of the underlying disease.
Amiodarone can be added in patients who remain symptomatic or who cannot tolerate beta blockers.(先用BB不行再用Amiodarone) Trials of amiodarone use in patients with VPBs post-MI (eg, CAMIAT and EMIAT) or with VPBs and heart failure (eg, CHF-STAT) have demonstrated a significant reduction in VPBs and in arrhythmic mortality, but routine amiodarone therapy is not recommended in asymptomatic patients because of the absence of a significant improvement in overall mortality. Subset analysis has suggested that overall mortality in post-MI patients may be significantly reduced when amiodarone is given to patients also treated with a beta blocker. These issues are discussed in detail separately.
Sotalol, dofetilide and, when available, azimilide do not appear to be harmful in patients who have had an MI. Although only limited data are available concerning the efficacy of these drugs for VPBs, they may be considered in patients who do not tolerate or respond to amiodarone.
Other therapies — Some alternative techniques that have been employed for VPB suppression include biofeedback, exercise, anxiolytics, and stress reduction. Whether these measures have a significant effect on the majority of patients, and if so, how much is a placebo effect, is not known. In addition, anxiolytics have the potential induce psychologic and physical dependence.
Frequent VPBs may be associated with worsening of systolic heart failure in patients with a dilated cardiomyopathy. Small studies have suggested that in selected patients, radiofrequency ablation of ectopic ventricular foci is associated with an improvement in left ventricular function and clinical improvement in symptoms [1,2,47,48].
The 2006 American College of Cardiology/American Heart Association/European Society of Cardiology (ACC/AHA/ESC) guidelines for the management of ventricular arrhythmias included suggestions regarding ablation therapy for VPBs [49]. They note that ablation of VPBs may be useful in the following settings:
• VPBs that are frequent, symptomatic, and monomorphic, if they are refractory to medical therapy or if the patient chooses to avoid long-term medical therapy.
Ventricular arrhythmia storm that is consistently provoked by VPBs of a similar morphology [50].

[CATH] BC + BMS + DES

BC: Ryujuin
Voyager
NC Voyager
Mercury
NC Mercury
Apex

BMS: Vision
Driver
MicroDriver
Jostent
Gazella
Zeta
Liberte
Tsunami
PC stent
Helistent
Blazer

DES: Cypher
Taxus
Endeavor
Resolute
Xience V
Promus
Coroflex

[Heart ECHO]Right ventricle systolic pressure

https://www.stanford.edu/group/ccm_echocardio/cgi-bin/mediawiki/index.php/Right_ventricle_systolic_pressure#.C2.A0Calculation_of_right_ventricle_systolic_pressure_.28RVSP.29


Right ventricle systolic pressure
From Echocardiography in ICU
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Contents [hide]
1 Calculation of right ventricle systolic pressure (RVSP)
1.1 Measurement of the pressure gradient between right ventricle (RV) and right atrium (RA)
1.2 Estimation of right atrium (RA) pressure
2 Example
3 Reference


Calculation of right ventricle systolic pressure (RVSP)
The right ventricle systolic pressure can be non-invasively measured by echocardiography.

It is obtained by the addition of the pressure gradient between the right ventricle and the right atrium, to the pressure in the right atrium.



Measurement of the pressure gradient between right ventricle (RV) and right atrium (RA)
The RV-RA pressure gradient is measured using the maximum velocity of the tricuspid regurgitation jet.

The maximum velocity measured as the peak regurgitation (systolic) is converted to pressure with Bernouilli law:

P = 4 V2

The maximum velocity of the tricuspid regurgitation can be measured from the parasternal short axis view or from the apical 4 chamber view. It is crucial to get a good envelope of the regurgitant jet, which means that the measurement is accurate.





Estimation of right atrium (RA) pressure
In patients with central venous lines, the RA pressure is easily measured: it is the central venous pressure (CVP).

In spontaneously breathing patients, the RA pressure is estimated from the measurement of the IVC size and collapsibility index:

(maximum diameter - minimum diameter) / maximum diameter.


Example
Apical 4 chamber view, color Doppler on tricuspid valve. Visualization of trace tricuspid regurgitation





Apical 4 chamber view, CW-Doppler aligned on tricuspid regurgitation. Measurement of maximum velocity: 228 cm/sec, translated into maximum pressure gradient between RV and RA: 21mmHg.






Subcostal view, Mmode on IVC. Measurement of maximum and minimum diameter.

--> Collapsibility index = (25.4-23.7)/23.7 = 7 %

--> RA pressure estimated at 20mmHg

Result: RVSP = 21 + 20 = 41 mmHg

Reference
Evaluation of size and dynamics of the inferior vena cava as an index of right-sided cardiac function. Moreno F.L., Hagan A.D., Holmen J.R., Pryor T.A., Strickland R.D., Castle C.H. Am J Cardiol (1984) 53 : pp 579-585

[PPM]ICD leads

3793316-7_20101012_CR_1001_1001

http://www.washingtonhra.com/22.html

[Abd CT]定位pancreas

1.[Splenic vein]
Splenic vein就在pancreas後面，有時候十分粗大。
Splenic vein在胰臟的neck背面和sMV匯合成portal vein。
2.[周邊]
pancreas的head緊靠12指腸環內側。
(pancreas的uncinate process可摺到SMV後方。)
pancreas的body位於SMA和SMV之前，並在胃部的後面通過。
pancreas的tail在splenic hilum附近。