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<channel>
	<title>Heart pearls! &#187; Dr Jayachandran Thejus MD</title>
	<atom:link href="http://www.heartpearls.com/author/admin/feed" rel="self" type="application/rss+xml" />
	<link>http://www.heartpearls.com</link>
	<description>For all cardiology enthusiasts! Bonjour! Click on the title above to go to site index so that you can browse the articles!</description>
	<lastBuildDate>Sun, 05 Feb 2012 16:42:30 +0000</lastBuildDate>
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		<item>
		<title>Levosimendan</title>
		<link>http://www.heartpearls.com/2012/02/levosimendan.html</link>
		<comments>http://www.heartpearls.com/2012/02/levosimendan.html#comments</comments>
		<pubDate>Thu, 02 Feb 2012 04:10:50 +0000</pubDate>
		<dc:creator>Dr Jayachandran Thejus MD</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://www.heartpearls.com/2012/02/levosimendan.html</guid>
		<description><![CDATA[Mechanism of action Calcium sensitizer- sensitizes myocardium to calcium Drug binds to troponin C- this stabilizes calcium induced change in tropomyosin- hence actin-myosin crossbridge formation is facilitated and prolonged Contractile apparatus is sensitized to available calcium Since calcium is not increased (unlike other inotropes)- Myocardial oxygen demand is not increased No increase in arrhythmias No [...]]]></description>
			<content:encoded><![CDATA[<ul>
<li>
<div>Mechanism of action
</div>
<ul>
<li>
<div>Calcium sensitizer- sensitizes myocardium to calcium
</div>
<ul>
<li>Drug binds to troponin C- this stabilizes calcium induced change in tropomyosin- hence actin-myosin crossbridge formation is facilitated and prolonged
</li>
<li>Contractile apparatus is sensitized to available calcium
</li>
<li>
<div>Since calcium is not increased (unlike other inotropes)-
</div>
<ul>
<li>Myocardial oxygen demand is not increased
</li>
<li>No increase in arrhythmias
</li>
</ul>
</li>
<li>No binding to troponin C during diastole when calcium level is low (binding to troponin C is dependent on calcium levels)- hence no diastolic dysfunction
</li>
</ul>
</li>
<li>
<div>Vasodilation
</div>
<ul>
<li>Decreases preload and afterload
</li>
<li>Increases coronary perfusion
</li>
<li>Chance of hypotension
</li>
</ul>
</li>
</ul>
</li>
<li>
<div>Advantages as an inotrope
</div>
<ul>
<li>No tachyphylaxis
</li>
<li>No arrhythmia risk
</li>
<li>Not antagonized by beta blockers
</li>
</ul>
</li>
<li>
<div>Studies
</div>
<ul>
<li>
<div>LIDO study
</div>
<ul>
<li>Compared levosimendan with dobutamine in heart failure
</li>
<li>Hemodynamic improvement was more with levosimendan
</li>
<li>Mortality was lower with levosimendan
</li>
</ul>
</li>
<li>
<div>RUSSLAN study
</div>
<ul>
<li>Compared levosimendan with placebo in post MI heart failure
</li>
<li>Levosimendan decreased mortality and worsening of heart failure
</li>
</ul>
</li>
</ul>
</li>
<li>
<div>Adverse effects
</div>
<ul>
<li>Hypotension
</li>
<li>Headache
</li>
</ul>
</li>
<li>
<div>Available product
</div>
<ul>
<li>Injection: 2.5 mg/mL (5 mL, 10 mL)
</li>
</ul>
</li>
<li>
<div>Dosage
</div>
<ul>
<li>6-24 mcg/kg over 10 minutes followed by a continuous infusion of 0.05-0.2 mcg/kg/minute, adjusted according to response.</li>
</ul>
</li>
</ul>
]]></content:encoded>
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		</item>
		<item>
		<title>Coronary guides</title>
		<link>http://www.heartpearls.com/2012/01/coronary-guides.html</link>
		<comments>http://www.heartpearls.com/2012/01/coronary-guides.html#comments</comments>
		<pubDate>Mon, 30 Jan 2012 19:43:38 +0000</pubDate>
		<dc:creator>Dr Jayachandran Thejus MD</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://www.heartpearls.com/2012/01/coronary-guides.html</guid>
		<description><![CDATA[Nged3chap3 General overview How to select guide? Size of ascending aorta Location of ostium Tortuosity proximal to target Calcification proximal to target Lesion characteristics Guide support Passive Due to design of guide Two components- Backup from opposite aortic wall Stiffness Active By operator manipulation Two components Making the guide conform to aortic root Deep engagement [...]]]></description>
			<content:encoded><![CDATA[<p><span style="font-size:8pt"><em>Nged3chap3<br />
</em></span></p>
<p>General overview
</p>
<ul>
<li>
<div>How to select guide?
</div>
<ul>
<li>Size of ascending aorta
</li>
<li>Location of ostium
</li>
<li>Tortuosity proximal to target
</li>
<li>Calcification proximal to target
</li>
<li>Lesion characteristics
</li>
</ul>
</li>
<li>
<div>Guide support
</div>
<ul>
<li>
<div>Passive
</div>
<ul>
<li>Due to design of guide
</li>
<li>
<div>Two components-
</div>
<ul>
<li>Backup from opposite aortic wall
</li>
<li>Stiffness
</li>
</ul>
</li>
</ul>
</li>
<li>
<div>Active
</div>
<ul>
<li>By operator manipulation
</li>
<li>
<div>Two components
</div>
<ul>
<li>Making the guide conform to aortic root
</li>
<li>Deep engagement
</li>
</ul>
</li>
</ul>
</li>
</ul>
</li>
<li>
<div>JL guide
</div>
<ul>
<li>
<div>Curves
</div>
<ul>
<li>Primary- 90 deg
</li>
<li>Secondary- 180 deg
</li>
<li>Tertiary- 35 deg
</li>
</ul>
</li>
<li>Engages LM easily
</li>
<li>Coaxial alignment is difficult due to 90 deg primary curve
</li>
<li>Often, support for PCI is inadequate
</li>
</ul>
</li>
<li>
<div>Amplatz guide
</div>
<ul>
<li>
<div>Secondary curve rests against
</div>
<ul>
<li>AL- non-coronary posterior cusp
</li>
<li>AR- left cusp
</li>
</ul>
</li>
<li>Good support for PCI
</li>
<li>
<div>Used for
</div>
<ul>
<li>Short LM
</li>
<li>Superior takeoff
</li>
<li>Downgoing LCx
</li>
<li>Downgoing RCA
</li>
</ul>
</li>
<li>Chance of ostial dissection due to downward tip
</li>
</ul>
</li>
<li>
<div>Multipurpose guide
</div>
<ul>
<li>Single minor bend at tip
</li>
<li>
<div>Uses-
</div>
<ul>
<li>High LM takeoff
</li>
<li>Downward RCA
</li>
</ul>
</li>
</ul>
</li>
<li>
<div>EBU-
</div>
<ul>
<li>Long secondary curve abuts opposite aortic wall- very good support
</li>
<li>Long tip forms straight line with coronary
</li>
</ul>
</li>
</ul>
<p>Guide manipulations
</p>
<ul>
<li>
<div>Standard safety techniques
</div>
<ul>
<li>
<div>After putting Y adapter-
</div>
<ul>
<li>First bleed back generously
</li>
<li>Then flush
</li>
<li>Then look for bubbles
</li>
</ul>
</li>
<li>
<div>During procedure
</div>
<ul>
<li>Frequently flush
</li>
<li>Always look for dampening
</li>
</ul>
</li>
<li>
<div>During injection    
</div>
<ul>
<li>Keep syringe pointed down, so air will not go in
</li>
<li>Always look for reflux
</li>
</ul>
</li>
<li>
<div>When withdrawing balloon/ stent/ TEC
</div>
<ul>
<li>Watch tip, especially if proximal plaque
</li>
<li>Look for dampening
</li>
</ul>
</li>
</ul>
</li>
<li>
<div>Tortuous iliac artery
</div>
<ul>
<li>
<div>If torque is not transmitting
</div>
<ul>
<li>Wait for torque to transmit
</li>
<li>Gently move guide in and out for a very short distance
</li>
</ul>
</li>
<li>Put long sheath (23 cm)
</li>
<li>Manipulate with 038 long J through Y adapter
</li>
</ul>
</li>
<li>
<div>Dampening of arterial pressure
</div>
<ul>
<li>Ventricularization- diastolic BP drop
</li>
<li>Dampening- systolic and diastolic BP drop
</li>
<li>
<div>Causes-
</div>
<ul>
<li>Ostial lesion- most common
</li>
<li>Coronary spasm
</li>
<li>
<div>Guide is too big for artery
</div>
<ul>
<li>Downsize guide or
</li>
<li>Put guide with side holes
</li>
</ul>
</li>
<li>Non- coaxial alignment
</li>
<li>
<div>Guide is deep in
</div>
<ul>
<li>Make guide out or
</li>
<li>Push in balloon/ stent/ TEC
</li>
</ul>
</li>
</ul>
</li>
<li>
<div>Guide with side holes
</div>
<ul>
<li>Suboptimal opacification
</li>
<li>More contrast needed
</li>
<li>Decreased backup from aortic root (rare)
</li>
<li>Kinking at sideholes (rare)
</li>
</ul>
</li>
</ul>
</li>
<li>
<div>Checking backup potential
</div>
<ul>
<li>
<div>Advance guide a bit
</div>
<ul>
<li>Further intubation- good backup
</li>
<li>Prolapsing out- poor backup
</li>
</ul>
</li>
</ul>
</li>
<li>
<div>Active intubation
</div>
<ul>
<li>Other names- active support, power position
</li>
<li>
<div>Do only if
</div>
<ul>
<li>Large artery
</li>
<li>No proximal lesion
</li>
</ul>
</li>
<li>Do only if coaxial alignment is not possible
</li>
<li>Chance of proximal dissection or thrombosis is high
</li>
<li>Osteoproximal stent placement may not be possible
</li>
</ul>
</li>
</ul>
<p>Judkins guide
</p>
<ul>
<li>
<div>JL
</div>
<ul>
<li>Size is cm between primary and secondary curves
</li>
<li>3.5 cm for Asians, 4 cm for Caucasians
</li>
<li>Enter by gentle counterclockwise rotation
</li>
<li>
<div>Size is determined by
</div>
<ul>
<li>Size of aortic root- lower size for smaller root and vice versa
</li>
<li>Direction of LAD- lower size for superiorly directed LAD
</li>
</ul>
</li>
<li>Smaller sized JL will point to superior wall and dissect here with injection, especially in elderly with unsuspected plaques
</li>
<li>Tip should point up. If it points down, the guide is too large.
</li>
<li>Small JL will double back
</li>
</ul>
</li>
<li>
<div>JR
</div>
<ul>
<li>Rotate clockwise while withdrawing to engage
</li>
<li>Check in RAO 30 deg- tip will be a head-on ring if coaxial
</li>
</ul>
</li>
</ul>
<p>Amplatz guide
</p>
<ul>
<li>
<div>Sizes
</div>
<ul>
<li>1- small root
</li>
<li>2- normal root
</li>
<li>3- large root
</li>
</ul>
</li>
<li>
<div>Relation between guide tip and ostium
</div>
<ul>
<li>Tip above ostium- larger than needed sized guide
</li>
<li>Tip into ostium- correct size
</li>
<li>Tip below ostium- lesser than needed size
</li>
<li>If size is not correct, do not attempt forceful engagement
</li>
</ul>
</li>
<li>If RCA ostium is very high, AL may be used
</li>
<li>
<div>Engaging-
</div>
<ul>
<li>Keep wire till guide reaches sinus
</li>
<li>Advance guide to reach ostium level
</li>
<li>For AL- rotate counter clockwise
</li>
<li>Then retract to engage
</li>
</ul>
</li>
<li>Optimal position- closed loop
</li>
<li>Undesirable position- open loop with tip pointing down inferior wall of ostium
</li>
<li>
<div>Disengagement
</div>
<ul>
<li>Be very careful
</li>
<li>Simple withdrawal is never to be done- tip advances further- dissection
</li>
<li>Advance guide to prolapsed out of ostium
</li>
<li>Then rotate guide to go away from coronary area
</li>
<li>Then withdraw
</li>
<li>Less likely to cause damage if retracted over a wire
</li>
</ul>
</li>
<li>
<div>Removing balloon
</div>
<ul>
<li>1<sup>st</sup> option- while pulling out balloon, simultaneously push the guide  to prolapsed it out, all the time watching fluoro
</li>
<li>2<sup>nd</sup> option- push balloon- guide goes back- pull balloon slowly watching whether guide comes in- if so, push balloon again- repeat this again and again
</li>
</ul>
</li>
</ul>
<p>Multipurpose guide    
</p>
<ul>
<li>
<div>For engaging left
</div>
<ul>
<li>30 deg RAO
</li>
<li>Place in posterior sinus
</li>
<li>Tip pointed to spine
</li>
<li>Advance till guide buckles
</li>
<li>Rotate clockwise
</li>
<li>Now guide enters left cusp
</li>
<li>Counter clockwise rotation to enter LAD
</li>
</ul>
</li>
<li>
<div>For engaging right
</div>
<ul>
<li>45 deg RAO
</li>
<li>Place in left cusp
</li>
<li>Tip pointed to anterior and right
</li>
<li>Rotate clockwise and slightly withdraw
</li>
</ul>
</li>
</ul>
<p>EBU
</p>
<ul>
<li>Keep wire till guide goes into sinus
</li>
</ul>
<p>
 </p>
<p>Diagnostic catheter for LM lesions
</p>
<ul>
<li>
<div>Suspect LM lesion when
</div>
<ul>
<li>Rest angina
</li>
<li>Angina at low level of activity
</li>
<li>Post prandial angina
</li>
<li>Angina at early stage of TMT
</li>
<li>Diffuse ST depression in TMT
</li>
<li>During TMT, BP does not increase or decreases
</li>
</ul>
</li>
<li>
<div>Tips
</div>
<ul>
<li>Use short tip JL
</li>
<li>Keep below ostium and inject 10 cc contrast
</li>
<li>Then slowly engage avoiding uncontrolled jump into LM
</li>
<li>Inject only if no ventricularization or damping
</li>
<li>Inject only 2 to 3 cc
</li>
<li>Only AP cranial and AP caudal views are needed for surgeon
</li>
<li>Do not hit and run- catheter tip may be under a plaque- dissection may occur
</li>
</ul>
</li>
</ul>
<p>Guide for LAD lesions
</p>
<ul>
<li>JL is a good option as it points superiorly
</li>
</ul>
<p>Guide for LCx lesions
</p>
<ul>
<li>Short LM and no acute angle of LCx origin- select JL.
</li>
<li>Long LM or acute angle of LCx origin- select EBU.  JL is not a good option as it points superiorly
</li>
<li>
<div>If JL is not hooking well
</div>
<ul>
<li>Rotate clockwise
</li>
<li>Select larger size
</li>
</ul>
</li>
<li>AL is also a good option.
</li>
<li>
<div>Power position for JL-
</div>
<ul>
<li>Better than this will be EBU or AL.
</li>
<li>Do over stent or balloon
</li>
<li>Gently push guide with gentle clockwise torque till whole curve sits well in left sinus.
</li>
<li>Now guide looks like AL.
</li>
<li>After purpose, remove by opposite torque and withdrawal
</li>
<li>Do only if no proximal or ostial disease
</li>
</ul>
</li>
</ul>
<p>Guide for RCA lesions
</p>
<ul>
<li>
<div>Takeoff
</div>
<ul>
<li>Horizontal- usual one
</li>
<li>Upward looking- shepherd&#8217;s crook
</li>
<li>Downward looking
</li>
</ul>
</li>
<li>
<div>Horizontal
</div>
<ul>
<li>First choice- JR, usually 4
</li>
<li>Second choice- AR
</li>
<li>Third choice- AL (with backup from opposite aortic wall)
</li>
</ul>
</li>
<li>
<div>Upward looking
</div>
<ul>
<li>AL
</li>
<li>Other choices- hockey stick, IMA guide, left venous bypass guide
</li>
<li>(JR will not give enough backup)
</li>
</ul>
</li>
<li>
<div>Downward looking
</div>
<ul>
<li>AR
</li>
<li>Multipurpose
</li>
<li>Right venous bypass
</li>
<li>(JR may dissect lateral wall)
</li>
</ul>
</li>
<li>
<div>Guide entering conus repeatedly
</div>
<ul>
<li>Engage by counterclockwise rotation
</li>
<li>Change over to higher sized guide
</li>
</ul>
</li>
<li>
<div>Deep seating RCA guide
</div>
<ul>
<li>Do not do if artery is small or if there is a proximal plaque.
</li>
<li>In LAO view, additional clockwise rotation will deep seat the guide
</li>
<li>If balloon or stent is in the coronary, the guide may be deep seated with gentle clockwise rotation. After purpose is served, guide should be withdrawn with counterclockwise rotation.
</li>
<li>When balloon or stent is advanced, assistant should hold the guide firmly near the femoral sheath
</li>
<li>When balloon or stent is advanced, assistant should pull back wire slowly to decrease friction between wire and balloon/stent.
</li>
</ul>
</li>
<li>
<div>Rotational Amplatz maneuver
</div>
<ul>
<li>JR guide is pushed with counterclockwise rotation- it forms a loop resting in the coronary sinus- looks like Amplatz
</li>
<li>Gives backup from opposite aortic wall
</li>
<li>Excessive push may prolapse guide into LV
</li>
<li>Do only with 6F or 5F- higher sized guides will prolapse into LV
</li>
<li>Like any power position, do not do if there is ostial lesion
</li>
</ul>
</li>
<li>
<div>Guide for aortic aneurysm and dissections
</div>
<ul>
<li>
<div>Aortic aneurysm
</div>
<ul>
<li>Guide may not seat well
</li>
<li>Guide may not be long enough
</li>
</ul>
</li>
<li>
<div>Aortic dissection
</div>
<ul>
<li>Guide may enter false lumen
</li>
<li>Guide may extend dissection
</li>
<li>Guide may perforate aortic wall, especially with injection
</li>
<li>Guide may dislodge thrombus distally
</li>
</ul>
</li>
<li>If there is BP difference between arms, use radial route in arm with higher BP
</li>
<li>If thoracoabdominal aorta is dissected or aneurismal, choose radial route
</li>
<li>If arch vessels are affected, choose femoral route
</li>
<li>If entire aorta is aneurismal, choose femoral route for better catheter manipulation
</li>
<li>Straight soft tipped catheters like Sones or Multipurpose are safer
</li>
<li>To make sure that catheter is in true lumen- enter LV or  cannulate coronaries
</li>
<li>Ascending aortogram- LAO view- 60 cc contrast at 25 to 40 cc/sec
</li>
<li>
<div>Never do ascending aortogram unless it is absolutely certain that guide is in true lumen
</div>
<ul>
<li>No delay in contrast washout
</li>
<li>No contrast swirling
</li>
<li>No dampening of pressures
</li>
<li>Brisk return of blood
</li>
</ul>
</li>
</ul>
</li>
</ul>
]]></content:encoded>
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		</item>
		<item>
		<title>Interpolated VPCs</title>
		<link>http://www.heartpearls.com/2012/01/interpolated-vpcs.html</link>
		<comments>http://www.heartpearls.com/2012/01/interpolated-vpcs.html#comments</comments>
		<pubDate>Tue, 24 Jan 2012 08:04:49 +0000</pubDate>
		<dc:creator>Dr Jayachandran Thejus MD</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://www.heartpearls.com/2012/01/interpolated-vpcs.html</guid>
		<description><![CDATA[]]></description>
			<content:encoded><![CDATA[<p><img src="http://www.heartpearls.com/wp-content/uploads/2012/01/012412_0804_Interpolate1.png" alt=""/></p>
]]></content:encoded>
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		</item>
		<item>
		<title>Atrial ectopic bigeminy</title>
		<link>http://www.heartpearls.com/2012/01/atrial-ectopic-bigeminy.html</link>
		<comments>http://www.heartpearls.com/2012/01/atrial-ectopic-bigeminy.html#comments</comments>
		<pubDate>Sat, 14 Jan 2012 04:53:02 +0000</pubDate>
		<dc:creator>Dr Jayachandran Thejus MD</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://www.heartpearls.com/2012/01/atrial-ectopic-bigeminy.html</guid>
		<description><![CDATA[    Bigeminal rhythm due to alternate atrial ectopic beats originating probably from near the AV node. Your thoughts are welcome.]]></description>
			<content:encoded><![CDATA[<p><img src="http://www.heartpearls.com/wp-content/uploads/2012/01/011412_0452_Atrialectop1.png" alt=""/>
	</p>
<p>
 </p>
<p>
 </p>
<p>Bigeminal rhythm due to alternate atrial ectopic beats originating probably from near the AV node.
</p>
<p>Your thoughts are welcome.</p>
]]></content:encoded>
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		</item>
		<item>
		<title>Courage and atheism</title>
		<link>http://www.heartpearls.com/2012/01/courage-and-atheism.html</link>
		<comments>http://www.heartpearls.com/2012/01/courage-and-atheism.html#comments</comments>
		<pubDate>Mon, 09 Jan 2012 15:14:57 +0000</pubDate>
		<dc:creator>Dr Jayachandran Thejus MD</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://www.heartpearls.com/2012/01/courage-and-atheism.html</guid>
		<description><![CDATA[Most atheists become theists when some tough situations surface in life- like impending death, a diagnosis of cancer etc. Indeed, during these times theists have more mental peace as they believe that life is not going to end and that their consciousness is not lost- they will be united with God, they will be reborn [...]]]></description>
			<content:encoded><![CDATA[<p>Most atheists become theists when some tough situations surface in life- like impending death, a diagnosis of cancer etc. Indeed, during these times theists have more mental peace as they believe that life is not going to end and that their consciousness is not lost- they will be united with God, they will be reborn etc. But for an atheist, death is the end of the beautiful journey called life. So he dreads death. Only the most mentally strong atheist can face death without converting to delusions of afterbirth, heaven etc. One shining example is Carl Sagan. Hats off to you Carl!</p>
]]></content:encoded>
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		</item>
		<item>
		<title>Pulse</title>
		<link>http://www.heartpearls.com/2011/12/pulse.html</link>
		<comments>http://www.heartpearls.com/2011/12/pulse.html#comments</comments>
		<pubDate>Thu, 15 Dec 2011 17:13:12 +0000</pubDate>
		<dc:creator>Dr Jayachandran Thejus MD</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://www.heartpearls.com/2011/12/pulse.html</guid>
		<description><![CDATA[Definition Waveform Carotids- Percussion wave due to LV ejection, then tidal wave which is a reflected wave from the periphery Radials- single sharp peaked wave Rate Rhythm Character Pulsus bisferiens Two systolic waves (percussion and tidal) Causes Severe AR AS with AR when AR is the predominant lesion HOCM- Often recorded, not palpated Dip is [...]]]></description>
			<content:encoded><![CDATA[<p>Definition
</p>
<p>Waveform
</p>
<ul>
<li>Carotids- Percussion wave due to LV ejection, then tidal wave which is a reflected wave from the periphery
</li>
<li>Radials- single sharp peaked wave
</li>
</ul>
<p>Rate
</p>
<p>Rhythm
</p>
<p>Character
</p>
<ul>
<li>
<div>Pulsus bisferiens
</div>
<ul style="margin-left: 72pt">
<li>Two systolic waves (percussion and tidal)
</li>
</ul>
<ul>
<li>
<div>Causes
</div>
<ul>
<li>Severe AR
</li>
<li>AS with AR when AR is the predominant lesion
</li>
<li>
<div>HOCM-
</div>
<ul>
<li>Often recorded, not palpated
</li>
<li>Dip is due to LVOT obstruction, second wave is tidal wave
</li>
<li>Can be precipitated by Valsalva maneuver and amyl nitrite
</li>
</ul>
</li>
<li>Large PDA
</li>
<li>AV fistula
</li>
<li>MVP- uncommon
</li>
</ul>
</li>
<li>
<div>Mechanism-
</div>
<ul>
<li>Large LV stroke volume rapidly ejected
</li>
</ul>
</li>
</ul>
</li>
<li>
<div>Dicrotic pulse
</div>
<ul style="margin-left: 72pt">
<li>A diastolic wave called dicrotic wave also after the normal systolic wave
</li>
<li>Difficult to distinguish from pulsus bisferiens at bedside
</li>
</ul>
<ul>
<li>
<div>Causes
</div>
<ul>
<li>Fever
</li>
<li>Heart failure
</li>
<li>Hypovolemic shock
</li>
<li>Cardiac tamponade
</li>
<li>Immediately after aortic valve replacement
</li>
<li>After exercise
</li>
</ul>
</li>
</ul>
</li>
<li>
<div>Waterhammer pulse or Corrigan pulse
</div>
<ul>
<li>Rapid upstroke, ill sustained peak, rapid downstroke
</li>
<li>Raise arm and feel
</li>
<li>Due to rapid ejection of large stroke volume and low systemic vascular resistance
</li>
<li>Seen in chronic severe AR
</li>
</ul>
</li>
<li>
<div>Pulse in severe AS
</div>
<ul>
<li>
<div>Anacrotic pulse
</div>
<ul>
<li>Anacrotic notch immediately after onset of upstroke
</li>
</ul>
</li>
<li>
<div>Pulsus parvus et tardus
</div>
<ul>
<li>Parvus refers to low volume
</li>
<li>Tardus refers to slow upstroke and delayed peak- peak is closer to S2 (normal pulse- closer to S1)
</li>
</ul>
</li>
<li>
<div>Carotid shudder
</div>
<ul>
<li>Thrill on ascending limb
</li>
</ul>
</li>
<li>Above findings may be absent in atherosclerotic carotids.
</li>
</ul>
</li>
</ul>
<p>Volume
</p>
<ul>
<li>High volume
</li>
<li>Low volume
</li>
<li>
<div>Pulsus alternans
</div>
<ul>
<li>Also called mechanical alternans
</li>
<li>Apply light pressure on a peripheral pulse
</li>
<li>Can be confirmed by BP measurement
</li>
<li>Alternate beats are strong and weak, rhythm is normal
</li>
<li>
<div>Causes
</div>
<ul>
<li>LV systolic failure
</li>
<li>Cardiac tamponade- rare
</li>
<li>Tachypnoea with respiratory rate half of pulse rate- rare
</li>
</ul>
</li>
<li>
<div>Mechanism
</div>
<ul>
<li>Alternating preload (Frank Starling mechanism)
</li>
<li>Incomplete relaxation
</li>
<li>Alternating afterload
</li>
<li>Alternating contractility- due to change in sarcoplasmic calcium pumps
</li>
</ul>
</li>
</ul>
</li>
<li>
<div>Pulsus paradoxus
</div>
<ul>
<li>Normal inspiratory fall is 8 to 12 mm Hg
</li>
<li>More than 20 mm Hg defines pulsus paradoxus
</li>
<li>Better appreciated with BP measurement
</li>
<li>Measure during normal respiration- not Valsalva
</li>
<li>
<div>Common causes-
</div>
<ul>
<li>Cardiac tamponade
</li>
<li>COPD
</li>
<li>Hypovolemic shock
</li>
</ul>
</li>
<li>
<div>Uncommon causes-
</div>
<ul>
<li>Constrictive pericarditis
</li>
<li>Restrictive cardiomyopathy
</li>
<li>Pulmonary embolism
</li>
<li>Pregnancy
</li>
<li>Marked obesity
</li>
<li>Partial SVC obstruction
</li>
</ul>
</li>
<li>
<div>Cardiac tamponade, but no pulsus paradoxus-
</div>
<ul>
<li>Severe AR
</li>
<li>ASD
</li>
</ul>
</li>
<li>
<div>Mechanism
</div>
<ul>
<li>Cardiac tamponade- Reverse Bernheim effect- venous return during inspiration shifts IVS to left- decreased LVEDV
</li>
<li>COPD- during exaggerated inspiratory effort, pulmonary venous return to left side of heart decreases
</li>
</ul>
</li>
<li>Reversed pulsus paradoxus- HOCM
</li>
</ul>
</li>
</ul>
<p>Condition of vessel wall
</p>
<p>Peripheral pulses
</p>
<ul>
<li>
<div>Decreased volume of a peripheral pulse may be due to
</div>
<ul>
<li>Atherosclerosis
</li>
<li>Embolism
</li>
<li>Takayasu arteritis
</li>
<li>Aortic dissection
</li>
<li>Aortic aneurysm
</li>
<li>Coarctation of aorta
</li>
<li>Supravalvular aortic stenosis (Coanda effect- selective streaming to right- right carotid and upper limb pulses are stronger)
</li>
<li>Cervical rib
</li>
</ul>
</li>
</ul>
<p>Radiofemoral delay
</p>
<ul>
<li>Coarctation of aorta
</li>
</ul>
<p>Radioradial delay
</p>
<ul>
<li>Takayasu arteritis
</li>
<li>Aortic dissection
</li>
<li>Aortic aneurysm
</li>
<li>Coarctation of aorta
</li>
<li>Supravalvular aortic stenosis (Coanda effect- selective streaming to right- right carotid and upper limb pulses are stronger)
</li>
<li>Cervical rib</li>
</ul>
]]></content:encoded>
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		</item>
		<item>
		<title>Pheochromocytoma</title>
		<link>http://www.heartpearls.com/2011/11/pheochromocytoma.html</link>
		<comments>http://www.heartpearls.com/2011/11/pheochromocytoma.html#comments</comments>
		<pubDate>Sun, 20 Nov 2011 04:55:57 +0000</pubDate>
		<dc:creator>Dr Jayachandran Thejus MD</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://www.heartpearls.com/2011/11/pheochromocytoma.html</guid>
		<description><![CDATA[Introduction Tumor of chromaffin cells of adrenal medulla Some also include catecholamine secreting paragangliomas Epidemiology &#60; 0.2 % of hypertensives have pheochromocytoma Most common in 4th and 5th decades, but may occur at any age Equal incidence in both sexes Clinical features Classic triad Episodic headache Sweating Tachycardia Hypertension Sustained or paroxysmal Absent in 5 [...]]]></description>
			<content:encoded><![CDATA[<p>Introduction
</p>
<ul>
<li>Tumor of chromaffin cells of adrenal medulla
</li>
<li>Some also include catecholamine secreting paragangliomas
</li>
</ul>
<p>Epidemiology
</p>
<ul>
<li>&lt; 0.2 % of hypertensives have pheochromocytoma
</li>
<li>Most common in 4<sup>th</sup> and 5<sup>th</sup> decades, but may occur at any age
</li>
<li>Equal incidence in both sexes
</li>
</ul>
<p>Clinical features
</p>
<ul>
<li>
<div>Classic triad
</div>
<ul>
<li>Episodic headache
</li>
<li>Sweating
</li>
<li>Tachycardia
</li>
</ul>
</li>
<li>
<div>Hypertension
</div>
<ul>
<li>Sustained or paroxysmal
</li>
<li>Absent in 5 to 10 %
</li>
<li>Orthostatic hypotension may occur
</li>
</ul>
</li>
<li>
<div>Other features
</div>
<ul>
<li>Palpitations
</li>
<li>Dyspnoea
</li>
<li>Weakness, weight loss
</li>
<li>Panic attacks
</li>
<li>Visual blurring, papilledema
</li>
<li>Polyuria, polydipsia, constipation
</li>
</ul>
</li>
<li>Cardiomyopathy due to cathecholamine excess
</li>
<li>Raised ESR, hyperglycemia, leucocytosis
</li>
<li>Secondary erythrocytosis due to increased erythropoietin
</li>
</ul>
]]></content:encoded>
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		</item>
		<item>
		<title>Hypertension</title>
		<link>http://www.heartpearls.com/2011/11/hypertension.html</link>
		<comments>http://www.heartpearls.com/2011/11/hypertension.html#comments</comments>
		<pubDate>Sat, 19 Nov 2011 14:26:57 +0000</pubDate>
		<dc:creator>Dr Jayachandran Thejus MD</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://www.heartpearls.com/2011/11/hypertension.html</guid>
		<description><![CDATA[Epidemiology Diseases caused by hypertension- Myocardial infarction Heart failure Atrial fibrillation Aortic dissection Peripheral vascular disease Stroke Hypertension is defined as BP of 140/90 mm Hg or above Hypertension is primary in 90 to 95% (rest- secondary) Behaviours which increase risk of hypertension Smoking Heavy drinking (3 drinks daily- one drink is 13.7 gm or [...]]]></description>
			<content:encoded><![CDATA[<p>Epidemiology
</p>
<ul>
<li>
<div>Diseases caused by hypertension-
</div>
<ul>
<li>Myocardial infarction
</li>
<li>Heart failure
</li>
<li>Atrial fibrillation
</li>
<li>Aortic dissection
</li>
<li>Peripheral vascular disease
</li>
<li>Stroke
</li>
</ul>
</li>
<li>
<div>Hypertension is defined as BP of
</div>
<ul>
<li>140/90 mm Hg or above
</li>
</ul>
</li>
<li>
<div>Hypertension is primary in
</div>
<ul>
<li>90 to 95% (rest- secondary)
</li>
</ul>
</li>
<li>
<div>Behaviours which increase risk of hypertension
</div>
<ul>
<li>Smoking
</li>
<li>Heavy drinking (3 drinks daily- one drink is 13.7 gm or 0.6 ounce of pure alcohol) (1 to 2 drinks decrease BP)
</li>
<li>Caffeine
</li>
<li>Obesity
</li>
<li>Excess calorie intake
</li>
<li>Excess sodium intake (potassium decreases BP)
</li>
<li>Physical inactivity
</li>
<li>Low intake of fresh fruits
</li>
</ul>
</li>
</ul>
<p>Mechanism of primary hypertension
</p>
<ul>
<li>
<div>Hemodynamic subsets of primary hypertension
</div>
<ul>
<li>
<div>Systolic hypertension in young adults
</div>
<ul>
<li>17 to 25 yrs
</li>
<li>Mechanism- sympathetic overactivity leading to increased cardiac output and stiffening of aorta
</li>
</ul>
</li>
<li>
<div>Diastolic hypertension in middle age
</div>
<ul>
<li>30 to 50 yrs
</li>
<li>Mechanism- elevated systemic vascular resistance due to vasoconstriction of resistance arterioles
</li>
</ul>
</li>
<li>
<div>Isolated systolic hypertension in older adults
</div>
<ul>
<li>&gt; 55 yrs
</li>
<li>Systolic BP increases with age. Diastolic BP increases till 55 yrs and then falls. Pulse pressure widens.
</li>
<li>Mechanism- aortic stiffening due to increased collagen- elastin ratio.
</li>
<li>More in women
</li>
</ul>
</li>
</ul>
</li>
<li>
<div>Neural mechanism- sympathetic overactivity
</div>
<ul>
<li>
<div>Seen in-
</div>
<ul>
<li>Systolic hypertension in young adults
</li>
<li>HT due to obesity (sympathetic stimulation to burn fat)
</li>
<li>HT due to sleep apnoea (daytime normoxia is misinterpreted as hypoxia, due to baroreceptor resetting, leading to sympathetic stimulation)
</li>
<li>HT with diabetes
</li>
<li>HT with CKD
</li>
<li>HT with heart failure
</li>
<li>HT due to cyclosporine
</li>
</ul>
</li>
<li>
<div>Mechanisms by which sympathetic overactivity contributes to hypertension-
</div>
<ul>
<li>Increased cardiac output
</li>
<li>Alpha mediated peripheral vasoconstriction
</li>
<li>Increased renin (beta 1 stimulation of juxtaglomerular apparatus)
</li>
<li>Renal sodium retention (alpha 1 stimulation of Na K ATP ase of collecting duct)
</li>
</ul>
</li>
<li>
<div>Adverse effects of sympathetic overactivity-
</div>
<ul>
<li>Norepinephrine causes alpha 1 mediated hypertrophy of myocardium leading to sudden cardiac death
</li>
</ul>
</li>
<li>
<div>Practical applications-
</div>
<ul>
<li>Carotid baroreceptor pacemaker
</li>
<li>Radiofrequency ablation of renal sympathetic nerves
</li>
</ul>
</li>
<li>
<div>Baroreceptors
</div>
<ul>
<li>In every hypertensive patient, baroreceptors are reset to higher BP.
</li>
<li>Baroreceptor control of sinus node is impaired in HT.
</li>
<li>
<div>Baroreflex failure-
</div>
<ul>
<li>
<div>Complete
</div>
<ul>
<li>Due to radiation for throat cancer
</li>
<li>Causes labile HT
</li>
</ul>
</li>
<li>
<div>Partial
</div>
<ul>
<li>Common in elderly hypertensives
</li>
<li>
<div>Triad
</div>
<ul>
<li>Supine hypertension
</li>
<li>Orthostatic hypotension
</li>
<li>Symptomatic post prandial hypotension- due to splanchnic pooling after carbohydrate rich meals
</li>
</ul>
</li>
</ul>
</li>
</ul>
</li>
</ul>
</li>
</ul>
</li>
<li>Renal mechanisms
</li>
</ul>
]]></content:encoded>
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		<item>
		<title>Takotsubo cardiomyopathy</title>
		<link>http://www.heartpearls.com/2011/10/takotsubo-cardiomyopathy.html</link>
		<comments>http://www.heartpearls.com/2011/10/takotsubo-cardiomyopathy.html#comments</comments>
		<pubDate>Sat, 15 Oct 2011 19:37:59 +0000</pubDate>
		<dc:creator>Dr Jayachandran Thejus MD</dc:creator>
				<category><![CDATA[Uncategorized]]></category>
		<category><![CDATA[apical ballooning syndrome]]></category>
		<category><![CDATA[clinical features of Takotsubo]]></category>
		<category><![CDATA[ECG of Takotsubo]]></category>
		<category><![CDATA[Echocardiogram of Takotsubo]]></category>
		<category><![CDATA[pathogenesis of Takotsubo]]></category>
		<category><![CDATA[prognosis of Takotsubo]]></category>
		<category><![CDATA[Takotsubo cardiomyopathy]]></category>
		<category><![CDATA[treatment of Takotsubo]]></category>

		<guid isPermaLink="false">http://www.heartpearls.com/2011/10/takatsubo-cardiomyopathy.html</guid>
		<description><![CDATA[Other names- (Takotsubo in Japanese- octopus trap) Stress induced cardiomyopathy Apical ballooning syndrome Broken heart syndrome Definition- Transient stress induced systolic dysfunction of apical or mid LV mimicking MI, but with normal coronaries. Pathogenesis- Cathecholamine excess leading to coronary microvascular spasm or direct myocardial toxicity Clinical features- More in women (&#62; 80%) Age- 60s and [...]]]></description>
			<content:encoded><![CDATA[<ul>
<li>
<div>Other names- (Takotsubo in Japanese- octopus trap)</div>
<ul>
<li>Stress induced cardiomyopathy</li>
<li>Apical ballooning syndrome</li>
<li>Broken heart syndrome</li>
</ul>
</li>
<li>
<div>Definition-</div>
<ul>
<li>Transient stress induced systolic dysfunction of apical or mid LV mimicking MI, but with normal coronaries.</li>
</ul>
</li>
<li>
<div>Pathogenesis-</div>
<ul>
<li>Cathecholamine excess leading to coronary microvascular spasm or direct myocardial toxicity</li>
</ul>
</li>
<li>
<div>Clinical features-</div>
<ul>
<li>More in women (&gt; 80%)</li>
<li>Age- 60s and 70s (post-menopausal)</li>
<li>
<div>Triggers-</div>
<ul>
<li>Not always present</li>
<li>Acute illness/ emotional trauma/ physical stress</li>
</ul>
</li>
<li>Presents with chest pain similar to MI</li>
</ul>
</li>
<li>
<div>Complications-</div>
<ul style="margin-left: 72pt;">
<li>Heart failure, shock</li>
<li>VT, VF</li>
<li>Bradyarrhythmias</li>
<li>MR</li>
<li>LVOTO</li>
<li>Apical thrombus, stroke</li>
</ul>
</li>
<li>
<div>Investigations-</div>
<ul>
<li>
<div>ECG-</div>
<ul>
<li>ST elevation- in half cases- precordial</li>
<li>T inversion with QT prolongation</li>
<li>Q waves</li>
</ul>
</li>
<li>
<div>Troponin-</div>
<ul>
<li>elevated, but only mildly- disproportionately low for chest pain and ECG changes</li>
</ul>
</li>
<li>
<div>Echo-</div>
<ul>
<li>Apical half to 2/3<sup>rd</sup> of LV is akinetic or dyskinetic (apical ballooning)</li>
<li>Apical sparing in some cases- mid ventricular</li>
<li>Systolic dysfunction is present</li>
<li>MR</li>
<li>LVOTO</li>
<li>Apical thrombus</li>
</ul>
</li>
<li>
<div>CMR-</div>
<ul>
<li>
<div>Useful in diagnosis-</div>
<ul>
<li>Takotsubo- no delayed (Gd) enhancement</li>
<li>MI- delayed enhancement in subendocardium</li>
<li>Myocarditis- patchy delayed enhancement</li>
</ul>
</li>
<li>May pick up RV involvement and apical thrombus not visible by echo</li>
</ul>
</li>
</ul>
</li>
<li>
<div>Mayo Clinic criteria- all four needed-</div>
<ul>
<li>Transient hypokinesia/akinesia/dyskinesia of mid LV</li>
<li>No obstructive CAD</li>
<li>ST elevation/T inversion or troponin elevation</li>
<li>No pheochromocytoma or myocarditis</li>
</ul>
</li>
<li>
<div>Treatment-</div>
<ul>
<li>Treatment of heart failure- diuretics, beta blockers, ACE inhibitors, dopamine/dobutamine, IABP</li>
<li>LVOTO- beta blockers, IV fluids</li>
<li>Anticoagulation if thrombus or severe LV dysfunction</li>
</ul>
</li>
<li>
<div>Prognosis-</div>
<ul>
<li>Ventricular function normalizes in 1 to 4 weeks</li>
<li>Mortality 0 to 8%</li>
</ul>
</li>
</ul>
]]></content:encoded>
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		<item>
		<title>Takayasu arteritis- treatment</title>
		<link>http://www.heartpearls.com/2011/10/takayasu-arteritis-treatment.html</link>
		<comments>http://www.heartpearls.com/2011/10/takayasu-arteritis-treatment.html#comments</comments>
		<pubDate>Sat, 15 Oct 2011 18:55:19 +0000</pubDate>
		<dc:creator>Dr Jayachandran Thejus MD</dc:creator>
				<category><![CDATA[Uncategorized]]></category>
		<category><![CDATA[Takayasu aortoarteritis]]></category>
		<category><![CDATA[Takayasu arteritis]]></category>
		<category><![CDATA[treatment of aortoarteritis]]></category>
		<category><![CDATA[treatment of Takayasu]]></category>

		<guid isPermaLink="false">http://www.heartpearls.com/2011/10/takayasu-arteritis-treatment.html</guid>
		<description><![CDATA[Glucocorticoids- First line treatment Arrests progression of disease Prednisone 45 to 60 mg/day is started Look for response- decreased symptoms, decrease in ESR and CRP Once response- decrease dose by maximum 10% per week- watch for exacerbations Response to glucocorticoids is inadequate in half cases- add another drug Methotrexate Azathioprine Anti-TNF agents- etanercept, infliximab Revascularization- [...]]]></description>
			<content:encoded><![CDATA[<ul>
<li>
<div>Glucocorticoids-
</div>
<ul>
<li>First line treatment
</li>
<li>Arrests progression of disease
</li>
<li>Prednisone 45 to 60 mg/day is started
</li>
<li>Look for response- decreased symptoms, decrease in ESR and CRP
</li>
<li>Once response- decrease dose by maximum 10% per week- watch for exacerbations
</li>
<li>Response to glucocorticoids is inadequate in half cases- add another drug
</li>
</ul>
</li>
<li>Methotrexate
</li>
<li>Azathioprine
</li>
<li>Anti-TNF agents- etanercept, infliximab
</li>
<li>Revascularization- PTCA or bypass grafts- chance of restenosis is greater with PTCA
</li>
<li>Aortic valve replacement or repair for AR</li>
</ul>
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