February | 2012 | Dr.S.Venkatesan MD

Archive for February, 2012

Basic lessons in STEMI :Does dying myocytes release potassium into the circulation ?

Posted in cardaic physiology, cardiac physiology, cardiology -ECG, cardiology -Therapeutics, cardiology- coronary care, Cardiology-Coronary artery disese, tagged beta blockers and hyperkalemia, betablockers in stemi and hyperkalemia, ecg tall t waves hyperacute mi, electrolytes in stemi, hyperacute stemi, nernst equation animation, potassium levels in acute stemi, pottasium and stemi, resting membrane potential, why tall waves in stemi on February 10, 2012| Leave a Comment »

Human life is a bundle of energy orchestrated by ions coming in and going out of every cell . Potassium is the life sustaining ion which determines the resting membrane potential of our cells.

When the heart suffers a massive necrotic attack what would happen to the potassium dynamics inside the myocytes ?

K + is the dominant intracellular cation , when about 100 million myocytes die suddenly , a chaos in the potassium metabolism is expected is it not ? .

When skeletal muscles dies it releases potassium . We know this from typical crush injuries and rabdomyolyis.

It is more of a common sense to expect this . . . from myocardium as well .

Source : http://nernstgoldman.physiology.arizona.edu

Which ion is responsible for the current of injury ?

We know a strong and continuous negative current that emanates from the necrotic zone after STEMI . (It is so powerful it shifts the baseline itself !), We do not know yet what exactly is causing this current of injury . It goes without saying sodium should sustain the depolarisation wave but potassium will also have a major role in the propagation of this injury current.

Do dying myocytes excrete the potassium into the circulation   ?

Is    k+ a marker of extent of MI ?

What is the mechanism of hyper acute tall T waves in MI ?

Questions galore . . . Answers struggle !

When a large area of cardiac muscle goes for necrosis it leads to leaking   of K +    . If it is true , it is expected to be a marker for extent of infarct. In reality it is not . Why ? This is because cardiac potassium pool is much small . A leak from an organ which weighs 400 grams do not elevate the ECF potassium . Still , there is ample evidence for   K + to accumulate in the local intracellular milieu. (Myocardial hyper-kalemia ) In fact , one of the mechanisms suggested for tall T waves in hyper-acute MI phase   potassium excess .

Image courtesey hqmeded-ecg.blogspot.in/2009/02/hyperacute-t-waves.html

http://hqmeded-ecg.blogspot.in/2009/02/hyperacute-t-waves.html

Potassium levels and incidence of ventricular tachycardia.

Many of the primary ventricular arrhythmias are due to acute ischemia . We have conflicting evidence for the effect of ischemia on QT interval. How does ischemia trigger VT ?
The answer to this question remain as a missing link ! . Grossly simplifying , one could suggest it is due to ischemic cell membrane damage that alters the ion channel function , resulting in intracellular accumulation of calcium and triggered activity .

What is the effect of potassium on cardiac contractility ?

Myocardial paralysis. (Please note it is the hypokalemia that primarily causes paralysis in skeletal muscles !)

It causes myocardial stunning a manifestation of local potassium leak ! A temporary myocardial paralysis.

What does the current guidelines of ACC/AHA state about potassium hemostasis in STEMI ?

It suggests a fairly aggressive maintenance of potassium levels to upper normal levels. Traditionally we are worried more about hypokalemia than the hyper. It is surprising we had the facts wrong . . . for so long !

What is new in the regulation of potassium level during STEMI ?

This landmark paper from JAMA seeks to set right the misconceptions about potassium during STEMI. It suggests K + levels has a U shaped morbidity curve in STEMI . One need to be cautious in correcting borderline hypokalemia . Serum K + is absolutely useless surrogate marker for myocardial K + . We do not know how K + behaves in the vicinity of MI zone . So extreme caution is required when giving IV K + supplements in coronary care units .

Watch out : Beta blockers /ACEI may worsen hyperkalemia

Early introduction of ACEI and ARBs is a strong risk factor for systemic as well as myocardial hyperkalemia . This is especially true in diabetic individuals who have low rennin levels due to diabetic micro circulation defect in kidneys .(Hypo-reninic hypo-aldosternosim )

Beta blockers are also known to raise potassium by two mechanism

1.Blocking rennin

2.Reduced uptake of K + in to the cells.

http://medicineforresidents.blogspot.in/2010/09/hyperkalemia-with-beta-blockers.html

Final message

In the management of STEMI , revascularization of the myocardium is considered as the only therapeutic aim . We need to realise it is much more than that . There are some subtle but important ways of resuscitating and protecting myocardium . Over indulgence in electrolytic management in coronary care is to be avoided.

Reference

Importance of sympathetic drive and potassium levels

http://www.nejm.org/doi/full/10.1056/NEJM198002213020803

http://ccn.aacnjournals.org/content/23/6/14.full.pdf+html

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Great men in medicine : Virchow is much . . . much greater than his “Lymph node and the Triad” he is known for !

Posted in general medicine, Great websites in cardiology, history of cardiology, tagged father of modern medicine, history of medicine, virchow virchow triad on February 8, 2012| 1 Comment »

Some scientists are known for their discovery , few are known for their vision few for their character .Here was a man who had all of them can be termed as father of modern medicine .

Rudolf Virchow - German pathologist( 1821-1902)

Unfortunately the current generation knows him for his concept and theory of blood clotting or lymph node in the neck .

Here is a reviews about this man who single handedly taught the world

He insisted , caring the sick and treating illness is more of a social science than medical one

We have probably not learnt a single lesson yet , from this master teacher is a different story !

Avid listeners to Virchow in Berlin university

My Virchowian thoughts

This man’s understanding of medicine was much . . . much sharper than us – 100 years ago , when cardiology was practiced with out even an ECG and X-ray chest . ( Is itn’t true today we struggle with loads of 3 dimensinal gadolinium enhanced cardiac MRI ! images )

Virchow’s concepts are most relevant in today’s world , where the corporate and capitalist culture has hijacked the noble profession . Inhabitants of this planet are threatened with eccentrically blown up healthcare system where the development of modern medical modalities is completely out phase of with what is required for the people .

We will pay a heavy penalty if this world continues to witness people die for as flimsy reasons like lack of oral re-hydration fluids , while the other section of society is marketing an exotic mitochondrial DNA slicers for prolonging a cancer victim life by few months .

In a global society where social , economic and environmental responsibilities and liabilities are shared , it would be disastrous if one country is simply not bothered about what is happening in other country.

WHO the world health organization came into being exactly for this reason .

We know . . . how it functions . It is the most abused united nation body . It has neither the required power nor the will to tell the world and insist them the righteous route for human health !

If the rich are not bothered about poor , it is certain the rich will also be eliminated from the planet for the same reasons . . . it’s just a matter of time !

Reference

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1305179/pdf/westjmed00323-0041.pdf

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

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What is the mechanism of deep q waves in volume over-load of left ventricle ?

Posted in Cardiology - Clinical, cardiology -ECG, tagged diastolic overload of left venticle, ecg basics, ecg in lv volume overload, lv diastolic overload, lv enlargment in ecg, lv systolic overload, lv voume overload, mq waves in v6 and voume overload of lv, q wave correspond to lvedp, volume overload of left ventricle on February 5, 2012| Leave a Comment »

Here is an X -Ray and ECG of a patient who came with palpitation , which he said descriptively

“I could feel it with my hands over chest “

He also had class 3 dyspnea and nocturnal chest pain . (Read here : What is the mechanism of nocturnal angina in AR ? )

Clinically it was classical severe aortic regurgitation .

His x – ray and ECG showed

q represents LV end diastole . The maximum diastolic stress point.
q indicate septal forces . When LV is dilated q also reflect cavity potential . Both gets summed up inscribing a classical deep q
In severe volume overload LV is not only dilated , it’s mass increases and is brought near the chest wall . Since the leas V 5 and V6 are the most proximal to LV both R and q increase correspondingly (Shall we call as reversed Brody effect ? )

Other findings of volume overload of LV are

While deep q is very valuable in LV diastolic volume over load there are other useful ECG signs.

Increased qrs amplitude (May be equally important like deep q . Both always go together )
Absence of typical ST/T changes (Systole is stress free !in pure AR/MR) . Still , ST/T changes can occur if there is associated LV dysfunction.
Left axis deviation.
Left atrial enlargement (In case of MR/ Large L-R shunts / or late stages of AR )
Rarely U waves are reported in LV volume overload*

Can we dignose volume overload without q waves in V 5 , V 6 ?

Most times no, but if there is associated incomplete LBBB q wave disappears.

Which is rare in pure volume over-load. In fact absence of q in isolated systolic overload of LV is attributed to the presence of incomplete LBBB by the ECG legend Shamroth !

Reference

* http://www.ccjm.org/content/78/8/505.full

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Importance of recognising type C RVH in clinical cardiology !

Posted in Uncategorized, tagged copd ecg, poor r wave progressin, right ventricular hypertrophy, rvh, type c rvh on February 5, 2012| 3 Comments »

RVH is traditionally categorized into three types . With the advent of echocardiography diagnosing RVH by ECG would appear redundant. Still , it gives vital information about the electro-physiologcal basis of RVH. Knowing different mechanisms of RVH helps us decode regional variations in RVH.

Type A , Type B are easy to diagnose as they fulfill the conventional criteria of tall R in lead V1

Type A RVH occur in severe pulmonary hypertension and critical valvular pulmonary stenosis.

Type B RVH occur in volume overload states like ASD and moderate forms of mitral stenosis.

( Severe MS may cause Type A pattern if RV pressure exceed systemic pressure)

Type C RVH has no classical signs of RVH. Here RVH is diagnosed by proxy . Look for RAE and a vertical QRS axis . ( For all practical purposes RAE will indicate RVH except in isolated tricuspid stenosis.

Type C RVH occurs classically in COPD and in some cases of acute pulmonary embolism .In other- words type C RVH reflects predominantly RV dilatation rather than hypertrophy.

Why Type C RVH is important ?

It is important for two reasons

It is basically a masked RVH .
It mimics Anterior MI

Missing the first one and erring in later both can have major implications in clinical cardiology especially during emergencies.

What is the mechanism of poor R wave in precardial leads in Type C RVH of COPD ?

The fact that poor R wave in precardial leads occur in most cases of COPD (whether or not RVH is present or not) convey an important message.

The lack of R wave progression is probably less to do with rotation of RV than the insulation effect lung . Further, the elongated lungs drags the heart down , and make it more vertical and in spite of RVH tall R is not picked up by v1 v2 .

Unlike primary PAH and critical MS where the RVH can dominate the LV , the quantum of RVH is never huge in pure COPD . However , presence of RBBB could alter the R wave amplitude .

ECG in acute pulmonary embolism

This resembles the type C RVH . The R waves in V 1 and V 2 can not gain the voltage acutely.

The S 1 . Q 3 , T 3 pattern if present indicate the acute RV strain and the resultant RV wall motion defect.

Clinical scenario : Practical utility of decoding RVH by ECG ?

A middle aged female came to our CCU with acute dyspnea with tachycardia .

Echo revealed a dilated RA and RV . She had mild TR and moderate to severe PAH (The TR jet measured 3.8m/sec)

The MPA showed a hazy shadow suspicious of thrombus . The patient had no evidence for DVT .

The fellows arrived at a conclusion about a severe PAH but , the etiology was debated.

One is chronic thrombo-embolic PAH . Other groups argued for acute massive pulmonary embolism and resultant PAH.

This raised an important therapeutic issue as one of them wanted to lyse the thrombus , the other argued for simple heparin .The argument continued as the first fellow reminded , presence of RA, RV dilatation is a sign of acute RV strain . The other countered the same as it could be a chronic response to pre existing PAH.

How do you know in an emergency , whether the RA, RV dilatation is new onset or a chronic one ?

In spite of good echocardiogram we were confused . Then it struck to us , ECG would solve our problem . It indeed helped us. She had a tall monophasic R in V1 indicating Type A RVH , which suggested chronic PAH and the thrombus in MPA in all likely hood was a sequel to PAH and not vice versa . A type C RVH would have voted in favor of acute pulmonary embolism.

Meanwhile a CT pulmonary angiogram report was available . It showed a small thrombus in MPA and LPA with no clearcut perfusion defects ruling out acute pulmoanry embolism . The thrombus was probably de-nova in- situ thrombus due to PAH.

Final message

It may appear funny for the present day cardiologists to waste so much time to analyze the RVH by surface ECG . But please remember ECG remain the only simple and cheap investigation that transmit live data from the heart instantly .Most importantly unlike other imaging modalities ECG data do not vary with person who records it !

Reference

A very good referen from Basic and Bedside Electrocardiography By Romulo F. Baltazar

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What are the mechanisms of “Nocturnal” Angina ?

Posted in cardaic physiology, Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, Clinical cardiology, myocardial disease, tagged angina during sleep, aortic regurgitation and nocturnal angina, nocurtnal angina, rem sleep associated angina on February 2, 2012| Leave a Comment »

Angina occurring at night is relatively uncommon . It is still more rare for angina to occur exclusively at night (With a possible exclusion of syphilitic aortits with AR !) The underlying conditions and mechanism of nocturnal angina are largely unexplored. In most clinical situations nocturnal angina is associated with day time angina as well .

Various mechanisms are proposed

It is primarily due to increased demand (Holter monitoring has documented brief bursts of HR acceleration just before nocturnal angina with manifest ST depression )
Increased demand during REM sleep .
Dreams related adrenergic surge has been implicated.
Rarely it is due to supply side defect .
Coronary vaso-spasm ( Mostly in a pre-exisiting lesion )
It could simply represent paroxysmal nocturnal dyspnea (pnd)
Sleep apnea can precipitate angina ( Ironically angina occur during re-breathing phase )
Altered hemo-rheology
Nocturnal gap in anti anginal medication *

* May be more common than we realise.

Cardio vascular hemo-dynamics at night

If we believe , sleep is the great relaxation , and the heart would enjoy the “night time” we are absolutely wrong . Even in sleep , heart has to pump the same 250 ml of blood every minute. Of course , the sleeping heart rate slows down considerably , still it is interspersed with spikes of activity. When the heart rate slows down , diastole is prolonged , coronary blood flow is expected to be copious unless there is critical CAD.

We know , sleep is not a passive process , even as the autonomic nervous system takes complete control over the somatic system .The true colors of our delicate autonomic system will come to light only during sleep.The muscle tone , the sympathetic drive fluctuates according a pre-set degree . Dreams and REM sleep disturbance can have considerable impact on the sympathetic nerve terminals which ooze catecholanines .

Sudden awakening from early sleep is vested with a risk of dangerous spikes of adrenaline release .This becomes especially important in compromised coronary circulation .In fact , this is commonest sleep -awake sequence in patients with nocturnal angina.

Silent ischemia at night

It is curious to note 24 hour Holter monitoring reveals most episodes of ST depression at night are silent. There must be a specific pain threshold above which a patient awakens with angina. The available studies do not answer this issue and are not perfect . We have no way to find true silent ischemia during sleep.(PET scan in thalamus ?)

Nocturnal angina in Aortic regurgitation

Aortic regurgitation has special relationship with dusk .For angina to occur AR must be severe and usually isolated .

Prolonged diastole at night -Regurgitation time is prolonged .
Dilated LV . Increased LV mass .Increased demand.
Raised LVEDP due high wall stress.
Diastolic coronary stealing . Venturi effect of AR jet

Nocturnal Angina : Is it stable or unstable ?

Most consider it as a type of stable angina .Now ,we have reasons to suspect it could a marker of unstable angina as it is an expression of rest angina .

Nocturnal angina vs nocturnal STEMI

How often an episode of nocturnal angina end up in STEMI ?

STEMI is more common in the early hours of the day and is more related to the hemo-rheological factors . Please note , STEMI is a supply side defect while most episodes of nocturnal angina is due to demand ischemia . However it is possible nocturnal angina episode can precipitate STEMI if vasospasm is the underlying mechanism and if it is prolonged can trigger thrombosis.

We do not know the answer as yet.

Nocturnal Angina : Can it be PND equivalent ?

Paroxysmal nocturnal dyspnea (PND) is a classic manifestation of episodic LVF. We know dyspnea can be an anginal equivalent. What prevents angina to become a dyspnea equivalent ! ( Especially the nocturnal ones , since the mechanism of generation of PND are very similar to the genesis of angina ). It is distinctly possible one may be mistaken for the other . Both occur when sudden hyper-adrenergic state is evoked which demands high MVO2 . An ischemic heart has every reason to respond with angina .

It is well known ischemia can result in transient diastolic dysfunction and elevate the PCWP simultaneously and PND would be the sequel . When we analysed the nocturnal calls ( Our fellows , do get lots of such calls from general wards at night ), many patients with LV dysfunction who complained of classic chest pain had some degree of dyspnea and few crackles over lung base as well .

Nocturnal angina and obstructive sleep apnea

The incidence of nocturnal angina is more common in obese population with obstructive sleep apnea.

The reason is two-fold

1 .Hypoxia mediated

2. Inappropriate tachycardia during recovery phase

Is there any specific management strategies to control nocturnal angina ?

General principles apply .
The timing of anti anginal medication can be adjusted . Long acting preparations taken in morning hours to be avoided as they do not cover night time.
A calcium channel blocker (with optional beta blocker ) at night may be the best bet to prevent nocturnal ischemia.
Dinner to sleep time to be widened.
Heavy diet at night to be avoided.
Sedatives role is not clear. (Can Diazepam suppress nocturnal angina ? If so . . . we can call it as anti anginal drug . . . is isn’t )

References