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Archive for the ‘Cardiology hypertension’ Category

We presume  ECG  fails miserably against echocardiography for assessing hemodynamics , while  echocardiogram  has  little value  when it comes to studying   electrophysiology .  Ironically ,  we often  ignore  the fact  ,   ECG can  provide  important long-term   hemodynamic  data . The pattern of  chamber enlargement  give us  vital clues to the prevailing hemodynamic  stress and loading conditions. While echo  can be termed as an  anatomical and  physiologic   modality  , ECG  apart from  its unique capacity to record cardiac  electrical finger prints ,  it  provides  useful ,  anatomical ,  hemodynamic information too !

While Doppler is a  fascinating modality to measure hemodynamic data in a moment to moment fashion it can never ever tell us  , what has been going around in the preceding months or years. This  is were chamber size helps which  give us chronic physiological information (Chronic  Doppler ?)

A simple E:A reversal  in  mitral inflow doppler can be a  innocuous  finding in isolation  . If it is associated with even   minimal grades of  LAE  it gains huge importance. That is why left atrial size is  funnily referred to as HB A1C of diastolic dysfunction ( A marker of chronicity  of  diastolic dysfunction)

If LAE is so important to diagnose diastolic dysfunction , why  we are so  obsessed  with doppler filling profiles  of mitral valve ,pulmonary veins, mitral annular tissue Doppler and what not ! .Many of these sophisticated doppler methods are extremely operator dependent  and are  subjected  to technical and mathematical errors. Especially , with  tissue doppler where we  magnify the errors as we  filter  extremely  slow tissue motion .

For  many  decades  we  have failed  to impress ourselves  , about the importance of subtle P wave abnormalities in the  ECGs   of  hypertensive patients.

In fact those  innocuous looking  slurs and notches   in P waves ,  suggest the left atrial  stress and a definite marker of underlying LV diastolic dysfunction .

P wave is the only electrical wave that occur in diastole .Hence there is no surprise  ,i  gives us enormous information about this phase of cardiac cycle .

If only we look  at them carefully, zoom it (Now it is made easy with so many softwares)  analyse critically we can find a wealth of information about the atrial behavior in hypertension.

Experience from our hypertension clinic  with periodic echocardiograms suggest ,  the following  ECG  findings   can be   good markers  of significant  diastolic dysfunction .

  1. Notched P wave
  2. Wide  P waves
  3. Slurred  P wave
  4. Bi-phasic P waves

* Surprisingly  , these abnormalities correlated with at least grade 1 diastolic dysfunction even in the absence of  for LAE or LVH by echocardiogram.

** In an  occasional patient  P waves  can widen due to inter atrial block or conduction delay. This a rare exception for wide P waves without LAE.

Final message

A well recorded and   analysed   ECG can  predict diastolic dysfunction  with fair  degree of accuracy .This fact need to be emphasized  by every one  .  Next to ECG ,  LA size and volume  by 2d echo are excellent parameters  to assess diastolic function in a long term fashion. Sophisticated  but  error prone ,  momentary doppler parameters are getting too much attention  at the cost of simple ,  shrewd ECG and 2D echo  !

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Blood pressure  measurement ,   probably  is the commonest investigation done  in our patients  in  the entire field of medicine . It is such a common thing ,  both physicians  and patients  fail to perceive  it as  an investigation . (It indeed is !)

Even though BP is  considered as a  clinical sign , measuring it requires a device called sphygmomanometer  . The BP apparatus has to be properly calibrated  with the mercury  , the tubing, the bladder  , inflation balloon  etc   need to be perfect.

The following fallacies are noted in the measurement of  blood pressure . Some of them are rampant* !

Patient

  • Posture of recording
  • Anxiety -White coat /Gender

Device

  • Cuff width/Length
  • Arm circumference

Ocular errors

It is surprising , such an important tool has a scale of 2mm markings which is prone for parallax errors of light with  mercury column undulating .

Physician factors*

  • Hasty cuff syndrome , Rapid deflation .
  • Absent minded recording – Failure to note phase 4 to phase 5  due to inattention
  • Failure to hear phase 4 muffling  (Aging  medico  -Auditory insufficiency !)

It is  not at all  surprising  to note,   two BP readings rarely match ,  even if it is recorded by the same person with  same machine at the same time !

There are many  articles that describe in detail  ,  how to record blood pressure properly. But this article from  a relatively unknown  journal   from Purdue university  ,  tells  us  most   scientifically  , what  has been taken for granted  by the medical  community for so long  .

Loose cuff  hypertension (Link to the journal of  Cardiovascular engineering )

How much  stiffness  is to be applied in  the arm for optimal pressure recording ?

What is the incidence of hypertension due to  loose cuff  ?

Final message

The BP apparatus ,  though appears  as  an   innocuous   machine ,   the readings  that emerge  from it  determines ,  how millions of our fellow human beings are going to be labeled  ! ( High pressured  humans ,  slaves to  anti hypertensive  drug marketeers    for  rest of their  life ) .

So , realise  how important  it is , to measure  the blood pressure properly    !  Never be casual . . . with  this  machine .

Experience has taught us ,  while  it is very easy to name an  individual  wrongly as hypertensive  , it  often needs  Herculean  efforts  to remove this medical tag from their neck . The reasonings  are  many .( Academic , non academic and patient factors included )

Finally , in this funny planet  it is  a personal observation ( Or is it  an imagination ?)    some  men and women   tend to  enjoy  ,   being  referred to  as  high pressured !   Loose cuff  or tight cuff   ,  it simply do not bother them  !

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It is traditionally believed  , renal blood flow is critically determined by the  luminal diameter  of  renal artery.But in reality  there are more important factors  other than renal  arterial diameter  that determine the glomerular  blood flow.  As in any vascular bed, it is the arterioles that determine the resistance and hence the flow . These arterioles  form the  critical  resistance  points and acts as   check  valves in this  “vascular  highway”  flowing across the renal terrain !

Unlike other micro-circulations ,  the kidney has a  special job to do ,  ie  filtering  the toxic  molecules.  Hence,   for the blood entering the kidneys  , even  nourishing the kidney seems ,  a less important  function !  The nephrons  of the kidneys are probably the most  “high – tech” cells in human body (Of course ,next only to brain cells ) .The vascular  tuft of glomerulus located within the bowman’s capsule  is perfused  by afferent arteriole and drained by efferent arteriole .

The entry of blood into glomerulus is regulated both by afferent and  efferent arteriolar  tone .These  two micro-circulaoty units  are under the  sensitive control of both neural  and humoral  signals. Glomerular circulation is meticulously  regulated by renal juxta glomerular apparatus.It modulates the glomerular  blood flow by secreting renin which  acts through Anigiotensin 2  on the   efferent arteriole .

The tone of the  efferent  arteriole  is thought to be the single important factor in this servo control mechanism.

What happens in bilateral renal arterial stenosis ?

When there is bilateral renal arterial stenosis the effective renal blood flow is not  significantly reduced , but maintained at  the cost of increasing the efferent arteriolar constrictor tone. It  is  like a  check valve at  the  exit point of a dam , which is partially closed to maintain the adequate pressure head (Here , intra-glomerular  pressure head )

What happens when ACEI are introduced ?

Once ACE inhibitor  is administered , the efferent arteriolar   tone is removed , this triggers  the intra glomerular pressure to drop  suddenly and filtration pressure reduces .

Note: ACEI does  not reduce the renal  blood flow  directly  but  the glomerular  perfusion pressure drops hence precipitating acute renal function deterioration.

What is your comment about the reno-protective effects of ACEI ?

The medical science’s  most  crucial  moments  occur  , when we confront  two diagonally opposite views  are  debated  and both  suggest , there is definite benefit for the patient ! Cardiologists and nephrologists were always  made to believe  ,  ACEI are  unfriendly to kidneys . But ,we now have  evidence , ACEI is not an untouchable molecule in renal  dysfunction.

This is based on  the observations made , over the years that  excess Angiotensin 2  is  ultimately a liability for the kidneys !

Looking at a  long  term perspective  , AT 2  increases the intra -glomerular hypertension and ACEI inhibitors reduce it.This  pr0tects the  nephrons from  hyper-filtration  mode ,  that accelerates the  glomerular  injury . So , the  current thinking  is  ACEI has a definite role in arresting the progress of  renal cell injury .

This is akin to beta blocker story in CHF which was initially contraindicated in CHF later became a definite indication

The only issue for ACEI is , it should not be continued if an ARF like picture sets in .(Acute deterioration ). Otherwise ,  in CRF at any  basal level of serum creatinine  , ACEI can be continued . Some think even an  increase by few mg of creatinine  can be allowed .

So the following can be a working guideline *

  • ACEI can be started  or continued at any level of creatinine in stable CKD with or without dialysis

But ,ACEIs need to be stopped in all of the following 

  • Acute renal failures
  • Acute on chronic renal  failure
  • Accelerated elevation of  creatinine  (As in bilateral renal artery stenosis)

How much elevation of creatinine is allowed in CKD  with ACEI  ?

This is   not answered yet .

*Caution : The above conclusions on ACEI and creatinine was  derived  by me , based on  with  personal discussions with my  Nephrology colleagues. It may  be subjected to correction.

//

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The much fancied criteria   “suspect secondary  HT” if the  onset of  hypertension  is   before 30 years   later than  55  years ,may be useful  .But a caution about this criteria  : It does not mean you should not hesitate to  diagnose renal HT  between 30 -55 years.  The  real onset may be   < 30years , but  the patient may report to the physician  late  in his /her  40 or 50s !

  1. Diastolic blood pressure > 120
  2. Sudden acceleration blood pressure
  3. Blood pressure which is  resistant to control with three or 4 drugs ,that shall typically include a  diuretic.
  4. An episode of left ventricular failure (Often referred to as  called flash pulmonary edema)
  5. Presence of  Hypertensive retinopathy
  6. Para umbilical bruit
  7. HT associated with significant CAD
  8. Marked LVH in echocardiography
  9. Finally , most importantly , worsening of renal function with ACE inhibitor is a  strong clue the kidney is under perfused  and  the   renal circulation  is dependent on  elevated angiotenisn 2 (Which ,if blocked worsens the GFR ).This implies every physician should take a baseline serum creatinine  and urea before starting them on ACEI.(Which is rarely followed , as far as my country is concerned !)

Is there any simple way to  differentiate  reno vascular from renal parenchymal HT ?

It is very difficult to differentiate between these two clinically. It makes things more difficult , as  combination of both occurs. Prolonged renal ischemia can result in parenchymal damage as well.

The simplest way is to do a rapid ultrasound imaging to assess kidney size and texture (Loss of cortical-medullary differentiation indicating early renal contraction phase ).Of course , our nephrology colleagues are always there to help you out .

* It need to be remembered the functional renal HT -Renal tubular acidosis,  Adrenal HT (Conn’s /chromo-pheocytomas  has to be ruled out , as these entities also occur in the same age group ).The combination of hypokalemia and mild alkalosis is a  good clue to rule out many of these  defects.

* The CT scan image used in the above illustration  courtesy

http://www.ajronline.org/cgi/content-nw/full/189/3/528/FIG21

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For medical science  to  defy   logic , is a not a great  new discovery . “Diabetes is a major  risk factor for heart disease   but controlling diabetes may not  remove this risk factor” Similarly  severe mulitvessel CAD  occurs without  any symptoms and compromise on LV function . It is a natural human  instinct  to open of  any thing  that is obstructing   on  their  path . The same logic applies in   physicians when we encounter blocks in the vascular highways  .

For a moment compare  it with an express way .

We realise many  roads have a  reserve capacity . Even if the road is  half  blocked , traffic  congestion  rarely happens  as the  original road’s width is  sufficiently  large for the projected traffic . Some other roads have emergency  service lanes (Collaterals) that can take care the flow of traffic.

Another  question to ask is , Where does the road  lead to ? and why  we are  traveling ?

If it leads to a “dead  sea”  or a “bottom less cliff’  there is no purpose  to travel further . Similarly , when you find a destructed kidney with little nephron mass( or dead myocardium  ) there is absolutely no purpose  in opening the block . (Some  may  believe  the act  of  opening  block , by itself   is a success /  sorry- story !)

This is what happened in the lase decade . Interventional    radiologists , vascularologists , cardiologists started  opening  renal artery obstructions , at their whims and fancies, in  many elderly and middle-aged population .To their surprise (This surprise is due to ignorance )  they found no worthwhile benefit  either in the BP reduction or worsening renal function .

Now comes the evidence  in  2009  as   ASTRAL  trial from UK . ( As usual   the evidence came   late after ,  few lakhs  of kidneys   been injured !*

* Renal interventions are notorious for many complications , which is often not reported . Read this article to know  it better.

http://www.nejm.org/doi/pdf/10.1056/NEJMoa0905368

Final message

Common sense can  work great wonders than the much hyped RCTs . (Except ASTRAL  of course !) In this era of scarcity of  such  sense we can expect another study soon , to nullify ASTRAL  and give us further license  to pursuit the  good old  human instinct  ! Already silent noises  are made in interventional  corridors questioning the  outcome of ASTRAL.

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  1. Do 64slice MDCT  in all patients who has  a coronary event and follow it up with catheter based CAG.
  2. Use liberally the new biochemical marker ,  serum  B-naturetic peptide (BNP) to diagnose cardiac failure in lieu of basal auscultation.
  3. Advice  cardiac resynchronisation therapy in all patients  who are in class 4 cardiac failure with a wide qrs complex .
  4. As it is may be considered a  crime to administer empirical  heparin, do ventilation perfusion scan in all cases with suspected pulmonary embolism.
  5. Do serial CPK MB and troponin levels in all patients with well  established  STEMI .
  6. Open up all occluded coronary arteries irrespective  of symptoms and muscle viability.
  7. Consider  ablation of pulmonary veins as an  initial strategy in  patients with recurrent idiopathic AF. If it is not feasible  atleast occlude their left atrial appendage with watch man  device.
  8. Never tell  your patients   the  truths  about the  diet , exercise &  lifestyle modification (That can  cure most of the early hypertension) . Instead encourage the  use of  newest ARBs  or even  try direct renin antoagonists   to treat all those patients in  stage 1 hypertension.
  9. Avoid regular heparin in acute coronary syndromes   as  it  is a disgrace to use it  in today’s world. Replace all prescription of heparin with  enoxaparine  or  still better ,  fondaparinux  whenever  possible.
  10. Finally never discharge  a  heftily  insured patient   until  he completes all the  cardiology investigations  that are available in your hospital  .

Coming soon :  10 more ways to  increase cost of cardiology care . . .beyond common man’s reach

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idh

  • Hypertension  is  major determinant of cardiovascular health  of our global population
  • Millions suffer,   hundreds of societies ,  and as many guidelines , and drugs are still struggling  to control the menace.
  • An important sub group of HT , (ie IDH ) population has been neglected and never received the scientific interest , which it deserves !
  • In our study it occured in 7.2% of all HT  patients.
  • JNC,  the world authority on HT never considered  IDH as a separate entity, and as of now there is no specific guidelines.
  • And the irony is complete . There is not  a  major study available to analyse the differential effects of anti hypertensive drugs on systolic and diastolic blood pressure.

If  a patient with the BP of 120/96 asks you , “Doctor , will the drug,   you have prescribed , selectively lower my diastolic blood pressure ” what will be your answer ?

A clear ,  I don”t know !

The following paper was presented in the World congress of cardiology Sydney  2002

Isolated  Diastolic Hypertension

S.Venkatesan,S.D.Jayaraj.Gnanavelu, Madras Medical College. Madras, India.

Abstract : Systemic  hypertension  continues to  be a major determinant of cardiovascular  morbidity. While isolated systolic hypertension(ISH) has been identified as a specific clinical entity, isolated  diastolic  hypertension(IDH) has not been reported as a separate group. When we analysed our data from our hypertension   clinic  we found  a distinct subgroup of patients who had  elevated  diastolic blood pressure   with  normal systolic pressure. We report the clinical profile of these patients. 440 newly registered hypertensive  patients between the year 1998-99  formed the study population. All  patients with secondary hypertension  were excluded.. IDH  was defined as  diastolic BP more than 90mmhg and systolic BP less than 140mmhg.

IDH was present in 32(7.2%) patients.  The male female ratio was 3:1, mean age was 42(Range32-56) The mean diastolic pressure was 96 mm (Range 90-110).The mean systolic pressure was 136mm(Range 128-140). LVH was observed in 4 patients(12.5%). Diastolic dysfunction was detected by echocardiography   in 20patients.(62%)

We conclude that isolated diastolic hypertension  constitute a  significant subset among  hypertensive  patients and they need further study regarding the pathogenesis, clinical  presentation and  therapeutic implication.

Link to PPT  will be available soon .

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