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Archive for the ‘Cardiology hypertension’ Category

Hypertension is  probably the most   important clinical entity for physicians
for decades .With the advent of modern interventional cardiology management of HT with  drugs have become a  less glamarous job for us. Still , the quantum of the problem and it’s impact on the  risk of CAD and progression   remain a major issue.
There many  different bodies periodically coughing  up guidelines  to manage HT.
  1. JNC from USA
  2. British Hypertension society from UK
  3. European society of cardiology
  4. World hypertension league
  5. Finally WHO guidelines* ( It is not a regular exercise ,WHO releases it  as and when it feels like !)

The stakes are high for the drug industry .Anti hypertensive drugs are the  major source of revenue  to them . Any dip in per capita consumption will have direct impact on their health ! ( WHO bothers about public health ? )

The so called scientific  guidelines,  are generally made balancing patients health vis a vis drug companies health .I have found more often than not it was tilted towards the industry .

The fact that there are multiple guideline with varying impact factors makes sure the confusion among the global physician intact . This is one of the aims of the pharma companies as they influence heavily  when to initiate the treatment ,  and what we are  supposed to prescribe.
Some of the guideline are notorious for insinuations . One example was about the definition of pre hypertension  few years ago .It has since been removed  from the literature after a critical debate .

* One may wonder why I’m focusing always  on non scientific  issues more than academics .(I some how feel non scientific factors are going to impact our health more than any other factor in the coming  generations  )

Now is the beginning of a balance .

European society of cardiology 2013 guidelines for hypertension
Among these guidelines  I would  think  ESC is close to reality and fairness.
Even    it was carrying dubious advices till recently .Now they have come out with new one in 2013.Most changes are  welcome.
  1. It is essentially about cleansing the contaminated guidelines
  2. Removing unnecessary medications
  3. Unified definition.
  4. More efforts to identify true secondary HT
The salient  points
There are  18 point update in the ESC 2013 . All of them are great . Essentially they are about the basics we have been  taught as we learnt in our final year MBBS. (The rest of our life we have to unlearn  the junk we have accrued over the years  from various CMEs )
I can modify it and  short list
  1. Do not start too early .Have universal definition (Now 140mmhg)
  2. Respect non drug treatment ,( However attractive the  gold tipped pen the  representative leaves  in your consulting suit !)
  3. Avoid using multiple drugs
  4. Never miss a secondary HT .( If  diastolic BP> 110mmh almost always a renal component would be there .Remember Conn syndrome (Primary aldosteronism )  is 10 times more common than much hyped pheochromocytoma ! Just do K+ levels to detect this )
  5. In CAD patients never treat HT in isolation .( Measure blood pressure with sugar and  lipid 120 /70 mg of LDL )
ESC 2013 is a commendable Initiative . It has  tried to remove most errors of the past .obviously  the pharma industry will be unhappy as it will definitely bring down  total drug consumption the  population.
Final message
HT  is an important target  for prevention and management of CAD
Thanks to the much maligned pharma industry  .
We have good drugs.Use it judiciously . Try to reduce the number of drugs .
If possible make them drug free.
If a patients taking   beta  blocker for associated  cardiac condition do not add another anti HT drug . (Recall  from your distant memory , beta blocker is a anti HT drug too !)
Simply follow common sense . (* If you think you  lack  it  ,  get  it from your learnt patients .Many  of them have in plenty . I often do that . One  question they keep asking  “Should I take this drug  life long doctor ?”  is a definite common sense booster!  )

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95 % of hypertension is designated as primary HT .What does it mean ?  It means  95 % of times  we do not   know what  exactly is the cause for raised blood pressure  . Simply stated  . . . it  reflects 95% ignorance .

So what is secondary hypertension ?

Secondary HT is the one,  in which we have specific reason for the raised BP.  The most important cause is Renal  ,  endocrine etc.

When will you suspect renal HT ?

https://drsvenkatesan.wordpress.com/2010/09/01/when-will-you-suspect-reno-vascular-hypertension/

How is secondary HT different ?

  • Occur at relatively at young age (<45)
  • It is generally more severe.
  • Diastolic BP is proportionately  higher ,
  • End organ damage is more.
  • It is very unlikely primary HT to present as acute LVF.  One rule of thumb is ,  if diastolic blo0d pressure is > 120 never diagnose  primary HT . Some amount of renal component is very likely.

Is stress related HT a form of secondary HT ?

https://drsvenkatesan.wordpress.com/2013/04/26/why-stress-obesity-related-hypertension-is-not-considered-as-secondary-hypertension/

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Answer

The tie is between “B” and “D ”

We know in hypertensive hearts LV primarily fails in diastole . Lungs get congested due to raised LVEDP .Here is a catch . . .  if diastole is  terribly dysfunctional  how can be systole be near  normal  ? (After all  . . . systole is not a  distant cousin of diastole !)

How is  that  high blood pressure maintained in spite of LV failure* ?

Is it due to  well-preserved  EF and cardiac Index ?  or Is it due to extreme levels of peripheral sympathetic activity mediated by catecholamine surge triggered by LVF.

We have attempted to measure  LVEF in patients with flash pulmonary edema and acute severe hypertension .It was a real messy echocardiography . We could not conclude much but one thing is  clear in acute hypertensive  LVF   the LV was vigorously contracting in , probably making the option D  more correct .

* The other way of  reasoning is    . . .  it is because  of high blood pressure the LVF  has occurred . LV contractility has no contribution in maintaining the high BP ( Not in line with  the age  old concept of LV contractility  a major determinant of systolic blood pressure !)

(Having said that  . . . we also see patients with severe LV dysfunction with  severely  stunned , ventricles in association with hypertension and LVF . In fact many of the reversible DCMs are due to sudden surge in blood pressure )

Other mechansims of LVF and lung congestion is

  • Extreme tachycardia and shortening of diastole
  • Mitral regurgitation
  • Assocaited  CAD unmasked by sudden raaise  in heart rate .

Postamble

If  this article has confused  you a little  , It has achieved  one of it’s  objective .  !  I expect more  from   young cardiology fellows to address the issue !

Reference

This NEJM article   authored by Sanjay  Gandhi  has almost answered the hemodynamics of acute LVF and HT .

mechanism of acute lvf in hypertension flash pulmonary edema lvedp in ht nejm 2005 sanjay gandhi

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It is tempting to fix the  “Force of cardiac  contractility” ,  to be the  prime determinant  of  systolic  blood pressure* .  Rather ,  it is  influenzed heavily  by   multitude of anatomical  and  physiological factors.

                                        ”  In most  life instances  the primary determinant  blood pressure  is not the state of cardiac contractility  “

                 For many ,  this  would  appear as  shocker of  a statement !

Fellows  should not be  confused with above inference  . What it means is ,  the  heart initiates  the blood pressure by a brief  period of  systole .The pulse wave attains a peak during ejection phase  . This is the peak systolic blood pressure  . There is nothing called  sustained  systolic  blood pressure .  The quantum and  duration of peak systolic pressure  contributed by the LV contraction  is  far less than we imagine .

If blood pressure is to be controlled   primarily  by  cardiac contractility , how is that ,  a  blood  pressure of   about 80mmhg is maintained throughout diastole when the heart is taking rest and the  aortic  valves  are closed  ?

The  major elastic blood vessels  aorta and the major branches use the potential  energy gained during systole  (Like a rubber band )  into   kinetic energy as vessels recoil during diastole . This recoil  imparts an   important component  to the  diastolic blood pressure  augmentation  and maintenance.

It is  prudent to note  since  diastole is  much  longer than systole  , integrity of the vascular tree  become  much more important  to maintain the blood  pressure  till the next systole arrives.

Note

*The cardiac contractility  , might  still be  important  in determining systolic BP  in  patients  with  severely compromised  LV function** For example ,  in  dilated cardiomyopathy  with  LV failure ,  systolic blood pressure will  be directly related to LV  function.  When LV function is critically  low , the elastic  blood vessels  fail  to  amplify the blood pressure  beyond  a limit.

**Still it is not  uncommon to find high systolic blood pressure  recorded in the back ground of with severe LV dysfunction especially hypertensive individuals.

What happens during aging ?

The  aorta and it’s major branches  gets thickened , the  vascular collagen  goes  cracking  with wear and tear of  life.  In effect , these vessels become less compliant . So , when blood is rapidly ejected  from the  left ventricle  into aorta  and their branches  it’s  distensibility   is  reduced  .This  fails to dampen the  pressure  wave  and  hence systolic  pressure spiking occurs. This we refer to systolic hypertension of elderly.

It is  important to  emphasise   major elastic arteries  has a big  say in fixing the systolic pressure. For the same cardiac output systolic pressure can surge in elderly this  is why we have kept the normal  in adults as 16o mmhg.

Another key point to be understood  is  ,  Aortic compliance  has an impact on diastole blood  pressure too ! . The  stiff vessels during diastole bring  less diastolic recoil. Diastolic recoil of large elastic arteries  determines the diastolic pressure . Hence there  could be  a mild fall in diastolic pressure with physiological aging when recoil is attenuated .  Since the  reduced diastolic  recoil ensures diastolic pressure from being elevated  the entity is aptly named as isolated systolic hypertension.(ISH)

Image courtesey :Norman M Kaplan, Lionel H Opie Lancet 2006; 367: 168–76

Final message

While the traditional  teaching  ramains  as  systolic blood  pressure  would be determined by cardiac contractility  / cardiac out put , while the   diastolic pressure is determined by peripheral  vascular  resistance .This is not an absolute reality ,  rather it is  too simplistic way of teaching circulatory physiology !

The  peak systolic blood  pressure is more often determined by the integrity of  Aortic  and major arteries   rather than cardiac contractility  and stroke volume. Similarly , aortic properties do have a  say in the diastolic pressure as well !

Further reading and debate

 The net effect of aging  on blood pressure :  Is it  physiological or pathological  ?

  Should we  treat  this  raised  pressure due to aging  related systolic hypertension  ?

There is a huge controversy going around ,  regarding the need  of  treating this mild elevation of systolic  blood pressure due to arterial stiffening .This will be addressed separately in this forum .

Reference

http://www.mayoclinicproceedings.com/content/85/5/460.full.pdf+html

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Q : Beta blockers reduce  blood pressure mainly through

  1. Reduction in Heart rate
  2. Reduction in cardiac output
  3. Negative Inotropic action
  4. Vascular sensitization to circulating catecholamines
  5. Blocks  Renin secretion and  reduce vascular tone.

Answer : (May be  4 as well !)

Our understanding of beta blocker’s  action  in SHT has changed considerably over the years .The  negative inotropic action on the myocardium  attributed for BP reduction ,  is no longer considered  important . Now we know , beta blockers can  reduce peripheral vascular resistance significantly.(There were days , we presumed  the opposite to be  true ,  ie when beta blockers are blocked , alpha action will overshoot to cause excess vascular resistance ! ) This  is more of  perceived fear.  This concept was never proved convincingly even in the  dreaded  Prinzmetal  angina* where beta blockers are  relatively contraindicated for fear of  aggravating vasospasm.

*Note : This is may  still be valid in selected few  who  show a  tendency for  Raynaud  phenomenon especially in peripheral vascular  system.


Additional  factors   influencing  beta blockers in SHT

  • Suppression  of  central adrenergic drive  ,  modulation of   brain stem vasomotor centre  are aslo considered vital . This action is linearly related to the ability of beta blockers to cross the blood brain barrier which is more with lipophilic drugs like metoprolol.
  • The role of beta blocker in isolated systolic hypertension in elderly  is unique.Here it reduces the myocardial dp/dt (ie contractility )  and hence help them prevent  systolic spikes of pressure and the resultant  stroke.
  • The newer  vasodilating beta blockers  like Nebivolol, (Nitric oxide mediated ?)  and Carvidilol may have additional advantage in controlling BP.
  • It needs to be appreciated , beta blockers combine well with  diuretics like  hydrochlorthaizide  .This  makes it easier to control severe forms of HT  especially volume dependent ones in  both young and elderly. (SHEP trial )

Final message

The modification of vascular response to catecholamines  is  the single most important mechanism of reduction of blood pressure.

This may be a direct consequence  of  1.  Blockade of  vascular  adrenergic receptors . Indirectly  through suppression of  Rennin secretion.

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Heart is a dynamic organ . It can alter  its force of contraction with every beat  according to the needs.Generally it responds to  length  of  previous  diastole.This is famously called frank starling law , ie the force of contraction is directly proportional to the end diastolic fiber length. So changing diastolic  duration as in atria fibrillation classically result in varying amplitude of LV contraction and pulse volume.

However , the commonest cause for  pulsus alternans  is  due to  severe left ventricular systolic dysfunction .There has  always been a suspicion about the existance of  beat to beat variation in  diastolic function as  well.  We have recently observed a  new* explanation for pulsus alternans .We know AV inflow is subjected to respiratory swings . Non  respiratory swings in mitral and tricuspid valves are rarely described. This pattern is now increasingly recognised.

These  non respiratory swings in the mitral inflow doppler pattern  is seen in  some of the  patients with hypertension and LVH.This  probably confirms the existence of  beat to beat variability of diastolic function . This phenomenon is relatively a new observation . Such pattern are common in patients who have had a recent hypertensive failure .

 

Here is a doppler of mitral inflow recorded from a patient with hypertension with LVH .

This is the doppler mitral inflow profile of a patient with Hypertension, LVH and class 2 dyspnea .Note the non respiratory swings in both "e" and "a" velocity

It is proposed  to  define  a new class of diastolic dysfunction that can be referred to as diastolic  mitral inflow  alternans .This phenomenon probably indicates a more severe grade of diastolic dysfunction.At the molecular level this is related to  undulating flux  in the calcium uptake from cytoplasm into SERCA .There is one more possible explanation for diastolic alternans  -Left atrial  dysfunction .

Occasionally one can visualise  a chaotic pattern of  diastolic filling waves  (e=a e>a a> e )  Such patterns are thought  to be markers of impending acute diastolic shutdown .

Further  analysis of  this  mitral doppler inflow pattern will be reported  later.

Reference

* Though we observed this for the first time , this is not a new phenomenon .There are few reports available in the literature.

http://www.sciencedirect.com/science/article/pii/S0735109785800358


http://www.sciencedirect.com/science/article/pii/S0894731706012818

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Is hypertension really a major risk factor for CAD ?

    1. Yes it is !
    2. No . . . it is not !
    3. May be !
    4. I don’t think so !

Ans : Any of the above can be a  right response , depending upon our basal and perceived  level of knowledge .

Answer analysis

  1. SHT  is  one of the risk factor for CAD  agreed ,  but definitely not a major one , as SHT per-se rarely precipitate a STEMI
  2. Unless SHT occurs with dyslipidemia, smoking or diabetes it is  rare to cause ACS.
  3. The only  adverse effect of SHT  is  , it has a potential  to aggravate atherosclerosis  by promoting epithelial injury and dysfunction.
  4. Hypertension is a well known  major risk factor for cerebro vascular disease while it is minor risk factor for CAD !
  5. We do not know yet why cerebral vessels are intolerant to high blood pressure while coronaries are pretty happy  with it !

Final comment

SHT is not a major risk factor  for CAD ! At worst , it can propagate chronic CAD. This sort of reasoning  may be considered a huge controversy  . . .but it is really not !

  • One evidence for the above observation is  , we  have  been struggling hard  for over a half a century  to prove a elusive  point that controlling blood pressure  to optimal levels  would  dramatically reduce  cardiac   events !
  • Further,HT’s  relationship with acute coronary syndrome especially STEMI  is vague , it is very rare for patients with accelerated hypertension or malignant hypertension to  present with STEMI *

* Caution :Young doctors should not get confused with this seemingly  controversial observation .This write-up , tries  to convey  a point  , SHT may not be that bad for coronary arteries when compared to cerebral arteries . However BP control remains  vital in  all patients who have  developed a cardiac  event or in patients with multiple risk factors .

Please note ** SHT is still  a powerful risk factor for cardiac failure.(Acute LVF to be precise ) ***SHT can aggravate unstable angina , but very  rare to precipitate unstable angina.**** SHT ./High intra-coronary  pressure can theoretically  dissect or fissure a plaque . (The fact that , HT is so prevalent in a community  but spontaneous  coronary  dissections are not !  should make us think further !)

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