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Posts Tagged ‘beta blockers’

What is the mechanism of Anti hypertensive action of beta blockers ?

Posted in cardiology -Therapeutics, Cardiology hypertension, tagged , , , , on October 17, 2011| 1 Comment »

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 : 5  (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 . 2  Indirectly  through suppression of  Rennin secretion.

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Can stable angina occur at rest ?

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , , , , , , , , on November 11, 2008| 1 Comment »

                                        Angina pectoris , classically occur on exertion and gets relieved on rest .This is called typical chronic stable angina as described by Heberden (CSA ) .  Unstable angina(UA), the term originally described by Noble O Fowler in early 1970s. ( Also being referred as  intermediate coronary syndrome , preinfarction angina etc).The definition for unstable angina has evolved  over the years  and currently  refers to .

 1.All new onset angina of any degree* Some include severe angina only ! New onset angina of very mild degree on exertion could be the onset of the first episode of  stable  angina. 

 2.Rest angina of more than >30 mts not relieved by taking sublingual nitroglycerine.

 3.All Post MI angina

 4.Any angina in patients who have been stented by PCI.

How to recognise a patient  who is shifting from  stable angina to  UA ? 
UA is  to be suspected when  a patient develops. 
5.More frequent episodes than usual
6.Angina occurring at lesser level of exertion than before 
7.Angina radiating to new site ( Example : Chest pain radiating  to jaw rather than to the usual left arm or vice versa)

Why the first episode of angina is given a special status and often considered critica ?

Angina is the  clinical expression of   myocardial ischemia.The course of  the  first  episode of angina , can not be predicted.It could be a the beginning of a chronic disease process, or it could be a progressive coronary occlusion as in unstable angina /NSTMEI , or the onset of even a STEMI.
In contrast a patient with chronic stable angina  has a predictable chest pain , at a particular level of exertion, radiation to same site, same character, and the patient knows for sure the pain  would promptly dissappear  when he takes rest or nitroglycerine  tablets.

What is the underlying pathology in UA ?  

Generally it is very rare for  a stable plaque to produce a  serious episode of unstable angina .It  requires  an unstable plaque* to  precipitate an unstable angina !
Unstable plaque refers to any plaque which is eroded, fissured, ruptured or  hanging  eccentrically ,  with
an active thrombus.

What is the significance of post PCI angina?

It is an irony, any angina following PCI is to be considered unstable as sudden occlusion of stent is quiet common.This is a paradox of sorts as one would wonder in a patient  with CSA who undergoes PCI with stenting  of left anterior descending coronary artery  (LAD)  all his subsequent episodes of angina  will be labelled as UA  even if a stable angina occur in his other coronary artery.And these patients would go for early invasive approach and potentially inappropriate interventions even if they are at low risk !

Is all angina at rest can be termed as unstable angina ?

No, but many times ,  rather most of the times  cardiologist believe all rest angina to be unstable.

What are the situations where stable angina can occur at rest?

An episode of angina during mental stress, or post prandial* state are very common in patients with CSA. This gets relieved after the stress. Some times  patients with CSA during episodes of fever may get angina at rest .These are considered variants of stable angina.
Post prandial angina , may be considered by some as unstable

How often a diagnostic confusion occur between CSA and UA ?

Generally, this issue is rarely addressed in cardiology literature , for the  simple reason it is never considered an  issue at all !
According to Canadian cardiovascular society grade 4 stable angina  is almost similar to unstable angina , as it denotes angina occurs with minimal effort or even at rest. In fact CCSC grade 4 should be termed as UA.

Can ECG be useful to identify stable angina from unstable angina ?

                                    ECG will some times  come to our rescue when one is confused between stable and unstable angina even though resting ST depression can occur in both stable and unstable angina . Statistically , if ST depression is noted during an episode of angina it is more likely to be UA rather than CSA. . Apart  from ECG , Troponin T or I levels may be elevated in some of the patients with unstable angina. Rarely stable angina can also show elevated troponin.

In patients with systemic hypertension and LVH or cardiomyopathy resting ST depression may not indicate UA 

So differentiation between, stable and unstable angina even though appear simple and  straight forward, it requires a diligent appraisal of history , physical examination (Aortic stenosis /HCM  may cause stable angina)  and ECG, enzyme evaluation.

Final message

In any coronary care unit ,  admissions with initial diagnosis of  ACS/UA/NSTEMI , subsequently turn out to be simple stable coronary artery disese . This error happens because the chest pain  or ECG changes  are aggravated by non cardiac factors like a mental stress or a post operative stress  or fever etc.
There could  be another school of thought, that is to err on the side of  safety, and manage all  rest angina as UA  .But the hazards of unwarranted therapy might exceed the risks of leaving these patients alone.
In this context ,there is a need for a new definition for unstable angina .
One ideal version could be . . .
  • Any angina , of any degree  which is caused  mainly by the supply side defect (By a acute thrombotic /disruptive plaque   occluding the  coronary lumen  with a imminent danger of myocardial infarction is to termed as real UA.
  •  All post MI and post PCI angina are unstable angina
  •  Rest angina which occurs due to increased demand situations need not be  labelled  as unstable angina for the simple reason  there is neither an active plaque nor a  fresh thrombus likely  in these patients. They rarely develop  recurrent angina or MI . The mechanism of angina at rest here is most often due to a tachycardia and resultant increase in MVO2 .(myocardial oxygen consumption) .Currently they are called as secondary unstable angina.In fact , anti thrombotic drugs are misused in these situations as they satisfy the criteria of UA/NSTEMI.

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