User Tools

Site Tools


beta adrenergic blockers


  • beta blockers are used for many therapeutic effects including lowering blood pressure, slowing the heart rate, reducing mortality after acute myocardial infarction (AMI/STEMI/NSTEMI), preventing migraine, symptomatic Mx of hyperthyroidism, etc.
  • they generally have the following potential adverse effects:
    • reduced exercise tolerance
    • worsening cardiac failure in those with poor cardiac function
    • risk of heart block in those at risk or with concurrent medications which block A-V conduction such as calcium channel blockers
    • risk of bronchospasm in those with asthma
    • exacerbation of peripheral vascular disease symptoms
    • metabolic effects including altered lipid profiles, glucose metabolism, and a mild increased risk of gout
    • obscuring the clinical features of hypoglycaemia which increases risk of unrecognised episodes in diabetics.
    • in addition, some, such as sotalol prolong QTc interval and may increase risk of torsades ventricular tachycardia (VT)
  • beta adrenergic blocker overdose can be fatal and difficult to Rx

General features of beta blockers:

Beta 1 adrenergic blockade:

  • bradycardia & negative inotropic effect ⇒ decreased cardiac output;
  • decreased BP if hypertension but full response may take several weeks:
    • (initial increase in peripheral resistance (beta2 block) which later normalises, then falls)
  • suppress exercise-induced tachycardia if therapeutic dose;
  • decreased renin secretion;
  • block catecholamine-induced tremor;
    • decreases spontaneous rate of depolarisation of ectopic pacemakers;
    • decreases conduction in atria & in AV node;
    • increases functional refractory period of AV node;
      • NB. some membrane-stabilising effect (Class Ia) in high [];
    • decreases angina by decreased HR, decreased contractility ⇒ decreased oxygen needs;
    • increased exercise tolerance if exertional angina;

Beta 2 adrenergic blockade:

  • bronchospasm
  • blockade of skeletal muscle vasodilatation;
  • adverse lipid profile?;
  • impaired glucose mobilisation & K+ entry into cells;

Intrinsic sympathomimetic activity (partial agonist):

  • May produce less decrease in HR & BP (but still block exertional increase in HR, CO):
    • ⇒ ? better for decreased cardiac reserve or tendency for bradycardia;
    • ⇒ not as good for Rx tachyarrhythmias, angina or post-AMI
  • May result in lower peripheral resistance in short term use (normally there is an increase);
  • May not effect plasma renin activity but still anti-HT effect;
  • May have less frequent adverse lipid profile alteration;
  • May have less tendency to bronchospasm;
  • eg. pindolol, penbutolol, acebutolol, (labetalol, celiprolol @ B2 only).

Membrane stabiliser (quinidine-like) activity:

  • Many beta-blockers have this activity but only had high doses, which may be important in overdose;
  • eg. propranolol, acebutolol, labetalol, metoprolol, pindolol;

Alpha-blockade activity:

  • May result in lower peripheral resistance in short term use (normally there is an increase);
  • May reduce vasoconstriction;
  • Eg. labetalol (alpha1);

Beta1-selective blockade:

  • Lessen adverse beta2-block effects of:
    • bronchospasm (but still use with great caution in asthmatics);
    • blockage of skeletal muscle vasodilatation;
    • adverse lipid profile?;
    • impaired glucose mobilisation & K+ entry into cells;
    • Eg. metoprolol; atenolol (Tenormin); acebutolol; betaxolol; esmolol; celiprolol; bisoprolol;

VW class III actions:

Direct vasodilating activity:

  • less vasodilating than labetalol though
  • eg. Carvedilol, bucindolol & celiprolol

Pharmacokinetics of beta blockers:

  • Most are well absorbed orally → peak plasma conc. @ 1-3hrs.
  • Most have high 1st pass effect → low bioavailability of 25-40%
    • EXCEPT pindolol, sotalol, betaxolol & penbutolol which are >90%.
  • Most are rapidly distributed with high Vd.
  • Only propranolol & penbutolol are highly lipid-soluble & penetrate blood-brain-barrier well.
  • Most have half lives in range 2-5hrs EXCEPT esmolol 10min, & sotalol 12hrs (& less common)
  • Most are extensively metabolised in liver
    • EXCEPT:
      • atenolol (Tenormin) & pindolol less extensive metabolised
      • esmolol is rapidly hydrolysed by RBC esterases
      • nadolol is excreted unchanged in urine → long half life of 14-24hrs

Clinical uses of beta blockers:


  • reduction of cardiac output without reflex increases in periph. vasc. resistance
  • reverses HT-related LVH although not as good as ACEI's
  • reduces mortality & morbidity
  • esp. useful if coexistent IHD or tachyarrhythmias
  • phaeochromocytoma:
    • an alpha-blocker usually commenced first to avoid unopposed alpha effects on periph. vasculature

exertional angina:

  • reduces exertion-induced rise in BP and HR
    • ⇒ longer diastolic filling time ⇒ increased oxygen delivery
    • ⇒ decreased oxygen consumption at a given cardiac workload


  • non-ISA beta blockers useful in:
    • reducing rate in sinus tachycardia
    • block AV node conduction in AF thus controlling ventricular rate
    • have little or no proarrythmic activity
  • sotalol has additional class III effect and is useful in:
    • suppression of non-sustained and sustained ventricular arrhythmias

reduction of mortality post-AMI:

  • have been shown to reduce mortality post-AMI presumably via:
    • reduced myocardial work
    • increased coronary perfusion via prolonging diastolic filling
    • inhibit catechol-stimulated rise in free fatty acid metabolism ⇒ improved myocardial metabolism
    • reduction of catecholamine-induced arrhythmias at time of AMI
  • since thrombolytic Rx introduced, have not been routinely used IV during AMI's although had been shown to be of benefit

systolic heart failure:

  • newer direct vasodilating beta blockers reduce systolic BP without negative inotropic activity being such a problem

various forms of diastolic heart failure:

  • acting by slowing heart rate & prolonging diastolic filling time
  • for pts who remain symptomatic despite standard Rx (ACEI, diuretics & digoxin)
  • must start at low doses & increase very carefully
  • vasodilating beta blockers may be better tolerated esp. at initiation of Rx

dissecting aortic aneurysm:

  • reduce systolic force generated within vessel

vasodepressor syncope:

  • sympathetic activation is an important triggering factor in this syndrome


  • adjunctive Rx in Mx of sympathetic effects

tremors, anxiety:

prevention of migraine


    • A cardioselective B1-blocker used topically to reduce intraocular pressure without producing bronchospasm as may topical timolol.

portal hypertension:

Chemical structure of beta blockers:

  • is generally of the form (except labetalol which is more like dobutamine):
    • R - benzene ring - O - CH2 - CHOH - CH2 - NH - R1
  • compare with:
    • catecholamines: catechol ring - CHOH - CH2 - NH - R
    • non-catechol sympathomimetics: R-benzene - CHOH - CHR1 - NH - R2
    • dobutamine catechol - CH2 - CH2 - NH - R - phenol
    • labetalol R-phenol - CHOH - CH2 - NH- R1- benzene
betablockers.txt · Last modified: 2012/01/24 23:52 by

Donate Powered by PHP Valid HTML5 Valid CSS Driven by DokuWiki