Pharmacology Flashcards
Beta adrenoreceptor agonists
Increase force, rate and cardiac output as well as O2 consumption
Reduce cardiac efficiency
Can cause disturbances in cardiac rhythm
Three Beta adrenoreceptor agonist
Dobutamine, Adrenaline, Noradrenaline
Adrenaline uses
Acute cardiac arrest, Anaphylactic shock
How can adrenaline be administered?
IM SC IV and IV infusion, in anaphylactic shock IM only IV if induced Cardiac arrest. Usually 500 micrograms
Adrenalines action
Beta 1 receptors positive inotropic chronotropic effect
Alpha 1 receptors vasoconstriction in gut skin
Beta 2 receptors dilation of coronary arteries
Adrenalines Half life
Roughly 2 minutes
Dobutamine uses
Acute potentially reversible heart failure, following cardiac surgery or during septic shock
How is dobutamine administered
IV infusion in high dependancy or critical units
Dobutamines action
Selective beta 1 agonist leads to increased contractile strength but not increased heart rate- unknown why
Rarely used only in short term
Three types of Beta antagonists
Non selective Propanol
Selective Atenolol Bisoprolol Metoprolol
Non selective partial agonists Alprenolol
Alprenolol and Non selective partial agonists
Weakly activate receptor yet prevent more potent agonist from binding, so slight rise in heart rate but block full effect
Effect of beta blockers at rest
Little effect as sinus rhythm, parasympathetic system, is dominant , Alprenolol will show slight rise
Beta blockers during exercise
reduced tolerance as rate force and CO are significantly lowered.
Overall effect of Beta blockers
Coronary Vessels constriction as B2 receptors blocked , however better oxygenation of myocardium as O2 requirement falls
Clincal usage of beta blockers
Arrythmias, Atrial fibrillation Supraventricular tachycardia , angina, and compensated heart failure.
With comorbidities e.g. angina can be first line for hypertension
Beta blockers in arrhythmia
Decrease excessive sympathetic drive to restore normal sinus rythm
Beta blockers in atrial fibrillation
Delays conduction through AV node preventing spread and helping restore normal sinus rhythm
Beta blockers in Angina
First line over Ca2+ blockers, helps reduce O2 consumption reducing waste product build up and in turn the symptoms
Beta blocker used in compensated heart failure treatment
Carvedilol, start low dose and increase slow
Carvedilol how does it work
Low dose reduces excessive sympathetic drive swell as alpha antagonist so vasodilation occurs less force required for same effect
Adverse effects of Beta blockers
Bronchospasms B2 receptor blockage, avoid asthmatics etc
Aggravation of non compensated heart failure as reliant or sympathetic drive for adequate CO
Hypoglycaemia B2 receptors activated release glucose from liver, no tachychardic warning signs either, avoid in poorly controlled diabetics
Fatigue CO reduced skeletal muscle perfusion B2 reduced
Cold extremities B2 mediated vasodilation
In what cases are the adverse effect negated if using selective agents e.g. atenolol
Bronchospasms and hypoglycaemia as use B2 receptors
Atropine
Non selective muscarinic ACh competative antagonist
Atropine clinical uses
Used to reverse symptomatic bradychardia as a result of a cardiac arrest
In anticholinesterase poisoning to reduce excessive parasympathetic activity
Atropine action
Increases heart rate at all but low doses
No effect on arterial BP as no parasympathetic innervation
No effect upon exercise resistance
Atropine for symptomatic bradycardia as a result of an cardiac arrest
300-600 microgram minimum dosage, titrate upwards. Too little has adverse slowing effect
Increased vagal tone as a result of cardiac arrest is reduced increasing heart rate
IV with constant monitoring for the adverse effects
Function of cardiac glycosides?
Increase contractility of the heart
Digoxin
Increases contractility of myocardium by increasing amount of Ca2+ in sarcoplasmic reticulum
Danger around digoxin
very low therapeutic ratio especially when coupled with low plasma K+
increases likely hood of ventricular fibrillation and tachycardia
Clinical use of digoxin
IV- acute heart failure
Oral in chronic heart failure if not responding to other drugs
Atrial fibrillation, as blocks of AV node preventing spread
Digoxin side effects
Can cause arrhythmias if lower AV conductance too low
Nausea, vomiting, colour vision disturbances
Levosimendan
Acute decompensated heart failure
Sensitises troponin C increasing contractility of myocardium
Dilates vascular smooth muscle by hyperpolarising membranes by opening k+ channels
Phosphodiesterase inhibitors
Amrinone and Milrinone
Action of Amrinone and milrinone
Inhibit PDE so increase conc of cAMP increasing contractility of the cardiac muscle
Reduced peripheral resistance
Clinical Usage of Amrinone and milrinone
Limited use as in long term increases mortality and morbidity, quality not quantity of life
IV for acute heart failure
Clinical use of organic nitrates
Acute angina, chest pain from acute MI, alongside other drugs treatment of pulmonary oedema
Action of organic nitrates
Broken-down in NO which activates guanylate cyclase, converts GTP into cGMP- relaxation pathway