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Positive iontrophs

Physiology and Pharmacology

QuestionAnswer
Effects of reduced cardiac output under perfusion of: Tissues - acidosis Brain - lethargy, cerebral damage Kidneys - acute tubular necrosis, renal failure
Uses of positive inotropes Cardiac failure - chronic, ischaemic - reduction in CO to the point that it does not satisfy requirements Hypovolaemia - actual e.g. haemorrhage or functional e.g. vasodilation
Effects of cardiac failure Hypotension Tachycardia Lethargy Exercise intolerance Breathlessness Oedema
Acute shock Hypovolaemic shock - haemorrhage Septic shock - toxic vasodilation Cardiogenic shock - myocardial infarction
Influences on cardiac output Cardiac input - venous return and circulating fluid volume Contractility Peripheral resistance
Effects of ischaemia on frank starling curve Shifts downwards Decreased coronary blood supply, decreased oxygen availability Decreases cardiac output for a given venous return
Causes of ischaemia Increased oxygen demand when this cannot be met - tachycardiac or increased contractility Reduced oxygen supply - coronary atherosclerosis and small vessel disease
Other causes of hypoxia Reduced oxygen carriage - anaemia Reduced oxygen exchange - asthma and COPD Does not cause build up of CO2 so does not disturb H and K gradients
Circle of cardiac failure Fall in cardiac contractility Fall in cardiac output Fall in coronary perfusion Cardiac ischaemia Circle repeats
Consequences of ischaemia Reduced contractility Dysrhythmias Infarction Death
Treatment of ischaemic failure Positive inotropic agent - with no increase in oxygen demand Cheat - vasodilate to increase cardiac output and limit work to match cardiac oxygen
Treatments for failure Must increase cardiac output Must not increase oxygen demand - no increase in ion pumping Should reduce outflow resistance slightly
Treatments for shock Must increase cardiac output Oxygen demand less critical - may use ion pumping and increase oxygen supply Must not vasodilate
Positive inotropes Sympathomimetics Glycosides Calcium sensitising agents Indirect - vasodilators
Effects of ischaemia on contractility Increased calcium all the time - cannot be taken up into SR Reduced contractility as less Ca to release and stiff walls Increased diastolic pressure
Effects of adrenaline on contractility Increased Ca in systole as more taken up into SR Increased contractility as more Ca to be released Decreased diastolic pressure
Alternative approaches vasodilators - for chronic ischaemic failure Vasoconstrictors for acute shock
Inotropic mechanisms Sympathetic stimulation - direct or indirect Altered contractile mechanism - calcium sensitization
Phosphodiesterase inhibitors Phosphodiesterase breaks down the second messenger of adrenaline signalling at beta receptors Inhibiting this via methyl xanthines e.g. aminophylline and theophylline increase the effects of sympathetic stimulation
Adrenaline effects Tachycardia Increased cardiac contractility Splanchnic vasoconstriction Skeletal muscle vasodilation at low conc and vasoconstriction at high conc - saturates beta due to high affinity then see alpha effects due to higher potency
Dopamine effects Increased cardiac output - beta 1 adrenergic Generalised vasoconstriction - alpha adrenergic and dopaminergic Vasodilation of gut and kidney - dopaminergic
Dopamine analogues Dobutamine - act via beta 1 receptors to increase contractility with limited vascular effects Dopexamine
Calcium sensitizers Levosimendan - binds to TnC Omecamtiv - myosin activator These increase contractility with no increase in ion pumping - although do have small effects
Glycoside actions Positive inotropic effect No increase in oxygen demand Diuretic effect Decreased sympathetic tone No decrease in life expectancy as is seen in other cardiac failure drugs Delay in onset Narrow therapeutic ratio - easy to overdose Highly toxic
Mechanism of glycosides Inhibit Na K pump Removes Na gradient Stops removal of Ca via Na Ca exchanger More Ca remains in cell to be taken up by SR
Endogenous glycosides Progesterone derivatives Hypertensive Absent in cardiac failure - may develop when glycosides stop being produced - potential treatment option
Endogenous inotropes Glycosides Apelin - don't fully know role in cardiac failure but seems to be absent - potential treatment option
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