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| Question | Answer |
| Drug effects on cardiac muscle: Heart-related diseases that can be treated by drugs | - Angina: temporary chest pain - Myocardial infarction 'heart attack': sustained chest pain and cell death due to coronary thrombosis - Arrythmias: lack of normal heart rythum - Heart failiures: insufficient cardiac output to meet body's needs - Hypertension: high blood pressure |
| Drug effects on cardiac muscle: ways drugs can improve heart function | 1. By acting on the cardiac muscle itself 2. By acting on the blood vessels eg coronary arteries, which in turn affects blood flow to the heart. |
| 2 types of action potential at the heart | 1. Pacemaker currents at the SA and AV nodes. Depolarisation caused by calcium entry, repolarisation caused by potassium loss. This is generated by the turning on of the If (funny current), because it's ion channels have unusual properties 2. Action potential at other areas eg in the ventricles; AP is caused by fast entry of sodium through voltage-gated sodium channels (Ina). This results in entry of Ca+, through voltage gated 'L-type' Ca channels before potassium loss causes repolarisation. |
| Endogenous regulation of the heart; Actions of the parasympathetic NS on the heart | - Acetylcholine is released from the vagus nerve into heart cells, deceases heart rate, having a negative chronotrophic effect. - -Acts on M2 muscarinic receptors in th SA node to open receptor operated K+ channels. - hyperpolarises receptor cells, as K+ ions leave the cells, slowing heart rate. - Has no effect on contractile force |
| Action of Ach on the SA node pacemaker | - During parasympathetic stimulation, there is hyperpolarisation and slower decay before another opening of Ca/K+ channels due to blocking of If, so the heart rate slows down |
| Cardiac actions of drugs that mimic or inhibit the parasymathetic ns: Muscarinic agonists | - not clinically used for cardiac effect - However may have a side effect of slowing the heart; particually anticholinestherases |
| Cardiac actions of drugs that mimic or inhibit the parasympathetic NS: Muscarinic antagonists | - Atropine; can be used in an emergency to increase a dangerously slow heart rate (bradyarrythmia) - Ivabradine; inhibits pacemaker 'funny current' If in SA node, slowing HR independently independently of Ach/PNS. Useful for treating heart failiure and angina, as it reduces cardiac O2 demand |
| Endogenous regulation of the heart; actions of the sympathetic NS: effect of adrenalina and noradrenaline on the heart | Noradrenaline from NTs and adrenal medulla and adrenaline from the adrenal medulla have a number of effects of the NS: - Increase HR - Increase contractile force, thus increasing stroke volume (volume pumped out per beat) - Increases cardiac output - Mediated cheifly by B1 adrenoreceptors on heart muscle cells - |
| Endogenous regulation of the heart: actions of the sympathetic NS: Mechanisms of NA and A | B1 adrenoreceptor stimulation leads to phosphorylation of intracellular proteins by protein kinase A (PKA): 1.. G protein in membrane binds to B1 receptor, causing alpha subunit to become detached from G protein, and attaches to adenyl cyclase also in the cell membrane 2. This activates adenyl cyclase, which then converts ATP to cyclic AMP- cAMP 3. cAMP activates PKA, which phosphorylates a set of proteins, altering their functions. |
| Actions of noradrenaline/adrenaline on the SA node pacemaker | - when NA/A activate the SA node pace maker there is faster diastolic desensitisation, meaning cells reach the threshold for opening of calcium channels more quickly, raising the HR. - This is partly due to an increase in the opeining of If |
| Cardiac excitation/contraction coupling | - calcium enters through the voltage gated calcium channel in the t-tubule, increasing calcium concentration in the cell. - this activates the opening of calcium channels at the sarcoplasmic reticulum, causing calcium to leak out, increasing calcium conc in the cell to increase further - calcium then binds to troponin, causing contraction - calcium is then pumped back into the sarcoplasmic reticulum via ATPase, as well as being pumped out of the cell. |
| B-adrenoreceptor stimulation increases force and relaxation of cardiac contraction | - Increase of force of contraction in cardiac muscle is driven by a rise in calcium - with sympathetic stimulation by the same thing occurs, but with more force and decays more quickly. -positive inotrophic effect- - this is due to an increased calcium entry into the cell during the action poteintial soa as a result more calcium is taken up into the SR, more calcium is released form the SR - faster ca uptake into the SR causes faster delay |
| Actions of drugs that mimic the actions of the sympathetic NS | B adrenoreceptor agonists eg isoprenaline and dobutamine: increase force and contraction in patients with acute heart failiure. |
| Actions of drugs that inhibit the actions of the sympathetic NS | EG Betablockers- beta-adrenoreceptor antagonists - Used in treating many cardiovascular diseases - Block the effect of sympatheicic stimulation on the heart Decrease HR and force, especially during exercise Decrease arterial BP (afterload) - Decrease carsiac work and O2 demand - Have little effect at rest EG Propanolol b1 and b2 adrenoreceptors bisoprolol- b1 selective |
| Cardiac glycosides | Positive inotropes; increase force of contraction EG Oubain- from the african 'posion arrow tree' Digitalis -from the foxglove Digitoxin- for some types of heart failiure |
| Mechanism of action of cardiac glycosides | - affect the Na/Ca exchange pump (NCX) Under normal conditions in the NCX: * Na flows into the cell; the energy it loses is coupled by NCX exchanger to drive calcium out against a large electrochemical gradient. The pumping out of the calcium utilises energy lost from sodium ions as they fall down their conc gradient in the cell* Effect of cardiac glycosides on the Na/Ca exchange pump: - Decrease sodium gradient by partially blocking Na/K ATPase leading to: - Increased Na in the cell, so less calcium is pumped out via NCX - This results in there being increased calcium in the cell - This results in more calcium being taken up into the sarcoplasmic reticulum. - Then , when SR is triggered to release calcium, more calcium is released, resulting in a strengthened heartbeat. |
| Ranolazine- mechanism and side effects/issues | Ranolazine represents a new class of antianginal drugs. It blocks late inward sodium currents in cardiomyocytes. ... By blocking late inward sodium currents, calcium overload and diastolic wall stress are reduced, leading to improved coronary blood flow. |
| Calcium channel blockers eg verapamil and nifedipine | - Both verapamil and nifedipine reduce Ca+ entry via voltage-gated calcium channels: * Verapamil does this in the heart * Nifedipine does this in smooth muscle - Reducing calcium entry results in decrease in contractile force in cardiac muscle (negative inotrope). - They are also used as anti-arrhythmic drugs due to thier effect on the AV node. - They also relax vascular smooth muscle, dilating arteries, making them useful in treating high blood pressure and angina |
| Arrythmias | - Arrythmias are mainly caused by ectopic sites of action potential generation - Are sorted into two classes: 'superventricular' (have origins in atrial tissue or AV node) or 'ventricular' (have origins in the ventricle) Arrythmias are typically the result of myocardial ischemia or structural abnormalities |
| Antiarrythmic drugs | - Most antiarrythmic drugs treat tachyarrythmias (HR too high), by decreasing the excitability of the tissue Therefore, there will be ectopic APs generated/conducted to the rest of the heart OR prolong the AP and thus refractory period resulting in the myocardium being less able to conducthigh-frequency APs |
| The 4 classes of antiarrythmic drugs | Class 1 eg Lidocane. Blocks fast Na+ channel, reducing excitability in the cardiac muscle but not SA/AV nodes as it doesnt affect Ca+ channel Class 2 eg Metaprolol. Acts as B1adrenoreceptor antagonists, reducing arrythmias due to sympathetic over-activity. Class 3 eg amiclarone. Blocks K+ channels from being repolarised. Prolongs AP and therefore refractory period. Class 4 eg verapamil. Blocks L-type Ca2+ channels, reducing excitability at SA and AV nodes. |
| Ways in which drugs can improve heart function: 1. By acting on the heart muscle itself | - Acting on the heart muscle itself, improving heart function by slowing or strengthening it |
| 2. Acting on blood vessels | Drugs can improve heart function by acting on blood vessels. For example vasodilators and thrombolytics can act on the coronary arteries to increase coronary blood flow and thus O2 supply - Can also decrease arterial resistance and dilate veins with nitrates to reduce cardiac work |
| Summary: Drugs can be used to alter cardiac function by directly affecting the actions of the autonomic nervous system on the heart: | - Mimicking the ANS- done by muscarinic receptor/ B1 adrenorecepor agonists - Blocking the ANS- done muscarinic receptor/B1 adrenoreceptor antagonists - Acting independently of the heart, altering blood vessel diameter, which indirectly affects cardiac function by changing blood flow to and from the heart |
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