1882355
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Flashcards by rachel-chads, updated more than 1 year ago
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Created by rachel-chads
almost 11 years ago
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| Question | Answer |
| What are the phases of a ventricular action potential? | Phase 1: - Fast depolarisation. - It - transient K+ channel - small reploarisation. Phase 2: - Plateau, - Opens Ca2+ channels - maintain depolarisation, - Loss of function = slow. Phase 3: - IKs and IKr - also ATP and ACh activated chanels, - Repolarisation. |
| How is the ventricular action potential duration different in long and short QT syndromes? | - Normal = 0.36s, extended suration compared to nerve AP. - Long = >>0.45s - Short = <<0.34s |
| Why is there the plateau phase of the ventricular action potential? | To prevent summation in the cardiac muscle. |
| What are the implications of QT syndromes? (Triggered activity) | Triggered activity After depolarisations reach threshold Additional beat (ectopic) Ventricular tachycardia Ventricular fibrillation |
| What are the implications of QT syndromes? (Re-entrant excitation) | Re-entrant excitation Different layers of cells impacted Spatial and temporal dispersion refractory perdios Re-entry and AP propagation Ventricular tachycardia Ventricular fibrillation |
| What are the details of Long QT syndrome? | - Prolonged QT interval. - Early death (30s), would run in families with no explanation. - Syncope (fainting.) - Increased risk of sudden death (torsades des pointes - twisting of ECG) - form VT and VF. - Incidence = 1:10,000 to 1:15,000. - 12 forms. - Can be gain of function or loss of function. |
| What is the channelopathy for Long QT Type 1? | Voltage gated K+ channelopathy - KCNQ1 Kv7.1 channel -4 subunits, each has 6 tmsd - loss of function mutations - can be recessive or dominant |
| As well as long QT, what symptoms can LQT1 and LQT5 have? Why? | Deafness. - LQT5 is a mutation in MinK (K+ channel that regualtes KCNQ1). - Mis-regulation of Kv7.1-alpha. - Therefore link between symptoms. |
| Why is the Kv7.1 channel (gene=KCNQ1 - LQT1) important in the ear? | - The channel is important in the production of endolymph (high K+). - K+ comes from cells in the stria vascularis - secrete by Q1/E1. - Reissenser's membrane collapses as there is not enough endolymph - so the person is deaf. (- Channel also in airway, kidney, GI system.) |
| What type of mutations affect which parts of contraction in LQT? | Plateau phase: - gain of function - Na+ and Ca2+ Repolarisation phase: - loss of function - K+ |
| How do K+ channel mutations affect LQT syndrome? | - loss of function - 100% K+ to 75% K+ - takes longer to repolarise as there is fewer channels - as there is still other types of K+ channels there is still repolarisation |
| How do loss of function Na+ channel mutations affect LQT syndrome? | - channels don't close when they should - takes longer to repolarise - Na+ coming in is stopping the K+ ions that are leaving from driving repolarisation |
| What are the treatments of long QT syndrome? | - Beta-blockers - class 2 antidysrhythmic drugs. - Antenolol - beta1 selective antagonist. (increases risk of brochoconstriction in person with asthma or other obstructive lung disease.) - cAMP linked receptor (LQT11 - important in cAMP regulation of channels. - Negative chronotropic and ionotropic actions. - Contra-indictions. |
| What are the details of short QT syndrome? | - Reduce QT interval. Symptoms: - arrhythmias, - palpitations, - syncope (fainting), - VT, VF and sudden death. - 5 forms. - Can also be gain or loss of function. - 75% of cases are in males - suggests it could be X-linked. - Appears in late adolescence. |
| Which mutations affect the plateau phase? and how? | - Loss of function Ca2+ channels. - Less Ca2+ coming in to maintain and drive depolarisation. |
| Which mutations affect the repolarisation phase? and how? | - Gain of function K+ channels. - More K+ leaving the cell. - Repolarisation quicker than normal. (- Gain of function mutations can also mean increased number of channels.) |
| What are the treatments for short QT syndrome? | - Implant defibrillator. - Research suggests quinidine (K+ channel blocker) may be effective. Issues with it as it isn't selective. |
| What is the equation for mean arterial blood pressure? | MABP = Cardiac output x total peripheral resistance |
| What are the likely suspect causes of essential hypertension? | - Cardiac dysfunction (increased response to stress and catecholamines.) - Vessel abnormalities. (eg. vessels constrict more, lack of NO) - Kidney dysfunction. (volume - induced hypertension) |
| Is hypertension genetic? | - EH is familial (not necessarily genetics - same habits). - However it does correlate with relatedness: twin studies, varies with race. - Known environmental risk factors (diet, obesity etc.) - Probably genetic predisposition and lifestyle/environment. |
| How big is the part played by genetic factors? | - Estimate 30-50% is genetic predisposition. - Multiple factors (possibly 5+ unproven key genes). - Best evidence for polymorphisms in: antiotensinogen, ENaC. |
| What are the causes of secondary hypertension? | - Renal disease. - Renal artery stenosis (compromises blood supply to kidneys, narrowing of the arteries, renin production and BP increase.) - Pheochromoctyomas (tumours of adrenal gland). - Hormone inbalance. |
| What are the consquences of hypertension? | - Flushing, sweating, blueered vision. - Arteriosclerosis/atherosclerosis. - Aneurysm. - Stroke. - MI. - Renal damage. |
| What are the non-pharmacological treatments for hypertension? | Lifestyle changes: - Weight loss. - Exercise. - Stop smoking. - Diet (reduce salt, alcohol, caffeine). - Relaxation. |
| What are the pharmacological treatments of hypertension? | - Diuretics. - Sympatholytics: reduce symp. NS impact - alpha blockers, clonidine decreases CNS sympathetic output, prazosin relaxes smooth muscle and decreases TPR. - beta blockers. - Ca2+ channel blockers (minoxidil - broad) (manidipine - selective) - ACE inhibitors (moexipil) - AGII receptor blockers (sartan family). |
| What is excitation-contraction coupling? | When an electrical event of the membrane of a muscle cell is converted into physical muscle contraction. |
| What specialisations rapidly transmit action potentials to the myocardium? | - T-tubules. - Intercalated disks (like gap junctions). |
| How does the Ca2+ concentration change after a muscle cell membrane is excited? | The intracellular calcium concentration rises during the plateau phase from 100nM to 1-10uM. |
| What happens when Ca2+ enters the muscle cell? | - Release of Ca2+ form intracellular organelles (eg. SR.) - Ca2+ binds to cytoskeleton, - Displaces troponin and tropomysocin complex from actin, - Allows myosin to contact actin, - Filament sliding commences. |
| What are the relationships between tension, crossbridges and sarcomere length? | - Muscle tension proportional to the number of cross bridges. - Cross bridges proportional to sarcomere length. - Tension should be proportional to muscle length. |
| How is the length-tension relationship tested? | - Use papillary muscles. - Measurements under isometric conditions (no change in length). - Tension is proportional to starting length. - Maximum tension and crossbridges at sarcomere length of 2.2um. |
| What is the force-velocity relationship? | - Muscle stretched by preload, then stimulated to lift afterload. - Rate it shortens. - Papillary muscle and isotonic contraction (no change in tension). |
| What are the force-velocity relationship experiment results? | - Measure the velocity of shortening with varied pre- and after-loads. - Increased pre-load gives increased maximal force (Po). - Increased pre-load also gives increased velocity - more stretch, stronger contraction. |
| What does contractility measure? | How well the actin and myosin crossbridges are working - quality rather than quantity. |
| When is a change in contractility seen? | - When an intact heart changes it output per beat when the end diastolic volume is constant. |
| What are inotropic effects? | Changes in contractility. They can be positive or negative inotropic effects. (drugs are positive or negative inotropes.) |
| How does noradrenaline impact maximal force (Po) and cardiac muscle contractility (Vmax)? | Noradrenaline increases both Po and Vmax. Positive inotropic (changes in contractility) and chronotropic (chnages in rate of contraction) effects. |
| What is the frequency-force relationship? | Interbeat duration influences the force of contraction. |
| How does Ca2+ relate to the frequency-force relationship? | Multiple systems are regulating Ca2+ (release and entry of Ca2+ from cells, and release from internal stores) Changes in Ca2+ availability alter the amount of calcium in the cytoplasm Responses due to different systems reacting |
| What needs to be measured in order to calculate cardiac output? | 1) Oxygen uptake rate by volume and oxygen content of expired air. 2) Concentration of oxygen in pulmonary artery, using pulmonary artery catheter. 3) Oxygen concentration in pulmonary vein - can be measured by measuring peripheral arterial blood. |
| What other methods can be used to measure cardiac output? | 1) Indicator dilution: - Inject indocyanine green tracer into vein or right atrium. - Sample arterial blood. - Output is proportional to 1/[tracer]. - Dilution will change as it goes through heart/lungs. 2) Thermodilution: - Increase in saline temperature. 3) Ultrasound - Non-invasive. |
| What are the homeometric intristic mechanisms that control cardiac output? | - Positive inotropic effects not related to endocrine/NS. - Treppe: - Strength of contraction increases as heart rate increases. - Increased heart rate also increases cardiac output. |
| What are the heterometric intristic mechanisms that control cardiac output? | End diastolic pressure in regulated by venous return: - As vascular storage decreases, venous return increases. - As blood volume increases, venous output and return increases. - As vascular resistance increases, venous return decreases. - Muscle pump action increases, venous return increases. - Venous return increases during inspiration. |
| How does the parasympathetic NS control cardiac output? | - Vagal firing decreases SA firing and conducting velocity. - Rates of pressure rise and fall decreases. - Cardiac rate and force per beat decreases (fewer, weaker beats). - ACh (released by vagus nerve) decreases sympathetic effects. |
| How does the sympathetic NS control cardiac output? | - Noradrenaline increases firing rate. - Rates of pressure rise and fall increases. - Systolic and diastolic times decrease. - Rate and force per beat increases - increased cardiac output. |
| What humoral factors control cardiac output? | - Adrenaline (+NA) increase rate and force but are minor compared to NS. - Insulin has positive inotropic effects - strength of contraction. - Thyroid hormones increase the rate and force. |
| How is tissue fluid formed? | - Net fluid transfer from capillaries to tissues by a balance of filtration and absorption. - Filtration can be between cells (paracellular) or through cells (transcellular). |
| What does tissue fluid formation depend on? | - Hydrostatic pressure difference between capillary and interstitial fluid. - Difference is colloid osmotic pressure, - Capillary filtration coefficient - ease of flow across vessel wall. |
| What are the humoral (extrinsic) factors involved in the control of circulation? | 1) Adrenal medullary hormones - Adrenaline (+NA): - Released from chromaffin cells, - Vasocontriction of skin/viscera, - Vasodilation of skeletal muscle/liver. 2) Kinins: - eg. Bradykinin, - Vasodilatory peptides. 3) Angiotensin II: - Powerful vasoconstrictor (increases BP significantly), - Formed by enzymes eg. renin - ACE inhibitors for high BP. |
| What are the local agent (extrinsic) factors involved in the control of circulation? | 1) Prostaglandins: - Most are vasodilators. 2) Serotonin: - Platelets release 5-HT to promote vasoconstriction at site of damage to vessel. 3) Histamine: - Promotes vasodilation, - Alters permeability of vessel walls, - Released by immune system (mast cells). 4) Endothelium derived hyperpolarising factors (EDHFs) 5) Endothelium derived relaxing factor (EDRF): - Nitric oxide. - Stimulates cGMP in muscle causing relaxation, increased flow and oxygen. - (viagra inhibits cGMP breakdown - prolonged vasodilation). - Nitroglycerin given to people with angina - general vasodilation including coronary arteries. |
| What are the autonomic (extrinsic) factors involved in the control of circulation? | - Most vessels have tonic (dimmer) sympathetic adrenaline constrictor input (alpha receptors). - Pre-capillary vessels in skeletal muscle, heart, lungs and kidneys have sympathetic ACh vasodilators. - Erectile tissue and glands have parasympathetic ACh vasodilators. |
| Where/why does the density of sympathetic constrictors vary? | - Density of innervation varies 1) Cutaneous = high: - high sympathetic control in order to maintain core body temperature by opening/closing capillary beds. 2) Cerebral = low: - Cerebral circulation must be maintained. - Never need to change amount of blood flow. - Tends to be autoregulated rather than depending on the autonomic NS. |
| What is myogenic regulation? | - It is an example of auto-regulation. - Stretch evokes a contraction. |
| What is the basal tone of vessels? | - Vessels have a resting tension - properties of the wall itself (muscle, elastic fibres etc.) - Low level control designed to give a constant flow - autoregulation. - But then is regulated by metabolites eg. PCO2, pH, PO2, temp, lactate. Those that increase as metabolism increases cause the blood vessels to dilate to get more blood to the area. |
| How can medullary neurones control circulation? | - They can act as sensors - They respond to changes in pH, PCO2 and PO2. - Increasing vasoconstriction, BP increases, bradycardia. - Increasing intracranial pressure decreases PO2 and increases PCO2. Cushing reflex is a physiological response to increased intracranial pressure. |
| What are the peripheral proprioceptors (relay to medulla) that control circulation? | 1) Baroreceptors: - Pressure receptors. 2) Stretch receptors: - Carotid and aortic bodies detect high pressure. - Atria, LV and pulmonary veins detect low pressure. 3) 'Buffer nerves': - Glossopharyngeal and vagus carry info to the brain. - Major roles is to buffer changes in BP. 4) Chemoreceptors: - Primary function in respiration. - Cardiac chemoreceptors - whether heart is receiving sufficient supply. |
| What is the mechanism of buffer nerves when there is an increase in arterial pressure? | Increases in arterial pressure increases firing. Decreased vasoconstrictors, increase cardioinhibition. Vasoldilation, bradycardia, decreased output and BP. Short term regulation (long term regulation by kidneys - control of blood volume.) |
| What are the higher brain regions involved in control of circulation? | 1) Hypothalamus: - Linked to cortex and limbic system. 2) Hypothalamus regulatory centres: - Cold and warm temperature responses. 3) Hypothalamus defence area: - Sympathetic dilation of skeletal muscle. 4) Medial preoptic area: - Sexual responses. 5) Anterior cingulated gyrus: - Bradycardia hypotension (playing dead). |
| What is the cycle of electrical activity in the heart? | - Starts at SA node (conduction = 0.05m/s) - Conduction 1.0m/s via atrial myocardium or bachmann's bundle to LA - AV node (conduction = 0.05m/s) - Fast conduction down bundle of His (1.0m/s) - septal activiation - Purkinje fibres, narrower, maximum conduction speed of 4.0m/s - Ventricular muscle (1.0m/s) |
| What is a pacemaker action potential like? (diagram) | |
| What is a pacemaker action potential like? | - No resting membrane potential. - A reduced maximum. - Starts from a higher voltage than a nerve (closer to -60mV). - Has its own endogenous rhythm. - Pre-potential (pacemaker potential): decreased K+ efflux, increased cation influx. - Threshold = -40 to -50mV, triggers Ca2+ channels to open, increased Ca2+ influx. - Increased K+ efflux causes repolarisation - membrane potential goes back to normal. - Broader peak - takes longer. |
| What is a cardiac muscle action potential like? (Diagram) | |
| What is a cardiac muscle action potential like? | - No automaticity - needs a trigger. - Low resting membrane potential, below -80mV like neurone or skeletal muscle. - Fast depolarisation and repolarisation but long plateau phase. - Atrial muscle - Purkinje fibres - Ventricular muscle |
| What are the ionic events of a cardiac muscle action potential? | - 60-70mV = Na+ channel activation and increased influx - Fast Na+ inactivation at -30 to -40mV, Ca2+ channel opening - Plateau phase - Delayed K+ opening then increases efflux and rapid replorisation. |
| How does ACh and NA control pacemaker cells? | Vagal stimulation: - ACh - hyperpolarisation of membrane and decreased prepotential slope - Slows firing rate. Sympathetic stimulation: - Noradrenaline - Increases prepotential slope - Increased firing rate. |
| What can cause heart block? | - Any part of the heart can be damaged, diseased or abnormally developed. - Impairment of conducting pathways, - Abnormal coronary distribution, - Infarct artery, disease etc. |
| What happens in first degree heart block? | - Slow SA-AV conduction - Increased PR interval on ECG - No symptoms, benign PR = 0.16-0.38s - Training effect in athletes, pathology or adaptation? |
| What happens in second degree heart block? | - Incomplete heart block - some of the SA activity is reaching ventricles, but some SA impulses fail to trigger QRS - Number of P waves exceed QRS complexes: Mobitz Type 1: - PR increase, sometimes no QRS - athletes - benign Mobitz type 2: - Repeated pattern - 2:1 or 3:1 etc. - May require pacing. |
| What happens in third degree heart block? | - Complete heart block as no SA impulses reach AV node. - Doesn't necessarily mean death as ventricles contract themselves. - Driven by alternative pacemakers. |
| What are the consequences of third degree heart block? | - Dissociation of chamber contraction: atria and ventricles not contracting in sync, atrial contraction greater than ventricular contraction. - Jugular A waves (atria) mismatch arterial pulse (radial). - Atria contraction against closed tricuspid valve - blood goes back into veins (cannon wave). - Compromised heart performance, - Reduced perfusion around body, - Dizziness and syncope (fainting). |
| What is seen on a ECG in bundle branch block? | - Tend to see broadening of QRS wave. - Delayed contraction. |
| What is sick sinus sydrome? | - Impaired SA node firing. - Shows periods of bradycardia and tachycardia. - More commonly seen in the elderly. - Familial and age dependent. |
| What is chronic cardiac failure? | - Inability to perfuse tissue at normal filling pressures. - Reduced contractility of the heart. |
| What is chronic cardiac failure evoked by? | - Damaged/dead from infarct - Poor blood supply - Poor energy supply/production/utilisation - Ca2+ transport - important in contraction of muscle |
| How does chronic cardiac failure affect exercise? | - Part of the body's compensation is to act as if it is exercising eventhough it is at rest. Stroke volume maintained until severe. - As a result the exercise response decreases: Body can't cope with exercise on top, Stroke volume cannot be raised, Noradrenaline circling around the body increases, Decreased catecholamine response, Plasma catecholamine increase, Top of Frank Starling curve, Sacromere length vs tension, overstretch muscles of the heart. |
| What are the early compensation mechanisms for chronic cardiac failure? | - Peripheral vasoconstriction, - Constrict veins to shift blood to atrial side, - Increased angiotensin II (vasoconstrictor), - Increased sympathetic activity, - To protect vital systems, - Increased plasma volume increases filling pressure and output, - Decreased renal flow evokes increases Na+/water retention, increasing plasma volume. |
| What is the progression of chronic cardiac failure? | - More blood left in heart after contractions, - Increased venous pressure, - Cardiac dilation impairs muscle and valve function - regurgitation of the blood (ventricles to atria), - Decreased plasma COP promotes oedema. |
| What are the phases of the cardiac cycle? | 1) Ventricular filling 2) Isovolumetric contraction 3) Ventricular ejection 4) Isovolumetric relaxation |
| What is the atrial effective refractory period? | - Allows time fore the artia to contract - Gap between P wave and QRS complex |
| What happens when ventricles contract? | - The increased pressure shuts the atrioventricular valve. - The papillary muscles and chordinae tendinae hold the valve in closed position, stopping backflow. - The valve closing causes the first sound (s1 - lup). - Increased volume in the ventricles but the volume doesn't change (isovolumetric contraction). |
| When does the aortic valve open? | - When the pressure in the ventricle is higher than the pressure in the aorta. - Blood shoots out of ventricle then reduces the rate at which it leaves. |
| What happens when the pressure in the aorta is greater than the pressure in the ventricle? | - Vigorous event - Valve shuts - Second sound (S2 - dub) |
| What happens when the pressure in the ventricles are below the pressure in the atria? | - Atrioventricular valves open - Refilling of blood - Can be vigorous causing turbulent flow and 3rd heart sound (S3). |
| Blood flow into the aorta | - Before the aortic valve opens, the flow is zero. - When the aortic valve opens, blood flows in the aorta shoots up and then drops. - Blood flow then goes negative - back flow into coronary arteries. |
| What are the phases of the jugular pulse? | A wave - atrial contraction (systole), returning blood filling up. C wave - ventricular contraction, tricuspid valve bulging back into right atrium. X descent - atria relaxation, eject blood, pressure decreases. V wave - filling (villing) of the right atrium (passive). Y descent - blood from atria into ventricle. |
| What are the asynchronies between the left and right sides of the heart? and why do they occur? | 1) Right atria contraction before left: - SA node on right side, wave of excitation spreads to left atrium. 2) Left ventricular contraction before right: - Layout of conduction fibres. 3) Right ventricular ejection before left: - Pressure difference between RV and pulmonary trunk less than difference in pressure between the LV and aorta. - Right side circuit works at a much lower pressure. |
| What is mitral stenosis? | - Narrowing/stiffening of the mitral valve. - Affects the sounds heard on an echocardiogram. |
| When does regurgitation occur? | - When the mitral valve doesn't shut properly - Backflow of blood from the ventricle to atria |
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