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Flashcards

CRH CARDIOVASCULAR

Dan Aduakwa Medicine Year 1 English 176 cards

Explain the action potential of a ventricular myocyte.

Cards in this deck (176)

  1. 1Where are spontaneously firing cells located in heart?Sino-Atrial Node
    Atrioventricular node
    Bundle of his
  2. 2Where is the SA node located?The wall of the right atrium just lateral to the sinus venarum at the junction where the superior vena cava enters the right atrium.
  3. 3Where is the AV node located?It is located at the centre of the heart, in the floor of the right atrium, between the atria and ventricles.
  4. 4Where are the bundle of his located?They are located at the inferior end of the inter-atrial septum, to the ventricles of the heart.
  5. 5What is the pathway of electrical excitation in the heart?1. SA node
    2. Rapidly though atria
    3. AV node (0.5 sec delay)
    4. rapidly through bundle of his, branches and purkinje fibre
    5. through ventricular muscle.
  6. 6What is one factor that aids in the rapid spread of excitation though the heart?The presence of intercalated discs between cardiac cells (they're microscopic identifying features of cardiac muscle).
  7. 7Define gap junction.A specialized intercellular connection between a multitude of animal cell-types. they provide a low resistance pathway for electrical impulses.
  8. 8What is myocardium?Heart muscle.
  9. 9What is the function of the delay in AV node?Enables efficient emptying of blood from the atria into the ventricles.
  10. 10What is the function of the ventricular excitation occurring synchronously?Enables ventricles to contract as co-ordinated units and hence expel blood efficiently.
  11. 11Explain the action potential of a ventricular myocyte.Explain the action potential of a ventricular myocyte.
  12. 12Function of the refractory period.The refractory period prevents fused contraction so that there are clear atrial and ventricular contractions.
  13. 13Describe the action potential of a SA node cell.Describe the action potential of a SA node cell.
  14. 14What is the effect of the increase in sympathetic nerve activity on the cardiac system?Increase heart rate by activation of beta-1 adrenoreceptors in the SA node.
  15. 15What is the effect of the increase in parasympathetic nerve activity on the cardiac system?Decrease in heart rate due to the activation of M2 muscarinic receptors in the SA node.
  16. 16Why would heart rate increase, were nerves to the heart to be cut?The parasympathetic nervous system dominates at rest.
  17. 17Which heart chamber has the most cardiac muscle?Left ventricle as it pumps blood to the whole body.
  18. 18Draw and label the arch of the aorta any subsequent blood vessels.Draw and label the arch of the aorta any subsequent blood vessels.
  19. 19What causes the aortic valve to open and stay open?If the pressure in the left ventricle exceeds aortic pressure, the aortic valve will open and as long as the ventricular pressure exceed aortic pressure the valve will remain open.
  20. 20How much blood is emptied from the ventricles in a single contraction?Only about half of the blood is ejected as it makes it easier to refill when its not completely empty.
  21. 21Outline the cardiac cycle.1. Atrial systole.
    2. Isovolumetric ventricular contraction
    3. Ventricular ejection
    4. Isovolumetric ventricular relaxation
    5. ventricular filling.
  22. 22What occurs in atrial systole?Rise in atrial pressure, A-V valves open and atria empty into ventricles.
  23. 23What occurs in Isovolumetric ventricular contraction?Increase in ventricular pressure closes the A-V valves. pressure is generated but no blood is ejected.
  24. 24What occurs in ventricular ejection?Ventricular pressure is greater than aortic pressure and thus, aortic valves open and blood is ejected.
  25. 25What occurs in Isovolumetric ventricular relaxation?Ventricular pressure drops below aortic pressure so the aortic valve shuts. Ventricular pressure is still higher than atrial pressure so the A-V valves stay shut.
  26. 26What occurs in ventricular filling?Ventricular pressure drops below atrial pressure and as such, the valves open and blood enters the ventricles. It does require atrial systole to start to fill up the ventricles, its a passive action.
  27. 27What do pulsations in the internal jugular vein reflect?Right atrial pressure changes
  28. 28What makes the low pitched LUB heart sound?A-V valve closure.
  29. 29What makes the high pitched DUP heart sound?Aortic/pulmonary valve closure.
  30. 30What makes the third heart sound?Vibration of ventricular call when filling
  31. 31What makes the fourth heart sound?Associated with ventricular filling during atrial systole.
  32. 32How does stenosis cause abnormal heart sounds?Stenosis (narrowing) which creates a steep pressure gradient across the valve. This causes a murmur when the valve opens, e.g. aortic stenosis.
  33. 33How do leaky/incompetent valves cause abnormal heart sounds?Flow can occur in different directions and as such there is a murmur when the valve should be closed, e.g. aortic regurgitation.
  34. 34What is the equation for cardiac output?What is the equation for cardiac output?
  35. 35What does cardiac output depend on?Factors affecting heart rate and stroke volume.
  36. 36What are the factors affecting heart rate?1. Sympathetic nervous system.
    2. Parasympathetic nervous system.
    3. Hormones.
    4. Extra/intracellular ions.
  37. 37Define stroke volume.The volume of blood ejected from the heart in a single heart beat.
  38. 38What factors affect stroke volume?1. Pre-load
    2. cardiac contractility
    3. After-load
  39. 39Define Pre-load.(Left ventricular end diastolic pressure)Amount of ventricular stretch at the end of diastole. Think of the heart loading up for the next big squeeze. Like blowing up a balloon, the more you blow, the more it stretches, the more pressure.
  40. 40Define After-load.(Systemic vascular resistance). The amount of resistance the heart must overcome to open the aortic valve. It is like the knot in the balloon. To get the air out you have to overcome the knot.
  41. 41If more blood is returned to the heart than usual, what happens in terms of the amount of blood pumped back out of the heart?More blood returned to the heart stretches the cardiac muscle so they contract with more force and pump out more blood.
  42. 42What is the effect of increased end diastolic volume (pre-load) on stroke volume?It leads to an increased stroke volume, as stretched cardiac muscles contract more forcefully, pushing out more blood.
  43. 43What is the effect of an increased aortic pressure (after-load) on stroke volume?It leads to a decreased stroke volume as more energy would be needed to overcome the aortic pressure so there is a delay before blood can start to be ejected and as such less blood is pushed out.
  44. 44What happens to the next heart beat after an increased aortic pressure.The next heart beat, the EDV is going to be higher and as a result there will be a higher stroke volume to restore the left ventricular volume back to normal.
  45. 45What is the result of increased cardiac contractility on stroke volume?It increases stroke volume.
  46. 46Define Haemodynamics.The physical laws governing pressure/flow relationships in blood vessels
  47. 47What is the equation for flow of blood?R- measure of the degree to which the tube (blood vessel) resists the flow of liquid.
    Delta P- Pressure difference between arteries and veins    What is the equation for flow of blood?
  48. 48What are the individual vessel diameters in decreasing size?Aorta>arteries>arterioles>capillaries< venules
  49. 49Rank the cross sectional vessel areas in increasing size.Aorta Venules>Veins>Vena Cava.
  50. 50What are the principles of Darcy's law of flow?1.Directly related to pressure difference
    2. Inversely related to the resistance.
  51. 51What are the principles of Poiseuille's law of flow?1. Directly related to pressure difference
    2. Inversely related to length of tube
    3. Inversely related to viscosity of fluid
    4. directly related to radius of tube.
  52. 52What is the equation for Poiseuille's law of flow?look on pg 33, 34 and 35 of book.
  53. 53What kind of flow needs a higher driving force to achieve flow?Turbulent flow.
  54. 54How is elasticity conferred to vessels?Elastin and Collagen
  55. 55Explain how skeletal muscle helps venous return.Leg muscles contract, squeezing blood from superficial veins to deep within the heart.
  56. 56Explain how respiration helps venous return.Respiration decreases intra-thoracic pressure and increases intra-abdominal pressure, hence provides a pressure gradient to assist blood flow back to the heart.
  57. 57What is the law of Laplace?The larger the vessel radius, the larger the wall tension required to withstand a given internal fluid pressure. For a given vessel radius and internal pressure, a spherical vessel will have half the wall tension of a cylindrical vessel.
  58. 58What is the function of surfactants of the lung?Decrease surface tension , they disrupt surface interactions in the lungs.
  59. 59Give an example of surfactants preventing lungs from collapsing.For example if there are two alveoli of different size, the small alveoli have high intra-alveolar pressure and the large alveoli have high intra-alveolar pressure. Air goes from high pressure to low pressure. small alveoli collapse, affecting lung function. surfactants reduce surface tension preventing this.
  60. 60What is infant respiratory distress syndrome? (neonatal respiratory distress syndrome)Insufficient surfactant production by foetus, meaning alveoli start to collapse and lungs are difficult to inflate.
  61. 61How do you treat IRDS?pre-birth: corticosteroids to speed up lung development.
    After-birth: surfactant replacement therapy.
    high levels of oxygen.
  62. 62What does a spirometer look like?What does a spirometer look like?
  63. 63Define tidal volume.The volume of air entering and leaving the lung with each normal breath = 0.5l
  64. 64Define inspiratory reserve volume.Extra volume of air inspired above the normal tidal volume with full force = 3.3l
  65. 65Define expiratory reserve volume.Extra volume of air expired by forceful expiration at the end of normal tidal expiration = 1.7l
  66. 66Define vital capacityMaximum amount of air expelled from the lungs after first filling the lungs to a maximum and then expiring to the maximum. (TV+IRV+ERV). = 5.5L
  67. 67Define functional residual capacity.The amount of air that remains in the lungs at the end of normal expiration. (ERV+IRV) = 3.5l
  68. 68Define total lung capacity.The maximum volume of air the lungs can hold. (VC+RV) = 7.3l
  69. 69Describe forced expiratory volume.Total volume exhaled = 5l
  70. 70Define FEV1.0Volume expired within the first second. typically 70% of FVC
  71. 71What is a lung restrictive deficit.1. Lung expansion is compromised- alterations in the lung parenchyma
    2. Lungs do not fill to capacity and hence are less full before expiration.
    3. pulmonary fibrosis and scoliosis.
  72. 72Define Parenchyma.The portion of the lungs intended for gas exchange, the alveoli, alveolar ducts and respiratory bronchioles.
  73. 73Define an obstructive lung deficit.Characterised by airway obstruction, if airways are narrowed they can still fill to capacity. Resistance is also increased on expiration. FEV1.0 will be reduced however forced vital capacity will stay approx. the same.
  74. 74Why is forced expiration so important?It is one of the most informative, yet simple tests to carry out.
  75. 75Which part of haemoglobin does oxygen attach to?The haem group.
  76. 76Which part of haemoglobin does CO2 attach to?The globin group
  77. 77What does a graph depicting Hb saturation of O2 over partial pressure of O2 look like?What does a graph depicting Hb saturation of O2 over partial pressure of O2 look like?
  78. 78What is the effect of raised temperature on affinity of haemoglobin to oxygen?It lowers the affinity of Hb for 02. graph shifts to right
  79. 79What is 2,3- DPGA glycolytic intermediate produced within the RBC that affects the affinity of Hb for oxygen. lowered Ph in RBCs decreases the mount of 2,3-DPG and vice versa. increases in 2,3-DPG shift oxygen dissociation curve to right (bad)
  80. 80What is the effect of decreased carbon dioxide on oxygen saturation in Hb?Increases oxygen saturation. Shift to left
  81. 81What is the effect of decreased H+ (higher Ph) dioxide on oxygen saturation in Hb?Increases oxygen saturation. Shift to left
  82. 82What is the difference between foetal haemoglobin and adult haemoglobin?Foetal haemoglobin has 2 gamma instead of 2 beta chains. They have a high affinity for oxygen , shift to the left .
  83. 83Define hypoxia.Inadequate supply of oxygen to body tissues.
  84. 84Define Hypoxaemic hypoxia.Interferance with ventilating, e.g. co2 poinsoning.
  85. 85Define anaemic hypoxia.Decreased amount of red blood cells, abnormal Hb.
  86. 86Define Ischaemic hypoxia.Impaired or blocked blood circulation.
  87. 87Define Histotoxic hypoxia.Body cells cant use O2 even if there is adequate supply, e.g. cyanide poisoning.
  88. 88Define cyanosis.1.Bluish discolouration of the skin and mucus membranes
    2. sign of heart failure, lung diseases, respiratory distress.
  89. 89CONTROL OF BLOOD VESSELSCONTROL OF BLOOD VESSELS.
  90. 90What are three main things that determine vascular resistance.Directly related to length of vessel.
    directly related to viscosity of fluid.
    INDIRECTLY related to vessel radius .
  91. 91What is the most important factor determining radius?arteriolar diameter.
  92. 92What does the vessel radius (diameter) depend on?Active tension exerted by smooth muscle
    passive elastic properties of the wall.
    blood pressure inside the vessel.
    Tissue pressure outside the vessel (veins)
  93. 93what balance maintains vessel Calibre?The balance between distending pressure and wall tension.
  94. 94Is wall tension bigger in larger or smaller vessels?Larger vessels
  95. 95What is the law of laplace?What is the law of laplace?
  96. 96What does active control of vessel calibre allow?Redistribution of blood flow,
    control of pre/post capillary sphincters
    regulation of vascular tone and control of blood pressure.
  97. 97Define Vascular toneThe degree of constriction/dilation.
  98. 98What factors affect vascular smooth muscle contraction?Sympathetic nerves
    hormones- e.g. noradrenaline/adrenaline (constrict/dilate)
    vasopressin, angiotensin (constrict)
    Bradykinin (dilate)
  99. 99What percentage of cardiac output is cerebral?14%
  100. 100What are the neural, local, hormonal and mechanical factors affecting coronary regulation?Neural: relatively minor control.
    Hormones: minor importance.
    Local: good auto regulation of flow. important metabolic control during mental activity, H+, K+, adenosine, hypoxia, all cause vasodilation.
    mechanical: in a rigid cranium, influenced by cerebrospinal fluid pressure. if inter cranial pressure increases cerebral blood flow is decreased
  101. 101define cardiac outputThe amount of blood put out by the left ventricle of the heart in one contraction is called the stroke volume. The stroke volume and the heart rate determine the cardiac output. A normal adult has a cardiac output of 4.7 liters (5 quarts) of blood per minute.
  102. 102BLOOD FLOW REGULATION IN SPECIFIC REGIONS.BLOOD FLOW REGULATION IN SPECIFIC REGIONS.
  103. 103What percentage of cardiac output is coronary?4%
  104. 104What are the neural, local, hormonal and mechanical factors affecting coronary regulation?neural: minor direct influence. secondary effect on flow due to changes in cardiac function.
    Local: major influence of metabolites: hypoxia, hypercapnia etc
    hormonal. adrenaline- vasodilator and stimulates metabolism.
    mechanical: major influence on flow during cardiac cycle; peak flow in early diastole
  105. 105What percentage of cardiac output is skin.4% at rest in thermoneutral environment.
  106. 106What are the neural and local factors affecting regulation of skin blood flow?neural: arterioles have a relatively weak innervation. A-V anastomosis have dense innervation.
    local: arterioles show some degree of myogenic auto regulation. A-V anastomosis show no auto regulation and no reactive hyperaemia.
  107. 107What are the hormonal and mechanical factors affecting regulation of skin blood flow?Hormonal: angiotensin, vasopressin, noradrenaline and adrenaline all cause vasoconstriction.
    Mechanical: minimal influence.
  108. 108What is a special factor affecting the regulation of skin blood flow?Primary function is thermoregulation. Sweat glands have sympathetic cholinergic innervation which can cause vasodilation via release of e.g. bradykinin.
  109. 109too long to write out, read pages 45-47too long to write out, read pages 45-47
  110. 110SYSTEMIC ARTERIAL BLOOD PRESSURE, BARORECEPTORS ETCSYSTEMIC ARTERIAL BLOOD PRESSURE, BARORECEPTORS ETC
  111. 111What are the average systolic, diastolic and normal blood pressures?Systolic BP= 120mmHg
    Diastolic BP= 70mmHg
    mean BP= DBP+ 1/3 PP (pulse pressure= SBP-DBP)
  112. 112What is systolic blood pressure determined by?Stroke Volume: ( amount of blood pumped from the heart per beat)- Increase in StV increase SBP
    Aortic elasticity: decrease in elasticity decreases DBP.
  113. 113What is diastolic blood pressure determined by?Peripheral resistance: Increase in TPR, increase DBP
    Aortic elasticity: decrease in elasticity, decrease in DBP
  114. 114What is the equation for mean arterial blood pressure?MAP= CO x TPR
  115. 115How is control of arterial blood pressure achieved?Pressure sensors (in circulation)
    Integration centres (in CNS)
    Effector mechanisms (via autonomic nervous system)
  116. 116What is another name for pressure sensors?Baroreceptors.
  117. 117Where are baroreceptors located?Arch of aorta and main arteries that supply the CNS and brain.
  118. 118What is the effect of the autonomic nervous system on the heart?Parasympathetic: Acetyl choline, muscarinic receptors decrease HR
    sympathetic (noradrenaline, B1 adrenoreceptors , increase HR and force (StV).
  119. 119OEDEMAOEDEMA
  120. 120Describe the structure of capillariesHave no smooth muscle in their walls, only endothelial cells are sites of exchange.
  121. 121Explain solvent movement across capillaries.It is not uniform. Depends on permeability which can vary between tissue. Determined by diffusion, filtration, pinocytosis
  122. 122what is bulk flow?Movement of a volume of protein free fluid out of the capillary (filtration) and back (reabsorbtion)
  123. 123What happens to pressure up and down stream if a capillary constricts?Increased pressure upstream
    decreased pressure downstream.
  124. 124Define oedema.a condition characterized by an excess of watery fluid collecting in the cavities or tissues of the body, causing swelling
  125. 125What are the possible causes of oedema?Lymphatic obstruction (reduced drainage)
    increased venous pressure
    hypoproteinaemia (e.g. renal damage)
    hypervolaemia
    inflammation (vasodilation and increased permeability)
  126. 126HEART FAILUREHEART FAILURE
  127. 127Define heart failure.Failure of the heart as a pump to meet circulatory needs. may be due to failure of the heart muscle or failure of the valves.
  128. 128What is heart failure precipitated by?Pregnancy
  129. 129What is often secondary to heart failure?Hypertension
    IHD
    Cardiomyopathies- disease of the cardiac muscle.
  130. 130Define IHD(Ischemic Heart Disease) Coronary artery disease is a blockage or narrowing (stenosis) of the arteries that supply blood to the heart muscle, often due to a buildup of fatty plaque inside the arteries. A severe enough blockage may cause a heart attack.
  131. 131What tends to cause right sided heart failure?It is often due to lung disease (cor pulmonale) and pulmonary valvular stenosis.
  132. 132Explain biventricular failure.Both chambers. The disease has affect both ventricles. LVF, leads to pulmonary congestion, which may lead to RVF.
  133. 133Symptoms of left ventricular failure.Pulmonary oedema
    dyspnoea
    cough
    orthopnea
    inspiratory crepitations
  134. 134Symproms of right sided ventricular failure.Raised venous pressure
    increased JVP
    Enlarged liver
    oedema- ankles. If lying down it spreads to the ankles.
  135. 135How do ACE inhibitors work?They reduce arterial and venous vasoconstriction (reduce after and pre-load). They reduce salt/water retention, hence reduce circulating volume. Inhibits RAS, prevents cardiac remodelling.
  136. 136What are some of the side effects and cautions of using ACE inhibitors?Monitor urea/ creatinine & K+ before and during treatment. may cause sever hypotension- Withdraw diuretic therapy a few days before. Can cause deterioration of renal function in pre existing renal disease.
  137. 137Give an example and function of angiotensin II receptor antagonistLOSARTAN
    Angiotensin II acts like AT1 receptors. AT1 receptor antagonists block the action of AII. They don't give rise to a cough. They are an alternative to ACE inhibitors.
  138. 138Describe beta blockers.Used to be contraindicated in CHF, now it is the first line. It is beta1 selective. e.g Metoprolol, bisoprolol. They reduce sympathetic stimulation, heart rate and O2 consumption. Especially useful in failure associated with ischaemia.
  139. 139Explain Diuretics.They reduce circulation volume by increasing urine production. It reduces preload on the heart. It also relieves pulmonary and peripheral oedema.
  140. 140Explain Digoxin.It is a cardiac glycoside
    Its a positive inotrope by inhibiting Na+/K+ ATPase, Na+ accumulates in the myocytes, exchanged with Ca2+ leading to increased contractility.
  141. 141Diagram on pg 71Diagram on pg 71
  142. 142What does the electrocardiogram give information about?Timing and direction of cardiac events.
    Rate/rhythm disturbances.
    Conduction abnormalities.
    Mass of active myocardium.
  143. 143What are important rules of positive electrodes for interpretation of an electrocardiogram.Depolarisation moving towards a positive electrode gives an upward deflection.
    depolarisation moving away from a positive electrode gives a downward deflection.
    If W.O.D is perpendicular to electrode, no deflection.
  144. 144What are important rules of negative electrodes for interpretation of an electrocardiogram.Depolarisation moving towards a negative electrode gives a downward deflection. Depolarisation moving away from a negative electrode gives an upward deflection.
  145. 145What is the effect of positioning of electrodes.A focally positioned negative electrode records the same thing as a diametrically opposite positive electrode. Combined measure of the change in potential difference means that bipolar recording configuration gives a deflection of a larger amplitude than unipolar.
  146. 146What are the rules for repolarisation in an electrocardiogram.The opposite than depolarisation.
  147. 147Why are there so many probes when doing an electrocardiogram?During excitation, wave fronts of depolarisation move through the atria and ventricles, in various directions. At any instant, the recorded potential difference is the vectorial resultant of several differently placed wave fronts.
  148. 148What is the cardiac cycle of excitation.SA Node- Atria- AV node- Ventricles
  149. 149What are the 4 phases (only 3 Visible)1.Atrial depolarisation
    2. Ventricular depolarisation (obscures atrial repolarisation)
    3. Ventricular repolarisation
  150. 150How are the P, Q, R, S, T waves labelled on the electrocardiogram.The first wave, irrespective of its polarity, is always called a P wave. The last wave I always called the T wave (unless Uwaves are present). First positive wave after P is R. Any negative wave after p, before R is Q. Any negative wave after R is S. Any positive wave after S is R'.
  151. 151HYPERTENSIONHYPERTENSION
  152. 152Define hypertension.A blood pressure associated with significant cardiac risk
  153. 153Goals of hypertensive treatment?Bring down blood pressure to NICE guidelines (SBP<140, DBP< 90)
  154. 154Read over all treatments on pg 86-89Read over all treatments on pg 86-89
  155. 155Function of ACE inhibitors. RAMIPRILReduction in angiotensin II which leads to reductions in arterial and venous vasoconstriction. Reduced aldosterone production leads to reductions in salt and water
  156. 156Function of AT1 receptor antagonists LOSARTANBlock the action of AII at the AT1 receptor. These agents have similar consequences as ACEI's but don't give rise to a cough.
  157. 157Function of Calcium channel blockers. VERAPAMIL.Inhibit voltage operated Ca2+ channels on vascular smooth muscle, leading to vasodilation and reduction in BP.
  158. 158Function of Diuretics. Thiazides.Third line antihypertensive. Inhibit Na+/Cl- in distal convoluted tubule, reducing the circulating volume. Has big side effects.
  159. 159What are the side effects of Diuretics?Hypokalemia
    postural hypotension
    impaired glucose control.
  160. 160Function of Alpha blockers. PRAZOZIN.These are competitive receptor antagonists of b1 adrenoreceptors. last choice antihypertensives,
  161. 161Function of B-Blockers. PROPANOLOL.Mechanism for action is unclear. Reduction in sympathetic drive to heart, reducing cardiac output. A reduction in sympathetically evoked renin release.
  162. 162FOETAL AND ADULT CIRCULATIONFOETAL AND ADULT CIRCULATION
  163. 163What is the function of the ductus arteriosus?Allows a shunt from the right ventricles straight into the aorta, by passing the lungs.
  164. 164What is the function of the foramen ovale?allows blood from right atrium to left atrium, by passing lungs
  165. 165What are the changes to circulation at birth?Closure of umbilical vessels
    closure of foramen ovale
    reduction of pulmonary vascular resistance
    closure of ductus arteriosus
    closure of ductus venosus
  166. 166Define Ischaemic heart disease.Ischemic Heart Disease, also known as Coronary Artery Disease, is a condition that affects the supply of blood to the heart. The blood vessels are narrowed or blocked due to the deposition of cholesterol on their walls
  167. 167What diseases can result from IHD?Angina and MI.
  168. 168Define Angina.A condition marked by severe pain in the chest, often also spreading to the shoulders, arms, and neck, owing to an inadequate blood supply to the heart,
  169. 169What are the pharmacological treatments for ischaemic heart disease?Beta- blockers
    Nitrates
    calcium channel blockers
    potassium channel activators
    antiplatelet drugs
    statins
  170. 170Describe Nitrates.Release of NO.
    Venodilation: leading to an decrease in preload and a reduction in cardiac work.
    Coronary vasodilation.
  171. 171Describe beta blockers.First choice drud for prevention. They black b2- adrenoreceptors. reduces cardiac work and symptoms.
  172. 172What group of people SHOULD NOT take B-blockers.Asthmatics shouldn't take beta blockers as they may still block b2 adrenoreceptors and cause smooth muscle constriction.
  173. 173Describe calcium channel blockers.Vasodilation and improve coronary blood flow, helping to alleviate symptoms.
  174. 174Describe antiplatelet drugs.They prevent thromboembolism, low dosage aspirin or clopidogrel.
  175. 175Describe statins.They are HMG-CoA reductase inhibitors. e.g. simvastatin. they reduce plasma cholesterol levels. This leads to an up regulation of hepatic LDL receptors, promoting LDL uptake.
  176. 176Which two drugs should you not combine?Don't combine a B-blocker with rate limiting agent, Ca channel blocker its fatal and can stop the heart.

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Year 1 Medicine (CRH) Flashcards on CRH CARDIOVASCULAR, created by Dan Aduakwa on 29/07/2016.
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