GoConqr has a new look! Let us know what you think.

Sign up free

Flashcards

L8+9 - Heart Failure

Jack Rowe CPP Year 1 English 116 cards

give the stages of pressure overload causing ventricular hypertrophy

Cards in this deck (116)

  1. 1define heart failureinability of the heart to supply adequate blood flow and O2 delivery to tissues and organs
  2. 2give some symptoms of heart failrue- rapid weight gain
    - shortness of breath
    - lower body swelling
    - dry cough
  3. 3give some structural changes which happen to the heart during heart failure- hypertrophy
    - dilation of chambers
  4. 4are the structural changes of the heart detrimental from the get go?no are beneficial initially but quickly become a hinderance
  5. 5what is used to evaluate and classify the type of heart failrethe ejection fraction
  6. 6give the different types of heart failure in terms of ejection fracrtion- HF with preserved EF
    - HF with mid range EF
    - HF with reduced EF
  7. 7which ventricle is looked at when measuring ejection fraction in heart failurethe left ventricular ejection fractoin
    (LVEF)
  8. 8what % of HF patients see a reduced EF?only around 50%
  9. 9what other tests can be done to diagnose HF?test for levels of ANP and BNP
    (naturetic peptides)
  10. 10what would the levels of naturetic peptides be in HF?elevated
  11. 11on a heart echo scan what structural changes could be seen in HF?- LV hypertrophy
    - hypertrophic L atrium
    - diastolic dysfunction
  12. 12which out of the 3 HF categories (in terms of EF) would beed naturetic peptides tests to diagnose HF?mid range or reduced EF
  13. 13what do ANP and BNP stand for?atrial naturetic peptide
    brain naturetic peptide
  14. 14what causes ANP to be produed?atrial stretching
    (shows why levels are elivated in HF)
  15. 15where does BNP come from?originates in the ventricles in response to stretch and damage
    (same as before about elivated in HF)
  16. 16what does ANP and BNP do?affects the vasculature function
  17. 17which category of HF is the most researched?HF with reduced EF
  18. 18what would be another way to classify HF?- assess a patients ability to do every day tasks
    - level 1 = no indication of HF
    - Level 5 = unable to carry out physical exersise
  19. 19what are the 3 primary causes of HF- pressure overload
    - volume overload
    - contractile dysfunction
  20. 20what could cause pressure overload of the heart- hypertension
    - aortic stenosis
  21. 21what is aortic stenosisdysfunction of the aortic valves
  22. 22what could cause volume overloadaortic of mitral valve regurgetation
    (blood goes back through the valve)
  23. 23give some causes of contractile dyfunsciotn- ischemic heart disease (lack of blood)
    - myocardial disease
    - pregnancy
    - congenital cardiomyopathies
  24. 24what is congenital cardiomyopahthy?irregular heart formation during development
  25. 25explain the implication of having larger ventricles on generation of pressure- larger ventricle has less contractile force meaning less pressure can be generated
    - like trying to blow up a balloon: its harder at the start bc smaller volume
  26. 26why does increased LV pressure cause hypertrophy?increases the stress and the stretching force on the wall
  27. 27give the stages of pressure overload causing ventricular hypertrophygive the stages of pressure overload causing ventricular hypertrophy
  28. 28what happens the ventricular radius during pressure and volume overloadf- increases despite ventricular wall hypertrophy
    - get a saggy heart
  29. 29why does the heart hypertrophy in pressure/ volume overload?the body is trying to compensate for the added load by increasing the muscle mass
  30. 30what is the issue with increased muscle mass of the ventriclesincreased suceptatibilty to ischemia + arrhythma
  31. 31why does increased muscle mass increase chance of ischameia?because there is more cells for the blood to deliver oxygen to increasing chance of deficit
  32. 32give the compensation mechanism used by the ANS in response to LV failre (HINT: thing about the change in CO in LV failre)- CO decreases --> BP falls --> barroreceptors --> increased symNS activity and decreased Para --> increased HR and contractility + vasoconstriction --> BP + CO returns to normal
  33. 33where does vasoconstriction happen during decreased CO/everywhere in the systemic circulation including the renal arteries
  34. 34what does sympathetic stimulation do to the renal arteriescauses vasoconstriction
  35. 35what is the effect of sym activity on renin and ang 2increased renin ang2 leading to increased aldosterone = further vasoconstriction
  36. 36during sym innervation of the kidney what happens to sodium and water retentionaldosterone increases sodium and therefore water retention which increases circulating volume
  37. 37what is the difference between heart failure and hypertrphy caused by exersiseexercise introduces adequate angiogenesis so there is enough blood supply to the new tissue
    - heart failure hypertrophy does not
  38. 38what is the result of insufficient angiogenisis of heart failure patients hearts?O2 imbalance causing ischemia
  39. 39what does ischemia do to contractilitydecreases contractility bc less energy available
  40. 40what happens during collegen deposition in HF patients?collagen is deposited causing fibrosis making the heart more stiff
  41. 41summarise the vicious cycle of heart failuresummarise the vicious cycle of heart failure
  42. 42what is physiological hypertrphywhen an athelete's heart gets stronger + more vasculated
  43. 43when referring to the angiogenesis of the heart by athelete's, what is the blood vessle type?coronary arteries
  44. 44what are the 2 types of pathogenic hypertrophy?concentric and eccentric hypertrophy
  45. 45what happens to the cardiomyocytes during concentric hypertrophy?the cells get shorter and fatter
  46. 46what happens to the cardiomyocytes during eccentric hypertrophythey become longer and thinner
  47. 47in both types of pathogenic hypertrohy, what are some key changes to the cells?- altered energy consumption
    - altered ion balance
    - increased expression of embryonic genes
  48. 48compare the changes in contractility with increased HR in health and in HF- in health increased HR increases Contractility
    - in pathology it initially increases contractility but then starts to fall soon after bc the myocytes cant keep up
  49. 49in health what is the purpose of cardiac fibroblaststhey produce collagen which builds a scaffold for myocytes to work on
  50. 50in HF what happens to the cardiac fibroblastsdisproportionate composision of fibroblasts with increased activity
  51. 51what type of collagen do healthy fibroblasts produce and what is produced in HFtype 1 in health
    type 3 in HF
  52. 52what happens to matrixmetalloprotein activity during HF and what is the result- their activity reduces so they dont regulate fibroblasts as well as in health
    - there is increased fibroblast activity and reduced removal of collagen
  53. 53what is replacement fibrosisin ischemia myocytes die and fibroblasts fill the gaps with collagen
  54. 54what is the initial benefit and the chronic cost of fibrosisinitially improves force generation but over time becomes more difficult so less blood is ejected
  55. 55how do cyardiomycocytes and fibroblatss communicatr- ion transfer
    - physical exchange
    - production of paracrine factors
  56. 56are paracrine factors long or short distance acting molecules?short distance
  57. 57what do paracrine factors initiate- hypertrophy
    - cell proliferation
    - fibrosis (excess collagen production)
  58. 58what happens to the interstitial space size during reactive fibrosisbecomes much thicker
    more collagen present
  59. 59what is the difference between reactive and replacement fibrosis- replacement is caused by myocyte loss so collagen fills in the space where they used to be
    - reactive doesnt need myocyte loss and is caused by something else instead
  60. 60give some of the causes of reactive fibrosispressure and volume overload
  61. 61what is perivascular fibrosiscollagen deposition in perivascular regions of vasculature caused y signalling molecules
  62. 62what signalling molecule is involved in perivascular fibrosisendothelin 1
  63. 63what is athrogenisisplaque formation
  64. 64can the vasculature get ischemia during HFyes
    can lead to necrosis and apoptosis
  65. 65what happens in HF to cause inapropreate vasoconstriction of the systemic?- increased production of ang2 and endothelin 1
    - decreased production of prostaglandins, NO and other vasodilative substances
  66. 66what happens to pre-load and after load during vasoconstrictionthey both increase
  67. 67define pre-load and after-load- pre load is the stretch on the sarcomeres caused by increased filling
    - after load is the pressure which the heart needs to work against to eject blood
  68. 68what causes the afterload to increase in HFincreased vasoconstriction increases the blood pressure so there is more work to overcome opening the aortic valve etc
  69. 69what is the normal hydrostatic and osmotic pressures at the capillerys? (in terms of net filtration vs reabsorption)- hydro pressure in caps higher than osmotic in interstitium at arteriole end
    - reverse seen at venous end    what is the normal hydrostatic and osmotic pressures at the capillerys? (in terms of net filtration vs reabsorption)
  70. 70give the net movement of fluid at the pulmonary capillaries and whynet out filtration as the osmotic pressure is higher than hydrostatic pressure the whole way across
  71. 71what happens to pulmonary capillery filtration during HF and whyincreased out filtration because pulmonary hydrostatic pressure increases so greater drive for outfiltration
  72. 72what does the greater outfiltration in the pulmonary caps causepulmonary congestion and oedema in extreme cases
  73. 73give the 2 stages of pulmonary oedema- pulmonary interstitial oedema
    - pulmonary alveolar oedema
  74. 74what happens to gas exchange during pulmonary oedemadecreases bc diffusion distance drastically increases
  75. 75how can drugs afftect the heart directly?they can affect HR, rhythm, force of contraction
  76. 76how can drugs affect the heart indirectly- can affect vasculature, blood volume/ composition
    - all will affect how well the heart pumps
  77. 77what are the 4 classes of drugs which can be used to treat heart failure- cardioinhibitory drugs
    - cardiostimulatory drugs
    - vasodilators
    - diuretics
  78. 78which of the 4 drugs are directly acting on the heart?cardio inhibitory and stimulatory
  79. 79what is the first line drugs for patiients with HFrEF (HF w reduced EF) (HINT: think of the common heart medicines used)- ACE inhibitors
    - Beta blockers
    - Diuretics
  80. 80how do beta blockers work on the heart?bind to B1 adrenoreceptors blocking sym activity
  81. 81where are NAD and adrenaline produced ?- NAD is produced by the neurones innervating the SAN and ventricles
    - adrenaline is produced by adrenal gland and circulates to the heart
  82. 82what sym effects are inhibited by beta blockers- ionotropy (contractility)
    - chronotropy (HR)
    - dromotropy
  83. 83what is dromotropyincreased electrical activity through the heart - e.g decreased conduction slowing at AVN
  84. 84how do B blockers affect the vasculature?cause mild vasoconstriction but dont have much affect at all
  85. 85what would you expect B blockers to do in HFREF patients? why is this actually a good thing?- despite the reduced ejection fraction there would be a further decrease in CO because the HR and contractility decrease
    - this is a good thing tho bc breakes the vicious cycle
  86. 86what does ACE inhibitors do to help with HFcause vasodilation by inhibiting conversion of ANG1 --> ANG2 so reduced vasoconstrictive effect
  87. 87how do the effects of ACE inhibitors help with HF treatment?decreased vasoconstriction decreases hypertension and therefore pressure overload of the heart
  88. 88how do angiotensin receptor blockershelp with HFtarget same pathway as ACE inhibitors but these instead prevent angiotensin binding rather than conversion
  89. 89what pathway is blocked by the angiotensin blockersblocks following pathway:
    - ANG binds to G protein causing increased IP3 and calcium release from the SR
    - calcimu release normally causes increased activity of MLK increasing smooth muscle contraction
  90. 90why might ang inhibitor be used over ACE inhibotrsfewer side effects
  91. 91how do Diuretics help with HF- increase volume expulsion at kidneys to decrease hypervolumia
    - decreases high volume on heart
  92. 92give some different diuretics which can be used- LOOP diurectics
    - thiazides
    - potassium sparing
  93. 93how do loop diuretics work- inhibit sodium - potsssium - chloride cotransporters in the ascending limb of loop
    - decreases ion reabsorption and therefore water reabsorption
  94. 94why might thiazide diuretics be preferred to loop?because they're less powerful so wont have as extreme a diuretic effect
  95. 95what 2 types of diuretic are often used in conjunction with each other and why?thiazides + K+ sparing to prevent hypokalemia
  96. 96what is digitalisa potent Na/K+ ATPase inhibitor that works in the heart
  97. 97what does digitalis do to sodium clacium exchange indirectly and what is the result of this?- increases sodium/ calcium exchange increasing contractility
    - so more calcium in cell less sodium in cell
  98. 98what does digitalis do to EF?increases it
  99. 99what are the parasympothomimietic properties of Digitalalisreduces HR so heart has more time to relax between beats
  100. 100why is it benificial for the heart to have more time to relax due to digitalis?has lower requirement for ATP bc has more resting time
  101. 101why isnt digitalis used anymore- easy to overdose which would kill you by causing calcium conc to increase too much causing arrythmia
  102. 102compared to the renin-angiotensin-aldosterone system, what does ANP and BNP dohas the opposite effect to the RAS system by causing vasodilation to reduce the amount of stretch applied to the heart
  103. 103what effect do ANP and BNP have on renin nad GFR at the kidneyreduced renin and GFR causing diuresis to lower circulating volume
  104. 104what drugs can be used with work with the ANP and BNP's to HFrecombinant human BNP used to increase their activity
  105. 105how do naturetic peptides cause vasodilationbind to receptor causing cGMP synthesis leading to dilation
  106. 106how do NP's compare to ACE inhibotprsNP's are more effective
  107. 107what is a funny currenta current which carries sodium into the myocyte during the pacemaker potential
  108. 108what transporter carries sodium into the cell during the pacemaker potentialHCN transporter
  109. 109what happens when the myocyte reaches thresholdL type calcium ion channels open causing influx of calcium
  110. 110how would inhibitors of funny current (HCN) treat HFdecreases membrane potential amplitude leading to slower HR
  111. 111what are nitrodilatorsdrugs which cause vasodilation e/g NO or enzymes that work in the pathway of NO
  112. 112give the actions of nitrodilators on the systemic vasculature, the cardiac cells and coronoary arteriesgive the actions of nitrodilators on the systemic vasculature, the cardiac cells and coronoary arteries
  113. 113give the different types of beta receptors locations and how their agonists affect the organgive the different types of beta receptors locations and how their agonists affect the organ
  114. 114give some emergency use drugs for heart failure- dopamine
    - adrenaline
    - noradrenaline
  115. 115why are phosphodiesterase inhibitors not used anymorebecause they can cause arrythmia
  116. 116give the effects of phosphodiestease inhibitors on systemic circulation and the cardiopulmonarygive the effects of phosphodiestease inhibitors on systemic circulation and the cardiopulmonary

Information

Description
Year 1 CPP Flashcards on L8+9 - Heart Failure, created by Jack Rowe on 22/12/2022.
Created by
Jack Rowe
Views
6
Rating

More on Heart Failure

Feedback

What is it about?

What do you think of the new look?

How do you like it?