Karteikarten
L8+9 - Heart Failure
Karten in diesem Stapel (116)
- 1define heart failureinability of the heart to supply adequate blood flow and O2 delivery to tissues and organs
- 2give some symptoms of heart failrue- rapid weight gain
- shortness of breath
- lower body swelling
- dry cough - 3give some structural changes which happen to the heart during heart failure- hypertrophy
- dilation of chambers - 4are the structural changes of the heart detrimental from the get go?no are beneficial initially but quickly become a hinderance
- 5what is used to evaluate and classify the type of heart failrethe ejection fraction
- 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 - 7which ventricle is looked at when measuring ejection fraction in heart failurethe left ventricular ejection fractoin
(LVEF) - 8what % of HF patients see a reduced EF?only around 50%
- 9what other tests can be done to diagnose HF?test for levels of ANP and BNP
(naturetic peptides) - 10what would the levels of naturetic peptides be in HF?elevated
- 11on a heart echo scan what structural changes could be seen in HF?- LV hypertrophy
- hypertrophic L atrium
- diastolic dysfunction - 12which out of the 3 HF categories (in terms of EF) would beed naturetic peptides tests to diagnose HF?mid range or reduced EF
- 13what do ANP and BNP stand for?atrial naturetic peptide
brain naturetic peptide - 14what causes ANP to be produed?atrial stretching
(shows why levels are elivated in HF) - 15where does BNP come from?originates in the ventricles in response to stretch and damage
(same as before about elivated in HF) - 16what does ANP and BNP do?affects the vasculature function
- 17which category of HF is the most researched?HF with reduced EF
- 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 - 19what are the 3 primary causes of HF- pressure overload
- volume overload
- contractile dysfunction - 20what could cause pressure overload of the heart- hypertension
- aortic stenosis - 21what is aortic stenosisdysfunction of the aortic valves
- 22what could cause volume overloadaortic of mitral valve regurgetation
(blood goes back through the valve) - 23give some causes of contractile dyfunsciotn- ischemic heart disease (lack of blood)
- myocardial disease
- pregnancy
- congenital cardiomyopathies - 24what is congenital cardiomyopahthy?irregular heart formation during development
- 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 - 26why does increased LV pressure cause hypertrophy?increases the stress and the stretching force on the wall
- 27give the stages of pressure overload causing ventricular hypertrophy
- 28what happens the ventricular radius during pressure and volume overloadf- increases despite ventricular wall hypertrophy
- get a saggy heart - 29why does the heart hypertrophy in pressure/ volume overload?the body is trying to compensate for the added load by increasing the muscle mass
- 30what is the issue with increased muscle mass of the ventriclesincreased suceptatibilty to ischemia + arrhythma
- 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
- 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
- 33where does vasoconstriction happen during decreased CO/everywhere in the systemic circulation including the renal arteries
- 34what does sympathetic stimulation do to the renal arteriescauses vasoconstriction
- 35what is the effect of sym activity on renin and ang 2increased renin ang2 leading to increased aldosterone = further vasoconstriction
- 36during sym innervation of the kidney what happens to sodium and water retentionaldosterone increases sodium and therefore water retention which increases circulating volume
- 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 - 38what is the result of insufficient angiogenisis of heart failure patients hearts?O2 imbalance causing ischemia
- 39what does ischemia do to contractilitydecreases contractility bc less energy available
- 40what happens during collegen deposition in HF patients?collagen is deposited causing fibrosis making the heart more stiff
- 41summarise the vicious cycle of heart failure
- 42what is physiological hypertrphywhen an athelete's heart gets stronger + more vasculated
- 43when referring to the angiogenesis of the heart by athelete's, what is the blood vessle type?coronary arteries
- 44what are the 2 types of pathogenic hypertrophy?concentric and eccentric hypertrophy
- 45what happens to the cardiomyocytes during concentric hypertrophy?the cells get shorter and fatter
- 46what happens to the cardiomyocytes during eccentric hypertrophythey become longer and thinner
- 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 - 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 - 49in health what is the purpose of cardiac fibroblaststhey produce collagen which builds a scaffold for myocytes to work on
- 50in HF what happens to the cardiac fibroblastsdisproportionate composision of fibroblasts with increased activity
- 51what type of collagen do healthy fibroblasts produce and what is produced in HFtype 1 in health
type 3 in HF - 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 - 53what is replacement fibrosisin ischemia myocytes die and fibroblasts fill the gaps with collagen
- 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
- 55how do cyardiomycocytes and fibroblatss communicatr- ion transfer
- physical exchange
- production of paracrine factors - 56are paracrine factors long or short distance acting molecules?short distance
- 57what do paracrine factors initiate- hypertrophy
- cell proliferation
- fibrosis (excess collagen production) - 58what happens to the interstitial space size during reactive fibrosisbecomes much thicker
more collagen present - 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 - 60give some of the causes of reactive fibrosispressure and volume overload
- 61what is perivascular fibrosiscollagen deposition in perivascular regions of vasculature caused y signalling molecules
- 62what signalling molecule is involved in perivascular fibrosisendothelin 1
- 63what is athrogenisisplaque formation
- 64can the vasculature get ischemia during HFyes
can lead to necrosis and apoptosis - 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 - 66what happens to pre-load and after load during vasoconstrictionthey both increase
- 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 - 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
- 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
- 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
- 71what happens to pulmonary capillery filtration during HF and whyincreased out filtration because pulmonary hydrostatic pressure increases so greater drive for outfiltration
- 72what does the greater outfiltration in the pulmonary caps causepulmonary congestion and oedema in extreme cases
- 73give the 2 stages of pulmonary oedema- pulmonary interstitial oedema
- pulmonary alveolar oedema - 74what happens to gas exchange during pulmonary oedemadecreases bc diffusion distance drastically increases
- 75how can drugs afftect the heart directly?they can affect HR, rhythm, force of contraction
- 76how can drugs affect the heart indirectly- can affect vasculature, blood volume/ composition
- all will affect how well the heart pumps - 77what are the 4 classes of drugs which can be used to treat heart failure- cardioinhibitory drugs
- cardiostimulatory drugs
- vasodilators
- diuretics - 78which of the 4 drugs are directly acting on the heart?cardio inhibitory and stimulatory
- 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 - 80how do beta blockers work on the heart?bind to B1 adrenoreceptors blocking sym activity
- 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 - 82what sym effects are inhibited by beta blockers- ionotropy (contractility)
- chronotropy (HR)
- dromotropy - 83what is dromotropyincreased electrical activity through the heart - e.g decreased conduction slowing at AVN
- 84how do B blockers affect the vasculature?cause mild vasoconstriction but dont have much affect at all
- 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 - 86what does ACE inhibitors do to help with HFcause vasodilation by inhibiting conversion of ANG1 --> ANG2 so reduced vasoconstrictive effect
- 87how do the effects of ACE inhibitors help with HF treatment?decreased vasoconstriction decreases hypertension and therefore pressure overload of the heart
- 88how do angiotensin receptor blockershelp with HFtarget same pathway as ACE inhibitors but these instead prevent angiotensin binding rather than conversion
- 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 - 90why might ang inhibitor be used over ACE inhibotrsfewer side effects
- 91how do Diuretics help with HF- increase volume expulsion at kidneys to decrease hypervolumia
- decreases high volume on heart - 92give some different diuretics which can be used- LOOP diurectics
- thiazides
- potassium sparing - 93how do loop diuretics work- inhibit sodium - potsssium - chloride cotransporters in the ascending limb of loop
- decreases ion reabsorption and therefore water reabsorption - 94why might thiazide diuretics be preferred to loop?because they're less powerful so wont have as extreme a diuretic effect
- 95what 2 types of diuretic are often used in conjunction with each other and why?thiazides + K+ sparing to prevent hypokalemia
- 96what is digitalisa potent Na/K+ ATPase inhibitor that works in the heart
- 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 - 98what does digitalis do to EF?increases it
- 99what are the parasympothomimietic properties of Digitalalisreduces HR so heart has more time to relax between beats
- 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
- 101why isnt digitalis used anymore- easy to overdose which would kill you by causing calcium conc to increase too much causing arrythmia
- 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
- 103what effect do ANP and BNP have on renin nad GFR at the kidneyreduced renin and GFR causing diuresis to lower circulating volume
- 104what drugs can be used with work with the ANP and BNP's to HFrecombinant human BNP used to increase their activity
- 105how do naturetic peptides cause vasodilationbind to receptor causing cGMP synthesis leading to dilation
- 106how do NP's compare to ACE inhibotprsNP's are more effective
- 107what is a funny currenta current which carries sodium into the myocyte during the pacemaker potential
- 108what transporter carries sodium into the cell during the pacemaker potentialHCN transporter
- 109what happens when the myocyte reaches thresholdL type calcium ion channels open causing influx of calcium
- 110how would inhibitors of funny current (HCN) treat HFdecreases membrane potential amplitude leading to slower HR
- 111what are nitrodilatorsdrugs which cause vasodilation e/g NO or enzymes that work in the pathway of NO
- 112give the actions of nitrodilators on the systemic vasculature, the cardiac cells and coronoary arteries
- 113give the different types of beta receptors locations and how their agonists affect the organ
- 114give some emergency use drugs for heart failure- dopamine
- adrenaline
- noradrenaline - 115why are phosphodiesterase inhibitors not used anymorebecause they can cause arrythmia
- 116give the effects of phosphodiestease inhibitors on systemic circulation and the cardiopulmonary
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- Beschreibung
- Year 1 CPP Karteikarten am L8+9 - Heart Failure, erstellt von Jack Rowe am 22/12/2022.
- Erstellt von
- Jack Rowe
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