| Term 
 | Definition 
 
        | a complex syndrome that can result from any structural or functional disorder that impairs the ability of the heart to function as a pump to support a physiological circulation |  | 
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        | Term 
 
        | What are some common causes of HF? |  | Definition 
 
        | - ischaemic heart disease (CAD) - cardiomyopathy
 - hypertension
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        | Term 
 | Definition 
 
        | - shortness of breath (dyspnoea) - swelling of the legs (oedema)
 - exercise intolerance
 - fatigue
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        | Term 
 
        | What are 5 tell-tale signs of HF? |  | Definition 
 
        | 1. pulmonary oedema 2. peripheral oedema
 3. ascites
 4. hepatomegaly
 5. raised jugular venous pressure
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        | Term 
 | Definition 
 
        | the gastroeneterological term for the accumulation of fluid in the peritoneal cavity |  | 
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        | Term 
 | Definition 
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        | Term 
 
        | What is the pattern of the NYHA classification? |  | Definition 
 
        | 1 = no limitations of phys activity, no normal activity 4 = severe of phys activity, symptoms at rest
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        | Term 
 | Definition 
 
        | maintained HF that is subdivided on basis of dominant feature systolic vs diastolic
 left vs right side
 congested
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        | Term 
 | Definition 
 
        | large dilated heart with impaired systolic performance decreased ejection fraction (less than 45%)
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        | Term 
 | Definition 
 
        | impaired diastolic filling (stiffness) |  | 
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        | Term 
 | Definition 
 
        | when impaired ventricular systolic function is present, this causes pooling of the blood in the periphery, which would normally be received by the RV |  | 
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        | Term 
 | Definition 
 
        | accumulation of fluid in the pulmonary circulation; much more common than right-sided heart failure but progresses to right sided heart failure |  | 
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        | Term 
 
        | What are the aims of HF treatment? |  | Definition 
 
        | - relieve symptoms - improve exercise tolerance
 - reduce mortality
 
 NO CURE
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        | Term 
 
        | What forms the basis of most HF treatment? |  | Definition 
 
        | primary malfunction leads to maladaptive secondary chnages. treatment corrects these changes
 
 however, some treatments do work by improving contractility of the heart
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        | Term 
 
        | Briefly state the autonomic dysfunctions and what they lead to |  | Definition 
 
        | - increased sympathetic activity - decreased parasympathetic activity
 
 leads to vasoconstriction -> increases afterload
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        | Term 
 
        | What does increased sympathetic activity cause? |  | Definition 
 
        | - increased force of contraction - increased heart rate
 - repolarisation and restoration of function following generalised cardiac depolarisation
 - reduced cardiac efficiency (O2 consumption is increased more than cardiac work)
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        | Term 
 
        | What does decreased parasympathetic activity cause? |  | Definition 
 
        | - cardiac slowing and reduced automaticity - inhibtion of AV conduction
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        | Term 
 
        | Briefly state the neurohumoral dysfunctions and what they lead to |  | Definition 
 
        | - renin-angiotensin system - vasopressin
 - aldosterone
 - endothelin
 
 leads to vasoconstriction, salt retention therefore fluid retention and increased preload
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        | Term 
 
        | What receptors do large coronary vessels posses? |  | Definition 
 
        | alpha-adrenoceptors that mediate vasocontriction |  | 
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        | Term 
 
        | What receptors do smaller coronary vessels posses? |  | Definition 
 
        | beta2-adrenoceptors that have dilatory effect |  | 
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        | Term 
 | Definition 
 
        | the pressure against which the heart has to pump (arterial pressure) |  | 
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        | Term 
 | Definition 
 
        | the amount the ventricle is stretched by at the end of diastole (EDV) |  | 
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        | Term 
 
        | How is the renin-angiotensin system linked to sympathetic stimulation? |  | Definition 
 
        | 1. increased noradrenaline from sympathetic NS 2. stimulates aldosterone secretion (enhances Na+ reabsorption)
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        | Term 
 | Definition 
 
        | ADH antidiuretic
 power vasoconstrictor in skin and other vascular beds
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        | Term 
 
        | What do V1 receptors mediate? |  | Definition 
 
        | vasoconstriction requires higher ADH levels
 activates PLC
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        | Term 
 
        | What do V2 receptors mediate? |  | Definition 
 
        | water retention requires lower levels
 activates adenylate cyclase
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        | Term 
 | Definition 
 
        | vasoconstrictors vasodilation (long lived)
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        | Term 
 
        | What are the structural changes in HF? |  | Definition 
 
        | myocytes : hypertrophy cardiac muscle : increased deposition of ECM components such as collagen
 blood vessel : changes in endothelial function
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        | Term 
 
        | What are the effects of reducing preload (with HF treatment)? 
 LOOK AT DIAGRAMS
 |  | Definition 
 
        | 1. fluid retention decreases 2. preload decreases
 3. pulmonary oedema decreases
 4. gas exchange increases
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        | Term 
 
        | What are the reducing of reducing afterload (with HF treatment)? 
 LOOK AT DIAGRAMS
 |  | Definition 
 
        | 1. vasodilation occurs 2. afterload decreases
 3. impedance to output of LV decreases
 4. cardiac output increases
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        | Term 
 
        | What are the 5 treatments for HF? |  | Definition 
 
        | 1. beta blockers 2. ACE inhibitors
 3. Diuretics
 4. Cardiac glycosides
 5. vasodilators
 
 these treatments are usually used in combination
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        | Term 
 
        | Why is the use of beta blockers in HF paradoxical? |  | Definition 
 
        | they slow the HR and reduce contractility, thus reducing the heart's ability to function as a pump. but we want to increase CO
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        | Term 
 
        | How a change in preload affect SV? |  | Definition 
 
        | in a CHF patient, preload changes has little effect on SV therefore causes congestion when pressure (ventricular) is so high |  | 
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        | Term 
 
        | How a change in afterload affect SV? |  | Definition 
 
        | in a CHF patient, SV is reduced dramatically as aortic pressure increases until SV is low it causes low output symptoms |  | 
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        | Term 
 
        | What is the outcome if ventricular filling pressure is high on the L-side? |  | Definition 
 
        | - left side receives blood from the lungs - congestion on this side
 - therefore congestion on the lungs
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        | Term 
 
        | What are the beneficial effects of beta blockers? |  | Definition 
 
        | - inhibition of central sympathetic outflow - direct vasodilation
 - prevention of remodelling (hypertrophy or fibrosis)
 - reduced dysrhythmias
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        | Term 
 
        | Describe first gen beta blockers |  | Definition 
 
        | non selective (binds to beta 1 and 2) eg propranolol |  | 
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        | Term 
 
        | Describe second gen beta blockers |  | Definition 
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        | Term 
 
        | Describe third gen beta blockers |  | Definition 
 
        | selective or non selective with additional desirable effects eg carvedilol |  | 
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        | Term 
 
        | what does alpha receptor stimulation cause? |  | Definition 
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        | Term 
 
        | what does beta receptor stimulation cause? |  | Definition 
 
        | vasodilation therefore beta blockers cause vasoconstriction
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        | Term 
 
        | Describe the effects of carvedilol |  | Definition 
 
        | causes vasodilation via alpha receptors block |  | 
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        | Term 
 
        | What are the adverse effects of beta blockers |  | Definition 
 
        | - bronchoconstriction (asthma) - cold extremities
 - fatigues
 - sleep disturbances (propranolol)
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        | Term 
 
        | Describe the Angiotensin system |  | Definition 
 
        | In low BP 1. angiotensin is converted into active form angiotensin I via renin
 2. ACE converts angiotensin I to angiotensin II
 3. Angiotensin II causes vasoconstriction, fluid retention and aldosterone release
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        | Term 
 
        | How is the RAS activated? |  | Definition 
 
        | mechanoreceptors detect: - decreased SV
 - decreased BP
 - decreased perfusion rate
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        | Term 
 
        | Give ACE inhibitor example |  | Definition 
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        | Term 
 
        | Adverse ACE inhibitor effects |  | Definition 
 
        | - hypotension - hyperkalaemia -> dysrhythmia
 - avoided in patients with impaired kidney function
 - cough
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        | Term 
 
        | When are AT1 receptor blockers used? |  | Definition 
 
        | instead of or in conjunction with ACE inhibitors block vasoconstriction and fluid retention
 they produce a more complete blockade of RAS than ACEI alone
 
 LOSARTAN
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        | Term 
 
        | What are the benefits of using AT1 alone? |  | Definition 
 
        | selective blockage of AT1 receptor preserves potentially beneficial effects of AT2 receptor stimulation |  | 
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        | Term 
 
        | What are the adverse effects of AT1 receptor blockers? |  | Definition 
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        | Term 
 | Definition 
 
        | drugs that increase the rate of urinary excretion and consequently reduce symptoms of oedema and improve exercise capacity |  | 
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        | Term 
 
        | How do diuretics achieve this? |  | Definition 
 
        | increase salt and water excretion decrease EDV
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        | Term 
 
        | How are diuretics classified? |  | Definition 
 
        | where they act within the kidney and their potency |  | 
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        | Term 
 | Definition 
 
        | most potent act on the loop
 eg furosemide
 
 for severe congestion
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        | Term 
 
        | Describe distal tubule diuretics |  | Definition 
 
        | non K+ sparing = chlorothiazide K+ sparing = amiloride
 
 mild oedema
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        | Term 
 
        | Adverse effects of diuretics |  | Definition 
 
        | volume depletion (hypoperfusion, dehydration postural hypotension) hypokalaemia
 hyperkalaemia
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        | Term 
 | Definition 
 
        | a significantly low level of perfusion |  | 
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        | Term 
 
        | Define postural hypotension |  | Definition 
 
        | blood pressure suddenly falls when standing up or stretching |  | 
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        | Term 
 
        | Example of cardiac glycoside |  | Definition 
 
        | digoxin 
 - reduces symptoms, improves exercise tolerance but does not increase survival
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        | Term 
 
        | What are the effects of cardiac glycoside |  | Definition 
 
        | 1. increase force of contraction 2. decrease sympathetic drive
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        | Term 
 
        | Describe how cardiac glycosides increase force of contraction |  | Definition 
 
        | 1. inhibit NaKATPase (which normally removes Na from the cell) 2. Increase [Na]i
 3. Na/Ca exchange
 4. Increase [Ca2+]i
 5. increased contraction
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        | Term 
 
        | Describe how cardiac glycosides decrease sympathetic drive |  | Definition 
 
        | 1. sensitisation of high pressure baroreceptors 2. reduces central sympathetic flow
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        | Term 
 
        | Which vasodilators are there? what do they do |  | Definition 
 
        | Nitrates (isosorbide dinitrate) and hydralazine 
 decrease ventricular preload and afterload
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        | Term 
 | Definition 
 
        | NO donors which cause vasodilation |  | 
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        | Term 
 
        | How does hydralazine work? |  | Definition 
 
        | reduces [Ca2+]i and may be an antioxidant |  | 
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