walker heart

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walker heart
2012-02-17 15:13:04

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  1. congestive heart failure definition
    syndrome involving right, left or both sides of the heart causes inadequate cardiac output
  2. low output failure
    • cardiac causes
    • 1.decreased contractility
    • 2. restricted volume
    • 3. valve dysfunction
    • post cardiac causes
    • 1.increased resistance to outflow
  3. high output failure
    • increased tissue demand
    • fluid dynamics-over hydration
    • vascular shunts
  4. compensitory reflex mechanisms
    • neuronal mechanisms
    • 1.increased sympathetic tone and increased hr&bp, re distribution of blood to vital organs
    • 2. reduced blood flow to kidnesy-->na & h2o retention
    • neuroendocrine mechanisms
    • 1.increased renin and erthropoiten release from kidney-->vasoconstriction--> elevated BP-->increased blood volume
    • increased aldosterone from adrenal gland-->increaased water retention
  5. autoregulatory mechanism of CHF
    • anoxia causes structures in the heart to secrete catecholamines-->self stimulation
    • atrium produces Atrial natuirueti factor
  6. mechainical factors leading to CHF
    • increased preload causes increased ventricular filling pressure
    • causes ventricular dialation, ventricular thinning and stretching and isotonic contraction with reduced ejection velocity
  7. symptoms of CHF
    weakness, fatigue, dyspenia, edema
  8. cardiac glycosides
    • alglycone and 1-4 sugars
    • obtained from floxglove plant
  9. digoxin
    • variable GI absoprtion
    • half life is 36 hours
    • peak effect 3-6 hours after oral administration
    • not metabolized and excreted unchanged from original state
  10. digitoxin
    • high absorption
    • long half life-5-7 days
    • peak effect-6-12 hours
    • metabolized by liver
  11. cardiac effects of cardioglycosides
    • increased velocity and maximum force of contraction
    • incrased cardiac output, decreased heart size and decreased venous and capillary pressure
  12. noncardiac effects of cardioglycosides
    • increased renal blood flow
    • incrased sodium and water excretion
    • decreased peripheral resistance adn venous tone
  13. clinical uses of cardioglycosides
    • low output cardiac failure
    • atrail fibrilation
    • paroxysmal atrial tachycardia
  14. dosing of cardiogylcosides
    • higher loading dose with a low maintance dose
    • narrow therapeutic index-patients need to be closely monitered
    • lethal dose is 5-10x minimal effective dose
    • toxic dose is 2-3x therapeutic dose
  15. adverse effects of cardioglycosides
    anorexia, nausea, vomiting, diarrhea, headache fatigue, malaise, neuralgias, delerium, vision changes
  16. adverse cardiac speecific effects of cardioglycosides
    • premature ventricular contractions
    • veentricular tachycardia and fibrillation
    • A-V dissociation and block
    • arrythmias and S-A block
    • atrail tachycardia
  17. amrione
    • used in advance CHF for short term application when other treatment methods are inneffective
    • given only via IV
  18. angina pectoris
    • type of chest pain characterized by sudden pressing substernal pain
    • radiates to left arm
  19. causes of angina
    • myocardial blood flow is insufficient to meet the oxygen demands of the heart
    • reduced blood flow cauesed by narrowing of the larger coronary vessels
    • mosy common cause is arteriolar sclerosis
  20. types of angina
    fixed, variant, unstable
  21. fixed angina
    • caused by arteriolar sclerotic narrowing of one or more of the coronary arteries
    • commonly occurs following activities that increases the heart oxygen demand
  22. variant angina
    • caused by a reduction of oxygen delivery
    • cuased by spontaneous spasms of coronary vessels
  23. unstable angina
    • change in character, frequency, duration and precipitating factors in patients with stable or variant angina
    • if the patient has unstable angina they are likely going to have a MI and should have vigorous therapy to prevent it
  24. classes of antiangial drugs
    • organic nitrates
    • beta blockers
    • calcium channel blockers
  25. organic nitrates general action
    • diulates both capcitance veins and peripher resistant vessels (arterioles) and coronary vessels
    • effect is most seen in veins-reduces its preload into the heart and leaes more blood in the veins
    • decreased platelet aggregation and adhesion
  26. mechanism of action of organic nitrates
    drugs interact wtih slfahydryl groups in vessel endothelial cells to produce NO which diffuses into the plateet cells and the arterial smooth muscle adn reduces the levles of intracellular calicum. with less intracellular calicum there is more muscle rleacation and vasodialation
  27. classification of organic nitrates
    • agents wiht rapid onset time adn short durations of actions are:
    • used to terminate acute anginal attacks
    • nitroglycerin-bipasses the first pass metabolism
  28. nitroglycerin
    • used as a rapid onset time organic nitrate
    • it bipasses the first pass metabolism by using sublingual or IV methods
  29. longer onset time organic nitrates
    • used to prevent anginal attacks adn are administered orally
    • nitroglycerin in a patch
    • isobide 5-mononitrate
  30. organic nitrate tolerance
    • a sulfahydryl groups are used up the organic nitrates lose their physiological effects
    • an incrasing dose is then needed to maintina the same clincal effect
    • the patient takes the drug duirng sleep so that the body has enough time to reincrease the sulfahydryl groups
  31. dependance on orgnic nitrates
    • too rapid of a withdrawl from these drugs after chronic administration canresult in acute MI, ischemia or even death
    • adverse rxns include:headache, flushing, orthostatic hypotension, nausea/vomiting
  32. drug interactions of organic nitrates
    can result in potentation of hypotensive effects
  33. beta adrenergic blockers
    • non-cardioselective-propranolol
    • cardioselective-atenolol, metopropolol
    • betal blockers wtih intrinisc sympathomimetic activity-pindlol and acebutolol
  34. calcium channel blockers general action
    • reduce angina by reducing the hearts work
    • dilation of peripheral resistance vesssels and relactation of cardaic muscle
    • increases oxygen supply to the heart
    • dilation of coronary arteries leads to direct dilation
  35. mechiams of action of calcium channel blockers
  36. movement of calcium and sodium ions into or moving potassium out of the cardiac and vascular smmoth muscle--> muscle contraction
    calcium channel vlocekrs blow the influx of calcium through voltage gated channels--> muscle relaxation
  37. nifedipine
    • primary action is on vascular smmoth muscle
    • used in variant angina
    • incrased blood glow into the coronary vessels reduces peripheral resistance
    • causes reflex tachycardia
  38. verapamil
    • effects both vascular smooth muscle and cardiac muscle
    • reduces hearts work, ocygen demand and peripheral resistance
    • increases blood flow to coronary vessels
    • no reflex tachycardia
    • must be careful if the patient is also taking digoxin
  39. dilizem
    • has effect on both vascular smooth muscle and cardiac muscle
    • less effect on cardiac muscle than verapamil and the same effect on cornomary smooth muscle as nifidepine
    • it is more favorable side effect profile compared to the two drugs because its more intermediate
    • used to treate variant and fixed angina
  40. determinants of blood pressure
    • stroke volume x heart rate=cardiac output
    • cardiac outputx peripheral resistance=atrial blood pressure
  41. classification of blood pressure
    • optimal <120/<80
    • prehypertension 120-139/80-89
    • hypertension
    • stage 1-mild 140-159/90-99
    • stage 2/moderate 160-179/100-109
    • stage 3/severe >180/>110
  42. types of hypertension
    • idiopathic-unknown cause-90% of cases
    • secondary-caused by another disease and once that disease is treated the blood pressure should return to normal elvels
  43. major risk factors leading to cardiovascular disease
    smoking, dyslipidemia, diabetes, age >60, family hisyory
  44. adrenergic neuronal blocking drugs- moa
    MOA-deplete NE, epinephrine, dopamine, seratonin by interfering with the storage or relase of amines
  45. reserpine
    • adrenergic neuronal blocking drug
    • inhibits the transport process of NY, epi, dopamine 5-HT by blocking the transport process of the amines into storage vesicles. makes the vesicles leaky
  46. guanethidine
    • adrenergic neuronal blocking drug
    • inhibits the transport process by competing with NE for storage sites in vesicles. when the neuron is depreted then there is less stored ne for release
  47. clincal uses of adrenergic neuronal blocking drugs
    • limited due to side effects
    • reserpine causes depression and peripheral effects like drowsiness and lethargy
    • guanethidine causes the same peripheral effects as reserpine but doesnt cause depression
  48. central sympatholytics
    • alpha 2 agonists of cns norepinephrine secreting neurons
    • results in decreased relase of epinephrine
    • used to moderate HTN when used wtih a dieuretic
    • adverse effects are sedation,edema, sexaul dysfunction
    • drugs-methyldopa, clonidine
  49. methyldopa
    a central spmpatholytic drug
  50. clonidine
    a central sympatholytic drug
  51. nonselective betal blockers
    • propanolol
    • timolol
    • nadolol
  52. selective beta blocker
    • metoproplol
    • atenolol
  53. partial agonist beta blocker
    • pindolol
    • acebutolol
  54. nonspecific alpha and beta blocker
  55. alpha adrenergic blockers-nonspecific
    phenoxybenzamine and phentolamine

    block alpha 1 and alpha 2 receptors cuases vasodialtion
  56. selective alpha adrenergic drugs
    • prazosin and terazosin, doxazosin
    • causes vasodialtion with reduced preload and afterload is reduced
    • to be used wtih a diuretic and beta blocker
  57. diruetic
    • thiazide type- hydrochlorothizide
    • loop diuretics-furosemide
    • potassium sparing type-sprionolactone
    • works by blocking sodium reabsoprtion from nephron--> na loss and diuresis
    • very important first line group of antihypertensive drugs
    • adverse effects regarding K
  58. hydrochlorozide
  59. furosemide
    loop diuretic
  60. sprionolactone
    potassium sparing diuretic
  61. angiotensin converting enzyme inhibitors
    • captopril
    • enalapril
    • blocks the conversion of inactive angiotensin 1 into active angiotensin 2 by clokcing the action of ACE
    • adverse effect is a dry cough
  62. captopril
    ACE inhibitor
  63. enalapril
    ace inhibitor
  64. direct renin inhibitor
    • aliskiren
    • decreases plasma renin activity and inhibits the conversion of angiotensiongen--> angiotensin 1
    • used for systemic htn
    • can cause birth defects
  65. aliskiren
    direct renin inhibitor
  66. angiotensin II receptor antagonists
    • end in -sartan
    • losartan, valsartan
    • competitively block angiotensin II receptors in blood vessels which blocks vasoconstriction.
    • used for mild to severe hypertension and congestive heart failure
    • can cause birth defects
  67. losartan
    angiotensin II receptor antagonist
  68. valsartan
    angiotensin II antagonists
  69. direct vasodilators
    • hydralazine and minoxidil
    • makes muscle relax, blood vessels get bigger,peripheral resistance decreases
    • not the first line of drugs used for nontherapy
    • adverse effects of reflex tachycradia, edema secondary to vasodialtion, lupus
  70. hydralazine
    • direct vasodilator
    • used to treat hypertension associated with preeclampsia
  71. minoxidil
    direct vasodialtor