cardiac lectures primary care I

Card Set Information

cardiac lectures primary care I
2012-04-29 10:22:23
medications cardiac primary care CHF Angina HTN

HTN, CHF, Angina, mostly treatment and medication
Show Answers:

  1. for persons over the age of 50 is SBP or DBP more improtant a a CVD risk factor?
    • SBP
    • until age 50 SBP and DBP rise in tandem. After age 50, SBP ontinuesw to rise steadily whereas DBP tends to fall. Soi, the prevalence of systolic HTN is directly proportional to age.
  2. What is Malignant Hypertension?
    a very elevated blood pressure >180/120 with TOD (organ damge in the eyes, brain, heart &/or kidneys) It is considered a hypertensive emergency.
  3. With an appropriate size BP cuff the cuff bladder encirlces what percentage of the arm?
  4. True or false
    HBPM (home blood pressure) monitoring is a better predictor of cadiovascular risk, TOD (target organ damage)
  5. True or False?
    HBPM (home blood pressure monitoring) helps reduce the white coat efect and determine the presence of masked HTN.
  6. True False?
    HBPM (home blood pressure monitoring) should be a routine componnet of BP measuirement for monitoring someone with known or suspected HTN.
  7. Which patients are not suitable candidates for HBPM?
    those with A-Fib or cardiac rhythm disturbances which make automatc BP readings unreliable.
  8. With HBPM how many reading do you need to make clinical decisions?
  9. With HBPM (home BP monitoring) what average is considered normal. parameters for normals.
  10. JNC BP reading parameters for normal, preHTN , stage I and stage 2 HTN.
    • normal <120/80
    • prHTN 120-139/80-89
    • Stage I 140-159/90-99
    • Stage II >160/100
  11. When the systolic an diastolic numbers fall into 2 different JNC catageories how do you base clinical decisions?
    use the higher reading and make clinical decisions based on that aberation.
  12. What is the BP goal for essential HTN?
    <140/90 except DM, CAD,Chronic renal Disease then <130/80
  13. What is the risk or concern with Pre Hypertension?
    • greater risk for CV events, especially in the presence of other risk factors. Risks more pronounced in AA.
    • identify these folks early, treat with lifestyle changes, lipid lowering agents, and start pharmacological therapy if 10yr risk is >20%, they are DM or have Chronic Kidney Disease.
  14. CV risk factors, list at least 5.
    • HTN
    • smoking
    • Obesity (BMI >30)
    • Dyslipidemia
    • Physical inactivity
    • DM
    • Family Hx (men <55 or women <65)
    • microalbuminuria or estimated GFR<60 ml/min
  15. What are the 6 complications of HTN?
    HINT: They relate to end organ damage, you should assess these organs with each visit.
    • Brain=stroke
    • Eyes=retinopathy
    • Vascular= PVD
    • Cardiac=LVH, CHD, CHF
    • Kidney=renal failure or proteinura
  16. HTN exam should include what when doing a physical exam?
    • BP both arms
    • height/weight/waist circumference
    • fundoscopic exam:
    • neck
    • heart
    • lungs
    • abdomen
    • extremities
    • neurological
    • Peripheral Vascular assessment
  17. HTN routine lab tests include?
    • EKG
    • UA
    • BG
    • BMP-elecrolytes, GFR
    • LIPID
  18. HTN risk stratification has 3 groups, A B & C
    what group is someone with DM (with or without any other issues)
    Group C
  19. HTN risk stratification has 3 groups, A B & C
    what group is someone without TOD/clinical cardiovascular disease and no known risk factors?
    group A
  20. HTN risk stratification has 3 groups, A B & C
    This person has a risk factor but no DM or TOD what group would he be assigned?
    Group B
  21. Treatment strategies and risk stratification
    Normal BP (120/80) what is the recommendation for Groups A, B & C?
    • Group A lifestyle modification
    • Group B lifestyle modification
    • Group C lifestyle modification (medication with DM, RI, HF)
  22. Treatment strategies and risk stratification
    Pre-HTN (120-139/80-89) what is the recommendationn for Groups A, B & C?
    • Group A lifestyle modification
    • Group B lifestyle modification (meds with multiple risk factors)
    • Group C Drugh therapy & lifestyle modification
  23. Treatment strategies and risk stratification
    Stage I HTN (140-150/90-99) what is the recommendation for Groups A, B & C?
    • Group A lifestyle modification
    • Group B drug therapy & lifestyle modifications
    • Group C drug therapy & lifesytle modifications
  24. Treatment strategies and risk stratification
    Stage 2 HTN (160/100+) what is the recommendation for Group A, B & C?
    all : drug therapy and lifestyle modification!
  25. Key messsaged from JNC 7
    • all pts with HTN or preHTN=lifestyle modifications
    • thiazide-type diuretics intitial drug therapy
    • certain high-risk conditions are compelling indications for other drug classess
    • most patient will require 2+ meds to achieve goal
    • if BP >20/10mmHg above goal, initiate therapy with 2 agents (one being thiazide)
  26. what are the recommended lifestyle modifications for HTN?
    • weight reduction
    • dash diet
    • sodium reduction >51 AA,HTN, CRI, DM <1500mg/day all others <2300mg/day
    • physical activity
    • moderate ETOH
    • stop smoking!
  27. what is the recommended sodium resitriction ?
    • 1500mg day with issues
    • 2300mg day without issues
  28. What is the DASH diet ?
    dietary approach to stop hypertension
    • 7-8 servings grains = energy & fiber
    • 4-5 servings of veggies and fruits= electolytes & fiber
    • 2-3 servings low-fat/non-fat dairy=protien & calcium
    • <2 servings meats= protien & magnesium
    • 4-5 servings WEEK nuts, seeds and legumes= energy, fiber, protien, magnesium & energy!
  29. If you follow DASH diet do you need to have weight management?
  30. what is the BMI goal for HTN and lifesyle modification
  31. ETOH cvonsumption guidlines with HTN?
    • men=24 oz beer=10oz wine=3oz liquior per day
    • women get 1/2 of this
  32. How to choose the right HTN medication?
    If no compelling indication choose what?
  33. How to choose the right HTN medication?
    if particular compelling indication then...
    • use the list from JNC 7 catagory ABC risk stratisfication chart
    • thiazide, and or ACE usually
  34. How to choose the right HTN medication?
    what are the five improtant classes of antihypertensives?
    • ACE-I
    • ARB
    • BB
    • CCB
  35. How to choose the right HTN medication?
    What is the A/CD straegy?
    ACE/ calcium channel blocker & diuretic!
  36. First line HTN agents according to JNC?
    • ABCD
  37. According to JNC 7 HF intial medication therapy options are?
    thiazide, BB, ACEI, ARB, Aldosterone antagonist
  38. According to JNC 7 Post MI initial medication therapy options are?
    BB, ACEI, Adosterone Antagonist
  39. According to JNC 7 persons with high CAD risks intial HTN medication include what meds?
    • ABCD
  40. According to JNC 7 persons with DM intial HTn therapy options inlcude?
    • THIAZ (1st or 2nd line therapy)
    • ACE,ARB (1st or 2nd line therapy)
    • BB (3rd or 4th line therapy)
    • CCB(3rd or 4th line therapy)
  41. According to JNC 7 those whith Chronic Kidney disease and HTN first line medications include?
    ACE (ARB)
  42. According to JNC 7 persons with stroke and HTn should have which meds initaly to prevent stroke recuurence?
    thiazide, ACEI
  43. How do diuretics work?
    decrease volume, reduce CVA, CHF mortality, montior electrolytes!
  44. Loop diuretic blocks the Na/K+/CL transprt in the luminal membrane of the ascending ____ __ _____ resulting in increased luminal concentration of Na, K, Mg Ca and diuresis. This enhances venodilation and decreases cardiac preload.
    loop of henle
  45. Thiazide inhibit the Na/Cl pump in the early part of the ____ _______ ____ resulting in a negative sodium balance.
    distal convoluted tubule
  46. Aldosterone antagonists inhibit aldosterone receptors in the ____ ____ which blocks the action of the Na/K/H pump resulting in decreased reabsortion of Na and reduced excretion of K+
    collecting tubule
  47. loop diuretics are efective in patients with.....
    • impaired renal function and CHF
    • Avoid in pregnancy
  48. Potassium sparing diuretics are used in what situations?
    Class III-IV CHF, post MI with LV dysfunciton
  49. what is the side effect of potassium sparing diuretics like aldactone?
    • they have a weak androgen effect which can cause gynecomastia and ED!
    • avoid if creat clearnace <20 (related to potassium sparing may increase risk of hyperkalemia)
  50. where are B1 cells?
    heart and kidneys
  51. where are Beta 2 cells?
    • Lungs, GI, Liver, Vascular Smooth Muscle, Uterus, Skeletal Muscle
    • beta blockers can cause bronchospasm and worsening PVD
  52. Where are Beta 3 cells?
    fat cells!
  53. how do Beta Blockers work?
    • block the action of endogenous catecholamines (epi and nor epi) ont he beta adrenergic receptors.
    • it lowers BP by reducing CO, reducing renin, decrasing sympathetic acivity.
  54. what are the compelling indications for considering Beta blockers?
    ischemic heart disease/ MI or CHF
  55. beta blocker side effects
    • ED
    • insomnia, wierd dreams, nightmare, depression
    • exacerbation of Raynaruds or increase in sx of PAD
    • bradycardia
    • fatigue
    • can increase triglycerides and decrease HDL
    • can mask signs of hypoglycemia
  56. ISA is intrinsic sympathomimtic activity, beta blockers with ISA have what characteristics?
    lower BP without reducing CO or producing significant bradycardia.
  57. ACEI prevent conversion of angiotension I to angiotnsion II by blocking angiotension converting enzme. This in turn increases bradykinin which is a vasodilator.
    True or false?
  58. ACEI blocks the effects of angiotension II a potentent vasoconstrictor. how does this effect heart, cornoary arteries, kidneys, adrenals and blood?
    • heart: reverse myocardial hypertrophy, interstitial fibrosis
    • Cornoary arterys: improve endothelial fx, vasodilation, decrease inflammation.
    • Kidnesy decrease glomerular pressure
    • adrenaldecreae aldosterone production
    • blood Decrease hypercoag states.
  59. ACEI are potent in what situations?
    high renin states, less effective in AA b/c they tend to have lower renin.
  60. ACEI are generally well tolerated, cost effective and long lasting. True or False?
  61. ACEI are used in what situations?
  62. ACEI common SE?
    • cought (d/t Bradykinin causing vasodilation, tissue edema bronchospasm
    • enutropenia
    • angioedema-rare but signifigant
    • rash
    • hyerkalemia
    • first dose hypotension
    • loss of taste
  63. Why an ARB?
    • ARB's avoid the ingibition of ACE, instead blocking the RAA cascade at angiotensin 1 receptors
    • by not leaving a lot of ACE floating around you don't have the build up of bradkinin whichis responsible for the cough associated with ACEI.
  64. If ARB's don't cause angioedema and no cough why not use them more?
    not as well studied, and they are costly. Losartan is the only generic currently available
  65. what are the indications for ordering an ARB?
    • same as ACEI: DM nephropathy, ACEI intolerance (cough), LVH, CHF, post MI
    • remember both ARB and ACEI are contraindicated in preganancy catogory C !
  66. what is another name for Losartan?
    Cozar, it is an ARB
  67. Tekturna (aliskiren) is what kind of anti-hypertensive?
    direct renin inhibitor: it inhibits the action of renin which convers angiotensinogen to angiotensin
  68. what do you know about Tekturna (aliskiren) regarding when not to use? (SE)
    • SE similar to other RAAS drugs
    • may cause cough or angioedema
    • most common SE is diarrhea,
    • avoid in pt with GFR> 30
    • contraindicated in pregnancy
    • can cause electolyte imbalances
  69. All CAB's inhibit cellular calcium influx reduing waht and what?
    • myocardial contractility as wall as inducing peripheral and coronary vasodilation
    • effective in low renin states (AA)
  70. CCAB's come in 2 versions: non dihydropyridines and dihydropyridines. which ones affect HR & BP?
    non's there are only 2 diltiazem and verapamil
  71. name the 2 nondihydropyridines (CCB's)
    cardizem and verapamil
  72. so how can you tell the nondihydropyridines from dihydropyridines?
    dihydropyridines end in "pine" and besides only 2 non's (cardizem and verapamil)
  73. what are the nondihydropyridines used for?
    rate control (a-fib) slowing HR but negative inotropic effect may exacerbate CHF so NOT with known LV dysfunction (check EF)
  74. What are the dihydropyridines used for?
    BP management
  75. which CCB is most cardiac specific and what are it's SE?
    • Verapamil is most cardiac specific causing
    • bradycardia
    • Heart Block
    • Hypotension and edema
    • constipation
  76. dihydropyridines have little or no effet on cardiac muscle contaction or AV conduction so they don't really affect HR, how and where do they act?
    • dihydropyridines at primarily on peripheral blood vessels
    • (amlodipine, nisoldipine, felodipine, nifedipine)
  77. which of the dihydropyridines, amlodipine, nisoldipine, felodipine, nifedipine have the most vasuclar speific effects?
    • nifedipine has the most vascular specifice SE things like;
    • hypotension, dizzyness, flushing , reflext tachy, peripheral edeamma and vascular headache.
  78. central acting A2 agonists are indicated mailnly for what situations?
    • resistat or malignant HTN or when multi drug therapy is needed.
    • (aldomet, catapres, wytensin, tenex)
  79. what kind of agent is clonidine?
    • also known as catapress
    • it is a central acting agent---A2 agonist
  80. what kind of anti-hypertensive is aldomet?
    • also known as a-methyldopa
    • it is a central acting agent----A2 agonist
  81. How/where do the A2 agonists work?
    • exert effects on vasomotor center of brain limiting sympathetic outlow to the heart and blood vessels.
    • little direct cardiac or renal effects so no lipid or electrolyte influence but lots of SE!
  82. So what are the SE associated with central acting A@ agonists? They reduce BP to normotensive in 30- 50% of persons when other meds don't; so why aren't they used more?
    • SE include sedation, postural hypotension, dry mouth, bradycardia, impotence, withdrawal syndromes, depression and dizzyness!
    • minimal potential for othostatic hypotensio but additive drug interactions especially with CNs depresants
    • remember clonidine should NEVER BE ABRUPTLY STOPPED!
  83. Name the protype peripheral Alpha 1 antagonist.
  84. Name the central Alpha 2 agonist?
    clonoDINE (catapress)
  85. how does Doxazosin, a peripheral A1 antagonist work?
    blocks sympathetically mediated vasocintriction responses and thereby reduces vascular resitance.
  86. when do you consider a drug like doxazosin?
    • consider a peripheral alpha 1 agonist as an "add on" treatment to other antihypertensives
    • SE include postural hypotension, syncope, tachy, dry mouth, fluid retenition, headache and dizzyness
  87. what kind of atihypertensives are minoxidil and hydralazine?
    • direct acting vasoldilators
    • very potent can cause fluid retention and tachycardia
  88. when are direct acting vasodilators like hydralazine used?
    in patients with CRF or refractory HTN
  89. hydralazine requires some special considerations, what are they?
    • address fluid and heart rate control
    • usually intiated by a subspecialist and
    • watch for a lupus like syndrome
  90. what are the prefered HTN drug treatment combinations?
    • ACEI/ARB + diuretic
    • ACEI/ARB + CCB

    • alternative acceptable
    • CCB + diuretic or BB+ diuretic
    • CCB (dihydropyridien) + BB
    • DRI +diuretic or DRI +ARB
  91. what are not likely to e effective combination therapies for HTN (what should not be ordered together)?
    • ACE+ARB can be used in selct CHF's with protienurea
    • RAAS+BB can be seen in CHF and CAD
    • BB+ Central A2 agents b/c both interfere with sympathetic nervous system an lead to brady and HB, rebound HTN if withdrawns abruptly.
  92. HTN and minorities:Although treatment is similar for all demographic areas, socioeconomic factors and lifestyle barries can influence BP control. What else should you be aware of when choosing medications for HTN management in minorities?
    • prevelance in AA is increased
    • AA demonstrate reduced BP response to monotherapy with BB, ACEIs or ARBs compared to diuretics or CCBs.
  93. what is LVH an independent risk factor for?
  94. regression of LVH occurs with aggressive BP management including lifestyle changes and all classess of drugs except....
    • hydralazine, minixidil and probably clonidine and prazosin.
    • ARB, ACEI, CCB most effective
  95. PAD is equivient in risk to ischemic heart disease. true or false?
  96. Any class of drugs can be used in most PAD patients. true or false?
  97. aging autonomic nervous system can lead to postural changes so monitor for side effects b/c this can increase comorbidity and mortality. true or false
  98. in the elderly discuss issues with diuretics, ACE.ARB and CCB
    • Diuretics: plateau in higher doses with more SE. avoid with hx of incontinence
    • ACEI/ARB: well tolerated, monitor renal fx
    • CCB, longer acting preparatons prefered, fewer SE
  99. oral contraeptives may increase BP but does HRT raise BP too?
    no HRT does not!
  100. what antihypertensives should be used for pregnant, or women who may become pregnant?
    • methyldopa, BB and vasodilators.
  101. ACEI & ARBS work well to control BP and slow progression of renal failure. true or false/
  102. is there a relationship between elevations in BP and renal failure?
  103. which class is first line for DM with HTN?
    ACEI or ARB
  104. dyslipidema and hypertension require agressive management. where is the emphasis of treatment?
    • weight loss
    • diet low sat fat, cholesterol, Na, ETOH
    • exercise
    • hyperlipidemic agents PRN
  105. client with essential tremor and HTN, what med should you consider to impact both of these issues?
    noncardioselecive b-blocker (inderal)
  106. what about persons with hyperthyroidism, what antihypertensive agent should you order?
    BB like propranolol
  107. how about with migraine and HTN?
    • noncardioselective BB inderal
    • nondihydropyridine CCB like verapamil, diltiazem
  108. with BPH and HTN what med can you consider?
    a-blockers doxazosin (cardura) or Tamsulosin (Flomax)
  109. what if someone has HTN and Raynaud's what med should you consider?
    CCB nifidipine (dihydropyrdine)
  110. what if they have OA and HTN? What medication can you consider to lower BP and affect OA?
    thiazide diuretics
  111. someone with peri-operative HTN should recieve what medication for their BP?
  112. those with dyslipidema and HTN, you should consider puttig them on what anti-hypertensive agent?
  113. Emergency medicine prinicple; who gets admitted?
    BP>180/120 with acute TOD or those without acute TOD?
    • TOD=target organ damage and inlcudes, eyes, brain, heart & kidney.
    • hsopitalize those with acute organ damage.
    • treat everyone with immediate combination of oral antihypersive and follow up for both. one in and one out within 7 days.
  114. what is the BP that would delay surgery?
    • 180/110 lower it then go to surgery.
    • lower it with BB
    • have them take BP medication right up until surgery and resume ASAP following surgery.
  115. what is pseudo HTN?
    oder patients typically can have this as a result of vascular stiffness.
  116. if BP cuff is too small BP will be too high or too low?
    • too high
    • cuff should be 80% of arm circumfrence.
  117. what is better, increasing dose or multidrug therapy?
    multidrug therapy. can consider combo pills to increase compliance but they may be more expensive.
  118. describe how to do home BP monitoring for somone with white coat HTN making office BP unrealiable to base treatment or treatment respose.
    • five consecutive days.
    • each day take 3 measurements 5 min apart in the am and pm
    • toss the first 2 days of measurements
    • average the remaining
    • average the first measurement of each triplicate set.
  119. define resistant HTN
    • BP that remains above goal despite the concurrent use of 3 anti-HTN agents of different classes.
    • one of these agents should be a diuretic
  120. evaluations of pt's with resitant HTN referrred to specialty clinics have consitently found tx resistance was in part due to improper use of diuretics. what should you consider reltated to diurteics and resitant HTN?
    • increase HCTZ from 12.5 to 25mg
    • change HCTZ to chlorthalidone
    • change to a loop if CR>1.5 or GFR<30mL/min
    • increase low dose loop to BID
    • use a mineralocorticoid receptor antagonisit like aldactone or amiloride
  121. what are common things that interfere with HTN medication efficacy?
    • ETOH use, NSAIDS
    • contraception
    • decongestants, diet pills, cocaine
    • stimulants
    • excess sodium.
  122. secondary causes of HTN (4)
    • obstructive sleep apnea
    • renal parenchymal disease
    • primary aldosteronism
    • renal artery stenosis
  123. what's the issue with sleep apnea and HTN?
    intermittent hypoxemia and or increased upper airwya resistance induces an increase in SNS.
  124. what is the BP control for patients with renal disease/
    • <130/80 or lower
    • use ACEI/ARBs they work and slow progressionof RF
    • a rise in cr. as amuch as 30% above baseline with ACEI/ARB is acceptable and not a reason to withold tx unless hyperkalemia develops (>5.5)
    • Na resitriction will help and use diuretics
  125. With an intra adrenal abnormality you will have an increase in aldosterone and electolye imbalance hypokalemia. Also you will see HTN and in younger persons. dx should be confirmed by CT if labs suggest primary hyperaldosteronism. what is the tx for bilateral adrenal hyperplasia?
    • spironolactone
    • if adenoma is found surgery will be requried.
  126. symptoms include:
    paradoxical worsening of HTN with ACEI
    recurrent pulmonary edema in moderate-severe HTN
    presence of abdomial bruit
    what should you consider?
    • reno artery stenosis!
    • dx with reanl duplex, spiral CT, MRI, renal angiogram
    • stop ACEI/ARB, PTCA stenting or surgery to improve renal perfusion and stop HTN!
  127. General treatment guidelines for mild HTN stage I.
    140-159/90-100 with no additonal risk factors, DM or TOD
    • lifestyle diet ,
    • DASH,
    • Exercise,
    • monthly BP re-eval in 6 months
    • consider 1st line Rx
  128. General treatment guidelines for mild HTN stage I
    140-159/90-100 with risk factors, or disease?
    • diet,
    • exercise,
    • DASH, monthly BP's re-eval in 3 months or less
    • start 1st line Rx
  129. General Treatment Guidelines for moderate HTN Stage II
    if risk factors TOD or DM start 1st line or combo after confirmation and diagnostic evaluation
  130. General Tx Guidelines for Severe HTN Stage II
    • start full dose of 1st line agent and a 2nd agent (diuretic)
    • re-eval in 1 week
    • if improved but elevated change to another 1st line agent at full dose.
    • reassess in 2-4 days if still elevated consider further titration or addtion of another agent
    • reasses weekly until DBP<100
  131. How often should newly dx HTN patient visit?
    • monthly until goal reached
    • then q 3-6 months
  132. how often to check potassium and creatine in HTN patients?
    1-2 times yearly
  133. can you consider reducing doses and number of agents afer 1 year below goal?
  134. when to refer to a specialist?
    • when a secondary cause of HN is suspected
    • if BP remains elevated after 6 mo of tx
    • outcomes do imrove when referred to a HTN specialist.
  135. CV disease lead to progressive LV disease which lead to ..
    heart failure
  136. NYHA Class is based on the patients current symptoms and describes the patient's functional limitations. As a dynamic scale the patients class may go up or down depnding on the improvement or worsening of his HF condition.
  137. The ACC/AHA heart failure stage A-D classifies and describes HF evolution progressively through the stages. not a dynamic scale it only goes one way (donwhill). Is the NYHA Class sytem incorporated into the A-D staging?
    why yes it is!
  138. If HF is not a disease state how is it described/
    • A clinical syndrome that is dynamic with signs and sx that wax and wane over time with tx.
    • the average life expectancy for a person with 1 hospitalization for HF is 5 years!
  139. what is this the definition of :
    structual or functional impairment of either venticle to fill or to eject blood--unable to meet metabolic needs of the body.
    • heart failure
    • CHF referst o LV systolic dysfunction: specifically an enlarge, blood congested LV
  140. these are the cardinal signs of something, what?
    dyspnea, fatigue, fluid retenion (pumonary &/or periphral)
    heart failure or CHF
  141. High out put HF--normal heart challenged with excessive metabolic demand and the heart fails to meet the need. what situations might you conside this situation?
    • hyperthyroidism
    • pregancy
    • anemais
  142. Low output HF cause about 90% of all HF cases. It occurs when diminished volume from a weakened heart muscle fails to meet normal metabolic needs. It may be left, right or biventrilcular.
    sytolic dysfuntion is seen with?
    diastolic dysfunction is seen with?
    • systolic dilated cardiomyopathy
    • disatolic impaired LV filling & relaxation (stenosis)
  143. LV dysfunction is most common usually after myocardial injury, infection, or valvular disorders. RV dysfunction may accompany LV with infaract or progression of left to right failure.
  144. HF is a clinical syndrome that represents the end point of many diseases name 5
    • HTN
    • CAD
    • Kidney disease
    • Pulmonary pathologies
    • DM (endocrine disturbance)
  145. how does HF begin?
    the process begins with an intial injury that leads to adaptation. Over time, what begins as normal adaptive proces results in LV remodeling, culminating in LV dysfunction and the development of HF
  146. what is this?
    abnormal dilation of the ventircles and resultant thinning of the myocardial wall with dereased stretch and contractile strength.
    dialted cardiomyopathy
  147. what is this?

    left and or right ventricular hypertrophy often asymmetrical, which usually involves the interventricular septem, impairing outflow through the aortic valve
    • HOCM: hypertrophic obstructive cardiomopathy
    • high risk for SCD d/t arrythmia
  148. what is this?
    Disease of myocardium that causes stiffening of the myocardium causing pressure within the ventricles to rise with small increases in volume. Thus, accentuated filling ocurs in early diastole. Reduced LV filling volume leads to reduced SV & low CO (fatigue, lethargy) whearas increased filling pressures cause pulmonary and systemic congestion.
    • RCM restrictive cardiomyopathy
    • S&Sx of left and right HF.
  149. what is arrhythmogenic RV cardiomyopathy?
    progressive fibrofatty replacement of the RV and to some degree LV myocardium which creates a proclivity for lethal arrhythmias, especially with exertion.
  150. what is octopus pot cardiomyopathy?
    • Takatsubo, similar to restrictive :bulging ventricle with limited outflow.
    • also know as stress cardiomyopathy.
    • most commo in midle-aged women
  151. which cardiomopathy is most common?
  152. what kind of murmur will you find with hypertrophic cardiomyopathy?
    • aortic stenosis murmur-sytolic murmur-turbulance.
    • diminishes with maneuvers to increase venous return like squating and increases with valsalva or position changes which decrease preload.
  153. what is systolic heart failure?
    • most common
    • develops form a weakened heart muslce and pump failures
  154. what causes diastolic heart failure
    results from end-organ damage as a result of long-standing HTN
  155. what is diastolic heart failure
    the venticle can't relax and accept an adequate volume of blood during diastole, EF will be normal or increase >55%
  156. describe restrictive heart failure.
    • rigid ventricles due to fibrosis (radiation therapy, sarring) or infiltration (amyloid, sarcoid) or scleroderma or tumor.
    • treatment options are very limited.
  157. The dilated cardiomyopathies tend to lead to what kind of dysfunction
    • systolic dysfunction
    • initially loss of LV contratile strength leads to pulmonary congestion
  158. diastolic failure takes place in the presnce of normal LV systolic function. True or False?
  159. you hear an S3 with increased end diatolic volume and client has EF <40% what type of dysfunction and where is it?
    sytolic dysfunciton d/t dilated LV
  160. client has normal herat size and contractility. normal or increased EF >45-75%. what type of pathology and dysfunction, why is the EF so high?
    • this is a diastolic dysfunction seen with normal LV systolic function.
    • the small LV chamer is able to eject a high fraction of the low volume it holds, that is why EF is high. it's all relative!
  161. Diastolic heart failure what sound will you hear? why?
    S4, increased filling (diastolic) pressure.
  162. what are the signs of diastolic heart failure?
    S4, JVD, liver enforgement/tenderness, LE edema, pulmonary congestion.
  163. what are the main components of diastolic HF? preload or after load?
    preload, even small amount of fluid creates high LVEDP.
  164. what are the main compnents of systolis heart failure?
    decreased contractility and afterload needs to be reduced.
  165. signs and sx of LV failure?
    • LVH,
    • hypotension
    • EF <40%
    • basilar crackles
    • S3 Tachycardia-reflex
    • increased BUN/CReatine from poor renal perfusion
    • DOE/SOB, orthopnea, PND, cough, weakness, fatigue, confusion
  166. what ate the signs and sx of RV failure?
    • peripheral edeama
    • weakness fatigue
    • weight gain,
    • JVD,
    • hepatomegaly
    • reflux
  167. what are the ompensatory mechanisms in Heart failure?
    • activate RAAS
    • increae HR increase myocardial O2 demand
    • retain Na+ and H20
    • LV remodeling
  168. what are the 3 main causes of heart failure?
    • CAD
    • HTN
    • DM
  169. recomendations for evidence what does each mean?
    Clas I
    Class IIb
    Calss III
    • Class I-SHOULD be done
    • Class IIa- REASONABLE to do
    • Class IIb- MIGHT BE tried
    • Class III- HARMFUL do not do it!
  170. when following guidelies, on generally stays with which 2 of the 4 classes for parctice excellence?
    Class I and IIa.
  171. when do you use NYHA classification and when do you use the ACC/AHA stages?
    • NYHA is used to describe functional limitations
    • ACC/AHA stages identifies risk factor level
  172. what are the classess of HFin the NYHA system
    • asymptomatic-no issues
    • mild-comfie at rest, some limitations
    • moderate -comfie at rest unable to engage in activities
    • severe - symptoms at rest
  173. what are the stages of the ACC/AHA HF system/
    • StageA-at risk but no structural changes or symptoms
    • Stge B- structural changes but no symptoms
    • Stage C- structural changes with symptoms (past or presnt)
    • Stage D-refractory HF requiring interventions
  174. In stage A HF: high risk w/o sx how do you treat?
    • systolic or diastolic HTN tx according to guidlien (JNC7)
    • if present lipid disorder tx
    • lifestyle modifications, smokeing, exercise, no etoh, diet
    • tx concomitant disease
    • angina=stnet, nitrate, BB &/or diuretics
    • A-Fib with prior DVT=anticoag rate control
    • metabolic syndrome=control weight, BG, lipids
  175. how do you tx treat stage B HF: structural changes w/o sx?
    • Class I recommendations: ACEI & BB if hx of MI regardless of EF (LVEF).
    • class IIa recommenations: ARB if ACEI not tolerated, consider ICD to prevent SCD from arrythmias (consider after 40 days post MI with EF <30%, consider after 3 months for those post CABG with EF<30%)
  176. How do you tx stage C HF: structural changes with past or current sx?
    • diuretics, ACEI, BB, Na+ restriction:*in select pt aldosterone antagonists, ARBs, hydralazine and isoosorbide dinitrate, routine exercise or digoxin may be considered.
    • consider ICD if EF <30% (40 days post MI, 3 mo post CABG)
    • CRT -cardiac resynchronization therapy- using biventricular pacing if NYHA class III or NYHA class IV ambulatory and in sinus with LVEF <35%
  177. how do you tx stage D HF: refractory HF requiring specilaized interventions
    • mechanical assist devices
    • chronic inotropes
    • heart transplant
    • hospice
  178. what dx test are ordered with HF?
    • 2D echo: most useful
    • CXR
    • 12 lead
    • cardiac testing nuclear/cardiac cath=EF, wall motion
    • BNP, CBC< CMP 24 thryroid panel UA
    • Pulse Ox
    • Pacemakers which measure intrathoracic impedance
  179. OPT?
    optimal pharmocological therapy
  180. ACEI recommendations for HF (Class Ia)
    • recommended for all patients with current or prior sx of HF and reduced LVEF
    • indicated in all patient with a recent or remote history of MI regardless of LVEF or presnce of HF
    • anyone with reduced LVEF with/without HF or MI
  181. What 3 BB are proven to reduce mortality in HF treatment?
    • bisoprolol
    • carvedilol
    • metoprolol succinate ER
  182. what are the recommendations for BB in HF?
    • recommended for allstable patients with current or prior sx of HF and reduced LVEF.
    • use bisprolol, carvedilol or Lopressor ER
    • ayone with a recent or remote hx of MI regarless of LVEF or HF
    • anyonw w/o hx of MI wh have a redued LVEF w/o HF sx.
  183. Aldosterone antagonists, like Inspra and spironolactone (aldactone), are a class IIb recommendations in HF. when and why should they be considered?
    • b/c aldosterone production in the adrenal cortex is stimulated by renin release in the kidneys from under perfusion. Aldosterone increases Na+ and water retention.
    • Inspra and spironoloactone block aldosterone recetors and promote Na+ and water excretion thereby reducing preload.
  184. what's the deal with ARB's and HF?
    use whenever ACEI would be used but can't be used d/t intolerance
  185. the recommendations for a hydralizine-nitrate addition to HF treatment is a class IIb "reasonable to consider". what do you need to know to consider this therapy? like when would you choose it?
    • reasonable in persons with rediced LVEF whae are already on ACEI/BBB for sx HF and still have sx
    • reasonalbe for AA who are NYHA III or IV and alredy on everything else.
    • might be ok in stage C HF with reduced LVEF who can't take ACEI/ARB b/c intolerance, hypotension or renal insufficiency.
  186. what about digoxin and HF?
    • can be beneficial stage C with reduced LVEF.
    • it is a sx improvement not a mortality benefit
    • does prevent hospitalizations but has a narrow theraputic window and requires really good management esp with renal issues to prevent toxicity.
  187. what is the salt restriction in HF?
  188. what is the diuretic recommendation for HF?
    for those who are stage C: diuretics and salt restriction are indicate in patients with current or prior sx of HF and reduced LVEF who have evidene of fluid retention
  189. ACC/AHA/NASPE recommend what in past-Mi patients with EF <30%?
  190. what are the current ICD indications based on NYHA functional class?
    • NYHA Class I: EF ,30%w/prior MI
    • NYHA Class II-III: EF <35%
    • NYHA class IV: if meet criteria for BV pacing
  191. LBBB is more prevalent with impaired LV systolic funtion, so what?
    leads to widened QRS and potentiates dyssynchrony and delayed ventriclar activation which means decreased jpumping efficiency in the already weak muscle.
  192. What will you find with syssynchrony as it relates to cardiac function and symtoms?
    • reduced diatolic filling time
    • weakened contractility
    • mitral regurg
    • post systolic regional contraction (contraction after aortic valve closes)
    • bottom line: decrease in SV!
  193. what besides ACEI can prevent or reverse LV remodeling in HF patients?
  194. Which HF patients needs CRT therapy?
    cardiac resynchronization therapy
    • have QRS duration >120 (cardiac dyssnynchrony)
    • EF <35%
    • are sx despite OPT
  195. in primary care if you suspect HF what is the clinical obligations?
    to determine the cause of the exacerbation and treat or admit.
  196. patient presents with
    new DOE, PND ororthopnea,
    liver congestion expressed as an elevated INR, abdominal tenerness or ascites-
    what should you be considereing for dx?
    • HF=acute HF syndrome=exacerbation of HF
    • if just volume it may not be cardiac, consider renal function as cause of fluid
  197. acute heart failure is caused by 3 overbearing cardiac conditions, what are they?
    • plumbing=CAD
    • structural+valvular heart disease
    • Electircal+ atrial arrhythmias/bradycardia
  198. name risk factors for the development of HF?
    • age
    • CAD
    • HTN
    • LVH
    • DM
    • Obesity:dietary indiscretion (sodium)
    • ETOH men>2drinks daily women>1 drink/day
    • smoking
  199. what are some differentials to consider with sx of HF:
    • MI
    • pulmonary disease (asthma, COPD, pul HTN, PE)
    • Sleep disorder
    • Obesity
    • Deconditioning/malnutrition
    • Anemia
    • liver/renal failure
    • hypoalbuminemia
    • venous stasis
    • depression
    • anxiety and hyperventiation syndromes
  200. what is the main reason for admission with HF?
    • cardiopulmonary congestion with high LV filling pressures
    • this leads to neurohormal activation-causing nor-epi release which causes vasoconstriction-which causes ishcemia- which worsens myocardial function. then LV dilation causes altered geometry of heart which causes valve distortion which leads to TV/MV regurge AKA valvular insufficiency which causes R sided failure
  201. acute HF syndrome-who should be hospitalized?
    • hemodynamically significant arrhythmia (A-Fib)
    • ACS: EKG changes or isoenzymes suggestive of MI
    • Dyspnea at rest: associated with resting tach not so much changes in pulse ox.
    • decompensation=hyptension, RF, cahnges in LOC
  202. What is the ER management of suspected acute HF?
    • medical hx
    • S&Sx, BP, HR, EKG, CXR, Renal fx, electolytes, pulse ox
    • BNP biochemical markers
    • echo
    • loop diuretic
    • nitro SL & or gtt (vasodilitation to decrease preload/afterload
  203. waht symtoms do you evaluate when considering Acute HF syndrome (AHFS)?
    • JVP
    • S3 gallop/murmurs suggesting vlavular dysfunction
    • rales
    • Hepatojugular reflux
    • ascites
    • edema
    • laterally displace or prominent PMI
  204. what is the recommendation for follow-up after dc from hospital for AHFS?
    • phone call within 3 days of dc
    • 7-10 days appointment
  205. what are the goals of therapy with diastolic HF wth preserved systolic function?
    • slow HR relax myocardium and enhance ventricur diastolic filling time so use BB.
    • achieve adequate BP control to prevent TOD (ACEI/CCB)
    • adequate diuresis to maintain euvolemia
  206. myocardial ischemia is related to what?
    O2 supply and demand
  207. which angina is this?
    predictable c/p with exertion
    stable angina
  208. when angina has accelrating symptoms what type of angina is it?
  209. what is vasopastic angina?
    this occurs with emotion and little or no activity
  210. there is a postprandial and a microvascular angina what are these?
    • postparndial occurs after eating
    • microvascular occurs with increases in myocardial well stress and strain like with HTN or aortic stenosis
  211. what are the unusual or minimal presentations of chest pain complaints in women compaired to men?
    • women fatugue SOB malaise "flu-like"
    • men chest squeezing, radiation to neck, jaw, arm
  212. What do you know about angina pain that would help you determine it c/p complaint is likely to be angina?
    • almost never is sharp or stabbing
    • does not change with postion or respiration
    • lasts minutes (dull ache lasting hours is not angina)
    • usually substernal can radiate but pain above the nadible, below epigastrium or localized ot a small area over the left alteral chest wall is rarely angina
    • precipated by eating, exertion or stress and relieved by rest (and nitro SL)
  213. patient complains of pain that increases with a deep breath what are you thinking?
    pleuritic pain
  214. what sympathetic nervous sytem repsonses are found during periors of true heart pain?

    • SOB
    • emotional repsonse to neurohumoral influences (anxiety, doom)
  215. Although a normal EKG does not exlude severe CAD it dose it imply what about cardiac function?
    normal LV with favorable prognosis
  216. most patients with chest pain/suspected angina do NOT neeed an ech. True or False?
  217. client with angina that occurs only with prolonged exertional activety and not at all with walking is what class of angian based on CCS classisfication scale?
    Cass I
  218. client with angian pain walking >2blocks or more than 1 flight of stairs wi is what angina class (based on CCS system)
    Class II
  219. client with anginal pain walking <2 blocks or <1 flight of stairs has what class on angina?
    Class III
  220. describe the client with class IV angina
    chest pain at rest
  221. A client with known stable angina complains of any of the following symptoms to you, the PCP, what are your concerns?
    new or worsening MR
    pulmonary edema/S3
    hypotension or tachycardia
    dynamic T-wave changes
    new dysrhythmia or EKG changes
    • high risk for MI
    • complaints of the above sx suggest unstable angina which is a medical emergency
  222. TIMI risk score has seven componants name them
    • AGe>65
    • >3 CAD risk factors
    • Prior coronary stenosis>50%
    • ST deviation
    • >2 anginal events in <24 hours
    • ASA in last 7 days
    • elevated cardiac markers
  223. when the pretest probability of severe CAD is high what test should you assign?
    coronary angiography-cathy lab
  224. what are the ACC/AHA Class I recommendations for initial management and anti-ischemic therapy of patients with unstable angina and NSTEMI?
    • best rest, telemetry, O2, IV nitro, morphine (pain)
    • BB
    • ACEI for persistent HTN in patients with LV systolic dysfunction or CHF
    • IABP for heodynamic instability
  225. what are contraindications to nitrates?
    • severe aortic stenosis
    • HOCM
    • erectile dysfunction treated wtih PDE5 inhibitors (viagra)
  226. what are clinical conditions that may limit use of BB ?
    • asthma
    • severe bradycardia
    • AV block
    • severe depression
    • raynaud's syndrome
    • sick sinus ysndrome
  227. CAD treatment is ABCDE
    • A=ASA and anti-anginal therapy
    • B=BB and BP control
    • C=cigatette smoking and cholesterol
    • D=diet and DM
    • E=education and exercise