Cardiology 3

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  1. Goals of Diagnosing HTN
    Detect & stage HTN severity; detect TOD; assessing overall CV risk; detect secondary causes of HTN
  2. HTN stats
    1 in 3 in US = HTN; 66 mil in US 20 yo & older; 95% are essential HTN; 2005 in US, direct & indirect cost of HTN = $59.7 Billion
  3. HTN pt awareness stats
    63% aware of the dx; only 45% receiving tx; 34% under ctrl using a threshold criterion of 140/90
  4. Factors of essential HTN:
    Genetic defect, inc dietary Na intake, intrinsic renal differences, stress, obesity, drug or substance abuse
  5. Primary HTN: other factors:
    Variable plasma renin activity; variable symp n.s. response & catecholamines; insulin resistance & DM; inadequate dietary K+ & Ca+ ; resistant vessels
  6. Renal artery stenosis in HTN: MOA
    Excessive renin release in response to decrease in renal blood flow & perfusion pressure
  7. Renal vascular HTN: 2 pathologic processes (resulting in stenosis)
    85% atherosclerosis of proximal renal arteries (pts usu also have CAD); 15% fibromuscular dysplasia (esp in F 15–50 yrs; genetic predisposition)
  8. Fibromuscular dysplasia (FMD) is characterized by:
    fibrous thickening of the intima, media, or adventitia of the renal artery
  9. Congenital abnormality which results in narrowing of the aorta, usually in the ascending region, which increase PVR due to the stenosis
    Coarctation of the Aorta
  10. Coarctation of the Aorta: incidence
    Rare (1:10,000) & usually accompanies other abnormalities such as bicuspid aortic valve or Turner Syndrome
  11. Hyperaldosteronism: most common etiologies:
    unilateral aldosterone-producing adenoma or bilateral adrenal hyperplasia
  12. If Pheochromocytoma undiagnosed:
    Outpouring of catecholamines during unrelated surgical/ radiologic procedure can lead to severe, abrupt hypertensive crisis & mortality rate over 80%
  13. Obstructive sleep apnea & HTN
    HTN = response to chronic, intermittent hypoxia during nocturnal apneic episodes
  14. Cushing Syndrome: tx for HTN
    HTN is reversible if cause is eliminated (ie, pituitary adenoma, corticosteroid Rx)
  15. HTN & chronic kidney dz: epidemiology
    HTN is second most common cause of chronic kidney disease (> 25% of cases)
  16. Most easily recognized treatable risk factor for stroke, MI, CHF, peripheral vascular dz, aortic dissection, atrial fibrillation & end-stage kidney disease
    HTN
  17. HTN in younger pts (< 50 yrs): Hemodynamic fault =
    vasoconstriction at the level of the resistance arterioles
  18. Isolated systolic HTN: associated risks
    BP of 160/60 (pulse pressure of 100 mmHg) carries 2x the risk of fatal coronary heart dz as 140/110 (pulse pressure of 30 mmHg) (PP = SBP – DBP)
  19. Diastolic BP age pattern
    Peaks in the early 50’s, then declines for men and women (Systolic BP continues to rise for both throughout life)
  20. Resistant Hypertension
    Defined as persistence of BP > 140/90 despite tx with full doses of 3 or more different classes of meds in rational combination (& including a diuretic); important to know pt is compliant
  21. 4 Categories of Resistant HTN
    Pseudoresistance; Inadequate medical regimen; Nonadherence or ingestion of pressor substances; secondary HTN
  22. Pseudoresistance:
    Usually caused by white coat effect superimposed on chronic HTN that is well controlled with meds outside the office
  23. Resistant HTN: Inadequate medical regimen
    Absence of appropriate diuretic; Renal fn impairment which affects drug clearance; monotherapy or inadequate dosing of meds
  24. Resistant HTN: Nonadherence or ingestion of pressor substances
    a. Medication nonadherence; b. Lifestyle modification noncompliance; obesity, high salt diet, excessive alcohol intake; c. Habitual use of tobacco, cocaine, meth, phenylephrine or NSAIDS (cause renal Na+ retention)
  25. Resistant HTN: Secondary HTN:
    If you’ve exhausted the first 3 categories, time to look for secondary cause of HTN
  26. Most commonly overlooked secondary causes of Resistant HTN:
    Chronic kidney dz & primary aldosteronism
  27. Hypertensive Urgency
    Severe elevation of BP; No evidence of progressive TOD; benefit from BP lowering in a few hrs; absence of raised intracranial pressure
  28. Hypertensive Emergency
    Acute, severe elevation in BP; evidence of rapidly progressive TOD (eg, MI, pulmonary edema or renal failure); requires immediate, gradual reduction of BP (NOT to the normal range); always look for secondary causes
  29. Hypertensive Emergency: tx
    Controlled, gradual lowering of BP; 10% decrease in first hour, then 15% over next 3–12 hrs to BP of no less than 160/110; rapid correction of BP to norm levels puts pt at high risk for worsening cerebral, renal or cardiac ischemia
  30. Malignant Hypertension:
    Type of Hypertensive Emergency; usually accompanied by other end organ damage
  31. Malignant Hypertension is most common in:
    Young adults, prior renal dz, AA males, PG, or collagen vascular dz
  32. Dz w/ Compelling Indications for tight HTN ctrl
    CHF; High Coronary Dz Risk; Chronic Kidney Dz; DM; Post-MI; Recurrent Stroke Prevention
  33. Beta blocker : MOA
    Blockade of parts of the symp NS (reduce PVR); Lowers HR; Initially lowers cardiac output; Reduces circulating renin
  34. Fn of Angiotensin II
    Normally stims release of Na+-retaining hormone aldosterone (adrenal corticol cells); normally amplifies vasoconstriction (systemic and renal)
  35. ACEI AEs
    Cough; Angioedema; Hyperkalemia; Rash; CI in PG; use cautiously in renal artery stenosis (RAS)
  36. ARBs: MOA
    Act to block Angiotensin II from binding points; same effect as ACEI, without some of the AEs
  37. ARBs AEs
    Hyperkalemia; Angioedema (rare, 10% cross-over); CI in PG; Cautious use in RAS
  38. Diuretics: MOA
    Act to block Na+ (and K+) from being absorbed, thus increasing urine Na+. Water follows Na+ out of the body. Blood volume is less (lowering BP)
  39. Diuretics: AEs
    Hypokalemia; Volume depletion; Gout; increased insulin resistance; hyponatremia; increased chol levels
  40. CCBs: MOA
    Blocks vascular smooth mx contractility (resulting in vasodilatation & afterload reduction). Also result in coronary vasodilatation & are used in coronary artery spasm
  41. CCBs: Dihydropyridines (DHPs) vs nonDHPs
    DHPs more vascular selective; nonDHPs are more cardio-selective with more inhibitory effects on the SA/AV node
  42. BP =
    CO X PVR
  43. Essential HTN =
    established primary HTN
  44. Hallmark of essential HTN =
    elevated peripheral vascular resistance
  45. Variations in BP determined by:
    variations in ECF volume, heart contractility, & vascular tone
  46. Def of HTN = repeated readings of:
    SBP over 140 &/or DBP over 90
  47. Evidence supports tx of high risk pts at lower threshold of:
    of 130/80 mmHg.
  48. HTN: High risk groups include:
    DM, chronic kidney dz, CV or Cerebrovascular dz, or LVH on EKG
  49. Factors of essential HTN affect:
    ECF volume, heart contractility, or vascular tone
  50. HTN contributes to what % of M/F AA deaths?
    30% M & 20% F
  51. Most common secondary cause of HTN
    Chronic renal dz (proteinuria, high creat)
  52. ?% of pts w/ chronic renal dz have HTN
    85%
  53. Chronic renal dz & HTN: MOA
    expanded plasma volume & peripheral vasoconstriction
  54. Renal artery stenosis prevalence in HTN pts
    less than 2%
  55. HTN pts w/ renal artery stenosis: proportions
    75% unilateral stenosis; 25% bilateral
  56. Problem w/ renovascular HTN
    Renal artery stenosis causes 30% of medically refractory HTN
  57. Catecholamine-producing large tumors of adrenals
    Pheochromocytoma
  58. HTN & CPAP use for OSA
    CPAP improves risk of developing HTN & CV dz
  59. HTN prevalence in DM pts
    75% of diabetics have HTN
  60. Aldosterone-like effect precipitates persistent HTN in:
    Cushing Syndrome
  61. Leading cause of death worldwide
    arterial HTN
  62. Using std size cuff on obese pt:
    Gives falsely elevated result
  63. Ambulatory BP monitor can detect:
    Lack of nocturnal dip (assoc w/higher CVD risk)
  64. BP & substances
    Avoid tobacco/caffeine 30 min prior; document if pt took meds
  65. Ambulatory BP monitor & TOD
    Better TOD predictor than office measurements
  66. Those that develop HTN before 50 yrs:
    SBP > 140 mmHg & DBP > 90 mmHg
  67. What symptom must be present for a dx of Malignant Hypertension?
    Papilledema
  68. Most patients who develop HTN after 50 yrs have:
    Isolated Systolic HTN
  69. Defn Isolated Systolic HTN
    systolic BP over 140 mmHg with diastolic BP <90 mmHg
  70. Isolated Systolic HTN: hemodynamic fault =
    decreased distensibility of the large conduit arteries
  71. Majority of uncontrolled HTN occurs among:
    older pts with isolated systolic HTN.
  72. JNC: SBP opinion
    In pts over 50, SBP over 140 is a more important CVD risk than DBP
  73. DHP CCBs: AEs
    Ankle edema; Flushing; HA; Increased HR
  74. Diltiazem/Verapamil: AEs
    Bradycardia; Constipation
  75. Most common cause of Hypertensive Emergency
    Acute CHF with pulm edema (37%)
  76. JNC7: tx of uncomplicated HTN for most pts
    thiazide diuretic
  77. HTN lifestyle mods
    Wt; ETOH; aerobic activity; Na+ to 2.4 mg/day; K+; DASH diet
  78. Most single HTN meds lower BP:
    at most 20/10 mm Hg (so most pts on more than 1 drug)
  79. Compelling Indications: CHF
    Diuretic; Beta-blocker; ACEI; ARB; AA
  80. Compelling Indications: High Coronary Dz Risk
    Beta; ACEI; CCB; Diuretic
  81. Compelling Indications: Post-MI
    Beta; ACEI; AA
  82. Compelling Indications: DM
    Beta; ACEI; Diuretic; ARB
  83. Compelling Indications: Chronic Kidney Dz
    ACEI; ARB
  84. Compelling Indications: Recurrent Stroke Prevention
    ACEI; Diuretic
  85. HTN eval labs
    UA; serum Cr, glu, K+, Na+ ; Lipids (TC, trigs, HDL, LDL); 12-Lead EKG (LVH)
  86. HTN TOD
    Neuro; Ophthalmologic; CV; Renal; Vascular
  87. First Line Tx for HTN
    *Thiazide* ; beta; ACEI; ARB; other diuretics; CCB
  88. ACEIs
    Block formation of angiotensin II; blocking Angiotensin II results in vasodilatation and Na+ loss
  89. Excessive Na+-K+ exchange which results in hypokalemia; associated with HTN
    Hyperaldosteronism
  90. Complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood (systolic or diastolic)
    CHF
  91. Clinical syndrome caused by a variety of underlying conditions that lead to inadequate cardiac output
    CHF
  92. Clinical syndrome of CHF =
    Body’s maladaptive response to a low-flow state which produces symptoms of dyspnea and volume overload
  93. 3 major adaptive mechanisms to compensate for CHF
    Frank-Starling mechanism (rapid); Neurohumoral system activation (rapid); Myocardial remodeling (slow)
  94. Frank-Starling mechanism
    Increased ventricular filling during diastole results in increased volume of ejected blood during systolic contraction (CO = HR x SV; norm is about 5L/min)
  95. Neurohumoral release
    Norepinephrine stimulates cardiac contraction & activation of renin-angiotensin-aldosterone system; fn = to maintain arterial pressure & perfusion of vital organs
  96. Cardiac Remodeling (decline in function)
    Compensatory response following injury to cardiac tissue; LV dilates, damaged area forms scar (over time progresses to noncompliance of ventricle, inhibiting relaxation & filling)
  97. ACEI effect on heart remodeling
    Decrease (reverse) remodeling, improving cardiac performance
  98. Diastolic Left Heart Failure:
    Relaxation or Filling: heart does not relax normally, filling pressures are high but EF is normal (over 55%)
  99. Systolic Dysfunction
    Defect is in the expulsion of blood from the left ventricle, leading to inadequate cardiac output
  100. Causes of Systolic Left Heart Failure
    Ischemic heart dz (most common) due to MI hit or chronic ischemia; Longstanding HTN; Valvular Heart Dz; Idiopathic; Myocarditis (L & R); Toxins (ETOH, Cocaine, Thyroid, Pb); Sepsis
  101. Relationship: CHF & age
    HF incidence due to Diastolic dysfunction increases with age (due to increasing noncompliance of LV from long-standing HTN)
  102. Systolic component of CHF caused by:
    chronic loss of contracting myocardium due to prior MI & acute loss of myocardial contractility induced by transient ischemia
  103. Diastolic component of CHF is due to:
    ventricles reduced compliance due to chronic scarring & acute loss of distensibility during ischemia
  104. Rare instances of high output HF is assoc with:
    Elevated cardiac index but low SVR; chronic activation of symp N.S. & RAA systems; chronic volume overload and remodeling; heart cannot meet the metabolic demands; ultimately result in same neurohormonal imbalances as low output HF
  105. Sudden triggers for Acute HF
    Massive MI; Tachyarrhythmia with a very rapid rate; rupture of valve secondary to infective endocarditis
  106. Causes of Right HF
    Left HF; Congenital Heart Lesion (ASD); Right Valve Dz (Tricuspid, Pulmonic); Pulmonary Dz
  107. Pulmonary Dz =
    COPD, Interstitial Lung Dz; Pulmonary emboli; Pulmonary HTN (idiopathic, connective tissue dz)
  108. Why do initial CHF S/S occur w/ exertion?
    Exertion: Decrease ventricular filling time; Increase HR; Inability to increase CO (end result = supply & demand mismatch); ischemia may worsen situation
  109. CHF S/S
    SOB/dyspnea on exertion; edema (LE, abdomen (ascites), sacral/low back if bedbound); PND; orthopnea; fatigue, weakness, anorexia, nausea, wt change; tachycardia/palpitations
  110. CHF Phys Exam findings
    Skin (pallor, cyanosis, cool/moist); Tachypnea/ accessory mx use?; JVP elevation; HJR, hepatomegaly
  111. Cardiac Exam: Right HF:
    Right sided S3 or S4; TR murmur, loud P2 (delayed closing of pulmonic valve
  112. CHF: Systemic Findings
    Hepatomegaly; Pulsatile liver, tender RUQ; Ascites, Abd Swelling; edema (Low Back or sacrum if in bed); diminished or bounding pulses; Pulse, Pressure, 02 sat, weight
  113. CHF: Cardiac Cath consists of:
    Left ventriculogram; Arch shot; Coronary angiography to assess for blockages
  114. Left ventriculogram:
    Evaluate LV fn w/ calculated EF, assess wall motion, look for evidence of Mitral Regurgitation
  115. Arch shot:
    Assess for Aortic Insufficiency, defects in aorta (dissection/aneurysm)
  116. CHR: Echo: Assess:
    Assess for EF (LV function); for LVH; RV & Pulmonary pressures; Cardiac valves/murmurs; diastolic fn/ relaxation; WMAs; Pericardium (for effusion or mass)
  117. Management Algorithm
    S/S; H&P; EKG /Labs (assess etiology); Echo (MRI): preserved EF (diastolic) or poor EF (Systolic); cardiac cath (r/o ischemia, assess valve gradients, filling pressures, consider bx; start acute or chronic tx; reduce concomitant risk factors
  118. Pharm mgmt of CHF
    ACEI; ARBs; Beta Blockers; Nitrates + hydralazine; AAs; diuretics; digoxin; statins
  119. CHF: Pharm mgmt w/ proven mortality benefit
    ACEI; ARBs; Beta Blockers; Nitrates + hydralazine; AAs
  120. CHF: Non-Pharm chronic tx
    Multi-disciplinary team approach; Wt mgmt (Na+ / Fluid balance; ETOH/Toxin avoidance; Behavioral/ Risk modification; Palliative Care/ Hospice when appropriate
  121. Exercise in CHF pts
    Pts limited in even daily activity by poor functional status; even if cannot fix heart make body more efficient at given work load to allow independence; allows for wt Loss, mx strength, rehab enough to be able to get transplant
  122. Resynchronization therapy (Biventricular pacing): indications
    If low EF, Wide QRS > 130 ms and Class III or IV
  123. Anticoagulation for CHF
    Consider Coumadin (chronically) for Low EF; Hosp pt: prophylactic anticoag; aspirin if CAD (but no evidence for non-ischemic)
  124. Anticoagulation for CHF: Chronic Definite Use (Unless CI)
    A-fib; LV Thrombus; Previous thrombo-embolic CVA; Coagulopathy; LV Aneurysm
  125. Decompensated CHF:
    Pt is clinically deteriorating or unstable; begin early & aggressive tx as sort out Etiology
  126. Acute CHF S/S
    Severe SOB, Rales, Hypoxic, Cyanotic, Pale; CP; Tachy, BP may be hyper or hypo; cool or not perfused, poor pulses; distress (tachypneic, accessory mx); poor mental status
  127. Tests to determine cause of Decompensated CHF
    EKG (ischemia), HTN, atrial or other arrhythmia; Echo to assist dx; CXR to assess pulmonary edema
  128. Acute Decompensated CHF: Tx
    Diuretics (Natriuretics); O2 (CPAP or BiPAP); morphine? ; Nitrates (Vasodilators); Inotropes (Dobutamine, Milrinone); Hold/Do not start Beta; ACE/ ARB or other afterload reduction; Balloon pump; ID & tx underlying cause
  129. Acute Pulmo Edema (flash Pulmo Edema)
    Overcome fluid balance btw vascular bed & lung interstitium; pts are tachypneic, tachycardic, hypertensive, hypoxemic, crackles; if hypotensive, grave sign
  130. Causes of Acute Pulmo Edema:
    MI; Acute Valvular lesion (MR, AI); HTN/Renovascular dz; End stage valvular dz (AS, MS); Systemic illness (sepsis, anemia, thyrotoxicosis, severe resp illness); poss other causes (PE, MI)
  131. Acute Pulmonary Edema: Rx
    IV Diuretics, nitrates, inotropes (or BNP nesiritide), pressors (BP support), ACE/ARB or hydralazine + nitrate; HOLD beta in acute phase; O2, Morphine, Anti-arrhythmics if indicated
  132. % of people with LV dysfn who are symptomatic
    50%
  133. Heart Contraction & Relaxation wrt energy
    Both are energy requiring
  134. Classifications of Left Heart Failure:
    Systolic & diastolic
  135. Systolic Left Heart Failure
    Contraction: heart does not squeeze well, low EF (<55%)
  136. CHF with preserved systolic function
    Clinical S/S similar to systolic dysfunction
  137. CHF risk factors
    Age; HTN; Tobacco; DM; Obesity; ETOH/Substance abuse
  138. Most common cause of Systolic Left Heart Failure
    Ischemic heart dz
  139. Can Systolic & Diastolic CHF coexist?
    yes
  140. Most common form of HF is caused by:
    chronic ischemic heart dz
  141. Prior histories most often assoc w/ systolic CHF
    CAD; valvular heart dz
  142. Prior histories most often assoc w/ diastolic CHF
    HTN
  143. Diagnostic features of systolic CHF
    Echo reduced EF; CXR Cardiomegaly; CXR Pulm edema
  144. Diagnostic features of diastolic CHF
    Echo LVH; EKG LVH; CXR Pulm edema
  145. Echo features present in systolic HF & absent in diastolic HF
    Reduced EF; LV dilation
  146. CHF & output
    Most right/ left heart failure is low output
  147. Most common cause of Right HF
    Left HF
  148. CHF pts w/low EF (<35%) are at risk of devt of:
    v-tach or v-fib
  149. JVP elevation:
    Assess R int jugular vein; Reflects right atrial pressure elevations
  150. HJR =
    Hepatojugular reflux
  151. CHF PE: First assess:
    Acute distress or chronically ill?
  152. Lung Exam: Left HF
    Crackles/Rales; poss wheezing; dullness at bases; sputum (frothy/pink)
  153. Lung Exam: Right HF
    Possibly clear; dullness at bases (consider pleural effusion)
  154. Cardiac Exam: Left HF:
    S3 or S4 or Summation gallop; MR murmur
  155. CHF: dx tests help to:
    classify dz; assess etiology
  156. What % of CHF patients have LVH?
    20%
  157. CHF: EKG
    Global low voltage possible in end stage CHF; Evidence of Ischemia or prior infarction (Q waves)
  158. CHF: Cardiac Biomarkers
    (CK/MB, Troponin levels): indicated if suspect ischemic etiology
  159. Cardiac Cath: Indicated in:
    MI, USA
  160. CHF: on CXR (PA/Lateral), what is important?
    Size & Shape of cardiac silhouette
  161. CHF: CXR findings
    Kerley B lines; Pleural effusions
  162. Kerley B lines =
    sharp, linear densities of interlobular interstitial edema
  163. Pleural effusions in CHF: caused by:
    increase in interstitial edema
  164. Pleural effusions most often assoc with:
    LV dysfunction
  165. CHF = most common cause of what pulmonary outcome?
    Pleural effusion
  166. Describe pleural effusions:
    Typically transudative, small to moderate in size, & free flowing (LLD view may be helpful)
  167. CHR: Echo provides:
    structural, anatomic & physiologic info about the heart
  168. BNP: CHF
    BNP secreted from ventricles under stress in CHF
  169. BNP Levels
    Levels vary dependent on alterations in intracardiac filling pressure
  170. BNP = proposed marker for :
    severity of CHF & potentially useful for Rx management
  171. BNP may be falsely elevated in:
    renal failure
  172. CHF Device Tx
    AICD; IABP; Ultrafiltration/hemofiltration to remove fluid; LVAD
  173. AICD criteria
    EF < 35% for most CHF etiologies
  174. AICD Purpose:
    Prevention of sudden death; also for some HCM
  175. IABP =
    Intra-aortic balloon pump, temporary measure for acute CHF in hospital
  176. AICD =
    Automatic Implantable Cardioverter Defibrillators
  177. CHF: Nonpharm tx
    Behavioral; Devices (AICDs, Pacing, LVADS or pumps); Transplant
  178. LVAD =
    Left Ventricular Assist Device
  179. LVAD is considered a ____ tx
    bridge therapy prior to heart transplantation
  180. Placement of LVAD
    May be internal or external
  181. Frequency of heart transplants for CHF
    2500/yr for CHF
  182. CHF Device Tx
    AICD; IABP; Ultrafiltration/hemofiltration to remove fluid; LVAD
  183. AICD for CHF = what type prevention?
    Primary or Secondary Prevention
  184. AICD indicated if:
    Previous V-Tach, SCD
  185. Effect of antiarrhythmics for VT/VF
    (Amiodarone, Dofetilide) do not improve survival
  186. Limitation in OHT (transplant) for CHF =
    donor organs
  187. OHT for CHF: Late Survival post one year:
    Determined by devt CAD or vasculopathy
  188. OHT for CHF: median survival =
    10 years
  189. OHT for CHF: one-year mortality predicted by:
    need for post-op dialysis or ventilation
  190. OHT for CHF: Hx of sepsis, CAD, DM, CVA predict:
    decreased 5 year survival
  191. Decompensated CHF: types
    Acute or Acute on Chronic
  192. Acute CHF: hypotension is:
    Ominous (if bradycardia this may be cause, as is inappropriate)
  193. Decompensated CHF: Phys Exam
    New murmur of MR or AI, worsened AS , rales
  194. Decompensated CHF: tx
    Tx early & aggressively; eliminate or control inciting factors
  195. Acute (flash) Pulmo Edema:
    S/S of rapid clinical deterioration

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Author:
 HuskerDevil
ID:
 94445
Filename:
 Cardiology 3
Updated:
2011-07-18 20:20:59
Tags:
DPAP2012 Cardiology
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