CLINICAL

 THERAPEUTICS  3A  –  MIDTERMS  CASE  3:  HEART  FAILURE,  HYPERTENSION&  

DYSLIPIDEMIA  
FEU-­‐NRMF  Institute  of  Medicine    
Microsoft  Office  User    
Medcine2017  
 
I.  Problem  1:  Chronic  Congestive  Heart  Failure  in  Acute  Exacerbation  
 
Although  there  is  no  precise  definition  of  heart  failure,  it  can  be  defined  as  a  progressive,  complex  clinical  syndrome  
characterized  by  dyspnea,  fatigue,  and  fluid  retention.  Patients  move  from  asymptomatic  left  ventricular  dysfunction  to  
symptomatic  heart  failure.    
Over   the   course   of   the   syndrome,   patients   will   not   always   have   symptoms   of   congestion.   Therefore,   the   term  
‘‘congestive  heart  failure’’  is  beginning  to  fall  out  of  favor;  rather,  ‘‘chronic  heart  failure’’  is  being  used  to  describe  this  
population.  
Patients  with  chronic  CHF  may  acutely  decompensate.  This  condition  may  result  from  either  a  natural  progression  
of   CHF   associated   with   a   decline   in   cardiac   function   or   some   identifiable   cardiovascular   precipitating   factors   such   as  
superimposed  ischemia  or  new  onset  atrial  fibrillation.  
Alternatively,   systemic   or   patient   related   precipitating   factors,   including   infection   or   medication   or   dietary  
noncompliance.  
 
A.  Basis  for  Diagnosis  
 
Table  1.  Signs  and  Symptoms  of  Heart  Failure,      
Table  2.  Risk  Factors  of  Heart  Failure  and  the  
Physical  Exam  Findings  and      
Risk  Factors  Present  in  the  Patient  
Clinical  Manifestation  Present  in  the  Patient    

S/Sx  and  PE  of  Heart   RISK  FACTORS  of  HF   Present  in  the  
Present  in  the  PATIENT   PATIENT  
Failure    

Fatigue  and  weakness   ✔     Hypertension   ✔     Hypertensive  

for  20  years  
Shortness  of  breath   ✔     RR-­‐  27cpm  
Diabetes   ✔   FBS:  189  
Swelling  (edema)  legs,   bilateral  up  to   mg/dL  
✔    
ankles  and  feet   knees  
Coronary  Artery   ✔    
Weight  gain   ✔     Disease  
Orthopnea   ✔     Obesity   ✔   BMI:  32  

Paroxysmal  nocturnal     Sleep  apnea   ✔    

✔  
dyspnea  
Advanced  age   ✔   66  years  old  
Crackles   ✔     bilaterally  
Valvular  Heart  DIsease   X    
Elevated  blood  pressure   ✔   154/92mmHg  
Smoking   X    
Murmur:  (+)  S3   ✔    
Severe  lung  disease   X    
PMI  displaced   ✔     laterally    
tachycardia   X     87  bpm    
 
Urinary  frequency   X      
 
 

  1  
B.  Classification  of  Heart  Failure  
   
The   patient   already   has   ventricular   hypertrophy,  
which   make   him   belong   to   the   AHA   stage   C  
(structural   heart   disease   with   prior   or   recurrent  
symptoms   of   HF).   He   was   symptomatic   even   at  
rest,  so  he  is  already  in  NYHA  functional  class  IV.  
 
 
 
 
 
 
 
 
 
 
 
C.  Pathophysiology  
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
   
  2  
 Several   generalized   pathophysiologic   conditions   Furthermore,   myocardial   contractility   is  
can   lead   to   HF   but   the   one   applicable   in   the   patient’s   enhanced   because   norepinephrine,   angiotensin   II,   and  
condition  is  the  pressure  overload  of  the  heart  due  to  his   endothelin-­‐1  are  positive  inotropic  agents,  the  former  via  
hypertension.   Clinically,   these   conditions   manifest   as   a   stimulation   of   A1   receptors.   Norepinephrine   also  
reduction  in  systolic  emptying  or  diastolic  relaxation  and   increases  heart  rate  (HR)  via  Beta  1  receptor  stimulation.  
filling.  Either  systolic  or  diastolic  dysfunction  can  lead  to  a    
decrease  in  stroke  volume  and  CO.     In   addition,   cytokines   such   as   TNF-­‐alpha   and  
  interleukin-­‐6,   the   former   become   elaborated   and  
The   decrease   in   CO   is   sensed   as   a   decrease   in   probably  play  a  role  in  facilitating  early  ventricular  dilation  
end-­‐organ   perfusion   pressure   principally   by   arterial   by   stimulating   increased   activity   of   matrix  
baroreceptors.  In  response  to  decreased  CO,  a  number  of   metalloproteinases   (MMPs).   MMPs   are   enzymes   that  
compensatory   responses,   many   of   which   are   degrade   extracellular   matrix,   thereby   augmenting   LV  
neurohormonally  mediated,  become  activated.     remodeling.    
   
Cardiac   myocyte   hypertrophy   or   an   increase   in   Thus,   neurohormonally   mediated   increases   in  
wall   thickness   also   occurs,   especially   in   response   to   the   contractility,   HR,   preload,   and   myocardial   hypertrophy,  
pressure   overload   of   HTN   or   aortic   stenosis,   and   is   the   along   with   cytokine   mediated   ventricular   remodeling,  
result  of  an  increase  in  the  diameter  of  myocytes  through   maintains  CO  after  initial  myocardial  injury.  
the  parallel  addition  of  new  sarcomeres.    
  In   the   peripheral   circulation   norepinephrine,  
Ventricular   remodeling   is   mediated   angiotensin   II,   and   endothelin-­‐1   promote   systemic  
predominantly   by   initial   activation   of   the   sympathetic   vasoconstriction   via   stimulation   of   vascular   alpha   1  
nervous  system  and  secondary  activation  of  the  RAAS.   receptors,   angiotensin   II   type   1   receptor   (AT1),   and  
  endothelin-­‐1   type   A   (ETA)   receptors,   respectively,   to  
Norepinephrine   and   decreased   renal   perfusion   maintain  perfusion  pressure.  
pressure   stimulate   the   release   of   renin   by   the   kidney.    
Renin,   both   systemically   and   locally   in   the   myocardium,   D.  Diuretic  Resistance  
first  acts  on  angiotensinogen  to  convert  it  to  angiotensin    
I.   Angiotensin   I   is   then   converted   to   angiotensin   II   by   In   the   ER,   the   patient   was   given   IV   boluses   of  
angiotensin-­‐converting  enzyme  (ACE).   Furosemide,   however,   no   much   response   was   noted.  
1.   Angiotensin   II   also   can   be   synthesized   locally   via   Later  on,  he  was  started  on  Furosemide  IV  infusion  at  5  
chymase,   an   ACE-­‐independent   pathway.   mg/hr.   After   3   hours,   No   symptomatic   relief   and   was  
Norepinephrine  and  angiotensin  II  act  as  mitogens  for   transferred   to   cardiac   intensive   care   unit   for   further  
cardiac   myocytes   to   increase   the   number   of   management.  This  is  called  diuretic  resistance.  
sarcomeres  (i.e.,  cardiac  hypertrophy).    
2.   Angiotensin  II  enhances  sympathetic  nervous  system   Diuretic   resistance   explains   why   some   patients  
activity   by   facilitating   presynaptic   norepinephrine   require   high   doses   of   diuretics   or   have   a   decreased  
release.   response   to   diuretics   over   time.   Several   mechanisms  
3.   Angiotensin   II   also   stimulates   the   release   of   contribute  to  diuretic  resistance.    
aldosterone   from   the   adrenals   and   facilitates   the   The   “braking   phenomenon”   refers   to   a   short-­‐
secretion  of  arginine  vasopressin.  In  turn,  aldosterone   term  resistance  following  a  bolus  dose  and  may  be  related  
and   arginine   vasopressin   trigger   renal   sodium   and   to   neurohormonal   activation   that   acts   to   preserve  
water   retention,   respectively.   Blood   volume   is   intravascular  volume.    
expanded,  so  preload  is  augmented.      
4.   Angiotensin   II   also   enhances   the   formation   of   A   longer   term   resistance   may   be   due   to  
preproendothelin   by   endothelial   cells.   compensatory   hypertrophy   of   the   distal   convoluted  
Preproendothelin  is  cleaved  by  endothelin-­‐converting   tubule,   which   avidly   reabsorbs   sodium   and   counteracts  
enzyme   to   form   endothelin-­‐1,   which   stimulates   the  natriuretic  effects  of  loop  diuretics.    
further   release   of   renin   and   aldosterone   as   well   as    
further  conversion  of  angiotensin  I  to  angiotensin  II  in    
endothelial   cells.   Therefore,   endothelin-­‐1   also    
promotes  sodium  retention.    
  3  
E.  Goals  of  Therapy   FOR  ACUTE  EXACERBATION:  
  ü   Diuretic  (IV  furosemide  or  another  loop  diuretic)  is  
Ø   Decrease  pulmonary  congestion   the  mainstay  of  treatment  for  acute  decompensation  
Ø   Reduce  the  Neurohormone  Activity   and  pulmonary  edema.    
Ø   Minimize  CHF  exacerbation   *The  venodilatory  action  of  IV  furosemide  is  observed  
Ø   Slow  the  CHF  progression   within  several  minutes  of  administration  and  precedes  
Ø   Improve  quality  of  life   its  natriuretic  effect  (fast  onset  but  short  duration).  
Ø   Increase  survival   Administration  should  not  be  delayed  due  to  the  
  immediate  unavailability  of  hemodynamic  monitoring  
Treatment  Strategies  &  Pharmacologic  Intervention   because  dramatic  relief  of  the  signs  and  symptoms  of  
  pulmonary  congestion  may  be  obtained.  
•   Decrease  pulmonary  congestion  à  Loop  diuretic,   ü   Spironolactone  is  added  since  the  patient  has  
Aldosterone  antagonist   transient  furosemide  resistance.  (can  decrease  
•   ↓  Neurohormone  activityà  ARBS,  Aldosterone   cardiac  remodeling  brought  about  by  aldosterone  &  K  
Antagonist   &  water  retention)  
•   ↓  preload  &  afterload  à  Loop  diuretic,  ARBS,    
Aldosterone  Antagonist     After  hemodynamic  and  clinical  stabilization  with  the  use  
•   ↓  catecholamine  effects  à  3rd  gen  B  blockers   of   intravenous   diuretics,   the   patient   is   transitioned   to   an  
•   Prevent  cardiac  remodeling    à  3rd  gen  B  blockers,   oral  regimen.    
Aldosterone  antagonist,  ARBS    
  FOR  MAINTENANCE,  
F.  Pharmacologic  Intervention   ü   ARBS   will   be   used   because   the   patient  
has  Benazepril  allergy,  so  we  will  not  use  
any  class  from  ACE  I.    

ARBs  ↓  preload  &  afterload,  

prevent  cardiac  remodeling  &  
↓neurohormonal  effects;  it  
manages  HTN  &  protects  from  CAD  
by  improving  hemodynamics,  also  
includes  renal  hemodynamics  so  
renders  protection  from  DM  

ü  When  the  patient  is  stabilized  to  

a  certain  NYHA  functional  class  with  
optimal,  conventional  medications,  
then  decisions  to  add  new  drugs  such  
as  Beta  -­‐blockers  or  to  evaluate  the  
patient  for  additional  non-­‐
pharmacologic  therapies  must  be  
made.  In  addition  to  that,  Digoxin  is  
used  when  the  ejection  fraction  is  ↓  .  

*β  blockers  only  added  when  there  

are  structural  abnormalities  
ü Carvedilol  
-­‐ Non  selective  α  &  β  antagonist  
    -­‐ Inhibits  mitogenesis  thus  
    prevents  cardiac  remodelling  
    ü Metoprolol  
    -­‐ Selective  β1  blocker  
    -­‐ Relieves  preload  &  afterload  

  4  
   Efficacy   Safety   Suitability   Cost    
 
Loop  Diuretics   ++++   +   ++++   20mg/2m  (P172.82  
 
/day)  
 
K  Sparing  Diuretics   ++++   +++   ++++   25  mg  (P15.34  /  day)    
ARB  (Cozaar)   ++++   +++   ++++   50mg  (P20.21)    
 
Beta  Blockers  
 
Carvedilol  (Karvil)   ++++   ++   ++++   6.25mg  (P  5.29/day)    
Metoprolol   +++   ++   +++   100mg  (P6.05  /  day)  
 
(Metoprim)    
G.  Non-­‐Pharmacologic  Intervention  
Ø   Lifestyle  Changes  
o   Avoiding  or  limiting  caffeine    
o   Eating  a  heart-­‐healthy  diet    
o   Being  physically  active    
o   Managing  stress    
o   Keeping  track    
o   Monitoring  your  blood  pressure    
o   Getting  adequate  rest    
o   Developing  support    
o   Avoiding  flu  and  pneumonia  with  vaccinations    
o   Following  heart  patient  guidelines  for  sexual  activity    
o   Selecting  appropriate  clothing  
Ø   Surgery  
o   Percutaneous  Coronary  Intervention/Angioplasty  
o   Coronary  Artery  Bypass  
o   Heart  Transplant  
o   Valve  Replacement  
o   Defibrillator  Implantation  
o   Cardiac  Resynchronization  
 
H.  Prescribing  the  drug:  
 
IV  FUROSEMIDE  
As  Heart  Failure  and  secondary  renal  dysfunction  progress,  increasingly  larger  and  more  frequent  doses  are  needed.  
Although  dosages  vary  widely,  patients  with  end-­‐stage  HF  may  need  two  or  three  oral  daily  doses  of  a  loop  diuretic  (e.g.,  
furosemide  160  to  400  mg).  A  good  rule  for  estimating  the  initial  dosage  of  furosemide.  
 

The   diuretic   most   commonly   used   for   congestive   heart   failure   is   a   loop   diuretic   like   furosemide,   which   is  
administered  IV,  in  a  dosage  of  40  mg,  followed  if  necessary  by  oral  administration,  20-­‐80  mg/24h.      
 
D:  Tab  Adult  Initially  ½  -­‐  1-­‐2  tab  daily.  Maintenance:  ½  -­‐  1tab  daily.  Inj  Adult  Initially  20-­‐40mg  IV/IM.  If  diuretic  effect  
is   not   satisfactory,   dose   maybe   increased   stepwise,   at   2   hrly   interval   by   20   mg   each   time   until   satisfactory   diuresis   is  
obtained,  the  dose  should  be  given  once-­‐bid.      
 
Allergic  and  Other  Reactions  
 

All  loop  diuretics,  with  the  exception  of  ethacrynic  acid,  are  sulfonamides.  Therefore,  skin  rash,  eosinophilia,  and  
less  often,  interstitial  nephritis  are  occasional  adverse  effects  of  these  drugs.  This  toxicity  usually  resolves  rapidly  after  drug  
withdrawal.  Allergic  reactions  are  much  less  common  with  ethacrynic  acid.  

  5  
 Because   Henle’s   loop   is   indirectly   responsible   for   water   reabsorption   by   the   downstream   collecting   duct,   loop  
diuretics  can  cause  severe  dehydration.  Hyponatremia  is  less  common  than  with  the  thiazides  (see  below),  but  patients  who  
increase  water  intake  in  response  to  hypovolemia-­‐induced  thirst  can  become  severely  hyponatremic  with  loop  agents.  Loop  
agents  can  cause  hypercalciuria,  which  can  lead  to  mild  hypocalcemia  and  secondary  hyperparathyroidism.  On  the  other  
hand,  loop  agents  can  have  the  opposite  effect  (hypercalcemia)  in  volume  depleted  patients  who  have  another—previously  
occult—cause  for  hypercalcemia,  such  as  metastatic  breast  or  squamous  cell  lung  carcinoma.  
 
SPIRONOLACTONE  
Adverse  Effects:  GI  symptoms,  Drowsiness,  Lethargy,  Headache,  Mental  confusion  
Ø   Stevens-­‐Johnson  syndrome  –  a  rare,  serious  disorder  of  your  skin  and  mucous  membranes  often  begins  with  flu-­‐like  
symptoms  followed  by  a  painful  red  or  purplish  rash  that  spreads  and  blisters  then  the  top  layer  of  affected  skin  dies  
and  sheds.  
Ø   Hyperkalemia  -­‐  Unlike  most  other  diuretics,  K  +  -­‐sparing  diuretics  reduce  urinary  excretion  of  K+  and  can  cause  mild,  
moderate,  or  even  life  threatening  hyperkalemia.  The  risk  of  this  complication  is  greatly  increased  by  renal  disease  (in  
which  maximal  K  +  excretion  may  be  reduced)  or  by  the  use  of  other  drugs  that  reduce  or  inhibit  renin  (β  blockers,  
NSAIDs,  aliskiren)  or  angiotensin  II  activity  (angiotensin-­‐converting  enzyme  inhibitors,  angiotensin  receptor  inhibitors).  
Since  most  other  diuretic  agents  lead  to  K  +  losses,  hyperkalemia  is  more  common  when  K  +  -­‐sparing  diuretics  are  used  
as  the  sole  diuretic  agent,  especially  in  patients  with  renal  insufficiency.  With  fixed-­‐dosage  combinations  of  K  +  -­‐sparing  
and  thiazide  diuretics,  the  thiazide-­‐induced  hypokalemia  and  metabolic  alkalosis  are  ameliorated.  However,  because  of  
variations  in  the  bioavailability  of  the  components  of  fixed-­‐dosage  forms,  the  thiazide-­‐associated  adverse  effects  often  
predominate.  Therefore,  it  is  generally  preferable  to  adjust  the  doses  of  the  two  drugs  separately.  
Ø   Patient  education  should  take  place  during  the  entire  hospitalization  with  a  specific  focus  on   salt  and  fluid  status  and  
obtaining  daily  weights,  in  addition  to  medication  schedules  
Ø   Criteria  for  discharge  should  include  at  least  24h  of  stable  fluid  status,  blood  pressure,  and  renal  function.  
Ø   Before  discharge,  patients  should  be   free  of  dyspnea  or  symptomatic  hypotension  while  at  rest,  washing,  and  walking  
on  the  ward.    
 
II.  Problem  2:  UNCONTROLLED  BP  DUE  TO  NON  COMPLIANCE  
 
A.  Basis  for  Diagnosis  
 
JNC   Guidelines   (JNC   8)   on   Hypertension   takes   a   rigorous,   evidence-­‐based   approach   to   recommend   treatment  
thresholds,  goals,  and  medications  in  the  management  of  hypertension  in  adults.  Evidence  was  drawn  from  randomized  
controlled   trials,   which   represent   the   gold   standard   for   determining   efficacy   and   effectiveness.   Evidence   quality   and  
recommendations  were  graded  based  on  their  effect  on  important  outcomes.  
 
Risk  factors  associated  in  the  case:    
 ü Age (66 y/o)
 ü Male
 ü past medical history: (+) Hypertension for
  20 years
 ü Family History: Father was known
hypertensive
 
ü BP findings: 154/92 mmHg
 
ü Shortness of breath
 ü (-) adherence to Anti – HPN medication
  (Amlodipine)
 ü Allergy to Benzapril (Cough)
 
                                                                       

  6  
Ø   In   general,   non   –   black   population,   including   those   with   Diabetes,   initial   hypertensive   treatment   should   include   a  
thiazide  –  type  of  diuretic,  Calcium  –  channel  blocker,  ACE  Inhibitor  or  Angiotensin  Receptor  blocker  
     
C.  Treatment  Goals  
 
Ø   Maximize   non-­‐pharmacologic   therapies   in  
combination  with  pharmacotherapy  based  on  
Ø   Individualize   all   therapies   based   on   compelling  
indications  and    
Ø   co-­‐morbid  condition  
Ø   Normalize  BP  based  on  recommended  target  JNC  8  
Ø   Prevent  complications,  MI  and  STROKE  
 
 
 
 
D.  Pharmacologic  Intervention  
Medications  to  consider  according  to  JNC  8:  
Ø   Thiazide  Diuretic  
-­‐  ↓  CO  &  indirectly  TPR  (↓Na  =  ↓  vascular  tone)  
Ø   ACE  Inhibitors    
Ø   ARBs  
Ø   Calcium  Channel  Blockers  
-­‐   Dihydropiridines(dipines):  ↓TPR  
-­‐   Non-­‐dihydropyridines  (diltiazem  &  verapamil):  
cardioprotective  by  ↓CO  
 
 
 
 
 
 
 
 
 
 
 
 
 
E.  Non-­‐Pharmacologic  Intervention  
Ø   Eat  a  better  diet,  which  may  include  reducing  salt  
Ø   Enjoy  regular  physical  activity  
Ø   Maintain  a  healthy  weight  
Ø   Manage  stress  
Ø   Avoid  tobacco  smoke  
Ø   Comply  with  medication  prescriptions  
Ø   If  you  drink,  limit  alcohol  
Ø   Understand  hot  tub  safety  
 
 
 

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DOC:  ARBs  
Drug  Interactions  
Ø   Potassium  sparing  diuretics  
Ø   Potassium  supplements    
 
Adverse  Effect  
Ø   Severe  hypotension  
Ø   Dry  cough  accompanied  by  wheezing    
Ø   More  aggressive  blood  pressure  targets  for  blood  pressure  control   (<130/80  mmHg)   are  generally  recommended  for  
patients  with  additional  cardiovascular  disease  risk  factors.  
Ø   Although  the  optimal  target  blood  pressure  in  patients  with  heart  failure  has  not  been  established,  a  reasonable  goal  is  
the  lowest  blood  pressure  that  is  not  associated  with  evidence  of  hypoperfusion.    
 
III.  Problem  3:  Dyslipidemia  
 
Dyslipidemia   is   an   abnormal   amount   of   lipids   in   the   blood,   usually   asymptomatic.   In   developed   countries,   most  
dyslipidemias   are   hyperlipidemias;   that   is,   an   elevation   of   lipids   in   the   blood.   Often   due   to   diet   and   lifestyle.   Prolonged  
elevation  of  insulin  levels  can  also  lead  to  dyslipidemia.    
Dyslipidemia  is  elevation  of  plasma  cholesterol,  triglycerides  (TGs),  or  both,  or  a  low  high-­‐density  lipoprotein  level  
that  contributes  to  the  development  of  atherosclerosis.  Causes  may  be  primary  (genetic)  or  secondary.  
 
Diagnosis   and   treatment   of   Dyslipidemia   is   a   step   by   step   process   according   to     The   National   Cholesterol   Education  
Program’s  Adult  Treatment  Panel  III  Guidelines  
(NCEP  ATP  III):  
 
1.   Determining  plasma  levels  of  complete  lipoprotein  profile  after  9-­‐  to  12-­‐hour  fast    
2.   Identifying  presence  of  clinical  atherosclerotic  disease  that  confers  high  risk  for  coronary  heart  disease  (CHD)  events  
(CHD  risk  equivalent)  
3.   Determining  presence  of  major  risk  factors  (other  than  LDL)  
4.   Assessing  10-­‐year  (short-­‐term)  CHD  risk  using  Framingham  tables  If  2+  risk  factors  (other  than  LDL)  are  present  
without  CHD  or  CHD  risk  equivalent  
5.   Determine  risk  category  
6.   Initiating  therapeutic  lifestyle  changes  (TLC)  if  LDL  is  above  goal  
7.   Considering  adding  drug  therapy  if  LDL  exceeds  levels  
8.   Identifying  metabolic  syndrome  and  treat,  if  present,  after  3  months  of  TLC  
9.   Treating  elevated  triglycerides  
 
STEP  1:    Determine  lipoprotein  levels  -­‐  obtain  complete  lipoprotein  profile  after  9-­‐  to  12-­‐hour  fast  
 
 
 
 
 
 
 
This  table  shows  that  the  patient  has  elevated  total  cholesterol,  borderline  of  LDL,  normal  HDL  and  elevated  Triglyceride.  
 

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STEP  2:  Identify  presence  of  clinical  atherosclerotic  disease  that  confers  high  risk  for  coronary  heart  disease  
(CHD)  events  (CHD  risk  equivalent)  
For  step  2  
positive  risk  
for  Coronary  
Artery  Disease  
and  Peripheral  
arterial  
disease  are  seen  in  the  patient  
 
STEP  3:  Determine  presence  of  major  risk  factors  (other  than  LDL)  
 
For  step  3,  the  
patient  has  2  of  
the  5  major  risk  
factor  for  
dyslipidemia  
which  are  
Hypertension  
>140/90  mmHg  
and  Age  >45  for  
men.  
 
STEP  4:  If  2+  risk  factors  (other  than  LDL)  are  present  without  CHD  or  CHD  risk  equivalent,  assess  10-­‐year  (short-­‐
term)  CHD  risk  using  Framingham  table  
 
According  to  Age:           According  to  Age  group  and  Total  Cholesterol  

 
According  to  Age  &  Smoking  

 
 
HDL  levels  
   
 
 
 
 
Systolic  Blood  Pressure  and  Treatment  Status:  
 
 
 
 
 

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10-­‐Year  Risk  by  Total  Framingham  Point  Scores:  
Total:  15  =  20%  Risk  
MODERATELY  HIGH  Risk  
10-­‐Year  Risk  by  Total  Framingham  Point  Scores   Patient’s  Score  
Age  Group   11  
Age  Group  and  Total  Cholesterol   1  
Age  and  Smoking   0  
HDL  Levels   1  
Systolic  Blood  Pressure  and  Treatment  status   2  
Total   15  
 
 
 
 
For  Step  4  MODERATELY  HIGH  Risk  in  developing  CHD  according  to  the  10-­‐Year  Risk  by  Total  Framingham  Point  Scores  
 
STEP  5:  Determine  risk  category:  
Establish  LDL  goal  of  therapy,  determine  need  for  therapeutic  lifestyle  changes  and  determine  level  for  drug  consideration  
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Patient  has  2  of  the  major  risk  factor  for  dyslipidemia  and  20%  Risk  in  10  years  by  Total  Framingham  Point  Scores,  
patient’s  LDL  goal  should  be  less  than  130  mg/dL.  
 
STEP  6:  Initiate  therapeutic  lifestyle  changes  (TLC)  if  LDL  is  above  goal:  
TLC  Diet:    
•   Saturated  fat  <7%  of  calories,  cholesterol  <200  mg/day.Consider  increased  viscous  (soluble)  fiber  (10-­‐25  g/day)  and  
plant  stanols/sterols  (2g/day)  as  therapeutic  options  to  enhance  LDL  lowering  
•   Weight  management  
•   Increased  physical  activity  
 
 
 
 
 
 
 
 
 

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STEP  7:  Consider  adding  drug  therapy  if  LDL  exceeds  levels  
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
STEP  8:  Identify  metabolic  syndrome  and  treat,  if  present,  after  3  months  of  TLC  
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
STEP  9:  Treat  elevated  triglycerides  
 
 
 
 
 
 
 
 
 
 
 
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A.  Pharmacologic  Intervention  
•   Most  effective  in  lowering  LDL:  Statins    
•   Most  effective  in  lowering  TG:  Fibrates    
•   Most  effective  in  increasing  HDL:  Niacin    
•   bile  acid  resins:  almost  NO  effect  on  TG  
•   Bile  acid  resins  along  with  ezetimibe  also  lower  LDL    
•   The  ones  that  primarly  lower  VLDL  are  nicotinic  acid,  fibrates  &  omega-­‐3  FA    
 
DRUG  OF  CHOICE:  Atorvastatin  20mg/tab  Every  Other  Day  
Adverse  Effects  
Ø   Potential  side  effects  include  dyspepsia,  headaches,  fatigue,  and  muscle  and  joint  pains.  
Ø   Severe  myopathy  and  rhabdomyolysis  (increased  in  old  age).    
Ø   Contact  physician  immediately  (Obtain  plasma  creatine  kinase  (CK)  level  to  document  myopathy)    
Ø   Serum  CK  levels  need  not  be  monitored  on  a  routine  basis  in  patients  taking  statins,  as  an  elevated  CK  in  the  absence  
of   symptoms   does   not   predict   the   development   of   myopathy   and   does   not   necessarily   suggest   the   need   for  
discontinuing  the  drug    
Ø   Elevation  in  liver  transaminases  (AST  and  ALT)  
*Patient   in   the   case   have   mild   elevation   of   liver   enzymes,   but   it   is   due   to   congestion   so   statins   not   yet  
contraindicated;  it  needs  to  be  3x  higher  than  normal  to  be  contraindicated  
Ø   Check  before  starting  therapy,  at  2-­‐3  months,  and  then  annually.      
Ø   Mild  to  moderate  (1  to  3  times  normal)  elevation  in  transaminases  in  the  absence  of  symptoms  need  not  mandate  
discontinuing  the  medication.  REMARKABLY  SAFE    
Ø   Maximum  effect  on  lipids  is  4-­‐6  weeks  (important  to  know,  so  physicians  will  know  when  to  monitor  lipid  profile.)  
High  intensity  statin  therapy  =  Daily  dose  lowers  LDL-­‐C  on  average,  by  approximately  >/=50%  
-­‐  Atorvastatin  (40)-­‐80mg  
Moderate   intensity   statin   therapy   =   Daily   dose   lowers   LDL-­‐C   on   average,   by   approximately   30%   to   <50%   -­‐   Atorvastatin   10  
(20)  mg  
 
B.  Non-­‐Pharmacologic  Intervention  
Ø   Lifestyle  Modification  
o   Weight  reduction  
o   Physical  exercise  –  20  to  30  minutes  a  day  for  at  
least  5  days  
o   Quit  smoking  
o   Decrease  alcohol  use  
 
Ø   Dietary  Modification  
o   DASH  (Dietary  Approaches  to  Stop  Hypertension)  
diet  
o   Low  fat  content  
o   Diet  rich  in  fruits  &  vegetables  
o   Dietary  sodium  restriction  to  2-­‐3  g/day  is  recommended  
o   Fluid  restriction  to  2  L/day  is  recommended  for  patients  with  evidence  of  hyponatremia  (Na  <  130  
mEq/dL)  
 
IV.  Follow-­‐Up  
 
Keep  scheduled  regular  visits  with  the  health  care   provider,  as  he  or  she  recommends,  because  congestive  heart  failure  is  
a  serious  medical  condition  that  requires  constant  monitoring.  Patients  need  to  educate  themselves  as  much  as  possible  
about  this  life-­‐threatening  condition  and  follow  these  suggestions:  
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 •   Establish  a  daily  routine  for  taking  medication  properly  and  on  schedule.  
•   Weigh   in   daily.   Every   morning,   record   the   weight   in   a   diary,   and   take   it   to   the   health   care   provider   every   visit.   An  
accurate   bathroom   scale   is   helpful   in   monitoring   weight   gain   or   loss   from   day   to   day   in   order   to   detect   fluid  
retention.  
•   Keep  a  list  of  all  medications,  with  the  exact  name  and  dose,  and  know  why  each  one  is  taken.  Bring  them  to  each  
follow-­‐up  visit  so  the  doctors  can  double  check  to  make  sure  patients  are  on  the  correct  medication  and  dose.  
•   Reminder  boxes  for  medications  are  helpful.  
•   Be   sure   to   keep   all   these   medications   away   from   small   children   who   may   accidentally   swallow   them.   Many   of   the  
drugs  prescribed  for  congestive  heart  failure  are  more  dangerous  in  overdose  than  other  medications  
•   After  starting  antihypertensive  drug  therapy,  the  patient  should  see  his  or  her  doctor  at  least  once  a  month  until  
the  blood  pressure  goal  is  reached.  
•   The  doctor  should  check  the  patient’s  serum  potassium  (diuretics  can  lower  this)  and  creatinine  (to  check  the  the  
kidneys)  once  or  twice  a  year.  
•   After   the   blood   pressure   goal   is   reached,   the   patient   should   see   the   doctor   every   three   to   six   months,   depending  
on  whether  he  or  she  has  any  diseases  such  as  heart  failure.  
•   After  starting  drug  therapy,  the  LDL  cholesterol  level  should  be  measured  in  about  six  weeks  and  again  in  12  weeks.  
Liver  function  and  other  tests  for  drug  toxicity  can  be  done  at  these  times.  If  the  LDL  goal  is  reached,  lipid  levels  
should  be  checked  every  six  to  12  months.  Follow-­‐up  analysis  should  occur  six  to  eight  weeks  after  a  change  in  drug  
therapy
 
I only edited the written report of my classmates
and added some notes.

Written Report by:

Batalla, Nico
Falcon, Mary Jane
Mirasol, John Christian
Pesebre, Angelie Lorraine
Sy, Fob Ian

 
 

Hi  Pau  Singh!  

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