Professional Documents
Culture Documents
S/Sx
and
PE
of
Heart
RISK
FACTORS
of
HF
Present
in
the
Present
in
the
PATIENT
PATIENT
Failure
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.
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
7
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.
8
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:
9
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
10
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
11
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:
12
• 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.
Hi Pau Singh!
13
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