PATHOPHYSIOLOGY

Predisposing
Age- 73 years old
Hereditary- HPN, DM
Gender- female
Hx of Cholecystectomy (NMMC; 1995)
Menopause (starts at age 42 years old; Menarche starts at age 13 yrs.old.)
DM II (1999; usual glucose level: 140-160mg/dL; highest level: 300mg/dL)

Precipitating
>HPN (37 yrs old; usual BP 140/90; highest BP is 200/110mmHg)
>Inc. serum Cholesterol level: 231mg/dL
>Lack of exercise/activity
>Obesity (BMI of 27 kg/m2, IBW: 48.96kg)

Increase shearing force of the arterial wall by the condition

of the blood

Diagnostic:
CBC:
Eosinophils-16.4%(0.006.00)
Diagnostic:
Blood Chemistry:
Cholesterol-231 mg/dl (0-200
mg/dl)
Triglycerides-191 mg/dL (0-150
mg/dl)
Medication:
>Atorvastatin Calcium (Lipitor)80mg 1 tab OD @ HS
(Antilipidemics)
>Enoxaparine Sodium
(Lovenox)-o.6ml SC q12
(Antilipemics)
>Aspirin
(Aspilet EC)-80mg 1tab od
(Nonopioid analgesics and
antipyretics; antiplatelet)
>Clopidogrel (Platexan)
75mg/tab, 4tabs now, then OD
(Adenosine diphosphate (ADP)
receptor antagonist

Nonspecific injury to arterial wall

(endothelial injury) in the
coronary artery

Desquamation of endothelial lining and

stimulation of Mast cells to produce
inflammation
Increase permeability/adhesion molecules,
Lipids (LDL, VLDL) and activation of platelets
assimilation into the area
Oxidized LDL attracts monocytes and
macrophages to the site and plaques begin to
form from cells and smooth muscle cells
develop to form foam cells into thrombus

Diagnostic:
>X-Ray Report (Chest AP- Sitting)
Impressions:
Medication: thoracic aorta.
Atherosclerosis
Besylate (Norvasc)> >Amlodipine
Color Flow Doppler
50mg 1 tab OD (Calcium-channel
Rupture of atherosclerotic plaque
Conclusion:
Antianginals)
(cap) and Increase adhesion of
a) blockers;
Segmental
wall motion abnormality
>Nitroglycerin
(Glyceryl
these molecules and increase
indicative
of coronary
artery disease
Signs/ symptoms:
Signs/
b) Trinitrate)-10mg
Aortic and Patch
mitral scleroses.
thrombus/blood clot formation
Right& left subcostal
(Nitrates/Vasodilators;
Coronary Ischemia and Ischemia
symptoms:
c)
Aortic regurgitation, 1+
margin chest pain-5-6/10
Antianginals)
>Cold,
d)
Mitral regurgitation, trivial
of tissue in the
region supplied by
Diagnostic:
pain scale; pain occur
>Isosorbide
Mononitrate
(Imdur)
Clammy skin Medication:
Interventions:even during exertion or
Diagnostic:
>ECG tracing:
the and
artery
Occlusion
stenosis/narrowing
of the
30mg 1 tab OD
>prolonged/d
>Obtained
a
12
lead heaviness
ECG as
> Metoprolol Tartrate
Clinical
Chemistry:
ST-depression &
Signs/ symptoms:
at rest;
and
coronary artery and leads to coronary
(Nitrates/Vasodilators;
ecreased
Signs/
prescribed
(Toprol-XL)
50mg
1tab
Decreased
Calcium
T
wave
>decreased capillary refill of 5
tightness
of
chest
with
Antianginals)
vasoconstriction
refillBID
Diagnostic:
Signs/
symptoms:
Interventions:
symptoms:
>Administered
O2 inhalation
via nasal
(beta-adrenergic
8.3
inversion capillary
secsmg/dl
dyspnea;
pain radiates
1tab
of and
5 seconds
Interventions:
Signs/
Signs/
demand
for oxygen
glucose
in
the >Aspirin(Aspilet EC) 80mg cannula
Clinical
Chemistry:
Dysrhythmias(bradycardia;
>O2 therapy
viasymptoms:
nasal
>Jugular Increase
vein
at 2L/min
blockers,
(8.4
10.2
mg/dl)
>Clinical
>RR: 26
cpm;
tachypneic
up
to
the
neck
and
chin;
od (Nonopioid
analgesics)
>increased
>O2
therapy via Interventions:
symptoms: cannula at
>tachycardia;
Urea
PR:49-59bpm;
tachycardia;
2L/min
distention
>Advised
to perform
deep
breathing
Anti-dysrhythmics)
Decreased
Peripheral
of nitrogenAnaerobic
metabolism
tissues andAltered
leads
Chemistry:
torepolarization
diminished
myocardial
>dyspnea
guarding
behavior,
facial
>Diazepam
(Valium)-5mg
1
tab
BP
of
nasal
cannula at NPO
>bradycardia;
PR:130-150bpm
Increased
22mg/dl
(7PR
(JVD)(Sept.4atvasoconstriction
8cm
Increase
Stimulation
of sympathetic
Stimulation
Increase
ofcaused
cardiac
Lactic
sensory
Acid
nerve
productionof
exercises
andgrimace;
used
of
pursed-lip
>Spironoloctone(Aldac
Hypokalemia
Cardiac
theCellular
and
myocardium
that
can
by
increased
oxygenation,
hypoxia
and
altered
cell130-150bpm);
>use of accessory
muscles
to
tachycarsia
BID (Anxiolytics)
170/110mmH
5,2009)
except
2L/min
PR:
49-59bpm
>palpitations
17mg/dL)
palpitations;
dizziness
noted
Decreased
Increase
myocardial
release
of
breathing
technique
tone)
25mg
1tab
OD
3.0
mmoL/L
nervous system to stimulate preload
endings
to transmit
with
kinins,
to for
the
potassium
central
ions,
nervous
Output
decreased
blood
lead
flow
to decreased
demand
O2
& glucose
breathe oxygen
membrane
integrity
130-150bpm;
mild
> Metoprolol Tartrate
(Toprol-XL)
Unstable
Angina
Decreased
left ventricular
>Elevated
HOB P.O meds Increased after
Increased
Heart
relaxing body
environment
(Potassium Sparing
(3.55.1 g
contractility
norepinephrine
needs
adrenal medullaand
system>maintained
to cause
prostaglandins
pain
>nasal flaring
anxiety;
weakness
to the kidneyscardiac
output
in the
tissues/hypoxia
50mg 1tab BID (beta-adrenergic
Pectoris
Atherosclerosi
s

Medication:
>Losartan Potassium
(Cozaar)-100mg 1tab OD
(Angiotensin II antagonists)
>Captopril(Capoten)-25mg
tab BID (Angiotensin II
antagonists)

Renin (released from kidneys) to

split off angiotensinogen to form
angiotensin I
Angiotensin-converting enzyme (ACE)
removes and converts Angiotensin I into
Angiotensin II which promotes
vasoconstriction
Antidiuretic hormone
Sodium retention
by
released
from
Angiotensin
stimulates
kidneys and IIpromotes
an
hypothalamus
to increase
adrenal
cortex
increased
plasma
reabsorption
ofrelease
water by
aldosterone
osmotic to
pressure
kidneys
increased blood

Medication:
>Spironoloctone
(Aldactone)
25mg 1 tab OD (Distal
Tubule Diuretics/
Potassium Sparing
Diuretics)

Constipation
prior to
admission
(resolved Sept
1,2009)

Medication:
Semma cone (Senokot)-30ml
OD PO
Lactulose (Chephulac)-30ml
od PO
Diarrhea resolved
(Sept. 3, 2009)

Interventions:
Hold laxatives
2xday
as indicated

for

BM

Increased blood
pressure

Signs/ symptoms:
>BP170/110mmHg(hypertensive)
>temp-36.8C
>Dizziness(10 days prior to
admission until assessment
day
>faintness(10days prior to
admission)

Diagnostic:
>Echocardiography
Conclusion:
Concentric left
ventricular
hypertrophy with left
ventricular diastolic
dysfunction

Overloading of blood in
the ventricles of the
heart

Excessive stretch and

decreased contraction
occur

Increase
workload of the
heart

Thickening of the cardiac

muscle that leads to Left
Ventricular Hypertrophy

Hypertensive
Cardiovascular
Disease (HCVD)

COMPLICATIONS:
Myocardial Infarction
Dysrhythmias
Cardiogenic shock
Pulmonary embolism
Recurrent
Myocardial Infarction
Ventricular
aneurysms
Rupture of the heart
Pericarditis
Death