CRISIS
A. HYPERTENSIVE CRISIS
1. Severe dan Abrupt Elevation è BP
-
Diastolic
BP 120 – 130 mmHg
-
Acut
target organ damage
-
Occurs
in patient – history of HT
2. Hypertensive Crisis è Classified :
-
Hypertensive
Emwergency
Develops è Hours –
Days – BP meningkat severe
Acut terget organ damage :
·
Hypertensive
encephalophaty
·
Intra
cranial hemorrhage
·
Acut
left. Fentr. Failure dan pulmonary oedema
·
Myocardial
infartion
·
Renal
failure
-
Hypertensive
Urgency
·
Clinical
3. Clinical Manifestation
-
Hypertensive
Encephalopati
·
Cerebral
oedema
·
Spam
of cerebral vessel
Sudden rise in arterial pressure
Headache, nausea, vomictingseizures, confusion,
stupor, coma, blurred vission dan transient bliness
-
Renal
in sufficiency
-
Cardiac
decompensation – pulmonary edema
Angina – infarction
dyspnea
-
Neurologic
dysfution
4. Hypertensive Crisis – often seen ( With CVA
5. Nursing dan Colaboratif Manajemen
-
Asses
è indicator HP Crisis
·
BP
meningkat dan Sign of progressive target organ damage or organ damage
-
HP
Emergency è Hospitalisasi
·
Intensive
care monitoring
·
IV è hypertensive drugs
-
Sodium
nitroprusside
-
Nitroglycerine
·
Evaluate
therapy è MAP
( mean arterial pressure )
MAP = DBP + Pulse pressure
Pulse pressure = Sistolic BP – Diastolic BP
Goal : Initial treatment
·
Decrease
– MAP è 10 – 20 %
LN 1 – 2
Hours menurun
·
Gradual
reduction – dext 24 hours
·
Monitor
vital sign è BP
2 – 3 minute è during treatment ( intra arterial line )
·
Excessive
reduction – BP è Stroke
è M I
è Visual changes
·
Hourly
urinary out put è Renal
dan Perfusion
·
Patient
receinving – anti hypertensive – IV
è Restricted to bed – getting up è cerebral ischemia
-
Frequent
neurologic cheks
·
Level
of conciousness
·
Pupillary
size dan reaction
·
Movement
of extremitas dan reaction
·
Detect
anychanges patient conditions
6. Myocardial Infartion
-
Ishemia
·
Ischemia
è Angina
è Cellullar anjury - reversible
-
Myocardial
Infaction
·
Cellullar
injury – Irreversible
·
Cellullar
Necrosis
-
Mortality
rate
·
30 –
50 %
·
In
the first 3 – 4 days
B. PATHOPHYSIOLOGY
-
Oxygen
in sufficiency
O2 supply menurun
O2 demand meningkat
-
Ischemia
è 20 – 30 mnt
-
Necrosis
( Infartion )
C. CLINICAL MANIFESTATION
1. Pain
-
Severe
not relieve with rest
-
Heaviness,
tightness
-
Subternal
è Radiating è meck, JAW & ARM, Back
-
retrosternal
2. Nausea dan Vomitng
3. Symphatetic nervour system – stimulation
-
Diaphoresis
-
Vasocontrictions
bloob vessel
-
Cold
sweat
4. Fever
-
The
forst 24 hours – 38 – 39 C
5. Cardiovascular Manifestation
-
BP
meningkat & HR meningkat mitially
-
BP
meningkat later è CO menurun
-
Crackles
è lung
-
JVP
meningkat
D. DIAGNOSTIK
1. Clinical presentation
2. ECG
3. Serum cardiac markers
E. COMPLICATIONS
1. Arrhytmias è 80 % MI
2. Life threatening : total AV Block
3. VT, VF è mostly – the first 4 hours
4. Cardiogenic shock
5. Papillary muscle dysfunction
6. Ventricular aneurysma
7. Pericarditis è 2 – 3 days after acut MI
8. Pulmonary embolic
F. COLABORATIVE
1. Patien MI è Cardiac care unit è monitor ECG
2. IV lines è Dsw è EMG
drugs
3. Mo è IV è Relief
of pain
4. Oxygen 2 – 4 l / mnt
5. Lidocaine – IV ( Prophylactic ) è 75 – 100 mg bolus – IV drip
( 500 ml Dsw + 2 % lidocaine )
6. Vital sign è 1 – 2 hr – firs 8 hr
7. Activity è Absolute bed rest, bed rest + ( Bed side commode)
passive ROM
8. Intake & out put – hourly
9. Thrombolytic care