PROVIDING PREHOSPITAL

PROMPT MEDICAL CARE

DURING THE MAIN MEDICAL-
SURGICAL EMERGENCIES
The Importance of Medical Emergencies in
Family Medicine
The family doctor as a first contact doctor has
a very well-defined role in determining the
diagnosis in medical-surgical emergencies, in
rapid assistance / first aid assistance in order
to save the patients life and in advising him
subsequently to go to hospital
 The Main Medical-Surgical Emergencies
Cardiovascular : chest pain (angina), heart
attack (myocardial infarction), arrhythmia,
hypertensive crisis, syncope ( fainting), near-
syncope (lipothimie), cardiac arrest.
Respiratory : bronchitic asthma attack, acute
pulmonary edema, pulmonary tromboembolism,
pneumothorax, haemoptysis, acute respiratory
failure.
Digestive: acute appendicitis, biliary colic, acute
pancreatitis, melaena, mesenteric infarction ,
acute peritonitis.
Renal : renal colic, acute pyelonephritis, acute
glomerulonephritis, acute urine retention, acute
renal failure.
 Neurological: sciatica crisis, vertiginous
syndrome (vertigo), convulsions,
meningitis, coma;
Gynaecological: ectopic pregnancy,
abortion, eclamsia, genital bleeding
Metabolical: dyspnea, hypoglycemia,
tireotoxica crisis
Dermatological: Erysipelas, Quinckes
edema, rashes specific to infectious and
contagious diseases
 Ophthalmology: red eye, glaucoma crisis
ENT: epistaxis, acute otitis, glottic edema
Intoxications : carbon monoxide poisoning,
organophosphorus poisoning, alcohol
intoxication, benzodiazepines, opiates
intoxication
Others: bleeding disorders, sepsis, burns,
frostbite, trauma
 The FD will have to determine an initial
diagnosis as sooner as possible
Therefore , in the case of a patient who
exhibits pale teguments (skin), cold
extremities, a thready pulse, profuse cold
sweating, polipnee, arterial hypotension ,
FD will indicate the diagnosis of shock.
By excluding other types of shock due to
burns, traumas, sepsis FD will take into
account the hypovolemic shock.
 Untill he establishes an etiological
diagnosis and the hospitalization of the
patient in a specialized department the FD
will have to alleviate rapidly the
hypovolemia, acidosis, hypoxia and
maintain the pressure of perfusion in the
tissues by applying a saline infusion,
sodium bicarbonate, glucose, oxygen and
vasoconstrictors (dopamine, dobutamine,
norepinephrine).
 The anaphylactic shock can occur in case
of insect bites or intravenous
administration of some particular
substances (penicilin) therefore the urgent
administration of adrenaline and
hydrocortisone hemisuccinat is necessary.
In acute intoxications the FD will have to
give immediately the adequate antidote to
the patient as , for example , atropine in
pesticide poisoning (organophosphorus
compounds) and perform gastric lavage.
 The family doctor is obliged to treat the
patient untill the moment of his
hospitalization in a specialized department
or untill the arrival of the ambulance which
takes over the patient .
To provide first aid in medical emergencies
MF must own a surgical emergency kit.
The emergency kit should contain:
- Drugs = nitroglycerin, Scobutil NO - SPA,
glucose, diazepam, phenobarbital, Miofilin
furosemide, hydrocortisone hemisuccinat
Algocalmin, adrenaline
 THE CARDIAC ARREST : It represents a clinical state
after the cessation of normal circulation of the blood due
to failure of the heart to contract effectively.

The diagnosis of cardiac arrest is established after the

following symptoms:
sudden pallor or cyanosis
absence of pulse in the large arteries (carotid or femoral)
absence of heart sounds
loss of consciousness (6-12 seconds after cessation of
oxygen supply to the brain)
the sudden cessation of respiratory movements ( in the
case of primary circulatory arrest, after 15-40 seconds)
the appearance of fixed mydriasis, dilated pupils , non-
reactive to light ( after 30 up to 90 seconds )
 THE RESUSCITATION PROCEDURE IN
CARDIOPULMONARY ARREST is done
in the first 3-5 minutes after the arrest,
when the patient is in clinical death,
afterwards if hes not resuscitated he
enters biological death the cessation of
brain functions when fixed midriasis ,
opaque cornea and cadaveric lividities
( livor mortis) occur.
 ABCD RULE

A Airways
The unobstruction of the respiratory ways;
The removal of foreign bodies from the
oropharyngian region , the head must be
kept in hyperextension and the mandible
will be held backwards with the chin pointig
upwards.
Esmarch maneuver
 Toracic blows will be carried out against
the back of the patient or abdominal
compression will be performed
( HEIMLICH manoeuvre) in the case of
foreign bodies aspiration. If the victim is
unable to breathe, the doctor will position
himself behind her back and will place his
fist with the thumb oriented towards the
victims abdomen above the navel and
under the ribs and sternum aria.
 He will grab his fist with the other hand
and he will pull both hands 4 times upward
and inward very fast and with an amount
of force.
This manoevre will increase the
pressure in the abdomen, causing the
pushing of the diaphragm upward.
Consequently, the diaphragm will
increase the air pressure in the lungs, and
the positive pressure will push the object
from the trachea through the superior air
ways.
 The ribs should not be squeezed
between the arms.

Only the fist pushed in the abdomen will

be used.

It isnecessary to repeat the manoevre 5

up to 10 times if possible.
 B Breath Ventilation

Mouth to mouth, mouth to nose , mouth to tube

( the SAFAR tube, the Guedel tube), mask
ventilation ( the AMBU type balloon).

If ventilation or intubation are not possible ( as in

the case of a glottic edema) the indispensable
tracheostomy will be used and urgent trachael
punction by placing a trachea stome between
thyroid and cricoid cartilage
 The efficiency of the ventilation will be
verified : the presence of breathing
movements; the cessation of cyanosis;
symmetrical vesicular murmur.
Rapid ventilation is attemped 2 times,
followed by a cardiac massage and
alternative ventilation in a 30/2 ratio.
The rate of thoracic compressions is 100
per minute.
The frequency of mouth to mouth ventilation
is 10-12 times per minute to an adult and
10-12 per minute to a child.
TECHNIQUES AND MEANS OF RESPIRATORY
ASSISTANCE

RECOGNITION OF ABSENCE BREATH. subluxation the mandible

ARTIFICIAL BREATHING : MOUTH TO MASK
MOUTH TO MOUTH
Heimlich MANEUVER IN THE CASE OF THE UPPER AIRWAY OBSTRUCTION AT
PATIENT IN SITTING POSITION STANDING POSITION
MANUAL EXTRACTION OF A THE RIGHT POSITION OF
FOREIGN BODY HANDS AND BODY IN TIME external
FROM THE upper airway cardiac massage
VENTILATION LARYNGEAL MASK ASSISTING KIT FOR RESPIRATORY
LARYNGO - TRACHEAL
AMBU TYPE BALLOON
VENTILATION

The mask will be applied with the thumb

and the index finger positioned above the
mouth and nose, the mandible will be kept
backwards and with the fingers left the
head will be placed in extension position.
C Circulation
The circulation of the blood in the case of each
cardiac arrest will be initiated immediately while
the precordial punch is being applied both ned
with cardiac massage.

External cardiac massage ( the patient in dorsal

decubitus, placed on a hard stand, is massaged
in the third inferior lower part of the sternum)
 The frequency of the massage : 100 strokes per
minute
the compression-decompression rate being >
50% compared to the compression plate, about 4-
5 cm.
Early defibrillation
If in the 15 minutes the massage lacks efficiency,
it can be continued for about 45-60 minutes in the
presence of the patients family or friends or untill
the arrival of the qualified ambulance.
in the case of ventricular fibrilation or T.P.S.V the
massage will be continued untill there will be
means for electrical defibrillation.
 DEFIBRILLATION AND EXTERNAL
CARDIOVERSION

indications : in cardiac arrest, ventricular

fibrilation, atrial fibrilation, T.P.S.V

device: electrical defibrilator provided with

2 metallic electrodes , its set up at the
lower part of the sternum and on the apical
(V5);
 before applying electric discharge, the
electrodes and the patients skin are
lubricated with an electroconductive paste,
the power of defibrillation is set at 200-360 J
for the thick wall, FV and 100-200 j for the
thin wall, FA, TPSV.

The discharge button is pressed and the

patients body is violently jolted while on the
monitor the E.K.G is changing
D- Drugs

The medical treatment

It is very important to achieve a peripheral
venous acces way.
Thus, intravenously or through endotrachael
tube in double or triple dose it can be
administered adrenaline 1 mg i.v. or 2-3 mg in 10
ml. s.f intratrachaelly, atropine 0.5-2 mg in case
of sinus bradycardia or asystole, lidocaine 1-
3mg/kg in order to prevent ventricular fibrilation
relapses, or sodium bicarbonate 8,4 % 50-100ml.
 PURSUED OBJECTIVES IN PROVIDING PREHOSPITAL
MEDICAL CARE
In tackling the issue of a medical-surgical emergency the
FD will have to take in consideration the following
objectives :
the evaluation of emergency at first sight : is it or is it not
an emergency?
The nature of the emergency
The cause
The gravity
The number of victims ( in case of casualities)
The measures that have to be undertaken
The succession of these measures
The estimated time since the occurence of emergency
untill the first taken measures.
Limiting the effect provoked by the primary agent
 The removal of the injured from the place of the
accident
Achieving a summary of the total injuries and a
sorting of them after their gravity
Establishing the intervention priorities in the order
of their vital urgency
The application of first aid measures
Positioning the victim in the right place, the
treatment of the serious injuries,
immobilization,hemostasis, sedation, s.a.
The appreciation of results after the undertaking
of measures
The FDs assuming of responsabilities to monitor
the patient or to send him to the hospital
The evaluation of the risk factors during the
transportation.
Acute myocardial infarction
Definition
Myocardial infarction (MI) is an ischemic necrosis
of a cardiac muscle, secondary to an obstruction
on a coronary artery which has as a consequence
a prolonged cellular hypoxia.

The myocardial necrosis determines :

a clinical syndrome
E.K.G modifications produced by the reduction or
even the cessation of coronary flow
the increase in the blood level of sensitive and
specific biomarkers ( cardiac troponin I or T ,
creatine kinase MB fraction, total creatine kinase,
myglobin, SGOT).
 The preffered marker for the myocardial
trouble is cardiac troponin (I or T) which
has almost complete cardiac specificity
and also, an increased sensitiveness.

The best alternative is CK-MB, which is

less specific then cardiac troponin, but it
exhibits a greater clinical specificity
concerning the irreversible injury.

morphopathological myocardial
modifications.
The Initial Diagnosis
A working diagnosis of myocardial infarction has
to be made in the first place.
This is usually based on the history of severe
chest pain that lasts 20 minutes or more and
which doesnt respond to nitroglycerine.
The most suggestive details are linked with an
earlier history of coronary illness, the way the
pain is radiated near the neck aria, in the
mandible or along the left arm.
The pain may not be severe and other
manifestations such as fatigue, dyspnea and
syncope are frequently encountered to older
patients mostly.
During the physical examination the following
aspects occur :
the pacient is anxious and troubled
pallor, cold and humid teguments;
sweating
bradycardial or tachicardic regular or erratic pulse
( arrhythmia)
subcrepitant rales in left ventricular insufficiency
(LVI)
wheezing in LVI
coughing combined with hemoptysis in pulmonary
embolism or acute pulmonary edema
Arterial hypotension appears in 3 circumstances

the extended anterolateral infarctions caused

by pumping dysfunction;

inferior infarctions of a vagal reflexive nature;

inferior infarctions with massive affectation of

the right ventricle,which leads to a deficit of
blood filling of the left ventricle.
ELECTROCARDIOGRAM
An electrocardiogram has to be obtained as soon
as possible.
Even in an early stage of infarction , the ECG
rarely looks normal.
In the case of ST segment denivelation or a
recently formed or presumed recently formed left
branch block, the therapy for reperfusion injury
has to be administered and measures for the
initiation of the treatment have to be undertaken
as soon as possible.
 Nevertheless, the ECG that is carried out in the
first hours it might not show the classical signs
of ST segment denivelation or of recently
emerged Q wave, even in confirmed infarction.
The ECG repeated recordings have to be
achieved and, when possible, the actual ECG
has to be compared with the previous lines.
Sometimes the recording of additional
derivations can be useful ( in subsequent
posterior infarctions V7, V8).
The monitoring with ECG has to be initiated as
soon as possible to all the patients in order to
detect the malignant arrhythmias.
The initial diagnosis of acute myocardial infarction :

history of pain/ chest (thoracic) discomfort

ST segment denivelation or left bunddle branch
block ( presumed to be recently formed) on the
ECG.
Repeated ECG recordings are often necessary.
increased myocardial necrosis markers ( CK-
MB, troponin).
The results for the initiation of reperfusion
treatment must not be waited for ( expected) !!

The two dimensional ecocardiography is useful

in the diagnosing the acute myocardial infarction
The amelioration of pain, dyspnea and anxiety
Relieving the pain is of maximum importance, not
only out of ethical reasons, but also because pain
is associated with the sympathetic activation
which produces vasoconstriction and increases
the burden of the heart rate.
Intravenous opioids , morphine, when it is
available, diamorphine, are the most frequently
used analgesics in this context, for exemple 4-8
mg of morphine with additional doses of 2 mg at
5 minutes intervals untill the pain subsides.
Repeated doses can be necessary.
 The side- effects include : nausea, and
possibly vomiting, hypotension combined
with bradycardia, respiratory depression.
The antiemetics can be administered
simultaneously with the opioids.
Hypotension and bradycardia usually react
to the administration of atropine while
respiratory depression to nalaxonum.
If the opioids do not succeed to calm down
the pain after repeated administrations,
intravenous beta-blockers or intravenous
nitrates are efficient in some cases
 Oxygen (2-4 l / minute on mask) has to be
administered to those who suffer of
dyspnea mostly or to those who exhibit
signs of cardiac insufficiency or shock.
Anxiety represents a natural reaction to
pain and to those circumstances that
accompany a coronary accident. Alleviating
the patients stress and their attendants is
extremely important. If the patient becomes
excessively agitated he can be given an
anxiolytic but opioids are usually enough.
 The alleviation of pain, dyspnea and
anxiety
Intravenous opioids ( for example 4-8 mg of
morphine) with additional doses of 2 mg at
intervals of 5 minutes
Oxygen (2-4 l/ min ) if the patient shows
signs of dyspnea or cardiac insufficiency
Beta-blockers or nitrates intravenously if
the pain does not subside after the
administration of opioids
Anxiolytics can be useful in this case.
Emergency conduct

The majority of deaths caused by AMI take place

in the first hours after the occurrence of the
infarction.
In the prehospital phase 2 objectives influence
the therapeutic attitude in the first hours of the
evolution of myocardial infarction.
1. the prevention of malignant arrhythmia
2. the early coronary reperfusion in the first 4-6
hours after infarction
 the prevention of malignant arrhythmia
( ventricular fibrilation, ventricular
tachycardia ) through lidocaine
administration , magnesium sulphate or
metoprolol in perfusion.
early coronary reperfusion in the first 4-6
hours through trombolytic agents
administration such as streptokinase,
urokinase, tissue plasminogen activator and
anticoagulants such as heparin in bolus
dose of 5000 UI followed by prolonged
perfusion in a dose of 1000 UI per hour.
 Although it has been proven that lidocaine
is able to reduce the incidence of
ventricular fibrilation during the acute stage
of myocardial infarction, this type of
medication increases significantly the risk
of asistolia.

Adjunctive antiplatelet therapy

Aspirin is better for the prevention of
recurrent clinical events, then in the
maintenance of vessel patency.
 The first dose of 150-325 mg has to be
chewed ( entersoluble capsules wont be
administered), the ulterior daily dose being
of 75-160 mg.

If their ingestion is not possible, the

treatment will be administered
intravenously (250 mg)
Antiarrhythmics Drugs

Beta-blockers: They are used due to their

potential of limiting the gravity of the infarction, of
reducing the rate of fatal arrhythmias and in order
to alleviate the pain.
The atrial fibrilation complicates about 15-20% of
myocardial infarctions and i tis frequently
associated with severe damages of the left
ventricle and with cardiac insufficiency.

Other supraventricular tachycardias are rare

and , usually, self-limited.
They can react to the compression of carotid
sinus
 If the rapid ventricular rate is one of the
reasons of cardiac insufficiency , prompt
medical treatment will be neccessary.
Beta-blockers and digoxine are efficient in
reducing the ventricular rate in many
cases, but amiodarone can be also
efficient in reducing arrhythmia.
The external electric shock should be used
if arrhythmia is poorly haemodinamically
tolerated.
Nitrates
the patient will receive a sublingual
nitroglycerin tablet immediately after the
onset of chest pain susceptible of
myocardial infarction,
if the pain did not give in five minutes,
repeat a second administration, and if the
chest pain persists after another 5 minutes
you can give the third tablet.
Patients treated with early intravenous
nitrate had a significant reduction (a third)
mortality.
Angiotensin converting enzyme inhibitors (ACEI)
It is now well established that you may give ACE
inhibitors to patients who have a decreased
ejection fraction or heart failure phenomena in an
acute phase.
A systematic review of trials with ACE inhibitors
administered early in the acute myocardial
infarction showed that this therapy is safe, well
tolerated and associated with a significant
reduction in mortality at 30 days with a maximum
of benefit observed in the first week.
It is now a general consensus to initiate
treatment with ACE inhibitors within the first 24
hours, in the absence of contraindications.
ACEI dose trials
GISS lysynopryl 5 mg initially to the 10mg/day
ISIS 6.25 mg captopryl initially 12.5mg after 2h,
10-25mg to 50mg x 12h 2/day
SMILE zofenopryl 7.5mg initially, repeated after
12h and administration ofrepeated double doses,
if tolerated up to 30mg x2/day
AIRE ramipryl 2.5mg x 2/zi, is increasing by 5mg
x 2/day
TRACE trandolapryl 0.5mg testing of up to
4mg/day
Glucose-insulin-potassium. The routine
administration of glucose insulin potassium
metabolism may favorably influence the ischemic
myocardium, thus leading to clinical benefit.
Criteria for evaluating the patient with myocardial
infarction risk
Chances of survival of patients with AMI depends on:
of the atmosphere and how is the patient's reaction
and his company reaction.
first measures applied to the patient's home and
during transport to hospital
quick and easy access of population to mobile
emergency care service (MECS)
specific technical equipment and training of the
MECS teams
CARDIOGENIC
PULMONARY EDEMA
DEFINITION:
Acute cardiogenic pulmonary edema (EPAC) is a
form of paroxysmal severe dyspnea due to
excessive accumulation of interstitial fluid and its
penetration into the alveoli.
EPA necardiogen occurs in organo-phosphorus
poisoning, in viral respiratory infection,
drowning,, neurological diseases stroke .
Most common precipitating factors encounter
in practice are:

Arrhythmias
Acute coronary syndrome (IMA)
Poorly controlled arterial hypertension
Discontinuation of dietary salt restriction in
ICC
Strenuous exercise
Clinic:
revealing anamnesis for a suffering cardiac
history
orthopnea and dyspnea with tachypnea
productive cough with foamy sputum, rosy-
like, abundant
cyanosis
profuse sweating
extreme anxiety
 EKG
- Paroxysmal arrhythmias
- Changes in ventricular hypertrophy
Acute coronary syndromes
cardio-pulmonary X-ray:
possible cardiomegaly
dilated vessels in the hilum with blurred
boundaries
fog lung fields especially in two thirds lower
infiltrative changes with imprecise edges
located perihilar (in butterfly wings)
any signs of pleural effusion in the pleural cavity
or fissure
dilated vessels in the HILUM with blurred boundaries
fog lung fields especially in two thirds lower
Cardiogenic pulmonary edema
 PULMONARY EDEMA TREATMENT
a. half-seated position:
- Is comfortable
- Allows easy breathing
- Facilitate expectoration
- Decreases venous return
- Usually in the EPAC is the only position that a
conscious patient may adopt.
b. the sputum is aspirated and the oropharyngeal
cavity of the patient is cleaned.
c. the preload is reduced by applying the tourniquet
to the limb level (3 of 4) and will be exchanged
within 10-15 minutes
d. Oxygen: it is continuously administered 6-
8 l / min.
e. Venous way stable, safe
f. Nitroglycerin:
- initially may be given 0.5 mg sublingual
every 5 minutes till the hemodynamics is
improved or the arterial hypotension
occurs (SBP <100 mm Hg)
Note that often the application only of
these therapeutic sequences is sufficient.
g. Diuretics:
most of them employed are the loop ones.
furosemide: 40-120 mg i.v.
is relying primarily on its effect venodilatator
which installs more quickly than the diuretic one,
the diuretic effect installs in 20-30 min.
h. The administration of digitalis is useful for EPAC
in atrial fibrillation with rapid ventricular heart
rate for the control of the ventricular allure at a
dose of 0.5 - 2 mg fractioned.
 i. In EPAC accompanied by
bronchospasm, Aminophylline 5 mg /
kgcorp (240-480 mg) i.v. in 10 minutes is
administered.

It is used with caution in cases of

coronary artery disease and myocardial
infarction because it increases the risk of
ventricular fibrilation.
HYPERTENSIVE EMERGENCIES

It represents the sudden rise and of variable

duration of the blood pressure which can cause
damage of the target organ.
hypertensive emergencies may occur in different
clinical contexts and were therefore divided into:
Hypertensive emergencies and Hypertensive
urgencies
The hypertensive emergencies are represented by
production increases in BP to the limit of
neurological damage, cardiovascular damage,
kidney and retina rapidly progressive damage,
with risk of death, so it is necessary to lower BP
within no more than an hour.
 Although blood pressure values are very
high, correlation between TA and target
organ damage is not directly proportional.
The hypertensive crisis, however, requires
the presence of organ damage rather than
the absolute level of BP.
So it is important to make a clinical
distinction between "hypertensive
emergencies (hypertension crisis) and
"hypertensive urgencies"
 The lesions are described as:
- Cerebrovascular = hypertensive
encephalopathy, intracranial hemorrhages
of that hypertensive subarahnoid or
intracerebral
- Cardiovascular = acute pulmonary
edema, aortic dissection, MI, unstable
angina pectoris
- Renal = hypertensive nephropathy ,
progressive renal failure
In this category of hypertensive emergencies
we describe:
Hypertensive encephalopathy - we have a
number of neurological signs and
symptoms: headache, mental status
changes - which occur early and consist of
drowsiness, dizziness, confusion,
disorientation, and progressing to coma,
signs of a stroke, blurred vision,
convulsions .
 hypertensive nephropathy with hematuria,
proteinuria, progressive renal failure.
pheochromocytoma crisis
malignant hypertension: encephalopathy or
nephropathy in the associated papilloedema
cerebral hemorrhage
acute aortic dissection
preeclampsia - eclampsia
EPA (acute pulmonary edema)
unstable angina
Acute myocardial infarction
 Hypertensive urgencies
There are situations in which there is a
sudden rise, severe BP (SBP> 220 or
DBP> 125 mmHg), without acute target
organ damage but their possibility in the
absence of medical intervention such as
cerebral edema.
In this case, blood pressure reduction
should be done gradually over several
hours because a sudden drop events
could cause hypotension.
TREATMENT
As a priority, the level of blood pressure
may be the same in both cases but
hypertensive emergencies requires a quick
reduction of blood pressure by
parenteral administration (iv) of
antihypertensive drugs, the patient being
monitored, while in an hypertensive
urgencies, BP control can be done in
hours or days, often using oral medication
(taken orally).
 treatment of hypertensive emergencies if
associates and hypertensive
encephalopathy is to decrease BP values
by 25% in minutes to a maximum of 1-2
hours, then the values of 160/100 mmHg
in the next 2-6 hours by application of
parenteral therapy. It is not indicated an
aggressive decrease of BP because
neurologic complications may occur by
the brain hypoperfusion .
 treatment of hypertensive emergencies is done
within intensive care units where
antihypertensive medication is administered
through an by automatic syringe and the patient
is monitored clinically, hemodynamic and ECG
because of the adverse effects of treatment that
may appear .
It uses a series of drugs like sodium
nitroprusside, diazoxide, nitroglycerin, labetalol,
Hydralazine, calcium channel blockers
(nicardipine) depending on clinical situation and
the main disease of the patient
 Hypertensive encephalopathy is caused by
the cerebral edema because lost
autoregulation function in clinical situations
with severe arterial hypertension.
HTA must be carefully reduced (SBP by
about 25% within 1-2 hours), otherwise an
aggressive decrease may lead to
neurological complications like cerebral
ischemia.

Nicardipine and labetolol are preferred .

Oral treatment

Nifedipine (adalat), calcium channel blocker, is

given initially at a dose of 10 mg repeated at 30
min.
Clonidine has sympatholytic action and it is given
an initial dose of 0.2 mg, then may increase by
0.1 mg / hour to 0.8 mg total dose. Side effects
are represented by drowsiness and rebound
hypertension after stopping treatment.
ACE inhibitors such as captopril at a dose
between 12.5 - 25 mg until 50 mg total dose is
given sublingually for decreasing blood
hypertension .
CONCLUSIONS:
Hypertensive crises represent a distinct
group of clinical and pathological entity
which requiring control of increasing BP ,
for to limit damage to the target organs.
This thing is best accomplished within
intensive care units where under close
supervision, hypotensive agents may be
administered by automatic syringe in a
strict dose .