Chest pain

FROM THE DISEASES WHICH CAN PRODUCE

CHEST PAIN, THE NEXT ONES HAVE
IMMEDIATELY LIFE THREATENING RISK:

ACUTE MYOCARDIAL INFARCTION

UNSTABLE ANGINA
AORTIC DISSECTION
PULMONARY EMBOLISM
CARDIAC TAMPONADE
PERICARDITIS
TENSION PNEUMOTHORAX
ACUTE MYOCARDIAL INFARCTION
Definition
◦ AMI is an ischemic necrosis of the myocardium more than 2 cm2 . Myocardial infarction
results when arterial blood flow to the myocardium is suddenly interrupted or decreased.
◦ Once the occlusion of the coronary artery appeared, necrosis occurs in a time-dependent
course, proceeding from endocardium to epicardium. Necrosis is almost complete within 4
hours if no reperfusions occurs. Where residual perfusion by collateral vassels is present or
lysis of thrombus occurs, there the myocardium will be saved.
◦ The earlier reperfusions -the more myocardium is saved.
ACUTE MYOCARDIAL INFARCTION
Possitive diagnosis
Possitive diagnosis of acute myocardial infarction is a paraclinical diagnosis (ECG, enzymes), but the clinical findings can
give the suspicion of diagnosis. The possitive diagnosis is based on some criterias:
1) Clinical manifestations:
A)coronarian pain:
-typical - chest pain localised retrosternal or precordial, radiated to the left arm or to the neck, with squeezing or
oppresive character, which worsens gradually.The pain lasts more than 30 minutes; this pain doesn’t disappear after NTG,
it can dissapear to opioids. It can associate anxiety, pallor,cold sweatening, tachycardia, tachypneea. Sometimes can
appear signs of cardiac failure, cardiogenic shock, arterial hypertension, digestive symptoms: nausea, vomiting.
-atypical : the pain is localised in epigastrium, irradiates to the back or to the precordial region, associated with nausea
or vomiting-like in abdominal disease, hypotension and bradicardia (due to a vagal mechanism). This is the inferior
myocardial infarction.
-silent myocardial infarction (painless)- to the diabetics, elderly pacients, drunkers. Appear atypical clinical manifestations,
chest pain is missing or has a little intensity.
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B)other clinical manifestations:
-syncope
-restlessness suddenly appeared
extreme anxiety
-pulmonary edema, pulmonary embolism
-tachy or bradiarrhytmias
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INFARCTION
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2) Electrocardioraphic findings
In myocardial infarction appear signs of necrosis, lesion, ischemia:
necrosis- electrically expressed by pathological Q wave :
width > 0,04 sec
amplitude>25% of R wave
persistent during deep inspiration.
Q wave doesnt appear from the first hours of evolution (sometimes in 2-3 rd day) or can be absent ( in case of
nonQ myocardial infarction).
Q wave without acute modifications of ST segment ( ST elevation with included T wave) is signs of old
myocardial infarction.
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INFARCTION
An amputated R wave (small amplitude) in some precordial leads (eg. V1-V4), with sudden increasing in
amplitude in V5, is equivalent with Q wave of necrosis.
 lesion- is expressed by ST segment modifications:
elevation of ST segment is the most often aspect – signifies subepicardial lesion
- depresion of ST segment- in subendocadial lesions
 ischemia- is expressed by modifications of T wave:
big T wave , simetrical, sharp ended- subendocardial ischemia
big negative T wave, simetrical- subepicardial ischemia.
Modifications of ST-T precede the appearance of Q wave
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Important for diagnosis of myocardial infarction is evolutivity of ECG aspects:
* the first ECG modifications (supracute modifications):
- high and simetrical T wave, sharp ended;
* the acute ECG modifications:
-ST elevation with the inferior concavity more than 1 mm in standard leads and more than 2 mm
in precordial leads; This elevation includes T wave and forms big monofazic wave, Pardee wave. This
aspect goes to ST depresion with big negative T wave. After few days, ST becomes isoelectric, and T wave
can become possitive in few weeks.
pathologic Q wave appear further, and can persist like marker of old myocardial infarction.
ACUTE MYOCARDIAL
INFARCTION
Non Q or subendocardial myocardial infarction is expressed on ECG by:
-elevation of ST segment in AVR associated with important ST depression with/or negative, high,
simetrical Twave in precordial leads and/or in standard leads.
-these modifications have recently appeared and are mentained more than 6 hours.
ACUTE MYOCARDIAL INFARCTION
Localisation of myocardial infarction:
The location of myocardial infarction will be established function of the ECG leads where the modifications
appears.
-inferior IMA: DII, DIII, aVF;
-anterior IMA: V1-V4;
-lateral IMA: D1,aVL,V5,V6;
-septal IMA:V3-V4;
-posterior IMA: high R wave in V1 with directly ECG signs in V7-V9;
-right ventricular infarction-V3R,V4R (simetrical with V3,V4 but on the right hemithorax.).
ACUTE MYOCARDIAL
INFARCTION
ACUTE MYOCARDIAL
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Nonspecific biological modifications:
-leucocitosis 12-20000l/mm3, appear in 2-3rd day, and it last arround 1 week; during this period exist
also small fever;
-increased ESR, fibrinogen, which come back to normal in 2-3 weeks.
-myocardial scintigraphy – this method is very useful for precocious diagnosis
-with tehnetium shows warm areas of infarction;
-with thalium shows hypocaptant zones for acute or old myocardial infarction.
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INFARCTION
3)Enzymatic:
A)Creatin-kinase CK. Normal value = 10-80 u/l.
Elevation begins after 6 hours and the maximum level is at 18-24 h. CK will be normal in 3-4 days. Specific for myocard
is isoenzyme CK-MB (N <10u/l).
b) Aspartat amino transferase / TGO/ ASAT. Normal value< 20 U/l
It startes increasing in 8-12 h after onset of infarction. Maximum is at 24-36 h and come back to normal in 3-4 days.The
fraction GOT/GPT is > 1 in IMA.
b) LDH Normal value =120-240u/l.
It starts increasing in 1-2 day after onset , maximum is at 3-6 days and normalises in 1-2 weeks. More specify has
isoenzyme LDH 1;
The presence of 2 criterias from the 3 (clinical, ECG, enzymatic) is sufficient for confirming the possitive diagnosis.
 ACUTE MYOCARDIAL
INFARCTION
Differential diagnosis
Is made with the others disseases which give chest pain, with life threatening risk;
1.Unstable angina - the chest pain-retrosternal, radiating to left arm, lasts up to 20-30 min, relieved by NTG. ECG can
be normal or with ischemical modifications. Very important is the absence of big values of the necrosis enzymes;
2.Dissection of thoracic aorta - the retrosternal pain has tearing character, maximal at onset, radiates to the back or
in inferior limbs. Exist inequality between the radial and the femural pulse, and appear murmurm of aortic
insufficiency. ECG and enzymatic modifications are absent
3.Pulmonary embolism - in this case exist an emboligenic status; the chest pain is associated with dyspnea, cough,
hemoptoic sputum. The chest pain is usually lateral thoracic localised, the duration is variable (minutes to hours).
On ECG appear typical modifications: Q wave with negative T in DIII, S I- Q III- sign of right ventricalur overloading.
But Q wave is absent in D III, so is differentiated from inferior myocardial infarction. Pulmonary scintigraphy (+/-
pulmonary arteriography) confirm the diagnosis.
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4.Cardiac tamponade - chest pain with signs of central plethora (distension of neck veins or signs of pulmonary
edema), hypotension or shock, faint of heart sounds, thin pulse pressure and paradoxal pulse. On ECG exist
diffused low voltage;
5.Pericarditis - prolonged retrosternal pain (hours-days) with pericardial friction, fever. On ECG exist difused ST
elevation with upper concavity in all leads, Q wave is absent, the necrosis enzymes values are normal.
Ecocardiography establishes the diagnosis.
6.Tension pneumothorax- exist a history of chest trauma frequently; chest pain is associated with dyspneea,
hiperressonance at the affected side, the absence of the vesicular murmur.
After excluding of these life threatening risk afections, we must think to the other diseases like:
pleumopulmonary diseases, gastric diseases, musculoskeletal disordes.
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Treatment
Further clinical evolution of patient with myocardial infarction depends on the treatment of
first 4-6 hours from onset. Exist 2 situations:
1) Acute myocardial infarction without complications;
2) Complicated acute myocardial infarction
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1)AMI without complications
I General measures:
-admision in hospital
-bed imobilisation
-oxygen 4-5 l/min
-cardiac monitor
-ECG in 12 leads or more
- establishe iv line, collecte blood for laboratory tests
-anxiolitic drugs: Diazepam 5-10mg. i.v.or i.m.. Avoid this drug in case of respiratory failure.
-Aspirin 300 mg chewed – like antiagregant.
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II.Treatment of pain- use the opioide drugs like:
- Morphyne 2-8 mg i.v or s.c.(1 f=20 mg) repeated to 5-15 minutes, until pain disappears or until
appear side effects (hypotension, vomiting, decreased activity of respiratory center).
Maximum dose for 1 day is 60 mg. The antidot for Morphyne is Naloxon=Nalorphine 0,4 mg i.v. or i.m. (1f).
Never give morphyne if blood presure is<90-100 mmHg.
Treat the hypotension and bradicardia with atropine 0,5-1,5mg i.v.
In case of vomiting give Plegomazin 1 f i.v./i.m. (or other antiemethic drug);
- Petidine (Mialgin, Demerol, Meperidina) 20-30 mg i.v. (1f=100mg), repeated after 10-15 minutes or
50-100 mg i.m.
- Penthazocine (Fortral) 20-30 mg i.v. or i.m. (1f=30 mg). This drug is preferated to a hypotensive
patient.
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III.Treatment for limitating the infarction zone
- Nitroglycerine - s.l., next intravenous perfusion (i.v.). For perfusion starte with 10 g /min and
progressivly increase the dose, until reducing the systolic blood pressure with 10% at a pacient with
normal blood pressure and with 30% at a hypertension patient.
NEVER reduce the systolic BP less than 90 mm Hg and never increase the pulse rate more than
110/min. Usually,NTG dose is 20-40 g /min,maximum 100-200. This perfusion is maintained for 12-24
hours.
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- Beta blockers will be administrated to all the patients who haven’t contraindications, after 4-6 hours.
C.I. are: -evidence of heart failure;
-systolic BP< 90-100mmHg;
-cardiac rate< 50-60/min;
-atrioventricular block II- III degree;
-bronchospasm;
-peripheral ischemic arteriopathy.
Drugs and dosages:
-Metoprolol (Lopresor) - 5 mg i.v.; repeated for three times to each 5 minute, with clinical monitorising (cardiac rate, blood
pressure dyspnea);
-Atenolol (Tenormin) 5-10 mg i.v. slowly;
-Propanolol 0,5-2 mg i.v., repeated three times to every 5 min.
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- Anticoagulants – Heparine 5000 U.I. bolus i.v. , followed by 1000 U.I/hour. It will be given until the anticoagulant efFect
( Howell time to be 2-4 times more than normal).
Contraindications:
-recently cranial or spinal trauma or surgical interventions
-any cerebrovascular event in last 3 months
-active gastroduodenal ulcer or with bleeding in last year
-age>75 years
-pregnancy
-arterial hipertension or suspicion of aortic dissection
-coagulopathy disorders.
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IV. Revascularization methods of infarcted zone
For a precocious reperfusio existthe next posibilities:
1. thrombolytic therapy i.v. or intracoronarian
2. angioplasty PTCA- percutan transluminal coronarian angioplasty
3. aortocoronarian by-pass.
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1. Pharmacologic thrombolysis is indicated as soon as possible in case of medium or big myocardial infarction, especially anterior ones.
The maximum benefit is obtained if it is started within 4 hours of chest pain onset. Then , efficiency decrease. Thrombolytic therapy can be
begun also later (12-24 hours) if the pain persists and ST elevation exists.
Contraindications:
-absolute C.I.: -any cerebrovascular event;
-surgery within 2 weeks;
-coagulopathy diseases, bleeding diathesis;
-recent head or spinal trauma in last 2 months;
-intracranial tumors;
-aortic dissection, malignant hypertension;
-previous allergy to thrombolytics;
-pregnancy
-cardiogenic shock
-
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-relative C.I. -activ peptic ulcer disease (in last 6-8 weeks);
-surgery or trauma in last 6 weeks;
-SK or APSAC in the last 6 month (use in this case rtPA);
-infective endocarditis;
-prolonged CPR with chest compression.
-conditions ssociated with a predisposition to bleeding
-advanced liver or kidney disease
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Drugs and dosages:
-Streptokinase- SK :1.500.000 units in 250 ml 5% Dextrose, p.i.v. in 20-30 min;
-Tissue plasminogen activator tPA : 60 mg. i.v. in the first hour, of which 10 mg over first 1-2
min., then 20 mg/hour.
-Urokinase UK: Loading dose =0,5 millions units over a 10 minutes period. This is followed by
infusion doses of 1,6-4,5 millions units over 18-24 hours.

Intracoronarian administration of thrombolytics, permit obtaining of similary results or more superior,

with small doses of drugs and small haemmoragic risk.
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The criterias for the efficiency of thrombolysis are:
a)clinical: -disappereance of the pain;
-sdr.bradicardia-hypotension;
b)ECG: -reduced ST elevation;
-apperance of reperfusion arrhytmias (VEx., accelerated idioventricular ritm).
c) biological: -partial thromboplastin time must be 2-3 times more than normal and the fibrinogen decreases with
20-80%.
2. For those pacient who have contraindications for thrombolysis or thrombolysis was inefficient, there are two
alternatives:
1.coronarian angioplasty (PTCA);
2.aorto-coronarian by pass.
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2)AMI with complications

I. In inferior myocardial infarction the pain can be localised in epigastric region or precordial
and can be accompanied with nausea, vomiting, arterial hypotension and bradycardia. On ECG
appear modifications in DII, DIII and AVF leads.
These symptoms are the expresion of increased the vagal tonus. To the clasical treatment
of myocardial infarction, give :
-Atropine – 0,5-1mg i.v. (not less);
-antiemetic drug- Prochlorperazine.
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II. Cardiogenic shock: Shock complicating myocardial infarction may be caused by extensive area of necrosis (> 40% of myocardium),
with decreased cardiac output.
Diagnosis: hypotension, tachycardia, decreased level of conciousness, cool skin, oliguria, methabolic acidosis, signs of increased central
venous pressure (+/- jugulare turgescence).
Treatment:-oxygen 5-10l/min
-i.v. line, blood tests
-monitoring:-clinical: signs of pulmonary edema, signs of central venous stasis
◦ -paraclinical: BP, cardiac rate, central venous pressure, central pulmonary (with a Swan Ganz catheter in pulmonary artery)
◦ -insert urinary Foley catheter and measure urine output

-give a fluid challenge- 250 ml saline i.v. over 30 min., with continous clinical and paraclinical monitoring of the patient (signs
of pulmonary edema, congestive heart failure). Repeat as needed if congestive heart failure doesn’t developp.
-give Dopamine 5-15 microg/kg. b.w.min. (medium dose),
-correct arrhythmias;
-vasodilator drugs with prudence, if mechanism of shock is inappropriate vasodilation (rare).
-PTCA-percutaneous transluminal coronary angioplasty
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III. Congestive heart failure
Diagnosis: dyspnea, anxiety, tachypnea, tachycardia, pulmonary rales or pulmonary edema,
hypoxemia, and typical findings on chest X ray, jugular distension, signs of right heart
failure:hepatomegaly, peripheral edema, elevated central venous pressure.
Treatment: -give oxygen 5-10 l/min.;
-monitor arterial blood gases;
-give Furosemide 20-40 mg i.v.bolus;
-give Morphyne 2-8 mg i.v.;
-give NTG in perfusion 10g / min and increase to 20-40.
-inhalatory sympathomimetics.
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IV.Acute pulmonary edema
Diagnosis: dyspnea, orthopnea, Wheezing may be present, cough with sputum (frothy, pink),
rales are present bilateral in the basis, tachycardia, anxiety.
Treatment:
- oxygen 10l/min
-diuretics –Furosemide 40-80mg i.v.
-opioids Morphyne 5-10mg i.v.
-nitrates given sublingually and intravenouslly 10-20 microg/min
-additional treatment.
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V.Arrhythmic complications
1.Ventricular extrasystole with risk for ventricular malignant arrhythmias are:
-VEx more than 5-6/ min;
-systematized V.Ex.: bigeminism, trigeminism.
-polymorphism V.Ex.;
-V.Ex. with R/T phenomen
Treatment: Lidocain 1-1,5 mg/b.w.bolus i.v., followed by continous infusion with 1-2 mg/min.
A second opinion is that ventricular extrasystole not require the treatment in all the cases. They are
treated if are symptomatic, if the hemodinamic status is decreased or if is impossible to have a ECG
monitor.
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2. Atrial fibrillation and atrial flutter with high ventricular response
This is the situation when the digitalic are indicated in case of myocardial infarction. Also cen be given
betablockers (Propranolol) or calcium blockers (Verapamil). If exist pompe insuficiency give diuretics and
vasodilators.
3.Supraventricular paroxistic tachycardia rarely complicates an myocardial infarction. It will be treated by
clasical algorithm; vagal manouvres, adenosine or fosfobion, Verapamil or Propranolol or Digoxin . If no
efficiency, D.C. shock.
4.Ventricular tachycardia with pulse wil be treated with Lidocaine 100 mg. bolus i.v., then perfusion with 1-
2mg/min; Avoid this drug in case of bradycardia, conductive disorders. If is not efficient, try Bretilium
Tosilate 1-2 mg/min. i.v. , procainamide, amiodarone.
5.Pulseless ventricular tachycardia and ventricular fibrilation will be treated from the algorithm of
cardiorespiratory arrest.
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6.Bradycardia
sinusal bradycardia with cardiac rate >40/min without symptoms, doesn”t need treatment.
I degree AVB- no treatment is necessary. If the patient usually take digitalic or betablokers, decrease the
dose .
II degree AVB type II and III degree infrahissian (wide QRS complexes and HR<40/min) appear usually in
anterior myocardial infarction and have bad prognosis due to their irreversibility. It is necessary permanent
cardiostimulation.
II degree and III degree AVB which complicate from the beginning inferior myocardial infarction , are due to
reflexed increased of vagal stimulation and inflamatory edema of AV node. These blocks are associated with
suprahissian escaping rithm: narrow QRS and HR>40/min.Treatment: Atropine 0,5-1 mg.i.v. repeated , max. 2
mg. Isoprenaline or temporary cardiostimulation.
Asistole – is a frequent complication of myocardial infarction. It produces cardiorespiratory arrest treated like
the algorithm.
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VI.Pericardial effusion and cardiac tamponade
A small quantity of fluid in the pericardial space appear to 25% of cases , especially in big myocardial infarction
associated with cardiac failure . Diagnosis: persistent chest pain which worsens by lying down possition. This pain
irradiates to the neck left shoulder. Appear pericardial friction rub. Diagnosis is confirmed on echocardiography.
Rarely is accumulating a big quantity of fluid in the pericardium, and produces cardiac tamponade Treatment:
oxygen, i.v. line pericardiocentesis ( if is decompensated) or with antiinflamatory drugs, corticotherapy if is
compensated.
VII. Recurent ischemia: precocious postmyocardial infarction angina and extension of necrosis area
Both are manifestated by recurent angor. The first one needs coronarography if can not be stabilized by medical
treatment.
Extension of necrosis area appear on ECG like extension of modifications and will be treated like a new infarction.
 UNSTABLE PECTORIS ANGINA-
UPA
Definition
UPA is also named preinfarction angina or intermediare syndrome or acute coronary insufficiency.
These signifie a clinical intermediate status between the stable effort angina and myocardial infarction.
Also this suggests the lability of clinical status, which can stabilize or can aggravate gradualy to
myocardial infarction, or can appear cardiac sudden death.
 UNSTABLE PECTORIS ANGINA- UPA
Unstable angina is defined on the next criterias:
1. clinical criterias:
One of the next manifestations can appear:
new-onset angina or novo angina - which have appeared in the last 2 months, with a small degree of effort
aggravated angina - a longer lasting effort angina, bigger intensity of pain, which appears to smaller degree of effort and has more difficult
response to nytroglicerine
rest angina
– subacute: pain in resting positionin the last 2 months, but not in the last 2 days
- acute: pain in resting position in the last 2 days.
Prinzmetal’s angina (variable angina) - the pain is associated with reversible ST elevation . It is determined by coronarian spasm appeared on
normal arteries or on artery with fixed ateroma lesions, without significant stenosis.
Precocious postinfarction angina - appears in the first 2 weeks after a myocardial infarction. It can clinically appear like:
- effort angina with small degree of effort
- rest angina
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UPA
2. ECG criteria – most of the times exist ischaemical modifications on ECG, but no that ones of myocardial
infarction

3. Enzymes criteria – dont appear big values suggestive for myocardial infarction.

Extracoranarian factors which can aggravate the ischaemia are: anemia, fever, infection, hypotension,
tahyarrythmias, tireotoxicosis, hypoxia by respiratory failure. This type of UPA has a good prognosis after the
treatement of cause.
The most severe is the acute rest angina (especially if it appears after myocardial infarction), without tratable
aggravating factors and which persists also with adequate treatement.
 UNSTABLE PECTORIS ANGINA-
UPA
Etiology
The pain in case of pectoris angina is caused by acute myocardial ischaemia which is not so prolonged
and so complete to produce necrosis of the myocardial cells like in myocardial infarction.
This ischaemia can be produced by:
-coronarian spasm or
-nonoclusive trombus or transitor plachetary agregates.
The ischaemic phenomen can occur on normal coronarian arteries, but usually this modifications occur on an
important coronarian atherosclerosis. Often exist three coronarian involving: right coronarian artery, anterior
descending coronarian artery and circumflexe artery.
 UNSTABLE PECTORIS ANGINA-
UPA
Paraclinical findings
1.E.C.G.
a. during the pain period, ECG shows: ST depression, T wave negative. These modifications dissapear
after the disparition of pain .
In Printzmetal’s angina is characteristic ST elevation, with ulteriorly normalizing .
b.effort E.C.G. can be made after the stabilisation of angina (minimum 2 days without pain in rest
possition).
The apparition of angina to a small degree of effort with ST depression, suggests important
coronarian lesion and requires a coronarography.
The patients with good tolerance of effort, without angina and without ST depression, have
better prognosis and they can be treatedwith drugs.
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UPA
2.Blood tests.
These test can show lipidic disturbances (hypercolesterolemia) or decreased tolerance to glucose.
The inflammatory tests (leucocites,VSH) are normal.
Myocardial enzymes have normal values.
3.Ecocardiography can show hypokinetic zones, reversible after the stabilisation of angina . If the
contractility abnormalties persist, they are factors of bad prognosis.
4.Myocardial scintigraphy with talium shows hypocaptation zones (hypoperfusion) . The presence and the
size of this areas are indicating the prognosis
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UPA
5.Coronarography is indicated to the next patients:
-patients with unstable angina who don”t responde to therapy. If the pain appears in rest position or to small
degree of effort inspite of adequate treatement of 2-7 days, coronarography will be effectuated immediately.
Preferable is the patient to be hemodinamical stabilized. Otherwise, the coronarography will be made under
the protection of contrapulsion aortic balon.
-the patients whose effort tests (after the stabilisation of angina) show a small degree of effort when appear
an important ischemia.
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UPA
The coronarography can show:
- left coronarian main injurie. It needs aortocoronarian by-pass in semiemergency (10 days after the
stabilisation)
- tricoronarian injuries. Also needs by-pass.
- uni- or bi-coronarian injuries with proximal stenosis. This requires coronarian angioplasty.
- permeable coronarian arteries (normal or with atheroma lesions, but without significant stenosis- less
than 50% of the diameter). These pacients have a better prognosis and they will get drug treatment .
 UNSTABLE PECTORIS ANGINA-
UPA
Differential diagnosis
- myocardial infaction: longer lasting pain, usually more hours, more severe in intensity. Also appear
E.C.G.and enzymes modifications, which are basic criterias for diagnosis.
- Noncoronarian retrosternal pain -see the differential diagnosis of myocardial infarction.
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UPA
Treatment
BE CARREFUL:
-diagnosis of unstable angina is a clinical one;
-hospitalise and monitorise any patient with suspicion of unstable angina
-dinamicaly monitorise the ECG and the enzymes;
-always correct the aggravating factors.
There are some steps you must follow:
- always hospitalise the patient
- give oxygen 5-10 l/min
- rest in bed
- treat the pain and anxiety
- treat the aggravating factors if exist: fever, infections, tachyarrythmias, anemia
- E.C.G. monitor and repeat miocardial enzymes determinations
UNSTABLE PECTORIS ANGINA-
UPA
the nitrates- are the first line of therapy. They can be administrated sublingual, transdermic, oraly,
or i.v. if is no efficiency.You must decrease blood pressure with 10% to normotensive patients and
with 30% to the hypertensive patients. The perfusion last maximum 24 hours, no more because the
pacient can developpe tolerance.
The oral nitrates :
- isosorbid dinitrate (Isodinit, Isoket, Maycor)
tb=20, 60, 120 mg dose =20-60 mg/2-3 times one day
- isosorbide 5 monohidrate (Isomonit)
tb=20, 60 mg dose= 10-20 mg/2-3 times one day
- pentaerytril tetranitrates (Pentalong, Nitropector)
tb=20 mg dose= 10-20 mg /3 times one day
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UPA
monitor the BP and pulse rate;
beta blockers are necessary because of decreasing the oxygene miocardic needs. They are contraindicated in case of heart
failure.Usually are used cardioselective drug like:
Propanolol tb=10 mg dose=20 mg/6 hours , max. 240mg/day.
Metoprolol, Beloc dose=100-200mg/day
Atenolol, Tenormin dose=50-100mg/day.
Side effects: bradicardia, mental disorders, hypotension.
Contraindications of betablockers are :
-history and ECG suggesting Printzmetal’s angina;
- bronchospasm;
- bradicardia < 55/min.
- AV block II-III degree
- hypotension
- diabetus mellitus
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UPA
calcium channels blockers- have a vasodilator effect on coronarian arteries and also on systemic arteries.
They decrease the cardiac output and the parietal pressure of left ventricule. They are the third line of
treatement.
Nifedipine tb=10, 20 mg dose=30-80mg/day
Diltiazem tb=60, 120 mg dose=90-240mg/day
Verapamil tb= 40-80 mg dose=120-240mg/day
Verapamil has the strongest antiarrythmic effect, also the strongest negative inotrop effect. So, avoid the
association with betablockers.
antiagregants- aspirin 300mg/day and anticoagulants-heparine 5000 UI i.v. next 1000 UI/ hour- will be
sistematically associated to the patients without specific contraindications.
the revascularisation methods (by-pass, angioplasty) are indicated in some cases, described anteriorly.
Printzmetal”s angina is usually treated with big doses of nitrates and calcium blockers.
 UNSTABLE PECTORIS ANGINA-
UPA
Prognosis
The factors of bad prognosis are:
- frequent subintrante crises of rest angina, which mentained inspite of medical treatement
- severe multicoronarian injuries evidentiated to coronarography
- left ventriculare failure
- intense possitive effort test.
In Printzmetal angina, after few months, the frequence of coronarian spasm can decrease; the
patient becomes asymptomatic for a long time, but can not exclude the relapse.