Lecture 8
AORTIC DISSECTION
Aortic aneurysm is a dilatation which includes all 3 elements of aortic wall, with loose
of paralelism between the layers.
The causes which can produce aneurysm are: lues, atherosclerosis, fibrinoin necrosis of
media, cystic necrosis of media, congenital aneurysms and traumatic.
Localisation of aneurisms:
- thoracic: from the origin to diafragmatic hole. This has 3 parts: ascendent (till
the aortic crosa with origin of the right brahiocephalic branch), aortic crosa (in
anteroposterior mediastinum) and descending aorta (in posterior mediastinum)
- abdominal- in retroperitoneal space.
Clinical findings:
- frequently are asymptomatic, discovered to Xray, doppler echography
- symptomatic by: - compression of organs
- dissection
- rupture
Aortic dissection is the appearance of the leaking in the aortic wall, which permits the
blood to enter between the layers of the aortic artery. In 90% of cases exist a transversal fissure
in intima. Appear a false lumen between the internal and external walls. To every cardiac beat
leaking increases and also the dissection .
Classification – De Bakey:
- proximal: dissection begins just distal to the aortic valves
type I- involves ascendent aorta and aortic crose
type II- limitated to ascendent aorta
- distal – type III- dissection begins in descending aorta, and progresses distally
or proximally.
The promoting factors are:
- arterial hypertension-by increased pressure over the walls. It is the most important risk factor.
- atherosclerosis-which favorises the rupture of the intima and the subintimale haemmorrage;
-cystic degenerescence of the media -which appears in Marfan syndrom or to the elderly patients
-aortic coarctation.
Clinical findings
The pain-is severe, with tearing character, appears brutally, like a rupture sensation. First, it is
localized retrosternal or interscapular, then it iradiates with the dissection:
-to the head and neck when the carotides are involved;
-to the superior or inferior limbs;
-to the lombar region in case of renal involving.
The pain is associated especially at the begining with vasovagal manifestations: sweatening,
nausea, vomiting,weakness, congestive cardiac failure.
Depending which vessels are compromised , can appear different clinical signs:
- Neurological signs: when the dissection involves carotidian arteries: stroke, syncope,
paraplegia.
- Pulse modifications: decreasing or dissapearance of pulse to the affected radial artery;
- Signs of aortic insufficiency: diastolic murmurs in aortic focus. Also left ventricular failure can
appears (dyspnea,ortopnea, acute pulmonary edema);
- Arterial occlusion of an extremity
- Abdominal or back pain with or without hematuria
- acute myocardial infarction.
- Blood pressure- usually is increased, even at the first look it seems that the patient is in shock
status (pale, sweatening, profound suffering).
If the hypotension exists, it can have the next causes:
- the rupture of the aorta in: -pericardium--cardiac tamponade;
-pleura-hemothorax;
-peritoneum-hemoperitoneum;
-involving the radial arteries which produce pseudo-hypotension.
Paraclinical findings
1.Chest X-ray: can show a widened mediastinum; the aortic enlargement, totaly or on certains
areas. Also can show pleural fluid
2.EKG - signs of left ventricular hypertrophy ( arterial hypertension)
3.Ecocardiography can show the blood flow in false lumen, the appearance of aortic
regurgitation, hemopericardium, division of aortic wall. Doppler echography shows also the
blood flow in the 2 lumens.
4.CT scan is less invasive and is a sensitive and specific diagnosis test. It sees all the zones of
the aorta and can differentiate the dissection from the fusiform aneurysm;
5. Transesophagian echography can show localisation and extension of dissection, entrance
orifice.
6.Aortic angiography with contrast substance is necessary .
Possitive diagnosis
Possitive diagnosis is suspicioned on clinical findings: arterial hypertension with Marfan
sd.,severe thoracic pain, irradiated to the back and to inferior, neurological signs, pulse
modifications, diastolic murmurs of aortic insuffiency.
The confirming diagnosis is made on the paraclinical methods: transesofagian
ecocardiography, CT, aorto angiography.
Treatment
The treatment is necessary from the moment of suspicion of diagnosis , untill definitive
diagnosis and beginning of surgical treatment.
Medical treatment is the only treatment in uncomplicated distal aortic dissection, also in
stable uncomplicated chronic dissections (more than 2 weeks).
The main goals of the treatment are:
- reduce the pain
- decrease hypertension
- reduce the speed of blood ejection from left ventrical to aorta.
1. reduce the pain – opioids
2. decrease the blood pressure to 100mm Hg or to the level which doesn’t produce
hypoperfusion disturbances in vital teritories (cerebral, coronarian, renal).
Use vasodilators drugs:
- Sodium nitroprusside 50-100 mg in 500 ml G5% ,p.e.v.20-400 g/min;
-Trimethaphan (ganglionar blocker) 500-2000 mg in 500 ml G5% - p.e.v. 1mg/min
-inhibitors of converting enzymes- Enalapril, 1-2 mg/6h;
-calcium channel blockers- Nifedipine s.l.
- nitrogycerine
3. blockers: Propranolol, Atenolol, Esmolol
- Propanolol 1 mg i.v. repeated every 5 min.until the heart rate is 60/min. Next 20-40mg/6h.
Be cautions with the contraindications of blockers ( bradycardia, bronchospasm, cardiac
failure).
Surgical treatment is performed in special cases:
- acute proximal aortic dissection;
- distal aortic dissection with complications:
- iminence of aortic rupture;
- retrograde extensions in ascending aorta;
- progression to a vital organ;
- Marfan sd.
The pacients with aortic dissection, even they had a surgical intervention, they will have a
chronic antihypertensive treatment, usually with the drugs which have also a negative inotrope
effect ( blockers, calcium blockers).They willl be periodical examined clinical, echographical,
biological.
Rupture of aortic aneuryism ( with or without dissection) produces clinical manifestations of
hipovolemic shock. Rupture can appear in : right bronchium, in traheea, pericardium, abdomen.
CARDIAC TAMPONADE
Definition
Cardiac tamponade or pericardic tamponade is an acute compression of the heart by fast
fluid collection in pericardic cavity, which produces a difficulty in diastolic loading, decrease the
cardiac output by increasing systemic and pulmonary venous pressure .
Etiology
a. Pericarditis
- viral
- tuberculosis
- bacterian (purulent)
- neoplasic
- uremic
- associated with acute myocardial infarction
- associated with imunologic diseases
b. Heart or vassels rupture
- rupture of free wall of the ventricle in myocardial infarction
- leaking of aortic anevrism in the pericardial cavity
- penetrating chest trauma or thoracic injuries
- iatrogenic rupture during the pericardic punction, heart catheter.
c. Postagressive imune reaction
- Dressler syndrome postmyocardial infarction
- postcardiotomy syndrome after heart surgical intervention
Pathogeny
Normally in pericardic cavity exist 15-50 ml serocitrin fluid to a pressure of –2-
3mmHg . Acumulation of fluid in pericardic cavity can be produced slowly, without significant
increasing pressure ( even 2 l). But fast acumulation more than 100-200 ml, produce increasing
of intrapericardic pressure to 15-30 mmHg, with some consequences:
- increased intraatrial pressure followed by difficulty of empting the veins in
right atrium, with jugulary turgescence, hepatomegaly
- compression of the ventricles (especially right), with difficulty of diastolic
filling and small cardiac output. Compensatory appear vasoconstriction and
tachycardia, mechanisms which will be further overtaken. Decrease
coronarian perfusion with severe subendocardial ischemia, electromechanical
dissociation and death without treatment.
- appearance of paradoxal pulse (increased physiological variation of pulse
amplitude with respiration).
Clinical findings
Exist 2 possibilities: -acute cardiac tamponade
-subacute cardiac tamponade
1. Acute cardiac tamponade has many causes like: trauma with hemopericardium, rupture of
ventricular wall or aortic aneurysm in pericardic cavity. So will collect a big quantity of blood
in a short time period and the pericardium will not be able to distend .
Clinical triade is:
- hypotension or shock
- turgescence of jugular veins
- faint of heart sounds with normal cardiac dulness
Patient has aspect of major acute suffering, with dyspneea, tachycardia, agitation, pallor,
cold and wet extremities, sometimes anuria.
If peripheral pulse can be palpated, this will be paradoxal pulse (this is a decreasing of
intensity or amplitudine of pulse during inspiration; also the peripheral pulse can be define like a
decreasing with more than 20 mmHg of the systolic blood pressure during normal inspiration).
2. Subacute cardiac tamponade usually appears in pericarditis of different ethiology. In this case,
the fluid collection is slowly acumulating, and the pericardium can be slowly distended. The
quantity of fluid can be more than 300 ml.
Clinical examination can find:
- chest pain with pericardic character (increases with cough and breathing; the pain decreases
intensity in“pillow position”or “mahomedan position”)
- dyspneea
- fever, tachycardia, viral status
- cardiac dullness is increased and the apexian point is localised inside the dullness
- cardiac friction can be heard
- signs of central plethora (turgescence of jugular veins, hepatomegaly, edema)
During the evolution, dyspneea and tachycardia increases and appear hypotension, paradoxal
pulse and faint of heart sounds.
Laboratory findings
1. ECG- Don”t exist specific modifications, but the following elements can be sugesstive for
diagnosis:
- sinusal tachycardia ( which exist also in case of pericarditis without tamponade)
- decreased voltage in all leads
- electrical alternance (modification of QRS amplitude to every 1-3 beats ), appeared on
old pericarditis is suggestive for cardiac tamponade
- nonspecific modifications of ST-T segment.
The evolution of typical modifications in pericarditis followes some steps:
- diffused ST elevation (in all leads)
- ST segment is getting closer to the isoelectric line and T wave is getting flatten
(differential diagnosis with myocardial infarction where T wave is negative before the ST
segment will be isoelectric)
- negativity of T wave
- normalising the aspect step by step.
2. Chest x-ray
In acute cardiac tamponade chest x-ray can be normal.
In subacute cardiac tamponade signs of pericarditis are present: increased cardiac opacity with
wipe off the cardiac aches shade .
3. Echocardiography can show important elements for diagnosis:
- presence of a transsonic space in front of right ventricle and posterior of left ventricle
- diastolic colapse of heart cavity ( first right atrium, next right ventricle,next left cavity).
Remember
The cardiac tamponade diagnosis is a clinical one. Echocardiography can help, but is not the first
criteria for diagnosis.
Differential diagnosis
In front of a patient with raised venous pressure, collapse, faint of cardiac sounds, eventually
paradoxal pulse, consider the next afections for differential diagnosis:
1.Acutisation of chronic cor pulmonale;
2.Massive pulmonary embolism;
3. Infarction of right ventricle;
4. Constrictive pericarditis;
5. Biventricular heart failure.
Ecocardiofraphy is very important for differential diagnosis, it is indispensable before
pericardiocentesis.
Treatment
I. Acute cardiac tamponade represents a major therapeutical emergency, due to the risk of
cardiac arrest by electromechanical dissociation. Until a decompressive method and
concomitent with this , treatment includes:
1. oxygen administration 5-10 l/min by face mask or nasal tube;
2. two big i.v. lines (>18) and administration of cristaloids, until decompression of pericardium.
3. administration of isoproterenol 2-4 microg/min. i.v. or dopamine 5-20 microg/kg/min.
Endovenous perfussion can sustain cardiac output until a pericardic decompression will be made.
Even patient with cardiac tamponade has signs of central plethora and signs of small cardiac
output (distension of jugular with hypotension or shock) do not administrate: diuretics and
digitalic drugs, because the contractility is normal and the increasing of venous central pressure
is a compensatory mechanism for assure a good ventricular loading and for maintaining the
circulatory flow.
Vasodilatation drugs will be avoided.
4. evacuation of fluid from pericardic cavity must be done as soon as possible. Pericardial
decompression methods are:
- Pericardiocentesis (with needle or catheter);
- Subxifoidian pericardiothomy with visual control (echography or x-rays);
- Surgical pericardectomy.
The first intention method is pericardiocentesis. This method without visual control has a
high risk of death, but in absence of equipment and when the patient status requires it, you must
to make this in emergency.
The ideal conditions for pericardiocentesis are: in the catheterism room, after
echocardiography, under fluoroscopic control, with monitoring the pressure in right heart
cavities and in pericardial cavity.
Technique :
- semisitting position
- asepsia with iodine
- local anestesia with Lidocain 1%
- subxifoidian abord
- use special needle for pericardiocentesis or needle for lombar punction.The needle
can be conected to an E.C.G. lead, to know when the heart is touched (appear ST
elevation or an extrasistolic arrythmias).
- the needle penetrates to 0,5 cm inferior and left of xifoid apendix, direction to posterior,
superior and right and aspirating in all this time.
The fluid must be studied : biochemical, cytological and bacteriological.
Surgical drennage are rarely practiced in emergency. The indications are:
-inefficiency of pericardiocentesis;
-tamponade recurence after pericardiocentesis;
5.After decompression the treatment involves surgical treatment of trauma, heart wounds, heart
ruptures or vessels rupture.
II. Subacute cardiac tamponade has next treatment:
1. oxygen 5-10 l/min.
2. continous ECG monitor and blood pressure measurements every 15 min.
3. invasive CVP – central venous pressure monitoring
4. peripheral i.v. line (>18), and fluid administration function BP values
5. confirming the presence of liquid in pericardic cavity by echocardiography in 1st hour
6. pericardiocentesis can be temporised or even avoided, etiological treatment can resolve the
situation:
- NSAI in idiopatic pericarditis
- Steroidian antiinflamatory
- Tuberculostatics in TBC pericarditis
- Antibiotics in purulent pericarditis
- Chimiotherapy in neoplasic pericarditis.
