Etiologies:
Heart failure (or ventricular) may be secondary to left:

• Hypertension by chronic increase of afterload with left ventricular hypertrophy
• A valvular (narrowing or aortic insufficiency or mitral)
• Ischemic heart disease (reduction or stoppage of blood flow in one or more arteries of the heart),
• Hypertensive cardiomyopathy, toxic, or deficiency (beri beri)
• Obstructive cardiomyopathy
• Myocarditis (myocarditis, inflammatory rheumatic or Chagas disease, common in South America)
• Arrhythmias,
• Profound anemia
• Hyperthyroidism
• Ischemic by coronary atherosclerosis

Heart failure (or ventricular) is right most often follows:

• Left heart failure + + +
• Pulmonary hypertension, itself caused by a lung disease (chronic bronchitis, emphysema, pulmonary embolism)
• CHD
• Mitral stenosis
• Chronic lung disease

Chronic heart failure:
Often a consequence of hypertension in the small or large circulation, during which the heart muscle to pump against the increased pressure in the vessels. The ventricle must provide more work.

The muscle fibers are modified, they become longer and thicker. It develops an enlarged heart muscle.

The ejection capacity of the heart is diminished. The excessive volume of blood that remains in the heart is dilated ventricles.

Symptoms and Signs:

Left heart failure:

1. Fatigue due to lower systemic flow
2. Dyspnea at rest and
3. Supine Dyspnea: one of the best signs of the evolution of IC is the increase in the number of pillows, changing the position of his body, increases the patient’s superior vena cava in venous return and thus pre load.
4. Cyanosis
5. Tachycardia, reflex acceleration of heart rate due to adrenergic hyperstimulation
6. Arrhythmias
7. Acute pulmonary edema, brutal and revealing
8. Sometimes, signs of cerebral in cerebral blood flow decline with confusion, insomnia, anxiety

In right heart failure, there creating an overpressure in the venous system. It follows:

• Dependent edema of the lower limbs
• Engorgement jugular
• Cyanosis
• Hepatomegaly and Splenomegaly (The venous territory touches the cellar, which increases the volume of the liver and spleen)
• Loss of appetite, nausea (for gastric reflux into the veins)
• + / – Inflammation of the gastric mucosa
• Insomnia
• Nocturia
• Ascites

Diagnosis:
According to the clinic:
By ECG to detect a possible etiology (myocardial infarction).

Chest radiography: It showed an increase in volume of the heart (cardiomegaly) and possible signs of lung overload.

Echocardiography: Assessing the size and function of the ventricles and diagnosed with valvular.

Other possible tests: cardiac catheterization, myocardial scintigraphy, CT …

Treatments:

• Treat symptoms and cause.
• Bed rest in a sitting position
• Diet low in salt, limit the amount of drink
• Avoid heavy meals
• Smoking cessation
• Avoid prolonged exposure to cold
• Limit physical exertion
• Weight Control
• Diuretics to reduce blood volume and water retention
• Improving the performance of the heart pump, trying to restore to normal myocardial contractility (inotropic agents)
• Reduction of cardiac load by reducing either the venous return (preload) or the resistance to ejection (afterload) (vasodilators)
• Digitalis in some cases (cardio tonics): they increase the contractility of the heart
• Calcium antagonists or inhibitors of converting enzyme (ACE) for dilation of arteries, decrease hypertension
• Necessary surgery for the treatment of the cause (valvular disease, ischemic heart disease …)
• Transplantation as a last resort, in patients under 65 years if the heart failure can be improved by other methods.

Causes:
The occlusion of one or more coronary arteries is almost always due to the formation of a thrombus (clot) on a plaque consisting of cholesterol deposits against the inner arterial wall. This condition occurs most often in patients with risk factors such as smoking, hypertension, high cholesterol, diabetes, sedentary lifestyle.

Symptoms
In half the cases, infarction occurs after a period shorter or longer during which the subject suffers from angina.
The pain (tightness, burning, sometimes crushing) are felt behind the breastbone (retrosternal), and can radiate to the left arm to the jaw, sometimes in the back. They disappear in a few minutes rest, sometimes with the use of a spray nitro.
In the other half of the cases, stroke is opening, that is to say that there are no warning signs. It manifests itself by severe pain sharp retro sternal (such as angina but longer and more intense). The pain may radiate to the arm, jaw and back. It is often constrictive and accompanied by anxiety and feeling of impending death.


About 20% of patients with myocardial infarction have little or no pain (silent infarction). Often in people with diabetes or the elderly.
Other signs may include:

• Nausea, vomiting
• Pale, grayish, cold sweats
• Death anxiety
• Dyspnea
• Sudden collapse with loss of consciousness
• Cardiogenic shock

Risk factors:

• Tobacco
• Diabetes
• Pill in women, smoking is associated with prothrombotic
• Overweight
• Hypercholesterolemia
• Sedentary lifestyle
• Coronary personal history or family
• Age> 65 years
• Male but caught by the female menopausal

Diagnosis:
The diagnosis is made in the presence of the following factors:
ECG qualifying myocardial typical of Pardee wave, Q wave of necrosis (ischemia old), in addition to raising at least 2 bypass the ST segment with sub-pass in the territories opposite (mirror) and loss of asymmetry of the T wave
Typical clinical symptoms but inconstant
Elevation of cardiac enzymes in the blood (enzymes released from myocardial cells, when destroyed):

• CPK MB: Threshold 10ng/ml (nonspecific)
• CTnI, the more specific negative short of 0.4 ng / ml, suspected angina between 0.4 and1 ng / ml, confirmed diagnosis beyond 1ng/ml. However, standards can vary between laboratories and sensitivity tests. Always ask about the standards of your lab
• Myoglobin (nonspecific), as advocated: threshold to 150ng/ml

Note that the threshold of detectability of these markers have a long and kinetic it is unnecessary to achieve within 2 hours after onset of pain.
Note also the need to take blood pressure in both arms to eliminate pain may find its origin in an aortic dissection, and temperature, to eliminate an infectious process such pericarditis, and this before therapy.
Care and treatment:
The No. 1 objective is to minimize the area of ischemia, to limit the loss of myocardial tissue and, ultimately, preserve ejection fraction of left ventricle.

• Emergency hospitalization in an intensive care unit with cardiac angiography table.
• Installation of 2 large peripheral venous channels (14-16G)
• ECG Monitoring 18 leads (devices, precordial, and right posterior), continues.
• Oxygenation systematically according to some authors, or SpO2> 95% according to other
• Antiplatelet therapy varies schools:
  • Aspirin 150 to 300mg IVD
  • clopidogrel 300 to 600mg depending on the orientation (trhombolyse gesture or angioplasty)
• Anticoagulation:
  • LMWH, sodium enoxarapine average 100ui/kg
  • Or unfractionated heparin in elderly patients (> 75 years) or renal inssufisant
• Use of nitrates and unless hypotension or infringement of the right ventricle
• Support for analgesia (morphine titration)
• Management of anxiety (1 to 2mg/kg hydroxyzine, alprazolam)
• The use of beta-blockers is possible if after the initial charge, the patient remained tachycardic and hypertensive, eg Atenolol 5mg / 5 minutes. However, the use of beta blockers should remain cautious (contraindicated in the COPD, the bronchospastic, AVB II or III, conduction disturbances, impaired ejection fraction …), as may unmask heart failure.

The focus of treatment will then be followed by availability of a table angioplasty.
If angioplasty quickly achievable, a preparation that will be conducted with a antiGpIIbIIIa: abciximab bolus of 0.25 mg / kg and then relay the 0,125 ug / kg / min in SAP (Tentative doses).
If the angioplasty is not feasible, thrombolysis in TNK-tPA (tenecteplase) 1000UI/10kg weight on a dedicated channel (interest VVP 2)
However, thrombolysis is subject to many cons-indications:

• hemorrhage less than a year
• Severe head injury less than three months
• Process active bleeding
• Abnormal hemostasis congenital or acquired
• Recent major surgery (<3 weeks)
• Pregnancy or recent birth (<1 week)
• Arterial dissection
• Severe uncontrolled hypertension
• Maneouvre resuscitation (external cardiac massage in prehospital example)

In addition, the nurse (e) will monitor this thrombolysis: bleeding from the puncture, gingival bleeding, epistaxis, neurological changes (pupillary reactivity, Isocore).
It goes without saying that the patient should remain at rest + + + to minimize oxygen consumption.
Evolution:
Monitor:

• The disappearance of pain
• The normalization of ST segment (low excess delay, disappearance of the mirror effect, resumed the asymmetry of the T wave)
• The appearance of a RIVA, Ventricular Rhythm Accelerated Idio is a rhythm disorder that does not deal with: there is indeed a good indicator of reperfusion. Other arrhythmias can be observed (extrasystoles, salvos of TV …)
• 15% of patients die before reaching hospital, 10% during hospitalization and 10% in the months that follow.
• After 3 to 6 hours, irreversible necrosis of muscle tissue reached settled.
• Necrosis can affect all layers of the heart wall (poor prognosis) or be limited to one part
• The evolution depends lesions. (Reached by 8% of akinetic muscle: reduced compliance, achieving 10% ejection fraction, 23% clinical heart failure)

Complications:

• heart failure
• heart rhythm disorder
• malfunction of the heart pump
• rupture of the myocardial wall by formation of aneurysm on the scars of scar tissue, or tamponade
• Cardiogenic shock
• PAO
• Recurrence in 1 / 4 to 1 / 3 cases

Prevention:
Removing risk factors:

• Quitting smoking
• Treatment of hypertension, diabetes and hypercholesterolemia
• Treatment of possible angina

After myocardial infarction, treatment with beta-blockers and aspirin 100mg daily reduces the risk of recurrence.
+ / – Administration of inhibitors of angiotensin converting enzyme and digitalis.

• the extent of necrosis of the left ventricular mass mainly
• a mechanical complications: cardiogenic shock secondary
• septal rupture responsible for CIV
• acute mitral regurgitation due to rupture or dysfunction pillar of mitral
• much more rarely, rupture of the free wall of left ventricle in charge of tamponade.
• the extension of an infarction less than the right ventricle

Symptoms:
In addition to signs of acute infarction, there are signs of tissue hypoperfusion:

• neurological signs: agitation, confusion, stupor,
• Signs peripheral coldness, pallor, mottling, cyanosis,
• Renal signs: oligo-anuria,
• hemodynamic signs: systolic blood pressure <90 mm Hg, toe pressure differential pressure, tachycardia with pulse spinning,
• signs of elevated filling pressures left (pulmonary edema, gallop …) and right (jugular turgor, hepato-jugular reflux).

Other etiologies:

• Severe pulmonary embolism thrombolysis in imposing an emergency,
• Tamponade to drain immediately in emergency
• Aortic dissection to be transferred in mid specialized medical and surgical cardiology.

more rarely:

• advanced dilated cardiomyopathy, hypertrophic or when crossing in TAP
• myocarditis (context associated infectious or pericarditis),
• advanced aortic stenosis,
• valve insufficiency in acute infective endocarditis,
• prosthetic valve dysfunction (thrombosis, avulsion …).
• myxoma of the left atrium (tumor)
• exceptionally: Beri beri, hyperthyroidism, arteriovenous fistula, myeloma.

Other statements of non-cardiogenic shock:
Septic shock
The table combines circulatory collapse by vasoplegia with hyperkinetic heart trim. In a second step, there is heart failure.
Hypovolemic shock
The most common cause is severe bleeding, internal or externalized.
Anaphylaxis
Typically occurs after contact with an allergen in a sensitized patient, resulting in hemodynamic failure due to a severe vasoplegia associated hypovolemia by capillary leak.

Treatment:

• The ECG monitoring and noninvasive blood pressure at first, as invasive as possible.
• The establishment of two peripheral venous channels.
• Treatment of any associated hypovolemia.
• The release oxygen.
• Assisted ventilation after intubation if necessary, the sedation and ventilation to reduce the metabolic needs
• The start of a positive inotropic (Beta +) dobutamine (2 to 40 mg / kg / min) which allows discrete alpha effect a reduction in cardiac afterload.
• Treating the cause
• Biological assessments in emergency (biological markers, blood gas, electrolyte blood, kidneys balance …)
• Maintain urine output (0.5-1 ml / kg / h minimum)
• Treatment of arrhythmias and conduction associated.

The phenomena of electrical stimulation:
The cells are pacemakers in the sinus node, the atrioventricular node and atrioventricular bundle (bundle of His). The sinus node is located in the wall of the right atrium. It is the primary pacemaker center: typically, the sinus node depolarizes spontaneously 70 times per minute, and mark the pace of all contractile cells.



This characteristic rhythm is called sinus rhythm and determines the basal heart rate.
The sinus node, the action potential (AP) propagates through the atria, where he borrows the internodal tract of the heart connecting the sinoatrial node to the atrioventricular node. (time: 0.04 s). At this node, the impulse is delayed by 0.1 s, allowing the atria complete their contraction. Then, the PA traverses the atrioventricular bundle, located in the interventricular septum, which ends in Purkinje fibers (also called cardiac conduction myofibres). The latter enter the apex and back into the walls to cause ventricular contraction. (T 0.22 s on average a healthy heart).


In case of failure of the sinus node, the atrioventricular node sets the rhythm at 40-60 beats per minute: this is called r ythme nodal rhythm.

Electrocardiogram:
To record the ECG, using 12-lead standard that provide a comprehensive picture of cardiac activity. Typically, it consists of 5 types of waves:

• The P wave of low amplitude due to depolarization of the atria, caused by the sinus node and has a duration of approximately 0.08 s.
• The QRS complex formed waves Q, R, S is related to the ventricular depolarization and a period of 0.08 s. The atrial repolarization is hidden
• T wave is caused by ventricular repolarization duration of 0.16 s.

All chest pain event related to a “narrowing of the size” of one or more coronary arteries. The coronary arteries are the arteries that supply blood to the heart muscle.

Clinical Data

Clinical examination was unremarkable.
The resting ECG was completely normal except for a painful crisis.
Any interrogation can find angina:
with chest pain to left arm
to pain on exertion and rest
pain in 3 to 4 minutes,
took to heart in a vise.

Pathophysiology

Suffering infarction: ischemia is associated with a mismatch between needs and the oxygen supply of heart muscle:
is the input can not increase in proportion to needs: angina of effort
is in constant need, contributions are reduced: spastic angina.
The decrease in arterial size is secondary to a “collection” by atherosclerotic plaques.

Definition of risk factors for cardiovascular

No tobacco
No diabetes
No dyslipidemia,
No hypertension
No overweight
No heredity
No inactivity.

Methods of diagnosis
Physical examination and ECG are quite normal, thus not contributing outside of a crisis.

Further examination

• Stress Test,
• scintigraphy,
• stress echocardiography,
• angiography.

Stress Test

On bicycle ergometer or treadmill.
Maintain a constant pedaling speed while pedaling resistance is overcome by increased every 2 minutes.
The goal is to increase the intake of myocardial O 2 and leading to a mismatch between needs and contributions, thus triggering pain and ECG changes.

Myocardial scintigraphy

Uses of the exercise test.
Using isotopes: technetium or technetium MIBI.
Check whether there are differences in determining the isotope of the photographic effort and after 4 hours of redistribution.

Coronary

Opacification of coronary arteries using a contrast agent based on iodine.
First, femoral, radial or humeral priority.
Lets make a simple “inventory” of places of the coronary circulation, therefore best to discuss the establishment of a treatment.

Coronary Anatomy

Presence of 3 coronary arteries:
_ The interventricular anterior
_ circumflex artery,
_ right coronary artery.

Treatment

• Medical:
  • nitrates,
  • Anti-calcium,
  • potassium channel activator,
  • beta-blockers,
  • antiplatelet,
  • statins, lipid-lowering,
• Percutaneous trans-luminal
• Bypass surgery.

Prejudices

Fight against cardiovascular risk factors:

• smoking cessation,
• equilibration Diabetes
• lipid-lowering diet,
• weight loss,
• fight against physical inactivity.

I-The pericardium:

The outer core is called the pericardium, made of dense and strong, protecting the heart, then two layers, one parietal and other visceral, defining a virtual cavity, where the cells produce pericardial fluid in serous for lubrication.

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II-The myocardium.

This is the tunic “through” the heart, composed mainly of cardiac muscle cells, and has the capacity to contract. They are entangled in a network of elastic fibers of connective tissue, forming the cardiac fibrous skeleton, thicker in places to form rings of support around the perimeter of valves and points of emergence of the great vessels.

III-The endocardium.

Corresponds to the inner layer made of a squamous epithelium, lining the heart chambers and is continuous with the endothelium of large vessels.

IV-cavities and great vessels.

The heart has four chambers, two atria and two ventricles.

From the right atrium entering three veins: the superior vena cava blood of bringing the regions above the diaphragm, the vena cava, bringing blood to areas under the diaphragm, and the coronary sinus, reducing the blood used by the myocardium itself.

From the left atrium arrive four pulmonary veins (attention to the confusion, however, the pulmonary veins bring oxygenated blood, but should not be called pulmonary arteries, which they bring the vitiated blood to the lungs).

Circulatory level, there are the lesser circulation or pulmonary circulation and the systemic circulation or systemic circulation:

The right heart is the pump of the pulmonary circulation, the oxygen-poor blood enters through the right atrium, then descends into the right ventricle, which propels the blood into the pulmonary trunk, from which both pulmonary arteries which carry the blood to cells. Then he goes back through the pulmonary veins to reach the left heart.

The left heart is the pump from the systemic circulation: the oxygen-rich blood from the lungs enters the pulmonary veins by the left atrium, before being expelled by the ventricle into the aorta, from which all branches to the different systems. Then he goes back through the venous system via the vena cava, the right heart.

The V-valve system.

Like any pump, the heart can not ensure its effectiveness in the presence of anti-reflux system, a role held in by four heart valves, two atrio ventricular valves, the aortic valve and the pulmonary trunk.

Atrio ventricular valves are located at the junction between the atrium and ventricle. The atrioventricular valve right ventricle, tricuspid valve is called the left is called bicuspid. Thin White cords of collagen anchor the valves and thus allow the sealing of these, but also prevent a reversal of the valve in his headset.

The valve of the aorta and pulmonary trunk has a role to prevent reflux into the ventricles