The aim of this article is to update the status of cardiogenic shock in particular detail in their diagnosis and especially in its current treatment on the stage of emergency. It was through the analysis of review articles that treat this condition as the main topic.

1. Update on diagnosis and management of emergencies in cardiogenic shock.
MSC. Dr. Gustavo Moreno Martín Head teaching assistant. UNIANDES University.
Intensivist physician. Ambato, Ecuador
Email: morenogmartin@gmail.com
OVERVIEW
The aim of this article is to update the status of cardiogenic shock in particular detail in their diagnosis and especially in its current treatment on the stage of emergency. It was through the analysis of review articles that treat this condition as the main topic. Currently it is considered that cardiovascular diseases are one of the leading causes of death in the world, being acute myocardial infarction the main contributor to this condition causes. The State of cardiogenic shock is the most critical expression of ischemic heart disease by its high morbidity and mortality. Although it occurs in less than 10% of the patients with coronary syndrome, its mortality rate reaches more than 80% if it is not treated early and appropriately. The clinical manifestations of tissue hypoperfusion defined diagnosis, and hemodynamic measurements allow us to elucidate the etiology of the State of shock, confirm the diagnosis and determine the strategy to follow. The handling with Catecholamines and Phosphodiesterase inhibitors are useful in the treatment but only survival is modified with the prompt restoration of coronary flow by bypass surgery or percutaneous coronary intervention. The use of the intra aortic balloon is also indicated. The success of the treatment involves the timely detection of the State of shock and the immediate restoration of the vascular flow. The goal of any therapy will be restore blood flow and prevent future damage to vital organs.
Key words: SHOCK CARDIOGENIC/syndrome coronary diagnosis/treatment/Control acute hemodynamic.
INTRODUCTION
Shock syndrome is characterized by a disorder of systemic perfusion leading to widespread cellular hypoxia and dysfunction of vital organs.
Although the clinical situation of shock is usually accompanied by low blood pressure, both terms are not synonymous. Hypotension can be attended with normal tissue perfusion through the establishment of compensating mechanisms, on the other hand the shock can occur with normal voltage figures.
The associated mortality is high, increasing the number of affected organs (kidney failure, respiratory distress, liver failure, etc.) from 21% with an organ failure, up to 76% when four organ failure or more; It will be essential, at the same time which carry out the relevant diagnostic procedures to reach etiology that has triggered this acute situation, the introduction of therapeutic measures urgent to prevent the progression of the condition.
Cardiogenic shock is an extreme form of acute heart failure, which is characterized by the persistent and progressive fall of blood pressure, with general and severe decrease in tissue perfusion, beyond the limits compatible with the function of vital organs at rest.
Because cardiogenic shock continues to be a major cause of death in patients with all types of acute coronary syndromes, there is a growing interest in the identification of patients at risk of developing this complication, and exploration of different therapeutic approaches aimed at preventing its development and improve the outcome when the shock is installed.
It is estimated his presentation as a complication of acute coronary syndromes up to 10% of cases, notably in the ST-segment-elevation acute coronary syndromes. This behavior has stabilized in the past 30 years, however, mortality has been reduced to 40-50%; so has determined the timely and every day more qualified medical attention,

2. including the coronary intervention procedures that provide immediate restoration of coronary flow, not to mention new technologies in pharmaceuticals and devices that are available in recent years.
Leading to higher mortality risk factors include advanced age, female gender, diabetes and properly coronary disease infarction of anterior wall as well as the presence of multiple diseased coronary vessels.
DEVELOPMENT
Definition.
Cardiogenic shock syndrome is characterized by a low cardiac index (CI) and by the presence of signs of hypoperfusion organic, despite the existence of a suitable intravascular volume (table 1).
In the shock cardiogenic you can define two stages:
1) Incipient or preshock, in which there is an IC low with a high full of left ventricular pressure but no manifest hypotension.
2) Installed or manifest, when a low IC (< 1.8 l/mto/m2) and the high pressure in the left ventricle full (> 18mmHg) added a decrease in systolic blood pressure below 90 mmHg or 30mmHg below basal levels, for a time equal to or greater than 30 minutes. Table 1. Definition of cardiogenic shock.
Cardiogenic shock is defined by the presence of a systolic blood pressure of < 90 mmHg for more than one hour to:
 Does not respond to the administration of fluids.
 It is secondary to cardiac dysfunction.
 He is associated with signs of hypoperfusion or IC < 1.8 l/mto/m2 and a pulmonary capillary pressure > 18mmHg.
Other considerations in this definition include:
 Patients requiring administration of inotropic drugs for more than one hour to keep a systolic blood pressure > 90 mmHg.
 Patients who die within an hour of the onset of hypotension but who meet other criteria of cardiogenic shock.
Etiology.
Different causes that can lead to a deterioration of cardiac function in a manner sufficient to induce the clinical picture of cardiogenic shock, however the most common cause is acute infarction myocardial extensive (AMI) (table 2).
The prior existence of cardiac pathologies such as aortic stenosis (EA) or mitral (EM) or cardiomyopathies can make to the susceptible heart to an insult in form of an acute ischemia. Around 40% of patients with shock cardiogenic as a complication of an Ami have a prior infarct that limits your booking myocardial.
For the purposes of this article, only reference is made to the cardiogenic shock complicating acute myocardial infarction. The most common cause of cardiogenic shock in emergency and intensive care area is Ami, being injury necrotic myocardial, involving an extensive area of the left ventricle (VI) - usually greater than the 40%-the most frequent etiology within it.
Table 2. Etiology of cardiogenic shock.
IAM.
 Critical loss of mass myocardial ischemia of VI.
 Extensive engagement of the right ventricle (RV).
 Mechanical complications: acute mitral insufficiency, cardiac rupture of the free wall with cardiac tamponade, rupture of the interventricular septum.
 IAM associated with sepsis, bleeding, anaphylaxis.

3.  Administration of metoprolol IV immediately to an IAM (Studio COMMIT).
Heart disease associated with ventricular commitment.
 Final stage of dilated cardiomyopathy.
 Severe myocarditis.
 Phase of severe valvular heart disease myocardial.
 Tachyarrhythmias or bradycardias.
 Postoperative cardiovascular surgery.
Heart blockage.
 Severe pulmonary hypertension.
 Coarctation of the aorta.
 Myxomas.
 Hypertensive pneumothorax.
Myocardial contusion.
Myxedema.
Aortic dissection.
Metabolic disorders: hyperkalemia, acidosis, hypoxemia.
Pathophysiology.
Shock early.
Ami complicated with shock cardiogenic cause of hospital admission is between 10 and 15% of all patients with cardiogenic shock.
According to the study, MILIS, pretrombolitica era cardiogenic shock diagnosed before 24 hours of hospital admission was 50% of the total, in contrast to the results of studies TIMI 2 (25%) and taste-1 (only 10%), belonging to the thrombolytic era.
Patients who develop cardiogenic shock in the first 24 h are characterized by:
 History of disease coronary (EC) severe.
 Proximal occlusion of an artery main epicardial and absence of collateral circulation.
 Elevated CPK levels.
 Large necrotic commitment of VI in autopsies.
 IAM with multiple vessel disease with areas of extensive isquemia-necrosis conditions of severe left ventricular dysfunction.
Late shock.
This group includes the majority of the patients (coronary angioplasty or thrombolytic era) with cardiogenic shock produced by Ami, developing after 24 h of the diagnosis of Ami.
They involved a series of conditions regardless of their origin, will lead to a further decrease of blood pressure with decline in coronary perfusion and greater ischemia and LV systolic dysfunction, among these are:
 Extensive ischemic commitment of VI.
 Dysfunction systolic and/or diastolic myocardial stunning secondary to reperfusion injury.
 Reinfarction.
 Ischemia residual or recurrent.
 Mechanical complications.
Reversible myocardial dysfunction.
In the non-infarcted area and with normal or limited blood flow, metabolic and functional alterations are also produced. This reversible dysfunction is evidenced in two ways: stunned myocardium and myocardial hibernated.
Stunned myocardium.
It represents a postischemic dysfunction that persists despite the restoration of normal blood flow after reperfusion with fibrinolytics, coronary angioplasty (PTCA) or bypass

4. surgery. Eventually, however, the myocardial performance recovers completely. The pathogenesis of this lesion appears to involve a combination of oxidative stress, disruption of homeostasis of calcium, and decrease in the response of myofilaments to calcium, all in the context of a preceding ischemia. Stunning intensity is mainly determined by the severity of the previous ischemic insult.
Myocardial hibernated.
It is a State of persistent dysfunction at home due to a severe reduction in coronary blood flow. Inherent in the definition of hibernated myocardium is the concept that the function can be normalized if the blood flow is improved. The hibernation should be considered as an adaptive response to reduce the hipoperfundido myocardial contractile function and restore the balance between the demand and the supply of nutrients, reducing the potential risk of necrosis. Hibernated myocardial revascularization is an improvement of the function, which is associated with a better prognosis.
Because the therapeutic implications of these conditions, consideration of stunned myocardium and myocardial hibernated is vital in patients with cardiogenic shock. Hibernated myocardial revascularization improve and the stunned myocardium retains an inotropic reserve and can respond to stimulation with inotropes.
Inflammatory response in septic shock.
Cardiogenic shock, suggests that a systemic inflammatory response, activation of complement, release of Inflammatory Cytokines, nitric oxide synthetase, inducible expression, and inappropriate vasodilation can play an important role not only in the genesis of the shock but also in its evolution.
These observations indicate that the paradigm cardiogenic shock should be expanded.
By introducing the inflammation as one pathogenetic event in cardiogenic shock, new therapies aimed specifically against certain proinflammatory pathways, such as antagonists of nitric oxide, antibodies anti C5, tilarginina, and Statins can be evaluated in the treatment.
Clinical picture.
The diagnosis is made after documenting the presence of myocardial dysfunction and exclude alternative causes of hypotension, such as hypovolaemia, hemorrhage, sepsis, pulmonary embolism, tamponade, aortic dissection and pre-existing valvular disease.
Preshock stage.
It is characterized by:
 Volume cardiac minute under, expressed by oliguria and tachycardia.
 Pulmonary congestion by increased pressure from end of diastole of the VI.
A number of endogenous vasopressors, including norepinephrine and Angiotensin II, maintain systemic vascular resistance too high, so at this early stage is not manifested hypotension.
Installed shock stage.
All manifestations of the process, which include are put in evidence:
 Systolic arterial hypotension held below 90 mmHg, which is indicative of the seriousness of the box.
 Pulmonary edema. Pulmonary congestion by increased pressure from full of VI is evidenced through of the hemodynamic monitoring and confirms the diagnosis of cardiogenic shock due to infarction of VI, excluding other causes of shock.
 Signs of low minute volume. They include sinus tachycardia, decreased urine output below 30 ml/h, presence of cold extremities and alterations in sensorium including agitation, restlessness or obtundation.

5. Complementary examinations.
Electrocardiogram.
The most common electrocardiographic presentation corresponds to acute coronary syndrome with segment elevation ST (STEMI), mainly from the former location. Acute coronary syndrome without elevation ST (NSTEACS) may result in slightly less than a quarter.
The IAM, shock cardiogenic and complete left bundle branch block is a predictive picture of poor prognosis with high mortality. The full bundle branch block right from emerging in the course of an anterior Ami is also a very severe because it is usually proximal occlusion of the anterior descending coronary artery, similar prognosis has Ami's previous face evolving infradesnivel of ST-segment on the underside.
In the shock cardiogenic is common the presence of ventricular arrhythmias such as frequent extrasystoles or ventricular tachycardias held or not held, which have a worse prognosis when appear 48 h after diagnosis.
Rx's chest.
The radiological signs of hypertension pulmonary venocapilar in different grades, highlight the alteration to the left ventricular full or diastolic failure: redistribution of pulmonary flow (grade I), interstitial edema (grade II) and alveolar oedema (grade III)
Most of the patients in cardiogenic shock with an Ami without prior history of angina or heart attack, have a chest x-ray characterized by oedema of lung related cardiothoracic preserved (acute oedema of lung with heart boy).
Echocardiogram.
Echocardiogram at the head of the patient is of fundamental importance for the diagnosis of the shock and for the evaluation of both systolic and diastolic left ventricular function. The systolic function estimated by calculating the fraction of ejection or shortening of the left ventricle is a prognostic value parameter. It can be underestimated in the first hours or days due to the phenomenon of stunning ischemic infarction. Diastolic function is altered.
Transesophageal echo to the patient's bedside is useful to evaluate the function of the right ventricle, calculate pulmonary pressures, and diagnose other causes of shock as the dysfunction of the mitral subvalvular apparatus at any level as a cause of acute failure, septal and free wall rupture, and cardiac tamponade. In the presence of ventricular hiperdinamia, the concomitant presence of hypovolemia should be suspected.
Hemoquimica.
Hyperglycemia by increasing the discharge of Catecholamines and the consequent reduction of release of insulin by the pancreas less irrigation. There will be an increase in creatinine, uric acid, hepatic transaminases as well as CPK and CPK-MB and troponin values. However the increased serum lactate and deficit of bases, they constitute the only biomarkers recommended with high level of evidence in this situation, the improvement of its values are unequivocal data of the recovery of the tissue hypoperfusion.
The coagulograma can detect dependent coagulation factors decrease disorders, disorders of platelet function and disseminated intravascular coagulation.
On the ionogram can reveal hyperkalemia and increasing osmolarity (> 295mmol/l). There may be a metabolic or lactic acidosis.
TREATMENT.
The management of cardiogenic shock involves the use of a series of General measures, measures of hemodynamic monitoring and specific treatments (table 3).
Table 3. Management of cardiogenic shock.
General measures.
 Monitoring heart rate, blood pressure and ST segment.
 Central venous access.

6.  Blood oxygenation and tissue proper (ARM).
 Correction of acid-base balance and electrolyte abnormalities.
 Correction of the hypovolemia.
 Treatment of pain.
 Treatment of arrhythmias heart.
 Placement of external or temporary pacemaker if necessary.
 Platelet antiplatelet therapy with aspirin.
 Anticoagulation with heparin.
Optimization of the preload and afterload.
 Administration of fluids.
 Intravenous infusion of diuretics.
 Administration of vasodilators.
Correction of metabolic alterations.
 Administration of glucose - potassium (GIK) *.
Measures to improve the systolic function of the VI.
 Administration of inotropes.
 Aortic counterpulsation balloon.
 Restoration of coronary flow (reperfusion/revascularization).
Thrombolysis.
Transluminal coronary angioplasty (ATC)
Coronary artery bypass grafting (CABG)
Diagnosis and correction of mechanical dysfunction of cardiac structures.
 Severe mitral regurgitation.
 Ventricular septal defect.
 Free wall rupture.
* Currently there is no indication for use.
Correction of the hypovolemia.
The hypovolemia is present in 30% of patients with cardiogenic shock, being produced by vomiting, sweating, use of diuretics, etc.
If not are evident signs of heart failure, physical examination or pulmonary congestion in the chest x-ray, prior to placement of the pulmonary artery catheter can try infusion of 100-300 ml of physiological solution. If improvement of blood pressure and urine output you do not get a pulmonary artery catheter should be placed to locate the patient in one hemodynamic groups. This will allow to define the therapeutic strategy to follow. The optimal pulmonary wedge pressure is that which relates to the increased heart rate. Usually this value is between 15-20mmHg.
In cases of Ami of the RV by proximal occlusion of the right coronary artery, arterial hypotension is accompanied by signs of venous hypertension. In these cases the diagnostic confirmation with electrocardiogram, Echocardiogram and through the hemodynamic monitoring is very important, since these patients usually require larger amounts of fluid.
Correction of metabolic alterations.
In the thrombolytic era and the spreading of the percutaneous coronary intervention, solutions polyelectrolytic formerly used to prevent complications such as arrhythmias, are not recommended, alterations documented in lab tests as they arise and must be treated.
Despite the fact that in several small studies it was observed a favourable effect on the metabolism of ischemic myocardium, high-dose glucose infusion - potassium (GIK) had a neutral effect on mortality rates, stop heart and cardiogenic shock in more than 20,000 patients evaluated in the study CREATE-ECLA. Therefore, there is no indication for this therapy in STEACS.

7. Use of pacemakers.
The IAM's front face with second degree or third degree AV block can be taken in many cases States of shock, and others of the AV conduction disorders are usually due to necrosis of the system exito-conductor so always external pacemaker placement will be indicated. Not so true AV blocks advanced in Ami's underside, which are due to ischemia, reason by which can be delayed for the placement of these devices as the optimization of the treatment antisquemico usually recover the disorder.
Use of inotropic drugs and vasopresoras.
Alterations circulation produced in shock, particularly hypotension with hypoperfusion of vital organs, they can be corrected with pharmacological methods (sympathomimetic drugs) or non-drug (aortic counterpulsation balloon).
Catecholamines and other agents increase the minute cardiac volume in acute form, but there is no evidence that can improve survival. It is suggested that excess of Catecholamines in the pathogenesis of the shock can accelerate the dysfunction of myocardial, with the consequent need for an escalation of doses. Inotrope drugs may have a role in the stabilization of the patients during the evaluation and transfers, and in situations in which identifies a reversible etiology; However, as isolated treatment should be considered as purely palliative.
We then relate the effects that possess about the stimulation of receptors (table 4).
Table 4. Effects of inotropes and vasopressors on receivers.
Receiver
Heart
Systemic
Pulmonary
Splanchnic

Contraction.
Contraction.
Contraction.
Contraction.

-
Dilatation.
-
Dilatation.

Chrono/inot. +
-
-
-

Chronotope. +
Dilatation.
Dilatation.
Dilatation.
1
Dilatation.
Dilatation.
-
Dilatation.
2
-
Dilatation.
-
Dilatation.
Dobutamine (Dobutrex).
1. Is an amine synthetic sympathomimetic that produces a powerful non-selective stimulation of adrenergic receptors. In its complex mechanism of action involves two stereoisomers with different affinity for different adrenergic receptors.
2. The dose usually ranges between the 2.5-15mcg/kg/mto and may is increased until the 20mcg/kg/mto, this is achieved to increase cardiac contractility and heart rate. Recommended starting dose 2-3mcg/kg/mto be increasing according to the hemodynamic response. The systemic vascular resistance (SVR) decreases moderately or remain unchanged.
3. Useful in the temporary inotropic support in hypotensive patients with heart failure sharply Decompensated, where TA is close to or above the 90 mmHg.
4. In patients with marked hypotension, the initial effect on the TA can be unpredictable, in this scenario it must be used together with a vasopressor, or use must be rejected. In hypovolemic patients exacerbates hypotension.
5. As with other inotropic agents, the increase in oxygen consumption can trigger or worsen myocardial ischemia. Tachycardia and arrhythmias may limit the dose increases, usually appears tachycardia with doses greater than 10mcg/kg/mto.
6. Prolonged infusion is associated with tolerance and partial loss of its hemodynamic effects. Also appears hypersensitivity myocarditis when used for prolonged periods (hemodynamic deterioration and peripheral Eosinophilia).
7. The alkaline pH inactive drug by which should not administer concomitantly to solutions such as bicarbonate.
8. Its withdrawal should be gradual, because otherwise there may be a sharp downturn of the hemodynamic parameters.
9. It should not be used in case of high levels of betabloqueo.

8. 10. Increases the AV conduction in atrial fibrillation (AF).
11. Has effect relatively weak beta-agonist, with modest reduction in pulmonary arterial tension, which is eliminated by combining the drug with inhibitor of Phosphodiesterase (levosimendan).
Levosimendan (Simdax).
1. Sensitising agent of calcium, which increases contractility myocardial without increased demands or myocardial2, causes coronary and systemic vasodilation. It is a well-tolerated drug with few interactions and Arrhythmogenic. Its inotropic effect, is mediated during systole through changes in the concentration of Troponin C calcium-dependent conformation. Its vasodilator effect depends on the opening of channels of potassium on vascular smooth muscle.
2. Is a metabolite of long duration with persistent hemodynamic effect up to about a week. After the infusion, its effect is persistent and requires can return again to dobutamine, at lower doses in order to wean definitely inotropic drugs.
3. In practice, it will be necessary to increase the dose of noradrenaline around 20% when you infuse levosimendan to hold the values of TA.
4. Begins to start with bolus IV 6-12mcg/kg administered in 10 minutes of continuing with a continuous infusion of 0.05-0.2mcg/kg/min. Bolus IV is optional since it may favor a significant hypotension.
5. Is useful in treatment of short-term failure cardiac acute (IC), associated with systolic dysfunction along with regular medication (ACE Inhibitors, diuretics, digoxin), when required without severe hypotension and inotropic support.
6. Although experience is limited, can be administered jointly to beta-blockers and other inotropes, resulting in additive effect.
7. Systolic less than 85mmHg are not recommended for use in patients with TA.
8. Is contraindicated for use in mechanical obstructions that hinder the ventricular filling-emptying, as well as patients with a clearance of creatinine clearance less than 30 ml/mto, severe liver damage, severe hypotension, tachyarrhythmias and history of torsion of tips.
Dopamine (Intropin).
1. It is an endogenous catecholamine, works as a synthetic precursor and central neurotransmitter norepinephrine in the path of synthesis of Catecholamines.
2. Stimulates receptors dopaminergic and adrenergic depending on the dose used, also stimulates the release of norepinephrine from nerve endings.
3. Dose:
  < 3mcg/kg/mto, leads to increase of splanchnic perfusion with limited effect on diuresis, without renal protective effect.
 3-10mcg/kg/mto, effect positive greater than dobutamine chronotope.
  > 10mcg/kg/mto, increases the RVS through peripheral vasoconstriction, this effect begins to occur with doses greater than 5mcg/kg/mto.
4. In the critical patient susceptibility to each dose is each patient's own, therefore using this drug should be titrated according to the hemodynamic response and not the numerical dose.
5. When we use dopamine, pulmonary artery wedge pressure measurement is not reliable since dopamine increases the same.
6. Not used as inotrope in patient with heart failure, only to increase RVS if it is decreased, and at a rate of > 10 mcg/kg/mto.
7. Dopamine currently not recommended at low doses (2mcg/kg/mto) as treatment to improve renal function in patients critically ill (including sepsis).
8. As agent with inotropic activity and vasopresora, moderately high doses has the versatility to be used as first line in unexplained hypotension. Or in combination

9. with other inotropes, moderate doses of dopamine, can be useful in hypotensive patients with sharply Decompensated HF management.
Epinephrine (Adrenalin).
1. Is a beta-agonist, dobutamine as endogenous catecholamine, producing relatively balanced between vasoconstriction and vasodilation effects. This balance is due to having equal and high affinities for1-β receptors, β2 and 1.
2. Low-dose β2 receptors are very sensitive to adrenaline and produce receivers increasing doses, systemic vasodilationΒ 1 activated and increases contractility and heart rate. At higher doses it appears the effect alfaagonista with vasoconstriction and increased blood pressure and heart rate.
3. Due to their adverse effects on splanchnic and renal blood flow, as well as the potential to induce tachyarrhythmias or myocardial ischemia, has been considered a drug of second line in the management of hypotension in septic shock.
4. Can be diluted in saline solution.
5. Dose:
 I stop cardiorespiratory (PCR): 1 mg/3-5mtos.
 Bradycardia: 2-10mcg/mto in continuous infusion.
 Anaphylaxis: 0.5-0. 3 mg intramuscular (IM) (1:1000) each 20mto, 0. 1 mg (1:10000) in 5mto, 1-4mcg/mto in continuous infusion.
Norepinephrine (Levophed).
1. Natural catecholamine effect on receptor  y. To differs from the adrenaline, β receptors are less sensitive to it and its effects in the clinic are mainly due to the activation of receptors .
2. Clinically differs from the adrenaline in his little effect in a wide range of doses, on heart rate, without losing in reality its inotropic effect much. Its main effect is then to increase the PAM.
3. Norepinephrine increases systolic and diastolic pressures, and in general, differential pressure.
4. Cardiac output remains unchanged or is decreased, and systemic peripheral resistance increases.
5. Increases splanchnic, renal vascular resistance, liver and striated muscle.
6. Increases coronary flow in significant degree, however in patients with Prinzmetal angina reduces coronary flow in a meaningful way.
7. Dose: 10-30mcg/mto (0.5-2mcg/kg/mto).
8. Is the drug of choice in septic shock (TA < 70mmHg).
Vasopressin (Pitressin).
1. Vasopressin or aintidiuretica hormone, has been one of the newest agents added to the arsenal available for treatment of hypotension (most recent levosimendan), their mechanism of action until recently little not was very clear. It operates through three different G-protein receptors called V1a, V1b and V2.
 V1a: Is located in the muscle cells smooth, half vasoconstriction through Phospholipase C and causes release of calcium by way of the phosphoinositol.
 V1b: Located in pituitary and half the production of ACTH through system G-protein and increase of intracellular camp.
 V2: Located in cells of the renal tubular manifold system. Half the reabsorption of water through increase of camp and adenylyl, which induces phosphorylation of aquaporins and formation of apical channels of water.

10. 2. In pathological conditions as in the case of shockhypovolemic, cardiac arrest, septic, shockshock cardiac post-surgery, refractory hypotension in patients under treatment with angiotensin-converting enzyme inhibitors or milrinone; shown partial deficiency or inappropriate levels of circulating vasopressin. Under these conditions despite the resuscitation maneuvers like repletion of volume, agents vasopressors such as norepinephrine or inotropes such as dobutamine, it's not possible to revert the State of shock patients and it has been shown that vasopressin through continuous intravenous infusions supplementation improves significantly the evolution of the sick.
3. Doserecommended in States of shock: 0.02 to 0.04 international units (IU) day in continuous infusion.
4. In PCR (Asystole/AES) can be administered a dose of 40UI instead of the first or second dose of epinephrine.
5. Large infusion rate, increases the risk of adverse effects related to the power of the drug as a vasoconstrictor, among these effects is ischemia myocardial, cutaneous, splanchnic, liver failure, pulmonary hypertension and platelet aggregation.
Isoproterenol (Isuprel).
1. Receptors, adrenergic stimulant (3-1 and 3-2, resulting in a rise in cardiac output, pulse pressure increases due to the increase in systolic pressure and the diastolic decrease).
2. Relaxing the pulmonary vasculature and bronchial smooth muscle.
3. Has very little affinity for receptors to.
4. Myocardial oxygen demands increase and also shortens the diastolic filling time, decreasing the coronary perfusion pressure.
5. Signs:
 Bradycardia with hemodynamic compromise, on a temporary basis while stands pacemaker (temporary or definitive).
 Status asthmaticus and pulmonary hypertension; It reduces postoperative pulmonary hypertension.
 Refractory twisted tips tachycardia, transient control in bradycardia with hemodynamic compromise in denervated hearts for transplant patients, while the pacemaker is installed.
6. Dose:Infusion 0.01mcg/kg/mto, can be adjusted to the desired effect. Kids: infusions of 0.05 to 0.1mcg/kg/mto.
7. Among the adverse effects issinus tachycardia, ventricular tachycardia, ischemia of the myocardium and acute infarction myocardial (AMI). Others are palpitations, headache, flushing, nausea, tremor, dizziness and weakness.
Phenylephrine (Neo-Synephrine).
1. Amine synthetic sympathomimetic that selectively stimulates adrenergic receptors, causing arterial vasoconstriction-dependent dose.
2. Is an interesting alternative in cases where tachyarrhythmias prevent the use of other agents.
3. High doses may cause excessive vasoconstriction, patients with LVEF committed can not tolerate it due to the increase of the post-load.
4. Dose: bolus of IV 50mcg, 100-180mcg/mto infusion, the usual dose once has fallen the TA is 40-60mcg/mto.
SELECTION OF FIRST-LINE AGENT.
So far there are no controlled studies on a large scale on the pharmacological management of hypotension. The consensus recommendations are based on small clinical studies and animal. Table 5 relate to the most common conditions that can be

11. processed with hypotension and first-line agent to use in each case. Below are some helpful considerations:
1. Taking advantage of the Pressor and inotropic properties of dopamine, moderate dose can be a reasonable choice in the initial handling of unknown cause hypotension. In the case of severe hypotension (systolic TA < 70mmHg), an adrenergic agonist effect more potent as norepinephrine may be considered.
2. Norepinephrine may be amine Pressor of choice in the management of vasodilation in septic shock.
3. In the moderately hypotensive patient, with commitment to the systolic function of the left ventricle (LVEF), dobutamine is the drug of choice. In Frank cardiogenic shock, or the combination of vasodilatation with pump failure, dopamine can be used as a single agent or in combination with other drugs such as dobutamine.
4. Vasopressin has emerged as an adjunctive agent useful for the treatment of the septic patient with hemodynamic collapse resistant to traditional sympathomimetics.
Table 5. Hemodynamic profile of hypotension and agent to be used in first line.
Cause of hypotension
Favorite actor
Unknown.
Dopamine.
Hypovolemia.
-
IC sharply unbalanced.
Dopamine-dobutamine.
Cardiogenic shock.
Dopamine.
Sepsis (hiperdinamia).
Norepinephrine-dopamine.
Sepsis with LVEF decrease.
Norepinephrine-dopamina+dobutamina.
Anaphylaxis.
Epinephrine.
Anesthesia-induced hypotension.
Phenylephrine.
Table 6 relate to the main inotropic agents according to their hemodynamic profile. Table 6. Inotropes and hemodynamic profile.
Drug
Cronotropismo
Inotropismo
Vasoconstriction
Vasodilation
Dopamine
++
++
++
-
Dobutamine
+
++++
+
++
Norepinephrine
++
++
++++
-
Adrenaline
++++
++++
++++
+++
Isoproterenol
++++
++++
-
++++
COMPLICATIONS.
The positive inotropic and vasopressor pose a potential of considerable toxicity mediated by the same mechanisms that produce the increase in Mt. They should be used with extreme caution and the lowest dose that maintains an adequate organ perfusion.
 Tachycardia or tachyarrhythmias may limit its use in patients with known heart disease.
 Commitment of LVEF resulting from the increase of the post-load or secondary to ischemia may develop.
 Ischemia myocardial may be due to vasoconstriction coronary or more commonly by increase in oxygen demand.
 Excessive arterial vasoconstriction may compromise the splanchnic perfusion and renal, and can occur in ischemia and necrosis in distal areas.
Monitoring.
 Patients should be treated in the emergency scenario, ensuring continuous monitoring of heart rate and urine output and arterial oxygenation.

12.  Intra-arterial catheterization and direct monitoring of the TA, is suggested during the prolonged use of vasopressors.
 Careful intravascular volume resuscitation and resuscitation with fluids are essential, as many patients with hypotension can stabilize only with the administration of fluids and use of vasopressors in hypovolaemia may worsen the tissue perfusion. Central or arterial venous catheter pulmonary to monitor pressures at those levels, is useful in many cases, however, the routine use of invasive hemodynamic monitoring is not necessary and can be harmful.
 Although the TAM in 60mmHg is usually required to maintain the self-regulation of the flow to vital organs, some patients require values higher or lower pressure. It is essential to monitor other indicators of global and regional as the level of consciousness and urine perfusion. Venous saturation of oxygen, serum lactate levels and by tonometry gastric intramucosal pH monitoring, can be helpful but its routine use is not recommended.
With few exceptions, these drugs have short half life, with a fast start and end of their pharmacological actions. Usually they begin without placing bowling IV and its decrease or abrupt withdrawal should be avoided to prevent a rebound hypotension.
These drugs show considerable variation in the initial dose required to properly restore the hemodynamics.
You should pay attention to potential drug interactions:
 Recent or current treatment with adrenergic antagonists may cause resistance to the action of dobutamine.
 Patients treated with MAOIS may experience an exaggerated response to some catecholamines, and must be treated with very low doses at the beginning.
These agents must generally be administered through a central venous catheter through an infusion or syringe infusion pump. In the event of extravasation of a vasopressor, an adrenergic antagonist in the area can infiltrate to limit local vasoconstriction and possible tissue necrosis.
CONCLUSIONS
Cardiogenic shock remains a condition of interest in the field of emergency, it is vital for the sake of a lower mortality, directly proportional stage to early diagnosis and effective treatment. Therefore, the current goal is early detection and even forecast the State of shock in patients with acute coronary syndromes. This goal will be accomplished only with the comprehensive care of the basic working group (physician, internist, clinical cardiologist and interventionist and intensivist) which will provide all available therapies in order to ensure a hemodynamics suitable to the patient, and primarily the recovery of blood flow in occluded coronary vessels.
REFERENCES
1. Report who (2009). Available at: URL: http://www.who.int/cardiovascular_diseases/en/
2. Nieminen MS, Bo¨hm M, MR Cowie, Drexler H, GS Filippatos, Jondeau G, et to the. (2005) Guidelines for the diagnosis and treatment of acute heart failure, European Society of Cardiology. European Heart Journal.
3. Van de Werf F, Bax J, Betriu A, Blomstrom-Lundqvist C, creates F, Falk V, et to the.(2009). guides for practice clinic of the European society of Cardiology (ESC). Management of acute myocardial infarction in patients with persistent ST-segment elevation. Revista Española de Cardiología.

13. 4. King SB III, Smith SC Jr., Hirshfeld JW Jr., Jacobs AK, Morrison DA, Williams DO. (2008). 2007 focused update of the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: (2007 Writing Group to Review New Evidence and Update the 2005 ACC/AHA/SCAI Guideline Update for Percutaneous Coronary Intervention). Journal of the American College of Cardiology
5. Antman EM, Hand M, Armstrong PW, Bates ER, Green, Halasyamani LK, et to the. (2008). 2007 focused update of the ACC / AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction). Journal of the American College of Cardiology.
6. Saunders, P (2011). Cardiovascular Medicine (8to Ed). Philadelphia.
7. Jessup M, Borozena S. (2003). Heart Failure. New England Journal of medicine, 348:2007-18.
8. Stomel, RJ, et to the. (1994). Treatment Strategies for Acute Myocardial Infarction Complicated by Cardiogenic Shock in a Community Hospital. Magazine Chest, 105 (4): 997-1002.
9. Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats TG, et to the. (2009). 2009 Focused update ncorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the International Society for Heart and Lung Transplantation. Journal of the American College of Cardiology.
10. McLaughlin VV, Archer SL, DB Badesch, Barst RJ, Farber HW, Lindner JR and et to the. (2009). 2009 ACCF/AHA expert consensus document on pulmonary hypertension to report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents and the American Heart Association developed in collaboration with the American College of Chest Physicians; American Thoracic Society, and the Pulmonary Hypertension Association. Journal of the American College of Cardiology.
11. F Haddad, Ashley EA, Michelakis E. (2010). New insights for the diagnosis and management of right ventricular failure, from molecular imaging to targeted right ventricular therapy (Unpublished manuscript). Boston, USA.
12. H. Mann, Nolan P. (2011). Update on the management of cardiogenic shock. Curr Opin Crit Care 12:431.
13. Jeger R., Harkness S., Ramanathan K. (2006). Emergency revascularization in patients with cardiogenic shock on admission: a report from the SHOCK trial registry and. European Heart Journal. 27:664.
14. White H., Assmann S., Sanborn T. (2005). Comparison of percutaneous coronary intervention and coronary artery bypass grafting after acute

14. myocardial infarction complicated by cardiogenic shock. Circulation 112:1992.
15. Sutton A., Hall j., Harcombe A. (2005). Predictors of outcome after percutaneous treatment for cardiogenic shock. Circulation 91: 339.