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The best approach to prevent measles is by active immunization. Ever since the introduction of the vaccine in the developed world, there has been a marked reduction in the incidence of measles, however, there are still some reported cases of the disease in low-incidence areas, usually imported from other countries by travelers. Because of this possible re-introduction of the virus, it is important to maintain a high level of immunity among the population in order to prevent outbreaks.

• The vaccination is generally not given earlier than this because children younger than 18 months usually retain anti-measles immunoglobulins (antibodies) transmitted from the mother during pregnancy.
• A "booster" vaccine is then given between the ages of four and five.
• Vaccination rates have been high enough to make measles relatively uncommon.
• Even a single case in a college dormitory or similar setting is often met with a local vaccination program, in case any of the people exposed are not already immune.

Measles vaccine (contained in MMR, MR and measles vaccines) can prevent this disease. The MMR vaccine is a live, attenuated (weakened), combination vaccine that protects against the measles, mumps, and rubella viruses. It was first licensed in the combined form in 1971 and contains the safest and most effective forms of each vaccine. It is made by taking the measles virus from the throat of an infected person and adapting it to grow in chick embryo cells in a laboratory. As the virus becomes better able to grow in the chick embryo cells, it becomes less able to grow in a child’s skin or lungs. When this vaccine virus is given to a child it replicates only a little before it is eliminated from the body. This replication causes the body to develop an immunity that, in 95% of children, lasts for a lifetime. A second dose of the vaccine is recommended to protect those 5% who did not develop immunity in the first dose and to give "booster" effect to those who did develop an immune response.

Children should get 2 doses of MMR vaccine

• The first dose at 12-15 months of age
• The second dose at 4-6 years of age

These are the recommended ages. But children can get the second dose at any age, as long as it is at least 28 days after the first dose.

Adults DO NOT need the measles, mumps, rubella vaccine (MMR) if:

• Blood tests show immunity to measles, mumps, and rubella.
• You are a man born before 1957.
• You are a woman born before 1957 who is sure she is not having more children, has already had rubella vaccine, or has had a positive rubella test.
• You already had two doses of MMR or one dose of MMR plus a second dose of measles vaccine.
• You already had one dose of MMR and are not at high risk of measles exposure.

Adults SHOULD get the measles vaccine if you are not among the categories listed above, and:

• You are a college student, trade school student, or other student beyond high school.
• You work in a hospital or other medical facility*.
• You travel internationally, or are a passenger on a cruise ship.
• You are a woman of childbearing age.

Random notes

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CS Ultrasound: Echocardiography is an important imaging modality in the evaluation of the patient with cardiogenic shock. In cardiogenic shock complicating acute-MI, findings such as poor wall motion may be identified. Mechanical complications such as papillary muscle rupture, pseudoaneurysm, and a ventricular septal defect may also be visualized. Valvular heart disease such as aortic stenosis, aortic insufficiency and mitral stenosis can also be assessed. Dynamic outflow obstruction such as HOCM can also be indentified and quantified. The magnitude of left ventricular dysfunction in patients with cardiomyopathy can be evaluated. It allows the clinician to distinguish cardiogenic shock from septic shock and neurogenic shock. In septic shock, a hypercontractile ventricle may be present.

• Differential diagnosis - "Cardiogenic shock may be difficult, at least initially, to distinguish from hypovolemic shock. Both forms of shock are associated with decreased cardiac output and compensatory upregulation of the sympathetic response. Both entities also respond initially to fluid resuscitation. The syndrome of cardiogenic shock is defined as the inability of the heart to deliver sufficient blood flow to meet metabolic demands. The etiology of cardiogenic shock may be intrinsic or extrinsic. In Case 1 , the development of class IV shock may be due to hemorrhage, such as an aortic injury, or may be cardiogenic, such as a myocardial contusion from blunt injury to the chest. Echocardiography would evaluate the possibility of intrinsic or extrinsic myocardial dysfunction. Intrinsic causes of cardiogenic shock include myocardial infarction, valvular disease, contusion from thoracic trauma, and arrhythmias. For patients with myocardial infarction, cardiogenic shock is associated with loss of greater than 40% of left ventricular myocardium. The normal physiologic compensation for cardiogenic shock actually results in progressively greater myocardial energy demand that, without intervention, results in the death of the patient . A decrease in blood pressure activates an adrenergic response that leads to increased sympathetic tone, stimulates renin-angiotensinaldosterone feedback, and potentiates antidiuretic hormone secretion. These mechanisms serve to increase vasomotor tone and retain salt and water. The resultant increase in systemic vascular resistance and in left ventricular end-diastolic pressure leads to increased myocardial oxygen demand in the face of decreased oxygen delivery. This, in turn, results in worsening left ventricular function, a perceived reduction in circulating blood volume, and repetition of the cycle."

Cardiogenic shock and Inflammatory Mediators

The Pathophysiologic "Spiral" of Cardiogenic shock

Among patients with acute MI, there is often a downward spiral of hypoperfusion leading to further ischemia which leads to a further reduction in cardiac output and further hypoperfusion. The lactic acidosis that develops as a result of poor systemic perfusion can further reduce cardiac contractility. Reduced cardiac output leads to activation of the sympathetic nervous system, and the ensuing tachycardia that develops further exacerbates the myocardial ischemia. The increased left ventricular end diastolic pressures is associated with a rise in wall stress which results in further myocardial ischemia. Hypotension reduces epicardial perfusion pressure which in turn further increases myocardial ischemia.

Patients with cardiogenic shock in the setting of STEMI more often have multivessel disease, and myocardial ischemia may be present in multiple territories. It is for this reason that multivessel angioplasty may be of benefit in the patient with cardiogenic shock.

The multifactorial nature of cardiogenic shock can also be operative in the patient with critical aortic stenosis who has "spiraled": There is impairment of left ventricular outflow, with a drop in cardiac output there is greater subendocardial ischemia and poorer flow in the coronary arteries, this leads to further left ventricular systolic dysfunction, given the subendocardial ischemia, the left ventricle develops diastolic dysfunction and becomes harder to fill. Inadvertent administration of vasodilators and venodilators may further reduce cardiac output and accelerate or trigger such a spiral.

Pathophysiologic Mechanisms to Compensate for Cardiogenic shock

Cardiac output is the product of stroke volume and heart rate. In order to compensate for a reduction in stroke volume, there is a rise in the heart rate in patients with cardiogenic shock. As a result of the reduction in cardiac output, peripheral tissues extract more oxygen from the limited blood that does flow to them, and this leaves the blood deoxygenated when it returns to the right heart resulting in a fall in the mixed venous oxygen saturation.

Pathophysiology of Multiorgan Failure

The poor perfusion of organs results in hypoxia and metabolic acidosis. Inadequate perfusion to meet the metabolic demands of the brain, kidneys and heart leads to multiorgan failure.

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Differential Diagnosis

Classification of shock based on hemodynamic parameters. (CO, cardiac output; CVP; central venous pressure; PAD, pulmonary artery diastolic pressure; PAS, pulmonary artery systolic pressure; RVD, right ventricular diastolic pressure; RVS, right ventricular systolic pressure; SVO2, systemic venous oxygen saturation; SVR, systemic vascular resistance.)

Type of Shock	Etiology	CO	SVR	PCWP	CVP	SVO2	RVS	RVD	PAS	PAD
Cardiogenic	Acute Ventricular Septal Defect	↓↓	↑	N — ↑	↑↑	↑ — ↑↑	N — ↑	↑	N — ↑	N — ↑
	Acute Mitral Regurgitation	↓↓	↑	↑↑	↑ — ↑↑	↓	↑	N — ↑	↑	↑
	Myocardial Dysfunction	↓↓	↑	↑↑	↑↑	↓	N — ↑	N — ↑	N — ↑	↑
	Right Ventricular Infarction	↓↓	↑	N — ↓	↑↑	↓	↓ — ↑	↑	↓ — ↑	↓ — ↑
Obstructive	Pulmonary Embolism	↓↓	↑	N — ↓	↑↑	↓	↓ — ↑	↑	↓ — ↑	↓ — ↑
	Cardiac Tamponade	↓ — ↓↓	↑	↑↑	↑↑	↓	N — ↑	↑	N — ↑	N — ↑
Distributive	Septic Shock	N — ↑↑	↓ — ↓↓	N — ↓	N — ↓	↑ — ↑↑	N — ↓	N — ↓	↓	↓
	Anaphylactic Shock	N — ↑↑	↓ — ↓↓	N — ↓	N — ↓	↑ — ↑↑	N — ↓	N — ↓	↓	↓
Hypovolemic	Volume Depletion	↓↓	↑	↓↓	↓↓	↓	N — ↓	N — ↓	↓	↓