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The Middle East respiratory syndrome coronavirus (MERS-CoV) is an emerging type of coronavirus, specifically a betacoronavirus of the lineage C. The MERS-CoV is a single stranded, positive sense virus, whose genome contains 30.119 nucleotides and encodes for structural and nonstructural proteins. The structural proteins located at the 3' end of the RNA chain are also seen in the genome of other coronaviruses and may include:

• Nucleocapsid protein.
• Glycoprotein for cell entry.
• 2 membrane proteins for virus structure and assembly.

Until May 23rd 2013, MERS-CoV was being described as a SARS-like virus or colloquially as "Saudi SARS. Since then it is known to be distinct, not only from SARS-CoV, but also from other known endemic coronaviruses, such as betacoronavirus HCoV-OC43 and HCoV-HKU1, as well as from the common cold coronavirus.

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Interspersed between and within these four structural proteins are five accessory proteins that are unique to MERS-CoV. Accessory proteins are encoded by all coronaviruses, are not essential for virus replication, may be structural or non- structural, and can be deleted without af- fecting pathogenesis (for examples, see references 7 and 8). A few are apparently involved in facilitating virus assembly or in immunoevasion, but the functions of the others are not known (9). MERS-CoV accessory proteins share no homology with any known host or virus protein, other than those of the closely related BtCoV-HKU4 and -HKU5 strains of bat coronavirus (4).

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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 — ↓	↓	↓