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There have been reported different stages of MERS-CoV infection in the discovered cases. These may range from asymptomatic patients to critically ill patients. According to the underlying comorbitdities of each patients, along with the evolution of the disease, there may be reported several complications, involving other organs systems, including:

• Acute respiratory distress syndrome
• Acute kidney injury
• Pericarditis

• Disseminated intravascular coagulation

Temporary

According to the progression of the disease, the physical findings will change and are usually suggestive of respiratory infection. However, in critically ill patients other systems may be affected, in which case, physical evaluation may include extrapulmonary findings. These findings may be suggestive of:

• Acute kidney injury
• Pericarditis
• Disseminated intravascular coagulation
• Shock

Vital Signs

• Hypotension
• Tachycardia
• Tachypnea, with evidence of increased respiratory effort
• Fever
• Decreased oxygen saturation

Most patients with MERS-CoV infection have been severely ill with pneumonia and acute respiratory distress syndrome, and some have had acute kidney injury [4,26,31-33,36,44,74]. Many patients have required mechanical ventilation and some have required extracorporeal membrane oxygenation. Other clinical manifestations that have been reported are gastrointestinal symptoms (anorexia, nausea, vomiting, abdominal pain, diarrhea), pericarditis, and disseminated intravascular coagulation [26,27,31,36,44]. Among 12 critically ill patients, 11 had extrapulmonary manifestations including shock (in 11) and acute kidney injury (in 7) [74]. One immunocompromised patient presented with fever, diarrhea, and abdominal pain but without early respiratory symptoms; pneumonia was identified incidentally on a chest x-ray [31,36].

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 — ↓	↓	↓