Anomalous trichromacy
Anomalous trichromacy is the mildest type of color deficiency, but the severity ranges from almost dichromacy (strong) to almost normal trichromacy (mild). In fact, many mild anomalous trichromats have very little difficulty carrying out tasks that require normal color vision and some may not even be aware that they have a color vision deficiency. The types of anomalous trichromacy include protanomaly, deuteranomaly and tritanomaly. It is approximately three times more common than dichromacy. Anomalous trichromats exhibit trichromacy, but the color matches they make differ from normal trichromats. In order to match a given spectral yellow light, protanomalous observers need more red light in a red/green mixture than a normal observer, and deuteranomalous observers need more green. This difference can be measured by an instrument called an Anomaloscope, where red and green lights are mixed by a subject to match a yellow light. Based on affected cone
There are two major types of color blindness: difficulty distinguishing between red and green, and difficulty distinguishing between blue and yellow. These definitions are based on the phenotype of the partial colorblindness. Clinically, it is more common to use a genotypical definition, which describes which cone/opsin is affected. Red–green color blindness
Red-green color blindness includes protan and deutan CVD. Protan CVD is related to the L-cone and includes protanomaly (anomalous trichromacy) and protanopia (dichromacy). Deutan CVD is related to the M-cone and includes deuteranomaly (anomalous trichromacy) and deuteranopia (dichromacy). The phenotype (visual experience) of deutans and protans is quite similar. Common colors of confusion include red/brown/green/yellow as well as blue/purple.
Care is directed to the dysfunctional organs (dialysis for the kidneys, mechanical ventilation for lungs dysfunction).Mortality rates have been decreasing in the United States. This is likely due to the rapid identification and treatment of the CS. Some studies have suggested that this possibly related to the increased use of coronary reperfusion strategies, like heart stents. Nonetheless, the mortality rates remain high. Multi-organ failure is associated with higher rates of mortality. Signs and symptoms
The presentation is the following:
Anxiety, restlessness, altered mental state due to decreased blood flow to the brain and subsequent hypoxia. Low blood pressure due to decrease in cardiac output. A rapid, weak, thready pulse due to decreased circulation combined with tachycardia. Cool, clammy, and mottled skin (cutis marmorata) due to vasoconstriction and subsequent hypoperfusion of the skin. Distended jugular veins due to increased jugular venous pressure. Oliguria (low urine output) due to inadequate blood flow to the kidneys if the condition persists. Rapid and deeper respirations (hyperventilation) due to sympathetic nervous system stimulation and acidosis. Fatigue due to hyperventilation and hypoxia. Absent pulse in fast and abnormal heart rhythms. Pulmonary edema, involving fluid back-up in the lungs due to insufficient pumping of the heart. Causes
Cardiogenic shock is caused by the failure of the heart to pump effectively. It is due to damage to the heart muscle, most often from a heart attack or myocardial contusion. Other causes include abnormal heart rhythms, cardiomyopathy, heart valve problems, ventricular outflow obstruction (i.e. systolic anterior motion (SAM) in hypertrophic cardiomyopathy), or ventriculoseptal defects.