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Increased urine output. In shock, particularly during the compensatory stage, urine output typically decreases as the body attempts to conserve fluids. Increased urine output would not be expected in this context.

Pale, mottled, or cyanotic skin. These skin changes are more characteristic of the progressive or irreversible stages of shock, indicating severe hypoperfusion and tissue hypoxia. In the compensatory stage, the skin is usually cool and pale, but not yet mottled or cyanotic.

Stupor and loss of reflexes. These neurological changes are more typical of the later stages of shock when perfusion to the brain is severely compromised. In the compensatory stage, mental status changes may be present but are less severe.

Afterload x preload. Afterload and preload are important factors influencing cardiac function but do not directly calculate cardiac output. Afterload refers to the resistance the heart must overcome to eject blood, and preload refers to the initial stretching of the heart muscle prior to contraction.

Ejection fraction x blood pressure. Ejection fraction is a measure of the percentage of blood ejected from the heart with each beat, and blood pressure is the force exerted by circulating blood on the walls of blood vessels. These factors influence cardiac function but do not directly calculate cardiac output.

Systolic x diastolic BP. Systolic and diastolic blood pressure are measurements of pressure during heartbeats and between beats, respectively. They are not used to calculate cardiac output.

Decreased systemic vascular resistance, decreased CVP. In hypovolemic shock, the body compensates by increasing systemic vascular resistance to maintain blood pressure. Therefore, decreased systemic vascular resistance is not consistent with hypovolemic shock. Central venous pressure (CVP) would be low due to reduced blood volume.

Increased systemic vascular resistance, increased CVP. While systemic vascular resistance increases, CVP is typically decreased in hypovolemic shock due to the lack of circulating blood volume.

Decreased systemic vascular resistance, increased CVP. Decreased systemic vascular resistance and increased CVP are not consistent with hypovolemic shock. These parameters might be seen in conditions with different hemodynamic profiles.

Rapid infusion of normal saline. While fluid resuscitation is important in managing anaphylactic shock, it is not the initial therapy of choice. Epinephrine should be administered first to counteract the allergic reaction.

Dobutamine. Dobutamine is used to support cardiac function in certain types of shock but is not the first-line treatment for anaphylactic shock.

Norepinephrine. Norepinephrine is a vasopressor used to treat severe hypotension and shock but is not the initial treatment for anaphylactic shock. Epinephrine is preferred to address the allergic reaction.
 

Oliguria. Oliguria, or reduced urine output, is a manifestation that occurs later as shock progresses and renal perfusion decreases. It is not typically seen in the initial stage of shock.

Hypotension. Hypotension generally appears in the compensatory and progressive stages of shock as the body's compensatory mechanisms begin to fail. In the initial stage, blood pressure may still be maintained by compensatory mechanisms.

Respiratory alkalosis. Respiratory alkalosis is more likely to occur during the compensatory stage of shock due to hyperventilation as the body attempts to compensate for hypoxia. It is not anticipated in the initial stage of shock.

Cyanosis. Cyanosis, or a bluish tint to the skin, indicates significant hypoxemia or poor oxygenation. While it can occur in severe anaphylaxis, it is not a primary integumentary manifestation.

Petechiae. Petechiae are small, pinpoint hemorrhages under the skin and are not typically associated with anaphylactic shock. They are more related to conditions involving bleeding or clotting disorders.

Ecchymosis. Ecchymosis, or bruising, is not a characteristic manifestation of anaphylactic shock. It is more related to trauma or bleeding disorders.

Respiratory acidosis. Respiratory acidosis occurs when there is inadequate ventilation, leading to increased carbon dioxide levels in the blood. Hyperventilation would not cause respiratory acidosis.

Metabolic acidosis. Metabolic acidosis results from an accumulation of acid or loss of bicarbonate in the body. It is typically seen in the later stages of shock when lactic acid builds up due to anaerobic metabolism.

Metabolic alkalosis. Metabolic alkalosis occurs due to an excessive loss of acids (e.g., through vomiting) or an accumulation of bicarbonate. Hyperventilation does not cause metabolic alkalosis.