Review Question - QID 100610

The clinical scenario is consistent with a patient in hypovolemic shock. Increased stroke volume is not a characteristic of hypovolemic shock.

Hypovolemic shock is characterized by increased systemic vascular resistance, decreased cardiac output, decreased stroke volume, decreased pulmonary capillary wedge pressure, and decreased central venous pressure. Fluid resuscitation with normal saline will reverse the process of hypovolemic shock, and lead to an increase in stroke volume (actively bleeding patients may also require blood transfusions).

Swedberg et al. report that shock is a consequence of insufficient blood flow for adequate oxygenation at the cellular level. Effective management of shock states includes early recognition and prompt volume repletion. Adequate arterial PO2 is also essential for maintaining appropriate cellular oxygenation.

Hanft et al. discuss the relationship between sarcomere length and cardiac function. Cardiac output is fine-tuned by ventricular filling volume, whereby an increase in end-diastolic volume leads to an appropriate increase in stroke volume. An increase in filling volume (i.e. preload) will stretch the myocytes leading to an increase in sarcomere length.

Illustration A depicts the changes in a sarcomere with increased or decreased ventricular filling. Illustration B shows the pathophysiology of hypovolemic shock in flow-chart form.

Incorrect Answers:
Answer 1: Confusion and irritability are common mental status changes seen in states of acute hemorrhagic shock.
Answer 2: Decreased preload would be expected with hypovolemic shock secondary to acute hemorrhage.
Answer 4: Decreased preload leads to decrease in sarcomere length.
Answer 5: Thomboxane A2 is a known vasoconstrictor that is important during tissue injury and inflammation and should be elevated in hemorrhagic shock.