Shock - Hypovolemic: Nursing

Hypovolemic shock is a life-threatening condition characterized by a decrease in intravascular volume in the cardiovascular system, which becomes insufficient to support adequate perfusion of the body tissues.

Now, let’s talk about the physiology of the cardiovascular system, which consists of the heart and blood vessels. The main job of the heart is to pump oxygenated and nutrient-rich blood through the arteries to the body tissues, and receive deoxygenated blood through the veins and pump it to the lungs to pick up more oxygen.

For this to be possible, there are three key factors to keep in mind: the cardiac output, which is the amount of blood pumped out by the heart per minute; the intravascular volume, which is the amount of blood in the client’s circulation; and the peripheral vascular resistance, which is the resistance of blood flow in peripheral arteries.

Normally, oxygen is delivered to the tissues because there’s enough pressure in the cardiovascular system to push blood through the body; so, blood pressure has a major effect on the amount of blood that reaches tissues and organs. For the most part, blood pressure is regulated by changes in peripheral vascular resistance and cardiac output, so that if one of them decreases, the other increases to try to compensate.

So, hypovolemic shock is caused by a significant decrease of intravascular volume, and can be classified as hemorrhagic and non-hemorrhagic. Hemorrhagic shock is the most common, and it’s usually caused by severe bleeding from postpartum hemorrhage, gastrointestinal bleeding, or traumatic injuries. On the other hand, non-hemorrhagic hypovolemic shock can be caused by anything that results in significant fluid loss, such as vomiting or diarrhea; renal losses, such as excessive diuresis in diabetic ketoacidosis or diabetes insipidus; excessive sweating, like in hyperthermia or hyperthyroidism; or third-spacing, which includes anything that causes intravascular fluid to shift into the interstitial space, like burns or acute pancreatitis.

Risk factors to look out for in hypovolemic shock include any conditions that could potentially worsen a hemorrhage, like having a clotting disorder or liver problems, as well as taking antiplatelet medications like aspirin, or anticoagulant medications like warfarin. Additional risk factors include anything that increases the risk of dehydration, such as persistent vomiting or diarrhea.

Now, the pathology of hypovolemic shock develops from a loss of intravascular volume, which in turn decreases the blood pressure and the venous return to the heart, decreasing cardiac output. So, in order to increase cardiac output, the body responds by releasing hormones into the bloodstream. This includes catecholamines such as epinephrine and norepinephrine which cause vasoconstriction, increase heart rate and contractility to maintain blood pressure and increasing blood flow; as well as ADH, which acts on the kidneys, increasing fluid retention and angiotensin II, which also constrict the blood vessels and causes sodium retention in the kidneys, raising blood pressure. As a result, the body may initially compensate by increasing peripheral vascular resistance and blood pressure, as well as the cardiac output. Additionally, vasoconstriction in the kidneys causes them to produce less urine in an attempt to retain as much fluid as possible, and thus maintain the intravascular volume.

However, if shock isn’t addressed quickly, these compensatory mechanisms may not be able to maintain blood pressure, and as a result, perfusion to the tissues decreases even more. If this occurs, the organs won’t get enough oxygenated blood, so they’ll need to switch to anaerobic metabolism, which eventually leads to metabolic acidosis, or excess acid in the body, leading to hyperventilation, confusion, or death, if severe. Finally, if shock persists for too long, vital organs such as the brain, heart, and kidneys may begin to shut down, leading to multiple organ failure.

The clinical manifestations of hypovolemic shock depend on the severity of the intravascular volume loss. During the initial stage, compensatory mechanisms such as increased heart rate and vascular constriction are sufficient to maintain cardiac output within the normal range. Cardiac output can best be seen by obtaining the mean arterial pressure, or the average pressure in one cardiac cycle, because it is a more accurate indicator of perfusion than a normal blood pressure measurement. In this stage, the MAP is decreased by less than 10 mmHg from baseline. Clients may experience tachycardia, but compensatory mechanisms keep blood pressure at around the normal range, so it may be difficult to detect shock at this stage.

During the compensation stage, the compensatory mechanisms are fully active but the MAP is decreased and is about 10-15 mmHg below baseline. The client’s skin can become cold and clammy, indicating that blood flow is being redirected to vital organs like the brain and heart. Other symptoms include pallor, severe hypotension and tachycardia, decreased peripheral pulses, and oliguria.

In the progressive stage, clients can develop organ failure because the compensatory mechanisms can no longer guarantee adequate blood flow to vital organs. The MAP is sustained at more than 20 mmHg below baseline. The client can experience anxiety, altered level of consciousness, cyanosis, increased respirations, decreased oxygen saturation from lung failure, profound hypotension, bradycardia, and irregular heart rhythm from heart failure, as well as anuria, which occurs due to kidney failure.

In the refractory stage, cell death occurs in the vital organs due to the lack of oxygen reaching the tissues. The MAP is still sustained at more than 20 mmHg from baseline. At this point, the damaged organs cannot respond to treatment, leading to multiple organ dysfunction. The client may experience a sudden loss of consciousness, shallow respirations, unmeasurable oxygen saturation, non-palpable pulses, or death.

The diagnosis of hypovolemic shock starts with the client’s history and physical assessment. The assessment identifies signs of hypoperfusion, including a drop in oxygen saturation, low or declining blood pressure, sudden changes in the ECG, or decreased urinary output. Additionally, laboratory tests can reveal decreased oxygen levels, metabolic acidosis, increased lactate levels, and coagulation abnormalities, which can be helpful to determine the evolution of shock and efficacy of treatment. Finally, imaging techniques, such as an ultrasound, chest X-ray, or CT scan can be performed to look for an internal source of hemorrhage.