Two factors determine oxygen delivery to tissues: (1) arterial oxygen content and (2) cardiac output. If there is normal oxygen delivery, then there will be enough oxygen content in the blood. Sufficient cardiac output means that there is adequate, appropriate blood flow distributed to the tissues. 

A healthy child maintains a higher oxygen concentration in the arterial circulation than the body needs. If an increase in oxygen demand ensues, the tissues utilize the excess oxygen in arterial blood. An increased oxygen demand will result in a reduced oxygen concentration of the arterial and venous circulation. Hypoxemia may still be apparent despite normal oxygen delivery if there is a compensatory increase in cardiac output. 

The central venous oxygen saturation (ScvO₂) assesses the balance between oxygen delivery and tissue demands. Monitoring the ScvO₂ of the patient in shock is just as crucial as monitoring arterial oxygen saturation.

If metabolic demand and oxygen content are constant, a fall in ScvO₂ indicates a drop in cardiac output because the tissues will pull out more oxygen to make up the deficit. As a result, less oxygen is left in the central venous blood entering the right side of the heart.  

The hemoglobin concentration represents the amount of oxygen in red blood cells. Chronic hypoxemia induces additional hemoglobin production so that the oxygen-carrying capacity of the body increases. This increases arterial oxygen to near-normal levels, even when the hemoglobin’s oxygen saturation is low, such as in cases of cyanotic congenital heart disease.

Cardiac Output

Cardiac output is a measure of blood flow to the tissues. Stroke volume and heart rate determine cardiac output. Stroke volume is the amount of blood that is ejected by the left ventricle after each contraction. Preload, contractility, and afterload are the prime determinants of stroke volume. 

The most common cause of compromised stroke volume is an inadequate preload. Hemorrhage, severe dehydration, or vasodilation are common causes of insufficient preload. Central venous pressure (CVP) monitoring can evaluate the status of the patient’s right ventricular preload.

Related Video – What is Cardiac Output?

Poor cardiac contractility also compromises stroke volume and results in cardiogenic shock. Myocardial dysfunction impairing cardiac contractility may be caused by myocarditis, hypoglycemia, or the ingestion of toxic substances (e.g., a calcium channel blocker overdose). 

Increased afterload can also cause a low stroke volume. An afterload increase creates resistance to flow after each contraction. Medical conditions such as pulmonary stenosis or systemic hypertension can cause increased afterload. One of the treatment regimens of cardiogenic shock is to reduce afterload. 

In general, an increase in stroke volume or heart rate increases cardiac output. However, if the heart rate is too fast, there may be insufficient time for the left ventricle to fill adequately, causing a significant decrease in stroke volume and thus a reduction in cardiac output. 

Vascular resistance can restrict blood flow to essential tissues and negatively affect tissue perfusion. If the blood vessel has a large diameter, then vascular resistance is low. If the diameter of blood vessels is small, then vascular resistance is high. Blood vessels can change their diameter based on the metabolic demands of the tissues. They increase in size if more blood flow is necessary and decrease when less blood flow is required. An abnormality in diameter (vasodilation or vasoconstriction) can compromise tissue perfusion despite adequate cardiac output.

Compensatory Mechanisms in Shock

The body works to improve tissue perfusion and oxygen delivery by increasing:

• Heart rate
• Systemic vascular resistance (SVR)
• The strength of cardiac contractions 
• Venous smooth muscle tone

Tachycardia is the first compensatory mechanism observed when a child is in shock. The heart rate goes up in an effort to increase cardiac output. The body then tries to divert blood flow to vital organs by selectively increasing vascular resistance in nonessential tissues. Clinically, the patient will have cool extremities and weak peripheral pulses as the body continues to direct blood flow preferentially to the heart and brain and perfusion to the kidneys declines, causing reduced urine output.

Related Video – What is the Cardiac Output Formula?

Effect on Blood Pressure

Two factors determine blood pressure: (1) cardiac output and (2) SVR. If there is a problem with cardiac output, the body increases the SVR to maintain the blood pressure. Children in shock will maintain normal or even slightly higher blood pressure in this way. 

Patients in shock will have a narrow pulse pressure if the compensatory increase in SVR causes the systolic and diastolic blood pressures to be closer to each other. For patients with sepsis, SVR is low, and diastolic blood pressure will significantly decrease compared to systolic blood pressure, and thus pulse pressure widens during sepsis. 

Tissue perfusion may be inadequate when there is a normal blood pressure because cardiac output in shock is still decreased despite increased SVR. Therefore, even though the patient has a normal to slightly elevated blood pressure, lactic acidosis and end-organ dysfunction remain significant concerns.

As shock progresses due to low cardiac output, SVR increases until it causes ischemia, and then blood pressure eventually declines. This advanced stage of shock means that oxygen delivery to the tissues is severely compromised. Patients will present with metabolic acidosis and other signs of end-organ failure. Advanced shock can lead to a depressed level of consciousness, decreased urine output, and myocardial ischemia or infarction. The result is often cardiac arrest and irreversible end-organ injury.