Shock defines a state of inadequate oxygen delivery to the tissues of the body. This can result from decreased tissue perfusion, or from inadequate blood oxygen content.
Shock defines a state of inadequate oxygen delivery to the tissues of the body. This can result from decreased tissue perfusion, or from inadequate blood oxygen content. Decreased tissue oxygen delivery results in tissue hypoxia and forces the cells to shift from aerobic respiration to anaerobic respiration for energy (ATP) production. Anaerobic respiration is less efficient than aerobic respiration and results in the generation of lactate and a systemic acidosis.
Lactate levels are expected to increase in any patient when the tissue demand for oxygen (oxygen consumption, VO2) exceeds the oxygen delivery (DO2). The level at which anaerobic respiration begins to produce measurable lactate concentrations is termed the critical oxygen delivery level (DO2crit). Lactate may also increase if an animal is struggling during venipuncture, and may result in an artificially increased value. Despite the possibility of hyperlactatemia with normal tissue perfusion, a finding of elevated lactate should prompt a more thorough survey for possible sources of hypoperfusion. Animals who have decreased tissue oxygen delivery due to decreased circulating hemoglobin (eg. from an acute hemolytic crisis) will also display hyperlactatemia.
The oxygen content of the blood is an equation with two components:
Hence, the overall equation for oxygen content of arterial blood (CaO2) is:
CaO2= 1.34 [Hb] * SaO2 + 0.003 * PaO2
This equation highlights the relative importance of hemoglobin levels in determining the oxygen content of the blood; the partial pressure of dissolved oxygen is important, but it contributes very little to the final CaO2 (although it does have an effect on the SaO2). Normal [Hb] is 15 g/dL, and normal PaO2 is 90 mm Hg, giving a normal CaO2 around 20.4 mL O2/dL
Pairing the oxygen content of blood with the rate at which it is delivered to the tissues (represented by cardiac output (Q)) gives the formula for oxygen delivery (DO2):
DO2 = Ca O2 * Q
Cardiac output is composed of two components: heart rate, and stroke volume, thus:
Q = HR * SV
If an animal needs to increase cardiac output, there are three ways that this may be accomplished: an increase in heart rate, an increase in stroke volume, or an increase in both.
Types of shock (with reference to above)
The classification of the different types of shock helps to describe individual mechanisms for syndromes of decreased oxygen delivery seen in veterinary patients. Although these describe generally discrete conditions, it is also possible to have more than one type of shock occurring at the same time.
Hypovolemic shock is one of the most common manifestations of shock seen in veterinary medicine. Perfusion is disturbed in these patients due to ineffective circulating blood volume (or, a low Q because of low stroke volume). Causes of hypovolemia include hemorrhage as well as third space losses such as edema or ascites. Animals with significant vomiting or diarrhea, or those with an obligate dieresis (e.g. from diabetes mellitus) may also become hypovolemic due to continued loss of fluid by these mechanisms.
Cardiogenic shock is caused by ineffective cardiac output, either due to decreased heart rate (e.g. third degree AV block) or decreased stroke volume (e.g. from dilated cardiomyopathy). This type of shock can be caused by myocardial failure, cardiac arrhythmias, or by cardiac tamponade as might be caused by a pericardial effusion. Regardless of cause, forward flow of blood from the heart is compromised. In addition, the backup of blood flow in the heart can cause pulmonary edema (congestive heart failure), and lead to a secondary hypoxic shock.
Distributive shock indicates a maldistribution of systemic blood flow. Under normal conditions, the vasculature and microvasculature vasoconstrict and vasodilate to meet individual tissue needs. In distributive shock, widespread vasodilation occurs, creating a relative hypovolemia. The primary cause of distributive shock in small animal patients is septic shock, although animals experiencing anaphylactic shock also have uncontrolled vasodilation.
Metabolic shock refers to any condition where the tissues of the body have an nadequate supply of nutrients for cellular energy production, but can also include scenarios where the cells are unable to use the delivered oxygen and nutrients. Patients with hypoglycemia are unable to create adequate cellular ATP levels because they have no substrate for the Krebs cycle. Patients with cyanide toxicity also technically have metabolic shock, as they have adequate oxygen delivery to the mitochondria, but are unable to use the electron transport chain to manufacture ATP.
Hypoxic shock is a decrease in the oxygen content of arterial blood (CaO2). This may be seen in patients with severe respiratory disease (low PaO2 and SaO2) or in patients with low blood oxygen content due to anemia (low Hb). Cellular energy generation is impaired due to lack of oxygen. This category can also include diseases with dysfunctional hemoglobin such as methemoglobinemia, or that caused by carbon monoxide inhalation, which impairs the ability of the hemoglobin to carry oxygen molecules.
Obstructive shock describes conditions where blood flow to a particular organ or organs is disturbed. Animals with thromboembolic disease or those with caval syndrome due to heartworm disease fit into this category. Some authors will also include diseases such as gastric dilatation volvulus (GDV) in this category due to the inhibition of adequate return of blood flow by the gas-filled stomach. Pericardial effusion is also included in this category sometimes due to the fact that the effusion is obstructive to adequate cardiac filling.
Diagnosis of shock
The clinical signs of shock reflect attempts by the body to maintain or regain homeostasis in the face of decreased oxygen delivery to the tissues. Cardiac output increases to maintain oxygen delivery, and patients with shock are usually tachycardic. Depending on the cause of shock, and the time course, cardiac stroke volume may be increased as well. In some animals where the ability to increase stroke volume is limited (e.g., pericardial effusion), an increased heart rate is the only way the heart can increase cardiac output. In cats who are experiencing shock due to a severe inflammatory stimulus (e.g., sepsis), they are equally as likely to be bradycardic on presentation to the hospital. A cat that is found to be bradycardic on initial physical exam warrants a thorough investigation into the possibility that systemic inflammation is present.
One method by which the body can increase the stroke volume is to increase the amount of blood that is returned to the heart (venous return). Vasoconstriction in some tissue beds (especially at the periphery) will increase the blood volume circulating in the central circulation. Animals with systemic vasoconstriction may display pale mucous membranes, and the extremities may be cold to the touch. By contrast, animals with septic (distributive) shock will frequently have bright red mucous membranes, reflecting uncontrolled (and inappropriate) vasodilation. CRT in patients with compensated distributive shock is usually faster than normal, which reflects both vasodilation and an increased cardiac output.
Impaired oxygen delivery results in an elevation of circulating plasma lactate concentrations. As a lactic (metabolic) acidosis develops, the body attempts to return the pH to normal by exhaling carbon dioxide. Decreased CO2 results from an increased respiratory minute volume (RMV = respiratory rate * tidal volume). Thus, many animals with shock will have elevated respiratory rates. Elevated respiratory rates can also be seen due to hypoxemia, as well as with elevated body temperature or endotoxemia.
Acidosis and decreased tissue oxygen delivery affect body systems beyond the cardiorespiratory system. The cells of the gastrointestinal mucosa have a high metabolic rate and consequently are very sensitive to decreases in oxygen supply. Animals with shock may show signs of small intestinal cell death (e.g., diarrhea) on presentation, or after they have been resuscitated. Severe acidosis may also cause ileus of the movement of the gastrointestinal track. This may predispose the patient to emesis or regurgitation, which may cause esophagitis or aspiration pneumonia. Decreased oxygen delivery to the liver can cause hepatocellular damage, leading to elevations in the hepatic enzymes (esp. alanine amino-transferase (ALT) and aspartate aminotransferase (AST)).
Decreased renal perfusion will lowers glomerular filtration rate (GFR) and cause elevations in serum urea nitrogen (BUN) and creatinine levels. Additionally, with decreased GFR, urine output will decrease, and renal failure may ensue. The kidney will activate the renin/angiotensin and aldosterone systems, causing the retention of sodium, and a modest degree of vasoconstriction, to help systemic perfusion.
Therapy for shock and hyperlactatemia consists of normalizing oxygen delivery. Therapies are directed towards the underlying cause; hypovolemic shock is treated by restoring circulating blood volume. Cardiogenic shock may be treated by the administration of drugs to increase cardiac output. Hypoxic shock is treated by improving blood oxygen content (e.g., with a blood transfusion), or improving blood oxygen levels (e.g., by use of oxygen cages or mechanical ventilation). Obstructive shock is treated by removing the obstruction (e.g., aspiration of a pericardial effusion). Distributive shock does not lend itself to a straightforward therapy. Vasoconstriction using either adrenergic drugs (e.g., dopamine) or non-adrenergic drugs (e.g., vasopressin) is usually necessary, in addition to normalization of intravascular volume and therapy for the inciting cause of the distributive dysregulation (e.g. surgery to remove the source of sepsis). Regardless, knowledge of how disease affects systemic oxygen delivery can lead to successful and tailored therapy of patients with shock.