Circulatory shock (Proceedings)
In general, shock is defined as abnormal oxygen delivery and/or oxygen utilization at the tissue level. Oxygen delivery to the tissues is one of the primary functions of the cardiopulmonary system and of primary importance to the patient manifesting signs of circulatory failure.
In general, shock is defined as abnormal oxygen delivery and/or oxygen utilization at the tissue level. Oxygen delivery to the tissues is one of the primary functions of the cardiopulmonary system and of primary importance to the patient manifesting signs of circulatory failure. If the defect in the transport of oxygen to the vital tissues can be identified and removed while the patient is supported, recovery is possible. Oxygen delivery is dependent on cardiac output (heart rate and stroke volume) and arterial oxygen content (hemoglobin concentration, hemoglobin saturation, and dissolved oxygen in the plasma). These proceedings will specifically focus on the cardiac output causes of shock, which leads to circulatory shock, and will not discuss the causes of shock caused by alterations in arterial oxygen content.
Pathophysiologic factors leading to shock
Based upon the definition of shock, oxygen delivery and cardiac output, there are several factors that can lead to circulatory shock:
1. Heart rate alterations
a. Severe tachycardia
b. Severe bradycardia
c. Arrhythmias
2. Decreased stroke volume
a. Inadequate preload (hypovolemia, inappropriate vasodilation)
b. Reduced myocardial contractility (DCM, sepsis)
c. Reduced myocardial relaxation (HCM, pericardial effusion)
d. Increased afterload (aortic stenosis, systemic hypertension)
Signs of circulatory shock
When focusing on just the cardiac output side of the oxygen delivery equation, circulatory shock is divided into 3 major classifications: cardiogenic shock (pump failure), hypovolemic shock (loss of effective circulating volume) and distributive shock (uneven distribution of blood flow). Though the mechanisms for each are distinctly different, each results in reduced oxygen delivery to tissues. Each type of shock stimulates the body to release neurohormones in an attempt to maintain blood pressure. Recall that blood pressure is the product of cardiac output and systemic vascular resistance. The primary systems that are stimulated are the renin-angiotensin-aldosterone system, release of antidiuretic hormone (vasopressin), and release of epinephrine/norepinephrine which will work in concert to retain water, retain sodium, vasoconstrict, increase heart rate, and increase cardiac contractility. When these neurohormonal systems are working properly, the animal compensates for the low blood pressure and oxygen delivery and is able to maintain homeostasis to some degree. However, if the compensatory shock stage is overlooked and the cause of the shock is progressive, then the animal can no longer compensate for the shock and decompensatory shock ensues. Signs of compensatory shock and decompensatory shock are important to recognize in order to treat an animal properly. Almost all signs of shock are secondary to epinephrine/norepinephrine release secondary to decreased oxygen delivery, hypotension, and possibly pain.
1. Signs of Compensatory Hypovolemic Shock
• Tachycardia
• Pale mucous membranes
• +/- Prolonged CRT
• Tachypnea
• Blood pressure is frequently normal to high in this stage
• Frequently mentally alert and able to walk around
2. Signs of Compensatory Cardiogenic Shock
• Tachycardia
• Pale mucous membranes
• +/- Prolonged CRT
• Tachypnea
• Respiratory distress if in CHF
• Blood pressure may be low in this stage due to pump failure
• Frequently mentally alert
3. Signs of Decompensatory Hypovolemic and Cardiogenic Shock
• Tachycardia
• Pale/White MM
• Prolonged CRT
• Tachypnea/Respiratory distress
• Weak pulses/Hypotension
• Hypothermia/Cold extremities
• Mental dullness
• Low urine output
4. Signs of Early Distributive Shock in Dogs
• Tachycardia
• Injected/Red mucous membrane
• Quick CRT
• Tachypnea
• Bounding pulses/Hypotension
• Pyrexia/Warm extremities
5. Signs of Late Distributive Shock in Dogs
• CRT prolongs
• Hypotension worsens
• Hypothermia
• Mental dullness
6. Signs of Distributive (Septic) Shock in Cats
• Bradycardia* (major difference compared to dogs)
• Pale/White MM
• Prolonged CRT
• Tachypnea
• Weak pulses/Hypotension
• Hypothermia/Cold extremities
• Mental dullness
Hypovolemic shock
The primary defect in hypovolemic shock is an inadequate circulating volume. This can be from sudden massive blood loss as in surgery or trauma, or fluid loss from vomiting, diarrhea, renal disease, severe burns, or severe respiratory water losses. Because cardiac output relies on stroke volume and heart rate, the patient with inadequate volume will be tachycardic in an attempt to compensate. Neurohormonal pathways detecting a drop in blood pressure will lead to increased vascular tone in an attempt to shunt circulation from the periphery to vital tissue beds. This results in cool extremities, tachycardia, prolonged capillary refill, oliguria and weakness.
Treatment should be directed at the primary source of fluid loss while correcting the fluid deficit. Crystalloid fluids can be used initially to restore circulating volume. Crystalloids will improve cardiac output and should not be withheld for fear of diluting the red blood cell mass. Oxygen delivery is a function not only of oxygen content but of cardiac output as well.
With a treatment goal of improving oxygen delivery to the tissues we can increase cardiac output by increasing stroke volume (fluids). Oxygen content can be increased by increasing the hemoglobin concentration (Red cell transfusion) and increasing oxygen saturation (Oxygen supplementation).
Volumes of fluid for resuscitation should be tailored to the individual patient. Shock doses of crystalloid fluids are based upon blood volumes. A full shock dose in the dog is 90 ml/kg/hr and in the cat it is 45-60 ml/kg/hr. Generally, it is best to start with ¼ shock dose over 10-15 minutes and titrate the fluids to effect. A full shock dose of fluids is often more than enough fluid and in extremely debilitated patients may lead to fluid overload (pulmonary and cerebral edema). Response to treatment should result in stronger pulses, a slower heart rate, improved mucous membrane color, improved capillary refill time, and improved mentation. If the patient is not responding, then continue with another ¼ shock dose.
Following the second dose of fluids the packed cell volume and total solids should be compared to pre-fluid values. If a patient receiving large quantities of crystalloids becomes anemic or hypoproteinemic, the fluid should be switched to an appropriate colloid such as whole blood, packed red blood cells, plasma or a synthetic product like hetastarch or dextrans. If the total solids has dropped to less than 50% of pretreatment a colloid should be considered for further resuscitation. If the PCV has dropped precipitously, whole blood and a search for the source of blood loss is indicated. Often, in the case of traumatic hemorrhage, correction of blood loss and pressure can open torn vessels leading to more hemorrhage. Therefore close attention is important.
Once the shock is controlled, fluid deficits can be replaced along with maintenance volumes and ongoing losses over the course of one to two days.
Cardiogenic shock
Cardiogenic shock occurs when the pumping function of the heart is severely impaired leading to circulatory failure. As with hypovolemic shock, the patient will be tachycardic, weak, oliguric, have cool extremities and weak pulses. The patient with cardiac failure may also have evidence of cardiac disease with a murmur, ascites, jugular venous distention, pulmonary edema, pleural effusion or cardiac arrhythmias. The primary defect in oxygen delivery is a reduced cardiac output. Stroke Volume is determine by preload, afterload, relaxation and contractility. Within limits, cardiac output increases as heart rate increases. Very high heart rates actually decrease cardiac output by impairing cardiac filling and subsequently stroke volume. Excessively fast heart rates may be the result of cardiac arrhythmias or physiologic responses to low volume. Specific anti-arrhythmic therapy and correction of underlying causes of tachycardia should be used to normalize heart rate. Clinically significant bradyarrhythmias are less common but include sick sinus syndrome and third degree atrioventricular block. It is uncommon for these slow heart rates to require emergency treatment. Often these patients have compensated with increased stroke volume and can be referred for pacemaker treatment.
Stroke volume is dependent upon four determinants of cardiac function: Preload, afterload, relaxation, and contractility. With congestive heart failure, the pump is failing due to decreased contractility or relaxation. The body attempts to compensate by increasing pre-load (sodium and fluid retention). Normally, the heart is able to pump all fluid presented to it through the Frank-Starling mechanism (increase stretch leading to increased contractility) so that by increasing pre-load, the heart will increase stroke volume. With failure however, the excess fluid cannot be moved and accumulates downstream of the failing ventricle. This results in pulmonary edema in the case of left-ventricular failure and ascites, pleural effusion and hepatic congestion in the case of right-ventricular failure.
Stroke volume (and cardiac output) can be maximized by recognizing and treating the primary defect. In the case of congestive failure, pre-load can be optimized by monitoring central venous pressure, administering diuretics like furosemide and venodilators such as nitroglycerine. With obstructive failure as is seen with pericardial effusion, removal of even a small amount of pericardial fluid will relieve the pressure on the right ventricle and allow more normal filling. Cardiac output can also be enhanced by decreasing afterload with calcium channel blockers or ACE inhibitors. These are especially useful in treating failure due to mitral insufficiency where contractility may be normal to increased but the cardiac output is going backwards into the left atrium instead of to systemic circulation. In documented myocardial failure, contractility can be enhanced with positive inotropic drugs such as digoxin or dobutamine.
Distributive shock
Distributive shock is probably the most challenging of the shock syndromes and one of the most difficult to reverse. The defect with distributive shock is an abnormal or systemic vasomotor response leading to peripheral vasodilation and a maldistribution of blood flow. There may also be increased vascular permeability. Both of these mechanisms result in decreased perfusion of vital tissues. The many primary causes of distributive shock are sepsis, endotoxemia, metabolic, toxic, and endocrine diseases.
There can be components of the other forms of shock. Fluid loss into body cavities and interstitial spaces results in a relative hypovolemia. The release of inflammatory mediators as in septic shock can depress the myocardium resulting in a cardiogenic component. Therapy must be directed at the underlying systemic defect. In the case of sepsis, drainage and control of the infected focus is necessary. Because systemic inflammation resulting from sepsis and other inflammatory disease can affect oxygen delivery in so many different places, serial monitoring of many variables becomes necessary to treat the variety of problems an individual may face.
Summary
It is important to constantly monitor and re-assess the shock patient. You need to learn to trust your physical examination, as stressful diagnostics like radiographs can push and animal into decompensatory shock. It is important to ensure that a complete physical examination is performed after the patient is stabilized.
Although various types of shock universally result in the same kind of cellular damage, the recognition of and treatment for the different types of shock varies tremendously. Differentiating hypovolemic vs. cardiogenic vs. distributive shock is key to successful outcomes
