Taking the shock factor out of shock Julie Antonellis, BS, LVT, VTS (ECC) Northern Virginia Regional Director for the VALVT Technician Supervisor VCA Animal Emergency Critical Care Business owner Antonellis Veterinary Consulting julieantonellis@gmail.com www.javetconsulting.com Objective: Shock is a widely used, but not always fully understood, term in veterinary medicine. Having a true understanding of what shock means and how our patients are affected by it can help us to better serve them. Without this knowledge we may miss very important and potentially subtle signs in our patients that should prompt us to either monitor more closely or treat earlier. In this lecture participants will be shocked about how much they will learn about this condition and the importance of early recognition and treatment. They will gain an understanding of the different types of shock that may affect their patients. They will learn how to recognize shock in their patients even when the signs may be subtle. Lecture participants will be advised on how to differentiate between the different stages of shock and when to become more vigilant in monitoring for changes in their patients. They will also gain an understanding of treatment options and monitoring in their patients and how those options may differ depending on the type and stage of shock the patient is in. The presentation will conclude with participants applying the information they learned to real life case reports that are presented. Definition of shock A condition in which vital organs and tissues in the body are not adequately perfused leading to widespread cellular hypoxia, cellular death and organ dysfunction. Without treatment it may ultimately lead to death. Components of the cardiovascular system Heart Intravascular volume Vascular tree *For effective tissue perfusion to take place the all of the components of the cardiovascular system must be functioning normally. Any dysfunction in any component of this system can result in poor tissue perfusion and/or shock. How does the body respond to shock? Altered tissue perfusion from dysfunction is picked up by sensors throughout the body A compensatory response is initiated Stretch receptors in the aorta and carotid arteries detect decreased cardiac output
Epinephrine and norepinephrine are released Sympathetic nervous system activity is increased Heart rate, cardiac contractility increase Vasoconstriction occurs Perfusion to tissues depend on their importance The brain and heart are able to autoregulate to maintain effective perfusion and oxygen delivery Other tissues are less effective at autoregulating and suffer severe consequences due to decreased perfusion as shock progresses Types of shock Hypovolemic decreased circulating blood volume most common type seen in veterinary medicine hemorrhage severe dehydration capillary leak hypoproteinemia Cardiogenic decreased cardiac output in the face of normal or increased vascular volume problem with the pump congestive heart failure myocardial abnormalities (dilated cardiomyopathy, hypertrophic cardiomyopathy) cardiac arrhythmias Obstructive blood flow is prevented from either leaving or returning to the heart pericardial effusion resulting in tamponade caval syndrome from heartworm disease GDV (caudal vena cava is obstructed due to dilation of the stomach) Distributive microcirculation is not functioning properly widespread and inappropriate vasodilation occurs resulting from inflammatory mediators that cause the production of nitric oxide (a potent vasodilator) systemic inflammatory response syndrome (SIRS) sepsis anaphylaxis How to recognize shock/clinical presentation Hypovolemic shock
pale mucous membranes prolonged CRT tachycardia poor pulse quality Cardiogenic shock tachypnea dyspnea abnormal lungs sounds cyanosis Obstructive clinical signs differ depending on cause pericardial tamponade lethargy/collapse tachycardia pulsus paradoxus muffled heart sounds caval syndrome dyspnea pale mucous membranes jugular distension weak femoral pulses GDV attempting to vomit tachycardia weak femoral pulses pale or muddy mucous membranes Distributive injected mucous membranes rapid CRT tachycardia hyperdynamic pulses Stages of shock and how to determine which one Compensatory the initial response of the body to whatever insult it is enduring see increases in systemic vascular resistance, heart rate and contractility to produce and increase in cardiac output patient is in a hypermetabolic state requiring large amounts of energy to maintain this state this stage cannot be maintained indefinitely easy to overlook clinical signs clinical signs: mild increase in heart rate
increased respiratory rate injected mucous membranes (may not see in cats) shorter than normal CRT normal to bounding femoral pulses Early decompensatory blood is redistributed to vital organs (heart, brain) anaerobic metabolism occurs in non perfused tissues lactic acidosis and tissue hypoxia occur bacterial translocation can occur through compromised mucosa of the intestines myocardial contractility decreases cardiac arrhythmias may occur renal blood flow is reduced and can result in oliguria and tubular necrosis clinical signs: tachycardia normal to decreased femoral pulses hypotension pale mucous membranes prolonged CRT decreased mentation decreased body temperature Decompensatory massive vasodilation occurs in all organs including the heart and the brain sympathetic center of the brain does not function circulatory collapse occurs death is imminent clinical signs: decreased heart rate in the face of low cardiac output severe hypotension pale or cyanotic mucous membranes weak or absent femoral pulses low body temperature anuria stupor or coma Treatment and monitoring Early recognition and treatment will greatly improve outcome in our patients. Oxygen therapy for all types of shock is beneficial patient may be hypoxemic (cardiogenic shock) poor perfusion leads to tissue hypoxia because of failure in the oxygen-hemoglobin transport system (can t get the oxygen where it needs to be) Intravenous access should be obtained avoid hind limbs due to diminished perfusion
cutdown may be necessary to visualize the vein consider jugular vein if cannot place in cephalic intraosseous is a good alternative in pediatric patients and neonates ideally use the shortest, largest bore catheter available if it is necessary to bolus large volumes of fluids quickly Crystalloids dosed as needed for the individual needs of the patient not indicated for cardiogenic shock used to increase intravascular volume temporarily and treat dehydration about 80% of crystalloids administered move to the interstitial space within the first hour they are given titrate to effect monitor heart rate, mucous membrane color, capillary refill time and blood pressure after each bolus Colloids may be considered if hypovolemic due to blood loss consider blood product replacement synthetic colloids should be used with caution but may be necessary titrate to effect monitor heart rate, mucous membrane color, capillary refill time and blood pressure after each bolus Hypertonic saline (7% NaCl) used to dramatically increase intravascular volume quickly pulls fluid into the intravascular space from the tissues due to the sudden increase in the osmotic gradient use in adequately hydrated animals effects last as long as that of crystalloids usually given with a synthetic colloid to help prolong effects administer slowly (over 5 minutes) if given too quickly can cause bradycardia, hypotension and bronchoconstriction closely monitor heart rate, blood pressure and respiratory effort after administration Drugs used to treat shock diuretics and vasodilators may be indicated in those animals suffering from cardiogenic shock dobutamine is a beta-agonist that improves cardiac contractility may be indicated for cardiogenic shock may be indicated for shock in which blood pressure and tissue perfusion are not improving despite adequate treatment with fluid and colloid boluses Side effects ventricular arrhythmias dopamine is an endogenous catecholamine that is a precursor to norepinephrine may be indicated for shock in which blood pressure and tissue perfusion are not improving despite adequate treatment with fluid and colloid boluses increases cardiac contractility, organ perfusion, renal blood flow and urine production
Side effects ventricular arrhythmias analgesics pain can be very detrimental to patients in shock can cause tachycardia, vasoconstriction and arrhythmias
References Patchtinger GE. The Many Types of Shock. Clinician s Brief Web site. 2013. Available at http://www.cliniciansbrief.com//article/many-types-shock#close. Accessed October 3, 2014. Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice 3rd ed. DiBartola SP, Shock Syndromes, St. Louis, Missouri, 2006 (540-562) Veterinary Emergency Critical Care Manual 2nd ed. Mathews KA, Shock, Ontario, Canada, 2006 (603-605)