Shock Recognition & Treatment PDF

Shock VETM 5291 At the end of the lecture, you should be able to list and describe 1. Definition of shock 2. Categories for causes of shock 3. Common examples of each category for each species 4. Parts of a triage exam 5. Stages of shock & signs associated with each...

Shock VETM 5291 At the end of the lecture, you should be able to list and describe 1. Definition of shock 2. Categories for causes of shock 3. Common examples of each category for each species 4. Parts of a triage exam 5. Stages of shock & signs associated with each 6. Basic treatments for shock and their mechanism of action 7. End points of shock resuscitation What is shock? Shock is defined as inadequate cellular energy production resulting from insufficient oxygen or nutrient delivery to meet cellular energy requirements. Oxygen delivery is a function of cardiac output (CO) and arterial oxygen content (CaO2): DO2 = CO x CaO2, where CaO2= (1.36 x SpO2 x Hb) + 0.003(PaO2). CO = heart rate x stroke volume (SV) and SV is determined by preload, afterload and cardiac contractility. In shock, energy deprivation leads to cellular dysfunction and ultimately, to cell death. At the tissue and organ level, shock can lead to organ dysfunction or failure. There are many causes of shock. Categories of Shock Causes of shock are divided into several categories including hypovolemic, distributive (including septic), cardiogenic, obstructive and metabolic. Some patients can have more than one type of shock. Hypovolemic shock is low effective circulating blood volume. Low blood volume reduces preload and thus decreases cardiac output. Hypovolemia can be caused by hemorrhage, loss of fluid via vomiting, diarrhea, polyurea, third space pooling of fluids into the chest or abdomen, or evaporative losses, all with inadequate fluid intake to meet those losses. Distributive shock is a state of relative hypovolemia due to vasodilation (also called vasodilatory shock) – that is, the blood volume does not fill the larger (arterial) vascular system. Vasodilation also causes reduced afterload. Distributive shock can occur with anaphylaxis, mast cell tumor degranulation, toxic doses of vasodilatory drugs, neurologic causes (brain injury, spinal injury affecting autonomic system), or hypoadrenocorticism. Septic shock is a specific subcategory of distributive shock. Septic shock begins Shock: Categories, stages, treatment principles – VETM 5291 Page 1 of 7 with an infection which leads to release of inflammatory mediators that subsequently cause vasodilation. Cardiogenic shock is low forward flow of blood due to heart-related problems. It may be caused by poor contractility (eg, dilated cardiomyopathy, late stage valvular disease or hypertrophic/restrictive cardiomyopathy, myocardial depression from sepsis or drug-induced), reduced preload (eg, hypertrophic cardiomyopathy, which causes poor relaxation, or tachycardias), or decreased heart rate (bradycardia) due to primary electrical system malfunction. Cardiac damage from trauma or toxins can also cause cardiogenic shock. Obstructive shock is caused by a physical obstruction impeding blood flow. To cause systemic shock, the obstruction to flow has to affect central circulation – the great arteries/veins or the heart. Pericardial effusion is a cause of obstructive shock because it impairs cardiac filling (cardiac tamponade), especially of the right side. Thromboembolic disease (vascular blood clots), masses impeding blood flow, and kinked or compressed vessels as occurs with GDV or colonic torsion are other examples of obstructive shock. Metabolic shock is caused by inadequate delivery of substrates needed to make energy. This shock is derived from abnormalities with the CaO2 side of the DO2 equation: severe anemia, hypoxemia (low PaO2) and hemoglobinopathies. Increased oxygen demand, as in sepsis or heat stroke (elevated metabolic rate exceeds body’s ability to deliver substrate), and inability to utilize oxygen properly, such as cyanide poisoning (interferes with mitochondrial energy production) and hypoglycemia are other causes of metabolic shock. Clinical Signs of Shock Patients with shock can present in several different ways, depending on how severe or advanced the condition is. Stages of shock include compensatory (or hyperdynamic), early decompensatory, or late decompensatory. Some of the findings are species-dependent. Compensatory shock occurs when compensatory mechanisms are adequate such that the patient can continue to meet metabolic oxygen demands of cells and tissues. Clinical signs of patients with compensatory shock may include an increased respiratory rate, increased heart rate, rapid capillary refill time, normal to dark pink mucous membranes, normal mentation, and normal blood pressure. Shock: Categories, stages, treatment principles – VETM 5291 Page 2 of 7 These clinical signs result when epinephrine and other catecholamines are released in response to a decrease in pressure detected by aortic baroreceptors leaving the heart, thereby increasing the strength of cardiac contraction, increasing heart rate, and increasing blood pressure by increased systemic vascular resistance (via vasoconstriction). Clinical signs in patients with early decompensatory shock include tachycardia (most species) or bradycardia (cats), prolonged capillary refill time, pale mucous membranes, decreased pulse quality, hypotension, decreased body temperature (smaller animals do this earlier), and mental depression. These clinical signs are the result of redistribution of blood flow to the vital organs (heart and brain) with subsequent decreased blood flow to other organs. The reduced oxygen delivery to non-vital organs leads to onset of anaerobic metabolism and lactic acidosis (a build up of lactate in the blood causing a low pH). Clinical signs in patients with late decompensatory shock include bradycardia, low cardiac output and severe hypotension, pallor or cyanosis, markedly prolonged to absent capillary refill time, weak or nonpalpable pulses, decreased cardiac sounds, hypothermia, oliguria to anuria, and stupor or coma. Cardiopulmonary arrest is imminent. These clinical signs are the result of failure of normal compensatory mechanisms due to ongoing lack of oxygen and nutrient delivery. This form of shock is often not responsive to even the most intensive therapy. Septic shock is unique in clinical signs of shock in that it is marked by hyperemic (red) or inappropriately pink (pink in the face of hypotension) mucous membranes and hypotension. Any animal in shock presenting with red mucous membranes should have sepsis as a top differential (except in the cat, which show pallor). Other types of vasodilatory shock should also be considered. Other signs of shock: Additional clinical signs may be seen during or after shock and are related to decreased oxygen delivery to specific tissues. For instance, bloody diarrhea and/or vomiting can result from poor perfusion of the intestinal tract. Acute renal failure can result from decreased renal perfusion, arrhythmias from poor perfusion of the coronary arteries, and leaky alveoli that fill with fluid (acute respiratory distress syndrome) may develop from damage to the lung. All organs and tissues have their own way of manifesting this shock. Shock: Categories, stages, treatment principles – VETM 5291 Page 3 of 7 Treatment for Shock Restoration of oxygen delivery and improving effective circulating volume are the main goals of treating shock. Circulating volume is determined by blood pressure and cardiac output. Blood pressure is determined by cardiac output and systemic vascular resistance (vascular tone) which are related by the equation: BP = CO x SVR. Cardiac output is determined by heart rate and stroke volume: CO = HR x SV. Stroke volume is determined by strength of cardiac contraction and circulating volume of blood. In treating shock, we can manipulate any of these parameters to try to improve effective circulating volume. Oxygen administration is implemented when physically possible. This will increase the PaO2. Oxygen is the mainstay of treatment for metabolic shock caused by hypoxemia. Fluid Therapy For most cases of shock, other than cardiogenic shock, fluid therapy is the first step in treatment. Shock fluid therapy involves quickly administering large quantities of intravenous crystalloid fluids or smaller quantities of hypertonic solutions or colloids. Fluid therapy improves stroke volume (remember the Starling law of the heart) which subsequently improves cardiac output and, therefore, blood pressure. The type and amount of fluids used depends on the underlying problem and the type and severity of shock present. Isotonic crystalloids (water based solutions containing small osmotically active particles that are permeable to cell membranes), hypertonic saline, and colloids (water based solutions containing large molecules that are restricted to the plasma compartment) can be used for fluid resuscitation (see fluid therapy lectures). Treatment of compensatory shock can usually be accomplished with isotonic replacement crystalloids alone. A combination of fluid types are often used for early and late decompensatory shock as well as for disease states complicated by brain or pulmonary disease where excess fluid could be detrimental. Resuscitation for catastrophic hemorrhage involves stopping hemorrhage and replacing intravascular volume and oxygen carrying capacity with a combination of blood products, colloids and crystalloids. Care should be taken to prevent rapid or extreme increases in hydrostatic pressure after hemorrhage, as blood clots may be dislodged and bleeding may begin again. Shock: Categories, stages, treatment principles – VETM 5291 Page 4 of 7 When administering fluids, calculate the shock dose, administer a portion of the full dose and reassess the patient. Not all animals need the entire shock dose. When using crystalloids in conjunction with colloids, the dose of crystalloids is usually initially reduced. See fluids lectures for more information. Sympathomimetics: Inotropes and pressors Patients that remain hypotensive despite intensive fluid therapy and adequate vascular volume may need pharmacologic support. Sympathomimetics ‘mimic’ the sympathetic nervous system, the hormonal system responsible for the “fight or flight” response. Sympathomimetics provide positive inotropic or pressor support and are only administered if the patient has adequate circulating volume. Positive inotropic drugs (β-agonists) increase strength of cardiac contraction; thereby improving cardiac output and, subsequently, blood pressure. Heart rate is also often increased. Examples of drugs used for their positive inotropic effects include dobutamine, mid-dose dopamine, and epinephrine. Vasopressors, including α-agonists (eg, phenylephrine, high-dose dopamine, epinephrine, norepinephrine) or vasopressin (V1 agonist), increase systemic vascular resistance by causing vasoconstriction, which increases blood pressure. Inotropes and pressors may be part of therapy in some cases of cardiogenic shock, especially those cases of myocardial failure (eg: dilated cardiomyopathy). Metabolic shock treatment is aimed at the specific underlying cause. For instance, animals in shock from anemia need red cell transfusions, animals with inability to carry oxygen on hemoglobin because of Tylenol toxicity need antioxidant therapy, hypoglycemic animals need glucose, hypoxemic animals need oxygen, etc. Other treatments for shock Fluids and sympathomimetics are the two main treatments to restore effective circulating volume. Other therapies are needed to combat the secondary effects that reduced oxygen delivery has on tissues. Warming Animals in shock are often hypothermic. This is especially true for cats and small exotics. The feline cholinergic receptors are not as responsive to catecholamines during hypothermia, which may contribute to the development and maintenance of hypotension in the cat. Compared to dogs and other larger animals, smaller aliquots Shock: Categories, stages, treatment principles – VETM 5291 Page 5 of 7 of fluids should be administered more slowly as the cat is actively rewarmed to a temperature of 99-100°F. If the cat is still hypotensive after full rewarming, additional fluids may be administered. Aggressive fluid resuscitation prior to rewarming can lead to volume overload once the cat is normothermic. Antibiotics are sometimes indicated as part of treating shock or its aftermath. Antimicrobials are always indicated in states of septic shock or if the animal has a documented infection. Evidence or suspicion of breach of normal body defenses, such as an animal that is sloughing its gut, is another clear indication for antibiotic therapy to prevent translocation of bacteria across the body surface and into the blood stream, causing a secondary sepsis. Corticosteroids are generally not indicated for shock except in two specific instances. The first is for patients with relative or absolute adrenal insufficiency. Relative adrenal insufficiency has been documented in septic patients. The second potential indication is in anaphylaxis for which steroids are sometimes given in conjunction with epinephrine. Endpoints of shock resuscitation The goal of shock therapy is to titrate fluids and medications to administer the minimum that is needed to reach resuscitation endpoints. Endpoints include restoration of effective circulating fluid volume as evidenced by pink mucous membranes with normal CRT, normal temperature and heart rate, strong pulse quality and normal blood pressure, improved mentation, and adequate urine output. Once endpoints have been achieved, additional fluid therapy should be instituted to maintain intravascular volume and perfusion and to address hydration and ongoing sensible and insensible losses. Type and rate of fluid administered depends on the underlying problem. Shock: Categories, stages, treatment principles – VETM 5291 Page 6 of 7 If endpoints are not achieved with fluid therapy, causes of nonresponsive shock should be investigated and treated. The most common causes of nonresponsive shock include inadequate volume replacement, ongoing losses (such as via hemorrhage or third spacing/extravasation) excessive vasodilation or vasoconstriction, hypoglycemia, electrolyte imbalances, underlying cardiac dysfunction or arrhythmias, ischemia/hypoxia, hypoadrenocorticism, hypothyroidism, or hypothermia. Monitoring Animals that are treated for shock and stabilized must be monitored to be sure they do not start to become critical again. Animals may respond initially to fluid boluses but then slip back into a state of shock as fluid leaks from vessels or is lost as hemorrhage or GI, urinary or third space losses. Intensive monitoring and treatment of other organ dysfunction is also important. Patients suffering from shock are at risk for a systemic inflammatory response syndrome (SIRS) which can progress to multiple organ dysfunction syndrome (MODS) and ultimately multiorgan failure syndrome (MOFS). Monitoring can help identify subtle changes in the patient that can be treated early. Monitoring vital parameters, (temperature, pulse respiratory rate and effort), pulse quality, mucous membranes and CRT, mentation), blood pressure, central venous pressure, and urine output give indications of adequacy of perfusion. Measurement of lactate can provide information on adequacy of oxygen delivery and utilization. Monitoring of glucose, oxygenation parameters, ECG, respiratory or gastrointestinal signs, clotting parameters, and neurologic status gives indication of other organ function. Shock: Categories, stages, treatment principles – VETM 5291 Page 7 of 7  1/2/25 Horses with sepsis develop a “toxic line” from endotoxin 54 Treatment for Shock n Increase oxygen delivery – Most commonly ______________________________ n Improve oxygen utilization – If applicable n Reduce excess oxygen consumption – Only if applicable 62 n 1  1/2/25 Treatment for Shock increase oxygen delivery DO2 = CaO2 x CO CO = HR x SV CO x SVR = BP CaO2 = (1.36 x SpO2 x Hb) + 0.003(PaO2) 63 Treatment for Shock increase oxygen delivery Inotropes/ DO2 = CaO2 x CO chronotropes: Pressors: β-agonists α-agonists CO = HR x SV Fluids CO x SVR = BP CaO2 = (1.36 x SpO2 x Hb) + 0.003 (PaO2) Oxygen 64 2  1/2/25 Treatment for Shock increase oxygen delivery n Oxygen n Improve effective circulating volume n Treat the underlying cause 65 Treatment for Shock increase oxygen delivery DO2 = CaO2 x CO CO = HR x SV CO x SVR = BP CaO2 = (1.36 x SpO2 x Hb) + 0.003 (PaO2) Oxygen 66 3  1/2/25 Treatment for Shock: Oxygen n Oxygen – When indicated – When practical 67 Treatment for Shock increase oxygen delivery DO2 = CaO2 x CO CO = HR x SV Fluids CO x SVR = BP CaO2 = (1.36 x SpO2 x Hb) + 0.003 (PaO2) Oxygen 68 4  1/2/25 Treatment for Shock: Increase CO n Increase blood volume § Bolus fluids § Give a portion of shock dose § REASSESS!! 69 Treatment for Shock increase oxygen delivery Inotropes/ DO2 = CaO2 x CO chronotropes: Pressors: β-agonists α-agonists CO = HR x SV Fluids CO x SVR = BP CaO2 = (1.36 x SpO2 x Hb) + 0.003 (PaO2) Oxygen 70 5  1/2/25 If Fluids Fail: Pharmacologic management of BP n Only after vascular volume normalized n Inotropes: increase cardiac contractility – β-agonists § Dobutamine, mid-dose Dopamine – Also increase heart rate n Pressors: cause vasoconstriction – α-agonists § NE, epi, high dose Dopamine, phenylephrine – Vasopressin (V1) agonist 71 Treatment for Shock increase oxygen delivery Inotropes/ DO2 = CaO2 x CO chronotropes: Pressors: β-agonists α-agonists CO = HR x SV Fluids CO x SVR = BP CaO2 = (1.36 x SpO2 x Hb) + 0.003 (PaO2) Oxygen 72 6  1/2/25 Address O2 carrying capacity PRN n Increase hemoglobin concentration – Red blood cell transfusion n Decrease metHB or carboxyHB conc 73 Treatment for Shock increase oxygen delivery Inotropes/ DO2 = CaO2 x CO chronotropes: Pressors: β-agonists α-agonists CO = HR x SV Fluids CO x SVR = BP CaO2 = (1.36 x SpO2 x Hb) + 0.003 (PaO2) Oxygen 74 7  1/2/25 Treating altered O2 utilization n Treating decreased capacity to use O2 § Hypoglycemia -> give Dextrose § Sepsis – antimicrobials and supportive care § Cyanide poisoning -> oxygen and antidote n Treating increased O2 demand § Heat stroke -> decrease body temperature § Sepsis -> treat underlying cause 75 Other treatments for shock n Rewarming – Especially cats, exotics n Antibiotics – Sepsis, infection – Breached defenses n Steroids – usually not indicated – Anaphylaxis – Adrenal insufficiency n Treat underlying cause… 76 8  1/2/25 Endpoints of Shock Resuscitation n Minimum treatment necessary to restore effective circulating volume – Pink mucous membranes, normal CRT – Normal heart rate, pulse quality and BP – Normal body temperature – Improved mentation – Adequate urine production 77 Monitoring n Even after stable n Signs of adequate perfusion n Signs of cell/organ dysfunction – may not appear for several days 78 9